micro

CAMPYLOBACTER

Campylobacter fetus ss. venerealis:



 Causes epizootic bovine infertility.

 It is an obligate reproductive pathogen.

 Transmission: Venereal, fomites.

 Bulls are non-clinical carriers.

 Causes infertility, abortions, still births, neonatal deaths.

 Recovered cows are carriers.

 DIAGNOSIS: collect specimens of cervical mucus, uterine discharges, fetal stomach contents.

Clinical picture plus direct exam. FA, elisa, agglutination test.

 Treatment: Streptomycin, tetracyclines, penicillins with streptomycin.

 Primary immunity is humoral.

 Bacterin used widely.

 Vaccine is used and annual vaccination is suggested.



Campylobacter fetus ss. fetus:



 Commensal in GI tract in cattle and sheep.

 Zoonotic pathogen.

 Causes sporadic abortions in cattle. Higher incidence of abortions in sheep. comparable to C.

jejuni abortions. Abortions in goats. endocarditis, meningitis, and diarrheal disease in

childern.

 Transmision: ingestion. No venereal transmission. Bacteremic spread to uterus. No early

abortions.

 Liver lesions in fetus are characteristic.

 Causes diarrheal disease in lambs and kids.

 Generalized immune response. Immunity is serotype specific.

 Multivalent bacterins are available.

 Treatment: penicillins are the drugs of choice combined with streptomycin. Can use

tetracyclines in feed.



Campylobacter jejuni:



 Commensal of GI tract in cattle, sheep, goats, pigs, horses, chicken, turkey, wild birds, dogs,

cats, primates, etc.....

 Very important food-borne zoonotic pathogen.

 Transmission is by ingestion of contaminated food.

 Equals or exceeds salmonella as a diarrheal pathogen.

 Produces LT-like toxin and others.

 In animals it causes gastroenteritis-colitis; cattle, sheep and goats, pigs, horses, dogs, cats,

poultry, non-human primates.

 May cause abortions in sheep and goats and many others.

 Causes Avian Vibrionic Hepatitis.

 In humans, it causes fever, malaise, abdominal pain, diarrhea (mucus or blood-tinged).

 Diagnosis: clinical picture plus exam of stained smears. Culture.

 immunity is primarily humoral.

 Treatment: Erythromycin, tetracyclines.



Porcine Proliferative Enteropathy (PPE)



 Caused by a campylobacter-like organism (Lawsonia intracellularis)

 Infection is by Ingestion of contaminated feed/water.

 Stress factors are important int his disease.

 Common in the midwast USA. Most common in 1-5 month old pigs.

 Lesions are typically seen in ileum and colon; less often in jejunum and cecum.



Porcine hemorhagic Enteropathy (PHE):

 thickening of the intestinal mucosa and massive hemorrhage in to the intestinal lumen.

 High Mortality.



Porcine Intestinal Adenomatosis (PIA):

 Chronic progressive proliferation ofintestinal epithelium.

 Low mortality. Chronic poor doers.

 Necrotic enteritis: PIA with extensive necrosis of mucosa

 Regional Ileitis: PIA with extensive granulomatous proliferation ofmucosa--”hose pipe

gut”

 Other species affected are dogs, foals,rabbits and hamsters.

 DIAGNOSIS: Clinical picture plus necropsy and direct examination.

 Treatment: Questionable if effective. Must control with All-in/All-out management and good

sanitation.



BRUCELLA

 Major economic losses to the livestock industry.

 Important zoonotic pathogens.

 Obligate pathogens

 Facultativeintracellular parasites.

 Classical species: B. abortus, B. melitensis, and B. suis. Current species: B. melitensis Biovar

abortus.

 Different biovars affect different species. Cattle, sheep and goats, and swine. Dogs and humans may

also ba affected.

 Infection may be by ingestion, inhalation, contact or venereal.

 Great efforts made to control/eradicate brucellosis.

 Treatment: Tetracyclines are drugs of choice with streptomycin (gentamicin)



BRUCELLOSIS IN CATTLE:



 Caused by Biovar abortus >>> Biovar suis and others.

 Typical manifestations of reproductive tract infections in both cows and bulls. Only occurs

in pregnant cows not repeat breeder syndrom asin borreliasis.

 semen quality is seriously compromised.

 DIAGNOSIS: Variety of serological tests. Collect specimens from fetal stomach contents,

lung,liver, spleen, fetal membranes and milk from affected herds (Brucella Ring test: add

stain Ag and ring will form at top.) Also blood or serum from suspected animals for Plate

agglutination test (an individual test that checks for serum agglutination. If positive, then do

tube agglutination test. If titer is greater than or equal to 1:100 then it is positive. If titer is

greater than or equal to 1:200 in vaccinated animal and then reactive and animals are

eliminated.

 Treatment: not practiced.

 Use strain #19 vaccine (ALV) in female calves 3-8 monthsof age. Not given to male calves or

pregnant animals because it causes orchitis and abortions.

 humans can get infected.

 use 45/20 vaccine (bacterin) for male r females or pregnant animals. Not permited in the

USA.

SWINE BRUCELLOSIS:



 Caused by Biovar suis >>>melitensis and abortus.

 infection is by ingestion and venereal transmission.

 Greater tendency for generalization...what ever that means.

 Common sites of infection are Bones and joints and respiratory.

 Causes abortions, still births, neonatal deaths and sterility. also spondylitis(inflamation of

vertebra.

 usually Cell mediated immunity.

 Agglutination test not reliable because of low titers.



BRUCELLOSIS IN DOGS:



 Caused by Biovar canis.

 epizootics in breeding kennels. Widely distriuted.

 Subclinical to clinical infections.

 Causes bacteremia with intermittent fever, abortions, stillbriths in females, and prostatitis,

epidymitits, and sterility in male dogs.

 DIAGNOSIS: Tube agglutination test (uses ovis or canis antigen)

 Treatment: Tetracyclines and Gentamicin (Controverisial) some recommend Euthanasia.

 No vaccines are available.



BRUCELLOSIS IN GOATS AND SHEEP:



 Goats:

 Caused by Bivar melitensis.

 Usually a mild disease. Occasional abortions.

 Most human infections occur via milk.

 prevalent in south western US and Swinebelt states.

 ALV (rev 1) available for females and Bacterin used for male goats.

 Sheep:

 Caused by Biovars melitensis and ovis.

 melitensis infetions similar to those in goats.

 Biovar ovis primarily infects rams causing epididymitis in breeding rams.



BRUCELLOSIS IN HORSES:



 Caused by Biovar abortus.

 Causes “Fistulous Withers” and “Pole Evil.” However, S. zooepidemicus and other

streptococci and staphylococci are found to be the major isolates of these diseases.

 Treatment is controversial and difficult.

 No vaccines are available. Strain #19 vaccine used by some, but is not approved by the

USDA and may be illegal.



BRUCELLOSIS IN HUMANS:



 Caused by Biovars abortus >> suis > melitensis > canis

 suis and melitensis cause more severe infections.

 Infections is by ingestion, inhalation, contact, conjuctiva.

 Causes Undulent Fever.

 No vaccines are available.

 Treatment: Tetracyclines plus gentamicin. Must be Long treatment.

Mycobacteria

 Major human and animal pathogens. Both domestic livestock and zoo animals and birds are

affected. Zoonotic pathogens.

 High lipid content in cell wall is very characteristic. ~60%; because of this:

1. acid fastness: attributed to mycolic acids.

2. resistance to acids and alkali and disinfectants. Treat suspected cases of

mycobacteria with alkali to eliminate all other organisms in order to get a pure

mycobacterial culture.

3. resistance to killing inside macrophage: virulence factors: Wax D and Cord Factor.

4. Slow growing: nutrients have difficulty diffusing through membrane

5. Slow response to antibiotics: use antibiotics that have lipid solubility characteristics

such as Rifampin.

 obligate aerobes. Acid-fast rods.

 facultative intracellular parasites. CMI response

 Classical Tuberculous Mycobacteria:

 M. tuberculosis. narrow spectrum. Humans, non-human primates, dogs, and swine.

One case in an elephant!!!

 M. bovis. Affects all vertebrate mammals including humans. main problem in zoo

animals. Reservoirs include cattle, exotic animals, bison, and feral swine.

-These are slow growers (4-6 weeks or longer) Cause typical TB. obligate pathogens. Animal to

animal, animal to human, or human to animal transmission. Susceptible to the antituberculous drug INH

(isoniazid).



