Feline Dermatology

Document Sample
Feline Dermatology Powered By Docstoc
					ESAVS YEAR 3 : 2005
Week 2
14th to 18th August

Pustules & infections;
Feline dermatology;
Dermatology of fish,
birds, reptiles & amphibia;
Equine dermatology;
Farm animal dermatology;
Pustule & tumour cytology.

David Lloyd
David Grant
Janet Littlewood
Murray Corke
Martin Lawton
Otto Fischer
Ilse Schwendenwein

                   WEEK 2: 14th - 18th August

Dear Friends,
We look forward to welcoming you to the final part of the ESAVS
Dermatology Course in Vienna.
This part of the programme deals with some unusual areas of
dermatology, and looks back on knowledge established earlier in the
course with an emphasis on differential diagnosis. Problem-based
learning is an important feature, which is integrated into all parts of the
The course timetable also allows time for review of distance learning
tasks and feed-back amongst participants.
The programme will be taught by David Lloyd and David Grant,
together with Janet Littlewood and Murray Corke, who will participate
in the large animal components, and Martin Lawton, who will cover
skin diseases of non-mammalian vertebrates. Practical classes on
cytology of pustular diseases and tumours will be taught by Otto
Fischer and Ilse Schwendenwein. This part of the programme has
been structured to allow for the fact that part of the class has already
studied tumour cytology
Textbooks recommended in the earlier parts of the course will be
relevant for much of this week also. Further advice on sources of
information in these areas and examples of textbooks on non-
mammalian dermatology will be provided during the course.

Textbooks, which are especially relevant to this week, are as follows.
   1. Guaguere, E & Prelaud, P. (eds.) A Practical Guide to Feline
      Derrmatology. Merial, 2000.
   2. Fournel-Fleury, C., Magnol, J-P. & Guelfi, J-F. Cytologie du
      Cancer Chez le Chien et le Chat (Color Atlas of Cancer
      Cytology of the Dog and Cat). Paris: PMCAC, 1994.
   3. Lloyd, D. H., Littlewood, J. D., Craig, A. M. & Thomsett, L. R.
      Practical Equine Dermatology. Oxford: Blackwell Science.
   4. Pascoe, R. R. R. & Knottenbelt, D. C. Manual of Equine
      Dermatology. London: W. B. Saunders, 1999.

See you soon!
                                         David Lloyd and David Grant.

             Year 3 of ESAVS Dermatology Course, WEEK 2, 2005
DATE                 TIME       TOPIC
Sun 14 Aug        08.30-10.00   Pustular diseases. D.L.
                  10.00-10.30   Refreshments
                  10.30-12.30   Antibiotic therapy. D.L.
                  12.30-13.30   Lunch
                  13.30-15.00   Pododermatitis. D.G.
                  15.00-15.30   Refreshments
                  15.30-17.30   Feline dermatology. D.G.
Mon 15 Aug        08.30-10.00   Cytology of pustular diseases and tumours. Part 1. I.S. & O.F.
                  10.00-10.30   Refreshments
                  10.30-12.30   Cytology of pustular diseases and tumours. Part 2. I.S. & O.F.
                  12.30-13.30   Lunch
                  13.30-14.00   Cytology of pustular diseases and tumours. Part 3. I.S. & O.F.
                  14.00-15.30   Cytology case challenges
                  15.30-16.00   Refreshments
                  16.00-17.30   Case presentations
Tues 16 Aug       08.30-9.00    Approach to equine dermatology. J.L.
                  9.00-10.30    Pruritic diseases. D.L.
                  10.30-11.00   Refreshments
                  11.00-12.00   Crusting dermatoses. J.L.
                  12.00-12.30   Pigmentary diseases. J.L.
                  12.30-13.30   Lunch
                  13.30-15.00   Equine ulcers & erosions. J.L.
                  15.00-15.30   Refreshments
                  15.30-16.30   Nodular diseases. D.L.
                  16.30-17.30   The equine foot. J.L.
Wed 17 Aug        08.30-9.00    Equine coat problems. D.L.
                  9.00-10.00    Farm animal pruritic & crusting diseases. Part 1. D.L.
                  10.00-10.30   Refreshments
                  10.30-11.00   Pruritic & crusting diseases. Part 2. D.L.
                  11.00-12.30   Nodules, ulcers & pigmentary problems. M.C.
                  12.30-13.30   Lunch
                  13.30-14.30   The teat & udder. M.C.
                  14.30-15.00   Alopecia. D.L.
                  15.00-15.30   Refreshments
                  15.30-16.15   The foot. D.L.
                  16.15-17.00   Case presentations
Thurs 18 Aug       08.30-9.00   Avian anatomy & physiology. M.L.
                  9.00-10.00    Avian parasitic & viral diseases
                  10.00-10.30   Refreshments
                  10.30-12.00   Avian bacterial and fungal diseases; feather loss. M.L.
                  12.00-12.30   Case challenge
                  12.30-13.30   Lunch
                  13.30-14.30   Reptilian anatomy & physiology; dysecdysis; shell trauma. M.L.
                  14.30-15.00   Reptilian bacterial diseases. M.L.
                  15.00-15.30   Refreshments
                  15.30-16.00   Reptilian viral & parasitic diseases. M.L.
                  16.00-16.30   Dermatology of fishes. M.L.
                  16.30-17.00   Case challenge

          Note: timing and sequence of individual components may be adjusted

Pustular Diseases __________________________________________________________________6
  Histological approach to pustular diseases ___________________________________________6
  Differential diagnosis of pustular diseases in dogs. ____________________________________6
  Subcorneal pustular dermatosis____________________________________________________7
  Canine linear IgA pustular dermatosis ______________________________________________7
  Sterile eosinophilic pustulosis ______________________________________________________7
  Reference ______________________________________________________________________7
Antibacterial and Immunostimulant Therapy ____________________________________________8
  Introduction ____________________________________________________________________8
  Discussion of Principles of Effective Antibiotic Therapy ________________________________8
  Antimicrobial Therapy/Management of Deep Infections ______________________________10
  Sampling Suspected Anaerobic Infection Sites _______________________________________10
  Therapy in Anaerobic Infections __________________________________________________11
  Immunostimulant Therapy_______________________________________________________12
  References and Further Reading __________________________________________________12
Pododermatitis ___________________________________________________________________14
  Approach and Assessment. _______________________________________________________15
  Perplexing cases of pododermatitis ________________________________________________16
Feline Dermatology _______________________________________________________________17
  Syndromes associated with systemic disease _________________________________________17
  Paraneoplastic syndromes in cats__________________________________________________17
  Superficial necrolytic dermatitis __________________________________________________17
  Feline paraneoplastic alopecia ____________________________________________________18
  Exfoliative dermatitis associated with thymoma _____________________________________19
  Degenerative Mucinous Lymphocytic Mural Folliculitis _______________________________19
  Acquired Cutaneous Fragility Syndrome ___________________________________________20
  Skin Infections _________________________________________________________________20
  Miscellaneous __________________________________________________________________25
  Idiopathic facial dermatitis in Persian cats. _________________________________________26
  Further Reading _______________________________________________________________27
Avian Dermatology ________________________________________________________________28
  Introduction ___________________________________________________________________28
  Avian Anatomy ________________________________________________________________28
  Avian Physiology _______________________________________________________________29
  Avian Parasitic Disease __________________________________________________________30
  Avian Viral Disease _____________________________________________________________31
  Avian Bacterial Disease__________________________________________________________34
  Avian Fungal Disease ___________________________________________________________35

  Feather Loss___________________________________________________________________36
  Establishing A Diagnosis_________________________________________________________36
  Behavioural Problems ___________________________________________________________36
  Feather Loss Without Plucking ___________________________________________________38
  Endocrine / Hypothyroidism. _____________________________________________________38
Reptilian Dermatology _____________________________________________________________39
  Introduction ___________________________________________________________________39
  Anatomy ______________________________________________________________________39
  Reptilian Physiology ____________________________________________________________41
  Shell Trauma __________________________________________________________________42
  Bacterial Diseases ______________________________________________________________43
  Viral Disease __________________________________________________________________44
  Parasitic Disease _______________________________________________________________45
  Fungal Infections _______________________________________________________________46
Fish Dermatology ________________________________________________________________46
  Integument Of Fish _____________________________________________________________46
  Bacterial Infections _____________________________________________________________47
  Viral Infections ________________________________________________________________47
  Parasitic Disease _______________________________________________________________48
  Fungal Infections _______________________________________________________________48
Equine Dermatology_______________________________________________________________49
  The Clinical Approach __________________________________________________________49
  Pruritic Diseases _______________________________________________________________51
  Crusting and Scaling Dermatoses _________________________________________________59
  Nodules and Swellings___________________________________________________________64
  Coat Problems _________________________________________________________________83
  Equine Ulcers and Erosions ______________________________________________________87
  Equine Pigmentary Diseases______________________________________________________93
  The Equine Foot _______________________________________________________________95
Farm Animal Dermatology ________________________________________________________101
  Clinical Approach _____________________________________________________________101
  Crusting & Scaling Diseases _____________________________________________________102
  Pruritic Skin Diseases __________________________________________________________118
  Nodules, ulcers and pigmentary disorders _________________________________________131
  The Foot _____________________________________________________________________141
  The Teat and Udder ___________________________________________________________145

Pustular Diseases
On clinical examination, a pustule is a small, circumscribed fluid-filled elevation of the epidermis
which contains pus. Pustules may be centred on hair follicles (so that a hair protrudes from the centre
of the lesion) or may affect the interfollicular epidermis. These lesions are often transient (due to the
thin epidermis of dogs and cats) and the predominant lesions in pustular diseases may be crusts,
epidermal collarettes or erosions.
Histologically, a pustule is an intraepidermal or subepidermal accumulation of inflammatory cells and
fluid. By contrast, a vesicle is a fluid-filled space within or beneath the epidermis, less than 1 cm in
diameter. Vesicles containing substantial numbers of leucocytes are known as vesicopustules. Some
diseases, which may be primarily “vesicular” in aetiology, may become vesiculopustular as
inflammatory cells are recruited to the site of inflammation. This review will focus primarily on
pustular diseases, and will include only vesiculopustular diseases where they are relevant in differential
In dogs, pyoderma is by far the most common cause of pustular lesions. However, pustules are the
primary lesions of some sterile inflammatory diseases such as drug eruptions, pemphigus foliaceus,
subcorneal pustular dermatosis and sterile eosinophilic pustulosis. Pyoderma is rare in cats and
pemphigus foliaceus is arguably the most common pustular disease in this species.

Histological approach to pustular diseases
This is based on the approach described by Yager and Wilcock (1994).
What level of the epidermis do the pustules / vesicopustules occupy?
Lesions are most commonly subcorneal in location. This location is typical of superficial pyoderma,
pemphigus foliaceus / erythematosus, and rare sterile neutrophilic (subcorneal pustular dermatosis) and
eosinophilic diseases (sterile eosinophilic pustulosis). Suprabasilar acantholysis is a cell-poor process
(vesicular) seen in pemphigus vulgaris. Subepidermal vesicopustules may be seen in cases of bullous
pemphigoid (although the lesions clinically is a vesicle).
What is the predominant cell type in the pustules / vesicopustule?
Neutrophilic pustules are most common and are seen in exudative diseases, especially microbial
infections and pemphigus foliaceus. The presence of acantholysis is suggestive of pemphigus foliaceus
/ erythematosus.
Eosinophilic pustules are seen in parasitic, allergic and immune-mediated / idiopathic diseases.
Eosinophilic micropustules may be seen at the site of insect bites. Sterile eosinophilic pustulosis
characterised by subcorneal and intracorneal pustules.
Mononuclear cell-rich pustules are rare and are most commonly seen in epitheliotropic lymphoma.
Clinically, pustular lesions are seldom seen in this disease.

Differential diagnosis of pustular diseases in dogs.

Disease                    Incidence      Cytology                    Biopsy
Pyoderma                   Common         Neutrophils (sick) and      Neutrophilic pusules / folliculitis
Pemphigus foliaceus        Rare           Neutrophils, free           Subcorneal pustules and
                                          epithelial cells            acantholysis
Drug eruption              Rare           Variable                    Variable
Subcorneal pustular        Very rare      Neutrophils but no          Subcorneal pustules with
dermatosis                                bacteria                    neutrophils
Canine linear IgA          Very rare      Neutrophils but no          Subcorneal pustules with
pustular dermatosis                       bacteria                    neutrophils

Sterile eosinophilic        Very rare      Eosinophils                  Subcorneal pustules with
pustulosis                                                              eosinophils

Clinical approach in dogs
•   Cytological examination of pustule contents (open with a needle and smear on a slide)
•   If cytology consistent with pyoderma, treat with antibiotics and re-examine after 10-20 days. Also
    take skin scrapings to exclude Demodex spp. as a cause of pyoderma.
If no response to antibiotics or cytology not consistent with pyoderma
•   culture for bacteria (antibiotic resistance if treatment failure)
•   obtain skin biopsies (necessary for diagnosis of all sterile pustular diseases). Ideally sample intact
    pustules. Include crust in the sample pot and do not prepare biopsy site prior to sampling.

Approach in cats
Because pustules are so unusual in this species, biopsy all cases but treat with antibiotics pending
biopsy results.

Subcorneal pustular dermatosis
This is a very rare, idiopathic neutrophilic subcornal pustular disease of dogs. It is most often reported
in Miniature Schnauzers. The pustular lesions are transient and therefore alopecia, erosions, scales,
collarettes and crusts may predominate. Dogs are otherwise healthy.
Diagnosis is based on exclusion of other diseases by laboratory tests and response to trial therapy.
Classically this disorder does not respond to antibiotics or steroids. Dapsone, an anti-inflammatory
drug which prevents neutrophil recruitment has been recommended as the drug of choice. The author
has only encountered one dog with a clinical presentation suggestive of subcorneal pustular dermatosis
but that responded to prednisolone!

Canine linear IgA pustular dermatosis
This is a very rare, idiopathic neutrophilic subcorneal pustular disease of Dachshunds. It is associated
with IgA deposition in the basement membrane (unlike subcorneal pustular dermatosis). This entity
should not be confused with linear IgA bullous dermatosis, which is associated with autoantibodies to
the bullous pemphigoid antigen.
Diagnosis is based on exclusion of other diseases by laboratory tests. Treatment comprises steroids or

Sterile eosinophilic pustulosis
This is a very rare, idiopathic eosinophilic pustular disease of dogs, characterised histologically by
intraepidermal eosinophilic pustules and eosinophilic folliculitis. The pustular lesions are transient
and therefore alopecia, erosions, scales, collarettes and crusts may predominate.
The diagnostic approach is as described for the other related diseases. Prednisolone is effective but
maintenance treatment may be required. The author has seen one dog with eosinophilic furunculosis of
the face which had widespread eosinophilic pustular lesions resembling sterile eosinophilic pustulosis.

Yager, J. and Wilcock, B. (1994) Colour atlas and text of surgical pathology of the dog and cat.
Volume 1. Dermatopathology and skin tumours. Mosby.

Antibacterial and Immunostimulant Therapy

Large amounts of antimicrobial drugs and other agents are used in veterinary dermatology, both
systemically and topically. During the initial week of the course we considered the commonly used
substances and their modes of application. At this point we wish to discuss three aspects of systemic
antimicrobial therapy in more detail:
         1. More efficient use of antibiotics
         2. Use of antibiotics against common but difficult organisms
         3. Therapy of deep microbial infections
These notes are designed to provide material for discussion of the principles of efficient antibiotic use
and the therapy of deep infections including those caused by anaerobes.

 Spectrum of Activity of Antimicrobial Drugs
 1. Narrow spectrum agents active against aerobes and facultative anaerobes

  Bacteria              Antimicrobial agents             Comments
  Mainly G+ve           lincosamides                     also very active against many obligate anaerobes
                        glycopeptides: vancomycin
  G+ve & fastidious     benzylpenicillin,                poor activity against beta-lactamase producing
  G-ves                 phenoxymethly-penicillin         staphylococci
                        cloxacillin, flucloxacillin      active against beta-lactamase producing
                        macrolides                       also active against Chlamidia & mycoplasmas
                        rifampicin                       also active against pox viruses, Chlamidia, some
                                                         protozoa and fungi (but antiviral & antifungal
                                                         activity not used clinically)
  Mainly G-ve           aminoglycosides:                 neomycin active against Pseudomonas
                        kanamycin, neomycin,             aeruginosa; aminoglycosides should usually be
                        streptomycin                     reserved for treatment of infections caused by
                                                         particularly resistant G-ve organisms
                        nalidixic acid
                        polymixins                     active against Pseudomonas aeruginosa; should
                                                       usually be reserved for treatment of infections
                                                       caused by particularly resistant G-ve organisms
            After Bishop, Y. (2001) Information for guidance only. Actual sensitivity may differ

Discussion of Principles of Effective Antibiotic Therapy
1. Selective and effective action against the probable (or confirmed) pathogen(s)
         • narrow spectrum
         • bactericidal action
         • correct target organism?
2. Minimal disturbance of the normal flora

3. No toxicity, side-effects; not likely to cause drug side effects or adverse reactions e.g.
         • vomiting with erythromycin, high doses of Synulox (?)
         • enrofloxacin, not to skeletally immature dogs, dogs with orthopaedic problems
         • trimethoprim sulphonamides - immune-mediated reactions
4. Consider problems of resistance induction
         • this animal; others in contact
5. Ensure good penetration into affected area; no inhibition by body fluids, exudate, necrotic tissue
6. Levels of antibiotic in tissue adequate and maintained for long enough
         • time or concentration dependent mechanisms of action
7. Drug is stable and can be conveniently administered
         • problem of generic or poorly formulated drugs
8. Economic and licensed for veterinary use
9. Remember that some underlying factor is likely to be involved and must be identified
10. Host systems must be encouraged to play their part; do not impair this with other therapy
11. Adjunctive and supportive therapy
12. Monitor response
13. If not effective question diagnosis, bacteriology, test result, dose and mode of administration,
    compliance - Consider reisolation and testing, more detailed work-up, concurrent disease

Spectrum of Activity of Antimicrobial Drugs
2. Broad spectrum agents active against aerobes and facultative anaerobes

 Bacteria              Antimicrobial agents             Comments
 Many G+ves &          aminoglycosides: amikacin,       sometimes active against Pseudomonas
 G-ves                 gentamicin, tobramycin           aeruginosa; should usually be reserved for
                                                        treatment of infections caused by particularly
                                                        resistance G-ve organisms
                       aminopenicillins                 poor activity against beta-lactamase producing
                       carboxypenicillins:              active against Pseudomonas aeruginosa; should
                       ticarcillin                      be reserved for treatment of infections caused by
                                                        particularly resistant G-ve organisms
                       cephalosporins                   3rd generation cephalosporins active against
                                                        Pseudomonas aeruginosa; should usually be
                                                        reserved for treatment of infections caused by
                                                        particularly resistant G-ve organisms
                       baquiloprim, trimethoprim,
 Many G+ves &          chloramphenicol                  also active against rickettsiae & Chlamidia
 G-ves, also some
                       fluoroquinolones                 also active against rickettsiae
 rickettsiae,          nitrofurans                      also active against protozoa
                       sulphonamides                    also active against protozoa & Chlamidia
                       tetracyclines                 also active against protozoa, rickettsiae &
          After Bishop, Y. (2001) Information for guidance only. Actual sensitivity may differ

14. Long-term or intermittent/pulsed therapy
          • consider carefully before consigning the animal to long-term therapy
          • is immunostimulation an alternative?

    Spectrum of Activity of Antimicrobial Drugs
    3. Antimicrobials for special organisms

     Bacteria             Antimicrobial agents            Comments
     Obligate             cephalosporins                  Bacteroides fragilis is resistant to all except
     anaerobes                                            cefoxitin
                          penicillins                     Bacteroides fragilis is resistant to all except
     Mycobacteria         rifampicin, streptomycin,
     Mycoplasma           fluoroquinolones                active against Pseudomonas aeruginosa; should
                                                          usually be reserved for treatment of infections
                                                          caused by particularly resistant G-ve organisms
                          lincosamides, macrolides,
                          nitrofurans, tetracyclines
              After Bishop, Y. (2001) Information for guidance only. Actual sensitivity may differ

Antimicrobial Therapy/Management of Deep Infections
•     Clinical and microbiological aspects of the deep microbial infections of the skin of dogs and cats
      are considered elsewhere.
•     It should be noted that many of the pathogens involved in the deep infections offer significant
      zoonotic risks.
•     Precautions should be taken and the advisability of therapy discussed with owners if dangerous
      infections are suspected or confirmed.
•     Sometimes the organisms involved will be difficult to grow, requiring special sampling, transport
      and cultural techniques.
•     Initial cytology will often allow the possible causes to be narrowed so that you can adopt a suitable
      sampling method and warn the laboratory of what to expect.
•     Failure by the laboratory to use appropriate methods may result in their reporting to you
      misleading information e.g. Staph. intermedius is present and reported but Actinomyces viscosus
      was missed.
•     In many deep infections surgical therapy will be a very important component and may be more
      significant than the use of antibiotics. This is particularly true of some of the deep granulomatous
      diseases and some anaerobic infections.

Sampling Suspected Anaerobic Infection Sites
          1. Obtain samples aseptically from deep within the lesion

                  • use a cuffed swab or catheter etc. if necessary
                  • aspirate pus from deep within the lesion
                  • obtain tissue by surgery
                  • bone biopsies, sequestra
         2. Prevent contamination by more superficial exudate
         3. Avoid fistulous tracts, if possible
         4. Transfer material to anaerobic medium or anaerobic transport device without delay
         5. Small specimens are most at risk
         6. Store at room temperature, if necessary

Therapy in Anaerobic Infections
1. It is vital to change the local microenvironment to as aerobic conditions as possible to inhibit the
   anaerobes and promote tissue health. Vigorous wound hygiene including effective drainage and
   debridement is essential and may need to be repeated on several occasions
2. High dose, long-term therapy is required except with simple, superficial abscesses.
3. Penicillins are often effective but where mixed infections with Gram -ve enteric organisms are
   involved, concurrent aminoglycoside therapy may be required.
4. Antibiotics effective against common anaerobes include: penicillins, chloramphenicol, clindamycin,
   metronidazole, cefoxitin.

Antimicrobial Agents and Doses for Cats
 Antimicrobial                           Route                   Dosage
 Penicillin G                            intramuscular           100 000 U/kg once or twice daily
 Clavulanate-potentiated amoxycillin     oral, subcutaneous      12.5-25 mg/kg twice daily
 Oxacillin                               oral                    11-35 mg/kg twice daily
 Cephalexin                              oral                    20 mg/kg twice daily
 Cefadroxil                              oral                    20 mg/kg twice daily
 Enrofloxacin                            oral, subcutaneous      5-20 mg/kg daily
 Marbofloxacin                           oral                    2-5 mg/kg daily
 Clindamycin                             oral                    5.5 mg/kg twice daily
 Lincomycin                              oral                    20 mg/kg twice daily
 Trimethoprim-sulphadiazine              oral                    15-20 mg/kg once or twice daily
 Trimethoprim-sulphamethoxazole          oral                    15-30 mg/kg once or twice daily
 Doxycyline                              oral                    5-11 mg/kg once or twice daily
 Minocycline                             oral                    5-11 mg/kg once or twice daily
 Tetracycline                            oral                    10-30 mg/kg twice daily
 Gentamicin                              intravenous             4 mg/kg daily
 Rifampicin                              oral                    10-20 mg/kg twice daily
 Clofazimine                             oral                    2-8 mg/kg daily
 Dapsone                                 oral                    1 mg/kg daily
                                          After Mueller, 2000.

Immunostimulant Therapy
A variety of agents have been used with the aim of stimulating immunity in animals but few have been
tested in properly controlled trials.
Agents used have included:
• Drugs
     ∗ Levamisole
         Believed to stimulate T-cell activity and phagocytic function. Anecdotal reports suggest a
         dose of 2.2 mg/kg every 48 hours with both higher and lower doses being
     ∗ Cimetidine
         Supposed to reverse T-suppressor-mediated immune suppression in chronic bacterial
         infection. Dose is 3-4 mg/kg/12 hours. Expensive
     ∗ Ketoconazole, hydroxyzine - efficacy unknown
• Vaccines
     ∗ Bacille Calmette-Guérin
     ∗ Propionibacterium acnes vaccine (Immunoregulin; Immunovet, Tampa, U.S.)
     ∗ Staphylococcal phage lysate (SPL; Delmont laboratories, Swarthmore, U.S.) containing lysed
       cultures of serotype 1 and 2 S. aureus lysed by a staphylococcal bacteriophage
     ∗ Autogenous staphylococcal vaccines
• Cytokines
     ∗ e.g. interleukins, interferons
         Efficacy unknown. Could be very useful but expensive.

Of these, only SPL and autogenous vaccines have been tested in controlled dermatological trials
•   For SPL, 40% efficacy demonstrated. This product is widely used in pyoderma in the U.S. SPL
    has also been used in canine IgA deficiency.
•   Autogenous vaccines have also proved useful and, if made from homologous S. intermedius have a
    theoretical advantage. There are major differences depending on how the vaccines are prepared.
    Controlled studies in the UK have shown efficacy in >50% of cases in superficial pyoderma.

IgA Deficient Dogs
    IgA deficiency is the most common primary immunodeficiency in man.. It can be partial, transient
    or severe.
    In dogs, IgA deficiency has been associated with chronic or recurrent skin infections, including
    otitis externa but this appears to be independent of the type of deficiency. Six dogs with IgA
    deficiency and treated with Staphylococcal Phage Lysate (0.5 ml/dog subcutaneously twice-a-
    week for 10 weeks or more showed increases in their mean serum IgA levels (13.8 to 41.8 mg/dl)
    and 4/6 showed regression of the pyoderma and decreased frequency of recurrence whilst off

References and Further Reading
Campbell, K. L., Felsburg, P. J. IgA deficiency and skin disorders. In: Kirk, R. D., Bonagura, J. D.
eds. Current veterinary therapy. XI. Small animal practice. pp. 528-32.

DeBoer, D. J. et al. Evaluation of a commercial staphylococcal bacterin for management of idiopathic
recurrent pyoderma in dogs. Am. J. Vet. Res. 1990; 51: 636-9.
Bishop, Y. (Ed.) The Veterinary Formulary. 5th Edition. London, Pharmaceutical Press, 2001.
Mueller, R. S. Bacterial dermatoses. In A Practical Guide to Feline Dermatology. Guaguere, E.,
Prelaud, P. Merial, 2000.

Pododermatitis simply refers to inflammation of the skin of the feet and is clearly not a diagnosis. The
differential list is often lengthy and cases of pododermatitis may be challenging and frustrating. This
section describes an approach to diagnosis, which is based on the pattern of the lesions on the feet.

Clinical presentations can be usefully divided into three types:
•      Pad only (single or multiple).
•      Pad + interdigital skin.
•      Interdigital skin only.

The differential lists for these three presentations are somewhat different.
Pad only
•     Plasma cell pododermatitis (cats)
•     Penetrating wounds
•     Neoplasia
•     Idiopathic digital hyperkeratosis
•     (Sterile pedal panniculitis / metatarsal fistulae: [however, lesion may discharge via haired skin])
•     (Familial vasculopathy of GSD)
Pad + interdigital skin
•     Necrolytic migratory erythema (NME)
•     Zinc-responsive dermatosis
•     Pemphigus foliaceus
•     Drug eruptions
•     Hookworm dermatitis
•          SLE
Interdigital skin alone
•     Atopy
•     Dietary sensitivity
•     Contact dermatitis

•     Demodicosis
•     Trombiculidiasis
•     Pelodera dermatitis

•     Dermatophytosis
•     Malassezia dermatitis
•     Deep pyoderma (furunculosis)
•     Eosinophilic granuloma
•     Sterile pyogranuloma
•     Trauma
•     Neoplasia

Approach and Assessment.
This section summarises the salient features of approach for the three categories:
Pad only
History and clinical signs.
Single pad or multiple?
Biopsy for diagnosis:
    •      neoplasia
    •      Sterile pedal panniculitis
    •      Familial vasculopathy
Inspection, surgery and response to treatment for foreign body.

Pad + skin disease.
History and clinical signs, checking especially for.
    •      Breed (zinc-responsive)
    •      Breed + environment (hookworm dermatitis occurs mainly in greyhounds on
                               earthen runs)
    •      Systemic disease (NME)
    •      Recent drug administration (drug reaction)

    •      Trial zinc-treatment (if zinc-responsive dermatosis is suspected)
    •      Haematology / biochemistry / ultrasound (if NME is suspected)
    •      Faecal examination (for strongyle [hookworm] eggs)
    •      Skin biopsies (especially if NME and autoimmune disease is suspected)

Interdigital skin only.

History + clinical signs.
Pruritus is likely to be significant in allergy, Malassezia dermatitis and some parasitic infestations.

Erythema alone:
    •      allergy ± Malassezia
    •      Trombiculidiasis
    •      Demodicosis

Erythema plus greasy exudation:
    •      Malassezia ± allergy
    •      bacterial infection ± allergy

    •    deep pyoderma
         – demodicosis?
         – dermatophytosis?
         – immunosuppression?
         - poor conformation?

    •    Neoplasia (primary or metastatic)
    •    Granulomata (sterile or infectious)
    •    Foreign bodies
    •    Poor conformation

Investigation of interdigital skin disease:
All cases:
    •    skin scrapes (parasites, including nematodes in case of Pelodera)
    •    cytology (Malassezia or bacteria; aspirates of nodules)

    •    microbial cultures

    •    biopsies

Perplexing cases of pododermatitis
Most clinicians will have encountered problematical cases of dogs presenting with recurrent interdigital
"cysts". These are not true cysts (as they do not have an epithelial lining) but represent deep
inflammation. Some have a bacterial pathogenesis but others fail to respond to antibiotics. Previous
episodes of furunculosis may trigger ongoing disease as a consequence of free hair shafts lying within
the dermis. Poor conformation, such as widely splayed toes may favour traumatic injury to the toe
webs. Radical surgical excision of interdigital skin may represent a last resort form of approach if
medical management fails.

Feline Dermatology

Syndromes associated with systemic disease
•   Endocrinopathy is uncommon.
•   Other syndromes increasingly recognised but many are as yet poorly described and may include
    distinct diseases. Watch for publication of well studied cases.
•   Understanding these diseases is important in differential diagnosis.

    Examples of Cutaneous Syndromes Associated with Systemic Disease

      Principal sign           Syndrome name
      Alopecias                Pancreatic paraneoplastic alopecia
                               Superficial necrolytic dermatitis (few cases)
                               Degenerative mucinous mural folliculitis
      Pruritus                 Paraneoplastic exfoliative dermatitis
                               Paraneoplastic pruritus (one case)
      Exfoliative              Paraneoplastic exfoliative dermatitis
      Skin fragility           Acquired cutaneous fragility syndrome
      Deposits in skin         Cutaneous xanthoma

Paraneoplastic syndromes in cats
Paraneoplastic syndromes are systemic, remote, complications of cancer not associated with the growth
of cancer cells in either primary or secondary sites. In some cases, the pathomechamisms are not well
understood. Paraneoplastic syndromes affecting the skin of cats include superficial necrolytic
dermatitis, feline paraneoplastic alopecia, and exfoliative dermatitis associated with thymoma. These
disorders are rare. However, a paraneoplastic disease should be suspected in cats which show unusual
skin lesions, especially if they are symmetrical, occur in older cats, are, or if there are signs of systemic

Superficial necrolytic dermatitis
(Synonyms: metabolic epidermal necrosis, necrolytic migratory erythema, hepatocutaneous syndrome)
An uncommon metabolic skin disease of dogs but very rare in the cat. Dogs develop symmetrical
periorificial crusting with fissures and ulceration (eyelids, muzzle, lips, perineum, scrotum) and
footpad hyperkeratosis and fissures (lameness is sometimes a presenting sign). Occurs in older dogs
usually in association with hepatic disease (vacuolar degeneration or cirrhosis) or rarely, pancreatic
tumours producing glucagon. Some dogs become overtly diabetic. Skin disease may precede or occur
at the same time as signs of internal disease (polyuria, reduced appetite, weight loss).
Patel et al. (1996) described this syndrome in an 11-year old cat with a pancreatic tumour.
•   Skin lesions comprised axillary alopecia, erythema, and exudation, and dorsal truncal scaling.
•   The footpads were not affected.
•   Skin biopsies showed a distinctive pattern comprising parakeratosis, upper epidermal pallor
    associated with oedema, and a superficial dermal infiltrate of mononuclear cells, which is
    diagnostic of this disease.

•   However, this cat did not display the periorificial and footpad pattern of distribution usually seen
    in affected dogs.
•   Although not reported in this feline case, abdominal ultrasonography in SND in dogs may reveal
    diffuse hepatic disease or a pancreatic tumour and its metastases.
The prognosis is often grave because the internal disease can seldom be corrected (unless a tumour
could be excised prior to metastasis) and therefore skin lesions tend to progress. Steroids sometimes
improve the skin lesions but are usually contra-indicated because of the metabolic disease. High
protein diets improve the skin lesions in some cases.

Patel, A., Whitbread, T. J., McNeil, P. E. (1996) A case of metabolic epidermal necrosis in a cat.
Veterinary Dermatology 7: 221-226.

Feline paraneoplastic alopecia

Paraneoplastic alopecia in cats has been reported in recent years (Brooks et al 1994; Pascal-Tenorio et
al. 1997; Godfrey 1998).
•   Old cats usually present with a short history (few weeks-months) of inappetance, weight loss, and
    progressive ventral and limb alopecia.
•   Alopecia may occur elsewhere in the body, notably around the medial canthi of the eyes. Affected
    skin may have a smooth, glistening appearance, or varying degrees of scale.
•   Footpads may be scaly, fissured or normal, and there may be nail fold exudation.
•   Most cases are associated with a pancreatic adenocarcinoma, although bile duct carcinoma have
    also been identified.
•   These lesions may or may not be palpable on abdominal examination, but ultrasonography may be
    useful in demonstration the primary lesion or hepatic metastases. Pulmonary metastases may also
•   Haematological and biochemical tests are generally not useful.
•   Skin biopsy specimens may show severe follicular and adnexal atrophy, minimal superficial
    perivascular lymphohistiocytic infiltration, mild acanthosis and absence of the stratum corneum.
•   Malassezia spp. yeast may be recovered in large numbers from affected cats.
The prognosis is generally grave due to the underlying malignancy. Tasker et al. (1999) reported
resolution of the alopecia within 10 weeks of the surgical excision of a pancreatic carcinoma.
However, weight loss and alopecia associated with hepatic, splenic and peritoneal metastases
necessitated euthanasia 8 weeks after the surgery.

Brooks, D. G., Campbell, K. L., Dennis, J. S., Dunstan, R. W. (1994) Pancreatic paraneoplastic
alopecia in three cats. Journal of the American Animal Hospital Association 30: 557-563.
Godfrey, D. A. (1998) A case of feline paraneoplastic alopecia with secondary Malassezia-associated
dermatitis. Journal of Small Animal Practice 39: 394-396.
Pascal-Tenorio, A., Olivry, T., Gross, T. L., Atlee, B. A., Ihrke, P. J. (1997) Paraneoplastic alopecia
associated with internal malignancies in the cat. Veterinary Dermatology 8: 47-52.
Tasker, S., Griffon, D. J., Nuttal, T. J., Hill, P. B. (1999) Resolution of paraneoplastic alopecia
following surgical removal of a pancreatic carcinoma in a cat. Journal of Small Animal Practice 40:

Exfoliative dermatitis associated with thymoma

Thymoma is a relatively uncommon tumour which is most likely to lead to dyspnoea (Day 1997).
However, there have been a number of reports describing an association between thyomoma and a
generalised exfoliative dermatitis (Scott et al. 1995; Day 1997; Forster Van-Hijfte et al. 1997).
•   Most cases have occurred in middle-aged or older cats.
•   The scaling disorder may initially affect the head or ears but then may extend to involve wide
    areas of the body.
•   Pruritus varies from none to severe.
•   Concurrent Malassezia proliferation may be a feature of some cases (Forster Van-Hijfte et al.
•   The disease is usually characterised by a cell-poor interface dermatitis with hydropic degeneration
    and apoptosis of cells in the basal layer and, to a lesser extent, the stratum spinosum (Scott et al.
    1995). Orthokeratosis and parakeratosis is accompanied by mild epidermal hyperplasia, and
    varying degrees of superficial perivascular dermatitis.
Therapy is based on surgical excision of the thymoma, which is usually benign, plus treatment of any
related M. pachydermatis dermatitis (Forster Van-Hijfte et al. 1997).

Day, M. J. (1997) Review of thymic pathology in 30 cats and 36 dogs. Journal of Small Animal
Practice 38: 393-403.
Forster-Van Hijfte, M. A., Curtis, C. F., White, R. N., (1997) Resolution of exfoliative dermatitis and
M. pachydermatis overgrowth in a cat after surgical thymoma resection. Journal of Small Animal
Practice 38: 451-454.

Scott, D. W., Yager, J. A., Johnston, K. M. (1995) Exfoliative dermatitis in association with thymoma
in three cats. Feline Practice 23: (4) 8-13.

Degenerative Mucinous Lymphocytic Mural Folliculitis

•   Not a single disease
•   Several different causes incriminated
•   Inflammatory reaction in outer root sheath of hair follicle
•   Incriminated factors: FIV infection, dermatophytosis, demodicosis, food allergy, drug reaction,
    pseudopelade, sebaceous adenitis, early (prodromal) epitheliotropic lymphoma, severe disease,
    high-dose glucocorticoids
•   Different syndromes may target different levels and components of the hair follicle unit

•   Seen in older cats
•   Alopecia, initially diffuse. Focal lesions have been described
•   Scaling, may be severe. Fine scaling in some cases

•   Pruritus variable
•   Otitis, bilateral, ceruminous, commonly occurs
•   Systemic signs may be present - malaise, dehydration

•   History, clinical signs, histopathology is important
•   Rule out possible underlying factors: infections, infestations, allergies, immune-mediated &
    autoimmune diseases, drug reactions, neoplasia, paraneoplastic syndromes
•   Routine tests: scrapings, hair plucks, bloods
•   Use sensitive techniques e.g. Mackenzie brush method for dermatophytes, histopathology of
    sequential biopsy samples (good dermatopathologist).

•   If underlying cause identified, correct if possible
•   Supportive therapy, improved nutrition, supplements; antibiotics, anti-inflammatory therapy ...
•   In idiopathic cases, prognosis is grave.

