Skip directly to search Skip directly to A to Z list Skip directly to page options Skip directly to site content

Volume 20, Number 6—June 2014

CME ACTIVITY - Synopsis

Adverse Pregnancy Outcomes and Coxiella burnetii Antibodies in Pregnant Women, Denmark

Stine Yde NielsenComments to Author , Kåre Mølbak, Tine Brink Henriksen, Karen Angeliki Krogfelt, Carsten Schade Larsen, and Steen Villumsen
Author affiliations: Aarhus University Hospital, Aarhus, Denmark (S.Y. Nielsen, T.B. Henriksen, C.S. Larsen); Statens Serum Institut, Copenhagen, Denmark (K. Mølbak, K.A. Krogfelt, S. Villumsen)

Cite This Article

Close

Highlight and copy the desired format.

EID Nielsen S, Mølbak K, Henriksen T, Krogfelt K, Larsen C, Villumsen S, et al. Adverse Pregnancy Outcomes and Coxiella burnetii Antibodies in Pregnant Women, Denmark. Emerg Infect Dis. 2014;20(6):925-931. https://dx.doi.org/10.3201/eid2006.130584
AMA Nielsen S, Mølbak K, Henriksen T, et al. Adverse Pregnancy Outcomes and Coxiella burnetii Antibodies in Pregnant Women, Denmark. Emerging Infectious Diseases. 2014;20(6):925-931. doi:10.3201/eid2006.130584.
APA Nielsen, S., Mølbak, K., Henriksen, T., Krogfelt, K., Larsen, C., & Villumsen, S. (2014). Adverse Pregnancy Outcomes and Coxiella burnetii Antibodies in Pregnant Women, Denmark. Emerging Infectious Diseases, 20(6), 925-931. https://dx.doi.org/10.3201/eid2006.130584.

Introduction

CME Logo

Medscape, LLC is pleased to provide online continuing medical education (CME) for this journal article, allowing clinicians the opportunity to earn CME credit.

This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of Medscape, LLC and Emerging Infectious Diseases. Medscape, LLC is accredited by the ACCME to provide continuing medical education for physicians.

Medscape, LLC designates this Journal-based CME activity for a maximum of 1 AMA PRA Category 1 Credit(s)TM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

All other clinicians completing this activity will be issued a certificate of participation. To participate in this journal CME activity: (1) review the learning objectives and author disclosures; (2) study the education content; (3) take the post-test with a 70% minimum passing score and complete the evaluation at www.medscape.org/journal/eid; (4) view/print certificate.

Release date: May 14, 2014; Expiration date: May 14, 2015

Learning Objectives

Upon completion of this activity, participants will be able to:

• Describe adverse outcomes of pregnancies with positive or increasing titers against C. burnetii, based on a case series from Denmark

• Distinguish the causal association between adverse pregnancy outcomes and C. burnetii infection

• Assess the overall risk for a Q fever–associated adverse pregnancy outcome.

CME Editor

Shannon O’Connor, ELS, Technical Writer/Editor, Emerging Infectious Diseases. Disclosure: Shannon O’Connor has disclosed no relevant financial relationships.

CME Author

Laurie Barclay, MD, freelance writer and reviewer, Medscape, LLC. Disclosure: Laurie Barclay, MD, has disclosed no relevant financial relationships.

Authors

Disclosures: Stine Yde Nielsen, MD, PhD; Kåre Mølbak, MD, DMSc; Tine Brink Henriksen, PhD; and Karen Angeliki Krogfelt, PhD, have disclosed no relevant financial relationships. Carsten Schade Larsen, DMSc, has disclosed the following relevant financial relationships: served as a speaker or a member of a speakers bureau for GlaxoSmithKline, Gilead; received grants for clinical research from CSL Behring. Steen Villumsen, MD, PhD, has disclosed the following relevant financial relationships: served as an advisor or consultant for and received grants for clinical research from Statens Serum Institut.

Abstract

A high risk for obstetric complications has been reported among women infected with Coxiella burnetii, the causative agent of Q fever, but recent studies have failed to confirm these findings. We reviewed national data collected in Denmark during 2007–2011 and found 19 pregnancies in 12 women during which the mother had a positive or equivocal test for antibodies to C. burnetii (IgM phase I and II titers >64, IgG phase I and II titers >128). Of these 12 women, 4 experienced obstetric complications (miscarriage, preterm delivery, infant small for gestational age, oligohydramnion, fetal growth restriction, or perinatal death); these complications occurred in 9 pregnancies (47% of the 19 total pregnancies identified). Our findings suggest an association between Q fever and adverse pregnancy outcomes, but complications were identified in only 9 pregnancies during the study’s 5-year period, indicating that the overall risk is low.

