Volume 15, Number 1—January 2009
Evidence of Maternal–Fetal Transmission of Parachlamydia acanthamoebae
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|EID||Baud D, Goy G, Gerber S, Vial Y, Hohlfeld P, Greub G, et al. Evidence of Maternal–Fetal Transmission of Parachlamydia acanthamoebae. Emerg Infect Dis. 2009;15(1):120-121. https://dx.doi.org/10.3201/eid1501.080911|
|AMA||Baud D, Goy G, Gerber S, et al. Evidence of Maternal–Fetal Transmission of Parachlamydia acanthamoebae. Emerging Infectious Diseases. 2009;15(1):120-121. doi:10.3201/eid1501.080911.|
|APA||Baud, D., Goy, G., Gerber, S., Vial, Y., Hohlfeld, P., & Greub, G. (2009). Evidence of Maternal–Fetal Transmission of Parachlamydia acanthamoebae. Emerging Infectious Diseases, 15(1), 120-121. https://dx.doi.org/10.3201/eid1501.080911.|
To the Editor: Parachlamydia acanthamoebae is a recently identified agent of pneumonia (1–3) and has been linked to adverse pregnancy outcomes, including human miscarriage and bovine abortion (4,5). Parachlamydial sequences have also been detected in human cervical smears (4) and in guinea pig inclusion conjunctivitis (6). We present direct evidence of maternal–fetal transmission of P. acanthamoebae.
We tested 78 amniotic fluid samples from patients who delivered prematurely (defined as spontaneous delivery before 37 weeks of gestation) at the Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland, from 2003 to 2006. DNA was extracted by using the QIAampDNA Mini kit (QIAGEN, Hilden, Germany) and was tested by using a specific Parachlamydia real-time PCR (7). One positive sample (threshold cycle of 34.2) was confirmed by using the 16SigF-Rp2Chlam PCR, which targets a large DNA segment of the 16S rRNA gene (8). Because these 2 PCRs target different DNA segments, the positive PCR results were not due to PCR contamination with amplicons. The sequence exhibited 99.6% similarity with P. acanthamoebae strain Hall’s coccus (1) (GenBank accession no. AF366365).
The sample was obtained from a 29-year-old woman during her second pregnancy, at 16 weeks of gestation. Amniocentesis was performed because a first-trimester test suggested a Down syndrome risk of 1/100. At the time of amniocentesis, the patient had cough and flu-like symptoms of 3 weeks’ duration, which resolved spontaneously in a few weeks. Cytogenetic analysis showed a normal 46XX karyotype; amniotic fluid culture remained sterile. The pregnancy ended prematurely at 35 weeks and 6 days with the vaginal delivery of a 2,060-g newborn (<5th percentile). The mother and child had an uneventful hospital course.
The role of Parachlamydia as the etiologic agent of premature labor and intrauterine growth retardation is likely because 1) all vaginal, placental, and urinary cultures were negative; 2) results of routine serologic tests were negative; and 3) only Parachlamydia was detected in the amniotic fluid. Intrauterine infection caused by Parachlamydia spp. may be chronic and asymptomatic until adverse pregnancy outcomes occur (4).
The infection of this pregnant woman might have occurred through zoonotic contact through her work as a butcher in a rural area known for cattle breeding. Of interest, a recent study of 482 healthy Swiss men found 3 who were seropositive for Parachlamydia sp., and all 3 came from the same rural area near Lausanne (within <20-km radius) (9). Moreover, the patient owns 2 guinea pigs, potential vectors of the bacterium (6). Other modes of transmission are possible, e.g., contaminated water (free-living amebae may serve as hosts for Parachlamydia spp. and are widespread in water networks) and ingestion of undercooked meat or contaminated cow milk.
A plausible pathogenic scenario for this case of possible maternal–fetal transmission of P. acanthamoebae might include bacteremia in the context of a lung infection. This could have resulted in intrauterine infection and intrauterine growth restriction.
We warmly thank Gabrielle Gerelle and Philip Tarr for reviewing the manuscript and Sandrine Gremlich-Irrausch and Françoise Damnon for technical help.
Research performed at the Center for Research on Intracellular Bacteria is mainly supported by grants from the Swiss National Science Foundation (no. FN3200B0-116445), the Faculty of Biology and Medicine of the University of Lausanne (Prix FBM 2006), and Coopération Européenne dans le Domaine de la Recherche Scientifique et Technique action 855. G.G. is supported by the Leenards Foundation through a career award entitled “Bourse Leenards pour la relève académique en médecine clinique à Lausanne.” This study was approved by the ethics committee of the University of Lausanne.
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Please use the form below to submit correspondence to the authors or contact them at the following address:
Gilbert Greub, Center for Research on Intracellular Bacteria, Institute of Microbiology, University Hospital Center and University of Lausanne, Bugnon 48, 1011 Lausanne, Switzerland;
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