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210 Cards in this Set
- Front
- Back
What are 3 examples of malabsorption?
|
rota, corona, cryptosporidiosis
|
|
Osmotic diarrhea can result from malabsorption of maldigestion. What are some examples?
|
-Magnesium sulfate
-Viral Diseases -Grain Overload -Poorly Digested milk Replacers |
|
Secretory diarrhea is caused by what? What are some examples?
|
-enterotoxins stimulate secretion by the intestinal cells by stimulating cyclic AMP (ETEC)
- or prostaglandin secretion as a result of inflammation can stimulate secretion ( Salmonella) |
|
Increased hydraulic pressure can result from what 3 things?
|
1 - decreased oncotic pressure (hypoalbuminemia)
2 - increased hydrostatic pressure ( heart failure) 3 - decreased lymphatic drainage due to blockage or inflammation (lymphoma) |
|
What are 6 keys to helping prevent neonatal diarrhea?
|
1 - clean birthing and housing environment (dry)
2 - clean dams utter 3 - proper colostrum intake 4 - keep age groups seperate 5 - vaccination of dam 6 - pigs esp: don't fluctuate the temp |
|
What is the proper amount of colostrum intake for calves?
|
6-8 liters/calf in the first 24 hours
|
|
What should the temp be for:
- baby pigs: -nursery pigs: |
- baby pigs: 90F
-nursery pigs: 85 F |
|
How do you vaccinate the dam to help prevent neonatal diarrhea?
|
- primiparous - 3 and 6 weeks
-pluriparous - 3 weeks prior to parturition - swine - feed dead piglets that died from diarrhea to prepartum dams |
|
When should samples of neonatal diarrhea be collected?
|
early in the disease - DON'T freeze
|
|
Where should samples be taken from in the case of neonatal diarrhea?
|
- always ileum
-also duodenum, jejunum, cecum, LI, mesenteric LN, abomasum |
|
Is the consistency and color of diarrhea diagnostic?
|
no
|
|
What is the agent for enteric colibacillosis?
|
Enterotoxigenic E. coli
|
|
What are the 2 main virulence factors for enteric colibacillosis?
|
1 - pilus or fibria that allows attachment to enterocytes (K99 - calf; K88 - pig; F41)
2 - heat stable enterotoxin (k99) and heat labile |
|
What is the most frequently isolated pathogen in diarrheaic neonates?
|
enteric colibacilosis
|
|
What is the age of animals that commonly get enteric colibacilosis?
What animals? |
1-4 days
- calves, lambs, kids, pigs |
|
What is enteric colibacilosis assoicated with?
|
lack of colostrum and or dirty environment
-complicates viral or parasitic enteric diseases |
|
What are the CS of enteric colibacillosis?
|
-profuse, watery diarrhea-
-no straining -dehydration and weakness |
|
What is the course of enteric colibacilosis?
|
rapid with death in 6-12 hours
|
|
What type of diarrhea will you see with enteric colibacilosis?
|
secretory due to secretion of enterotoxins
-absorptive capicity is intact, but overwhelmed |
|
What are the lab findings with enteric colibacilosis?
|
- hypoglycemia
- hyperkalemia (results in cardiotoxicity) -acidosis -dehydration -total body decrease in Na and Cl, although may appear normal |
|
How do you diagnose enteric colibacilosis?
|
-culture of E. coli with presence of pilus antigen
-ElISA or latex agglutination test on feces - Florescent AB testing of intestinal tissues |
|
What is seen on histopath with enteric colibacilosis?
|
1 - min. inflammation in the SI
2 - mild villous atrophy 3 - sheets of gram negative bacilli adhered to the villious enterocytes of the SI mucosa |
|
What is the treatment for enteric colibacilosis?
|
-fluid therapy
-colostrum feeding -EARLY --> Ceftiofur, Spectinomycin, Sulfas |
|
How do you prevent enteric colibacilosis?
|
1 - proper colostrum management
2 - birth in clean environment 3 - vaccination of dam with pili antigen vaccine (K99, K88, F41) 4 - monoclonal antibody (Genecol 99) |
|
What type of virus is Rotavirus?
|
reoviridae
|
|
What group of animals get the following type of rotavirus diarrhea?
A B ABCE Which is the predominant serotype? |
A is predominant
A - calves B - lambs (atypical rotavirus, pararotavirus) ABCE - swine |
|
What is the distribution of rotavirus?
