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complicated in structure; consisting of interconnected parts; "a complex set of variations based on a simple folk melody"; "a complex mass of diverse laws and customs"
a compound described in terms of the central atom to which other atoms are bound or coordinated (同)coordination_compound
a conceptual whole made up of complicated and related parts; "the complex of shopping malls, houses, and roads created a new town" (同)composite
(psychoanalysis) a combination of emotions and impulses that have been rejected from awareness but still influence a persons behavior
located or occurring within a cell or cells; "intracellular fluid"

PrepTutorEJDIC

『いくつかの部分から成る』,複合の,合成の / 『複雑な』,入りくんだ,こみいった(complicated) / 複合体,合成物 / コンプレックス,複合(抑圧されて心に残った複雑なしこり)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/01/30 12:54:51」(JST)

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Mycobacterium avium complex (MAC) is a group of genetically related bacteria belonging to the genus Mycobacterium. It includes Mycobacterium avium and Mycobacterium intracellulare.^[1]^[2]

Some sources also include Mycobacterium avium subspecies paratuberculosis (MAP).^[3]

Mycobacterium avium complex (MAC) include ubiquitous atypical bacteria found in the environment which can infect patients with HIV and low CD4 cell count (below 100/microliter); mode of infection is usually inhalation or ingestion.

MAC causes disseminated disease in up to 40% of patients with human immunodeficiency virus (HIV) in the United States, producing fever, sweats, weight loss, and anemia.^[4]^[5]^[6] Disseminated MAC characteristically affects patients with advanced HIV disease and peripheral CD4+ T-lymphocyte counts less than 100 cells/uL. Effective prevention and therapy of MAC has the potential to contribute substantially to improved quality of life and duration of survival for HIV-infected persons.^[7]

Diagnosis

Disseminated MAC is most readily diagnosed by one positive blood culture. Blood cultures should be performed in patients with symptoms, signs, or laboratory abnormalities compatible with mycobacterium infection. Blood cultures are not routinely recommended for asymptomatic persons, even for those who have CD4+ T-lymphocyte counts less than 100 cells/uL.^[7]

Prevention

Patients with HIV infection and less than 50 CD4+ T-lymphocytes/uL should be administered prophylaxis against MAC. Prophylaxis should be continued for the patient's lifetime unless multiple drug therapy for MAC becomes necessary because of the development of MAC disease.^[7]

Clinicians must weigh the potential benefits of MAC prophylaxis against the potential for toxicities and drug interactions, the cost, the potential to produce resistance in a community with a high rate of tuberculosis, and the possibility that the addition of another drug to the medical regimen may adversely affect patients' compliance with treatment. Because of these concerns, therefore, in some situations rifabutin prophylaxis should not be administered.^[7]

Before prophylaxis is administered, patients should be assessed to ensure that they do not have active disease due to MAC, M. tuberculosis, or any other mycobacterial species. This assessment may include a chest radiograph and tuberculin skin test.^[7]

Rifabutin, 300 mg by mouth daily, is recommended for the patient's lifetime unless disseminated MAC develops, which would then require multiple drug therapy. Although other drugs, such as azithromycin and clarithromycin, have laboratory and clinical activity against MAC, none has been shown in a prospective, controlled trial to be effective and safe for prophylaxis. Thus, in the absence of data, no other regimen can be recommended at this time.The 300-mg dose of rifabutin has been well tolerated. Adverse effects included neutropenia, thrombocytopenia, rash, and gastrointestinal disturbances.^[7]

Treatment

Although studies have not yet identified an optimal regimen or confirmed that any therapeutic regimen produces sustained clinical benefit for patients with disseminated MAC, the Task Force concluded that the available information indicated the need for treatment of disseminated MAC. The Public Health Service therefore recommends that regimens be based on the following principles:^[7]

Treatment regimens outside a clinical trial should include at least two agents.
Every regimen should contain either azithromycin or clarithromycin; many experts prefer ethambutol as a second drug. Many clinicians have added one or more of the following as second, third, or fourth agents: clofazimine, rifabutin, rifampin, ciprofloxacin, and in some situations amikacin. Isoniazid and pyrazinamide are not effective for the therapy of MAC.
Therapy should continue for the lifetime of the patient if clinical and microbiologic improvement is observed.

