Problems in the Management of TB Among HIV Patients - Research Paper Example

Introduction Human Immunodeficiency Virus (HIV) is one of the major health problems being faced by the general population. It is a major cause of worry for health administrators and health professionals in various parts of the world. In 1981, symptoms which were typical of this disease first manifested in homosexual men in Los Angeles and New York (Daar & Marks, 2010). They manifested with lung-infection type of a disease and rare skin tumours known as Kaposi’s sarcomas. This disease was later diagnosed in the rest of the US, then in Western Europe, and Africa. It was in 1983 when this disease was described and named as AIDS as caused by the HIV virus. Tests to confirm the presence of this disease later became known in the medical world and in the general population (Daar & Marks, 2010). As a result of this disease, a variety of opportunistic infections have been known to arise. One of these infections is known to be tuberculosis. This paper shall now discuss the proper management of tuberculosis (TB) among HIV-positive patients. A physiology of HIV shall first be presented, followed by a discussion on the physiology of TB. A discussion on TB as an opportunistic infection shall also be set forth. The diagnosis and screening of TB on the HIV-positive patients shall also be emphasized, as well as the management of TB on these HIV-positive patients. The prevention of transmission of TB among these patients shall be discussed, and finally the barriers to proper management shall be set forth in this paper. This paper is being conducted in order to come up with a comprehensive and thorough discussion on TB and HIV. It shall serve to provide academic and evidence-based information on the management of this disease as well as the management of the barriers to its effective management. With this discussion, it is hoped that data established herein can be used to guide practitioners in caring for TB/HIV patients. Physiology of HIV The physiology of HIV is composed of eight stages. The first stage is the viral binding stage (Kartikeyan, 2007, p. 47). The surface of cell membranes is full of receptors and the HIV virus often binds to atleast two of these receptors. This starts the infection process and with the tight binding of the virus with the receptors, fusion with the cell is achieved (Mohammed & Nasidi, n.d, p. 135). During the entry and coating stage, the viral core and its RNA enters the cell. The coating of the RNA dissolves and a partial uncoating leads to the release of the viral RNA inside the cell. The third stage – the reverse transcription stage – converts the RNA to DNA through the process of reverse transcriptase (Mohammed & Nasidi, n.d, p. 135). This process would copy the sequence of the viral RNA entering the cell and convert it into a DNA sequence. This virus then uses the viral proteins to make copies of the RNA. This reverse transcription is however faulty and prone to error (Levy, 2009, p. 150). Such defects and errors in transcription make it difficult for scientists to combat HIV because frequent errors in transcription lead to further mutations in the virus; and this makes it difficult for scientists to come up with treatment measures for this virus because it keeps on mutating (Kotz, Treizel, & Townsend, 2009, p. 507). The next stage is the integration into the host chromosomal DNA. In this stage, viral DNA is placed into the host cell DNA through the viral enzyme integrase (Mohammed & Nasidi, n.d, p. 135). The synthesis of viral DNA follows next. In this stage, when the infected cells are activated, the viral DNA is transcribed with the host DNA into messenger RNA. The new viral RNA is the genetic material for the next batch of viruses (Mohammed & Nasidi, n.d, p. 135). The translation and production of viral proteins leads to the creation of polypeptide sequences and each area of the mRNA matches a protein which is the building block for new HIV proteins (Mohammed & Nasidi, n.d, p. 135). The next stage is the assembly of virus and budding from the host cell. New virus proteins known as the virion forms at this stage and is preceded by the formation of viral proteins. As the RNA and other proteins are released from the surface of the cell as viruses, they also include a small part of the cellular membrane which already contains viral surface proteins (Porth & Matfin, 2007, p. 365). The viral proteins serve to envelope the new viral particles and these proteins then