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[A rare cause of myocarditis in a 30-year-old patient].

CASE REPORT: A 30-year-old male was admitted to hospital because of chest pain and raised cardiac enzymes. Coronary heart disease was excluded by coronary angiography. Assuming myocarditis serological testing was performed and showed markedly raised antibody titers against Coxiella Burnetii. We treated the patient with doxycycline, 2 times 100 mg daily for 5 months. CONCLUSION: Acute Q-fever should be considered as a possible cause of myocarditis, especially in rural areas.

Adult↗

The in-vitro anti-rickettsial activity of macrolides.

The anti-rickettsial activity of azithromycin and clarithromycin was studied in Vero cells. The rate of rickettsial inhibition-growth caused by both macrolides was determined using rickettsial counts and ELISA. Both macrolides inhibited > 50% the growth of Rickettsia conorii and Rickettsia typhi at concentrations of 1.0 and 0.1 mg/L, respectively. The growth of Coxiella burnetii was inhibited to a rate of > or = 50% at the concentrations of 0.01 and 1.0 mg/L of azithromycin and clarithromycin, respectively.

Animals↗

[A case of Q fever infection causing acute exacerbation of chronic respiratory failure].

The authors report a case of Q fever infection that caused acute exacerbation of chronic respiratory failure, which had developed as a sequela of pulmonary tuberculosis. This case was found on wide-ranging serological screening for respiratory infection performed in order to investigate the prevalence of Q fever in Japan. A 73-year-old man who had been treated for hypertension and sequelae of pulmonary tuberculosis was admitted to our hospital because of fever, productive cough, and dyspnea on effort. Hypoxia and right heart failure were detected on arterial blood analysis and ultrasonography. The acute exacerbation was triggered by respiratory infection and although the infection improved on azithromycin treatment after admission, respiratory failure continued for the period of admission. Home oxygen therapy was required for the management of chronic respiratory failure on discharge. Paired serum samples were tested for antibodies against Coxiella burnetii by indirect immunofluorescence, showing an elevated antibody titer in the convalescent phase. We believe that Q fever infection caused acute exacerbation of chronic respiratory failure, and that C. burnetii is an agent that might influence the clinical course of chronic respiratory failure.

Acute Disease↗

Acute hepatitis with or without jaundice: a predominant presentation of acute Q fever in southern Taiwan.

Acute Q fever was previously regarded as an uncommon infectious disease in Taiwan but has been increasingly recognized recently. Acute febrile illness, hepatitis, and pneumonia are the 3 most common manifestations of this condition, whereas jaundice is rarely reported among patients with acute Q fever. We report 2 cases of acute Q fever with jaundice and multi-organ involvement. The first patient presented with fever, severe headache, and acute abdomen necessitating laparotomy and was complicated with acute cholestatic hepatitis, acute non-oliguric renal failure and disseminated intravascular coagulation. The second patient had acute cholestatic hepatitis and thrombocytopenia, and the latter was likely related to the infection of bone marrow by Coxiella burnetii, as evidenced by the presence of C. burnetii DNA detected by nested polymerase chain reaction. The incidence and clinical significance of hyperbilirubinemia was also determined by review of medical records of 35 cases of acute Q fever cases diagnosed serologically at National Cheng Kung University Hospital from 1994 to 2001. All had biochemical hepatitis and 23% had hyperbilirubinemia (serum bilirubin > or =2 mg/dL). The febrile course before admission and the period between the initiation of effective medication to defervescence were longer in patients with hyperbilirubinemia than in patients without hyperbilirubinemia, although this difference was not significant. Our results suggest that the predominant presentation of acute Q fever in southern Taiwan is acute febrile illness with hepatitis and that jaundice is not uncommon. Due to the clinical polymorphism of acute Q fever, the threshold of surveys for C. burnetii infections should be low for febrile patients with elevated transaminases or hyperbilirubinemia of unknown cause.

Abdominal Pain↗

Q fever during pregnancy: diagnosis, treatment, and follow-up.

BACKGROUND: Q fever, caused by Coxiella burnetii, may result in abortions, premature deliveries, and stillbirths in infected pregnant women. OBJECTIVE: To evaluate the best treatment strategy for Q fever during pregnancy. METHODS: We evaluated the prognosis of 17 pregnant women who developed Q fever with and without co-trimoxazole (trimethoprim-sulfamethoxazole) treatment. RESULTS: The outcome of the pregnancy was found to depend on the trimester. Abortions occurred in 7 of 7 insufficiently treated patients infected during the first trimester vs 1 of 5 patients infected later. Co-trimoxazole given until delivery protected against abortion (0/4) but not against the development of chronic infections, and it did not significantly reduce the colonization of the placenta (2/4 vs 4/4). CONCLUSIONS: Our results show that C burnetii infections cause abortion and that women who develop Q fever while pregnant should be treated with co-trimoxazole for the duration of pregnancy, specifically when infected during the first trimester.

Acute Disease↗

Q fever epidemiology and pathogenesis.

The lungs are a port of entry and primary infectious focus of Coxiella burnetii, the obligate intracellular contagium of the worldwide zoonosis Q fever. The infectious process and immune response are characterised by studies in cell culture and animal systems. Following endocytosis, replication exclusively occurs in the phagolysosome. Several potential virulence factors are described.

Animals↗

Ongoing queries: Interpretation of serology in asymptomatic or atypical chronic Q fever.

