DIAGNOSIS & MANAGEMENT OF ACUTE GASTRO-INTESTINAL TRACT DISEASE
Remo Lobetti
BVSc (Hons) MMedVet (Med) PhD Dipl. ECVIM (Internal Medicine)
Bryanston Veterinary Hospital
PO Box 67092, Bryanston, 2021, South Africa
Email: rlobetti@mweb.co.za
INTRODUCTION
There are a large number of potential causes of acute vomition and/or diarrhoea but whether an
absolute diagnosis is pursued, and when symptomatic therapy is instituted, are clinical and
sometimes economic judgments. In many cases of acute GI tract disease, an aetiological agent is not
identified. Similarly 80% of human cases of acute haemorrhagic diarrhoea lack a diagnosis. While
academically unsatisfying, the lack of a definitive diagnosis in dogs and cats does not matter if the
problem resolves and does not recur. Important causes of acute GI tract disease in young animals
include dietary, infectious, toxins, foreign bodies, and intussusception.
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Dietary:
 Food intolerance.
 Sudden diet change.
 Food poisoning:
 Poor quality.
 Spoiled foods.
 Bacteria.
Viral.
Bacterial.
Helminths.
Protozoa.
Trauma:
 Foreign bodies.
 Intussusception.
Acute gastro-enteritis can be further characterised and prioritised as follows:
 Non-fatal and often self-limiting:
 Uncomplicated parasitism.
 Dietary indiscretions or intolerance.
 Drug-induced.
 Exogenous toxins.
 Acute diarrhoea resulting from systemic infections such as infectious canine hepatitis,
distemper, leptospirosis.
 Severe and potentially life-threatening:
 Enteric infections (Enteroviruses, salmonellosis)
 Intestinal obstruction (foreign body, intussusception)
Animals that are bright, alert, and not dehydrated often require no further investigation besides a full
faecal analysis. However, further investigation of acute gastro-intestinal disease is indicated if the
animal:
 Is listless, febrile, dehydrated, and either tachycardic or bradycardic.
 Has abdominal discomfort, melena, bloody mucoid stools, or frequent vomiting.
 Has an obvious intestinal mass or intestinal plication.
INFECTIOUS AETIOLGIES
Feline astrovirus
Astrovirus can cause subclinical infections and also diarrhoea, particularly in kittens that may last as
long as two weeks.
Feline coronavirus
Feline corona viruses are divided into two groups: The pathogenic strains that cause feline infectious
peritonitis (FIP) and those feline enteric corona viruses (FECV) that cause a subclinical or mild enteric
infection. Viruses of these two categories are closely related.
Feline panleukopenia
Feline panleukopenia virus, a parvovirus, is a highly contagious, frequently fatal, viral disease of cats.
The disease is seen most frequently in cats 3 - 5 months of age and is associated with high mortality.
The virus is present in nasal secretions, faeces and urine and is transmitted by contact with infected
animals via fomites. Infection of kittens in utero or within a few days of birth leads to cerebellar ataxia.
Clinical signs include pyrexia, anorexia, depression, weakness, sternal recumbency, nasal discharge,
conjunctivitis, vomiting, and diarrhoea.
Canine parvovirus
The origin of CPV-2 has been speculated to be from FPV, although differences between FPV and
CPV-2 suggest that CPV-2 originated from an antigenically similar ancestor, such as a wild carnivore.
To date, the exact evolution and origin of CPV-2 remains elusive. Initially the emergence of CPV-2 in
the naïve canine population resulted in high morbidity and mortality. In the 1980s a new strain of
CPV-2 emerged, which was designated CPV-2a. That strain then mutated into CPV-2b, and more
recently into CPV-2c. This latter strain was first reported in Europe and then in the USA. This strain is
highly virulent and associated with high morbidity and rapid death.
The disease is seen in household dogs and may involve whole litters and kennels. Young and elderly
dogs and Doberman pinschers and Rottweilers are most susceptible. Clinical signs include vomiting,
haemorrhagic diarrhoea, fever, dehydration, and marked leukopenia. Up to the last 5-6 years, CPV
infection has remained a relatively treatable and preventable disease with severe morbidity and
mortality rates occurring in animal shelters and in unvaccinated dogs. Recently, however, CPV has
become an issue in well-managed and well-vaccinated dogs. The emergence of CPV-2c is the most
challenging as its detection appears to be limited with the currently available antigenic detection kits,
current vaccines have questionable protection, and the general canine population remains relatively
naïve lacking circulating antibodies.
