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Welcome to Dr. Sweeney's Bovine Extravaganza
There is a 
fairly large amount of information under the topic of "bovine," more than 
we can cover in a couple of hours or an hour and a half, so this will be 
quick and dirty; first clue shoudl be that there is a handout! Those of 
you not here, 100 copies were made so people from VHUP can bring them 
back to you. The handout contains the information from the slides. We are 
going to go over diseases very superficially, to jog your memory, not to 
go into detail tonight. If you fall asleep, you still have the handout.


RESPIRATORY DISEASE

-Bovine Respiratory Disease Complex aka "shipping 
fever" (BRDC) - acute fulminant bronchopneumonia
-Enzootic Calf 
Pneumonia- chronic insidious pneumonia
-Atypical Pneumonia/ARDS/ABPE - 
not due to bacteria
-Lungworms - not seen much about here but could be on 
boards.
-Allergic alveolitis "Farmer's Lung"

If you are presented with 
an animal that has respiratory distress or fever and cough or just cough, 
these are the main differentials. 

BRDC

-acute pneumonia, typically 
seen in 6-18 month old cattle. 
-stress plays major role: shipping, 
sales, regrouping, weaning
-etiology multifactorial:
-viral infxns: 
BVD/PI3/BRSV/IBR (infxs bovine rhinotracheitis) - these viruses damage 
the mucosa or cause immunosuppression
-secondary bacterial infxn: 
P.hemolyticum (makes leukotoxin which destroys neutrophils which set up 
severe inflammatory cascade) and P. multocida
-depressed, febrile, 
anorexic, abnormal lung sounds, consolidation
-acute fibrinous 
pleuropneumonia
-tx: ceftiofur (only one good for lactating dairy cows), 
tilmicosin, oxytet, florfenicol, enrofloxacin (these four are only for 
beef cattle)
-prevention: preconditioning which means weaning and getting 
animals on solid feed prior to shipping, vaccinating them against viruses 
before shipping - that will lower incidence of shipping fever.

ENZOOTIC 
CALF PNEUMONIA:

-low grade bronchopneumonia
-especially a management 
disease, seen in young dairy calves raised indoors in adult cow barn or 
other barn with no windows, often in winter 
-poor ventilation plus 
stress eg weaning, regrouping, FPT
-virus: IBR, BVD, PI3, BRSV

-mycoplasma is a main agent - slow, progressive, low grade fever, cough 
eventually, early on no signs
-secondary p. multocida, actinomyces 
pyogenes causing abscess in chronic case
-tx more difficult b/c chronic, 
but - same as for shipping fever
-prevention: adequate passive transfer, 
good ventilation, calf hutches

ACUTE BOVINE PULMONARY EDEMA/EMPHYSEMA, 
"Fog Fever"

-another differential for a bunch of dyspneic cows
-often 
called "atypical pneumonia"
-dairy or beef cattle turned out early 
spring/summer or fall on lush green pasture
-pasture high in tryptophan

-tryptophan converted by rumen bacteria to 3-methyl-indole, a pneumotoxin

-3MI activated by c P450 in type I alveolar cells and clara cells and 
causes necrosis of those cells
-severe interstitial edema in lung, 
proliferation of type II cells with chronicity, respiratory distress, 
emphysema
-herd problem, dyspnea, SQ emphysema, death
-tx: people have 
tried NSAIDs, Steroids but no specific antidote exists and stress of 
handling may precipitate death in severe cases
-similar syndrome caused 
by perilla mint (ketone in the mint is pneumotoxin) and moldy sweet 
potatoes
-prevention: limit exposure to lush pasture

LUNGWORMS:


-dictyocaulus viviparous
-if you have an outbreak of coughing, consider 
this
-adults live in airway, larvae pass in feces, ingested, migrate to 
bronchi via circulation, 21 day prepatent period from ingestion of larvae 
to mature worm.
-usually late summer/fall in northern hemisphere
-caudal 
ventral consolidation, unlike most bacterial pneumonias
-coughing is 
often a prominent clinical sign, more than fever
-dx: baermann or 
tracheal wash
-tx and prevention: ivermectin, fenbendazole, levamisole


ALLERGIC ALVEOLITIS "farmer's lung"

-might be on boards, prob not CCT

-hypersensitivity to mold
-micropolysporum faenii and thermactinomyces 
vulgaris - grow in hay
-adults exposed to moldy hay in barn in winter

-spores small, penetrate far into airways
-alveolar inflammation and 
fibrosis in chronic cases 
-also happens to people, hence "farmer's lung"


END RESPIRATORY DISEASES!