bind to the receptors of other immune cells. Consequently, infection easily pervades the body and the cells. Once viral replication becomes extensive and as it affects the CD4 and the lymphocytes, HIV will then destroy the cells and then further reproduce (Brenchley, Price, & Douek, 2006, p. 235). These CD4 + cells are then unable to fulfill their functions in fighting infection which leaves the body vulnerable to opportunistic infections. The last stage is the maturation stage. This stage is where the virus becomes infectious. In this stage, once the protease enzymes bud from the host cell, the protease then binds to the polypeptides. This processing step leads to the maturation of the infectious virion (Mohammed & Nasidi, n.d, p. 135). Physiology of Tuberculosis Tuberculosis is one of the oldest diseases known to man. At one point in our history, this disease has managed to devastate and decimate large groups of people. It is caused by the bacteria from the genus Mycobacterium; and Mycobacterium tuberculosis is the bacteria known to cause this disease (Covert, 2010). When these particles are inhaled, the droplets settle in the upper airways where the goblet cells reside (Knechel, 2009, p. 35). When the bacteria would make it through the mucociliary system, the bacteria enters the system and is immediately phagocytized or consumed by the white blood cells in the immune system (Covert, 2010). These mucus cells would initially fight off these bacteria through the process of coughing and expectoration. Phagocytosis however would not kill or decimate the bacteria; instead, these bacteria would now live inside the cells and multiply until the white blood cells would be destroyed (Covert, 2010). Attempts by the cell to fight off bacteria through the production of proteolytic enzymes and cytokines are initiated by the WBC. The cytokines attract the T lymphocytes which then help in cell-mediated immunity (Knechel, 2009, p. 35). The macrophages present with mycobacterial antigens to the T-cells and after about 2-12 weeks, the bacterium becomes detectible through skin tests. The cell-mediated immunity would help create granulomas around the bacteria. Nodular-type lesions accumulate from the T-lymphocytes and macrophages which then form an area which restricts replication and limits the spread of the bacteria (Knechel, 2009, p. 34). Such an area would kill the macrophages and create decay at the centre of the lesion. The bacteria would however be able to adapt and survive such an environment. These bacteria can continue to adapt and survive and form caseous necrosis, low oxygen levels, low pH, and limited nutrients (Braun, 2006, p. 327). Lesions would later calcify for those with a sufficient immune system and such calcification would help control the infection. Those with an inadequate immune system would experience primary progressive tuberculosis (Knechel, 2009, p. 34). Tuberculosis as an opportunistic infection TB is considered to be an opportunistic infection among HIV/AIDS patients. The infection process discussed above mostly affects the lungs; however, it can also affect other parts of the body, such as the kidneys or the spine. Among HIV patients, TB takes advantage of their weakened immune system (Bobak, 2009). In 2007 alone, there were about 1.37 million HIV patients diagnosed with TB and about 450,000 of them died (Thomas, 2009). Tuberculosis infection may either be latent or active. In latent infection, the bacterium is inside the body but does not manifest any symptoms; whereas for active TB, symptoms manifest and multiply in the person’s body (Kauffman & Walker, 2009, p. 192). In the early stages of HIV, TB is often expected among infected individuals without HIV and upper lung infiltrates on their chest X-ray. When the HIV becomes more progressive, the patients become more vulnerable to miliary TB and to manifest changes in their X-rays which can often be mistaken for bacterial pneumonia (Jarvis, 2010). HIV-related Tuberculosis Experts believe that HIV increases vulnerability to the M.tuberculosis bacteria and the progression of the bacteria to TB (WHO, 2004). Such vulnerability also increases as the patient is more immunocompromised. HIV also increases the rate of recent or latent M.tuberculosis infection (WHO, 2004). Furthermore, as HIV progresses, the CD4 T-lymphocytes decrease in number and function. This is an unfortunate consequence because these cells are important in securing the body against the M. Tuberculosis bacteria (WHO, 2004). In other