How long can it survive in the environment? |
80-100%
9 months |
|
When are most calves affected by rotavirus?
Lambs and kids? |
calves - 4 -14 days
lambs and kids - less than one week |
|
When do CS of rotavirus develope?
|
When colostral immunity declines
|
|
Why does rotavirus spread quickly among neonates?
|
due to the large number of virus particles that are shed in the diarrhea
|
|
What are the severity of CS dependent on with rotavirus and what does the poop look like with calves, lambs and kids?
|
depend on animal's immunity and the presence of secondary invaders (diarrhea may last 1-2 days or 3-5 days if secondary bacterial invaders are involved)
- bright yellow or green pudding then water |
|
When do most cases of pig rotavirus occur?
|
1-6 weeks, but mostly around weaning when lactogenic immunity declines
|
|
What are CS of rotavirus in pigs?
|
watery to puding diarrhea with poor weight gain
(exacerbated by E. coli) |
|
What type of diarrhea is seen with rotavirus?
|
malabsorptive - vilus tip of SI affected
-lack of enzymes results in fermention of products in LI reulting in -osmotic diarrhea |
|
What is seen on necrospsy with rotavirus?
|
-moderatly distended intestines
- thinning of gut wall -absent lacteals |
|
What does histopath look like with rotavirus?
|
shortening and blunting and fusion of villi with loss of columbar villous epithelium in SI only
|
|
What does the fecal ELISA detect with rotavirus?
|
rotazyme for group A rotavirus only
|
|
What are 3 ways to diagnose rotavirus?
|
1 - electron microscope
2- Florescent antibody test 3 - fecal ELISA |
|
How do you treat rotavirus?
|
-fluids
-antibiotics (ruminants if secondary bacterial invaders) -pigs - increase temp in nursery |
|
What are 4 ways to prevent rotavirus?
|
1 - vaccination
2 - colostrum (dairy calves 2 weeks post calving) 3- clean environment 4 - pigs - antibiotics at weaning |
|
Why is the oral MLV rotavirus vaccine not recommended?
When is parenteral vaccination most used? |
have to delay feeding colostrum
-dairy calves |
|
What is the agent of TGE in swine?
|
coronavirus
|
|
IS the morbidity and mortality of TGE high or low?
What alters the severity of disease? |
high in naive herds
- variations in dam immunity |
|
What are carriers or excretors of TGE of swine?
|
dog, cat, starlings, flies
|
|
What are the CS of neonates with TGE?
|
<2 weeks old
- Diarrhea (profuse white to yellow with very wet tails), dehydration, vomiting, excessive thirst, DEATH |
|
What is the predominant group of pigs affected by endemic TGE?
|
post-weaning age
|
|
What is the CS of growers, finishers, and adults with TGE?
|
-anorexia, vomiting, and fever, +/- diarrhea
|
|
What type of diarrhea occurs with TGE?
|
malabsorptive
|
|
What is found on necropsy with TGE?
|
- fluid distention with jejunal and ileal intestinal thinning
-no visible lymphatics in mesentary in area of fluid distension and thinning |
|
What does histopath look like with TGE?
|
-fusion and blunting of SI villi (SEVERE VILLOUS ATROPHY)
-villous to crypt length ration is 1:1 (normal is 7:1) |
|
What is the treatment for TGE?
|
-rehydration and allowing neonates water and electroytes
- keep floor temp above 90F |
|
How do you prevent TGE?
|
vaccination
|
|
How do you diagnose TGE?
|
histopath, electron microscope, FA
|
|
What is the morbidity and mortality rate of coronavirus in calves?
|
morbidity - 15-25%
case fatality - 5-10% |
|
When do asymptomatic cows shed coronavirus?
What is the prevalence of antibodies? |
around parturition
100% |
|
When are most cases of coronavirus in calves observed?
|
5-30 days old
|
|
What is in the feces of calves with coronavirus?
|
mucus, milk curd, +/- blood
|
|
What is more severe - rotavirus or coronavirus?
|
corona - after 2-4 days they can be depresed, weak, and gaunt near death
|
|
What part of the GI tract is affected by coronavirus in calves?
|
SI and colon
-absorptive columnar epithelial cells |
|
What cells does the coronavirus attack in calves and why is this imortant?
|
undifferentiated epithelial cells, fibroblasts, and endothelial cells, making recovery longer compared to rotaviurs
|
|
What is the treatment for coronavirus?
|
fluids
|
|
What is seen on histopath with coronavirus?
|
severe blunting and fusion of vili of the distal SI and colon
|
|
How is coroona in calves diagnosed?
|
FA, TEM , histopath
|
|
What agent causes Clostridial scours in pigs?
|
C. perfringens type C
|
|
What age pigs are affected by Clostridial scours and what pigs get it the worse?
|
1-14 days
worst - 1-5 days |
|
What are the CS of clostridial scours?
