Chlamydia pneumoniae
Scientific classification
Domain:	Bacteria
Kingdom:	Pseudomonadati
Phylum:	Chlamydiota
Class:	Chlamydiia
Order:	Chlamydiales
Family:	Chlamydiaceae
Genus:	Chlamydia
Species:	C. pneumoniae
Binomial name
Chlamydia pneumoniae Graystonet al. 1989
Synonyms
Chlamydophila pneumoniae(Grayston et al. 1989) Everett, Bush & Andersen 1999

Chlamydia pneumoniae^[1] is a species ofChlamydia, anobligate intracellular bacterium^[2] that infects humans and is a major cause ofpneumonia. 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.^[3] Briefly, it was known asChlamydophila pneumoniae, and that name is used as an alternate in some sources.^[4] In some cases, to avoid confusion, both names are given.^[5]

Chlamydia pneumoniae has a complex life cycle and must infect another cell toreproduce; thus, it is classified as anobligate intracellular pathogen. The fullgenome sequence forC. pneumoniae was published in 1999.^[6] It also infects and causes disease inkoalas,emerald tree boas (Corallus caninus),iguanas,chameleons, frogs, and turtles.

The first known case of infection withC. pneumoniae was a case ofconjunctivitis inTaiwan in 1950. There are no known cases ofC. pneumoniae in human history before 1950. This atypical bacterium commonly causespharyngitis,bronchitis,coronary artery disease andatypical pneumonia in addition to several other possible diseases.^[7][8]

Chlamydia pneumoniae is a small gram-negative bacterium (0.2 to 1 μm) that undergoes several transformations during its life cycle. It exists as anelementary body (EB) betweenhosts. The EB is not biologically active, but is resistant toenvironmental stresses and can survive outside a host for a limited time. The EB travels from aninfected person to thelungs of an uninfected person in smalldroplets and is responsible for infection. Once in the lungs, the EB is taken up bycells in a pouch called anendosome by a process calledphagocytosis. However, the EB is not destroyed by fusion withlysosomes, as is typical for phagocytosed material. Instead, it transforms into areticulate 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 sameorganism or in a new host. Thus, the lifecycle ofC. 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 a new infection.^[9]

Chlamydia pneumoniae is a common cause of pneumonia around the world; it is typically acquired by otherwise-healthy people and is a form ofcommunity-acquired pneumonia. Its treatment and diagnosis are different from historically recognized causes, such asStreptococcus pneumoniae.^[10] Because it does not gram stain well, and becauseC. pneumoniae bacteria is very different from the many other bacteria causing pneumonia (in the earlier days, it was even thought to be a virus), the pneumonia caused byC. pneumoniae is categorized as an "atypical pneumonia".^[11]

Chlamydia pneumoniae infection was first associated with wheezing, asthmatic bronchitis, and adult-onsetasthma in 1991.^[12] Subsequent studies of bronchoalveolar lavage fluid from pediatric patients with asthma and also other severe chronic respiratory illnesses have demonstrated that over 50 percent had evidence ofC. pneumoniae by direct organism identification.^[13][14]C. pneumoniae infection triggers acute wheezing, if it becomes chronic then it is diagnosed as asthma.^[15] These observations suggest that acuteC. pneumoniae infection is capable of causing protean manifestations of chronic respiratory illness which lead to asthma.^[16]

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^[17][18] and two randomized controlled trials^[19][20] of azithromycin treatment for asthma. One of these RCTs^[20] and another macrolide trial^[21] suggest that the treatment effect may be greatest in patients with severe, refractory asthma. These clinical results correlate with epidemiological evidence thatC. pneumoniae is positively associated with asthma severity^[22] and laboratory evidence thatC. pneumoniae infection creates steroid-resistance.^[23] A 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.^[24] More recent positive results of long-term treatment with azithromycin on asthma exacerbations and quality-of-life in patients with severe, refractory asthma^[25][26] have resulted in azithromycin now being recommended in international guidelines as a treatment option for these types of patients.^[27]

A recent case series of 101 adults with asthma reported that macrolides (mostly azithromycin) and tetracyclines, either separately or in combination, appeared to be dramatically efficacious in a subgroup of "difficult-to-treat" (i.e., not necessarily refractory to high-dose inhaled corticosteroids but who did not take them) patients with severe asthma, many of whom also had the "overlap syndrome" (asthma and COPD).^[28] Randomized, controlled trials that include these types of asthma patients are needed.

ChronicC. pneumoniae infection has been documented via direct organism detection (PCRTooltip polymerase chain reaction and/orculture) insputum andbronchoalveolar lavage (BAL) of children with chronic respiratory conditions including asthma,^[29][30][31] and in peripheral blood of healthy blood donors.^[32]C. pneumoniae has also been detected byimmunohistochemical staining in themonocytes residing within the lungs of 100% of patients undergoing lung resection for cancer; patients with comorbid COPD had significantly higher infection burden than those without COPD. The same study found that 44% of young and middle aged accident victims were also chronically infected, albeit with significantly lower infection burden.^[33]

Onemeta-analysis ofserological data comparing priorC. pneumoniae infection in patients with and without lung cancer found results suggesting prior infection was associated with an increased risk of developing lung cancer.^[34][35][36]

In research into the association betweenC. pneumoniae infection andatherosclerosis andcoronary artery disease,serological testing, direct pathologic analysis of plaques, andin vitro testing suggest infection withC. pneumoniae is a significant risk factor for development of atheroscleroticplaques and atherosclerosis.^[37]C. pneumoniae infection increases adherence ofmacrophages toendothelial cellsin vitro and aortasex vivo.^[38] However, most current research and data are insufficient and do not define how oftenC. pneumoniae is found in atherosclerotic or normalvascular tissue.^[39]

Chlamydia pneumoniae has also been found in the cerebrospinal fluid of patients diagnosed with multiple sclerosis.^[40]

Chlamydia pneumoniae infection has been associated withschizophrenia.^[41] Many other pathogens have been associated with schizophrenia as well.^[41] ChronicChlamydia pneumoniae infection has also in some cases been found to be a cause ofchronic fatigue syndrome (CFS) that can be resolved with antibiotics.^[42][43]

Thefirst-lineantibiotics for treatment ofChlamydia pneumoniae are themacrolideerythromycin and thetetracyclinestetracycline anddoxycycline.^[44] The macrolidesclarithromycin andazithromycin are also effective.^[44]Chlamydia pneumoniae shows resistance topenicillin,ampicillin, andsulfa drugs, and hence these antibiotics are not recommended.^[44] Other antibiotics which may be effective includefluoroquinolones likelevofloxacin,gatifloxacin,gemifloxacin, andmoxifloxacin.^[44] Symptoms ofChlamydia pneumoniae often reappear after short or conventional courses of antibiotics.^[44] As a result, following confirmation of persistent infection with culture, intensive long-term treatment is recommended.^[44]

There is currently no vaccine to protect againstChlamydia pneumoniae. Identification of immunogenicantigens is critical for the construction of an efficacious subunit vaccine againstC. pneumoniae infections. Additionally, there is a general shortage worldwide of facilities that can identify/diagnoseChlamydia pneumoniae.^{[citation needed]}

• Chlamydia Pneumoniae cpnhelp.orgArchived 2022-07-05 at theWayback Machine
• Type strain ofChlamydopila pneumoniae at BacDive - the Bacterial Diversity Metadatabase

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• Pathogenic bacteria

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