-Atypical mycobacteria: Based on the rate of growth and pigmentation of the colonies, four

groups (Runyon groups) are recognized (please see page 144) These are slow or fast growing. disease

may or may not resemble classical TB. Free living organisms. Many species show no animal to animal

transmission. Resistant to INH. these are now important in AIDS patients. Treatment is a problem.



Group I (photochromogens): colonial growth in 7-15 days or longer. colonies non-

pigmented in dark but turn yellowish orange up on exposure to light. M. kansassii causes

the most important infections in Humans and many infections in animals.

Group II: not clinically significant: (scotochromogens)

Group III: Most grow in 10-21 days, soft and light tan or colorless. Very important

group. M. avium complex belong to this group. [M. avium complex is now classified as

non-tuberculous mycobacteria. Affect birds (serotypes 1,2,3) and mammals.]

Group IV: Fastest growing. Good colonial growth in 3-7 days. M. fortuitum belongs to

this group.



TUBERCULOSIS IN CATTLE:



 Caused by M. bovis (rarely M. avium)

 Inhalation: tubercles in lungs, pleura, regional lymph nodes. Metastasis to other organs.

 Ingestion: Liver, spleen, lymphnodes, lungs and pleura. metastasis to other organs.



DIAGNOSIS:

1. Tuberculin Test: widely used

2. Bovine Purified protein derivative (PPD): given in the tail fold or side of the neck.

swelling > 10 mm in 72 ht is +.

3. Comparative cervical test: used for confirmation.

4. Bovine and avian PPD is given separately on two sides of the neck. If the reaction is

higher with bovine PPD, then it is positive. This is because some animals may be

sensitized (pre exposed) to M. avian which will cause a delayed response to Bovine

PPD. so unless you provide the avian PPD the test will not be accurate.

CULTURE AND IDENTIFICATION



DNA probes and PCR: detects as few as 10 organisms in a clinical material



 BCG: is an avirulent live M. bovis strain which is used as human vaccine but not approved for

use in animals.

 NO TREATMENT practiced in the USA. Test and slaughter recommended. Only in special

occasions is treatment attempted; as in the case of very rare zoo animals. Classical

antituberculous drugs are used (Rifampin, ethambutol, isoniazid, ethionamide, pyrazinamide,

sparfloxacillin and streptomycin). Highly recommended that you do not treat animals OR

humans with just one drug. This is because the treatment is prolonged and thus resistance may

result if only one drug is used.

 Phenolic disinfectants are effective but NOT quaternary ammonium compounds. Bleach is

very good.

 Slides:

 granulomatous lesions

 grape-like clusters subtuberculous nodules.

 One of the good ways to identifying tuberculous organism is infecting lab animals.

guinea pigs are very good specimens.

 tuberculosis is mostly detected at the time of necropsy because of the limited

resources available for identification while the animal is still alive.

 Tuberculous milk from infected cow is an important source of culture.

 In Acid fast stain, they look as slender RED RODS. Red because of Red fuschism

(carbon fixate) and counter stain is methylene blue.



SWINE TUBERCULOSIS:



 most infections by Ingestion

 M. avium infections are most common and least severe. next is M. tuberculosis

 M. bovis infections are least common but causes progressive generalized tuberculosis.



TUBERCULOSIS IN HORSES:



 Rare M. bovis > M. avium.

 infection by ingestion.

 Progressive generalized tuberculosis.



TUBERCULOSIS IN SHEEP AND GOATS:



 Rare. M. avium > M. bovis.

 M. avium causes mild infections while M. bovis infections are severe

 TB in goats is RARE. M. bovis.



TUBERCULOSIS IN DOGS AND CATS:



 2/3 infections in dogs are due to M. tuberculosis.

 1/3 infections are due to M. bovis

 Infection by inhalation

 Pulmonary form is common. Radiography useful in diagnosis

 M. bovis is the most common cause in cats.

 M. tuberculosis is rare in cats.

 Abdominal form of the disease is more common

Slides:

 M. bovis: lungs are prominently involved

 Highly vascular organs are mostly affected.

 In horses the tuberculous lesions are big tumor-like instead of small tuberculous

lesions in other domestic animals. mostly M. bovis in equines.

 Lowenstein-Jensen medium is used to grow M. bovis: slow growing organism ; at 30

days, almost no growth.

 In acid fast stain of M. bovis, you find clusters of the organism in a serpentine

fashion. This is due to the Chord Factor.

 M. tuberculosis also exhibits this serpentine pattern, but at 30 days, it shows

significant growth in the L-J medium.



TUBERCULOSIS IN CHICKENS:



 Economically significant

 M. avium complex >>>> M. tuberculosis

 Infection is usually by Ingestion

 Intestines, liver, spleen and lymph nodes

 Lung lesions are less common

 Slides:

 In Acid fast stain you see ????

 bones and joints are the other common places you see tuberculosis:



ATYPICAL MYCOBACTERIA:



M. kansassii: Rapid growth (10-15 days). Lymphadenitis in cattle and swine. Severe pulmonary

disease in humans.

M. fortuitum: Rapid growth in lab media (3-7 days). Primarily subcutaneous infections in dogs

and cats. Usually in the head and limb regions. Chronic. Need prolonged therapy.

Recommended Antibiotics are TETRACYCLINES (preferred) and Gentamicin.

Cat Leprosy organism: very similar to M. fortuitum. Subcutaneous nodules and abscesses. Not

cultivated in the lab (can‟t use ordinary lab media). Dapsone used in treatment. Same drug used

in treatment of human leprosy.

SLIDES:

 M. kansassii: is a photochromogen; yellow colonies

 M. marinum: affects fish species, reptiles also a photochromogen. „Swimming pool

know that these two

granuloma‟

are photochromogens

 M. fortuitum: Grows readily and fast in lab media. Creamy and thick pus is

characteristic.

 Cat leprosy organism: affects tissues of the head. Lesions are harder and more of a

tumor-like type of appearance.

 Skin tuberculosis of Cattle: organism has not been isolated. lesions are usually in the

limb regions.

 Armadillo: Is the only animal which is affected by human tuberculosis in the same

manner.



JOHNE’S DISEASE: (Paratuberculosis)



Slide: characteristic picture: great volume of fluid coming out of the anus. Persistent Chronic

diarrhea. „bony self‟. Lots of dehydration and marked emaciation and death. Almost always fatal

disease. whole animal is soiled with feces. Rough coat and hair loss, sunken eyelids.

 Infection is most often by ingestion, but transplacental infection has been shown.

contaminated food by feces, or ingestion of contaminated milk.

 Caused by Mycobacterium paratuberculosis

 Obligate pathogen

 chronic, progressive, granulomatous

 Inflammation of intestinal mucosa

 Severe watery diarrhea

 Protein losing enteropathy

 Dehydration, emaciation, death.

 EPIDEMIOLOGY:

 Up to 11% slaughter cows show infection; Economic losses of ~1.5 billions

 Most of the time, cows are infected at a very early age. Believed to be because of

ingestion of contaminated milk form contaminated mother.

 However, clinical signs don‟t appear until ~2 years of age. So incubation period is of

about 2 years.

 Peak incidence is in animals from 2-4 years

 Most frequent in dairy cattle than in beef cattle because of the way they are managed.

 Susceptible animals are: Buffaloes, Sheep, goats, wild ruminants.

 Disease is less severe in sheep and goats.

 DIAGNOSIS:

 Clinical and necropsy picture; Acid fast rods in mucosal scrapings and

impression smears

 @necropsy: greatly thickened mucosa in ileum, cecum and colon;

“corrugated look”. Congestion of the ileocecal valve and mesenteric

lymphadenitis.

 Serological tests: ELISA considered desirable with acceptable sensitivity

and specificity.

 Culturing is the gold standard for diagnosis

 DNA probes plus PCR appears promising

 No treatment is practiced.

 Bacterins approved in some state. Reduces losses in severely infected

herds. They do not prevent infection, but do decrease incidence of infection.

There are some problems with bacterin: Potential problem of infection to

humans--if human is accidentally infected with bacterin, it will cause

nodular painful inflammations.



NOCARDIA ASTEROIDES:



 Partially acid-fast, gram-positive filaments

 Strict Aerobe. Soil saprophyte

 Opportunistic pathogen

 Malignancies, chronic debilitating diseases and immune suppression are predisposing factors.

 most infections via inhalation (pulmonary--lung abscesses) or via skin injuries (localized skin

infections).