Acquired Cutaneous Fragility Syndrome

•   Syndrome with several possible underlying causes; commonly idiopathic
•   Incriminated factors: iatrogenic (glucocorticoid, megestrol acetate); spontaneous
    hyperadrenocorticism; diabetes mellitus; hepatic lipidosis; bile duct adenocarcinoma
•   Cause postulated to be dermal weakness (asthenia) due to metabolic dysfunction

•   Skin becomes thin and then tears very easily
•   Little haemorrhage or pain
•   Signs associated with underlying disease

•   History; clinical signs are clear; biopsy (care), histopathology shows atrophy
•   Differentiate from “cutaneous asthenia”- appears in very young animals. Do not attempt to
    determine skin extensibility!
•   Careful approach to identify underlying cause(s).

•   Treat underlying disease. Repair wounds; slow healing. Guarded prognosis.

Skin Infections

Mycobacterial Diseases

•   Taxonomy: Bacteria; Firmicutes; Actinobacteria; Actinobacteridae; Actinomycetales;
    Corynebacterineae; Mycobacteriaceae; Mycobacterium - over 100 species.

•   Pathogenicity:
    1.   Causing tuberculosis. M. tuberculosis, M. bovis. Grow slowly in culture (growth not visible
         for 2-6 weeks, photochromogenic, strongly acid fast. Obligate pathogens.
    2.   Causing leprosy. M. lepraemurium - causes leprosy in rats; probable cause of feline leprosy
         (confirmed in presumptive feline leprosy by PCR). Very difficult to grow, scotochromogenic.
    3.   Opportunistic mycobacteria (less strongly acid fast)
         i           Infect cold-blooded animals only. Slow growing (>7 days), non-chromogenic
         ii          Facultative pathogens. M. avium, M. kansasii, M. marinum, M. ulcerans. Slow
                     growing (2-6 weeks), non-chromogenic.
         iii         Atypical group. Includes M. chelonae, M. fortuitum, M. phlei,, M. smegmatis, M.
                     thermoresistible, M. xenopi. Fast growing (2-7 days). May be pigmented or non-

             Photochromogenic - produce yellow pigment when exposed to light but not in the dark
             Scotochromogenic - produce pigment in the light and in the dark
             Non-photochromogenic - light has no effect on pigment production
             Non-chromogenic - do not produce pigment

Feline Tuberculosis

•   M. tuberculosis or M. bovis. Cats may be more susceptible to M. bovis.
•   Depends on exposure. In cities - human disease; in rural areas, bovine disease.

•   Onset often insidious in cats
•   Principal signs are generally related to the respiratory and gastrointestinal tracts
•   Skin lesions often on head, neck, limbs, include nodules, plaques, abscesses, ulcers; malodorous
    green pus

•   History; clinical signs. Culture from lesions, diagnostic imaging, histopathology, lymphocyte
    blastogenesis. BCG and PPD tests are not reliable in the cat.
•   PCR is now available in some laboratories and can greatly shorten the time to diagnosis
•   Check reporting regulations

•   Not normally treated - euthanasia.

Variant Tuberculosis of Cats


•   Organism matching M. bovis and M. tuberculosis DNA with intermediate cultural characteristics
•   Suggested infection occurred in hunting cats via wounds

•   Nodules on face, thorax, limbs, perineal region, sometimes ulcerating, non-healing; regional
•   Generalised disease also occurred

•   Differentiate by PCR or culture

Feline Leprosy

•   Not known for certain. M. lepraemurium apparently responsible
•   Long incubation. Disease appearing in winter with possible transmission by biting arthropods
    (mosquitoes, flies, ticks) in summer
•   A similar disease (canine leprosy) has been described in dogs in Zimbabwe and in Australia and
    transmission of the causative agent by biting flies has been suggested.

•   2/3 cases in cats 1-3 years old
•   Cutaneous nodules, may ulcerate; non-healing abscesses and/or fistulae, do not spread; oral and
    nasal mucosae may be affected.
•   Often regional lymphadenopathy
•   No systemic illness.

•   History; clinical signs. Acid-fast short rods in smears and histopathology.
•   Culture tissue and inoculate guinea pigs to check for tuberculosis, opportunistic mycobacteria,
    fungi, other bacteria
•   Other differentials include: foreign bodies, neoplasia

•   Surgical excision if localised. May recur.
•   Chemotherapy with: clofazimine, dapsone, rifampicin
    → e.g. clofazimine - 2-8 mg/kg daily (may turn skin and mucosae red)
•   May recover spontaneously.

Opportunistic (atypical) Mycobacterial granuloma

•   Atypical group. M. chelonae, M. fortuitum, M. phlei,, M. smegmatis, M. thermoresistible, M.
•   Soil and water organisms. Infect via wounds.
•   Concurrent infection with other organisms may occur.

•   Lesions most often in abdomen, perineum, lumbar regions.
•   Slow development (weeks) - nodules and non-healing wounds leading to abscesses, ulcers and
    draining tracts.
•   Extensive lesions in immunosuppressed animals
•   Cat not systemically ill unless lesions extensive. Lymph nodes may be enlarged.

•   History; clinical signs. Acid-fast rods in smears (aspirates are good) and histopathology, may be
    difficult to find.
•   Culture tissue (deep dermis and subcutis are best) on mycobacterial media. Results in c. 7d
    normally. Continue cultures for weeks to detect slow-growing species.

•   Surgical excision, including all associated fat. Start chemotherapy before surgery.
•   Long term chemotherapy if excision not complete or lesions extensive. Base this on sensitivity.
    Treat for months. Continue for 6 weeks after lesion resolution.
    → doxycycline - 5 mg/kg daily
    → enrofloxacin - 5-20 mg/kg daily
    → clofazimine - 2-8 mg/kg daily (may turn skin and mucosae red)
•   More complex combination protocols may be used
•   Spontaneous recovery may occur after months to years.

Malassezia Dermatitis
•   M. pachydermatis appears to be a relatively infrequent pathogen in cats, at least when compared
    with dogs. This may reflect the lower carriage rates seen in healthy cats (Baxter 1976; Hajsig et al.
    1985; Hajsig et al. 1990; Bond et al. 1995; Bond et al. 1996; Bond et al. 1997).
•   Ceruminous otitis externa responsive to antifungal ear drops is the commonest clinical presentation
    of M. pachydermatis -associated skin disease in cats.
•   Occasional cases of localised or generalised M. pachydermatis -associated dermatitis have been
    described in cats (Carlotti et al. 1993; Mason and Stewart 1993). Exfoliative erythroderma, greasy
    exudation and varying degrees of pruritus may be seen.
•   Cats with exfoliative dermatitis associated with thymoma and paraneoplastic alopecia may have
    concurrent proliferations of Malassezia (Forster-Van Hijfte et al 1997; Godfrey 1998).

Cats also differ from dogs in that they may be colonised by at least two lipid-dependent species, M.
sympodialis and M. globosa (Bond et al 1996; Bond et al. 1997). Crespo et al. (1999) reported the
isolation of M. furfur from the external ear canal of one out of 33 healthy cats. In most cases, M.
pachydermatis is isolated from cats with disease and the pathogenicity of lipid-dependent Malassezia
in cats has not yet been fully determined. Crespo et al. (2000) reported the isolation of M. sympodialis
the external ears canals of 2 cats with otitis externa. The author is aware of sporadic unpublished cases
where M. sympodialis has been implicated in more generalised dermatitis in cats.

The factors which determine the variability in skin carriage of Malassezia spp. amongst different
mammalian hosts are not well understood although differences in skin lipid composition have been
suggested as one possible factor. We hypothesised that variability in the species of Malassezia yeasts
recovered from various mammalian hosts might reflect differences in the adhesive capacities of

corneocytes (stratum corneum cells) between host species. Therefore, the abilities of M.
pachydermatis and M. sympodialis to adhere to corneocytes derived from healthy dogs, cats and
humans were compared using an assay in vitro (Bond et al 2000).
Corneocytes were collected from six Irish setter dogs, six domestic short-haired cats and six humans.
Corneocytes were obtained from the ventral abdomen of each dog and cat, and from the forearm of
each human using double-sided adhesive tape mounted on glass slides. Populations of Malassezia spp.
were assessed in skin adjacent to the sites from which corneocytes were obtained using 28 mm contact
plates containing modified Dixon's agar. Two strains of M. pachydermatis were used; CBS 1879 and
BH4L The two strains of M. sympodialis used were CBS 7222 and F7, a strain from our collection
obtained from a healthy cat.
M. pachydermatis was isolated in small numbers from two dogs and one cat only. Lipid-dependent
Malassezia spp. were not isolated from any of the subjects. Malassezia spp. were not observed in any
of the control corneocyte preparations which were not inoculated with yeast cells. M. pachydermatis
CBS1879 adhered best to corneocytes derived from cats and humans, whereas adherence to canine
corneocytes was significantly (P<0.01) lower. M. pachydermatis BH4L adherence to feline
corneocytes exceeded (P<0.05) that of canine and human corneocytes. The adherence of M.
sympodialis CBS 7222 and F7 to canine corneocytes was significantly lower (P<0.01) in comparison to
human and feline corneocytes. M. sympodialis F7 adherence to human corneocytes exceeded (P<0.01)
that of feline cells.
A clear relationship between adherence of the two M. pachydermatis strains tested in vitro and the
susceptibility to colonisation of dogs, cats and humans by this yeast species in vivo was not
demonstrated. The relatively low level of adherence of M. pachydermatis CBS 1879 to dog squames,
and the relatively high adherence shown by M. pachydermatis BH4L to cat cells does not parallel the
relative frequency of isolation of the yeast from these host species. The ability of the M.
pachydermatis strains tested to adhere to human corneocytes in vitro suggests that other physical or
chemical factors must account for the rare isolation M. pachydermatis from human skin and favour the
colonisation by the other Malassezia spp.
In contrast, the relatively low adherence of both M. sympodialis strains tested to canine corneocytes
more closely parallels the situation in vivo. However, the overall difference in counts of M.
sympodialis between the three mammalian donor species, although statistically significant, was not
high. Reduced adherence may, in part, limit the potential for colonisation of canine skin by M.
sympodialis but other factors must be responsible for the absence of this yeast from canine skin. The
results of this study suggest that variability in the adhesive capacities of corneocytes between host
species does not explain the marked differences in the Malassezia spp. flora of dogs, cats and humans.
•   Diagnostic and therapeutic measures are similar to those used in dogs.
•   Cytology should be routinely used to assess yeast populations and trial therapy should be given if
    populations seem abnormally high. M. pachydermatis is readily cultured using standard
    mycological techniques but other Malassezia spp. are more fastidious and they require lipid-
    supplemented culture media.
•   Most veterinary diagnostic laboratories are probably unfamiliar with the techniques required to
    isolate and identify lipid-dependent Malassezia spp. Specialist laboratories, human diagnostic
    centres and mycological reference laboratories should be consulted if lipid-dependent Malassezia
    are suspected.
•   Modified Dixon's agar and Leeming's medium are appropriate; plates should be incubated at 32-
    37oC for at least 7 days.

Baxter, M. (1976). The association of Pityrosporum pachydermatis with the normal external ear canal
of dogs and cats. Journal of Small Animal Practice 17: 231-4.
Bond, R., Anthony, R. M., Dodd, M., Lloyd, D. H. (1996). Isolation of Malassezia sympodialis from
feline skin. Journal of Medical and Veterinary Mycology 34: 145-147.

Bond, R., Howell, S. A., Haywood, P. J., Lloyd, D. H. (1997). Isolation of Malassezia sympodialis
and Malassezia globosa from healthy pet cats. Veterinary Record 141: 200-201.
Bond, R., Wren, L. & Lloyd, D.H. (2000) Adherence of Malassezia pachydermatis and Malassezia
sympodialis to canine, feline and human corneocytes in vitro. Veterinary Record 147: 454-455
Carlotti, D. N., Hubert, B., Delmas, H., Magnol, J. P. (1993). Les mycoses superficielles chez le chat.
Practique Medicale et Chirurgicale de L'animal de Compagnie 28: 241-257.
Crespo, M. J., Abarca, M. L., Cabanes, F. J. (1999) Isolation of M. furfur from a cat. Journal of
Clinical Microbiology 37: 1573-1574.
Crespo, M. J., Abarca, M. L., Cabanes, F. J. (2000) Otitis externa associated with M. sympodialis in
two cats. Journal of Clinical Microbiology 38: 1263-1266.
Forster-Van Hijfte, M. A., Curtis, C. F., White, R. N., (1997) Resolution of exfoliative dermatitis and
M. pachydermatis overgrowth in a cat after surgical thymoma resection. Journal of Small Animal
Practice 38: 451-454.
Godfrey, D. A. (1998) A case of feline paraneoplastic alopecia with secondary Malassezia-associated
dermatitis. Journal of Small Animal Practice 39: 394-396.
Hajsig, D., Hajsig, M., Svoboda Vukovic, D. (1990). Malassezia pachydermatis in healthy cats.
Veterinarski Arhiv 60: 69-73.
Mason, K. V., Stewart, L. J. (1993). Malassezia and canine dermatitis. In: Advances in veterinary
dermatology, Volume 3. Eds P. J. Ihrke, I. S. Mason and S. D. White. Oxford, Pergamon Press.

Viral Diseases of the Face and Head

This was covered in last year’s module

Hargis et al (1999) recently described an ulcerative dermatitis of the nasal planum or haired skin of the
face, associated with intranuclear inclusion bodies compatible with herpes virus.
•   Clinically lesions consisted of vesicles, ulcers and crusts
•   An eosinophil-rich necrotising dermatitis was seen histologically
•   Intranuclear inclusion bodies may be found in adnexal epithelial cells
•   PCR amplification of viral DNA yielded sequences consistent with Feline Herpes Virus 1
•   Latent viral infection or stress may be risk factors for this disease
•   Alpha-interferon may be of therapeutic value but this needs further assessment


Plasma Cell Pododermatitis

•   Unknown cause; suspected immunemediated cause. FIV infection may be a factor in some cases.

•   Normally affects several pads - usually central metacarpal and/or metatarsal pads - on several feet.
•   Pads swollen, soft (“mushy”), often have a violet tint with white striations.
•   Asymptomatic unless ulceration and secondary infection occur; may be haemorrhagic when

•   No systemic signs, normally.
•   Rarely also plasma cell stomatitis, renal amyloidosis, immunemediated glomerulonephritis

                                                                                                              Kommentar: Many are Mott’s
•   History; clinical signs, cytology and culture of aspirates (plasma cells, sterile); histopathology        cells i.e. distended by Russell bodies
                                                                                                              - globular inclusions composed of
•   Rule out neoplasia, granulomas and pyogranulomas (infectious, sterile, eosinophilic), arthropod           aggregates of immunoglobulins
    bite reactions - all normally affect a single pad
•   Blood biochemistry typically shows hypergammaglobulinaemia - polyclonal gammopathy

•   Is it necessary? May regress spontaneously.
•   Doxycycline 5-10 mg/kg per day for up to 8 weeks. Tetracycline also said to be effective.
•   Prednisolone, 4 mg/kg daily - response in 3 weeks, maximal at 14 weeks. Dexamethasone, 0.5 mg
    per cat daily if not responsive to prednisolone.
•   Surgical removal of the footpad
•   Chrysotherapy has been used.

Idiopathic facial dermatitis in Persian cats.

An idiopathic facial dermatitis of Persian cats has been recognised in the U.K (Bond et al 2000).
Anecdotal reports suggest that a similar entity has been seen in North America. In a series of 13 cases,
8 male and 5 female Persian cats aged between 10 months and 6 years (median 2.5 years) were studied.
Each cat was presented with a history of progressive, predominately facial skin disease of 3 months to
4 years duration (median 12 months).
•   The age at onset reported by the owners ranged from 4 months to 5 years (median 12 months).
•   The first abnormality noted by the owners was the presence of a black material which matted the
    hairs of the periocular, perioral or chin areas.
•   Pruritus was not reported early in the course of the disease. However, the affected areas became
    progressively inflamed and pruritus became moderate or severe, despite a variety of symptomatic
•   Affected cats were otherwise reported to be in good general health. All cats were routinely fed on
    standard commercial diets.
•   Similar clinical signs were seen in each case. A black waxy material, which matted the distal
    portions of the hair, was present in a symmetrical pattern on the face of each cat.
•   In most cases, the chin, perioral and periocular areas were affected. Erythema and exudation were
    often observed in the facial folds but the lesions were clearly present in non-intertriginous areas.
•   Moderate to severe erythema was observed in the areas of exudation and also in the preauricular
•   A bilateral erythematous otitis externa with accumulation of black waxy material within the
    external ear canal was seen in 7 cats. Excoriations were observed in severely affected cases.
•   Apart from a submandibular lymphadenopathy, which was present in 5 cats, general physical
    examinations showed no other abnormalities.
•   Histopathological examination of skin biopsy specimens showed marked acanthosis with crusting,
    hydropic degeneration and dyskeratotic basal epithelial cells, a mixed diffuse superficial
    inflammatory infiltrate and sebaceous hyperplasia.

•   Malassezia pachydermatis yeasts and various bacteria were isolated from the lesions in some of
    the cats but in no case was antimicrobial therapy curative.
•   The response to glucocorticoids was variable and often poor.
•   Elimination diets and intradermal tests, when done, were unrewarding.
•   No satisfactory therapeutic regimen could be identified and the cause of the disorder is unknown
    although a genetic basis is possible.
•   Four cats were euthanased because of severe, uncontrolled pruritus.

Bond, R., Curtis, C.F., Ferguson, E.A., Mason, I.S. & Rest, J. (2000) An idiopathic facial dermatitis of
Persian cats. Veterinary Dermatology 11, 35-41

Further Reading
Guaguère, E., Prélaud, P. A practical guide to feline dermatology. Merial, 2000.
Scott, D. W., Miller, W. H., Griffin, C. E. Muller & Kirk’s Small Animal Dermatology. 6th Edition.
Philadelphia: W. B. Saunders, 2001.

                                    Avian Dermatology

                                             Martin Lawton
 BVetMed; CertVOphthal; CertLAS; CBiol; MIBiol; DZooMed; FRCVS, RCVS Specialist in Exotic
                                    Animal Medicine.
                       12 Fitzilian Avenue, Harold Wood, Essex, UK, RM3 0QS


The Class of Aves (birds) contains over 9000 species and some 28 Orders (too many to list here!).
Birds are kept for either for
         1)          Food eg. Galliformes (Game birds), Struthioniformes (Ostriches), and some
                     Anseriformes (Ducks and Geese),
         2)          Sport eg. Falconiformes (Falcons & Hawks), Columbiformes (Doves & Pigeons),
                     and Strigiformes (Owls),
         3)          Companionship eg. Passeriformes (Canaries) and Psittaciformes (Parrots and

Avian Anatomy

The skin of birds is much thinner than that of mammals. It also has less attached muscles. There are
boney attachments at the distal wing and the feet. The skin has an epidermis, dermis and subcutaneous
layer with neurovascular component. The Stratum Germinativum produces new cells, which are
pushed to the surface. The dermis is also thin but has the dermal papilla from which feathers grow.

The beak (or bill) is a horny keratinised epidermal layer known as the Rhamphotheca. It is continuous
with the periosteum of the premaxilla or mandible. On the basal surface there are folds or papillary
pegs within which there are mechanoreceptors and sensory receptors.


The characteristics of all birds are that they have feathers. Feathers are important for the insulation of
the bird, as well as aiding in flight. The feathers over different parts of the body vary. The contour
feathers cover the whole body. The contour feathers may also become specialised as the flight feathers
(Remiges) or the tail feathers (Rectrices). Remiges are dived into primary and secondary. Contour
feathers are laid in tracts (Pterylae) with spaces in between (Apteryia) which may or may not have
down. Smaller feathers (Filoplumes) are found in close association with the follicle of each contour
feather. Filoplumes have unmyelinated nerve endings in their follicles.

The feather emerges from the skin as a calamus (quill). This then gives rise to the shaft (scapus or
rachis) as the main body of the feather which itself gives rise to numerous vanes (vexilla). Fine

branches (barbs or plumes) arise from the shaft at 45° on either side and from these barbs arise smaller
branches (barbules) at an angle of 45°. Flight feather barbules are locked together by small hooks
which form an interlocking structure resulting in the flat but firm feather. If the barbules are not
locked together then the feather will appear as a "fluffy" feather. Feathers with damage to the barbs
and barbules may cuase difficulty in flight, water proofing or lack of insulation. Barbules are absent in
Semiplumes which often lie along the margin of the pterylae.

Preening by the bird is essential for the general cleaning and protection of all the feathers as well as re-
engaging any unhooked barbules to restore the normal conformation.

Down feathers are not semiplumes. The shaft is shorter then the barbs. Powder down feathers may be
any feather and not just down feathers. The powder is produced by disintegration of the tips (keratin) of
the powder down feathers. This powder helps to make the rest of the feathers waterproof and also
helps to lubricate them. Down feathers cover the whole body in penguins and ducks but are absent in
ratites, passerines and pigeons.

Uropygial Gland

Also known as the Preen gland. The uropygial gland is absent in a number of birds, including the
Amazon parrot, emus and ostriches. There is variable presence among the pigeons, other parrots and

This is an oil producing gland and is particularly important in water fowl. It is located on the dorsal
base of the tail. The papilla of the uropygial gland is covered by a tuft of prominent feathers. There
may be single or multiple ducts. The secretion consist of extruded cells with a lipid component. The
beak is used for spreading this over the feathers in the process of preening. When neoplastic (or
infected) this will become very enlarged and should be surgically removed.

Avian Physiology


In order for a new feather to grow, the old feather has to be extruded (Moulted). There is a periodic
shedding (moulting) of the old feathers.

The new feathers (pin feathers) can grow from the existing feather follicle (an invagination of the
skin). The epidermal cells grow from a cap covering the dermal papilla which is at the bottom of the
follicle and receives its blood supply from the underlying dermis. The new pin feather has a central
dermal pulp which has an axial artery and a vein (blood feather). Initially there is an outer keratin
sheath. Eventually the blood vessels die back when the feather is at its normal length, leaving the
keratin sheath around the feather. As part of the natural grooming, the bird breaks down this sheath
(desheathing) to release the feather.

The growth and development of feathers are affected by light and hormones. Changes in day length can
trigger the moult. The connection between the photoperiods and the endocrine system are not fully
understood. Thyroid hormones do not simply or directly control moults and there does appear to be an

interaction between thyroid activity and gonadal cycles. Moults often precedes migration and follows
breeding. Gondal hormones (oestrogens and androgens) appear to inhibit moult but are not essential for
a moult, as caponized cocks will continue to moult on schedule.

The increased metabolism associated with a moult is not just associated with new feather growth but
also increased cardiovascular activity, increased amino acid production, increased skin keratin
production, calcium distribution changes. Only 7% of the increased energy requirements are
incorporated into the new feathers.

A bird which is failing to have a normal moult (growth cycle) should have been identified by the
condition of the feathers. The retained feathers become dull, dirty and often of ragged asymmetrical
appearance, there is also a lack of pin feathers. Often feathers are missing, these have been moulted and
not yet replaced. This may be associated with hypothyroidism and although blood samples may be
taken they are often difficult to interpret, especially as normal values may not be available for all the

Avian Parasitic Disease


These are rare in psittacines and noted only in heavy infestations. They are commoner in Pigeons and


These are more frequently seen and include the mange mite (Myidlges spp) which causes pruritus and
feather picking in the face of grey cheeked parakeets.

Cnemidocoptes spp are the most common of the mites that are encountered in bird. The parasite
Cnemidocoptis piliae produces classic hyperkeratosis of the skin and excessive scaliness, usually
around the beak and eyes or legs and feet, and resulting in a substantial feather loss. Passerines
may be infested with Cnemidocoptes mutans or Cnemidocoptes jamaicensis. C. laevis is the
depluming mite of parrots (especially Macaws (Ara spp.)). This mite is found within the feather
follicle. Quill mites (Csyringophilus bipectinatus and Dermoglyphys elongatus) destroy feathers
early in development by entering the feather shaft. They may also cause dermal cysts. The mites
are easily seen as they are quite large, living on the bird, their eggs being deposited along the feather
shaft. Although definitive diagnosis can be made on a biopsy (a scraping is often unrewarding as it
is difficult to actually demonstrate the mite), a final diagnosis is often made retrospectively on
response to treatment. C. piliae spends its life cycle of 3 weeks in the skin of the host. There is often
a carrier state which produces clinical signs during times of stress such as poor nutrition, poor
husbandry or infectious disease.

Cnemidocoptes spp. are now easily treated by the use of ivermectin injection (200mcg/kg)
although unlicensed and may require repeated doses on a fortnightly basis. The use of benzyl
benzoate is now not recommended as firstly, it does not penetrate the thickened skin to the mite and
secondly, it is toxic.

Dermanyssus gallinae is the red mite, this is mainly an aviary problem. The mite only feeds at night.
During the day it is within the cage in recesses or even under droppings. Diagnosis during the day

requires very careful examination of the cage. Nocturnal examination of the bird may demonstrate
the mite. Even without seeing the mite, there is often signs of pruritus and restlessness in the bird.
Treatment of the environment with Vapona (Dichlorovos; Shell) for 3 days, repeating each 2 weeks
usually eliminates the mites.


The protozoal organism Giardia spp have been reported as a cause of pruritus of the head and neck in
cockatiels which is thought to be a hypersensitivity reaction causing feather picking.

Avian Viral Disease

There are two main viral conditions which will result in feather loss, these are Circovirus and
Polyomavirus. In general the abnormalities that will occur will depend on the species infected and on
the stage of feather development when viral infection occurs. There can therefore be acute and chronic
forms. The acute form is more likely to be associated with Polyomavirus and the chronic form with
Circovirus. However, Circovirus can also cause an acute problem in Budgerigars.

Diagnosis of a Viral Condition

    1) Cytology/ histopathology.
                 This can be of the skin, feathers or ideally both. Feather pulp examination is often
         rewarding and where ever possible the sample should include a pin feather with the follicle.
         Although routine H & E staining, and light microscopical examination is helpful, electron
         microscopy is invaluable for diagnosing viral causes (Psittacine Feather and Beak Disease).

    2) PCR/ ELISA.
             There are now an increasing number of tests that are becoming available for diagnosing
    infectious diseases. These include tests for Chlamydia, Polyoma and Psitaccine Beak and feather
    disease. All birds should be tested for Chlamydia, as a routine, especially as there are zoonotic

Psittacine Beak and Feather Disease

         Historically this was first reported in Australian Cockatoos in 1970 and for many years was
known as Cocaktoo Feather and Beak Disease. When it was established that other psittacines could be
infected it was nenamed Psittacine Beak and Feather Disease (PFBD). It is usually fatal in
cockatoos (Cacatua spp.) (in which it was first reported in 1970) and parakeets (Agapornis spp.). In
budgerigars (Melopsittacus undulatus) it tends to rarely be fatal, just interfering with ability to fly.
Affected birds are often referred to as "creepers" or "crawlers" to reflect their mode of transport.
Previously it has been considered to be a parvovirus or papovavirus-like organism, then a
polyomavirus. It is a nonenveloped virus 14 to 17nm. It haemagglutinates erythrocytes. On the basis of
size and other similarities it has been placed in Circoviridae, and it is now well accepted that a
Circovirus is the cause of Psittacine Beak and Feather Disease (PBFD), indeed a suggested new title is
Psittacine Circovirus Disease (PCD). The presence of the virus can be suspected when Basophilic
intranuclear and intracytoplasmic inclusion bodies have been found.

We now know more about the Circovirus family. In pigs there is a pathogenic and apathogenic
circovirus and the same is now thought to be occurring with PBFD. Some tests have been shown to be
more specific and may only pick up certain variants. It should be remembered that not all circoviruses
in the birds are PBFD. PCR is showing that there is two variants, PBFD 1 & 2. The affected species is
most likely to have a mixed infection of PBFD 1 & 2. although different variants may effect different
psittacine species. There may even be more than two variants and as also be shown in other avian
species and mammals. The PBFD virus(es) that affects different hosts are antigenically similar. Lesions
have now been described in 42 species of psittaciformes. In a recent survey of an outbreak of 9 lorries
that were shown to be all positive in the feathers for PBFD but were all negative on blood, when the
blood was sent to another lab (using a slightly different probe) and they were shown to be positive.
This is thought to be due to a lorry variant which has been confirmed in Australia and it appears that a
percentage will recover from this virus. However, most clinically apparent forms of PBFD are
considered fatal.

Virus shedding is from feather dander, crop and faeces. Vertical transmission occurs. It is a progressive

In the acute form, it is noted during the first feather formation in the young or fledgling birds. The
feathers may be abnormal, often with necrosis or haemorrhage, gross feather lesions may be quite
subtle. Crop stasis and diarrhoea can also occur before death. On PM there can also be evidence of
hepatitis and high levels of virus can be detected in the livers and bile.

The Chronic form occurs in Nature and adult birds. Chronic PBFD is characterised by the progressive
appearance of abnormally developed feathers during each successive moult. The dystrophic feathers
will stop growing shortly after emerging from the follicle, and their number increases with each
successive molt. The powder down feathers, located over the hips and flanks are typically the first to
show signs of dystrophy. The disease progresses to involve the body contour feathers followed by
changes in the primary, secondary and the crest Feathers. Primary feathers are usually the last to
manifest the disease. Feather dystrophy and loss are roughly symmetrical. Changes include feather
sheath retention, pulp cavity hemorrhage, fracture of the proximal rachis, and failure of developing
feathers to desheathe. Short clubbed feathers, deformed curled feathers, stress lines within vanes, and
circumferential constrictions may be observed

Histology of circovirus (PBFD) shows a necrosis of the stratum germinitivum and inflammation within
the feathers and this is usually diffuse and severe. Epidermal hyperplasia and hyperkeratosis will be
very much in evidence. Necrosis varies from multifocal involvement of the basal feather epithelium to
difuse involvement of the pulp cavity. Characteristic findings include basophilic to amphophilic
nuclear and cytoplasmic inclusions both within hematoxylin and eosin-stained tissue sections. Large
intracytoplasmic inclusions within the macrophages is considered to be characteristic of the disease. On
direct electron microscopy aggregates of circoviruses can be identified amongst cellular debris

Beak changes include progressive elongation, fractures, palatine necrosis and oral ulceration. If the
powder down feather are dystrophic then the beak becomes very shiny.

Immunosuppression from damage to the thymus or bursa (of Fabricius) is thought to occur. In the
PBFD positive bird has the inclusion bodies in the nucleus of infected epithelial cell, they may
spontaneously recover while as if the inclusion bodies are intracytoplasmic in the macrophages then
they will succumb to disease. An age-related susceptibility has been suggested. The minimum
incubation period is 21 to 25 days while as the maximum may be years. Most birds that are affected are
under 2 years of age and it has proved difficult to reproduce the disease in adult birds, however all age
groups should be considered as susceptible.

The treatment is supportive, to make the bird comfortable. Unfortunately, there is no cure for this

disease. There is also evidence to support a vertical transmission to offspring, via the egg. In contact
birds can be screened to see whether or not they are likely to develop the disease by electron
microscopy of a biopsy sample. There has also been some reported success of the use of autogenous
vaccines in affected birds, although this author has had no such success with this technique. The
outcome will depend on which species of bird is actually affected. It is usually fatal in cockatoos
(Cacatua spp.) (in which it was first reported) and parakeets (Agapornis spp.).

Diagnosis is most easily done on DNA probe (PCR and DNA dot-blot assay) of blood sample or
feather pulp. On DNA probe testing, a positive with clinical signs shows that PBFD is the cause of the
disease. A Positive bird which is showing no clinical signs means it is recently infected and viraemic or
has latent infection and should be retested after 90 days, in which case if it is still positive it has a
latent infection. In flocks of wild cockatoos, it was found that there was a disease prevalence of 20%
and a seroprevalence of 60 to 80%.


Polyomavirus is a Papovaviridae (Papovavirus) and was first called budgerigar fledgling disease. In
Budgerigars there may just be fledgling death (highest in birds less then 15 days old but most deaths
occur 20 to 56 days of age), or clinical signs including distended abdomens, subcutaneous
haemorrhages, tremors, ataxia and reduced formation of the contour feathers or dystrophic feathers (see
later). Neonates presented for PM after sudden death are usually in good condition with full crops.
Some asymptomatically infected adults produce persistently infected young or some that produce
clinical signs. Infection by ingestion and aerosol.

In larger psittacines there can be acute death or chronic signs of diarrhoea, dehydration, delayed crop
emptying, subcutaneous haemorrhages, dyspnoea and polyuria. Neurological signs have been
described. The feather abnormalities that are seen in budgerigars are less frequently seen in the other

The acute form of the feather disease in budgerigars is often referred to as French molt (an Australian
term) although strictly speaking it describes both the acute form of Circovirus or polyomavirus in
young budgerigars. These two infection can occur concurrently in the same bird. It is usually seen in
young birds during their first molt, and can be observed in chicks within 25 to 40 days following
inoculation. Although the exact incubation period is not known and the virus typically rests in a latent
state until there is some stressors. The hatchlings may have reduced formation of down and contour
feathers. While as the Juveniles that survive early infection may exhibit symmetric feather
abnormalities characterized by dystrophic primary and tail feathers, lack of down feathers on the back
and abdomen, and lack of filoplumes on the head and neck.

Diagnosis is on DNA probe. Cloacal swabs are preferred as they are easier to collect in young birds. It
should be noted that at a recent AAV conference Dr Branson Ritchie reported that the DNA probes that
are designed to detect polyoma in psittaciformes do not detect some strains of polyomavirus from


Avipoxvuruses are epitheliotropic and cause local tumors in nonfeathered areas of the skin.
Avipoxvirus (Poxvirus) in the dry form manifests itself as nodular and papalar lesions on nonfeathered
skin, especially around the eyes; beak and nares. The dry form is most common in passerines but can
also be found in amazons. There are many species of Avipox that are not host specific and will cause

disease (often milder) in a non-host species. Canary poxvirus is considered the most virulent of the
avipoxviruses which can result in 100% mortalities, mainly from internal diphtheritic lesions.

The antigenic relationship between the avipoxviruses are complicated. Often infection with one type
will not produce protection against another type. Psittacine poxviruses are antigenically distinct from
quail, fowl or pigeon poxviruses.

Histopatholgy shows epithelial hyperplasia and the Intracytoplasmic inclusions (Bollinger bodies)
which are pathognomonic of this virus. Bollinger bodies are referred to as Borrel bodies on impression

Lesions will usually resolve within 4 weeks. Surgery can be undertaken where there are large lesions.
Antibacterial therapy is advised to reduce down the occurrence of secondary infections.


Herpesvirus can cause a dry proliferative lesions on the toes of cockatoos, but this can also be found on
the feet and legs.


Papillomavirus are the second group of Papovaviridae (Papovavirus) and can be ssociated with the
formation of benign epithelial tumors on skin and epithelial mucosa. Cloacal papillomata are common.
Histopathology shows hyperplasia and hyperkeratosis of epidermal tissue.

Avian Bacterial Disease

Bacterial Folliculitis and pulpitis are rare, however, it can be diagnosed on examination of biopsy
specimens, or a Gram stain of the feather pulp. Clinicians often find difficulty in differentiating
between primary and opportunistic invaders. These bacterial infections can be caused by the Gram-
negative organisms (e.g., Aeromonas spp., Psesudomonas spp.), Gram-positive organisms (e.g.,
Staplrylococcas spp., Streptococcus spp.) or Mycobacteria spp. (very uncommon). Where ever a
bacterial involvment is suspected, it is important to take samples for culture and sensitivity.

The presenting clinical signs are Perifollicular and follicular reddening and necrosis with crust
formations. Sometimes there may be abnormal odours. On histopathology there is a heterophilic
inflammatory infiltrate with or without the presence of bacteria.

In the case of Mycobacterial granulomatous dermatitis there is a lump or multiple lumps comprising
large macrophages, containing acid- fast bacteria and a amiable number of heterophils and plasma cells

Chronic ulcerative dermatitis

Causes of ulcerative lesions include Trauma or those associated with bacterial infections.

Trauma can be self induced, such as the lesions that are associated with feather picking syndromes and
self-mutilation as seen in Moluccans (Keel feather and muscle mutilation, ulcerative disease),
Lovebirds (wing web area mutilation), Cockatiels (feather mutilation syndrome) and African greys
(Incessant split keel).

Repeated trauma can leave to chronic ulcerative dermatitis (CUD) which is characterized by
septicemia, edema, hyperemia, and ulceration of the skin. CUD has been associated with tumors
(xanthomata), abscesses, and mycobacterosis, among other conditions. Failure to prevent keel lesions,
cauased from repeated hard landings on hard surfaces can also become CUDs.

Surgery is required for the keel injuries while as appropriate behavioral modification is required for the
self mutilators.

Another big group of ulcerative lesions are those of the feet which are often associated with incorrect
perchs. These are grouped together as Bumblefoot lesions. The underlying pathology is related to
repeated trauma to the foot or toe which will lead to superficial damage to the skin which can then
become infected (various organisms) and result in scab formation and ultimately ulceration and
deepening of the lesion. The treatment is aimed at improving the perching environment, improving
hygiene and treating the lesion.

Superficial lesions can be treated with antiseptics and antiinflammatories. More sever lesions will need
surgery but often radiography may be required in order to rule out bone or joint involvement, which
carries a poor prognosis.


Bacterial dermatitis or folliculitis can be treated with an appropriate antibiotic (such as cephalexin
10mg/kg PO tid, enrofloxacin 15mg/Kg PO bid or doxycycline 10mg/kg PO od), but this should be
based on the results of culture and sensitivity.

Avian Fungal Disease

This is very uncommon in birds, unlike mammals.

Candia spp. have been associated with feather and skin lesions in gallinaceous birds, especially with
feather loss in the vent area, and with some pet avian species in the head.

Dermatophytes (mainly Miscrosporum gallinae) can affect fowl (Galliformes), ducks
(Anseriforms), pigeons (Columbiforms) and turkeys (Galliformes), but are very rare. Dermatophytes
can cause patchy Feather loss, especially on the head, neck, and breast; dermatophytes include
Microsporum gallinae (fowl, canary, duck, pigeon and Turkey), Mirosporum Museum (fowl, parrot),
Trichophyton verrucosum (fowl, canary), and Trichophyton spp. (robin).

Lesions are limited to fleshy or thin skinned areas of the head and are seen as scabs, crust or alopecia.
Candida albicanas can cause similar lesions but may also show a white powdery type deposit.
Microsurgical examination of skin scrapings gives a definitive diagnosis.

Feather Loss

The feather can be damaged due to physical trauma, nutritional problems or illness all which results in
deformed feathers or fret lines. Infections (viral, bacterial and parasitic) can all affect either the
development of the feather, or loss and damage to the feather itself.

