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57 Cards in this Set
- Front
- Back
Describe genus Clostridium. |
Gram-positive Spore-forming Strict anaerobes Pathogenic species are exotoxigenic. |
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How are clostridia often acquired? |
From the environment, via trauma or ingestion |
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What do the alpha, beta, gamma, and delta toxins do with C. septicum? |
Alpha - hemolysin Beta - DNAse, leukocidin Gamma - hyaluronidase Delta - hemolysin |
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Which toxin is crucial for malignant edema caused by C. septicum? |
Alpha toxin - activated by proteolysis, causing pore forming. |
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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 |
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What is braxy? |
Compromise of the abomasal lining and invasion by Clostridia, resulting in hemorrhagic, necrotic abomasitis and fatal bacteremia. |
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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. |
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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) |
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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). |
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What toxins does C. novyi have? |
Alpha and beta Different expression in different types of the bacteria (types A, B, D) |
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What does Type A C. novyi cause? |
Wound infections Bighead (rams) Fast-spreading edema of head, neck, and cranial thorax after damage by fighting |
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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 |
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Why is it called "black disease"? |
Due to the characteristic darkening of the underside of the skin from venous congestion. |
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What does Type D C. novyi cause? |
Red water disease - bacillary hemoglobinuria from beta toxin. |
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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. |
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What disease does Clostridium chauvoei cause? |
Blackleg (necrotizing emphysematous myositis) |
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What's the common route of infection for C. chauvoei? |
Ingestion |
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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. |
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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. |
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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 |
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What are the clinical signs (antemortem) of blackleg? |
Fever Depression Lameness Anorexia Discolored, dry, or cracked skin Crepitating swellings (esp on hips and shoulders) |
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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 |
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How can you prevent Clostridial infections? |
Vaccines! Antitoxin and antibiotics are ineffective. |
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What does Moraxella bovis cause? |
Pink eye in cattle |
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Describe genus Actinobacillus. |
Gram-negative, pleomorphic nonmotile rods. Commensal and obligate symbiont. |
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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. |
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An important predisposing factor for Actinobacillus is... |
Trauma! Needs penetration of the mucosal or epithelial barrier. |
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How would you diagnose Actinobacillus lignieresii? |
Biopsy or exudate > histology Culture of exudates |
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How do you treat an Actinobacillus ligieresii infection? |
Surgery Iodide Antibiotics |
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Describe genus Actinomyces. |
Gram-positive rods with a fungi-like branched network. |
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What disease does Actinomyces bovis cause? |
Lumpy jaw
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Describe the pathogenesis of Actinomyces bovis. |
Wound in oral mucosa > bacteria enter > local pyogranulomatous lesions > proliferation of connective tissue with abscesses (usually in jaw) |
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What causes Johne's disease? |
Mycobacterium avium subsp paratuberculosis |
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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. |
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When is Johne's typically contracted? |
Up to a year of age, but affects adults. |
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How is Johne's classified with regards to reportability? |
Notifiable |
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Describe MAP. |
Obligate pathogen, facultative intracellular pathogen. Resistant to disinfectants and degradation. |
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How does MAP avoid production of antibodies against it? |
Lives intracellularly, specifically in macrophages. Prevents antigen presentation by the macrophages. |
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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. |
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What are the clinical signs of Johne's? |
Chronic, non-responsive diarrhea (with no appetite loss) Muscle wasting Severe loss of body condition Death |
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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 |
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How is MAP transmitted? |
Oral ingestion Shed in feces, persists in environment Also present in milk (though lower) Transplacental transmission |
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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 |
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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. |
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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 |
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What are the four groups of animals with regards to infection with MAP? |
Non-infected Infected but not shedding Infected and shedding Clinically infected |
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What is the gold standard test for Johne's? |
Tissue culture |
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What's the biggest general recommendation for controlling Johne's? |
Minimizing contact between infected cows and susceptible young stock. |
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How else can you help control Johne's spreading? |
Culling infected (clinical) animals Environmental cleanup Segregate calves Controlled herd additions |
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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. |
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What disease is caused by Coxiella burnetii? |
Q fever |
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True or false: Q fever only affects cattle. |
False! It's zoonotic and also affects other ruminants.
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How can C. burnetii be transmitted? |
Ticks Oral Inhalation |
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What symptoms do ruminants with Q fever show? |
Usually no symptoms, except abortion or some general symptoms or conjunctivitis. |
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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 |
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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 |
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How would you diagnose C. burnetii? |
Cytologic exam of specimens Serology (ELISA) PCR Modified Ziehl-Nielsen stain |