Q fever is a zoonotic infection caused by Coxiella burnetii. Findings of adverse pregnancy outcome in infected women, high seroprevalence in animal studies, and large human outbreaks have placed increasing focus on Q fever in several European countries, including Denmark (14). In ruminants, infection with C. burnetii is associated with high numbers of bacteria in the placenta, and the infection is known to cause abortion, retained placenta, endometritis, and infertility (5,6). Humans are infected with C. burnetii predominantly by inhalation of contaminated aerosols, and persons who have contact with livestock are at highest risk for exposure (7). Among pregnant women, >90% of those who show antibodies for C. burnetii that suggest recent infection may remain asymptomatic (8). Case series from France have associated symptomatic and asymptomatic C. burnetii infection during pregnancy with obstetric complications, including miscarriage, preterm delivery, and fetal death (911). In contrast, population studies from northern Europe have not found an association between C. burnetii and adverse pregnancy outcomes (1215).

Cattle are the main reservoir for C. burnetii in Denmark. A recent study of the seroprevalence of C. burnetii in cattle found that bulk-tank milk samples tested positive for C. burnetii at 59 of 100 randomly selected farms (16). In addition, the reported prevalence of antibodies to C. burnetii among veterinarians in Denmark ranges from 36% to 47% (1,2,17). These findings show that exposure to C. burnetii is common in this country in the animal reservoir and in those who are occupationally exposed to livestock or who live in rural areas with livestock contact. However, the risk for and implications of infection with C. burnetii among pregnant women have not been exhaustively described (12,15). Because of this, and because findings from the case series in France conflict with results from population-based studies from the Netherlands and Denmark, we reviewed national data from Aarhus University Hospital, Aalborg University Hospital, Hospital of Southwest Jutland, Viborg Regional Hospital, Regional Hospital West Jutland, and Hilleroed Hospital in Denmark to identify women who had elevated antibodies to C. burnetii during pregnancy. We evaluated the course of infection, effects of treatment with cotrimoxazole (trimethoprim-sulfamethoxazole), and pregnancy outcomes for these women.

Materials and Methods

Every resident in Denmark is provided with a unique civil registration number that enables individual-level linkage between national registries. Data from health records at obstetric and infectious disease departments were thereby linked to civil registration numbers from women (18–45 years of age) who had positive or equivocal tests at the Statens Serum Institut for antibodies to C. burnetii during 2007–2011. Using these data, we identified pregnant women who could be included in the study on the basis of positive serologic test results for C. burnetii and availability of titers from throughout pregnancy to enable evaluation of infection in paired samples.

Detection of Antibodies against C. burnetii

In Denmark, C. burnetii serologic testing is performed only at the Statens Serum Institut by indirect immunofluorescence assay (IFA; Focus Diagnostics, Cypress, CA, USA), according to the manufacturer’s instructions. C. burnetii expresses 2 antigens, phase I and phase II. During active infection, phase II IgG and IgM are elevated; these results may remain positive for months to years. In acute Q fever, primarily antibodies against phase II antigens are raised, and these titers are higher than for antibodies against phase I antigens; IgM antibodies appear first. In chronic forms of the disease, antibodies against phase I antigens are elevated.

A local cutoff value adjusted to the population of Denmark has defined negative, equivocal, and positive titers (18); we included patients with equivocal and positive titers in our study. A sample was considered IFA-positive when IgM for phase I or phase II titers was >64 or IgG for any of the phases was >128. A 4-fold increase in titers between 2 paired samples was defined as diagnostic for recent or acute C. burnetii infection.

PCR Analysis

DNA from urine samples was subjected to a Chelex 100-based DNA extraction method as described (19). DNA from placenta and bone marrow samples was extracted by using the DNeasy Blood and Tissue Kit (QIAGEN, Hilden, Germany) according to the manufacturer’s instructions. DNA from the cream layer of fresh breast milk samples was extracted by using a previously described protocol that included washing with phosphate-buffered saline and subsequent extraction with the DNeasy Blood and Tissue Kit (20). PCR was conducted with primers targeting the multicopy gene IS1111 as described (21).

