Many primary bacterial enteropathogens have been implicated as a cause of gastrointestinal disease in dogs. In clinical practice it can be difficult to prove that they are actually causing the enteropathy, since many of these bacteria occur as a normal component of the indigenous intestinal flora. Routine faecal culture, the method most commonly used to identify enteropathogens, is therefore limited by the difficulty in interpreting the results. In vitro methods applying molecular approaches for identification of toxic genes from bacterial isolates are a promising alternative to provide a more accurate diagnosis. This is especially true for E. coli, which is a major component of the intestinal flora and commonly present in the faeces.

Regulation of Gastrointestinal Bacteria

The normal regulation of the gastrointestinal microflora depends on complex interactions between host and microbial factors. These factors are also important in preventing transient pathogenic bacteria from colonising the bowel. Bowel colonisation is necessary for such bacteria to become truly pathogenic.

Host factors include peristaltic activity, which sweeps the gut, supported by the antibacterial activities of gastric acid, bile and pancreatic juice. Protection at the mucosal surface consists of the epithelial barrier and its covering of secretory immunoglobulins (particularly IgA) which entrap bacteria. Cellular responses in the lamina propria can finally help to eliminate microorganisms that have penetrated the epithelial barrier.

Microbial interactions also play an important role, favouring only the growth of the normal microflora. These include the production of bactericidal agents by the normal flora and competition between bacteria depleting nutrients that are essential for the growth of some microorganisms.

A change in any of these homeostatic mechanisms can cause sufficient disruption of the normal microflora and/or local immune system to allow for colonisation by pathogenic bacteria, leading to signs of disease.

Properties of Bacterial Enteropathogens

Pathogenic enteric bacteria are disseminated in faeces from infected animals and are most likely to be acquired by consuming contaminated food or water. Their survival time varies significantly, which contributes to the likelihood of acquiring infections. Campylobacter can survive for days in surface water and as long as 4 weeks in faeces; in addition, the duration of excretion in infected dogs and cats can be as long as 4 months. Salmonellae can also survive for prolonged periods outside the host, especially in aquatic environments; shedding may continue for 3 to 6 weeks, and can be reactivated at a later date by any intercurrent stress.

Once access to the gastrointestinal tract has been achieved they have to survive the natural host defences and compete with the established non-pathogenic flora in order to become established. Colonisation factors are an important component of pathogenicity and include flagellae, adherence factors and enzymes. Enteropathogens are also distinguished by virulence factors that enable them to cause primary intestinal damage, such as invasion, secretion of cytotoxins or enterotoxins, and resistance to phagocytosis.

Invasive bacteria, including Salmonella sp., Campylobacter sp and enteroinvasive E. coli (EIEC), can invade the mucosa of the distal small bowel and colon causing acute enterocolitis. This is typically manifest as diarrhoea accompanied by passage of blood and mucus, and may result in a potentially fatal septicemia if the organisms penetrate the intestinal barrier.

Cytotoxins are secreted by enteric pathogens including enterohaemorrhagic E. coli (EHEC), cytotoxic necrotising factor (CNF)-secreting E. coli and Clostridium perfringens. Cytotoxins are lethal to intestinal epithelial cells, causing haemorrhage and ulceration, potentially mimicking the severe enterocolitis caused by invasive bacteria.

Enterotoxins do not cause intestinal damage, but have a specific biochemical effect. They are secreted for example by enterotoxigenic E. coli (ETEC) and act as secretagogues resulting in a watery electrolyte-rich diarrhoea.

Attaching-effacement of microvilli in the small intestine is caused by enteropathogenic E. coli (EPEC) resulting in osmotic diarrhoea due to compromised absorptive function.

Many of these enteric pathogens cause acute clinical disease. However, properties such as adherence to the surface or invasion of the mucosa can promote long-term colonisation by certain enteropathogens, predisposing to chronic disease or carrier status. The outcome depends also on host reaction, particularly the ability to mount an effective immune response.

Diagnosis of Bacterial Enteropathogens

Diagnosis of bacterial intestinal infections cannot just be based on isolation of a potential enteropathogen by faecal culture. The significance of an isolate such as Campylobacter or Salmonella needs to be evaluated in light of the animal's age, immune status, and environmental stresses such as housing conditions and hospitalisation. Faecal cultures tend to be most relevant in animals with a history of bacterial exposure to bacterial pathogens, outbreaks of diarrhoea in more than one animal per household, or onset of diarrhoea after kennelling. Acute onset of bloody diarrhoea in association with evidence of sepsis, or presence of large numbers of faecal neutrophils also warrants faecal culture.

