End-stage Acquired Immunodeficiency Syndrome Research Articles

Acute respiratory distress syndrome (ARDS) is a serious complication of sepsis. Only a few cases of non-tuberculous mycobacteria complicated by ARDS have been discussed in the literature to date. Mycobacterium kansasii is the most pathogenic non-tuberculous mycobacterium affecting the lung. In the late stages of acquired immunodeficiency syndrome (AIDS), it may also present as disseminated disease. The clinical course is usually chronic, and the time to clinical diagnosis can sometimes be long, requiring a careful and meticulous search for the pathogen. To our knowledge, this is the first case report of disseminated M. kansasii infection complicated by ARDS and acute liver failure in a patient with end-stage AIDS.

INTRODUCTION : Infection with Human Immunodeficiency Virus (HIV) and its end stage Acquired Immunodeficiency Syndrome (AIDS) is the major public challenge of Modern times, with over 25 million persons already dead and over 30 million Living with HIV / AIDS, the majority of whom are without access to therapy. Opportunistic infection continue to cause morbidity and mortality in Patients with human immunodeficiency virus infection throughout the world. Although the incidences of opportunistic infections have been reduced Around the globe by Highly Active Anti Retroviral Therapy (HAART), the situation remains the same in most developing countries including India. This is due to the fact that some patients do not have access to the treatment and others do not have sustained response to antiretroviral drugs for multiple reasons including poor adherence, drug toxicities, drug interactions or initial acquisition of a drug resistant strains. Oropharyngeal candidiasis is the most common opportunistic infection Observed in AIDS patients, occurring in an estimated 80 to 95% of these patients when the CD4 T lymphocyte counts are below 200 cells /mm3. Increased retroviral replication and an associated decline in immune defences render these patients more susceptible to oropharyngeal candidiasis. Considering the above the facts, the present study was conducted to determine the species distribution and antifungal susceptibility profiles of the Candida isolates from HIV patients with Oropharyngeal Candidiasis. AIMS AND OBJECTIVES : 1. To isolate Candida species from HIV patients with oropharyngeal Candidiasis. 2. To speciate the Candida isolates. 3. To determine the antifungal susceptibility pattern of the isolates by disk diffusion and microbroth dilution method. 4. To find out the correlation of various Candida isolates and their antifungal susceptibility pattern to the CD4 count of the patients. MATERIALS AND METHODS : Statistical analysis were carried out using statistical package for Social sciences and Epi- software by statistician .The proportional data of this cross sectional study were tested using Pearson’s Chi Square Analysis test and Binomial Proportion test. Study group includes 150 HIV positive patients presenting with clinical picture of oral candidiasis. Inclusion Criteria: 1. HIV positive patients: Seropositivity status of the patients were determined as per NACO guidelines. 2. Patients with clinical picture of candidiasis on the oral /pharyngeal mucosa. 3. Patients above 18 years of age group. 4. Both Males and Female were included in the study. 5. Not on any antifungals or corticosteroids 30 days prior to the study. Patients were included in the study only after getting informed written consent. All patients satisfying the inclusion criteria were only once documented and were assigned serial numbers. Patients were interviewed by structured questionnaire and their hospital records were used to know about the previous episodes of Oropharyngeal Candidiasis, use of any antifungal agents and past medical conditions.Oropharyngeal specimens were collected by firmly swabbing the lesion site with two steile cotton swabs under strict aseptic precautions. Samples were transported immediately to the laboratory and subjected to various mycological tests. Blood was collected in EDTA vacutainer tubes from each patients for enumeration of their CD4 count using BD FACS Counter. CONCLUSION : In conclusion, Candida albicans is the most frequently isolated species from HIV seropositive patients with primary as well as recurrent Candidiasis. Non- albicans Candida species are emerging as important pathogens with increasing rates of azole resistance and with increased immunosuppression. Since oral candidiasis may be considered as indirect marker of immunosuppression in HIV patients, regular oral check up of these patients could be an indicator of immunosuppression. Further the increasing rates of resistance particularly among the non- albicans Candida spp. emphasizes the need for speciation and determination of antifungal susceptibility pattern of the oral candida isolates from HIV patients with oropharyngeal candidiasis.

African primates are naturally infected with over 40 different simian immunodeficiency viruses (SIVs), two of which have crossed the species barrier and generated human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2). Unlike the human viruses, however, SIVs do not generally cause acquired immunodeficiency syndrome (AIDS) in their natural hosts. Here we show that SIVcpz, the immediate precursor of HIV-1, is pathogenic in free-ranging chimpanzees. By following 94 members of two habituated chimpanzee communities in Gombe National Park, Tanzania, for over 9 years, we found a 10- to 16-fold higher age-corrected death hazard for SIVcpz-infected (n = 17) compared to uninfected (n = 77) chimpanzees. We also found that SIVcpz-infected females were less likely to give birth and had a higher infant mortality rate than uninfected females. Immunohistochemistry and in situ hybridization of post-mortem spleen and lymph node samples from three infected and two uninfected chimpanzees revealed significant CD4(+) T-cell depletion in all infected individuals, with evidence of high viral replication and extensive follicular dendritic cell virus trapping in one of them. One female, who died within 3 years of acquiring SIVcpz, had histopathological findings consistent with end-stage AIDS. These results indicate that SIVcpz, like HIV-1, is associated with progressive CD4(+) T-cell loss, lymphatic tissue destruction and premature death. These findings challenge the prevailing view that all natural SIV infections are non-pathogenic and suggest that SIVcpz has a substantial negative impact on the health, reproduction and lifespan of chimpanzees in the wild.

