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Herein, we describe the first case of mammary implant infection caused by Coxiella burnetii, resulting in delayed diagnosis and treatment and an in-hospital cross-transmission of Q fever to medical personnel.

Background: Evidence on the effectiveness of first-line treatment for chronic Q fever, tetracyclines (TET) plus hydroxychloroquine (HCQ), and potential alternatives is scarce., Methods: We performed a retrospective, observational cohort study to assess efficacy of treatment with TET plus quinolones (QNL), TET plus QNL plus HCQ, QNL monotherapy, or TET monotherapy compared to TET plus HCQ in chronic Q fever patients. We used a time-dependent Cox proportional hazards model to assess our primary (all-cause mortality) and secondary outcomes (first disease-related event and therapy failure)., Results: We assessed 322 chronic Q fever patients; 276 (86%) received antibiotics. Compared to TET plus HCQ (n = 254; 92%), treatment with TET plus QNL (n = 49; 17%), TET plus QNL plus HCQ (n = 29, 10%), QNL monotherapy (n = 93; 34%), or TET monotherapy (n = 54; 20%) were not associated with primary or secondary outcomes. QNL and TET monotherapies were frequently discontinued due to insufficient clinical response (n = 27, 29% and n = 32, 59%). TET plus HCQ, TET plus QNL, and TET plus QNL plus HCQ were most frequently discontinued due to side effects (n = 110, 43%; n = 13, 27%; and n = 12, 41%)., Conclusions: Treatment of chronic Q fever with TET plus QNL appears to be a safe alternative for TET plus HCQ, for example, if TET plus HCQ cannot be tolerated due to side effects. Treatment with TET plus QNL plus HCQ was not superior to treatment with TET plus HCQ, although this may be caused by confounding by indication. Treatment with TET or QNL monotherapy should be avoided; switches due to subjective, insufficient clinical response were frequently observed., (© The Author 2017. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.)

A meta-analysis of 136 Q fever pregnancies, including 4 new cases and 7 population-based serological studies, revealed significant increases in fetal death and malformation after Q fever during pregnancy. This poor obstetric outcome is prevented by antibiotic treatment., (© The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

Background:  The prevention of Q fever endocarditis through the use of systematic echocardiography and antibiotic prophylaxis in patients with acute Q fever and valvulopathy has never been validated in a cohort study., Methods:  From 2007 to 2012, all patients followed at the French National Referral Center for acute Q fever were included in a cohort study. The prevention of endocarditis included a systematic transthoracic echocardiography (TTE) and a 12-month course of doxycycline and hydroxychloroquine prophylaxis in patients with significant valvulopathy. Transesophageal echocardiography (TEE) was performed in patients with a negative TTE and a rapid rise of phase I immunoglobulin G titers., Results:  Seventy-two patients were included with a median follow-up time of 22 months. A valvulopathy was identified in 31 patients (43%), being previously unknown in 24 (33%) and diagnosed only upon TEE or a second TTE in 7 (10%). The major determinants associated with endocarditis were age (hazard ratio [HR], 1.07; 95% confidence interval [CI], 1.006-1.13; P = .03), aortic regurgitation (HR, 10.2; 95% CI, 3.2-32.2; P < .001), and mitral regurgitation (HR, 4.78; 95% CI, 1.4-16.0; P = .01). Antibiotic prophylaxis was highly effective (HR, 0.002; 95% CI, .00-.77; P = .04) for the 31 patients with valvulopathy., Conclusions:  Acute Q fever could be associated with an increased prevalence of valvulopathy. The evolution from acute Q fever to endocarditis is associated with age and valvulopathy and can be entirely prevented by antibiotic prophylaxis. Although the name "chronic Q fever" suggests otherwise, rapid evolution (<1 month) was observed.

Q fever is a zoonosis caused by Coxiella burnetii, a unique bacterium that is widespread but infrequently associated with human illness or outbreaks. We report on evidence of infection with C. burnetii in a small group of regular consumers of raw (unpasteurized) milk from the same dairy in Michigan.

Background: Q fever is a zoonosis caused by Coxiella burnetii. During pregnancy, it may result in obstetric complications, such as spontaneous abortion, intrauterine growth retardation, intrauterine fetal death, and premature delivery. Pregnant women are exposed to the risk of chronic Q fever., Methods: We included 53 pregnant women who received a diagnosis of Q fever. We compared the incidence of obstetric and maternal Q fever complications for women who received long-term cotrimoxazole treatment (n=16) with that for women who did not receive long-term cotrimoxazole treatment (n=37); long-term cotrimoxazole treatment was defined as oral administration of trimethoprim-sulfamethoxazole during at least 5 weeks of pregnancy., Results: Obstetric complications were observed in 81.1% of pregnant women who did not receive long-term cotrimoxazole therapy: 5 (13.5%) women experienced spontaneous abortions, 10 (27%) experienced intrauterine growth retardation, 10 (27%) experienced intrauterine fetal death, and 10 (27%) experienced premature delivery. Oligoamnios was observed in 4 patients (10.8%). Obstetric complications were found to occur significantly more often in patients infected during their first trimester of pregnancy than in those infected later (P=.032). The outcome of the pregnancy was found to depend on placental infection by C. burnetii (P=.013). Long-term cotrimoxazole treatment protected against maternal chronic Q fever (P=.001), placental infection (P=.038), and obstetric complications (P=.009), especially intrauterine fetal death (P=.018), which was found to be related to placental infection (P=.008)., Conclusions: Q fever during pregnancy results in severe obstetric complications, including oligoamnios. Because of its ability to protect against placental infection, intrauterine fetal death, and maternal chronic Q fever, long-term cotrimoxazole treatment should be used to treat pregnant women with Q fever.

