Case Presentation: Patient is a 15 yo boy with PANDAS, epilepsy, ADHD, and developmental delay presented with 9 days of decreased ambulation, abdominal pain, headache, and fatigue. Initially, his symptoms were attributed to recent fall and recent IVIG infusion. However, the patient then developed anorexia, weight loss, and aggressive behavior prompting admission. On exam, he was irritable and uncooperative without focal abnormality. Over the next 2 days, he developed nuchal rigidity. Initial CBC was normal except for a mild left shift and mild eosinophilia. Inflammatory markers were elevated. CT and MRI of the spine and pelvis noted to be normal.Brain MRI showed leptomeningeal enhancement and evidence of increased intracranial pressure. LP was significant for an opening pressure of 32, glucose of 33, protein 93, RBC 90, WBC 116, 0% Neutrophil, 63% Lymphocyte, 20% Eosinophil. CSF bacterial and fungal cultures were negative. Multiple infectious labs were sent, all of which were negative. The patient was presumed to have aseptic meningitis secondary to recent IVIG infusion and was given a 5 day course of prednisone, after which patient returned to baseline. A week later, patient presented to the hospital with similar presentation with addition of right leg numbness and tingling as well as horizontal nystagmus. Patient underwent repeat LP, which demonstrated findings similar to original. Repeat Brain MRI demonstrated multiple hemorrhages throughout the brain and brainstem. Flow cytometry of CSF was negative for malignancy. Ultimately a brain biopsy was obtained, which demonstrated necrotizing granulomas, perivascular inflammation without inflammation of vessel walls, numerous eosinophils, and overall inflammation of lesion with predominance of CD4 cells. Eventually, Angiostrongylus Cantonensis PCR of CSF returned positive from CDC. Patient then received steroid course with taper, but ultimately, we decided not to administer albendazole. Patient subsequently returned to baseline and has remained well to date.

Discussion: The causes of eosinophilic meningitis are few, and include parasitic cerebral infection, lymphoma, leukemia, medications, and hypereosinophilic syndrome. Angiostrongylus Cantonensis, commonly called the rat lungworm, has a lifecycle that involves rats and snails. Humans are an incidental host and cannot transmit the parasite to other humans. While typically seen in SE Asia, there have been increasing reports in the US, particularly in the south. Our case makes the fourth patient reported in the literature from the Houston, Texas, area since 2016. Typically, adults with Angiostrongylus Cantonensis infection will be asymptomatic. However, children with this infection have a more severe presentation including headache and fever. Other symptoms can include meningitic signs, weakness, encephalitis, and ataxia. It is presumed that this increased clinical severity is secondary to higher larval burden in children relative to adults. Angiostrongylus infection is typically treated with steroids and albendazole, though anthelmintic medications are controversial due to the fact that inflammation caused by dying larvae may worsen symptoms. Therefore, it is reasonable to consider treating with steroids alone.

Conclusions: The presentation of Angiostrongylus Cantonensis may require brain biopsy to ultimately make the diagnosis. In the setting of eosinophilic meningitis, it is important to consider Angiostrongylus Cantonensis infection if practicing in the southern U.S.