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Ovid: Oxford Handbook of Tropical Medicine

Editors: Eddleston, Michael; Pierini, Stephen; Wilkinson, Robert; Davidson, Robert Title: Oxford Handbook of Tropical Medicine, 2nd Edition Copyright ©2005 Oxford University Press (Copyright 2005 by M. Eddleston, S. Pierini, R. Wilkinson, and R. Davidson) > Table of Contents > Chapter 2 > Chapter 2D – Diarrhoeal diseases > Acute diarrhoea with blood Acute diarrhoea with blood The presence of blood in diarrhoea (dysentery) usually signifies ulceration of the large bowel. The most common bacterial agents causing dysentery in the tropics are Shigella (bacillary dysentery) and Campylobacter. Shigellosis can be a serious infection that progresses to complications and death. Dysentery should be treated on clinical diagnosis with antibiotics that cover Shigella. If the patient does not improve after 48 hours, the antibiotic should be changed taking into account stool culture findings if available. If culture results are negative or not available, change the antibiotic (e.g. from co-trimoxazole to nalidixic acid or ciprofloxacin). Bacillary dysentery (shigellosis) Shigella dysenteriae, Sh. flexneri, Sh. Boydii, and Sh. sonneii cause the disease known as bacillary dysentery, with the former two species responsible for most morbidity and mortality (which may reach 20% in untreated cases). The disease may occur both endemically and epidemically, with children most frequently affected. The incubation period in humans (the only natural host) is 1–5 days following direct person to person contact (from cases of asymptomatic excreters) or ingestion of contaminated water and food. Clinical features: range from mild disease in which there is intermittent watery diarrhoea alone, to severe systemic complications. In severe cases, onset is usually rapid, with tenesmus, fever, and passage of frequent (up to 100/day) bloody mucoid stools. Intestinal complications include: toxic megacolon, perforation, and protein-losing enteropathy. Systemic complications include: dehydration, hypoglycaemia, and electrolyte imbalance (particularly hyponatraemia), haemolytic-uraemic syndrome, convulsions (particularly in children, often before the onset of diarrhoea), Reiter’s syndrome, thrombotic thrombocytopenic purpura, pneumonia. Invasive disease may give ‘rose spots’ — crops of 2–4 mm papules which fade on pressure, usually appearing on the upper abdomen and lower chest. Diagnosis: the clinical distinction between bacillary and amoebic dysentery is usually impossible. Stool microscopy may show leukocytes and haematophagus trophozoites of amoeba. Management

  • Oral rehydration is sufficient for mild disease.
  • In severe disease, ampicillin or trimethoprim (or co-trimoxazole) should be given, although resistance is common in many places; quinolones such as ciprofloxacin are an alternative. Antimicrobial sensitivities should be sought from individual cultures wherever possible.

Prevention: no vaccine is currently available. P.123
Causes of acute diarrhoea with blood

  • Bacillary dysentery (shigellosis)
  • Enterohaemorrhagic E. coli
  • Campylobacter enterocolitis
  • Salmonella enterocolitis
  • Yersinia enterocolitis
  • Amoebic dysentery
  • Balantidium coli enterocolitis
  • Massive Trichuris infection
  • Antibiotic-associated colitis (pseudomembranous colitis)
  • S. mansoni or S. japonicum infection

Enterohaemorrhagic E. coli (EHEC) These bacteria produce vero cell cytotoxins similar to the toxin produced by Shigella dysenteriae. The most common EHEC is E. coli 0157. These bacteria have been associated with a number of outbreaks of inflammatory, haemorrhagic colitis and are implicated in the haemolytic-uraemic syndrome (HUS). Infections occur most frequently in the summer months. Contaminated food, particularly ground beef in hamburgers or milk, is the most common cause; cider, fruit, and vegetables may be contaminated by animal faeces. Cross-contamination of meat products has been responsible for outbreaks. Clinical features: the illness may start with watery diarrhoea, blood appearing after 2–3 days. Vomiting and abdominal tenderness are common and the infection may be confused with appendicitis, intussusception, or inflammatory bowel disease. HUS is a serious life-threatening complication that occurs in 8–10% of children with known E. coli 0157 infection usually about a week after onset of diarrhoea. It is characterized by thrombocytopaenia, renal failure, and CNS involvement. Diagnosis: stool culture is necessary to make the definitive diagnosis but is not generally available. The presence of an outbreak and exposure risk should be sought in the history. Management

  • Oral rehydration and supportive care.
  • Antibiotic treatment is not indicated and has been associated with increased duration. Some, but not all, studies suggest that antibiotic use may increase the risk of the HUS. Antimotility drugs should be avoided.

