2003 Clinical Vignette Abstract Winner

Parainfluenza Type 3 Meningoencephalitis Following Plasmodium Falciparum Malaria Infection. Aaron From, M3, and Deana Hoganson, M3, University of Iowa Carver College of Medicine, Iowa City, IA, Joel A. Gordon, MD, Mentor

A 19-year-old female was transferred from her local hospital after nine days of nausea, vomiting, spiking fevers, constant headache and intermittent confusion. She denied cough or dyspnea. Five days prior to the onset of symptoms she finished a seven day course of intravenous doxycycline and quinine to treat a Plasmodium falciparum malaria infection with pulmonary edema acquired during a four week visit to Uganda, Africa.

Physical exam on day one revealed a pale, well oriented female. She was hypersensitive to light, sound and touch. There was no nuchal rigidity. Liver and spleen edges were palpable and tender. Laboratory analysis showed a white blood cell count of 2,200/mm3 without a left shift and hemolytic anemia. CSF sampling was consistent with viral infection. Prior to transfer, MRI of the brain was unrevealing. The findings were consistent with a previous malarial infection and a current CNS viral infection.

On day two of her hospital stay she was found unresponsive with opisthotonic posturing and dilated, reactive pupils. The patient was transferred to the ICU for endotracheal intubation. Subsequent CT and MRI of the brain revealed focal lesions and general edema consistent with encephalitis. Biopsy of brain tissue revealed Parainfluenza type 3 virus and showed no demyelination. After five days the patient was extubated and treated symptomatically for control of seizures with phenytoin. Upon discharge on day 15 the patient was afebrile with no neurological abnormalities and normal laboratory values.

The four serotypes of Parainflueza virus, members of the family Paramyxoviridae, account for 1.1% of viral neurologic infections with 65% of those cases caused by Parainfluenza type 3.1

Pulmonary intravascular inflammatory changes and immune suppression with post-malarial infection are both documented consequences of malarial infection.2,3 Our patient displayed both sequelae demonstrating pulmonary edema while infected and a low leukocyte count post-infection. This breakdown of physical and immunological barriers may explain the rare cause of encephalitis.

References:
1. Assaad F, et. al. Bull WHO. 58:297-311. 1980
2. Zombrano-Villa S, et. al. Trends Parasit. Vol. 18 No. 6. 2002
3. Wilson A, et. al. J Inf. 40(2):202-4. 2000

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