Chlamydophila pneumoniae: Infectious substances pathogen safety data sheet

For more information on Chlamydophila pneumoniae, see the following:

Section I – Infectious agent

Name

Chlamydophila pneumoniae

Agent type

Bacteria

Taxonomy

Family

Chlamydiaceae

Genus

Chlamydophila

Species

pneumoniae

Synonym or cross-reference

Originally named Chlamydia strain TWAR, in 1989 it was reclassified as a new species, Chlamydia pneumoniaeFootnote1. In 1999 the genus was renamed Chlamydophila, but the change was not universally adopted. C. pneumoniae is commonly referred to by both genus namesFootnote 2.

Characteristics

Brief description

C. pneumoniae is a non-motile, gram-negative obligate intracellular bacterium. The genome is approximately 1.23 MbpFootnote 3. C. pneumoniae has two developmental forms: a metabolically inactive and infectious elementary body, which is adapted for extracellular survival, and a metabolically active, non-infectious reproductive reticulate bodyFootnote 4. C. pneumoniae elementary bodies are usually pear-shaped, whereas elementary bodies of other members of the genus are typically roundFootnote 3. The elementary bodies are smaller in size (0.2 µm) while the reticulate bodies are larger in size (0.8 µm)Footnote 5. Three C. pneumoniae biovars have been identified: human, koala, and equineFootnote 3Footnote 6.

Properties

C. pneumoniae can be cultured in yolk sacs of chicken embryos and some cell lines such as HL (human line) and Hep-2 cellsFootnote 3. C. pneumoniae replicate in the cytoplasm of host cells within membrane-bound vacuoles (inclusion), until they occupy most of the cytoplasm, C. pneumoniae is then released from the cell either by extrusion or cell host lysis to infect neighbouring cellsFootnote 5. C. pneumoniae is able to systematically spread to other tissues outside the lungs through peripheral blood mononuclear cells, and can multiply in various cell typesFootnote 5. C pneumoniae can survive under stressful conditions as a non-infectious persistent form and remain in the host cell as reticulate bodies before reactivationFootnote 5.

Section II – Hazard identification

Pathogenicity and toxicity

C. pneumoniae causes upper and lower respiratory tract infections (e.g., pharyngitis, sinusitis, bronchitis, community-acquired pneumonia) in humansFootnote1. In most individuals, infection is asymptomatic, or mild and self-limitingFootnote 7Footnote 8. Initial symptoms include rhinorrhea, headache (25-60%), fever (25-45%), hoarseness (65-75%), and sore throat (70-80%)Footnote8. These symptoms usually resolve after one week and are followed by a dry cough (75-90%) that can persist for weeks to monthsFootnote7Footnote8Footnote 9. Although C. pneumoniae can cause a severe form of pneumonia, fatalities are rareFootnote 10Footnote 11.

C. pneumoniae appears to be capable of persisting in the body after acute infectionFootnote7, and has been associated with various chronic conditions in adults including atherosclerosisFootnote 12Footnote 13Footnote 14, cardiovascular diseaseFootnote5, neck vein obstructionFootnote 15, asthma onset and exacerbationFootnote 16Footnote 17, chronic obstructive pulmonary diseaseFootnote 18, late onset dementiaFootnote 19, arthritisFootnote 20Footnote 21, multiple sclerosisFootnote 22 and, skin and mucous membrane eruptionsFootnote 23.

Atherosclerosis is the buildup of plaque in arteries and is a precursor to cardiovascular disease. In vascular cells, C. pneumoniae induces oxidative stress and inflammatory proteins which accelerates atherosclerotic lesion developmentFootnote 24. The prevalence of C. pneumoniae in atherosclerotic plaques is 40-50%Footnote 25.

C. pneumoniae can promote asthma onset by inducing high counts of eosinophils and neutrophils in the airways. If not treated, C. pneumoniae can cause chronic infection that induces more inflammatory responses. The reported prevalence of asthmatics with C. pneumoniae infection is variable, ranging from 15-92%Footnote 26.

Furthermore, C. pneumoniae can infect the brain and central nervous system, possibly through the olfactory nerves, and increase the risk factor for dementia by promoting amyloid beta deposits in the brainFootnote 27. 80-90% of patients with late-onset dementia contained C. pneumoniae in their brain tissueFootnote 27.