Prevention: improve animal management practices, food preparation, and food storage. P.124
Campylobacter enterocolitis C. jejuni, C. coli, or C. laridis cause frequent epidemics in nurseries or paediatric wards and are common in the community in developing countries. Infective bacteria may continue to be excreted in the faeces up to 3 weeks after the cessation of diarrhoea. Campylobacter infect most mammals and birds and transmission may be by contact with animal or poultry excreta or contaminated food or water. Clinical features: the disease is normally self-limiting in 5–7 days. Severe, disseminated infection can occur with concurrent malnutrition, hepatic dysfunction, malignancy, diabetes mellitus, renal failure, and immunosuppression. Complications include bacteraemia, meningitis, deep abscesses, cholecystitis, and reactive arthritis. Diagnosis: clinically, the enterocolitis often starts with fever, abdominal pain, and watery diarrhoea, followed by bloody diarrhoea in some cases when it becomes indistinguishable from Shigella and Salmonella infections. Abdominal pain may be prominent and continue after diarrhoea settles. Diagnosis depends on Gram stain or dark field microscopy of faecal smears +/- culture. In severe disease, colonoscopic biopsy may be needed. Prevention: Campylobacter infection is an almost ubiquitous zoonosis. Prevention depends on breaking the chain of food and water contamination. No vaccine is currently available. Yersinia enterocolitis Yersinia enterocolitica is a rare cause of diarrhoea in the tropics. There may be low-grade fever, bloody diarrhoea, and abdominal pain affecting mainly children <5 yrs, plus nausea, vomiting, headache, or pharyngitis. Infection may spread to cause: septicaemia; peritonitis; hepatic, renal and splenic abscesses; pyomyositis; and osteomyelitis, although such complications are more common in immunocompromised adults or in patients who are iron overloaded (e.g. haemochromatosis). Diagnosis: culture from stool or other focal sites of infection. Balantidium enterocolitis Balantidium coli is a rare protozoal pathogen of humans. It exists in cyst and trophozoite forms, the former being responsible for transmission. Trophozoites invade the intestinal mucosa producing inflammation and ulceration. Clinical features: infection closely resembles amoebic colitis and may take one of three forms:

  • Asymptomatic carrier state (80%).
  • Acute dysentery that may be associated with nausea, abdominal pain, and weight loss. This is potentially fatal.
  • Chronic diarrhoea, frequently without blood.

Diagnosis: rests upon identification of the trophozoite in the faeces. P.125
Management Careful rehydration and symptomatic relief is usually sufficient for all three infections. Severe disease may require antibiotics:

  • Campylobacter enterocolitis

In severe dysenteric type disease, use erythromycin. Resistant strains (especially C. coli) may need trimethoprim (or co-trimoxazole) or ciprofloxacin.

  • Yersinia enterocolitis

In complicated disease, use combinations of gentamicin, cefotaxime, ciprofloxacin, or doxycycline.

  • Balantidium enterocolitis

If necessary, tetracycline 500 mg PO qds for 10 days in severe disease. The parasite is also sensitive to ampicillin and metronidazole. P.126
Salmonella enterocolitis Salmonella typhimurium and S. enteritidis enterocolitis is an important public health problem in the developing world. Transmission is faeco-oral, usually by ingestion of contaminated food (they survive freezing at 20°C). The organisms are widely distributed among wild and domestic animals. The incubation period is 24–48 hrs (up to 72 hrs); bacteria are then excreted in the faeces for up to 8 weeks following infection. There are associations with both malaria and HIV infection. Clinical features: range in severity according to the serotype involved. Two (often overlapping) clinical syndromes are seen.

