Intestinal bacteria in dogs

After birth, gastrointestinal is colonised by various micro-organisms. The number of organisms increased from approximately 10²-10⁵ colony forming units (CFU) /ml in proximal small intestine to 10⁵-10⁹ CFU / mI in the distal small intestine, and then increased dramatically in the large intestine to approximately 10¹⁰-10¹¹CFU/ml in colon. This quantitative proximal-distal gradient is accompanied by complex qualitative changes from a predominantly aerobic flora in the small intestine to the large anaerobic flora in the large intestine. There is wide variation in the bacterial flora of normal individuals, and the concentration of May will be affected by various conditions including the environment, diet, scavenging and coprophagia. Increasing the number of bacteria in the small intestine carry an increase risk of damage the outcome. Whether this is a real clinical will depend on individual circumstances, including the composition of the diet that the bacteria can convert to potentially harmful metabolites. Nature of host response to the increased load may also be particularly important, and this May involve stimulation of immunoglobulin and mucus production, suppression of the potential damage to the cell mediated immune response, a compensatory production of structural and functional epithelial cell protein, and increased epithelial cell turnover. Threshold between the real normality and clinical disease in May therefore differ between individuals and is influenced by a complex balance between the microflora and the host. Clinical disease associated with bacterial overgrowth are common problems in dogs and occurs when this balance is tipped against the host.

Primary enteric bacterial pathogens can also cause acute clinical disease since they have the virulence factors that have Adverse effects on the gut. Adherence to the surface or invasion of the mucosa to facilitate long-term colonization by specific enteropathogens, predisposing to the carrier status or chronic disease, the result may depend on expression of virulence determine and host response.

Small intestinal bacterial

Small intestinal bacterial overgrowth (SIBO) is emerging as an important condition in dogs and emphasizes the potentially harmful effects of normal gut flora when the symbiotic relationship with the host is disrupted. This typically presents in young animals as chronic intermittent small bowel diarrhea, which in May accompanied by the loss of body weight or failure to gain weight. SIBO is ii a particular problem in many large breeds of dog, including German shepherd dogs Labradors and Golden retrievers, and colony dog appears to be particularly at risk.

The cause of bacterial

In most cases, it can not be identified, but a host of factors known to be a tendency for bacterial overgrowth, including disability gastric acid secretion, interference with normal motility or stasis, and disabled local immunity. The latter has been implicated in the German shepherd dog with 51,130, because this dog of a low serum and intestinal concentration of immunoglobulin A (Iga) that are important secreted protectant on the surface of the intestine. Other factors, stich as a potential stress or contaminated environment, diet and coprophagia, May also play a role and can contribute to the relatively high number of bacteria reported in kennelled dogs. Damaged as a result of overgrowth can involve competition by bacteria for calories and essential nutrients, production of harmful metabolites, and direct damage to the intestinal mucosa interfere with bowel function. Histological changes in gut biopsies from partial villus atrophy and lymphocyte / plasma cell infiltrate is present in 30% of cases, and in most cases, damage to the mucosa can not be seen by conventional light microscopy.

Diagnosis of bacterial

Diagnosis of SIBO in dogs is difficult and etirrently the assay of serum folate and cobalamin (B12) is the only practical screening test. An increased serum folate or reduced cobalamin concentration can provide indirect evidence of SIBO in dogs, and this has a reasonable specificity, although sensitivity is low. Increased sensitivity was achieved by hydrogen breath test following the oral administration of sugars. These sugars are metabolised by the bacteria present in the proximal small intestine in the SIBO resulted in the increase of breath hydrogen within 2 hours that do not occur in dogs with SIBO. Microbiological culture of duodenal juice obtained endoscopically or at laparotomy is needed to confirm the diagnosis of SIBO, and must show> 10⁵ colony formed units per ml. This is generally a mixture of flora, the most frequent isolates usually including enterococci and E. coli in dogs with aerobic overgrowth, and Clostridia in dogs with anaerobic overgrowth. Faecal culture does not help the diagnosis of overgrowth since the number and type of bacteria present in faeces are dominated by contributions from the large intestine.

Management of bacterial

Treatment with long-term oral broad spectrum antibiotics have proved to be effective, but there is a need for an alternative approach to the chronic management of dogs that relapse when antibiotics are withdrawn. Probiotics can theoretically help, but there are no objective studies that demonstrate efficacy as an approach. The management of SIBO with a low fat diet can help, because this can minimize the secretory diarrhea caused by bacterial metabolism of fatty acid and bile salt. Diet should also contain highly digestible carbohydrate and protein to minimize the availability of substrate for bacteria that will promote their life and can have other unpleasant consequences since intestinal gas is produced. A beneficial role for dietary fiber has not been documented, but it is clear that fiber-containing diets designed for weight reduction should not be used in these dogs that already have a compromised gut function as this could result in sufficient weight loss.

Pathogenic enteric Bacteria

Pathogenic stomach bacteria have colonization factors that encourage them live in the intestine and virulence factors that allow them to cause major intestinal disease. A number of potential enteropathogens were isolated from dogs, most especially Salmonella sp. and Canipylobacter sp. Their clinical importance is not yet fully defined, but clearly that some can cause clinical disease and may also represent zoonotic risk.

