痤疮丙酸杆菌与痤疮

痤疮丙酸杆菌的结构、分布和生理特点决定其在痤疮发病中的重要作用,尤其与痤疮的炎症损害及严重程度密切有关.目前,针对痤疮丙酸杆菌的痤疮治疗方法众多,包括应用四环素类、克林霉素、红霉素等治疗和过氧苯甲酰或5-氨基酮戊酸光动力疗法等.由于耐药性痤疮丙酸杆菌的出现,抗生素与非抗生素类药物的联合疗法已被证明为最佳治疗手段.痤疮丙酸杆菌全部基因组序列的测定使针对痤疮的菌苗疗法成为可能.     

痤疮丙酸杆菌致病机制研究进展

痤疮的发病机制较为复杂.研究表明,痤疮丙酸杆菌与痤疮的发生有重要的关系,在多个致病因素中起核心作用,然而痤疮丙酸杆菌在痤疮中的作用尚不完全清楚.随着医学研究的不断发展,痤疮丙酸杆菌基因功能的破解、痤疮丙酸杆菌生物膜致病耐药机制的不断完善、痤疮丙酸杆菌表面唾液酸酶为靶位的疫苗研发等为了解痤疮丙酸杆菌的致病机制和治疗提供线索.     

痤疮患者中痤疮丙酸杆菌对抗生素的耐药性

寻常性痤疮是一多因素疾病,其中厌氧类白喉痤疮丙酸杆菌在本病炎症的发生中起重要作用.对于痤疮丙酸杆菌用抗生素治疗已成为主要的有效疗法之一,临床医师及患者常提出痤疮丙酸杆菌对抗生素是否会产生耐药性.过去的研究,在全身性抗生素疗法无效的病人身上,未能发现痤疮丙酸杆菌对抗生素耐药的证据.根据这些以及其他一再发现痤疮丙酸杆菌对抗生素具有易感性的研究,从而得出     

痤疮患者痤疮丙酸杆菌耐药性的研究进展

痤疮丙酸杆菌在痤疮发生中起重要作用。局部或系统使用抗生素治疗痤疮的炎症性损害，取得了很好的疗效。然而，近年来有关痤疮丙酸杆菌耐药导致痤疮治疗失败的报道逐年增多。概述了痤疮丙酸杆菌在痤疮发生中的作用、耐药现状及其发生机制，以及如何能够尽可能减少或避免耐药菌的产生，从而提高药物疗效。     

痤疮患者痤疮丙酸杆菌耐药性的研究进展

痤疮丙酸杆菌在痤疮发生中起重要作用。局部或系统使用抗生素治疗痤疮的炎症性损害 ,取得了很好的疗效。然而 ,近年来有关痤疮丙酸杆菌耐药导致痤疮治疗失败的报道逐年增多。概述了痤疮丙酸杆菌在痤疮发生中的作用、耐药现状及其发生机制 ,以及如何能够尽可能减少或避免耐药菌的产生 ,从而提高药物疗效。     

痤疮的抗生素治疗及耐药现状

痤疮丙酸杆菌在痤疮发生、发展过程中起着重要作用,外用或口服抗生素对痤疮炎性皮损有肯定疗效。然而随着抗生素的广泛使用,耐药问题日益严峻,研究表明超过50%的痤疮丙酸杆菌出现了耐药,尤其是对大环内酯类抗生素。本文对抗生素治疗痤疮的作用机理与使用现状、耐药机制与耐药现状进行综述。     

420nm强脉冲光治疗寻常痤疮的疗效观察

痤疮是一种多因素导致的发生于毛囊皮脂腺的慢性炎症性皮肤病,不但影响容貌,而且还可以使患者产生焦虑、抑郁等心理问题[1],对患者的工作、学习造成了较大的影响.传统药物治疗存在着一定的不足, 比如耐药痤疮丙酸杆菌菌株的出现、长期口服异维A 酸和抗生素的不良反应等.     