  • Acute enterocolitis: nausea and vomiting, headache, fever, and malaise, rapidly progressing to diarrhoea with cramping abdominal pains. Initially voluminous and watery, the stool changes to ‘colitic stool’ with blood and mucus as the disease progresses. There may be LIF pain and rebound tenderness. Infrequently, ileal involvement is dominant with symptoms mimicking appendicitis. Severe colitis may be complicated by toxic megacolon.
  • Invasive salmonellosis: bacteraemia rates of 8% have been recorded, with higher rates for certain serotypes. Predisposing factors are: extremes of age, immunosuppression, malignancy, gastric hypoacidity (e.g. antacid use), concurrent severe disease, bartonellosis, and sickle cell disease. Systemic illness is characterized by swinging fevers, rigors, and general toxicity accompanying the diarrhoea, or a typhoid-like illness characterized by sustained fever, splenomegaly, rose spots, and minimal diarrhoea. There may be metastatic spread to meninges (almost exclusively in children < 2 yrs old), bones and joints, lungs, endocardium and arteries, liver, spleen, ovaries, or kidneys. A reactive arthritis is infrequently seen. Patients with chronic schistosomiasis are prone to 2° Salmonella bacteraemia since the bacteria live within the helminth and are protected from antibiotics.

Diagnosis: requires isolation of the bacteria from faecal samples or blood cultures. Sigmoidoscopy may be used in severely ill patients. Salmonella typhi does not usually present with diarrhoea and should not be confused with Salmonella enterocolitis. Management

  • Careful rehydration and supportive care is usually sufficient.
  • Most antibiotics do not influence the clinical course and may prolong bacterial carriage.
  • To patients with severe colitis and/or invasive disease, plus those in whom the risk of developing severe disease is high (eg. neonates, immunosuppressed, and elderly), give ciprofloxacin 500 mg PO bd for 5 days.
  • Chloramphenicol, amoxicillin, or trimethoprim (or co-trimoxazole) may be effective in systemic disease, but local resistance is increasing. Cefotaxime is highly effective, where available.

Amoebic dysentery Around 480 million people worldwide are infected by the protozoan Entamoeba histolytica and, although only about 10% are symptomatic, it is the third leading parasitic cause of death after malaria and schistosomiasis, with an annual mortality of ~100,000. Severe infection occurs in pregnant women, very young children, the malnourished, and people on steroids. Transmission: occurs via the faeco-oral route, usually through food and drink becoming contaminated with human faeces. Prevalence is highest in areas where human faeces are used as fertilizer. Sexual transmission also occurs. Cysts are ingested and pass into the small and large intestine, dividing to form metacysts and trophozoites which produce further cysts. These are evacuated in the stool and remain viable and infective for several days (up to 2 months in cool, damp conditions). E. histolytica has the capacity to destroy almost any tissue in the body, with amoebic liver abscess being the most common extra-intestinal manifestation. Clinical features: range from the asymptomatic carrier state to fulminant colitis with perforation and multi-organ involvement. Intestinal amoebiasis usually has an insidious onset with abdominal discomfort and diarrhoea becoming increasingly bloody and mucoid as severity increases. Tenesmus occurs in half the patients and is always associated with rectosigmoid involvement. On palpation, there is frequently tenderness over the caecum, transverse, and sigmoid colon and the liver may be enlarged and tender. Colonoscopy may reveal hyperaemic, necrotic ulcers covered with a yellowish exudate, particularly in the region of the flexures. Following repeated amoebic infection, an amoebal granuloma (amoeboma) may develop (most frequently at the caecum) where it may be palpable and mistaken for a malignant mass. Extra-intestinal amoebiasis: the most common form is a liver abscess which may in turn give rise to pericardial, pleuropulmonary, cerebral, genitourinary, or cutaneous disease. It may occur without dysentery. Diagnosis: is often difficult. Examine at least 3 stool samples using concentration and permanent stain techniques, preferably before administration of medications or contrast media since these interfere with amoebae recovery. The presence of E. histolytica trophozoites containing ingested erythrocytes is diagnostic of amoebiasis. However, the demonstration of cysts in a patient with GI symptoms does not necessarily indicate that amoebiasis is causing these symptoms. The cysts of the lumen-dwelling amoeba E. dispar is identical to invasive E. histolytica and cannot be distinguished microscopically. Techlab Entamoeba 11® is a faecal ELISA based on lectin detection that will differentiate invasive E. histolytica cysts or trophozoites from those of E. dispar. Prevention: improved hygiene; no vaccine is yet available. Management