Care must be taken on handling birds to prevent damage to the feathers. Likewise, when preparing a
bird for surgery it is keep the removal of the feathers to the minimum so that the insulation properties
of the feathers are not lost.

The plane of nutrition of the bird is important in the development of all feathers. On lower planes of
nutrition, or if the bird is ill, the developing feather is affected and often there are lines running through
it (fret lines). These are caused by disruption of the epidermal collar possibly due to release of natural
corticosteroids during times of prolonged stress. Up to 85% of pet psittacines have deficient diets,
which often result in poor feather quality.

Establishing A Diagnosis

It is often possible to establish a definitive diagnosis after taking the case history and clinical
examination. If the bird is showing classic self-inflicted trauma, with the presence of perfect feathers
on the head, while there is loss over the body, then it is nearly always a behavioural problem.
However, owners are often convinced that their bird is not suffering from such a problem, but has a
parasitic infestation; this should always be ruled out by routine microscopy, examination of the bird
and environment. A bird which is failing to have a normal moult (growth cycle) can be identified by
the condition of the feathers. The retained feathers become dull, dirty and often of ragged
asymmetrical appearance, there is also a lack of pin feathers. Often feathers are missing, these have
been moulted and not yet replaced. This may be associated with hypothyroidism and although blood
samples may be taken they are often difficult to interpret.

Behavioural Problems

Neurosis and other behavioural problems result in feather chewing or feather plucking and are the
most difficult feather loss conditions to manage. Initially, if the cause of the neurosis is established,
appropriate measures should be taken in order to eliminate it. Often there are many factors involved
in the original neurosis. If the bird has been recently moved from a site in which it was previously
happy, then it should be moved back. This is less easy if the owners have recently moved house or
flat. Birds being within sight or sound of other birds but not having contact with them may also
be a causal factor. Sometimes the introduction of another bird will stop the vice, at other times it
may cause the new bird to learn the vice and the result will be two feather plucking birds.

In all cases it is a good idea to advise the owner to allow the bird to have access to water, and either to
have regular baths or be sprayed on a daily basis. This is particularly important for African Gray
parrots (Psittacus erithacus) that tend to produce a large amount of down powder, and are
therefore prone to developing an irritant dermatitis which results in over grooming which may

become excessive, and later on may develop into feather plucking.

Nervous birds should be provided with some sort of "hide" and if necessary be given a "quiet time"
during some stage of the day. Birds that are left alone for long hours during the day, should either
have the radio or television left on to give them company, or be given new toys on a regular basis;
older toys should be removed at the same time In this way a new stimulus for them to play with or
explore is provided. Change feeding regimes to make the bird work for its food by (a) not giving ad
libitum food and (b) adding stones or marbles (too big to be eaten) will make the bird hunt for food
leaving less time for feather plucking.

If more than 12 hours of daylight (including artificial light) is provided, then it is advisable to reduce
this to about 12 hours of light, 12 hours of darkness.

The bird that is feather plucking in front of the owner for attention is more difficult to deal with.
This involves convincing the owner that they must not rush up to the bird and scold it (or pay any
other form of attention) when it plucks a feather, as this positively reinforces the behaviour by
rewarding the bird for pulling out feathers, thus making the problem worse. It is good policy to
develop a reward and punishment regime, punishment involves walking up to the bird (without
speaking to it), and either covering it up with a very thick blanket or curtain, or putting it under
the stairs, in a cupboard, or another darkened area. Initially do this for five minutes, on subsequent
occasions gradually increase by a minute each time, up to a maximum of 15 minutes. Isolating the
bird out of the client's "love", or putting it into a darkened area, is a big punishment, especially to
the attention seeking bird.

If environmental and managemental methods do not improve the condition, the use of a neck collar
to physically prevent the bird from chewing and plucking its feathers is very useful. This is
frequently used in combination with Medication. Often the collar has to be left in place for at least 3-4
months (sometimes substantially longer). However, unless changes are made to the management and
environment of the bird, and the neurosis controlled, then as soon as the collar is taken off the bird can
revert to the previous vice.

1) Hormonal Treatment. The use of hormonal therapy with megoestral acetate (2.5mg/kg daily to
start with) has been reported to be of value in some cases. Thyroxine (100mcg/kg each 48 hrs
for 2 weeks) can induce moulting. However, hypothyroidism usually presents as dyspnoea with
change of voice and strange head posture well before any clinical signs associated with
feathering is noted.

2) Diazepam (Valium, Roche)         0.6mg/ Kg p/o, i/m, i/v. two drops (5mg/ml) per 30ml of drinking
water is a Short-term only treatment used to allow healing and until underlying cause or problem is
treated. This treatment may cause sedation and ataxia at effective doses

3) Phenobarbitone (0.3mg/100g bid) has also been reported as helpful to control neurosis, although
as in humans it is possible that this could cause long term harmful effects to the bird and is therefore
best to be avoided.

4 ) Fluoxetine (Prozac, Dista) is a psychotropic Drug which was developed in man for the treatment of
Obsessive Compulsive Behaviour (OCB). As feather plucking/ chewing can very much become an
OCB, then it is often indicated in the treatment of birds with this condition. It has been used at 0.4mg/
kg p/o od or bid, but has to be used for a minimum of 6 weeks in order to have maximum effect (or be
deemed not have the desired effect). It has the advantage that it is not meant to cause sedation, but has

been associated with causing loss of speak or reduction of speaking to the owner. Its use should be
reserved for when there is no evidence of physical trauma.

5) Tricyclic antidepressants. Where there is evidence of iritation or self mutilation then the use of the
tricyclic Antidepressants may be useful. This class of drugs has antihistaminic, Anticholinergic and
Local Anaesthetic properties which make them ideal for pruritic conditions. The main two are
Amitryptyline (Lentizol, Parke-Davis) 1 - 5mg/ kg p/o bid and Doxepin (Sinequan, Pfizer) 0.5 -
1mg/ kg p/o bid, both of which can be mixed in fruit drink or Millupa

6) Antipsychotics. Where there is evidence of behavioural problems and self mutilation, then
Haloperidol (Dozic, R.P. Drugs) 0.4 - 1 mg/ kg p/o od or bid should be considered. This is an
Antipsychotic, Neuroleptic and Dopamine Antagonist which is used in man to treat psychomotor
agitation. The Dopamine Antagonist action is particularly useful as the Neuropeptides (Dopamine) play
a part in self-mutilation. However, the use of this drug is more likely to cause sedation or even
extrapyramidal centre effects - Parkinson-like symptoms which will disappear on drug withdrawal.

Feather Loss Without Plucking

This group of conditions should be considered as manly the “non-behavioural” causes of feather loss.
These are usually either 1) parasitic 2) viral 3) neoplastic or 4) endocrine. Those conditions that are
also associated with crusting or ulceration will be dealt with later (ie Parasitic conditions).

Endocrine / Hypothyroidism.

This is very uncommon in avian cases and has only been well-documented in a scarlet macaw.
Thyroxine is important in the initiation of molting. Normal T4 values range from 0.1 to 1.1 ug/dl in
Amazons to 0.2 to 4.3 ug/dl in lovebirds

The classic clinical signs are a Non-pruritic feather loss where there is no evidence of pin feathers as
the molting has ceased and the feathers therefore may be in a “tatty” condition reflecting their age.
There may be Obesity and a thickened or fat-laden, skin.


Cases of true hypothyroidism, where there is a failure to moult, may be treated with thyroxine 0.025mg
daily; this usually causes the bird to moult within 30 days of treatment. Thyroxine therapy should be
continued until the bird has moulted out. Continued therapy with thyroxine (as in the norm in
mammals) can cause continuous moulting.

If a moult is required to be induced (other than for treatment of hypothyroidism) the Thyroxine at
100mcg/kg each 48 hrs for 2 weeks, can induce moulting.

                                 Reptilian Dermatology

                                         Martin P.C. Lawton
 BVetMed; CertVOphthal; CertLAS; CBiol; MIBiol; DZooMed; FRCVS, RCVS Specialist in Exotic
                                    Animal Medicine.
                      12 Fitzilian Avenue, Harold Wood, Essex, UK, RM3 0QS


        The older Class of Reptilia consists of approximately 6,547 species. It therefore greatly out
numbers the Class Mammalia. The reptilian Class is divided into:-

                 1. Order Squamata (6280 species) (includes Snakes and Lizards).
                 2. Order Chelonia (244 species) (Tortoises, Turtles and Terrapins).
                 3. Order Crocodilia (22 species) (Crocodiles and Aligators).
                 4. Order Spenodontia (1 species) (Tuartarta).


    The reptilian integument consists of the epidermis and the dermis. The outer layer of the
    epidermis has a covering of keratin. The keratin can be thick forming scales or dorsal ornamental
    structures. The Keratin consists of three layers

                 1) The Oberhauchen (Outer) layer,
                 2) The beta-keratin layer
                 3) The inner alpha-keratin layer.

These three layers of dead cells are known as the horny layer (Stratum corneum). This layer has been
designed to prevent desiccation, although in some species there is a high degree of permeability.
Against ultraviolet radiation. There is also very good protectionUnder the keratin layer is the stratum
germinativum. The stratum corneum and stratum germinativum form the epidermis

The dermal-epidermal boundary is marked by the basement membrane of the epidermis. The dermis
consists of mainly connective tissue, blood and lymph vessels and nerves. The dermis is usually thicker
then the epidermis. There may be dermal bones (osteoderms). Osteoderms are metabolically active.

Chromatophores are present in the dermis of many lizards that can allow a change of skin colour,
such as that seen in Chamaeleo spp. Control may be hormonal, neurological or both. They may also

react to stimulation from light or temperature. There are a mixture of melanophores, erythrophores,
xanthophores and iridophores.

In reptiles the skin commonly forms scales. The snake is covered completely by scales which over the
sides and dorsal surface are relatively small and are arranged like a mosaic but in an overlapping
fashion. These are just folds of skin that form a thin hinge between the scales. Ventrally there are large
belly scales (gastrosteges) which overlap the next caudal scale. Immediately in front of the cloaca
there is a pair of scales instead of a single scale. All the others underneath the tail are also paired. These
are called sub-caudals.

The skin of the head of crocodilians are fused to the cranial and facial bones. The skin of all
crocodilians is composed of separate, rough, leather-like scales. The scales are joined by elastic
connective tissue. The dorsal hide is cornified and lies above bony plates (osteoderms) the best
developed of these are in the cervical region. In Caiman there are also ventral osteoderms.

In all snakes and some lizards (ie geckos), There are no moveable eyelids but a fusion of the eyelids to
form a transparent area of the general integument known as a Spectacle (eye cap or brille).

Chelonian Shell

In Chelonia, large amounts of dermal bone have fused with the ribs and spinal column to form the
shell, which gives a protective advantage. The shell consists of the Carapace, which is the dorsal part of
the shell and ventrally the Plastron.

During embryonic development, the thick layer of integument that is to be the carapace grows laterally
until its rim projects from each side of the developing trunk. It is attached to the neural spines of the
trunk vertebrae. The lateral ends of the ribs become attached to or very closely associated with the
thickened dermis. As this grows laterally it raises the ribs and carries them up and over the limb
girdles, resulting in the unusual situation of the pectoral and pelvic girdles being medial to rib

Bony plates develop in the deepest part of the dermis from separate centres of ossification during late
embryonic and early post-natal life. Those associated with the ribs begin around these structures and
spread outwards from them. The plastron develops as a series of bony bars; elements of the limb
girdles become included.

While these dermal bones are developing the germinative layer covering them is producing the
epidermal cells which become heavily keratinised to form the horny laminae of the shell surface
(shields or scutes). The outlines of the shields seldom coincide with those of the bony plates and it is
thought this overlap increases the strength of the shell. Development of the shell is incomplete at

The carapace and plastron are continuous at the lateral bridges but separated widely cranially for the
neck and forelimbs and caudally for the tail and hindlimbs. In some species parts of the plastron are
hinged and allow slight movement. In a number of species the plastron may be reduced or it may be
modified to form a hinge to provide extra protection.

Skin glands of reptiles

There are very few skin glands when compared to mammals or amphibians. The relative lack of glands
results in the dry skin. Where they occur, they are dermal derivatives and have chemosensory, social
and recognition functions (producing phermones).

Crocodilians have two glands on the underside of the jaw. There are two musk glands in the cloaca.
These act to attract mates or ward off predators. Snakes have almost no skin glands although there are
two anal scent glands, located ventrally in the tail base.

Many lizards have femoral pores, but other glands in the skin are few. The femoral pores of Iguanids
produce a secretion which fluoresces under Ultraviolet light and is though to provide a visual method
of marking territory.

Reptilian Physiology


All reptiles are able to shed their skin (Ecdysis) although this is to a variable extent in the class of
Reptilia. Crocodilians and chelonians shed infrequently, squamates shed periodically. Thyroxine plays
a variable role in ecdysis. In Lizards, throxine stimulates shedding while as it inhibits shedding in

During ecdysis, the epidermis is shed. Factors that influence ecdysis include species, age, nutrition
plane, reproductive state, parasitic load, hormonal balance, health, ambient temperature and humidity.
Snakes need to shed their skin to allow growth. Young snakes moult soon after they are born or
hatched, and in the first year of life when growth is most rapid, there may be up to 7 moults or more.

In mammals, there is a continuous loss of the epidermal cornified layers and new generation of cells
from the germinative layers. In reptiles the Stratum germinativum is only periodically active. In
ecdysis, cells of the intermediate zone (upper stratum germinativum) replicate and form a new three
layer epidermis (inner epidermal generation), upon completion of this, lymph diffuses into the area and
enzymatic action results in the formation of a cleavage zone between the new inner epidermal
generation and the older outer epidermal generation, which eventually leads to a sloughing of the outer
epidermal generation. At the time of the lymph diffusing into the cleavage zone there is a bluing of the
skin and particularly of the spectacles, which is known as going opaque. This in an indication of an
impending slough. On the clearing of the lymph, shedding usually occurs 5 to 8 days later. In
squamates, there is a vascular change in the head which results in the blood vessels and sinuses
underlying the cranial epidermis to swell and the fracture the cleavage zone between the outer and
innner epidermal generations.

There is increase permeability of the skin during the growth and shedding phase. The shedding phase
requires about 2 weeks and then there is a resting phase which may vary from days to months.

In land Chelonia there is often a retention of the shed Keratin shields (scutes) which are seen as
sequential growth lines on these shields. The horny shields grow by increment of new substance to
their deeper surfaces, each newly formed layer being larger than and so visible round the periphery of
the last. There is a seasonal growth cycle, a layer being added each year as a general rule. However,
this is not closely followed and many factors can influence the scute production. The early layers,
which are therefore the more central and the more superficial, do also become detached. This makes

estimation of age from the rings very imprecise.

    In rattlesnakes, the last scales do not shed, but stay to produce the rattle. In other snakes the
    terminal scale is normally a hollow cone that is shed with the rest of the snake skin, but in the
    rattlesnake each moult leaves the old hollow cone in place and increases the length of the rattle.


Dysecdysis is the inability to shed normally. This is a multifactor condition. Failure to maintain the
humidity at between 50 to 65% will predispose to the retention of skin and failure to shed. Once the
skin has been retained 24hours beyond when it should have been shed, it will become dehydrated and
may cause constriction and interference of the blood supply to distal extremities.

Sick reptiles, especially those with hypoproteinaemia, will be unable to produce the full complement of
enzymes necessary to complete the breakdown between the new and old epidermal generations and this
will lead to a retardation of ecdysis or total failure.

Treatment is correction of the environmental conditions and treating any underlying causes (ie
parasites, bacterial infections).

Shell Trauma

Congenital Abnormalities

Congenital abnormalities in Chelonia are common, but are usually minor. They usually involve
additional shields or failure of fusion of the dermal plates.   It is common for hatchlings to have an
umbilicus and even a yolk sac attached which, over a period of 48 hours, should disappear leaving only
an umbilical scar which will be difficult to see after a month.


Although the shell is protective in nature, trauma is all too common. The degree of damage varies from
that just to the keratin (such as caused by over amorous male Testudo spp.) to more serious damage
resulting in penetration of the dermal bone (such as lawn mower injuries or dog bites). Traumatic
wounds to the skin should be cleaned and sutured when infection is either not present or has been

Assessment has to be made as to treatment. Often simple cleaning with povidone iodine is all that is
required, however, shell repair may also be necessary. Extensive wounds (such as full thickness) and
they are contaminated then shell repair may have to be delayed. When there is obvious infection, it is
best to take a swab for bacterial culture and sensitivity. Antibiotics by topical and sometimes systemic
route should be used on sensitivity. The use of wet to dry bandages is often useful in order to control
infection and remove infected tissue as well as providing protection to the exposed areas, especially if
full thickness. The use of silver sulphasalazine (Flamazine; Smith & Nephew) promotes granulation
but also has an anti psuedomonal activity.

Whenever the shell has to be repaired, it is best done under general anaesthesia and only after all
underlying infection has been controlled. Repair materials includes fibreglass, epoxy resin and light
curing material. The use of wire sutures may be employed to reconstruct shell. Where skin has been
avulsed from the shell, then drilling allows the placement of sutures to reappose the skin back onto the
shell. Healing of the shell is slow and may take several years.

Although the shell is protective in nature, trauma is all too common. The degree of damage varies from
that just to the keratin (such as caused by over amorous male Testudo spp.) to more serious damage
resulting in penetration of the dermal bone (such as lawn mower injuries). Assessment has to be made
as to treatment. Often simple cleaning with povidone iodine is all that is required, however, shell repair
may also be required. When ever the shell has to be repaired, it is best done under general anaesthesia
and only after any underlying infection has been controlled. Repair materials includes fibreglass, epoxy
resin and light curing material. Healing of the shell is slow and may take several years.

Bacterial Diseases

Where there is infection of the shell, it may be necessary to remove varying amounts of the overlying
keratin shields in order to explore the extent of the infection and allow treatment. Wherever possible
samples should be taken for cytology, culture and sensitivity. Some “shell rots” may be so extensive as
to result in large areas of death of the dermal bone and this requires the surgical removal of these
sequestrum in order to deal with the deep seated infection. Once the infection has been eliminated then
shell repair may be necessary.

Subcutaneous abscesses are extremely common, They can be as a result of bites, penetrating wounds or
iatrogenic injections or microchip implantation. The abscess is inspissated. The lack of lysozymes in
the granulocytic leukocytes cases caseous exudate formation. Chronicity causes a mononuclear
response and giant cell formation and some also develop a fibrous connective tissue capsule. Whatever
the cause of the abscess, surgical removal is the treatment. The fibrous capsule (of various thickness)
should also be removed. In sever cases there may be miliary and diffuse and difficult to remove in toto,
these may be associated with a septicaemic episode.

Cases of moist eczema may be associated with septicaemic disease and such cases should always have
a white blood cell count. Moist eczema may also occur in cases of hyeprvitaminosis A.

Cutaneous atypical mycobacteria (M. chelonei) have been associated with either primary or secondary
skin disease.

Dermatitis, although can be associated with parasitic infections, where there are blisters, ulcerations or
necrosis, this is usually associated with bacterial infections. This is often associated with a dirty
environment. The treatment should therefore include advise on improving hygiene.

Treatment of the underlying infection requires cleaning with antiseptic solutions and use of topical or
systemic antibiotics (ideally based on sensitivity), depends on the extent of the infection. Where there
is extensive loss of skin, treatment for fluid loss and dehydration may have to be undertaken.

Septicaemic Cutaneous Ulcerative Disease

SCUD is associated with Citrobacter freundii and Serratia spp. It is mainly seen in fresh water
Chelonia. The genera mainly infected are Trionyx, but it can also be seen in Chysemys and Trachemys.
Ulcers occur on the skin and the shell. These ulcers can become necrotising lesions. The infection often
becomes septicaemic. This may be a cause of paralysis, liver or kidney failure or septicaemic death.
Serratia spp. is thought to be a contributing bacteria as it has lytic activity and the Citrobacter sp. The
cause of the speticaemia.

Treatment requires cleaning of the lesions and systemic antibiotics (based on sensitivity). The main
prevention is improvement of the water quality.

Ventral Dermal Necrosis

This is seen in snakes and is thought to be associated with a necrotising skin lesion from a thermal burn
associated with heat mats or appropriate heating of the vivaria. A common organism is Pseudomonas

The early signs are petechiation , oedema or blister formation. If the dermal infection is not treated at
this time, then ecchymotic haermorrhages and sloughing of the top dermal layers will occur. With
progression of the disease, then infection may progress to a full thickness necrotising dermatitis go
through the dermal layer and into the underlying muscle massesand eventually result in septicaemia
and death.

Ear Abscesses

Although this is strictly a middle ear infection, the presenting signs are associated with a stretching of
the tympanic. This is an enlarged cutaneous scale or transparent tympanum caudoventral to the eye. In
severe cases there is not just a stretching of the skin but often an ulceration or rupture of the skin
exposing the inspisated mass within the middle ear.

It is thought that the majority of infected Chelonia are immunosupressed (due to suboptimal
temperatures) and they get a secondary infection. Hypovitaminosis A may also predispose.

Viral Disease

Gray Patch Disease of Green Sea Turtles

This is caused by a Herpesvirus and is seen in green sea turtles (Chelonia mydas). This virus mainly
affects young turtles between 56 to 90 days of age. The skin lesions start as a small circular papular
lesion containing epidermal cells with basophilic intranuclear inclusions. Epizootics occur in the


First described in crocodilians (Caiman & Nile Crocodiles. It causes a greyish circular lesions scattered
over the skin. Lesions can also involve the oropharynx. Large eosinophilic intracytoplasmic inclusions
are seen on histopathology.

It has also been reported in an amelanotic California desert tortoise (Xerobates agassizi). Multiple
raised papular to vesicular lesions of the skin on the head, neck, legs were found.

Papillomavius has been isolated from skin lesions in Boolivian side necked turtles (Platemys sp) as
well as the European green lizards (Lacerta viridis). In the European green lizard there is a sex linked
distribution of the lesions; in the females the lesions are in the caudal part of the body (mainly tail base)
while as in the males they are around the face (particularly the eyelids). Papillomata of the ventral
scales are not seen.

Parasitic Disease


These external parasites can be responsible for skin irritation. They can also be responsible for the
transmission of disease, especially Aeromonas hydrophilla. The snake mite, Ophionassus natricis, is
particularly a problem and can be very difficult to eliminate. The eggs are layed off the host and
contaminate the environment. The life cycle is temperature dependant and can be between 10 to 32
days. The mites may be difficult to see especially as then tend to lie inbetween scales and in the sulcus
formed between the spectacle and the periocular scales.

It must be remembered that these mites are an environmental problem and therefore treatment must be
aimed at treating the environment as well as the animals themselves. Treatment depends upon the
parasite found. Although ivermectin can be used in Squamata, it should never be used in Chelonia, as
this drug can induce an irreversible hindlimb paralysis. Ivermectin or a suitable ectoparasite can be
used for mites both on the animal and the environment.


Hard ticks are of the genera Ixodes. Soft ticks of the genera Argasidae and Ornithodoros. Some species
are host specific, many are not. Ticks can cause damage to the host’s skin, transmit blood parasites,
viruses or bacteria. These are mainly seen in imported species.

Visceral Larval Migration

Various nematodes, such as Kalicephalus spp. Can undergo percutaneous migration. This can result in
blistering of the skin and may lead to a secondary infection.

Filarial nematodes can cause a dermal necrosis from the physical effect of blocking blood vessels and
lymphatic vessels.

Subcutaneous swellings can be associated with spiruroid nematodes or pleurocercoids of tapeworms.

Myiasis ??

Fly strike and the presence of maggots are frequently seen in summer affecting debilitated reptiles with
wounds or diarrhoea.

Fungal Infections

Clinical signs are similar to bacterial dermatoses. There are relatively few reports of cutaneous mycotic
disease in chelonia. However, fungal association with shell necrosis is more common. Often there is a
mix infection with Enterobacteriaceae present as well.

Dermatophytes that are frequently encountered include Mucor spp., Fusarium spp., Trichosporon spp.,
and Geotrichum spp. while as rarely isolated are Microsporum spp., Trichophyton spp. Algae are also
frequently seen on the shells of aquatic and semiaquatic species, but seldom causes any problems.

Fungal culture is required to make the diagnosis or on cytology or histopathology and seeing the fungal
hyphae. Like bacterial dermatoses, the majority of infections are secondary to poor captive husbandry
and in particular poor water quality for aquatic species. Treatment requires improving the environment
and cleaning with povidone iodine (which does have some antifungal activity) and where necessary,
the use of topical antifungal creams and ointments.

                                     Fish Dermatology

                                           Martin P.C. Lawton
 BVetMed; CertVOphthal; CertLAS; CBiol; MIBiol; DZooMed; FRCVS, RCVS Specialist in Exotic
                                    Animal Medicine.
                       12 Fitzilian Avenue, Harold Wood, Essex, UK, RM3 0QS

Integument Of Fish

Like that of any other vertebrate the skin, that of fish also consists of epidermis and dermis. The
stratified squamous epithelium of the epidermis differs from that of mammals in consisting at all levels
of living cells, capable of active division. Mucus secretory cells are also present. The outer surface of
the integument is covered by a very thin mucopolysaccharide layer that may be referred to as the
cuticle. It contains sloughed cells, secretions from the surface epithelial cells and also mucus. In
addition to reducing body friction in the water, it is protective and is also thought to have anti-pathogen

The dermis can be divided into two; a relatively thin outer layer of loose connective tissue, the stratum
spongiosum and a thick deeper one, the stratum compactum. The stratum spongiosum contains the
pigment cells (chromatophores). The pigments are mainly carotenoids from the food as the fish
cannot manufacture them. Some chromatophores contain the purine crystals responsible for the
reflective iridescence of parts of the skin.

The scales are also in the stratum spongiosum. There are no scales on the head or on the fins. Scales are
flat, nearly circular plates of bone, which is laid down in concentric rings, representing differential
seasonal growth rates. They overlap one another from cranial to caudal so that only a small caudal part
lies immediately under the epidermis: the rest is deep to the scales in front. The scales of trout which
have a smooth contour are known as cycloid, while as species with stiff spikes projecting caudally
from the exposed edge of the scale are known as ctenoid. During growth, scales increase in size but not
in number.

The deeper stratum compactum of the dermis is a thick matrix of dense collagenous tissue and this
provides most of the strength of the skin. The deepest parts form the more loosely arranged
hypodermis, and this binds the rest of the integument to the underlying muscles. It may itself be quite
vascular and contain adipose tissue.

Bacterial Infections

This can be primary or secondary pathogens. Excess mucus (“slime disease” ) will often be seen as this
is a sign of an unhealthy skin layer. Long term infections will lead to loss of mucus and a roughened
appearance which will predispose to further infection. Ulceration of the skin is common and can lead
to septicaemia and death. Mycobacterium sp. is the commonest organism encountered. Pseudomonas
spp. Aeromonas sp. Nocardia asteroids and Flavobacterium sp. are also found.

Acute Systemic disease is usually a secondary infection of a debilitated fish but can also be a primary
pathogen. The presenting signs are ulceration, eryhtema and petechiation of the skin and fins. Death if
usually from either severe osmoregulatory disorder or the septicaemia. Aeromonas spp. Are associated
with Spring Viraemia of Carp (caused by a Rhabdovirus).

Viral Infections

Carp Pox
Herpesvirus cyprini is the cause of Carp Pox. This is a chronic disease affecting mainly the older fish.
In the early stages the lesions are seen as whitish/ grey plaques. The are benign epidermal hyperplasia
and are restricted to the epidermis although they can get quite big and develop into tumors and can
cover large areas by coalescing. The infection can be latent and immunological response towards these
lesions is weak.

Lip fibromata have been associated with retrovirus like particles. Papillomata are also frequently

Parasitic Disease

Signs of parasitic disease may be “flashing” or ulceration and secondary infections. Protozoal
infections are very common.

Protozoal infections

Ichthyophthirius multifiliis and Tricodin Trichodenella and Tripartiell are all too frequently involved.

Ichthyophthirius multifiliis is a ciliated protozoa that causes white spot (“Ich”) in fish. This is not just
restricted to the skin and there is penetration of the epidermis and the gills. The life cycle is
temperature dependant and is between 6 to 15 days

Anchor Worm

Lernaea cyprinacea is a parasite of carp. It causes irritation and even small number can cause serious
damage. The female attaches by the head which causes an intense inflammation which could progress
to a granuloma or necrosis of tissue. A egg sac is readily visible. It is unable to complete its life cycle
with water temperatures less then 15oC.

Fungal Infections

It is not uncommon to see “cotton wool” like lesions associated with superficial fungal infections or
myxobacterial infections. This is usually secondary and requires damaged tissue. Aphanomyces sp,
Rhizopus sp., Phoma sp, Saprolegnia sp. and Achyla sp. are often found.

Ichthyophonus sp. invades the body and will cause granulomatous lesions within the body. The damage
to the skin lead to loss of the mucus layer and dark colour lesions which form abscesses or may

Equine Dermatology

The Clinical Approach
To the clinician unfamiliar with equine patients, the horse with skin disease can be a daunting
challenge. However, for the experienced dermatologist this need not be so, since the principles
involved in the approach to a horse with a skin problem are essentially similar to those applied to small
animal cases. Just as in the canine and feline patient, the history of the case obtained from the owner or
person caring for the horse is vital. It is worth noting that the owner may not be the person having day
to day care of the horse and it is essential to obtain details of history and management from the
person(s) having that frequent daily contact with the animal. After obtaining the history, a thorough
clinical examination is conducted, a problem list created and potential differential diagnoses considered
prior to undertaking further investigations. If a definitive diagnosis is reached specific therapy can be
instituted, or appropriate empirical or symptomatic therapy whilst the results of diagnostic tests are

Age, sex, breed and type of horse, the duration of ownership and the purpose for which it is kept should
be established, and where possible details of previous medical history. The nature of the problem at
onset and progression of the disease are obviously important and, in particular, the time of year and any
seasonality that may have been noted. Presence or absence of pruritus is an important diagnostic
consideration. The management of the horse,
•   whether stabled full time, or out at pasture;
•   contact with other horses and whether in contact animals show any signs of disease;
•   nature and type of bulk and concentrate foods;
•   type of bedding used in stables;
•   whether tack and grooming kits are shared
all may have a bearing on the skin lesions present.
It is particularly important with equine patients to attempt to gain information on all treatments or
medications that have been used and whether there was any improvement or deterioration noted with
any. Horse owners often try a number of over-the-counter or alternative remedies in addition to
prescribed treatments and it is not unusual to have the input of more than one veterinarian. It can
sometimes be difficult to obtain a clear picture of the plethora of medicaments that may have been
used! Details of general health of the animal and any previous medical problems should also be
obtained. A pro-forma sheet is most helpful in obtaining and recording the pertinent points of history

A general clinical examination should be conducted, although rectal examination may only be
performed if other findings indicate it to be necessary. Particular note should be taken of the superficial
lymph nodes. If sedation is anticipated the cardiovascular system should be evaluated.
Dermatological examination is facilitated by the use of an outline diagram, which can be combined
with the history form. The nature and distribution of all lesions should be recorded, making note of
primary and secondary lesions. Special attention should be paid to the mucocutaneous junctions and
junctions with other specialised cutaneous structures such as the coronary band, frogs, chestnuts and

It is helpful to make a problem list from the information obtained thus far and then draw up a list of
differential diagnoses, starting with the most likely. The list will usually extend to half a dozen
conditions in the first instance, allowing selection of appropriate diagnostic tests, but may need to be
modified or extended, depending upon results. This is the juncture at which communication with the
owner is of great importance. There is often pressure to come up with a diagnosis, there and then, but
this is not usually possible without some further investigation. Sometimes the client needs to be
educated about the concept of differential diagnoses and the importance of reaching a definitive
diagnosis, since only with this can a proper plan for specific therapy be prescribed and a prognosis

There is a large amount of additional information that can be obtained relatively easily by the
performance of a few simple diagnostic procedures (2). The choice will depend upon the nature of the
lesions present, and may direct the need for further tests, but in nearly every case microscopical
examination of material is indicated. The procedures that may be employed are outlined below:

Procedure                          Indications                            Comments
Skin scrapings: superficial/deep   Crusting and scaling lesions           Use wooden spatula or comb for
                                                                          collection of surface material; view
                                                                          directly or mounted in liquid paraffin
Adhesive tape strip preparations   Scaling lesions                        Good technique for capturing
                                                                          chorioptic mange mites; may identify
                                                                          fungal elements on stained preparations
Hair plucks                        Alopecia                               Use forceps, but with protected jaws.
                                                                          Assess anagen/telogen roots and
                                                                          condition of hair tips. Examine for
                                                                          fungal elements - hyphae and
Cytology                           Crusting lesions, pustular lesions,    Stain with a rapid stain and examine
                                   exudative lesions, exfoliative         for inflammatory cells, acanthocytes,
                                   cytology of surface of masses or       micro-organisms. Wet preparations in
                                   biopsy samples                         saline helpful for dry crusts, good for
                                                                          identification of Dermatophilus
Bacterial culture                  Exudative lesions, draining tracts     Helpful to submit tissue samples as
                                                                          well as swabs for culture. Need special
                                                                          conditions for isolation of
Fungal culture                     Alopecia, crusting, scaling, papular   Scalp brush useful for sampling.
                                   lesions                                Inoculate both DTM and Sabouraud’s
                                                                          dextrose agar; note -some fungi
                                                                          sensitive to cycloheximide. Some
                                                                          strains of T. equinum need extra B
Skin biopsy                        Nodules, masses, vesicular and, or     Best taken early in course of disease,
                                   ulcerated lesions, unusual or severe   no surgical preparation, multiple
                                   dermatoses                             samples, punches or excisional.
                                                                          Provide full history.
Allergy tests                      Recurrent urticaria, pruritus          Dietary restriction and provocation,
                                                                          environmental changes. Intradermal
                                                                          skin testing


With a careful and thorough approach as outlined above, the information gained will enable the
clinician to reach a definitive diagnosis, discuss the prognosis and therapeutic options with the owner
and initiate an appropriate plan for treatment. Ongoing monitoring and reassessment may indicate the
need for further investigations during the course of the disease and modification of the diagnosis, and
for some of those really challenging cases involvement of a specialist may be helpful!

1.   Lloyd D H, Littlewood J D, Craig J M and Thomsett L R. Practical Equine Dermatology.
     Blackwells Science (In Press)
2.   Littlewood J D. Diagnostic procedures in equine skin diseases. Equine vet Educ 9: 174-176 (1997)
3.   Evans A G and Stannard A A. Diagnositic approach to equine skin disease. Compend Contin Educ
     Prac 8: 652-661 (1986)
4.   Scott D W. Large Animal Dermatology W B Saunders Co (1988)

Pruritic Diseases
Pruritus is the commonest presenting sign in equine skin disease. Signs may include:-
         • Behavioural changes: irritability, restlessness, kicking and stamping, rubbing, biting
         • Physical signs: excoriation, exudation, crusting, bruising, swelling, haematoma, hair loss,
           broken hair, skin thickening, scaling
Severity may be difficult to gauge from the history. Pruritus needs to be differentiated from pain; both
may be present. Approached horses with painful lesions with great care. Sedation may be necessary.

Contagious Conditions



Clinical Features
•    Mild to severe pruritus, patchy alopecia, excoriation, exudation, in-contacts affected; ill temper,
     loss of condition and, if severe, anaemia (sucking lice only)

     Werneckiella (Damalinia) equi
     Biting louse: small (c. 1.8mm long), rounded head, usually many lice; affects dorso-lateral trunk
     and neck, especially under the mane, and the head

     Haematopinus asini
     Sucking louse: large (c. 3.2mm long), more visible, fewer lice; usually affects base of mane, tail,
     fetlocks. Populations high and extensive in long winter coats

•    Signs, history (underlying problem causing debility?)
•    Find lice and nits, and identify microscopically

Treatment & Control
•    Topical insecticides containing cypermethrin (Deosan Deosect, Fort Dodge ; Barricade, Sorex),
     permethrin (Fly Repellent Plus for Horses - Coopers, Schering-Plough Animal Health) and
     pyrethrins (Dermoline Shampoo for Horses, Day Son & Hewitt); pruritus stops in <36h, transient
     urticaria has been reported.

•   1% selenium sulphide shampoo (Seleen, CEVA Animal Health) shown to work for biting lice.
    Whole body shampooing on 3 occasions at 10 day intervals, contact time 5 - 10 min before rinsing.

•   Ivermectin 200µg – 300µg/kg repeated after 14 days for sucking lice.
•   Fipronil spray can be used but volume required can be considerable.
•   Treat in-contacts, rugs, harness, saddlery



Clinical features
•   Infestation with Chorioptes equi affects the distal parts of the limbs but may spread to other
    regions. The hind legs are more often involved and heavily feathered legs are especially
•   The problem is clinically apparent particularly during the colder times of the year.
•   Affected animals show signs of pruritus with stamping, and rubbing or biting at the affected areas
•   Lesions include scaling and crust formation in the pastern, fetlock and cannon regions
•   Exudative, proliferative dermatitis with secondary bacterial infection (“Grease”) may develop in
    severe cases

•   History and signs.
•   Demonstrate the mite in scrapings from fresh lesions which can often be found on edges of more
    chronically affected skin

Treatment (no licensed products)
•   Topical
    Clip the affected area first. The following treatments have been reported effective:
    1% selenium sulphide shampoo whole body washes (Seleen, CEVA Animal Health), repeated
    three times at 5 day intervals, allowing a skin contact time of 10minutes prior to thorough rinsing .
    Fipronil (Frontline Spray; Merial Animal Health) applied to dampen haircoat and skin surface;
    may need to repeat.
    6% Flumethrin (Bayticol Scab and Tick Dip, Bayer). Dilute 1:900 (66µg/ml), apply up to 2mg/kg
    (30ml/kg), repeat after 14 days
•   Systemic
    Ivermectin (Eqvalan Paste for Horses, Merial; Furexel, Janssen; Panomec Paste for Horses,
    Merial) at 200µg – 300µg/kg orally, may provide relief in 4-7 d and needs to be repeated after 10-
    14 d. Treatment reduces the mite load by over 95% and provides an efficient means for the
    treatment of large groups of horses
•   Treat in-contacts and dispose of bedding to prevent reinfestation

• May occur in imported horses; very rare in Western Europe
•   Sarcoptes scabiei causes pruritus with papules, crusts, alopecia, excoriation and lichenification
    beginning on the head and neck and extending caudally
•   Psoroptes equi causes severe pruritus, crusting and alopecia, especially of the head (ears), mane
    and tail. Rapid transmission occurs

•   Can be found in horses ears and may cause no problems or lead to head shaking, and ear rubbing.
    Affected animals may have a lop-eared appearance.