Colonization with stomach Pathogens

Pathogenic enteric bacteria are disseminated in the feces of infected animals and is most likely acquired by consuming contaminated food or water. Once access to the gastrointestinal tract has been achieved they then have to survive natural host defenses, including gastric acid, enzymes, mucus and local immunity. They also must compete with established non-pathogenic flora in order to ensure that they were standing on their predilection site. Colonization factors is therefore important component of pathogenicity and May include flagellae, chemotactins, mucinases, and fimbriae are hair-like projections that attach to specific receptors on the surface of the intestinal cells.

Virulence factors and clinical signs

Stomach bacteria cause clinical disease by many different mechanisms that may involve direct interaction with the intestinal mucosa and secretion of cytotoxins or enterotoxins. Various kinds of pathogenic E. coli, which is very popular in other species and emerge as important enteropathogens in dogs, illustrates the spectrum possible mechanisms. Invasive bacteria such as Salmonella sp., Campylobacter sp., Yersinia sp., Shigella sp. and enteroinvasive E. coli (EIEC) can invade the mucosa of the distal small intestine and colon causing acute enterocolitis. This is usually manifest as diarrhea accompanied by the passage of blood and mucus, and May lead to potentially fatal septicaemia if the organisms penetrate the intestinal barrier into the blood stream. Enteropathogenic E. coli (EPEC) also interacts directly with the mucosa of the small intestine, but cause more subtle damage than this professional invaders, resulting in a loss of microvilli from absorpsi epithelial cells in the small intestine. This compromises absorpsi function and causes the osmotic small bowel diarrhea.

Cytotoxins is secreted by a number of enteric pathogens including enterohaemorrhagic E. coli (EHEC), cytotoxic necrotising factor secreting E. coli and Clostridium perfringens. Cytotoxins is lethal to intestinal epithelial cells, causing bleeding and ulceration, potentially mimicking a severe enterocolitis caused by invasive bacteria. If EHEC to enter the circulation they can also damage endothelial cells and precipitate the haemolytic-uraemic syndrome. This mechanism has been responsible for the well-publicised human fatalities in Scotland and Japan following the food poisoning with the 0157 strain is usually derived from bovine products. In contrast to the cytotoxins, enterotoxins do not cause intestinal damage, but has a specific biochemical effect. They secreted eg by enterotoxigenic E. coli. (ETEC) and act as secretagogues resulted in a watery electrolyte-rich diarrhea. 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 colonization by specific enteropathogens, predisposing to chronic disease or carrier status. The result may depend not only on the expression of virulence set but also on the host reaction, especially the ability to mount an effective immunological response.

Identification of stomach pathogens

Detection of enteropathogens in faecal samples initially involves conventional microbiological techniques, including biochemical characterisation and serotyping when appropriate. Identification of genes encoding virulence determine the new molecular approaches that proved invaluable, especially to distinguish between nonpathogenic E. coli. the main component normal intestinal flora, and different types of pathogenic E. coli of wolves in sheeps' clothing.

Main enteropathogens most frequently identified in dogs are Salmonella sp. and Campylobacter sp. This has been clearly associated with acute and chronic disease, usually causing haemorrhagic enterocolitis, but it can also be present in the clinical health service which potentially risks other animals and people. There is relatively little information on the prevalence of pathogenic E. coli. in dogs, although individual reports have isolated EPEC and ETEC from dogs with diarrhea. Our own studies have used gene probes to investigate E.coli. in faecal samples from dogs with diarrhea and clinical healthy dogs, all kept in the home environment. Results beginning shows that significantly more affected dogs were excreting pathogenic E. coli that hybridised with probes for EPEC and verocytotoxin. These findings support the possibility that pathogenic E. coli. can play a role in the pathogenesis of acute and chronic diarrhea in dogs. Additional preliminary studies of kennelled dogs suggest their May act as a carrier of pathogenic E. coli that can be transmitted and cause clinical disease in susceptible individuals. Vulnerability can involve environmental factors such as stress, but also an innate inability to mount an effective mucosal immune response to this organism.

Treatment and prevention of infection

Treatment acute cases, depending on the severity of clinical signs. Mild cases require little or no treatment, whereas parenteral antibiotics and intensive fluid therapy is indicated in severe cases, especially when there is evidence of septicaemia or endotoxaemia. Chronic cases can he difficult to manage and this may be due to a number of factors including poor support from the down host response, antibiotic resistance, the failure of antibiotics to reach invasive enteropathogens, or Reinfection from the environment.

There are obviously a force the argument for the administration of antibiotics in severe cases, but their use is controversial, especially in the clinically-healthy carriers. Options May be guided by antibiotic sensitivity testing, but generally antibiotic selection for clinical disease and to eliminate carrier status is enrofloxacin for salmonellosis and erythromycin for campylobacteriosis. Clearly, attention should also he given to the identification of sources of infection and the introduction of effective management procedures to prevent infection, especially if the dogs are housed together in the community. In an assessment 7oonotic potential it is relevant to consider that approximately 100,000 salmonella, but as few as 500 campylohacter organisms may be needed to cause clinical disease. The zoonotic implications of pathogenic E. coli infection in dogs is not well understood, but the infected animals should be considered a potential risk to relevant information to the contrary is available.