C. pneumoniae infections have been identified in koalas, horses, bandicoots, amphibians, and reptilesFootnote 18. While clinical features in other animals are less known, C. pneumoniae causes respiratory tract infections in koalas; infections can be asymptomatic or koalas may present symptoms similar to those observed in humansFootnote3Footnote 28.

Epidemiology

C. pneumoniae causes respiratory tract infections in children and adults worldwide. Primary infection occurs mainly in school-aged children, whereas reinfection occurs in adults. Seroprevalence is approximately 50% by age 20, 80% in elderly males, and 70% in elderly femalesFootnote 18. Incidence of community-acquired pneumonia in adults requiring hospitalization in the United States is approximately 24.8 cases per 10,000 people per yearFootnote 29. C. pneumoniae is responsible for 6-20% of community-acquired pneumonia casesFootnote 8, and 5% of bronchitis casesFootnote 7. Individuals with untreated HIV have higher risk of C. pneumoniae infection than healthy individualsFootnote 30. Disease can be more severe in elderly individuals and those with cardiopulmonary diseaseFootnote 8. Fatalities due to C. pneumoniae respiratory infections are rareFootnote 10Footnote 11. Sporadic outbreaks of respiratory tract infection caused by C. pneumoniae have been reported in long-term care facilities, correctional centres, and military basesFootnote 31Footnote 32Footnote 33.

Host range

Natural host(s)

HumansFootnote1, horsesFootnote 6, koalasFootnote28, Western-barred bandicootsFootnote 34, reptiles (snakes, iguanas, chameleons, turtles)Footnote 35, birdsFootnote 36 and amphibians (frogs)Footnote36.

Other host(s)

Mice, rabbits, toads, hamsters and non-human primates have been experimentally infectedFootnote 37Footnote 38Footnote 39Footnote 40.

Infectious dose

Unknown.

Incubation period

Approximately 21 daysFootnote7.

Communicability

Transmission of C. pneumoniae occurs via exposure to contaminated surfaces and subsequent transfer to mucosal tissuesFootnote 41Footnote 42. Transmission can also occur via exposure to infectious aerosols through close person-to-person contact, but this does not appear to be an efficient mode of transmissionFootnote42.

Section III – Dissemination

Reservoir

HumansFootnote 43.

Zoonosis

None. However, findings of animal genotypes in humans suggest the possibility of zoonosisFootnote 44.

Vectors

None.

Section IV – Stability and viability

Drug susceptibility/resistance

C. pneumoniae growth is inhibited by tetracyclines, macrolides, azalides, ketolides, chloramphenicol, rifampin, and fluoroquinolones in vitroFootnote3. The developmental cycle is interrupted in the presence of beta-lactam antibioticsFootnote3. Recently, Lefamulin has been shown to effectively inhibit protein synthesis in pulmonary organisms, including C. pneumoniae, and has been approved by FDA (Food and Drug Administration), EMA (European Medicines Agency), and Health Canada to treat against community-acquired pneumoniaFootnote 45.

C. pneumoniae is not susceptible to sulphonamidesFootnote2Footnote3Footnote 46. The TW-183 strain of C. pneumoniae has shown some in-vitro resistance to rifampin and rifalazil due to gene mutationsFootnote 47. Mutated CV-6 strain of C. pneumoniae has shown in-vitro resistance to quinolonesFootnote 48.

Susceptibility to disinfectants

Topical application of the oxidant N-chlorotaurine (0.1%) has been shown to effectively inactivate intra-cellular C. pneumoniae in-vitroFootnote 49. Bleach (0.25%), ethanol (70%), glutaraldehyde (2%), hydrogen peroxide (7.5%), peracetic acid (0.2%), and orthophthalaldehyde (0.55%) are effective against other members of the Chlamydophila genusFootnote 50.

Physical inactivation

C. pneumoniae is sensitive to heat and UV radiationFootnote 51. C. pneumoniae can be inactivated by heat treatment at 90°C for 30 minutes and by exposure to 30W UV light source for 30 minutes from a distance of 15 cmFootnote51Footnote 52.

Survival outside host

C. pneumoniae can persist on a dry inanimate surface for up to 30 hoursFootnote41. C. pneumoniae can survive in liquid medium at 15°C for 2 weeksFootnote 53, and on hands for 10-15 minutesFootnote41.

