JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
with visual disturbances due to larval invasion of the ocular structures.6,11
These percentages of the signs and symptoms of eosinophilic meningitis caused by A. cantonensis found by McBride, et al., are consistent among many other research articles in similar regards.1,2,8,14 However, other associated signs and symptoms were noted elsewhere. One case report followed an outbreak of eosinophilic meningitis first noted on April 29, 2000 of 23 travelers.8 Twelve of the 23 travelers met diagnostic criteria for eosinophilic meningitis – headache beginning 35 days after the trip plus: nuchal rigidity, or visual disturbances, or altered cutaneous sensations.8 Of these 12 individuals, 100% (n=12) presented with a headache, 92% (n= 11) presented with visual disturbance or photophobia, 83% (n=10) presented with fatigue and nuchal rigidity, 67% (n=8) presented vomiting, and other associated symptoms included muscle pain (50%, n=6), fever (42%, n=5), muscle weakness (33%, n=4), and diarrhea (17%, n=2).8 Although, some isolated case reports exhibit atypical presentations to the aforementioned similarly to the patient in this case. A case report on eosinophilic meningitis caused by A.cantonensis in 2011 found a 24-year-old male with later confirmedeosinophilicmeningitis tohavepresentedwithmerely a persistent headache for three days with associated episodes of nausea without vomiting.14 This patient did not experience or exhibit signs of myotonia, speech difficulty, weakness, abnormal cutaneous sensations, or focal neurologic deficit.14
DEMOGRAPHICS
Angiostrongylus cantonensis was first described as a human pathogen in China in 1945.9 Today, numerous countries have experienced severe outbreaks including China, Taiwan, Jamaica, and Thailand.5,8 While A. cantonensis is prevalent in Southeast Asia and the Pacific Islands, there have been increasing numbers of documented cases in the continental U.S. The current theory of introduction into the continental U.S. begins in the 1980s from rats aboard ships arriving into New Orleans, Louisiana. Since then, a few numbers of cases have presented in the southeastern U.S. including Louisiana, Texas, and Florida.9,10 One study conducted by Walden, et al., sought PCR positivity in vectors such as snails and Rattus rats in multiple Florida counties to confirm the roundworm’s migration to the continental U.S. They established that A. cantonensis was found in 5 of the 18 counties tested.10 Walden, et al., necropsied 171 Rattus Rattus and found 22.8% (n=39) showed PCR positivity while only 1.9% (n=27, of 1,437) of gastropods were positive for A. cantonensis . Other mammalian hosts have been documented in the southeastern U.S. including a horse in Picayune, Mississippi, a captive howler monkey, wild wood rat, and four wild opossums in New Orleans, Louisiana, and a captive white- handed gibbon in Miami, Florida.9 With readily available global transportation, other cases of eosinophilic meningitis caused by A. cantonensis have been noted in other regions of the U.S. as well. One case documented in 2002 by Slom, et al., documented a large outbreak among a group of U.S. citizens that traveled from Jamaica to the U.S. and presumably occurred after eating salads in Jamaica.8 Of the 12 patients that demonstrated illness in this study, 75% (n=12) were male with a median age of 22. Conversely, another larger study conducted in Vietnam by McBride, et al., also demonstrated a slight male predominance with an infected population of 59.4% male (n=51) and a median age of 31.21-44
IMAGING AND LABORATORY INVESTIGATION
Investigatory laboratory studies and diagnostic imaging are crucial in the diagnosis of eosinophilic meningitis. Beyond basic hematologic laboratory investigations, a CT, MRI, and lumbar puncture should be considered in patients with meningeal irritation symptoms. In theory, a hallmark eosinophilic meningitis presentation should presumably show evidence of increased opening pressure on lumbar puncture, PCR positivity for A. cantonensis , and eosinophilia in the blood or CSF.2,8 McBride, et al., in a very large retrospective studies of eosinophilicmeningitis, conducted a study of 69 individuals with eosinophilic meningitis and found an elevated CSF leukocyte count/mm³ median of 564 (347-1015) with a CSF eosinophilia differential median of 39% (27-52%), and an elevated opening pressure median of 23 cm H20 (17-33 cm H20). Additionally, they also found an elevated CSF protein median of 0.8 g/dL (0.5-1.2), an elevated CSF glucose median of 2.5 g/dL (1.9-2.8), and an elevated CSF lactate median of 2.8 mmol/L (2.2-3.9).2 They also noted that PCR positivity correlated with an increased duration of illness at presentation (median of 14; 10-20 vs. nine days, P=0.027). Severity, however, was unrelated to PCR positivity. Some of the findings they found on MRI and CT imaging include cerebral edema (45%), meningeal inflammation (36.4%), and focal parenchymal hyper-intense lesions on T2-weighted FLAIR MRI (45%).2
PRESENTATION AND CLINICAL FEATURES
The most common symptoms of meningitis are headache, fever, and nuchal rigidity that develop within a few days of the infection. In cases of typical bacterial meningitis, roughly 44-46% of patients present with all three classical features.13 However, eosinophilic meningitis caused by A. cantonensis can demonstrate an atypical presentation as in this case. One infectious disease report published in 2017 of 69 adults in southern Vietnam has shown that patients who meet diagnostic criteria for eosinophilicmeningitis present with headache (n=63, 96.9%), fever (n=58, 84.1%), and vomiting (n=39, 62.9%).2 Their observations have also shown that 72.5% (n=50) of patients initially presented with nuchal rigidity, 37.7% (n=20) initially presented with a fever of 38°C or above, and 12.1% (n=9) initially presented with cranial nerve palsy – most commonly CN VI.2
Another larger study after an outbreak in Jamaica found to have a median opening pressure of 24 cm H20 (12-55 cmH20), an
J La State Med Soc VOL 170 MAY/JUNE 2018 85
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