Oral, Gastrointestinal & pancreas

ORAL INFECTIONS

DIAGNOSTICS

The most common conditions are gingivitis, periodontitis, stomatitis and tooth root abscess. Predisposing factors can contribute (dental plaque or calculus, viral infections, immunosuppression).

Gingivitis: localised inflammation of the gingiva, often caused by dental plaque or calculus

Periodontitis: inflammation of the periodontium leading to irreversible tissue loss around the tooth

Stomatitis: inflammation of the oral mucosa, often accompanied by secondary bacterial infection. Chronic stomatitis is more often seen in cats than dogs and is often idiopathic.

Diagnosis is made on presenting symptoms and oral examination. Radiographs may assist, especially for tooth root abscesses.

TREATMENT

Following removal of plaque / calculus, many cases of gingivitis and periodontitis can be treated with topical therapies alone. Antimicrobials are only indicated in cases with local or systemic signs of infection. Culture and sensitivity should be considered, especially in cases that do not respond to empirical therapy. Clindamycin or amoxycillin have adequate spectrum to cover the most likely pathogens29,30.

DURATION OF THERAPY

7 days is generally adequate however, if osteomyelitis is present, longer durations will be required (21-28 days often quoted).

 

ACUTE GASTROENTERITIS

DIAGNOSTICS

There are many possible causes of acute gastroenteritis that are not bacterial in origin and therefore do not require antimicrobial therapy. These are not covered in this document. The major bacteria implicated in the syndrome are covered below:

Campylobacter: infection rarely causes clinical disease and the bacteria is frequently isolated from healthy animals. Attempts to induce enteritis in puppies with C. jejuni have been equivocal31. C. upsaliensis may be more pathogenic in dogs but is not zoonotic32,33. Clinical signs still tend to be relatively mild34. Concurrent infection with another pathogen is likely in animals with clinical signs. C. jejuni inoculum for human infection is very low35 so both asymptomatic carriers and diarrhoetic dogs pose a zoonotic risk. Diagnosis can be made by examining stained faecal smears, however other Campylobacter-like organisms may be present leading to false-positives. Faecal PCR or culture can be performed however results need to be interpreted with caution.

Salmonella: clinical salmonellosis is rare and asymptomatic carriers are common with international studies suggesting up to 44% of healthy dogs36,37 and 14% of healthy cats38 may carry Salmonella. Infection can result in severe gastroenteritis with or without septicaemia. Isolation of the organism in faeces, in conjunction with clinical signs of disease, is generally used to make a diagnosis, however the organism can be isolated from healthy animals so caution should be used in interpreting results.

Clostridium difficile & C. perfringens: clinical signs are variable, from mild and self-limiting to potentially fatal acute haemorrhagic diarrhoea, and the clinical significance is unknown. C. perfringens can be found in ~15%, and C. difficile in up to 40%, of non-diarrhoetic dogs39,40. Detection of a enterotoxigenic isolate, in combination with positive ELISA for the clostridial toxin, is required for a diagnosis of C. perfringens. C. difficile is more difficult to diagnose as culture is not useful, the toxin tests are not validated for use in dogs and have given high numbers of toxin-positive, culture-negative results39. Faecal lactoferrin has been used in humans, as a marker of intestinal inflammation, in combination with toxin testing. This has not yet been evaluated for the diagnosis of C. difficile infection in dogs.

E. coli: the significance of enteropathogenic (EPEC) or enterotoxin-producing (ETEC) E. coli in diarrhoea in dogs and cats unknown. ETEC has been incriminated in diarrhoea in young dogs41,42. Enteroinvasive E. coli has a role in the development of histiocytic colitis in young boxers43. PCR is the most common method for detecting and differentiating pathogenic strains of E. coli.

TREATMENT

Campylobacter: Macrolides are most appropriate (erythromycin)44,45. High rates of mutational resistance can occur during treatment with fluoroquinolones; these are not recommended. Tetracyclines are a suitable alternative if erythromycin cannot be used, although tetracycline resistant strains exist.

C. perfringens: amoxycillin or metronidazole are generally effective, although resistant strains have been identified46.

C. difficile: metronidazole is recommended, resistant strains have not been reported in dogs46.

E. coli: Antimicrobial therapy is controversial as the disease is generally self-limiting. In addition, antimicrobial therapy may enhance toxin synthesis or release leading to a decline in clinical status47. There is also a relatively high incidence of inherent resistance48. In severe cases, with secondary sepsis, amoxycillin or 1st generation cephalosporins are a reasonable choice.

Salmonella: Therapy should be based on culture and susceptibility testing. Empirical therapy with amoxycillin or trimethoprim / sulphonamide is probably reasonable while awaiting culture results.

DURATION OF THERAPY

Campylobacter & Salmonella: 10 days

Clostridial diarrhoea: 5-7 days

ACUTE HAEMORRHAGIC DIARRHOEA SYNDROME

DIAGNOSTICS

Faecal culture and diagnostic panel for common pathogens is always indicated.

TREATMENT

Treatment with amoxycillin / clavulanate does not reduce the duration of disease in patients without sepsis49. Appropriate supportive care & close monitoring for signs of sepsis is recommended. Animals generally fall into one of 3 groups:

1. Mild haemorrhagic diarrhoea with no evidence of hypovolaemia or other systemic effects No antimicrobials indicated
2. Severe haemorrhagic diarrhoea with hypovolaemia but no evidence of sepsis Supportive care and monitoring, no antimicrobials indicated
3. Severe haemorrhagic diarrhoea with hypovolaemia and signs of sepsis Antimicrobials always indicated. Intravenous ampicillin or amoxycillin is usually sufficient. Intravenous metronidazole can also be used if the animal fails to respond to initial therapy or condition worsens.

DURATION OF THERAPY

Dependent on pathogen, see above.

INFLAMMATORY BOWEL DISEASE

This syndrome incorporates a group of chronic inflammatory conditions of the GI tract. Several types have been identified:

  • Lymphoplasmocytic enteritis / colitis
  • Eosinophilic enteritis / colitis
  • Lymphangectasia
  • Histiocytic (granulomatous) colitis

DIAGNOSTICS

Based on GI biopsies. Histiocytic ulcerative colitis in Boxers can be diagnosed by histopathology (FISH test) of colonic biopsies.

TREATMENT

Prednisolone alone is as effective as prednisolone in combination with metronidazole50 so solo therapy with prednisolone is recommended as first line. The first choice antimicrobial for non-responsive cases is tylosin51. If tylosin is not available, alternatives are oxytetracycline or lastly metronidazole. Histiocytic ulcerative colitis in Boxers can respond to long-term antimicrobial therapy43. Resistance development is widespread so therapy should be based on susceptibility testing rather than empirically.


DURATION OF THERAPY

2-8 weeks have been described.

SMALL INTESTINAL BACTERIAL OVERGROWTH AND ANTIMICROBIAL-RESPONSIVE DIARRHOEA

DIAGNOSTICS

This syndrome usually has an underlying cause and identification of the primary disorder is recommended prior to antimicrobial therapy.

TREATMENT

Tylosin is recommended, with oxytetracycline and metronidazole as acceptable alternatives if tylosin is not available.


DURATION OF THERAPY

SIBO: 2-4 weeks

ARD: 4-6 weeks

 

PANCREATITIS

DIAGNOSTICS

Diagnosis is generally made from serum biochemistry results.

TREATMENT

Antimicrobial therapy is not indicated.

 

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