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Table of Contents    
Year : 2020  |  Volume : 68  |  Issue : 3  |  Page : 684-687

Secondary Bacterial Infection of a Solitary Cysticercus Granuloma

1 Department of Neurological Sciences, Christian Medical College, Vellore, Tamil Nadu, India
2 Department of Pathology, Christian Medical College, Vellore, Tamil Nadu, India

Date of Web Publication6-Jul-2020

Correspondence Address:
Prof. Ari George Chacko
Department of Neurological Sciences, Christian Medical College, Vellore - 632 004, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.288991

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 » Abstract 

The most common presenting form of neurocysticercosis in the Indian subcontinent is a solitary cysticercus granuloma (SCG). Patients with typical SCGs almost never require any form of surgical intervention. Herein, we report an extremely rare case of bacterial superinfection of a left frontal SCG in a 23-year-old female, resulting in severe perilesional edema and mass effect. The patient had to undergo an emergency left decompressive hemicraniectomy and excision of the infected granuloma. Serum enzyme-linked immunoelectrotransfer blot (EITB) for cysticercal antibodies was positive and histopathological examination of the lesion revealed a cysticercus. The culture of the pus from within the lesion grew vancomycin-resistant Enterococcus spp. for which she was treated with linezolid for 6 weeks. At 6 months follow-up, she had residual motor dysphasia, right homonymous hemianopia, and right hemiparesis but was steadily improving. Secondary bacterial infection of an SCG is very uncommon and can be devastating. A high index of suspicion is therefore required when there is disproportionate perilesional edema and mass effect.

Keywords: Bacterial, neurocysticercosis, solitary cysticercus granuloma, superinfection
Key Messages: Bacterial superinfection of a solitary cysticercus granuloma is possible and if not treated aggressively, can be fatal.

How to cite this article:
Abraham AP, Bindra MS, Chacko AG. Secondary Bacterial Infection of a Solitary Cysticercus Granuloma. Neurol India 2020;68:684-7

How to cite this URL:
Abraham AP, Bindra MS, Chacko AG. Secondary Bacterial Infection of a Solitary Cysticercus Granuloma. Neurol India [serial online] 2020 [cited 2020 Sep 21];68:684-7. Available from:

Neurocysticercosis (NCC) refers to infection of the central nervous system by the larval stage of the helminth Taenia solium. One of the presenting forms of NCC is a solitary cysticercus granuloma (SCG), which represents a single, degenerating parenchymal cyst; usually less than 20 mm in diameter.[1] Secondary bacterial infection of a cysticercus granuloma is extremely uncommon and may have devastating consequences.

 » Case Report Top

A 23-year-old female presented to our outpatient clinic with refractory generalized seizures for 2 years. She had no known comorbid illnesses and had no history of any immunosuppressive therapy. She complained of occasional headaches but had no focal neurological deficits or papilledema on examination. Plain computerized tomography (CT) of the brain done 2 months previously showed a left frontal slightly hyperdense lesion with central hypodensity. It measured 15 mm in size and had perilesional edema but no mass effect [Figure 1]a and [Figure 1]b. A preliminary diagnosis of a SCG was made. Her antiepileptic drugs were titrated, blood was drawn for the detection of cysticeral antibodies by enzyme-linked immunoelectrotransfer blot (EITB) and she was advised to review with a contrast-enhanced magnetic resonance imaging (MRI) of the brain. She was not started on anticysticercal therapy.
Figure 1: (a and b) Plain CT brain showing a left frontal hyperdense lesion with a hypodense center. There is mild perilesional edema but no mass effect; (c and d) repeat plain CT brain done 2 months later at our institution, showing an increase in edema with a significant midline shift to the right. An evolving left posterior cerebral artery territory infarct can also be seen

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However, 2 days after her visit to the outpatient clinic, she developed fever, severe headache, and vomiting. Within the next 48 h, her sensorium deteriorated and she was brought to the emergency room with a Glasgow coma scale (GCS) score of 7/15 and right hemiparesis. She was intubated and a plain CT brain was done. It showed extensive left frontoparietal edema causing significant midline shift and left uncal herniation along with an evolving left posterior cerebral artery (PCA) territory infarct [Figure 1]c and [Figure 1]d. Total and differential leukocyte counts and serum electrolytes were normal. She underwent an emergency left decompressive hemicraniectomy. A 2 cm lesion with a central hypoechoic area was localized with ultrasonography just beneath the cortical surface in the left posterior frontal region that we excised in-toto. The lesion had a thick wall and contained green pus. The bone flap was not replaced at the end of surgery because the brain remained tense and bulging.

