Case Presentation: A 29-year-old Caucasian male lettuce farmer with no significant past medical history presented to our ED with acutely worsening holocranial throbbing headache, polyarthralgias, intermittent migrating burning rashes, and severe paresthesia to tips of all toes. He reported a three-week history of neck pain, excruciating hyperesthesias to light touch, diffuse abdominal pain, and constipation. Nine days prior to admission, he was evaluated for similar complaints and was suspected to have rat lungworm disease (RLWD), a parasitic eosinophilic meningitis familiar to the region, after initial studies identified peripheral eosinophilia. However, CSF studies lacked the characteristic eosinophilic pleocytosis and PCR testing for the parasite was negative so a diagnosis remained elusive. Upon admission, however, there was increasing suspicion of RLWD in light of the patient’s occupation as he regularly consumed unwashed produce- namely lettuce- and animals from the farm. Repeat studies revealed eosinophilic CSF pleocytosis, curvilinear tracts on brain MRI, and PCR positivity for the rat lungworm to confirm diagnosis. Patient was treated with multimodal pain management, corticosteroids, periodic removal of CSF, and later, an antihelminthic, with partial success.
Discussion: Eosinophilic meningitis is a rare clinical entity characterized by meningeal inflammation and eosinophilic CSF pleocytosis. Among infectious causes, the rat lungworm parasite Angiostrongylus cantonensis, is the most common worldwide. Humans are incidental hosts and become infected by ingestion of raw or undercooked snails, slugs, or contaminated produce that contain the infective, neurotropic larvae. Typical presentation includes symptoms of bacterial meningitis, such as nausea, vomiting, neck stiffness and headaches. Diagnosis is based upon clinical presentation, CSF eosinophilia (>10 eosinophils/mm3) and history of possible exposure. Peripheral eosinophilia is also commonly seen, but does not correlate with CSF eosinophilia or clinical course. Treatment is supportive. Antihelminthics are not routinely used as they may elicit an inflammatory response due to dying organisms, potentially worsening neurologic symptoms. In the absence of reinfection, most infections resolve without specific treatment as the migrating larvae die. However, serious complications leading to neurologic dysfunction or death can rarely occur.
Conclusions: RLWD should be considered in patients who present with headache, meningismus, and nonspecific neurologic symptoms in the setting of possible exposure. Given the rarity of this disease and the fact that characteristic laboratory features may be absent at initial encounter, it is important to maintain a high-index of suspicion for RLWD, especially in endemic areas. While most patients will have a self-limited course and recover completely, there is potential for severe debilitation as highlighted by this case. Early recognition may factor into recovery of long-term recovery of patients, although studies on this are limited.