Tuberculous brain abscess in an immunocompetent adolescent.

Tuberculous brain abscess (TBA) is one of the rare forms of central nervous system tuberculosis. A case of tuberculous cerebellar abscess in a young immunocompetent adult male is being described. There was no clinical or radiological evidence of active tuberculosis elsewhere in the body. The diagnosis of tubercular abscess was confirmed by demonstration of acid fast bacilli in the abscess material aspirated via a burr hole. High index of suspicion and timely intervention is required to diagnose and treat this potential fatal but easily treatable condition.

INTRODUCTION

Virtually, all organs in body are affected by tuberculosis. Central nervous system tuberculosis constitutes approximately 10% of extra pulmonary tuberculosis and presents mainly as meningitis, tuberculoma of brain or spinal cord and tubercular abscess. Tuberculous brain abscess (TBA) is one of the rare forms of central nervous system tuberculosis with only few cases documented in the literature. It has been reported rarely even in country where tuberculosis is an alarming public health problem.[1] With the advent of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS), more cases are being diagnosed, but very few have been reported in immunocompetent HIV negative patients. We present a case of tuberculous cerebellar abscess in an 18-year-old immunocompetent male without any clinical or radiological evidence of tuberculosis elsewhere in the body. The diagnosis of tubercular abscess was confirmed by demonstration of acid fast bacilli in the abscess material aspirated via a burr hole. The patient responded very well to anti-tubercular treatment after the aspiration of the abscess.

CASE REPORT

An 18-year-old male presented with complaints of sub-acute onset, moderate to severe, occipitonuchal headache associated with vomiting and low grade fever 1 year back. He was initially evaluated and treated by a primary care physician. The treatment records were not available with the patient. With some symptomatic relief after initial 2 months of treatment, he discontinued medications without any medical advice or further follow-up. For another 9 months he continued to have recurrent off and on headache at irregular intervals which used to get relieved with over the counter medications. Over the last 6 months he had symptoms suggestive of progressive gait ataxia and right upper limb intentional tremors. For last 1 month he had resurgence of the symptoms in the form of severe holocranial headache, vomiting and fever. There was no history of seizures, loss of consciousness, any bulbar symptoms, diplopia, facial numbness or weakness. There was no significant past medical history. He was unmarried, rural dweller with agriculture as main vocation. There was no history of any high risk sexual behaviour. His mother took treatment for pulmonary tuberculosis for 9 months, 15 years back. Her exact medication records were not available.

On examination the general physical examination was unremarkable. He was conscious and well oriented to time place and person. All the cranial nerves including fundus were within normal limits. There was horizontal nystagmus in right eye on right lateral gaze with fast component towards the side of gaze. There was hypotonia on right side with grade power five in all limbs. Deep tendon reflexes were bilaterally grade two. Pendular right knee jerk was observed. Sensory examination was normal for touch, pain temperature, joint position, and vibration sense. Right sided cerebellar signs were present in the form of intentional tremors, dysdiadokokinesia, past pointing, and dysmetria. Gait was ataxic, wide based with tendency to sway on right side. Rest of the other systemic examination was normal.

Clinically, space occupying lesion in the right cerebellum-infective granuloma/benign or low grade malignancy was suspected. Routine hematological and biochemical investigations including hepatorenal functions were within normal limits. No abnormality was detected on chest roentgenograph. Enzyme-linked immuno sorbent assay for the HIV was negative. Induration of 16 mm in diameter was noted on a tuberculin skin test. The Magnetic resonance imaging of cranium revealed Intra axial T2 hyperintense and T1 hypointense parenchymal lesion in right cerebellum [Figure 1]. The gadolinium contrast revealed ring enhancement and there was restriction on diffusion weighted image [Figures 2a and 2b]. The Magnetic resonance spectroscopy study showed lactate and lipid peak [Figure 3]. In view of the radiological abnormalities, possibility of tubercular or pyogenic abscess was kept. Aerobic and anaerobic culture of pus drained from the burr hole was sterile. The microscopic examination of the pus smear demonstrated acid fast bacilli [Figure 4]. The pus culture using Lowenstein jensen media for mycobacteria was sterile after 7 weeks. Histopathology of abscess wall showed chronic inflammatory infiltrate without evidence of caseating granuloma or fungal elements. After drainage of the pus, anti-tubercular therapy was started which resulted in clinically significant resolution of the symptoms. He still continues to be on anti-tubercular therapy and is under regular clinical follow up.

Figure 1

The Magnetic resonance imaging of cranium showing Intra axial T2 hyperintense parenchymal lesion in right cerebellum

Figure 2a

The Gadolinium contrast enhanced Magnetic resonance imaging of cranium showing ring enhancement of the same parenchymal lesion

Figure 2b

The same lesion showing restriction on diffusion weighted image

Figure 3

Magnetic resonance spectroscopy of the lesion showing and lactate and lipid peak

Figure 4

The microscopic examination of the pus drained from the burr hole demonstrating acid fast bacilli

DISCUSSION

Tuberculous brain abscess is a rare and unusual expression of tuberculosis of central nervous system (CNS) and probably is the result of an altered host response to invasion by tubercular bacilli. It is characterized by an encapsulated collection of pus, containing viable tubercular bacilli without evidence of tubercular granuloma, but if present, are not in the form of organized follicles.[2] Abscess walls are usually devoid of epitheloid and giant cells, which are characteristic of tuberculoma.[3] It is not known why abscesses form instead of the usual tuberculoma, but many factors like host immunity, dose of infecting agent, nature of the involved tissue and anti-tuberculosis therapy perhaps decide the type of tissue reaction.

TBA is more commonly seen in immune compromised patients who are unable to mount a granulomatous inflammatory response. It has been reported in 20% of the cases of CNS tuberculosis with HIV.[4] Very few cases of TBA in immunocompetent individuals have been reported in literature. In developing countries TBA have been reported from 4% to 7.5% of patients with CNS tuberculosis without HIV.[5] In one of the study, tuberculosis accounted for 4% of the all the cases of intracranial abscesses.[6]

In 1978, Whitner proposed following criteria for establishing diagnosis of TBA-(i) Macroscopic evidence of a true abscess formation within the brain as confirmed during surgery or autopsy, (ii) Histological proof of presence of inflammatory cells in the abscess wall and (iii) Demonstration of Acid Fast bacilli AFB in the pus or abscess wall.[7] The diagnosis of TBA is usually suspected in immune-compromised patients with or without HIV infection or in an immunocompetent patient from an endemic region with a pulmonary focus of infection. The pulmonary focus of infection may be demonstrated in only one third of the cases.[5] Our patient too did not have any demonstrable pulmonary focus of infection. Perhaps tuberculosis in mother lead to early child hood exposure to infection in our patient. The latent tuberculosis was supported by the strongly positive tuberculin skin reaction. In the absence of an extracranial focus of infection, it is difficult to suspect TBA on the basis of clinical and routine magnetic resonance imaging (MRI) features, as these are nonspecific. A relatively long clinical history, contrast enhanced MRI showing enhancing capsule with thick wall and characteristic magnetic resonance spectroscopic findings were suggestive of TBA in our case. Although, the culture was negative for mycobacteria, proof of tubercular origin of abscess was demonstrated by acid fast bacilli in drained pus.

This case report underscores the importance of prudent utilization of the limited clinical and radiological information, supplemented with a simple procedure like burr hole aspiration for timely diagnosis and treatment of TBA. Early detection and intervention prevents further spread of infection and mortality. Though a rarity, physicians should be aware of this easily treatable entity.