GASTROINTESTINAL DISEASES:

-Diarrhea: adult 
and neonatal
-Abdominal distension
-Miscellaneous

CALF DIARRHEA: CAUSES:


neonatal calf - under 4 weeks - mainly these top three.

-enterotoxigenic 
e.coli
-rotavirus/coronavirus
-cryptosporidium

-BVD can be any age

-Salmonella can be septicemia or colitis, neonates or adults
-Clostridium 
perfringens remember - enterotoxemia, type B, D, etc.
-Attaching and 
effacing e. coli can cause blood in feces.

-Coccidia not in calves under 
3 weeks b/c of incubation period. 21 d prepatent period. hallmark signs 
of coccidia are hematochezia and tenesmus. you won't see this in calves 
in hutches, it's seen in groups.

ENTEROTOXIGENIC E. COLI: few days to a 
week of age

-similar to cholera in people
-not invasive bacteria. they 
do not penetrate mucosa or cause inflammation
-simply attach to mucosal 
surface, in first few days of life.
-binds to intestine with pili (K88, 
K99) after ingestion
-secretes exotoxin (Enterotoxin) that stimulates 
adenyl cyclase causing increased cAMP in enterocytes
-enterocytes secrete 
electrolytes and water into gut lumen
-dx: culture. if you do a gram 
stain you may see bacteria on gut wall but not inflammation or blunted 
villi. on CCT can submit ligated section of gut and have them culture for 
ETEC not for regular e.coli

QUESTION: on CCT, how much diagnostics do 
you do on a calf with diarrhea?
ANSWER: do a post on dead animals, always 
submit samples for e.coli, rotavirus, crypto. that's not too expensive. 
this is if it is a herd problem. 

-treatment of individual animal: 
fluids! most important. oral or IV. if animal is mildly dehydrated, oral 
is ok- Na+, Glucose must be in there with the water, because glucose 
absorption is comediated by sodium, and water is absorbed with these 
across the GI tract. K+ and other things may be in there too. If 
recumbent or cold extremities, need IV fluids. 
-dehydration, acidosis 
due to bicarb loss in intestine.
-after you dx ETEC, you need to prevent 
it in subsequent calves. 
-prevention: colostrum management - ensure 4 L 
in first 12 hrs of life - 2 L right away and 2 more in next 8 hrs. also 
can vaccinate moms during dry period against the pilus, so they have high 
colostral antibody. there is an ecoli vaccine and a rotavirus vaccine. 
also, improve environmental hygeine - clean calving stall, don't let calf 
suck dirty udder. 

ROTAVIRUS/CORONAVIRUS: up to a month of age

-attacks 
epithelial cells on tips of villi
-villi blunted, epi cells slough, brush 
border enzymes lost and decreased absorptive surface area
-maldigestion, 
malabsorption
-osmotic diarrhea
-signs same as for e.coli, clinically.  
also cryptosporidium. none of these have bloody feces. 
-dx: live animal: 
submit feces for rotazine test to id rotavirus. no such test for 
coronavirus. can do electron microscopy. for dead animal: submit 
intestine not fixed in formalin, they do fluorescent antibody stain for 
these viruses

CRYPTOSPORIDIUM 

-protozoan parasite, important gi 
pathogen, one of BIG THREE of calf diarrhea
-complex life cycle
-affected 
calves pass oocysts in feces that are immediately infective
-5 day 
incubation period from ingestion to onset of diarrhea
-secretory 
diarrhea, prostaglandin mediated (inflammatory process)
-malabsorption 
from blunted villi as well
-zoonotic! handlers are susceptible. early 
cases were vet students. if you are immunocompetent it is self limiting 
but unpleasant, lasting 1-2 wks. if immunocompromised, it can be fatal. 