•   Signs and history indicate an ear problem. Mites can be obtained from deep within the ear and are
    visible as white moving dots. They can be identified by microscopy. Sedation and otoscopy may
    be necessary.

•   Clean debris and wax from ears. Instil eardrops containing acaricide and repeat after 10 days.

Free-living mites


Clinical Features
•   Larvae usually acquired from infested pasture in late summer or autumn
•   Can cause severe pruritus often indicated by stamping
•   Signs include papules, wheals and alopecia which may affect limbs, head and sometimes the
    ventral abdomen
•   Larvae may be visible as red dots (<0.5 mm) on affected skin

•   History, signs, demonstration of the 6-legged larvae in scrapings

•   Larvae drop off after feeding but therapy is usually warranted. A single treatment with a topical
    antiparasitic preparation e.g. fipronil (Frontline Spray, Merial), cypermethrin (Deosan Deosect,
    Fort Dodge ; Barricade, Sorex), permethrin (Fly Repellent Plus for Horses, Coopers, Schering-
    Plough Animal Health) or pyrethrins (Dermoline Shampoo for Horses, Day Son & Hewitt) is
•   Areas infested with these mites should be avoided in the late summer and autumn, if possible

•   These free-living mites e.g. Pyemotes or Acarus spp., may be present in hay and bedding
•   Can cause papular and crusty lesions, which may be pruritic, in areas of skin in contact with the
    contaminated material (e.g. feet, muzzle)

•   Differentiate from other papular and crusting conditions affecting feet, muzzle
•   Demonstrate mites (0.3-0.6mm long) in skin scrapings and samples of hay and bedding

•   Replacement of contaminated material leads to recovery in a few days

•   The red mite of poultry attacks at night and generally causes pruritus of the head and limbs. The
    mites are not normally present on the horse during the day

•   Signs together with a history of contact with poultry housing is usually highly indicative
•   Mites are just visible with the naked eye. Examine scrapings and coat brushings taken at night

•   As for Neotrombicula autumnalis infestation
•   Exclude contact with poultry. Horses may need to be moved away if the mite infestation cannot be

Helminth infestation


Clinical Features
•   Female worms emerge from the rectum and lay cream-coloured eggs in perineum causing pruritus
•   The horse rubs its tail (rat tail) and becomes restless or ill tempered
•   Infestation occurs especially in stabled horses where rapid transmission of the eggs can occur; eggs
    are sensitive to desiccation

•   Signs are highly suggestive. Examine eggs using tape strip samples from the perianal region
•   Differentials: Culicoides hypersensitivity, other allergies, lice

Treatment & Control
•   Improve stable hygiene. A normal equine worming routine should give good control.
•   Dealing with a specific infestation: ivermectin paste (Eqvalan Paste for Horses, Merial; Furexel,
    Janssen; Panomec Paste for Horses, Merial) given at 200-300 µg/Kg orally given twice at 3-6
    week intervals, or moxidectin gel (Equest, Fort Dodge) at 0.4 mg/kg orally every 12 weeks.


Clinical Features
•   Now uncommon
•   Hypersensitivity (types I and III) to microfilariae affecting ventral midline, chest and withers
•   Pruritus, patchy alopecia, small papules, thickened dry scaly skin, poor hair regrowth, concentrated
    in ventral midline.
•   If severe, marked pruritus, excoriation, crusts. Tail rubbing is rare.
•   A summer problem

•   History, signs.
•   Biopsy and presence of helminth larvae (in skin with characteristic lesions).
•   Can examine minced skin, suspended in PBS for 3h at 37oC, filter coarsely, centrifuge 5 min at
    3,000 rpm, examine deposit at 60-100 x magnification for larvae.
•   Differentials: sweet itch, trombiculidiasis. N.B. Insect hypersensitivity and onchocerciasis can both
    be associated with Culicoides and so may coexist.


•     Ivermectin paste (Eqvalan Paste for Horses; Merial, Furexel; Janssen, Panomec Paste for Horses;
      Merial) given at 200-300 µg/Kg every 6-8 weeks or moxidectin gel (Equest, Fort Dodge) 0.4
      mg/kg every 12 weeks (Monahan et al. 1995) is effective in killing the larvae. Most cases resolve
      with one treatment, however, regular treatment is needed as the adult worms are not killed by
      ivermectin and thus condition may recur (Lyons et al.1988)
•     Acute exacerbation said to be encountered sometimes in first few days, may need glucocorticoids.


Clinical Features
•     Under unhygienic conditions (muddy yards, contaminated bedding) free-living nematode larvae
      can invade equine skin and cause irritation
•     Marked pruritus, papules, pustules, ulcers, crusts, alopecia, erythema of limbs, ventrum.

•     Demonstrate motile nematode larvae in skin scrapings; biopsy specimens.

•     Clean and disinfect skin (e.g. can use antimicrobial cream). Signs regress over days to weeks.
      Clean and rectify environment.

Microbial Infections
Microbial infections in which pruritus may be a feature are listed in the table.

    Fungal Disease     Causative Organism            Bacterial Disease       Causative Organism
    Superficial        Trichophyton and              Folliculitis and        Pathogenic
                       Microsporum.                  furunculosis            staphylococci;
    Deep               e.g. Pythium insidiosum,      Dermatophilosis         Dermatophilus
                       Basidiobolus haptosporus,                             congolensis.
                       Rhinosporidium seeberi

Non-Contagious Conditions

Clinical features
•     Insects involved: horse fly (Tabanus), stable fly (Stomoxys), midges (Culicoides), horn fly
      (Haematobia), black fly (Simulium), mosquitoes, wasps, bees
•     Signs may include:
      Bite marks (Figure 13[CD6]), bleeding, presence of a sting, pain, swelling
      Stamping, restlessness, irritability. Horses may choose to stand in smoke which drives away flies

Treatment & Control
•     Depends on severity and pain
•     Tabanus and Stomoxys
      Topical anti-inflammatory or analgesic cream
      Sedation e.g. acepromazine 10mg/125kg i/m

•   Generally
    Repellents and/or persistent insecticides e.g. synthetic pyrethroids
    Change environment - dispose of manure, cut vegetation, use environmental insecticides,
    depending on the life cycle of the insect(s) responsible e.g. for Tabanus remove decaying
    vegetation and manure

Synonyms: sweet itch, insect-bite hypersensitivity

Clinical Features
•   Occurs in areas where Culicoides spp. attack occurs. Populations and attack are promoted by
    waterlogged ground and low wind speeds. Biting is diurnal and restricted to early morning and late
    afternoon in the summer and autumn in the U.K.
•   Hypersensitivity occurs principally in horses over 6 months of age
•   Signs include
    Pruritus indicated by rubbing and the presence of broken hairs especially in the mane and tail (rat
    Papules, crusts, exudation and skin thickening dorsally (ears to tail); ventral lesions can occur.
    Note that some spp. of Culicoides bite ventral areas
    Horses may show irritability, restlessness and weight loss

•   History, signs, presence of midges in the environment
•   Feeding midges burrow into mane and forelock to feed - part hair and search
•   Intradermal tests - cross-reaction occurs between different Culicoides spp. Culicoides extracts not
    readily available.
•   Differentials: Oxyuris equi infestation, bites or hypersensitivity to other insects, atopy (may co-
    exist), contact dermatitis

•   Prevent access to horses by Culicoides
    Stable horses 4 p.m. to 8 a.m.
    Cover horses with rugs and hoods
    Fine mesh screen for stables or install fans in stables to create a breeze.
    Repellents and insecticides such as cypermethrin (Deosan Deosect, Fort Dodge: Barricade, Sorex),
    permethrin (Switch, Day Son & Hewitt: Fly Repellent Plus for Horses, Coopers, Schering-Plough
    Animal Health), residual insecticides, light oil, citronellol with permethrin or alone (Fly Repellent
    Plus for Horses, Coopers, Schering-Plough Animal Health; Extra Tail, Kalium).
    Consider moving horses away from infested area
•   Anti-inflammatory and antipruritic therapy
    Antihistamines have limited effect. Hydroxyzine hydrochloride (Atarax, Pfizer) 200-60 mg/kg
    orally, divided into two or three daily doses, said to be effective Other antihistamines that have
    been tried are: pyrilamine maleate, 1 mg/kg bid; diphenhydramine 0.75-1 mg/kg bid; doxepin
    hydrochloride 0.5-0.75 mg/kg bid; chlorpheniramine 0.25 mg/kg bid.
    Prednisolone or methylprednisolone at 1 mg/kg once daily until control achieved, reducing to
    alternate day therapy when necessary

    Topical soothing creams containing benzoyl benzoate (Sweet itch plus, Pettifer; Killitch, Carr &
    Day & Martin), shampoos containing colloidal oatmeal (Dermasoothe, Vericore VP; Episoothe ,

Clinical Features
•   Reactions to a wide variety of agents including pollens, moulds and dusts, and forage mites
•   Signs
    Recurrent pruritus and/or urticaria; variable seasonality. No other primary signs.
    Secondary lesions: excoriation, scaling, alopecia, papules, lichenification, skin thickening,

•   History, signs; eliminate other pruritic diseases
•   Intradermal tests
•   Biopsy: superficial perivascular dermatitis, predominantly eosinophilic.
•   Differentials: food hypersensitivity, ectoparasites, Oxyuris irritation, insect bite hypersensitivity,
    contact dermatitis.

Treatment and Management
•   Allergen avoidance e.g. change bedding material, accommodation....
•   Anti-inflammatory therapy
    Prednisolone at 1 mg/kg SID until control achieved then reduce to lowest dose alternate day
    regimen. Alternatively, dexamethasone 0.02 – 0.1 mg/kg orally or intramuscularly as a loading
    dose with maintenance at 0.01-0.02 mg/kg every 48h-72 hours
    Antihistamines: not generally successful but hydroxyzine (200-400 mg/kg twice daily, orally) may
    be useful in chronic pruritus and urticaria
•   Immunotherapy can be effective
•   Essential fatty acids do not seem useful generally but may help some horses

Clinical features
•   A poorly documented disease
•   May cause urticaria and pruritus
•   Diagnosis is rarely confirmed

•   Exclude other pruritic and urticarial diseases
•   Carry out food exclusion trial for at least three weeks e.g. only alfalfa hay
•   Confirm by provocative challenge

Treatment and Management
•   Change diet

Clinical Features

•   Local lesions; allergic and irritant reactions may co-exist
    pruritus ; maculopapular rash, vesicles, exudation, crusting
•   Contact sites affected. May relate to harness and tack. Promoted by moisture (sweating) and can
    affect both haired and hairless areas
•   Sensitisers include: dyes and preservatives, soaps, topical medicaments (insect repellents), plants
    and forage

•   Signs, sites; confirm by biopsy, patch tests, exclusion of suspected agent

•   Remove source of allergen
•   Clean sites and apply topical glucocorticoids - short term
•   Systemic prednisolone at 1 mg/kg orally once daily until control achieved if allergen cannot be

Clinical Features
•   Urticaria (Figure CD12): wheals, varying in extent, which pit on pressure and are transient. In
    inhalant allergy they resolve within 12 - 24 hours after exposure to the relevant allergen.
•   Angio-oedema: large oedematous swellings involving leakage of serum or blood
•   Lesions especially on neck, trunk, head but can affect any part of the body. May be pruritic
•   Causes: hypersensitivity, physical factors (light, heat, exercise, pressure), stress, topical and
    systemic drugs, chemicals (including soaps, leather conditioners) insect bites, infections (e.g.
    strangles, dermatophytosis), vaccines, feed.

•   History, signs, urticarial lesions pit on pressure, presence of causative factors, rule-outs. Biopsy
    not diagnostic but helps with rule-outs.

•   Eliminate cause
    Prednisolone at 1mg/kg once daily until control achieved. Alternatively, dexamethasone 0.02 – 0.1
    mg/kg as loading dose then maintained at 0.01-0.02 mg/kg every 48-72 hours
•   Hydroxyzine hydrochloride (Atarax, Pfizer) 200-400 mg/kg bid may help
•   Prognosis
    Urticaria: good but often difficult to identify cause and may recur
    Angio-oedema: variable depending on severity and location

References & Further Reading
Paterson S & Orrell S., 1995. Treatment of biting lice (Damalina equi) in horses using selenium
sulphide. Equine Veterinary Education 7, 304-306
Curtis CF., 1999. Pilot study to investigate the efficacy of a 1% selenium shampoo in the treatment of
chorioptic mange. The Veterinary Record, 144, 674-675.
Littlewood JD, 1999, Control of ectoparasites in horses, In Practice, 21(8), p418-424,).
Littlewood JD, Rose JF & Paterson S., 1995, Oral ivermectin paste for treatment of chorioptic mange
in horses, Veterinary Record 137, 661-663.

Littlewood JD, 2000, Chorioptic mange: successful treatment of a case with fipronil. Equine Veterinary
Education, 12 (3) 144-146.

Crusting and Scaling Dermatoses

Crusts are formed as a result of drying of exudate over erosions or ulcerations. Scales are the result of
abnormal keratinisation of the epidermis and may be due to primary defects or secondary to other
disease processes. Crusting and scaling lesions are commonly encountered in equine skin diseases.

Primary keratinisation disorders are uncommon in the horse. A few syndromes are recognised where no
underlying disease process can be identified.
Cannon keratosis is an idiopathic condition affecting the anterior aspect of the metatarsal and, or, the
metacarpal regions, the major differential for which is dermatophilosis. It is not related to urine
splashing since it occurs in both sexes and on forelimbs as well as hind. A further differential is photo-
activated vasculitis. Management is symptomatic with use of topical therapies.
Linear keratosis is characterised by a unilateral, linear, vertical band of hyperkeratosis over the neck
or trunk. The lesion is asymptomatic The condition may have a genetic component since it is most
frequently recognised in Quarter horses and the lesion may be manifestation of an epidermal nevus.
Topical symptomatic therapy may be used to reduce the surface hyperkeratosis.

Mane and tail seborrhoea is charecterised by the presence of scale in the mane and , or tail , which may
be dry or oily. Treatment consists of frequent and regular washing with keratolytic shampoos and use
of emollient conditioners.

Idiopathic generalised seborrhoea is a rare condition, which can only be diagnosed after ruling out all
causes of secondary seborrhoea. Treatment is symptomatic.

Initially thought to be related to urine splashing affecting the cranial aspect of the metatarsal regions
(Stud crud) , there is no sex, or breed or age, predisposition. The condition is typified by areas of
scaling and crusting with variably hair loss, usually asymptomatic, affecting both hind cannon regions.
The cause is unknown and treatment is symptomatic and lifelong, consisting of application of
keratolytic shampoos or ointments. Topical glucocorticoids may be helpful.

The aetiology of this condition is unknown, but the lesion may be manifestation of an epidermal nevus.
Histologically a lymphocytic, murine folliculitis is seen.. Quarter horses are predisposed, usually young
adults. The lesion appears as an asymptomatic, unilateral linear band of hyperkeratosis with variable
alopecia, predominantly affecting the neck and lateral trunk.
        Treatment with keratolytic shampoos or ointments and topical glucocorticoids usually results
in improvement.

Infectious causes

A number of dermatophytes have been isolated from horses with clinical disease:
•   Trichophyton equinum is the most common.
•   T. mentagrophytes is less common
•   T. verrucosum may cause lesions in horses in contact with cattle
•   Microsporum equinum , which is one of the dermatophytes that causes fluorescence of infected
    hairs under a Wood’s lamp
•   M. canis and M. gypseum infection may also occur, although earlier reports of M. canis isolation
    may actually have been M. equinum.

Clinical signs
Scaling and crusting are consistent features, though of variable severity. Early lesions may be urticarial.
The hairs are typically raised; lesions extend peripherally. The crusting can be quite variable, with
subsequent hair loss and broken hairs. Pruritus may sometimes be present, particularly when the girth
region is involved. Infected horses represent a zoonotic risk as well as a source of infection for other
horses. The incubation period is usually about 10days but may be up to 4 weeks.

Management of outbreaks of dermatophytosis can present a significant challenge and some racehorse
yards accept infection of young horses coming into training as an inevitability. The disease is usually
self-limiting in otherwise healthy animals, but topical therapy is indicated to limit spread and
environmental contamination. Topical chlorhexidine - miconazole shampoos have been shown to be
extremely helpful in the control of infection in groups of horses, used as a whole body shampoo twice
weekly until resolution. Other topical antifungal agents include natamycin (0.01% solution applied by
spray or locally , repeat after 4-5 days and 14 days if necessary) and enilconazole (wash with 0.2%
solution every 3-4 days on 4 occasions).
          Griseofulvin 10mg/kg is a registered product, with recommendation to treat for 7 days, but 3-
12 weeks may be needed to achieve mycological cure. The product is contra-indicated in the presence
of renal or hepatic impairment and in pregnant animals.
         Infected animals should be isolated from others. Environmental decontamination can be
achieved with hypochlorite bleach, gluteraldehyde disinfectants, horticultural miconazole foggers and
formaldehyde fumigation. To limit spread, tack and grooming equipment should be restricted to
individual animals, with provision of separate protective clothing for personnel.

Infection of the epidermis by Dermatophilus congolensis requires the presence of moisture and surface
damage in addition to the spores, which are ubiquitous and long-lived. The condition can be considered
to be endemic in certain areas. Synonyms for the disease are rain scald affecting the dorso-lateral trunk
and mud fever or rash, involving the limbs. The problem is prevalent in wet autumn and winter
months and predisposed by minor trauma from gravel, soil, grooming and clipping. Several horses in a
group are likely to be affected.

Clinical signs
The primary lesions are follicular and non-follicular papules and pustules, which exude and then crust.
Lesions are often more severe in non-pigmented skin.. The crusts typically extend over a number of
follicles causing tufting of hairs or more extensive scabs. Lesions are more severe in non-pigmented
skin. In some animals urticaria may be a feature and in severe cases oedema and cellulitis of the limbs
may be seen. Detachment of the crusts is accompanied by epilation, leading to alopecia.
        The underside of crusts is typically concave and in the early phase of infection the moist
underside provides ideal material for cytological examination. Older scabs are dry and should be
macerated in saline prior to fixing and staining. The appearance of Dermatophilus is diagnositic, with

Gram positive branching filaments breaking up into multiple rows of cocci, giving the characteristic
railway track appearance. The organism has special cultural requirements (microaerophilic with
increased carbon dioxide concentrations) and is very susceptible to overgrowth by other organisms.
 Affected horses should be stabled and kept away from waterlogged ground. Therapy should consist of
vigorous and thorough cleansing of affected areas with an antibacterial shampoo such as chlorhexidine,
with careful disposal of crusts. Careful drying and use of stable bandages is helpful. Some cases will
require systemic antibiotics, which should be continued until after resolution of clinical lesions.
Prophylactic chlorhexidine washes are indicated in susceptible animals at the first sign of crusting
lesions. Topical antibiotic- steroid preparations may also be beneficial.

Pastern folliculitis can present with very similar lesions to dermatophilosis of the distal limbs. The
organism most frequently isolated is coagulase positive staphylocci, (Staph. intermedius, Staph.
aureus,) but mixed growth of organisms (including streptococci) is not unusual. Treatment should
consist of a minimum of 3 weeks of systemic antibiosis, to continue beyond clinical resolution, in
addition to topical therapy as above.

Immune mediated causes

Pemphigus foliaceus commonly presents as a crusting and scaling disease, although the primary lesion
is a vesico-pustule.

Clinical signs
The lesions can be generalised, or may be restricted to mucocutaneous and other junctional areas. The
disease in older horses is often confined to the coronary band, but may involve other specialised
structures such as the frog, chestnut and ergot. Mucosal lesions are sometimes present.
          If intact pustules are present, cytological examination of pustule contents is extremely
helpful, looking for non-degenerate neutrophils and, or, eosinophils, acanthocytes and absence of
bacteria. Histopathological examination of skin biopsies reveals the presence of intra-epidermal to
subcorneal clefts containing acanthocytes and neutrophils and, or, eosinophils. Intra-epidermal deposits
of immunoglobulin and complement may be demonstrated by immunohistochemical staining.

Treatment consists of use of glucocorticoids at immunosuppressive doses (prednisolone 2-4mg/kg,
dexamethasone 0.1-0.2mg/kg) until no new lesions are developing, followed by gradual reduction in
dose by about 20% per week. Long term maintenance therapy is usually required, except for cases of
juvenile onset where complete recovery may occur. The change to alternate day therapy is best done
gradually, with increase of dosage on one day and reduction of dosage on the next day, until the horse
is receiving double the previous daily dose, and nothing on the intervening day. In cases refractory to
steroid therapy alone, injectable gold salts may be used and there are anecdotal reports of azathioprine
being used with success in equine patients.

Classically lupus erythematosus is divided into two syndromes, systemic lupus erythematosus (SLE)
and discoid lupus erythematosus, probably better called chronic cutaneous lupus erythematosus
(CCLE). SLE has been rarely recognised in horses, with polyarthritis, thrombocytopenia, proteinuria ,
fever, depression and weight loss reported inaddition to cutaneous signs. The cutaneous manifestations
are similar in the systemic and benign form of the disease. The pathogenesis is poorly defined, with
genetic factors, hormonal influences, viral infection and ultraviolet light all potentially playing a part in
the immunological disorder resulting in the presence of various auto-antibodies.

Clinical signs

Various degrees of patchy erythema, depigmentation and scaling are seen, particularly affecting the
skin around the eyes, lips and nostrils, and also neck and trunk. Chronic cases may have the appearance
of wrinkled parchment paper. Alopecia is usually cicatricial (scarring) and permanent. Other cutaneous
signs may include panniculitis and oedema of the limbs.
Histopathological changes involve the dermo-epidermal junction with
•   hydropic degeneration of the basal cell layer of the epidermis
•   vacuolar degeneration of the basement membrane zone
•   thickening of the basement membrane zone
•   pigmentary incontinence
•   presence of apoptotic keratinocytes (Civatte or colloid bodies) in the basal epidermis
•   deposition of fibrinoid material in the superficial dermis and around superficial blood vessels
Deposition of immunoglobulin and complement at the basement membrane zone is demonstrable
(lupus band).
In most cases a positive anti-nuclear antibody (ANA) titre is demonstrable. Routine haematology,
biochemistry and urinalysis should be performed to rule out systemic involvement.


For cutaneous LE, treatment should consist of sunlight avoidance, topical sunscreens and the use of
topical glucocorticoids. Refractory cases may require systemic glucocorticoids (prednisolone 1mg/kg
per os bid; dexamethasone 0.2mg/kg orally once daily) reducing to lowest possible alternate day
dosage for maintenance. Systemic therapy is indicated for SLE and other immunosuppressive drugs
may be needed in addition to glucocorticoids. The prognosis for SLE is unpredictable.

The aetiology of the condition is not fully understood, but the presence of changes typical of vasculitis
in skin biopsies suggests an immune-mediated basis. Immunoglobulin and or complement deposits
have been identified in the vessel walls in a few horses. Photoactivation may have a role, since the
lesions are usually confined to non-pigmented skin. However, affected horses have no known exposure
to photosensitising agents and liver function tests are normal.

Clinical signs
The condition is characterised by the presence of tightly adherent crusts, sometimes with a warty
surface affecting the distal limbs.

Glucocorticoids, initially at high anti-inflammatory doses for two weeks followed by gradual reduction
over the next two to four weeks, together with preventing exposure to sunlight. Wet soaks aid in gentle
removal of crusts. The majority of cases respond well and relapse is rare.

This is an uncommon but characteristic skin condition of horses, with an association with the use of
rhinopneumonitis vaccine in some cases.

Clinical signs
Single or multiple focal crusts from 1-5 mm in diameter are found on the dorsal midline, accompanied
by marked pain. White hairs appear in the crusting lesions, which persist after the disease has run its
course and the crusting has subsided.
         Histologically severe subepidermal oedema and clefting is seen with variable numbers of
apoptotic keratinocytes and intraepidermal oedema to vesiculation , soemtimes with pigment

The disease is self-limiting, with glucocorticoids of only marginal value.

Generalised granulomatous disease is characterised by the presence of granulomatous lesions in the
skin and internal organs. The histopathological appearance is similar to that of human sarcoidosis. It is
presumed that the condition represents an abnormal response to some as yet unidentified antigen.

Clinical signs
The cutaneous lesions are characterised by widespread scaling and crusting with variable alopecia.
More rarely nodular lesions may be present. Other organ systems involved, in order of frequency are
lungs, lymph nodes, gastro-intestinal tract, spleen, kidney, bones and CNS. Associated clinical signs
may include peripheral lymphadenopathy, weight loss, diarrhoea, icterus and lameness. Blood samples
may reveal leucocytosis, mild anaemia and hyperglobulinaemia.
         The diagnosis is confirmed by demonstration of typical non-caseating granulomata
histologically, with epithelioid cells and giant cells and small numbers of neutrophils, lymphocytes and
plasma cells. Skin and lymph node biopsies are of greatest value. Other causes of granulomatous
changes must be ruled out by searching for micro-organisms by special stains and culture. Serology for
Lyme disease (borreliosis) should be checked.

Although the prognosis appears to be more guarded than in the human disease, some cases do well with
corticosteroid therapy.

(exfoliative eosinophilic dermatitis & stomatitis)
Multisystemic eosinophilic disease is a rare condition of unknown aetiology. The condition is
characterised by marked infiltration of epithelial tissues with eosinophils, suggesting a possible
immune-mediated aetiology. Tissues involved include the skin, gastrointestinal tract, bronchial and
biliary epithelium.

Clinical signs
Skin lesions consist of scaling, crusting and oozing dermatitis with fissures, initially affecting face and
or coronets then becoming generalised with hairloss, ulceration and exudation. Oral ulceration is an
early feature, together with facial and coronary band involvement. Severe, progressive weight loss,
often without diarrhoea, is seen. Loose faeces may be passed. Dependent oedema may be seen.
Hypoproteinaemia is common.

The prognosis is grave, with progression of clinical signs in spite of high doses of systemic

Environmental and nutritional causes

Various topical medicaments or chemicals used in stables or on tack and harmess, particularly if
incorrectly diluted, may result in inflammation of the skin. Severity of clinical signs is variable
depending upon the nature of the insult, but low grade inflammation with a secondary seborrhoea and
some hair loss is common.. The history and clinical signs are usually indicative of the aetiology.
Symptomatic treatment is indicated, with topical bathing to remove irritant chemicals and emollients as


Toxicosis usually follows excessive administration of iodides to treat cutaneous mycoses. Clinical
signs are generalised dryness and scaling with variable alopecia, and watering of the eyes and nose.
Iodine is rapidly metabolised and the condition resolves once further administration or contact with the
source of iodine is prevented.


Nutritional deficiencies are rare in horses. However, severe endoparasitism may be accompanied by
poor skin and coat condition with scaling. Severe hepatic disease may affect lipid metabolism and give
rise to generalised seborrhoea in affected horses.

Grease heel syndrome or greasy heel is a clinical syndrome typified by varying degrees of crusting and
scaling affecting the distal limbs and pastern regions. It is a multifactorial condition with the possible
involvement of a number of distinct diseases including
•   chorioptic mange
•   harvest mites (trombiculidiasis)
•   dermatophytosis
•   dermatophilosis
•   bacterial folliculitis
•   photoactivated leucocytoclastic vasculitis
•   photosensitisation
•   irritant contact dermatitis
•   canon keratosis
•   chronic fibrosis or keloids (grapes)
•   neoplasia (warts, sarcoids)
•   idiopathic causes
When presented with a case of a dermatosis affecting the distal limb, the clinician should always
attempt to make a definitive diagnosis, by taking appropriate samples for laboratory investigation
(superficial scrapes, cytology, bacterial and, or fungal culture, biopsy). Once a definitive diagnosis has
been confirmed, then appropriate specific therapy can be employed, in addition to necessary
symptomatic management. Failure to reach a diagnosis and reliance on symptomatic proprietary
therapies alone may result in prolonged disease, which is a welfare issue for the patient and a cause of
frustration and dissatisfaction for owner and veterinarian alike.

Nodules and Swellings
Nodular diseases are quite common and can arise from a variety of different causes. A careful
diagnostic approach is essential.
History. Important factors to consider are age and speed of onset, breed, sex, coat and/or skin colour,
seasonality and history of systemic disease or recent treatment.
Complementary examination. Fungal culture, bacteriology, cytology of exudates and needle aspirates
are often indicated. Nn most cases, histopathology is necessary for definitive diagnosis.

Physical conditions


Clinical features
•   Bruising: swelling and discolouration of skin.
•   Haematoma: firm to hard subcutaneous swelling.

•   Diagnostic indicators
    History of trauma, physical appearance, skin usually pits on pressure.
•   Confirmatory tests
    Needle aspirate.
•   Differential diagnoses
    Abscess, neoplasia, cyst, urticaria.

•   Rest. Hot and cold compresses.

Infectious diseases


•   The most common equine neoplasm.
Clinical features
•   Age, breed, sex, colour incidence controversial.
•   Often multiple. May occur anywhere, especially on head, legs and ventral trunk.
•   Verrucous, fibroblastic, flat (occult), mixed and malevolent forms.
•   Probably papovavirus combined with a genetic predilection; familial tendency may exist.
•   Verrucous: slow growing, warty proliferations of skin.
•   Fibroblastic: proud flesh, most severe form of sarcoid; locally invasive but no metastasis.
•   Flat (occult): single or multiple patch of alopecia, scaling and crusting. May stay static and then
    develop papules or nodules within alopecic areas. Will often become locally aggressive. Verrucous
    and flat lesions may progress to fibroblastic.
•   Mixed: rare - may be transitional between verrucous and fibroblastic.
•   Malevolent: multiple very invasive tumours found along lymphatic vessels and local lymph nodes.
•   Diagnostic indicators
    Speed of onset and physical appearance.
•   Confirmatory tests
    Skin biopsy - but may encourage local aggression (contra-indicated in lesions that have not
    increased in size over a long period).
•   Differential Diagnoses
    Verrucous: papillomatosis, squamous cell carcinoma

    Fibroblastic: squamous cell carcinoma, exuberant granulation tissue, habronemiasis, infectious
    granulomas, fibroma, fibrosarcoma, neurofibroma, neurofibrosarcoma.
    Flat: dermatophytosis, dermatophilosis, demodicosis, folliculitis, onchocerciasis, alopecia areata.
    Malevolent: lymphangitis

•   Therapeutic approach
•   Therapy needs to be tailored to each case depending on availability of treatment, location of
    tumour, size of tumour, cost and risk. Specialist advice should be sought.
    Ligatures: elastrator rings, lycra or elastic bands.
    Conventional surgery: 50% recurrence. Improved success with electrocautery, cryosurgery.
    Sarcoid cream (AW-3-Ludes; Knottenbelt, Liverpool Veterinary School, UK), arsenic trioxide,
    podophyllin, 5-fluorouracil. Applied daily or every 2 days onto small superficial tumours, until
    Intralesional implants and injections may be effective. Active agents include; cisplatin mixed with
    sesame seed oil, carboplatin, 5-Fluorouracil and bleomycin. Injections of cisplatin are given at 1
    mg/cm3 of tissue 2 weeks apart for 4 injections. Cysplatin is mutagenic and carcinogenic and
    extreme care should be exercised during preparation, handling and administration.
    Immune stimulation: e.g. BCG (bacillus Calmette-Guerin) vaccination. Administration of BCG
    may result in severe hypersensitivity and anaphylactic reactions, thus systemic steroids are given
    prophlactically. Peri-ocular sarcoids are most responsive to this method of treatment
    Radiation using implanted radon22, gold198, radium226, cobalt60 or iridium192. Good results have
    been demonstrated using iridium192 with periocular sarcoids. Radiofrequency hyperthermia and
    CO2 laser reported effective but expensive
•   Prognosis
    Static occult and verrucous: probably best left alone as surgery or biopsy may lead to enlargement
    and local spread. Fibroblastic will normally need removal. Combination therapy improves
    probability of successful resolution. Repeated treatment often needed.


Clinical features
•   Common especially in horses younger than 3 years old. Incubation period 2-6 months.
•   Transmission: direct and indirect. Predisposing factors: skin damage e.g. insect or ectoparasite
    bite, UV.
•   Self-limiting.
•   Believed to be a host-specific papovavirus.
•   Single or multiple raised, verrucous proliferations of epidermis; 1 mm-2 cm.
•   Most commonly seen around the eyes, muzzle, lips, distal limbs and external genitalia.

•   Age of onset, location on body and physical appearance; biopsy, but not usually necessary.
•   Differential diagnoses
    Sarcoid, viral papular dermatitis, equine molluscum contagiosum.

•   Leave alone.
•   Surgery or cryosurgery (may lead to scarring and depigmentation)
•   Topical cytotoxic agents
•   Autogenous vaccines but no evidence of efficacy in horses
•   Prognosis
    Spontaneous regression may take from 1 to 6 months. Horses normally develop complete
•   Prophylaxis
    Disinfection of premises, avoid contact with affected horses - hard to carry out

•   Synonyms: aural flat warts, papillary acanthoma, hyperplastic dermatitis of the ear, squamous

Clinical features
•   Common skin disease of adult horses, caused by a DNA papovavirus.
•   No sex or breed predisposition; rare in horses less than 1 year old. Transmission may be associated
    with black fly.
•   Signs
    Greyish-white papules coalesce to form hyperkeratotic plaques affecting the medial pinnae. No
    discomfort in most cases. Occasionally occur around the anus, vulva and inguinal regions.

Diagnostic indicators
•   Age of onset and physical appearance; histopathology of shave skin biopsy specimens but not
    usually necessary.

•   No effective treatment available; lesions tend to persist indefinitely.


Clinical features
•   An unclassified pox virus
•   Initially - small non-pruritic papules on the trunk, neck and legs. At 7 days - crusting, after about
    14 days - annular alopecia and scaling

•   Speed of onset and physical appearance. Virus isolation and skin biopsy.
Differential diagnoses
•   Staphylococcal folliculitis, dermatophilosis, dermatophytosis, demodicosis.

•   No specific treatment. Spontaneous remission usually within 4-6 weeks.


Clinical features
•   An unclassified poxvirus.
•   Multiple waxy papules may coalesce and produce a caseous discharge. Lesions on penis, prepuce,
    scrotum, mammary glands, thighs, axillae and muzzle.

•   Location of lesions and physical appearance. Skin biopsies
Differential diagnoses
•   Papillomatosis, viral papular dermatitis

•   No specific treatment. Regression may take years


• See crusting and scaling


Clinical features
•   Rare, no age or sex predilection. Poorly defined, severe, deep, suppurative infection involving the
    subcutaneous tissues.
•   Staphylococci or anaerobic bacteria often involved. Commonly inThoroughbred racehorses in
    active training. No obvious association with trauma or infections.
•   Severe and painful swelling of one (often hind) limb with extreme lameness. Pyrexia, tachycardia
    and distress. Complications include necrosis, sloughing, laminitis of affected or contralateral limb,
    osteomyelitis and bacteraemia.

Diagnostic indicators
•   Sudden onset of severe lameness and physical appearance

Therapeutic approach
•   Prolonged systemic antibiotics
    If mild, trimethoprim sulphadiazine, 15-30 mg/kg BID by mouth or procaine penicillin, 15-20
    mg/kg BID im
    Ceftiofur 2 mg/kg im once daily
    If severe, gentamicin 6 mg/kg (iv or im) TID + procaine penicillin G (20mg/kg BID im)
    Longer term therapy: oral enrofloxacin (not immature horses) Baytril 10% Oral Solution 5.0 – 7.5
    mg/kg SID. Note this is a poultry preparation.

•   Non-steroidal anti-inflammatory drugs.
•   Support bandages on the affected and contralateral limb.
•   Guarded.


Clinical features
•   Localised, fluctuant to solid lesions consisting of dead cells, debris and liquefied tissue.
•   Contamination of skin wounds, vaccination sites.
•   Corynebacterium pseudotuberculosis, Clostridium spp. and staphylococci often involved.
•   Circumscribed, subcutaneous accumulations of pus

•   Clinical signs. Stained smears of needle aspirate, bacterial culture. Ultrasound
Differential diagnoses
•   Cysts, haematomas, mycetomas, neoplasia

•   Surgical drainage and debridement. Flushing and packing with topical antimicrobial agents.
    Systemic antibiotics based on sensitivity testing; not before the abscess matures.
•   Usually good
•   General hygiene


Clinical features
•   Very rare.Contamination of skin wounds. Transmission by direct contact or insect vectors;
    possibly contaminated soil. 3-4 week incubation period reported for Corynebacterium
•   Usually Corynebacterium pseudotuberculosis and/or Pseudomonas aeruginosa
•   Painful, discharging nodules on distal hind limbs - unilateral or bilateral. Pyrexia common.
    Regional lymphatics may show enlargement, hardening and ulceration leading to lameness and
    debility. New lesions may continue to appear for years.
•   Sometimes fatal.

•   Clinical signs. Stained smears and skin biopsies for culture and histopathology
Differential diagnoses
•   Sporotrichosis, actinomycosis, nocardiosis, mycobacterial infections.

•   Surgical drainage, hydrotherapy, exercise. Prolonged high doses of procaine penicillin (20 000-80
    000 IU/kg twice daily). Autogenous bacterins - of doubtful efficacy.
•   Cure is unlikely in the later stages, when fibrosis is present.
•   Good hygiene and management; early wound treatment and effective insect control.


Clinical features
•   Chronic sub-cutaneous infection where bacteria are present in tissues as granules or grains.
•   Actinomycotic mycetoma: Actinobacillus, Nocardia and Actinomyces spp. Other bacteria e.g.
    staphylococci, Pseudomonas spp.
•   Ulcerative nodules with draining tracts and usually tissue granules (grains)

•   Clinical signs. Bacterial culture, stained smears of needle aspirates and skin biopsies with special
Differential diagnoses
•   Fungal granulomas, habronemiasis, exuberant granulation tissue, neoplasia.

Therapeutic approach
•   Prolonged antibiotics based on sensitivity; radical surgical excision.
•   Antibacterials include:
    Ceftiofur (Excenel Sterile Powder, Pharmacia & Upjohn) 2 mg/kg i/v sid (2 ml of reconstituted
    solution / 50 kg horse).
    Procaine penicillin 22,000 IU/kg bid im
    Trimethoprim-sulphadiazine: 15-30 mg/kg bid orally
    Oral enrofloxacin (not immature horses) Baytril 10% Oral Solution 5.0 – 7.5 mg/kg SID. Note this
    is a poultry preparation.