Canine parvovirus 1
Canine parvovirus 1 (CPV-1) is related to bovine parvo-virus and usually results in enteric and/or
respiratory disease in puppies less than 4 weeks of age and reproductive failure in pregnant bitches.
A number of puppies in a litter may be infected and the outcome may be fatal. Clinical signs include
dullness, anorexia, diarrhoea, vomiting and dyspnea. Unless a particular cell line (Walter Reed canine
cell line) is employed for isolation or special immunological reagents employed, laboratory diagnosis
is usually unsuccessful.
Canine coronavirus
Canine coronavirus infection is a relatively mild enteric disease of mainly young dogs although all
ages may be infected. The virus is relatively labile and can survive outside the animal for 1 - 2 days.
Clinical signs are anorexia, depression vomiting, and diarrhoea.
Rotavirus
Rotavirus occurs widely in the intestine of dogs but infections are generally subclinical. Feline
rotaviruses can cause subclinical infections and occasionally mild enteritis in kittens, but not the
severe infection seen in the young animals of other domestic species. Rotavirus can be detected in
faeces with electron microscopy.
Campylobacteriosis
Campylobacteriosis is a contagious disease caused by Campylobacter jejuni and characterized by
enteritis and diarrhoea of variable duration and severity, although dogs and cats can carry and shed
C. jejuni, without showing clinical signs. C. jejuni is a small, fragile, gram-negative rod. Dogs less than
six months of age are more severely affected and there is some question as to whether this organism
causes enteritis and diarrhoea in normal cats other than kittens. Debilitated cats and those with
parasitic or microbial infections are more susceptible. Although C. coli and C. upsaliensis can
occasionally be recovered from the faeces of cats, their significance is not clear.
Salmonellosis
Salmonellosis is a contagious disease of animals and humans caused by many varieties of the enteric
gram-negative bacterium Salmonella. Over 2000 serotypes of Salmonella have been implicated as
causes of salmonellosis. The most common serotype recovered from dogs and cats is S.
typhimurium. Concurrent enteric infection and immunosuppression may predispose to clinical
salmonellosis. Salmonellosis is manifested by one of the following three syndromes: septicaemia,
acute enteritis and chronic enteritis. Young animals most frequently develop the septicaemic form,
whereas acute and chronic enteritis is seen most commonly in adult animals. Cats are highly
resistant to salmonellosis but there are reports of outbreaks in kittens and infrequent clinical disease
in adult cats. A considerable number of dogs and cats are carriers. Clinical signs vary with the severity
of the infection and include acute to chronic gastroenteritis, episodes of fever, vomiting, depression,
occasionally pneumonia and sometimes abscesses in lymph nodes and liver.
Coccidiosis
Several species of Isospora have been associated with diarrhoea in dogs and cats, particularly in
puppies and kittens; however, most infections are subclinical. Infection is by ingestion of sporulated
oocysts found in faeces contaminated feed, water, and soil. Dogs and cats usually become infected
before one year of age and may remain sub-clinically infected for long periods. Overcrowding, poor
sanitation, nutrition, impaired immunity, and other stresses predispose to clinical coccidiosis. Clinical
signs are intermittent diarrhoea for several days and haematochezia.
Cryptosporidiosis
This is a widespread, worldwide infection of humans and domestic animals, caused by the coccidian
parasite, Cryptosporidium parvum. Infection is by the oral-faecal route. Most infections are subclinical
with clinical disease rare in dogs and cats. Kittens and puppies are most susceptible. When it occurs
there may be predisposing underlying disease, e.g., FeLV or FIV infections. The organism invades
the microvillus border and there is mild to severe villous atrophy. Both the intestine and colon are
affected. Clinical signs are mild to severe diarrhoea.
Giardiasis
Giardiasis is a protozoal intestinal infection, caused by Giardia duodenalis. This flagellated protozoan
inhabits the lumen of the small intestine where it produces microscopic lesions on villi. Transmission
takes place when cysts are passed in faeces and ingested. Contaminated food and water are
frequently the source of infection. Cysts are resistant and can survive for long periods outside the
host. Infections in adult dogs and cats are usually subclinical but clinical disease is also seen. Acute
and chronic diarrhoea occurs mainly in kittens and puppies. Clinical signs include diarrhoea, poor hair
coat, flatulence, and loss of or failure to gain weight.