Testing Indications and Pregnancy Outcomes

The indication for Q fever testing for most of the women was exposure to livestock. Two of the women were tested in a subsequent pregnancy because of a previous adverse pregnancy outcome; none were tested because of symptoms. Adverse pregnancy outcomes were defined as miscarriage, preterm delivery, single fetal death with a surviving co-twin, infant small for gestational age, oligohydramnion, fetal growth restriction, and perinatal death.

Results

We identified 12 women with equivocal and positive antibody titers for C. burnetii infection who underwent 19 pregnancies during the 5-year study period. All women were farmers or veterinarians and resided in rural areas of Denmark. Obstetric complications were recorded in 9 (47%) of the 19 pregnancies (Table 1). None of the women were found to be IgM positive for pathogens regarded as classic causes of infection of the developing fetus during pregnancy; these pathogens included Toxoplasma gondii, parvovirus B19, rubella virus, cytomegalovirus, and herpes simplex virus. However, not all women were exhaustively tested during pregnancy. For all women tested during pregnancy, C. burnetii serologic test results were available from no later than pregnancy week 13 (Table 2).

Two patients (1 and 10) reported dry cough and short episodes of fever; both had antibody titers during the first trimester consistent with acute infection. These patients were treated with cotrimoxazole beginning in gestational week 15 or 10, respectively; patient 1 was treated throughout pregnancy and patient 10 until gestational week 39. Patent 1 had a PCR-positive urine sample in gestational week 10, but results of PCR on a bone marrow biopsy from gestational week 15 and PCR on amniotic fluid and placenta were negative. For patient 10, no C. burnetii DNA was detected by PCR from placental tissue or breast milk; for her second pregnancy, serologic test results for C. burnetii were negative, PCR on placenta was not performed, and the pregnancy had a healthy outcome.

Patient 2 reported weeks of dry cough without fever during the weeks just before the first pregnancy that ended with miscarriage. She had 3 miscarriages and an extrauterine pregnancy within 2 years, and the titers that were found indicate that she was acutely infected weeks before the first miscarriage. Her antibody titers reached a maximum level after the second miscarriage. No embryo material was tested from any of her miscarriages.

Patients 3, 5, and 12 had serologic profiles with IgG phase I titer of 1,024 at the end of pregnancy; 2 of the patients were treated during pregnancy, but none had symptoms, received a diagnoses of endocarditis, or received long-term postpartum treatment. Patient 12 had a serologic profile indicating reactivation of C. burnetii infection, but her antibody titers had been negative in a previous pregnancy 2 years earlier.

Patient 4 seroconverted before her second pregnancy, during which she experienced a single fetal death around gestational week 8 and a surviving co-twin. She had a decrease in IgG phase I during pregnancy; the surviving twin was delivered healthy and at term.

Patient 5 was treated for acute Q fever before her second pregnancy. Her antibody titers were stable during the second pregnancy, and her baby was full-term but slightly small for gestational age. After a short interpregnancy interval, she had a significant increase in IgG phase II titers during her third pregnancy; because of fetal growth restriction and oligohydramnion noted during gestational week 28, she had a cesarean section during gestational week 38. The placentas from these 2 pregnancies were not tested.

Patient 8 had rising antibody titers during her first pregnancy, and because of bleeding and contractions, she had an acute cesarean section in week 27 and gave birth to a severely growth retarded and malformed infant who lived only a few hours. The fetus and placenta were not tested for C. burnetii, but results of testing for toxoplasmosis, cytomegalovirus, and parvovirus B19 were negative, as were results of genetic testing for neuromuscular diseases. Her titers decreased slightly postpartum, but during her second pregnancy, titers increased significantly, and treatment with cotrimoxazole was initiated around gestational week 22. In gestational week 30, she spontaneously went into labor and gave birth to a healthy baby. Treatment was terminated immediately postpartum, and her antibody levels decreased, indicating that she was not chronically infected. Thus, patients 5 and 8 had serologic indication of a reactivation of infection with C. burnetii: a postpartum decline in antibody titers followed by a >4-fold increase in titers during the next pregnancy.

Three of the remaining pregnancies (in patients 6, 9, and 11) had an uncomplicated course with a healthy pregnancy outcome. Patient 7 had an acute cesarean because of rupture of the uterus; she had had a cesarean in her first pregnancy.