Clinical manifestations of disseminated MAC—such as fever, weight loss, and night sweats—should be monitored several times during the initial weeks of therapy. Microbiologic response, as assessed by blood culture every 4 weeks during initial therapy, can also be helpful in interpreting the efficacy of a therapeutic regimen.Most patients who ultimately respond show substantial clinical improvement in the first 4–6 weeks of therapy. Elimination of the organisms from blood cultures may take somewhat longer, often requiring 4–12 weeks.^[7]

HIV-infected children

HIV-infected children less than 12 years of age also develop disseminated MAC. Some age adjustment is necessary when clinicians interpret CD4+ T-lymphocyte counts in children less than 2 years of age. Diagnosis, therapy, and prophylaxis should follow recommendations similar to those for adolescents and adults.^[7]

References

This article incorporates public domain material from the Centers for Disease Control and Prevention document "Recommendations on Prophylaxis and Therapy for Disseminated Mycobacterium avium Complex for Adults and Adolescents Infected with Human Immunodeficiency Virus".

^ White, Lois (2004). Foundations of Nursing. Cengage Learning. p. 1298. ISBN 978-1-4018-2692-5.
^ "Disease Listing, Mycobacterium avium Complex". CDC Bacterial, Mycotic Diseases. Retrieved 2010-11-04.
^ Irving, Peter; Rampton, David; Shanahan, Fergus (2006). Clinical dilemmas in inflammatory bowel disease. Wiley-Blackwell. p. 36. ISBN 978-1-4051-3377-7.
^ Horsburgh CR (May 1991). "Mycobacterium avium complex infection in the acquired immunodeficiency syndrome". N. Engl. J. Med. 324 (19): 1332–8. doi:10.1056/NEJM199105093241906. PMID 2017230.
^ Chaisson RE, Moore RD, Richman DD, Keruly J, Creagh T (August 1992). "Incidence and natural history of Mycobacterium avium-complex infections in patients with advanced human immunodeficiency virus disease treated with zidovudine. The Zidovudine Epidemiology Study Group". Am. Rev. Respir. Dis. 146 (2): 285–9. doi:10.1164/ajrccm/146.2.285. PMID 1362634.
^ Havlik JA, Horsburgh CR, Metchock B, Williams PP, Fann SA, Thompson SE (March 1992). "Disseminated Mycobacterium avium complex infection: clinical identification and epidemiologic trends". J. Infect. Dis. 165 (3): 577–80. doi:10.1093/infdis/165.3.577. PMID 1347060.
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ U.S. Public Health Service Task Force on Prophylaxis and Therapy for Mycobacterium avium Complex (June 1993). "Recommendations on prophylaxis and therapy for disseminated Mycobacterium avium complex for adults and adolescents infected with human immunodeficiency virus". MMWR Recomm Rep 42 (RR-9): 14–20. PMID 8393134.

"Mycobacterium avium complex". NCBI Taxonomy Browser. 37162.

UpToDate Contents

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1. HIV陰性患者における非結核性抗酸菌感染症の概要 overview of nontuberculous mycobacterial infections in hiv negative patients
2. HIV感染患者におけるMycobacterium avium complex (MAC）感染症 mycobacterium avium complex mac infections in hiv infected patients
3. HIV陰性患者における肺非結核性抗酸菌感染症の治療 treatment of nontuberculous mycobacterial infections of the lung in hiv negative patients
4. 非結核性抗酸菌の微生物学 microbiology of nontuberculous mycobacteria
5. 非結核性抗酸菌感染症の疫学 epidemiology of nontuberculous mycobacterial infections

English Journal

Changes in serum immunomolecules during antibiotic therapy for Mycobacterium avium complex lung disease.

Kim SY1, Koh WJ, Park HY, Jeon K, Kwon OJ, Cho SN, Shin SJ.Author information 1Division of Pulmonary and Critical Care Medicine, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea.AbstractLittle information is available regarding changes in immune status for patients with Mycobacterium avium complex (MAC) lung disease during antibiotic therapy. Serum immunomolecules from 42 patients with MAC lung disease were assayed comparatively using an array-based system according to (i) patients with MAC lung disease at the time of diagnosis versus healthy controls and (ii) alterations after 12 months of antibiotic therapy in the MAC lung disease group. In addition, cytokine analyses were performed to determine whether cytokine responses were associated specifically with the disease phenotype, treatment outcome and aetiological agent. Notably, the serum concentrations of type 1 cytokine-associated molecules, such as CD40L, interferon (IFN)-γ, interleukin (IL)-8 and IL-23, were decreased significantly in patients at the time of diagnosis, suggesting that these molecules may serve as indicators of host susceptibility to MAC disease. Although the overall serum level of T helper type 1 (Th1)-related molecules, such as CD40L and IFN-γ, was restored after treatment, Th17-related cytokines, such as IL-17 and IL-23, were down-regulated significantly at 12 months post-treatment compared to pretreatment. Furthermore, these cytokine patterns differed among patient subgroups. Decreased serum concentrations of IL-17 and/or IL-23 were associated with failure of sputum conversion, the fibrocavitary disease phenotype and M. intracellulare lung disease. Thus, the reciprocal balance between Th1 and Th17 immunity during antibiotic therapy for MAC lung disease is critical for dictating the treatment response. In conclusion, a low level of Th1-related immunomolecules may perpetuate MAC lung disease, and the serum concentrations of Th17-related cytokines can reflect the treatment outcome, disease phenotype and aetiological agent.
Clinical and experimental immunology.Clin Exp Immunol.2014 Apr;176(1):93-101. doi: 10.1111/cei.12253.
Little information is available regarding changes in immune status for patients with Mycobacterium avium complex (MAC) lung disease during antibiotic therapy. Serum immunomolecules from 42 patients with MAC lung disease were assayed comparatively using an array-based system according to (i) patients
PMID 24354934

