M. avium

• マイコバクテリウム・アビウム

関

Mycobacterium avium

WordNet

1. the 13th letter of the Roman alphabet (同)m
2. the imperial dynasty of China from 1368 to 1644 (同)Ming dynasty
3. a form of address for a woman (同)Ms.

PrepTutorEJDIC

1. Mach number / mark[s] / Monsieur
2. (中国の)明,明朝(1368‐1644)
3. mendeleviumの化学記号

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/08/21 22:57:53」(JST)

wiki en

[Wiki en表示]

Mycobacterium avium complex (MAC) is a group of genetically related bacterium belonging to the genus Mycobacterium. It includes Mycobacterium avium and Mycobacterium intracellulare.

Some sources also include Mycobacterium avium subspecies paratuberculosis (MAP).

Mycobacterium avium complex (MAC) include ubiquitous atypical bacterium 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. 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.

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.

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.

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.

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.

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.

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:

• 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.

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.

See also

• Mycobacterium avium-intracellulare infection

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".

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

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

• 1. 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
• 2. 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
• 3. 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
• 4. 小児における非結核性抗酸菌性肺感染症の概要 overview of nontuberculous mycobacterial pulmonary infections in children
• 5. 非結核性抗酸菌感染症の疫学 epidemiology of nontuberculous mycobacterial infections

English Journal

• Mycobacterium avium Biofilm Attenuates Mononuclear Phagocyte Function by Triggering Hyperstimulation and Apoptosis during Early Infection.

• Rose SJ, Bermudez LE.Author information Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, Oregon, USA.AbstractMycobacterium avium subsp. hominissuis is an opportunistic human pathogen that has been shown to form biofilm in vitro and in vivo. Biofilm formation in vivo appears to be associated with infections in the respiratory tract of the host. The reasoning behind how M. avium subsp. hominissuis biofilm is allowed to establish and persist without being cleared by the innate immune system is currently unknown. To identify the mechanism responsible for this, we developed an in vitro model using THP-1 human mononuclear phagocytes cocultured with established M. avium subsp. hominissuis biofilm and surveyed various aspects of the interaction, including phagocyte stimulation and response, bacterial killing, and apoptosis. M. avium subsp. hominissuis biofilm triggered robust tumor necrosis factor alpha (TNF-α) release from THP-1 cells as well as superoxide and nitric oxide production. Surprisingly, the hyperstimulated phagocytes did not effectively eliminate the cells of the biofilm, even when prestimulated with gamma interferon (IFN-γ) or TNF-α or cocultured with natural killer cells (which have been shown to induce anti-M. avium subsp. hominissuis activity when added to THP-1 cells infected with planktonic M. avium subsp. hominissuis). Time-lapse microscopy and the TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) assay determined that contact with the M. avium subsp. hominissuis biofilm led to early, widespread onset of apoptosis, which is not seen until much later in planktonic M. avium subsp. hominissuis infection. Blocking TNF-α or TNF-R1 during interaction with the biofilm significantly reduced THP-1 apoptosis but did not lead to elimination of M. avium subsp. hominissuis. Our data collectively indicate that M. avium subsp. hominissuis biofilm induces TNF-α-driven hyperstimulation and apoptosis of surveilling phagocytes, which prevents clearance of the biofilm by cells of the innate immune system and allows the biofilm-associated infection to persist.
• Infection and immunity.Infect Immun.2014 Jan;82(1):405-12. doi: 10.1128/IAI.00820-13. Epub 2013 Nov 4.
• Mycobacterium avium subsp. hominissuis is an opportunistic human pathogen that has been shown to form biofilm in vitro and in vivo. Biofilm formation in vivo appears to be associated with infections in the respiratory tract of the host. The reasoning behind how M. avium subsp. hominissuis biofilm is
• PMID 24191301

• Comparison of Mycobacterium lentiflavum and Mycobacterium avium-intracellulare Complex Lymphadenitis.

• Jiménez-Montero B, Baquero-Artigao F, Saavedra-Lozano J, Tagarro-García A, Blázquez-Gamero D, Cilleruelo-Ortega MJ, Ramos-Amador JT, Galé-Ansó I, Marín N, Gómez-García R, Santiago-García B, Garrido J, López G.Author information From the *Department of Pediatrics, Hospital Infanta Sofía, San Sebastián de los Reyes; †Division of Pediatric Infectious Diseases, Hospital Universitario La Paz; ‡Division of Pediatric Infectious Diseases, Gregorio Marañón Hospital; §Division of Pediatric Infectious Diseases, Hospital Universitario 12 de Octubre; ¶Department of Pediatrics, Hospital Puerta de Hierro- Majadahonda; ‖Department of Pediatrics, Hospital de Getafe; and **Department of Microbiology, Hospital Universitario La Paz, Madrid.AbstractBACKGROUND: Mycobacterium lentiflavum is considered a rare pathogen causing nontuberculous mycobacterial (NTM) lymphadenitis.
• The Pediatric infectious disease journal.Pediatr Infect Dis J.2014 Jan;33(1):28-34. doi: 10.1097/INF.0000000000000007.
• BACKGROUND: Mycobacterium lentiflavum is considered a rare pathogen causing nontuberculous mycobacterial (NTM) lymphadenitis.METHODS: A multicenter, retrospective study was performed in immunocompetent children <14 years of age with microbiologically confirmed NTM lymphadenitis treated at 6 hospi
• PMID 24064561

• Stability of genotyping target sequences of Mycobacterium avium subsp. paratuberculosis upon cultivation on different media, in vitro- and in vivo passage, and natural infection.

