Chlamydia pneumoniae is a common intracellular bacterial pathogen causing a range of respiratory infections such as pneumonia, bronchitis, sinusitis, and pharyngitis.
It is widely prevalent globally, transmitted through respiratory routes, and has a high reinfection rate throughout life.
While often asymptomatic or mildly symptomatic, C. pneumoniae can lead to severe respiratory illnesses in about 30% of cases.
Beyond respiratory infections, it has been implicated in chronic conditions like asthma, chronic obstructive pulmonary disease (COPD), and even cardiovascular diseases such as atherosclerosis and coronary heart disease.
The bacterium's persistence in the body, despite antibiotic treatment, poses significant challenges, necessitating further research into its pathogenesis and effective treatment strategies.
Chlamydophila pneumoniae IgM antibodies are essential for diagnosing acute infections, appearing 2-3 weeks after symptom onset and peaking at 4-5 weeks. Despite challenges like false positives in chronic lung disease patients, IgM detection via ELISA remains valuable for diagnosing community-acquired lower respiratory tract infections, particularly in children.
Chlamydophila pneumoniae is a common intracellular bacterial respiratory pathogen with a unique biphasic life cycle [6.].
It is widely distributed globally and transmitted from human to human via the respiratory route, infecting the majority of the world's population; it has a high prevalence of reinfection throughout life [1., 6.].
C. pneumoniae causes about 10% of community-acquired pneumonia and 5% of pharyngitis, bronchitis, and sinusitis [2.].
In Western countries, new infections are most common between ages 5 and 15, and seroprevalence is higher in adult males [1.].
Most infections (70%) are asymptomatic or mildly symptomatic, but about 30% can cause severe respiratory illnesses [6.].
C. pneumoniae can cause various respiratory illnesses, including pneumonia, bronchitis, sinusitis, and pharyngitis [6.].
After an acute infection, C. pneumoniae can persist in a form that is resistant to antibiotics and potentially contributes to chronic respiratory conditions such as asthma, chronic bronchitis, and COPD [6.].
Additionally, evidence suggests a potential link between C. pneumoniae infection and atherosclerosis as the bacterium has been found in atherosclerotic plaques. It is also associated with coronary heart disease and acute myocardial infarction [1.].
It has also been implicated in other conditions like erythema nodosum and sarcoidosis [2.].
Chlamydia pneumoniae is part of the Chlamydiae order, which contains obligate intracellular pathogens.
The order initially comprised one genus, Chlamydia, with four recognized species: C. trachomatis, C. psittaci, C. pneumoniae, and C. pecorum.
Recent taxonomic analysis has led to a proposed reclassification, suggesting the division of the genus Chlamydia into two genera: Chlamydia and Chlamydophila.
Under this new classification, C. trachomatis would be joined by two new species, Chlamydia muridarum and Chlamydia suis.
The genus Chlamydophila would include C. pecorum, C. pneumoniae, and C. psittaci, along with three new species derived from C. psittaci: Chlamydophila abortus, Chlamydophila caviae, and Chlamydophila felis. Despite ongoing controversy regarding this reclassification, the term Chlamydia is still commonly used.
Chlamydia pneumoniae, also known as TWAR, is distinguished from C. trachomatis and C. psittaci by its unique elementary body morphology and less than 10% DNA homology.
The symptoms of C. pneumoniae infections are similar to those caused by other respiratory pathogens but often present a subacute onset with pharyngitis that may resolve before bronchitis or pneumonia develops. A prolonged cough and slow recovery, even with antibiotic therapy, are common.
C. pneumoniae is associated with the following conditions:
Chlamydophila pneumoniae IgM antibodies are used to diagnose acute infections, but their interpretation can be challenging. Studies have shown that IgM antibodies typically appear 2-3 weeks after illness onset, peak at 4-5 weeks, and become undetectable after 3-5 months [12.].
However, false-positive IgM results can occur in patients with chronic lung diseases, potentially leading to misdiagnosis of acute infections [11.].
In some cases, individuals may exhibit atypical immune responses, producing predominantly IgM antibodies in both primary and repeated infections [14.].
The optimal time for serum collection is 3-6 weeks after symptom onset when using a single sample, while paired sera should be obtained at least 4 weeks apart [12.].
Despite these challenges, serological detection of C. pneumoniae IgM antibodies using ELISA can be useful in diagnosing community-acquired lower respiratory tract infections, particularly in children [9.].
C. pneumoniae is often tested by assessing the presence of antibodies against this organism. Often, IgG, IgM, and IgA antibody levels are tested.
Serology tests can describe the timeline of infection, with the presence of IgM antibodies indicating a current or recent infection, and IgG antibodies indicating a past infection. IgA antibodies typically confirm an immune response in mucosal tissue, often from the respiratory or digestive tract.
However, there may be some nuance to the presence of IgM antibodies.
Chlamydophila pneumoniae IgM antibodies are used to diagnose acute infections, typically appearing 2-3 weeks after illness onset, peaking at 4-5 weeks, and disappearing after 3-5 months.
