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Chronic Strongyloidiasis – Don't Look and You Won't Find

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Chronic Strongyloidiasis – Don't Look and You Won't Find CLINICAL Chronic strongyloidiasis – Don’t look and you won’t find Wendy Page, Rick Speare Background hronic strongyloidiasis in humans is immunosuppressive therapy (especially caused by the remarkably persistent corticosteroids and chemotherapy), Strongyloidiasis is one of the most C roundworm Strongyloides as this can cause the hyperinfective neglected tropical diseases and it exists stercoralis, distinguished by its syndrome. in Australia. Patients may have acquired unique autoinfective lifecycle. General Patients who are immunocompromised, their initial infection while in an endemic practitioners (GPs) have an important such as those with diabetes, systemic area. Because of the autoinfective role in diagnosing and treating chronic lupus erythematosus (SLE), human cycle of Strongyloides stercoralis, the strongyloidiasis to prevent cases of fatal T-cell lymphotropic virus type 1, or organ causative agent, these patients may hyperinfection. Unless strongyloidiasis is transplant recipients, as well as patients remain infected for life unless effectively deliberately considered, the diagnosis is who are malnourished and infected, treated. Corticosteroids have precipitated 8 death in more than 60% of disseminated unlikely to be made. are at risk of dissemination. Aboriginal strongyloidiasis cases. and Torres Strait Islander patients from Epidemiology rural and remote areas in Australia Objective An estimated 370 million people should not be given immunosuppressive worldwide are infected with S. stercoralis.1 treatment without being tested or treated The aim of this article is to raise Strongyloidiasis is endemic in tropical and prophylactically for strongyloidiasis.9 awareness of the unique features of subtropical regions of the world where S. stercoralis and outline the important warmth, moisture and poor sanitation Life cycle role that general practitioners (GPs) favour its spread. A prevalence greater The traditional mode of S. stercoralis have in diagnosing and treating chronic than 5% is considered hyperendemic.2 infection is penetration of the skin by strongyloidiasis, as well as in preventing Some remote Aboriginal and Torres Strait microscopic, infective filariform larvae. cases of fatal hyperinfection. Islander communities in Australia have The larvae are then carried in the Discussion had prevalences up to 60%.3 In Australia, bloodstream to the right side of the heart. strongyloidiasis should be considered in They exit the pulmonary capillaries, enter Chronic strongyloidiasis is not an overt residents of endemic areas, immigrants the alveolar spaces in the lungs, ascend disease – if you don’t look for it, you (including older patients from southern the bronchial tree and are swallowed by won’t find it. In particular, patients who Europe), refugees, war veterans (World the host. In the small intestine, the larvae have lived in an endemic area or have War II and Vietnam War), and workers and mature into adult female worms (2–3 mm unexplained eosinophilia must be checked travellers returning from endemic areas with long) and penetrate the mucosa of the for the presence of the parasite before ‘a souvenir you don’t want to bring home’.4–7 proximal small intestine, where they can initiation of steroid or immunosuppressive lay up to 40 eggs a day. This occurs 17–28 therapy. These patients, if infected, may Who is at risk? days after the initial infection. The eggs develop hyperinfective syndrome, which Although history is important to identify hatch in the intestinal mucosa to release has a high fatality rate. those at risk of strongyloidiasis, the initial rhabditiform larvae that migrate to the exposure to infective larvae may have lumen of the intestine.2 occurred decades earlier. Doctors should The life cycle of S. stercoralis has three consider infection with S. stercoralis unusual features that make its eradication in all patients who are to receive difficult: 40 REPRINTED FROM AFP VOL.45, NO.1–2, JAN–FEB 2016 © The Royal Australian College of General Practitioners 2016 CHRONIC STRONGYLOIDIASIS CLINICAL • Autoinfective larvae: these can • Skin: larva currens is the only • Multiple end-organ failure: this penetrate the colonic wall or perianal pathognomonic sign in patients with is an outcome of disseminated skin, and enter the body to repeat the S. stercoralis infection. Erythematous strongyloidiasis with a poor prognosis migration that establishes ongoing serpiginous lesions appear and move despite treatment.2,14,24 internal reinfection. This autoinfective rapidly (2–10 cm per hour). This is cycle allows strongyloidiasis to persist more commonly seen on the trunk Early diagnosis improves for decades after the host has left