痤疮与皮肤微生物

痤疮的四大发病机制是皮脂腺过量分泌脂质、毛囊皮脂腺导管角化异常、痤疮丙酸杆菌等皮肤微生物增殖、发炎与免疫反应.本文结合国内外研究进展,对痤疮的发病机制中皮肤常驻微生物,包括痤疮丙酸杆菌、表皮葡萄球菌、马拉色菌的作用进行综述,同时综述耐药性痤疮丙酸杆菌的耐药机制,及在耐药率不断升高下,替代治疗以及物理疗法的发展.     

女性青春期后痤疮研究进展

女性青春期后痤疮可分为迟发性痤疮及持续性痤疮,发病率有升高趋势.临床表现多为轻至中度痤疮,主要为炎性损害,多分布于下颏、口周等部位.女性青春期后痤疮可能的发病机制为皮肤雄激素增多,痤疮丙酸杆菌耐药菌株的存在及大然免疫的慢性刺激.各种原因引起的性激素水平改变、血清胰岛素样生长因子-1升高、精神压力、吸烟等为其诱发或加重因素,部分患者可有潜在内分泌疾病需注意排查.治疗方面可考虑加用抗生素类,低剂量异维A酸间歇治疗.对治疗较抵抗的患者抗雄激素治疗是重要手段之一,主要药物有螺内酯、氟他胺、醋酸环丙孕酮及口服避孕药.     

光动力疗法治疗痤疮

<正>0197浅谈5-氨基酮戊酸光动力疗法治疗痤疮的影响因素王艳青(山西医科大学第二医院皮肤科),冯文莉,吴媛…//山西医药杂志.-2014,43(19).-2296~2297痤疮是一种累及颜面、前胸和后背的毛囊皮脂腺的慢性炎症性疾病,皮脂腺功能亢进和痤疮丙酸杆菌的增多是其发病的重要原因。痤疮丙酸杆菌是痤疮重要的病原菌,也是5-氨基酮戊酸光     

Acne and Propionibacterium acnes

The involvement of microorganisms in the development of acne has a long and checkered history. Just over 100 years ago, Propionibacterium acnes (then known as Bacillus acnes) was isolated from acne lesions, and it was suggested that P. acnes was involved in the pathology of the disease. The 1960s saw the use of antibiotics to treat acne, and the consequent clinical success combined with reductions in P. acnes gave new impetus to the debate. Over the past two decades, the inevitable emergence of antibiotic-resistant strains of P. acnes as a consequence of acne therapy not only has reopened the debate as to the role of P. acnes in acne, but also has created some serious health care implications.     

Nadifloxacin, an antiacne quinolone antimicrobial, inhibits the production of proinflammatory cytokines by human peripheral blood mononuclear cells and normal human keratinocytes

BACKGROUND: Acne vulgaris is a chronic inflammatory disease involving colonization of Propionibacterium acnes (P. acnes), activation of neutrophils and lymphocytes. Circumstantial evidence suggests that antigen-independent and -dependent immune responses against P. acnes are involved in the pathogenesis of inflammatory acne. Epidermal keratinocytes are also suggested to be involved in initiation and progression of cutaneous inflammation. Nadifloxacin, a fluorinated quinolone, has potent antimicrobial activities against Gram-negative and -positive microbes and is used to treat multiple inflamed acne lesions. However, its effect on immune conferring cells such as mononuclear cells and keratinocytes has not been examined. OBJECTIVE: To evaluate the possible involvement of potential anti-inflammatory activity of nadifloxacin in its therapeutic effect on inflammatory acne, we examined the effects of nadifloxacin, in comparison with other antibiotics used to treat acne vulgaris, on cytokine production by human peripheral blood mononuclear cells (PBMC) and keratinocytes. METHODS: Cytokine production by PBMC was determined after treatment with heat-killed P. acnes in the presence or absence of antimicrobials using a real-time PCR and ELISA. Cultured human epidermal keratinocytes were stimulated by IFN-gamma plus IL-1beta and the effects of antimicrobials were examined by using ELISA. RESULTS: Nadifloxacin as well as macrolide antibiotics and clindamycin inhibited IL-12 and IFN-gamma production by PBMC stimulated by heat-killed P. acnes. The drug also inhibited the IL-1alpha, Il-6, IL-8 and GM-CMS production by keratinocytes treated with IFN-gamma plus IL-1beta. CONCLUSIONS: Inhibitory effects of nadifloxacin to activate T cells and keratinocytes may be involved at least in part in the mechanism of its therapeutic effect against inflammatory acne.     

