Diarrhoea is the passage of fluid faeces. The immediate cause is generally an excess of fluid entering the intestinal tract, inability of the intestinal tract to absorb all of the fluid in the lumen, increased contractility of the intestines which reduces time for absorption to occur, or increased fluid secretion from the gut wall into the lumen.
Failure to absorb fluid may be caused by excess food material escaping from the small bowel to the large bowel and attracting water, as occurs with carbohydrate overload (ruminal acidosis). Atrophy or erosion of the large intestinal epithelium may also inhibit normal absorptive capacity.
Diarrhoea also commonly results from inflammation of the bowel that results in leakage or increased secretion of fluid from the bowel wall to the gut lumen. The main causes of inflammation are bacteria, protozoa or gastrointestinal worms.
The most likely causes of diarrhoea in the live export process include:
Diarrhoea may be accompanied by abdominal pain, tenesmus (straining), dehydration, loss of body condition and heavy faecal contamination of hindquarters depending on cause and severity. Speed of onset, the numbers affected, and the feeding conditions should be taken into account when determining the cause. See sections on specific diseases for more information.
Specimens from live animals for laboratory differentiation include chilled faeces for bacteriology, virology and parasitology, and serum for virology. Specimens from dead animals should additionally include sections of abdominal viscera chilled for bacteriology, and in buffered formalin for histology.
Because of the potential for acidosis to occur in export animals, it is advisable to have test strips readily available for measuring pH of rumen fluid. Acidosis should be suspected if the pH is less than 5.5 (normal levels are >5.9).
Non-specific therapy for diarrhoea is based on ensuring access to plentiful clean water and providing fluid therapy (oral or intravenous) with electrolytes if necessary. Non-steroidal anti-inflammatory drugs may be useful if animals are febrile and also to counteract potential effects of endotoxin production associated with infectious enteritis. Replacing grain or concentrate diets with roughage (chaff or hay) helps to restore or maintain appetite and restore normal digestive function.
Additional medications may be appropriate depending on cause and clinical signs.
Dietary change to reduce concentrate and increase roughage is important if diet is thought to be contributing to diarrhoea. Alkinising agents may be administered for rumen acidosis, and anthelmintics if parasitism is suspected.
The use of antibiotics in ruminants with diarrhoea is widespread but may not be very efficacious. Oral antibtiotics are not recommended because they may disrupt normal populations of bacteria in the gastrointestinal tract and increase the risk of proliferation of pathogenic bacteria. Systemic administration of broad-spectrum antibiotics may be helpful in animals that are systemically ill and where septicaemia may be suspected.
Choice of preventative measures is dictated by the diagnosis and risk factors predisposing to the current disease event.
Options available in the live export process include providing adequate dietary fibre, changing diets incrementally, reducing faecal contamination of feed and water, and minimising stress. Ionophores such as monensin and lasalocid can be added to diets to prevent coccidiosis.
Pre-export testing and animal selection may reduce the risk of some diseases that cause diarrhoea such as Johne's disease and bovine virus diarrhoea virus. Vaccines are available to protect against bovine virus diarrhoea virus and salmonellosis.