  • Metronidazole 800 mg PO tds for 5 days followed by
  • Diloxanide furoate 500 mg tds for 10 days.
  • If there are signs of peritonism, add a broad spectrum antibiotic.

(Metronidazole is effective against the trophozoite, but because it has little effect on the cysts treatment should be followed by a luminal amoebicide such as diloxanide). P.128
Trichuriasis (whipworm) Thought to infect up to 25% of the world’s population, Trichuris trichuria are 3–4 cm long and colonize the colon and rectum after ingestion of faecally contaminated soil. Life cycle: ingested eggs hatch in the small intestine releasing larvae which mature in the villi for ~1 week before colonizing the caecum and colorectum. Released eggs pass out in the stool and can resist low temperatures, but not desiccation. The time from ingestion to appearance of eggs in the faeces is ~60 days. The perianal area is covered with eggs and autoinfection occurs by the eggs being carried from the anal margin directly to the mouth. Clinical features: are often absent in mild infections. However, co-infection with Ascaris lumbricoides or hookworms (which is common) may result in RIF pain, vomiting, distension, flatulence, and weight loss. Heavy worm burden can result in lower GI haemorrhage, mucopurulent stool, and dysentery, with rectal prolapse. 2° infection with E. histolytica or B. coli can aggravate mucosal ulceration and exacerbate dysentery. In such cases there may be finger clubbing and growth retardation in children. Diagnosis: is by detection of eggs in the stool. An egg count may be done and indicates the degree of infection (>30,000/g stool is heavy infection, implying the presence of several hundred adult worms). There may be anaemia and hypoalbuminaemia, though eosinophilia usually indicates concomitant Toxocara infection. Proctoscopy may reveal worms attached to a reddened, ulcerated rectal mucosa. AXR can show changes similar to those seen in Crohn’s disease. Management: mebendazole 500 mg or albendazole 400 mg, both PO once, are equally effective, although there may be regional differences in albendazole sensitivity. 3 day courses may be used for heavy infections. Prevention: control is as for other soil-transmitted helminths. Antibiotic-associated colitis This condition was previously called pseudomembranous colitis or Clostridium difficile colitis. It is caused by infection with C. difficile following disruption of the normal bowel flora by broad-spectrum oral or IV antibiotic therapy. It is apparently rare in the tropics but is one of the most common causes of hospital acquired diarrhoeal infection in developed countries. Clinical features: vary from the asymptomatic to toxic megacolon and are due to the production of toxins. Sigmoidoscopy shows characteristic yellow plaques (pseudomembranes) on the mucosa. Management: metronidazole 800 mg PO stat, then 400 mg PO tds for 10 days. Oral vancomycin (0.5–2 g PO daily in 3–4 divided doses for 7–10 days) is an expensive alternative. Prevention: careful use of broad-spectrum antibiotics. P.129

Fig. 2D.5 Life cycle of T. trichiura

Clindamycin Because it is associated with potentially fatal antibiotic-associated colitis, clindamycin has few primary indications (staphylococcal joint and bone infections; intra-abdominal sepsis). However, the WHO considers clindamycin to be a valuable drug that should be used when other antibiotics are known to be ineffective or inappropriate for a given individual. It should be stopped immediately that diarrhoea occurs. It should also be borne in mind that in western countries the most common antibiotics associated with the development of antibiotic-associated colitis are the broad-spectrum β-lactams.

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