MARY S.STONEMDSOONBAHRAMIMDCARRIE ANN R.CUSACKMDSENAIT W.DYSONMDMOLLY A.HINSHAWMDVINCENTLIUMD
Microscopic examination showed epidermal bulla formation with underlying basophilic helminthic organisms located in the superficial dermis and subcutaneous fat. Notably, there was no inflammatory response or granuloma formation. Organisms were also present in the brain, lungs, and gastrointestinal tract. The nematodes were consistent with Strongyloides stercoralis, and the diagnosis was disseminated strongyloidiasis.
Strongyloides is endemic in the United States, particularly in the southeastern and Applachian regions.1-4 Typically, the worms penetrate the foot from contaminated soil and enter the bloodstream. Then, they travel to the lungs, invade capillary walls, and enter alveolar spaces. Next, they migrate up the trachea, are coughed up, and are then swallowed, after which they attach to the small intestines and produce rhabditiform larvae. Then, 1 of 2 things can happen: the rhabditiform larvae can get excreted back into soil and complete a free-living cycle, or they can transform into infectious filariform larvae within the host, penetrate the intestinal mucosa and/or perianal tissue, reenter the bloodstream, and reinfect their host. The latter process, which is called autoinfection, is unique to S stercoralis.1 Autoinfection results in chronic infection that typically persists in the host for decades, causing no symptoms until the host becomes immunocompromised, most commonly by the use of systemic steroids.3,5 Once the host is immunosuppressed, disseminated disease ensues, potentially affecting any organ in the body and causing hyperinfection.1 Furthermore, these parasites carry enteric organisms with them as they infiltrate the tissues, causing superinfections such as bacteremia, meningitis, and endocarditis.1,3 Forty-five percent of the patients with dissemination develop superinfections,1 and their mortality rate is close to 80%.2-4 The patients present with nonspecific gastrointestinal and/or respiratory symptoms, depending on the extent of involvement.1,3 Immunocompetent patients with uncomplicated parasitic infections typically present with eosinophilia; however, eosinopenia is more common in patients who have been treated with steroids and is a poor prognostic factor.1 Stool sampling for ova and parasites is the most cost-effective diagnostic tool.1 One stool examination has only 30% sensitivity1-3; therefore, obtaining 3 stool samples is recommended to increase the sensitivity to 50%.3 Additional diagnostic studies include sputum sampling, bronchial washings, cerebrospinal fluid analysis, tissue biopsy,1 and serologic tests (available only in commercial laboratories). There are 2 skin manifestations associated with Strongyloides. Larva currens, which is present in immunocompetent individuals, is considered by some to be pathognomonic for strongyloidiasis.4-6 It is a serpiginous, erythematous rash caused by larval migration through the skin3,4,7 that rapidly migrates 5 to 15 cm/h.4,7 The second manifestation, which is associated with immunocompromised patients, involves a purpuric eruption that occurs on the abdomen and thighs as a result of vessel destruction from the invasive organisms.4,5 These rashes can strikingly resemble a drug eruption; therefore, recognizing disseminated strongyloidiasis as a cause of purpuric rash may be lifesaving.
Purpuric Eruption in a Patient Treated With Systemic Steroids—Diagnosis. Arch Dermatol. 2010;146(2):191–196. doi:10.1001/archdermatol.2009.364-b
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