 BOVINES:

1. MASTITIS: can metastasize to lungs

2. Bovine Farcy: lymphangitis (hind legs) and regional lymphadenitis. can metastasize

to lungs. Pulmonary form is refractory to treatment and FATAL

 DOGS AND CATS:

3. Pulmonary nocardiosis: metastatic spread to other visceral organs

4. Mycetoma: chronic indurative lesions of the feet

 Other Animals: Pulmonary nocardiosis in non-human primates, marsupials, and horses

 Mastitis in goats (and sheep); abortions in sows.

 Humans: Disease is similar to that in dogs. Pulmonary form is often FATAL.

 Diagnosis: Clinical picture, Direct examination, and culturing.

 Treatment: tetracyclines, sulfonamides; sulfadiazine and sulfisoxazole; trimethoprim-sulfa.

 Prolonged therapy is needed.

 No vaccination is available.

 Predominantly CMI

 SLIDES:

 Gram positive filaments

 Grows well in blood agar.



DERMATOPHILUS CONGOLENSIS:



 Primarily a Skin disease

 broader than nocardia.

 Gram-positive filamentous rod showing characteristic transverse and longitudinal

fragmentations. Upon exposure to moisture (very important for the organism to cause

disease; if the moisture is not there, the organism cannot cause disease.), each fragment

becomes a motile zoospore which is the actual infectious stage.

 Obligate Pathogen

 Infections via Skin, contact or Flies

 DERMATOPHILOSIS: Exudative pustular dermatitis. Exudate becomes dry and you find

scabs and crusts.

 CATTLE AND HORSES: commonly seen. Discrete small elevated lesions: crusts and scabs;

extensive confluent lesions along the back, neck and sides.

 SHEEP: relatively less common.

 “Lumpy wool disease”

 dermatitis of the face and scrotum

 strawberry foot-rot

 DOGS, CATS, PIGS, DEER, AND HUMANS: Rare; similar to the disease in cattle.

 Diagnosis: Clinical picture plus examination of Stained Smears of exudate or smears from

moistened crusts (or scabs) or skin scrapings is very useful for diagnosis. FA test available.

Culturing.

 Treatment: Penicillin plus streptomycin plus topical iodine (or copper sulfate or penicillin)

 NO vaccination practiced.

 Drying is very important for recovery; must keep area and animal dry.

 SLIDES:

 Long filament; you can see striations; they look like long chromosomes.

 each „striation‟ will become a zoospore

 zoospore is flagellated and looks like a coccus

 you can see crusty appearance of affected area. If you pull hair, some scabs come

off. Moisten scabs and smear for diagnosis.

 In addition to the head, neck and back, another area where you see lesions is in the

distal limbs. some of these bleed and may have secondary infections as well.



SPIROCHETES

 spiral shaped organisms; spirals are very tight. the number of spirals and length of organism are

important distinguishing features.

 Borrelia anserina:

 Cause of Avian borreliosis

 Vectors: ticks (or mites). ingestion of the eggs of the tick.

 Ingestion is the common mode of infection

 Acute septicemic disease with profuse diarrhea

 High morbidity and mortality

 Severe enteritis, hepatomegaly and spleenomegaly.

 Diagnosis: clinical picture plus spirochetes (loose spirals) in blood. FA test. hardly any

culturing is done because there is no other poultry spirochete.

 Treatment: Penicillins are the drugs of choice (tetracyclines also) given parenterally or in

water (tetracycline only)

 Prevention: Bacterins or avirulent live vaccine; Tick control.

 Animals that recover are immune.

 Typically Humoral Immunity.

 SLIDES:

 You can see lots of spirochetes in blood; rampant infection.

 if collect blood at acute phase, you see lots of spirochetes in blood, however, at later

stages, the organisms decrease and/or disappear from the blood. Usually you see

clumping of the spirochetes together.

 Borrelia burgdorferi: read book closely.



 Causes “Lyme Disease” a tick borne disease

 Life cycle: larval, nymphal, adult stages of the tick (vector)

 Most infections are due to nymphal infection, less so by adults.

 larval stages infect birds

 white tailed deer is preferred host of B. burgdorferi.

 Fall season is the time of highest infection because of tick life cycle.

 In dogs, Arthritis is the most common manifestation: 2 stages:

1. Stage 1: almost asymptomatic.

2. stage 2: Severe arthritis (most common), Cardiac manifestations, neurological

manifestation.

 if arthritis is the case, then you collect joint fluid for examination.



LYME BORRELIOSIS UPDATE:



 No definitive serological test although ELISA is being used frequently.

 No direct correlation between clinical disease and antibody titers

  1:160 titer considered seropositive. (not disease)

 paired sera and four fold increase in titer indicate recent infection but not necessarily

clinical disease (note: some dogs serocnvert but show no clinical disease.)

 high incidence of seropositive dogs in enzootic areas

 False positives because of cross reactions.

 B. burgdorferi bacterin is USDA licensed and is reported to reduce the incidence of the

disease in vaccinated dogs by about 78% as compared to unvaccinated controls.

 the gene for outer surface protein A (Osp A) of B. burgdorferi has been cloned and expressed

in E. coli and inoculation of susceptible mice with recombinant E. coli or with purified Osp A

protein produced antibodies to Osp A and were protected from challenge exposure to several

strains of B. burgdorferi.

 Administration of monoclonal antibody to Osp A to experimental immunodeficient mice

protected them against development of arthritis or greatly reduced the severity of clinical signs

when challenge infected with B. burgdorferi.

 SLIDES:

 Loose spiral shaped organism

 usually big joints are affected (in cattle)

 in humans the first signs of the disease is the Bull‟s Eye Rash (Erythema

Chronicum Migrans) -->characteristic of Lyme disease. Also see arthritis in

humans as well as neurological signs (Bell‟s pulsi)

 You can actually recover the organism from the brain in some cases.

 Fluorescent antibody is used to demonstrate organism.

 Serpulina hyodysenteriae:



 Very important Swine disease. Causes “Swine Dysentery” in feeder swine

 Anaerobic, -hemolytic spirochete.

 Loose spirals. Small number of spirals.

 Severe disease requires contribution by other anaerobes such as Fusobacterium and

Bacteroides.

 infection by ingestion

 Morbidity and mortality are high in new herds; low mortality in enzootic herds.

 Severe mucohemorrhagic diarrhea (bloody scours.)

 SLIDES:

 bloody scours, black scours, ugh!

 Diagnosis:

 Hemmorrhagic inflammation of colonic mucosa, colonic malabsorption, dehydration

and death.

 Necropsy: hemorrhagic colitis

 chronic poor doers. carriers are important

 Clinical picture and necropsy.

 Exam of stained smears of feces and mucosal scrapings

 FA test is used.

 Culturing required for definitive diagnosis.

 Treatment: Antibiotics in feed (Lyncomycin or tylosin) and good management. Can use

many kinds of antibiotics.

 Prevention: Use Autogenous bacterins

 Typically a Humoral immunity, but some CMI also.

 SLIDES:

 Severe hemorrhagic type of colitis; see mucous and blood tinged material when open

colon.

 Bloody and congested mucosa.

 Take mucosal scrapings show very high concentrations of spirochete. Looks similar

to campylobacter--> must differentiate.

 The spirochetes burrow into the tissue

 Use silver stain to show spirochete





LEPTOSPIRA



 Important animal pathogens

 Zoonotic

 aerobic

 tightly coiled

 hook at one or both ends

 L. interogans: Includes all pathogenic leptospires.

 Many serovars: Pomona, canis (canicola), hardjo, etc...

 Obligate pathogens

 many infections are subclinical

 infection: via mucous membranes (oral, nasal, conjunctiva), skin, venereal, congenital.

 LEPTOSPIROSIS: Cattle, swine, and dogs.

 Localization: Kidney, liver, reproductive tract, udder, meninges, intestines and eye.

 DIAGNOSIS:

 clinical picture plus demonstration of leptospires in stained smears or by histopath

 Serology-- Agglutination test; ELISA

 Culturing

 DNA probes

 Treatment: penicillin and streptomycin; tetracyclines.

 Immunity: Humoral. serovar specific

 Prevention: Multivalent bacterins used.



CANINE LEPTOSPIROSIS



 commonly seen serovars Canicola and Copenhegeni of the icterohemorrhagiae serogroup

 Host adapted serovar: Canicola

 A host adapted serovar in general causes milder infection and has a prolonged

infection. Therefore animals may be shedding the organism for long periods of time

and maybe for the rest of the animal‟s life.

 Copenhegeni is not host adapted. Usually dogs get infected through rat urine.