The main enteropathogens that are most commonly identified in dogs are Salmonella sp and Campylobacter sp. These have been clearly associated with acute and chronic disease, typically causing diarrhoea that often contains blood or mucus and is associated with tenesmus. Vomiting, inappetence, malaise, lethargy and abdominal pain are more variably encountered. Salmonellosis in cats may also present as a chronic non-febrile illness without gastrointestinal signs. However, these organisms can also be present in clinically healthy carriers that potentially present a risk to other animals and humans. Active carriers tend to shed organisms continuously or intermittently, while latent carriers shed only when under stress.

Diagnostic evaluation usually includes a baseline laboratory evaluation and faecal analysis for parasites (especially Giardia, coccidian, whip- and hookworms) to detect or exclude other potential causes of diarrhoea. In young or unvaccinated animals with bloody diarrhoea a faecal ELISA test for parvovirus may be submitted. Further tests depend on clinical status. In animals with acute diarrhoea, vomiting and/or abdominal pain these may include determination of amylase and lipase, to detect pancreatitis, and abdominal imaging to help detect partial obstructions, pancreatitis and peritonitis. In dogs with chronic diarrhoea further tests may include measurement of serum TLI, folate and cobalamin, and intestinal biopsy, to detect or rule out non-infectious chronic enteropathies.

A tentative diagnosis of bacterial gastroenteritis usually rests on a positive faecal culture in an animal with appropriate clinical signs. It is important to realise that this may occur in association with underlying or other diseases, which also should be treated.

Identification of genes encoding virulence determinants can contribute particularly to the detection of pathogenic E. coli. There is relatively little information on the prevalence of pathogenic E. coli in dogs, but there is good evidence that they may play a role in the pathogenesis not both acute and chronic diarrhoea in dogs. In common with other enteropathogens, some dogs may act as carriers, and the development of clinical disease may involve environmental factors such as stress and an innate inability to mount an effective mucosal immune response.

Treatment and Prevention of Infection

Treatment of acute cases depends on the severity of the clinical signs. Mild cases need minimal or no treatment, whereas parenteral antibiotic and intensive fluid therapy is indicated in severe cases, particularly when there is evidence of septicaemia or endotoxaemia. Chronic cases can be difficult to manage and this may be due to a number of factors including poor support from a defective host response, antibiotic resistance, failure of antibiotic to reach invasive enteropathogens, or re-infection from the environment.

The use of antibiotics is controversial, particularly in clinically-healthy carriers. The choice may be guided by antibiotic sensitivity testing, but generally the antibiotics of choice for clinical disease and to eliminate carrier status are enrofloxacin for salmonellosis and erythromycin for campylobacteriosis.

The source of infection needs to be identified and effective management procedures to prevent re-infection should be introduced. It is important to realise that approximately 100,000 salmonella, but as few as 500 Campylobacter organisms may be needed to cause clinical disease. Animals that are shedding organisms in the faeces should be kept away from children and immune-compromised people. The zoonotic implications of pathogenic E. coli infection in dogs are not well understood, but infected animals should be considered a potential risk until relevant information to the contrary is available.

Key issues for the future are characterisation of the host response to infection, and the development of effective strategies for the prevention of infection and elimination of chronic colonisation, exploring potential applications of prebiotics, probiotics and vaccination.

References

1.  Batt RM, Rutgers HC, Sancak AA. Enteric bacteria - friend or foe ? J Small Anim Pract 1996;37: 261-267.

2.  Hall EJ, Simpson KW. Diseases of the small intestine. In:Textbook of Veterinary Internal Medicine, 5^th ed., Ettinger SJ and Ettinger EC (eds.). WB Saunders, Philadelphia, 2000. pp 1182-1238

3.  Hart CA, Batt, RM, Saunders JR. Diarrhoea caused by Escherichia coli. Ann Trop Paediat 1993; 13: 121-131.

4.  McDonough PL, Simpson KW. Diagnosing emerging bacterial infections: Salmonellosis, Campyolobacteriosis, Clostridual toxicosis, and Helicobacteriosis. Sem Vet Med Surg 1996; 11:187-197