Inflammation of the stomach is manifested clinically by vomiting and is commonly associated with enteritis in gastroenteritis.
Gastritis may be acute or chronic but both forms of the disease may be caused by the same etiological agents acting with varying degrees of severity and for varying periods. The inflammation may be associated with physical, chemical, bacterial, viral or metazoan agents.
Diseases of the rumen and abomasum are presented in Chapter 6. For comparative purposes the causes of abomasitis are listed here. For sheep there is no information other than about parasites. They are listed with cattle for convenience sake.
Physical agents such as frosted feeds affect only the rumen. In calves, gross overeating and the ingestion of foreign materials may cause abomasitis. In adults, there is a very low incidence of foreign bodies in the abomasum,1 half the cases being associated with traumatic reticulitis.
All the irritant and caustic poisons, including arsenic, mercury, copper, phosphorus and lead, cause abomasitis. Fungal toxins cause abomasal irritation, especially those of Fusarium spp. and Stachybotris alternans. Acute lactic acidosis due to engorgement on carbohydrate-rich food causes rumenitis with some run-off into the abomasum and the development of some abomasitis/enteritis.
Only the viruses of rinderpest, bovine virus diarrhea and bovine malignant catarrh cause abomasal erosions. Bacterial causes are very rare – sporadic cases of extension from oral necrobacillosis, hemorrhagic enterotoxemia due to C. perfringens types A, B, C, rarely as an adjunct to colibacillosis and its enteric lesion in calves. Fungi, e.g. Mucor spp. and Aspergillus spp. complicate abomasal ulcer due to other causes.
Foreign bodies, bedding, frosted feeds, moldy and fermented feeds are all possible causes.
Physical and chemical agents as listed under cattle may cause gastritis rarely. Infectious causes of gastritis are rare in the horse but emphysematous gastritis associated with C. perfringens has been recorded.
Metazoan agents causing gastritis in horses include massive infestation with botfly larvae (Gasterophilus spp.); Habronema muscae and Habronema microstoma infestation; Habronema megastoma causes granulomatous and ulcerative lesions and may lead to perforation and peritonitis.
Gastritis does not often occur in animals without involvement of other parts of the alimentary tract. Even in parasitic infestations where the nematodes are relatively selective in their habitat, infestation with one nematode is usually accompanied by infestation with others, so that gastroenteritis is produced. It is dealt with as a specific entity here because it may occur as such, and enteritis is common without gastric involvement. The net effects of gastroenteritis can be determined by a summation of the effects of gastritis and enteritis.
The reactions of the stomach to inflammation include increased motility and increased secretion. There is an increase in the secretion of mucus, which protects the mucosa to some extent but also delays digestion and may allow putrefactive breakdown of the ingesta. This abnormal digestion may cause further inflammation and favors spread of the inflammation to the intestines. In acute gastritis, the major effect is on motility; in chronic gastritis, on secretion. In acute gastritis there is an increase in motility, causing abdominal pain and more rapid emptying of the stomach, either by vomiting or via the pylorus in animals unable to vomit. In chronic gastritis, the emptying of the stomach is prolonged because of the delay in digestion caused by excessive secretion of mucus. This may result in chronic gastric dilatation. The motility is not necessarily diminished and there may be subacute abdominal pain or a depraved appetite due to increased stomach contractions equivalent to hunger pains.
When the inflammation is severe, pigs and, rarely, horses and ruminants vomit (or ruminants regurgitate excessive quantities of rumen contents). In monogastric animals, such as pigs, the vomitus contains much mucus, sometimes blood, and is small in amount, and vomiting is repeated, with forceful retching movements. The appetite is always reduced, often absent, but thirst is usually excessive and pigs affected with gastroenteritis may stand continually lapping water or even licking cool objects. The breath has an offensive odor and there may be abdominal pain. Diarrhea is not marked unless there is an accompanying enteritis but the feces are usually pasty and soft. Additional signs are usually evident when gastritis is part of a primary disease syndrome. Dehydration and alkalosis with tetany and rapid breathing may develop if vomiting is excessive.
Chronic gastritis is much less severe. The appetite is depressed or depraved and vomiting occurs only sporadically, usually after feeding. The vomitus contains much viscid mucus. Abdominal pain is minor and dehydration is unlikely to occur, but the animal becomes emaciated through lack of food intake and incomplete digestion.
Anorexia, tympanites, gastritis, pyloric stenosis and gastric ulcers are the clinical manifestations of abomasal foreign body in cattle.
Specimens taken for laboratory examination are usually for the purpose of identifying the causative agent in specific diseases. Estimations of gastric acidity are not usually undertaken but samples of vomitus should be collected if a chemical poison is suspected.
The signs of inflammation vary in severity from a diffuse catarrhal gastritis to severe hemorrhagic and ulcerative erosion of the mucosa. In the mucosal diseases there are discrete erosive lesions. In parasitic gastritis there is usually marked thickening and edema of the wall if the process has been in existence for some time. Chemical inflammation is usually most marked on the tips of the rugae and in the pyloric region. In severe cases the stomach contents may be hemorrhagic; in chronic cases the wall is thickened and the contents contain much mucus and have a rancid odor suggestive of a prolonged sojourn and putrefaction of the food.
It is important to differentiate between gastritis and the erythematous flush of normal gastric mucosa in animals that have died suddenly. Venous infarction in the stomach wall occurs in a number of bacterial and viral septicemias of pigs and causes extensive submucosal hemorrhages, which may easily be mistaken for hemorrhagic gastritis.
• Gastritis and gastric dilatation have many similarities but in the latter the vomitus is more profuse and vomiting is of a more projectile nature, although this difference is not so marked in the horse, in which any form of vomiting is severe
• Gastritis in the horse is not usually accompanied by vomiting but it may occur in gastric dilatation
• In esophageal obstruction, the vomitus is neutral in reaction and does not have the rancid odor of stomach contents
• Intestinal obstruction may be accompanied by vomiting and, although the vomitus is alkaline and may contain bile or even fecal material, this may also be the case in gastritis when intestinal contents are regurgitated into the stomach
• Vomiting of central origin is extremely rare in farm animals
• Determination of the cause of gastritis may be difficult but the presence of signs of the specific diseases and history of access to poisons or physical agents listed under etiology above may provide the necessary clues
• Analysis of vomitus or food materials may have diagnostic value if chemical poisoning is suspected
Treatment of the primary disease is the first principle and requires a specific diagnosis. Ancillary treatment includes the withholding of feed, the use of gastric sedatives, the administration of electrolyte solutions to replace fluids and electrolytes lost by vomiting, and stimulation of normal stomach motility in the convalescent period.
In horses and pigs, gastric lavage may be attempted to remove irritant chemicals. Gastric sedatives usually contain insoluble magnesium hydroxide or carbonate, kaolin, pectin or charcoal. Frequent dosing at intervals of 2–3 hours is advisable. If purgatives are used to empty the alimentary tract, they should be bland preparations such as mineral oil to avoid further irritation to the mucosa.
If vomiting is severe, large quantities of electrolyte solution should be administered parenterally. Details of the available solutions are given under the heading of disturbances of body water. If the liquids can be given orally without vomiting occurring, this route of administration is satisfactory.