 Wide Spread

 latent to severe (more often)

 Infected Shedders.

 In general, there are more infections in males than in females.

 hemorrhagic, icteric, and uremic (chronic uremic form usually caused by Canicola) forms of

the disease.

 DIAGNOSIS:

 clinical and necropsy picture.

 demonstration in tissue sections and in Urine.

 Microscopic agglutination test. Paired sera. 4 to 5 rise in sera is positive.

 FA test; ELISA; DNA probes.



BOVINE LEPTOSPIROSIS:



 Commonly caused by HARDJO (Host adapted), POMONA (Very potent; common in cattle,

swine, equines; in practically all cases, pomona causes a severe disease), GRIPPOTYPHOSA

and others.

 Infection is commonly from contact with infected urine of cattle, pigs, other animals.

 Varying severity.

 Fever, icterus, hemoglobinuria, nephritis, and death.

 Drop in milk yield; yellow or blood-tinged milk.

 Abortions and still-births.

 Animals who recover are immune.

 Prevention: Mixed bacterins are used. Annual vaccination recommended.

 Treatment: Tetracyclines are the drug of choice. Also amoxicillin or penicillin plus

streptomycin also used.



PORCINE LEPTOSPIROSIS:



 Serovars Bratislava (host adapted), pomona, canicola, icterohemorrhagiae, and

grippotyphosa.

 Pigs are important reservoirs of leptospirosis

 Mostly latent infections

 but when clinical manifestations occur, those are very similar as those in cattle.

 In the case of pigs, the most important area of localization in the body, is the reproductive

tract as opposed to liver in dogs.



EQUINE LEPTOSPIROSIS:

 Uncommon. Often serovar POMONA and others.

 Disease similar to that in cattle.

 Eye manifestations frequent in equines. (Uveitis and iridocyclitis)



LEPTOSPIROSIS IN SHEEP:



 Uncommon. Serovar AUTRALIS (host adapted), POMONA, HARDJO and others.

 Signs similar to those in other animals, but milder.

 Severe hemolytic disease in lambs.



HUMAN LEPTOSPIROSIS:



 most infections are latent or self-limiting.

 A few are fatal. Depends on individual

 Fever, icterus (higher mortality), hemorrhagic rash (higher mortality), nephritis. Death in

some cases.

 human to human transmission is rare.

 Treatment same as in other species.

 occupational hazard to veterinarians, pet owners, miners, packing house workers, and farmers.

SLIDES:

 Highly coiled long organism. Hook at one or both ends.

 icterohemorrhagia in mucous membranes. Yellowish mucosa and hemorrhage.

 urine is yellowish red.

 L. canicola usually causes uremic type of disease. Degeneration of kidneys.

 Pomona serovar tend to be rather severe. Abortions.

 You can see hemorrhages in fetal skin. In some aborted fetuses you can see necrotic lesions.



RICKETTSIA

 FAMILY: Rickettsiaceae

 Tribe: Rickettsiae

 Genera:

 Rickettsi:, Rickettsia rickettsi

 Coxiella: Coxiella burnetii

 Tribe: Ehrlichiae

 Genera:

 Ehrlichia: E. canis, E. chaffeensis; E. risticii; E. equi; E. platys.

 Cowdria: C. ruminantium

 Neorickettsia: N. helminthoeka

 Obligate intracellular parasites. Parasites of arthropods.

 Animals and humans are accidental hosts and suffer the clinical disease.

 Two genera: Rickettsia and Coxiella.

 Zoonotic.



ROCKY Mountain Spotted Fever



 Least frequently in Rocky mountains!!

 Most frequently reported rickettsial disease.

 Caused by R. rickettsii.

 Vectors: Ticks (Dermacentor and Amblyomma)

 DOGS: Fever, anorexia, severe depression, petechial hemorrhages on mucous membranes,

abdominal discomfort, jaundice, and neurological signs (head tilt, circling, incoordination.)--

[not always seen, but can be striking.]

 HUMANS: Flu-like, skin rash, abdominal pain, stupor, coma, and seizures. Some deaths if

not treated as soon as possible, the treatment response is very good.

 Treatment: Tetracyclines are drugs of choice.

 DIAGNOSIS: IFA, Micro-FA, and CF tests.

 Protective immunity is CMI

 Recovered animals are immune

 Bacterins are used in humans; effectiveness is disputed.

 Inactivated tissue culture vaccines effective.



Q FEVER:



 Coxiella burnetii: Obligate intracellular pathogen.

 Prevalent World wide: in Michigan---several outbreaks.

 Ticks are the natural host.

 look at diagram for transmission*****

 Cattle, sheep, and goats.

 Most often than not, they do not show clinical signs.

 HUMANS: influenza-like disease (self-limiting; most commonly); nausea, vomiting,

pneumonitis; abortions in women; rarely endocarditis which is often fatal. also encephalitis

and meningitis.

 Transmitted by: Droplet infection, milk, fomites.

 Tetracyclines are the drugs of choice for humans.

 Bacterins are used in humans in limited manner.

 A single gram of aborted tissue can have greater than (some enormous number)

 DIAGNOSIS: CF and IFA tests; giemsa stained sections of tissues. ELISA test is

recommended for detecting carriers.

 Treatment: not practiced in animals

 No commercial vaccines used in animals.



 SLIDES:

 typical petechial type of rash in the skin; rocky mountain spotted fever.

 also see rash in the face.

 In dogs you look for hemorrhages in the mucous membranes, elevation of liver enzymes.

Retinal hemorrhages (e.g.) in a dog. Vasculitis.

 In case of animals infected with Q fever you will find large intracytoplasmic inclusion

bodies. these are large colonies of organisms and eventually burst out.



Ehrlichia canis:



 Now an important disease; about ten years ago it was hardly noticed.

 Causes Canine Ehrlichiosis or Tropical canine pancytopenia.

 dog is main; host and reservoir.

 Tick transmission (Rhipicephalus sanguineus)

 Acute phase in dogs: fever, anorexia, depression, thrombocytopenia, lymphadenopathy,

recovery or progression to chronic phase.

 Chronic phase: [weeks even months, even a year later] Anemia, leukopenia,

thrombocytopenia, EPISTAXIS (classic signs of thrombocytopenia), internal hemorrhages,

death. Enlarged spleen and L. nodes.

 HUMANS: Caused by Ehrlichia chaffeensis. Nausea, vomiting, weight loss, Pancytopenia.

 DIAGNOSIS: IFA and look for intracytoplasmic inclusions in monocytes.

 Treatment: Tetracyclines are drugs of choice; no vaccines.

 Recovered animals are CARRIERS!! and NOT Immune can be readily re-infected.

 SLIDES:

 Associated with heavy tick infection.

 Epistaxis is typical

 Look for intracytoplasmic inclusion bodies in monocytes.



Ehrlichia risticii:



 Causes “Potomac Horse Fever” or Equine Monocytic Ehrlichiosis

 Highest incidence from July to august.

 mechanism of transmission is not known. There is no proof involving ticks.

 Cats and dogs may be reservoirs debated

 Clinical Signs: Fever, anorexia, depression, leukopenia, severe diarrhea (ehrlichial colitis)

[almost like salmonella--must differentiate--severe colic], laminitis, limb edema, and death.

30% Mortality.

 DIAGNOSIS: demonstration of cytoplasmic inclusion bodies in monocytes. IFA test--> Less

than 50% infected give positive test. Titers of 1:120 plus clinical signs considered positive.

Not a very reliable test.

 Treatment: Tetracyclines are drugs of choice and widely used.

 Bacterins are used in prophylaxis---not that great.[about 75-80%] Even animals which are

vaccinated can be reinfected after 6 months or even less.

 Recovered animals may be immune for about a year.

 Annual vaccination is recommended.



Ehrlichia platys:



 Causes Canine Infectious Cyclic Thrombocytopenia

 There is a spike of thrombocytopenia every Ten days. Eye is Prominently involved.

 signs: Fever, thrombocytopenia, and anemia. Uveitis, corneal edema, iridial congestion.

 Diagnosis: intracytoplasmic inclusion bodies in Platelets.

 Treatment: Tetracyclines are drugs of choice. Topical neomycin-polymyxin for eye.



Ehrlichia equi:



 Causes Equine Ehrlichiosis

 Fever, anorexia, depression, subcuataneus hemorrhages and edema in legs.

 Neutropenia, lymphopenia, thrombocytopenia, icterus and ataxia.

