Strongyloides stercoralis Causing Polymicrobial Empyema in a Cancer Patient

Hung D. Tran, MD, Sinai Hospital, Baltimore; John N. Greene, MD, and Ramon L. Sandin, MD, MS, both from the University of South Florida College of Medicine and H. Lee Moffitt Cancer Center and Research Institute, Tampa; and Albert L. Vincent, PhD, H. Lee Moffitt Cancer Center and Research Institute, Tampa


Infect Med. 2001;18(1) 

In This Article


S stercoralis is a significant cause of pulmonary infection in the tropics and subtropics, as well as in the southeastern United States -- notably, Louisiana, Tennessee, and Kentucky. Also affected are Puerto Rico, some parts of Europe, Southeast Asia, South America, and sub-Saharan Africa.[1,2,3] The reported prevalence of infection in the United States is 0.4% to 4%.[1]

Initially, infection is acquired when the infective filariform larvae in the soil penetrate the skin and reach the lung via the lymphatic or venous system. Once there, they traverse through the alveolar walls and ascend the trachea to the glottis, where they are swallowed. The larvae then develop in the wall of the duodenum and proximal jejunum, molting into adults. Mature females produce eggs, which soon hatch into noninvasive rhabdoid larvae. This feeding stage is passed in the feces and develops directly in the soil into infective filariform larvae. Alternatively, under favorable conditions, they may give rise to an entirely free-living life cycle in the soil.[4,5,6,7] In yet another variant of the life cycle, rhabdoid larvae may transform into the filariform stage without leaving the host of origin, but they directly penetrate the bowel wall, completing the transpulmonary migration and molting into new adult worms in the duodenum. This capacity for autoinfection is rare among helminths but undoubtedly accounts for Strongyloides infections that may persist for half a century.[7] More significantly, it sets the stage for dissemination of larvae in overwhelming numbers.[8]

The hyperinfection syndrome of S stercoralis is unlikely to be seen in the healthy, immunocompetent host. Predisposing factors include immunosuppression by chemotherapy or corticosteroids, Hodgkin or non-Hodgkin lymphoma, chronic infections, alcoholism, or other conditions.[2,4,8,9,10,11] Corticosteroids, given systemically, topically, or under the
conjunctiva, have been held responsible for most cases of hyperinfection in the United States.[7]

The syndrome may initially develop with increased total worm burden but without spreading into organs beyond their usual migratory routes -- the gut, cardiovascular system, and respiratory tract.[1,5] Clinically, there may be asthma, bronchitis, hemoptysis, or adult respiratory distress syndrome.[6,10] Progressive abdominal pain, nausea, vomiting, and diarrhea are increasingly evident as greater numbers of worms disrupt the bowel mucosa.[2] Signs of invasion into the liver, urinary tract, and brain indicate an ominous progression of the disease.[2,12]

Complications of overwhelming strongyloidiasis include bacteremia, pneumonia, urinary tract infection, endocarditis, and peritonitis. The
bacteria isolated are usually enteric pathogens, such as gram-negative bacilli -- Escherichia coli, Klebsiella pneumoniae, P aeruginosa, Enterobacter cloacae, and enterococci. These probably gain access to the blood by adhering to the cuticle of the parasite.[1,12]

In the case presented here, the patient initially showed neither signs nor symptoms of infection by S stercoralis. Filariform larvae were an incidental finding in a viral culture. Failure to identify and treat the underlying strongyloidiasis allowed for persistence of the empyema from enteric organisms. DeVault and colleagues[1] found that immunosuppressive chemotherapy increases the translocation of GI flora to the reticuloendothelial system in experimentally infected mice.

Although relatively uncommon, latent strongyloidiasis is dangerous and should always be remembered by the clinician contemplating an immunosuppressive regimen. Often, fortuitous diagnoses do not come soon enough -- mortality may exceed 80%.[7] In an adult with recurrent gram-negative sepsis, a history suggestive of Strongyloides hyperinfection would include institutionalization, being a prisoner of war or concentration camp survivor, exposure to dog feces, and residence in a warm climate, even if in the distant past. Laboratory findings may include leukocytosis, increased serum IgE levels, and eosinophilia. While eosinophilia is a near-universal expectation in tissue helminthiases, corticosteroid therapy may produce the opposite effect.[13]

Larva currens, or "racing larva," is a rapidly progressive creeping eruption with an urticarial perianal band that although infrequently seen, is highly suggestive of strongyloidiasis. Infective larvae burrow in the stratum corneum outward from the anal area and onto the thighs or toward the axilla, leaving approximately linear urticarial trails in their wake. Other clinical manifestations of disseminated strongyloidiasis include fleeting pulmonary infiltrates and necrotic skin lesions, probably from local enteric bacterial proliferation.

Even the most sensitive of stool examination techniques, a stool funnel, may fail in latent strongyloidiasis.[14] Parasites may also be sought in duodenal aspirates, jejunal biopsy samples, pleural fluids, or sputa.[8,10] Grocott-Gomori methenamine-silver nitrate stain or Papanicolaou stain of sputum may detect the larval forms in the lungs. Culture of sputum after several days of bacterial growth may show serpiginous trails of bacterial colonies following the burrowing larvae across the agar plate (Figures 2 and 3). Larvae of S stercoralis may be an unexpected finding in various laboratory tests, including both vaginal and ascitic smears.[15] Serologic tests to detect antibodies to S stercoralis by enzyme-linked immunosorbent assay (ELISA) are now available in some commercial laboratories and from the CDC and NIH. Liu and Weller[2] have reported that the sensitivity of the ELISA is about 85% to 90%. Cross-
reactivity with other nematode infections is minimal.[2]

Serpiginous movement of the larval forms of Strongyloides can be seen as the bacterial colonies of normal oral flora are formed along the moving trail on a chocolate agar sputum culture. This sample was obtained from a patient who died of disseminated strongyloidiasis while receiving corticosteroids for a primary brain tumor.

Close-up view of Figure 2 clearly delineates the bacterial colonies following the Strongyloides larval trails.

The mainstay of treatment for strongyloidiasis has been thiabendazole, 25 mg/kg orally in 3 divided doses daily for 2 or 3 days. For patients with hyperinfection syndrome and disseminated strongyloidiasis, treatment should be continued for 7 to 10 days or longer as needed. Serious adverse reactions, occurring in as many as 30% of patients, include nausea; dizziness; drowsiness; visual disturbances; hypotension; and neuropsychiatric symptoms, such as disorientation and delirium in severe reactions.[2] Relapses occur in up to 30% of cases, necessitating careful follow-up.[6] Albendazole has replaced thiabendazole because the former has equal efficacy but less toxicity. Our patient was successfully treated with albendazole, 400 mg/d orally for 3 days. Liu and Weller[2] reported that albendazole has a cure rate of 81% if given at 400 mg/d for 3 days. Nausea and diarrhea are the principal adverse effects. Our patient tolerated treatment with no evidence of adverse reactions. Ivermectin appears to be as effective as either thiabendazole or albendazole, with fewer side effects.[2,3,6,10]


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