- Dietary diarrhoea
- Canine parvoviras
- Other canine viral enteritides
- Feline enteritis
- Other feline viral infections
- Acute bacterial enteritis
- Tyzzer’s disease
- Haemorrhagic gastroenteritis (HGE)
- Intestinal obstruction
Dogs in particular will tolerate a wide variety of diets, while cats tend to be fastidious and require a high protein diet. If the diet is changed suddenly, especially from a dried to a tinned food, then diarrhoea often follows for several days which will be self-limiting. Unfortunately most owners on observing the diarrhoea then change the diet, further exacerbating the problem. This leads to episodes of apparent relapsing acute diarrhoea although there is a history of frequent diet changes. Treatment simply involves the selection of a suitable standard diet fed at the correct rates without change or supplementation.
Dogs are frequently fed high carbohydrate diets usually in the form of biscuit, potato or bread. High levels of cereal or potato in the diet, especially if not precooked will often lead to diarrhoea. This is because the carbohydate is not as digestible when uncooked and may reach the distal ileum and colon where bacterial fermentation occurs. The problem should be recognized from a careful history, and is easily corrected by changing the dietary management.
Milk is renowned for causing diarrhoea in adult dogs and occasionally cats, although it is not common in the authors’ experience. The problem is often referred to as a ‘milk allergy’ when in fact it is a ‘milk intolerance’ and occurs because there is a deficiency of the brush border enzyme lactase. The diarrhoea is sudden and acute but rapidly settles when milk is withdrawn from the diet. The problem is simply treated by removal of milk from the diet. Those adult dogs and cats which tolerate milk in the diet have usually been fed milk since weaning and therefore appear not to develop a lactase deficiency.
Preparation of homemade diets is often associated with enteric problems. Overcooking meat often reduces its digestibility, feeding raw egg introduces trypsin inhibitors and excessive cereals leads to bacterial fermentation in the colon and increased faecal bulk. Feeding fresh meat alone often induces foul-smelling diarrhoea and is also low in calcium. Feeding of tinned meats rich in liver, kidney or heart may also induce diarrhoea in individual cases.
Scavenging can be a major problem and one which is sometimes difficult to detect. It is not uncommon for responsible owners to be totally unaware that their dog is scavenging. In such situations there is recurrent diarrhoea which settles immediately the dog is hospitalized. The problem often recurs as soon as the dog returns to its own environment. Macroscopic examination of the faeces may help to reveal the type of rubbish the dog has eaten.
A further dietary problem may arise from owners simply overfeeding their puppy or kitten with the result that the next meal is ingested before the first meal has undergone complete digestion and absorption. In this situation the previous meal is moved to the colon before complete absorption has occurred, with subsequent bacterial fermentation leading to an osmotic or secretory diarrhoea.
Many diets are low in fibre, leading to low food residues in the distal ileum and colon. This fails to stimulate peristalsis and chyme is retained for long periods in the colon allowing a greater opportunity for bacterial fermentation and subsequent diarrhoea. The inclusion of fibre in the diet will quickly resolve the problem.
True dietary allergies have been described, often manifest by acute relapsing diarrhoea. Other cases present as chronic diarrhoea with other manifestations including dermatitis and chronic otitis. Irish Setters with gluten sensitivity have been described. This may be reversible when a gluten-free diet is fed (). Other commercial foods and table scraps have been implicated as possible dietary allergens. Such allergens may cause vomiting and/or diarrhoea and are frustrating to identify, as this can only be achieved by laborious dietary exclusion. Very often the clinician is faced with trying foods which are thought to be rarely implicated in food allergy, in the hope of obtaining a remission of symptoms. Foods such as fresh mutton, rice and chicken are good choices. If the dog responds, then one of the original foods is introduced per week till the offending food is identified. When the offending food is detected it is necessary to determine which component of the food is responsible. It may be protein, carbohydrate, fat or a preservative. Some foods such as soya bean contain trypsin inhibitors which actively prevent the protease enzymes from digesting proteins.
