---start---
dr palmer
the continuing saga 

Diarrhea in Foals

it turns 
out that acute diarrhea in foals is one of the most common health 
problems of foals; few foals survive childhood without at least one bout 
(the other thing is respiratory dz...)
70-80% of foals < 6 mos have 
diarrhea at some point
majority are in the first week and are self 
limiting
if it isn't self limiting though, there is a high fatality rate

it is hard to tell apart the ok kind and the deadly kind, though. that's 
the problem. 

Foal Heat Diarrhea
mare has a heat at about 9 days 
postpartum; that's when this occurs
usually 6-14 days of age
always self 
limiting
occurs at about the time of the mare's heat
probably unrelated 
to that but possible etiologies:
hormonal changes (not likely)
milk 
composition from colostrum to postcolostrum to full milk? unlikely

*coprophagy - this does occur and can cause diarrhea
*genital d/c from 
mare - can occur
roughage ingestion - probably not cause
irritants - 
probably not cause
*strongyloides - foals do get this, but not likely 
cause
physiological changes occuring as foal changes from milk to some 
solid food
* these things can cause diarrhea, but the foal heat diarrhea 
occurs in foals without these factors present as well.

anyway, this 
isn't that important of a problem. Foals do ok with this. 

signs and 
course:
soft to watery diarrhea
diarrhea not "profuse" - very liquid, but 
not huge amounts
attitute, appetite, temperature normal - hard to do PE, 
foal wants to play
lasts 2-4 days, a couple of times a day
monitor 
closely, do not treat

Nutritional diarrheas:

irritants/diet changes:

foals have an inquisitive nature, so they go and try to chew and eat 
everything they see. they engage in unselective feeding, feeding 
frenzies. they find something like mom's tail, or bedding, or whatever, 
and they spend all day eating it. they ingest irritating things, and this 
sudden change in diet causes diarrhea.

coprophagy:
a normal phenomenon 
for foal to eat mom's fresh feces. they don't like stale feces. if you 
put a bunch of different mares' feces in stall, foal will choose mom's. 
this is a source of excessive roughage. not a source of parasites - foal 
eats it fresh, before infective stage develops. coprophagy may be very 
important for establishing/developing the normal GI flora, so don't 
discourage it. but some foals get carried away and eat too much and get 
diarrhea.

Excessive milk intake: some mares make a lot of milk, more 
than foal is ready for, and foal overeats. heavily producing mares; mares 
who are separated from their foals (eg, mare is shipped to be bred and 
foal is left home 6 hrs, mare comes back engorged); overly tube feeding 
sick foals; bottle feeding orphan foals (foal normally eats every 20 
minutes but we feed larger feedings every hour); over supplementation; 
etc. Excessive milk overwhelms the absorbing capacity of small intestine; 
overflow of milk to colon which isn't adapted for absorbing things yet 
--> diarrhea. Again, generally a self-limiting problem. 

sand or dirt 
diarrhea: sometimes foals eat dirt, they get into this habit. dx by fecal 
floatation and identification of geosediment. Rx: try to remove 
opportunity for foal to eat dirt. 

CHO intolerance: nonspecific 
malabsorption or malabsorption of everything as occurs secondary to 
rotavirus. self limiting, no therapy. may be hard to dx though. 

lactose 
malabsorption: lactase deficiency. dx: lactose absorption test after 
glucose absorption test. rx: remove lactose from diet if possible, which 
means early weaning. this is a bit of a problem b/c most energy dense 
foal food has lactose in it. 

Parasitic diarrheas:

strongyloides 
westeri: comes from mom's milk - hides in the CT of mammary gland, 
recall. heaviest shedding 2-3 weeks postpartum. probably rarely a cause 
of diarrhea in foals, though gets a lot of blame. experimentally you need 
100x the amount shed in mare's milk to cause clinical diarrhea in foals. 
subclinical infections are common. tx: ivermectin, thiabendazole, 
cambendazole, oxibendazole, given just prior to foal heat diarrhea 
period. this prevents s.westeri from establishing itself, but foal still 
gets foal heat diarrhea :)

cyathostomiasis (small strongyles): poorly 
described, not really in such young foals; may cause typhlitis/colitis, 
colic or diarrhea; dx by finding L4 or L5 in feces. not important in 
foals, poorly described.

Viral diarrheas are important - most common 
infectious ones of foalhood. three occur:

Adenovirus: only in 
immunodeficient animals?
coronavirus: hard to find
rotavirus - easiest to 
detect, know most about it

probably another 8 or 9 occur but we aren't 
aware...

