Test 1 Old exam questions Flashcards
you have confirmed that a local farmer that you work with has an outbreak of botulism on his farm. In 7 days he has had 34 affected animal, all of which have died. You explain to the owner that botulism is caused by Clostridium botulinum which is an obligate anaerobe commonly found in soil, animal feces, carrion or in improperly baled hay.
Briefly (1 sentence) explain what an obligate anaerobe is?
Obligate anaerobes are bacteria that lack catalase and superoxide dismutase and are therefore susceptible to killing by oxygen free radicals. Needs CO2 for growth.
you have confirmed that a local farmer that you work with has an outbreak of botulism on his farm. In 7 days he has had 34 affected animal, all of which have died. You explain to the herd owner that the clinical signs in affected animals are caused by botulinum toxin.
Is this an Endotoxin? or an Exotoxin
Exotoxin
you have confirmed that a local farmer that you work with has an outbreak of botulism on his farm. In 7 days he has had 34 affected animal, all of which have died. Based on history provided by the owner you suspect this is a case of botulinum intoxication.
Briefly describe (1 sentence) what is botulinum intoxication?
Ingestion of preformed botulinum toxin via feed
you have confirmed that a local farmer that you work with has an outbreak of botulism on his farm. In 7 days he has had 34 affected animal, all of which have died. Your colleague tells you that in addition to intoxication there are two additional routes of entry of botulinum toxin and that it is important to exclude these in this case.
LIST and briefly describe (1-2 sentences each) the two other possible routes of entry for botulism.
a. Toxicoinfectious botulism: Ingestion of spores with subsequent germination in the GI tract (in intestinal wounds, ulcers, etc) and elaboration of toxin
b. Wound botulism: Infection of a wound with Clostridium botulinum and elaboration of toxin (also toxicoinfectious)
you have confirmed that a local farmer that you work with has an outbreak of botulism on his farm. In 7 days he has had 34 affected animal, all of which have died.
In 1 to 2 sentences describe what would be your approach to demonstrate (or prove) that the route of entry in this outbreak is indeed intoxication?
Submit feed samples (or intestinal material) for botulinum toxin detection and neutralization bioassay.
Briefly (4 to 5 sentences) describe how botulinum toxin causes flaccid paralysis i.e. what is the mechanism of action of toxin?
Botulinum toxin is absorbed into the bloodstream and is distributed to neuromuscular junctions (peripheral nervous system). The toxin enzymatically cleaves polypeptides essential for exocytosis of neurotransmitter vesicles, thus preventing the release of acetylcholine from presynaptic vesicles at neuromuscular junctions. The end result is flaccid paralysis. Note: It DOES NOT block ACH receptors. It DOES NOT do direct damage to the NMJ.
you have confirmed that a local farmer that you work with has an outbreak of botulism on his farm. In 7 days he has had 34 affected animal, all of which have died. Although clearly not the problem on this farm, tetanus is caused by a similar organism (Clostridium tetani). However, tetanus is a very different disease than botulism.
Briefly (4 to 5 sentences) describe the pathogenesis and clinical signs of tetanus:
C. tetani spores gain entry into a wound (i.e. puncture wound to the foot) and germinates to vegetative cells in an anaerobic environment (necrotic tissue, deep puncture, etc). Replicating C. tetani bacteria produce two toxins (i) tetanolysin which causes further necrosis and anaerobiosis and (ii) tetanospasmin (tetanus toxin), which binds to peripheral nerves and ascends to the spinal cord via retrograde axonal transport. The toxin blocks the release of inhibitory neurotransmitters from inhibitory interneurons in the central nervous system (spinal cord and brain). Excitatory and inhibitory effects of motor neurons become unbalanced and the end result is rigid muscle contraction (spastic paralysis/tetany).
you have confirmed that a local farmer that you work with has an outbreak of botulism on his farm. In 7 days he has had 34 affected animal, all of which have died. and currently 4 more are recumbent.