During convalescence, the animal should be offered only soft, palatable, highly nutritious foods. Bran mashes for cattle and horses and gruels for calves and pigs are most suitable and are relished by the animal.
In the pig, simple gastric distension is usually readily relieved by vomiting.
This is a much more serious problem.1 Torsion is thought to occur because the sow eats a large, sloppy meal very quickly. The occurrence is specifically related to intense excitement and activity occurring at feeding time. Death occurs 6–24 hours after the pig’s last meal. At necropsy the stomach is enormous (50–60 cm diameter), with engorgement of vessels and hemorrhagic effusion into the stomach, which contains much gas and usually a lot of food. Rotation varies in degree from 90–360° and is usually to the right. The spleen is markedly displaced, the liver is bloodless and the diaphragm encroaches deeply into the chest.2
Acute dilatation also occurs in pigs secondarily to acute obstruction of the small intestine. The obstruction may be as far down as the ileocecal valve. The oral segment of intestine dilates and fills with fluid, and refluxes into the stomach, filling it. In the pig vomiting follows. The outcome depends on whether sufficient gastric motility returns to evacuate the stomach.
Some causes of intestinal obstruction are:
• Torsion of the coiled colon about its mesentery occurs in adult pigs
• Obstruction of the terminal small colon in young piglets causes very hard fecal balls, or barley chaff used as bedding may be implicated in obstruction
• Heavy feeding on lactose1 causes a dilatation and atony of the intestine in the same way as grain feeding does in ruminants.
• In pigs impaction of the colon and rectum occurs sporadically, usually in adult sows that get little exercise and are fed wholly on grain. The disease also occurs in pigs that are overcrowded in sandy or gravelly outdoor yards
• A special occurrence in young weaned pigs causes obstruction of the coiled colon
• A presumed inherited megacolon of fattening pigs is reported as a cause of abdominal distension, constipation and wasting. There is no anal stricture.1
In impaction of the large intestine the effects appear to be due largely to autointoxication, although the commonly occurring posterior paresis seems more likely to be due to pressure from inspissated fecal material.
Retention of the meconium has no specific signs. There is anorexia and dullness and the pig is recumbent much of the time. Feces passed are scanty, very hard and covered with mucus. Weakness to the point of inability to rise occurs in some cases. Hard balls of feces in the rectum are usually detected when a thermometer is inserted.
In paralysis of the rectum there is inability to defecate and usually some straining. The anus and rectum are ballooned and manual removal of the feces does not result in contraction of the rectum. Spontaneous recovery usually occurs 3–4 days after parturition.
• Primary tympany occurs with ingestion of excess whey. Recorded in adult dry sows. Distension of proximal colon causes rupture with death from endotoxic shock1
• Secondary large bowel tympany – usually secondary to acute intestinal obstruction.
The term enteritis is used to describe inflammation of the intestinal mucosa resulting in diarrhea and sometimes dysentery, abdominal pain occasionally, and varying degrees of dehydration and acid–base imbalance, depending on the cause of the lesion, its severity and location. In many cases, gastritis also occurs together with enteritis.
There are several diseases of the intestines of farm animals in which diarrhea and dehydration are major clinical findings, but classical inflammation of the mucosa may not be present. The best example of this is the diarrhea associated with enterotoxigenic E. coli, which elaborate an enterotoxin that causes a large net increase of secretion of fluids into the lumen of the gut, with very minor, if any, structural changes in the intestinal mucosa. This suggests that a word other than enteritis may be necessary to describe alterations in the intestinal secretory and absorptive mechanisms that result in diarrhea but in which pathological lesions are not present. However, with the above qualifications, we have chosen, for convenience, to continue to use the term enteritis to describe those diseases in which diarrhea is a major clinical finding due to malabsorption in the intestinal tract.
There are many causes of enteritis or malabsorption in farm animals and the disease varies considerably in its severity depending upon the causative agent. Enteropathogens include bacteria, viruses, fungi, protozoa and helminths. Many chemicals and toxins can also cause enteritis (Tables 5.12-5.15). In addition to the primary etiological agents of enteritis, there are many epidemiological characteristics of the animal and the environment that are important in facilitating or suppressing the ability of the causative agent to cause enteritis. Thus newborn calves and piglets that are deficient in colostral immunoglobulins are much more susceptible to diarrhea, and with a high mortality rate from diarrhea, than animals with adequate levels. Enteric salmonellosis is commonly precipitated by the stressors of transportation or deprivation of feed and water. The stress of weaning in pigs is a risk factor for postweaning diarrhea. The prolonged use of antimicrobials orally in all species may alter the intestinal microflora and allow the development of a superinfection by organisms that would not normally cause disease.
Table 5.12 Epidemiological and clinical features of diseases of cattle in which diarrhea is a significant clinical finding
| Etiological agent or disease | Age and class of animal affected and important epidemiological factors | Major clinical findings and diagnostic criteria |
|---|---|---|
| Bacteria | ||
| Enterotoxigenic E. coli | Newborn calves < 3–5 days of age, colostral immune status determines survival. Outbreaks common | Acute profuse watery diarrhea, dehydration and acidosis. |
| Culture feces for enteropathogenic type | ||
| Salmonella spp. | All ages. Outbreaks occur. Stress-induced | |
| Clostridium perfringens types B and C | Young well nourished calves < 10 days of age | Severe hemorrhagic enterotoxemia, rapid death. Fecal smear |
| Mycobacterium avium subsp. paratuberculosis | Mature cattle, sporadic, single animal | |
| Proteus spp. and Pseudomonas spp. | Calves treated for diarrhea with prolonged course of antibiotics | Chronic to subacute diarrhea, poor response to treatment, progressive loss of weight. Culture feces |
| Fungi | ||
| Candida spp. | Young calves following prolonged use of oral antibacterials | Chronic diarrhea, no response to treatment. Fecal smears |
| Viruses | ||
| Rotavirus and coronavirus | Newborn calves, 5–21 days old, explosive outbreaks | Acute profuse watery diarrhea. Demonstrate virus in feces |
| Winter dysentery (Coronavirus) | Mature housed cows, explosive outbreaks | Acute epizootic of transient diarrhea and dysentery lasting 24 hours. Definitive diagnosis not possible currently |
| Bovine virus diarrhea (mucosal disease) | Young cattle 8 months to 2 years. Usually sporadic but epidemics occur | Erosive gastroenteritis and stomatitis. Usually fatal. Virus isolation |
| Rinderpest | Highly contagious, occurs in plague form | Erosive stomatitis and gastroenteritis. High morbidity and mortality |
