哮喘肺炎衣原体感染:临床意义。

Mesut Gencay, Michael Roth
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引用次数: 5

摘要

肺炎衣原体是一种细胞内病原体,已被认为在哮喘病理中起作用。然而,到目前为止,没有一项研究提供明确的证据证明肺炎支原体感染在哮喘中的致病作用,尽管毫无疑问,慢性肺炎支原体感染确实会加重哮喘,应该进行治疗。肺炎支原体感染的诊断仍然是一个值得关注的问题,因为它依赖于训练有素的熟练人员,并且在不同的诊断实验室之间可能存在很大差异。这一事实也是比较流行病学研究时遇到的主要问题之一,这些研究调查了肺炎支原体感染的可能作用及其对其他疾病发病机制的影响。在治疗方面,长期使用大环内酯类药物治疗是根除肺炎原体的最佳方法。然而,肺炎原体的成功治疗也可能因新发感染的高可能性而变得复杂,因为流行病学研究表明,在所有研究人群中,肺炎原体抗体的流行率随着年龄的增长而增加。在北半球,肺炎原体的流行也受到季节条件的影响。从赤道带国家得出任何结论还为时过早。热带国家关于肺炎原体的现有数据表明,成年早期的感染率要快得多,25岁以上人群的血清学患病率为100%。如果得到证实,这一数据将反驳肺炎原体引起哮喘的说法,因为这些国家的哮喘患病率并没有以平行模式增加。对大多数研究的另一种解释可能是,哮喘患者中肺炎衣原体感染率的增加是由于宿主细胞生理学的未知变化导致对微生物的易感性改变。应该记住的是,肺炎支原体感染的患病率增加并不局限于哮喘。需要进一步的研究来了解肺炎支原体,特别是慢性感染,在炎症性疾病的发病机制中的作用,特别关注微生物在受感染宿主细胞中引发的作用。只有当我们了解肺炎球菌对其宿主细胞的作用时,我们才能判断其对受感染患者整体状况的影响,而这些知识将有助于我们开发成功的治疗方法。
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Chlamydia pneumoniae infections in asthma: clinical implications.

Chlamydia pneumoniae is an intracellular pathogen that has been suggested to play a role in the pathology of asthma. However, so far none of the studies have provided clear evidence for a causative role of C. pneumoniae infections in asthma, although there is little doubt that chronic C. pneumoniae infection does aggravate asthma and should be treated. The diagnosis of C. pneumoniae infection is still a matter of concern for it is dependent on trained skilled personnel and can vary significantly between different diagnostic laboratories. This fact is also one of the major problems encountered when comparing epidemiological studies investigating the possible role of C. pneumoniae infections and their impact on the pathogenesis of other diseases. With regard to therapy, long-term treatment with macrolides is the best available method to eradicate C. pneumoniae. Successful therapy for C. pneumoniae, however, can also be complicated by the high possibility of de novo infection as epidemiological studies have shown that the prevalence of antibodies to C. pneumoniae increases with age in all populations studied. In the northern hemisphere the prevalence of C. pneumoniae is also affected by seasonal conditions. It is too early to draw any conclusions from the equatorial belt countries. The available data on C. pneumoniae in tropical countries indicate a much faster infection rate during early adulthood with 100% serological prevalence at an age greater than 25 years. This data, if confirmed, would argue against C. pneumoniae causing asthma since the asthma prevalence in those countries does not increase in a parallel pattern. An alternative interpretation of most studies could be that the increased rate of C. pneumoniae infections in patients with asthma results from a modified susceptibility towards the microorganism, due to yet unknown changes of the host cell's physiology. It should be kept in mind that increased prevalence of C. pneumoniae infection is not restricted to asthma. Further studies are needed to understand the role of C. pneumoniae, especially of chronic infection, in the pathogenesis of inflammatory diseases with a specific focus on the effect that the microorganism triggers in the infected host cell. Only when we understand what C. pneumoniae does to its host cell will we be able to judge its impact on the overall status of an affected patient, and this knowledge will help us to develop a successful therapy.

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