Rotavirus: 30% of foals with diarrhea have this; 90-100% of 
adults have rotavirus antibodies. 
source: subclinical adult carriers; 
recovered foals shed up to 8 mos; virus can survive 9 mos. 
rotavirus 
epidemics occur late in foaling season: population pressure, management - 
often favors heavy contamination. early in foaling season, a few foals 
are affected, they shed, they contaminate environment, more foals get it, 
heavier and heavier contamination occurs until everyone gets it. almost 
all mares have Ab in their colostrum, and it's a neutralizing Ab...but 
passive protection is overwhelmed by huge environmental contamination. 

note that only a certain % (40%?) of foals show clinical signs. 100% of 
foals are infected in an epidemic, though. there is a vaccination that 
may help, btw. 

signs: < 2 mos old (often < 1 month); depression, 
failure to nurse (mare gets engorged), then 12-24 hrs later: profuse, 
nonfetid diarrhea, secondary bacterial infections with fever and 
leukopenia (if no bacterial infection, no fever or leukopenia occurs), 
weight loss, debilitation. 

diagnosis of rotavirus:
electron microscopy 
- good if heavy infection
rotazine test (human test - detects some equine 
types
latex agglutination - detects about 80% of equine types

immunofluorescence - rarely used
immunoelectronmicroscopy - rarely used

PCR- rarely used
virus isolation - rarely used

interpreting results: 
finding virus does not mean the virus is the cause of the problem. many 
foals have rotavirus and have no clinical signs. there can be other 
pathogens there. so don't overinterpret a positive result. 

treatment - 
fluids, electrolytes. keep letting foals nurse (some people say not to) 
because it's stressful on you, mom, and foal to try to prevent nursing. 
also milk has good electrolyte balance, good source of fluids. also foals 
this age require lumenal nutrients for the GI tract to heal. may need to 
supplement with more fluids b/c nursing may produce more profuse 
diarrhea, but the benefits seem to outweigh this. can place IV cath and 
have owners give boluses of IV fluids. 

vaccination - field trials are 
promising - may be helpful. 
prevention - primarily management

Other 
diarrheas - 

bacterial:
salmonella
e.coli - no enteropathogenic strains 
of this in the horse; probably enteroinvasive forms or septicemia forms 
are what cause diarrhea in foals
clostridium
Rhodococcus equi - diarrhea, 
pneumonia
campylobacter spp
klebsiella pneumoniae
bacteroides fragilis

streptococcus durans

so a lot of things may be there; you only have 
whatever your diagnostic lab tells you as far as diagnoses...the 
principles of therapy are very similar, though.

Clostridium difficile 
has been found to be important cause of equine diarrhea lately. age of 
onset 20-60 hours old! duration of illness 3-7 days. can be dehydrating 
enough to kill the foal without fluid replacment, though. mixed 
infections occur. multifactorial: some foals born into heavily 
contaminated stalls do NOT develop disease. 
signs: dehydration, colic, 
abdominal distension, diarrhea - watery, malodorous, yellow/brown. 

depression, leukopenia, anorexia, rapid weight loss, fever uncommon
rx: 
butorphanol (they seem to like that sort of drug)(:))

outbreak on 5 
farms 2 yrs ago in NY:
33 foals affected; one death (fungal aspiration 
pneumonia)
C. difficile toxin positive: 82% of foals, 51% dams
fecal 
pathogens: 
25% foals culture positive for C. difficile (on 
antimicrobials)
35% also grew C. perfringens
47% also rotavirus positive 
by EM

this vet started everyone on metronidazole after the first few 
came down with it; that may account for low culture positive rate.
these 
pathogens often potentiate each other; one alone is less problematic.


treatment: fluids w/KCl, bicarb; bismuth subsalicylate; metronidazole 
(drug of choice in humans with c.difficile but in CA many strains are 
resistant) or vancomycin (for resistant strains - this is scary to do 
though, b/c we use vanc to tx MDR microbes in people in ICU...methicillin 
resistant staph, etc...so don't use vancomycin in these horses unless you 
*absolutely* have to), probiotics (GI flora can outcompete the pathogens 
- problem is that we don't have the right combination of flora all ready 
to go). 

prophylaxis: if you have an outbreak, how do you keep new cases 
from happening?:
metronidazole
probiotics
remove mare's feces pre/post 
foaling
bathe mare at stage I labor (questionable)
good hygiene, 
disinfection

C. perfringens B and C:
peracute death - within hours

bloody diarrhea
sometimes mild forms - more often than not - orange 
feces, fever
signs and course similar to c. difficile

---end of testable 
material from that handout!

read rest of foal handout if you want to; it 
won't be on the test.