| Bovine malignant catarrh | Usually mature cattle, sporadic but small outbreaks occur | Erosive stomatitis and gastroenteritis, enlarged lymph nodes, ocular lesions, hematuria and terminal encephalitis. |
| Transmission with whole blood | ||
| Helminths | ||
| Ostertagiasis | Young cattle on pasture | |
| Protozoa | ||
| Eimeria spp. | Calves over 3 weeks old and cattle up to 12 months of age. Outbreaks common | Dysentery, tenesmus, nervous signs. Fecal examination diagnostic |
| Cryptosporidium spp. | Calves 5–35 days of age | Diarrhea. Fecal smear and special stain |
| Chemical agents | ||
| Arsenic, fluorine, copper, sodium chloride, mercury, molybdenum, nitrates, poisonous plants, mycotoxicoses | All ages, history of access to substance. | All severities of diarrhea, dysentery, abdominal pain, in some cases nervous signs, dehydration, toxemia. Fecal and tissue analyses |
| Outbreaks occur | ||
| Physical agents | ||
| Sand, soil, silage, feed containing lactic acid (sour brewers’ grains) | Usually mature cattle, history of access. Outbreaks occur | |
| Nutritional deficiency | ||
| Copper deficiency, conditioned by excess molybdenum | Usually mature cattle on pasture with high levels of molybdenum | Subacute and chronic diarrhea, osteodystrophy, no systemic effects, hair color changes. Liver and blood analyses |
| Dietary | ||
| Overfeeding | Young calves overfed on milk | Mild diarrhea, feces voluminous and pale yellow. Clinical diagnosis |
| Simple indigestion | Change of ration of mature cows (hay to silage) or grain to feedlot cattle | Subacute diarrhea. Normal in 24 hours. Clinical diagnosis usually sufficient |
| Inferior milk replacers | Heat-denatured skim milk used in manufacturing of milk replacers for calves | |
| Miscellaneous or uncertain etiology | ||
| Intestinal disaccharidase deficiency | May occur in young calves. Sporadic | Subacute diarrhea unresponsive to usual therapy except withdrawal of milk. Lactose digestion tests |
| Congestive heart failure | Sporadic. Mature cattle. | Profuse watery diarrhea associated with visceral edema. |
| Toxemia (peracute coliform mastitis) | Sporadic | Acute diarrhea due to endotoxemia from peracute mastitis. |
| Culture milk | ||
Table 5.13 The epidemiological and clinical features of horses with diarrhea
| Etiological agent or disease | Age and class of animal affected and important epidemiological factors | Major clinical findings; diagnostic criteria |
|---|---|---|
| Bacteria | ||
| Salmonella spp. | Young foals; mature horses, following stress | Acute profuse diarrhea, severe dehydration, foul-smelling feces; leukopenia and neutropenia, culture feces, hyponatremia |
| Rhodococcus equi | Foals 2–5 months of age, some with history of respiratory disease | Diarrhea associated with R. equi pneumonia; culture respiratory tract |
| Clostridium perfringens or C. difficile | Mature horses administered antibiotics. Young foals | Profuse, watery diarrhea, hypovolemia, hyponatremia. Fecal culture and demonstration of toxin in feces |
| Aeromonas spp. | Adult horses, tends to be more common in summer. Often isolated from horses with diarrhea. | Febrile, acute diarrhea. Culture feces |
| Definitive etiological role not proved | ||
| Viruses and rickettsia | ||
| Neorickettsia risticii (formerly Ehrlichia risticii) | Endemic to certain regions in North and South | Profuse watery diarrhea, fever, laminitis. IFA, PCR |
| America and Europe. Ingestion of organism spread by insects (mayflies) | ||
| Parasites | ||
| Cyathostomes and large strongyles | Acute to chronic diarrhea. Patent infections evident by fecal examination for parasite eggs | |
| Physical | ||
| Sand accumulation | Individual horses or farm problem. Ingestion of sand or gravel | Watery diarrhea, not malodorous, not profuse. Abdominal radiography or ultrasonography, examination of feces |
| Overdosing of cathartics (DSS, MgSO4, NaSO4, castor oil) | Treated animals | Moderate to profuse diarrhea. Historical confirmation of administration of compounds |
| Miscellaneous or unknown | ||
| Colitis X | Single animal. Adult horses. High death rate | Acute, pyrexic diarrhea, hypovolemia, leukopenia. Post mortem examination |
| Granulomatous or eosinophilic colitis | Single animal. Adults | Chronic diarrhea. Necropsy or colonic biopsy |
| Right dorsal colitis/phenylbutazone toxicity | Administration of NSAIDs in large doses or prolonged administration | Mild diarrhea. Low grade fever. Mild colic. Hypoproteinemia, hyponatremia. Necropsy, surgery |
| Antibiotic-induced diarrhea | History of antimicrobial administration. High case fatality rate | Acute onset diarrhea with or without fever. Leukopenia, hypovolemia. History |
DSS, dioctyl sodium sulfosuccinate; IFA, indirect fluorescence antibody test; NSAIDs, nonsteroidal anti-inflammatory drugs; PCR, polymerase chain reaction.
Table 5.14 Epidemiological and clinical features of diseases of the pig in which diarrhea is a significant clinical finding
| Etiological agent or disease | Age and class of animal affected and important epidemiological factors | Major clinical findings and diagnostic criteria |
|---|---|---|
| Viruses | ||
| Classical and African swine fever | Hemorrhagic diarrhea at any age | Many other signs(pyrexia) variety of lab tests (isolation, ELISA, PCR etc.) |
| Transmissible gastroenteritis (TGE) | Explosive outbreaks in newborn piglets. High morbidity and mortality | Acute diarrhea, vomition, dehydration and death. No response to treatment (lab tests include virus isolation, ELISA, EM, FATs) |
| Rotavirus and coronavirus (Epidemic diarrhea) | Acute diarrhea and dehydration. May continue to suck the sow. Death in 2–4 days. Virus isolation and pathology of gut, EM, FATs (PED), PAGE for rotavirus | |
| Bacteria | ||
| Enterotoxigenic E. coli | Common disease of newborn, 3-week-old and weaned piglets. Outbreaks. Colostral immune status important | |
| Salmonella spp. | All ages. Most common in feeder pigs | Acute septicemia or chronic diarrhea. Responds to early treatment. Culture and serotyping |
| Clostridium perfringens type C | Newborn piglets. High mortality | Acute and peracute hemorrhagic enterotoxemia. Toxin demonstration and culture |
| Clostridium perfringens type A | Slightly older pigs, first week of life, lower mortality | As above |
| Clostridium difficile | Diarrhea in preweaned pigs | Smears of colon wall, culture, FAT, PCR |
| Brachyspira hyodysenteriae (swine dysentery) | Usually feeder pigs. Outbreaks common | |
| Lawsonia intracellularis (PIA, PHE) | Growing and mature pigs. Outbreaks common | Acute dysentery and death. MZN on mucosal smears, PCR, silver-stained sections |
| Brachyspira pilosicoli | Usually weaned pigs | PCR |
| Protozoa | ||
| Isospora spp. | Newborn piglets 5–14 days of age. High morbidity, low mortality | Acute diarrhea. Poor response to therapy with amprolium. |
| Fecal examination for oocysts | ||
| Other species (Eimeria) | In older pigs | Histology of gut sections |
| Parasites | ||
| Ascaris suum and A. lumbricoides | Mild diarrhea for few days. Worm egg count | |
| Trichuris suis | Diarrhea, dysentery and loss of weight. Fecal examination and gross pathology | |
| Nutritional deficiency | ||
| Iron deficiency | Young piglets 6–8 weeks. Not common in well managed swine herds | Mild diarrhea and anemia |
ELISA, enzyme-linked immunoassay; EM, electron micrograph; FATs, fluorescence antibody transfer; MZN, Modified ziehl-neilson; PAGE, Poly acrylamide get electrophoresis; PCR, polymerase chain reaction; PED, Porcine epidemic diarrhea.
