Angiostrongylus cantonensis in Hawaii: A Parasite to Consider in Meningitis Patients
Abstract & Commentary
By Brian G. Blackburn, MD, Clinical Assistant Professor of Medicine, Division of Infectious Diseases and Geographic Medicine, Stanford University School of Medicine
Dr. Blackburn reports no financial relationships relevant to this field of study.
Synopsis: Angiostrongylus cantonensis is endemic to Hawaii and carries the potential for outbreaks; physicians caring for patients who live in or have recently traveled to Hawaii should be cognizant of this entity as a possible cause of meningitis.
Source: Hochberg NS, et al. Distribution of eosinophilic meningitis cases attributable to Angiostrongylus cantonensis, Hawaii. Emerg Infect Dis. 2007;13:1675-1680.
Eosinophilic meningitis is a distinct clinical syndrome characterized, in part, by an eosinophilic pleocytosis in the cerebrospinal fluid (CSF). Although intracranial hardware is the most common cause of this syndrome in the United States, Angiostrongylus cantonensis (the rat lungworm) is the most common etiology worldwide.1 This nematode is acquired by humans most commonly via ingestion of intermediate hosts such as slugs and snails, and paratenic hosts such as freshwater crustaceans.2 Although it has been reported elsewhere, A. cantonensis is endemic primarily to the Pacific basin, with several outbreaks described in the literature.3-5 A. cantonensis classically causes eosinophilic meningitis, typically a self-limited illness. However, patients can be left with persistent neurological symptoms, and rarely can die from this infection.
Prompted by a cluster of five voluntarily reported cases of eosinophilic meningitis in the state of Hawaii, Hochberg and colleagues ascertained cases of eosinophilic meningitis (and subsequently A. cantonensis) to determine whether this temporal clustering represented an outbreak. Because hospitals and clinics in Hawaii utilize a limited number of laboratories, Hochberg et al were able to obtain data on nearly all lumbar punctures (LPs) performed in the state from 2001-early 2005. Eighty-three patients were identified from these data who met the criteria for eosinophilic meningitis (CSF leukocyte counts > 6 cells/mm3, with > 10% eosinophils and/or eosinophil counts > 10 cells/ mm3 in patients that did not have intracranial hemorrhage). Although intracranial hardware was the most common cause of eosinophilic meningitis during the study period, Hochberg et al identified 24 cases of A. cantonensis infection (29% of the eosinophilic meningitis cases), defined as patients clinically suspected of having A. cantonensis who were > 2 months of age, without intracranial hardware or an alternative diagnosis that accounted for their meningitis. A. cantonensis case-patients had higher CSF eosinophil counts than patients with other causes of eosinophilic meningitis.
The statewide incidence of A. cantonensis infection increased from a baseline of 0.3 per 100,000 person-years to 2.1 (P < 0.001) during the study period (November 2004-February 2005), confirming the presence of the hypothesized outbreak. This increase was primarily due to cases on the Big Island of Hawaii and secondarily on Maui, but not Oahu. During the outbreak, 69% of eosinophilic meningitis cases in Hawaii were due to A. cantonensis. While eosinophilic meningitis was uncommon overall (representing less than 1% of the LPs performed during the study period), A. cantonensis was confirmed as a common cause of this syndrome when identified.
Commentary
This is the first systematic study of A. cantonensis incidence in an endemic area, and was possible, in part, because the state of Hawaii consolidates laboratory work to only a few providers, allowing for complete data capture. This methodology could also prove useful for study of infectious disease epidemiology in other settings. Although Hochberg et al relied mostly upon a clinical definition for A. cantonensis cases (only one was parasitologically confirmed), this is a largely unavoidable limitation in studying A. cantonensis epidemiology, given the lack of a reliable confirmatory test in most cases. Despite this, the absence of an alternative diagnosis, the fact that Hawaii is hyperenzootic for A. cantonensis but not Gnathostoma spinigerum or Baylisascaris procyonis (two other parasitic causes of eosinophilic meningitis), and that patients met clinical criteria consistent with A. cantonensis, makes it likely that the patients included in this study did truly have A. cantonensis infection.
These data confirm not only the endemnicity of A. cantonensis in Hawaii, but also its outbreak potential there. It is important for physicians caring for patients who live in, or have recently traveled to, Hawaii to consider this infection as part of the differential diagnosis for patients with meningitis, in particular those with eosinophilic meningitis.
References
- Re VL, Gluckman SJ. Eosinophilic Meningitis. Am J Med. 2003;114:217-223.
- Koo J, et al. Angiostrongylus (Parastrongylus) eosinophilic meningitis. Rev Infect Dis. 1988;10:1155-1162.
- Tsai TH, et al. An outbreak of meningitis caused by Angiostrongylus cantonensis in Kaohsiung. J Microbiol Immunol Infect. 2001;34:50-56.
- Tsai HC, et al. Outbreak of eosinophilic meningitis associated with drinking raw vegetable juice in southern Taiwan. Am J Trop Med Hyg. 2004;71:222-226.
- Slom TJ, et al. An outbreak of eosinophilic meningitis caused by Angiostrongylus cantonensis in travelers returning from the Caribbean. N Engl J Med. 2002;346:668-675.
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