A thirteen year old boy presented with acute progressive paraplegia and bladder incontinence. MRI revealed affection of spinal cord from the level of T1 to conus medullaris. CSF examination was normal. Diagnosis of acute demyelinating myelitis was made. Child was treated with intravenous methyl prednisolone for five days which was followed by oral prednisolone for three weeks. He recovered completely and steroid was tapered over next three weeks. However, at the end of six weeks after starting steroids, child presented with abdominal pain and distension, and vomiting. Clinical and abdominal examination were unremarkable. Hemogram revealed a total count of 15,000/cmm with 60% neutrophils, 36% lymphocytes and 4% eosinophils. HIV serology was negative. Urine microscopy revealed pyuria and urine culture grew E.coli in significant colony count. Child was started on intravenous antibiotics Amikacin and Ceftriaxone as per sensitivity report. While on day seven of antibiotics, child developed headache and meningeal signs. CSF examination revealed polymorphic pleocytosis with normal sugar and mildly elevated protein; Gram staining, AFB staining and culture were negative. CT scan of head was normal. Child continued to have abdominal distention, vomiting and developed persistent diarrhea. Stool routine evaluation was normal, there were no ova, cysts or pus cells, and no fat globules or reducing substances. There was no growth on stool culture. Child was treated with parenteral fluids and electrolytes as serum sodium remained persistently low. Repeat stool routine examination, and USG abdomen and erect X-ray abdomen were normal. Child underwent upper GI endoscopy and duodenal biopsy was taken. The condition of the child progressively worsened with development of severe malnutrition, malabsorption and anasarca. Child gradually progressed to hypotension and muffled heart sounds with left ventricular failure. Echocardiography revealed mild to moderate pericardial effusion. However, the child expired before a pericardiocentesis could be done. Duodenal biopsy report later revealed blunting with abundant rhabditiform larvae of S. stercoralis.

S. stercoralis usually persists and replicates in a host for a decade without symptoms. However when the host becomes immunocompromised, it can lead to fatal conditions like hyper-infection syndrome and disseminated strongyloidiasis. The disease should be suspected in an immunocompromised host who comes from an area endemic for Strongyloides stercoralis. In endemic areas, a prevalence of as high as 40% is observed in general population. However, disseminated strongyloi-dasis is very rare in immunocompetent host. Clinical manifestations of disseminated strongyloidosis are nonspecific. The onset is usually sudden with generalized abdominal pain, distension and fever, associated with indigestion, vomiting, diarrhea, steatorrhoea, protein losing enteropathy and weight loss. There is remarkable absence of eosinophilia. Steroids may not only affect the host’s cellular immunity, but also mimic an endogenous parasitic-derived regulatory hormone. Strongyloides were noticed to produce more eggs in the presence of exogenous steroids. Due to immuno-suppressant therapy, there is a larger proportion of the rhabditiform larvae which mature into the filariform larvae within the host. This leads to a greater larval load and dissemination. It involves widespread dissemination of larvae to extra intestinal organs (CNS, heart, urinary tract, endocrine organs) which are not ordinarily part of parasitic lifecycle. The enteric organisms either carried by the larvae or through intestinal ulcers, cause bacteremia.

Hyperinfection implies confinement of the Strongyloides larvae to the organs normally involved in the pulmonary autoinfection cycle (i.e., GI tract, lungs, and peritoneum). Disseminated strongyloidiasis is defined as larvae migrating to end organs not usually involved in the normal cycle of the parasite, such as brain and skin. The definitive diagnostic test is identification of S. stercoralis larvae in stool examination. Single stool examination has low sensitivity (30%). Hence multiple examinations are recommended. In children with hyper-infection syndrome, larvae may be found in samples from sites of potential larva migration like duodenal aspirate, sputum, BAL fluid, lung biopsy and rarely in small intestine biopsy specimens. Stool microscopy done twice, in this child, during the illness did not reveal the larvae. This child developed left ventricular failure on the last day and there was significant pericardial effusion. The reason for heart failure was presumed to be due to disseminated strongyloidiasis. Myocardial involvement in disseminated strongyloidiasis has been described in literature [7].

Funding: None.

Competing interest: None stated.

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