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Dr Sweeney
Bovine gastrointestinal system 

diseases of the 
forestomach

quick reminder of rumen physiology

esophagus --> reticulum 
--> ventral sac --> dorsal sac --> cardia. the rumen is a fermentation 
vat. there is a layer of liquid covered with a mat of fibrous material. 
there are bacteria and protozoa in there doing the actual digesting. 


water, food and saliva get put in, they meet the bacteria and protozoa 
and get made into VFAs (volatile fatty acids, which are absorbed and sent 
to liver) and gases (which are eructated), and then stuff passes down 
into abomasum for further digestion. the rumen bacteria and protozoa are 
vital to digestive process.

the input, the rumen motility and the rumen 
flora are all tightly related so if any one changes, the others need to 
change too. any sudden changes can perturb the system. if a cow gets 
mastitis, and stops eating, the flora die, and then when she starts 
eating again it's all messed up.

analysis of rumen contents: 

how do 
you collect the rumen contents?
more common, less invasive way: per 
stomach tube - use one with a seive on the end. pass tube and then attach 
syringe to suck out stuff.
growing popularity technique: rumenocentesis - 
surg prep of small area, stick in 3-4 inch needle through flank into 
ventral sac, collect contents.

pros and cons of each - with 
rumenocentesis, you drag needle out through the skin and there is a good 
chance for developing localized abscess or localized peritonitis. usually 
rapidly walled off, but risk exists. 

pH measurement is important. 
normal pH of saliva is very alkaline. contaminating rumen contents with 
saliva in the tube results in falsely high pH. 

once you collect the 
sample, you can run tests: two most important tests rae to measure the pH 
- should be acid, 6-7. there is a syndrome of overfed cows where pH drops 
to about 5, or in cows who don't eat, pH goes up to about 7.5 or so. so 
pH is important. when you give symptomatic tx to correct the rumen 
problem, you want to know if you need to acidify or neutralize.

next 
thing - directly assess rumen flora (or fauna?). the protozoa are fragile 
and die quickly when animal stops eating. then animal won't want to start 
eating again b/c can't digest.

so put drop of rumen contents on a slide, 
and view under 10x - should be teeming with protozoa. should be swimming 
all around. you want to see big ones and little ones. if you don't, you 
have to fix it. take rumen stuff from fistulated cow and put it into sick 
cow's rumen. 

specific diseases to be discussed wrt the rumen are:

1. 
Simple indigestion (2 minutes)
2  Grain Overload (rumen acidosis)
3  
Bloat

Simple indigestion: if anything changes - increased feed intake, 
change in feed component, change in feed pH, etc - the rumen flora aren't 
adapted - so for a couple of days the cow won't eat as well, rumen 
contraction will drop, milk production will drop - all sort of minor. if 
several cows suddenly back off feed and you can't find a problem with 
them but you know farmer just opened a new silo, or whatever, this is the 
most likely diagnosis. no real tx - just give a couple of days to adapt. 
if after 2-3 days they aren't eating again, look for another cause. this 
is malfunction of rumen fermentation process due to recent feeding 
change.

Grain Overload (rumen acidosis): a more severe form of 
indigestion. the fermentation products of CHOs are VFAs, and a little 
lactate. the VFAs go to liver, the lactate is used by ther rumen bacteria 
as a carbohydrate source. sometimes the animal  (cow, sheep, goat) is 
exposed to a sudden increase or overdose of soluble CHO. this problem is 
caused by excessive CHO intake. sometimes on the weekend there is a 
feeding accident, ration isn't mixed up correctly....ok, so causes are: 
human error (feeding accident), bovine error (cows get loose and break 
into feed room or cereal grain pasture), iatrogenic (when beef animals 
are put onto feedlot). the dose needed to cause disease is variable 
animal to animal - depends on previous diet. so you can gradually 
increase the grain portion of diet and flora adapt and the animal can eat 
a lot of CHO. but if an animal has been eating only grass and hay and 
then you start giving 20 lbs of grain/day, it gets sick. so when calves 
are put onto feedlots, if grain isn't introduced gradually, they can get 
this syndrome. so key points are excessive grain consumption (relative to 
what animal has had in the past).