Mycobacterium avium Complex in Day Care Hot Water Systems, and Persistence of Live Cells and DNA in Hot Water Pipes.

Bukh AS1, Roslev P.Author information 1Section of Biology and Environmental Science, Department of Biotechnology, Chemistry and Environmental Engineering, Aalborg University, Sohngaardsholmsvej 57, 9000, Alborg, Denmark.AbstractThe Mycobacterium avium complex (MAC) is a group of opportunistic human pathogens that may thrive in engineered water systems. MAC has been shown to occur in drinking water supplies based on surface water, but less is known about the occurrence and persistence of live cells and DNA in public hot water systems based on groundwater. In this study, we examined the occurrence of MAC in hot water systems of public day care centers and determined the persistence of live and dead M. avium cells and naked DNA in model systems with the modern plumbing material cross-linked polyethylene (PEX). The occurrence of MAC and co-occurrence of Legionella spp. and Legionella pneumophila were determined using cultivation and qPCR. Co-occurrences of MAC and Legionella were detected in water and/or biofilms in all hot water systems at temperatures between 40 and 54 °C. Moderate correlations were observed between abundance of culturable MAC and that of MAC genome copies, and between MAC and total eubacterial genome copies. No quantitative relationship was observed between occurrence of Legionella and that of MAC. Persistence in hot water of live and dead M. avium cells and naked DNA was studied using PEX laboratory model systems at 44 °C. Naked DNA and DNA in dead M. avium cells persisted for weeks. Live M. avium increased tenfold in water and biofilms on PEX. The results suggest that water and biofilms in groundwater-based hot water systems can constitute reservoirs of MAC, and that amplifiable naked DNA is relatively short-lived, whereas PEX plumbing material supports persistence and proliferation of M. avium.
Current microbiology.Curr Microbiol.2014 Apr;68(4):428-39. doi: 10.1007/s00284-013-0493-4. Epub 2013 Nov 23.
The Mycobacterium avium complex (MAC) is a group of opportunistic human pathogens that may thrive in engineered water systems. MAC has been shown to occur in drinking water supplies based on surface water, but less is known about the occurrence and persistence of live cells and DNA in public hot wat
PMID 24272032

In Vitro Activity of Amikacin against Isolates of Mycobacterium avium Complex with Proposed MIC Breakpoints and Finding of a 16S rRNA Gene Mutation in Treated Isolates.

Brown-Elliott BA1, Iakhiaeva E, Griffith DE, Woods GL, Stout JE, Wolfe CR, Turenne CY, Wallace RJ Jr.
Journal of clinical microbiology.J Clin Microbiol.2014 Apr;52(4):1311. doi: 10.1128/JCM.00224-14.
PMID 24619984

Japanese Journal

肺野末梢に孤立性結節影を呈した Mycobacterium avium intracellulare complex (MAC) 肺感染症に腺癌を合併した1例

太田英樹,河合秀樹
日本呼吸器外科学会雑誌 = The journal of the Japanese Association for Chest Surgery 26(4), 481-485, 2012-05-15
NAID 10030435876

非結核性抗酸菌症に対する手術療法の意義

本野望,保坂靖子,富樫賢一
日本呼吸器外科学会雑誌 = The journal of the Japanese Association for Chest Surgery 26(1), 17-20, 2012-01-15
NAID 10030025912

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★リンクテーブル★

リンク元	「マイコバクテリウム・アビウムコンプレックス」「Mycobacterium avium-intracellulare」「マイコバクテリウム・アビウム・イントラセルラーレ複合体」
関連記事	「complex」「complexed」「intracellular」「complexes」「avium」