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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 > Persistent or chronic diarrhoea Persistent or chronic diarrhoea Persistent is the preferred term for episodes starting acutely and associated with gastrointestinal infections. Defined as diarrhoea lasting >2 weeks. Causes of persistent or chronic diarrhea

  • Secondary events
    • Subclinical malabsorption
    • Hypolactasia (1° and 2°)
    • Tropical sprue
    • Cow’s milk protein intolerance
  • Continuing infection
    • Strongyloidiasis
    • Cryptosporidiosis
    • Enteropathogenic E. coli
    • Intestinal flukes
    • Chronic intestinal schistosomiasis
  • Delayed recovery
    • Malnutrition
    • Zinc deficiency
  • Sequential new infections
  • Others
    • HIV enteropathy
    • Chronic calcific pancreatitis
    • Short bowel disease (e.g. recovered pigbel disease)
    • Ileocaecal TB
    • Lymphoma — Burkitt’s and Mediterranean
    • Acute and chronic liver disease
    • Inflammatory bowel disease and coeliac disease

Malabsorption and steatorrhoea May be due to a wide range of causes. The key signs and symptoms are:

  • Diarrhoea: stool is typically loose, bulky, offensive, greasy, light coloured, and difficult to flush away.
  • Abdominal symptoms: discomfort, distension, flatulence.
  • Nutritional deficiencies: e.g. glossitis, pallor, muscle pain bruising, hyperpigmentation, CNS or PNS signs, skeletal deformity.
  • General ill health: anorexia, weight loss, lethargy, dyspnoea, fatigue.
  • Features related to underlying cause: surgical scars, systemic disease.

Investigating malabsorption Do FBC, U&Es ESR, LFTs, stool culture, and microscopy. Others include faecal fat, INR (deficiency of fat-soluble vitamins), carbohydrate absorption (after glucose or xylose), Schilling test (as measure of ileal function) Clinical malabsorption 1° hypolactasia (a lactase deficiency of genetic origin) is a common non-infectious cause of watery diarrhoea occurring after consumption of milk. 2° hypolactasia results from brush border damage during GI infection; it may persist afterwards. Incomplete hydrolysis of lactose results in osmotic P.145
diarrhoea, abdominal pain, distension, and flatulence. Colonic bacteria may produce lactic acid by hydrolysing lactose — this can also cause an irritative diarrhoea. Diagnosis: rests upon detection of worsening symptoms with increased lactose intake (lactose tolerance test), acid stools with positive reducing substances, the hydrogen breath test, or a lactase assay in jejunal biopsy. Management: consists of reducing lactose in diet, giving only small amounts of lactose at a time. Yogurt may be substituted for milk; cereal-milk mixtures have also been used successfully. In severe cases it may be necessary to eliminate lactose-containing products from the diet. They may be gradually reintroduced after 6 weeks without symptoms. Care should be taken to ensure that reduction or elimination of lactose containing foods does not reduce energy and nutrient intake. Possible mechanisms for persistent diarrhoea Different mechanisms may prolong diarrhoea. In areas where sanitation and clean water are lacking and diarrhoea incidence is high, most persistent diarrhoea seems to be attributable to frequent new infections combined with delayed recovery (3 and 4). Delayed recovery is often due to nutrient deficiencies. Persistent diarrhoea is associated with malnutrition and high mortality in children. Dietary management with continued feeding, correction of micronutrient deficiencies, antimicrobial treatment of concomitant infections and dysentery — as well as rehydration if necessary — has been shown to be effective in 80% of children. Causes of malabsorption

  • Infective: acute enteritis, intestinal TB, parasitic infections, traveller’s diarrhoea, Whipple’s disease.
  • Anatomical/motility: blind loops, diverticulae, strictures, fistulae, small bowel lymphoma, systemic sclerosis, diabetes mellitus, pseudo-obstruction, radiotherapy, amyloidosis, lymphatic obstruction (TB, lymphoma, cardiac disease).
  • Defective digestion: chronic pancreatitis, cystic fibrosis, food sensitivity (lactose, gluten), malnutrition, gastric/intestinal surgery, Zollinger–Ellison syndrome, pancreatectomy, biliary obstruction, terminal ileal disease/resection (short bowel syndrome), parenchymal liver disease, bacterial overgrowth.
  • Drugs: antibiotics, cholestyramine, metformin, methyldopa, alcohol, antacids, purgative misuse, paraaminosalicylic acid.