You decide to collect clinical material (e.g., blood, serum and fecal material) from all 4 affected animals. What is the most appropriate test that you would recommend for the CONFIRMATORY diagnosis of botulism in this case? Circle one best option
a. Gram staining for the identification of gram positive rods of C. botulinum.
b. Isolation of C. botulinum from clinical material.
c. Detection of botulinum toxin by mouse inoculation test and toxin neutralization assay.
Briefly JUSTIFY your answer
c. Detection of botulinum toxin by mouse inoculation test and toxin neutralization assay.
Gram staining is not confirmatory test because it will not identify the causative organism. Isolation of C. botulinum from the given clinical material is likely to be unproductive because in this case the outbreak is caused by ingestion of preformed toxin, not due to the bacterial infection. Thus, detection of toxin form samples is the most appropriate test for confirmatory diagnosis.
you have confirmed that a local farmer that you work with has an outbreak of botulism on his farm. In 7 days he has had 34 affected animal, all of which have died, and currently 4 more are recumbent.
You realize that the prognosis for the 4 recumbent animals is poor. However, you decide to treat all sick animals.
a. Will you use an antitoxin or a toxoid?
b. Define antitoxin:
c. Define toxoid:
Antitoxin.
Note: toxoid is also routinely administered to boost immunity (to help protect against subsequent exposure), but this would not be therapeutic for the current bout of botulism in sick animals.
Define antitoxin: Specific antibody against a specific toxin.
Define toxoid: An inactivated toxin that induces an antibody response against the toxin.
you have confirmed that a local farmer that you work with has an outbreak of botulism on his farm. In 7 days he has had 34 affected animal, all of which have died, and currently 4 more are recumbent. you start treatment with an antitoxin.
Will toxin typing be necessary for optimal treatment of sick animals? YES or NO Briefly explain your answer:
YES
Unlike C. tetanum which has only 1 toxin type, there are 8 different strains and 8 toxin types of C. botulinum. These toxins are not cross protective and therefore toxin typing will be necessary for treatment of sick animals with specific antitoxin.
you have confirmed that a local farmer that you work with has an outbreak of botulism on his farm. In 7 days he has had 34 affected animal, all of which have died, and currently 4 more are recumbent. You start treatment with a antitoxin.
Will this treatment reverse the clinical signs in sick animals?
YES or NO
Briefly justify your answer:
NO The antitoxin will only bind to free toxin, preventing further toxin from binding to nerves, but does nothing for toxin already internalized and bound within nerves. The goal is to prevent further worsening of clinical signs, not to reverse the current clinical s
. You are a large animal veterinary practitioner. It is late spring and you are called out to investigate an outbreak of generalized muscle weakness, evidenced by recumbency and flaccid paralysis in a dairy herd consisting of 85 Holstein cows and heifers. Over 7 day period, 34 affected animals have died and on the day of your visit there are 4 animals with active signs of illness. Your physical examination on these 4 animals reveals signs of abdominal breathing, decreased rumen sounds, and decreased tongue and tail tone. Upon your inquiry, the herd owner recalled removing a dead rabbit from first-cut hay 3 days prior to the onset of disease outbreak. Owner also reported that all of the animals are fed with the same haylage and there were no other management changes in past one month. You begin your investigations of the outbreak. Based on your knowledge of clinical bacteriology, you suspect this as an outbreak of botulism.
Will you treat sick animals with antibiotics?
YES or NO
Briefly justify your answer:
NO
This outbreak is due to ingestion of preformed toxin, there is no infection. If you said YES and justified your answer, I gave you credit.
you have confirmed that a local farmer that you work with has an outbreak of botulism on his farm. In 7 days he has had 34 affected animal, all of which have died, and currently 4 more are recumbent. you have started treatment with an antitoxin.
The owner is very upset and does not want to go through this again with his other animals. You recommend vaccinating all the remaining animals with a botulinum vaccine. Will your strategy of vaccinating prevent C. botulinum infection in his other animals?
YES or NO
Briefly justify your answer:
NO
Botulinum vaccine is a toxoid. Toxoids specifically generate antibody response against specific toxin and not specific bacteria. Therefore, botulinum vaccine will not prevent infection, but will prevent disease due to neutralization of botulinum toxin.
