Ulcers Leishmaniasis by lXK4rdzv


									SKIN ULCERS
 Causes / Types of Skin Ulcers

Department of Pathology, AGU

Infection of the Monocyte / Macrophage
System (i.e. RES) caused by a protozoan
of Leishmania species

20 million people infected worldwide
     Determinant Factors in Worldwide
 Geographic Variations of Leishmaniasis

1. Infectious Agent
Protozoan - Genus: Leishmania
Numerous species differ in
    1. Natural habitat differ in various geographic
    regions / countries
    2. Different host / reservoirs
    3. Type of disease produced a spectrum of
    clinical syndromes from indolent self resolving
    ulcer to fatal disseminated disease
2. Reservoir / Host (animal, man or both)
Leishmania is primarily a parasite of wild animals and
  man becomes accidental host when intruding into the
  “natural habitat” of these animals i.e. “Zoonotic
  Different Leishmania species may have different
  specific zoonotic reservoirs eg
  a. Dogs in Visceral Leishmaniasis in Mediterranean
  b. Wild rodents in Mexican cutaneous Leishmaniasis
  c. Common reservoirs hosts: Rodents, dogs, foxes,
  d. Potential hosts include cattle, horses, wild canine,
3. Habitat
   Physical geomorphological
  characteristics of Vector and Reservoir
  eg landscape, vegetation, etc
  Environmental characteristics eg wind,
  temperature, humidity, light etc
4. Vector: Leishmaniasis transmitted by
  bites of female Phlebotomus sandflies.
  Sandflies acquire infection from feeding
  on infected animals.
  Physiological age movements
  Time of activity
  Flying range
  Feeding habits
  Reproductive activity
  Condition of alimentary canal

Sandfly bite ►►Leishmania (promostigotes)
 phagocytosed by histiocytes ►►
 reproduced within macrophage
 ►►Daughter amastigotes rupture from
 cell ►► spread to other macrophages

 1. Immunological capabilities of the host
 2. Infecting species of Leishmania

  Central + South America, Middle East, India, China,
  Northern Africa
  Localised cutaneous disease – “Aleppo, Baghdad,
  oriental, tropical sore”.

  Amastigote-filled macrophages  ulcerates overlying
  Oval amastigotes 2m containing 2 internal structures, a
  nucleus and kinetoplast
  Amastigotes in macrophages appear as multiple
  cytoplasmic dots “Leishman–Donovan Bodies”
Progressive development of CMI to the
parasite  Macrophages activated  Kill
intracellular parasites  Amastigote-
filled macrophages  Granulomatous
reaction  Ulcer
Lesion starts as small itching solitary
papule  erodes to form shallow ulcer
(sharp raised borders)  Extension of
ulcer (6-8 cm)  Satellite lesions
develop along draining lymphatics.
Ulcer resolve in 3 – 6 months and heals
Diffuse Cutaneous Leishmaniasis
 Enormous numbers of macrophages
 containing large numbers of Leishmania
 Develops in patients who lack specific cell-
 mediated immune response to
 Begins as single nodule – extensive
 ulceration developing into satellites along
 draining lymphatics
Late complication of cutaneous
Leishmaniasis .
Species: L.Braziliensis
Geography: Central & South America
Reservoir: Rodents, sloth
 Early course and pathologic changes similar to
 Localizes Cutaneous Leishmaniasis i.e.
 solitary ulcer appears, expands and then
 resolves spontaneously.
 Years after healing of primary  ulcer
 develops at mucocutaneous junctions (e.g.
 nasal septum, anus, vulva)  slowly
 progressive, highly destructive, disfiguring 
 erodes mucosal surfaces and nearby tissues.
 Destruction of nasal septum  Nose deformity
 MCL ulcers may  obstruct airways
Potentially fatal disseminated infection of
macrophage / monocyte system caused by
several subspecies of L. donovani.
Reservoirs in susceptible age groups vary in
different parts of the world eg
Humans in India
Foxes in S. France, Central Italy, S. America
Dogs in Mediteranean basin, China, S. America
Jackals M. East, Central Asia
  Sandfly bite  localized collection of infected
  macrophages ►ulcer
  95% infected persons can contain the disease,
  destroying L. Donovani by CMI.
   5% Young children, malnourished persons  failure
  to mount adequate CMI response
  Mononuclear phagocytes full with proliferating L.
  amastigotes  replacing normal architecture of liver,
  spleen, LN leading to their massive enlargement
  BM is replaced by filled with proliferating amastigots
  Eventually mononuclear phagocytes accumulate in
  other organs e.g. heart, kidney.
           Skin Ulcers - Causes
1. Trauma + Thermal injuries, burns, scalds,
  chemical, injection ulcers, erythrocyanosis
2. Infection:
  a. Viral + Bacterial:
       Acute: ‘desert sore’, gas gangrene
       Chronic: Buruli ulcer, tuberculosis, leprosy,
       swimming-pool granuloma, osteomyelitis
  b. Anaerobic: Meleney’s ulcer, synergistic
  bacterial gangrene (with streptococcus)
  c. Mycotic: Superficial and deep fungus
  d. Spirochaetal: Syphlis and yaws
  e. Protozoans: Leishmaniasis
3. Infestation, bites, spiders, scorpions, snakes
4. Metaboloic: Diabetes, gout, Necrobiosis lipoidica
5. Vasculitis: Rheumatoid disease, SLE, immune
  complex disease, pyoderma gangrenosum, temporal
6. Vascular: Varicose veins, congenital absence of
  veins, post-thrombotic , atrophie blanche,
  arteriovenous ulcers, hypertension (Martorell’s),
7. Ischaemic : Scars, fibrosis, radiodermatitis,
  Necrobiosis lipoidica,
8. Skin diseases: Pemphigoid, psoriasis, tinea,
  summer ulcers
9. Neuropathic “trophic”, Diabetes mellitus, leprosy,
  tabes dosralis, syringomyelia, neuropathic,
10. Blood diseases: Polycythaemia, spherocytosis,
  sickle-cell anaemia
11. Neoplastic: BCC, SCC, Malignant Melanoma,
  Kaposi’s sarcoma, leukaemia, lymphoma

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