Table 5.15 Epidemiological and clinical features of the diseases of sheep and goats in which diarrhea is a significant clinical finding
| Etiological agent or disease | Age and class of animal affected and important epidemiological factors | Major clinical findings and diagnostic criteria |
|---|---|---|
| Bacteria | ||
| Enterotoxigenic Escherichia coli (colibacillosis) | ||
| Clostridium perfringens type B (lamb dysentery) | Newborn lambs up to 10 days of age. Overcrowded lambing sheds | Sudden death, diarrhea, dysentery, toxemia. Fecal smear |
| Clostridium perfringens type D (enterotoxemia) | Adult lactating does | Peracute, acute and chronic forms occur. Enterocolitis. Watery diarrhea with feces containing blood and mucus, weakness, abdominal colic |
| Salmonella spp. | Newborn lambs. Adult sheep in pregnancy | Acute diarrhea and dysentery in lambs. Acute toxemia, diarrhea in ewes followed by abortion. Fecal culture and pathology |
| Mycobacterium paratuberculosis | Mature sheep and goats; several animals may be affected | Loss of weight, chronic diarrhea, long course, no response to therapy. Serological tests |
| Viruses | ||
| Rotavirus and coronavirus | Newborn lambs. Many lambs affected | Acute profuse watery diarrhea. No toxemia. Usually recover spontaneously if no secondary complications. Virus isolation |
| Parasites | ||
| Nematodirus spp. | Anorexia, diarrhea, thirsty, 10–20% of lambs may die if not treated. Fecal examination | |
| Ostertagia spp. | Lambs 10 weeks of age and older lambs and young ewes on grass. Types I and II | Many lambs develop diarrhea, weight loss. Abomasitis |
| Trichostrongylus spp. | Older lambs 4–9 months of age | Dull, anorexic, loss of weight and chronic diarrhea. Fecal examination |
| Protozoa | ||
| Eimeria spp. | Overstocking on pasture and overcrowding indoors, poor sanitation and hygiene. Commonly occurs following weaning and introduction into feedlot | |
| Cryptosporidium | Lambs 7–10 days of age | Dullness, anorexia, afebrile, diarrhea, may die in 2–3 days, survivors may be unthrifty. Examination of feces and intestinal mucosa. No specific treatment |
The salient epidemiological characteristics and clinical findings of the diseases in which diarrhea, due to enteritis or malabsorption, is a principal clinical finding in each species are summarized by species in Tables 5.12-5.15 There are many other diseases in which diarrhea may be present but in which it is only of minor importance.
Under normal conditions, a large quantity of fluid enters the small intestine from the saliva, stomach, pancreas, liver and intestinal mucosa. This fluid and its electrolytes and other nutrients must be absorbed, mainly by the small intestines, although large quantities move into the large intestine for digestion and absorption, especially in the horse. The brush border membrane of the villous epithelial cells is of paramount importance for the absorption of water, electrolytes and nutrients.
Details of the physiology and pathophysiology of epithelial secretion in the gastrointestinal tract are becoming clear, leading to new models of the mechanisms underlying diarrhea.1 The enteric nervous system is a critical component of the mechanism regulating fluid secretion in the normal intestine and a key element in the pathophysiology of diarrhea. Neural reflex pathways increase epithelial fluid secretion in response to several enteric pathogens of veterinary importance such as Salmonella spp., Cryptosporidium parvum, rotavirus and C. difficile. The enteric nervous system also has an important role in epithelial secretion triggered by products of activated leukocytes during inflammation.
Any dysfunction of the intestines will result in failure of adequate absorption and diarrhea. Depending on the causative agent, intestinal malabsorption may be the result of at least four different mechanisms:
There may be an osmotic effect when substances within the lumen of the intestine increase the osmotic pressure over a greater than normal length of intestine, resulting in an osmotic movement of an excessive amount of fluid into the lumen of the intestine. The fluid is not reabsorbed and accumulates in the lumen. Examples include saline purgatives, overfeeding, indigestible feeds and disaccharidase deficiencies. A deficiency of a disaccharidase leads to incomplete digestion and the accumulation of large quantities of undigested material, which acts as a hypertonic solution.
Malabsorption is associated with several epitheliotropic viruses that affect the villous absorptive cells, causing a disaccharidase deficiency. Examples include the TGE (transmissible gastroenteritis) virus in newborn piglets, and rotavirus and coronavirus infections in newborn calves and other species. The usual pathogenetic sequence of events is selective destruction of villous absorptive cells, villous atrophy, loss of digestive and absorptive capacities (malabsorption), diarrhea, crypt hyperplasia and recovery. Recovery depends on the severity of the lesion, the relative injury done to the villous cells and crypt epithelium, and the age of the animal. Newborn piglets affected with TGE commonly die of dehydration and starvation before there is sufficient time for regeneration of the villous cells from the crypt epithelium. In contrast, older pigs have greater capacity for regeneration of the villous cells and the diarrhea may be only transient.
Acute or chronic inflammation or necrosis of the intestinal mucosa results in a net increase in fluid production, inflammatory products, including loss of serum proteins, and a reduction in absorption of fluids and electrolytes. Examples include many of the diseases associated with bacteria, viruses, fungi, protozoa, chemical agents and tumors that are summarized in Tables 5.12-5.15 The classic example is enteric salmonellosis, in which there is severe inflammation with the production of fibrinous, hemorrhagic enteritis. Other notable examples include swine dysentery, bovine virus diarrhea and inorganic arsenic poisoning.
A secretory–absorptive imbalance results in a large net increase in fluid secretion with little if any structural change in the mucosal cells. The enterotoxin elaborated by enterotoxigenic E. coli results in intestinal hypersecretion. The villi, along with their digestive and absorptive capabilities, remain intact. The crypts also remain intact; however, their secretion is increased beyond the absorptive capacity of the intestines, resulting in diarrhea. The increased secretion is due to an increase in cyclic adenosine monophosphate, which in turn may be stimulated by prostaglandins. The integrity of the mucosal structure is maintained and the secreted fluid is isotonic, electrolyte-rich, alkaline and free of exudates. This is useful diagnostically in enterotoxic colibacillosis.
An important therapeutic principle can be applied in secretory diarrhea disease. Whenever possible, because of the cost of parenteral fluid therapy, fluids and electrolytes should be given orally. The mucosa remains relatively intact and retains normal absorptive capacity. Fluid replacement solutions containing water, glucose and amino acids can be given orally and are absorbed efficiently. Glucose and amino acids enhance the absorption of sodium and water, thus replacing or diminishing fluid and electrolyte losses.
There is also evidence that active electrolyte secretion occurs in enterocolitis due to salmonellosis in several species of animal. In diseases such as swine dysentery, the permeability of the colon may remain normal or even decrease, but the absorption of water and electrolytes is decreased. This suggests that the primary cause of fluid and electrolyte loss in some diseases of the colon may be failure of the affected epithelium to absorb fluids and electrolytes.
Hyperexcitability, convulsions and the stress of unexpected sudden confinement may result in diarrhea, which may be due to increased peristalsis, resulting in ‘intestinal hurry’ and reduced intestinal absorption due to rapid passage of intestinal fluids in an otherwise normal intestine. This can occur in animals that are being assembled for transportation and during transportation.