In summary, 3 patients (1, 2, and 10) reported symptoms of acute Q fever. At least 1 (patient 8) appeared to have seroconverted without symptoms close to the beginning of her first pregnancy.

For 7 of the 19 pregnancies, treatment with cotrimoxazole was initiated in the patient; 6 of these pregnancies resulted in healthy, full-term babies, and no mention of severe side effects was found in the mothers’ medical records. One of the women who had obstetric complications received treatment with cotrimoxazole (patient 8, in her second pregnancy). By comparison, among the 12 pregnancies in which no treatment was given, 8 resulted in obstetric complications. The effect of treatment with cotrimoxazole on complications was tested, but the difference was not significant (p = 0.057 by Fisher exact test; data not shown).

PCR was performed on placentas from 10 pregnancies and in 4 of these, breast milk was also tested; no results were positive. For 7 of the 10 pregnancies in which placentas were tested, the woman had received treatment with cotrimoxazole during pregnancy.

Discussion

Adverse pregnancy outcome was observed in 9 of 19 pregnancies among 4 of the 12 pregnant women in which equivocal or positive tests for C. burnetii antibodies were found. One woman had 3 miscarriages and an extrauterine pregnancy, 1 experienced preterm delivery, 1 had a single fetal death with a surviving co-twin, and 1 delivered a small-for-gestational-age baby. Oligohydramnion and fetal growth restriction were found in 2 pregnancies; 1 had a healthy outcome, but in the other, the baby died a few hours postpartum.

The observed complication rate of 47% may seem high, but the causal relationship of this finding may not be clear. For example, none of the tested placentas were examined by histopathology, and all of the 10 placentas tested by PCR were negative for C. burnetii. Furthermore, not all of the women were thoroughly tested for other infections. One possible explanation for the lack of findings related to the placenta in 7 of the cases could be the patient’s treatment with cotrimoxazole or focal placental infection. Nonetheless, we did observe adverse pregnancy outcome in 8 (67%) of 12 pregnancies in which the women were not treated with cotrimoxazole, which supports the beneficial effects of treatment.

Among the cases we reviewed, none of the 4 breast milk samples tested by PCR were positive for C. burnetii. This bacterium has been found in human milk (22,23), but the implications for the breastfed child are unclear. Because of the lack of evidence, breastfeeding has been deemed safe according to the obstetric guidelines in Denmark for the treatment of C. burnetii–seropositive pregnant women and their newborns.

Two studies, in the Netherlands (24) and Canada (25), have suggested a low rate of placental C. burnetii infection in asymptomatic women and that obstetric complications in symptomatic cases may be explained by massive placental necrosis following a higher bacterial load in the placenta, systemic infection, or both. A study in France (26) found that untreated Q fever in 1 pregnancy may be reactivated in a subsequent pregnancy, a result found in 3 patients in our study (patients 5, 8, and 12).

The evidence for an adverse pregnancy outcome in humans in relation to Q fever mainly originates from case studies from France of referred, infected, pregnant patients, as well as pregnancies in which a diagnosis of Q fever was reached retrospectively, after an adverse outcome (911). Carcopino et al. reported clinical symptoms in 32 (60.4%) of 53 cases and a chronic serologic profile in more than half of patients and concluded that Q fever in pregnancy may cause severe complications (10). The Netherlands has recently experienced an unprecedented Q fever outbreak that has prompted 2 large studies in pregnant women. One study, a population-based study of 1,174 serum samples collected at the twelfth week of pregnancy, found no association between antibodies to C. burnetii and adverse pregnancy outcome among women living in the area with the highest Q fever incidence. The other study, a randomized, controlled trial, tested 1,229 pregnant women living in high-risk areas during the outbreak; 15% of the women were seropositive in both the intervention group and the control group, and no difference was found in obstetric complications (13). Hence, the findings from France were not reproduced in the Netherlands. Likewise, a recent study in Denmark assessed the association between presence of antibodies to C. burnetii, seroconversion, and pregnancy outcome and found that seropositivity was not associated with miscarriage, preterm birth, or low birthweight (15).

Differences in findings among these various studies may be explained in part by differences in study design. The indication for serologic testing is a crucial point; in our study, the indication for testing was exposure to livestock for most of the women. In contrast, the women in the case series in France were primarily tested because of pathologic conditions during pregnancy or clinical symptoms (e.g., fever, hepatitis) or retrospectively because of an adverse pregnancy outcome. Angelakis et al. (11) found that 17 of 30 C. burnetii seropositive pregnant women were asymptomatic; only 2 of these had an uncomplicated pregnancy, but no placentitis or isolation of C. burnetii was found in 14 available biopsy specimens. These authors suggested that the different rates of obstetric complications found in various geographic areas could be related to strain specificity, potentially because of differences in plasmid types.