She was sedated and ventilated for 2 days after which her sensorium and right hemiparesis began to improve. Histopathological examination of the surgical specimen revealed parts of a cysticercus surrounded by a palisade of histiocytes with dense infiltrates of lymphocytes, plasma cells, and neutrophils [Figure 2]. The culture from the pus within the cyst grew vancomycin-resistant Enterococcus spp. while the blood culture remained sterile. EITB detected the presence of cysticercal antibodies in her blood. She was started on a 6-week course of linezolid 600 mg twice daily (2 weeks intravenous and 4 weeks oral). A plain CT brain done 1 week after surgery showed no obvious residual lesion, a significant decrease in the perilesional edema, and an established ipsilateral PCA territory infarct [Figure 3]a and [Figure 3]b. Echocardiography, ultrasonography of the abdomen, otoscopy, naso-pharyngo-laryngoscopy, and a dental assessment ruled out pyogenic foci elsewhere. Serum enzyme-linked immunosorbent assay (ELISA) for human immunodeficiency virus (HIV) was also negative.
Figure 2: Photomicrographs of hematoxylin and eosin-stained sections showing (a) a cysticercal cyst with multiple layers and an intense surrounding inflammatory response; (b) adjoining areas show abscess formation surrounded by a palisade of histiocytes with dense infiltrates of lymphocytes, plasma cells, eosinophils, and neutrophils

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Figure 3: (a and b) Plain CT brain done 1-week postop showing an established left posterior cerebral artery territory infarct, a resection cavity in the left frontal lobe and a hemicraniectomy defect with adequately decompressed brain; (c) T2-weighted, (d and e) T1-weighted gadolinium-enhanced and (f) susceptibility-weighted (SWI) MRI sequences done 6 months later showing gliosis in the left frontal lobe with no contrast enhancement, edema or mass effect. There is a small, nodular, T2-hypointense lesion in the resection cavity with corresponding signal dropout on SWI suggestive of hemosiderin staining or calcification

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Six months later her GCS was 15/15 with mildly impaired fluency of speech and naming ability. She had right homonymous hemianopia and subtle right hemiparesis but had started performing most of her daily activities independently. Contrast brain MRI showed gliosis in the left frontal region with no edema or mass effect. There was however a small, nodular, T2-weighted hypointense, faintly contrast-enhancing lesion in the resection cavity which also demonstrated signal dropout on susceptibility-weighted imaging suggestive of either hemosiderin staining or calcification [Figure 3]c, [Figure 3]d, [Figure 3]e, [Figure 3]f. It is a possibility that this may have been a small residual lesion. However, since there was no perilesional edema or mass effect and the patient was clinically improving, we decided to keep her on surveillance. She was asked to review with repeat imaging after 6 months.

 » Discussion Top

NCC is an endemic problem in several developing countries. SCG is the most frequently reported type of NCC in India and many other Southeast Asian countries.[2] The clinical features supportive of a diagnosis of SCG are focal seizures with or without secondary generalization. CT findings compatible with SCG are size <20 mm, contrast enhancement, mild or no perilesional edema, and minimal mass effect with no midline shift.[3],[4] The EITB, developed for the detection of cysticercal antibodies, is an excellent supportive serological test with its sensitivity and specificity of nearly 100%.[5] Based on these criteria, our patient at initial presentation was diagnosed to have SCG.

