Chlamydia muridarum

{{Short description|Species of bacterium}}

{{Speciesbox

| taxon = Chlamydia muridarum

| authority = Everett et al., 1999{{cite journal|last1=Everett|first1=K. D. E.|last2=Bush|first2=R. M.|last3=Andersen|first3=A. A.|title=Emended description of the order Chlamydiales, proposal of Parachlamydiaceae fam. nov. and Simkaniaceae fam. nov., each containing one monotypic genus, revised taxonomy of the family Chlamydiaceae, including a new genus and five new species, and standards for the identification of organisms|journal=International Journal of Systematic Bacteriology|volume=49|issue=2|year=1999|pages=415–440|issn=0020-7713|doi=10.1099/00207713-49-2-415|pmid=10319462|doi-access=free}}

}}

Chlamydia muridarum is an intracellular bacterial species that at one time belonged to Chlamydia trachomatis. However, C. trachomatis naturally only infects humans and C. muridarum naturally infects only members of the family Muridae (includes both mice and hamsters, Alderton, 1996).

Two strains of Chlamydia muridarum, MoPn (originally named Nigg) and SFPD,{{Cite journal | last1 = Zhang | first1 = YX. | last2 = Fox | first2 = JG. | last3 = Ho | first3 = Y. | last4 = Zhang | first4 = L. | last5 = Stills | first5 = HF. | last6 = Smith | first6 = TF. | title = Comparison of the major outer-membrane protein (MOMP) gene of mouse pneumonitis (MoPn) and hamster SFPD strains of Chlamydia trachomatis with other Chlamydia strains. | journal = Mol Biol Evol | volume = 10 | issue = 6 | pages = 1327–42 |date=Nov 1993 | doi = 10.1093/oxfordjournals.molbev.a040079| pmid = 8277858 | doi-access = free }}

have been isolated from mice and hamsters. Glycogen production by both strains has been demonstrated. The chromosome and extrachromosomal plasmid of MoPn have been sequenced.

Chlamydia muridarum MoPn binds mAbs recognizing Chlamydia trachomatis MOMP vs4 core epitope (T) LNPT (IA).{{Cite journal | last1 = Peterson | first1 = EM. | last2 = Cheng | first2 = X. | last3 = Markoff | first3 = BA. | last4 = Fielder | first4 = TJ. | last5 = de la Maza | first5 = LM. | title = Functional and structural mapping of Chlamydia trachomatis species-specific major outer membrane protein epitopes by use of neutralizing monoclonal antibodies. | journal = Infect Immun | volume = 59 | issue = 11 | pages = 4147–53 |date=Nov 1991 | doi = 10.1128/IAI.59.11.4147-4153.1991| pmid = 1718870 | pmc=259009}}

DNA sequence analysis indicates that these mAbs should recognize SFPD and that Chlamydia trachomatis B-serogroup mAbs specific for the vs4 epitope IAGAG should recognize SFPD.{{Cite journal | last1 = Batteiger | first1 = BE. | last2 = Lin | first2 = PM. | last3 = Jones | first3 = RB. | last4 = Van Der Pol | first4 = BJ. | title = Species-, serogroup-, and serovar-specific epitopes are juxtaposed in variable sequence region 4 of the major outer membrane proteins of some Chlamydia trachomatis serovars. | journal = Infect Immun | volume = 64 | issue = 7 | pages = 2839–41 |date=Jul 1996 | doi = 10.1128/IAI.64.7.2839-2841.1996| pmid = 8698520 | pmc=174151}} MoPn was isolated in 1942 from the lungs of asymptomatic albino Swiss mice and was subsequently shown to be capable of producing disease in mice.{{Cite journal | last1 = Nigg | first1 = C. | title = An Unidentified Virus Which Produces Pneumonia and Systemic Infection in Mice | journal = Science | volume = 95 | issue = 2454 | pages = 49–50 |date=Jan 1942 | doi = 10.1126/science.95.2454.49-a | pmid = 17773453 | bibcode = 1942Sci....95...49N | s2cid = 34446808 }} SFPD was obtained from a hamster, concurrent with a causative agent of proliferative ileitis. MoPn has been shown to be sensitive to sulfadiazine. In contrast to Chlamydia trachomatis, Chlamydia muridarum lacks a tryptophan operon.{{Cite journal|last1=Farris|first1=Christina M.|last2=Morrison|first2=Richard P.|date=Mar 2011|editor-last=Andrews-Polymenis|editor-first=H. L.|title=Vaccination against Chlamydia Genital Infection Utilizing the Murine C. muridarum Model|journal=Infection and Immunity|language=en|volume=79|issue=3|pages=986–996|doi=10.1128/IAI.00881-10|pmid=21078844|issn=0019-9567|pmc=3067520}} Due to this, Chlamydia muridarum responds to interferon gamma (IFN-γ) differently than Chlamydia trachomatis, which effects the degree to which the two different Chlamydia strains are inhibited in infected mice and humans, respectively.{{Cite journal|last1=Farris|first1=Christina M.|last2=Morrison|first2=Richard P.|date=Mar 2011|editor-last=Andrews-Polymenis|editor-first=H. L.|title=Vaccination against Chlamydia Genital Infection Utilizing the Murine C. muridarum Model|journal=Infection and Immunity|language=en|volume=79|issue=3|pages=986–996|doi=10.1128/IAI.00881-10|pmid=21078844|issn=0019-9567|pmc=3067520}}{{Cite book|url=https://linkinghub.elsevier.com/retrieve/pii/C20101677449|title=Molecular Medical Microbiology|date=2015|publisher=Elsevier|isbn=9780123971692|language=en|doi=10.1016/c2010-1-67744-9}}