 Cytoplasmic inclusion bodies are in the Neutrophils and eosinophils.

 Treatement: Tetracyclines. No vaccines are used

 Recovered animals are immune.



[Bovine and ovine ehrlichiosis are caused, respectively, by E. bovis and E. ovis. Causing a febrile disease

with cytoplasmic inclusion bodies in monocytes.]



Neorickettsia helminthoeka:



 Causes “salmon poisoning” in the dog family and a variety of wild mammals.

 flukes are prominently involved. These are infected with Neorickettsia and mature in the

intestines of dog and release Neorickettsia which colonize RES.

 Generalized infection of lymphoid tissues.

 Fever, anorexia, depression, persistent vomiting, bloody diarrhea, dehydration and death in 2

weeks.

 Hemorrhagic gastroenteritis, lymphoid hyperplasia, monocytic meningitis. 90% mortality in

untreated.

 Unless treated prominently, mortality is increased.

 DIAGNOSIS: demonstration of flukes and fluke eggs. Cytoplasmic inclusions in monocytes

and neutrophils; to demonstrate inclusion bodies usually take an aspirate from a swollen

mandibular lymph node is often used.

 TREATMENT: Tetracyclines or chloramphenicol.

 Recovered animals are immune.



Elokomin Fluke Fever:



 Caused by: N. elokominica

 Canids, bears, raccoons, ferrets.

 infectious period: 1.5 to weeks

 Fever, generalized lymphadenopathy, weight loss, some neural signs. NO Bloody diarrhea

 Mortality is lower than N. helminthoeka, about less than 10%



CHLAMYDIA

 No life cycle in arthropods.

 obligate intracellular parasites

 Developmental cycle in host cell---read that in blue book.



Chlamydia :

 only species we will be dealing with

 chlamydiosis

 Avian and many mammalian serotypes. Different serotypes cause specific diseases in animals

and birds.

 Two major antigens:

1. Lipopolysaccharide antigen: elicits a group specific antibody. reactive in CF, FA,

agglutination and agar gel precipitin tests.

2. Cell Wall protein antigen elicits protective immunity. Immunity is serotype

specific.

 Route of infection is through ingestion or inhalation, but the clinical signs are the same.

 Sites of localization:

 Liver, spleen, kidneys, lungs and intestines (important in birds especially)

 in some animals you can see CNS and joint diseases.

 in others, EYE can be affected.

 Reproductive tract. (e.g. in sheep) in others.

 In some species, they can affect all these systems.



 AVIAN Diseases:

 Psittacosis: chlamydiosis of psittacine birds

 ornithosis: chlamydiosis of Turkeys, chicken, sparrows, pigeons, etc....

 latency in an important feature of the disease. Some of these birds can have latent

infections for months. So Fecal shedding by these latent animals are important in the

spread of the disease.

 Stress is an important factor in activating the disease

 Mortality can vary from 70-90% in young birds.

 Anorexia, depression, conjunctivitis, Pneumonitis, Severe Diarrhea, dehydration, and

Death.

 Acute or chronic. In any given species there can be acute or chronic infections.

At necropsy you find: pneumonitis, enteritis, pericarditis, peritonitis, hepatomegaly,

spleenomegaly, and necrotic foci in liver. This are not unique signs; they can be seen

in other septicemic diseases of birds.

 TREATMENT: Tetracyclines are the drug of choice; erythromycin also.

 Cell mediated Immunity is protective; some humoral, but not protective involved

in serological tests.

 CHLAMYDIOSIS DIAGNOSTIC TESTS:

 Clinical setting:

 cloacal swab:

 latex agglutination test (LA)[more dependable]; clear view-

commercial.

 ELISA: (Sure Sell-commercial)

 FA on direct smear (not dependable)

 Necropsy Specimens: Lungs, liver, spleen, kidney; make impression smears.

 FA test useful on direct smear

 LA and ELISA can be done.

 Clinical Setting:

 Cloacal swabs (3 cloacal swabs in three successive days): need to use

transport medium; provided free by AHDL.

 Cultured in McCoy cells

 FA test done.

 MAMMALIAN DISEASES:

 Enzootic abortion of Ewes:

 severe outbreaks in goat and sheep herds

 infection by ingestion

 also tick transmission; venereal

 abortions, stillbirths, neonatal deaths.

 Diagnosis: Demonstration of chlamydia in fetal tissue and uterine

discharges.

 Bacterin is used

 Asymptomatic shedders are a problem.

 Sporadic Bovine Encephalomyelitis (Buss disease)

 Primarily by Ingestion; inhalation and contact infections can also happen.

 widespread in young calves ( 70 species. (i.e. host specificity as well as tissue specificity)

 Stress factors are important. And quite often it is the stress factors that initiate the disease.

 Both Humoral and cell mediated immune responses.

 DIAGNOSIS: Serological.

 Culturing is impractical for most of them.

 CF, HI, and ELISA

 Growth and Metabolic Inhibition tests: If growth inhibition in presence of a specific antibody

 Important diseases in: Poultry, swine, cattle, goats and sheep.



Mycoplasma gallisepticum:



 Chronic Respiratory disease (CRD) in chicken and Infectious Sinusitis of Turkeys (IST);

same thing, but different species.

 Sinus involvement is very prominent in Turkeys.

 birds 4-8 weeks age.

 Obligate parasite.

 Transmission: Aerosol, egg transmission and contact. Aerosol is most common.

 Signs: sinusitis, tracheitits, bronchitis, airsacculitis. Some pneumonitis and synovitis.

 high morbidity and low mortality

 secondary infections increase severity. It is the secondary infections in some cases that causes

the serious problems. e.g. E. coli septicemias or some other severe type of infections.

 Recovered animals are carriers.

 DIAGNOSIS: Hemoagglutination inhibition test (HI) and slide Agglutination Test (SAT)

 Treatment: Tylosin, tetracyclines, or lincocin in feed or water.

 Egg dipping--in tylosin or erythromycin

 heat treatment of eggs: 12-14 hrs at 46C

 Federally approved Bacterin is used.

 Development of Mycoplasma free flocks.



Mycoplasma synoviae:



 Causes infectious Synovitis: infectious disease.

 Chicken and Turkeys are the main economically important species affected.

 Obligate parasite

 Transmission is similar to CRD: Aerosol, egg transmission and contact.

 Synovitis of hock and wing joints is main symptom

 lameness

 Mortality is insignificant.

 DIAGNOSIS, treatment and control similar to CRD.



Mycoplasma meleagridis:



 True Venereal disease.

 Tom Turkeys are non-clinical carriers.

 Not a major disease, but especially as the M. gallisepticum infections have gone down, these

infections have risen.

 Air sacculitis of turkeys as well as other mild respiratory infections.

 Generally Mild disease.

 Obligate parasite.

 Venereal transmission and egg transmission is considered more important. Aerosol

transmission as well.



Mycoplasma hyopneumoniae:



 enzootic pneumonia of pigs (EPP) or Mycoplasma pneumonia of swine (MPS)

 [[Other major pneumonic bacteria in swine----A. pleuropneumonia, Pasteurella multocida,

Streptococcus suis, Salmonella cholerasuis.]]

 Widespread in pigs 3-10 weeks.

 Carrier swine are prominently involved in transmission of this disease.***

 Transmission: Aerosol or contact infection.

 High morbidity and low mortality unless infected by a more severe secondary pathogen.

 A prominent feature of this disease is Chronic non-productive cough. Poor weight gains.

 Pneumonia is variable.

 should be looking at the herd as a whole in order to make proper diagnosis.

 70% positive for M. horhinis. M. horhinis contributes to infection?

 DIAGNOSIS: clinical picture, ELISA, CF, culture (very little is done).

 Treatment: Tetracyclines, tylosin, tiamulin (miracle drug?), lincomycin. not sure if treatment

with these antibiotics is useful at all. So must focus on disease free herds.

 Focus on M. hyopneumoniae-free herds.



Mycoplasma hyosynoviae:



 Arthritis and synovits in 3-6 month old pigs.

 Severe lameness. so severe that some animals die of starvation. They just don‟t move. Low

weight gains.

 Transmission: Aerosols, or direct contact.

 Localized in the tonsils

 Stress activates disease.

 DIAGNOSIS: clinical picture plus culture. collect paired sera and do CF or metabolic

inhibition test, but these are not very useful.

 Treatment: injectable tylosin or lincomycin plus Steroids. Steroids for lameness.

 In about 4-6 weeks the disease goes away. Can be self-limiting. But because of the extreme

pain, you must treat the animals.



