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A diagnosis of A. cantonensis is strongly suggested when symptoms suggest bacterial meningitis but testing reveals eosinophilia either in the blood (>5%) or in cerebrospinal fluid (>10%) and travel history reveals recent travel to endemic areas of the world. History of ingestion of raw or undercooked intermediate hosts or possibly transport hosts is a crucial clue as well. However, ill persons may not be aware of ingestion of foods that could lead to infection. Examination of the CSF can reveal eosinophilia (>10% eosinophils), elevated protein, and low or normal CSF glucose. It is important to note, however, that eosinophilia in the CSF and in the blood may not be present on initial presentation or in late stages of infection. The CSF pressure is generally elevated. Recovery of A. cantonensis from the CSF confirms the diagnosis; however, the organism is rarely detected on microscopy as it can adhere to the meninges.
Serologic tests have been developed but are not commercially available. A few specialty or research laboratories offer serologic tests, but the sensitivity and specificity of the tests may not be optimal and the infection is often identified only on convalescent sera. In addition, some research laboratories have developed PCR tests for use with CSF and tissue. Because of the difficulty in making the diagnosis, it is important to rule-out other causes of eosinophilic meningitis. Neuroimaging studies can be useful as there usually is an absence of focal lesions on CT scan, which helps to distinguish A. cantonensis eosinophilic meningitis from focal lesions which may be seen in neurocysticercosis and gnathostomiasis. Because eggs are not passed in the feces, a stool examination is not useful for diagnosis.
Although several serologic tests have been developed by researchers, they are not readily available. Cases are often diagnosed postoperatively by examination of surgical specimens. Most patients have leukocystosis, often with a high percentage of eosinophils (>10%). Radiologic examination of the gastrointestinal tract may demonstrate edema and spasticity in the areas of inflammation. Because eggs are not passed in the feces, a stool examination is not useful for diagnosis. The parasitic differential diagnosis includes anisakiasis and toxocariasis.
Treatment is usually supportive with the use of analgesics for pain and corticosteroids to limit the inflammatory reaction. Careful removal of CSF at frequent intervals can help to relieve headache in patients with elevated intracranial pressure. No anti-helminthic drugs have been proven to be effective in treatment, and there is concern that anti-helminthics could exacerbate neurological symptoms due to a systemic response to dying worms. The effectiveness of any regimen may vary by endemic region. One randomized, placebo-control study of a 2-week course of prednisolone (60 mg per day in 3 divided doses) found that the corticosteroids reduced the median length of headache from 13 days to 5 days and reduced the need for repeat lumbar puncture. Additionally 9.1% of treatment patients compared to 45.5% of controls still had headache at 2 weeks.
In two small cases series (41 and 26 adults, respectively) adult patients were given prednisolone 60 mg/day and an anti-helminthic (mebendazole 10 mg/kg/day or albendazole 15mg/kg/day two weeks, respectively), resulting in resolution of headache in a median of 3 days in the mebendazole case-series and 4 days in the albendazole case-series without serious side effects. As there was no control group, it is difficult to determine if the anthelminthic provided additional benefit. Comparing the results from the placebo-control trial to the 2 case-series, 9.1% of prednisolone monotherapy patients, 9.8% of prednisolone-mebendazole patients, and 11.5% of prednisolone-albendazole patients still had headache after 2 weeks. One small trial that directly compared prednisolone monotherapy to prednisolone-albendazole combined therapy found no benefit of adding albendazole to the regimen.
Additional symptomatic treatment may also be required for nausea, vomiting, and in some cases chronic pain due to nerve damage and muscle atrophy.
There is no proven treatment for illness caused by A. costaricensis and there is some concern that treatment with anthelminthics could result in worsening of the disease. Acute episodes may resolve spontaneously or require surgical treatment for intestinal inflammation.
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