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57 Cards in this Set

  • Front
  • Back

Describe genus Clostridium.

Gram-positive


Spore-forming


Strict anaerobes


Pathogenic species are exotoxigenic.

How are clostridia often acquired?

From the environment, via trauma or ingestion

What do the alpha, beta, gamma, and delta toxins do with C. septicum?

Alpha - hemolysin


Beta - DNAse, leukocidin


Gamma - hyaluronidase


Delta - hemolysin

Which toxin is crucial for malignant edema caused by C. septicum?

Alpha toxin - activated by proteolysis, causing pore forming.

Describe the onset of pathogenesis by C. septicum.

Found in the soil and intestinal contents of animals.


Traumatic wound > myonecrosis (toxicogenesis) > hemorrhage, edema, necrosis as spreading along muscle fascia > death


Aka malignant edema

What is braxy?

Compromise of the abomasal lining and invasion by Clostridia, resulting in hemorrhagic, necrotic abomasitis and fatal bacteremia.

What clinical signs would you see with C. septicum infection?

Fever, depression, weakness, muscle tremors and weakness, and soft doughy swelling and erythema around the site of infection.

What would you see postmortem with C. septicum infection?

Gangrene around the infection site


Foul odour


Gelatinous exudate in SQ and IM connective tissue


Subserosal hemorrhage


Serosanguineous fluid in body cavities


Dark red muscle tissue (but usually no gas)

How do you diagnose C. septicum?

Difficult; looks like blackleg.


Use laboratory confirmation: fluorescent antibody staining (but not if dead >24h).


If in horses and pigs, more likely septicum (not susceptible to blackleg).

What toxins does C. novyi have?

Alpha and beta


Different expression in different types of the bacteria (types A, B, D)

What does Type A C. novyi cause?

Wound infections


Bighead (rams)


Fast-spreading edema of head, neck, and cranial thorax after damage by fighting

What does type B C. novyi cause?

Black disease of sheep and cattle (infectious necrotic hepatitis)


Spores germinate in liver tissue, often damaged by fluke migration


Acute or peracute death

Why is it called "black disease"?

Due to the characteristic darkening of the underside of the skin from venous congestion.

What does Type D C. novyi cause?

Red water disease - bacillary hemoglobinuria from beta toxin.

Describe the pathogenesis of C. novyi type D.

Type D spores or vegetative cells ingested > deposited in digestive tract and liver > (fluke migration through liver > hepatic necrosis/hypoxia) >spores germinate > release beta toxin > hepatic necrosis > disseminated in blood, intravascular hemolysis and hemorrhage.

What disease does Clostridium chauvoei cause?

Blackleg (necrotizing emphysematous myositis)

What's the common route of infection for C. chauvoei?

Ingestion

Blackleg is more commonly seen in ______-fed animals than in _______-fed animals.

Blackleg is more commonly seen in grass-fed animals than in stall-fed animals.

Where do you see the most significant lesions with C. chauvoei?

Hindquarters


Will have infiltrated, necrotic muscle with gas bubbles and a characteristic rancid smell.

Describe the pathogenesis of C. chauvoei.

Spores enter bloodstream > organs and tissues (muscles) > dormant until trigger (injury) > decreased blood flow/O2 > bacteria multiply, release toxins

What are the clinical signs (antemortem) of blackleg?

Fever


Depression


Lameness


Anorexia


Discolored, dry, or cracked skin


Crepitating swellings (esp on hips and shoulders)

What are the postmortem findings with C. chauvoei?

Laying on one side with affected leg stuck out


Carcass bloated, blood-stained frothy exudate from orifices


Dark red to black muscle of loin, back, leg


Gas bubbles SQ

How can you prevent Clostridial infections?

Vaccines!


Antitoxin and antibiotics are ineffective.

What does Moraxella bovis cause?

Pink eye in cattle

Describe genus Actinobacillus.

Gram-negative, pleomorphic nonmotile rods.


Commensal and obligate symbiont.

What can Actinobacillus lignieresii cause?

Proliferation of fibrous connective tissue and formation of small abscesses.


Formation of hard, tumourous masses in the tongue > wooden tongue.