Other canine viral enteritides
Both rotavirus and coronavirus infections have been detected in dogs, but their true role as primary pathogens is still questioned ().
Coronavirus is another epitheliotrophic enterovirus which has been implicated in acute enteritis followed by villus atrophy and malabsorption. Enteritis is very similar to that observed with parvovirus so the two conditions can only be differentiated by faecal isolation or serology. Coronavirus may occur simultaneously with parvovirus making it difficult to decide which is the significant pathogen. In coronavirus infection an ocular and nasal discharge may also be present. Treatment is very similar to that for parvovirus infection. Control is more difficult as a vaccine is not available.
Very little is known about rotavirus infection although it has been isolated from dogs with acute enteritis. Unlike parvovirus and coronavirus this virus attacks the cells at the tip of the villi not the crypt cells. The clinical signs are normally less severe than those observed with parvovirus and coronavirus. A watery mucoid diarrhoea lasting some 10 days is observed with little vomiting, anorexia or pyrexia. Treatment is again along the lines used for dogs with parvovirus.
Feline enteritis is also known as feline panleucopenia and feline parvovirus infection. In addition to gastroenteritis the virus may cause stillbirths, abortion and fetal resorption in pregnant queens and cerebellar hypoplasia in neonatal kittens. All forms of the condition are seen less frequently because of effective vaccination, but gastroenteritis is still seen in isolated situations. The virus has preference for rapidly dividing cells and following ingestion establishes in the pharyngeal lymphoid tissue prior to dissemination via the circulation to the bone marrow and intestinal crypt cells. The virus can cross the placenta and in early gestation leads to fetal death and resorption. Infection in the second half of gestation may result in cerebellar hypoplasia in neonates.
The virus is very resistant and can survive for up to 1 year in infected premises. Formaldehyde, gluteraldehyde and hypochlorite disinfectants are required to clean infected premises.
The symptoms may vary from mild enteritis to peracute gastroenteritis and sudden deaths. Following a 2 to 10 day incubation period the first signs observed are lethargy, anorexia and pyrexia. The cat may appear very thirsty, sitting over the water bowl, but often fails to drink. Vomiting starts before diarrhoea and is persistent. Acute abdominal pain is observed and the intestines feel fluid and gas-filled. The temperature often falls if the animal survives more than 3 days and the diarrhoea becomes fluid and contains blood. There is severe dehydration and the mortality rate can reach 75%. Secondary bacterial infection is likely due to the immunosuppression and physical damage to the intestine.
Diagnosis is often based on clinical findings and a history of inadequate vaccination. Examination of oropharyngeal swabs and faeces for virus or serology may be employed to confirm the diagnosis. Histological examination of the intestine reveals dilation of the crypts, destruction of enterocytes and the presence of inclusion bodies in surviving cell nests at the base of the mucosa with epithelial proliferation in surviving areas. Changes are most marked in the ileum.
This is very similar to that employed for canine parvovirus infection. Intensive fluid therapy using lactated Ringer’s solution followed by dextrose saline should be given intravenously. Oral fluids and food should be withheld until vomiting has stopped. Broad spectrum antibiotics such as ampicillin (Amfipen; Gist-Brocades Pharmaceuticals) are essential as is metaclopramide (Emequell; SmithKline Beecham Pharmaceuticals) as described for canine parvovirus infection. Vaccination of healthy cats using a live vaccine will provide good protection against infection. For pregnant queens and unweaned kittens a dead vaccine is also available.
Other feline viral infections
Feline coronavirus is closely related to feline infectious peritonitis (FIP). It may cause a mild self-limiting diarrhoea in kittens but is not pathogenic to adult cats (). A non-fatal acute enteritis may be seen in kittens from weaning to 12 weeks of age. Cross-reaction of serology with FIP is common, making a definitive diagnosis difficult. FIP is thought to be a mutant of enteric coronavirus ().