Section V – First aid/medical

Surveillance

C. pneumoniae can be detected in clinical specimens using culture-based, antigen detection, antibody detection, and molecular methodsFootnote 54. C. pneumoniae antigens can be detected in cells using a peroxidase or fluorescent markerFootnote 55. Antibodies against C. pneumoniae can be detected using micro-immunofluorescence antibody assays (MIF) and ELISAsFootnote 9. Commercial PCR assays such as FilmArray® Respiratory Panel (BioFire Diagnostics, Salt Lake City, UT) and NxTag® Respiratory Pathogen Panel (Luminex Inc., Austin, TX) have been approved by the FDA for C. pneumoniae detectionFootnote9Footnote29Footnote55. Molecular methods, including PCR assays, is considered the "gold standard"Footnote 56.

Note: The specific recommendations for surveillance in the laboratory should come from the medical surveillance program, which is based on a local risk assessment of the pathogens and activities being undertaken, as well as an overarching risk assessment of the biosafety program as a whole. More information on medical surveillance is available in the Canadian Biosafety Handbook.

First aid/treatment

The first-line treatment for C. pneumoniae are macrolides. The most active is clarithromycin with a minimum inhibitory concentration of 0.004-0.03 µg/mL. Others include azithromycin (0.05-0.25 µg/mL) and erythromycin (0.015-0.25 µg/mL)Footnote47. Infections are also commonly treated with tetracyclines, such as doxycycline and minocycline, which have a minimum inhibitory concentration of 0.015-0.25 µg/mLFootnote47. Quinolones show inhibitory activity against C. pneumoniae as well with varying levels of inhibitory concentrations, such as garenoxacin (0.015-0.03 µg/L), gemifloxacin (0.06-0.25 µg/L), or levofloxacin (0.25-1 µg/L)Footnote 47. Treatment regimens usually involve multiple drugs due to complexity of eradicating chronic infectionFootnote2.

Note: The specific recommendations for first aid/treatment in the laboratory should come from the post-exposure response plan, which is developed as part of the medical surveillance program. More information on the post-exposure response plan can be found in the Canadian Biosafety Handbook.

Immunization

None.

Note: More information on the medical surveillance program can be found in the Canadian Biosafety Handbook, and by consulting the Canadian Immunization Guide.

Prophylaxis

None.

Note: More information on prophylaxis as part of the medical surveillance program can be found in the Canadian Biosafety Handbook.

Section VI – Laboratory hazard

Laboratory-acquired infections

Two laboratory workers developed asymptomatic respiratory tract infection with C. pneumoniae after exposure to aerosolized infectious materialFootnote 57. Four laboratory technicians presented with C. pneumoniae pneumonia after cultivating an isolate in the laboratoryFootnote 58. One laboratory technician presented with fatigue, fever, and severe pneumonia after aerosol exposureFootnote 59.

Note: Please consult the Canadian Biosafety Standard and Canadian Biosafety Handbook for additional details on requirements for reporting exposure incidents. A Canadian biosafety guideline describing notification and reporting procedures is also available.

Sources/specimens

Nasopharyngeal swab or aspirate, lung and vascular biopsy specimens, blood, atherosclerotic plaques, brain tissueFootnote2Footnote25Footnote27.

Primary hazards

Autoinoculation with infectious material and exposure of mucous membranes to infectious material, including infectious aerosolsFootnote42.

Special hazards

None.

Section VII – Exposure controls/personal protection

Risk group classification

C. pneumoniae is a Risk Group 2 Human Pathogen and Risk Group 2 Animal PathogenFootnote 60Footnote 61.

Containment requirements

Containment Level 2 facilities, equipment, and operational practices outlined in the Canadian Biosafety Standard for work involving infectious or potentially infectious materials, animals, or cultures.

Protective clothing

The applicable Containment Level 2 requirements for personal protective equipment and clothing outlined in the Canadian Biosafety Standard are to be followed. The personal protective equipment could include the use of a labcoat and dedicated footwear (e.g., boots, shoes) or additional protective footwear (e.g., boot or shoe covers) where floors may be contaminated (e.g., animal cubicles, PM rooms), gloves when direct skin contact with infected materials or animals is unavoidable, and eye protection where there is a known or potential risk of exposure to splashes.

Note: A local risk assessment will identify the appropriate hand, foot, head, body, eye/face, and respiratory protection, and the personal protective equipment requirements for the containment zone and work activities must be documented.

