Mycobacterium avium Complex Infection in Patients with the Acquired Immunodeficiency Syndrome

Wallace, Jeanne M.; Hannah, James

doi:10.1378/chest.93.5.926

Cited by 156 publications

(61 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In contrast, M. avium appears to have a particular predilection for infecting and disseminating within HIV-infected patients. (186,287,342,436,466) and the respiratory tract as a secondary and significantly less frequent portal of entry (4,231,257,388). Disseminated disease in AIDS patients is frequently preceded by gastrointestinal tract colonization (22,87,231,388) as evidenced by the relatively high frequency of positive stool cultures (22,120,202,231,342,436) and the high frequency of gastrointestinal involvement, with large numbers of mycobacteria infiltrating the intestinal mucosa and submucosa (120,186,287,406).…”

Section: Pathogenesismentioning

confidence: 99%

The Mycobacterium avium complex

1993

View full text Add to dashboard Cite

Mycobacterium avium complex (MAC) disease emerged early in the epidemic of AIDS as one of the common opportunistic infections afflicting human immunodeficiency virus-infected patients. However, only over the past few years has a consensus developed about its significance to the morbidity and mortality of AIDS. M. avium was well known to mycobacteriologists decades before AIDS, and the MAC was known to cause disease, albeit uncommon, in humans and animals. The early interest in the MAC provided a basis for an explosion of studies over the past 10 years largely in response to the role of the MAC in AIDS opportunistic infection. Molecular techniques have been applied to the epidemiology of MAC disease as well as to a better understanding of the genetics of antimicrobial resistance. The interaction of the MAC with the immune system is complex, and putative MAC virulence factors appear to have a direct effect on the components of cellular immunity, including the regulation of cytokine expression and function. There now is compelling evidence that disseminated MAC disease in humans contributes to both a decrease in the quality of life and survival. Disseminated disease most commonly develops late in the course of AIDS as the CD4 cells are depleted below a critical threshold, but new therapies for prophylaxis and treatment offer considerable promise. These new therapeutic modalities are likely to be useful in the treatment of other forms of MAC disease in patients without AIDS. The laboratory diagnosis of MAC disease has focused on the detection of mycobacteria in the blood and tissues, and although the existing methods are largely adequate, there is need for improvement. Indeed, the successful treatment of MAC disease clearly will require an early and rapid detection of the MAC in clinical specimens long before the establishment of the characteristic overwhelming infection of bone marrow, liver, spleen, and other tissue. Also, a standard method of susceptibility testing is of increasing interest and importance as new effective antimicrobial agents are identified and evaluated. Antimicrobial resistance has already emerged as an important problem, and methods for circumventing resistance that use combination therapies are now being studied.

show abstract

Section: Pathogenesismentioning

confidence: 99%

The Mycobacterium avium complex

1993

View full text Add to dashboard Cite

show abstract

“…Disseminated M. avium disease usually occurs late in the course of AIDS and is associated with severe immunosuppression. Although only 3-4% ofAIDS patients have disseminated M. avium infection as their initial opportunistic infection, 46-56% of AIDS patients have evidence of disseminated M. avium infection at the time of death (3,4). High tissue burdens ofM.…”

Section: Introductionmentioning

confidence: 99%

“…10-,ul aliquots of each dilution were plated in triplicate on Middlebrook 7H 10 agar supplemented with oleic acid-albumin-dextrose-catalase (Difco Laboratories, Detroit, MI). The agar plates then were incubated at 37°C for [4][5][6][7] Expression ofcytokine mRNA. Adherent monocytes were precultured in a 60-mm petri dish ( 1007; Falcon Labware, Oxnard, CA) with or without gpl20 (1 ,g/ml) for 2 d and then infected with M. avium.…”

Section: Introductionmentioning

confidence: 99%

Modulation of the effector function of human monocytes for Mycobacterium avium by human immunodeficiency virus-1 envelope glycoprotein gp120.