Tritrichomonas
Tritrichomonas foetus is a microscopic single-celled flagellated protozoan parasite that has
traditionally been identified as a cause of reproductive disease in cattle (infertility, abortion and
endometritis). In cats the organism is an important cause of diarrhoea. It can infect and colonises the
large intestine, resulting in prolonged and intractable large bowel diarrhoea. With severe diarrhoea the
anus may become inflamed and painful, and in some cases faecal incontinence can develop.
Although the diarrhoea may be persistent and severe, most affected cats are otherwise well, and
show no significant weight loss.
Although cats of all ages can be affected, it is most commonly seen in young cats and kittens, the
majority being under 12 months of age. Infection is most commonly seen in colonies of cats and
multi-cat households, where the organism is presumably spread between cats by close and direct
contact. There has been no evidence of spread from other species, or spread via food or water.
Toxoplasmosis
This is a widespread, frequently subclinical, protozoal disease of many warm-blooded animals and
humans throughout the world. Toxoplasma gondii, a coccidia-like protozoan, completes its life cycle in
epithelial cells of the intestine of the cat. Cats are the definitive host and serve as the main reservoir.
Clinical disease may develop as a result of stress, impaired immunity and concurrent disease. In cats
intestinal infections are usually subclinical with mild diarrhoea infrequently seen. Cysts in tissues do
not usually result in clinical signs; however, they cause diarrhoea, vomiting, fever, anorexia, dyspnea,
icterus, ocular disease, and neurological dysfunction. In dogs infections are acquired from eating
uncooked meat and ingesting food and water that has been contaminated with faeces. Infections are
usually asymptomatic. Some of the conditions attributed to toxoplasmosis are: neurological infections
with abnormal reflexes, ataxia, paralysis, but rarely with ocular involvement; infections of the
myocardium and skeletal muscle; pneumonia and hepatitis.
DIAGNOSITIC APPROACH
The diagnosis is often based on history and clinical examination, without any detailed work-up,
however, in all cases a review of the vaccination status, diet, and possible exposure to toxin or
infectious disease should be done as well as a full faecal analysis (floatation, wet prep, and smear) as
parasites should always be considered a possible cause until proven otherwise. Additional diagnostic
tests that may be considered are survey abdominal radiographs, abdominal ultrasonography,
haematology, and serum biochemistry.
THERAPY
The initial management of acute gastro-intestinal disease is symptomatic and supportive. It is started
on the basis of clinical findings, in particular the presence of dehydration. It is important that the
animal is regularly re-evaluated to monitor the response to therapy and to detect the development of
other clinical signs.
Fluid therapy
Oral fluid and electrolyte replacement therapy may be sufficient if acute diarrhoea is associated with
only mild or insignificant dehydration and vomiting is infrequent or absent. Mixed solutions containing
glucose and electrolytes—sometimes with added glycine, glutamine, or peptides can be used.
However, when there is significant vomition, diarrhoea and/or dehydration, parenteral fluids should be
administered at a rate that replaces deficits, supplies maintenance needs, and compensates for
ongoing losses. Animals with marked hypovolaemia require more aggressive support. The type of
fluid and the requirement for potassium supplementation is best judged by performing a minimum
database and serum electrolytes. Parenteral fluids are best given intravenously, however, the
intraosseous route can be used if venous access is unavailable, but subcutaneous fluids are likely to
be inadequate.
Diet
Current recommendations are to feed a bland diet, given little and often, for 3-5 days; thereafter the
original diet is gradually reintroduced. Common choices are commercially available diets or homecooked consisting of boiled chicken or white fish or low-fat cottage cheese with boiled rice. Cats seem
to have a lower tolerance to dietary starch and may benefit from a diet with a higher fat content. Little
attention is paid to the overall nutritional adequacy of home-prepared bland diets when fed in the
short term.
This dogma of “intestinal rest” has been challenged by studies that demonstrate that feeding human
infants during infectious, secretory diarrhoea promotes recovery. However, in dogs and cats,
secretory diarrhoea is less common, the resultant increased volumes of diarrhoea may be
cosmetically unacceptable, and the presence of vomiting may preclude this approach. The inclusion
of glutamine, a nutrient utilized preferentially by enterocytes, may also promote recovery and
decrease bacterial translocation.
Theoretically, any intestinal disease may predispose the animal to the development of food sensitivity;
therefore the feeding of a novel protein source during these periods may preclude the development of
sensitivity to the staple diet. However, evidence for this concept of feeding a “sacrificial protein” is only
circumstantial.