-no specific chemotherapeutics exist
-tx fluids, supportive care, no 
vaccination exists, no drugs that work
-prevention: hygeine, good 
management of colostrum
-dx: fecal flotation for oocysts, or acid/fast 
stain to see oocysts because hard to see on float; also histopath will 
show oocysts in small intestine.

COCCIDIA: older calves

-post weaning, 
grouped in pens somehwere, exposed to oocysts 
-Eimeria is most common 
one 
-21 day ppp, 14 day incubation
-tenesmus, bloody diarrhea
-tx 
amprolium orally
-prevention: docoquinate, monensin -- coccidiostats


SALMONELLA: any age

-enteric (more in adults) or septicemic (calves)

-any age
-s.typhimurium most common; s. dublin can have carrier state for 
a very extended period of time with no clinical signs - can colonize 
udder and shed in the milk(host adapted strain)
-fecal/oral transmission

-invasive, colonic inflammation, colitis, leakage of fluids across 
damaged mucosa and enterotoxins, secretory diarrhea
-vaccines exist but 
are not effective
-shed in milk, feces - ZOONOTIC
-on CCT, if there is a 
choice, remind owner it is zoonotic and sheds in milk and it is common on 
farms for people to drink the raw milk so tell them not to.
-antibiotics 
helpful for septic form, not usually used in adults with enteric form b/c 
won't change course of disease.  choose one effective against gram negs 
like ceftiofur or flurfenicol :)

Other cause of Adult Cattle Diarrhea:


ACUTE ADULT DIARRHEA

salmonella

BVD: two types:
1. classic form: 
inapparent infection or fever, diarrhea, oral erosions, abortion, birth 
defects. most animals infected with type I will survive. 
2. more 
recently reported: high fever, respiratory signs, death - often mimics 
pneumonia, and no GI signs seen. also, thrombocytopenia occurs, may see 
ecchymoses, bleeding diathesis. often no diarrhea but may have diarrhea. 
often these will die.
3. persistent infection: "mucosal disease" requires 
series of events. need persistently infected calf. nonimmune pregnant cow 
exposed to non-cytopathic BVD virus at 50-125 days gestation, virus 
crosses placenta, infects fetus. fetus sees virus as self, born viremic 
with no antibody production against virus. can be born normal or be 
chronically ill/unthrifty. this calf is a source of infection to 
herdmates. later, if exposed to cytopathic strain of BVD, develops 
MUCOSAL DISEASE with severe fulminant GI ulceration and death. 
other 
main problem is many persistently infected calves are normal and are 
constantly infecting other animals on the farm. or may be unthrifty. 

dx 
of BVD: 
acute: live animal - viral isolation on whole blood, buffy coat; 
serum neutralization with paired sera; fluorescent antibodies on necropsy 
tissues (LN, GI)
persistently infected: microplate agglutination test to 
detect virus in serum

BVD prevention:
MLV vaccine - is abortigenic. good 
immunity with single dose
killed vaccine - won't cause abortion. requires 
2 doses 4 wks apart first time around to ensure anamnestic response. some 
give it q 6 mos but that won't work at first
dairy cow recommendations: 
give MLV at 6 mos of age, and in case of maternal antibody interference 
revax at 15 mos before first breeding, then annual reboost prior to 
breeding each year. 
-biosecurity: screen animals before adding to herd 
to avoid PI animals.
-BVD is ruleout for diarrhea/fever in any age 
animal.

Winter Dysentery: rule out for diarrhea in adult cattle.