This has been really busy week for you. It’s Sunday and a time have some fun at the pool. However Jeff, who is the owner of Wilson dairy farm and one of your very important client, calls to tell you that 8 of his calves (all
Based on your knowledge of the clinical syndrome caused by ETEC, list two independent CLINICAL SIGNS exhibited by the calves that are CONSISTENT with ETEC.
1) Watery diarrhea
2) Dehydration (depression, weakness, anorexia, and moribund would also be consistent with advanced cases)
I was not looking for ANIMAL or MANAGEMENTAL factors here (only clinical signs), however I gave points to those who mentioned age of animals (too young animals,
Briefly explain the pathogenesis of ETEC diarrhea. Include in your answer, factors pertinent to the ability of the bacteria to cause disease, and the specific mechanism of the diarrhea.
Enterotoxigenic E. coli bind to the intestinal epithelial cells via fimbriae (or pili). They DO NOT invade the cells. The receptors bound by these fimbriae are expressed on intestinal epithelial cells in very young animals (generally
Assuming that some calves that you care for have ETEC infection, how would you confirm the diagnosis of ETEC? Include in your answer specific information about what samples to collect, what test will be done and what the test will detect.
Perform fecal culture and confirm the presence of F5 fimbrial and enterotoxin genes on E. coli isolates using PCR or latex agglutination test.
Based on your understanding of the mechanism of diarrhea associated with ETEC infection, describe the important components (apart from antibiotic therapy) of your treatment protocol and briefly (1 to 2 sentences) explain your rationale for each;
1) Fluid and electrolyte therapy: Essential to reverse hypovolemia due to severe diarrhea in which both water and electrolytes are being lost. Accepted others (glucose/dextrose) if well justified.
2) Monoclonal antibodies: These will only help to neutralize free toxin that is not absorbed by the intestine. (I accept this although it is too late for an oral antibodies to do much good in this case).
You are also concerned about salmonellosis. Prior to obtaining a definitive diagnosis, you would like to rule out Salmonellosis. List (a simple listing is sufficient) two independent clinical signs (or observations) that are most likely observed in Salmonellosis but ARE NOT CONSISTENT with ETEC.
1] Fever
2] Blood and mucus in feces
Again, I was not looking for ANIMAL or MANAGEMENTAL factors here (only clinical signs), however I gave points if you mentioned age of animals (all age groups affected).
Briefly explain the pathogenesis of diarrheal syndrome caused by Salmonella. Include in your answer, three important components of diarrhea and briefly describe the specific mechanism of the diarrhea
1] Malabsorption: Salmonella invades enterocytes and replicates, causing direct cell damage. An intense inflammatory response ensues, which causes further damage to villous epithelium. Villous damage results in decreased absorption of water. The loss of epithelium and the severe inflammation in the lamina propria results in loss of cells and hemorrhage into the lumen.
2] Exudation: The severe inflammation results in leakage of inflammatory cells and protein-rich fluid (exudate) into the lumen, contributing to the diarrhea.
3] Hypersecretion: Inflammatory response in the lamina propria results in release of prostaglandins and bradykinins. These activate adenylate cyclase, causing inhibition of sodium and chloride uptake in villous cells and increased secretion of chloride in crypt cells and resulting in net EFFLUX of water.
Based on the information provided in the clinical scenario, should you also include C. perfringens type C in your list of differentials?
YES or NO
Briefly justify r answer as to why or why not?
No
The clinical signs of nectrotic enterocolitis and hemorrhagic diarrhea are consistent with C. perfringens Type C infection. None of the calves are showing these clinical signs. If you said YES and justified you answer, I gave you credit.
let’s assume that you are considering C. perfringens type C as one of your DfDx. List two most important PATHOGEN factors of C. perfringens Type C that cause damage to the host and briefly (1 to 2 sentences) describe the mechanism of the damage cause by these pathogen factors.
a. Production of alpha toxin: cytolytic, responsible for lysis of leukocytes and red blood cells
b. Production of beta toxin: necrotic, responsible for most of the damage to the intestinal villi leading to nectrotic enterocolitis
I was looking for PATHOGEN factors, NOT animal or management factors.
