Shigellosis is an acute self-limiting intestinal infection caused by one of four species of Gram-negative nonspore- forming bacilli. These include Shigella dysenteriae, S. flexneri, S. boydii and S. sonnei. While all of them are enteroinvasive, S. dysenteriae type 1 and some strains of S. flexneri and S. sonnei have been demonstrated to elaborate a toxin that is enterotoxic, neurotoxic and cytotoxic. Like salmonellosis, shigellosis is found worldwide and is more prevalent in areas with poor hygiene and overcrowding. Transmission is by the faecal-oral route.
The incubation period is short, usually 2 days. The onset is acute, with fever, malaise, abdominal pain and watery diarrhoea. As the disease increases in intensity, bloody diarrhoea with mucus, tenesmus, faecal urgency and severe cramping abdominal pain becomes prominent. Nausea, vomiting, headache and convulsions (in children) may occur and have been attributed to the neurotoxin. When the disease is due to S. dysenteriae, which is responsible for the more fulminant forms of shigellosis, a cholera- like picture is occasionally seen. Sigmoidoscopy shows the presence of a markedly hyperaemic and inflamed mucosa, with transversely distributed ulcers with ragged undermined edges. The appearances are often indistinguishable from other dysenteric infections and from non-specific inflammatory bowel disease. Complications may be mild (arthritis, conjunctivitis, morbilliform rash) or life-threatening, such as colonic perforation, septicaemia and the haemolytic uraemic syndrome.
The diagnosis is made on the basis of a stool culture.
Treatment is symptomatic. In severe cases, trimethoprim 200 mg twice daily or ciprofloxacin 500 mg twice daily are used. Public health measures, particularly the disposal of excreta and the provision of potable water, prevent infection. Outbreaks in schools can only be controlled by good hygiene.
Campylobaeter jejuni is a Gram-negative, motile, curved spiral rod that is microaerophilic and thus fails to multiplyunder aerobic or strict anaerobic conditions. C. jejuni causes acute diarrhoea, sometimes with blood, and is now one of the most common causes of acute gastroenteritisin the UK. In developing countries asymptomatic carriers occur in young children.
Symptoms begin 2-5 days after eating infected material (usualIy chicken or milk), the commonest being fever, headache and malaise. These are followed rapidly by diarrhoea, often with blood, and quite severe cramping abdominal pain. The patient generalIy appears unwell. Sigmoidoscopy can show the changes of acute colitis, which may be indistinguishable from those of ulcerative colitis. Complications include cholecystitis, pancreatitis, a reactive arthritis, the Guillain-Barre syndrome and the haemolytic uraemic syndrome.
Direct phase microscopy of a wet mount of stool may reveal the motile curved rods resembling ‘flying birds’. The organism may be cultured on special media within 48 hours. In severe infections the organism may be cultured from the blood.
In the majority of cases, Campylobacter enteritis is a selflimiting illness, resolving in 5-7 days. Although the organism is sensitive to erythromycin, there is no evidence that treatment with this antibiotic alters the natural history of the infection. However, if systemic symptoms continue in association with persistent bacteraemia, antibiotics are usualIy administered.
Helicobacter pylori, a curved Gram-negative organism, colonizes the gastric epithelium beneath the mucus layer and in areas of gastric metaplasia such as occur in the duodenum. H. pylori is noted for its ability to produce urease, which is thought to be involved in the pathogenesis of disease.
The only three major human pathogens are Y. pseudotuberculosis and Y. enterocolitica, which cause mesenteric lymphadenitis and enterocolitis, respectively, and Yersinia pestis, which causes plague. Yersinia enterocolitica and Yersinia pseudotuberculosis infections These result in a number of clinical syndromes depending on the host’s age and immune status. Patients may present with enterocolitis, acute mesenteric lymphadenitis or terminal ileitis. Enterocolitis is characterized by the presence of fever, diarrhoea and severe abdominal pain, which may lead to a mistaken diagnosis of appendicitis. Arthritis and erythema nodosum are seen and are immunologically mediated. This is usually a self-limiting disease and no treatment is required. In very severe cases, tetracycline 1 g daily may be given.
Plague is caused by Y. pestis, a Gram-negative, pleomorphic bacterium. Nowadays it is mainly limited to animals, but sporadic cases of plague, as well as occasional epidemics, occur worldwide in humans. The major reservoirs are woodland rodents, which transmit infection to domestic rats (Rattus rattus). The vector is the rat flea, Xenopsylla cheopis. These fleas bite humans when there is a sudden decline in the rat population. Occasionally, spread of the organisms may be through infected faeces being rubbed into skin wounds or through inhalation of droplets. Virulence is attributed to the presence of the endotoxin, exotoxin and fraction I (a soluble protein that prevents phagocytosis of the organism). Clinical manifestations are attributed to the lipopolysaccharide endotoxin.
Four clinical forms are recognized-bubonic, pneumonic, septicaemic and cutaneous plague.
BUBONIC PLAGUE is the commonest form and occurs in about 90% of infected individuals. The incubation period is about 1 week. The onset of illness is acute, with high fever, chills, headache, myalgia, nausea, vomiting and, when severe, prostration. This is rapidly followed by the development of lymphadenopathy, most commonly involving the inguinal lymph nodes (buboes). Characteristically these are matted and tender, and suppurate in 1-2 weeks. Petechiae, ecchymoses and bleeding from the gastrointestinal tract, the respiratory tract and the genitourinary tract may occur. Mental confusion follows the development of toxaemia.
PNEUMONIC PLAGUE is characterized by the abrupt onset of features of a fulminant pneumonia with bloody sputum, marked respiratory distress, cyanosis and death in almost all affected patients.
SEPTICAEMIC PLAGUE presents as an acute fulminant infection with evidence of shock and Ole. If left untreated, death usually occurs in 2-5 days. Lymphadenopathy is unusual.
CUTANEOUS PLAGUE presents either as a pustule, eschar or papule or an extensive purpura, which can become necrotic and gangrenous.
The diagnosis is easily established by demonstrating the organism in lymph node aspirates, in blood cultures or on examination of sputum.
Treatment is urgent and should be instituted before the results of culture studies are available. Several antimicrobial drugs are effective, including streptomycin 0.5 g i.m. every 4 hours for 48 hours followed by 0.5 g every 6 hours for 5 days, or tetracycline 2-3 g daily for 14 days.
PREVENTION AND CONTROL
Prevention of plague is largely dependent on the control of the flea population and the use of potent antiflea agents such as 2% aldrin. Outhouses, or huts, should be sprayed with insecticides that are effective against the local flea. Rodents should not be killed until the fleas are under control as the fleas will leave dead rodents to bite humans. Tetracycline 500 mg four times daily or sulphonamides 2-4 g daily for 7 days are effective chemoprophylactic agents. Patients themselves can be infective when the buboes break down; patients with pneumonic plague can spread the organism by droplets. A partially effective formalin-killed vaccine is available for use by travellers to plague-endemic areas.