Other precautions

A biological safety cabinet (BSC) or other primary containment devices to be used for activities with open vessels, based on the risks associated with the inherent characteristics of the regulated material, the potential to produce infectious aerosols or aerosolized toxins, the handling of high concentrations of regulated materials, or the handling of large volumes of regulated materials.

Use of needles and syringes to be strictly limited. Bending, shearing, re-capping, or removing needles from syringes to be avoided, and if necessary, performed only as specified in standard operating procedures (SOPs). Additional precautions are required with work involving animals or large-scale activities.

Additional information

For diagnostic laboratories handling primary specimens that may contain C. pneumoniae, the following resources may be consulted:

Section VIII – Handling and storage

Spills

Allow aerosols to settle. Wearing personal protective equipment, gently cover the spill with absorbent paper towel and apply suitable disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up (Canadian Biosafety Handbook).

Disposal

All materials/substances that have come in contact with the regulated materials should be completely decontaminated before they are removed from the containment zone or standard operating procedures (SOPs) to be in place to safely and securely move or transport waste out of the containment zone to a designated decontamination area / third party. This can be achieved by using decontamination technologies and processes that have been demonstrated to be effective against the regulated material, such as chemical disinfectants, autoclaving, irradiation, incineration, an effluent treatment system, or gaseous decontamination (Canadian Biosafety Handbook).

Storage

Containment Level 2: The applicable Containment Level 2 requirements for storage outlined in the Canadian Biosafety Standard are to be followed. Primary containers of regulated materials removed from the containment zone to be labelled, leakproof, impact resistant, and kept either in locked storage equipment or within an area with limited access.

Section IX – Regulatory and other information

Canadian regulatory information

Controlled activities with C. pneumoniae require a Human Pathogens and Toxins licence issued by the Public Health Agency of Canada. C. pneumoniae is a terrestrial animal pathogen in Canada; therefore, importation of C. pneumoniae requires an import permit under the authority of the Health of Animals Regulations (HAR), issued by the Public Health Agency of Canada. The Agency issues a "Pathogen and Toxin Licence document" for both a Humans Pathogens and Toxins Licence and HAR importation permit.

The following is a non-exhaustive list of applicable designations, regulations, or legislations:

Last file update

September, 2023

Prepared by

Centre for Biosecurity, Public Health Agency of Canada.

Disclaimer

The scientific information, opinions, and recommendations contained in this Pathogen Safety Data Sheet have been developed based on or compiled from trusted sources available at the time of publication. Newly discovered hazards are frequent and this information may not be completely up to date. The Government of Canada accepts no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information.

Persons in Canada are responsible for complying with the relevant laws, including regulations, directives and standards applicable to the import, transport, and use of pathogens and toxins in Canada set by relevant regulatory authorities, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment and Climate Change Canada, and Transport Canada. The risk classification and related regulatory requirements referenced in this Pathogen Safety Data Sheet, such as those found in the Canadian Biosafety Standard, may be incomplete and are specific to the Canadian context. Other jurisdictions will have their own requirements.

Copyright © Public Health Agency of Canada, 2023, Canada

References

Footnote 1

Grayston, J. T., C. C. Kuo, L. A. Campbell, and S. P. Wang. 1989. Chlamydia pneumoniae sp. nov. for Chlamydia sp. Strain TWAR. Int J Syst Bacteriol. 39:88.

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Footnote 2

Blasi, F., P. Tarsia, and S. Aliberti. 2009. Chlamydophila pneumoniae. Clin. Microbiol. Infect. 15:29-35.

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Footnote 3

Kuo, C. C., R. S. Stephens, P. M. Bavoil, and B. Kaltenboeck. 2012. Genus I. Chlamydia, p. 846. N. R. Krieg, J. T. Staley, D. R. Brown, B. P. Hedlund, B. J. Paster, N. L. Ward, W. Ludwig, and W. B. Whitman (eds.), Bergey's Manual of Systematic Bacteriology. Volume Four, 2nd ed.,. Springer.

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Footnote 4

Miyashita, N., and A. Matsumoto. 2005. Morphology of Chlamydia pneumoniae, p. 11. H. Friedman, Y. Yamamoto, and M. Bendinelli (eds.), Chlamydia pneumoniae Infection and Disease. Springer.

