1. Salmonellosis in Horses
Description
Salmonellosis (see Salmonellosis) is one of the most commonly diagnosed infectious causes
of diarrhea in adult horses. Clinical manifestations range from no abnormal clinical signs
(subclinical carrier) to acute, severe diarrhea and even death. The disease is seen
sporadically but may become an epidemic, depending on the virulence of the organism,
level of exposure, and host factors
Etiology
Salmonella enterica of the serogroup B includes S enterica serovar typhimurium and S enterica agona
Transmission
Infection can occur via
-contamination of the environment, feed, or water
- contact with animals actively shedding the bacteria
Clinical Findings
Three forms of salmonellosis have been recognized in adult horses.
1st
form - subclinical carrier
-which may or may not be actively shedding the organism but has the potential to transmit the
bacteria to susceptible animals either by direct contact or by contamination of the environment,
water, or feed sources.
2nd
form
- characterized by a mild clinical course with Signs of : fever, anorexia, and soft but not
watery feces, absolute neutropenia
- Self limmiting after 4-5 days
3rd
form
- characterized by an acute onset of severe depression, anorexia, profound neutropenia, and
frequently abdominal pain
- Diarrhea develops 6–24 hr after the onset of fever; feces are fluid and foul smelling
- Affected horses dehydrate rapidly, and metabolic acidosis and electrolyte losses occur as
the horse deteriorates.

2. - Clinical signs of sepsis and hypovolemic shock can progress rapidly
- signs of abdominal discomfort, straining, or severe colic secondary to ileus, gas distension,
and colonic inflammation and possible infarction.
- If untreated, this form of salmonellosis is often fatal.
Diagnosis
- Diagnosis is based on clinical signs, severe neutropenia, and isolation of salmonellae from
feces, blood, or tissues
- Culturing of rectal mucosal biopsies
- PCR test
Treatment
- polyionic isotonic fluid is used for volume replacement
- IV fluid volumes of 40–80 L/day may be necessary
- Lipid soluble antibiotics
- GI protectants
- NSAID
- Ploymixin B
Prevention
- Biosecurity
- Serotyping, antimicrobial susceptibility profiles and genotyping by pulse field
electrophoresis, plasmid profile analysis, and phage typing can be used to determine
whether isolates are genetically related and help determine whether infection is
nosocomial.
- Owners should be made aware of the zoonotic risk of S enterica infection. People working
with infected animals should practice strict hygiene.
Actinobacillosis in horse
Etilogy
Actinobacillus equuli

3. Disease in foals may manifest as diarrhea, followed by meningitis, pneumonia,
purulent nephritis, or septic polyarthritis (sleepy foal disease or joint-ill).
Epidemiology
Infection may be acquired through a contaminated umbilicus or by inhalation or ingestion.
Lesion
Abortions, septicemia, nephritis, peritonitis, and endocarditis
Diagnosis
- Isolation
Treatment
Antibiotic therapy
- chloramphenicol, gentamicin, or third-generation cephalosporins, depending on the
nature of the infection and the ability to achieve therapeutic concentrations at the site
of infection. β-Lactam antibiotics and potentiated sulfonamides have been
recommended; however, resistance to both of these types of antibiotics is
occasionally reported.
PREVENTION
The incidence of foal infection is reduced with greater attention to sanitation in the birthing
environment, and maternal antibodies in colostrum are often protective.
Potomac Horse Fever

4. (Equine monocytic ehrlichiosis, Ditch fever, Shasta River crud, Equine
ehrlichial colitis)
Description
is an acute enterocolitis syndrome producing mild colic, fever, and diarrhea in horses of all ages, as well
as abortion in pregnant mares
Etiology
Neorickettsia risticii
- gram-negative obligate intracellular bacterium with a trophism for monocytes
Transmission
inadvertent ingestion of hatched aquatic insects that carry N risticii in the metacercarial stage of a
trematode
Clinical findings and lessions
- initially by mild depression and anorexia, followed by a fever of 102°–107°F (38.9°–41.7°C)
- diarrhea
- leukopenia and thrombocytopenia
- abortion due to fetal infection
- Fetal lesions include colitis, periportal hepatitis, and lymphoid hyperplasia of mesenteric lymph nodes
and spleen.
Prevention
- whole-cell vaccination
- Minimizing insect ingestion in stabled horses by turning off barn lights at night, which normally attract
the insects, has been suggested.
Coronavirus in Horses
Clinical signs
-include anorexia, lethargy, and fever. Colic and changes in fecal consistency are seen in some cases.
Occasionally, rapid progression leads to death (or euthanasia), but most cases resolve with supportive
care.