Mycoplasma hyorhinis:



 Affects 3-10 week old piglets.

 very frequent in swine respiratory infections

 Transmission: Aerosol or contact infections.

 Localized in tonsils.

 Stress triggers the disease.

 Associated with polyserositis and arthritis alone or in co-infections with Haemophilus

parasuis. Milder disease in pure culture. Secondary involvement in M. hyopneumoniae and

Bordetella, and Pasteurella infections.

 Fastest growing of Mycoplasmas. Also easy to grow.

 DIAGNOSIS: Culture and identification.

 Treatment: Prophylactic use of tylosin or lincocin on a herd basis lower incidence---not

effective as cure.

SLIDES:

 When you cultivate mycoplasma, they have a fried egg appearance.

 Infectious sinusitis; M. gallisepticum. Really big sinuses.

 Prominently infected infraorbital sinus. bloody serous exudate

 Varying amounts of respiratory distress. You can see the tremendous difference in terms of

weight gain.

 M. synoviae: infectious synovitis;

 The two major joints affected hock and wing joints

 Swine disease M. hyopneumoniae.

 One characteristic feature of EPP is the tremendous difference between the affected area and

not affected area of the lungs. Liver like consistency.

 M. hyosynoviae; severe lameness in affected animals. can affect one or more joints.

So painful to get up, the have a „dog-like‟ sitting position. One or several legs may

be affected.

 Polyserositis and arthritis; peritonitis, pancreatitis. M. hyorhinis.



RESPIRATORY MYCOPLASMOSIS IN CATTLE



 Most infections are caused by Mycoplasma mycoides ss mycoides (SC)[small colony form]

 Causes Contagious Bovine Pleuropneumonia (CBPP)

 Eradicated from US ~100 years.

 Pleuritis and pneumonitis.

 High mortality.

 Prevention: Attenuated Live vaccine.

 M. bovis (moderate), M. bovirhinis (mildest), M. dispar(mild), aand Ureaplasma diversum are

frequent isolates from bovine pneumonic disease.

 Most importan is M. bovis. M. dispar is second most important, and the third one is

Ureaplasma diversum.

 60-90 of the pneumonic cases yield mycoplasma. Primary pathogens or mixed infections.

---------Addendum--------------------------BOVINE MYCOPLASMA-----------------------------------------

Mycoplasma mycoides ss. mycoides (SC):

Obligate pathogen; high pathogenicity-Contagious Bovine Pleuropneumonia in cattle world wide.

Eradicated from the USA. ALV is effective.

Mycoplasma californicum;

Obligate pathogen. High pathogenicity. Bovine mastitis.

Mycoplasma canadensei:

Respiratory and urogenital commensal. Moderate pathogenicity. Mastitis; arthritis, repiratory

infections.

Mycoplasma alcalescens:

Respiratory and urogenital commensal. Moderate pathogenicity. mastitis; arthritis in calves.

Mycoplasma dispar:

Respiratory commensal. Moderate pathogenicity. Calf pneumonia.

Mycoplasma bovigenitalium:

Urogenital commensal. moderate pathogenicity. mastitis, vulvovaginitis; seminal vesiculitis.

Mycoplasma bovirhinis:

Respiratory commensal. Low pathogenicity. mastitis and respiratory infections.

Mycoplasma bovoculi:

Moderate. Conjuctivitis; keratitis; mixed infections with Moraxella bovis.

---------------------------------------------------------------------------------------------------------------------EOF

MYCOPLASMA MASTITIS IN CATTLE: (Discussed in Class)

 M. bovis and M. californicum are the two organisms that cause the most severe mastitis. M.

bovis is the most severe.

 M. bovirhinis(mild), M. canadense(moderate), M. bovigenitalium(mild) and M.

alkalescens(moderate).

 Occurs mainly during winter months.

 Several characteristics of this mastitis that are different from other mastitis.

 M. bovis causes more generalized infection with a very decreased milk production.

 Fever, decreased milk production, discooration of milk (flaky sediments). Severe

swelling; nodules and abscesses; purulent discharge; secretory tisse replaced by

fibrotic tissue; Permanent loss of udder function. Calves may show septicemia,

arthritis and pneumonia.

 Carriers are carriers for life

 Poor response to treatment.

 Must seggregate or cull infected animals. The disease results in substantial losses.





MYCOPLASMA IN GOATS:





 Respiratory infections:

 M. mycoides ss mycoides (LC)[large colony form]; M. capricolum M. agalactiae, ,

and M. ovipneumoniae are involved. these two cause the most

 Transmisison: Droplet or ingestion. severe infections.



 Septicemia, pneumonia, and arthritis. Severe disease with significant mortalities.

Milk borne outbreatks in kids with high mortalities.

 On necropsy you find Polyserositis and pneumonitis.

 Carriers are a serious problem.

 DIAGNOSIS: Culture and serology.

 Culling of infected animals or seggregation is recommended.

 Mastits Infections:

 ss. mycoides (LC): severe mastitis. Generalized infection including viscera.

Arthritis Stress factor contribue to the disesse. High mortalities.

 M. capricolum: Acute mastitis and polyarthritis in goats. Sporadic.

 M. putrefaciens; usually subacute or chronic mastitis in goats. some polyarthritis

may be seen.

 SLIDES:

 (SC) ss. mycoides: causes severe respiratory disease and distributed world wide.

 necropsy features: rough surface of the lung, lots of liquid. Very severe thickening of

interlobular septum.

 ss. mycoides (LC) causes severe mastitis infections in goats.

 Arthritis can be found in mastitis cases of ss. mycoides.

 M. capricolum mastitis is acompanied by severe polyarthritis. knees are less affected.





Clinical Example: 2 year old english setter; fever, anorexia, depression, lethargy, and vomiting.

Conjuctivits and petechial hemorrhages. Sensitive to abdominal palpation. What is it? Rocky mountain

spotted fever caused by R. rickettsii. Owner of dog contracted the disease neurological signs.

Tetracyclines are the drugs of choice.

clinical example: Cat with conjuctivits, coughing, and sneezing. varying degrees of pneumonitis...died

after 4 days. considerable weight loss. Feline pneumonitis caused by Chlamydia psittaci. Tetracyclines

are antibiotics of choice.

Clinical Example: collie dog; listlessness, anorexia, weight loss, coughing and general malaise. Epistaxis,

feer, subcutaneous hemorrhages on the abdomen and enlarged parotic glands. E. canis. Tetracyclines are

durgs of choice, but only helpful if an acute disease.

Clinical Example: equine; fever, leukopenia, profuse diarrhea, signs of colic. laminits, distal edema of

limbs. All animals showed varying degrees of anorexia and depression. More than .225 of the affecteed

animals died. E. risticii. Potomac horse fever.





Bacillus Piliformis: Not a true bacillus!!!!(misnomer)





 Gram negative rod.

 Causes tyzzer’s disease.

 Obligate pathogen.

 Infection by Ingestion of infected feed or water.

 epizootics in colonies of rats, mice and rabbits. sporadic infetions in foal, dogs, cats,

monkeys, etc....

 Sudden deaths, fever, depression, icteric, or hemorrhagic MM, diarrhea, dehydration and

death.

 Many mortalities despite therapy.

 DIAGNOSIS:

 @necropsy:

 severe hemorrhagic enteritis or enterocolitis

 hepatitis with grayish white necrotic foci

 clusters of long tapered cells in parallel and criss cross bundles within

hepatocytes.

 Not cultivable on normal lab media; thus, grown in yolksac of embryo or in mice.

 Treatment: Tetracyclines are durgs of choice usually given in the water. Can give parenteral

tetracyclines to individual animals.





Streptobacillus moniliformis:





 Causes Rat-Bite fever in humans (most of the infections). thus, zoonotic pathogen

 Commensal in nasopharynx of rats (other rodents.)

 Septic arthritis , focal necrosis of the liver and spleen, and lymphadenitis in mice.

 HUMANS: Infetion by rat bite or ingestion of milk or water contaminated with rat urine.

 Septicemia, polyarthritis, petechial skin rash, fever, chills, vomiting, head and back aches.

 Mortalities up to 10% in untreated cases.

 DIAGNOSIS: Very easy to culture in blood or joint fluid. Also use mouse inoculation test.

Serum agglutination test.

 Treatment: Penicillis are drugs of choice. Tetracyclines can be used.[L-forms first discovered

with this organism----specimens without cell wall thus, penicillin recistance. Usually, the

animal recovers after treatment with penicillins, but after about two weeks, there is a relapse

this is because of these L-forms. At this point, Tetracyclins are recomended for treatment.]





