A bronchoscopy with BAL has revealed organisms that are consistent with Pneumocystis carinii (Kovacs et al., 2001, 2450-2460).
Analysis: His long-drawn disease is consistent with HIV infection that has turned into AIDS over last 2 months leading to most probably an opportunistic infection of the gastrointestinal tract leading to disturbing diarrhea associated with nausea and vomiting. His decreased leukocyte count and pulmonary infection with Pneumocystis carinii indicates opportunistic pulmonary infection that is very characteristic of immunodeficiency associated with AIDS and consequent diminished CD4 count (Newton et al., 2003, 185-186).
Thus the original disease that the patient is suffering is AIDS, the hallmark of which is immune deficiency. The treatment with antibacterial agents thus has a chance to break down. This has been ascribed to the profound deficiency in immune function that eventually develops in an infected individual. The virus, HIV suppresses immune function since this has a predilection to infect the immune system, and as a result of continued infection, these cells are eventually destroyed (Adler, 2001, 12-17).
The most significant targets of this virus are a subset of thymus derived lymphocytes that carry surface molecule CD4. CD4 has been demonstrated to bind to the envelop glycoprotein of the HIV. Many other cells and tissues, such as, monocytes and macrophages also bear CD4 receptors. Coupled with G-protein coupled receptor family co-receptors, the processing of chemokines in these cells are affected, leading to defective migration, differentiation, and function of leukocytes during immune response to any infective process in the body. Two specific receptors, CCR5 and CXCR4 are important particularly. CCR5 are expressed widely on cells of the immune system that fight disease, such as, lymphocytes, macrophages, and dendritic cells. When the virus strains infect the primary macrophages through these co-receptors, the macrophages which are prime immune cells themselves are rendered defunct (Adler, 2001, 12-17).
From that point of view, the CD4 lymphocytes or T helper cells have known significant and central roles in immune functions, and as a result of HIV infection, these cells are destroyed. In consequence, the body immune response of affected, and these in part explain the immunosuppressive effects of the virus. These cells are normally stimulated by antigen contact, and normally they respond through enhanced cell division and synthesis and release of lymphokines, namely, interferons, tumor necrosis factors, interleukins, and other chemotactic factors that are involved in recruitment of more immune cells. The whole cascade of these phenomena are affected, and as a result the functions of the lymphokines to act as promoters of cytotoxic or suppressor CD8 cells and their maturation and behaviour are all affected, culminating into suppressed synthesis of antibody from the B lymphocytes. Other cells participating in the process of this innate immunity against diseases functionally contribute to the process. These are monocytes, tissue macrophages, and dendritic cell, and hence with an infection with HIV, the total immune system is compromised. Macrophages and particularly dendritic cells are