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Footnote 5

Di Pietro, M., S. Filardo, S. Romano, and R. Sessa. 2019. Chlamydia trachomatis and chlamydia pneumoniae interaction with the host: Latest advances and future prospective. Microorganisms. 7.

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Footnote 6

Storey, C., M. Lusher, P. Yates, and S. Richmond. 1993. Evidence for Chlamydia pneumoniae of non-human origin. J. Gen. Microbiol. 139:2621-2626.

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Footnote 7

Burrillo, A., and E. Bouza. 2010. Chlamydophila pneumoniae. Infect. Dis. Clin. North Am. 24:61-71.

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Footnote 8

Blasi, F., R. Cosentini, P. Tarsia, and L. Allegra. 2005. Pneumonia caused by Chlamydia pneumoniae, p. 57. H. Friedman, Y. Yamamoto, and M. Bendinelli (eds.), Chlamydia pneumoniae Infection and Disease. Springer.

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Footnote 9

Arnold, F. W., J. T. Summersgill, and J. A. Ramirez. 2016. Role of Atypical Pathogens in the Etiology of Community-Acquired Pneumonia. Semin. Respir. Crit. Care. Med. 37:819-828.

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Footnote 10

Cilloniz, C., S. Ewig, E. Polverino, M. A. Marcos, C. Esquinas, A. Gabarrus, J. Mensa, and A. Torres. 2011. Microbial aetiology of community-acquired pneumonia and its relation to severity. Thorax. 66:340-346.

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Footnote 11

Valade, S., L. Biard, V. Lemiale, L. Argaud, F. Pene, L. Papazian, F. Bruneel, A. Seguin, A. Kouatchet, J. Oziel, S. Rouleau, N. Bele, K. Razazi, O. Lesieur, F. Boissier, B. Megarbane, N. Bige, N. Brule, A. S. Moreau, A. Lautrette, O. Peyrony, P. Perez, J. Mayaux, and E. Azoulay. 2018. Severe atypical pneumonia in critically ill patients: a retrospective multicenter study. Ann. Intensive Care. 8:81-018-0429-z.

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Footnote 12

Kuo, C. C., A. Shor, L. A. Campbell, H. Fukushi, D. L. Patton, and J. T. Grayston. 1993. Demonstration of Chlamydia pneumoniae in atherosclerotic lesions of coronary arteries. J. Infect. Dis. 167:841-849.

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Footnote 13

El Yazouli, L., A. Criscuolo, H. Hejaji, M. Bouazza, N. Elmdaghri, A. Aroussi Alami, A. Amraoui, N. Dakka, and F. Radouani. 2017. Molecular characterisation of Chlamydia pneumoniae associated to atherosclerosis. Pathog. Dis. 75:10.1093/femspd/ftx039.

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Footnote 14

Ngeh, J., and S. Gupta. 2005. Chlamydia pneumoniae and Atherosclerosis - an Overview of the Association, p. 113. H. Friedman, Y. Yamamoto, and M. Bendinelli (eds.), Chlamydia pneumoniae Infection and Disease. Springer.

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Footnote 15

Thibault, P. K. 2018. Neck vein obstruction: Diagnosis and the role of chronic persistent Chlamydophila pneumoniae infection. Phlebology. 268355518804379.

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Footnote 16

Webley, W. C., and D. L. Hahn. 2017. Infection-mediated asthma: etiology, mechanisms and treatment options, with focus on Chlamydia pneumoniae and macrolides. Respir. Res. 18:98-017-0584-z.

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Footnote 17

Hahn, D. 2005. Role of Chlamydia pneumoniae as an Inducer of Asthma, p. 239. H. Friedman, Y. Yamamoto, and M. Bendinelli (eds.), Chlamydia pneumoniae Infection and Disease. Springer.

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Footnote 18

Cheong, H. C., C. Y. Q. Lee, Y. Y. Cheok, G. M. Y. Tan, C. Y. Looi, and W. F. Wong. 2019. Chlamydiaceae: Diseases in primary hosts and zoonosis. Microorganisms. 7.

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Footnote 19

Balin, B. J., C. J. Hammond, C. S. Little, S. T. Hingley, Z. Al-Atrache, D. M. Appelt, J. A. Whittum-Hudson, and A. P. Hudson. 2018. Chlamydia pneumoniae: An Etiologic Agent for Late-Onset Dementia. Front. Aging Neurosci. 10:302.

