tuberculosis granuloma structure

Meningitis can develop tuberculosis granuloma structure latent local focus, in the distance, for example, lung abscess or paravertebral through hematogenous spread, or as a result of miliary tuberculosis. Histologically, only a small number of living bacilli visible in the parenchyma and serous meningitis may be no obvious organism. Early TB meningitis is dangerous, with a prodromal period of 2 weeks before the onset of meningeal symptoms.

tuberculosis granuloma structure

Clinical manifestations include fever, anorexia, malaise, nausea, vomiting, headache, apathy and mental disorders.

tuberculosis granuloma structure

Physical findings include neck stiffness, decrease in basilar cranial nerve, focal neurological deficits, pupillary changes, changes in the fundus, optic disc edema and peripheral lymphadenopathy. Most cases of TB meningitis progress through three stages. The first stage is done with a mild fever, personality changes, and irritability, and takes 1-2 weeks. Confusion can be an early sign of the parents. During the second phase, increased intracranial pressure and nausea, vomiting, stiff neck, photophobia, seizures and cranial nerve palsies (third, sixth, seventh) were generated. The last phase involves high fever, confusion, stupor, and coma. Decortication and eventually can lead to hernias. In a study of 199 patients with tuberculosis and HIV infection, 14% had a disorder of the central nervous system (Shafer, et al, 1991). The presence of peripheral intrathoracic and intra-abdominal lymphadenopathy was more common in patients with HIV infection. Patients with low CD4 + lymphocytes also have a poorer prognosis.
TB meningitis (TBM) caused by Mycobacterium tuberculosis (M. tuberculosis) and is the most common form of central nervous system (CNS), tuberculosis (TB). TPM is associated with a high incidence of neurological complications and death if not promptly [1-5] treated. TPM is rare in developed countries, with about 100 to 150 cases occur each year in the U.S., less than 3% of the nearly 4100 years, cases of bacterial meningitis [6, 7]. This disease occurs when the subpial or subependymal nodules, also known as the “rich points” bacillemia sown during primary infection or disseminated disease, rupture into the subarachnoid space [8]. The people most at risk, including children with tuberculosis and TBM patients with primary immunodeficiency caused by aging, malnutrition, or diseases such as HIV and cancer [9, 10]. With the help of anti-tumor necrosis factor alpha (TNFa) antibodies has also been associated with an increased risk of TPM, including pulmonary tuberculosis [11]. Most of them do not have a known history of tuberculosis, but the evidence extrameningeal diseases (eg, lung) can be found in nearly half of the patients [3, 4]. tuberculosis granuloma structure Positive tuberculin test is only 50% of patients with TPM. In areas with a low prevalence of tuberculosis, TPM more frequent reactivation of tuberculosis.

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