-explosive herd outbreak, whole herd in 10 days.
-bloody diarrhea
-most 
often in northern US and in wintertime
-high morbidity, adult cattle, 
mortality rare
-recovery w/in few days
-reduced appetite, dropped milk 
production
-spontaneous recovery
-coronavirus recently isolated as 
etiologic agent

MCF malignant catarrhal fever 
-diarrhea, oral 
ulceration
-virus, transmission unclear
-associated w/sheep in US, 
wildebeest in africa
-cattle associating with sheep
-sporadic - 2 animals 
in a herd, not whole herd
-oral erosions, corneal edema, marked nasal d/c 
and lacrimation, diarrhea
-enlargement of prescapular LNs
-high 
mortality, about uniformly fatal

CHRONIC DIARRHEA in adults:

Johne's 
Disease: NUMBER ONE ddx!
-mycobacterium paratuberculosis (now renamed 
m.avium paratuberculosis)
-main susceptibility in terms of establishing 
infxn in young calves
-calving stall is important
-infected adults shed 
in feces, calves suck dirty udder or ingest in calving stall.
-long, 
clinically silent incubation period with no shedding or signs - totally 
undetectable. during this time, bacteria proliferate in ileum and 
mesenteric LNs, causing granulomatous enteritis, eventually protein 
losing enteropathy
-after 2 yrs of age, cow will break with pipestream 
watery or pea soup diarrhea with rapid weight loss (due to PLE), 
excellent appetite, and edema 
-dx: fecal culture to detect asymptomatic 
carriers (takes 12 - 16 wks); serology (ELISA and AGID) - these tests are 
cheaper but require more advanced dz because less sensitive, fecal PCR 
(faster than culture), intestinal and ileocecal LN biopsy - in very 
important cow!.
-no practical treatment
-antimycobacterial drugs can be 
used in rare cases
-shed in feces and in milk - possible source of infxn 
for calves, people. resists pasteurization as well, so can be killed with 
high temps but some older methods of lower temp pasteurization do not 
kill it.
-this may be related to crohn's dz in people, some of whom have 
had this bug isolated from them.

Ostertagia ostertagi:

-strongyle type 
nematode
-larvae ingested at pasture
-L4 enters abomasal gastric gland, 
damages it
-acid production impaired, abomasal pH increases, pepsinogen 
not activated
-cell junctions weakened, albumin leaks into lumen, 
pepsinogen leaks into blood
-diarrhea (bright green), weight loss, edema 
due to protein losing enteropathy
-usually younger than Johne's dz - 
under 2 yrs of age
-dx: measure serum pepsinogen (increased with this 
problem)
-type I infection: less than 2 yrs of age, ingestion of larvae 
on pasture
--type II: usually 2-4 yrs old. L4 emerge from gastric glands 
after hypobiosis, usually in spring around here, when conditions are 
good. emergence causes severe inflammation and damage to lining of 
abomasum and diarrhea as above. 
tx: ivermectin, fenbendazole


Copper 
deficiency

OTHER MISCELLANEOUS:

LUMPY JAW:
mandibular or maxillary 
(usually mandible) osteomyelitis due to actinomyces bovis. usually broken 
tooth, or abrasion in oral mucosa - bacteria invade into bone. very hard 
swelling usually ventral aspect of mandible. may open and drain. pus on 
slide will reveal "sulfur granules" with little yellow thingys that look 
like sulfur. tx difficult - penicillin and isoniazid, surgical debulking. 
may be able to arrest disease but won't make swelling go away.

VESICULAR 
STOMATITIS:

viral infection of horse and cow
oral, teat and digital 
vesicles. cow very lame. vesicles very painful. vesicles rupture early 
and then mimic ulcers but usually some cows in herd will still have 
vesicles. signs include smacking lips, reduced appetite, decreased milk 
production and lameness. mortality is not high. economic impact is due to 
quarantine and milk losses. 
r/o foot and mouth disease (doesn't occur in 
US)(VS does occur in US)
if you see any vesicular dz in cow you will call 
the feds to investigate!
recent outbreaks in CO and CA
r/o FMD, BVD, MCF, 
papular stomatitis (causes mild erosions on nose, no fever or anything, 
clinically not a big deal)

ABDOMINAL DISTENSION:

