**1. Introduction**

376 Current Topics in Tropical Medicine

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Strongyloidiasis is an intestinal parasitosis found in tropical and subtropical areas, where the warm climates are suitable for parasite survival (Barr, 1978). It is a common cause of morbidity and mortality, particularly in developing countries, and infects over one-quarter of the world's population (Genta, 1989). Approximately 52 species are known to infect mammals, birds, reptiles and amphibians (Speare, 1989). The most common globally distributed human pathogen of clinical importance is *Strongyloides stercoralis* (Schad, 1989). Another species, *Strongyloides fuelleborni,* is a zoonotic parasite that infects primates and is found sporadically in humans in Africa (Pampiglione & Ricciardi, 1972). *S. stercoralis* is a ubiquitous soil-transmitted intestinal nematode that was first reported in 1876 in French soldiers working in Vietnam. It is unique among helminths in that it completes its life cycle inside a single human host. A unique feature of strongyloidiasis is the ability of the parasite to autoinfect the host, which makes *S. stercoralis* a significant public health problem (Grove, 1989).

#### **2. Epidemiology**

The epidemiology of *Strongyloides* infection is poorly understood because it is difficult to detect and can be underestimated (Albonico et al., 1999; Viney & Lok, 2007). However, it is estimated that from 30 a 100 million people are infected worldwide with *Strongyloides*, and can range from asymptomic to multiorgan failure (Genta, 1989). *Strongyloides* is found in tropical and subtropical areas and requires specific soil and climate conditions for its development. In North America, Latin America, Africa and Southeast Asia, the infection is endemic (Roxby et al., 2009). The risk of acquiring strongyloidiasis is higher in rural areas, among people who work with soil, and among lower socioeconomic groups *(*Vadlamudi et al., 2006; Viney & Lok, 2007*).* Walking barefoot in areas where human faeces containing the parasite are deposited increases the probability of acquiring the infection (Grove, 1994).

#### **3. Parasite**

*S. stercoralis* has free-living and parasitic life cycles, and the morphology of each differs. Parasitic worms are female adults that reproduce by parthenogenesis and measure approximately 1 - 10 mm in length by 27 -95 μm in width. Free-living adults are

Hyperinfection Syndrome in Strongyloidiasis 379

The infective larvae reach the small intestine, where they moult twice to become female adult worms. These females reproduce in the absence of males by parthenogenesis. The females are embedded in the intestinal mucosa and produce eggs in the duodenum. The rhabditiform larvae emerge from the hatching eggs and migrate into the intestinal lumen, then pass into the external environment with the faeces. Depending on temperature and humidity, the rhabditiform larvae may have two different life cycles in the environment: an indirect (heterogonic) life cycle, in which the rhabditiform larvae differentiate into freeliving adults and release eggs that hatch and transform into infective larvae, or a direct (homogonic) life cycle, in which the rhabditiform larvae may moult directly into filariform

One characteristic that differentiates *S. stercoralis* from almost all other worms is its capacity to replicate within the host. Rhabditiform larvae in the bowel lumen transform into filariform larvae before excretion and invade the intestinal wall or the perianal skin, permitting ongoing cycles of autoinfection, an important feature of strongyloidiasis (Concha

The clinical presentation of strongyloidiasis varies with the status of the host´s immune system, and the infection is classified as acute, chronic or severe. Acute infections of strongyloidiasis manifest as a wide spectrum of clinical features ranging from asymptomatic disease to cutaneous (larva currens and urticaria), pulmonary (cough and tracheal irritation), and gastrointestinal symptoms (diarrhoea and constipation), although the

The ability of *S. stercoralis* to establish a cycle of autoinfection within the host results in chronic infections that can persist in an individual for decades. Chronic infections are often asymptomatic, but when symptoms occur they are usually mild, episodic and prolonged, including nausea, vomiting, diarrhoea, constipation, weight loss or cutaneous reactions

Uncontrolled autoinfection of *S. stercoralis* is more likely to occur in immunosuppressed patients, leading to hyperinfection syndrome. The pulmonary phase of hyperinfection due to migrating larvae resembles Löffler syndrome with coughing and wheezing, asthma-like symptoms, haemorrhaging and pneumonia. In the intestine, symptoms include diarrhoea, nausea, vomiting, abdominal pain, and weight loss (Concha et al., 2005; Viney & Lok, 2007). Bacteremia is a common complication of hyperinfection syndrome and is caused by filariform larvae that may lead bacteria from the bowel to the bloodstream with subsequent secretion into the host circulation (Bamias et al., 2010). Pathogens such as *Streptococcus bovis, Escherichia coli, Klebsiella pneumonia* or *Enterobacter cloacae* are found during fatal complications of strongyloidiasis (Link & Orenstein, 1999). The mortality rate of dissemination associated with bacterial infections can reach approximately 90% (Igra-

Dissemination occurs upon larval migration to organs beyond the range of the pulmonary phase, such as the liver, heart, lymph nodes, gallbladder, kidneys, pancreas, and brain (Keiser & Nutman, 2004). Petechiae and purpura have also been reported in disseminated cases as a result of larval migration through vessel walls, which promotes haemorrhage (Basile et al., 2010). Others complications of disseminated strongyloidiasis can occur and include syndromes such as cholecystitis, pancreatitis, paralytic ileus, intestinal perforation

larvae and repenetrate the host skin, restarting the cycle (Schad, 1989).

majority of *S. stercoralis* infections are resolved (Mahmoud, 1996).

et al., 2005).

(Grove, 1989).

Siegman et al., 1981).

**5. Clinical manifestation** 

approximately 1 mm, live in the soil, and reproduce sexually; females are slightly larger than males (Speare, 1989). Embryonated eggs are thin-shelled and measure approximately 55 - 60 μm in length and 28 - 32 μm in width. Rhabditiform larvae are the first-stage larvae (210 μm) and develop into free-living larvae or third-stage infective larvae that measure approximately 490-630 μm and are capable of infecting the host (Schad, 1989).