pathogenesis of rumen acidosis: you 
should understand this
what happens when the cow consumes the sudden 
bolus of grain? well, initially the rumen pH might be about 6.5; the 
normal protozoa and bacteria are making VFA and lactate. as CHO intake 
goes up, VFA and lactate production increases. this lowers the pH of the 
rumen. it may approach 5. at this pH, a lot of gram negative bacteria are 
starting to die. protozoa died too. the problem with this is the gram 
negs are the most avid lactate consumers. now you have increase in 
lactate production, and decreased lactic acid consumption b/c of gram 
negatives dying off. also at this pH, strep bovis starts to proliferate - 
this is another lactic acid producer. so it's a vicious positive feedback 
cycle. pH may drop as low as 4.0 at which point almost all bacteria die, 
you have a very high concentration of lactic acid in there. (in the lumen 
of the rumen). now the cow will get really sick and here's why. you know 
about osmosis. water moves into area of high solute concentration. well, 
now you have this rumen full of lactic acid. water goes into the rumen to 
dilute stuff out. water comes from ECF and blood. so: 
1. water enters 
rumen --> severe dehydration
2. lactic acid is absorbed into systemic 
circulation --> metabolic acidosis
3. acid damages rumen wall --> 
increased permeability --> endotoxemia --> circulatory collapse, 
laminitis

these are very important concepts.

clinical signs of acute 
rumen acidosis:

the first and most important as far as animal's well 
being goes is severe dehydration due to sequestration of fluid in rumen. 
so you see sunken eyes.
the second thing you see is a distended rumen. it 
will be a very fluid distension. it will be ventral distension b/c it is 
fluid. it will be on left but also on the right often; massive abdominal 
distension with a fluid wave.

those are the two specific signs of this 
condition. dehydration and large distended splashy rumen. other signs are 
secondary to dehydration and acidosis:

high heart rate
depression

recumbency
may exhibit signs of abdominal pain: bruxism, treading, 
groaning
loose yellow foul smelling foamy feces
CNS signs - ataxia, 
seizures, death - with severe acidosis

so you see a severely dehydrated 
animal with big distended rumen, really really sick, not comfortable. 
that's acute grain overload/rumen acidosis.

there is a subacute or 
chronic form - seen usually in dairy cows. instead of one big bolus of 
grain and severe acute illness, they're just chronically fed a diet with 
a little too much CHO and not enough fiber, that they can't really adapt 
to, and they have slightly low pH but not really sick. will have low 
milkfat in their milk, and they are predisposed to laminitis. 

back to 
the acid - it can really cause necrosis of rumen mucosa as seen in this 
slide. this allows bacteria, endotoxin, etc to be absorbed into blood 
much more easily. 

if your tx is successful and animal survives, there 
are these sequelae to worry about - mostly having to do with damge to the 
rumen. 

b/c the rumen is damaged, you can get fungal infection in the 
wall of the rumen - mycotic rumenitis. if they have this they won't eat. 
fatal complication. 

the second common sequela - where do bacteria go 
when they leave the rumen via damaged wall? into the portal vein. 
straight to liver. there, they form hepatic abscesses. liver abscesses 
are a common sequela to rumen acidosis. fusobacterium necrophorum (sp?) 
are the main bacteria that do this; also actinomyces pyogenes. another 
sequela is laminitis.

normally you think of laminitis as the devastating 
dz of horses; but also can occur in cattle. poor perfusion to capillary 
beds in feet combined with endotoxin effects; necrosis of laminae, 
laminitis. not always fatal. 