Clinical features
•   Skin involvement very rare.
•   Mycobacterium intracellulare, M. avium and M. smegmatis have been isolated.
•   Scaling, alopecia, nodules and ulceration; systemic signs include fever, diarrhoea, weight loss and


•   History of contact with infected animal, physical examination, clinical signs, radiography.
    Mycobacterial culture, serology and skin biopsies with special stains. 70% of normal horses show
    positive intradermal reactions to purified mammalian and avian tuberculin.

•   Euthanasia


•   See crusting and scaling


Clinical features
•   Chronic sub-cutaneous infection where fungi present in tissues as granules or grains.
•   Soil-living fungal spp. Curvularia geniculata and Pseudoallescheria boydii have been isolated
•   Chronic subcutaneous nodules, often ulcerative, with draining tracts and tissue granules or grains
    in discharge

•   Clinical signs. Stained smears of needle aspirates, fungal culture.
Differential diagnoses
•   Bacterial mycetoma, bacterial and fungal pseudomycetoma, phaeohyphomycosis.

Therapeutic approach
•   Surgical removal.
•   Iodides
    Sodium iodide: 50 mg/kg iv as 3.5% solution in normal saline. Two doses, 3-7 days apart.
    Potassium iodide: 10g/450 kg BID orally for 10 days or until iodism occurs. Signs of iodide
    toxicity: dry scurfy skin, watery eyes and nose, enlarged thyroid gland, depression, weight loss,
    anorexia, fever, coughing, alopecia.
•   Guarded. Medical therapy often unsuccessful.
•   Good hygiene and management; early wound treatment and effective insect control.


Clinical features
•   Usually occurs through wound contamination.
•   Drechslera spicifera, Alternaria alternata and other ubiquitous saprophytic fungi.

•   Plaques, papules and pustules. Slow-growing, solitary or multiple, sub-cutaneous masses often
    ulcerated. Found on neck, body, legs.

•   History and clinical signs. Smears of discharge (organised in septate hyphae, not into granules),
    skin biopsy and fungal culture.
Differential diagnoses
•   Collagenolytic granuloma, mycetomas.

Therapeutic approach
•   Systemic iodides,
    Sodium iodide: 50 mg/kg iv as 3.5% solution in normal saline. Two doses 3-7 days apart.
    Potassium iodide: 10 g/450 kg BID orally for 10 days or until iodism occurs. Signs of iodide
    toxicity: dry scurfy skin, watery eyes and nose, enlarged thyroid gland, depression, weight loss,
    anorexia, fever, coughing, alopecia.
•   Ketoconazole (Nizoral, Janssen-Cilag): 30 mg/kg SID or BID. Itraconazole (Sporanox, Janssen-
    Cilag): 3 mg/kg BID for < 2 months.
•   Amphotericin B (Fungizone, Squibb): 0.3 mg/kg/day in 1 litre of 5% dextrose given slowly iv.
    Daily dose increased to a maximum of 1 mg/kg for < 30 days.
•   Good hygiene and management; early wound treatment and effective insect control.


Clinical features
•   Rare; zoonotic; usually occurs through wound contamination.
•   Only one horse in a herd is usually infected.
•   Sporothrix schenckii, ubiquitous saprophytic fungus.
•   Hard subcutaneous nodules which ulcerate and produce creamy pus
•   Lymphatics often affected on medial legs.
•   Sometimes systemic involvement.

•   History and clinical signs. Stained smears of discharge, fungal culture, serology.
Differential diagnoses
•   Mycetomas, phaeohyphomycosis, abscess and neoplasia.

Therapeutic approach
•   Surgical removal of masses
•   Systemic iodides:
    Sodium iodide: 50 mg/kg iv as 3.5% solution in normal saline. Two doses 3-7 days apart.
    Potassium iodide: 10 g/450 kg BID orally for 10 days or until iodism occurs. Signs of iodide

    toxicity: dry scurfy skin, watery eyes and nose, enlarged thyroid gland, depression, weight loss,
    anorexia, fever, coughing, alopecia.
•   Ketoconazole (Nizoral, Janssen-Cilag): 30 mg/kg SID or BID. Itraconazole (Sporanox, Janssen-
    Cilag): 3 mg/kg BID for < 2 months.
•   Amphotericin B (Fungizone, Squibb): 0.3 mg/kg/day in 1 litre of 5% dextrose given slowly iv.
    Daily dose increased to a maximum of 1 mg/kg for < 30 days.
•   Lesions should regress after 3-4 weeks of antifungal therapy.
•   Good hygiene and management; early wound treatment and effective insect control.



Clinical features
•   Eradicated from UK but may occur in imported horses. Anaphylaxis reported following death or
    rupture of larvae. Cattle are primary hosts. Seasonal incidence around spring.
•   Infestation by larvae of warble fly (Hypoderma bovis, H. lineatum)
•   Subcutaneous nodules and cysts over dorsum. Opening or breathing pore frequently develops.
    Sometimes pruritic.

•   History (imported animals) and clinical signs. Demonstration of larvae
Differential diagnoses
•   Infectious granulomas, cysts, neoplasia, collagenolytic granuloma, demodicosis

Therapeutic approach
•   Removal of larva - surgical removal of entire nodule.
•   Fair.
•   Effective insect control.


Clinical features
•   Rare in horses.
•   Demodex equi and D. caballi. Immunosuppression may be a factor.
•   Alopecia, scaling and variable pyoderma. Papular to nodular form is less common.

•   History and clinical signs. Mites in scrapings or material expressed from nodules.
Differential diagnoses
•   Infectious granulomas, hypodermiasis, cysts, neoplasia, collagenolytic granuloma

Therapeutic approach
•   Correction of underlying immunosuppressive factor. Incision of nodule. Topical antimicrobials.
•   Amitraz may cause death in horses and is completely contraindicated.
•   Fair to guarded depending on underlying factors

See under ulcers and erosions


•   See viral nodules and swellings

Clinical features
•   Very common especially on grey and white coated horses. About 67% of cases malignant. Rarely
    seen in horses under 6 years old. No sex predilection.
•   Small hard tumours in subcutis. Slowly increase in size but rapidly fatal once vital organs are
    involved. Sometimes ulcerative with a black discharge.
•   Anus, vulva and tail commonly involved (Figures 54[CD51] & 55[CD52]). Less commonly male
    genitalia, limbs, ears, eyelids and neck. May be associated with dystocia or problems in defecation.

•   History and clinical signs. Stained smears of fine needle aspirate, skin biopsy.
Differential diagnoses
•   Melanocytic tumours recently differentiated into 4 syndromes: melanocytic nevus; anaplastic
    malignant melanoma; dermal melanoma; dermal melanomatosis.

Therapeutic approach
•   Radical surgical excision, cryotherapy.
•   Cimetidine at 2.5 mg/kg TID for at least 3 months OR 4mg/kg TID orally for 3mths, if tumour
    regresses continue at 2.5mg/kg orally.
•   Cisplatin, 1 mg/cm3 of tissue every second week for 4 treatments.
•   Poor


Clinical features
•   Rare. Usually forms part of multicentric, alimentary or thymic lymphoma. May arise at any site in
    the body where there is lymphoreticular tissue. Accounts for only 1-3% of all tumours but is one of
    the most common causes of neoplasia associated deaths in horses.
•   Seen in all ages. Possibly more common in males than females. Primary cutaneous form recently
    reported in UK.
•   Multifocal, firm subcutaneous nodules without inflammation or alopecia. Systemic signs, weight
    loss, diarrhoea etc. Clinical course usually rapid and disease fatal.

•   History and clinical signs. Skin biopsy and immunohistochemical staining.
Differential diagnoses
•   Collagenolytic granuloma, sterile panniculitis, sarcoid, fibroma, mastocytosis, melanoma,
    squamous cell carcinoma, amyloidosis.

•   Euthanasia in multicentric, alimentary or thymic forms. Surgical removal of individual lesions is
    palliative. Glucocorticoids and progestagens have been used successfully in the primary cutaneous
•   Poor.

Clinical features
•   Second most common equine tumour (accounts for 20% of all equine tumours). Most common
    periocular and periadnexal tumour and most common tumour of stomach.
•   Mean age incidence of 12 years; males maybe predisposed; no breed predilection.
•   Associated with chronic exposure of unpigmented, poorly haired skin to ultra violet light.
•   Smegma implicated in development of penile and preputial lesions.
•   Head (conjunctiva and eyelids), mucocutaneous junctions and external genitalia are common sites.
•   Lesions usually proliferative with secondary ulceration; sometimes primarily erosive. May present
    as chronic non-healing ulcer. Haemorrhage and secondary infection may occur.

•   History and clinical signs. Biopsy
Differential diagnoses
•   Habronemiasis, exuberant granulation tissue, fibroblastic sarcoid and other cutaneous neoplasms.

•   Wide surgical excision, cryosurgery.
•   Radiotherapy - brachytherapy using radioisotopes including gold, strontium, iridium
•   Chemotherapy: intralesional cisplatin at 1 mg/cm3 of tissue 2 weeks apart for 4 injections and 5-
    fluorouracil; topical 5-fluorouracil daily for 3-4 months until tumour regression.
•   Intralesional BCG also reported to work.

•   Lasers may reduce recurrence and spread.
•   Locally aggressive and may later spread to lymph nodes and lungs.
•   Penile and preputial lesions tend to be more aggressive.


See ulcers and erosions

•   See pruritus

Clinical features
•   Affects skin and upper respiratory tract. No age, breed or sex predilection. Slow, progressive
    development of lesions.
•   Unknown
•   Multiple, hard, non-painful cutaneous nodules, papules and plaques 0.5-10 cm in diameter.
    Overlying skin usually normal. Initial lesions sometimes resemble urticaria and may resolve
•   Anterior parts of the body often affected. Dyspnoea may result when involvement of nasal mucosa
    is severe. Internal organs rarely involved.

•   History, clinical signs. Skin biopsies with special stains (Congo red, crystal violet, thioflavin T).
Differential diagnoses
•   Neoplasia, collagenolytic granuloma, mastocytosis, mycetoma

•   None likely to be effective. Tracheotomy to ensure patent airway
•   May be best not to breed from affected horses (some human forms have genetic basis).
•   Disease often prolonged and progressive.


•   Eosinophilic granuloma, nodular necrobiosis with collagen degeneration, acute collagen necrosis.

Clinical features
•   Common; no age, breed or sex predilection. Occurs mostly in spring and summer. May resolve
    spontaneously but recurrence common.

•   Unknown cause and pathogenesis - possible multiple aetiology including hypersensitivity to insect
•   Single or multiple dermal lesions, variable diameter (0.5 - 10 cm). Often in saddle area but also
    neck and flanks.
•   Rounded, well circumscribed, firm, non-alopecic, non-ulcerative, non-painful and non-pruritic.
    Overlying skin surface and hair usually normal unless traumatised. Mineralisation in chronic

•   History and clinical signs. Stained smears of needle aspirate, skin biopsy.
Differential diagnoses
•   Hypodermiasis, viral papular dermatitis, unilateral papular dermatosis, staphylococcal folliculitis
    and furunculosis, dermatophytosis, neoplasia, calcinosis circumscripta.

•   Leave alone. Surgical excision - if single or few lesions.
•   Systemic, intra-lesional or sub-lesional injections of glucocorticoid.
    Prednisolone: 1 mg/kg SID orally for 2-3 weeks
    Dexamethasone (Opticorten, Novartis): 0.1 mg/kg SID, as an oral solution, as a loading dose then
    0.04 mg/kg or less every 72-96 h for 2-3 weeks
    Methylprednisolone acetate: 5-10 mg/lesion. Repeat after 2 weeks if necessary.
    Triamcinolone acetonide: 3-5 mg/lesion. No more than 20 mg/horse. Repeat after 2 weeks if
•   Glucocorticoids probably ineffective in later stages after mineralisation. Treatment unlikely to
    produce permanent remission.

Clinical features
•   Rare condition affecting mature working and non-working horses. Only one out of a group
•   Unknown.
•   Usually unilateral, single or multiple. Round, firm, well-circumscribed, non-alopecic, non-
    ulcerative, non-painful, non-pruritic sub-cutaneous nodules near girth and axillae. Size of nodules
    varies between 1-5 cm.

•   History and clinical signs. Stained smears of needle aspirate, skin biopsy, bacterial and fungal
    culture to rule out differentials.
Differential diagnoses
•   Collagenolytic granuloma, pressure sores, infectious granuloma, cutaneous amyloidosis,
    mastocytosis, lymphosarcoma and other neoplastic conditions.

•   Surgical excision, systemic or sub-lesional glucocorticoids.
    Prednisolone: 1 mg/kg SID orally for 2-3 weeks
    Dexamethasone (Opticorten, Novartis): 0.1 mg/kg SID, as an oral solution, as a loading dose then
    0.04 mg/kg or less every 72-96 h for 2-3 weeks
    Methylprednisolone acetate: 5-10 mg/lesion. Repeat after 2 weeks if necessary.
•   Triamcinolone acetonide: 3-5 mg/lesion. No more than 20 mg/horse. Repeat after 2 weeks if
•   Uncertain. Variable response to glucocorticoids.

Clinical features
•   Uncommon; reactive or hyperplastic process rather than neoplastic; metastasis not reported.
•   Usually a single cutaneous nodule often located on the head or legs. May also present at birth with
    multiple masses which may regress and reform. Size 2-20 cm diameter. Surface may be normal,
    hairless or ulcerated. May become mineralised
•   Regression spontaneously and after biopsy has been reported.

•   History and clinical signs. Stained smears of needle aspirate, skin biopsy.
Differential diagnoses
•   Collagenolytic granuloma, neoplasia, cutaneous amyloidosis, mycetomas

•   Surgical excision; rarely recurs after excision.
•   Systemic or intralesional glucocorticoids.
    Prednisolone: 1 mg/kg SID orally for 2-3 weeks
    Dexamethasone (Opticorten, Novartis): 0.1 mg/kg SID, as an oral solution, as a loading dose then
    0.04 mg/kg or less every 72-96 h for 2-3 weeks
    Methylprednisolone acetate: 5-10 mg/lesion. Repeat after 2 weeks if necessary.
    Triamcinolone acetonide: 3-5 mg/lesion. No more than 20 mg/horse. Repeat after 2 weeks if
•   Radiotherapy.

Clinical features
•   Uncommon.
•   Multifactorial aetiology including contact with bedding, insect bites, peripheral neuropathy,
    infectious agent.
•   Unilateral papules. Usually neither pruritic nor painful. No systemic illness.

•   Characteristic unilateral presentation and skin biopsy.
Differential diagnoses
•   Collagenolytic granuloma, viral papular dermatitis, staphylococcal folliculitis and furunculosis,
    dermatophytosis, neoplasia, calcinosis circumscripta.

•   Leave alone.
•   Systemic glucocorticoids.
    Prednisolone: 1 mg/kg SID for 2-3 weeks
    Dexamethasone (Opticorten, Novartis): 0.1 mg/kg SID, as an oral solution, as a loading dose then
    0.04 mg/kg or less every 72-96 h for 2-3 weeks
•   Some cases resolve after a few weeks or months. Sometimes recurrent. Glucocorticoids may
    hasten recovery.
•   Insect control.

•   See crusting and scaling

•   Epithelium-lined cavities containing fluid or solid material. Smooth, well-circumscribed, fluctuant
    to solid mass. Uncommon.

•   Synonyms: atheroma, epithelial inclusion cyst.

Clinical features
•   Subcutaneous nodule found unilaterally (rarely bilateral) in or over false nostril (false nostril cyst);
    this may be congenital but not noticed until horse is 3-6 months old. Does not usually cause
    respiratory noise or obstruction. May occur around base of the ear and may produce mucoid
    secretion (dentigerous cyst).
•   Congenital or acquired through occlusion of hair follicle or traumatic implantation of epidermis.
•   Solitary or multiple. Well-circumscribed, firm, non-alopecic, non-ulcerative, non-painful and non-
    pruritic nodule. Progressive exfoliation of keratinised material leads to enlargement of cyst.
    Overlying skin surface and hair usually normal unless traumatised.

•   History and clinical signs. Needle aspirate - no evidence of pus. Skin biopsy.
Differential Diagnoses
•   Abscess, foreign body, fistula, other cysts, neoplasia.

•   Leave or surgical excision.

•   Unlikely to resolve without therapy.

Clinical features
•   Congenital or hereditary. Age range of 6 months to 9 years. Wall contains epidermal appendages.
    Lumen contains hair and secretions from sebaceous and sweat glands in addition to keratin.
•   Embryonic displacement of ectoderm into subcutis.
•   Solitary or multiple. Dorsal midline between withers and rump. Well circumscribed, firm, non-
    alopecic, non-ulcerative, non-painful and non-pruritic nodule. Overlying skin surface and hair
    usually normal unless traumatised.

•   History and clinical signs. Needle aspirate. Skin biopsy.
Differential Diagnoses
•   Abscess, foreign body, other cysts, neoplasia.

•   Leave or surgical excision.
•   Unlikely to resolve without therapy.

Clinical features
•   Rare; no age, breed or sex predilection.
•   Developmental defect.
•   Fluctuating non-painful swelling. Solitary, occurs near base of the ear, may discharge a mucoid

•   History and clinical signs. Needle aspirate. Skin biopsy.
Differential Diagnoses
•   Abscess, foreign body, fistula, dentigerous cysts, neoplasia.

•   Leave or surgical excision
•   Unlikely to resolve without therapy.

Synonym: tumoral calcinosis

Clinical features
•   Formation of calcified granular deposits in subcutis. Age incidence typically 12-18 months. Most
    commonly reported in young male Standardbreds.
•   Unknown. Maybe associated with prolonged or repeated trauma or with error in phosphorus
    metabolism inherited as an autosomal recessive gene.
•   Hard, well-circumscribed, subcutaneous nodules about 3-12 cm in diameter. Single or multiple.
    Non-painful and non-pruritic. Overlying skin normal.
•   Frequently occurs near joints or tendon sheaths especially over lateral stifle (unilateral or bilateral).
    No lameness associated.

•   History and clinical signs. Skin biopsies and radiography.
Differential diagnoses
•   Neoplasia, collagenolytic and infectious granulomata, mastocytosis, amyloidosis.

•   Leave alone or surgical excision.
•   Postoperative wound breakdown is common.

Synonyms: proud flesh, excessive granulation tissue.

Clinical features
•   Overgrowth above adjacent epithelium of normal granulation tissue following injury or trauma.
•   Often associated with chemical irritants, bacterial infection or contamination with debris such as
    hair, dirt, gravel, buried sutures and inappropriate wound management.
•   Can be promoted by bandaging and casting
•   Unknown
•   Proliferation of granulation tissue with no healing or epithelium production. Tissue is pink to red
    coloured, firm and granular. Frequently occurs on distal limbs.

•   History, clinical signs, lesion location. Skin biopsies.
Differential diagnoses
•   Fibroblastic sarcoid, habronemiasis, squamous cell carcinoma, infectious granulomata.

Therapeutic approach
•   Surgical trimming/excision; avoid casting and tight/heavy bandaging if possible; keep wound
    moist with hydrogel dressing and protect with foam polymer e.g. Intrasite Gel covered with
    Allevyn foam (Smith & Nephew)

•   Physiological saline for lavage, with antiseptics if necessary e.g. chlorhexidine at 0.05% or
    povidone iodine at 0.1%
•   Topical glucocorticoids can suppress granulation tissue formation but also inhibit healing; best
    used once a granulation bed has established.
•   Graft skin if the wound is large and contraction will be insufficient to achieve closure
•   Limb immobilisation aids closure; is most effective in acute wounds or where secondary closure is
    being attempted.
•   Chemical cauterisation and cryotherapy cause tissue necrosis and delay healing; they should be
•   Guarded. Surgical trimming followed if necessary by grafting can be very effective.
•   Prompt attention to wounds with good hygiene and wound care.

Clinical features
•   Rare inflammatory condition affecting subcutaneous fat. No age, breed or gender predilection.
•   Multifactorial: skin infections, immune mediated conditions (lupus, drug eruption, vasculitis),
    physicochemical factors (trauma, pressure, cold, foreign body, injection of bulky, oily or insoluble
    liquids), systemic disease (pancreatitis), glucocorticoid therapy, nutritional (vitamin E) deficiency,
•   Sometimes idiopathic.
•   Single or multiple nodules affecting trunk, neck and proximal limbs. Ulceration and draining tracts
    may develop.
•   Variable pain and texture. Variable systemic signs - anorexia, pyrexia, lethargy, depression

•   History and clinical signs. Skin biopsy and stained smears of needle aspirate. Special histological
    stains and microbial culture to rule out differentials.
Differential diagnoses
•   Neoplasia, cysts, amyloidosis, collagenolytic and infectious granulomata.

•   Identify and treat specific cause.
    High doses of glucocorticoids, Prednisolone: 1 mg/kg SID orally for 2-3 weeks. Dexamethasone
    (Opticorten, Novartis): 0.1 mg/kg SID, as an oral solution, as a loading dose then 0.04 mg/kg or
    less every 72-96 h for 2-3 weeks
•   Prognosis
•   Variable response to glucocorticoids.

•   Nettles, wasps, bees, biting flies, spiders and snakes. Signs vary according to agent, amount of
    venom injected, host factors.

Clinical Features

•   Papules, wheals and plaques; variable pain and pruritus; necrosis and sloughing, anaphylaxis.

•   History and clinical signs.
Differential diagnoses
•   Other causes of urticaria, collagenolytic granuloma, unilateral papular dermatosis, viral papular
    dermatitis. Haematoma, abscess, cysts. Poisoning.

•   Leave. Glucocorticoids, antihistamines. Insect repellents.
•   Varies according to source of bite/sting and host factors.

Coat Problems
•   Normal coat density is dependent upon ordered cyclic activity of hair follicles which pass through
    a cyclical growth phase - anagen, a phase of maturation - catagen and a third or resting phase -
    telogen when the mature hair is shed.
•   Under certain circumstances of environmental or nutritional stress or a disease process, telogen
    hair loss becomes synchronised and abnormal hair loss occurs. This is referred to as telogen
    effluvium, and may occur several months after the causative event.
•   Conversely hair loss during the growth phase - anagen effluvium - may be precipitated by more
    severe disease processes and some forms of medication. This may be seen within a short time of
    the stressful event.


•   Rarely if ever recorded in the horse.

•   Virtually any inflammatory disease of skin will precipitate hair loss. Examples are:
    Parasitic infestation: chorioptic mange, pediculosis, larval nematode dermatitis (Pelodera
    strongyloides, Strongyloides westeri), onchocerciasis, ticks
    Immunological reactions: Culicoides hypersensitivity, cutaneous lupus erythematosus, atopy,
    chronic eosinophilic enteritis, systemic granulomatous disease, alopecia areata,
    Drug reactions
    Contact dermatitis
    Infections: dermatophilosis, dermatophytosis
    Functional disorders - seborrhoea
    Toxicoses: heavy metal poisoning, selenium

•   Crusting and scaling are also prominent signs in addition to alopecia in chemical toxicoses


Clinical Features
•   Selenium toxicosis can result from the ingestion of grasses and cereal grains containing excessive
    selenium due to high soil content of selenium or the presence of selenium concentrating plants.
•   Occasionally concentrate feeds may be over-supplemented with selenium. Feed concentrations
    should not exceed 5 ppm.
•   Cutaneous changes are more likely to be seen in chronic toxicity.
•   Signs:
    Whilst a rough, dry haircoat with some skin scaling is seen, the predominant signs are coronary
    band inflammation, hoof changes and accompanying lameness and progressive loss of mane, tail
    and fetlock hair. Generalised alopecia may develop.
    Systemic signs may occur including lethargy, weight loss and ultimately death.

•   History, clinical examination
    Selenium levels in blood, hoof and hair. Toxic tissue concentrations of selenium are typically 1-
    4ppm in blood, 11-45ppm in hair and 8-20ppm in hoof. Selenium may also be found in the urine.
•   Differentials: heavy metal toxicity.

•   There is no specific treatment for chronic selenosis.
•   Change diet to reduce intake.
•   Five ppm. inorganic arsenic added to drinking water.
•   Diet high in sulphur containing aminoacids, e.g. methionine supplements 2-3 g daily.
•   Recovery is prolonged and euthanasia may be indicated in animals with severe hoof deformities

Clinical Features
•   Now rare.
•   Cutaneous absorption of arsenic causes irritation, drying and fissuring of the skin.
    Hair loss, typically over the mane and tail is seen, although on occasions a hirsute appearance
    results. Scaling and greasiness and sometimes ulceration..

•   Based on history, clinical signs and renal or hepatic arsenic concentrations >10ppm.
•   Differentials: selenosis, mercury and other toxicoses, Cushing’s disease, malnutrition

•   D-penicillamine at a dose of 11mg/kg orally four times daily for 7-10 days and removal of the
    source of arsenic.
•   Alternative choices of therapy are: sodium thiosulphate (10-30g intravenously then 20-60g PO
    four times daily for 3-4 days); and dimercaprol (3-5mg/kg intramuscularly four times daily for 2
    days then bid for 8 days).

Clinical Features

•   Ingestion of grain treated with organic mercurial substances such as anti-fungals may result in
    chronic mercury poisoning. Topical mercury-containing skin dressings may be licked off and may
    be absorbed percutaneously.
•   Signs:
    Chronic mercury poisoning results in progressive generalised alopecia and exfoliation, without
    hoof involvement.
    Systemic signs include gastro-enteritis, weight loss and lameness.

•   Mercury is concentrated in the kidneys and chronic poisoning may be confirmed post-mortem by
    tissue concentration > 100 ppm.

•   The source of mercury must be identified and removed.
•   Sodium thiosulphate and dimercaprol are recommended for treatment (see dose rates above) and
    potassium iodide 4g orally daily for 10-14 days is reported to be of benefit.

Clinical Features
•   A rare cell-mediated skin disease - within the autoimmune category
•   T lymphocytes congregated against the hair matrix and epithelium of the root sheath of the hair
•   Signs:
    Appearance of non-scaling, circumscribed areas of alopecia which may be bilaterally symmetrical
    Trimming of mane and tail hair
    Possibility of leukotrichia and/or hoof deformity
    Intermittent periods of remission and recrudescence may occur.

•   Histopathology of biopsy specimen from a new lesion to confirm lymphocytic attack on anagen
    phase hair bulbs.
•   Differentials: other non inflammatory alopecias

•   Corticosteroids are of uncertain efficacy. Systemic, topical, or intralesional
    Prednisolone: 1 mg/kg SID for 2-3 weeks
    Dexamethasone (Opticorten, Novartis): 0.1 mg/kg SID, as an oral solution, as a loading dose then
    0.04 mg/kg or less every 72-96 h for 2-3 weeks
    Methylprednisolone acetate: 5-10 mg/lesion. Repeat after 2 weeks if necessary.
    Triamcinolone acetonide: 3-5 mg/lesion. No more than 20 mg/horse. Repeat after 2 weeks if

•   Treatment may be ineffectual. Spontaneous hair growth is likely, initially with white hair

Clinical Features

•   Hyperadrenocorticism (HAC) is most commonly found in cases with an adenoma of the pars
    intermedia of the pituitary.
•   The exact mechanisms involved are uncertain, but hypersecretion of pro-opiolipomelanocortin
    (POLMC) which is insensitive to corticosteroid negative feedback is thought to be responsible.
•   Processing of POLMC results in the production of melanocyte stimulating hormone,
    corticotrophin-like intermediate lobe peptide, beta-endorphins and ACTH.
•   A condition of older horses and ponies.
•   Skin signs: The most striking feature is hirsutism and affected animals show an excessively long,
    dense and curly haircoat which is not shed normally. The mane and tail are usually unaffected.
    Skin is often moist and greasy. Skin and other infections may be present.
•   Systemic signs: Lethargy, pot-bellied appearance, muscle wasting, polydipsia and polyuria,
    infections. A bulging supraorbital fat pad may be present. Laminitis may be a serious

•   Commonest blood abnormalities are elevated alkaline phosphatase and hyperglycaemia.
•   Intercurrent diabetes mellitus is common. Plasma insulin concentrations are elevated.
•   Neutrophilia, eosinopenia and lymphopenia may also be found together with elevation of liver
•   Dynamic hormone tests:
    A variety of tests has been employed to confirm the diagnosis including ACTH stimulation tests
    and dexamethasone suppression tests, but there is considerable risk associated with the latter of
    precipitating laminitis.
    An alternative test, which is diagnostic in most cases, is the cortisol response to thyrotropin
    releasing hormone (Protirelin).
        Blood samples are taken before and 30 minutes after intravenous injection of 1mg of
        Protirelin (Cambridge). Normal horses show no alteration in baseline cortisol concentrations
        whereas affected horses show a mean increase in cortisol of 62-120%. The test is less
        sensitive in animals with elevated baseline cortisol concentrations.

•   Many animals will respond to treatment with pergolide, a dopaminergic agonist which interferes
    with peptide secretion by the pituitary tumour. The recommended dose rate is 5mg per horse daily
    orally, but beneficial responses may be obtained at lower doses.
•   Bromocriptine mesylate (0.02 mg/kg intramuscularly twice daily) has been used successfully. .
•   Cyproheptadine (Periactin), a serotonin antagonist which probably acts by interfering with ACTH
    secretion, may also be beneficial. Initial dose rates of 0.15-0.25 mg/kg orally daily are
    recommended reducing to alternate day therapy after 3 months.
•   Treatment with either of these drugs is expensive and often prohibitive.
•   Affected animals are often debilitated and require a high plane of nutrition. Laminitis may develop
    suddenly and often necessitates euthanasia.

Equine Ulcers and Erosions

An ulcerated lesion is one in which the full thickness of the epidermis is damaged and lost, penetrating
through the basement membrane zone to expose the superficial dermis. The damage is less extensive in
an erosion, where the basement membrane of the epidermis remains intact. Erosions and ulcers may
arise as a result of a number of primary insults, including direct injury to the epidermal surface,
intraepithelial and subepithelial vesicles and bullae or clefts and pathological processes in the dermis
that give rise to necrosis and sloughing of the overlying epidermis. Ulcers and erosions are often
covered with crusts of dried exudate and some of the diseases covered below may present with greater
or lesser degrees of erosion or ulceration and may be primarily crusting at presentation. In some cases
of primary dermal pathology, there may be nodular lesions which become ulcerated.

Infectious causes


This disease is rare in the UK, seen usually in warmer temperate and tropical climates. The larvae of
the helminth parasites Habronema muscae, H. microstoma and H. megastoma deposited in faeces of
horses infested with adult parasites in the stomach are ingested by flies (Musca domestica, Stomoxys
calcitrans) and then deposited around the lips, mucocutaneous junctions or in damaged skin of horses.
The normal life cycle of the parasite is completed when horses swallow the infective larvae, but
cutaneous disease results from aberrant parasitism when larvae are deposited in damaged skin, or
possibly at other mucocutaneous sites.

Clinical signs
Areas of ulceration, possibly with granulation tissue, usually containing small, gritty yellow nodules
may be seen at the medial canthus of the eye or in the conjunctivae, involving male genitalia,
particularly the urethral process, or wounds of the distal limbs or ventrum. Disease may occur within a
sarcoid or squamous cell carcinoma and biopsy may be necessary do differentiate causes.

Lesions can be surgically debulked, but complete excision is seldom possible. Inflammation can be
reduced with topical or intralesional glucocorticoids, or oral prednisolone for large or multiple lesions,
approximately 1mg/kg daily for 2 weeks, then halving the dose for a further 2 weeks. Strict fly control
and wound care is needed to prevent recurrence.
Ivermectin will kill larvae. Topical Ivomec Pour On (5mg/ml, 0.5% w/v) mixed 1:1 with artificial tears
has been used for ocular lesions. Glucocorticoid ophthalmic preparations are contraindicated if there is
corneal erosion or ulceration.

Deep bacterial and fungal infections may well present with ulcerated lesions, but there is usually a pre-
existing nodule or mass which subsequently becomes ulcerated.


Equine herpes virus (EHV) 3 infection can be spread by fomites and insects as well as by venereal

Clinical signs

The virus causes ballooning degeneration of basal epithelial cells and vesicle formation. Papules and
vesicles which become ulcerated and may crust are found on the penis, prepuce and scrotum of males
and vulva and perineum of females. The lips, mouths and nostrils may be affected, particularly in
young foals suckling infected mares. Healing usually occurs over 2-3 weeks, although focal
depigmentation may persist. Secondary bacterial infection may complicate the primary lesions and
require specific therapy. Lesions may recur if the animal becomes a carrier of the virus.
Intranuclear viral inclusion bodies may be seen in biopsies. The diagnosis can be confirmed by virus
isolation, identification of viruses by electron microscopy or demonstration of a rising EHV-3 antibody

Animals should be rested from coitus for a minimum of 4 weeks. Any secondary infection should be
treated appropriately. Topical antiseptic bathing and use of emollient creams may be beneficial.

A rare benign disease in mainland Europe, not reported in the UK for some time, caused by and
unclassified pox virus, antigenically related to the cowpox virus (orthopox).

Clinical signs
Three presentations are described - oral lesions; pastern and fetlock lesions; vulvar lesions. Lesions
consist of vesicles, umbilicated pustules and crusts affecting skin and mucosal surfaces. There may be
mild pyrexia and lameness.
Ballooning degeneration of epidermal cells with intracytoplasmic inclusion bodies and intraepidermal
vesicle formation are seen on biopsy. Demonstration of pox virus particles by electron microscopy or
virus isolation confirm the diagnosis.

The natural course of disease is 2-4 weeks, recovery conferring long-term immunity.

Another unclassified poxvirus causes this mild, self-limiting cutaneous infection, also recognised in
humans. The lesions consist of multiple, well-circumscribed, smooth, gray-white papules with a waxy
surface. These progress to become umbilicated, with a central pore containing a caseous plug.
Histologically the appearance is pathognomonic, with epidermal hyperplasia and swelling of
keratinocytes which contain large intracytoplasmic inclusions (molluscum bodies). These eosinophilic
aggregations grow as the keratinocytes move up to the surface and become increasingly basophilic,
compressing the cell nucleus. The infected cells exfoliate through the central pore of the lesion. There
is an absence of an associated dermal reaction.

Immune mediated causes

This is a rare disease of the horse, resulting from auto-antibodies directed against antigens in the
basement membrane zone. In man and animals the main bullous pemphigoid antigens are epitopes on
the collagen XVII molecule (BP180, BPAG II), a transmembrane protein produced by basal epithelial
cells, which comprise part of the anchoring filaments of the lamina lucida arising from the
hemidesmosomes and connecting with anchoring fibrils in the lamina densa of the basement

Clinical signs
Dermo-epidermal separation results in formation of supepidermal vesicles or bullae, which rapidly
ulcerate, affecting the oral cavity, mucocutaneous junctions and skin. Cutaneous lesions most

commonly affect the axillae and groin. Variable pain and pruritus may be evident. Affected horses may
be depressed, febrile and anorexic, with excessive salivation if there is significant oral involvement.
Biopsies reveal subepidermal vesicular dermatitis and immunohistochemistry may demonstrate linear
deposits of immunoglobulin and usually complement at the dermo-epidermal junction.

High doses of corticosteroids are indicated (prednisolone 1mg/kg bid per os; dexamethasone 0.2mg/kg
once daily per os), possibly with other immunosuppressive agents. The prognosis is grave.

A rare, acute cutaneous eruption of horses, the lesions may be urticarial, maculopapular or vesico-
bullous in nature. A number of triggering factors have been implicated including infections,
pregnancy, neoplasia, systemic disease and drugs, but in many cases the cause is not identified. The
pathogenesis is poorly understood.
Eruptions are usually asymptomatic, bilaterally symmetrical and initial lesions often spread
peripherally, with central clearing, resulting in annular, arciform shapes, which persist for days to
weeks. Histologically hydropic interface dermatitis is seen with apoptosis of keratinocytes. The
vesicular lesions result from extensive epithelial necrosis and, or massive subepidermal oedema.
If the underlying cause is evident, this should be addressed and the lesions should resolve
spontaneously. Symptomatic therapy for the skin lesions is not usually required.

Cutaneous vasculitis is uncommon in horses, assumed in most cases to involve type I and type III
hypersensitivity reactions. Lesions are characterised by purpura, oedema, necrosis and ulcerations of
the extremities and oral mucosa. The formation of immune complexes as a sequel to infection is the
most commonly recognised aetiology, particularly Streptococcus equi, but in many cases the aetiology
is not identified.
Equine purpura haemorrhagica following respiratory infection is of low incidence, with signs appearing
within 2-4 weeks of respiratory signs. Urticaria, pitting, oedema, petechiation, exudation and sloughing
are seen, with variable systemic signs of depression, difficulty breathing, Prompt therapy is required,
with antibiotics, diuretics and glucocorticoids.
If the underlying cause is not evident, symptomatic use of glucocorticoids may secure resolution.

A review of adverse cutaneous drug eruptions involving 22 horses revealed that lesions developed
within 1-3 weeks of exposure in the majority of cases, with a delay of up to 2 months in one case. The
drugs implicated were:
•   antibiotics
    •    potentiate sulphonamides (4 cases)
    •    procaine penicillin (4 cases)
    •    ciprofloxacin, metronidazole, gentamycin (each 1 case)
•   non-steroidal anti-inflammatories
    •    phenyl butazone (3 cases); flunixin (1 case)
•   anaesthetic agents
    •    guafenesin +/- thiamylal (2 cases)
•   ivermectin (2 cases)
•   multivitamin preparation (1 case)
•   multiple systemic or topical drugs (5 cases)

Clinical signs
The skin lesions described included:
•   urticaria (7 cases);
•   erythema multiforme,
    •    urticarial (3 cases), urticarial and vasculitic (1 case), necrotising (1case)
•   exfoliative dermatitis
    •    alone (2 cases), with ulceration (2 cases), exudation (1 case)
•   pyogranulomatous dermatitis
•   papulocrustous pruritic dermatitis
•   papulonecrotic dermatitis
•   hypotrichosis and trichorrhexis
•   contact dermatitis
Most cases resolved with removal of the suspected agent, considerable improvement seen in 7-14 days,
but in two cases taking 6-10 weeks. Definitive identification of the causal agent requires rechallenge,
but this may be hazardous and is not recommended.

If a drug eruption is suspected, drug therapy should be discontinued. If continuing treatment for an
underlying disease is essential, then unrelated drugs should be substituted. Symptomatic measures may
be appropriate, including bathing, control of secondary infection, and in some cases with pruritus or
severe immune-mediated reactions glucocorticoid therapy may be indicated.

Congenital and hereditary causes

A rare, inherited defect of foals, caused by a single autosomal recessive trait, affected animals are born
with sharply demarcated areas of absence of skin and appendages. The distal limbs are most frequently
affected, with bleeding from the underlying dermis. Secondary infection ensues, with septicaemia and
death, since there is no effective therapy. Sire and dam of affected foals should not be bred from again.