words, the immune system cannot effectively “prevent the growth and local spread of M. Tuberculosis” (WHO, 2004). Diagnosis and Screening of TB among HIV-positive patients HIV patients are cautioned to immediately undergo a tuberculin skin test or Mantoux test in order to detect for TB (Van Dyk, 2008, p. 65). Regardless of their CD4 count, HIV patients are required to undergo a complete assessment in order to detect active of latent TB. Through the Mantoux test, the patient is injected with PPD tuberculin and among latent TB infection patients, they will usually manifest with sensitivity to PFD tuberculin which is seen as a reddish lump in the injected site within 48-72 hours from the administration of the tuberculin test (Jarvis, 2010). Clinical features which may suggest TB and HIV coinfection may involve the following clinical history: sexually transmitted infection; herpes zoster, recent or recurrent pneumonia, severe bacterial infections, and recent related TB (WHO, 2004). Symptoms like weight loss, diarrhoea, pain on swallowing, burning sensation of feet; and signs like scar of herpes zoster, pruritic popular skin rash, Kaposi sarcoma, oral candidiasis, necrotizing gingivitis, and persistent painful genital ulceration all indicate a possible HIV and TB coinfection (WHO, 2004). For HIV patients with mild immunosuppression, TB may present a clinical picture which is similar to post-primary pulmonary TB; a positive sputum smear test; and typical chest X-ray with upper lobe infiltrates or bilateral infiltrates; cavitation, pulmonary fibrosis, and shrinkage (Matji, n.d). For HIV patients with severe immunosuppression, their TB presents symptoms similar to primary TB with their sputum smears often testing negative; chest X-rays showing interstitial infiltrates in the lower zones and without showing any cavitation and fibrosis; chest x-rays looking exactly similar to bacterial pneumonia; higher number of extrapulmonary manifestations with the immune system less able to control the growth and spread of M.tuberculosis (Matji, n.d). Management of Tuberculosis on the HIV-positive patients In order to address TB/HIV coinfection, the WHO recommends a coordinated approach wherein interventions and activities are implemented simultaneously in order to prevent and control HIV and TB (Narain & Lo, 2004). In the regional level, the WHO is generating its programmes on advocacy and is mobilizing partnerships and resources in order to educate communities in the management of TB. On the national level, the treatment protocols for both HIV and TB are now being closely coordinated with each other in order to achieve maximum efficacy and promote effective management. In general however, HIV/TB patients must coordinate with their district medical officer before undergoing the treatment process (Action Nigeria, n.d). Their initial treatment phase for the first 2 months is focused on the killing of the bacilli and in this phase 2-3 drugs (Isoniazid, rifampicin, pyrazinamide, and ethambutol) are administered to the patient. Their treatment is considered up to 4-6 months where the type and number of drugs (Isoniazid and ethambutol) are reduced and this phase is aimed at eliminating the remaining bacteria (Action Nigeria, n.d). The DOT strategy (Directly Observed Treatment) is applied to these patients. Highly active retroviral therapy (HAART) has proven to be a beneficial in managing HIV coinfection. The application of anti-TB treatments alongside HAART has also ensured that HIV-TB coinfection is adequately managed (Narain & Lo, 2004). Studies however note the pharmacokinetic interactions between the rifamycin element of anti-TB meds and the antiretroviral drugs, more particularly protease inhibitors (PIs) and non-nucleoside drugs reverse transcriptase inhibitors (NNRTIs (Piscitelli & Gallicano, 2001). The principles behind the treatment of TB/HIV emphasize that the treatment of TB is prioritized over the treatment of HIV; among patients under HAART, such therapy has to be continued with the necessary adjustments in the HAART and the TB treatment; in patients not receiving HAART, the initiation of the treatment has to depend on the short-term risk assessment of the disease (Narain & Lo, 2004). Some studies believe that if the CD4+ counts of the patient are >200/mm3, the HAART can be initiated after the TB treatment has been completed and if the CD4 counts+ are 100-200/mm3, the HAART can be initiated after the first two months of TB treatment; and when the CD4 counts are Read More