Gastro-intestinal infections

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37 Gastro-intestinal infections

Gastro-intestinal infections represent a major public health and clinical problem worldwide. Many species of bacteria, viruses and protozoa cause gastro-intestinal infection, resulting in two main clinical syndromes. Gastroenteritis is a non-invasive infection of the small or large bowel that manifests clinically as diarrhoea and vomiting. Other infections are invasive, causing systemic illness, often with few gastro-intestinal symptoms. Helicobacter pylori, and its association with gastritis, peptic ulceration and gastric carcinoma, is discussed in Chapter 12.

Epidemiology and aetiology

In Western countries, the average person probably experiences one or two episodes of gastro-intestinal infection each year. Infections are rarely severe and the vast majority of cases never reach medical attention. Nevertheless, they are of considerable economic importance. In the UK, viruses such as rotaviruses, adenoviruses and noroviruses are probably the most common causes of gastroenteritis. Campylobacter, followed by non-typhoidal serovars of Salmonella enterica, are the most common reported causes of bacterial gastroenteritis. Cryptosporidiosis is the most commonly reported parasitic infection. In developing countries, the incidence of gastro-intestinal infection is at least twice as high and the range of common pathogens is much wider. Infections are more often severe and represent a major cause of mortality, especially in children.

Gastro-intestinal infections can be transmitted by consumption of contaminated food or water or by direct faecal–oral spread. Air-borne spread of viruses that cause gastroenteritis also occurs. The most important causes of gastro-intestinal infection, and their usual modes of spread, are shown in Table 37.1. In developed countries, the majority of gastro-intestinal infections are food borne. Farm animals are often colonised by gastro-intestinal pathogens, especially Salmonella and Campylobacter. Therefore, raw foods such as poultry, meat, eggs and unpasteurised dairy products are commonly contaminated and must be thoroughly cooked to kill such organisms. Raw foods also represent a potential source of cross-contamination of other foods, through hands, surfaces or utensils that have been inadequately cleaned. Food handlers who are excreting pathogens in their faeces can also contaminate food. This is most likely when diarrhoea is present, but continued excretion of pathogens during convalescence also represents a risk. Food handlers are the usual source of Staphylococcus aureus food poisoning, where toxin-producing strains of S. aureus carried in the nose or on skin are transferred to foods. Bacterial food poisoning is often associated with inadequate cooking and/or prolonged storage of food at ambient temperature before consumption. Water-borne gastro-intestinal infection is primarily a problem in countries without a sanitary water supply or sewerage system, although outbreaks of water-borne cryptosporidiosis occur from time to time in the UK. Spread of pathogens such as Shigella or enteropathogenic Escherichia coli by the faecal–oral route is favoured by over-crowding and poor standards of personal hygiene. Such infections in developed countries are most common in children and can cause troublesome outbreaks in paediatric wards, nurseries and residential children’s homes.

Table 37.1 Important causes of gastro-intestinal infection, their modes of spread and pathogenic mechanisms

Causative agent Chief mode(s) of spread Pathogenic mechanisms
Bacteria
Campylobacter Food, especially poultry, milk Mucosal invasion
    Enterotoxin
Salmonella enterica, non-typhoidal serovars Food, especially poultry, eggs, meat Mucosal invasion
    Enterotoxin
Salmonella enterica serovars Typhi and Paratyphi Food, water Systemic invasion
Shigella Faecal–oral Mucosal invasion
    Enterotoxin
Escherichia coli
Enteropathogenic Faecal–oral Mucosal adhesion
Enterotoxigenic Faecal–oral, water Enterotoxin
Enteroinvasive Faecal–oral, food Mucosal invasion
Verotoxin-producing Food, especially beef Verotoxin
Staphylococcus aureus Food, especially meat, dairy produce Emetic toxin
Clostridium perfringens Food, especially meat Enterotoxin
Bacillus cereus
Short incubation period Food, especially rice Emetic toxin
Long incubation period Food, especially meat and vegetable dishes Enterotoxin
Vibrio cholerae O1, O139 Water Enterotoxin
Vibrio parahaemolyticus Seafoods Mucosal invasion
    Enterotoxin
Clostridium difficile Faecal–oral (nosocomial) Cytotoxin
    Enterotoxin
Clostridium botulinum Inadequately heat-treated canned/ preserved foods Neurotoxin
Protozoa
Giardia lamblia Water Mucosal invasion
Cryptosporidium Water, animal contact Mucosal invasion
Entamoeba histolytica Food, water Mucosal invasion
Viruses Food, faecal–oral, respiratory secretions Small intestinal mucosal damage

Treatment with broad-spectrum antibiotics alters the bowel flora, creating conditions that favour superinfection with micro-organisms (principally Clostridium difficile) that can cause diarrhoea. C. difficile infection (CDI) may be associated with any antibiotic but clindamycin, the cephalosporins and the fluoroquinolones are most commonly implicated. CDI is most common in patients with serious underlying disease and in the elderly. Although some sporadic cases are probably due to overgrowth of endogenous organisms, person-to-person transmission also occurs in hospitals and care homes, sometimes resulting in large outbreaks.