Junctional epidermolysis bullosa (EB) has been described in the Belgian horse breed, recently
identified as a defect in the laminin V gene affecting the anchoring filaments. Separation occurs within
the lamina lucida of the basement membrane zone, leaving the lamina densa overlying the dermis.
Affected foals show lesions at birth or shortly after, with involvement of skin, mucosae and other
junctions. Collapsed bullae with whitish flaps are seen in the oral cavity, with expanding erosions to
ulceration of the skin. Separation of the hooves at the coronary band is consistently present, with
dystrophic teeth also commonly seen. A positive Nikolsky sign (dermo-epidermal separation with
application of transverse pressure) may be elicited.
There is no treatment. Sire and dam should be removed from breeding programmes.

The disease has been reported in Quarter horses and an Arab crossbred. Various defects of collagen
synthesis may occur, but the condition in most species of animals has not been well characterised. It is
inherited as an autosomal recessive trait in the horse. The defect(s) result in connective tissue
dysplasias characterised by loose, hyperextensible, fragile skin that is easily torn. Clinical signs were
noted at 6-12 months of age, with thin to hyperextensible skin, tearing with minor trauma and healing
slowly, with poor suture holding and scarring.
Histological examination of affected skin may show a thin dermis or disorganisation and fragmentation
of collagen fibres, with foci of degeneration and phagocytosis of fibrils.

There is no effective therapy and affected animals and relatives should not be bred.

Environmental and nutritional causes

Traumatic injury from ill-fitting and poorly maintained tack is common in horses. The extent of the
lesions depends on the nature and duration of frictional forces applied and may range from acute
erosions or ulcerations of the skin, with exudation due to sudden, considerable force or hyperkeratosis,
hair loss and callus formation resulting from repeated, low grade pressure. Prolonged pressure may
result in ischaemic damage and sloughing. Scar tissue with alopecia, atrophic epithelium and
depigmentation are the sequel. Saddle sores and girth galls typify these reactions.
The cause of the damage should be identified and corrected. Mild changes may resolve, but ischaemic
changes are permanent. Surgical removal of calluses or associated dermal nodular reactions (corns, sit-
fasts) should be avoided since greater problems may ensue.

Thermal and chemical insults may result in burn damage. The lesions are classified according to depth
and severity of damage.
•   first degree burns: erythema, superficial oedema and marked pain, resolving after superficial
•   second degree burns: hair loss, superficial blistering, epidermal necrosis with pain; healing in 7-10
    days with no permanent damage
•   third degree burns: severe blistering with loss of epidermis and superficial dermis with absence of
    pain except at edges of lesions; healing is slow with scarring
•   fourth degree burns: loss of full skin thickness and involvement of deeper tissues; serious scarring
    and functional impairment follow prolonged healing.
Considerable loss of plasma protein may accompany second, third and fourth degree burns and
secondary infection is common.

Prompt application of cold water for at least 20-30 minutes will limit further tissue damage.
Intravenous therapy may be required. Antibiotic cover is indicated. Adequate analgesia should be
provided and sedation or anaesthesia prior to wound cleansing and debridement. Non-adherent, semi-
occlusive dressing should be applied where possible. Skin grafting may be indicated in due course.
Involvement of extensive areas of the body surface is likely to be fatal, and if burns are deep and
functional impairment is likely, or there is significant ocular or respiratory involvement then euthanasia
may be indicated.

Actinic dermatoses
Ultraviolet (UV) light may damage the skin acutely or chronically. Even in apparently undamaged skin
UV light has a deleterious effect on the skin immune system, depleting Langerhans cells and
lymphocytes, rendering non-pigmented areas of skin more susceptible to infections and influencing
other aspects of immune surveillance.

Acute, excessive exposure to sunlight may result in sunburn damage to skin that is poorly haired and
non- or lightly pigmented. Affected skin is erythematous, and may be painful and oedematous.
Blistering may occur but is uncommon. Resolution follows superficial scaling.

The presence of photo-active compounds in the skin may result in tissue damage on exposure to UV
light (wavelength 320-400 nm). Cutaneous absorption occurs where pigment is lacking and there is no
or only a thin haircoat, but may extend to lightly pigmented skin with sufficient exposure.
Photoallergic mechanisms involving immunological hypersensitivity reactions are recognised in
people, but poorly defined in animals and most cases in animals are of phototoxicity. Photodynamic
agents may reach the skin by systemic routes or by contact. Energy is absorbed by the photodynamic
molecules and released into the tissues via free radical formation, causing damage to the epidermis,
superficial dermis and blood vessels.

Most cases of contact photosensitisation have occurred in horses grazing pastures containing clover.
The incidence of cases on a particular pasture is variable from year to year, being more common in
seasons with a wet spring and lush growth. The actual nature of the photodynamic agent is not known.

Clinical signs
Contact areas only are affected, with lesions on non-pigmented areas of the lips, muzzle, face and distal
limbs. Several animals in a group would be expected to show lesions, but liver function tests should be
undertaken, since all may have been exposed to an agent causing hepatotoxicity. Lesions consist of
erythema, oedema, superficial necrosis, crusting and sloughing.

Affected animals should be stabled to prevent further exposure to sunlight and to remove them from
the source of the photodynamic agent. Non-steroidal anti-inflammatory drugs, glucocorticoids and
symptomatic topical therapy may be employed.

This results from ingestion of plants or drugs containing photodynamic agents, which are absorbed and
enter the circulation. Examples include St John’s sort (hypericin), perennial rye grass (perloline),
phenothiazines, thiazides, sulphonamides, tetracyclines, methylene blue.

Phylloerythrin is a photodynamic metabolite of chlorophyll produced in the gut by bacterial
fermentation. It is usually excreted in bile, but in cases of chronic hepatic damage or biliary obstruction
it may accumulate in the tissues. Liver damage in horses is frequently the result of ingestion of ragwort
(Senecio jacobea), usually in hay rather than direct from pasture, but other plant alkaloids and diseases
may damage the liver sufficiently to give rise to photosensitisation

Clinical signs
The clinical appearance is similar in both primary and secondary photosensitisation. Liver function
tests should be run on all animals, since the prognosis is poor in hepatogenous photosensitisation.
Lesions are found on any sun-exposed skin that is non-pigmented and poorly haired, but may extend to
lightly pigmented areas. Signs are variable, ranging from erythema, oedema and scaling, to exudation
and crusting, with necrosis and sloughing in severe cases.
Horses with secondary photosensitisation may show signs referable to the underlying liver pathology,
including weight loss, hypoproteinaemia, hepatic encephalopathy.

Management is as for contact photosensitisation, but the prognosis is poor in hepatic photosensitisation,
and the extent of liver damage may well necessitate euthanasia.

Equine Pigmentary Diseases

Melanocytes are of neural crest origin; the melanoblasts migrate to peripheral sties and differentiate in
to melanocytes Proliferation can occur at the final sites. The formation of pigment involves
melanosome formation and synthesis of melanin from tyrosine and transfer of mature melanosomes via
dendritic processes into surrounding keratinocytes.

Congenital and hereditary conditions
Defects may occur at any of the above stages and result in abnormalities of cutaneous pigmentation.
Some of these abnormalities are acceptable variations of normal in some domestic species.

A defect in stem cell factor (SCF) / c-kit receptors, which are important in the proliferation and
survival of melanoblasts in embryogenesis, results in absence of melanocytes in affected sites. The
patchy amelanosis is considered a normal variant of coat colouration in the horse.

Classical albino, white with pink eyes, does not occur in the horse. Generalised but incomplete
albinism, a white haircoat with pigmented irides, is inherited as an autosomal dominant trait (allele W).
Mating of heterozygotes results in 25% of the offspring being non-viable homozygous embryos.
An autosomal recessive disorder resulting from the breeding of two American overo paint horses, with
affected foals having non-pigmented coats and congenital defects of the gastro-intestinal tract. This is
an example of Waardenburg type 4 defect of melanoblast proliferation and differentiation.

Various breeds of horses may be fully coloured at birth, but subsequently acquire increasing numbers
of white hairs with age. This has been associated with the presence of the G allele and examples are the
Leppizaner and Percheron breeds. In Camargue horses the degree of coat pigmentation has been found
to correlate with α-MSH concentrations. Progressive patchy depigmentation is a feature of the
Appaloosa breed, also due to the effect of mutant genes.
Pigmentation references: see and for detail and discussion on equine coat colour.

Vitiligo is an acquired depigmentation of skin and hair which is reported in horses and may be
hereditary, autoimmune forms or idiopathic. The condition is most commonly seen in Arabian horses
and is also known as Arabian fading syndrome, Arabian pinky syndrome and juvenile Arabian
leucoderma. Circulating antibodies against melanocytes were identified in one report of the condition
Affected animals are mostly young and show symmetrical macular depigmentation (leucoderma)
affecting the periocular skin, lips, muzzle and sometimes perineal and genital areas. Occasionally
horses will repigment, and the condition may wax and wane in severity.
There is no evidence that vitamin-mineral supplements have any influence on the course of the disease.
In view of the possible hereditary nature of the condition affected animals should not be bred.

Post-inflammatory conditions
Leukoderma and leukotrichia are common sequelae of inflammatory condition s in the horse. Melanin
synthesis is inhibited by tumour necrosis factor (TNF) α, interleukin (IL) -1 and IL-6. Upregulation of
ICAM-1 by TNF α and interferon (IFN) γ may facilitate leucocyte attachment and damage in the basal
epithelium and subsequent pigmentary incontinence that is a feature of diseases affecting the basement
membrane region.


Saddle sores and wounds are frequently followed by permanent loss of pigment in the skin and hair.

Permanent damage to the melanocytes in the basal epidermis at sites of application of freeze brands is
the desired effect, to give permanent leukotrichia. Prolonged application of the brand may cause
excessive damage with scarring and hairloss and a thin epidermis at the site of damage.

Irritant contact dermatitis may cause sufficient damage to result in leukoderma and leukotrichia, which
may be temporary or permanent. Leukoderma of the lips is well recognised sequel to contact reactions
due to vulcanised rubber bits in certain individuals.

Depigmentation may follow various infections, including viral infections (papillomatosis, coital
exanthema), deep bacterial and fungal infections and parasitic infestations (trypanosomiasis,
oncherchiasis, fly bites, cutaneous larval migrans of Parafilaria).

Reticulated or variegated leukotrichia (tiger stripe) has been reported in quarter horses in the USA,
thoroughbreds and standardbreds in Australia and rarely in other breeds. The pathogenesis is unclear.
The leukotrichia is preceded by linear crusts in ante-like or cross-hatched pattern over the dorsum and a
temporary alopecia. The leukotrichia is permanent.

This is an idiopathic condition of mainly Arab horses, characterised by development of white spots of
hair, especially over the rump and sides of the trunk, usually with no leukoderma. The condition is
asymptomatic, may resolve if leukoderma is absent, but may be permanent.

This condition presents with painful crusting lesions and was considered in the section on crusting

Depigmentation is a common feature of cutaneous lupus erythematosus, together with erythema and
scaling. The disease was covered in detail in the section on crusting dermatoses.

Leukotrichia is a common sequel to this primarily hyperkeratotic to crusting dermatosis.

Increased pigmentation may be triggered by inflammatory processes, melanin production being
stimulated by a number of cytokines including leukotriene B4 and vasoconstrictive peptide. Focal
darkening of hair - melanotrichia - may be seen after fly bites or other local inflammation.

Conditions Affecting Non-pigmented Skin
Non-pigmented skin is susceptible to actinic damage due to ultraviolet light exposure. Sunburn and
photosensitisation are covered in detail in the section on ulcerative and erosive diseases. Photoactivated
vasculitis presents primarily with crusting. Non-pigmented skin is more prone to infections with
organisms such as Dermatophilus congolensis, covered in crusting dermatoses.

The Equine Foot

The hoof of the horse is a specialised keratinised structure encasing the third phalanx and distal part of
the second phalanx (coffin and short pastern bones respectively), the sesamoid bone (navicular)
associated with the distal interphalangeal (coffin) joint and the lateral cartilages, insertions of the
superficial and deep digital flexor tendons and the digital extensor tendon as well as suspensory

Structure and growth
The dermis of the foot is contiguous with the periosteum of the phalanges. Dermal rete ridges are
elongate into papillae that project proximo-distally. Perpendicular to this, projecting cranio-caudally
are the laminae. The hoof consists of the wall, sole, frog and white line. The epidermal tissue giving
rise to the horn capsule interdigitates with the dermal papillae and laminae.
The region at the junction of haired skin and the hoof is known as the coronary band or coronet, and is
the major site of growth of the hoof wall. The keratinocytes are arranged such that they give rise to
tubules of horn and also intertubular horn, visible when the wall is cut in cross-section. The tubules are
produced from the cells overlying dermal papillae and the intertubular horn from cells in the
interpapillary regions. The full thickness of the wall can be divided into three layers, stratum externum,
stratum medium and stratum internum. The stratumexternum is also known as the periople, which has
high lipid content and is thought to be important in protection. The stratum internum is the area of
specialised dermo-epidermal connection, with the large interlocking surface area conferring firm
bonding between the hoof wall and underlying structures and giving rise to the specialised processes of
keratinisation. It gives rise to a proportion of horn growth, contributing to the hoof wall. The hoof horn
consists of a high proportion of hard keratins, intermediate filaments with a high sulphur content and
greater cross-linking within the molecules and reduced water content, although analysis of hoof wall
keratins has shown them to be more similar to those described in human keratinising epidermis than to
those identified in the human fingernail. The anatomical features of the wall allow it to deal effectively
with multidirectional forces generated during weight bearing and locomotion. The hoof wall can be
divided into the toe, quarters and the heels. Good farriery practices are essential to maintain the health
of the hoof and whole foot.
The sole is also composed of tubular and intertubular horn and is produced from tissue overlying the
base of the pedal bone. It is usually concave, and flattening of the sole is considered a conformational
defect. The frog is a V-shaped structure with a grooved central sulcus and flanked by grooves called
the collateral sulci. It is composed of rubbery horn and is thought to function as an anticoncussive
device, anti-slip device and possibly as an aid to blood circulation within the foot and limb. It may also
help facilitate expansion of the heel under loading.
The white line is the junction between the horn of the wall and the sole, and consists of interdigitating
components of each. It is thought to allow independent movement between the sole and the wall under
loading forces.
Hoof horn grows at approximately a half a centimetre per month and requires trimming every 4-6
weeks. Replacement of the wall takes between nine and twelve months. The growth rate is slower in
older animals. Genetic factors, nutritional factors, work and management practices all influence hoof
quality and growth. The practice of working horses on hard ground necessitates the use of shoes, to
protect against excessive wear and splitting of the wall. Usually made of metal, these are attached by
nails placed in the ground-contacting surface of the wall, adjacent to, but peripheral to the white line,
thus avoiding the laminar structures deep to the wall.
Experimental work has demonstrated that the arrangement of horn tubules in the stratum medium
allows it to act as a quadrilaminar ply with respect to structural qualities, allowing stress transfer within
the hoof wall. Interestingly the hoof of the donkey was found to differ from that of ponies, lacking the
four-zoned arrangement observed. Evening primrose oil supplementation had no significant effect on
the rate of horn growth, but differences in lipid content were noted between treatment and control
groups and between different parts of the hoof. Biotin supplementation was associated with a
significant increase in growth rate of hoof horn and more hoof growth at the midline after 5 months
supplementation at a dose rate of 0.12mg/kg bodyweight. Farrier’s Formula, a proprietary feed

supplement, has also been shown to have a beneficial effect on gross and microscopic structure of hoof
horn in horses with various defects.
Other specialised keratinised structures of the distal limb of the horse that may be involved in
cutaneous disease are the ergots, considered to be vestiges of the second and fourth digits, and the
chestnuts, considered to be vestiges of the first digit. These horny structures may flake off of their own
accord as they grow, but in heavier and draught breeds may require trimming.

Examination of the foot
The hoof wall should be examined visually for symmetry and conformation, evenness of wear and
obvious wall defects. The coronary band should be palpated to assess the presence of any irregularities
or lesions, and the hoof wall to detect areas of heat. The digital arteries should be examined for pulse
character, altered in laminitis, and possibly in inflammatory conditions of the foot. The presence of
pain in the foot may be assessed with hoof testers. Radiographic examination may be helpful,
particularly in cases of laminitis.

Congenital and inherited disorders

Covered in more detail in ulcerative conditions, this autosomal recessive condition often involves the

Junctional EB of the Belgian horse consistently involves the feet, with separation of the hooves at the
coronary band.

Flat feet and thin walls and soles predispose to damage to the hoof, make shoeing difficult and can
predispose to lameness and restrict the usefulness of the animal.

Acquired disorders

The foot is very prone to traumatic damage, which may manifest in a number of ways.

Bruising of the sole may result from exercising on uneven ground or contact with sharp objects.
Bruising may also result from bad shoeing and may also be a sequel to laminitis.
Signs vary with the severity of the injury,, with blood streaking in the solar horn, to bleeding under the
sole, which may result in separation of the sole from underlying tissues. In severe cases there may be
under running, secondary infection and exudation at the coronary band.
Treatment consists of relieving pressure by paring of the sole, treatment of secondary infection, and
application of a protective pad under shoes until the area has fully healed. Dietary supplements may be

Areas of hyperkeratosis at the angle of the heel and wall junction, adjacent to the lateral sulci of the
frog, may result from poor shoeing, with excessively long quarters to the shoes, which impinge on the
softer horn at this junctional region. Proper farriery attention and careful shoeing are indicated both to
treat and prevent the condition.


Penetration of sharp objects, including shoeing nails, may result in damage to the sole and laminae of
the wall, with the risk of infection and abscess formation.
Drainage should be encouraged by paring, hot soaking of the affected foot (tubbing), and application of
poultices. Systemic antibiotics may be indicated.

Cracks may affect the wall, heels, toes, quarters and soles of the feet. Cracks are usually vertical, but
transverse cracks may occur. Deep cracks may involve the sensitive laminae and cause lameness.
Factors that may contribute to cracked hooves include genetic factors, bad foot care, traumatic damage,
nutritional status and systemic disease. A recent study looking at fungal isolates from hoof horn found
that 66.7-80% of samples from animals with hoof wall defects yielded keratopathogenic fungi or
dermatophytes compared to 9% of samples from healthy animals.
Management involves specialised farriery procedures, often on a long-term basis. Dietary supplements
may be beneficial. On the basis of the fungal culture study, topical antifungal treatment may well be of
benefit also.

Hoof rings
Variation in the production of wall keratin at the coronary band is manifest as visible rings on the hoof
wall. Some seasonal effect horn growth may be due to nutritional changes, but more marked rings may
result from a period of systemic illness, from inflammation of the coronary band (coronitis) and
particularly in cases of laminitis.

This is a condition characterised by inflammation of the laminae of the hoof wall. It can be reproduced
by carbohydrate loading, with an increase in blood flow at the midmetacarpal region, but reduced
laminar perfusion, with shunting of blood away from the laminar capillary network at the onset of
lameness. Several hypotheses were put forward to explain the laminar hypoperfusion, including
endotoxin -induced microthrombosis, vasoconstriction, perivascular oedema and arteriovenous
shunting. Movement of fluid out of the vascular compartment may cause tissue pressure to increase,
subsequently impairing blood flow in the digital microcirculation, bypassing the dermal laminae and
allowing stagnation of blood in the area, allowing for development of microthrombi.
Damage to the laminae results in breakdown of the interdigitation between the hoof wall and the
underlying dermal laminae (corium) and the distal phalanx beneath separates from the hoof wall. The
acute phase of the condition is characterised by acute pain. The chronic sequelae to the acute
inflammatory phase include rotation of the distal phalanx, marked abnormalities of growth of the wall
of the hoof with hoof rings, tipping up of the toe and possible penetration of the distal phalanx through
the sole of the foot.
Treatment of the acute phase invloves use of non-steroidal antiinflammatory drugs to decrease
inflammation, oedema and pain and prevent progressive laminar damage. Flunixin is probably the drug
of choice, although ketoprofen may have more potent anti-inflammatory effects on lipoxygenase and
prostaglandin pathways of the arachidonic acid cascade. Aspirin, heparin and vasodilators may also be
employed to improve perfusion. Xanthine drugs (pentoxyfylline, oxypentofylline) may also be
indicated. Corrective farriery is essential. The prognosis is dependent upon the severity of the initial
damage to the laminae, and may be so severe as to necessitate euthanasia.

Selenium toxicity may result from accidental over-supplementation of concentrate rations, but may also
be seen in horses grazing plants that concentrate selenium from the soil (not encountered in the UK,
seen in parts of Ireland and the USA). Chronic toxicity in the horse results in coronitis with swelling
and exudation of the coronary band. Defective horn is produced, which grows distally. Deep transverse
cracks appear around the hoof wall, associated with lameness. Affected horses may become recumbent
with decubitus ulcers and myositis as potential sequels. Other clinical signs include loss of the mane
and tail hair and serum exudation and lesions on the mucosae of the lips, nostril and perineum.
Inappetance and weight loss result due to the lameness preventing horses from feeding.

Dietary recommendations for selenium are up to 0.3 ppm (0.3mg/kg dry weight). Dietary levels of
more than 5 ppm cause chronic toxicosis, higher concentrations resulting in clinical signs more
quickly. Levels of 5-20 ppm are found in the hoof and hair of affected animals, with post mortem liver
concentrations of 2-20 ppm (compared to 0.5-2 ppm in normal adult livers).
The prognosis for recovery is not good, and euthanasia is often indicated on welfare grounds. Removal
of the source of selenium, provision of a low selenium diet, use of analgesics, addition of arsanilic acid
50-100ppm of food to increase biliary excretion of selenium and hoof care may be successful and if
horses survive to the point of sloughing of abnormal tissue, recovery may ensue.

Coronary band disorders

The coronary band can be involved in any of the inflammatory conditions that may affect the distal
limb, such as chorioptic mange, dermatophytosis, dermatophilosis, etc. A number of conditions
particularly affect this region, sometimes with few signs elsewhere on the limbs or rest of the body.
Irritant contact dermatitis may affect this area, resulting from accidental contact with chemicals or
agents that the horse walks through or occasionally may be iatrogenic, due to chemicals in bedding, or
materials applied to the hoof, or topical therapies. Inflammatory and, or infective conditions involving
the deeper structures of the hoof may result in exudation or discharge of purulent material at the
coronary band.
Any horse presenting with a coronitis must be thoroughly examined to establish the extent of disease
both within the foot and distal limb, and also elsewhere on the body. The same diagnostic procedures
can be conducted as for dermatoses at other sites, including biopsy. The best biopsy samples are
procured by a shave technique at the caudal aspect of the foot, above the heels. Wedge biopsies and
punch biopsies are accompanied by copious haemorrhage, making second incisions and suturing
extremely difficult. Pressure bandaging is the best way of achieving haemostasis and biopsy sites heal
well, usually with no residual effect on hoof growth.

This is a specific entity in the horse, affecting all or part of the coronary bands of multiple feet, of
unknown aetiology, but thought to be a defect of cornification. The condition is characterised by
proliferative lesions of the coronary band that may initially be exudative, followed by hyperkeratosis.
Severely affected horses may be lame, although often there is no lameness. The ergots and chestnuts
may be involved.
Other causes of secondary seborrhoea should be ruled out, and the diagnosis is one made by exclusion.
Biopsy reveals non-specific hypertrophic hyperkeratosis.
Treatment is symptomatic.

Pemphigus foliaceus in the older horse often presents with lesions primarily, or even exclusively,
affecting the coronary band. The ergots and chestnuts are frequently involved in addition to the
coronary band. There may be lesions elsewhere on the body, including mucocutaneous junctions and
mucosal surfaces. Lesions of the coronary band consist of swelling, crusting, erosions, sometimes with
some minimal exudation. Variable discomfort may be evident.
The diagnosis should be confirmed by histological examination of shave biopsies;
immunohistochemistry may be helpful in demonstrating the presence of intraepithelial deposits of
Treatment with systemic glucocorticoids will often secure complete remission, but long-term alternate
day maintenance therapy is usually required to prevent relapse. Many cases will return to useful work,
with no significant adverse effects from steroid therapy.

An exudative, ulcerative coronitis is seen in some horses with severe liver pathology, sometimes with
lesions also affecting the skin and mucocutaneous areas of the face. Affected animals usually show

clinical signs referable to the liver, with weight loss, hypoproteinaemia, elevated liver enzymes and
abnormal liver function tests. Hepatic encephalopathy may be present.
The histopathological changes are similar to the condition in other species, with epidermal oedema and
necrosis accompanied by superficial dermal inflammation and marked parakeratosis.
The prognosis is grave, since the associated hepatic damage is usually irreversible.

(eosinophilic enteritis-dermatitis-stomatitis)
The coronary bands are consistently involved in this multisystemic disease with lesions evident early in
the course of the disease. The lesions are exudative and erosive, with fissuring also seen, in addition to
exfoliation and hair loss. (See section on crusting dermatoses).
The prognosis is grave, with poor response to even high doses of glucocorticoids.

Cracked heels may be seen in a number of dermatoses covered above, and may be a part of, or
considered in a similar way to greasy heel syndrome. The term does not imply a definitive diagnosis,
but is merely a descriptive term, and the clinician should employ all the tools required to identify
specific aetiological factors. Having acknowledged that many cases may be part of any of the diseases
that may contribute to greasy heel syndrome, the management practice of frequent washing of the distal
limbs of the horse may result in excessive wetting of the distal pastern and heels, which then
predisposes to secondary infection. Attention to stable management practices and use of antibacterial
washes and emollient creams, perhaps with barrier creams to prevent over-wetting, can be employed. It
is often white heels that are more frequently and more severely involved in this syndrome.

Conditions of the frog

This is a necrotic condition of the horn sulci, extending to involve the rest of the frog, associated with
infections with Fusobacterium necrophorum. Infection becomes established due to poor management
factors, including standing in soiled, wet bedding or muddy, waterlogged pasture and failure to clean
out hooves regularly.
The hind feet are more frequently and more severely affected than the fore feet, with a distinctive, foul,
necrotic odour evident when the foot is examined. Affected sulci exude a thick, black, moist,
malodorous discharge. Probing with a hoof pick reveals that the sulcus is deeper than normal due to
loss of necrotic tissue. Most horses show no lameness.
Treatment includes rectifying stable management, with provision of clean, dry bedding. Necrotic tissue
should be pared away and astringent dressings and topical antibacterials applied. Regular foot hygiene
and foot care should be employed. Special shoeing may be needed.

This is of unknown aetiology, with rapid and excessive growth of the frog epithelium. Excessive
thickness of the frog, without adequate wear, is detrimental to foot balance and ultimately foot
conformation, and should be managed by regular, judicious paring of excess tissue by the farrier.

Some cases of pemphigus foliaceus may involve the epithelium of the frog, with softening and
sloughing of the superficial layers. A consistency similar to cream cheese may be seen. Minimal
lameness may be evident, in spite of apparently severe pathology. Other clinical signs are usually
evident at the coronary bands and elsewhere. A good response to treatment may be seen in spite of
severe presenting signs.

Neoplastic Conditions of the Foot

This is an unusual to rare tumour of the inner hoof wall, arising from the basal keratinocytes. An
expanding lesion results, with a core of abnormally keratinising tissue impinging on the underlying
pedal bone and causing localised, variably circumscribed alterations in the surface contours of the hoof
and horn quality. Radiography will reveal the extent of damage to the inner structures of the foot.

Surgical ablation, with resection of the hoof wall is the treatment of choice, with appropriate surgical
shoeing to support the remaining wall and use of resin to fill the defect until healing occurs. The
tumour has a relatively high rate of occurrence, probably related to failure to entirely remove the mass
at initial surgery.

This presents as a soft, fleshy mass, well circumscribed, with well-defined margins, affecting any part
of the frog, but may extend to the sole.
Complete surgical removal is usually very effective, although deep dissection may be required.

Farm Animal Dermatology

Clinical Approach
•   In a single day it is not possible to present a comprehensive view of farm animal skin diseases. We
    have therefore selected important and key illustrative diseases which will introduce you to the
    subject and provide a basis for understanding and further study.
•   This course will focus on the ruminant, using cattle and the goat to illustrate how general
    dermatology and knowledge of the cutaneous diseases of other species can be employed to
    investigate, diagnose and treat farm animal dermatoses.
•   A structured approach is essential. Vital information is usually obtained during the history taking
    process and sufficient time must be allowed for this. Accurate information on management is
    particularly important. Clinical examination must include systemic and skin components.

Taking the History
•       The approach is similar to that adopted in the horse. Points to include are:
        ∗        Breed, age and sex, origin. Consider these aspects carefully. In many conditions these
                 simple data will have a major impact on your diagnostic considerations.
        ∗        Type of husbandry and use
                 •        Intensive, extensive, variable
                 •        Type of housing; construction, hygiene, contamination
                 •        Conditions in pastures and holding areas
                 •        Seasonal changes in management
                 •        Feeding regimen; routine management procedures, vaccination
                 •        Contact with other animals, other species; evidence and opportunities for
                          transmission; lesions in humans in contact
•       History of the current skin problem
        ∗        First signs, progression, response to treatment and management changes
        ∗        Seasonal effects
        ∗        Any diagnostic test results
        ∗        Current or recent therapy; include questions about farm remedies
        ∗        Current status of the animal
•       General health

Clinical Examination
• A full clinical examination of both the general clinical status and of the skin is necessary in most
  cases. Ensure that the animal is adequately restrained and you have sufficient light. You may need
  to clean the skin to observe some lesions. In some instances sedation may be necessary.
• A record of the distribution and severity of primary and secondary lesions should be kept. Forms
  including an animal outline make this much easier.
• It may be necessary to visit and examine the pasture(s) used

Diagnostic Tests
The history and clinical examination should enable you to formulate a list of differential diagnoses
and to decide on appropriate diagnostic procedures. Tests may include the following:
1. Hair plucks, skin scrapings, coat brushings, tape strippings.
2. Mackenzie brush samples for dermatophytosis
3. Crusts or swabs for culture (bacteria or fungi) or smear preparation
4. Impression and pus or exudate smears
5. Biopsy sampling for histopathology; several samples, including primary lesions; use a punch larger
   than 6mm if possible, or take an excision biopsy.
6. Collection and examination and/or analysis of herbage and other materials available to the animals

Crusting & Scaling Diseases

•        Scaling and crusting are indications of changes in the behaviour of the epidermis usually
         involving hyperkeratosis (increased thickness of the stratum corneum), which may be
         orthokeratotic or parakeratotic (nuclei retained in the stratum corneum).
•        Dyskeratosis (defective premature keratinisation) may also be involved and is often present
         together with parakeratosis.
•        Crusting occurs when exudation has taken place. Exudates may be serous, haemorrhagic,
         cellular (leucocytes) or serocellular (commonest) and the nature of the exudate determines the
         appearance of the crust. In infectious conditions the crust will contain micro-organisms and,
         usually leucocytes. In autoimmune disease, such as pemphigus foliaceous, acanthocytes may
         be present.
•        Thus it is important to differentiate between scaling and crusting diseases and where crusts are
         present to determine the nature of the crust. Laboratory studies of crusts (smears, cultures,
         histopathology) are often rewarding.
•        These notes will cover the principal scaling and crusting conditions of farm animals but will
         omit those in which the these signs form a minor part of the disease process.

Sunlight & Photosensitisation
•   This is covered under pigmentary disease.

Mite Infestations - Residents

Clinical Features
•        Infestation with Sarcoptes scabiei
•        Burrowing mite, feeds on tissue fluid +/- epidermis
•        Incubation: days-weeks
•        Tends to be species specific; cross infections uncommon
•        Severe, chronic disease associated with poor management, malnutrition
•        Need not affect all animals in herd or flock
•        Transmission by direct and indirect contact

•      Signs:
       ∗        Very pruritic papular disease with production of thick crusts, lichenification
       ∗        Often starts on head and neck, then extends over back; may generalise
       ∗        Chronic disease leads to debility

•      Prevalence may be increasing in U.K.
•      Signs:
       ∗        lesions as in cattle; affect principally the head, neck, limbs
       ∗        also usually a peripheral lymphadenopathy
       ∗        often leads to general debility

•      Very rare in U.K.

•      Occurs in most herds; passed from sow to piglets
•      Progression of disease:
       ∗        First signs are crusting and excoriation of ears; signs fade after 3-4 months
       ∗        Papular rash extends over trunk
       ∗        Thick crusting of ears (hyperkeratotic form) may occur in some adults especially if

•      History, signs
•      Scrapings; may need to crush large crusts and clear with KOH
•      May be difficult to find in pigs. Examine crusts and wax from ears
•      Differentials:
       ∗        other crusting, pruritic diseases
       ∗        in pigs - a wide range of possibilities

•      Ruminants: amitraz, ivermectin, phosmet
•      Pigs: ideally eradication
       ∗        Treat females during gestation e.g. Ivermectin, 300ug/kg s/c once 8-37 d before
       ∗        Quarantine new stock

Clinical Features
•      Caused by Chorioptes bovis (cattle), C. caprae (goats), C. ovis (sheep)
•      Species specific, surface-living mites which feed on epidermal debris.
•      C. bovis can survive up to 69 d off host experimentally
•      Clinical and sub-clinical infestation of goats relatively common

•        Populations are higher in winter (temperature & humidity effect)
•        Although the disease generally regresses spontaneously in summer, the mite may still be
         detectable around the coronet
•        Signs:
         ∗        Pruritus, papules, crusts, alopecia, exudation, ulceration
         ∗        Lesions are often caudal: hind feet/legs, groin, udder scrotum, perineum, tail; can
                  affect flanks & neck
         ∗        In sheep thick scrotal crusts and exudate can cause temporary infertility

•        Scrapings and crusts from edges of lesions
•        Differentials: sarcoptic and psoroptic mange; Psorergates

•        As for sarcoptic mange but eprinomectin pour- on is easier
•        Ensure animals in contact are treated simultaneously

Clinical Features
•        Surface-living mites which feed on tissue fluid
         ∗        P. ovis - body mange of cattle & sheep (the status of P. bovis is uncertain)
         ∗        P. caprae - body & ears of goats
         ∗        P. cuniculi - ear infestation in rabbit, goat, sheep
•        Transfer occurs between these species but not to man
•        Can survive off host for 2 weeks or more: survival has been recorded experimentally for 7 and
         12 weeks respectively for P. ovis and P. cuniculi

•        Infestations worst in winter; P. ovis persists in summer in skin folds of the face, perineum,
         inguinum and interdigital spaces

•        Commonly associated with Psoroptes cuniculi and perhaps P. caprae

         ∗        Head shaking, pruritus; pinnal crusting & alopecia, increased cerumen
         ∗        If severe can cause otitis media or interna and spread to head, pasterns and
                  interdigital spaces
         ∗        May not cause any signs

•        Since 1992 dipping has not been compulsory and the UK prevalence has increased greatly
•        Signs:
         ∗        Marked pruritus chiefly of dorsal trunk
         ∗        Pustules, crusting (yellow/brown), wet & matted coat, alopecia, excoriation

        ∗        Hyperaesthesia, mouthing
        ∗        Secondary infection including dermatophilosis

•       Based on history, clinical signs
•       Scrapings, scab or crust samples from body surface, ears
        ∗        For ear infestations collect deep ear debris - otoscopy + sedation
•       Mites seldom found in biopsy specimens
•       Differentiate from other pruritic ectoparasitic diseases

•       P. cuniculi (caprae)
•       Otic drugs as in small animals - twice weekly for 3 weeks (goats)
•       Sheep scab
        ∗        Organophosphate dips (diazinon, propetamphos): precautions must be taken in the
                 use of these substances (severe neuropathies, joint disorders in man; certificate of
                 competence required to carry out dipping with organophosphates)
        ∗        References:
                 •        Pesticides: code of practice for the safe use of pesticides on farms and
                          holdings. London: HMSO, 1997.
                 •        Safe use of organophosphorus sheep dips: Important instructions for
                          farmers and operators. NOAH/VMD, April 1993.
        ∗        Pyrethroid - Flumethrin dip
        ∗        Ivermectin or moxidectin 2 injections or doramectin injection. Treat in-contacts
        ∗        Possible future role for Serratia marcesens in control?
•       Cattle
        ∗        Ivermectin s/c v. effective @ 200ug/kg

Clinical features
• Found more commonly in America and South Africa.
• Recently reported in UK,
• Life cycle completed in 4-5 weeks.
• Transmitted by direct contact.
• Small mites with radially arranged legs.

• Psorergates bovis (Psorobia bovis).

• Variable pruritus.
• Alopecia, scaling and skin thickening.
• Most areas of the body affected.

Diagnostic indicators
• History and clinical signs.

Confirmatory tests
• Skin scrapings.

• Topical acaricides.
• Ivermectin, moxidectin, doramectin.

• Infestation may persist within herd if all animals not treated.

Clinical Features
•       Mites are normal residents of skin and transferred to offspring from dam
•       Not considered contagious
•       Onset of Disease
        ∗        often associated with underlying problems:
        ∗        malnutrition; stress factors; immunosuppression by disease or drugs
        ∗        genetic predisposition may exist
•       Cattle
        ∗        3 species are found in cattle
                 •         D. bovis - eyelids and body, 200-240um long
                 •         Unclassified Demodex - eyelids and body, 195um long
                 •         D. ghanensis - eyelids, 400um long
•       Goats
        ∗        D. caprae, 224-315um long
•       Sheep
        ∗        D. ovis, 240-280um long
•       Pigs
        ∗        D. phylloides, 230-265um long
•       Signs
        ∗        Follicular papules & nodules; may form a central crust; affect especially dorsal trunk,
        ∗        Severe infections - crusting, deep pyoderma
        ∗        Goats:
                 •         Facial involvement more common
        ∗        Sheep:
                 •         Rare, alopecia, scaling, erythema;
                 •         lesions of face, neck, dorsum, can affect limbs, coronary bands
        ∗        Pigs:

                •        Snout, eyelids, ventral neck & trunk, medial thighs;
                •        lesions are papules, pustules, nodules; usually sub-clinical

•      History, clinical signs
•      Squeeze skin and scrape deeply; biopsy
•      Differentiate from other causes of folliculitis: staphylococcal, dermatophytosis,
       dermatophilosis - Note that pyoderma may be secondary to infestation

•      Correct underlying problems
•      Treat infections; specific therapy rarely attempted
•      Cull affected animals?