Spirillum minor:





 Another cause of rat bite fever; less frequent in USA, but frequent in Asia.

 Rat bite results in speticemic disease. Relapsing fever, skin rash, regional lymphadenitis.

 DIAGNOSIS: not cultivable on lab media. isolated by guinea pig or mouse inoculation.

demonstration of spirillum in blood or lymph node aspirate.

 Treatment: penicillin is the drug of choice.





Other Miscellaneous pathogens:





 Vibrio species: Capable of causing serious infections in marine, aquarium and other cultured

fish. usually a hemorrhagic disease.

 Aeromonas species: hydrophila; typically septicemic disease. salmonicida; fatal septicemic

disease in salmonid fish as well as many other fresh water and marine fish.

 Edwardsiella: Causes serious enteric septicemia in commercial cat fish farms.

 Acinetobacter: Gram negative; very much like a pseudomonsas. sporadic infections. Can

cause Bovine mastitis, and occasional Septicemias in dogs and poultry.

Capnocytophaga canimorsus and C. cyanodegmis:





 Gram negative rods

 Facultative Intracellular Parasites

 Both are commensals in the oral cavity of dogs and cats. Human disease results from dog

bite (mostly).

 Local inflamatory reaction in the majority of cases; self-limiting. Important in individuals

with compromised immune systems. In those cases, severe septicemia may occur. Petechial

and ecchymotic hemorrhages on face, extremities and trunk.

 Organism is seen inside neutrophils.

 Endocarditis, purulent meningitis, and septic arthritis.

 Treatment: Pen-G and third generation cephalosporins are the drugs of choice.





 Clinical Example: A 28-year-old woman, employed as a dog groomer in a veterinary practice,

was bitten on the forearm by a 2-year-old Cocker Spaniel. The puncture wounds were cleaned

with providone-iodine and a dressing was applied. Three days later, the woman left work

complaining of chills, malaise, weakness, and increasing pain at the bite site. In the next 12

hours, she became progressivel depressed and was taken to emergency in a state of collapse

after two gran mal seizures. Physical exam revealed necrotizing cellulitis at the bite site.

Petechial and ecchymotic hemorrhages were noticed on the face,

SLIDES:

 tyzzer’s disease in a foal: the liver is covered with grayish white necrotic foci. Primarily in

lab animals, but other species can have it. It is NOT a zoonotic disease.

 In histopath look for long elongated liver cells with criss crossing bundles inside. Long

needle shaped bacteria present in the hepatocyte.

 Colonies of Streptobacillus moniliformis. The name comes from the bead shaped long

filaments.





CAT SCRATCH DISEASE:





 Caused by a Rickettsia: Bartonella (rochalimaea) henselae

 Non contagious, non suppurative or suppurative regional lymphadenitis following a cat

scratch or bite. Depending on site of scratch or bite.

 Skin rash, encephalopathy, arthritis-arthralgia, hepatitis, and pneumonia in

immunocompromised patients. Strictly a zoonotic disease (cat-humans, not cat-cat).

 Small rod shaped organisms in stained sections of lymph nodes; (skin or conjuctiva)

 usually a self limiting disease.

 Treatment: Ciprofloxacin or tetracyclines.(??)

 SLIDES:

 Severe swelling of lymph nodes!!! really big.

 Sometimes can be harmless.; but varies a great deal.

 Rash all over the body, seen in septicemic disease agressive treatment. occurs in

immunocompromised individuals.

Clinical Example: 12 year old son of aveterinarian became ill two weeks after being bitten by ticks on the

Georgia coast. The child saw a physician with a three dya history of fever, chills, headache, and myalgia.

The boy had a temperature of 102.8 F. blood analysis revealed mild thrombocytopenia as wellas

leukopenia. Human ehrlichiosis: E. chafeenis.





MYCOLOGY LECTURE SERIES



My-1 handout: look at it. Dichotomous key to the filamentous fungi:

 under heading “phycomycetes” add Rhizopus

 under the heading of fungi imperfecti all the rest fall: Penicillum, fusarium, aspergillus.

 you may find out that Microsporum and Trichophyton are ascomycetes, but they have

different names for their sexual forms eg. nannizia for Microsporum.

 Asexual spores are often refered to as conidia by mycologists. (conidium--singular) There is

a tendendy now to change all the previously named asexual spores into „something-conidium‟

 often two names prevail for the asexual reproductive bodies:





Clinical Aspect Of The Fungi:





The two types of manifestations that occur in clinics are intoxications and infections. In

the case of the fungi, we have two forms of intoxications. The first one is called mycetismus; this

is „mushroom poisoning‟ This is due to ingestion of poisonous mushrooms. A couple of them are

Amanita phalloides: called the „Death Cap‟ and A. verna; called the “Destroying angel”. these are

the most common. The other type of poisoning is much more important Mycotoxicoses:

caused by small molecular weight compounds known as mycotoxins. mycotoxins are produced in

imporperly stored grains. (i.e. warm, moist grains) It turns out that almost all animals and birds are

suceptible to the action of these toxins. And I include humans under the heading of animals here.

The first example is the Aflatoxins: Produced by Aspergillus flavus. These were first discovered

when a 100,000 turkeys died in 1960‟s from “Turkey X disease”. Caused by aflatoxin in peanut

grains. Aflatoxins are important in peanuts and corn. Important in poultry, cattle, sheep, swine,

dogs. also some problems in humans. Mycotoxins used as biological warfare??? Aflatoxins are

Carcinogenic. Mayor manifestation that one sees is Hemorrhagic Hepatitis prolonged clotting

times, and liver necrosis. Another type comes from fusarium and depending on what species of

fusarium, these are broken up into two chemical categories, the first one known as the

tricothecene types. The first one of the tricothecenes is called food refusal factor (vomitoxin).

This turns up primarily in the case of pigs. the pigs will refuse to eat the food that has this and will

not eat it untill they are starving, and then they end up with vomiting and diarrhea. Another type is

called T2. Cases have been reported in cattle, horses, swine, poultry. Symptoms associated with

T2 are inappetence, diarrhea, staggers, and agalactia. Pathologically, here one sees skin necrosis

and necrosis of the mucous membranes. So it is a fairly wide ranging problem. There is another

type called zearalenone (F2). this particular toxin, causes estrogenism in pigs.---Precocious

sexual development. Another is rhizoctonia leguminicola; this is a plant pathogen which affects

legumes. When it infects the plants, it releases a toxin which then affects whomever ingests the

legume. The disesae in plants is called “Black patch disease”; Causes black reproductive bodies

called Sclerotia. This is particullarly common in red clover. The mycotoxin, which is produced in

the sclerotia, is called slaframine (or Slobber factor). The disease is called “Slobbers” and

causes excessive saliva production drooling. Also see bloat, and diarrhea. Table in Merck Vet

manual gives more infor on mycotoxins.

The Superficial infections are called dermatomycoses. General comments: the

organisms are reffered to as dermatophytes („skin plants‟) and there are three mayor genera that

are important. Epidermiphyton, Microsporum, and Trichophyton. All of these can affect to

some degree all animals and birds. The mayor ones that you find in animals are microsporum and

trichophyton. They are restricted to infecting skin, hair, and nails (hoof and horn) and feathers as

well. Thus, these organisms are Keratinophilic since all these structures are high in keratin. Now

not all species will infect all of those, some will infect skin only, some hair only, etc.... The Ring

worm lesion in skin has an area of inflamation and a scaly center of healing skin. You may have a

secondary infection. Another thing you may have within the center of region is Alopecia. To

confirm the lesion is of Ring Worm origin, one thing that you can do is use fluorescence. another

thing you could do is microscopic examination from skin scrapings in 10% KOH. Also can use

Lactophenol cotton Blue stain, but this works best for culture. In addition the lesions are

sometimes called tinea (worm) examples are „tinea corporis‟, „tinea capitus‟, „tinea barba‟,

„tinea pedis‟ and „tinea cruis‟(Jock itch!). these infections also carry with them yet another

name.....Favus. What you get here, is a crusty white lesion. And you see this particularly in

fowl comb and twettles will be white and encruste. If this condition is unchecked, then it can

spread to the feathers and surrounding skin as well. Generally speakin you hear the term favis in

infections involving fowl, but sometimes in mice as well.