Background: Q fever is a zoonosis caused by Coxiella burnetii. After a large outbreak occurred in the Chamonix Valley in the French Alps in 2002, an extensive surveillance was conducted, to describe the variations in the clinical expression of acute Q fever according to host factors, as well as to monitor the risk of evolution of acute Q fever to chronic Q fever in patients at risk., Methods: Three groups of patients with risk factors for evolution of acute Q fever to chronic Q fever were considered: 376 pregnant women, 19 immunocompromised patients, and 91 patients with valvular or vascular abnormalities. A group of 578 people without risk factors for evolution of acute Q fever to chronic Q fever was also tested. Diagnosis of Q fever was based on serologic testing by immunofluorescence assay., Results: Between 30 August 2002 and 31 July 2003, a total of 1946 serum samples obtained from 1064 persons were tested. A total of 101 patients (9.3%) had acute Q fever diagnosed, and 5 patients (0.5%) had chronic Q fever diagnosed. A diagnosis of acute Q fever was established for 11 pregnant women (2.6% of 379 pregnancies), 5 patients with valvular disease (5.5%), and 85 people without risk factors (14.7%) (71 [27.9%] of 254 symptomatic patients and 14 [4.3%] of 324 asymptomatic patients). A new pregnancy in a woman with negative results of serologic tests for Q fever exposes the woman to a new risk for acute Q fever able to evolve to chronic Q fever. The rates of clinical expression were 90.6% in adult men, 75% in adult women, and 33.3% in children, and they were significantly lower (9.1%) in pregnant women. Evolution to chronic Q fever was observed in 5 patients., Conclusion: This study emphasizes the importance of active surveillance in postepidemic conditions, especially among patients at risk, as well as the importance of systematic serologic testing during pregnancy.

Large numbers of armed forces personnel returning from southwest Asia may present with infections that are not endemic to the United States or that occur rarely and are underdiagnosed in the United States. We report 2 cases of acute Q fever in members of the US Military recently returned from Iraq. Because a number of recent reports suggest that the risk of Q fever may be higher than initially thought among US forces deployed to this region, clinicians need to have a high index of clinical suspicion, an understanding of the available diagnostic tests, and knowledge regarding the methodology and capabilities of the laboratory to which specimens are submitted.

We report here 63 sporadic urban cases of acute Q fever diagnosed in 1985-1997. Fifty-eight men and five women were included; the mean age (+/- SD) was 35.6 (+/- 10.2) years. Twenty-six patients had pneumonia, 30 had hepatitis, and 7 had a self-limited febrile illness. The most frequent radiological abnormalities were lobar or segmental alveolar opacities involving right lower lobes. Chronic bronchitis was significantly more frequent among patients with pneumonic Q fever (P = .01). Thirty-two patients' illnesses were diagnosed through seroconversion, 12 by a fourfold increase in serum antibody titer, and 19 by initial high titers. Patients who initially received doxycycline had a significantly shorter duration of fever than those treated with erythromycin or other antibiotics (P = .0001 and P = .0004, respectively). No patient died. Acute Q fever affects mainly urban men, most frequently causing hepatitis, except in those with chronic bronchitis, who more frequently develop pneumonia. Hepatic Q fever presented with more pronounced increases in liver function test values than did pneumonic Q fever. Treatment with doxycycline caused a significant reduction in the duration of fever.

Chronic Q fever has been associated with endocarditis, granulomatous hepatitis, and osteomyelitis but only rarely with pregnancy. The apparent predilection of Coxiella burnetii, the organism causing Q fever, for the human placenta suggests that chronic Q fever of pregnancy is due to placentitis. We describe a patient with chronic, clinically apparent Q fever in pregnancy and a successful outcome. The diagnosis was made both by serology and by isolation of C. burnetii from the patient's serum and placenta. Therapy with erythromycin and rifampin contributed to the delivery of a healthy baby. The mother's infection was clinically cured by subsequent therapy with doxycycline and rifampin.

We describe an 11-year-old boy with acute Q fever complicated by hemophagocytosis. In addition to pancytopenia, the boy presented with hyponatremia, hypofibrinogenemia, and changes in lipid metabolism. Examination of a bone marrow aspirate revealed striking hemophagocytosis. All of the pathological changes were caused by an activated macrophage system. We also discuss the possible role that pathogenetic mechanisms play in these changes.

A retrospective study was undertaken in Crete, Greece, to investigate the epidemiologic, clinical, and therapeutic aspects of Q fever. Over a period of 5 years (1989-1993), 1,298 patients were examined and 98 cases were identified. Individuals who were aged 20-29 years and 30-39 years appeared to have an increased risk of infection. Contact with animals was found to be a major risk factor for acquisition of Q fever. The predominant clinical manifestations of the infection were fever (91.7% of patients) and respiratory disease (88.5%), whereas hepatitis was the dominant feature in only a minority (7.1%) of patients. Chest radiographs frequently revealed pulmonary interstitial changes (36.4% of patients) and alveolar changes (34.4%). Abnormal echocardiographic findings were also observed. There was no difference in the duration of fever whether the patient received therapy with tetracycline or erythromycin, a finding that may be explained by the delay in initiating tetracycline therapy.

Acute infection with Coxiella burnetti usually results in a self-limited illness requiring a high index of clinical suspicion for diagnosis. Although headache is a common presentation of acute infection with this agent, focal neurological deficits are considered to be limited to chronic infection, most commonly caused by emboli from endocarditis. We report the case of a soldier returning from Desert Storm who presented with headache and a crescendo pattern of transient ischemic attacks and had serology consistent with an acute Q fever infection. The English-language literature on central nervous system infection caused by Coxiella burnetti is reviewed.