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 Infections of the Gastrointestinal Tract). These infections spread by direct contact or the fecal-oral route. Some infections are the result of overgrowth of specific organisms in the normal GI microbiome (eg, Clostridium perfringens in dogs, salmonellosis in horses after transportation, extended anesthesia, or surgery).
Common Infections of the Gastrointestinal Tract
Pathogen | Cattle, Sheep, and Goats | Pigs | Horses | Dogs and Cats |
|---|---|---|---|---|
Viruses | 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 |
Rickettsiae | Neorickettsia risticii (Potomac horse fever [equine monocytic ehrlichiosis]) | Neorickettsia helminthoeca (salmon poisoning in dogs) | ||
Bacteria | 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, Clostridium difficile, Lawsonia intracellularis | Salmonella spp, Campylobacter jejuni, Clostridium spp, , Mycobacterium spp, S, adherent invasive E coli, |
Protozoa | Eimeria spp, Cryptosporidium spp | Eimeria spp, Isospora suis | Eimeria spp, Cryptosporidium spp | Isospora spp, Sarcocystis spp, Toxoplasma sp, Giardia sp, Tritrichomonas spp, Cryptosporidium spp, Neospora sp |
Fungi | Candida spp (cattle) | Candida spp | Aspergillus fumigatus | Histoplasma capsulatum, Aspergillus spp, Candida albicans, phycomycetes |
Algae | Prototheca spp | Prototheca spp | Prototheca spp | Prototheca spp |
Parasites (helminths) | See page Gastrointestinal Parasites of Ruminants. | See page Gastrointestinal Parasites of Pigs. | See page Gastrointestinal Parasites of Horses. |
Definitive etiologic diagnosis of infectious disease of the GI tract depends on demonstrating the organism 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).
Gastrointestinal Parasitism in Animals
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.
To estimate parasite load, see Internal Parasite (Endoparasite) Diagnosis in Livestock:.
Treatment of Infectious Diseases of the GI Tract in Animals
Supportive care
Antibiotics or anthelmintics may be needed, depending on the specific diagnosis
Supportive care for GI infections may include oral or parenteral fluids and electrolytes to correct imbalances caused by vomiting or diarrhea, nutritional support, anti-emetics, and prokinetics to help restore the normal intestinal microbiome.
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 of the GI Tract in Animals
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
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 systemic immunity provides little protection against the infectious enteritides in most cases. 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.