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Footnote 20

Ma, J., D. Johnson, and V. Gainers-Hasugluw. 2018. Association of Chlamydophila pneumoniae Infection With Symptomatic Erosive Osteoarthritis of the Hand. J. Clin. Rheumatol. 24:275-277.

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Footnote 21

Whittum-Hudson, J. A., H. R. Schumacher, and A. P. Hudson. 2005. Chlamydia pneumoniae and Inflammatory Arthritis, p. 227. H. Friedman, Y. Yamamoto, and M. Bendinelli (eds.), Chlamydia pneumoniae Infection and Disease. Springer.

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Footnote 22

Stratton, C. W., and S. Sriram. 2005. Chlamydia pneumoniae as a Candidate Pathogen in Multiple Sclerosis, p. 199. H. Friedman, Y. Yamamoto, and M. Bendinelli (eds.), Chlamydia pneumoniae Infection and Disease. Springer.

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Footnote 23

De Luigi, G., L. Zgraggen, L. Kottanattu, G. D. Simonetti, L. Terraneo, F. Vanoni, I. Terrani, M. G. Bianchetti, S. A. G. Lava, and G. P. Milani. 2020. Skin and Mucous Membrane Eruptions Associated with Chlamydophila Pneumoniae Respiratory Infections: Literature Review. Dermatology. 237:230-235.

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Footnote 24

Di Pietro, M., S. Filardo, F. De Santis, and R. Sessa. 2013. Chlamydia pneumoniae Infection in Atherosclerotic Lesion Development through Oxidative Stress: A Brief Overview. International Journal of Molecular Sciences. 14:15120.

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Footnote 25

Honarmand, H. 2013. Atherosclerosis Induced by Chlamydophila pneumoniae: A Controversial Theory. Interdisciplinary Perspectives on Infectious Diseases. 2013:941392.

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Footnote 26

Calmes, D., P. Huynen, V. Paulus, M. Henket, F. Guissard, C. Moermans, R. Louis, and F. Schleich. 2021. Chronic infection with Chlamydia pneumoniae in asthma: a type-2 low infection related phenotype. Respiratory Research. 22:72.

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Footnote 27

Chacko, A., A. Delbaz, H. Walkden, S. Basu, C. W. Armitage, T. Eindorf, L. K. Trim, E. Miller, N. P. West, J. A. St John, K. W. Beagley, and J. A. K. Ekberg. 2022. Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer's disease risk. Sci. Rep. 12:2759-9.

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Footnote 28

Jackson, M., N. White, P. Giffard, and P. Timms. 1999. Epizootiology of Chlamydia infections in two free-range koala populations. Vet. Microbiol. 65:255-264.

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Footnote 29

Jain, S., D. J. Williams, S. R. Arnold, K. Ampofo, A. M. Bramley, C. Reed, C. Stockmann, E. J. Anderson, C. G. Grijalva, W. H. Self, Y. Zhu, A. Patel, W. Hymas, J. D. Chappell, R. A. Kaufman, J. H. Kan, D. Dansie, N. Lenny, D. R. Hillyard, L. M. Haynes, M. Levine, S. Lindstrom, J. M. Winchell, J. M. Katz, D. Erdman, E. Schneider, L. A. Hicks, R. G. Wunderink, K. M. Edwards, A. T. Pavia, J. A. McCullers, L. Finelli, and CDC EPIC Study Team. 2015. Community-acquired pneumonia requiring hospitalization among U.S. children. N. Engl. J. Med. 372:835-845.

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Footnote 30

Head, B. M., A. Trajtman, Z. V. Rueda, L. Vé lez, and Y. Keynan. 2017. Atypical bacterial pneumonia in the HIV-infected population. Pneumonia (Nathan). 9:12-017-0036-z. eCollection 2017.

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Footnote 31

Miyashita, N., K. Ouchi, H. Shoji, Y. Obase, M. Fukuda, K. Yoshida, Y. Niki, and M. Oka. 2005. Outbreak of Chlamydophila pneumoniae infection in long-term care facilities and an affiliated hospital. J. Med. Microbiol. 54:1243-1247.

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Footnote 32

Conklin, L., J. Adjemian, J. Loo, S. Mandal, C. Davis, S. Parks, T. Parsons, B. McDonough, J. Partida, K. Thurman, M. H. Diaz, A. Benitez, T. Pondo, C. G. Whitney, J. M. Winchell, N. Kendig, and C. Van Beneden. 2013. Investigation of a Chlamydia pneumoniae outbreak in a Federal correctional facility in Texas. Clin. Infect. Dis. 57:639-647.

