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Query: UMLS:C0026916 (MAC)
 5,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection due to the Mycobacterium avium complex (MAC) accounts for the most frequent AIDS-related opportunistic infections, but MAC infection is usually not the first AIDS-defining event that a patient infected with HIV experiences. The incidence increases linearly over time, at a rate of 20 to 25% per year, after a patient's first AIDS-defining event, and the incidence increases exponentially as the CD4+ cell count approaches zero. There is evidence that MAC may eventually infect most if not all HIV-infected patients who do not die from another HIV-related event. Since MAC infection contributes substantially to the morbidity and mortality of AIDS patients, prophylaxis appears to be mandatory. Rifabutin was the first drug which was shown to be effective in preventing MAC infection, and, recently, prophylaxis with clarithromycin was also found to prevent the disease. The optimal approach to prophylaxis still needs to be defined. Since a large majority of MAC infections occur in patients with CD4+ cell counts below 50/microliter, recommendations regarding the prophylaxis of patients with a history of an AIDS-defining opportunistic event and a CD4+ cell count between 50 and 200/microliter can be individualized, depending for example on how well the patient seems to be responding to antiretroviral treatment. Prophylaxis against MAC should be provided for any HIV-infected patient with a CD4+ cell count less than 50/microliter.
Infection
PMID:Prophylaxis against Mycobacterium avium-intracellulare complex infections in human immunodeficiency virus-infected patients. 903 47

Tuberculosis (TB) is still a major health problem, both as a single disease entity and as a cofactor in AIDS. The interaction between macrophage and Mycobacterium tuberculosis (MTB) is a critical step in the establishment of an early chronic infection. This study analyses the capacity of MTB to induce apoptosis in cells obtained by broncho-alveolar lavage (BAL) from patients with reactive pulmonary tuberculosis and from AIDS patients with disseminated pulmonary tuberculosis. Apoptosis was increased three-fold in BAL cells obtained from patients with pulmonary tuberculosis and even more markedly in alveolar macrophages of MTB-infected AIDS patients, compared with controls. Apoptosis was analysed and characterized by propidium iodide (PI) incorporation, terminal deoxy transferase (TDT)-mediated dUTP-biotin nick end labelling (TUNEL), and tissue transglutaminase (tTG) expression. The MTB-macrophage interaction was also investigated in vitro by infecting monocyte-derived macrophages (MDM) with MTB (virulent strain H37Rv). The induction of apoptosis by MTB required viable bacteria, was dose-dependent, and was restricted to H37Rv. Infection with either Mycobacterium avium complex (MAC) or HIV-1 and treatment with heat-killed MTB failed to induce apoptosis.
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PMID:Apoptosis of human monocytes/macrophages in Mycobacterium tuberculosis infection. 907

Infections caused by organisms of the Mycobacterium avium complex occur in approximately 50 to 60% of patients with AIDS. M. avium is an intracellular pathogen that survives and multiplies within mononuclear phagocytes. In this study, we investigated the uptake of M. avium grown within macrophages (intracellular growth M. avium [IG]) by a second macrophage compared with M. avium cultured in broth (extracellular growth M. avium [EG]). The results showed that IG was six- to eightfold more efficient than EG in entering macrophages. In addition, while an anti-CR3 antibody was able to inhibit approximately 60% of EG uptake by macrophages, it failed to inhibit the entry of IG. In contrast to EG, IG uptake into macrophages was significantly inhibited in the presence of anti-beta1-integrin and anti-transferrin receptor antibodies. Entry into macrophages by alternate receptors was associated with resistance to tumor necrosis factor alpha (TNF-alpha) stimulation. While stimulation with TNF-alpha resulted in inhibition of the growth of EG, it was not associated with inhibition of intracellular growth of IG. Investigation of the reason why M. avium is able to sense the changes in the intracellular environment triggering a change to the invasive phenotype suggests a direct relationship with macrophage apoptosis. These results suggest that intracellular growth is associated with novel mechanisms of M. avium uptake of macrophages and that those mechanisms appear to offer advantages to the bacteria in escaping the host defense.
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PMID:Growth within macrophages increases the efficiency of Mycobacterium avium in invading other macrophages by a complement receptor-independent pathway. 912 80