Surgical intervention is almost never required for patients who present with such typical SCGs.[6] A short course (1–2 weeks) of albendazole (with or without corticosteroids), may be prescribed but treatment is mainly with antiepileptic therapy.[4] However, there is a small subgroup of patients who can present with “atypical” SCG prompting surgery; having severe headache and/or persistent focal neurological deficits and atypical radiological features such as enlarging lesions with extensive perilesional edema.[7]

Superinfection of hydatid cysts is known to occur in about 7% of cases even in the absence of immunosuppression such as diabetes, malignancy, and steroids. The pyogenic organism typically implants itself on the parasite by local spread when present in the lung or liver; however, in the central nervous system, it is likely to occur from bacteremia.[8]

On reviewing the literature regarding superinfection of cysticercal cysts of the brain, we found only one case reported by Britton et al.[9]; that of a 7-year-old immigrant boy from India who was ultimately diagnosed to have a pyogenic right parietal brain abscess but also had positive serology to Taenia solium. The histopathological examination of the abscess, however, did not reveal a cysticercus, and mere positive serology does not prove NCC.

Our case on the other hand, conclusively proves that secondary infection of SCG with pyogenic organisms through a hematogenous route does occur, with dangerous consequences. An emergency decompressive hemicraniectomy along with excision of the granuloma and abscess resulted in a good outcome. The strong inflammatory host response to the degenerating cysticerci with resultant disruption of the blood-brain barrier and neuronal death could have provided an ideal milieu for bacterial seeding and eventual abscess formation. This case also throws light on a possible mechanism for the disproportionate perilesional edema and mass effect in a minority of SCGs. Pyogenic superinfection of a preexisting parenchymal cysticercus may be considered in some of these cases if the patient is resident in a region endemic for cysticercosis.

Our patient was not immunocompromised. She did not have history or blood investigations suggestive of sepsis and a thorough evaluation to look for a primary focus of infection was negative. Yang et al.[10]reported that in up to 40% of patients with brain abscesses, no systemic source of infection could be found, as seems to have been the case with our patient.

In conclusion, bacterial superinfection of an SCG is a rare but potentially fatal complication of the disease which should be suspected in any patient with disproportionate perilesional edema and mass effect.[11]

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Conflicts of interest

There are no conflicts of interest.

 » References Top

Rajshekhar V. Etiology and management of single small CT lesions in patients with seizures: Understanding a controversy. Acta Neurol Scand 1991;84:465-70.  Back to cited text no. 1
Garg RK, Malhotra HS. Solitary cysticercus granuloma. Expert Rev Anti Infect Ther 2012;10:597-612.  Back to cited text no. 2
Rajshekhar V, Chandy MJ. Validation of diagnostic criteria for solitary cerebral cysticercus granuloma in patients presenting with seizures. Acta Neurol Scand 2009;96:76-81.  Back to cited text no. 3
Singh G, Rajshekhar V, Murthy JMK, Prabhakar S, Modi M, Khandelwal N, et al. A diagnostic and therapeutic scheme for a solitary cysticercus granuloma. Neurology 2010;75:2236-45.  Back to cited text no. 4
Del Brutto OH, Nash TE, White AC, Rajshekhar V, Wilkins PP, Singh G, et al. Revised diagnostic criteria for neurocysticercosis. J Neurol Sci 2017;372:202-10.  Back to cited text no. 5
Rajshekhar V. Surgical management of neurocysticercosis. Int J Surg 2010;8:100-4.  Back to cited text no. 6
Rajshekhar V, Chandy MJ. Enlarging solitary cysticercus granulomas. J Neurosurg 1994;80:840-3.  Back to cited text no. 7
García MB, Lledías JP, Pérez IG, Tirado VV, Pardo LF, Bellvís LM, et al. Primary super-infection of hydatid cyst--clinical setting and microbiology in 37 cases. Am J Trop Med Hyg 2010;82:376-8.  Back to cited text no. 8
Britton PN, Chaseling R. Brain abscess in a recent immigrant. J Paediatr Child Health 2013;49:E176-8.  Back to cited text no. 9
Yang SY, Zhao CS. Review of 140 patients with brain abscess. Surg Neurol 1993;39:290-6.  Back to cited text no. 10
Rajshekhar V. Cerebral cysticercus granuloma associated with a subdural effusion. Neurol India 2001;49:182-4.  Back to cited text no. 11
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