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Indian Pediatr 2011;48: 974-975 |
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Disseminated Strongyloidiasis in a
Immunocompromised Host |
Suneel C Mundkur, Shrikiran Aroor and K Jayashree
From the Department of Pediatrics, Kasturba Medical
College, Manipal, India.
Correspondence to: Dr Suneel C Mundkur, Associate
Professor, Pediatrics, KMC Manipal, Karnataka, India.
Email: [email protected]
Received: December 12, 2009;
Initial Review: February 09, 2010;
Accepted: August 23, 2010.
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Strongyloidiasis in an immunocompromised patient has the potential to
be life threatening. We describe a boy who was on steroids for acute
demyelinating myelitis and receiving antibiotics for E.coli UTI
and meningitis. He developed anasarca, malabsorption, malnutrition and
left ventricular failure. Duodenal biopsy revealed abundant
rhabditiform larvae of Strongyloides stercoralis. The diagnosis
went unsuspected and proved fatal. This emphasizes the need to have a
high index of suspicion and early intervention for S. stercoralis
in immunosuppressed persons who present with refractory
gastrointestinal symptoms.
Key words: Immunodeficiency, Strongyloidiasis.
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Strongyloidiasis is an intestinal
infestation caused by the nematode Strongyloides
stercoralis, common in endemic areas of tropical and subtropical
countries. In an immuno-compromised patient, it has the potential to
cause life threatening conditions like hyper-infection syndrome and
disseminated strongyloidiasis. Severe strongyloidiasis has a high
mortality of up to 80% as the diagnosis is often delayed. We
describe a boy who was immuno-compromised secondary to systemic
steroid therapy, in whom the diagnosis was delayed.
Case Report
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.
Discussion
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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