Antibiotic susceptibility of Propionibacterium acnes isolated from acne vulgaris in Korea

Propionibacterium acnes plays an important role in the development of acne, and inflammatory lesions are improved by antibiotics. Long-term use of antibiotics may result in development of resistant strains and treatment failure. The aim of the present study was to investigate the isolation rate of P. acnes and to evaluate its antibiotic susceptibility to widely used antibiotics in acne in Korea. Among 46 patients, 31 P. acnes strains were cultured. Isolated P. acnes was measured for minimum inhibitory concentration (MIC) of tetracycline, doxycycline, minocycline, erythromycin and clindamycin using an Epsilometer test. Age, disease duration and previous history of antibiotic therapy for acne were compared in relation to the MIC. The mean MIC of tetracycline, minocyclines, doxycycline, clindamycin and erythromycin were all below the breakpoint of antibiotic resistance. The patients with acne vulgaris with disease duration of more than 2 years documented higher MIC values in doxycycline, erythromycin, and clindamycin than those of less than 2 years. The patients who were previously treated with topical or systemic antibiotics showed higher MIC in doxycycline. Antibiotic resistance of P. acnes is still low in Korea, but at this point, there is an increasing trend of MIC. Caution and acknowledgement of increased risk of antibiotic resistant P. acnes should be advised in acne antibiotic treatment to minimize and avoid the emergence of the resistant strain.     

Propionibacterium acnes resistance to antibiotics in acne patients

The minimal inhibitory concentration (MIC) of Propionibacterium acnes in seventy-five acne patients receiving long-term antibiotic therapy demonstrated the emergence of resistant strains. The mean MIC in thirty-three patients receiving long-term tetracycline was four to five times higher than that found in control groups of acne patients not receiving antibiotic therapy and controls free of acne. The average MIC for erythromycin was more than 100 times higher in those receiving long-term antibiotic therapy. In a second group of sixty-two patients, the clinical course and number of P. acnes were correlated with the presence of "resistant strains" defined as P. acnes with a tenfold increase in MIC to tetracycline or erythromycin. Patients with resistant strains had higher counts of P. acnes and clinically were not doing as well as those with sensitive strains.     

The evolving role of Propionibacterium acnes in acne

Propionibacterium acnes is a member of the resident cutaneous flora. Sebaceous follicles involved in acne are characterized by the accumulation of abnormally desquamated corneocytes and excess sebum-the microcomedo. This environment provides ideal growth conditions for P acnes. Several orders of magnitude level of P acnes are found in microcomedos. P acnes produces a variety of chemotactic factors and proinflammatory molecules that are responsible for the inflammatory phase of acne. Antibiotic therapy works by reducing the viable number of P acnes as well as by reducing the production of inflammatory stimuli. Antibiotic therapy has been a mainstay of treatment for more than 30 years. In the last decade, decreased sensitivity to antibiotics has developed and clinical resistance has been described. This development threatens the usefulness of antibiotic therapy in the future.     

Effects of Roxithromycin on the production of lipase and neutrophil chemotactic factor by Propionibacterium acnes

BACKGROUND: The macrolide antibiotic roxithromycin is effective against acne associated with inflammation, but the mechanism by which this is achieved has not been clarified. OBJECTIVE: We studied the effects of roxithromycin on the production of lipase and neutrophil chemotactic factor by Propionibacterium acnes in vitro. RESULTS: Roxithromycin significantly inhibited the production of lipase and neutrophil chemotactic factor by P. acnes at a concentration one eighth of the MIC, at which the growth curve of P. acnes is not affected. CONCLUSION: One mechanism of the effectiveness of roxithromycin in acne therapy is thought to be the inhibition of bacterial lipase and neutrophil chemotactic factor production by P. acnes.     