--break--

Acute diarrhea - Adult horses
different 
from foal diarrhea. in adults, acute diarrhea is fairly rare and usually 
important

Causes:

Salmonellosis
Potomac Horse Fever
Colitis X

Clostridiosis
Parasitic Enteritis
Antibiotic Associated Enteritis
NSAID 
toxicity
Fungal colitis
Toxic insults (arsenic, blister beetle)

an 
etiologic dx is only made in 30-50% of acute diarrhea cases in adult 
horses.
lately we've seen very few <knock wood> salmonella cases -a  few 
per year; historically we've seen 100/yr.

clostridia seems to be the 
enteric equine pathogen of the 90s. Some folks from Auburn have been 
seeing some weird ones. since the microbiologists get better, probably 
we're just finding it more, it's not new or anything.

Colitis X: in the 
60s (mid-late 60s) horses were dying at racetracks, some of the best 
horses in country, were getting acutely ill w/diarrhea and dying within 
hours. when expensive, well  known horses have this problem, people pay 
to find out the cause. One pathologist named Jim Rooney (sp?) went to do 
necropsies and stuff and there was a lot of press interest in the matter, 
so he figured that to keep the interest going and to get funding to find 
the root of the problem, it would be good to give it a catchy name. so he 
called it "colitis X". we still don't know the cause. it's a sporadic 
disease of racehorses at tracks but also elsewhere. acute to peracute - 
usually death within hours. "very fatal." usually death at 3-24 hrs. if 
they recover, possibly they didn't have this disease. 95% die rapidly. 

Authors have confused this syndrome by calling any acute diarrhea in 
horses "colitis X" and saying that 80% of horses with colitis x live. 
that's not so. Colitis X has high mortality.
synonyms: Acute Colitis 
Syndrome, Hemorrhagic Edematous Colitis b/c colon is edematous and 
hemorrhagic, Post Stress Diarrhea b/c some feel stress is cause; Equine 
Anaphylaxis (people thought that's what it was for a while).

history:

"stress" 10-24 days prior to onset: shipping, respiratory dz, heavy 
training, sudden diet change, protein rich diet, etc - some horses have 
no history of recognizable "stress"
any age, breed, sex 
no seasonality

sporadic outbreaks on racetracks occur
most common in young, fit race 
horses

signs:
sudden onset of severe disease
hypovolemic shock and 
endotoxic shock
febrile (up to 106) or hypothermic
profound depression

complete anorexia
abdominal distension
mild/severe colic
red/purple mms

CRT >4 sec, up to 10, or never refills
mms dry, tacky
weak, rapid pulses

poor jugular fill (poor venous return)
tachypnea

diarrhea not always 
present - often they die prior to diarrhea occuring; find liquid feces in 
colon on necropsy. when it does occur, very profuse, watery, foul 
smelling; not bloody. contains protein and horse suffers dramatic 
hypoproteinemia
Rectal exam is very difficult (as in any enteritis horse) 
b/c very painful and horse is straining. when you do the rectal exam, 
colonic and cecal wall edema will be present - maybe 2-3 inches thick. 
mesenteric/colonic LN edema, very edematous/friable rectal mucosa - may 
come out with blood all over your sleeve not form perforation but b/c 
mucosa bleeds when you touch it. 

etiology:
has been kicked around a 
while. many theories.
used to think: endotoxic shock - but that looks 
different
used to think: anaphylaxis - but that looks different too

"Exhaustive shock" - Rooney's theory: a horse that had some stress 10-24 
days ago, and then some secondary stress came on top of that, like the 
straw breaking camel's back, too much to handle, causes shock.
C. 
perfringens type A - is isolated in some cases, histologic findings 
correlate.
Peracute salmonellosis - sometimes isolated

diagnosis: 
clinical course, postmortem findings. if horse is sick and gets better, 
not colitis x. if acutely ill, dying, etc - could be. necropsy findings: 
lesions in cecum/colon, mucosa hyperemic, petechia, green/black necrosis, 
DIC. lesion starts in colon, is very segmental, well demarcated. not due 
to torsion or vascular occlusion but looks like it is b/c so segmental. 


tx: fluids, fluids, and more fluids. then, you should give some fluids. 
give pain relief too - often horse is in pain. some people give steroids 
- not that great a help. 90% die anyway. most die on their way here. what 
analgesic do you give? well, ask the horse. try something. if it doesn't 
work, try something else. probably more important to be humane than worry 
about side effects. detomidine, butorphanol/detomidine, morphine, 
demerol. those last two seem fairly potent combined with xylazine, 
detomidine (isn't there some weird thing about narcotics in horses 
though?)