All the women in this case series had contact with livestock in Denmark, and it is reasonable to assume that these women were occupationally exposed to endemically occurring C. burnetii infections among cattle. However, the observations by Angelakis et al. suggest that strains of C. burnetti in Denmark, and possibly cattle in general, might be less virulent than that seen when the infection is acquired from other animal reservoirs (e.g., goats). In France, goats and sheep have been the main source of C. burnetti infection. The recent outbreak in the Netherlands was detected shortly after a large number of dairy milk farms had changed from cattle to goats as production animals. In Denmark, goat and sheep farms are rare, and despite high clinical awareness during the past 7 years, no reports have described a microbiologically verified outbreak of Q fever in humans or a case of chronic Q fever that was definitely acquired in Denmark. However, a large percentage of dairy cattle in Denmark shed C. burnetii, and a high prevalence of antibodies has been found among pregnant women who had exposure to cattle (16,17). These observations could, in part, be an explanation for the discrepancies in rates of serious adverse pregnancy outcomes among studies from different countries.

In conclusion, we evaluated risks and implications in 19 pregnancies with positive or rising titers against C. burnetii from Denmark, a country that has high seroprevalence of C. burnetii but low prevalence of clinical Q fever and for which cattle are the primary bacterial reservoir. In this case series, almost half of the women had obstetric complications, which is comparable to previous case series. We found complications in 8 out of 12 untreated pregnancies; 7 pregnant women received long-term treatment with cotrimoxazole. In this study, serologic signs of Q fever were associated with adverse pregnancy outcome. However, in none of the cases could we identify a definite causal relationship between C. burnetii seropositivity and adverse pregnancy outcome. Because only 9 cases of adverse pregnancy outcome were found over 5 years, despite increased awareness among the relevant risk groups, and because community studies in Denmark and the Netherlands have failed to confirm this association, the overall risk for a Q fever–associated adverse pregnancy outcome in Denmark is likely to be low.

Dr Nielsen is a physician in the Department of Clinical Microbiology, Aarhus University Hospital, and a postdoctoral scholar at the Department of Occupational Medicine, Hospital Region West, Herning, Denmark. Her research interests include infections, obstetrics, pediatrics, and microbiology.