Which litters get it more? |
-bloody diarrhea (rare), sudden death
-gilt litters |
|
What is the pathophysiology of Clostridial scours in pigs?
|
-release of enterotoxin resulting in necrosis of the SI microvilli and desquamation of epithelial cells
-hemorrhage into the lumen and necrosis of the SI resulting in peritonitis |
|
What lesion is pathopneumonic for the acute/peracute disease of clostridial scours in pigs?
|
- subserosal and luminal bleeding
-excessive blood tinged pleural peritoneal fluids |
|
What is seen on histopath with clostridial scours in pigs?
|
- necrosis and hemorrhage of the mucosa with gram positive colones
|
|
What do you do if you encounter an outbreak of clostridial scours?
|
-give antitoxin and penicillin to piglets (orally or injection)
|
|
How do you prevent clostridial scours in pigs?
|
give type C bacterin to dams
|
|
What is the most common cause of hemorrhagic enteritis in the first week of life in food animals?
|
Clostridial scours in pigs
|
|
What causes enterotoxemia in ruminants?
|
toxigenic type Clostridium perfringens
(C and D) |
|
What are the characteristics of C. perfringens?
|
- Gram positive bacillus, secrete enterotoxin, normal gut flora
|
|
Why does C. perfringens produce toxin with enterotoxemia in ruminants?
|
in response to notmal flora changes due to increased intake of carb and protein rich foods.
-includes calves sucking on high producing dams |
|
Why type of toxin causes type C enterotoxemia?
type D? |
C - Beta
D - Epsilon |
|
What is the most common cause of acute fatal hemorrhagic enteritis of neonatal lambs, kids, and calves?
What age? |
enterotoxemia in ruminants - type C
1-10 days |
|
What is another name for type D entertoxemia?
|
overeating disease in lambs (also cattle goat and sheep)
|
|
What are the CS of type C enterotoxemia?
|
-diarrhea, dysentery, colic, opisthotonus, tetany (many die before diarrhea develops)
|
|
What are the lesions of type C enterotoxemia in ruminants?
|
-hemorrhagic inflammation of the jejunum and ileum and LN
-large numbers of gram positive rods in the intestine |
|
What are CS of type D enterotoxemia in ruminants?
|
-sudden death usually
-neuro signs (mania, ataxia, blind, recumbent, convulsions) -renal damage, hyperglycemia, hypertension, edema -glycosuria in sheep |
|
What is seen on necrospsy in animals that die from type D enterotoxemia?
|
pleural and pericardial fluid with petechial hemorrhages on serosa of intestine, diaphragm, endocardium, pericardium with fibrin
|
|
What is used to ID type D toxin with enterotoxemia?
|
mouse inoculation tests
|
|
What is the treatment for type D enterotoxemia?
|
most are dead already
- hyperimune serum, antibiotics, fluids |
|
When should you vaccinate lambs and calves for type D enterotoxemia?
|
calves - week 8 and 12 and before feedlot
lambs - two weeks before weaning and before feedlot |
|
What is the agent of cryptosporidiosis?
|
C. parvum
|
|
When do oocysts sporulate with cryptoand what does this mean?
|
at time of passage so they are infective immediately
|
|
Do crypto oocytsts survive freezing?
|
no, but are hardy and can build up over time
|
|
What are CS to crypto?
|
diarrhea, tenesmus, anorexia, weight loss, depression
|
|
What age does crypto occur?
|
1-3 weeks (at 10 days)
|
|
What type of diarrhea is seen with Crypto and why?
Where? |
malabsorptive - attach to BB and prevent absorption
-in distal SI |
|
How do you diagnose Crypto?
|
- fecal float
-Histopath |
|
What is the treatment for crypto?
|
fluids
vit A supportive care |
|
How do you prevent Crypto?
|
-sanitation
-drying -movement of housing |
|
What are the agents of coccidiosis in:
-calves -kids -lambs |
calves - Eimeria bovis and zuernii
kids - Eimeria arloingi lambs - Eimeria ovina |
|
What is associated with ruminant coccidiosis?