finally the effect of the problem on 
nutrition - thiamine is usually made in the rumen by bacteria, but you 
have had death of bacteria and may have thiamine deficiency, which causes 
CNS problems - polioencephalomalacia. so you can see 
polioencephalomalacia as sequela to grain overload. 

prior to tx - 
confirm your dx via history, PE, rumen content analysis. 
note that rumen 
pH is stable for a few hours after death of cow so you can measure pH 
postmortem to determine if rumen acidosis was present. 

often, this 
condition occurs in multiple animals. so you have to practice triage. in 
WWI when wounded soldiers came to hospital they were divided into three 
groups: the dead and definitely dying, on whom time was not wasted; the 
living who would survive with or without tx; and those who will survive 
with tx but will die without tx. so the cows with HR >120, recumbent, 
moribund - probably should euthanize. the ones that are standing but very 
dehydrated and painful - treat. the ones that you think got into the 
grain, but don't seem sick - monitor closely. 

the principles of tx are 
twofold - 
first, get bad stuff out of rumen
second, correct existing 
metabolic problems
the best way to empty the rumen is via rumenotomy. 
people talk about stomach tubes, lavage, blah blah. it is time consuming, 
you risk aspiration, it's stressful and surgery doesn't take any longer 
so rumenotomy is best. empty the rumen, wash the wall of the rumen, look 
in there well, and put in fresh ingesta from a normal cow, some feed 
substrate. that's the best tx. sometimes you can't do that. you don't 
know how, or don't have equipment. can try stomach tube, siphoning off 
contents, lavage, infusing in bicarb...but isn't as good as doing a 
rumenotomy.

then correct dehydration with fluids, correct acidosis with 
bicarbonate, treat to prevent sequelae - PCN to reduce liver abscess 
risk, thiamine to prevent polio. restrict access to grain, give water and 
hay, gradually reintroduce grain after a few days. 

any advantage to 
giving something against the gram negatives?well, they are already dead. 
you might give some drugs to combat the effects of endotoxin, like NSAIDs 
like banamine or something to combat the endotoxemia. but you're not 
going to have live gram negative bacteria in the blood. the anaerobes and 
gram positives are what cause liver abscess. 

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ok, so - 

regarding rumenotomy - usually done standing in cattle under local 
anesthetic. in goats, usually general anesthesia b/c less stoic, struggle 
more, can protect airway in case of regurgitation. 

next on our list is 
bloat; this is a highly scientific term referring to Gas Distension of 
the Rumen! :)

remember the 5 Fs of abdominal distension:
1. Fat
2. Fetus

3. Feces/feed
4. Fluid
5. Flatus

Gas distension is dorsal distension as 
opposed to the ventral distension of fluid. is gas distension of rumen 
due to increased gas production or decreased eructation? most commonly, 
reduced eructation is the culprit. he can't emphasize that enough. 
failure of eructation is the problem, in the majority of cases. the avg 
cow produces 300 L of gas per day, and has to eructate it. of that, about 
200 L is CO2 produced by reaction of bicarb from saliva with acid in 
rumen. About 50 L of CO2 is produced by fermentation. also about 50 L of 
methane are produced. so there is alot of gas, but cow has huge capacity 
to eructate. you could increase gas 3-4x and cow would not get distended 
unless she lost capacity for eructation.

what makes a cow lose ability 
to eructate? 
botulism -> pharyngeal paralysis
tetanus 
other paralysis

obstruction - abscess, tumor, foreign body (potato)
fluid in area of 
cardia - cow lying on back or side, overfull rumen.

there is a specific 
syndrome called "Frothy Bloat" which we'll discuss now. in this 
condition, the gas is trapped in foam, like a meringue, and can't be 
eructated. why does the foam form? well. normally during fermentation gas 
bubbles are produced ventrally and they rise to the surface, rupture and 
become free gas in the dorsal sac. in frothy bloat, something has changed 
- the diet is different or something - and the surface tension of the 
liquid in the rumen is different, such that the bubbles stabilize at the 
gas/liquid interface and do not burst. now they can't get out. they are 
trapped. they call this frothy bloat. 