and buttocks (Figure 1). Other signs outcome an endemic area. Hyperinfection or include pruritus, recurrent urticaria or Prevention of high morbidity and disseminated strongyloidiasis occurs a ‘rash that comes and goes’.2,4,14 A mortality from strongyloidiasis is because large numbers of parasitic ‘rapidly progressive purpuric petechial dependent on clinicians’ awareness. females develop in the small intestine eruption with a reticulated pattern’ Most cases of disseminated and thousands of autoinfective larvae has been described in disseminated strongyloidiasis are diagnosed at autopsy migrate through the organs.2 Prescribing strongyloidiasis.16 or in the late disseminated phase, when immunosuppressants, especially • Respiratory: pulmonary millions of parasites are in the body, corticosteroids, to undiagnosed strongyloidiasis manifestations which means they are more easily patients who are infected is a include dyspnoea, bronchospasm, identified in body fluids. Unfortunately, common precipitant for disseminated haemoptysis, bronchopneumonia, this is too late for the majority, who will strongyloidiasis because it stimulates pleural effusion, lung abscess and die from this disease. All individuals the autoinfective cycle.2,8,10 interlobular septal fibrosis.14,17 There who are infected, including those who • Parthenogenesis: the ability of the are reported cases of immigrants are asymptomatic, should be treated parasitic female to reproduce without in Australia with cavitary lesions on because hyperinfection is unpredictable a male contributes to the challenges of chest X-ray that mimicked tuberculosis and potentially fatal.14,15 successful treatment in humans. One but resolved after treatment with GPs have an important role in the remaining female parasite can result in anthelmintics.18 diagnosis, treatment and follow-up of recrudescence of infection. • Gastrointestinal: manifestations may patients with chronic strongyloidiasis by: • External phase of life cycle and free- include diarrhoea, hypokalaemia, • identifying patients at risk (who may living adults: S. stercoralis has the ability protein-losing enteropathy, be asymptomatic) to produce one generation of short- malnutrition, wasting, epigastric • considering strongyloidiasis as a lived, free-living adult male and female pain and tenderness that simulates differential diagnosis or underlying worms in the external environment. peptic ulcers, subacute obstruction cause for non-specific clinical Only one generation of free-living adults or segmental ileus, paralytic ileus, manifestations as outlined above. are produced by S. stercoralis and they ulcerative enteritis with intestinal Gram-negative sepsis should be a die within 10 days.2,11,12 The infective perforation and peritonitis, melaena, prompt to consider strongyloidiasis as larvae can survive in the soil for several and haematochezia.14,15,19 an underlying factor11,23,24 weeks if the environment is moist and • Genitourinary: manifestations may temperature is suitable (23–28°C).11 include nephrotic syndrome and renal abscess.15,20 Clinical presentations • Hepatic: manifestations may include The autoinfective larvae of S. stercoralis hepatomegaly and hepatic abscess.15,21 can invade any organ of the body, • Cardiac: manifestations may include including the central nervous system, pericardial effusion.22 through random migration.2,13–15 The • Haematological: eosinophilia is present symptoms of chronic strongyloidiasis may in 10–70% of chronic strongyloidiasis be protean, non-specific and intermittent, cases, but is less prevalent in making the underlying diagnosis elusive. disseminated strongyloidiasis. Signs and symptoms vary with the • Central nervous system (CNS): location and number of worms, and manifestations may include bacterial Figure 1. Larva currens on the trunk of female whether the autoinfective larvae have meningitis and abnormal CNS patient from northern New South Wales carried bacteria to extraintestinal locations. signs.2,13,23 These erythematous, serpiginous lesions appear and move rapidly (2–10 cm per hour), and are the • Sepsis: Gram-negative septicaemia or The following clinical presentations may pathognomonic sign of strongyloidiasis. alert the clinician to consider the diagnosis sepsis in any organ may occur due to Source: W. Page of strongyloidiasis: enteric bacteria.15,24 © The Royal Australian College of General Practitioners 2016 REPRINTED FROM AFP VOL.45, NO.1–2, JAN–FEB 2016 41 CLINICAL CHRONIC STRONGYLOIDIASIS • screening patients who are at risk Faecal testing has been the mainstay of strongyloidiasis and hyperinfection.27 False and advising prophylaxis prior to testing for ova, cysts and parasites. The negatives can occur when new cases have immunosuppressant therapy8,9,25 presence of live larvae, rather than eggs, not yet seroconverted. Also, patients who
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