Other Mites - Visitors

Clinical Features
•      Found chiefly in autumn; in animals grazing in chalky areas, grassland ...
•      Principally a problem of sheep
•      Signs:
       ∗        Papules, wheals, distal limbs, face, ventrum
       ∗        May lead to exudation, crusting , ulceration, weight loss, wool loss

•      History, signs, response to treatment
•      Mites may be difficult to find in chronic lesions



Clinical Features
•      Members of the family Acaridae - Tyroglyphus and Acarus are synonyms
•      Present in hay/straw bedding; recently shorn sheep are more susceptible
•      Signs:
       ∗        Sheep shorn recently
       ∗        Wool loss, alopecia; flanks, backs

•      Forage heavily infested with mites
•      Differentiate from stress-associated wool loss


Geophilic Dermatophytes - soil inhabitants

Clinical Features
•      Sporadic outbreaks
•      Signs: thick, circumscribed, adherent, pale grey-brown crusts
•      M. gypseum - infections in cattle, horses, sheep, goats, pigs, man
•      M. nanum - infections in pigs, cattle, man

Clinical Features
•      Commonly isolated from soil; found as skin contaminant
•      Can be isolated from soil, dung
•      Wild animal reservoir exists in rodents and foxes
•      Signs:
       ∗        circular crusted lesions with broken hairs;
       ∗        can be v. inflammatory; follicles, papules
       ∗        Infections in cattle, man, goats, sheep, pigs, horses

Zoophilic Dermatophytes - adapted to animals

Clinical Features
•      Transferred between animals, fomites important; uncommon in large animals
•      Signs:
       ∗        circular crusted lesions with broken hairs;
       ∗        variable crust thickness
•      T. equinum infections in horses, man, cattle
•      M. canis infections in cats, man, dogs , horses , cattle, sheep, goats, pigs

Clinical Features
•      Transfer between animals and to/from man; fomites are important
•      Can be isolated from soil and dung
•      Signs:
       ∗        thick, adherent, circumscribed, circular greyish, crusted lesions
       ∗        infections in cattle, man, goats, sheep, pigs, horses

•      History and clinical signs

•      Woods lamp (M. canis, T. equinum);
•      KOH preparations of hair/crusts; culture, biopsy

Treatment and Management
•      Spontaneous recovery in 4-16 w normally
•      Therapy not well validated
•      Topical therapy is advisable to reduce contamination
       ∗        Enilconazole, natamycin registered for topical use in cattle
•      Systemic therapy
       ∗        Cattle:
                •         Griseofulvin 7.5mg/kg oral powder/granules;
                          duration 7 d on label but 3-12 weeks needed
       ∗        Sheep, goats, pigs:
                •         Griseofulvin 10mg/kg orally
•      Prophylaxis - cattle, calves
       ∗        T. verrucosum LTF-130 intramuscular living attenuated vaccine available; has been
                very effective in Russia and Scandinavia

Yeast Infections

Clinical Features
•      Infections in degraded skin; predisposed by stress, immunodeficiency; can be severe but rare
•      Goats
       ∗        Protein deficiency reported to predispose to candidiasis
       ∗        Signs: extensive alopecia, scaling, crusting, greasiness, lichenification
       ∗        Budding yeasts and pseudohyphae found in specimens from skin but not cultured
•      Candida albicans infection of Pigs
       ∗        Signs: greyish, exudative dermatitis, ventral lichenification
       ∗        Associated with maceration following feeding and lying on rubbish
       ∗        Resolution occurred with provision of dry bedding over a period of weeks

•      Smears (Methylene blue, Diff-Quik), cultures, biopsy

Dermatophilus congolensis infection

Clinical Features
•      Life cycle and epidemiology
       ∗        Motile infective cocci (zoospores) of Dermatophilus congolensis escape from scabs
                attached to skin or coat and are transferred to other animals or swim to adjacent areas
                of skin.

      ∗        They are attracted by CO2 to breaks in the stratum corneum where they germinate and
               invade the living epidermis. Hence any factors, which abrade the skin, will
               predispose to infection.
      ∗        Invasion provokes a neutrophilic response with hyperkeratosis, forming the scab.
      ∗        Continued wetting leads to a chronic infection but drying of the skin usually leads to
               resolution within about 3 weeks. Persisting disease can occur in stressed or
               immunosuppressed animals.
      ∗        Crusts are firmly attached to the hairs and provide a source of infection which persists
               until the next period of wet weather.
•     Pathogenesis is not understood

•     Sheep
      ∗        Syndromes: Lumpy wool, Strawberry foot rot (association with Orf virus)
      ∗        Infects most/all U.K. flocks; more severe in lowland flocks
      ∗        Infection passed from ewes to lambs during suckling and lesions often appear first on
               head and extend progressively over the trunk each year.
      ∗        In dry years tends to remain subclinical in most or all of the flock but can result in
               high morbidity outbreaks following prolonged wet weather or short periods of high
               intensity rainfall
      ∗        Signs:
               •        Wooled skin - crusts of varying thickness (3mm-1.5cm), may become
                        macerated if wet; tend to be less dense than on haired skin; large areas can
                        be affected, especially dorsal head and trunk following prolonged wet
                        weather which soaks the fleece
               •        Haired skin - more focal, denser crusts, 3mm or more in diameter, can be
                        very thick and may form horn-like structures (1cm or more, long) in chronic
                        lesions which provide reservoirs of infection, often on the ears. Haired skin
                        is affected particularly after intense rainfall.
               •        Severe infections can occur on the scrotum and adjacent skin in rams.
               •        Strawberry foot rot - an association of Orf and Dermatophilus with lesions
                        affecting the lower parts of the limbs. Crusts get rubbed off the granulating
                        lesions giving them a strawberry-like appearance.
•     Cattle
•     Bovine dermatophilosis is rarely reported in the UK but infections have been reported in:
      ∗        Milk scald of calves fed from the bucket
      ∗        Lesions of the trunk and limbs are rare or unrecognised. Leather processors report
               anecdotally hide damage in UK cattle which is indicative of dermatophilosis.
•     Pigs, goats can be affected. Infection can be transmitted to man and has been reported in a
      very wide range of vertebrates; it has been diagnosed in the fox and cat in Great Britain

•     History, signs; Smears from scabs stained with Gram’s stain, Giemsa or Methylene blue will
      reveal the characteristic branching (Gram-positive) filaments which break up into multiple
      rows of cocci.
•     Culture is difficult as Dermatophilus grows slowly and is easily swamped by other organisms


•      Bring affected animals into a dry environment
•      Investigate and correct underlying problems which may predispose to infection
•      Systemic antibiotic: e.g.
       ∗        intramuscular penicillin and streptomycin at normal doses daily for 5 days
       ∗        single high dose of penicillin (70,000 IU/kg) and streptomycin (70 mg/kg)
       ∗        a single dose of long-acting oxytetracycline (20 mg/kg)
•      Topical Cu SO4 at 0.2%
•      Dips containing 0.5% ZnSO4; 1.0% potash alum

•      Potash alum powder in fleece - small flocks

Fleece Rot

Clinical Features
•      Also called “wool rot” and “canary stain” (because affected wool is stained yellow)
•      Possibly associated with dermatophilosis but probably involves pigment producing bacteria
•      Can predispose to fly strike
•      Downgrades wool value
•      In Australia
       ∗        Can be a severe problem;
       ∗        Pseudomonas aeruginosa shown to be important
       ∗        Vaccines against the Pseudomonas aeruginosa developed

Staphylococcal Disease

Clinical Features
•      Caused by infection with coagulase positive staphylococci; spread by milkers, cloths
•      Affects goats, sheep, cattle
•      Signs:
       ∗        non-follicular pustular dermatitis; pustules develop yellowish-brown crusts; erosions
                may occur subsequently in more severe cases
       ∗        normally affects the udder, especially the teat bases and intramammary sulcus
       ∗        may spread to the ventral abdomen, thighs, perineum, ventral tail;
       ∗        can lead to mastitis

•      Daily antiseptic washes (chlorhexidine; iodophores)
•      Autogenous vaccines have been used
•      Milk affected animals last


•      Occurs in goats (acne), sheep; is rare in cattle, pigs
•      Underlying problems can often be identified
•      Signs:
       ∗        paintbrush lesions, papules which may lead to exudation, pustules and ulceration
       ∗        in more severe cases there may be furunculosis, nodules and fistulous tracts
       ∗        during the healing phase epidermal collarettes with central hyperpigmentation often


Clinical Features
•      A common infection with Staphylococcus aureus
•      Sometimes called “Goat pox” but this capripox disease is absent from the U.K.
•      Occurrence:
       ∗        often in females after first kids
       ∗        spread at milking on hands, cloths
•      Signs:
       ∗        affects especially the udder, teats, groin; also the ventral abdomen medial thighs,
                perineum, tail
       ∗        pustules, up to 4cm in diameter, are not pruritic or painful, and rupture to form scales
                and crusts
       ∗        milk yield is unaffected
       ∗        Severe infection may lead to mastitis and can cause systemic signs including fever,
                malaise and septicaemia


Clinical Features
•      Occurrence:
       ∗        3-4 week old lambs
                •        develop a benign pustular dermatitis of lips & perineum
                •        regresses in 3 weeks
       ∗        All ages, especially ewes just prior to lambing
                •        Severe facial or periorbital dermatitis; also involves the pinnae and horn
                         base; legs (thistle damage may predispose to limb lesions)
•      May be contagious; possibly spread by fighting and during feeding at trough

Diagnosis of Folliculitis and Furunculosis
•      Signs, rule-outs, biopsy, culture

•      May recover spontaneously
•      Topical antiseptics and drying - daily for 1 week then every 3-4 days
•      Systemic antibiotics if severe

       ∗        procaine penicillin 22,000 i.u./kg bid for 7-10 d
       ∗        long-acting oxytetracycline in sheep (10-20mg/kg) used in limb infection

•      Improve management, reduce abrasions;
•      Try to identify and eliminate source of infection

Clinical Features
•      Staphylococcus hyicus infection;
•      An epidermolytic toxin is produced which causes epidermal splitting and appears also to
       damage other epithelia including the ureters when the toxic passes through the skin
•      Occurrence:
       ∗        sporadic, in litters of sucking piglets up to 7 weeks, normally;
       ∗        incubation period is about 3 days
       ∗        morbidity and mortality up to 90%
•      Syndromes:
       ∗        Peracute
                •          greasy, brown exudate on face, esp. behind ears, vesicopustular eruptions
                           esp. coronets; epidermal splitting
                •          becomes generalised with systemic signs and death in 3-5 days
       ∗        Acute
                •          signs as for the peracute disease but also skin thickening and crusting; death
                           4-8 days
       ∗        Subacute
                •          lesions on the head and ears and can may involve the limbs;
                •          pigs may recover spontaneously but usually are stunted

•      History, signs, biopsy, culture

Treatment and Prevention
•      Early treatment important; isolate affected piglets; treat those in contact
•      Penicillin - 5000 i.u./kg bid for 3-5 days
•      Topical cleaning helpful;
       ∗        benzoyl peroxide shampoo (for dogs) has been used but skin can be fragile
•      Improve management
•      Bacterial interference using an avirulent S. hyicus isolate shown effective in preventing the
       disease experimentally

Clinical Features
•      Beta-haemolytic streptococci

       ∗        including Str. zooepidemicus and Str. equisimilis associated with abscesses and
                porcine ear necrosis
       ∗        including Lancefield group C streptococci associated with “Contagious pustular
                dermatitis of sucking pigs”
       ∗        Signs:
                •        fever, depression, anorexia then ventral and periocular erythema sometimes
                         with petechiae
                •        pustules in groin, axilla, lumbosacral and periocular regions
                •        ulcers may affect face, tail, legs and feet
                •        epidermal collarettes and pruritus are features of the recovery phase

•      Penicillin or tetracyclines
•      Improve hygiene and minimise skin injury; bacterins may be useful

Vitamin & Mineral Deficiencies

•      An histopathological reaction pattern: thickened corneum with retention of nuclei
•      Diagnostic significance when pattern is diffuse and there is follicular involvement

•      Failure of intestinal absorption of Zinc
•      Signs: symmetrical scaling & crusting; wasting syndrome

•      In growing pigs; related to nutrition
•      Signs: generalised crusting without pruritus

See notes on bovine chlorinated naphthylene toxicity

       ∗        Pigs: alopecia, hoof problems

       ∗        Pigs: weight loss, diarrhoea, neurological

       ∗      Calves: vitamin C-responsive dermatosis

       ∗        Goats: vitamin E and Se-responsive dermatosis
       ∗        Calves fed high fat milk substitutes: response to Vitamin E or low-fat milk substitute

Caprine Seborrhoea

Clinical Features
•      Syndrome in older male goats, particularly the British Toggenburg and British Alpine
•      Aetiology unknown but possibly associated with:
       ∗        nutritional deficiency (Zinc suggested) in the breeding season
       ∗        Urine scald
       ∗        Rubbing but not generally pruritic
•      Signs: thickened, scaly skin, especially of the head and dorsal trunk

•      Treat with shampoos; Zinc supplements have been tried

Urine Scald in Male Goats

Clinical Features
•      Urination on caudal forelegs, face and beard
•      During the breeding season
•      Signs:
       ∗        staining of coat and hair loss; may also lead to scalding of skin
       ∗        scald also caused by unhygienic housing and recumbancy

Milk Scald - Muzzle Alopecia
•      Seen in bucket fed calves
•      Persistent wetting causes scaling, hair loss and erythema of the muzzle
•      May predispose to dermatophilosis

Labial Dermatitis of Kids
•      Facial and labial erythema, alopecia
•      May be associated with S. aureus infection
•      Differentials: early stages of orf virus infection; dermatophilosis

Congenital and Hereditary Diseases

•       Also known as “Sticky kid”
•       Autosomal recessive inheritance
•       Signs: goats are born with greasy, matted coats; lifelong

•       Familial; unknown aetiology
•       Signs: crusty, non-pruritic lesions around head - eyes, nose, ears; also affects the axilla, groin
        and perineum

•       Seen in a number of bovine autosomal recessive traits

•       Affected calves skin covered by thick scaly plates
•       Born dead or die soon after

•     Generalised hyperkeratosis and alopecia at birth or within weeks
•       Microtia and cataracts
•       Also reported in pigs

Clinical Features
•       Autosomal recessive trait reported in female Holsteins;
•       thought to be lethal to homozygous males
•       Signs:
        ∗        Calves loose condition at 1-2 months of age
        ∗        Skin thickened, scaly, wrinkled in patches
        ∗        Affects: periocular regions, neck, withers, elbows, stifles, hocks; curled tips of ears
        ∗        Generalised hair loss
        ∗        Eventually excessive salivation, emaciation, death

Clinical Features
•       Occurs in cattle, sheep and pigs
•       Associated with congenital connective tissue disorders
•       Signs: fragile hyperextensible skin; lax joints

•       Cattle, sheep - severe, fatal

•      Pigs, horses - mild to moderate

•      Do not breed from affected animals

Clinical Features
•      Autosomal recessive inheritance; apparent at birth or less than 3 weeks of age
•      Signs:
       ∗        symmetrical erythematous maculopapular lesions of ventral abdomen, medial thighs
                which develop dark crusts
       ∗        lesions of hoof & coronary band
       ∗        pneumonia
       ∗        Affected animals become stunted; most die at less than 6 weeks

•      History, Rule-outs, Biopsy

•      Also known as “Pityriasis rosea”
•      White piglets (especially Landrace) 3-14 weeks old;
•      Affects one to several in a litter; resolves after 3-10 weeks
•      Signs:
       ∗        symmetrical erythematous maculopapular lesions of ventral abdomen, medial thighs.
                May be generalised
       ∗        develop to form crateriform lesions and scales, and then heal
       ∗        may be preceded by transient inappetance, vomiting, diarrhoea

•      History, rule-outs, biopsy

Organic Chemical Toxicosis

•      Used as lubricants & preservatives and have contaminated feeds
•      Pathogenesis:
       ∗        direct toxic effects and also interfere with conversion carotene to vitamin A leading
                to deficiency
•      Signs:
       ∗        Generalised hyperkeratosis but no pruritus, eventually wasting and

•      Accumulate in fat & persist
•      Poisoning described in cattle

         ∗        anorexia, decreased milk, then haematomas, abscesses, abnormal hoof growth, coat
                  matting, alopecia and lichenification of the lateral trunk region

•        Problems caused by inappropriate supplementation or nutritional excess
•        Skin Signs:
         ∗        severe seborrhoea sicca; there may be hair loss
         ∗        chiefly affects dorsum
•        Other Signs:
         ∗        lachrimation and nasal discharges, cough; inappetance; joint pain

•        Restore iodine intake to normal
•        Rapid recovery

Pruritic Skin Diseases


Parasitic infestations
•        common and often produce considerable irritation

Clinical Features
•        Linognathus vituli, Haematopinus eurysternus and Solenopotes capillatus (sucking)
•        Bovicola (Damalinia) bovis (biting)
•        Obligate parasites, host specific and entire life cycle spent on host
•        Eggs (nits) stick to hairs
•        Life cycle may take several weeks
•        Transmission mostly by direct contact
•        Usually a winter problem - close contact and because colder temperatures. Warm
         temperatures are fatal
•        Serious cause of economic loss to UK bovine leather industry
•        Signs:
         ∗        pruritus, poor coat, alopecia, excoriation and damage to hide
         ∗        restlessness, poor feeding
         ∗        reduced milk production
         ∗        calves may develop hair balls from excessive licking
         ∗        severe infestations with sucking lice may cause anaemia
•        Solenopotes capillatus, rare, found around the eyes

•       History, physical examination and demonstration of lice or nits
•       Differentials: mite infestation; pyrexia, pruritus, haemorrhagic syndrome; dietary sensitivity;
        other causes of anaemia

•       insecticides (organophosphates, pyrethroids, amitraz - sprays, pour-ons and spot-ons, also
        injectable ivermectin, doramectin and moxidectin)
•       treat all in-contacts

•       Chorioptes, Psoroptes Sarcoptes and Psorergates found in the UK.
•       All may cause severe pruritus and are more common in winter.

See notes on Crusting and Scaling Diseases
•       Ixodes ricinus, Haemaphysalis punctata found in coastal regions of UK; Dermacentor
        reticulatus is rare.
•       3 host life-cycle of Ixodes
•       Signs:
        ∗        heavy infestations may cause anaemia, irritation and skin lesions
        ∗        transmission of babesiosis (red water fever), tick borne fever and zoonoses - Lyme
                 disease and Q fever

•       amitraz, organophosphates or synthetic pyrethroids
•       pasture management

•       Signs:
        ∗        fly worry
                 •         may produce tear scalding under the eyes and to the face
        ∗        fly worry and irritation
                 •         Hippobosca equina feeds on blood from perineal and inguinal regions of
        ∗        blow fly strike
                 •         Lucilia sericata or Phormia terra-novae less common than in sheep. May
                           occur when adult cattle are dehorned in summer
        ∗        superficial skin damage
                 •         Tabanus (horse fly), Musca autumnalis, Morrelia simplex and Hydrotoea
                           spp (head fly)
        ∗        nodules
                 •         Haematobia (horn flies), Stomoxys calcitrans (stable fly) and Tabanus.
        ∗        painful vesicles
        ∗        Simulium

        ∗           open wounds
                    •      Haematobia irritans, Hydrotoea irritans
•       warble fly Hypoderma bovis eradicated in UK

•       good hygiene, insecticides, repellents, good pasture management


Type 4 hypersensitivity reactions have been induced experimentally in cattle

not documented in cattle

incriminated substances include wheat, maize, soyabean, rice bran and clover hay

not documented in cattle

rarely recognised


•       probably common but undiagnosed
•       chronic diarrhoea may lead to sore, cracked skin and alopecia in the perianal region. Dried
        faeces around the tail may lead to tissue necrosis
•       urine scald, pruritus and moist dermatitis in unhygienic conditions

•       rare in cattle, but has been reported in association with arthropod bites and stings, infections,
        systemic medications, vaccines, feeds and plants such as nettles
•       ears, face and trunk affected
•       Milk allergy a unique autoallergy of cattle, especially Jerseys and Guernseys. Believed to be
        hereditary and triggered by circumstances that cause milk retention or udder engorgement
•       Signs: urticaria and respiratory distress

•       history, physical examination, neutrophilia and eosinopaenia, intradermal test with own milk

•       milk out regularly and avoid over-filled udders; dry out gradually

•       variable cutaneous eruptions

•      first reported in UK in 1976 in dairy cows
•      occurs in silage fed cattle during winter and has a mortality rate of 90% in severely affected
•      aetiology unknown, mycotoxins suspected
•      Signs: pruritus, pyrexia and blood loss; excoriation and hair loss

•      history, physical examination, rule out of differentials
•      Differentials: pediculosis, mite infestation, dietary sensitivity

•      supportive
•      give good quality feed with no mycotoxins

•      one case reported in 1992
•      Signs: pruritus and excoriation

•      identify predisposing factor and correct if possible


Parasitic infestations
•      common and often produce considerable irritation

•      Linognathus ovillus, Linognathus pedalis (sucking)
•      Bovicola (Damalinia) ovis (biting)
•      Linognathus pedalis may cause lameness

see under cattle for general details
•      Signs:
       ∗        pruritus, wool loss, excoriation, fleece staining
       ∗        restlessness, poor feeding, loss of condition
       ∗        severe infestations with sucking lice may cause anaemia

•      history, physical examination and demonstration of lice or nits
•      Differentials: mite infestation, ked infestation, tick infestation, other causes of anaemia,

•      insecticides (organophosphates, pyrethroids, amitraz - dips, sprays, pour-ons and spot-ons,
       also injectable ivermectin)

•       treat all in-contacts
•       spring shearing and warmer temperatures reduce ked populations

See notes on crusting and scaling diseases
see cattle
(see cattle)

•       Hydrotoea irritans
•       non-biting fly; swarms around the head and causes annoyance, interrupts grazing and may lead
        to excoriations
•       may lead to secondary infection, fly strike and economic loss
•       attracted by wounds
•       lays eggs in damp vegetation in spring, adult flies emerge in June and July and persist until
        September or October
•       may help transmit August Bag (C. pyogenes summer mastitis), keratoconjunctivitis, infectious
        vulvovaginitis and possibly border disease

•       difficult ; keep flocks 15 m from woods and large hedges
•       insect repellents: cypermethrin pour-on or deltamethrin spot-on are used but are not 100% (1-2
        applications during June/July may be effective)
•       physical barrier repellents are helpful but need frequent reapplication.

•      Oestrus ovis
•       Eggs/larvae deposited in the nose of sheep
•       autumn infestations overwinter in the ewe while early summer infestations develop rapidly
•       infestation sporadic but may be severe in some flocks
•       Signs: nose rubbing and nasal discharge
•       Differential diagnosis: scrapie

•       ivermectin or closantel at any time of year
•       all neighbouring flocks should be treated simultaneously

•       wingless, hairy leathery insects 4-7 mm long, blood feeding
•       obligate parasites, entire life cycle (5-6 weeks) spent on the host
•       adult female attaches larvae to hair and wool

•     transmission by direct and indirect contact
•     engorged females can live 8 days off the host
•     more prominent in autumn and winter
•     poorly fed and debilitated animals are particularly susceptible
•     increased incidence recently because of less dipping
•     Signs:
      ∗         intense pruritus affecting principally neck, sides, rump and abdomen
      ∗        excoriation and broken wool ensue
      ∗        ked excrement can stain wool
      ∗        heavy infestations can cause anaemia
      ∗        may transmit blue tongue virus (notifiable in UK)

•     as for lice

•     fatal neurological disease
•     subacute transmissible spongiform encephalopathy
•     viral or prion aetiology
•     infection usually occurs in lambs
•     long incubation period and signs present in sheep between 2 and 4 years
•     lambs born to affected ewes may develop the disease through contact or through hereditary
•     Signs:
      ∗        change in temperament
      ∗        pruritus, excoriations and wool loss
      ∗        trembling, nibbling reflexes and incoordination

•     post-mortem examination of brain necessary for definitive diagnosis
•     history and physical examination suggestive
•     no serological tests

•     cull, using only rams with resistant genotypes

Seasonal allergic dermatitis
•     recurrent seasonal pruritus and dermatitis on teats, udder and ventral abdomen reported in area
      where Culicoides obsoletus found


Parasitic infestations
•       common

•       Linognathus stenopsis (sucking)
•       Bovicola (Damalinia) caprae (biting)
•       Bovicola (Damalinia) limbatus, Holakartikos (Damalinia) crassipes in Angoras

see under cattle for general details
•       Economically devastating in Angora goats.
•       Signs:
        ∗        mostly neck, trunk and groin
        ∗        pruritus, wool loss, excoriation and damage to the hide
        ∗        restlessness, poor feeding and reduced milk production
        ∗        severe infestations with sucking lice may cause anaemia

•       history, physical examination and demonstration of lice or nits
•       Differentials: mite infestation, other causes of anaemia, scrapie

•       see sheep

See notes on Crusting and Scaling Diseases
•       (see cattle)

•       (see sheep)

•       (see sheep)

•       (see sheep)
•       may occur in goats which have not been in contact with sheep, possibly through eating
        contaminated foodstuffs
•       incubation period may be shorter than in sheep
•       pruritus and nervous signs may be less marked than in sheep

Labial dermatitis
•      a dry pruritic dermatitis sometimes seen around the mouth of milk fed kids (mainly when
       bucket fed)

•      wipe face after feeding

Urine scald
•      moist dermatitis of face, lips and front limbs due to licking at the stream of their urine

•      frequent washing with a mild soap
•      application of Vaseline or other water repellent ointment
•      habit of licking at urine stream is difficult to cure once started


Lice (pediculosis)
•      (see under cattle for general details)
•      Haematopinus suis (sucking); may temporarily feed on humans
•      second most common ectoparasitism of pigs
•      may transmit swinepox and contribute to ear and tail biting behaviour
•      Signs:
       ∗        ears, neck, axillae and groin
       ∗        pruritus and anaemia
       ∗        restlessness, poor feeding

Mange (sarcoptic mange)

See notes on Crusting and Scaling Diseases

Yeast associated otitis
•      uncertain importance of yeast in pathogenesis of otitis externa
•      Malassezia pachydermatis isolated from ears in 86% of 4,600 pigs with otitis
•      Malassezia ovalis and Candida catenulata have also been isolated from pigs ears
•      Signs:
       ∗        head shaking
       ∗        ear rubbing
       ∗        excess cerumen production

•      history, physical examination, smears of cerumen, culture
•      Differential diagnosis: pediculosis, mange

•        ear drops with efficacy against yeasts

Other Porcine Problems

•        probably common but undiagnosed

•   in unhygienic conditions

A common problem. Can be due to:
•        Failure to produce a hair follicle - rare.
         ∗        Usually congenital e.g. underfeeding of ewe 110-130 days gestation
•        Failure of follicle to produce a hair - uncommon.
         ∗        Mainly congenital, follicular infection or cicatrition from scarring after deep skin
                  wounds destroy the hair follicles
•        Loss of preformed follicles - common.
         ∗        Often follows rubbing/pruritus. Infections, parasites, nutrition, metabolic problems,
                  toxicities, physical (urine scald etc)
Alopecia can also occur with:
• pruritus, eczema, parakeratosis, hyperkeratosis, pachydermia, dermatitis, seborrhoea

Congenital problems

This is possibly inherited in some cattle breeds and in sheep due to plant intoxication resulting in
prolonged gestation. Calves are small and suffer varying abnormalities e.g. hypotrichosis

Inherited problem in the Holstein with alopecia, loss of condition and failure of horns to grow. Hooves
overgrow and there is reduction in joint mobility

Seen in lambs and calves, epidermal bullae develop on the skin surface and in the mouth leading to loss
of hair. The hoof separates at the coronary band

Probably inherited in calves and results in defective collagen bridges in the deeper dermal layers. Skin
is shed over the knee, and coronary band with separation of the hoof.

Seen occasionally in most species as a partial or complete absence of the hair coat. There is no defect
of horn or hoof growth. The degree and distribution of hair loss is variable in different breeds.

Seen in cattle and also called fish scale disease with the animal partially or completely hairless with
plates of horny scales separated by fissures.

A symmetrical loss of hair in calves

Seen only in Scottish blackface sheep and a few days after birth there is shedding of the skin on the
limbs, the ear and also horn. Probably inherited.

Aetiology and epidemiology
•        All species due to deficiency of iodine in the feed of the dam
•        High dietary intake of calcium reduces iodine absorption.
•        Problems also arise from
         ∗        Brassica spp e.g. cabbage, rape, kale probably due to a glucosinolate which produces
                  thiocyanate in the rumen
         ∗        High levels of linseed meal, soya bean by-products as well as sewage sludge

Clinical signs
• There is an increase in stillbirths, delayed parturition, abortion and birth of weak animals
• Partial or complete alopecia occurs and the thyroid glands are enlarged

1. Signs in the new born animal
2. Blood iodine levels thyroxine (T4) often used but difficult to interpret

1. Provision of iodine to the young should allow survival
2. Ensure adequate iodine intake for adults
3. Iodine in water
4. Iodine injections

Aetiology and epidemiology
1. An increasing problem where non proprietary feeds used and not sufficiently supplemented
2. Green feeds are high in carotene but this may not be transferred across the placenta to the foetus
3. Heating, storage, and pelleting diets reduce vitamin A levels. Vitamin C and E help prevent loss of
   vitamin A in feedstuffs during digestion
4. High phosphate diets, chlorinated napthalenes and mineral oils can all reduce vitamin A levels

Clinical signs
1. Problems occur most commonly in the new-born or fast growing animal
2. There is a reduction in appetite, poor growth, night blindness, reproductive disorders
3. Xerophthalmia occurs in the calf
4. The skin becomes dry, rough and hooves become dry and cracked
5. Heavy deposits of brown bran-like scales occur in cattle. Occasionally there is hair loss

1. Signs are helpful
2. Vitamin A blood levels. Normal level above 0.42 mmol/l
3. Squamous metaplasia of the parotid salivary gland ducts on post mortem

• Increase vitamin A content of diet. Daily allowance growing animals 40 iu vitamin A/kg BW,
  pregnancy (cattle, sheep), lactation (cattle sheep pigs), feed lot 80 iu/kg BW

• Inject 10 times normal daily requirement i.e. 440 iu/kg BW

Aetiology and epidemiology
1. An uncommon condition seen in calves in the period before rumination
2. Vitamin C is synthesised in the tissues
3. Blood vitamin C levels fall after birth but start to rise at about three weeks
4. Vitamin C is involved in collagen metabolism and antagonism to histamine

Clinical signs
1. There is alopecia, dermatitis, a heavy dandruff followed by a waxy crust
2. Usually this commences on the ears or limbs, lesions may spread to the cheeks, crest of neck and
3. Lesions may be erythematous

• Signs
• Response to treatment
• Often self limiting and spontaneous recovery
• 3 gm ascorbic acid given subcutaneously is helpful

Metabolic Problems/Undernutrition

Aetiology and epidemiology
1. It can occur in any species but is most commonly apparent in the sheep. Poor continuous nutrition
   especially in pregnancy makes the hair brittle resulting in loss of coat
2. In fat cow syndrome the coat can become oily and matted.

Aetiology and epidemiology
1. Seen in sheep following housing and shearing
2. The wool is lost two or three weeks after shearing
3. It is thought to be the result of stress resulting in a prolonged rise in corticosteroid levels following
   housing and then shearing

Clinical signs

• Wool may be lost from most or parts of the body
• The bald areas have normal skin and the hair regrows

•   Histology
• Signs

• If shearing is to be undertaken it should be done at the same time as housing to provide all stresses
  at one time

• Outbreaks of alopecia in calves fed milk substitute have occurred but are not fully understood.

• In all species diarrhoea tends to adhere to the hair over the buttocks. If this continues and
  prolonged matting occurs, it will often result in a loss of hair from the buttocks. This will regrow.

• Continued wetting of the skin with urine results in a loss of hair.
• Most commonly seen in the male calf involving the medial aspects of the limb. It is mostly a
  problem where there is a weak calf, one which is recumbent, or has a pervious urachus, nephritis or
• Occasionally seen in the heifer and alopecia is in the perineal region.

Aetiology and epidemiology
1. Very rare but could arise from chronic oversupplementation of the feed
2. Cases could arise where selenium in the feed is above 5 ppm (normal supplementation level is 0.1
3. Most cases are acute and develop nervous signs
4. Skin lesions could develop in chronic cases

Clinical signs
• Signs are chronic and involve loss of condition, dullness, rough coat, stiffness, lameness
• There may be a generalised alopecia (pigs) or more localised e.g. hairs at the base of tail (cattle)

• History
• Signs
• Selenium assay
    ∗ Blood levels of 3 mg/kg are associated with illness
    ∗ Hair samples with selenium levels of 5.0-10.0 mg/kg suggest possible toxicity and above 10
      mg/kg indicate toxicity

1. Remove source of selenium
2. High protein diets help to protect
3. Inclusion of arsanilic acid at 0.01 - 0.02% in pig diets is helpful

1. Very rare, mercury was used as an antifungal agent for grain but now prohibited
2. Signs of acute poisoning involve acute gastro-enteritis
3. Chronic cases can lead to skin lesions

Clinical signs
1. Depression, anorexia, emaciation, a stiff gait possibly progressing to paresis, chronic diarrhoea,
   petechiation and tenderness of the gums
2. Alopecia with scabby lesions around the anus and vulva can occur. Pruritus is present

• Mercury levels in the kidney

1. Intravenous injection of sodium thiosulphate. Cattle - 15-30 g in 100-200 ml water 30-60 g orally
   every 6 hours
2. Remove mercury source

Aetiology and epidemiology
1. Uncommon but may occur in calves on milk substitute
2. Alpha tocopherol is high in green grasses but lower in hay
3. Vitamin E levels falls with propionic acid use, storage, heating and rancidification
4. Vitamin E prevents fatty acid hydroperoxide formation
5. Signs of deficiency are usually similar to these with selenium deficiency
6. Problems need to be further assessed

Clinical signs
1. Skin lesions are not normally associated with vitamin E deficiency. Usually they involve muscular
   dystrophy, unthriftiness, reproductive problems or reduced resistance to infectious disease
2. Groups of calves on milk substitute have developed alopecia on the muzzle, around the eyes, base
   of ears and hind limbs. Scurfiness of skin may occur

1. Signs but may need to be reassessed
2. Blood vitamin E levels (normal levels above 1.2 mmol/l)
3. Response to therapy

1. Injection of vitamin E may be helpful
2. Change of milk powder or addition of vitamin E may prevent the problem

Nodules, ulcers and pigmentary disorders

Nodular Diseases

Trauma may result in haemorrhage, bruising, swelling and inflammation. Secondary infection is a
common sequel. Common causes include inadequate space and poor design of housing, fighting, rough
handling, injury during transportations, penetrating wounds, dirty injections.
Haematomata are usually the result of trauma, but haemorrhagic disorders may result from ingestion of
toxic factors such as bracken poisoning, dicoumarol poisoning including chronic toxicity due fungal
action on sweet clover and related species. Occasionally drugs and mycotoxins may cause
thrombocytopenia. An inherited clotting factor defect is recognised in Holstein-Friesian cattle, factor
XI deficiency.

Clinical signs
Sudden appearance of swelling, may continue to enlarge, often painless, may pit on pressure, may
organise into firmer clot and serous fluid, sometimes bruising visible through the skin. Needle
aspiration will aid in differentiation from abscesses, use ultrasound if concerned about hernia or
rupture, blood samples to demonstrate platelet deficiency and clotting screening tests.

Need to identify and deal with underlying cause if possible. Drainage of haematomas under farm
conditions may result in local infection. Transfusion may be economically viable in some farm animals
where appropriate.

Herniation may occur at natural orifices in the abdominal wall - umbilical, inguinal, scrotal. Familial
factors are likely to be involved. Umbilical hernias often become infected.
Traumatic ruptures may occur with tearing of abdominal musculature.

Swelling over joints or bony prominences due to inflammation of underlying bursae, can result from
localised trauma, but may become infected. Chronically infection of bursae by Brucella abortus may
occur in affected herds. May be aspirated - aseptically, correct underlying predisposing causes, use
antibiotics if infected, may not resolve completely.


Usually follow trauma, penetration by sharp objects, may be iatrogenic (dirty needles, contaminated
solutions, inappropriate site of injection). Bacteria commonly involved are streptococci, staphylococci,
clostridial species, Arcanobacterium pyogenes (formerly Actinomyces /Corynebacterium) pyogenes),
Fusobacterium necrophorum.

Clinical signs
Variable sized swelling, often acute and usually painful, initially firm but will result in pitting and
pointing and may rupture spontaneously. Some abscesses fail to drain and become chronic and hard.
Local drainage lymph nodes may be enlarged. Aspiration reveals purulent material.


Hot compresses to encourage pointing, lance and drain, with copious lavage. Systemic antibiotics may
be necessary.

 Often seen in neonatal calves, lambs and kids. The infection may be localised to the cord itself or in
the subcutaneous tissues and abdominal muscles. Bacteraemia may result and weakening of the
abdominal wall may result in herniation. Organisms involved include Arcanobacterium pyogenes,
staphylococci, Escherichia coli, and Proteus. The problem in a herd or flock may increase over the
calving or lambing season.

Clinical signs
Swollen, fleshy umbilicus, which may be painful on palpation and pus may be expressed. The animal
may be dull and pyrexic.

Parenteral antibiotics, may need surgical attention.
Prevent by improving hygiene at parturition, with treatment of navel with iodine dip.

Diffuse swelling and inflammation of subcutaneous tissues, often secondary to trauma.
Infection with Clostridium chauvoei may cause "Blackleg" in all farm species, and gas gangrene or
false blackleg resulting from Cl. septicum ,Cl, novii or Cl. sordelli. These anaerobes are found in the
soil, and probably enter the animal via the gut, with localisation in damaged tissues. Any muscles
maybe involved, but the limb muscles are usually affected. Periparturient injuries in sheep and goats
are particularly susceptible.

Clinical signs
Swelling, heat and pain, later cold, painless and emphysematous. Animal is lame, depressed and
pyrexic. Death is common in 12-36 hours.

High doses of penicillin, initially crystalline, then procaine penicillin. Prophylactic vaccination should
be given to other animals.

Caused by Corynebacterium pseudotuberculosis, seen in sheep and goats. Infection may enter via skin
wound, but no lesions at this site, with enlargement of local lymph node weeks to months later.
Haematogenous spread may occur to lungs, liver etc. Lymph nodes become abscessated, semi-solid
and later caseous, with thick fibrous capsule, rendering systemic treatment of little value. Can lance
and drain lesions. Can cull infected animals on basis of ELISA test to eliminate disease. Need to
differentiate from Actinobacillus lignieresi lesions. Vaccination available in Australia.