-surgical obstruction 
(LDA/RDA/cecal volvulus) (RDA will have hypochloremic hypokalemic 
metabolic alkalosis, like a vomiting dog). these occur in early 
postpartum period in dairy cows, may be associated with excess grain, 
lack of fiber; also may see concurrent ketosis, metritis, mastitis

if 
rumen distension: one of these:

-frothy bloat: cattle on lush legume 
pasture; soluble chloroplast protein changes surface tension and 
viscosity of fluid, gas is trapped within fluid and can't be eructated, 
froth is produced within rumen. see rumen distension, pressure on vena 
cava and diaphragm. rumen pushing on vena cava may cause blanching of 
esophagus, a "bloat line." tx and prevention: poloxalene, which acts on 
surface tension, "bloat gard" given orally to affecteds or pretreat 
before turnout. to tell from free gas bloat - pass stomach tube, if gas 
comes off, it was free gas.

-free gas bloat: due to reduced eructation


-vagal indigestion: forestomach emptying dysfunction due to irritation of 
vagus nerve (due to pneumonia, hardware) or mechanical obstruction or 
adhesion. gradual onset of rumen distension, anorexia, scant feces. Left 
side looks like apple, right like pear - "papple cow", L shaped rumen, 
splashy sounds. if adult look for hardware dz or cranial abdominal 
abscess. tx surgical, px guarded.

-rumen acidosis aka grain overload: 
ruminants who eat extra carbohydrate (grain), normally grain is fermented 
to VFA and lactic acid which is consumed by rumen bacteria but if they 
eat extra grain/CHO, too much VFA and lactic acid build up, pH lowers, 
lactate consumers die, lactic acid producing bugs grow, pH drops more, 
down to under 5 and almost all bacteria are killed and now the rumen is a 
bag of acid. acid is absorbed through damaged rumen wall causing 
acidosis, and acid pulls water into rumen osmotically from vascular space 
causing dehydration. tachycardia, tachypnea, sunken eyes, distended 
fluidy rumen, groaning, kicking at belly, pasty loose yellow feces; 
ataxia and death in severe cases. sequelae in survivors: laminitis due to 
endotoxin crossing abnormal rumen wall, polio (thiamin deficiency since 
bacteria are gone from rumen)(clinical signs of polio are opisthotanos, 
blindness. polio ddx lead poisoning)(listeria causes asymmetric cranial 
nerve signs, not blindness), liver abscesses due to bacterial 
translocation, mycotic rumenitis.
tx: rehydrate via IV fluids with bicarb 
to correct acidosis, rumenotomy is preferred over gavage with orogastric 
tube which takes a long time. penicillin to prevent liver abscesses and 
thiamine to prevent polio.

MASTITIS:

subclinical: milk normal, 
production decreased. increased SCC, positive CMT, positive culture. milk 
can be sold, but will increase bulk SCC
clinical: milk has clots, flakes, 
watery. cow sick or not sick. milk can't be sold. most often, cow is not 
sick but milk is abnormal. may be able to palpate abnormal mammary gland.


many farms are on monthly testing to detect subclinical mastitis.
if bulk 
scc increases too much, none of the milk can be sold.

contagious 
mastitis:
-bacteria reside only in udder
-transmitted by milkers and 
equipment
-staph aureus, strep agalactia, mycoplasma
-staph often relapse 
after tx, not that responsive to abx - cull staph cows or milk last; 
mycoplasma untreatable, rare; strep agalactia relatively easy to 
eliminate, responds to abx.

environmental mastitis:
-bacteria in stall, 
manure, bedding
-organic bedding eg straw, shavings support more 
bacteria; sand doesn't.
-strep "non ag" - strep uberis, strep 
dysgalactiae
-coliforms (e.coli, klebsiella pneumonia (associated with 
wood shavings))
-abx controversial - studies show no improved response to 
gentamicin tx for cows with e.coli mastitis; for streps generally 
frequent stripping is usual tx, for coliforms sometimes abx are used.

-with streps, cows aren't sick; with coliforms, cows get sick, 
endotoxemic, febrile, milk is watery, gland is warm and swollen or hard, 
wont' eat, get recumbent. coliform mastitis is also sometimes called 
septic mastitis and is seen in immediate postpartum period.

