Tropical Sprue

Tropical sprue is a chronic malabsorptive syndrome of uncertain but presumed infective or postinfective aetiology. It occurs in residents of, or travellers returning from, defined tropical and subtropical regions, notably parts of South Asia, Southeast Asia and the Caribbean.

It is characterised by small intestinal villous abnormality, malabsorption of multiple nutrients, and a generally good response to prolonged antibiotic and folate based therapy.

This distinguishes it as a distinct clinical entity from coeliac disease despite some overlapping histological and clinical features.

Pathophysiology

• The precise aetiology remains incompletely understood. The prevailing hypothesis implicates chronic small intestinal bacterial overgrowth, potentially triggered by an initial acute infective gastroenteritis episode.
• Bacterial toxin production and chronic mucosal inflammation then drive progressive villous blunting and malabsorption along a variable length of small bowel.
• The condition is defined by its geographic and temporal association with residence in, or travel to, an endemic tropical region. Symptoms generally develop after residence or travel of at least several weeks to months. This distinguishes it from acute traveller's diarrhoea and other more transient enteric infections.

• The typical presentation is chronic diarrhoea, often with steatorrhoea, abdominal bloating and cramping, with progressive weight loss and fatigue. It develops over weeks to months following the relevant tropical exposure.
• Specific nutrient malabsorption develops over time. It includes folate deficiency (often an early and prominent feature), vitamin B12 deficiency (particularly with more extensive or prolonged small bowel involvement) and iron deficiency. In more severe or prolonged disease, other fat soluble vitamin deficiencies occur.
• Glossitis and angular cheilitis, reflecting the associated haematinic deficiencies, may accompany the core gastrointestinal symptoms. So may peripheral oedema in more severe protein losing states.
• A clear history of residence in, or travel to, a recognised endemic region is essential. It is generally for a period of at least one month. Symptom onset may be during this period or, notably, sometimes only after return home.
• This history supports the diagnosis and distinguishes it from other causes of chronic diarrhoea and malabsorption.

• Diagnosis relies on a compatible clinical picture, the relevant geographic exposure history, and exclusion of alternative causes of malabsorption. It also needs small intestinal biopsy showing villous blunting.
• The villous changes are generally less severe and more patchy than the diagnostic changes of coeliac disease. Considerable histological overlap can occur, so the distinction can be genuinely challenging on histology alone.
• Actively exclude coeliac disease, given overlapping clinical and histological features. Use coeliac specific serology (tissue transglutaminase antibodies).
• Where diagnostic uncertainty persists, assess clinical and histological response to a gluten free diet. Coeliac disease would be expected to respond to gluten exclusion, whereas tropical sprue would not.
• Laboratory testing typically shows evidence of malabsorption: reduced serum folate and vitamin B12, and iron deficiency. Where more extensive assessment is undertaken, it may show reduced fat soluble vitamin levels, and evidence of fat malabsorption on stool fat quantification where performed.
• Perform stool microscopy and culture, with specific testing for recognised intestinal parasites (Giardia and others). This excludes a specific, identifiable ongoing infective cause of the malabsorption. Such a cause would be managed specifically rather than with the broader antibiotic and folate approach used for tropical sprue.

• Folic acid 5 mg orally once daily is a central component of treatment. It corrects the frequently significant associated folate deficiency. Historically, many patients improved substantially with folate alone, even before antibiotic therapy was added.
• Give tetracycline 250 mg orally four times daily alongside folic acid. Doxycycline 100 mg twice daily is a more convenient and better tolerated modern alternative. Treatment continues for a prolonged period, typically three to six months, reflecting the presumed bacterial overgrowth contribution to the pathophysiology.
• Guide treatment duration by clinical and, where feasible, histological response.
• Vitamin B12 replacement is an essential component of management, as detailed under that condition. It is typically intramuscular hydroxocobalamin where deficiency is confirmed. Correct other identified nutrient deficiencies (iron, fat soluble vitamins) alongside the folate and antibiotic based treatment.
• Give nutritional support and dietary advice. A generally normal, well balanced diet is used, rather than any specific restrictive approach. This is in clear distinction from the gluten free diet required for coeliac disease. It reinforces the importance of confidently excluding that diagnosis before committing to tropical sprue management.
• The majority of patients show substantial clinical improvement within weeks of starting treatment. Full histological recovery generally follows over a more prolonged period of months.
• Relapse after apparently successful treatment is recognised, particularly with re exposure to the same endemic region. It warrants further treatment.
• Specialist gastroenterology input is generally appropriate. The diagnosis is rare outside endemic settings and overlaps with other causes of malabsorption. Input confirms the diagnosis, excludes alternative or coexisting pathology, and guides treatment approach and duration.