• Kasnitz N, Köhler H, Weigoldt M, Gerlach GF, Möbius P.Author information Institute of Molecular Pathogenesis, Friedrich-Loeffler-Institut (Federal Research Institute for Animal Health), Naumburger Str. 96a, 07743 Jena, Germany.AbstractMycobacterium (M.) avium subsp. paratuberculosis - the causative agent of paratuberculosis (Johne's disease) - affects domestic and wild ruminants worldwide. Recently, different typing techniques have been combined to provide sufficient discriminatory power for the differentiation of isolates and for epidemiological studies. In order to challenge the reliability of this approach the stability of different M. avium subsp. paratuberculosis genotypes determined after primary isolation was investigated after sub-cultivation on six different media (A), twelve in vitro passages (B), or a singular in vivo passage (C). In addition, different isolates from a single animal or herd were investigated (D). Sub-cultures of type- and reference strains, re-isolated inoculation strain after in vivo passage, and 23 field isolates were genotyped by mycobacterial interspersed repetitive unit-variable-number of tandem-repeat (MIRU-VNTR)-, short-sequence-repeat (SSR)-, and IS900-based restriction-fragment length-polymorphism (IS900-RFLP)-analyses and compared with initial genotypes. MIRU-VNTR-alleles (at loci 292, X3, 25, 47, 7, and 32) were stable after in vitro cultivations and after animal passage. Results of SSR analysis at Locus 1 with 7G nucleotides and at Loci 8 and 9 (tri-nucleotides) were also stable. At Locus 2 9G repeats changed into 10G after goat passage. After in vitro subculture (A+B) but not after animal passage (C) IS900-RFLP-typing revealed changes of BstEII-patterns for 3 of 23 strains (including ATCC 19698). Multiple isolates from individual animals or from a single cattle herd with natural infection (D) which exhibited identical IS900-RFLP- and MIRU-VNTR- genotypes, showed different G repeat numbers at SSR locus 2. This implies strand slippage events during chromosomal duplication of bacteria in the course of bacterial spreading within hosts and herds. Consequently, SSR-Locus 2 is not suitable as genome marker for epidemiological studies.
• Veterinary microbiology.Vet Microbiol.2013 Dec 27;167(3-4):573-83. doi: 10.1016/j.vetmic.2013.09.008. Epub 2013 Sep 13.
• Mycobacterium (M.) avium subsp. paratuberculosis - the causative agent of paratuberculosis (Johne's disease) - affects domestic and wild ruminants worldwide. Recently, different typing techniques have been combined to provide sufficient discriminatory power for the differentiation of isolates and fo
• PMID 24095568

Japanese Journal

• 画像診断 気管支中心性肉芽腫像を呈した肺Mycobacterium avium症の1例

• 日本呼吸器学会誌 = Annals of the Japanese Respiratory Society 5(2), 106-109, 2016-03-10
• NAID 40020765226

• 肺MAC症に対する手術前後および再燃再発時におけるMAC抗体の変動 : MAC抗体は術後の再燃再発の指標になりうるか?

• 結核 91(2), 41-44, 2016-02
• NAID 40020740438

• キャピリアMAC抗体検査の精度評価と患者背景の臨床的検討

• 結核 91(2), 27-32, 2016-02
• NAID 40020738581

Related Links

• 新結核用語事典・M. avium complex感染症

［infections caused by M. avium complex］ 分類学上極めて近縁のM. aviumとM. intracellulareの２菌種が原因菌となる感染症を指す。わが国の非定型抗酸菌症の70％ 前後を占める。日和見感染症の傾向が大きく，M. kansasii感染症に比べて，肺結核遺 残 ...

• Mycobacterium avium complex - Wikipedia, the free encyclopedia

Mycobacterium avium complex (MAC) is a group of genetically related bacteria belonging to the genus Mycobacterium. It includes ... intracellulare. Some sources also include Mycobacterium avium subspecies paratuberculosis (MAP).

---

★リンクテーブル★

リンク元	「マイコバクテリウム・アビウム」
関連記事	「avium」「Md」「M」

「マイコバクテリウム・アビウム」

　　[★]

ラ

Mycobacterium avium、M. avium

「avium」

　　[★]

• Mycobacterium avium、Bordetella avium

「Md」

　　[★] メンデレビウム mendelevium 　

「M」

　　[★] メチオニン methionine