Where are infections often picked up? |
-crowed unsanitary conditions in times of stress
-infection picked up near water due to concentration of infective oocyts |
|
When are clinical signs of ruminant coccidiosis seen?
|
3-4 weeks of age and older
-most at weaning |
|
What are CS of coccidiosis in ruminants?
|
-diarrhea
feces with mucus and +/- blood (usually not with kids or lambs) -dehydrates and listless, weak and emaciated -ROUGH hair coat -tenesmus with rectal prolapse |
|
What is the malabsorption due to with coccidiosis?
|
destruction of enterocytes
|
|
How do you diagnose coccidiosis in ruminants?
|
-fecal exam
necropsy -histopath |
|
Where are the lesions with coccidiosis in cattle and sheep and goats?
|
cattle - LI
sheep and goats - SI |
|
What is the treatment for coccidiosis in ruminants?
|
-amprolium (thiamine def) - need 3-5 x dose with SR
- sulfaquinoxaline - supportive care - fluids and secondary invaders |
|
How do you prevent coccidiosis in ruminants?
|
-avoid wet environements
-feed supplements (amprolium and ionophores) |
|
What is the agent for swine coccisiosis?
|
Isospora suis
|
|
When are most signs of coccidiosis in pigs?
|
7-11 days
but can occur anywhere between 5 days to 3 weeks |
|
Coccisiosis in pigs is sporadic. Why is it important if morality is low?
|
unthrifty and poor growth - economically important
|
|
What are the CS to coccidiosis in pigs?
|
-yellow to tan to gray pasty diarrhea becoming watery, dehydration, unthrifty
-rapid onset |
|
Where are lesions in pig coccidiosis?
|
SI
|
|
What is treatment for pigs with coccidiosis?
|
questionable
|
|
How do you prevent pig coccidiosis?
|
-all in, all out; clean farrowing crates
-wash sows before entering farrowing house |
|
What is the agent that causes Swine Dysentery?
|
Brachyospira hypdysenteria
|
|
How long can swine dysentery be shed by carriers and survive in lagoon water?
|
-90 days - birds, rodents, dogs and flies for 30 days
-2 months |
|
How is swine dysentery normally brought in?
|
new pigs, equipment, boots, contaminated with feces
|
|
What age is swine dysentery common in?
|
post-nursery age group - grower and finisher
|
|
HOw do you treat and control swine dysentery?
|
feed grade antibiotics
|
|
How do you prevent swine dysentery?
|
subunit vaccine and strict biosecurity
|
|
HOw do you diagnose swine dysentery?
|
-necropsy
culture |
|
Where are the lesions with swine dysentery?
|
cecum and spiral colon
-mucus adherent to mucosa early then bloody and fibrinous later -multifocal areas of petechial to paint brush hemorrhages on mucosal surfaces |
|
Why is there malabsorption assoicated with swine dysentery?
|
failure of epithelial transport mech
|
|
What are the CS of swine dysentery?
|
gray mucoid feces first then bloody, mucoid diarrhea (undigested blood)
-emaciation and POOR GROWTH -sporadic diarrhea and reduced weight gain |
|
What is the agent that causes Swine paratyphoid?
|
-Salmonella. cholerasuis (60-70%); Salmonella typhimurium
|
|
How might swine paratyphoid come to the farm?
|
via feedstuffs
- high protein supplements of animal origin (blood meal) - Ca: Phosphorus supplements of animal origin (bone meal) |
|
What are epidemics of Swine paratypoid assoicated with?
|
stress
|
|
Can healthy animals be carriers of Swine paratypoid?
|
yes
|
|
What is the morbidity and mortality of swine paratyphoid?
|
high
|
|
What are the CS of swine paratyphoid?
|
-watery, yellow diarrhea often with necrotic debris, diarrhea may be bloody
-febrile, anorexic and occasionally septicemic signs predominate -pneumonia - survivors may be stunted pigs (poor growth) and have rectal strictures |
|
Survivors of swine parathyphoid may have what?
|
-stunted pigs
-poor growth - rectal strictures |
|
What type of diarrhea is seen with swine paratyphoid?