Ulcerative lymphangitis is a rare condition of cattle caused by Corynebacterium pseudotuberculosis,
infection via skin wounds, which causes lymphangitis of the lower limbs, with nodules up to 5cm
diameter which may discharge clear gelatinous exudate. Local lymph nodes may be enlarged.
Diagnosis is by signs and detection of organism, treatment with systemic antibiotics. Different
pathogenesis to caseous lymphadenitis in sheep and goats, and does not occur in association.

Subacute infections in pigs infected with Erysipelothrix rhusiopathiae may present with palpable
urticarial like swellings on the belly, neck and ears, preceding the appearance of the classical red or
purple diamonds. In severe cases the diamonds may coalesce, harden and slough. Similar skin lesions
may be seen in Swine Fever or African Swine Fever. , Acute erysipelas may result in sudden death,
while lameness or endocarditis may occur in chronically affected animals. Systemic penicillin, possibly
in combination with anti- serum is usually successful in acute and subacute cases. The organism may
be present in the soil or in carrier pigs, so vaccination is indicated on affected properties .
Erysipelothrix rhusiopathiae can cause cellulitis with extension to the laminae of the feet in sheep,
after dipping in soil contaminated dips which contain no bacteriostat.


Caused by Mycobacterium bovis, may cause disease in all species, but commonest in cattle and is a
zoonotic risk. Relatively rare, but pockets of infection exist, thought to be in association with reservoir
of infection in badgers. Many cases are detected before clinical signs present, by tuberculin testing. The
disease is notifiable.

Clinical signs
May involve respiratory signs, loss of condition, variable appetite. Superficial lymph nodes may be
painlessly enlarged and may occasionally rupture to the surface. Skin involvement is rare. Diagnosis is
confirmed by presence of acid fast bacteria in discharge. Infection of milk may occur in advanced

Infected animals and those reacting to the tuberculin test are slaughtered. The herd undergoes periodic
tuberculin testing until clear of infection.

Papular and nodular lesions found on the lower limbs of cattle, suggests contamination of cutaneous
wounds with gram-positive acid-fast organisms, found in smears and biopsies. Organisms implicated
include M. kansasii and M. farcinogenes. Lesions are often in chains along lymphatics, may extend up
limbs to abdomen and may rupture and discharge thick pus. Regional lymph nodes are not usually
involved. Treatment not usually instituted, poor response to antibiotics. Affected animals may give an
inconclusive or positive tuberculin reaction. Although humans and other species may be affected by
these opportunistic organisms, the condition is not thought to be contagious.

Infection with Actinobacillosis lignieresi can occur in cattle, sheep, goats and man.

Clinical signs
In cattle usually causes “wooden tongue” with swelling of the tongue and presence of nodules and
abscesses, which later becomes shrunken and fibrotic. Cutaneous lesions occur in sheep, especially
jaw, face, nose and neck folds; the tongue is rarely affected. Enlargement of maxillary and parotid
lymph nodes may occur with or without tongue involvement.

Systemic antibiotics usually effective, but need prolonged course (penicillins, streptomycin,
sulphonamides). If prolonged courses fail to secure resolution then iodides can be helpful. Infected
animals are a source of infection to others and should be isolated and subsequently culled.

Infection with Actinomyces bovis is seen mainly in cattle, occasionally in pigs and may infect man. A
common inhabitant of the oral cavity, causes “lumpy jaw” osteomyelitis of the maxilla or mandible.
Pain on eating leads to wasting. In pigs granulomatous lesions can occur with visceral involvement.
The bony lesions may rupture and discharge small amounts of thick pus. Usually responds to long
courses of antibiotics with iodides, but can act as source of infection, so isolate infected animals and
cull when appropriate.

Also known as Necrotic ulcer. Caused by a spirochaete organism, Borrelia suilla, with lesions on the
face of sucking pigs and also abdomen of sow. Small hard fibrous swellings ulcerate and produce a
persistent ulcer with a centre of granulomatous tissue covered by thick grey pus. Lesions may expand
and cause tissue loss. Treatment consists of systemic penicillin or topical antibiotics.

The severe form of this disease of cattle is caused by a member of the capripox genus of viruses,
known as the Neethling pox virus, which occurs in Africa including Egypt, and Israel. A milder form
of the disease is caused by the Allerton herpes virus, BHV-2 (see bovine mammillitis).

Clinical signs
Sudden appearance of cutaneous nodules 1-4 cm diameter, often with regional lymphadenopathy. In
severe form animals are pyrexic, with oculo-nasal discharge, lameness and may abort.

Infected animals should be separated. Secondary bacterial infection may need treatment. A vaccine is
available for the severe form.

Granulomatous lesions containing a fungal mycelium, occur most commonly in warm wet areas such
as the southern USA, Europe and India (organisms include Cladosporium sps, Curvularia geniculata,
Fonsecaea pedrosoi, Helminthosporium sps, Petriellidium boydii, and Philalophera sps) which
probably enter the skin through a small wound.

Clinical signs
Subcutaneous nodules which may be accompanied by lymphangitis (Sporotrichium sps), or larger
granulomata, Ulceration and discharge of pus containing fungal elements may occur.

Systemic ketoconazole or iodide therapy, surgically de- bulking the granuloma if large, together with
systemic therapy.

Neoplastic conditions

Papillomatosis is caused by host-specific DNA papovaviruses. In cattle papillomatosis is common.
There are at least six different types of BPV, which tend to have site specificity and a degree of lesional
specificity. Several strains of BPV may cause lesions on the teats of cattle.
•   BPV-1 causes the typical fibropapillomas on the teats and penis of animals under 2 years of age.
    Lesions usually regress within 1-12 months

•   BPV-2 cause fibropapillomas on the head, neck, dewlap and occasionally legs and teats of
    animals less than 2 years old. Lesions often spontaneously regress, but immunity is not complete
•   BPV-3 causes atypical warts in cattle of all ages. Lesions are low, flat, circular, non-pedunculated,
    with frond-like projections; may occur anywhere on the body surface including teats, and do not
    regress spontaneously
•   BPV-4 causes lesions in the gastrointestinal tract
•   BPV-5 causes rice-grain warts on the teats of cattle of all ages, which do not regress spontaneously
•   BPV-6 is associated with proliferative, fronded lesions.

Interdigital papillomatosis are suspected to have a viral aetiology.
Ocular papillomas in cattle may also have a viral aetiology, with virions identified by electron
microscopy and spontaneous resolution occurring in 25-50% of cases. May also be precursors of
squamous cell carcinoma.

Squamous cell carcinoma affecting the eyelids and ocular tissues of white faced cattle is known as
"Cancer Eye" and may progress from a papilloma virus associated plaque-like to papillomatous lesion
to invasive neoplasia of epidermal tissues of the skin, eyelids, conjunctiva and cornea, induced by
exposure to ultraviolet light. Treatment is by surgical removal, where possible. Use of BCG vaccine as
immunotherapy has also been reported to be helpful.
Squamous cell carcinoma may also affect sheep and goats, with lesions usually seen on ears, but also
nose and occasionally perineum of goats. Proliferative growths with ulcerated surfaces seen. Surgical
removal of ear pinna effective when lesions small.

Caused by a retrovirus, resulting in multicentric lymphosarcoma in adult cattle. The disease affects
cattle mostly 4-8 years of age and is rare under 2 years old. The condition is uncommon in Britain with
only a few infected herds, but common in North America and some European countries, and was
originally imported with Holstein Friesian cattle. The disease is notifiable (all neoplasms apart from
papilloma, haemangiomata and haemangiosarcoma should be reported to relevant authorities).

Clinical signs
Superficial lymphadenopathy is present in most cases, with other signs (alimentary, neurological etc)
depending on site of involvement. Systemic signs of anorexia and weight loss are common. Viral
aetiology confirmed by blood test and ELISA. Immunological studies indicate it is primarily a B-cell

Notifiable disease, with confirmed cases resulting in imposition of movement restriction off farm,
encouraging slaughter of affected cases and testing of rest of herd.

An antigenically similar retro-virus is associated with lymphosarcoma in sheep.

Most cases of cutaneous bovine lymphosarcoma are sporadic, non-BLV related, occurring in young
adult animals 1-4 years of age.

Clinical signs

Lesions are usually multiple and plaque-like, with normal overlying skin or alopecia to hyperkeratosis.
Often lesions spontaneously regress, but remission is usually followed by relapse and internal
involvement. A juvenile form occurs in calves, with multiple lymphadenopathy and systemic dullness,
pyrexia and weakness. Thymic lymphosarcoma occurs in 1-2 year old cattle. Some cases show

Cases should be notified to the authorities, but usually there are no preventive measures. Some cases of
thymic lymphosarcoma may have an inherited basis.

Ulcerative Diseases

Accidental exposure to agricultural and medicinal compounds in concentrated form may result in
chemical damage to cutaneous and deeper tissues. Examples would include caustic dehorning paste in
calves, and incorrectly diluted formalin foot baths, chemicals added to forage or grain.

Clinical signs
Depend upon site of contact and nature of chemical. Ingested chemicals may cause lesions around the
mouth, foot baths or chemicals on pasture or bedding would give rise to lesions of the feet, coronary
band and interdigital areas. Chemical burns are usually painful, oedematous and result in necrosis and

Symptomatic treatment and antibiotic cover to control secondary infections. Prevention of further
damage by proper attention to dilution of chemicals, appropriate storage of concentrated solutions etc.

A common problem seen in all species, but particularly sheep. Species of fly involved include
•   Lucilia sericata chief species in UK, also L. cuprina , L. caesar, L. illustirs - primary flies which
    initiate strike by laying egges on living animals
•   Calliphora erythrocephala, C. vomotoria - secondary flies which usually lay their eggs on animals
    already struck, the larvae extending the injury done by the larvae of the primary flies
•   Phormia spp, Musca domestica - tertiary flies, whose larvae do little further damage
The problem is most common in warm wet summers. Blow flies are attracted to faecal or urine soiled
area, particularly around the perineum and buttocks, and also to wounds. Strike may also be a sequel to
infections with dermatophilosis or wool rot. The problem has become more common since compulsory
dipping for sheep scab has been discontinued.

Clinical signs
The earliest lesions are easily overlooked. Affected animals become restless, inappetant, may rub and
bit at the area. Affected area becomes discoloured and malodorous. On examination eggs and maggots
are found on inflamed and ulcerated skin. Animals may become dull, pyrexic and toxic and may die.
Recovery may be protracted with scarring.

Clean area, remove maggots, apply larvicidal powder to area. Other sheep should be treated with
appropriate insecticide to prevent further cases. Docking of lambs’ tails reduces faecal soiling of
perineum and buttocks. Wool should be removed from the crutch area as a preventative in spring -
before full shearing is due. All wounds should be dressed appropriately with powder containing
antibiotic and larvicide.

Frostbite damage is relatively uncommon, but may affect the extremities of any species, particularly
young animals. Very low temperature causes vasoconstriction and subsequent ischaemic necrosis, with
sloughing of devitalised tissue. The ear tips, tail and occasionally distal limbs may be affected. The
condition should be prevented where possible by housing animals in extreme weather conditions. If
animals are accidentally exposed, symptomatic treatment with debridement to remove necrotic tissues
and routine wound care with antibiotic cover is indicated.

Vasoconstriction results from ingestion of the alkaloid produced by the fungus Claviceps purpurea
(ergot of rye) in high concentration or in cumulative small doses over a long period. Arteriolar spasm
and endothelial damage result in vascular occlusion, ischaemia and necrosis.

Clinical signs
The ear tips, tail and distal extremities are affected, with initial signs of swelling, erythema, hair loss,
hypothermia of tissues followed by blackening, drying and separation of necrotic tissue. In some cases
the animal may also show diarrhoea.

If the limbs are involved, euthanasia is indicated. Otherwise removal of necrotic tissue if necessary,
and prevention of exposure to ergot.

Dry gangrene of ear tips, tail, distal limbs below fetlock may occur in calves as a sequel to
salmonellosis, which may not have been recognised at the time, but the history indicates diarrhoea has
been present in some of the calves previously. Isolation of salmonella spp. by the time of appearance of
the skin lesions is unlikely. If limbs are involved, euthanasia is indicated.

Rare, acute, self-limiting urticarial, maculopapular or vesico-bullous dermatosis reported in cattle.
Lesions are usually symmetrical, annular, persist longer than classical urticaria and lack the scaling,
crusting and alopecia usually seen with other causes of superficial annular lesions. No cause has been
established for the cases reported in cattle, but immune-mediated aetiology triggered by drugs,
infectious or other internal disease should be suspected.
The condition is usually benign and self-limiting.

Viral infections

Caused by a picornavirus, endemic in some parts of the world, with sporadic outbreaks in Europe,
recent outbreak in UK and Netherlands in 2001. Transmission by inhalation and ingestion, incubation
2-7, up to 14 days. Notifiable disease, with slaughter policy of affected herds and adjacent herds in UK,
movement restriction orders in infected areas and export of animals, semen and meat prohibited.
Vaccination used in some countries as routine or as part of disease control to reduce spread. Use of
vaccine resisted in recent UK outbreak because of delay in ability to declare country free of disease
(difficulty in differentiating between infected and vaccinated animals) and return to normal export

Clinical signs

Most severe in cattle:
•   pyrexia up to 48 hours followed by epithelial lesions
•   vesicles affecting tongue, hard palate, dental pad, muzzle, lips, coronary band, interdigital space
    with under-running of horn, teat lesions
Sheep and goats less severely affected:
•   lesions less vesicular, more under-running
•   affects mucous membranes, mouth -particularly dental pad, interdigital space, coronet, heels
•   differentiate from ulceration of mouth due to hard, poor quality feedstuffs
Pigs shed large amounts of virus, important in wind borne transmission:
•   sudden lameness, painful feet
•   whitening of epithelium followed by ulcers on tongue and snout, interdigital space and around
    supernumerary digits, under-running of horn causing “thimbling”

If disease is suspected, notify authorities and stay on premises.

Worldwide infectious disease of cattle caused by a pestivirus (RNA, Togaviridae). Transmission by
direct contact and inhalation.

Clinical signs:
•   discrete erosions, which may coalesce and lead to necrosis
•   lesions found on muzzle, lips and nostrils, may also occur on vulva, prepuce, coronet and
    interdigital space with subsequent lameness
•   occasionally crusts, scales and alopecia occur on perineum, medial thighs, neck
•   systemic signs of anorexia, followed by diarrhoea
•    abortion may occur in pregnant animals or still born calves. Live calves with congenital
    abnormalities may be born, or calves that are immunotolerant to the virus initially and then break
    with severe, usually fatal disease (Mucosal Disease) between 6 and 24 months of age.

Sporadic, acute, often fatal systemic disease of cattle in most parts of the world.. Exists in at least two
forms, wildebeest-associated form in Africa caused by bovine herpesvirus (BHV) 3 and sheep-
associated form whose precise aetiology is undetermined. Incubation period is extended, 18-73 days.

Clinical signs:
•   erythema, scaling, necrosis, and ulceration of muzzle and face, occasionally udder teats , vulva and
•   cutaneous lesions of purplish discoloration, papules, crusts, thickening , oozing and necrosis may
    affect perineal, axillary, inguinal and dorsal skin
•   may have lesions at coronet and result in sloughing of horn
•   systemic signs of anorexia and high fever, scleral congestion and keratitis, severe respiratory
    enteric and neurological signs and death

Parapoxvirus infection of cattle of all ages and breeds around the world, but more common in animals
under one year of age. Morbidity 10-100%, mortality rare. Incubation period 3-5 days. Disease of
limited economic significance. Agent may be identical to that causing pseudocowpox, but there are
several strains.

Clinical signs:
•   erythematous macules which evolve into papules and undergo central necrosis, become crusted
    and papillomatous (ie proliferative rather than erosive)
•   lesions commonly on muzzle, nostril and lips and occasionally on lateral trunk, abdomen, hind
    legs, scrotum and prepuce
•   cows nursing infected calves may develop teat lesions
•   lesions may persist for weeks to months in otherwise healthy animals
•   may cause lesions on fingers and hands of humans (milkers nodules) identical to pseudocowpox
    and contagious pustular dermatitis virus lesions

Worldwide common disease of sheep and goats, occasionally of cattle, caused by a parapoxvirus. Also
transmissible to man. Transmitted by animal to animal contact, shed scabs and fomites. Incubation 2-3
days. High morbidity, low mortality unless secondary infection intervenes, rapid spread, virus very
persistent in environment.

Clinical signs:
•   primarily disease of lambs and kids
•   lesions on lips, muzzle, nostrils and eyelids
•   in severe cases lesions also on genitalia, perineum, coronets, interdigital spaces, pasterns, fetlocks
    and oral cavity
•   lesions may occur on teats and udders of nursing ewes and nanny goats and also of cattle
•   lesions follow typical pock progression (early vesicle-pustule-rupture-crust), quite proliferative,
    with healing usually in 4 weeks
•   recovery produces immunity, but no colostral transfer of antibodies so newborn animals are
•   considerable economic significance because of failure to thrive due to inability to suckle and graze
•   zoonotic
Disease is self-limiting. On farms where orf is a problem, control by vaccination of ewes at least 6
weeks before lambing, live vaccine applied by scarification. Can vaccinate lambs from birth.


Orthopoxviruses, latter being laboratory propagated virus formerly used for prophylactic vaccination
against human smallpox. Cowpox may be misnamed as the virus is endemic in wild rodents (such as
Microtus spp.) in Britain and Europe, but is rare in cattle. Disease has not been recorded in UK for
several decades. When virus is introduced into susceptible herd, rapid spread occurs within 2-3 weeks,
transmitted via teat cup of milking machine and milker’s hands. Classical lesions of thick, red, crusted
pocks 1-2cm in diameter, affecting teats and udder, and in severe cases, medial thighs, perineum ,
vulva, scrotum and mouth of nursing calves.

Pigmentary Disorders

Sudden exposure to large amount of sunlight may results in sunburn damage to white skinned, sparsely
haired areas of any species, particularly light-skinned dairy goats and white pigs. Phototoxic damage is
a reaction to ultraviolet (UV) light of wavelength 230-320nm , UV-B.

Clinical signs
Erythema, scaling, sometimes with exudation, crusting and necrosis.

Gradual exposure or limited exposure to sunlight and use of sunscreens

The presence of a photodynamic agent in the tissues may result in non-pigmented and thin-coated skin
when exposed to UV-A light (320-400nm). The UV light results in the production of free radicals and
subsequent tissue damage and release of enzymes and other mediators. Photodynamic agents may
reach the skin after ingestion, injection or by direct contact. Cutaneous gangrene may occur in severe
cases if the animal is not removed from sunlight.
Primary photosensitising agents include
•   plants eg Hypericum (St Johns Wort), Lolium perenne (perennial ryegrass)
•   chemicals eg phenothiazine, sulphonamides, tetracyclines
Secondary (hepatogenous) photosensitisation is the commonest form encountered in farm animals.
Abnormal liver function results in failure to excrete phylloerythrin, which is produced by enteric
bacterial breakdown of chlorophyll, and is photodynamic. Liver damage can result from poisonous
plants such as ragwort (Senecio jacobea) or bog asphodel (Narthecium ossifragum), mycotoxins such
as aflatoxin or that produced by Pithomyces chartarum which grows on moist dead plant material, or
chemical toxicity, or from infections or tumours. A congenital hyperbilirubinemia occurs in Southdown
Photodermatitis results from direct contact of the skin with the sap of some plants such as
Ranunculacae (Buttercups) and the Umbelliferae, Heracleum mantegazzianum (Giant Hogweed) and
Anthriscus sylvestris (Cow Parsley), which locally sensitise the skin to UV light. Lesions occur
principally in non haired and non pigmented areas of the dorsal and lateral regions. This results
erythema and pruritus in the affected areas. Oedema of the head, ears and teats may occur. Lesions on
the muzzle may be confused with viral vesicular diseases.
Bovine congenital porphyria (pink tooth) is the result of accumulation of uroporphyrin I and
coproporphyrin I in tissues due to aberrant haem synthesis, inherited as an autosomal recessive trait.
The porphyrins are photodynamic. Affected animals have discoloured teeth, reddish urine and anaemia
and may develop photosensitisation. Orange-red fluorescence of teeth and urine is seen under
ultraviolet light.
Idiopathic photosensitisation is seen in groups of animals on lush pastures containing particularly
clover, but also lucerne (alfalfa), vetch and oats. The pathogenesis is not understood and the incidence
is sporadic, occurring in certain pastures in some years and not others, often after a wet spring.

Photoallergy is recognised in humans, where sensitised individuals after contact with certain plants
followed by UV light exposure develop lesions, but this mechanism of damage has not been well
described in animals.

Clinical signs
The damage occurs in non- or lightly-pigmented skin that is sparsely-haired, but can extend to dark-
skinned areas. Areas typically affected are the eyelids, face, ears, perineum and coronary band. Initial

signs of acute swelling, erythema and pain or pruritus may lead on to vesicles or bullae, oozing and
         The number of animals in a group that are involved will usually point to either primary or
secondary aetiology, together with history of pasture, drug usage etc. Liver function testing is
indicated, since the long term prognosis is poor in cases of secondary hepatogenous photosensitisation.

Removal of the source of the photodynamic agent, avoidance of UV light and symptomatic therapy -
analgesics, anti-inflammatory agents, debridement, antibiotic cover as needed. Animals with chronic
liver disease are usually culled.

Dietary requirement for copper for cattle and sheep is approximately 8-9mg/kg dry matter feed.
Inadequate concentrations of copper in the diet, or excess molybdenum inhibiting copper absorption
and storage, results in copper deficiency. Copper is essential for certain oxidative enzyme activity,
particularly tyrosinase, which is vital for synthesis of melanin.

Clinical signs
Young cattle are particularly susceptible, with faded coat colour, especially periocular producing
typical “spectacled” appearance. Varying degrees of itching and coat licking may occur. Dairy herds
with copper deficiency often have a history of lameness associated with exfoliative dermatitis and heel
cracks. Diarrhoea is also seen. Sheep show changes in wool texture, with steely wool and loss of crimp,
since alignment of keratin fibrils and disulphide group cross-linking is abnormal in copper deficiency.
Anaemia and loss of condition also occur. Affected animals have blood copper levels <0.7 µg/ml and
liver levels < 20ppm dry matter.

Avoid pasture and forage high in molybdenum. Copper supplementation orally (sheep 4g of copper
oxide needles, cattle 8-24g depending on size and severity of the deficiency) or by injection (copper
edetate in cattle, copper methionate or heptonate in sheep). (Note that excessive supplementation in
calves and sheep can results in copper toxicity, causing jaundice, haemoglobinuria,
methaemoglobinaemia and death).

This is an autosomal recessive partial oculo-cutaneous albinism that has been described in Hereford
cattle. In addition to the absence of pigment in the skin and eyes, abnormalities of white cells and
platelets are present. Affected cattle have photophobia, increased susceptibility to infections,
haemorrhagic tendencies and reduced life expectancy. Microscopical abnormalities include large and
clumped melanosomes, which are not delivered normally to keratinocytes and enlarged cytoplasmic
granules in leucocytes. These are enlarged lysosomes, thought to be due to abnormal membrane fusion.

The Foot
Pedal problems are of great importance in farm animals. Lameness can be a major constraint on farm
profitability and may cause considerable pain. Thus it is both an economic problem and a welfare
This section will consider only foot problems related to the skin but it should be remembered that
orthopaedic conditions are also important. We will describe the most significant pedal infections of
cattle sheep and goats.



Also known as: interdigital necrobacillosis, Foul in the foot, interdigital pododermatitis

•   Acute or subacute necrotising bacterial infection of interdigital skin and subjacent tissues
•   Involves infection by gram-negative anaerobes: Fusobacterium necrophorum, Dichelobacter
    (Bacteroides) nodosus and Bacteroides melaninogenicus
•   Bacterial invasion occurs following damage to the interdigital skin - trauma, maceration, ice

•   Very common cause of foot lameness of cattle. This is a first rule out.
•   Sporadic but can be epidemics; commonest in wet weather and in dairy cattle; can recur - little
    immunity develops
•   Sudden onset, mild to severe.
•   Characteristic odour and location; presence of interdigital fissures. may affect more than one foot.
•   May extend to involve deeper tissues and lead to swelling of pastern and fetlock
•   Systemic signs may be present: inappetance, loss of weight, reduced milk production, pyrexia

•   History, signs: location, odour
•   Culture seldom necessary

•   Clean foot, debride necrotic tissue, disinfect
•   Give systemic antibiotics, e.g. penicillin, tetracycline, sulphonamide. Note: choice of antibacterials
    will depend on whether beef or dairy
•   Prognosis. Rapid recovery in 2-3 days unless joint or tendon involvement.
•   Prevention and control. Remove causative factors, use footbaths.

Also known as: hairy warts, digital papillomatosis ...

•   Not warts! Appears to be caused by a spirochaete
•   Transmissible and can be introduced to a farm by bringing in clinically normal cattle from infected

•   Warty or hairy, cauliflower-like proliferation and inflammation of skin above heels adjacent to
    interdigital space. Exudate may mat surrounding hairs. “Hairy” keratin fronds develop in later
    stages (up to 1.5 cm).
•   Lameness absent to severe. Lesions are quite painful.

•   Typical clinical appearance. Histopathology may confirm.

•   Clean lesions and apply topical antibiotic e.g. oxytetracycline
•   Introduce footbaths - maintain long-term. Otherwise recurrence within 2 months likely.

•   Surgery was used in the past.
•   Prognosis. Quite good with good management.

Also known as corns, interdigital fibroma

•   Chronic irritation - poor conformation? Inherited in Herefords? Poor foot trimming
•   Interdigital proliferative reaction
•   Often infected with F. necrophorum

•   Quite common. Affects dorsal or middle if interdigital space. Generally causes no lameness but
    can be severe if large - pressure from claws. May become infected - very painful

•   Characteristic appearance

•   Clean and treat with local or systemic antibiotics; hold animal in clean environment
•   If lame and large - surgical removal. Dress wound and hold animal in clean area for 2 weeks
•   Prognosis. If deeper tissues not involved, generally rapid recovery (a few days). May recur
    especially in Hereford bulls.

Sheep and goat generally share the same problems. However, goats are generally more severely

Also known as: contagious foot rot, hoof rot ...

•   Multifactorial. Damage to interdigital skin and infection by F. necrophorum (present in gut and
    environment) facilitates infection with D. nodosus (specific pathogen, habitat ruminant hooves,
    survival in soil only 7 days).
•   D. nodosus infection introduced by bringing in sheep from infected flocks. Readily transferred
    between sheep and goats
•   Role of spirochaets controversial.

•   Degree of lameness and extent of outbreak depends on severity but not every animal may be
•   Severely affected sheep are recumbent, loose weight, may suffer decubitus and then fly strike.
    Wool production, fertility affected.
•   Severe lesions involve separation of soft horn of heel and sole and necrosis of affected tissues;
    characteristic smell.
•   Disease divided into benign (BFR) and virulent (VFR) forms

•   History, signs. Gram-stained smears of necrotic tissue show D. nodosus.
•   VFR is caused by virulent variants of D. nodosus and can be characterised by lab tests (e.g.
    elastase, gelatinase) but animals may have both benign and virulent isolates simultaneously so
    must test multiple isolates.

•   Evaluate proportions of sheep severely and mildly affected and estimate stage of outbreak to
    determine the need for individual animal or whole flock treatment.
•   BFR. Foot bathing is sufficient. Baths 6m long by 10 cm deep with 5% formalin or 10% zinc
    sulphate. May need to repeat weekly until local conditions improve or animals recover.
•   VFR. If topical treatment, pare hooves to remove necrotic tissue first. Foot baths then work well
    but is very labour intensive. Systemic antibiotics are more efficient. Combination therapy gives
    90-95% success. Cull animals not responding at 3-4 weeks.
•   Vaccination can be used to control the disease.
•   Eradication is justifiable if VFR is present.

•   Invasion of interdigital skin by F. necrophorum in sheep continuously exposed to wet pasture
•   No D. nodosus

•   Mild dermatitis of one or more interdigital spaces. Sometime also erosion or ulceration.
•   Minor problem but can lead to foot-rot or foot abscess (F. necrophorum invades subcutis and
    terminal interphalangeal joint).

•   History, signs, smears of affected skin - no D. nodosus

•   Not warranted

•   Dermatophilus congolensis with orf virus and wet weather

•   Crusted granulomatous lesions of the feet.
•   If secondary infection occurs there may be purulent exudate
•   Regression over 8 weeks. Little lameness

•   History, signs. Demonstrate D. congolensis

•   Seldom warranted.
•   Foot baths and D. congolensis treatments can be used (see lumpy wool)

The Teat and Udder

Periparturient oedema
Marked oedema of the udder and ventral abdomen may occur at the end of gestation especially in
primiparous cattle. Oozing of serous fluid through the skin may occur in some cases. Thought to be due
to a combination of hormonal effects preparing the gland for lactation, and also pressure effects of the
foetus in the caudal abdomen affecting venous return. The problem will resolve after parturition, but
may need appropriate symptomatic therapy.

Suspensory ligament rupture
The suspensory ligaments of the udder may rupture in older dairy cows with large udders - no effective

The udder is susceptible to traumatic injury from hazards in the environment such as barbed wire. In
sows, sharp teeth of piglets may inflict damage to the udder.

Injury from cows treading on the udder, may be self-inflicted in animals with pendulous udders, or
from other cows when housed together.

Frost bite
In extreme weather conditions, the distal teat of cows may be susceptible to cold damage, which is
ischaemic in aetiology. Severity of lesions, - scabs, erosions, ulcerations, necrosis, depends upon
degree of freezing.

Exposure to hot sunshine may result in burn damage to udder and teats of cattle, milking sheep, goats
and pigs. Clinical signs of reddening through to blistering and peeling may be seen. Must be
differentiated from contact irritant dermatitis. Signs are less severe than those associated with true

The non-pigmented skin of the udder and teats may be involved in photosensitisation (see Pigmentary

Contact dermatitis
Usually associated with contact with chemicals. Most commonly in dairy cows, and to lesser extent
ewes and goats as the result of incorrectly diluted teat dips or udder wash solutions, especially
iodophors. In nursing sows, contact with wet, highly alkaline concrete can cause dermatitis and
erosions to teat and udder skin.

Chapped teats
Chapping of the teats is a problem of dairy cows and potentially of milking ewes and goats. The
problem is due to poor milking practices, with over-milking, use of poor quality teat cup liners or
failure to replace liners frequently, inadequate drying of udder and teats after washing and before
application of teat cups, failure to use emollient teat dip after milking, all predisposing to the
development of dry teat skin and horizontal skin cracks. Affected cows are predisposed to develop

Hyperkeratosis of teats
May be the chronic sequel to the factors cited above.

Eversion of teat canal
Over-milking and use of old teat liners can lead to eversion of the teat canal epithelium, predisposing to
infection and mastitis.

Black spot ('pox')
An erosive disease of the teat orifice of cattle caused by infection by Staphylococcus aureus,
characterised by a crateriform ulcer with raised edges and a central black spot on the tip of the teat.
Involvement of the teat orifice may result in mastitis. May be refractory to treatment, but attention to
milking technique, hygiene, use of antibacterials is indicated.

Pustular dermatitis affecting the udder, base of the teats and intramammary sulcus, occasionally
spreading to the teats, ventral abdomen, medial thighs, perineum and underside of the tail, seen in all
species, but particularly sheep and goats. Subcorneal pustules rupture to leave erosions and yellow-
brown crusts. Animals show little if any discomfort, unless mastitis ensues. In sheep and cattle,
Staphylococcus aureus is the causal organism, but in goats S. intermedius has also been implicated in
two thirds of cases. Can be secondary to parapox infection in sheep and goats. The infection can be
spread during milking. Topical chlorhexidine or iodophors usually result in rapid healing and systemic
antibiotics are rarely indicated.

Mastitis can be caused by a number of bacterial organisms and may be sub-clinical, associated with
increased numbers of leucocytes and small clots in the milk, with no obvious external clinical signs.
Clinical mastitis cases show obvious clots in the milk, in addition to signs of heat, pain or swelling of
the gland; in more severe cases the animal may show pyrexia and systemic signs of illness. Clinical
signs vary with virulence of organisms and species involved, and the stage of the lactation.
 Peracute mastitis most commonly occurs in early lactation in dairy cows or goats associated with
Staphylococcus aureus infection, which may result in gangrenous mastitis and severe toxaemia, or E.
coli infections which results in endotoxaemia and drying off of the quarter if the animal survives.
Chronic mastitis may result in induration or hypertrophy of the quarter as a result of microabscesses or
fibrosis of the gland . Hypertrophy of the gland may be seen in goats with Caprine Arthritis
Encephalitis and in sheep with Maedi Visna.
Many infective agents have been implicated in mastitis in dairy cows, including Strep. agalactiae,
Strep. dysgalactiae, Staphylococcus aureus, Mycoplasma bovis and advanced cases of Mycobacterium
bovis. Strep. uberis, Strep. dysgalactiae, Escherichia coli and Klebsiella spp are environmental
organisms, may cause mastitis in cattle. Non lactating dairy or beef cattle may develop mastitis due to

Arcanobacter pyogenes (formerly Actinomyces or Corynebacterium) pyogenes,) infection often with
other bacteria, so-called summer mastitis. Infection results in loss of the infected quarter, and
uncommonly the death of the animal. Mannheimia (Pasteurella) haemolytica and Staph. aureus are
the principle agents in sheep. Dairy goats and sheep are affected by a similar spectrum of agents to
dairy cows. Pigs are susceptible to E.coli and Klebsiella mastitis with endotoxaemia at parturition,
chronic mastitis due to A. pyogenes, staphylococci and streptococci may occur in one or more glands,
often associated with teat damage.
The treatment of dairy cow mastitis cases with intramammary antibiotics during the lactation are
successful in producing a bacteriological cure in about 70% of cases only. Systemic antibiotics with
good udder penetration and possibly non steroidal antiinflamatory agents are indicated in cases with
systemic signs. Long acting intramammary preparations used during the dry period may be successful
in resolving chronic infection and protect against new infections before calving.
A wide range of factors may affect the development of mastitis, the investigation of a case must take
into account the organism involved, the stage of lactation, the environment and any damage to the
teats. In dairy animals the milking machine and milking routine may be critical to the spread of

Viral diseases
A number of viral diseases may involve the teats and udder.

See section on ulcerative diseases.
Teat lesions may occur in infected cattle.

See section on ulcerative diseases.
Erosive lesions may occur on the udder, medial thighs, perineum and vulva.

See section on ulcerative diseases.
Erythematous, scaling, ulcerative and necrotic lesions occasionally involve the udder, teats, and vulva

Acute viral infection of udder and teats caused by bovine herpesvirus (BHV) 2, which may also cause
pseudo-lumpy skin disease. Bovine herpes mamillitis (BHM) has been reported in most parts of the
world. In the USA a syndrome of mammary pustular dermatitis has been associated with BHV 4,
which is normally associated with respiratory disease. BHM is seasonal - August to December, sudden
onset with rapid spread to all susceptible milking cattle. Incubation period 3-7 days

Clinical signs:
•   lesions may be confined to one teat or involve several and extend to udder
•   sudden acute onset with swollen, tender teats
•   vesicles may be seen, or ulceration to exposed inflamed dermis with exudation and crust formation
•   severity varies from lines of erythema, often in circles, to annular plaques which evolve in to
    shallow ulcers to large areas of discolouration, necrosis, slough and ulceration.
•   milking and suckling resented due to painful lesions
•   suckling calves may develop similar lesions on muzzle and mouth

•   healing usually occurs in 2-3 weeks, recovered animals have long-standing immunity

No specific treatment, condition is self-limiting, hygiene precautions of limited benefit in preventing
spread of disease. Symptomatic treatments include emollients, antiseptics, local anaesthetic ointments,
mastitis prophylaxis

Several strains of BPV may cause lesions on the teats of cattle.
•   BPV-1 causes the typical fibropapillomas on the teats of animals under 2 years of age. Lesions
    usually regress within 1-12 months
•   BPV-2 causes fibropapillomas occasionally on teats of animals less than 2 years old. Lesions often
    spontaneously regress, but immunity is not complete
•   BPV-3 causes atypical warts in cattle of all ages. Lesions ar low, flat, circular, non-pedunculated,
    with frond-like projections; may occur anywhere on the body surface including teats, and do not
    regress spontaneously
•   BPV-5 causes rice-grain warts on the teats of cattle of all ages, which do not regress spontaneously
•   BPV-6 is associated with proliferative, fronded lesions.

See section on ulcerative diseases.
Cows nursing infected calves may develop teat lesions. Humans in contact with affected dairy cows
may develop lesions on fingers and hands (milkers nodules) identical to pseudocowpox and contagious
pustular dermatitis virus lesions

See section on ulcerative diseases.
Primarily a disease of lambs and kids, lesions occur on lips, muzzle, nostrils and eyelids. Lesions may
develop on teats and udders of nursing ewes and nanny goats and also of cattle. Zoonotic.

Orthopoxviruses, the latter being laboratory propagated virus formerly used for prophylactic
vaccination against human smallpox. Cowpox may be misnamed as the virus is endemic in wild
rodents (such as Microtus spp.) in Britain and Europe, but is rare in cattle. Disease has not been
recorded in UK for several decades. When virus is introduced into susceptible herd, rapid spread occurs
within 2-3 weeks, transmitted via teat cup of milking machine and milker’s hands. Classical lesions of
thick, red, crusted pocks 1-2cm in diameter, affecting teats and udder, and in severe cases, medial
thighs, perineum , vulva, scrotum and mouth of nursing calves.

Dermatophilosis may cause crusted hyperkeratotic scabs on udder and teats of ewes, transmitted from
raised kerion-like lesions on muzzle and lips of lambs.
Dermatophytosis caused by Trichophyton verrucosum or T. mentagrophytes may cause raised, scaly
and crusted lesions on skin of udder and, or teats of cattle, sheep and goats. In pigs Microsporum
nanum causes diffuse, circular reddish brown rings with light brown scale or scab that may involve
udder as well as other parts of the body.
Mite infestations may involve udder in all species, particularly chorioptic mange of cattle

Further Reading
Howard, J. L., Smith, R. A. Current Veterinary Therapy: Food Animal Practice. Fourth Edition.
Philadelphia: W. B. Saunders, 1999.
Linklater, K. A., Smith, M. C. Diseases and Disorders of the Sheep and Goat. London: Mosby-Year
Book, 1993.
Martin, W. B., Aitken, I. D. (Eds.) Diseases of Sheep. Third Edition. Oxford: Blackwell Science, 2000.
Matthews, J. G. Diseases of the Goat. Second Edition. Oxford: Blackwell Science, 1999.
Rebhun, W. C., Guard, C., Richards, C. Diseases of Dairy Cattle. Baltimore: Williams & Williams,