Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
70 Cards in this Set
- Front
- Back
|
What can happen to the villi in a case of chronic diarrhea? |
Clubbing and blunting. |
|
|
What causes the wt loss seen in chronic diarrhea? |
1. Chronic nutrient malassimilation 2. Protein loss |
|
|
What are some important DDX for chronic diarrhea? |
1. parasites 2. IBD 3. Increased hydrostatic pressure 4. Chronic BVD 5. Granulomatous enteritis 6. Cu deficiency |
|
|
What are some of the initial tests that you will collect when working up a chronic diarrhea? |
1. history - feed and disease 2. BW - checking for inflammation, protein 3. Edema present? 4. Fecal O&P 5. Rectal scrape |
|
|
What are HOT complex worms? |
Haemonchus, ostertagia, trichostrongyles/teladorsalis -- those that inhabit the abomasum |
|
|
Where is Giardia maintained in animals |
in wildlife and domesticated spp --> everyone can get it!!!! |
|
|
Define Type II Ostertagiasis |
the mass development of hypo biotic larvae of ostertagia that have been encysted in the abomasum. Occurs in the first or second winter of life. |
|
|
What does the en mass development of the ostertagia larvae do to the gastric glands and their secretions? |
Destroys the glands, reducing their production of acid and pepsin |
|
|
Can we see ova during this type II ostertagiasis |
No - this is the pre patent period, so there are no ova being shed. |
|
|
What can we see a few weeks post worm ingestion on clinical pathology? |
An increase in blood pepsinogen and a small increase in gastrin -- presumably stays high throughout infection. |
|
|
What about during the emergence of encysted larvae? |
Similar to that of a new infection - increase in pepsinogen and gastrin. |
|
|
What is Type I ostertagiasis? |
the first wave of infection and damage. |
|
|
How do we diagnose ostertagia? |
Fecal Egg counts after pre patent period, necropsy, hypoproteinemia, hyperpepsinogenemia. |
|
|
What is the treatment for ostertagia? |
Antiparasiticals, and management changes. |
|
|
What is the causative agent of Johnes? |
Mycobacterium avium subspecies paratuberculosis. |
|
|
How long can johnes survive in the environment? |
up to 4 months -- better in acidic, cool, damp soils. |
|
|
Can mycobacterium survive pasteurization? |
YES -- the conventional pasteurization |
|
|
Who is susceptible to Johnes? |
Anything with two toes -- Ruminants, camelids, camels, rodents (?) and people (?) |
|
|
How many strains are there of Johnes? |
2 - Ovine and Bovine |
|
|
Who gets the ovine strain of johnes? |
Sheep and goats |
|
|
Who gets infected with the bovine MAP? |
Everyone else and goats. |
|
|
How is MAP transmitted? |
1. Fecal oral (primary) 2. some milk 3. Some utero (goes to UT) 4. Some semen transmission |
|
|
How is bacteria introduced to an environment |
Fomites or shedding animals. |
|
|
How is Johnes brought to a naive herd? |
By a non clinical shedding animal. Or bringing your animals to a contaminated field/facilities |
|
|
Can a non clinical animal shed the MAP? |
Yes - just generally not in as high an amount as clinical animals. Shedding will usually increase with duration of disease. |
|
|
What period of life do most infections occur? |
Newborns |
|
|
If you have a clinical carrier, what are the chances that you have a lot more non clinical ones? |
VERY HIGH (usually assume for every 1 clinical animal there are 1-2 non clinical) |
|
|
What are the primary colonization areas for MAP? |
The ileocecal mucosa and the mesenteric lymph nodes. Other areas (LN and urogenitals) are 2º |
|
|
What if I am infected and have a poor immune function? How likely is it that I am shedding? |
1. Slow development of disease w/ intermittent shedding 2. RAPID disease development with MASSIVE shedding. |
|
|
What is the basic lesion of MAP? |
Granulomas -- these are intracellular bacterium. |
|
|
How long does it take clinical signs to develop? |
1.5-2 years |
|
|
Can a 6 month old calf show signs |