Intestinal Clostridiosis - closely related to Colitis X?? used 
to think so. used to think of this as peracute, fulminating dz, but some 
are mild and recover. caused by clostridium perfringens type A and 
clostridium difficile.
dx: clostridia in feces, clostridia toxin in 
feces. you can grow clostridia from unaffected horses, and sometimes find 
the toxin in there too...when you find both in an affected horse, that's 
a confirmatory sign. histo: large gram positive rods associated with 
mucosa, damaged mucosa.
in horses, usually have not had abx prior to 
illness, whereas in humans, most with clostridia isolated have had abx 
before. but in horse, occurs spontaneously. although, abx related 
enteritis in horse often does involve clostridia, too. 

pathogenesis: 
normal horse resistant to colonization with clostridia but with change in 
flora can get established. in people, abx do this. in horse - stress, 
feed change, dietary factors, abx...protein supplements (lysine, 
methionine) are associated with colonization by clostridia.

young race 
horses seem predisposed esp if on alfalfa hay - those will have 
clostridia in feces but may not get sick (finding it doesn't mean it is 
sick)
a high colony count can occur in absence of disease
abx: 
tetracyclines in particular change the flora and promote clostridial 
growth; also lincomycin. will find increased c.perfringens/difficile 
counts in feces after giving these drugs.

experimental dz induction: 
broth cultures are used, requires huge numbers of bacteria to induce - 
produces mild signs in 1/3 of horses. so normal horses are resistant and 
don't seem to get that sick. 

history: usually acute onset, a few hours 
prior may be prodromal signs - depression, decreased appetite - sudden 
onset severe diarreha then occurs.

signs: acute toxic enteritis. colic, 
fever, variable diarrhea severe, watery, dark, foul smelling with drop in 
protein. normal feces decreased in volume may occur. listlessness, 
fetid/semisolid feces
dehydration is proportional to diarrhea but some 
toxins can cause depression, other signs.

lab findings:
early 
leukopenia, late leukocytosis
increased PCV/TP early; later TP drops

prerenal azotemia, may become renal
DIC
dx requires both fecal culture of 
clostridia, and identification of toxin in feces - assay for toxin A or B 
of c. difficile and enterotoxin of c. perfringens. 
postmortem lesions 
are helpful as well. 

therapy:
fluids, supportive care - lots of fluids!

antibiotics - metronidaole probably most effective. vancomycin in CA. 
bacitracin which is pretty toxic given systemically can be used orally 
for clostridia with good success. probiotics - anything with good 
bacteria. in Europe there is a product called "Sour Milk" which is 
basically fermented buttermilk which can experimentally inhibit or kill 
clostridia. 

Parasitic diarrhea

strongylus vulgaris
diarrhea:
mild, 
chronic, intermittent, or watery, profuse, acute diarrhea
fulminant 
colitis, infarcts
fever, colic, weight loss, poor hair coats, very 
painful, very necrotic colon.

Cyathostomes/small strongyles: 
horse 
under 5 or aged
sometimes fever, colic, wt loss in history
usually sudden 
onset as with salmonella, clostridia
usually late winter, early spring

recall hypobiosis of early L3 - in lumen, crypts, or mucosa/submucosa; 
may last up to three years. encysted late L3 and L4 stages also occur. 

encysted cyathostomes - to see on necropsy, hold mucosa up to light and 
you can see these little areas where they are. too small to see 
otherwise.
pathology: larvae rupture from cysts in large numbers at once, 
causing physical damage. the cysts contain excretory/secretory products 
that affect motility, as well as irritants, and immunogens.

response to 
infection: depends on pattern of exposure/resistance
heavy exposure - 
disease in young horses
moderate exposure after "clean environment" in 
nonresistant horse - severe disease. these are the horses kept on farms 
with good management, pasture rotation, etc - horse that hasn't been 
exposed to these before - suddenly exposed and gets sick
aged horses: 
waning immunity - develop disease on well-managed farm
may have > 100,000 
luminal forms with no disease problems. 
for a long time, this fooled us. 
we'd see these parasites in healthy horses and so we thought they were 
not pathogenic. however, the pathology is related to immunity of 
individual as relates to number of parasites. so now, we think small 
strongyles are a common cause of colic and undiagnosed diarrhea.