The importance of rotavirus is not entirely clear. The virus has been isolated from cat faeces but it is not necessarily a primary pathogen. It is thought to cause a mild self-limiting enteritis in cats.
Acute bacterial enteritis
Although bacteria are frequently implicated as causing enteritis in dogs and cats, there are very few documented cases. Bacteria such as E. coli (toxigenic), Campy lob acter spp., Salmonella spp., Staphylococcus spp., Yersinia spp. and Klebsiella spp., have been documented (). The importance of E. coli as a cause of acute diarrhoea is still debatable, for even though it may be isolated on faecal culture, it does not: confirm the diagnosis. The situation is further complicated by the knowledge that faecal culture does not necessarily reflect the population in the small intestine ().
Yersinia may give rise to a mild enteritis and lymphadenopathy of the mesenteric lymph nodes together with weight loss. The organism is carried by birds and small mammals and so is more likely to involve cats rather than dogs. Although rare, Tyzzer’s disease in kittens due to Bacillus piliformis has also been recorded.
Campylobacter jejuni was previously known as Vibrio spp. and has only been recognized as a pathogen in man since 1977. It is so common in man that it may overtake Salmonellosis as the commonest cause of food poisoning. The organism is widely distributed throughout the world in animals and birds. No cultural difference has been found between the organism causing human enteritis and that found in pets (). Carrier states exist and although dogs and cats may act as a reservoir, it is thought that very few cases of human enteritis originate from household pets (). The main sources of infection include raw milk, undercooked meat, especially poultry, and water ().
Campylobacter is excreted more frequently from stray dogs than pet-owned dogs and there is a poor correlation between excretion and the presence of diarrhoea (). Excretion is also intermittent and repeated culture may be required for its detection (). The organism is an opportunist and takes advantage of a favourable environment such as those under stress or with concurrent viral infection which allow the organism to establish (). Excretion in cats is variable with surveys revealing from 10.7 to 45% of cats positive on faecal sampling ().
It has been stated that cats rarely have diarrhoea associated with Campylobacter (). However we have seen many cases which present with an acute self-limiting infection which lasts some 10 days. Pyrexia, depression, abdominal pain and diarrhoea, occasionally with blood, may be present. Vomiting is not common and mortality rate is low. Flattening of the villi, reduced numbers of goblet cells and infiltration of inflammatory cells are found on histology of the intestine. Relapses appear to be quite common.
When the organism is isolated from faecal samples, treatment with tylosin (Tylan; Elanco Products) at 20 to 40mg/kg/day orally should be instituted, as it is often successful. Erythromycin at 40mg/kg for at least 10 days may also be used especially in young animals and is available as a paediatric suspension (Erythroped; Abbott Laboratories).
There are over 1800 serotypes of salmonella known to cause food poisoning. Animals and man may carry the organism without showing clinical signs, and excrete it intermittently for months. Salmonella tends to lodge in the mesenteric lymph nodes especially after short-term antibiotics have been given and is then difficult to eliminate (). It is an important zoonosis and rivals Campylobacter jejuni as the commonest cause of food poisoning, and like Campylobacters the source of outbreaks is often never determined. Many salmonella organisms which cause food poisoning in man may not show signs in dogs or cats, but are simply carried by these species.
The major sources of infection include raw milk, uncooked meat especially poultry, poor slaughterhouse hygiene and use of recycled slaughterhouse waste as animal feed. Human infection attributable to pets is very rare compared with the above sources ().
In one study salmonella was isolated intermittently from the faeces of stray dogs with only 3.8% excreting the organism (). Other surveys however reveal up to 30% excretion in dogs (). Cats have also been studied and from 159 sampled cats only 2% were positive ().
Varying severity of enteric infection has been observed. Subclinical disease is common while clinical disease is more frequent in young, old or debilitated dogs or cats. Cats appear to be more resistant to infection than dogs. Pyrexia, abdominal pain, profuse watery diarrhoea occasionally with blood, together with vomiting may be observed.
