Case Report: A rare case of Intracranial tuberculous granuloma (tuberculoma) in a 19-year -old male

Introduction

Mycobacterium tuberculosis, an infectious disease of pandemic size, causes tuberculosis (TB). It has consistently been among the top 10 infectious agents causing death for many years.¹ TB cases have decreased in some regions of the world, but the emergence of drug-resistant TB has created new problems. The most severe form of TB, known as CNS-TB, affects the central nervous system and accounts for 1% of all reported cases of TB, despite the fact that it can also affect other organs of the body. Tuberculosis (TB) is primarily a pulmonary disease.²

The formation of tuberculosis granulomas, the histopathological hallmark of the disease, is typically a defining feature of Mycobacterium tuberculosis infection, which kills hundreds of thousands of people annually. Our understanding of granulomas, which are a biologically diverse body of pro and anti-inflammatory cells from the host immune response, is primarily based on examination of lungs in studies on both humans and animals, but little is known about their counterparts from other organs of the TB patient, such as the brain.³

Granulomas are reactions of the body to protracted exposure to antigenic stimuli. They serve as a histopathologic hallmark of TB because they are the body’s initial response to Mycobacterium tuberculosis infection they are composed of a mixture of specialized immune cells that are affected by both pro and anti-inflammatory responses.⁴

The quantity and distribution of these cells, as well as other underlying diseases in the host, can have an impact on granuloma formation. For example the release of cytokines by a high number of B lymphocytes contributes to the development of tuberculous granulomas.¹

Case report

A 19-year-old male patient was treated in a hospital for fever and chills, generalized weakness, body pain, restlessness, nausea and vomiting, constipation, and abdominal pain. According to the patient’s complaints, he had a history of tonic-colonic seizures, typhoid fever, sickle cell disease, and AS pattern. He received treatment from a civil hospital, and there was no record of syncopal episodes at home. When the patient was admitted, he underwent several invasive and non-invasive investigations, including a CT brain plane and an MRI brain with contrast.

A computed tomography (CT) brain scan showed a chronic lacunar infarct in the left corona radiata (Figure 1).

Figure 1. CT scan of brain.

MRI with contrast findings showed acute infarct in the right corona radiata, abnormal meningeal enhancement on post-contrast with meningitis, multiple ring-enhancing lesions in the bilateral cerebral hemisphere, cerebellum, corpus callosum, and intracranial tuberculous granuloma. chronic infarct in the left corona radiata (Figure 2).

Figure 2. MRI of brain.

After admission, the patient also underwent various investigations such as CSF microscopy and culture, complete blood count (cbc), APTT ESR, LFT, KFT lipid profile, and CSF analysis showed that glucose-CSF 20 and protein-CSF 141, ph-7.2, no pus cell, and no RBC, culture-growth of Achromobactin xyloidine gram-negative bacteria. CBC investigation finding shows that HB% -11.4, WBC- 13800, MCHC -32.4, MCV -70.6, MCH -22.8, total platelet count- 2.68, haematocrit (HCT)- 35.2, KFT finding shows that Urea -15 mg/dl, Creatinine- 0.6 mg/dl, sodium (Na)-132 meq/lit, potassium(k)m- 4.6 meq/lit, LFT finding shows that ALT-12 U/lit, AST -34 U/lit total protein -7.6 gm/dl, globulin-4.3 gm/dl total bilirubin 0.9 gm/dl, APTT-36.4, ESR -13.

All investigations were performed after all patients were diagnosed with intracranial tuberculous granuloma (tuberculoma) and were on medical treatment, such as antitubercular therapy, antibiotic therapy, anticonvulsant therapy, antiplatelet therapy, steroid therapy, antipyretic, and analgesic therapy. In the CNS examination, the patient is oriented to the time place and person, the patient is in a mild confusion state, there is no type of injury, rashes, pigmentation, or scar formation, and symmetrical in size and shape of head, hearing activity was normal, eye examination revealed blurred vision at night, and he was instructed to have a CT brain and MRI brain with contrast. The patient was given the opinion of a neurophysician after all assessments and investigations had been completed.

The main goal is to prevent the development of infection by using all sterile technique procedures, article and equipment, and patients on a Foley catheter (2-way catheter 14 No.), catheter care given every 4–6 hours, and maintaining negative intake and output balance by monitoring the patient’s intake and output chart on an hourly basis. Every 4 hrly, vital parameters such as temperature, pulse, respiration, and blood pressure were monitored. Antitubercular, antibiotic, anticonvulsant, antiplatelet, steroid, antipyretic, and analgesic therapies.

Inj.Piptaz 4.5 gm intravenous 8 h, Inj. Streptomycin 150 mg once a day (OD), Tab levofloxacin 150 mg once daily, Tab Ethambutol 800 mg once daily, Inj. Dexamethasone 6 mg once daily, Inj. Pantoprazole 40 mg once daily (OD), Tab Acetazolamide 250 mg 8 hrly, Tab Sodium bicarbonate 2 tab once a day, Tab Aspirin 75 mg once a day.

Discussion

Since the development of anti-tuberculosis drugs, the risk of mortality and morbidity from tuberculosis has decreased dramatically. However, central nervous system involvement continues to bear the weight of mortality and neurological morbidity. As a highly oxygenated organ, the brain is the target of Mycobacterium Tuberculosis, an aerobic organism. The innate immune system is activated, and granulomas are produced as a result of the interaction between the organism and alveolar macrophages in the lung after it has been acquired and deposited there.⁵

The development of tuberculous foci in the brain parenchyma, meninges, or spinal cord is the first step in the development of central nervous system tuberculomas. The most common manifestation of central nervous system tuberculosis (TB) is tuberculous meningitis. Microglial cells are the primary target cells of the central nervous system are microglial cells.⁵

The clinical presentation was confirmed by radiological investigations. When used alone, a brain CT scan has an 80% false-positive rate for the diagnosis of tuberculoma owing to its relatively low specificity (13). Treatment for symptoms, anti-tuberculosis medication, and potential surgical resection of the lesion is all part of the management of intracranial tuberculomas. Clinically, the use of glucocorticoids, such as dexamethasone, is advised to reduce cerebral edema, inflammation risk, and intracranial pressure.⁶

The symptoms of a 19-year-old male patient being treated in a hospital included fever and chills, generalized weakness, body pain, restlessness, nausea and vomiting, constipation, and abdominal pain. According to the patient’s complaints, he had a history of tonic-clonic seizures, typhoid fever, and sickle cell disease as well as an AS pattern.

Consent

Written informed consent for publication of their clinical details as obtained from the patient study.