Transmission and spread of these things......First of all, infected hairs, skin bits (dander/dandruff),

feathers, and if the fungi happen to be growing around, hyphal fragments and spores can spread

them. These infected material will be introduced into skin breaks microscopical or

otherwise...that‟s the usual mode of entrance. In the case of athlete‟s foot, the cracks are

microscopical. all you need is suitable incubation conditions which usually come into the heading

of warm and moist.



Treatment:

First of all, you must isolate the patient and clean the contaminated surroundings

thoroughly. for dogs and cats you can use sytemic griseofulvin after you can use some

topical ointment such as desenex, Micatin, Tinactin. alternatively, you can dip the animal

in captan (an agricultural fungicide) or you can use an iodine shampoo. In guinea pigs,

systemic griseofulvin again and tolnaftate powder (tinactin). Cattle and pigs, remove

crsts, scrub with iodine or sodium caprylate. Horses you wash with captan, followed by

daily iodinescrubs. chicken remove crusts and scrub with iodine.



Important Dermatophytes: My-2



 Microsporum (hair and skin):

 M. canis: 98% (cat) 70%(dogs)[fluorescence]

 M. gypseum: 1%(cats), 20%(dogs)

 Trycophyton (hari, skin, nail)

 T. mentagrophytes: 1%(cat), 10%(dogs)

 T. verrucosum: cattle

 T. equinum: horses.



Life cycle of Microsporum:

 Find them in soil. Behave the same way as in culture.

 there they will form the micro or macroconidia (multiloculate)

 For microsporum, the type of hair infection is called ectothrix(Artrhoconidia

asexual) because only the surface of the hair is involved. As oposed to endothrix

where the conidia grow inside the hair.

 Esentially, every other cell in the septate hypha becomes an arthroconidium.

 If the hair sloghs off and/or comes in contact with another animal, the infection then

is transfered. then you have a cycle of repetitive infection of the hair.

 Or if the arthrospores fall into the soil, then the arthrospores grow there too. So the

reservoir for the disease is the soil.

 if they come in contact with skin, the first thing that happens, the hyphae penetrate

the skin. This is what creates the itching.

 the hypha absorb all the goodies out of the cells and then it differentiates into a

chlamydospore. When the skin is sloghed off, the chlamydospore is infectious and

some other unsuspecting individual may be infected.



Esentially, trichophyton has the same life cycle.



Subcutaneous infections are usually self limiting type of diseases, but on rare occasions become

disseminated. Major example is sporotrichosis: characterized by formation of subQ nodules.

nodules eventually ulcerate and discharge pus (chancre,boil) Sporothrix schenckii: Cigar shaped

yeast in tissues and pus. hyphae in culture (less than 30C, corn meal agar) Clusters of

(sympodulo) conidia on short stalks and will also form chlamydospores in old cultures. organism

is common in plant material. Entry is usually by wound, often from thorns. Usually in the neck,

face and hands, and paws. Horses and dogs, followed by humans, most often infected. diagnosis

is by microscopic examination of pus. diagnose also by fluorescent antibody supported by culture.

There are a wide variety of fungi that create subQ infections, but sporotrichosis is the most

important one.

Systemic infections (deep mycoses) These clinical manifestations will vary depending on the

organism involved. generally lesions form in different organ systems depending on fungus. Can

group them as Opportunistic pathogens. Example 1 is candidiasis: Caused by Candida albicans,

but there are other candida species as well. Now, candida is an important human pathogen

(vaginitis [inflammation, mucous and pus], thrush[infection of new borns in mouth] white fuzzy

patches in the tounge and cheek of the baby). Candidiasis usually causes mucous membrane

inflammations. An interesting example: 2 dogs presented with vaginitis caused by candida. The

source of the infection turned out to be the owner. she liked to bathe with her dogs. In cattle there

are occasional cases of mastitis due to Candida. This is also a problem in chickens and other fowl.

And what you see here are crop and mouth lesions (budding yeast form). The only problem is that

you see them at post mortem since major sign of disease is Death. it turns out the major cause is a

vitamin deficiency which predisposes the birds to Candida infection. To prevent or eliminate this,

you should put stuff in drinking water such as CuSO4, nystatin or amphotericin B. Candida is the

classic dimorphic or (Diphasic) fungus. At 37-37C you get the nice yeasts in blood agar, and in

room temperature (below 30C) on corn meal agar, you get mycelial form. But in the case of

candida it is a false mycelial not a true mycelial. At the tip you can see the chlamydospore and on

the edges you see the smaller blastospores. The structure where the spores form is called a

pseudohyphae. For treatment you use one of the “azole” drugs such as Myconazole,

ketoconazole, and clotrimazole. Another type of opportunistic pathogen is Aspergillosis: This is

an infection with a particular pathogen Aspergillus fumigatis. one of the major manifestations is

that they should be long infections usually due to the amount of spores that these infections

produce. An example is air sac infections in fowl and you can also get respiratory infections.

Penguins seem to be particularly susceptible to this disease and this is due because of the

tremendous stress that they undergo when passing through the tropic when coming/going to some

other country. Occasionally, Aspergillus spp. cause abortions in cattle and some other species.

They form “flask” shaped conidiophores. The recomended treatment is amphotericin B with or

without 5-fluorocytosine sometimes called flucytosine.



FRANK PATHOGENS:



 coccidioidomycosis: Do NOT confuse it with coccidiosis (parasitic caused by Eimeria sp.)

 also sometimes called coxy, “Valley Fever”, “San Joaquin fever”

 It is a disease important in humans, horses and dogs.

 distribution: Southern California, south western USA especially in Arizona.

 If you do a skin test for it, in Arizona about 60-80% of the populatino is positive.

 In Michigan cases are due to transportation of horses through infected areas. Thus,

Prior history is important.

 First of all, often the majority of cases are either inapparent or very mild respiratory

infections. The data for humans say that about 0.2% develop one of the more serious

forms of the disease. One is called primary pulmonary coccidioidomycosis or

granulomatous form and the other is called secondary disseminated form or

suppurative form.

 Agent is Coccidioides immits: infact it is a phycomycete. The hyphal form grows in

the soil. This is a very unusual dimorphic fungus. It likes dry condtions (south west)

and when the hyphae age, they form arthrospores that can be easily air borne (dusts,

winds out west) and they can enter the body through the lungs. Nobody grows

arthrospores because they are very dangerous (deadly). Once they get into the body,

what happens is that these arthrospores undergo a series of differentiations if you will

and they form spherules with endospores. You can find them in the sputum, and

pus. They look like a fat droplet, so they‟re very difficult to distinguish from fat

droplets until they are fully differentiated and you can see the endospores celarly.

This is the diagnostic feature. These are not infectious by the way. But what

happens is when the animal hacks up the spherules in the sputum or when the animal

dies, these spherules fall on the soil and they convert to the hyphal form again to

form the arthrospores thus, reinitiating the cycle.

 DIAGNOSIS: Look for spherules in sputum, pus, urine, and various tissue sections.

Also can use a skin test and the agent that‟s used is called coccidioidin.

 Treatment: Amphotericin B or Ketoconazole.

 Cryptococcosis: typical yeast but it has a big thick polysaccharide capsule. You can find it in

cerebral fluid.

 manifestations include meningitis, and brainstem infections. Occasionally some

cases of mastatitis are seen.

 The agent is Cryptococcus neoformans: it is a true yeast and is encapsulated. So

that‟s much different than the other fungi we‟ve been talking about.

 For diagnostic purposes, you find these yeast with capsules in tissue, CSF and other

materials

 Treatment: Amphotericin B and 5 fluorocytosine.

 This particular disease has world wide distribution, but it is relatively rare in in the

US.

 Blastomycosis: usually called North American blastomycosis. one of the important things

about this disease is its distribution. And there are a lot of cases in the Upper Peninsula (MI).

This are Large Yeast and that will help distinguish from the yeast of histoplasmosis.

 Histoplasmosis: small yeasts. Differentiate from large blastocycotic yeasts. One important

thing on histoplasmosis is the development of tuberculate disease.

 read everything else on the notes.

Antibiotics: They are surface active and the structure is such that one side is hydrophobic and the other is

hydrophilic. And they also attach to aldosterone in the membranes. amphotericin b and nystatin will bind

to the same particular sterol in cell membrane. Griseofulvin only binds to cell walls that have chitin.

Primarily, griseoufulvin is an anti-mitotic agent. Use of the 5-fluorocytosine is only on the yeasts candida

and cryptococcus. Cyclohexamid is used as a selective agent to cut down the growth of fungi in

bacteriological media.