An important predisposing factor for Actinobacillus is...

Trauma! Needs penetration of the mucosal or epithelial barrier.

How would you diagnose Actinobacillus lignieresii?

Biopsy or exudate > histology


Culture of exudates

How do you treat an Actinobacillus ligieresii infection?

Surgery


Iodide


Antibiotics

Describe genus Actinomyces.

Gram-positive rods with a fungi-like branched network.

What disease does Actinomyces bovis cause?

Lumpy jaw

Describe the pathogenesis of Actinomyces bovis.

Wound in oral mucosa > bacteria enter > local pyogranulomatous lesions > proliferation of connective tissue with abscesses (usually in jaw)

What causes Johne's disease?

Mycobacterium avium subsp paratuberculosis

In one sentence, describe Johne's and its progression.

A progressive, debilitating, emaciating disease of ALL adult ruminant animals for which there is no treatment.

When is Johne's typically contracted?

Up to a year of age, but affects adults.

How is Johne's classified with regards to reportability?

Notifiable

Describe MAP.

Obligate pathogen, facultative intracellular pathogen.


Resistant to disinfectants and degradation.

How does MAP avoid production of antibodies against it?

Lives intracellularly, specifically in macrophages. Prevents antigen presentation by the macrophages.

How does Johne's cause emaciation?

Over time, causes movement of macrophages to the ileum. The ileum swells and becomes corrugated, resulting in malabsorption and emaciation.

What are the clinical signs of Johne's?

Chronic, non-responsive diarrhea (with no appetite loss)


Muscle wasting


Severe loss of body condition


Death

What histologic lesions would you see with Johne's?

Thickened, corrugated, highly folded intestine


Diffuse granulomatous or histiocytic enteritis


No necrosis/fibrosis


Swollen lymph nodes

How is MAP transmitted?

Oral ingestion


Shed in feces, persists in environment


Also present in milk (though lower)


Transplacental transmission

Describe the pathogenesis of Johne's.

Ingestion of MAP > ileum infected (Peyer's patches) > inflammation over 2-5 years > survival of MAP within macrophages > intestinal thickening and loss of function > malabsorption and emaciation

Why do animals affected by Johne's disease have bottlejaw (submandibular) edema?

Due to protein-losing enteropathy causing loss of oncotic pressure and leakage of fluid from vessels.

How do you diagnose Johne's disease?

It is difficult! Takes a long time for shedding and antibody responses.


By clinical signs


No one really good diagnostic test, but can use rectal/fecal smear (acid-fast stain), fecal/environmental culture, serology, gamma interferon, PCR

What are the four groups of animals with regards to infection with MAP?

Non-infected


Infected but not shedding


Infected and shedding


Clinically infected

What is the gold standard test for Johne's?

Tissue culture

What's the biggest general recommendation for controlling Johne's?

Minimizing contact between infected cows and susceptible young stock.

How else can you help control Johne's spreading?

Culling infected (clinical) animals


Environmental cleanup


Segregate calves


Controlled herd additions

Describe Coxiella burnetii.

Polymorphic gram negative microorganism.


Obligate intracellular.


Has two growth types, large and small variants - small variant resemble spores and are what is released from cells and infectious.

What disease is caused by Coxiella burnetii?

Q fever

True or false: Q fever only affects cattle.

False! It's zoonotic and also affects other ruminants.

How can C. burnetii be transmitted?

Ticks


Oral


Inhalation

What symptoms do ruminants with Q fever show?

Usually no symptoms, except abortion or some general symptoms or conjunctivitis.

Describe the pathogenesis of C. burnetii.

Binds to human monocytes >phagocytosed > phagolysosomes fuse and form large vacuoles (C. burnetii withstands low pH) > slow intracellular multiplication

What are the two antigenic phases of C. burnetii? Explain.

Phase I and phase II (yeah really)


Acute: phase II antibodies higher and then decrease


Chronic: eventually phase I antibodies appear after prolonged exposure to the antigen

How would you diagnose C. burnetii?

Cytologic exam of specimens


Serology (ELISA)


PCR


Modified Ziehl-Nielsen stain