Pathophysiology

Development of symptoms after ingestion of gastro-intestinal pathogens depends on two factors. First, sufficient organisms must be ingested and then survive host defence mechanisms, and second, the pathogens must possess one or more virulence mechanisms to cause disease.

Host factors

Healthy individuals possess a number of defence mechanisms that protect against infection by enteropathogens. Therefore, large numbers of many pathogens must be ingested for infection to ensue; for example, the infective dose for Salmonella is typically around 105 organisms. Other species, however, are better able to survive host defence mechanisms; for example, infection with Shigella or verotoxin-producing E. coli (VTEC) can result from ingestion of fewer than 100 organisms. VTEC (principally E. coli O157) are especially important because of the risk of a life-threatening complication, haemolytic uraemic syndrome (HUS).

Organism factors

The first requirement of gastro-intestinal pathogens is that they are able to adhere to the gut wall and colonise the intestine. The symptoms of gastro-intestinal infection can then be mediated by various mechanisms (see Table 37.1).

Clinical manifestations

Many cases of gastro-intestinal infection are asymptomatic or cause subclinical illness. Gastroenteritis is the most common syndrome of gastro-intestinal infection, presenting with symptoms such as vomiting, diarrhoea and abdominal pain. The term ‘dysentery’ is sometimes applied to infections with Shigella (bacillary dysentery) and Entamoeba histolytica (amoebic dysentery), where severe colonic mucosal inflammation causes frequent diarrhoea with blood and pus. Table 37.2 shows the most important causative agents of gastroenteritis together with a brief description of the typical illness that each causes. However, the symptoms experienced by individuals infected with the same organism can differ considerably. This is important because it means that it is rarely possible to diagnose the cause of gastroenteritis on clinical grounds alone.

Table 37.2 Characteristic clinical features of various causes of gastroenteritis

Causative agent Incubation period Symptoms (syndrome)
Campylobacter 2–5 days Bloody diarrhoea
    Abdominal pain
    Systemic upset
Salmonella 6–72 h Diarrhoea and vomiting
    Fever; may be associated bacteraemia
Shigella 1–4 days Diarrhoea, fever (bacillary dysentery)
Escherichia coli
Enteropathogenic 12–72 h Infantile diarrhoea
Enterotoxigenic 1–3 days Traveller’s diarrhoea
Enteroinvasive 1–3 days Similar to Shigella
Verotoxin-producing 1–3 days Bloody diarrhoea (haemorrhagic colitis)
    Haemolytic uraemic syndrome
Staphylococcus aureus 4–8 h Severe nausea and vomiting
Clostridium perfringens 6–24 h Diarrhoea
Bacillus cereus
Short incubation period 1–6 h Vomiting
Long incubation period 6–18 h Diarrhoea
Vibrio cholerae O1, O139 1–5 days Profuse diarrhoea (cholera)
Vibrio parahaemolyticus 12–48 h Diarrhoea, abdominal pain
Clostridium difficile Usually occurs during/just after antibiotic therapy Diarrhoea, abdominal pain, pseudomembranous enterocolitis
Giardia lamblia 1–2 weeks Watery diarrhoea
Cryptosporidium 2 days–2 weeks Watery diarrhoea
Entamoeba histolytica 2–4 weeks Diarrhoea with blood and mucus (amoebic dysentery), liver abscess
Viruses 1–2 days Vomiting, diarrhoea
    Systemic upset

Gastro-intestinal manifestations of infection with VTEC range from non-bloody diarrhoea to haemorrhagic colitis. In addition, VTEC are the most important cause of HUS, a serious complication which is most common in young children and the elderly. HUS is defined by the triad of microangiopathic haemolytic anaemia, thrombocytopenia and acute renal dysfunction. The mortality is about 5% and up to half the survivors suffer long-term renal damage.

The clinical spectrum of CDI ranges from asymptomatic carriage to life-threatening pseudomembranous colitis (so-called because yellow-white plaques or membranes consisting of fibrin, mucus, leucocytes and necrotic epithelial cells are found adherent to the inflamed colonic mucosa).

Enteric fever, resulting from infection with S. enterica