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Abstract & Commentary
Synopsis: Angiostrongyliasis, the most common cause of eosinophilic meningitis, has been recognized in a number of travelers to endemic areas.
Source: Re III VL, Gluckman SJ. Eosinophilic meningitis due to Angiostrongylus cantonensis in a returned traveler: Case report and review of the literature. Clin Infect Dis. 2001;33:e112-e114.
Re and Gluckman in Philadelphia describe a 37-year-old woman who presented to them with a 4- week history of headache, paresthesias, and a 2-week history of unilateral hearing loss beginning while traveling in Tonga. She was originally seen in Auckland, New Zealand, on the 11th day of her illness, at which time she had a peripheral WBC of 7100 cells/µL with 8% eosinophils and a cerebrospinal fluid (CSF) WBC of 246 cells/µL with 3% eosinophils, as well as CSF protein of 100 mg/dL, glucose of 36 mg/d; opening pressure was 21 cm H2O. Five days later, her CSF WBC was 302 cells/µL with 16% eosinophils and her CSF opening pressure had increased to 26 cm H2O. By the time she presented in the United States 4 weeks after the onset of illness, her hearing loss had resolved, but the other symptoms persisted. Her CSF protein and glucose were normal and her CSF WBC had decreased to 13 cells/µL with 2% eosinophils. MRI was normal, as it had been in New Zealand. No parasites were detected in her CSF, but serological tests were consistent with seroconversion to antigens of Angiostrongylus cantonensis. She recalled having eaten fresh lettuce while in Tonga.
Comment by Stan Deresinski, MD, FACP
Angiostrongyliasis may be acquired in many areas of the world, including Hawaii and other Pacific islands, Southeast Asia, Africa, India, and the Caribbean.1 Within the Caribbean, Jamaica has recently emerged as a hot spot for infection with A cantonensis infection. In March of this year, a woman who spent 6 days in Ocho Rios, Jamaica, where she ate mostly salads and seafood at a hotel restaurant buffet, presented 3 weeks later with symptoms of meningitis, with later symptoms including facial pain and paresthesias involving the hands, legs, and circumoral area.2 CSF examination revealed a protein of 218 mg/dL, glucose 38 mg/dL, and WBC of 507 cells/µL with 47% eosinophils. Paresthesias and malaise were still present 2 months after the onset of illness. While serological tests were still pending, a presumptive diagnosis of eosinophilic meningitis due to A cantonensis was made. Independently of this case, 5 of 22 first-year Northwestern University medical students acquired eosinophilic meningitis due to this organism during their 2001 spring break in Montego Bay.3 It is believed that a Caesar salad eaten at an "expensive restaurant" was the source of infection.
Infection has also been acquired in the continental United States—a patient with angiostrongyliasis, apparently acquired by ingestion of raw snails—has been reported in New Orleans.4 Spread of the pathogen to this unique city on the Mississippi River delta, as to many other regions of the world, is thought to have resulted from transportation by ship of infected rats, the primary hosts of the parasite; 20% of wharf rats in "The Big Easy" have been reported to be infected.
After infection of the rat, sexually mature worms lay eggs in their site of residence in their pulmonary arteries. Upon hatching, larvae migrate out of the lungs via the trachea, are swallowed, and excreted in feces. Snails and slugs, the intermediate hosts, ingest the larvae-infested rat feces and then serve as the site for maturation of the larvae into the infective form. Humans are infected as the result of ingestion of the infective larvae present in raw snails, on contaminated vegetables, or in freshwater crabs or shrimp that have ingested the infective larvae. The organism finds its way into the bloodstream and, ultimately, to the central nervous system, where, it dies.
The incubation period is reported to range from a few days to a month. In addition to headache, many patients develop paresthesias that may persist for months after other symptoms have resolved. Extraocular of facial nerve palsy rarely occur. Blindness may occasionally occur as the consequence of migration of the parasite to the eye, where it may cause retinal hemorrhage and/or detachment.
Tsai and colleagues recently reviewed their experience with 17 Thai laborers who developed eosinophilic meningitis due to the parasite as the result of eating raw golden apple snails in Taiwan.5 The mean incubation period in these cases was 13 ± 7 days. All complained of headache and only 11 (65%) had neck stiffness. Fever was present in 11 (65%), but only 2 (12%) complained of paresthesias. Four (24%) had skin rash. Each of the following findings were observed in 1 person: abducens nerve palsy, facial nerve palsy, and "transient labyrinth insufficiency." Muscle weakness was reported by 8 (47%) and elevated serum creatine kinase levels were observed in 7 patients. Brain MRI demonstrated meningeal enhancement, and 9 of 13 (69%) were felt to have abnormal enhancement of the globus pallidus. All 17 patients recovered with "minimal neurologic sequelae" after a mean duration of illness of 20 ± 14 days.
While as many as one third of patients may lack peripheral eosinophilia, CSF eosinophilia usually ranges from 20% to 70%. The parasite is seldom visualized in CSF, and the diagnosis is generally confirmed by serological testing. Antihelminthic treatment is not known to have efficacy in this disease, but a randomized trial has demonstrated benefit from a 2-week course of prednisolone at a dose of 60 mg daily.6
Some potential causes of CSF eosinophilia are listed in the Table. Of these, gnathostomiasis, caused by Gnathostoma spingerum, is the primary alternative diagnosis in its endemic region of endemic in Southeast Asia, Japan, and China. This organism causes eosinophilic myeloencephalitis, and symptoms may include painful radiculitis as well as limb motor paralysis; subarachnoid hemorrhage may occur.
|Some Reported Causes (Pathogens) of CSF Eosinophilia|
|Angiostrongyliasis (A cantonensis)|
|Cysticercosis (C cellulosae, the larval form of Taenia solium)|
|Gnathostomiasis (G spingerum)|
|Schistosomiasis (S mansoni, S japonicum)|
|Paragonomiasis (P westermanii)|
|Echinococcosis (E granulosus, E multilocularis)|
|Toxocariasis (T canis, T cati)|
|Baylisascariasis (B procyonis)|
|Trichinosis (Trichinella spiralis)|
|Coccidioidomycosis (C immitis)|
|CNS Hodgkin’s disease, nonHodgkin’s lymphoma|
|Tuberculosis (M tuberculosis)|
|Neurosyphilis (T pallidum)|
|Phaeohyphomycosis (Wangiells dermatitidis)|
|Ventriculoperitoneal shunt malfunction and/or infection|
|Neonatal intraventricular hemorrhage—late finding|
|Reaction to cadaveric dural graft|
|Reaction to intraventricular administration of vancomycin|
1. Pien FD, Pien BC. Angiostrongylus cantonensis eosinophilic meningitis. Int J Infect Dis. 1999;3: 161-163.
2. King CH. ProMED-mail post. www.promedmail.org. Accessed November 21, 2001.
3. Pollack MP. ProMED-mail post. www.promedmail.org. Accessed November 21, 2001.
4. New D, et al. Angiostrongylus cantonensis infection from eating raw snails. N Engl J Med. 1995;332: 1105-1106.
5. Tsai HC, et al. Eosinophilic meningitis caused by Angiostrongylus cantonensis: Report of 17 cases. Am J Med. 2001;111:109-114.
6. Chotmongkol V, et al. Corticosteroid treatment of eosinophilic meningitis. Clin Infect Dis. 2001;31: 660-662.
Dr. Deresinski, Clinical Professor of Medicine, Stanford; Director, AIDS Community Research Consortium; Associate Chief of Infectious Diseases, Santa Clara Valley Medical Center, is Editor of Infectious Disease Alert.