The location of the lesion in the intestinal tract may also influence the severity of the enteritis or malabsorption. Lesions involving the small intestine are considered to be more acute and severe than those in the large intestine because approximately 75–80% of the intestinal fluids are absorbed by the small intestine and much lesser quantities by the large intestine. Thus, in general, when lesions of the large intestine predominate, the fluid and electrolyte losses are not as acute nor as severe as when the lesions of the small intestine predominate. However, the horse is an exception. The total amount of fluid entering the large intestine from the small intestine, plus the amount entering from the mucosa of the large intestine, is equal to the animal’s total extracellular fluid volume, and 95% of this is reabsorbed by the large intestine. This illustrates the major importance of the large intestine of the horse in absorbing a large quantity of fluid originating from saliva, the stomach, liver, pancreas, small intestine and large intestine. Any significant dysfunction of the absorptive mechanism of the large intestine of the horse results in large losses of fluids and electrolytes. This may explain the rapid dehydration and circulatory collapse that occurs in horses with colitis-X. Moderate to severe ulcerative colitis of the right dorsal colon in horses treated with phenylbutazone results in marked dehydration, endotoxic shock and death.2
The net effect of an increase in the total amount of fluid in the intestinal lumen and a reduction in intestinal absorption is a loss of fluids and electrolytes at the expense of body fluids and electrolytes and the normal intestinal juices. The fluid that is lost consists primarily of water, the electrolytes sodium, chloride, potassium and bicarbonate, and varying quantities of protein. Protein is lost (protein-losing enteropathy) in both acute and chronic inflammation, leading to hypoproteinemia in some cases. The loss of bicarbonate results in metabolic acidosis, which is of major importance in acute diarrhea. The loss of sodium, chloride and potassium results in serum electrolyte imbalances. In the horse with enteric salmonellosis, there is severe dehydration and marked hyponatremia. In the calf with neonatal diarrhea there are varying degrees of dehydration and a moderate loss of all electrolytes. With acute severe diarrhea, there is severe acidosis and reduced circulating blood volume, resulting in reduced perfusion of the liver and kidney and of peripheral tissues. This results in uremia, anaerobic oxidation and lactic acidosis, which accentuates the metabolic acidosis. Hyperventilation occurs in some animals in an attempt to compensate for the acidosis.
In acute diarrhea, large quantities of intestinal fluid are lost in the feces and large quantities are present in the intestinal lumen (intraluminal dehydration), which accounts for the remarkable clinical dehydration in some affected animals. The fluid moves out of the intravascular compartment first, then out of the extravascular compartment (interstitial spaces), followed lastly by fluid from the intracellular space. Thus in acute diarrhea of sudden onset the actual degree of dehydration present initially may be much more severe than is recognizable clinically; as the diarrhea continues, the degree of clinical dehydration becomes much more evident.
In chronic enteritis, as a sequel to acute enteritis or developing insidiously, the intestinal wall becomes thickened and mucus secretion is stimulated, the absorption of intestinal fluids is also decreased but not of the same magnitude as in acute enteritis. In chronic enteritis there is a negative nutrient balance because of decreased digestion of nutrients and decreased absorption, resulting in body wasting. The animal may continue to drink and maintain almost normal hydration. In some cases of chronic enteritis, depending on the cause, there is continuous loss of protein, leading to clinical hypoproteinemia. Intestinal helminthiasis of all species, Johne’s disease of ruminants, and chronic diarrheas of the horse are examples. Lymphocytic plasmacytic enteritis causing chronic weight loss occurs in the horse.3
Regional ileitis is a functional obstruction of the lower ileum associated with granulation tissue proliferation in the lamina propria and submucosa, with or without ulceration of the mucosa, and a massive muscular hypertrophy of the wall of affected areas of the intestine. It has been recognized with increased frequency in recent years in pigs, horses and lambs. The lesion undoubtedly interferes with normal digestion and absorption but diarrhea is not a common clinical finding.
The villous absorptive epithelial cells of the small intestine are involved in almost every type of enteritis or malabsorptive syndrome. These cells that line the villi and face the lumen of the intestine contain important digestive enzymes such as the disaccharidases. They are also involved in absorption of fluids, electrolytes, monosaccharides such as glucose, and amino acids, and in the transport of fat micelles. Their replacement time is up to several days in the newborn calf and piglet, and only a few days when these animals are older (at 3 weeks). This may explain the relatively greater susceptibility of the newborn to the viral enteritides, such as TGE in piglets and rotavirus infection in all newborn farm animal species. Almost any noxious influence can increase the rate of extrusion of these cells, which are then replaced by cells that are immature and not fully functional. The villi become shortened (villous atrophy) and chronic malabsorption similar to the ‘sprue gut’ of humans may be the result. The destruction of villous epithelial cells explains the long recovery period of several days in some animals with acute enteritis and the chronic diarrhea in others with chronic villous atrophy.
The literature on the mechanisms of intestinal mucosal repair has been reviewed.4
Neutrophils are critical elements of the cascade of events that culminates in mucosal injury in many inflammatory diseases of the gastrointestinal tract, including ischemia and reperfusion injury.5 Neutrophils mediate their detrimental actions by several mechanisms, especially physical disruption of the epithelium. These findings have resulted in consideration of strategies to attenuate neutrophil-mediated mucosal injury by preventing neutrophil transendothelial migration into the intestinal mucosa and subsequent activation during inflammation. Newer pharmacological drugs that inhibit beta-2-integrin activation, and therefore beta 2-integrin function, may be useful clinically to inhibit neutrophil-mediated injury during inflammation.5
The motility of the intestinal tract in animals with enteritis has not been sufficiently examined and little information is available. It was thought for many years that intestinal hypermotility, and increased frequency and amplitude of peristalsis, was present in most enteritides as a response to the enteritis and that the hypermotility accounted for the reduced absorption. However, when the pathogenesis of the infectious enteritides is considered, for example the unique secretory effect of enterotoxin, it seems more likely that, if hypermotility is present, it is a response to the distension of the intestinal lumen with fluid rather than a response to irritation. With a fluid-filled intestinal lumen, very little intestinal peristalsis would be necessary to move large quantities of fluid down the intestinal tract. This may explain the fluid-rushing sounds that are audible on auscultation of the abdomen in animals with enteritis. It is possible that the intestines may be in a state of relative hypomotility rather than hypermotility, which makes the use of antimotility drugs for the treatment of enteritis questionable.
Gastritis commonly accompanies enteritis but does not cause vomition except perhaps in the pig. Gastritis (or abomasitis) may also be the primary lesion, resulting in a profuse diarrhea without lesions of the intestines. Examples are ostertagiasis and abomasal ulceration in cattle. Presumably the excessive amount of fluid secreted into the affected abomasum cannot be reabsorbed by the intestines.
Enteritis may alter the pharmacodynamics of orally administered drugs. In acute diarrheal states there is delayed or impaired absorption, resulting in subtherapeutic plasma concentration. In chronic malabsorption states, decreased, increased or delayed absorption may occur, depending on the drug. Also, gastric antacids, anticholinergic drugs and opiates, administered orally for the treatment of diarrhea, may impair absorption of other drugs by altering solubility or delaying gastric emptying time.
