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Infectious Diseases of the GI Tract


Stanley I. Rubin

, DVM, MS, DACVIM, Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois at Urbana-Champaign

Last full review/revision Dec 2013 | Content last modified Dec 2013
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The GI tract is subject to infection by many pathogens, which are a major cause of economic loss due to illness, suboptimal performance, and death (see Table: Common Pathogens of the Gastrointestinal Tract). These infections spread by direct contact or the fecal-oral route. Many of the pathogens are part of the normal intestinal flora, and disease develops only after a stressful event, eg, salmonellosis in horses after transportation, extended anesthesia, or surgery. The intestinal flora becomes established within a few hours after birth, which emphasizes the importance of the early ingestion of colostrum to provide protection against septicemia and intestinal infection.


Common Pathogens of the Gastrointestinal Tract


Cattle, Sheep, and Goats



Dogs and Cats


Bovine viral diarrhea, rotavirus, coronavirus, rinderpest, malignant catarrhal fever, bluetongue, foot-and-mouth disease

Transmissible gastroenteritis, porcine circovirus type II, porcine epidemic diarrhea virus, rotavirus, foot-and-mouth disease, vesicular stomatitis, vesicular exanthema

Rotavirus, vesicular stomatitis, coronavirus

Canine parvovirus, canine coronavirus, feline panleukopenia virus, feline enteric coronavirus, canine and feline rotaviruses, canine and feline astroviruses


Neorickettsia risticii (Potomac horse fever [equine monocytic ehrlichiosis])

Neorickettsia helminthoeca (salmon poisoning in dogs)


Enterotoxigenic Escherichia coli, Salmonella spp, Mycobacterium paratuberculosis, Fusobacterium necrophorum, Clostridium perfringens (types B, C, and D), Actinobacillus lignieresii, Yersinia enterocolitica, Campylobacter jejuni

Enterotoxigenic E coli, Salmonella spp, Brachyspira hyodysenteriae, Clostridium perfringens types B and C, Lawsonia intracellularis, Clostridium difficile

Enterotoxigenic E coli, Salmonella spp, Rhodococcus equi, Actinobacillus equuli, Clostridium perfringens types B and C, Clostridium difficile, Lawsonia intracellularis

Salmonella spp, Yersinia enterocolitica, Campylobacter jejuni, Clostridium spp, Clostridium piliforme, Mycobacterium spp, Shigella spp, adherent invasive E coli, Brachyspira spp


Eimeria spp, Cryptosporidium spp

Eimeria spp, Isospora suis

Eimeria spp, Cryptosporidium spp

Isospora spp, Sarcocystis spp, Besnoitia spp, Hammondia sp, Toxoplasma sp, Giardia sp, Tritrichomonas spp, Entamoeba histolytica, Balantidium coli, Cryptosporidium spp, Neospora sp


Candida spp (cattle)

Candida spp

Aspergillus fumigatus

Histoplasma capsulatum, Aspergillus spp, Candida albicans, phycomycetes


Prototheca spp

Prototheca spp

Prototheca spp

Prototheca spp

Parasites (helminths)

Definitive etiologic diagnosis of infectious disease of the GI tract depends on demonstrating the pathogen in the tract or in the feces of the affected animal. In herd epidemics, such as an outbreak of acute undifferentiated diarrhea in newborn calves or piglets, the best opportunity to establish a diagnosis is in the earliest stage of the disease by selecting untreated animals and submitting them for necropsy and detailed microbiologic examination of the intestinal flora. When selective necropsy is not an option, a series of carefully collected daily fecal samples should be submitted to a diagnostic laboratory with a request for special culture techniques, depending on the infectious disease suspected. Molecular technologies, including ELISA and PCR, have been developed to demonstrate the presence of viral, bacterial, or protozoal proteins or nucleic acids within the feces, which can provide a definitive diagnosis (eg, canine parvovirus, salmonellosis, cryptosporidiosis).

Overview of Gastrointestinal Parasitism

The GI tract may be inhabited by many species of parasites. Their cycles may be direct, in which eggs and larvae are passed in the feces and stadial development occurs to the infective stage, which is then ingested by the final host. Alternatively, the immature stages may be ingested by an intermediate host (usually an invertebrate) in which further development occurs, and infection is acquired when the intermediate host or free-living stage shed by that host is ingested by the final host. Sometimes, there is no development in the intermediate host, in which case it is known as a transport or paratenic host, depending on whether the larvae are encapsulated or in the tissues. Clinical parasitism depends on the number and pathogenicity of the parasites, which depend on the biotic potential of the parasites or, when appropriate, their intermediate host and the climate and management practices. In the host, resistance, age, nutrition, and concomitant disease also influence the course of parasitic infection. The economic importance of subclinical parasitism in farm animals is also determined by the above factors, and it is well established that lightly parasitized animals that show no clinical evidence of disease perform less efficiently in the feedlot, dairy, or finishing house.

