Introduction
Acquired immunodeficiency syndrome (AIDS) is a stage of advanced HIV infection. At this phase of HIV infection, an individual develops various symptoms and signs. These clinical manifestations sometimes resemble common illnesses but then progresses unusually to contribute to a serious destruction of the CD4 cells which are critical in the immune system. The HIV targets and weakens the immune system, hence exposing the body to a series of opportunistic infections which lead to a general health deterioration or death. Therefore, AIDs is chronic and life-threatening hence the need to properly manage the strength of the virus and maintenance of the amount of the virus in the body (viral load) at lower levels (Moylett & Shearer, 2002). There are various clinical manifestations of AIDs, but these signs and symptoms rely on various factors such as the baseline immunity of an individual.
Pathophysiology of AIDs
The human immunodeficiency Syndrome is a disease which results from the destruction of the body immune system by human immunodeficiency virus (HIV). Once inside the body of an individual, the HIV uses ribonucleic acid and the deoxyribonucleic acid of an infected person form a viral DNA. This viral DNA has a long incubation period (clinical latency) but ultimately manifests in various signs and symptoms (Moylett & Shearer, 2002). The fact that the virus targets and damages the immune system contributes to a drastic health decline. The fact that HIV replicates by using the DNA of CD4+ cells destroys the overall immune system. Most importantly for an individual to be diagnosed with AIDS, he or she must be having a condition that points to an HIV infection or has a CD4 count of fewer than 200 cells/mm3. The CD4 count is the ultimate determinant of whether someone has AIDS irrespective of whether the person has AIDS-defining conditions or not (Schuitemaker & Miedema, 2000).
Clinical Manifestations of AIDs
The primary manifestations of AIDs are the occurrence of fever which cannot be traced to any infection. The mild signs of the virus may be easily misconstrued to be any other disease. However, the manifestations progress to acute viral syndrome after a period of between 2 to 4 weeks of contracting HIV (Calles, Evans, & Terlonge, 2010). However, depending on the health status of the patient, the acute viral syndrome may occur even after six weeks of exposure to the virus. During this period, infected people experience fever, myalgia, general fatigue, chronic cough, loss of weight and headache (Boniphace, Omari, Fred, Ferdinand, & Marcel, 2011). The acute viral syndrome also manifests in the form of effect on the skin such as rashes which may occur in any part of the body such as the face, trunk, palms, and sole of the feet.
Gastrointestinal manifestations also dominate the acute viral syndrome phase of AIDs. These include pain in the abdomen, vomiting, nausea, and diarrhea. These are the primary gastrointestinal manifestations of AIDs. These signs are associated with profound depreciation in the number and functionality of the CD4 cells (white blood cells which fights virus) (Boniphace et al., 2011). It also has a series of metabolic manifestations such as hyperlipidemia, body fat redistribution, and insulin resistance.
There are also various oral signs and symptoms of AIDs. Even though an HIV infected person may not necessarily have all of them, he or she will have at least one of the oral manifestations at some stage in the course of the disease. Candidiasis of the oral cavity is one common oral infection among AIDs patients. The risks of such oral complications associated with HIV increases with the declining levels of immunodeficiency (Moylett & Shearer, 2002). The oral manifestations of AIDs result from five primary causations which include fungi, bacteria, virus, neoplastic and miscellaneous lesion. Some of the specific oral manifestations include Aphthous ulcers, Candidiasis, linear gingival erythema and salivary gland disease (Galanda, 2009). However, the probability of these signs occurring depends on other CD4+ T cells count in an individual's body.
AIDs also manifest on the skin surface. These can be divided into 5 primary categories including infestations, infectious, inflammatory, papulosquamous and neoplasm. Some of these include herpes virus infections which are often resistant to the first line of therapy among people infected with HIV (Galanda, 2009). These cutaneous infections may occur in the genitals or perianal areas. The acute HIV syndrome which progresses to full-blown AIDs is associated with aggressive rashes on the skin, sore throat, and painful mouth sores.
The severe destruction of the immune system generally exposes the body to a series of opportunistic infections whose signs may be a clear manifestation of AIDs. AIDs may not necessarily present itself as a disease of its own but rather a combination of symptoms of other diseases which proliferate under conditions of depressed immunity (Calles, Evans, & Terlonge, 2010). For instance, AIDs manifest in the form of pneumonia, tuberculosis, neurological changes and infections in the esophagus. These are attributable to the fungi, bacteria and viruses which thrive in an environment where the HIV has drastically reduced body immunity. For instance, pneumonia in people living with AIDs results from Pneumocystis jiroveci which is a bacteria that is rare among people with normal immune systems (Galanda, 2009).
References
Boniphace, I., Omari, M., Fred, R. S., Ferdinand, M., & Marcel, T. (2011). HIV/AIDS clinical manifestations and their implication for patient clinical staging in resource limited settings in Tanzania. The open AIDS journal, 5, 9. Doi: 10.2174/1874613601105010009.
Calles, N. R., Evans, D., & Terlonge, D. (2010). Pathophysiology of the human immunodeficiency virus. HIV Curriculum, 7. https://bipai.org/sites/bipai/files/HIV_Curriculum_Web.pdf#page=15
Galanda, C. D. (2009). AIDS-related opportunistic infections. New York: Nova Biomedical Books.
Moylett, E. H., & Shearer, W. T. (2002). HIV: clinical manifestations. Journal of Allergy and Clinical Immunology, 110(1), 3-16. DOI: 10.1067/mai.2002.125978
Schuitemaker, H., & Miedema, F. (2000). AIDS pathogenesis. Dordrecht; Boston, Kluwer Academic.
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