what is it in the diet that 
changes the surface tension? well, there is evidence now that there is a 
protein in chloroplasts called ribulose diphosphate carboxylase (dno't 
need to know that) that is highly soluble, and is present especially in 
lush, lagoon pasture. so cow consumes this lush grass, high in soluble 
protein, and this alters the surface tension such that froth forms. 


this is a disease of cattle on pasture, esp lush, lagoon pasture like 
clover or alfalfa. usually multiple animals are affected. in some areas 
in australia, they used to broadcast bloat warnings on the radio - when 
pastures were lush they would alert the farmers about this problem. 


clinical signs: initially some distension of the dorsal sac of the rumen 
b/c of gas accumulation; initially not a major concern, animal may stop 
eating but it is bright, alert. but as it goes on, rumen gets more 
distended and compresses diaphragm, limits respiration, compresses 
abdominal vena cava, causes impaired venous return and circulatory 
collapse. untreated, the animal will die of respiratory and circulatory 
failure. 

so, if you are presented with an animal with dorsal distension 
of the rumen on the left the first thing to do is figure out of there is 
foam/froth or if there is free gas bloat. how do you do that? pass a 
stomach tube, if not in resp distress. if the gas all comes off, you know 
that was free gas with failure of eructation. vagal nerve problem, one of 
those other things we mentioned - figure that out. but if gas doesn't 
come out and tube comes out covered in froth, it's frothy bloat. in an 
emergency situation, if you have cow in respiratory distress, tx is to 
trocharize the rumen - stab large needle in through paralumbar fossa - to 
relieve pressure. then of course you worry about peritonitis but that's 
later. this is to save life immediately. in cases less severe than that, 
you can use chemical agents - surfactants - to change the surface tension 
and destabilize the foam, allowing bloat to be alleviated. we use 
poloxalene - that's the generic name. The brand name is TheraBloat. Or 
BloatGuard. easy to remember. these are oils that change the surface 
viscosity. 
obviously, you'd rather prevent this than treat it. a few 
preventive tricks:
prior to allowing cattle onto lush pasture, feed hay 
to fill them up so they don't pig out, also will stimulate saliva 
production which has some surfactant properties, also can pretreat with 
poloxalene in salt licks, drenches, molasses licks. avoid/limit access to 
really lush pasture

slide: calf with free gas bloat - distended left 
dorsal abdomen. this calf couldn't eructate due to inflammation of vagus 
nerve secondary to pneumonia

slide: cow with frothy bloat - distended 
dorsally on left, a bit on right too. this cow had a ping present. not 
all these cows have pings, though, b/c the foam compartmentalizes the 
gas. because saliva has antifoam properties, one old fashioned treatments 
is to tie a stick in her mouth, to induce salivation. nowadays, that's 
less common, but sometimes people still do it.
people also use mineral 
oil, vegetable oil, turpentine. poloxalene probably best. other oils may 
work too.

people often give oral abx or other things like turpentine to 
kill bacteria and inhibit gas production -but gas overproduction isn't 
the problem so that's not the best plan.

Ok, one more disease. 
Peritonitis. 

Cattle peritonitis: most commonly caused by hardware 
disease 
this is infection w/in abdominal cavity, often involving 
omentum, serosal surfaces, etc. usual source of bacteria is the GI tract. 
common causes:
in order of likelihood:

hardware disease
perforated 
abomasal ulcer
perforated uterus related to parturition or intrauterine 
infusions
miscellaneous
[we don't see strangulating intestinal lesions so 
much due to short mesentery, but could see intussusception, iatrogenic 
puncture of spiral colon during IP injection, rumenocentesis]
way down on 
the list would be surgical wound infection or other penetrating wound. 
peritonitis is very very rarely associated with wounds in cattle. 

if 
you see a cow with clinical signs of peritonitis, consider above causes.