This article reviews the importance of preventing illness in HIV-infected patients. The indications and medication regimens for preventing several common opportunistic complications are discussed. Infections addressed include pneumocystis pneumonia, Mycobacterium avium complex, toxoplasmosis encephalitis, and tuberculosis, among others. Other preventive interventions such as routine immunizations are addressed briefly as well. Diagnosis and treatment of five of the most common HIV-associated opportunistic infections are reviewed.
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PMID:Prevention and treatment of common HIV-associated opportunistic complications. 927 92

Infection with HIV-1 results in pronounced immune suppression and susceptibility to opportunistic infections (OI). Reciprocally, OI augment HIV-1 replication. As we have shown for Mycobacterium avium complex (MAC) and Pneumocystis carinii, macrophages infected with opportunistic pathogens and within lymphoid tissues containing OI, exhibit striking levels of viral replication. To explore potential underlying mechanisms for increased HIV-1 replication associated with coinfection, blood monocytes were exposed to MAC antigens (MAg) or viable MAC and their levels of tumor necrosis factor alpha (TNFalpha) and HIV-1 coreceptors monitored. MAC enhanced TNFalpha production in vitro, consistent with its expression in coinfected lymph nodes. Using a polyclonal antibody to the CCR5 coreceptor that mediates viral entry of macrophage tropic HIV-1, a subset of unstimulated monocytes was shown to be CCR5-positive by fluorescence-activated cell sorter analysis. After stimulation with MAg or infection with MAC, CCR5 expression was increased at both the mRNA level and on the cell surface. Up-regulation of CCR5 by MAC was not paralleled by an increase in the T cell tropic coreceptor, CXCR4. Increases in NF-kappaB, TNFalpha, and CCR5 were consistent with the enhanced production of HIV-1 in MAg-treated adherent macrophage cultures as measured by HIV-1 p24 levels. Increased CCR5 was also detected in coinfected lymph nodes as compared with tissues with only HIV-1. The increased production of TNFalpha, together with elevated expression of CCR5, provide potential mechanisms for enhanced infection and replication of HIV-1 by macrophages in OI-infected cells and tissues. Consequently, treating OI may inhibit not only the OI-induced pathology, but also limit the viral burden.
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PMID:Mycobacterium avium complex augments macrophage HIV-1 production and increases CCR5 expression. 977 May 27

Infections caused by nontuberculous mycobacteria (NTM), although rare in immuno-competent individuals, can potentially produce problems in immunocompromised patients such as those with acquired immunodeficiency syndrome (AIDS). In this study, hemocultures for mycobacteria using radiometric BACTEC 13A media were taken from 334 patients with known human immunodeficiency virus infection admitted to four referral hospitals with fever of unknown site of infection and negative blood cultures for pathogenic bacteria. The mycobacterial hemocultures were positive for Mycobacterium avium complex (MAC) in 58 patients (17.4%) and positive for Mycobacterium tuberculosis in 34 patients (10.2%). The results of this study have proved that MAC infection, indeed, exists among Thai AIDS patients. The prevalence of MAC infection in Thailand is very high and comparable to that in the western countries. Physicians taking care of AIDS patients in Thailand should be aware of potential MAC infection, particularly in advanced cases. Considering the high prevalence of infection, primary prophylaxis against MAC infection in advanced AIDS patients is recommended.
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PMID:Prevalence of disseminated Mycobacterium avium complex infection in Thai AIDS patients. 1051 64

The bacterial growth and the production of tumor necrosis factor alpha (TNF-alpha) and TNF receptors (TNF-Rs) in the spleen and blood of BALB/c mice challenged with Mycobacterium avium complex (MAC) were monitored. Infection developed in two phases: the first, up to day 21, was associated with rapid MAC multiplication in the spleen and a drop in the mycobacteremia, and the second was associated with control of the infection in both compartments. In the spleen, TNF-alpha and TNF-RII mRNA levels peaked on day 21 and then slowly decreased; however, no increase in the level of TNF-RI mRNA was observed throughout these experiments. The level of circulating soluble TNF-RII (sTNF-RII) was transiently increased after day 21. In a model in which overproduction of bioactive TNF-alpha was triggered in response to a second infection with MAC, an increased production of sTNF-RII by cultured splenocytes was also observed. Administration of an antagonist anti-TNF-RII monoclonal antibody (MAb 6G1) to infected mice inhibited the bacterial growth in the spleen, suggesting that the TNF-RII and/or sTNF-RII was functionally involved in the mechanisms that control the infection. Overall, these observations suggest that upregulation of TNF-RII or sTNF-RII contributes to modulation of the TNF-alpha antibacterial activity in MAC infections.
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PMID:Upregulation of p75 tumor necrosis factor alpha receptor in Mycobacterium avium-infected mice: evidence for a functional role. 1053 Dec 26