The bacteriology of acne vulgaris and antimicrobial susceptibility of Propionibacterium acnes and Staphylococcus epidermidis isolated from acne lesions

We examined the species of bacteria aerobically and anaerobically isolated from 30 acne lesions and determined antimicrobial susceptibilities of Propionibacterium acnes (P. acnes) and Staphylococcus epidermidis (S. epidermidis) using nine antimicrobial agents. Among the bacteria isolated, S. epidermidis was most dominant. Both P. acnes and S. epidermidis were isolated from half of the acne lesions. The MIC of seven antimicrobials (ampicillin, erythromycin, roxithromycin, clindamycin, tetracycline, minocycline, nadifloxacin) against P. acnes was under 3.13 micrograms/ml. There were very few resistant strains of P. acnes, but many of S. epidermidis. More than 30% of the S. epidermidis isolates were resistant to erythromycin, roxithromycin, and clindamycin. After long-term systemic antibiotic therapy, the resistant strains of S. epidermidis increased, but P. acnes resistance was still limited. When we use antimicrobial agents for the treatment of acne, it should be noticed that not only P. acnes but also S. epidermidis in the acne lesions may acquire resistance to antimicrobials.     

Benzoyl Peroxide-Based Combination Therapies for Acne Vulgaris

Benzoyl peroxide, with its broad-spectrum antimicrobial activity, is among the most widely used topical agents in the treatment of inflammatory acne vulgaris. Benzoyl peroxide is marketed either alone or in combination with other topical antibiotics; namely, erythromycin and clindamycin. The combination products confer specific advantages over benzoyl peroxide alone, particularly in decreasing the in vivo follicular counts of Propionibacterium acnes, the anaerobic bacterium implicated in the pathogenesis of acne. In addition, the topical treatment of inflammatory acne has been complicated by the development of P acnes resistance to topical erythromycin and clindamycin. Combination products containing benzoyl peroxide and the topical antibiotics have been shown to both: (i) prevent the development of antibiotic resistance in acne patients; and (ii) confer significant clinical improvement to patients who have already developed antibiotic resistance.     

我国痤疮患者皮损中痤疮丙酸杆菌对抗生素耐药性的Meta分析

目的：系统评价我国痤疮患者的皮损分离的痤疮丙酸杆菌(P.acnes)对抗生素的耐药情况，为痤疮抗生素合理治疗提供临床依据。方法：计算机网络检索中国知网(CNKI)、中文科技期刊文数据库(VIP)、万方数据库和PubMed中的相关研究，收集痤疮皮损分离痤疮丙酸杆菌对四环素类、大环内酯类等抗菌药物耐药率的相关研究，对符合纳入标准研究资料进行提取，采用R语言3.3.2 Meta程序包进行Meta分析。结果：共纳入文章13篇，合计1770例痤疮患者，共分离痤疮丙酸杆菌合计1259株。对我国P.acnes的抗生素耐药率进行单组率Meta分析，结果显示P.acnes对红霉素、克拉霉素、阿奇霉素耐药率分别为：45%（95% CI 0.35～0.58)，74%（95% CI 0.51～0.89)，59%（95% CI 0.33～0.84)；对米诺环素、多西环素、四环素耐药率分别为：2%（95% CI 0.00～0.07)，6%（95% CI 0.00～0.26)，8%（95% CI 0.00～0.24)；对甲硝唑耐药率为96%（95% CI 0.80～1.00）。不同抗生素之间存在交叉耐药。结论：我国痤疮患者皮损分离的P.acnes对大环内酯类及甲硝唑耐药率高，对四环素类、喹诺酮类抗生素较为敏感，其中以米诺环素敏感性最高。