Clostridial Diseases Flashcards
____ should be considered a differential for all cases of sudden death in cattle
clostridium
why is clostridium “everywhere”?
it is present in soil and water, and it is a part of the intestinal microflora
true or false: the prescence of clostridium is enough to cause disease
false! but proliferation is dangerous
clostridium produces exotoxins. What does this mean?
exotoxins are soluble proteins that produce toxic effects causing clinical disease
how do exotoxins get access to the host?
cows ingest the bacteria and disrupt GIT microflora and proliferate and release toxins, usually after a tissue infection or insult
list some risk factors of clostridiosis in cattle?
young animals, failure of passive transfer, open and non opened wounds providing an anaerobic environment, umbillical cord infections or recent castration
contaminated pastures and facillities, unhygenic conditions, soil disturbance
changes in nutrition/changes in pH, excess starches
horses are most at risk of what clostridial disease? sheep?
horses: tetanus
sheep: C perfringens type D
most common clinical sign of clostridiosis? how is diagnosis made?
sudden death! particularily in spring born calves that are well fed and doing well. diagnosis is mostly done via gross pathology
why do you want to collect samples from freshly dead animals or moribund (about to die) animals?
because clostridiosis infected cows autolyze quickly and the bacteria can be hard to actually detect so you need to catch it fast!!
how should you perform a culture when you suspect clostridiosis?
sample 5mls of terminal small intestine content in a sterile container and fill it to the brim! You want to remove air because the pathogen is anaerobic.
how do you definitively diagnose a clostridium pathogen? 2 ways
fluorescent antibody test (FAT) and PCR
exotoxin ID: for C perfringens, usually only done in academic situations
when you suspect clostridial disease, what are important history questions to ask the producer?
-the animals breed, age, etc
-number of animals affected, how many are dead, and what animals are at risk still
-clinical signs of the animal
-vaccine history: has it been given in past 12 months, how many doses, how far apart, how is vaccine stored, given, etc
-any treatments or handling in the last month
-housing of the animals
-feeding: any extra supplements, are the animals grazing?
what are the current guidlines for clostridial vaccines in cattle?
vaccines are usually bacterin toxoids usually in combo with many species. requires a booster, and boosting yearly or more frquently depends on the farm’s needs and risks. they CAN cause anaphylaxsis
if you’re faced with an outbreak of what you think is clostridial disease, what are some things you can do right away?
revaccination of the herd to prevent more cases in future
can give antibiotics like penicillin, but rarely works
treat with an anti-toxin if available (like tetanus)
tetanus causes ________ disease due to _____ and is often associated with ____
spastic paralytic disease due to tetanospamin
associated with wounds
how does tetanus cause paralysis?
toxin blocks neurotransmitter release from inhibitory neurons=spastic paralysis
clinical signs of tetanus?
fever, sweating, convulsions, stiffness, tremors, ataxia, prolpase of 3rd eyelid, rigid limbs, bloat, and eventual respiratory arrest
you are presented with a cow that is ataxic, temoring, has muscle stiffness, and is bloated. The cow was castrated 2 weeks ago. Differential and how will you treat this animal?
anti toxin, penicillin and sedatives like ace, keep in a dark bedded place. Most animals die
pathogenesis of botulism?
C. botulinum type C and D produce toxins that attach to motor neurons and inhibit acetylcholine release–>flaccid paralysis
how do cows get infected with botulism?
phosphorus deficinecy + licking bones with decaying material, access to dead birds
you are presented with a cow that has progressive muscle weakness for the past 2 hours and is now down. On closer examination, the cow’s tongue is sticking out of it’s mouth. differential? how will you treat?
botulism!
could try antitoxin if available and supportive care but often not successful
blackleg disease is caused by ______. what is the pathogenesis?
clostridium chauvoei
causes a clostridial myositis
spores are ingested, replicate in the GI and are absorbed and travel into skeletal and cardiac muscle and remain dormant until there is a traumatic event that allows for anaerobic conditions.
you are presented with a herd of cows, some of them acutely died and the farmer found them dead. One cow still alive has a massively swollen right forelimb and is severely lame. Upon palpation there is some crepitation in the limb. top differential? how will you confirm your diagnosis?
blackleg (C. chauvoei)
could be malignant edema
i would like to do a necropsy and maybe a FAT to confirm
you are investigating a cow that actuely died, an on necropsy you find black rancid gas filled muscles in the limbs, in the heart, and some in the diaphragm too. differential?
blackleg/C chauvoei
if you suspect a cow has blackleg disease and is still alive, what treatments can you offer?
penicillin and a fasciotomy
vaccinate the rest of the herd
malignant edema is caused by
clostridium septicum (also apparently novyi, sordellii, and perfringens can be involved)
pathogenesis of malignant edema
wound contamination or iatrogenic bacteria contamination and proliferation, toxin production, and cellulitis/necrotizing myositis
trauma usually involved can be: parturition, necrotizing vulvovaginitis and metritis
you are presented with a cow that recently gave birth, and has localized swelling and emphysema. top differential?
malignant edema
could also be black leg
how to treat malignant edema?
penicillin and fasciotomy
make sure vaccines are UTD before calving or any surgery
what causes black disease and what is the pathogenesis?
C. novyi type B
liver flukes migrating through the liver causing liver damage, C novyi proliferates in the liver and produces alpha toxins, leading to acute necrotising hepatitis. liver lesions are pale yellow to white necrotic areas surrounded by dark red to black hyperemia.
why is it called “black disease”?
carcasses are highly congested and have a dark appearance/ often serous blood tinged fluid in body cavities including the pericardial sac.
red water disease is actually called ____ and is caused by____
bacillary hemoglobinemia
clostridium haemolyticium
pathogenesis of bacillary hemoglobinemia? what is the primary pathologic lesions?
release of beta toxin causes intravascular hemolysis, anemia, hemoglobinuria, and jaundice
primary lesions is hepatic necrosis (can look like black disease)
which clostridial speies causes necrotic hemorrhagic enteritis and enterotoxemia?
clostridium perfringens
which types of C perfringens do cows get?
type A: clostridial abmasitis and necrohemorrhagic enteritis
type D: enterotoxemia
hemorrhagic enteritis is thought to be caused by ____ but this is controversial. why?
C perfringens type A
it is a commensal of the intestine so we dont actually know…
what is the pathogenesis of c perfringens type A?
favorable conditions in the gut such as high starches cause germination and release of alpha toxins which causes fatal hemorrhagic enteritis
clinical signs of clostridium perfringens type A?
abdominal distension, colic, depression, anorexia, or sudden death
what clostridial species commonly causes enterotoxemia?
C perfrinens type D–>epsilon toxin causes the enterotoxemia
which cows are at risk of developing clostridial enterotoxemia?
cattle on high grain rations or high protein diets, and those in stressful environments
you’re out on a farm and there are some well fed calves that have suddenly dropped dead. On talking with the producer, the calves showed colic signs last night with some respiratory distress but waited to call you until this morning and now they are dead. On necropsy, you note necrohemorrhagic enteritis, excessive pericardial fluid, friable pulpy kidneys, and some pulmonary edema. Differential?
enterotoxemia from clostridium perfringens type D