two types of peritonitis exist: localized and diffuse. mostly, when a cow 
gets a leakage from hardware or ulcers or whatever, usually, the cow does 
a great job of walling it off and keeping it localized. occasionally, the 
cow is not able to do it, and it becomes diffuse, causing basically 
septic shock, with bacteria throughout abdomen. 

clinical signs: (type)

fever (both) 
abdominal pain - remember cows are STOIC so if painful, 
signs minimal... 
elbows abducted, stiff gait (both)
positive grunt test 
(both)(esp with hardware, ulcer)
positive scooch/wither pinch test 
(failure to ventroflex) (both)
free gas bloat (some local)
scleral 
injection (diffuse)
dehydration (diffuse)
tachycardia (diffuse)
sunken 
eyes (diffuse)
abdominal distension from abdominal fluid, ileus (diffuse)

very sick cow (diffuse)
elevated fibrinogen (both)
we don't do much 
labwork, but if you could do one to look for infection, what would it be? 
fibrinogen.
leukocytosis or neutrophilia (some local)
leukopenia (most 
diffuse)
normal abdominocentesis (local, unless you happen to tap 
affected area)
increased protein and WBC (neutrophils) of peritoneal 
fluid (diffuse)
high PCV, low TP (diffuse)(dehydration + protein losses 
into abdomen) key sign

Hardware disease specifically - this is a pretty 
common cause for a cow to be off feed. Cows are not discriminating 
eaters. these days, you have total mix rations where all stuff is mixed 
together, even chopped hay, it's easy for hardware to get into the mix. 
cows don't notice and they eat it. a wire is swallowed. drops into 
reticulum. sits there, doesn't bother anyone. after 6-8 weeks or 12 mos 
for a nail, it will corrode and be gone. but sometimes it will penetrate 
through the wall of the reticulum. but the pain isn't from the wire or 
nail poking through the stomach. the pain is due to the inflammatory 
response from the infection around the leaking reticulum. 

Ok, you think 
you have a cow with localized peritonitis due to hardware disease. how to 
confirm this? clinically, looks like abomasal ulcer. so you have to 
radiograph to tell for sure. can't do that with a portable unit. rads are 
useful in hospital situation though. in practice, it's a clinical 
diagnosis and you treat based on your best guess, unfortunately. tx for 
hardware disease - surgical or medical. most respond to medical tx. use 
surgery for those that don't respond to medical tx is what dr sweeney 
prefers, others disagree. but you want to prevent further migration of 
wire and pull it back into reticulum. give cow a magnet per os. it will 
go into reticulum and hold wire in place. tx infection with antibiotics. 
penicillin, ceftiofur are common choices (ceftiofur is good for lactating 
dairy cows - no milk problems). analgesics so cow continues to eat and 
feels ok - aspirin or flunixin meglumine. restrict exercise so you don't 
encourage hardware to move around. 

rumenotomy is the surgical option. 
cure rates are about the same w/or w/o surgery though. hmm. 

possible 
sequelae to hardware dz: 
traumatic reticuloperitonitis - not common

damaged/inflamed vagus nerve, interruption of normal rumen 
motility/eructation (vagal indigestion)

slides: metal foreign bodies in 
the reticulum (note reticulated pattern of mucosa). nails, wires. not 
causing problems - not penetrating wall. 
slide: cow with elbows akimbo 
(indicates cranial abdominal pain), arched back
slide: positive grunt 
test - cow has mouth open and tongue out while someone is pushing on her 
xiphoid.
slide: cow with diffuse peritonitis - abdominal distension, IV 
fluids running in.
slide: loose feces - sign of diffuse peritonitis - 
scant, loose feces. can try tx with fluids, abx, NSAIDs but px for 
diffuse peritonitis very poor. drainage, lavage, we've tried, very rare 
success, very poor prognosis.
brisket edema, submandibular edema - 
traumatic pericarditis causing venous distension. 
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