All Species Flashcards
Blackleg agent
Clostridium chauvoei
Blackleg description
Bacteria in anaerobic environment in the muscle –> bruised or damaged muscle tissue
Can be due to wound or ingestion of spores and deposit in muscle
Can have crepitus on palpation, die acutely, lameness, fever, anorexia
On post-mortem, have black and necrotic muscle with gas bubbles –> foul, sweet odor
Redwater disease agent
Clostridium haemolyticum
Bacillary hemoglobinuria
Redwater disease
Endospores ingested and deposit in liver –> have liver fluke (Fasciola hepatica) –> damage from fluke create anaerobic environment –> bacteria proliferate –> release toxin that targets RBC
Clinical signs: hemoglobinuria, red water (red urine and water blood), anemia, icterus, labored breathing, dehydration, fever
Cattle and sheep
Can see large necrotic area on necropsy
Treat with penicillin and oxytetracycline, antitoxin serum
Common things with Clostridium
Gram positive, anaerobes
Often treat with penicillin
Often vaccine preventable
Black disease agent
Clostridium novyi type B
Infectious Necrotic Hepatits
Black disease description
Endospores ingested –> go into liver –> get liver fluke –> damage liver and cause bacteria to grow –> toxin targets liver –> severe liver damage and some RBC destruction
Mainly sheep (acute death), some cattle with high grain (mainly lethargic)
Liver appears gray to black with a foul smell
No treatment bc acute
Prevent with 7-way vaccine
Tetanus agent
Clostridium tetani
Tetanus description
Horses and pigs most susceptible
Get spores from puncture wounds, castration sites, banding, dehorning
Clinical signs: sawhorse stance, lock jaw, difficulty chewing food, stiff tail, prolapsed eyelid, flared nostrils, muscle tremors/spasms, sensitivity to noise and movement
Treat with tetanus antitoxin, penicillin, supportive care
Botulism agent
Clostridium botulinum
Botulism description
Get from contaminated feed (pre-formed toxin in there) in spoiled silage or feed with dead animals in it
Foals can get toxicoinfectious form –> ingest bacteria and form toxin in their GI tract –> Shaker Foal syndrome
Clinical signs: ascending paralysis; start with muscle tremors and fasciculations and end with respiratory paralysis and death; dilated pupil, ptosis (dropped eyelid), weak tongue
Not many effective treatment
Overeating Disease agent
Clostridium perfringens type D
Pulpy kidney disease
Malignant Edema agent
Any Clostridia in 7-way vaccine
Bighead in sheep is from Clostridium novyi type A
Malignant Edema description
Cattle, sheep, goat, horse
Open wound gets infected with bacteria –> injury, castration, difficult parturition, fighting
Clinical signs: localized swelling and edema, depression, anorexia, high fever, can lead to death in 24-48 hrs if not treated
Necropsy: dark area with foul odor; swelling with no gas accumulation
Can prevent with 7-way vaccine, treat early with penicillin
Overeating Disease
Normal flora of GI tract –> lots of grain or fattening diet –> release of toxin
Clinical signs: decreased appetite, weakness, incoordination, diarrhea, nervous signs, death, glucosuria common
Can prevent with 7-way vaccine
Pulpy kidney disease in sheep –> from rapid carcass decomposition
Enterotoxemia agent
Clostridium perfringens type B, C, E
Enterotoxemia description
Calves, lambs, piglets, foals less than 7 days old
Normal GI tract inhabitant with overgrows due to increased dietary intake
Clinical signs: weakness, abdominal distention, bloody diarrhea, convulsions; can be sudden death but often fatal once signs show
Necropsy: purple gut –> reddened sections of fluid filled small intestines
Treatment: can try fluids, electrolyte, antitoxin, antibiotics but often not successful
Prevent: herd vaccination; give antitoxin at birth, vaccinate dam twice
Clostridium perfringens type A diseases
Jejunal hemorrhage syndrome (JHS); hemorrhagic bowel syndrome; hemorrhagic enteritis in adult cattle
Yellow lamb disease
Intestinal clostridiosis in horses
Clostridium perfringens type A description
Cows with JHS: can be found acutely dead or have increased HR, normal to low temp, enlarged abdomen from ileus, digested/clotted blood in feces
Diagnosis: abdominal US to find increased SI diameter; hyperglycemia, low sodium/chlorine/potassium, high magnesium
NO VACCINE
Yellow lamb disease: show icterus, weakness, rapid death
Have hemolysis, anemia, hemoglobinuria, icterus, fever
Giardia spp. description
Definitive host: dog and cats
Most common species: G. duodenalis in dog
Have assemblages
Clinical signs: diarrhea, colitis, weight loss, decreased appetite, asymptomatic
Fecal-oral transmission of a cyst
Diagnosis: direct smear with saline mount, fecal flotation with centrifugation (zinc sulfate), fecal ELISA, fecal PCR
Treatment: metronidazole, fenbendazole
Should re-test after treatment
No zoonotic from animals to human
Coccidiosis in Small Animal
Cystoisopora spp. mainly affect dog and cat
Clinical signs: diarrhea, colitis; puppy/kitten can be life-threatening with weight loss, dehydration
Transmission: infective sporulated oocysts or transport host ingestion
Diagnosis: fecal flotation
Treatment: sulfadimethoxine (approved), ponazuril, TMS
Not zoonotic
Feline Tritrichomonas Infection
Agent: Tritrichomonas blagburni (T. foetus)
Transmission: feco-oral
In cats, colon and cecum
Clinical signs: Chronic or intermittent diarrhea
Diagnostics: direct smear (can be confused with Giardia but this has jerky and random motions vs Giardia with falling leaf motion), PCR, culture
Treatment: Ronidazole; can have drug resistance and neuro side effects
Kittens can grow out of it
Toxoplasma gondii in cats
Transmission: congenital from dam to offspring via placenta or mammary; acquired from infected tissue of IH or oocysts
Diagnosis: fecal flotation, serology like IFA or ELISA (get convalescent titers), PCR
Treatment: clindamycin (treatment of choice), TMS, pyrimethamine + sulfonamide
Zoonotic risk to humans cause it causes congenital defects
No clinical signs usually in cats unless immunocompromised
Neospora caninum in dog
Definitive host is dog
Acquired transmission (ingest oocyst or infected cattle tissue), congenital (placenta transmission)
Clinical signs: young dogs (ascending paralysis); older dogs (neurologic, respiratory and/or dermatological signs)
Diagnosis: fecal flotation, serology like IFA/direct agglutination/ELISA (convalescent titers), PCR, cytologic or histologic exam
Treatment: clindamycin, TMS + pyrimethamine