References

  1. Bacci S, Villumsen S, Valentiner-Branth P, Smith B, Krogfelt KA, Molbak K. Epidemiology and clinical features of human infection with Coxiella burnetii in Denmark during 2006–07. Zoonoses Public Health. 2012;59:618. DOIPubMed
  2. Bosnjak E, Hvass AM, Villumsen S, Nielsen H. Emerging evidence for Q fever in humans in Denmark: role of contact with dairy cattle. Clin Microbiol Infect. 2010;16:12858. DOIPubMed
  3. Roest HI, Tilburg JJ, van der Hoek W, Vellema P, van Zijderveld FG, Klaassen CH, The Q fever epidemic in the Netherlands: history, onset, response and reflection. Epidemiol Infect. 2011;139:112. DOIPubMed
  4. European Centre for Disease Prevention and Control. Annual epidemiological report on communicable diseases in Europe 2010 [cited 2012 Dec 4]. http://www.ecdc.europa.eu/en/publications/Publications/1011_SUR_Annual_Epidemiological_Report_on_Communicable_Diseases_in_Europe.pdf
  5. Berri M, Rousset E, Champion JL, Russo P, Rodolakis A. Goats may experience reproductive failures and shed Coxiella burnetii at two successive parturitions after a Q fever infection. Res Vet Sci. 2007;83:4752. DOIPubMed
  6. Bildfell RJ, Thomson GW, Haines DM, McEwen BJ, Smart N. Coxiella burnetii infection is associated with placentitis in cases of bovine abortion. J Vet Diagn Invest. 2000;12:41925. DOIPubMed
  7. Parker NR, Barralet JH, Bell AM. Q fever. Lancet. 2006;367:67988. DOIPubMed
  8. Tissot-Dupont H, Vaillant V, Rey S, Raoult D. Role of sex, age, previous valve lesion, and pregnancy in the clinical expression and outcome of Q fever after a large outbreak. Clin Infect Dis. 2007;44:2327. DOIPubMed
  9. Carcopino X, Raoult D, Bretelle F, Boubli L, Stein A. Q Fever during pregnancy: a cause of poor fetal and maternal outcome. Ann N Y Acad Sci. 2009;1166:7989. DOIPubMed
  10. Carcopino X, Raoult D, Bretelle F, Boubli L, Stein A. Managing Q fever during pregnancy: the benefits of long-term cotrimoxazole therapy. Clin Infect Dis. 2007;45:54855. DOIPubMed
  11. Angelakis E, Million M, D’Amato F, Rouli L, Richet H, Stein A, Q fever and pregnancy: disease, prevention, and strain specificity. Eur J Clin Microbiol Infect Dis. 2013;32:3618. DOIPubMed
  12. Nielsen SY, Hjollund NH, Andersen AM, Henriksen TB, Kantso B, Krogfelt KA, Presence of antibodies against Coxiella burnetii and risk of spontaneous abortion: a nested case-control study. PLoS ONE. 2012;7:e31909. DOIPubMed
  13. Munster JM. Effectiveness of a screening program for Q fever during pregnancy: a clustered randomised controlled trial. Presented at: European Scientific Conference on Applied Infectious Disease Epidemiology; Stockholm, Sweden; 2011 Nov 6–8.
  14. van der Hoek W, Meekelenkamp JC, Leenders AC, Wijers N, Notermans DW, Hukkelhoven CW. Antibodies against Coxiella burnetii and pregnancy outcome during the 2007–2008 Q fever outbreaks in the Netherlands. BMC Infect Dis. 2011;11:44. DOIPubMed
  15. Nielsen SY, Andersen AM, Molbak K, Hjollund NH, Kantso B, Krogfelt KA, No excess risk of adverse pregnancy outcomes among women with serological markers of previous infection with Coxiella burnetii: evidence from the Danish national birth cohort. BMC Infect Dis. 2013;13:87. DOIPubMed
  16. Agger JF, Christoffersen AB, Rattenborg E, Nielsen J, Agerholm JS. Prevalence of Coxiella burnetii antibodies in Danish dairy herds. Acta Vet Scand. 2010;52:5. DOIPubMed
  17. Nielsen SY, Molbak K, Nybo Andersen AM, Brink Henriksen T, Kantso B, Krogfelt KA, Prevalence of Coxiella burnetii in women exposed to livestock animals, Denmark, 1996 to 2002. Euro Surveill. 2013;18:20528 .PubMed
  18. Villumsen S, Jorgensen CS, Smith B, Uldum S, Schiellerup P, Krogfelt KA. Determination of new cutoff values for indirect immunofluorescence antibody test for Q fever diagnosis in Denmark. Diagn Microbiol Infect Dis. 2009;65:938. DOIPubMed
  19. Jensen JS, Bjornelius E, Dohn B, Lidbrink P. Comparison of first void urine and urogenital swab specimens for detection of Mycoplasma genitalium and Chlamydia trachomatis by polymerase chain reaction in patients attending a sexually transmitted disease clinic. Sex Transm Dis. 2004;31:499507. DOIPubMed
  20. Angen Ø, Stahl M, Agerholm JS, Christoffersen AB, Agger JF. Dynamics of relationship between the presence of Coxiella burnetii DNA, antibodies, and intrinsic variables in cow milk and bulk tank milk from Danish dairy cattle. J Dairy Sci. 2011;94:57509. DOIPubMed
  21. Koch A, Svendsen CB, Christensen JJ, Bundgaard H, Vindfeld L, Christiansen CB, Q fever in Greenland. Emerg Infect Dis. 2010;16:5113. DOIPubMed
  22. Kumar A, Yadav MP, Kakkar S. Human milk as a source of Q-fever infection in breast-fed babies. Indian J Med Res. 1981;73:5102 .PubMed
  23. Prasad BN, Chandiramani NK, Wagle A. Isolation of Coxiella burnetii from human sources. Int J Zoonoses. 1986;13:1127 .PubMed
  24. Munster JM, Leenders AC, Hamilton CJ, Hak E, Aarnoudse JG, Timmer A. Placental histopathology after Coxiella burnetii infection during pregnancy. Placenta. 2012;33:12831. DOIPubMed
  25. Langley JM, Marrie TJ, Leblanc JC, Almudevar A, Resch L, Raoult D. Coxiella burnetii seropositivity in parturient women is associated with adverse pregnancy outcomes. Am J Obstet Gynecol. 2003;189:22832. DOIPubMed
  26. Raoult D, Fenollar F, Stein A. Q fever during pregnancy: diagnosis, treatment, and follow-up. Arch Intern Med. 2002;162:7014. DOIPubMed

