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In March 2005, we reviewed a 38-year-old Malawian university student referred by an ear, nose, and throat surgeon after investigation of recent bilateral conductive hearing loss and diffuse sinus mucosal thickening. A biopsy revealed non-specific lymphoid hyperplasia. He was found to be HIV antibody positive.
He had arrived in Australia 12 months previously and claimed to have had negative HIV serology in Malawi in 2003. He denied risk factors for HIV acquisition but did report a dental procedure before traveling to Australia. Within weeks of arrival, he was admitted to hospital for treatment of pneumonia, which responded to conventional antibiotics.
On examination, there was generalized shotty lymphadenopathy, seborrheic dermatitis, and papular eruption. There was no hepatosplenomegaly or signs of chronic liver disease. Further study revealed a Human Immunodeficiency Virus ribonucleic acid (HIV RNA) load of 395,000 copies/mL, CD4 count of 120 cells/mL, Hepatitis B virus surface antigen (HBVsAg) positive, Hepatitis B virus envelope antigen (HBVeAg) positive, and an Hepatitis B virus deoxyribonucleic acid (HBV DNA) load of > 200,000 copies/mL. He had normal hepatic aminotransferases and liver function. Full blood count showed normal hemoglobin, platelets, and white cell count but abnormal white cell differential, showing marked eosinophilia (3.9 x 109/L; normal range: 0–0.4 x 109/ L). Tuberculin skin test was non-reactive; serum rapid plasma regain (RPR) was negative; and serum cryptococcal antigen titer was 1:2.
Anti-retroviral therapy was initiated with efavirenz 600 mg, lamivudine 300 mg, and tenofovir 300 mg once daily. Within days of starting therapy, he complained of headaches, and a lumber puncture was performed. This showed mild Cerebrospinal fluid (CSF) lymphocytosis (10/µL), negative India Ink stain, and negative cryptococcal antigen. The headaches persisted but resolved 1 week after replacing efavirenz with nevi-rapine.
Because of the patient’s eosinophilia and geographic origin, he underwent stool examination for the presence of intestinal parasites. Strongyloides filariform and rhabditiform larvae and eggs were identified (Figure 1
–3). The patient was treated with ivermectin 200 µg/kg on 2 consecutive days, which was repeated 3 weeks later. Peripheral eosinophilia reduced 4-fold within 1 month of treatment.
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The impact of Strongyloides infection on HIV infection is debated. Some have suggested that the immune activation stimulated by helminth infestation may contribute to HIV disease progression and the excess morbidity of HIV in the developing world.3 Strongyloides stercoralis is endemic to tropical regions, and ivermectin is the treatment of choice.4 Infection is frequently asymptomatic but can cause a syndrome of hyper-infection in the immunodeficient host. The dearth of reports of hyper-infection in HIV despite the co-endemicity of strongyloides and HIV in sub-Saharan Africa have led some to question the risk posed by HIV co-infection.5
This case highlights the need for clinicians to maintain a high index of suspicion for diseases that are more prevalent overseas. In addition, some patients will be infected with more than one pathogen, and knowledge of the global epidemiology of infectious diseases should help direct investigation.
Received October 19, 2005. Accepted for publication July 13, 2006.
* Address correspondence to Thomas Snelling, Department of Microbiology, The Children’s Hospital at Westmead, Locked Bag 4001, West-mead, New South Wales, Australia 2145. E-mail: tom.snelling{at}gmail.com 
Authors’ addresses: Thomas Snelling, Chris Ossowicz, and Mark Boyd, Department of Microbiology and Infectious Diseases, Flinders Medical Centre, Bedford Park, South Australia, Australia 5042.
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