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Post-infective malabsorption (PIM or tropical sprue) A better name for this syndrome of diarrhoea, malabsorption, and weight loss is post-acute infective malabsorption, since a chronicity of at least 2 months is required for the diagnosis. Malabsorption of nutrients is quantitatively more important than that of water or electrolytes in this condition. It produces an estimated 10% deficit of dietary energy. It is therefore obvious that its impact on individuals (particularly children) living on marginal diets is significant and that it will quickly exacerbate malnutrition. PIM is common in central America, northern South America, and Asia; it also occurs around the Mediterranean and in the Middle East. Aetiology: is thought to involve:

  • Genes — an association with certain HLA antigens has been found
  • Infection — Klebsiella pneumoniae, Enterobacter cloacae, and E. coli are the organisms most commonly isolated from mucosal biopsy or luminal fluid; they may persist in overgrowth for many months
  • Jejunal morphology — partial villous atrophy, crypt hyperplasia, elevated jejunal surface pH, and changes in gut hormones and colonic function have been found.

Clinical features: chronic diarrhoea of >2 months duration with large, pale, fatty stools and often flatulence. Other features include weight loss, glossitis, megaloblastic anaemia, fluid retention, depression, lethargy, amenorrhoea, and infertility. Serum folate and vitamin B12 may fall to very low levels. Hypoalbuminaemia and oedema are late signs. Investigations: 1-hr blood xylose concentration following a 5g or 25g loading dose; 72-hr faecal fat estimation; Schilling test; serum B12; RBC folate; serum globin; and albumin. Exclude faecal parasites. Barium meal and follow-through will show dilated loops of jejunum with clumping of barium. Jejunal biopsy may show a ridged or convoluted mucosa, depending on the duration of the disease, with T lymphocyte infiltration. Management

  • Eliminate bacterial overgrowth with tetracycline 250 mg PO qds for at least 2 weeks.
  • Aid mucosal recovery by providing folate supplements.
  • Provide a suitable diet to promote weight gain.
  • Give symptomatic relief in the acute stages:
    • Codeine phosphate 30 mg PO tds or
    • Loperamide 4 mg PO initially, then 2 mg after each loose stool. Usual dose 6–8 mg od; maximum dose 16 mg od.

Tropical enteropathy and subclinical malabsorption Repeated low-grade viral, bacterial, and parasitic infections may also cause damage to the small intestinal mucosa of individuals living in the tropics. Concurrent systemic infections (e.g. TB, pneumococcal pneumonia), malnutrition, and pellagra have also been implicated in causing subclinical malabsorption. Xylose, glucose, and vitamin B12 are most commonly malabsorbed. P.147

Fig. 2D.7 Distribution of post-infective malabsorption.
Fig. 2D.8

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Other causes of malabsorption Whipples disease: a rare malabsorptive condition characterized by transient migratory polyarthritis, fever, lymphadenopathy, and cardiac and neurological complications. It is caused by Tropheryma whippelii. Treatment is with penicillin, tetracycline, or co-trimoxazole; many patients relapse. Lymphangiectasia: either 1° or following an abdominal malignancy, it results in lacteal dilatation. Clinically there is peripheral oedema secondary to hypoproteinaemia owing to a protein-losing enteropathy. Diagnosis requires small bowel biopsy. Treatment is with a low-fat diet. Abetalipoproteinaemia: a rare AR disorder, usually presenting in childhood due to defective triglyceride transport from the liver and gut. Eventually neurological dysfunction (peripheral neuropathy, cerebellar ataxia) may follow. Diagnosis is by small bowel biopsy and symptomatic treatment is with low-fat diet and vitamin supplementation. Other causes of chronic diarrhoea