Feed conversion in light to moderate parasitism is adversely affected and is primarily due to reduced appetite and poor use of absorbed protein and energy. Carcass quality and size also are reduced, which further reduce financial returns. Endoparasites of companion animals can cause severe disease or unthriftiness and are aesthetically undesirable. Furthermore, some of these parasites also infect people.

Because parasitism is easily confused with other debilitating conditions, diagnosis depends heavily on the seasonal character of parasitic infection; previous farm history; and examination of feces for evidence of oocysts, worm eggs, or larvae. Increased serum pepsinogen levels can support the diagnosis of some abomasal infections, as can increased serum liver enzymes for liver fluke infection. ELISA are being used, and other serologic (including monoclonal antibody) techniques are under development; serodiagnosis will likely be used more frequently as the specificity of the tests improves. These tests should be particularly useful in companion animals harboring parasites incriminated in zoonoses.

Advances in epidemiology (particularly regarding factors affecting seasonal development of the free-living stages and their survival), coupled with the discovery of highly efficient broad-spectrum anthelmintics, have made successful treatment and control of GI parasites both possible and practical. Response to therapy is usually rapid, and single treatments usually suffice unless reinfection occurs or the lesions are particularly severe. Preventive control in large animals is generally achieved by integrating grassland management with the use of anthelmintics. Improved methods of administering anthelmintics (eg, the pour-on method or sustained or pulsed-release devices) have also helped. Strategies to prevent parasitism and related production losses are part of any modern herd-health, flock, or stud program. Similar preventive programs are equally important in controlling parasitism in pet animals. Control by vaccination is limited to lungworms; vaccine for cattle is available in several European countries, and vaccine for sheep is available in parts of eastern Europe and in the Middle East.

Treatment of Infectious Diseases

Antimicrobial agents are used for the treatment of bacterial diseases, and anthelmintics for parasitic diseases. There is no specific therapy for treatment of viral diseases. Antimicrobials are commonly given PO daily for several days until recovery is apparent, but there is little objective evidence of efficacy. There is evidence that overdosage or prolonged oral treatment may be detrimental (eg, bacterial overgrowth, villous atrophy). Parenteral administration of antimicrobials is indicated when septicemia is apparent or may occur. The choice of antimicrobial agent depends on the suspected disease, previous results, and cost. In herd epidemics, antimicrobials may be added to the feed or water supplies at therapeutic levels for several days, followed by preventive levels for an extended period, depending on the infection pressure in the population. The feed and water supplies of in-contact animals also may be medicated in an attempt to prevent new cases from developing. (Also see Systemic Pharmacotherapeutics of the Digestive System.)

Control of Infectious Diseases

Effective control of the common infectious diseases of the GI tract depends on practicing good sanitation and hygiene, developing and maintaining nonspecific resistance in the animal, and in certain cases, providing specific immunity by vaccinating the pregnant dam or susceptible animal.

Effective sanitation and hygiene is achieved primarily by providing adequate space for animals and by regular cleaning of pens and efficient removal of manure from the immediate environment. Development and maintenance of nonspecific resistance depends on the genetic selection of animals that have a reasonable degree of inherent resistance and on the provision of adequate nutrition and housing, which minimizes stress and allows the animals to grow and behave normally. The development of infected but clinically healthy animals, which can shed pathogens for weeks or months, is a major problem with some infectious diseases of the GI tract, eg, salmonellosis. Ideally, these carrier animals should be identified by microbiologic means and isolated from the rest of the herd until free of the infection or culled.

Certain diseases (eg, enterotoxigenic colibacillosis in calves and piglets) can be controlled by vaccination of the pregnant dam several weeks before parturition. This method depends on achieving a protective level of antibodies in the colostrum. There are exceptions but, in most cases, systemic immunity provides little protection against the infectious enteritides; effective immunity against GI disease depends on stimulation of local intestinal immunity after the neonatal period. During the neonatal period, protection can be provided through the local action of maternally derived antibodies. For example, secretory IgA progressively increases in sow’s milk from the time of farrowing until weaning, which provides the piglet with daily protection during the nursing period.

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