et al. 1994

View full text Add to dashboard Cite

Disseminated Mycobacterium avium infection in AIDS is associated with high tissue burdens (109-10i1 mycobacteria/g tissue) of organism. The basis for the extraordinary susceptibility of AIDS to M. avium infection is unclear. HIV or its constituents may alter mononuclear phagocyte functions resulting in enhanced intracellular M. avium growth. The effects of an envelope glycoprotein (gpl20), a transmembrane protein (pl21), and core proteins of HIV-1 on M. avium infection of human monocytes were examined. Preculturing monocytes with gp120 inhibited M. avium phagocytosis and consistently enhanced intracellular growth of six M. avium strains. Pretreatment with p121, gagS, or p24 did not inhibit phagocytosis nor enhance intracellular growth of M. avium. Incubation of gpl20 with soluble CD4 before addition to monocyte cultures or pretreatment of monocytes with OKT4A abrogated gp120 effects on M. avium phagocytosis and intracellular growth. gp120 also augmented cytokine production by infected monocytes. These results suggest that gpl20, but not p121 or core proteins, modulate monocyte phagocytosis and enhance intracellular growth of M. avium at least in part through monocyte CD4 receptors. Direct effects of HIV-1 products may, therefore, contribute to the diathesis of AIDS to develop disseminated M. avium infection and to the extensive replication of the organisms within tissue macrophages. (J. Clin. Invest. 1994. 93:885-891.)

show abstract

“…Patients with M. avium infection usually have disseminated disease with bacteremia and frequently liver, spleen, bone marrow, and lymph node involvement. In addition, a variable percentage of these patients can have invasive infection in the brain (6,11,12,15,17,27).Murine models of disseminated M. avium infection have been developed since 1983 (2, 3, 10) and used extensively in the investigation of host response and in the screening of active therapeutic agents (1). In these models, bacterial burden and histopathology changes in the abdominal organs and lymph nodes had been thoroughly studied, but the neuraxes have not been evaluated.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

Invasion of the Brain and Chronic Central Nervous System Infection after SystemicMycobacterium aviumComplex Infection in Mice

Wu¹,

Kolonoski²,

Chang³

et al. 2000

Infect Immun

View full text Add to dashboard Cite

Central nervous system (CNS) infections caused by nontuberculous mycobacteria have been described previously, especially in patients with AIDS. To investigate specific aspects of the pathogenesis of this entity, C57BL bg ؉ /bg ؊ mice were infected intravenously with Mycobacterium avium, and cultures of blood and brain as well as histopathology examination of brain tissue were carried out at several time points up to 6 months after infection. Low-grade inflammatory changes with small aggregates of lymphocytes and macrophages as well as perivascular cuffing were seen early in the infection. A small number of bacteria could be observed in the parenchyma of the choroid plexus. Six months after infection, numerous bacteria were present within the foamy macrophage of the granulomatous lesions along the ventricle and meninges. None of the mice developed clinical signs of meningitis or encephalitis or even died spontaneously during the period of observation. Use of CD18؊/؊ knockout mice indicated that transport of the bacterium within neutrophils or monocytes into the brain is unlikely. Mild chronic CNS infection developed in the mice during sustained systemic M. avium infection, similar to what has been reported in most human cases.Central nervous system (CNS) infections due to nontuberculous mycobacteria (NTBM) usually manifest as meningitis or meningoencephalitis, but occasionally pure encephalitis or abscesses along neuraxes are found (5, 9). NTBM brain diseases are most often described in patients with AIDS or other immune-compromised patients, but it had also been reported in individuals without obvious underlying disease (5,26,28). CNS infections with NTBM can sometimes be misdiagnosed as Mycobacterium tuberculosis infection, resulting in incorrect treatment and death (11,28). As the epidemic of human immunodeficiency virus infection and the application of immunosuppressive treatment expand, it has become more likely that doctors might come in contact with these usually infrequent infections. A suitable animal model may therefore help us to understand the immunopathophysiology of this disease, as well as to develop an effective therapy.The Mycobacterium avium complex is the most common organism causing systemic opportunistic bacterial infections in patients with AIDS (13,14,29). It is also the leading cause of the NTBM brain disease in this population (5). Patients with M. avium infection usually have disseminated disease with bacteremia and frequently liver, spleen, bone marrow, and lymph node involvement. In addition, a variable percentage of these patients can have invasive infection in the brain (6,11,12,15,17,27).Murine models of disseminated M. avium infection have been developed since 1983 (2, 3, 10) and used extensively in the investigation of host response and in the screening of active therapeutic agents (1). In these models, bacterial burden and histopathology changes in the abdominal organs and lymph nodes had been thoroughly studied, but the neuraxes have not been evaluated.The CNS is confined to an ...

show abstract

Mycobacterium avium Complex Infection in Patients with the Acquired Immunodeficiency Syndrome

Cited by 156 publications

References 13 publications

The Mycobacterium avium complex

The Mycobacterium avium complex

Modulation of the effector function of human monocytes for Mycobacterium avium by human immunodeficiency virus-1 envelope glycoprotein gp120.

Invasion of the Brain and Chronic Central Nervous System Infection after SystemicMycobacterium aviumComplex Infection in Mice

Contact Info

Product

Resources

About