Chlamydophila pneumoniae is a species of Chlamydophila, an obligate intracellular bacterium that infects humans and is a major cause of pneumonia. It was known as the Taiwan acute respiratory agent (TWAR) from the names of the two original isolates – Taiwan (TW-183) and an acute respiratory isolate designated AR-39. Until recently, it was known as Chlamydia pneumoniae, and that name is used as an alternate in some sources. In some cases, to avoid confusion, both names are given.
C. pneumoniae has a complex life cycle and must infect another cell to reproduce; thus, it is classified as an obligate intracellular pathogen. The full genome sequence for C. pneumoniae was published in 1999. It also infects and causes disease in koalas, emerald tree boas (Corallus caninus), iguanas, chameleons, frogs, and turtles.
The first known case of infection with C. pneumoniae was a case of conjunctivitis in Taiwan. This atypical bacterium commonly causes pharyngitis, bronchitis and atypical pneumonia, mainly in elderly and debilitated patients, but in healthy adults, also.
Life cycle and method of infection
Chlamydophila pneumoniae is a small gram negative bacterium (0.2 to 1 μm) that undergoes several transformations during its life cycle. It exists as an elementary body (EB) between hosts. The EB is not biologically active, but is resistant to environmental stresses and can survive outside a host for a limited time. The EB travels from an infected person to the lungs of an uninfected person in small droplets and is responsible for infection. Once in the lungs, the EB is taken up by cells in a pouch called an endosome by a process called phagocytosis. However, the EB is not destroyed by fusion with lysosomes, as is typical for phagocytosed material. Instead, it transforms into a reticulate body (RB) and begins to replicate within the endosome. The reticulate bodies must use some of the host's cellular metabolism to complete its replication. The reticulate bodies then convert back to elementary bodies and are released back into the lung, often after causing the death of the host cell. The EBs are thereafter able to infect new cells, either in the same organism or in a new host. Thus, the lifecycle of C. pneumoniae is divided between the elementary body, which is able to infect new hosts but cannot replicate, and the reticulate body, which replicates but is not able to cause new infection.
C. pneumoniae is a common cause of pneumonia around the world; it is typically acquired by otherwise-healthy people and is a form of community-acquired pneumonia. Its treatment and diagnosis are different from historically recognized causes, such as Streptococcus pneumoniae. Because it does not gram stain as well as gram-negative and gram-positive organisms and because C. pneumoniae bacteria is very different from the many other bacteria causing pneumonia (in the earlier days, it was even thought being a virus), pneumonia caused by C. pneumoniae is categorized as an "atypical pneumonia".
In addition to pneumonia, C. pneumoniae less commonly causes several other illnesses. Among these are meningoencephalitis (infection and inflammation of the brain and meninges), arthritis, myocarditis (inflammation of the heart), and Guillain-Barré syndrome.[who?]
Multiple studies have evaluated prior C. pneumoniae infection and a possible connection to lung cancer. One meta-analysis of serological data comparing prior C. pneumoniae infection in patients with and without lung cancer found results suggesting prior infection was associated with a slightly increased risk of developing lung cancer.
In research into the association between C. pneumoniae infection and atherosclerosis and coronary artery disease, serological testing, direct pathologic analysis of plaques, and in vitro testing suggest chronic infection with C. pneumoniae may be a risk factor for development of atherosclerotic plaques. C. pneumoniae infection increases adherence of macrophages to endothelial cells in vitro and aortas ex vivo. However, the current data do not define how often C. pneumoniae is found in atherosclerotic or normal vascular tissue, nor does it allow for determining whether C. pneumoniae infection has a causative effect on atheroma formation or is merely an "innocent passenger" in these plaques. The largest trials that studied the use of antibiotics as a prevention for diseases associated with atherosclerosis, such as heart attacks and strokes, did not show any significant difference between antibiotics and placebo.
C. pneumoniae has been found in the cerebrospinal fluid of some patients diagnosed with multiple sclerosis.
C. pneumoniae infection was first associated with wheezing, asthmatic bronchitis, and adult-onset asthma in 1991. Subsequent studies of bronchoalveolar lavage fluid from pediatric patients with asthma and also other severe chronic respiratory illnesses have demonstrated that over half had evidence of C. pneumoniae by direct organism identification. Acute C. pneumoniae infection can trigger acute wheezing that becomes chronic and is diagnosed as asthma. These observations suggest that acute C. pneumoniae infection is capable of causing protean manifestations of chronic respiratory illness, and may lead to asthma is a small minority of cases.
Macrolide antibiotic treatment can improve asthma in a subgroup of patients that remains to be clearly defined. Macrolide benefits were first suggested in two observational trials and two randomized controlled trials of azithromycin treatment for asthma. One of these RCTs and another macrolide trial suggest that the treatment effect may be greatest in patients with severe, refractory asthma. These clinical results correlate with epidemiological evidence that C. pneumoniae is positively associated with asthma severity and laboratory evidence that C. pneumoniae infection creates steroid-resistance. A recent meta analysis of 12 RCTs of macrolides for the long term management of asthma found significant effects on asthma symptoms, quality of life, bronchial hyper reactivity and peak flow but not FEV1. Evidence from macrolide RCTs of patients with uncontrolled severe and refractory asthma will be critical in defining the role of macrolides in asthma.
There is no vaccine to protect against Chlamydophila pneumoniae. Research is on-going. Identification of highly immunogenic antigens is critical for the construction of an efficacious subunit vaccine against C. pneumoniae infections.
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