5. Diagnosis
-is by detection of the organism in feces by real-time PCR, electron microscopy, and virus isolation.
Viral Diarrhea in Foals
Etiology
Rotavirus
Charcteristic
characterized by depression, anorexia, and profuse, watery, malodorous feces. It is usually
seen in foals <2 mo old; younger foals typically have more severe clinical signs. The diarrhea
usually lasts 4–7 days, although it can persist for weeks.
Pathogenesis
Rotavirus destroys the enterocytes on the tip of the villi in the small intestine, which results in
malabsorption
Clinical signs
depression, anorexia, and profuse, watery, malodorous feces
Diagnosis
dentification of virus in the feces by electron microscopy or commercial immunoassay kits
designed for detection of human rotavirus
Treatment
-Supportive
- vaccine for pregnant mares to induce colostral antibodies directed at reducing the risk of
rotavirus infection in their foals is available.
Prevention
-Sick foals are highly contagious and should be isolated in the stall in the barn in which the foal
originally became ill or moved to a designated isolation facility.
-Personnel should wear disposable gloves and cleanable boots and wash their hands with soap
before and after handling diarrheic foals.
- Disinfection
- Fecal material of sick foals removed from stalls should not be spread on pastures used for
horses and foals, and care should be taken to avoid fecal contamination of alleyways.

6. Equine proliferative enteropathy (Lawsonia
intracellularis Infection)
Etiology
Lawsonia intracellularis
http://www.merckmanuals.com/vet/digestive_system/intestinal_diseases_in_horses_and_foals/bacteri
al_diarrhea_in_foals.html
Enterotoxemia Caused by Clostridium in Foals
Etiology
Clostridium spp. (C. perfringens)
CS
severe inflammation of the intestines, abdominal pain, and release of toxins that are responsible
for severe intestinal damage and high mortality in foals
Treatment
dministration of antibiotics by mouth to destroy the C. perfringens in the intestine, giving fluids to
compensate for losses due to diarrhea, and appropriate use of drugs to relieve pain.
Physical
Acute Intestinal obstruction
Etiology
a) Intestinal obstruction
- Messenteric torsion of the small intestine
- Strangulation of Inguinal hernia

7. - Intussuception
b) Luminal blockage
c) Excessive trauma
Pathogenesis
In horses, obstruction of the small intestine or colon usually kills within 24 hrs. Distention of the bowel
causes reflex cardio vascular effects, peripheral circulatory failure and collapse. In the most severe
lesion infarction devitalize the gut completely, and the two factors of fluid loss and toxemia and further
insult.
Clinical signs
a) Acute obstruction of the small intestine
Foal Heat Diarrhea
Etiology
Unknown
Pathogenesis
it may be associated with alterations in the foal's intestinal microbial flora or alteration in
diet as the foal begins to eat small amounts of hay and grain. Coprophagy may also
have a role.
Clinical signs
Feces are semiformed to watery and not malodorous
Recurrent Diarrhea in Horses
Small-Intestinal Fibrosis in Horses
Etiology
Unknown