A 36-Year-Old Woman With a Unilateral Breast Mass

Two neuropathological changes that are linked with biological and pathological aging were examined in subjects with end-stage acquired immunodeficiency syndrome (AIDS). Autopsy brain specimens were examined from 25 people who died from complications of AIDS and 25 comparison subjects who were human immunodeficiency virus (HIV)-negative, matched for age, gender, ethnicity, and postmortem time interval. These adults were stratified into three age groups: elderly (62 to 75 years), intermediate (55 to 60 years), and young (21 to 42 years). Ubiquitin-stained dotlike deposits (Ub-dots) and diffuse extracellular plaques containing the beta-amyloid (Abeta) fragment of the amyloid precursor protein (Abeta plaque) were both increased significantly in the hippocampal formation of older subjects. In subjects with AIDS, Ub-dots were increased whereas Abeta plaque counts were not significantly different. Western blotting confirmed that high-molecular-weight ubiquitin-protein conjugates (HMW-Ub-conj) were increased in AIDS. The band intensity of one HMW-Ub-conj species with an approximate molecular mass of 145 kDa was correlated significantly with increased acute phase inflammatory protein (a-1-antichymotrypsin) and decreased synaptophysin and growth-associated protein-43 band intensities. These results raise the possibility that HIV-related brain inflammation disturbs neuronal protein turnover through the ubiquitin-proteasome apparatus, and might increase the prevalence of age-associated neurodegenerative diseases by decreasing synaptic protein turnover through the proteasome.

To test the hypothesis that CD4+ T lymphocytes accumulate in brains of end-stage acquired immunodeficiency syndrome (AIDS) patients, we examined T-lymphocyte subsets in the CA1, CA3, and CA4 regions of the hippocampus of AIDS patients with (n = 10) and without (n = 11) human immunodeficiency virus encephalitis (HIVE) plus controls (n = 7). HIV p24 antigen was common in monocytic cells and rare in activated/memory CD45RO+ lymphocytes. Hippocampal activated/memory CD45RO+ T lymphocytes significantly increased (P <.001) in seven of the eight hippocampal subregions with hippocampal HIVE (1.14 +/- 1.4 T cells/high-power field [hpf]), but AIDS hippocampus without HIVE were similar to controls (0.03 +/- 0.07 T cells/hpf and 0.03 +/- 0.09 T cells/hpf, respectively). CD45RO+ and CD3+ lymphocytes were similar in numbers and distribution, whereas CD4+ and CD8+ lymphocytes were weakly immunoreactive and less frequent. All four lymphocyte subtypes were present in perivascular spaces and microglial nodules of HIVE, and had direct contact with neurons. Monocytes, microglia, and multinucleated giant cells were immunoreactive for CD4 in AIDS cases with hippocampal HIVE but microglia in remaining AIDS cases and controls were CD4-. CD68+ macrophages significantly increased in hippocampus of HIVE patients (P <.05) and were predominately perivascular in the absence of local HIVE. These studies show that CD4+ T lymphocytes, as well as CD8+ T lymphocytes, participate in the local inflammatory response of HIVE in end-stage AIDS patients, and suggest that their recruitment requires local HIV infection. The perineuronal location of CD4+ cells provides the potential for lymphocyte-mediated neuronal injury or trans-receptor-mediated neuronal infection.

Challenges in Pain Management Among Persons with AIDS in a Long-Term-Care Facility

Peripheral neuropathy is common in human immunodeficiency virus type-1 (HIV-1) infection. Peripheral neuropathies complicate all stages of the HIV-1 disease and cause considerable morbidity and disability in HIV-1 infected individuals and acquired immunodeficiency syndrome (AIDS) patients. Whereas symptomatic neuropathies occur in approximately 10% to 15% of HIV-1-infected patients overall, pathologic evidence of peripheral nerve involvement is present in virtually all end-stage AIDS patients. There are 6 major clinical types of HIV-associated neuropathies that are regularly seen in large HIV-1 clinics. Distal sensory polyneuropathy (DSP) is the most common among the HIV-1-associated neuropathies. DSP generally occurs in later stages of HIV-1 infection and it follows an indolent and protracted clinical course. The dominant clinical features in DSP include distal pain, paresthesia and numbness in a typical length-dependent fashion with proximal to distal gradient. Whereas toxic neuropathies--secondary to certain antiretroviral agents--are clinically similar to DSP, their temporal relation to neurotoxic medication helps distinguish them from other HIV-1-associated neuropathies. DSP and toxic neuropathy may coexist in a single patient. Acute and chronic inflammatory demyelinating polyradiculoneuropathies (AIDP and CIDP) produce global limb weakness. AIDP may occur at seroconversion and it can therefore be the initial manifestation of HIV-1 infection. CIDP generally occurs in the mid to late stages of HIV-1 infection. Progressive polyradiculopathy (PP) occurs in patients with advanced immunodeficiency and is generally caused by the opportunist cytomegalovirus (CMV) infection. Mononeuropathy multiplex (MM) in early stages of HIV-1 infection is immune mediated, whereas in advanced AIDS it is caused by the CMV infection. Finally, subclinical autonomic nervous system involvement is common in all stages of HIV-1 infection. Because HIV-1-associated neuropathies are diverse in their etiology and pathogenesis, a precise clinical diagnosis is required to formulate a rational therapeutic intervention.