Infections caused by non-tuberculous mycobacteria and multidrug-resistant Mycobacterium tuberculosis are difficult to treat. New compounds potentially active against these bacteria are therefore constantly being sought. Among them is grepafloxacin, a new C5 fluoroquinolone. A panel of 130 isolates of mycobacteria including 33 M. tuberculosis isolates and 97 isolates of different species of atypical mycobacteria were analysed for susceptibility to grepafloxacin, ofloxacin and ciprofloxacin. The MICs of these fluoroquinolones were determined using the agar-dilution method. Different mycobacterial species showed different degrees of susceptibility to grepafloxacin, ofloxacin and ciprofloxacin but little difference was observed between the MICs of the three antibiotics against strains of the same mycobacterial species. In addition, to evaluate the intracellular activity of these drugs, six strains of mycobacteria were studied using a human-macrophage infection model. Preliminary results of macrophage experiments showed that grepafloxacin was more active than ofloxacin and ciprofloxacin, particularly against Mycobacterium kansasii and, to a lesser degree, against Mycobacterium avium complex and Mycobacterium marinum. However, the three fluoroquinolones had comparable activities against M. tuberculosis.
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PMID:Comparative antimycobacterial activities of ofloxacin, ciprofloxacin and grepafloxacin. 1055 81

Mycobacterium avium complex (MAC) can induce upregulation of HIV. To investigate the underlying mechanisms, the effect of MAC-induced cytokines on HIV replication was first studied. Semiquantitative RT-PCR, followed by Northern blot analysis, revealed that mRNA encoding IL-6 and TNF-alpha was induced by MAC. However, production of these cytokines was undetectable and the addition of anti-cytokine antibodies to coinfected cells could only minimally block the MAC effect on HIV. Infection of U38 cells with MAC resulted in enhancement of HIV-1 LTR-CAT transcription. In addition, transient transfection of U937 cells with full-length wild-type as well as NF-kappaB-binding site-deleted mutant HIV-1 LTR-CAT constructs revealed that MAC-induced HIV-LTR CAT is NF-kappaB dependent. These findings, together with our previous work, indicate that MAC-induced cytokine expression increases the formation of NF-kappaB, which in turn enhances HIV-1 LTR-CAT transcription. However, additional factor(s) yet to be elucidated may play a more significant role in MAC-mediated HIV-upregulation.
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PMID:Mycobacterium avium induces HIV upregulation through mechanisms independent of cytokine induction. 1077 29

The purpose of the present study was to elucidate the role of oestrogen in the pathogenesis of Mycobacterium avium complex (MAC) pulmonary disease, which occurs most frequently in postmenopausal women. The study was carried out in a murine infectious model using ovariectomized DBA/2 female mice. Infection with MAC was established by intratracheal administration of bacilli. In some experiments, ovariectomized mice were treated with exogenous 17 beta-estradiol (E2). The number of bacilli in the lungs of infected mice which received ovariectomy was significantly larger than that in the lungs of sham-operated control mice, and treatment of ovariectomized mice with exogenous E2 restored the burden of bacilli to the same level as that in the sham-operated control mice. We next examined the effect of E2 in vitro using bone marrow-derived macrophages obtained from DBA/2 female mice. The macrophages showed bacteriostatic activity against MAC after treatment with interferon-gamma (IFN-gamma) and this activity was further enhanced by the exogenous addition of E2 to the culture medium. In parallel with these findings, E2 augmented the production of reactive nitrogen intermediates (RNI) by macrophages pretreated with IFN-gamma and stimulated with MAC, as shown by evaluating nitrite production and inducible nitric oxide synthase mRNA expression. These findings taken together suggest that absence of endogenous oestrogen appears to be responsible for the development of MAC pulmonary disease in this mouse model and that the enhancement by E2 of anti-MAC activity of murine macrophages induced through increased RNI production may play some role in resistance to MAC infection.
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PMID:Effect of oestrogen on Mycobacterium avium complex pulmonary infection in mice. 1129 30


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