Tables

Follow Up

Earning CME Credit

To obtain credit, you should first read the journal article. After reading the article, you should be able to answer the following, related, multiple-choice questions. To complete the questions (with a minimum 75% passing score) and earn continuing medical education (CME) credit, please go to www.medscape.org/journal/eid. Credit cannot be obtained for tests completed on paper, although you may use the worksheet below to keep a record of your answers. You must be a registered user on Medscape.org. If you are not registered on Medscape.org, please click on the New Users: Free Registration link on the left hand side of the website to register. Only one answer is correct for each question. Once you successfully answer all post-test questions you will be able to view and/or print your certificate. For questions regarding the content of this activity, contact the accredited provider, CME@medscape.net. For technical assistance, contact CME@webmd.net. American Medical Association’s Physician’s Recognition Award (AMA PRA) credits are accepted in the US as evidence of participation in CME activities. For further information on this award, please refer to http://www.ama-assn.org/ama/pub/category/2922.html. The AMA has determined that physicians not licensed in the US who participate in this CME activity are eligible for AMA PRA Category 1 Credits™. Through agreements that the AMA has made with agencies in some countries, AMA PRA credit may be acceptable as evidence of participation in CME activities. If you are not licensed in the US, please complete the questions online, print the certificate and present it to your national medical association for review.

Article Title:
Adverse Pregnancy Outcomes and Coxiella burnetii Antibodies in Pregnant Women, Denmark

CME Questions

1. Your patient is a 28-year-old pregnant Danish woman with positive titers against Coxiella burnetii. According to the case series by Dr. Nielsen and colleagues, which of the following statements about adverse pregnancy outcomes is correct?

A. Approximately three fourths of women with positive titers against C. burnetii had obstetric complications

B. No deaths occurred in this case series

C. Oligohydramnios was not reported

D. Adverse pregnancy outcomes included miscarriage, extrauterine pregnancy, preterm delivery, and delivery of an infant small for gestational age

2. According to the case series by Dr. Nielsen and colleagues, which of the following statements about the causal association between adverse pregnancy outcomes and C. burnetii infection is correct?

A. Findings from this case series prove that C. burnetii infection causes adverse pregnancy outcomes

B. Other infections were conclusively ruled out in all the women

C. Adverse pregnancy outcome occurred in 8 of 12 pregnancies in which the women were not treated for C. burnetii infection, supporting a possible causal association

D. All placentae tested by polymerase chain reaction tested positive for C. burnetii infection

3. According to the case series by Dr. Nielsen and colleagues, which of the following statements about the overall risk for a Q fever associated adverse pregnancy outcome would most likely be correct?

A. The investigators found 9 cases of Q fever–associated adverse pregnancy outcomes in Denmark during a period of 5 years

B. Lack of awareness of Q fever–associated adverse pregnancy outcomes in the relevant risk groups means that the true risk is much higher than found in this study

C. Cases in this series came from a wide variety of occupations and communities

D. Community studies in Denmark and the Netherlands have confirmed the association between Q fever and adverse pregnancy outcomes

Activity Evaluation

1. The activity supported the learning objectives.

Strongly Disagree

Strongly Agree

1

2

3

4

5

2. The material was organized clearly for learning to occur.

Strongly Disagree

Strongly Agree

1

2

3

4

5

3. The content learned from this activity will impact my practice.

Strongly Disagree

Strongly Agree

1

2

3

4

5

4. The activity was presented objectively and free of commercial bias.

Strongly Disagree

Strongly Agree

1

2

3

4

5

Cite This Article

DOI: 10.3201/eid2006.130584

Table of Contents – Volume 20, Number 6—June 2014

Article Navigation

Comments

Please use the form below to submit correspondence to the authors or contact them at the following address:

Stine Yde Nielsen, Department of Clinical Microbiology, Aarhus University Hospital, Brendstrupgaardsvej 100, 8200 Aarhus N, Denmark


character(s) remaining.

Comment submitted successfully, thank you for your feedback.

TOP