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Footnote 33

Clemmons, N. S., N. N. Jordan, A. D. Brown, E. M. Kough, L. A. Pacha, S. M. Varner, A. W. Hawksworth, C. A. Myers, and J. C. Gaydos. 2019. Outbreak of Chlamydia pneumoniae Infections and X-ray-Confirmed Pneumonia in Army Trainees at Fort Leonard Wood, Missouri, 2014. Mil. Med.

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Footnote 34

Kutlin, A., P. M. Roblin, S. Kumar, S. Kohlhoff, T. Bodetti, P. Timms, and M. R. Hammerschlag. 2007. Molecular characterization of Chlamydophila pneumoniae isolates from Western barred bandicoots. J. Med. Microbiol. 56:407-417.

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Footnote 35

Burnard, D., and A. Polkinghorne. 2016. Chlamydial infections in wildlife-conservation threats and/or reservoirs of 'spill-over' infections? Vet. Microbiol. 196:78-84.

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Footnote 36

Frutos, M. C., M. S. Monetti, J. Mosmann, A. X. Kiguen, F. R. Venezuela, V. E. Re, and C. G. Cuffini. 2016. Molecular characterization of Chlamydia pneumoniae in animals and humans from Argentina: Genetic characterization of Chlamydia pneumoniae. Infect. Genet. Evol. 44:43-45.

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Footnote 37

Fong, I. W., B. Chiu, E. Viira, M. W. Fong, D. Jang, and J. Mahony. 1997. Rabbit model for Chlamydia pneumoniae infection. J. Clin. Microbiol. 35:48-52.

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Footnote 38

Kuo, C. C., H. H. Chen, S. P. Wang, and J. T. Grayston. 1986. Identification of a new group of Chlamydia psittaci strains called TWAR. J. Clin. Microbiol. 24:1034-1037.

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Footnote 39

Fratzke, A., L. L. Howard, M. E. Tocidlowski, A. Armién, F. Oliveira, B. Ritchie, E. Berlin, and E. Snook. 2019. Chlamydia pneumoniae Polioencephalomyelitis and Ganglionitis in Captive Houston Toads (Anaxyrus houstonensis). Vet. Pathol. 56:789-793.

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Footnote 40

Marangoni, A., V. Sambri, M. Donati, K. Di Leo, and R. Cevenini. 2005. Development of a hamster model of Chlamydophila pneumoniae infection. Vet. Res. Commun. 29 Suppl 1:61-70.

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Footnote 41

Falsey, A. R., and E. E. Walsh. 1993. Transmission of Chlamydia pneumoniae. J. Infect. Dis. 168:493-496.

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Footnote 42

US Department of Health & Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institutes of Health. 2009. Agent Summary Statements - Chlamydia psittaci (Chlamydophila psittaci), C. trachomatis, C. pneumoniae (Chlamydophila pneumoniae), p. 131. L. C. Chosewood and D. E. Wilson (eds.), Biosafety in Microbiological and Biomedical Laboratories, 5th ed.,. HHS Publication No. (CDC) 21-1112.

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Footnote 43

Gnarpe, J., H. Gnarpe, and B. Sundelof. 1991. Endemic prevalence of Chlamydia pneumoniae in subjectively healthy persons. Scand. J. Infect. Dis. 23:387-388.

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Footnote 44

Cochrane, M., P. Walker, H. Gibbs, and P. Timms. 2005. Multiple genotypes of Chlamydia pneumoniae identified in human carotid plaque. Microbiology (Reading) 151:2285-2290.

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Footnote 45

Mercuro, N. J., and M. P. Veve. 2020. Clinical Utility of Lefamulin: If Not Now, When? Curr. Infect. Dis. Rep. 22:25.

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Footnote 46

Hammerschlag, M. R. 2005. Antibiotic Susceptibility and Treatment of Chlamydia pneumoniae Infections, p. 45. H. Friedman, Y. Yamamoto, and M. Bendinelli (eds.), Chlamydia pneumoniae Infection and Disease. Springer.