However, false-positive results can occur in patients with chronic lung diseases, leading to potential misdiagnosis.
Some individuals may show atypical immune responses, producing IgM antibodies in both primary and repeated infections.
The optimal time for serum collection was reported as 3-6 weeks after symptom onset for a single sample, with paired sera collected at least 4 weeks apart, by one group of study authors [12.].
Despite these challenges, IgM detection via ELISA remains valuable for diagnosing community-acquired lower respiratory tract infections, particularly in children [9.].
In contrast, C. pneumoniae IgG antibodies can persist for months to years. Seroprevalence studies show 50-70% of adults have IgG antibodies, indicating frequent reinfections [13.].
Antimicrobial treatment of C. pneumoniae often consists of:
Each of these has shown 70-90% success in eradicating C. pneumoniae from the respiratory tract in cases of pneumonia.
Macrolides, ketolides, tetracyclines, quinolones, and rifamycins have all shown effectiveness in vitro [7.].
Click here to compare test options and order testing for C. pneumoniae.
[1.] Blasi F, Tarsia P, Arosio C, Fagetti L, Allegra L. Epidemiology of Chlamydia pneumoniae. Clinical Microbiology and Infection. 1998;4:4S1-4S6. doi:https://doi.org/10.1111/j.1469-0691.1998.tb00697.x
[2.] Campbell LA, Kuo CC, Grayston JT. Chlamydia pneumoniae and cardiovascular disease. Emerg Infect Dis. 1998 Oct-Dec;4(4):571-9. doi: 10.3201/eid0404.980407. PMID: 9866733; PMCID: PMC2640250.
[3.] CDC. Laboratory Testing for Chlamydia pneumoniae. Chlamydia pneumoniae Infection. Published 2024. Accessed August 6, 2024. https://www.cdc.gov/cpneumoniae/php/laboratories
[4.] Cheok YY, Lee CYQ, Cheong HC, Looi CY, Wong WF. Chronic Inflammatory Diseases at Secondary Sites Ensuing Urogenital or Pulmonary Chlamydia Infections. Microorganisms. 2020;8(1):127. doi:https://doi.org/10.3390/microorganisms8010127
[5.] Choroszy−Król I, Frej−Mądrzak M, Hober M, Jolanta Sarowska, Agnieszka Jama-Kmiecik. Infections Caused by Chlamydophila pneumoniae. Advances in Clinical and Experimental Medicine. 2014;23(1):123-126. doi:https://doi.org/10.17219/acem/37035
[6.] Hahn DL, Azenabor AA, Beatty WL, Byrne GI. Chlamydia pneumoniae as a respiratory pathogen. Frontiers in Bioscience: A Journal and Virtual Library. 2002;7:e66-76. doi:https://doi.org/10.2741/hahn
[7.] Hammerschlag MR. Advances in the management of Chlamydia pneumoniae infections. Expert Review of Anti-infective Therapy. 2003;1(3):493-503. doi:https://doi.org/10.1586/14787210.1.3.493
[8.] Hammerschlag MR. Chlamydia trachomatis and Chlamydia pneumoniae Infections in Children and Adolescents. Pediatrics in Review. 2004;25(2):43-51. doi:https://doi.org/10.1542/pir.25-2-43
[9.] Kumar S, Saigal SR, Sethi GR. Detection of IgM and IgG antibodies to Chlamydophila pneumoniae in pediatric community-acquired lower respiratory tract infections. Indian J Pathol Microbiol. 2011 Oct-Dec;54(4):782-5. doi: 10.4103/0377-4929.91501. PMID: 22234110.
[10.] Kuo CC, Jackson LA, Campbell LA, Grayston JT. Chlamydia pneumoniae (TWAR). Clinical Microbiology Reviews. 1995;8(4):451-461. doi:https://doi.org/10.1128/CMR.8.4.451
[11.] Miyashita N, Yasushi Obase, Fukuda M, et al. Evaluation of Serological Tests Detecting Chlamydophila pneumoniae-specific Immunoglobulin M Antibody. Internal Medicine. 2006;45(20):1127-1131. doi:https://doi.org/10.2169/internalmedicine.45.6074
[12.] Miyashita N, Kawai Y, Tanaka T, et al. Antibody responses of Chlamydophila pneumoniae pneumonia: Why is the diagnosis of C. pneumoniae pneumonia difficult? Journal of Infection and Chemotherapy. 2015;21(7):497-501. doi:https://doi.org/10.1016/j.jiac.2015.03.003
[13.] Peeling RW. Laboratory diagnosis of Chlamydia pneumoniae infections. Can J Infect Dis. 1995 Jul;6(4):198-203. doi: 10.1155/1995/696950. PMID: 22514397; PMCID: PMC3327923.
[14.] Tuuminen T, Salo K, Surcel HM. A casuistic immunologic response in primary and repeated Chlamydophila pneumoniae infections in an immunocompetent individual. J Infect. 2002 Oct;45(3):202-6. doi: 10.1016/s0163-4453(02)91021-2. PMID: 12387780.