Treatment is controversial, as the infection is normally self-limiting, and because of the risk of carrier states and resistance. Unless the dog or cat is severely ill no antibiotics should be used (). Routine screening should be performed until three clear negative faecal samples have been obtained. Non-antibiotic symptomatic treatment may be given as required.
This is an uncommon disease which has been recorded in mice, rabbits, gerbils, hamsters, dog, foxes, wild cats as well as domestic cats. It is caused by a pleomorphic bacterium, Bacillus piliformis which is an obligate intra-cellular pathogen.
Outbreaks of disease have been recorded in laboratory animals (mice and rabbits especially) where carriers are apparently common. It is not known if the carrier state exists in cats. Morbidity and mortality in cats is greatest in kittens. Stress, immunosuppression, feline leukaemia virus (FeLV), overcrowding and poor hygiene appear to be important in feline outbreaks.
Clinically in the kitten, Tyzzer’s disease may appear like feline panleucopenia. There may be sudden deaths together with kittens which have subnormal temperatures, palor of mucus membranes, tachycardia, dyspnoea, abdominal distention and pain. Vomiting occasionally occurs while profuse diarrhoea is always present and may contain blood. Icterus has been reported in some cases ().
Laboratory tests may reveal anaemia, leucopenia, hepatic jaundice and elevated serum alanine aminotransferase levels. Affected cats should be checked for the presence of FeLV and feline immunodeficiency virus (FIV).
Post-mortem examination usually reveals multiple areas of necrosis in the liver, and occasionally periportal fibrosis with proliferation of biliary duct epithelium. The organism is found within hepatocytes. A myocarditis with areas of cardiac muscle necrosis may also be observed with evidence of the organism in the cardiac muscle cells. The intestinal tract may show inflammation and evidence of the organism within the cells.
This is very unlikely to be effective so the prognosis must always be extremely guarded. Those that do survive may remain in poor condition and susceptible to infection, ultimately leading to the need for their humane destruction.
Haemorrhagic gastroenteritis (HGE)
This is a condition which is observed in the small and toy breeds of dog, especially the King Charles Spaniel, Sheltie, Pekinese and Poodle. Although dogs of any age may be affected, those between 2 and 4 years of age are most frequently involved. It is not unknown for dogs to have a relapse (15%) at any time in the future. Although the aetiology is not known, there is no evidence of inflammation on histological examination of the intestine. It is generally thought that the cause is an anaphylactic reaction, possibly to bacterial endotoxin. In particular Clostridium perfringens has been implicated in some clinical cases.
There is usually a sudden onset of acute vomiting and diarrhoea which develops to the stage where large amounts of fresh blood are produced. Clients are often very alarmed as they find the dog collapsed and passing quite large amounts of blood. Although mild forms of the condition may occur most are very acute and the dogs rapidly become shocked, dehydrated, collapsed and should be treated as real medical emergencies. Examination will often reveal tachycardia, pallor of mucous membranes, normal to subnormal temperature, depression and a characteristic fetid smell on the breath.
The condition must be differentiated from parvovirus infection, infectious canine hepatitis, acute pancreatitis and intestinal obstructions which may appear very similar in the early stages. There are no diagnostic tests to confirm the presence of HGE, so differentiation is based on elimination of other conditions. The packed cell volume (PCV) is often greater than 60% with a proportional rise in serum proteins. White cell counts vary considerably and clotting factors may be abnormal.
Intravenous fluids, as compound lactated Ringer’s solution, should be administered immediately to counter the state of shock and to replace the fluid and electrolyte loss. Broad spectrum antibiotic cover should also be provided, ideally as ampicillin in combination with aminoglycosides, to protect against Gram-positive and -negative bacteria. Corticosteroids may be helpful in those cases which are severely shocked.
The dog should be kept warm, in a quiet and stress-free environment. The response to treatment should be monitored carefully and adjusted as required. Although many cases appear critically ill and the prognosis must always be guarded, it is likely that most cases seen early and given adequate treatment will survive.
Selections from the book: “Digestive Disease in the Dog and Cat” (1991)