8. Description
Extensive fibrosis of the submucosa of the small intestine has been associated with weight loss and recurrent
colic in adult horses on pasture
Gastrointestinal Neoplasia in Horses
Description
Squamous cell carcinoma of the stomach and the alimentary form of lymphosarcoma are
the most common forms of neoplasia involving the GI tract in horses.
Clinical signs
Chronic weight loss may be the primary clinical sign. Chronic diarrhea and
hypoalbuminemia may develop when lymphosarcoma has infiltrated the wall of the
intestine.
Lesions
Squamous cell carcinoma in the stomach
enlarged mesenteric lymph nodes or thickened bowel
Diagnosis
-Exclusion of other cause of weight loss
-histopathologic examination of the tissue collected by duodenal or rectal mucosal
biopsy during exploratory laparotomy or at necropsy
- gastroscopy
- rectal palpation
- ultrasonographic examination
- biopsy
Treatment
-No attempted
- Chemotherapy may be an option for some horses, and corticosteroid therapy may
prolong survival time in some cases.

9. Inflammatory Bowel Disease in Horses
This collection of diseases includes granulomatous enteritis (GE), lymphocytic-plasmacytic enterocolitis (LPE),
multisystemic eosinophilic epitheliotropic disease (MEED), and idiopathic focal eosinophilic enterocolitis (IFEE).
Disease is characterized by infiltration of the small and large intestine with inflammatory cells, including
lymphocytes, plasma cells, macrophages, and eosinophils. The inflammatory condition may be limited to only a
short segment of the bowel or be more diffuse. Malabsorption and a protein-losing enterocolopathy result.
Diarrhea may or may not be a clinical feature. Inflammatory bowel disease should be considered in the
differential diagnosis of horses with weight loss, recurrent colic, or hypoproteinemia, as well as in some horses
with generalized skin disease.
Diagnosis is based on clinical signs, low serum protein concentration, possible thickened bowel (identified by
ultrasonography or on rectal palpation), malabsorption, and intestinal or rectal biopsy. Malabsorption of
carbohydrates occurs secondary to severe villous atrophy throughout the small intestine. Failure to absorb oral
glucose or D-xylose verifies malabsorption from the small intestine.
Histologic diagnosis is subjective and should be performed by a pathologist experienced in reading equine
intestinal biopsies. Rectal mucosal biopsy is useful in the diagnosis of ~50% of cases of GE and MEED but is
rarely helpful in the diagnosis of LPE and IFEE. High numbers of eosinophils and lymphocytes can be identified
in the intestinal wall of normal horses, but overinterpretation should be avoided. The presence of eosinophilic
granulomas, vasculitis, and fibrinoid necrosis of intramural vessels is diagnostic of MEED. Horses with MEED
may have severe dermatitis, eosinophilic infiltrations in the liver or pancreas, and sometimes marked
eosinophilia. Horses with IFEE have eosinophilic infiltration restricted to the intestine and have a better
prognosis for survival. Full-thickness intestinal biopsies can be obtained by using a laparoscopic procedure via
a flank incision or by ventral midline celiotomy. Because most of the horses have severe hypoproteinemia at
the time of diagnosis, incisional healing can be problematic.
The pathophysiology of the various syndromes is not well understood. An altered immune response to a
common intestinal factor (eg, feed, parasites, bacteria) has been suggested. Histopathologic similarities exist
between GE in horses, Johne disease in cattle, and Crohn disease in people. Standardbreds seemed to be
predisposed to GE and MEED, which suggests possible genetic predisposition.

10. Various medical treatments have been tried with limited success. Corticosteroids, dietary alterations,
metronidazole, and the antimetabolite azathioprine have been used. Hypereosinophilic syndrome in
people often responds to hydroxyurea or vincristine, and sometimes interferon-α and cyclosporine are
used. Supportive nutritional care should involve frequent feeding of good-quality, high-energy feeds.
The prognosis is grave. If only a limited and accessible section of the bowel is affected, surgical
removal may be successful. This is more common in IFEE, in which horses commonly present with
colic rather than weight loss. Focal thickening, sometimes restricted to circumferential mural bands, is
detected via exploratory laparotomy or necropsy; a diagnosis can be made by subsequent
histopathology. Horses with IFEE respond to surgical resection of the diseased segment of intestine.
Medical treatment with corticosteroids and feeding small frequent meals has also led to resolution of
clinical signs after small-intestinal decompression without resection.