The major clinical finding in enteritis or malabsorption is diarrhea. Dehydration, abdominal pain, septicemia and toxemia with fever occur commonly and their degree of severity depends on the causative agent, the age and species of the animal and the stage of the disease.
In acute enteritis, the feces are soft or fluid in consistency and may have an unpleasant odor. They may contain blood (dysentery), fibrinous casts and mucus or obvious foreign material such as sand. The color of the feces will vary considerably: they are usually pale yellow because of the dilution of the brown bile pigments but almost any color other than the normal is possible and, with the exception of frank blood (hematochezia) or melena (black tarry feces), the color of the feces is usually not representative of a particular disease. When the feces are watery, they may escape notice on clinical examination. Some indication of the nature of the enteritis may be obtained from the distribution of the feces on the animal’s perineum. Thus, in calves, the smudge pattern may suggest coccidiosis when both the staining that accompanies it and the feces are smeared horizontally across the ischial tuberosities and the adjoining tail, or helminth infestation when there is little smearing on the pinbones but the tail and insides of the hocks are liberally coated with feces. Straining may occur, especially in calves, and be followed by rectal prolapse, particularly when the lesions are present in the colon and rectum. Intussusception may occur when the enteritis involves the small intestine.
There are a number of diseases in which dysentery with or without toxemia occurs and death may occur rapidly. These include lamb dysentery, hemorrhagic enterotoxemia of calves, acute swine dysentery and hemorrhagic bowel syndrome of pigs.
Acute intraluminal hemorrhage due to ulceration of unknown etiology in the small intestine has been recorded in adult cows.6 Duodenal ulceration may also occur in cattle in association with left-side displacement of the abomasum.7
The systemic effects in enteritis vary considerably. Septicemia, toxemia and fever are common in the infectious enteritides. An increased body temperature may return to normal following the onset of diarrhea or if circulatory collapse and shock are imminent. Dehydration will vary from being just barely detectable at 4–6% of body weight up to 10–12% of body weight, when it is clinically very evident. The degree of dehydration can be best assessed by tenting the skin of the upper eyelid or neck and determining the time taken for the skin fold to return to normal. The degree of recession of the eyeball is also a useful aid. In the early stages of acute enteritis, the degree of clinical dehydration may be underestimated because of the time required for fluid to shift from the interstitial and intracellular spaces to the intravascular space to replace fluids already lost. Dehydration is usually evident by 10–12 hours following the onset of acute enteritis and clinically obvious by 18–24 hours. Peripheral circulatory collapse (shock) occurs commonly in acute and peracute cases. There may be tachycardia or bradycardia and arrhythmia depending on the degree of acidosis and electrolyte imbalance. In acute enteritis, there may be severe abdominal pain, which is most severe in the horse and is often sufficient in this species to cause rolling and kicking at the abdomen. Abdominal pain in enteritis is unusual in the other species although it does occur in heavy inorganic metal poisonings, such as arsenic and lead, and in acute salmonellosis in cattle. Some severe cases of enteric colibacillosis in calves are characterized by abdominal pain evidenced by intermittent bouts of stretching and kicking at the abdomen. The passage of intestinal gas also occurs commonly in horses with acute and chronic diarrhea.
Auscultation of the abdomen usually reveals sounds of increased peristalsis and fluid-rushing sounds in the early stages of acute enteritis. Later there may be paralytic ileus and an absence of peristaltic sounds with only fluid and gas tinkling sounds. The abdomen may be distended in the early stages because of distension of intestines and gaunt in the later stages when the fluid has been passed out in the feces. Pain may be evidenced on palpation of the abdomen in young animals.
In chronic enteritis, the feces are usually soft and homogeneous in consistency, contain considerable mucus and usually do not have a grossly abnormal odor. Progressive weight loss and emaciation or ‘runting’ are common and there are usually no systemic abnormalities. Animals with chronic enteritis will often drink and absorb sufficient water to maintain clinical hydration but there may be laboratory evidence of dehydration and electrolyte loss. In parasitic enteritis and abomasitis there may be hypoproteinemia and subcutaneous edema. In terminal ileitis, there is usually chronic progressive weight loss and occasionally some mild diarrhea. The lesion is usually recognized only at necropsy. Intestinal adenomatosis of pigs, rectal strictures in pigs, granulomatous enteritis of horses and lymphosarcoma of the intestine of horses are examples of enteric disease causing chronic anorexia and progressive weight loss, usually without clinical evidence of diarrhea. These are commonly referred to as malabsorption syndromes.
The laboratory testing of animals to obtain an etiological diagnosis of enteritis can be a complex and expensive procedure, which requires careful consideration of the history, the clinical findings and the number of animals affected. In outbreaks of enteric syndromes, it may be important to submit samples from both affected and normal animals. The details of the sampling techniques and the tissues required for the diagnosis of diseases of the digestive tract caused by feeding mismanagement, infections, toxins and other agents have been outlined and this is recommended as a reference.8
Examination of the feces to determine the presence of causative bacteria, helminths, protozoa, viruses and chemical agents is described under specific diseases throughout this book. It is important that fecal specimens be taken as the differentiation of the etiological groups depends on laboratory examinations. In outbreaks of diarrhea, fecal samples should also be taken from a representative number of normal animals in the same group as the affected animals. Comparison of the fecal examination results between affected and normal animals will improve the accuracy of interpretation.
Fecal samples can be examined for the presence of leukocytes and epithelial cells, which occur in exudative enteritis.
In outbreaks of diarrhea, especially in neonates, it may be useful to do necropsies on selected early untreated cases of acute diarrhea. The lesions associated with the enteropathogens are well known and a provisional etiological diagnosis may be possible by gross and histopathological examination of the intestinal mucosa.
With increasing sophistication in diagnostic laboratories and in large-animal practice, it is becoming common to do considerable laboratory evaluation to determine the actual changes that are present, for purposes of a more rational approach to therapy. For each specific enteritis there are changes in the hemogram and serum biochemistry that aid in the diagnosis and differential diagnosis. In bacterial enteritis, such as acute enteric salmonellosis in the horse, there may be marked changes in the total and differential leukocyte count, which is a useful diagnostic aid. In most cases of acute enteritis there is hemoconcentration, metabolic acidosis, an increase in total serum solids concentration, a decrease in plasma bicarbonate, hyponatremia, hypochloremia and hypokalemia. However, abnormalities in body fluid compartments caused by diarrhea depend on the pathogenetic mechanisms involved and the duration of the diarrhea. In horses with diarrhea of less than 6 days’ duration, the most common abnormality may be a combined anion gap, metabolic acidosis and metabolic alkalosis characterized by hyponatremia, hypochloremia and hyperkalemia. The acid–base imbalances may vary considerably from case to case and it is suggested that optimal fluid therapy should be based on laboratory evaluation of the animal’s blood gas and electrolytes. Hyperkalemia may occur in severe acidosis. An increase in serum creatinine may be due to inadequate renal perfusion associated with the dehydration and circulatory failure.
Digestion and absorption tests are available for the investigation of chronic malabsorptive conditions, particularly in the horse. Intestinal biopsy may be necessary for a definitive diagnosis of chronic intestinal lesions that cannot be determined by the usual diagnostic tests. Examples include intestinal lymphosarcoma, granulomatous enteritis and perhaps Johne’s disease. Serum electrophoresis and the administration of radioactively labeled albumin may be necessary to determine the presence of a protein-losing enteropathy.