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Footnote 47

Kutlin, A., S. Kohlhoff, P. Roblin, M. R. Hammerschlag, and P. Riska. 2005. Emergence of Resistance to Rifampin and Rifalazil in Chlamydophila pneumoniae and Chlamydia trachomatis. Antimicrobial Agents and Chemotherapy 49:903-907.

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Footnote 48

Rupp, J., A. Gebert, W. Solbach, and M. Maass. 2005. Serine-to-asparagine substitution in the GyrA gene leads to quinolone resistance in moxifloxacin-exposed Chlamydia pneumoniae. Antimicrob Agents Chemother 49:406-7.

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Footnote 49

Bellmann-Weiler, R., V. Maass, R. Arnitz, G. Weiss, M. Maass, and M. 2. Nagl. 2018. The endogenous antiseptic N-chlorotaurine irreversibly inactivates Chlamydia pneumoniae and Chlamydia trachomatis. Journal of Medical Microbiology,. 67:1410-1415.

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Footnote 50

Coulon, C., M. Eterpi, G. Greub, A. Collignon, G. McDonnell, and V. Thomas. 2012. Amoebal host range, host-free survival and disinfection susceptibility of environmental Chlamydiae as compared to Chlamydia trachomatis. FEMS Immunol. Med. Microbiol. 64:364-373.

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Molestina, R. E., D. Dean, R. D. Miller, J. A. Ramirez, and J. T. Summersgill. 1998. Characterization of a strain of Chlamydia pneumoniae isolated from a coronary atheroma by analysis of the omp1 gene and biological activity in human endothelial cells. Infect. Immun. 66:1370-1376.

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Footnote 52

Yaraei, K., L. A. Campbell, X. Zhu, W. C. Liles, C. Kuo, and M. E. Rosenfeld. 2005. Effect of Chlamydia pneumoniae on cellular ATP content in mouse macrophages: role of Toll-like receptor 2. Infect. Immun. 73:4323-4326.

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Footnote 53

Matsuo, J., M. Kobayashi, S. Nakamura, Y. Mizutani, T. Yao, I. Hirai, Y. Yamamoto, and H. Yamaguchi. 2010. Stability of Chlamydophila pneumoniae in a harsh environment without a requirement for acanthamoebae. Microbiol. Immunol. 54:63-73.

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Footnote 54

Hammerschlag, M. R., S. A. Kohlhoff, and C. A. Gaydos. 2015. Chlamydia pneumoniae. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 2174-2182.e2.

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Footnote 55

Babady, N. E., M. R. England, K. L. Jurcic Smith, T. He, D. S. Wijetunge, Y. W. Tang, R. R. Chamberland, M. Menegus, E. M. Swierkosz, R. C. Jerris, and W. Greene. 2018. Multicenter Evaluation of the ePlex Respiratory Pathogen Panel for the Detection of Viral and Bacterial Respiratory Tract Pathogens in Nasopharyngeal Swabs. J. Clin. Microbiol. 56:10.1128/JCM.01658-17. Print 2018 Feb.

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Footnote 56

Stivala, A., C. Genovese, C. Bonaccorso, V. Di Salvatore, G. Petronio Petronio, A. Garozzo, and M. Salmeri. 2020. Comparison of Cell Culture with Three Conventional Polymerase Chain Reactions for Detecting Chlamydophila pneumoniae in Adult's Pharyngotonsillitis. Curr. Microbiol. 77:2841-2846.

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Footnote 57

Hyman, C. L., M. H. Augenbraun, P. M. Roblin, J. Schachter, and M. R. Hammerschlag. 1991. Asymptomatic respiratory tract infection with Chlamydia pneumoniae TWAR. J. Clin. Microbiol. 29:2082-2083.

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Footnote 58

Surcel, H. M., H. Syrjälä, M. Leinonen, P. Saikku, and E. Herva. 1993. Cell-mediated immunity to Chlamydia pneumoniae measured as lymphocyte blast transformation in vitro. Infect. Immun. 61:2196-2199.

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Footnote 59

Tuuminen, T., K. Salo, and H. Surcel. 2002. A Casuistic Immunologic Response in Primary and Repeated Chlamydophila pneumoniae Infections in an Immunocompetent Individual. J. Infect. 45:202-206.

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Footnote 60

Government of Canada. Jan 2019. ePATHogen - Risk Group Database. Feb 2019:.

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Footnote 61

Public Health Agency of Canada. 2018. Human Pathogens and Toxins Act (HPTA) (S.C. 2009, c.24).

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