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Biology- Research Assignment - Essay Example

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One infectious disease that affects the urinary, nervous, and endocrine systems is extra-pulmonary tuberculosis (EPTB), caused by the organism Mycobacterium tuberculosis (Fauci et al., 2008). M. tuberculosis is an acid-fast, non-spore forming, rod-shaped bacterium that possesses…
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Biology- Research Assignment
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Extrapulmonary Tuberculosis: Urinary, Nervous, and Endocrine Systems Infection One infectious disease that affects the urinary, nervous, and endocrine systems is extra-pulmonary tuberculosis (EPTB), caused by the organism Mycobacterium tuberculosis (Fauci et al., 2008). M. tuberculosis is an acid-fast, non-spore forming, rod-shaped bacterium that possesses a mycolic acid-rich cell wall which confers low permeability to antibiotics (Fauci et al., 2008). Although most cases of tuberculosis infection worldwide manifest primarily as lung disease, one-third of the cases actually affect other organs (Fauci et al, 2008). M. tuberculosis may lodge in any part of the genitourinary tract such as the kidneys, ureters, or bladder.

Clinical symptoms of genitourinary TB include hematuria (blood in the urine), flank pain, urinary frequency, and painful urination (Herchline, 2012). Meanwhile, tuberculous meningitis results when the subependymally-located pathogen affects the subarachnoid space (Mohan and Sharma, 2004). Symptoms indicative of this disease presents with a 2-3 week exanthema consisting of low-grade fever, body malaise, and headache, which evolves to cause damage to the cerebral arteries and cranial nerves (Golden and Vikram, 2005).

This may lead to hemeparesis, seizures, increased intracranial pressure, and coma. A common endocrine organ infected by M. tuberculosis is the adrenal glands, causing tuberculous Addison’s disease (Kelestimur, 2004). This results in adrenocortical deficiency which presents as body fatigue, loss of appetite, weight loss, nausea, decrease in blood pressure, and skin hyperpigmentation. Non-pulmonary tuberculosis is acquired when an individual is exposed to aerosols of a person with active pulmonary tuberculosis such as during sneezing, talking, or coughing (Fauci et al., 2008). When the organism is inhaled, it gets deposited in the airways but may not necessarily establish infection there.

It may be carried hematogenously or through the lymphatics to the other parts of the body and infect other organs. In addition, primary pulmonary tuberculosis can spread to different organs via hematogenous dissemination especially in immunocompromised individuals like HIV-infected patients (Golden and Vikram, 2005). Once inside the body, the organism activates a macrophage-activating cell-mediated immune (CMI) response and tissue-damaging response (Fauci et al., 2008). The CMI results in activation of macrophages to engulf and supposedly kill the pathogen.

However, M. tuberculosis is equipped with mechanisms that allow it to survive and multiply within the macrophages. Meanwhile, the tissue-damaging response is a delayed-type hypersensitivity (DTH) reaction as a result of the antigens secreted by the pathogen. Its function is to destroy the infected macrophages, causing necrosis of the involved tissues leading to granuloma formation (Fauci et al., 2008). The inflammation and granuloma formation involved in the pathogenesis of M. tuberculosis infection cause destruction of the organs.

Recommendations for the treatment of extrapulmonary tuberculosis include a 2-month intensive phase treatment with daily or 3 times/week administration of isoniazid, rifampicin, pyrazinamide, and ethambutol (Mohan and Sharma, 2004). This is followed by a 6-month continuation phase consisting of izoniazide and ethambutol treatment (Mohan and Sharma, 2004). Extra-pulmonary tuberculosis causes a myriad of complications. For instance, genitourinary TB may result in infertility and obstruction of ureters while neurologic complications may include cranial nerve palsies and visual loss (Mohan and Sharma, 2004).

Permanent hormone imbalance may result from endocrine affectations. Fauci, A., Kasper, D., Longo, D., Braunwald, E., Hauser, S., Jameson, J., and Loscalzo, J. 2008. Harrison’s Principles of Internal Medicine. 17th edition. The McGraw-Hill Companies. Ch 138Golden, M., and Vikram, H. 2005. Extrapulmonary Tuberculosis: An Overview. Am Fam Physician. 72(9):1761-1768Kelestimu, F. 2004. The endocrinology of adrenal tuberculosis: the effects of tuberculosis on the hypothalamo- pituitary-adrenal axis and adrenocortical function.

J Endocrinol Invest.;27(4):380-6.Mohan, A., and Sharma, S. 2004. Extrapulmonary tuberculosis. Indian J Med Res. 120: 316-353

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