Pseudomembranous colitis

Pseudomembranous colitis is caused by the A and B toxins produced by C. difficile. It usually occurs a few days after institution of antibiotic therapy, although it has been known to occur even a month after discontinuing antibiotics. Clindamycin has been most frequently implicated, but ampicillin” tetracycline and the cephalosporins have also been causally related to some cases. Fever, diarrhoea (rarely with blood) and abdominal cramps are usual. Sigmoidoscopic examination may reveal a markedly erythematous, ulcerated mucosa covered by a membrane- like material, although in about 20% of patients only the ascending colon is involved. A normal sigmoidoscopy therefore does not exclude infection. The presence of this membrane is not essential to the diagnosis.


Identification of the toxin (by observing its cytopathic effect on cells in tissue culture or by ELISA) in stool specimens is usually diagnostic but the test can be unreliable. Culture of the organism alone is insufficient as 5% of healthy adults carry C. difficile. Both the organism and its toxin are commonly found in healthy neonates in whom it has no pathological significance.


All suspected antibiotics should be discontinued and this alone may result in the diarrhoea stopping. Vancomycin 125 mg orally, four times daily, for 10 days is often used but metronidazole is also effective and considerably less expensive. Relapses are common. There is no evidence that changing chemotherapy helps. Patients should be isolated to try and prevent spread to other susceptible individuals.


Anthrax is caused by Bacillus anthracis. Its spores are extremely hardy and withstand extremes of temperature and humidity. The organism is capable of toxin production and this property correlates most closely with its virulence. The disease occurs worldwide. Epidemics have been reported in The Gambia, in both North and SouthAmerica and in southern Europe. Transmission is through direct contact with an infected animal and is seen in farmers, butchers and dealers in wool and animal hides. Spores can also be ingested or inhaled.


The incubation period varies from 1 to 5 days.

THE CUTANEOUS FORM is the commonest mode of presentation and is seen most frequently in the tropics. It is self-limiting in the majority of patients. Typically, a small erythematous, maculopapular lesion is present that subsequently vesiculates and undergoes ulceration, with formation of a central black eschar. Occasionally the perivesicular oedema is marked and toxaemia may be present.

RESPIRATORY INVOLVEMENT (woolsorter’s disease) due to inhalation of spores results in a non-productive cough, fever and retrosternal discomfort. Pleural effusions are common. In some patients there is apparent clinical improvement followed by the abrupt onset of dyspnoea, marked cyanosis and death.

GASTROINTESTINAL ANTHRAX presents as severe gastroenteritis. Haematemesis and bloody diarrhoea may occur.


Diagnosis is established by demonstrating the organism in smears or by culture. Detection of a fourfold increase in antibodies measured by indirect microhaemagglutination or ELISA in paired sera (i.e. acute and convalescent samples) is diagnostic.


Penicillin is the drug of choice. In mild cutaneous infections, phenoxymethylpenicillin 500 mg four times daily for 2 weeks is adequate. In more severe infections, e.g. when septicaemia is present, up to 24 g of intravenous penicillin is required daily. Sulphonamides, chloramphenicol and tetracycline have also been used successfully. The role of steroids in fulminant anthrax infections is questionable.
Any infected animal that dies should be burned and the area in which it was housed disinfected. Where animal husbandry is poor, mass vaccination of animals may prevent widespread contamination. Vaccination of exposed workers is effective. Bacillus cereus infection This Gram-positive, aerobic, spore-forming bacillus can cause food poisoning  often from contaminated rice. It also causes wound sepsis.


Cat-scratch disease Between 7 and 14 days after a scratch or bite, a small red papule appears at the site associated with regional lymphnode enlargement. Lymphadenopathy may persist for several weeks and suppurate in up to 40%. The disease may progress systemically with encephalitis, neuroretinitis, arthritis, hepatitis, osteolytic bone lesions and pleurisy. A cell wall defective Gram-positive bacilli has been tentatively identified as the cause and serologically there is a humoral response to Rochalimaea henselae suggesting that this or a closely related organism is the aetiologic agent. The organism is sensitive to some cephalosporins (cefoxitin, cefotaxime) and aminoglycosides (gentamicin, tobramycin).

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