  • Chronic calcific pancreatitis A syndrome of pancreatic calcification associated with both exocrine and endocrine impairment, commonly encountered in the tropics, especially equatorial Africa, southern India, and Indonesia. Its aetiology is unknown, although childhood kwashiorkor, gastroenteritis, excessive alcohol consumption, dehydration, and ingestion of cassava (Manhiot esculenta) have all been implicated. Clinical features: are of chronic malabsorption with weight loss, often associated with DM (10% of diabetes in E&W Africa) and (sometimes severe) pain. There is an association with pancreatic malignancy. Management: consists of diabetic control, a low-fat diet, and enzymatic supplementation (e.g. pancreatin BP 6g orally with food). Pancreatic dysfunction may also result from schistosomiasis, trichinellosis, cysticercosis, clonorchiasis, opisthorchiasis, and hydatid disease. Obstruction is commonly a complication of A. lumbricoides infection.
  • Intestinal lymphoma Wide varieties of lymphomas affect the GI tract, originating in either intestinal lymph nodes (e.g. Hodgkin’s lymphoma) or mucosa-associated lymphoid tissue (MALT lymphomas). Weight loss is a common feature and nodal disease may be confused with intestinal TB, as X-ray changes appear similar. Diagnosis requires biopsy.
  • Intestinal parasites Many parasites such as Giardia, Cryptosporidium, Trichuris, and Strongyloides cause diarrhoea and have been described above. Other intestinal parasites are described below.

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Fig. 2D.9 Mechanisms of Steatorrhoea.

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Intestinal flukes These pathogens are common throughout Asia (particularly S.E. Asia), where their prevalence may reach 30% in certain populations. Children are more heavily infected and prone to symptoms.

  • Fasciolopsiasis Caused by Fasciolopsis buski, infection is via consumption of metacercaria attached to the seed pods of water plants contaminated by human and pig faeces.
  • Echinostomiasis At least 15 Echinostoma spp. infect humans via the consumption of raw or undercooked freshwater snails, clams, fish, and tadpoles. In N.E. Thailand, it is commonly associated with Opisthorchis infection.
  • Heterophyasis Numerous species of the small (2.5 mm) Heterophyes flukes infect humans following consumption of raw aquatic foods and/or insect larvae.

Clinical features: the attachment of parasites to the intestinal mucosa results in inflammation and ulcer formation. Infections are frequently asymptomatic; when symptoms do occur, they are usually mild and non-specific — diarrhoea, flatulence, mild abdominal pains, vomiting, fever, and anorexia. Fasciolopsiasis may produce severe disease with ascites, oedema, anaemia, and symptomatic malabsorption. Eggs (and sometimes adult worms) of Heterophyes spp. may enter the lymphatics after mucosal penetration and be transported to other sites (notably heart, spinal cord, brain, lungs, liver, and spleen) where they cause granulomatous reactions. Myocarditis and neurological deficits may result. Diagnosis: faecal examination for eggs, after concentration. Differentiation between F. hepatica, F. buski, and echinostomes is often difficult. Similarly, heterophydiae eggs closely resemble those of Clonorchis and Opisthorchis. Recovery of adult worms from post-treatment faeces allows a definitive diagnosis, although in the case of the heterophyids this is difficult owing to their small size. Extraintestinal cases of heterophyiasis are also difficult to diagnose — they are often only revealed during surgery or autopsy. Management

  • Praziquantel is the drug of choice, with high efficacy at 25 mg/kg as a single dose.
  • Mebendazole or albendazole may be used for echinostomiasis although praziquantel is recommended in areas where other trematodes are present, due to its broad efficacy.

Prevention: should concentrate on breaking the faeco-oral cycle (e.g. stopping the use of human and pig excreta as fertilizer) possibly combined with community-based praziquantel treatment and education regarding the consumption of raw/undercooked foodstuffs. P.151

Fig. 2D.10 Eggs of Fascilopsis buski (top, 140×85µm) and Heterophyes heterophyes (below, 25×15µm)

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