HEART 
DISEASE:
think of three main diseases if you see heart failure:


pericarditis (hardware) (NB: pericarditis is a rare complication of 
hardware dz)
lymphosarcoma (right atrium) (look for enlarged LNs 
elsewhere)(BLV negative will rule out lsa)
vegetative endocarditis - hx 
of chronic infection somewhere else is likely. signs are fever, 
tachycardia, pounding heartbeat, half of these cows have murmurs, px 
poor, dx via ultrasound.
if you are out west, there is another ddx - high 
altitude disease, aka brisket disease. caused by vasoconstriction of 
pulmonary arterioles due to hypoxia. this reflex occurs to avoid v/q 
mismatch but it's bad when it occurs in ALL the alveoli! causes pulmonary 
hypertension, cor pulmonare/right sided heart failure. locoweed 
predisposes to this disease. that's a good board question.

KETOSIS:


-underfeeding: reduced energy intake causing mobilization of body fat. 
primary: inadequate feed offerred; secondary: anorexia due to illness eg 
LDA
-spontaneous: increased energy output in milk - healthy cow in peak 
lactation, unable to eat enough feed to keep up with production 
either 
form can cause nervous ketosis!

peripheral fat mobilized
lipid breakdown 
products overwhelm krebs cycle
acetylCoA diverted to ketone production 
(acetate, acetoacetate)
chronically will cause fatty liver

tx: fix 
underlying problem; give IV 50% dextrose 500 ml bolus which will cause 
temporary resolution to problem; then give propylene glycol PO - this is 
a glucose precursor. insulin will inhibit hormone sensitive lipase and 
can be used in resistant cases to stop breakdown of peripheral fat; also 
dexamethasone to stimulate gluconeogenesis and decrease milk production.


MILK FEVER/parturient paresis

hypocalcemia due to Ca drain at onset of 
lactation
usually within 48 hrs before or after parturition
NEVER EVER 
EVER in first calf heifers. never. ever. do not dx it in first calf 
heifer. old age predisposes.
high Ca in dry period reduces ability to 
mobilize Ca from bone via PTH modulation. so feed LOW calcium diet in dry 
period! even though it's counter intuitive. do it.
signs: initially 
hyperirritable, then flaccid paralysis, poor perfusion, cold ears, 
sluggish pupils, bloat, rumen atony, recumbency, can lead to downer cow 
syndrome. tx iv 23% calcium borogluconate, also some oral products exist 
but once recumbent need IV due to inability to eat, swallow or absorb. 
prevention: dry period diet low calcium, also anionic salts like sulfates 
will promote acidoses and aid calcium mobilization from bone. 

other 
diseases to study:
renal: pyelonephritis (corynebacterium renale) with 
bloody/pus filled urine, straining to urinate urolithiasis in feedlot 
cattle with ruptured bladder or waterbelly due to ruptured urethra; 
BLV/LSA - remember most infected cows not sick, only 5% get LSA, 
predilection site of tumors are LN, heart, abomasum, uterus. Also REPRO - 
you're on your own. review repro estrus cycle, abortion differentials, 
those are also important. 
also study maybe the night before the exam if 
you have a merck manual, there is a whole chapter of infectious diseases, 
like 10 clostridial diseases - chauvei, hemolyticum, etc - it's good to 
match the bacteria with the disease like blackleg, redwater, black diseas 
e- review those. 
neuro: polio, listeria, TEME caused by hemophilus 
somnus.
toxicology: lead, nitrates, Organophosphates, ergot alkaloid with 
ishchemic necrosis of extremitis
White muscle disease - vit E/selenium 
deficiency

anaplasmosis is a red blood cell protozoal parasite, seen in 
south, transmitted by ticks, not seen here too much, causes hemolytic 
anemia - extravascular. icteric, no red urine. dx on smear, take blood 
from ear b/c that is where you find parasites more easily. tx with 
oxytetracycline, there is a vaccine. mostly in south. 
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