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Gi disorders in horses
Gi disorders in horses
Gi disorders in horses
Gi disorders in horses
Gi disorders in horses
Gi disorders in horses
Gi disorders in horses
Gi disorders in horses
Gi disorders in horses
Gi disorders in horses
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Gi disorders in horses

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  • 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.

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