|
-malabsorption from intestinal damage
- secretory due to inflammatory products |
|
How do you diagnose swine paratyphoid?
|
-culture
-necropsy |
|
What does a pig with swine parathyroid look like on necropsy?
|
-inflamed and thickened ileum and colon (small and large intestine) with fibrinous adhesions and mucosal hemorrhages
-button ulcers |
|
What part of the intestine is affected by swine paratyphoid?
|
small and large intestine
|
|
What is treatment for swine paratyphoid?
|
antibiotics and supportive care
|
|
How do you prevent swine paratyphoid?
|
closed herds
-avirulent live culture vaccine of S. choleraesuis, administered intranasally or via water |
|
What is the agent that causes Salmonellosis?
|
Salmonella typhimurium, dublin, newport, muenchen, copenhagen
- S. dublin is host adapted to cattle |
|
What are the 4 ways animals can acquire Salmonellosis?
|
-environment
- carriers - feed -water |
|
How do carriers spread Salmonellosis?
|
recrudescence at times of stress
-S. dublin infected cattle may shed organism in the milk and feces periodically |
|
How do animals acquire Salmonellosis in the feed?
water? |
-contamination by feces (rodent, wildlife)
-runoff |
|
Does sunlight kill salmonella?
|
yes
|
|
What type of diarrhea is associated with Salmonella?
|
Malabsorptive and Secretory
secretory - prostaglandin synthesis from endotoxin effects malabsorptive - destruction of microvillous and inflammatory reaction in the bowel |
|
What is the age of animals affected with Salmonellosisi?
|
10 days to 3 months, but all ages can be affected
|
|
What are the CS to Salmonellosis?
|
-enteritis, fever, inappetance, depression, dehydration
- initially diarrhea is watery, but as disease progresses, diarrhea may contain shreds of mucosa, fibrin casts or frank blood -putrid foul odor - acute PLE and weight loss - abortions |
|
What repro problem is seen with Salmonellosis?
|
abortions
|
|
What is seen on necrospy in animals with Salmonellosis?
|
-fibrin tags on the intestines along with excessive peritoneal fluid
-mesenteric LN are enlarged and often hemorrhagic -bowel contents may have blood, mucus, fibrin tags, fluid feces - fibrin and mucosal casts are often found in both the SI and LI |
|
What is the enrichment media for Salmonellosis?
|
Brilliant green agar, selenite broth
|
|
What do you use to culture Salmonella?
|
feces, LN, bile and portions of affected GI tract
|
|
How do you treat Salmonellosis?
|
-fluids (oral or IV)
-antibiotics (Ceftiofur, TMS) -NSAIDS - banamine |
|
How do you prevent Salmonellosis?
|
-clean the environment, proper nutrition, reduce stress
-vaccination --> commercial or autogenou; J5 vaccination, EndoVac Bovi |
|
What is the agent that causes porcine proliferative enteritis?
|
Lawsonia intracellularis
|
|
What age pigs is porcine proliferative enteritis normally seen in?
|
grower and finishing pigs (6-20 weeks)
|
|
What are the CS of porcine proliferative enteritis?
|
-diarrhea may be mild or have a watery mucoid to bloody diarrhea
-Poor Growth, Chronic Wasting -Sudden Death with intestinal hemorrhage in breeding age animals (PHE) |
|
What is the pathophysiology?
|
malabsorption
|
|
How do you diagnose porcine proliferative enteritis?
|
-necropsy
- PCR or immunoflourescence assays (works well) |
|
What does the necropsy look like on porcine proliferative enteritis?
|
-areas of small and large intestine, ileum, cecum and upper spiral colon look like large stuffed sausages --> garden hose gut
- substantial granulation tissue proliferation leading to muscular hypertrophy causing thickened and rugated mucosa |
|
What is the treatment for porcine proliferative enteritis?
|
antibiotics in the feed, various antibiotic regimens
- vaccine |
|
What are the factors that cause gastric ulcers in swine?
|
-stress
-finely ground grain -Vit E and Se def. -copper toxicity -irregular feedings |
|
What are the CS to swines with gastric ulcers?
|
-apparently healthy animal found dead
- animals may be pale, anemic, weak with increased respiratory rate -grinding teeth, anorexia, bloody tarry feces - off and on anorexia and weight loss and intermittent tarry feces |
|
How do you diagnose gastric ulcers in swine?