The increasing use of highly active antiretroviral therapies (HAARTs) has changed the course of AIDS-related illnesses and enhanced the quality of life of patients infected with human immunodeficiency virus (HIV) and may have changed the causes of deaths in patients with acquired immunodeficiency syndrome (AIDS). The aim of the present study was to investigate causes of deaths in long-term care hospital patients with late-stage AIDS who expired at the Coler-Goldwater Memorial Hospital in New York City in 1995, and in 1998 and 1999, that is, immediately before and the two most recent years after the advent of HAART. Analysis of causes of deaths as recorded on the death certificates of 232 AIDS patients. The overall mortality rate declined from 75.6 deaths per 100 person-years in 1995 to 33.2 deaths per 100 person-years in 1998-1999 (P < .001). The number of AIDS patients who expired because of sepsis and opportunistic infections, which included Pneumocystis carinii pneumonia (PCP), decreased significantly from 30 (26.1%) and 24 (20.9%) in 1995 to 15 (12.8%) and 10 (8.5%) in 1998-1999, respectively (P < .05). In contrast, deaths from hepatic failure increased from 0 (0%) in 1995 to 7 (6%) in 1998-1999 (P < .05). Increases, although not significant statistically, were associated with pneumonias excluding PCP, end-stage AIDS, renal failure, and malignancies. Analysis of cause-specific mortality by gender between 1995 and 1998-1999 revealed very little difference between men and women. This analysis showed, however, that the infectious processes taken together (pneumonias excluding PCP, sepsis, and opportunistic infections including PCP) were significantly less frequent causes of death in 1998-1999 than in 1995 (P < .01). These findings indicate that HAART affected the causes of deaths in patients with AIDS, with "traditional" opportunistic infections diminishing in importance relative to chronic medical conditions and malignancies.

HIV and Women

Homeless people are often thought not to adhere to therapy. Should we try to make protease inhibitors available to them? The new therapies for human immunodeficiency virus (HIV) infection are expensive, and their use may lead to the development of drug resistance. Do these drawbacks outweigh the ethical imperative to make effective drugs available to an underserved population? In late 1995, the first protease inhibitor was licensed by the Food and Drug Administration for persons infected with HIV. In combination with reverse transcriptase inhibitors, protease inhibitors give unprecedented improvements in CD4+cell count, viral load, morbidity, and mortality.1One press report used the term Lazarus effect2to describe the return to functional status of some patients with end-stage acquired immunodeficiency syndrome (AIDS). Driven by both science and enthusiasm, the standard of care for HIV-infected patients has quickly become combination antiretroviral therapy with a protease inhibitor.1,3The price

Advance medical directives are designed to allow a patient to choose a designated agent to make his or her medical decisions should the patient lose decisionmaking capacity. Problems can arise, however, in determining when and if the patient has lost the capacity to make such decisions. We examine a case in which a man with end-stage acquired immunodeficiency syndrome was admitted to the hospital because his agent and family could no longer provide adequate health care at home. While the patient was hospitalized, a conflict about aggressive vs comfort care arose between his physicians and his agent and family, both sides claiming that they knew best what his health care wishes were. At present, there are no clear guidelines as to who evaluates decision-making capacity; therefore, this judgment often falls to psychiatrists or ethics committees or even to the courts. We offer a systematic approach to resolving these conflicts. The

Advance medical directives are designed to allow a patient to choose a designated agent to make his or her medical decisions should the patient lose decisionmaking capacity. Problems can arise, however, in determining<i>when</i>and if the patient has lost the capacity to make such decisions. We examine a case in which a man with end-stage acquired immunodeficiency syndrome was admitted to the hospital because his agent and family could no longer provide adequate health care at home. While the patient was hospitalized, a conflict about aggressive vs comfort care arose between his physicians and his agent and family, both sides claiming that they knew best what his health care wishes were. At present, there are no clear guidelines as to who evaluates decision-making capacity; therefore, this judgment often falls to psychiatrists or ethics committees or even to the courts. We offer a systematic approach to resolving these conflicts. The