A Case Series of Eosinophilic Meningitis from Kerala

Sir, Eosinophilic meningitis is a rare entity with unique pockets of distribution in areas of poor hygiene. There are very few case reports from India.[1-4] The cause of eosinophilic meningitis in the previous two case series from middle Kerala was due to ingestion of monitor lizard.[2,5] We report 3 cases of eosinophilic meningitis from south Kerala [Table 1]. All three patients were women, presenting with symptoms and signs of raised intracranial pressure without lateralizing deficits. All had eosinophilic meningitis and there was a history of exposure to snails in their kitchen and backyard within three months of presentation. They responded to prednisolone 1 mg/kg in two weeks and then tapered off. MRI brain of one patient showed linear blooming on SWI, giving a track like appearance Figure 1.Table 1: Clinical details of three cases of eosinophilic meningitisFigure 1: SWI showing focal linear hemorrhages forming a track like appearanceWe present three cases of eosinophilic meningitis which responded to steroids. We speculate the contamination of food by snails to be responsible for eosinophilic meningitis. The recent increase in eosinophilic meningitis could be due to an increase in the snail population following glitches in waste disposal in Thiruvananthapuram city following the shutdown of the only waste disposal facility in Vilapinshala. All three cases were reported between August 2018 and November 2018; the snail population increases from June to August during the monsoon season. During this period snails swarm the damp areas of the habitats. Women were exclusively affected probably due to the higher risk of exposure to snails in the kitchen and domestic waste disposal areas. There was no history of exposure to drugs, or evidence of CNS fungal infections nor other non-infectious aetiology for eosinophilic meningitis like lymphoma, leukemia, or sarcoidosis. Eosinophilic meningitis could be due to infectious or noninfectious causes.[6] However, the most frequent causes of eosinophilic meningitis are angiostrongylus cantonensis (rat lungworm), Gnathostoma spinigerium and Baylisascaris procyonis. Rat is the definitive host where the sexual reproduction of the nematode occurs. The larval form of the nematode enters the intermediate host Mollusks (snail/slug) by ingestion of the rat faeces.[7] The third larval stage which develops in the intermediates hosts is the infective form which is ingested by the definitive hosts (rat) or the accidental host (human beings). The contamination of food by the slime of the infected snail or slug is enough for transmission. The ingested larvae penetrate the small intestinal mucosa and enter the bloodstream. A minority enter the central nervous system causing an immune reaction or mechanical damage.[7] The limited studies on histopathology of the brain show meningeal infiltration by eosinophils, macrophages and lymphocytes, tracks within the brain parenchyma associated with cell debris, microthrombi, and granulomas surrounding dead worms.[8] There are previous reports of eosinophilic meningitis following contamination from snails.[9,10] The snails reported to be involved in eosinophilic meningitis are Pila ampullacea and Pomacea canaliculate.[11,12] Eosinophilic meningitis can result from ingestion of transport hosts like freshwater shrimp, frogs, land crabs, and planarians which are not required for reproduction of the nematode but capable of transmission of infection to humans if eaten raw or undercooked. Other rare causes were ruled out: no cystic lesions on brain imaging suggesting neurocysticercosis, negative VDRL, no history of illicit drug abuse, patients not on medications causing eosinophilic meningitis, no evidence of lymphadenopathy or organomegaly suggesting lymphoma, no history of bathing in pond predisposing to schistosomiasis, not consumed crustaceans nor pulmonary involvement implicating paragonimiasis. Our patients presented with symptoms of raised intracranial pressure without lateralizing deficits. We investigated the patients considering chronic meningitis, cerebral venous sinus thrombosis and idiopathic intracranial hypertension as the differential diagnosis. The most common symptom is a headache and the most frequently affected cranial nerve is the abducens nerve palsy.[13] CSF of our patients was consistent with eosinophilic meningitis. The key to the diagnosis of eosinophilic meningitis is >10 eosinophils/μL in the CSF or at least 10% eosinophils. However, eosinophilia may not be seen in the initial CSF study.[14] Absolute peripheral eosinophilia more than 1,500 cells/cubic mm also suggests parasitic infestation. CSF may be xanthochromic or blood-tinged. Two of our patients showed hypoglycorrhachia mimicking tuberculous, cryptococcal, and malignant meningitis. CSF glucose is usually only mildly reduced, but it may rarely be too low, which further adds to the diagnostic dilemma. Protein is mildly elevated.[13] Large volumes of CSF may even demonstrate the larvae. The MRI findings are varied and non-specific: leptomeningeal enhancement, ventricular enlargement, hyperintense signal lesions on T2W sequences or ring/disc enhancing lesions.[15] The presence of hemorrhagic tracts, seen in our patient, is possibly produced by migrating worms which is of diagnostic value.[3,16] All patients responded to the steroid, headache subsiding within two weeks of oral prednisolone.[16] In animal studies dexamethasone significantly decreased the expressions of 14-3-3 isoform proteins and damage to the blood-brain barrier.[17] Steroids induce the apoptosis of eosinophils and inhibit brain apoptosis in mice with eosinophilic meningitis.[17] Hence the role of steroids is vital and tapered based on the clinical response.[17] It is essential to look for eosinophils in the CSF to detect eosinophilic meningitis. This practice will help avoid unnecessary antibiotics, anti-fungal and empirical antituberculous treatment. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.