|
CS
necropsy - ulcers in the pars esophagus with blood clots within the stomach |
|
How do you treat for gastric ulcers in swine?
|
-aluminum hydroxides and magnesium silicate
- reduce stress -Tagamet - oats/alfalfa hay -Omeprazole |
|
How do you prevent gastric ulcers in swine?
|
-adequate vit. E and Se
-reduce stress -consistent feeding intervals and increase coarseness of feed - give hay |
|
What causes winter dysentery?
|
coronavirus
|
|
What are the CS with winter dysentery?
|
-acute diarrhea that is contagious
- explosive, light tan to dark brown diarrhea with +/- blood -anorexia, depression, and acute drop in milk -afebrile |
|
What age animals get winter dysentery?
|
adults, usually dairy that are confined
|
|
What is the percentage of a herd that is affected the first day and then the seconda day with winter dysentary?
How long is the herd affected? |
first day - 10-15%
second day - 20-40% herd affected for 2 weeks |
|
What is the morbidity/mortality of winter dysentery?
Who is more severely affected? |
-high morbidity
- low mortality - first lactation animals |
|
What is the treatment for winter dysentery?
|
supportive, oral fluids, kaolin
|
|
What is the agent for Johnes?
|
Mycobacterium paratuberculosis
- slow grower (4-16 weeks to grow in culture) -intracellular, acid fast organism |
|
Can there be cross species infection with M. paratuberculsosi?
|
yes - domestic and wild
|
|
What is the prevalence of Johnes in dairy and beef cows?
|
dairy - 22%
beef - 8% herd 1-26% |
|
What is the age of clinical onset of Johnes disease?
What is the clinical onset of disease assoicated with? |
2-5 years old
(range form 4 months to 15 years) -associated with a stressful event |
|
What age are calves susceptible to infection with Johnes?
How is the disease transmitted? |
3-4 months old are most susceptible
fecal oral (most); 25-33% are in utero infections -organisms are shed in milk and colostrum |
|
How long can M. paraTB survive?
|
11 months in feces and 5-9 months in pond water
|
|
What age do CS of Johnes show up?
|
2-5 years old with Chronic weight loss in cattle
- 1 year or older with chronic weight loss in small ruminants |
|
What are CS of Johnes in cattle?
|
-good appetite and intermittent to persistent diarrheawith Chronic weight loss
-maybe a fever -advanced: debilitation, dehydration, weakness and ventral edema; anemia |
|
What are CS of Johnes in sheep?
|
- usually NOT diarrhea (only a terminal signs)
-chronic weight loss -feces may be normal or intermittently be pasty of clumpy |
|
What is the pathophysiology of Johnes?
|
-Protein Losing enteropathy,
-malabsorption (due to infiltration of macrophages) - granulomatous enteritis |
|
How do you diagnose Johnes?
|
-CS: chronic diarrhea with good appetite
- Serological Tests: CF, AGID, ELISA (MOST Sensitive) --> sen increases when animals shedding a lot with diarrhea, not very accurate with subclinical or asymptomatic infections -SR - AGID is as sensitive as sulture (45%) |
|
How do you definitively diagnose Johnes disease?
|
-isolation of M. paraTB at PM, biopsy of gut or associated LN, or rectal scraping followed by histopath
-culture takes 1-4 months (don't call negitive for 6 months) - acid fast bacteria and granulomatous histopath changes |
|
What does Johnes look like on necropsy?
|
-intestines are thick, edematous, and corrugated
-illeum is most affected -SR: gross lesions are not as distinct as in bovines, granulomatous LN |
|
HOw do you diagnose a herd with Johnes?
|
fecal culture, DNA probe
|
|
How do you treat JOhnes Disease?
|
rifampin and isoniazide
-extralabel -relapses occur after treatment stops |
|
How do you prevent Johnes disease?
|
-replacement animals should come from certified free herds
-prevent run off from adult herds into water sources or pastures - don't spread manure on fields that are used for grazing - Newborns: raise calves separate from adults; hygienic calving area; colostrum from know negative cows on pasteurized colostrum; calves from infected cows should be culled |
|
What happens when cows are vaccinated against Johnes?