in the worst possible scenario - yes. |
|
|
What are the clinical signs of Johnes? |
Emaciation, peripheral edema, profuse pea green watery diarrhea (non hemorrhagic) |
|
|
Does johnes cause a rapid or slow decline in milk production? |
SLOW |
|
|
If a cow has MAP are they still eating? |
YES |
|
|
How long can it take for signs to develop in a clinically sick animal? |
up to 6 months. |
|
|
Is Johnes reportable? |
YES |
|
|
What is the most sensitive, specific test for MAP? |
Histopath - but is $$$ for live animal or it has to be a dead animal. |
|
|
Which test is 100% specific and sensitive for testing a HERD for MAP? |
Fecal Culture |
|
|
What is the problem with fecal culture? |
Takes up to 4 months for results! |
|
|
Can fecal culture detect low volume shedders? |
YES |
|
|
Which test is usually required by Regulatory bodies? |
Complement fixation |
|
|
What is the problem with CF? |
It only has a 70% specificity so it is a poor screening test (too many false positives) |
|
|
What is the sensitivity/specificity of the AGID? |
>90% |
|
|
Which test is fastest and cheapest? |
ELISA (2 hour turn around) |
|
|
What is the specificity of the ELISA for clinical and non clinical animals? |
> 95% |
|
|
Which test is not affected by vaccination? |
Fecal PCR |
|
|
Which level of shedding will the fecal PCR catch? |
light, moderate and high shedding animals |
|
|
What tests would you use to confirm a diagnosis? |
ELISA, PCR, necropsy +histopath |
|
|
What about herd screening/estimation? |
ELISA, PCR |
|
|
What must a producer decide to do with their testing results? |
Decide if they are just controlling or eradicating the disease |
|
|
What do you need to choose for a test for ERADICATION |
Something that is very SPECIFIC *you are going to be culling all POSITIVES* |
|
|
What age of cow is included for herd certification? |
any animal > 20 months old. |
|
|
How do you get the probable positive prevalence in the herd? |
Take the # positive on testing and x 2 |
|
|
How is a certification level determined |
How many years there have been all negative tests (up to 4)( -- so that first year - cull all + animals, retest 1 year - if negative you are a level 1) |
|
|
What basic principles must be adhered to to control Johnes? |
Keep cow/calf contact at minimum, do not feed calves milk straight from dams, sanitize EVERYTHING, no manure spreading, immediately remove all suspect animals. |
|
|
Are there any vaccines for MAP? |
Yes - MLV vacc - for calves 7-35days old. Does not reduce infection, only the shedding and the clinical rates. |
|
|
What other major disease testing can MAP vaccines interfere with? |
TB testing!! |
|
|
Which is better? MAP vacc or control? |
CONTROL (they have about the same efficacy, but the control does not interfere with TB testing!) |
|
|
What are the two major ways our cattle get copper deficiency? |
1. Primary Cu deficiency in feed stuffs (poor soil) 2. Molybdenum excess (or sulfur,Zn, Fe, Pb) |
|
|
Why is Cu so darn important? |
Super oxide dismutase and ceruloplasmin. Essentially oxidative metabolism of cells. |
|
|
What are the CxS of Cu deficiency? |
D+, anemia, dilute hair coat, loss of crimp in sheep fiber, good appetite! |
|
|
How do you dx Cu deficiency? |
Testing the feed, liver or blood. Also need to consider the other metals when looking at the dietary copper. |
|
|
Treatment for Cu deficiency |
Cu capsules (oxide or sulfate). |
|
|
How much Cu should be in forages? |
> 10mg/kg (>5 for those sensitive sheep), less molybdenum. |
|
|
What ratio of Cu:molybdenum is best? |
5:1
|
|
|
What are some microscopic signs of IBD on histology? |
Eosinophils anywhere but the crypts of the villi, dilation of the lacteals, edema of the villus |
|
|
What are the hallmark signs of IBD in cattle |
Wt loss, good appetite, D+ |
|
|
What is the major ddx for IBD? |
JOHNES |
|
|
Where are the characteristic changes in the villus in IBD? |
in the immune cells (submucosa) or the villus tips |