response to deworming:
7-10 days after deworming, horse develops diarrhea 
or colic
deworming kills luminal forms, triggers hypobiotic larvae to 
emerge en masse.
so a heavily parasitized animal with lots of hypobiotic 
larvae present that is suddenly dewormed can get really sick. 

diarrhea 
may be severe with periods of apparent remission
large numbers of L4-L5 
may be found in feces (if you're lucky) (have to look for them, 
though)(see little black threads, moving around.)
PLE: profound 
hypoproteinemia occurs due to GI protein loss
great individual variation 
with same challenge - strict control can predispose to severe disease if 
control efforts are interrupted.

prevention: good management
not 
overcrowding
weekly removal of feces from pasture (pasture vacuum has 
been invented! it's like a lawnmower with a wagon behind it. if you use 
it weekly, you have lower parasite load than if you aggressively 
deworm!!)
harrowing to break up feces
pasture rotate with sheep or cattle

rest pastures over summer
good anthelmintic program
be wary of changing 
from strict to lax control

Larvicidal therapy:
repeat q 2 weeks

Fenbendazole - 10 mg/kg for 5 days in a row: effective against encysted 
late L3/L4? not sure. resistance may make it less efficacious. techniques 
used in the early studies are being questioned.
Oxfendazole @ 10 mg/kg 
day 1 and day 3
Ivermectin @ 200 micrograms/kg, PO: not good for 
hypobiotic or encysted forms, some resistance exists. very good for 
luminal forms, though. 

Moxidectin: effective against encysted late L3 
early L4 larvae? inconsistent data at this time. company says it is. 
studies are not convincing; often not statistically significant, often 
inconsistent results.
effective against hypobiotic forms (early L3)?? 
encysted - data inconsistent (3 studies say yes, four say no). luminal 
hypobiotics - variable effect
therapy may stimulate development of 
hypobiotic larvae
effective against lumenal L4 and adults for sure
shares 
resistance with ivermectin
anecdotal reports of colic post moxidectin 
therapy

pyrantel tartrate: daily deworming to kill L3 before they 
invade. more preventive. prevents infection by L3 and protects against 
disease unless resistance occurs. decreases incidence of colic. very 
effective control method. for a while they were selling this stuff with 
an "insurance policy" offer of $2500 to the owner if colic surgery was 
required. the problem with this drug is that if your horse is on this 
oral anthelmintic therapy (which is a good idea on boarding farms, etc) 
this is very strict control. if you use it for 10 years and then decide 
to stop it, you are setting horse up for disease.

antibiotic associated 
diarrhea (occurs in foals and adults)
most commonly associated with 
oxytetracycline, tmp sulfa, ceftiofur sodium
any antimicrobial *can* 
cause this problem. in one area one drug might cause it and in another 
area that drug may not cause a problem. here, in the mid 80s we saw 
problems with TMP sulfa, in other areas in early 90s, now it isn't so 
much a problem. Ceftiofur sodium has caused problems in some areas but 
not others. we don't see a problem with it here. at local racetracks, 
they do. depends on local flora and their susceptibilities, among other 
things. abx associated diarrhea then is a complication that could occur 
with any drug. here, now, oxytet and TMPsulfa are unlikely to cause 
problems.

other associated abx:
erythromycin - if you have a foal with 
rhodococcus, erythromycin and rifampin are often used - mares who suckle 
those foals get erythromycin induced diarrhea somehow, even though their 
exposure is very small. the pathogen in this diarrhea is clostridia 
difficile
high levels of penicillin
lincomycin
metronidazole

cephalosporins


history, signs:
abx therapy
diarrhea after starting tx

diarrhea after ending tx
all degrees of severity

erythromycin induced 
cases can be really bad.

seems to occur on some farms more than others.


can only make tentative dx by association
disturbance of intestinal flora

sensitive organisms are decreased, eliminated
pathogens overgrow

TMP 
sulfa will kill enterobacteriacea, enterococci, clostridia, variably 
affect anaerobes and e.coli. after cessation there is reconstitution with 
new serotypes

tetracycline suppresses anaerobic flora, causes 
proliferation of clostridium perfringens A and others. 

tx: remove 
offending abx, avoid other abx if possible, supportive therapy, 
transfaunation. consider parenteral aminoglycoside - those don't get into 
GI tract. 



---end---