The pathology of enteritis or malabsorption varies considerably depending on the cause. There may be an absence of grossly visible changes of the mucosa but the intestinal lumen will be fluid-filled or relatively empty, depending on the stage of examination in enterotoxigenic colibacillosis. When there is gross evidence of inflammation of the mucosa there will be varying degrees of edema, hyperemia, hemorrhage, foul-smelling intestinal contents, fibrinous inflammation, ulceration and necrosis of the mucosa. With acute necrosis there is evidence of frank blood, fibrinous casts and epithelial shreds. The mesenteric lymph nodes show varying degrees of enlargement, edema and congestion, and secondary involvement of spleen and liver is not unusual. In chronic enteritis, the epithelium may appear relatively normal but the wall is usually thickened and may be edematous. In some specific diseases there are lesions typical of the particular disease.
• The approach to the diagnosis of diarrhea requires a consideration of the epidemiological history and the nature and severity of the clinical findings. With the exception of the acute enteritides in newborn farm animals, most of the other common enteritides have reasonably distinct epidemiological and clinical features
• In some cases, a necropsy on an untreated case of diarrhea in the early stages of the disease can be very useful
• If possible, a hemogram should be obtained to assist in determining the presence or absence of infection
• The gross appearance of the feces may provide some clues about the cause of the diarrhea. In general, the diarrheas caused by lesions of the small intestine are profuse and the feces are liquid and sometimes as clear as water. The diarrheas associated with lesions of the large intestine are characterized by small volumes of soft feces, often containing excess quantities of mucus
• The presence of toxemia and fever-marked changes in the total and differential leukocyte count suggest bacterial enteritis, possibly with septicemia. This is of particular importance in horses and cattle with salmonellosis
• The presence of frank blood and/or fibrinous casts in the feces usually indicates a severe inflammatory lesion of the intestines. In sand-induced diarrhea in horses the feces may contain sand
• A chronic diarrhea with a history of chronic weight loss in a mature cow suggests Johne’s disease
• Chronic weight loss and chronic diarrhea, or even the absence of diarrhea, in the horse may indicate the presence of granulomatous enteritis, chronic eosinophilic gastroenteritis, alimentary lymphosarcoma, tuberculosis and histoplasmosis
• In dietary diarrhea the feces are usually voluminous, soft and odoriferous, the animal is usually bright and alert and there are minimal systemic effects. An examination of the diet will usually reveal if the composition of the diet or irregular feeding practices are responsible for the diarrhea. Analysis of samples of new feed may be necessary to determine the presence of toxic chemical agents
• Arsenic poisoning is characterized by dysentery, toxemia, normal temperature and nervous signs
• Copper deficiency conditioned by an excess of molybdenum causes a moderately profuse diarrhea with soft feces, moderate weight loss and there is usually normal hydration and possibly depigmentation of hair
• In cattle, the oral cavity must be examined for evidence of lesions characteristic of viral diseases
• Many diseases of the stomach, including ulceration, parasitism, gastritis and tumors, may result in diarrhea and must be considered in the differential diagnosis of chronic diarrhea
• The soft scant feces associated with some cases of incomplete obstruction of the digestive tract of cattle affected with the complications of traumatic reticuloperitonitis must not be confused with diarrhea
The principles of treatment of enteritis are:
Specific treatment is usually directed at intestinal helminthiasis with anthelmintics, antiprotozoan agents against diseases such as coccidiosis and antimicrobial agents against the bacterial enteritides. There are no specific treatments available for the viral enteritides in farm animals.
While considerable investigations have been done on the enteritides on farm animals, the emphasis has been on the immunology, pathology, microbiology and body fluid dynamics, each with different emphasis in different species. For example, there is considerable information on the microbiology and immunology of the common enteritides in calves and piglets in addition to the extensive knowledge of the body fluid dynamics in calves. In the horse there is some information on body fluid dynamics but the microbiology of the diarrheas is not well understood. In none of the species is there sufficient information on the effects of antibiotics on the intestinal microflora.
The use of antimicrobials, either orally or parenterally, or by both routes simultaneously, for the treatment of bacterial enteritides is a controversial subject in both human and veterinary medicine. Those who support their use in acute bacterial enteritis claim that they are necessary to help reduce the overgrowth of pathogenic bacteria responsible for the enteritis and to prevent or treat bacteremia or septicemia that may occur secondary to an enteritis. Those who suggest that they are contraindicated or unnecessary in bacterial enteritis suggest that the drugs may eliminate a significant proportion of the intestinal flora in addition to the pathogenic flora. This may reduce the effect of competitive antagonism in the intestine, which in turn may permit the development of a superinfection (the appearance of bacteriological and clinical evidence of a new infection during the chemotherapy of a primary one). Also, the use of antimicrobials in infectious enteric disease allows the development of multiple drug resistance, which is a major public health concern. The use of antimicrobials may also increase the length of time over which affected animals excrete the organisms which, for example, may occur in enteric salmonellosis.
Many different antimicrobial preparations for both oral and parenteral administration are available. The choice will depend on previous experience, the disease suspected and the results of culture and drug sensitivity tests. Parenteral preparations are indicated in animals with acute diarrhea, toxemia and fever. Many antimicrobials, when given parenterally, are excreted by the liver into the lumen of the intestine and oral preparations may not be necessary. In cases of subacute diarrhea with minimal systemic effects, the use of an oral preparation may be sufficient. However, oral preparations should not be used for more than 3 days to avoid a superinfection. The preparations and doses of the antimicrobials commonly used in bacterial enteritides are described under each disease.
Mass medication of the drinking water supply with antimicrobials for the treatment of outbreaks of specific infectious enteritides in animals is used commonly and with success. One of the best examples is the use of antimicrobials in the drinking water of pigs affected with swine dysentery. However, not all affected animals will drink a sufficient quantity of the medicated water and daily intake must be monitored carefully. Severely affected animals in an outbreak need individual treatment.
If the cause of the diarrhea is dietary in origin the feed should be removed until the animal has fully recovered; feed should then be replaced by another source or reintroduced gradually. The question of whether or not a normally digestible diet should be removed temporarily or the total daily intake reduced in animals with acute enteritis is a difficult one. The rationale is that in acute enteritis the digestibility of nutrients is reduced considerably and undigested feed provides a substrate for fermentation and putrefaction to occur, the products of which may accentuate the malabsorptive state. However, temporary withdrawal of feed presents practical problems, especially in the young. For example, the temporary removal from the sow of newborn piglets affected with acute enteritis presents practical problems and is of doubtful value; similarly with beef calves nursing cows on pasture. With foals it is relatively easy to muzzle them for 24 hours. With weaned piglets affected with weanling diarrhea and feeder pigs with swine dysentery, it is common practice to reduce the normal daily intake by half for a few days until recovery is apparent. Mature horses affected with diarrhea should not have access to any feed for at least 24 hours. During the period of temporary starvation, the oral intake of fluids containing glucose and electrolytes is desirable and necessary to assist in maintaining hydration. In newborn calves with diarrhea, if oral fluid intake is maintained, the total loss of water from feces and through the kidney is not significantly greater than in normal calves because in diarrheic calves the kidney will effectively compensate for fecal losses. When recovery is apparent, the animal’s usual diet may be reintroduced gradually over a period of a few days.