Protectants and adsorbents
Bismuth subsalicylate, kaolin-pectin, montmorillonite (a refined form of kaolin), activated charcoal and
magnesium, and aluminium and barium products are often administered in acute diarrhoea to bind
bacteria and their toxins and to protect the intestinal mucosa. They also bind water and may be antisecretory. Therapy should not exceed 3 days if there is no improvement.
Antiemetics
These may be beneficial to reduce fluid loss and patient discomfort but may mask signs of intestinal
obstruction.
Motility and secretion modifying agents
Anticholinergics and opiates or opioids (loperamide, diphenoxylate) are indicated for the short-term
symptomatic management of acute diarrhoea in dogs; anticholinergic agents can potentiate ileus and
are not recommended. Opiate analgesics stimulate segmental motility, thereby slowing transit, and
also decrease intestinal secretion and promote absorption. They are contraindicated in cases
involving obstruction or an infectious aetiology, and loperamide may have central nervous system
side effects in dogs with the multidrug resistance 1 (MDR-1) gene mutation.
Antimicrobials
Antimicrobials are indicated only in animals with GI tract disease with a confirmed bacterial or
protozoal infection and in animals in which a breach of intestinal barrier integrity is suspected.
Leukopenia, neutrophilia, pyrexia, the presence of blood in the faeces, and shock all are potential
indications for prophylactic antibiotics in animals with GI tract disease. Initial choices in these
situations include amoxicillin or a cephalosporin effective against gram-positive and some gramnegative and anaerobic bacteria. If systemic translocation of enteric bacteria is suspected,
antimicrobials effective against anaerobic organisms, such as metronidazole or clindamycin, and an
aminoglycoside effective against “difficult” gram-negative aerobes, are indicated. To reduce renal
sided effects aminoglycosides should not be given until the animal is fully hydrated.
Probiotics and prebiotics
Probiotics are orally administered living organisms that exert health benefits beyond those of basic
nutrition. In addition to direct antagonistic properties against pathogenic bacteria, they modulate
mucosal immune responses. In other words, they can switch off expression of TNF-α through NF-κB
and alter intestinal permeability. The evidence shows that the positive effect of probiotics is species
specific and present only while the probiotic is administered. The traditional practice of feeding live
yogurt as a way of repopulating the intestine with beneficial lactobacilli after an acute GI upset or
antibiotics is unlikely to work, but probiotics are now available for use in dogs and cats.
Prebiotics are selective substrates used by a limited number of “beneficial” species, which therefore
cause alterations in the luminal microflora. The most frequently used prebiotics are non-digestible
carbohydrates—such as lactulose, inulin, and FOS—and immunomodulators such as lactoferrin. Their
use combined with probiotics to encourage the growth of organisms is termed symbiosis.
Therapy of parvo virus
The treatment of CPV is mainly supportive – managing dehydration, controlling secondary infections,
reducing the intestinal signs, and ensuring adequate nutrition.
Antibiotics
 Amoxicillin
 Gentamycin:
o 6 mg/kg oid for 3-5 days.
o Only once patient is rehydrated.
o Check for RTE cells in urine.
Fluid therapy
 Replacement or maintenance fluids.
 Colloids.
Anti-emeticss
 Metaclopramide
 0.2 -0.4 mg/kg tid-qid.
 1-2 mg/kg/day as a constant rate infusion.
 Cerenia® at 1 mg/kg oid.
 Prochlorperazine at 0.5 mg/kg tid or a piece of a suppository. Has no prokinetic effect.
 Ondansetron at 0.1-1 mg/kg bid-qid.
Nutrition
 Feed once rehydrated, which should be approximately 4-12 hours after admission.
 Feed minimum of 1/3 of nutritional requirements in first 24 hours.
 With severe vomition, skip out 1-2 hours and/or reduce quantity.
 Naso-oesophageal tube if necessary.
Additional therapy
 Plasma transfusion at 10-20 ml/kg if albumin < 20 g/l.
 Blood transfusion if not improving and Ht <15–20%.
 Deworming as needed.
 Sucralfate 1ml/3kg tid-qid with severe vomiting to control flux oesophagitis.
 Cimetidine 10 mg/kg tid or ranitidine 2 mg/kg bid.
 Buprenorphine 0.01mg/kg tid with severe abdominal pain.
Monitoring
 Body weight.
 Blood glucose.
 Haematocrit.
 Total serum proteins.
 Serum potassium.