JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
cerebrospinal fluid (CSF), the closing pressure was measured at 26 cm H20. All symptoms improved significantly after the procedure. On laboratory testing a complete blood count showed a mild leukocytosis at 11.8 × 109 cells/L (reference range 4.5–11.0 × 103/UL) with 11% eosinophils, an elevated absolute eosinophil count at 1.3 (reference range 0.0–0.6 × 103/UL). Sedimentation rate and C-reactive protein were both within normal limits. Human immunodeficiency virus (HIV), syphilis antibody, hepatitis panel, and interferon gamma release assay for tuberculosis were all non-reactive. Analysis of the CSF revealed elevation of leukocyte count at 383 UL (reference range 0-5 UL) with 62% eosinophils, elevated protein at 63.8 mg/dl (reference range 15.0 - 45.0 mg/dl), and normal glucose at 50 mg/dl. Cultures and gram stains of the CSF were negative for bacteria, acid-fast bacilli, and fungi. Malaria antigen was negative. Pathology review of the blood was negative for Plasmodium, Babesia, and other parasites. A. cantonensis polymerase chain reaction (PCR) on the CSF resulted positive indicating infection by A. cantonensis . The patient was discharged on acetazolamide 500 mg twice a day to manage intracranial hypertension and two weeks of prednisone 60 mg daily with an eight-day taper. She had full resolution of papilledema, right CN VI palsy, headaches, and nuchal rigidity at her one-month clinic follow-up. After discharge, serum Strongyloides Stercoralis immunoglobulin – G (IgG) by enzyme-linked immunosorbent assay (ELISA) resulted positive at 1.56 IV (Reference range <= 0.99). Per infectious disease recommendations, the patient was prescribed ivermectin at 200 mcg per kilogram daily for two days after Strongyloides Stercoralis IgG was found to be positive. It was thought that the S. stercoralis IgG positivity was indicative of a prior infection or exposure; however, initiation of steroid therapy warranted anitparasitic treatment for S. stercoralis .
Humans occasionally serve as incidental hosts of the organism, in which eosinophilic meningitis can present. The transmission of A. cantonensis to humans is usually via consumption of the undercooked larvae-infected snails or mollusks (i.e. fresh- water shrimp, crabs), or via undercooked vegetables, prawns, crabs and frogs that become contaminated by the mucus of infected slugs, or snails.5,7 The onset of clinical symptoms of infection due to A. cantonensis usually arises between 1-4 weeks from exposure.8 Once ingested by a human host, the larvae of A. cantonensis cannot complete its life cycle, and it will typically die within the gastrointestinal system, which can cause eosinophilic gastroenteritis.4 However, the larvae can invade the vasculature of the digestive tract, and migrate within the blood.3,4 Usually, the larvae tend to migrate to the brain and spinal cord of human hosts, where they develop further only to be extinguished by the activation of cytokines and eosinophils of the human host. A. cantonenensis is unique in the human host as the eyes can also be involved. Once the human host has elicited an immune response to eliminate the CNS pathogen, inflammatory symptoms of eosinophilic meningitis may ensue due to direct physical larval damage and immune reaction.3,9 Such symptoms include headache, visual disturbances, nuchal rigidity, fever, nausea, and vomiting. Death may occur in severe infections.10 The symptoms most often resolve spontaneously after 7-14 days, however headaches and paresthesias can take longer to resolve, varying from weeks to months.8,11,12 The most common presentations in a case series of 34 patients were: headache (90%), stiff necks and emesis ( 56%), paresthesias (54%) and fever (41%).11 Infection has been found to involve the cranial nerves, although less common, as well as the eyes Figure 1: The life cycle of this parasitic nematode includes an intermediate host of raw land and freshwater snails and a definitive host of rats or other rodents where the adult rat lungworms live and lays eggs in the pulmonary arteries of rodents. 2,6 Humans occasionally serve as incidental hosts of the organism.
LITERATURE REVIEW
Angiostrongylus Cantonensis (A. cantonensis) , or “rat lungworm,” is one of the most known infectious causes of eosinophilic meningitis. It is a parasitic nematode that is widely found in endemic areas such as Southeast Asia, the Pacific Islands, and the Caribbean.1,2 Although, the area of distribution of A. cantonensis has drastically increased over time to areas including Africa and the U.S. due to global transport networking. To date, thousands of cases have been reported worldwide.3,4,5 The life cycle of this parasitic nematode includes an intermediate host of raw land and freshwater snails and a definitive host of rats or other rodents where the adult rat lungworms live and lays eggs in the pulmonary arteries of rodents.2,6 After the eggs hatch, the larvae migrate into the pharynx of infected rats and are swallowed, subsequently passing in the rodent’s feces. Snails and slugs then ingest the larvae becoming infected. When rats subsequently ingest infected snails and slugs, the larvae can then mature to adult worms in the rodents (Figure 1).
84 La State Med Soc VOL 170 MAY/JUNE 2018
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