The initial goals of fluid and electrolyte therapy for the effects of enteritis are: the restoration of the body fluids to normal volume, effective osmolality, composition and acid–base balance. The quality and quantity of fluids required to achieve these goals depend on the characteristics of the dehydration and acid–base electrolyte imbalance. Under ideal conditions when a laboratory is available, the determination of packed cell volume, total serum proteins, plasma bicarbonate, blood pH, serum electrolytes and a hemogram would provide the clinician with a laboratory evaluation initially and throughout the course of therapy, to assess the effectiveness of the treatment. However, such laboratory service is expensive and usually not readily available. The clinician must therefore assess the degree of clinical dehydration and, based on the history and clinical findings, estimate the degree of acidosis and electrolyte deficits that are likely to be present. A practical approach to fluid therapy in the horse has been described. Fluids should be given orally whenever possible to save time and expense and to avoid the complications that can arise from long-term parenteral fluid therapy. Also, fluids should be given as early as possible to minimize the degree of dehydration. With good kidney function there is a wider safe latitude in the solution used.
The three major abnormalities of dehydration, acidosis and electrolyte deficit are usually corrected simultaneously with fluid therapy. When severe acidosis is suspected, this should be corrected immediately with a hypertonic (5%) solution of bicarbonate given intravenously at the rate of 5–7 mL/kg BW at a speed of about 100 mL/min. This is followed by the administration of electrolyte solutions in quantities necessary to correct the dehydration. With severe dehydration, equivalent to 10% of BW, large amounts of fluids are necessary.
| Animal | Dehydration (%) | Fluid deficit (L) |
|---|---|---|
| 500 kg horse | 10 | 50 |
| 75 kg foal | 10 | 7.5 |
| 45 kg calf | 10 | 4.5 |
The initial hydration therapy should be given over the first 4–6 hours by continuous intravenous infusion, followed by maintenance therapy for the next 20–24 hours, or for the duration of the diarrhea if severe, at a rate of 100–150 mL/kg BW/24 h. Horses with acute enteritis have severe hyponatremia and following fluid therapy may become severely hypokalemic, as evidenced by weakness and muscular tremors. The hypertonic solution of sodium bicarbonate will assist in correcting the hyponatremia but potassium chloride may need to be added to the large quantity of fluids given for dehydration; 1 g of potassium chloride added to each liter of fluid will provide an additional 14 mosmol/L (14 mmol/L) of potassium. In preruminant calves with diarrhea, the fluids and electrolytes required for maintenance may be given orally in divided doses every few hours. In the early stage of acute diarrhea and for animals that are not severely dehydrated, the oral route can also be used successfully to correct dehydration and prevent it from becoming worse. The formulae of oral glucose–electrolyte solutions are given in the section under colibacillosis. Piglets and lambs affected with dehydration are most effectively treated using balanced electrolyte solutions given subcutaneously at the dose rates of 20 mL/kg BW every 4 hours and orally at 20 mL/kg BW every 2 hours. Details of the treatment of fluid and electrolyte disturbances are given under that heading in Chapter 2.
Kaolin and pectin mixtures are used widely to coat the intestinal mucosa, inhibit secretions and increase the bulk of the feces in animals with enteritis. In children with diarrhea, kaolin and pectin will result in formed rather than watery feces, but the water content of the feces is unchanged. It is not possible at this time to make a recommendation on their use in animals.
Anticholinergic drugs and opiates are available to decrease intestinal motility. The anticholinergic drugs block the action of acetylcholine on smooth muscle and glands. This results in decreased gastric secretion and emptying and a reduction on both segmental and propulsive movements of the intestines. Dosages of anticholinergics necessary to produce effectiveness may also cause side effects such as xerostomia, photophobia, tachycardia, urinary retention and neuromuscular paralysis. The opiates function by producing an increase in segmentation while reducing propulsive movements in the intestine. The net effect is an increase in resistance to passage of intestinal contents and more complete absorption of both water and nutrients occurs with a subsequent decrease in the frequency of defecation. There are no published reports of clinical trials using antimotility drugs for the treatment of diarrhea in farm animals and at the present time, therefore, they cannot be recommended with any assurance of effectiveness.
Antisecretory drugs are also available for the treatment of diarrhea due to the hypersecretory activity of enterotoxin produced by bacteria such as enterotoxigenic E. coli. Loperamide hydrochloride given orally to calves with experimentally induced diarrhea can delay the onset of diarrhea by its inhibition of fluid secretion. Antisecretory drugs include chlorpromazine, opiates, atropine and prostaglandin inhibitors. These have not yet been adequately evaluated and the provision of balanced fluids and electrolytes, containing sodium chloride, sodium bicarbonate, potassium chloride and glucose, given both parenterally and orally, are considered to be adequate and effective for treating the effects of the hypersecretion.
Because prostaglandins have an important reparative role in the intestine, NSAIDs may retard recovery of ischemic-injured intestine and are contraindicated.9
The control and prevention of enteritis in farm animals is a major topic and activity of large-animal practice. The control of each specific enteritis is presented under each specific disease in Part II of this book. The principles of control include the following:
• Reduce infection pressure by controlling population density
• Ensure adequate nonspecific resistance by adequate colostrum intake of neonatal farm animals and maintaining adequate nutritional status
• Vaccinate for those diseases for which there is an effective vaccine
• Minimize managemental and environmental stressors
• Monitor morbidity and mortality and ensure that a diagnosis is obtained so that control measures for newly introduced diseases into a herd can be instituted.
Blikslager AT, Roberts MC. Mechanisms of intestinal mucosal repair. J Am Vet Med Assoc. 1997;211:1437-1441.
Blanchard PC. Sampling techniques for the diagnosis of digestive disease. Vet Clin North Am Food Anim Pract. 2000;16:23-36.
Waters WR. Immunology of inflammatory diseases of the bowel. Vet Clin North Am Food Anim Pract. 2001;17:517-534.
Jones SL, Blikslager AT. Role of the enteric nervous system in the pathophysiology of secretory diarrhea. J Vet Intern Med. 2002;16:222-228.
Tomlinson J, Blikslager A. Role of nonsteroidal anti-inflammatory drugs in gastrointestinal tract injury and repair. J Am Vet Med Assoc. 2003;222:946-951.
1 Jones SL, Blikslager T. J Vet Intern Med. 2002;16:222.
2 Karcher LF, et al. J Vet Intern Med. 1990;4:247.
3 MacAllister CG, et al. J Am Vet Med Assoc. 1990;196:1995.
4 Blikslager AT, Roberts MC. J Am Vet Med Assoc. 1997;211:1437.
5 Gayle JM, et al. J Am Vet Med Assoc. 2000;217:498.
6 Ruggles AJ, et al. Cornell Vet. 1992;82:181.
7 West HJ, Baker JR. Vet Rec. 1991;129:196.
8 Blanchard PC. Vet Clin North Am Food Anim Pract. 2000;16:23.
9 Tomlinson J, Blikslager A. J Am Vet Med Assoc. 2003;222:946.