When is it given? |
they become TB reactors
to calves at 35 days |
|
What is the disadvantage to the Johnes vaccine?
|
-decreases incidence of clinical disease and shedding
- doesn't eliminate infection |
|
What is the agent of BVDV?
|
pestivirus, RNA virus (similar to Border Disease Virus, Hog Cholera Virus)
|
|
What are the 2 biotypes of BVDV?
|
-cytopathic
-noncytopathic |
|
Either biotype of BVDV can cause what?
|
- clinical disease in young or older cattle
- abortion or fetal malformations |
|
What is necessary for the development of mucosal disease?
What it that? |
infection with both biotypes
chronic BVDV |
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Can noncytopathic BVD mutate to cytopathic?
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yes
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Is antigenicity dependent on or linked to biotype?
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no
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Persistent infection as a sequela to in utero infection only involves which biotype?
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noncytopathic
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How is noncytopathic biotype of BVDV detected?
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by immunoflourescence or interference tech
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What is the seroprevalence of BVDV and how many show clinical disease?
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50-90% (endemic), but low in isolated herds so that they are at high risk for an outbreak
- 5% may show CS |
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What are most infections of BVDV due to?
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noncytopathic BVDV
-because this is the biotype that is shed by persistently infected cattle (0-2% of the population) |
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What are CS of subclinical infection with BVD?
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-most common
- anorexia, fever, serous nasal discharge and leukopenia -recover in 10 days, unless secondary invaders |
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Where is acute or classic BVD common?
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feedlot situations due to stress and increased exposure
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What are the CS of classic or acute BVD?
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-acute gasteroenteritis (watery diarrhea +/- blood; fever 104-106F, no rumen motility, splashy gut sounds, oral mucosal lesions, blunting of buccal papillae
-most recover in 10 days - respiratory (may see primary respiratory disease without GI involvement) |
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What happens when naive, pregnant cattle get BVD during their first trimester?
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decreased conception, abortion/resorption/repeat breeder
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What happens when naive, pregnant cattle get BVD during their 2nd/3rd trimester?
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fetal anomalies
-cerebellar hypoplasia -dysmyelinogenesis -lenticular cataracts - microophtalmia -hydran and hydrocephalus |
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What happens when naive, pregnant cattle get noncytopathic BVD between 80-120 days?
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-may be aborted or resorbed
-may become immunotolerant |
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Cows that get noncytopathic BVD between 80-120 days can have calves that are immunotolerant. What do these animals look like clinically?
|
-stunted and tough looking, poor doers - however some may appear normal
-lymphopenic -persistently viremic and viral sheders -serologically negative to infecting strain but may develop low titers to other BVD serotypes -50% die in first 2 months (less than 10% make it to breeding age) -infected bulls may have decreased sperm quality |
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What happens when naive, pregnant cattle get noncytopathic BVD after 150 days?
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-either die and are aborted
-or survive and develop humoral response and are seropositive at birth |
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In what types of animals does mucosal disease occur?
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only in immunotolerant animals to non-cytppathic BVD
|
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When do signs of mucosal disease arise and how?
|
6-18 months due to the decline of maternal antibody
- calf encounters cytopathic virus or noncytopathic converts to cytopathic (most common) |
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What are symptoms of mucosal disease?
|
-depressed, intermittent fevers
-diarrhea and oral lesions -mucopurulent ocular nasal discharge -nasal mucosa crusty with a thick layer of dry purulent discharge -lame - coronitis and interdigital ulcers - not responsive to antibiotics -become debilitated and die |
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What is the temp of a cow with TYPE II BVD?
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106-107
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What are CS of BVD?
|
-high temp (106-107)
-anorexia, decreased milk production -respiratory distress -death in 48 hours -no mucosal lesions -may or may not have diarrhea (usually NOT present) -higher mortality in calves vs. adults |
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What is the different between a necrospy on type I BVD vs. type II?
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type I - multifocal erosion of all segments of the GI tract, esp. the esophagus and SI; necrosis of Peyers patches and depletion of lymphoid follicles in the spleen and LN
type II - viral septicemia, pulmonary hemorrhages and edema |
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How do you diagnose BVD?
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1 -serology
2 - virus isolation from serum 3 - white blood cells 4 - secretions 5 - immunohistochemistry (ear notch) 6 - immunoflourescence |
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How do you treat BVD?
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-supportive, prophylactic antibiotics, NSAIDs,
mucosal disease - none - euthanize |
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Can the MLV of BVD cause mucosal disease?
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yes in immunotolerant animals
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