Neurocysticercosis is a common parasitic infection of the brain. It can occur intra-parenchymal, intraventricular, within the subarachnoid cistern or spine. CT/MRI is the standard modality to detect NCC. On imaging, five stages are recognized: non-cystic, vesicular, colloidal-vesicular, granular-nodular, and calcified-nodular stage (Lucato et al. 2007; Zhao et al. 2015). The colloidal vesicular stage mimics pyogenic brain abscess. On MRI, the signal in the cystic lesion is hyperintense on T2 in comparison to CSF and with peripheral enhancement suggestive of fibrosis. The colloidal vesicular stage signifies loss of immune tolerance to the larva (Kimura-Hayama et al. 2010).
Reports of cysticercal abscess are rare in literature. Kapu et al reported a single case of spinal cysticercal abscess. MRI showed T1W isointense lesion with central hypointensity and enhancement at the periphery. The abscess was excised, and the yellowish fluid was sent for culture. Histopathology of the wall showed fibrocollagenous tissue with foamy histiocytes mixed with lymphocytes. The characteristics of the parasitic wall with tegumentary layer, subtegumentary cytons, and inner loose reticular layer were suggestive of cysticercal cyst, although no scolex was identified. The yellowish fluid was sterile on culture (Kapu et al. 2012). Abraham et al. recorded bacterial superinfection of solitary cysticercal granuloma confirmed by culture. The source of the infection was presumed to be hematogenous, although the blood culture was sterile. The biopsy revealed a cysticercal granuloma within the luminal aspect and an adjoining palisade of histiocytes, infiltrated by lymphocytes, plasma cells, and neutrophils like our cases. Hence, abscess formation can be either primary or secondary from other sources like blood (Abraham et al. 2020). The chances of superinfection are greater in the presence of associated immunocompromised conditions like diabetes, malignancy, or retro positive patients. In our series, the first patient (case 1) had uncontrolled diabetes. The previously reported case of spinal cysticercal abscess was without a preexisting immunocompromised condition (Kapu et al. 2012).
The cysticercal brain abscess closely mimics a chronic abscess. Clinically both present with signs of inflammation and neurological deficits due to mass effect. Radiologically, both are identical with peripheral ring enhancement and non-enhancing center. If the cysticercal cyst wall is not found on histology, the differential diagnosis includes pyogenic abscess, tubercular abscess, and fungal abscess (Table 1). The histological clues to the diagnosis include a serpiginous or stellate outline of the cavity walled by several multinucleated giant cells, and an infiltrate rich in eosinophils. Calcospherules are rare. These features should prompt the pathologist to assiduously search for remnants of the parasite. Viable cysts do not produce an inflammatory response. A degenerating cyst elicits an inflammatory response with surrounding fibrosis. As the cysticercus dies, its structure becomes less distinct and usually starts to calcify, producing small calcospherules that aid in diagnosis even in the absence of a parasite wall. The eosinophil rich infiltrate and granulomatous response with foreign body giant cells mimics fungal granulomas or tuberculoma. Stains for fungal hyphae such as Periodic acid Schiff (PAS) and Gomori Methenamine Silver (GMS) help in ruling out fungal etiology. Culture remains the gold standard to prove the sterile nature of cysticercal abscess, and to exclude pyogenic and tubercular etiologies.
Table 1
Histological differential diagnosis of cysticercal abscess.
| Nature of lesion | Layers |
| Pyogenic abscess | 1. Central necrosis 2. Inflammatory granulation tissue composed of neutrophils and lymphomononuclear cells 3. Fibrous capsule 4. Gliosis |
| Tuberculoma | 1. Caseous necrosis with acid-fast bacilli on Ziehl Neelsen stain 2. Epithelioid granulomas with Langhan’s giant cells 3. Fibrous capsule 4. Gliosis |
| Fungal granuloma | 1. Central necrosis with fungal hyphae highlighted on PAS and GMS stains 2. Granulomas with foreign body type of giant cells engulfing the fungal hyphae. Eosinophils present 3. Fibrous capsule 4. Gliosis |
| Cysticercal abscess | 1. Central necrosis with serpiginous borders lined by palisade of epithelioid cells. Degenerating cysticercal cyst 2. Inflammatory granulation tissue rich in eosinophils along with foreign body type of giant cells 3. Fibrous capsule 4. Gliosis |
In the lesions described here, histologically, the lesion revealed layers of an abscess with central necrosis, the wall of granulation tissue, and varying degrees of fibrosis. However, in distinction from a pyogenic abscess, these lesions displayed the presence of four-layered organization with central necrosis having characteristic serpiginous borders, surrounded by mixed inflammatory granulation tissue with palisading epithelioid cells along with multinucleated giant cells and several eosinophils, which was in turn surrounded by fibrous granulation tissue and dense gliosis. These provided a clue that the lesion was not a pyogenic abscess. Detection of parasitic remnants aided the diagnosis. The detection of cysticercal antibodies in serum can provide supportive evidence. Pathogenetic events that lead to the formation of abscess are unclear and maybe governed by factors such as the host immunity and the number of antigens exposed following degeneration of the cysticercal cyst. The possibility of bacterial superinfection has been proposed based on the culture of the abscess contents (Abraham et al. 2020).
There is no standard protocol for management as the reported cases are few (Kapu et al. 2012; Britton and Chaseling 2013; Abraham et al. 2020). The reported cases in the literature were treated with surgical excision followed by anti-helminthic drugs albendazole with or without a short course of steroid, similar to our series (Kapu et al. 2012). The patient with a spinal cysticercal cyst was treated with eight weeks of albendazole and steroid. As the culture was sterile, the patient was not treated with antibiotics. Secondary bacterial infection of solitary cysticercal granuloma can be managed with appropriate antibiotics. Abraham et al used linezolid as the microorganism was vancomycin-resistant Enterococcus spp (Abraham et al. 2020). In our series, cases 2 and 3 were treated with two weeks of albendazole with a short course of oral steroids. As bacterial cultures were sterile, no antibiotics were added in the postoperative period.