Chronic Q fever, predominantly associated with endocarditis, can develop insidiously. Although the diagnosis may be straightforward with a typical clinical presentation, incidental discovery of positive Coxiella burnetii serology poses a difficult clinical challenge. We describe the cases of two such patients and review the literature on the serological diagnosis of chronic Q fever.

Anti-Bacterial Agents↗

Q fever pneumonia in children in Japan.

The prevalence of Q fever pneumonia among children with atypical pneumonia from whom only an acute-phase serum sample was available was traced by using an indirect immunofluorescence (IF) test, nested PCR, and isolation. Twenty (34.5%) of 58 sera were found to have both polyvalent and immunoglobulin M antibodies to the phase II antigen of Coxiella burnetii by the IF test. Q fever pneumonia was present in 23 (39.7%) of 58 patients as determined by both the nested PCR and isolation and in 20 patients as determined by the IF test. The sensitivities for nested PCR and isolation were 100%, and that for the IF test was 87%. Our results indicate that nested PCR was faster and more sensitive than isolation and the IF test in the diagnosis of acute Q fever when a single acute-phase serum was available. These findings suggest that C. burnetii is an important cause of atypical pneumonia in children in Japan.

Antibodies, Bacterial↗

Short report: Q fever and Plasmodium falciparum malaria co-infection in a patient returning from the Comoros archipelago.

Although Plasmodium falciparum malaria and Q fever are both prevalent in Africa, there have been no reports of co-infection to date. We report a case who returned from the Comoros archipelago diagnosed by serologic analysis as well as detection of Coxiella burnetii DNA in acute-phase serum. Thus, Q fever may be associated with malaria infection in travelers returning from disease-endemic countries. This diagnosis should be considered when the response to malaria treatment is incomplete.

Adult↗

Seroepidemiologic study of three zoonoses (leptospirosis, Q fever, and tularemia) among trappers in Québec, Canada.

This study was undertaken to evaluate the prevalence of antibodies against Francisella tularensis, Coxiella burnetii, and certain serovars of Leptospira interrogans among trappers in Québec, Canada. Muskrat trapping was identified as a risk factor for F. tularensis infection, whereas having a cat at home apparently protected trappers against infection by L. interrogans. High percentages of control sera were positive for antibodies against C. burnetii (15%) and L. interrogans (5%), most frequently serovar bratislava. This is the first report of human infection by serovar bratislava in North America.

Adult↗

Vaccines against Coxiella infection.

Coxiella burnetii is an obligate intracellular bacterium that causes a worldwide zoonotic disease, Q fever. Since C. burnetii infection is an occupational hazard and could develop into severe chronic disease in humans, vaccination should be considered to protect individuals at-risk of contact with naturally infected animals or exposure to the agents. Although several vaccines produced from Phase I whole-cell C. burnetii are effective in protecting against the infection in humans, vaccination of previously sensitized people can induce severe local and occasional systemic reactions. Safe use of these vaccines requires screening of potential vaccinees by skin tests, serological tests, or in vitro lymphocyte proliferation assay. Since these procedures are time-consuming and costly, they limit the use of whole-cell vaccines in a mass vaccination program. Efforts have been underway to develop a safer, more effective new-generation vaccine that will not cause adverse reactions when given to someone with pre-existing immunity. This article describes new information relating to the characterization of acquired immunity to C. burnetii infection that will provide a fundamental understanding of the development of protective immunity against Q fever. Recent works focused on development of recombinant vaccines against this pathogen offers promise in the pursuit of a new Q fever vaccine.

Animals↗

Q fever outbreak in industrial setting.

An outbreak of Q fever occurred in South Wales, United Kingdom, from July 15 through September 30, 2002. To investigate the outbreak a cohort and nested case-control study of persons who had worked at a cardboard manufacturing plant was conducted. The cohort included 282 employees and subcontractors, of whom 253 (90%) provided blood samples and 214 (76%) completed questionnaires. Ninety-five cases of acute Q fever were identified. The epidemic curve and other data suggested an outbreak source likely occurred August 5-9, 2002. Employees in the factory's offices were at greatest risk for infection (odds ratio 3.46; 95% confidence interval 1.38-9.06). The offices were undergoing renovation work around the time of likely exposure and contained straw board that had repeatedly been drilled. The outbreak may have been caused by aerosolization of Coxiella burnetii spore-like forms during drilling into contaminated straw board.

Case-Control Studies↗

A dog-related outbreak of Q fever.

Coxiella burnetii pneumonia developed in all three members of one family 8 to 12 days following exposure to an infected parturient dog. The dog gave birth to four pups; three died shortly after birth, and the fourth died within 24 hours of birth.

Adolescent↗

Identification, cloning, and expression of potential diagnostic markers for Q fever.

The clinical diagnosis of Q fever is difficult. Whole cell antigens are currently used in several serological methods, but antigens are limited due to the hazardous nature of Coxiella burnetii cultivation. In this report, we described the method of detecting immunodominant antigens of C. burnetii by using proteomic techniques with patient sera, and cloning and expressing the selected antigens using a novel vector known for its ease of expression, purification, and downstream application.

Antigens, Bacterial↗

Cardiac valves in patients with Q fever endocarditis: microbiological, molecular, and histologic studies.

The pathologic features of Q fever endocarditis, which is caused by Coxiella burnetii, were histologically evaluated in cardiac valves from 28 patients. We used quantitative image analysis to compare valvular fibrosis, calcifications, vegetations, inflammation, and vascularization due to Q fever endocarditis with that due to non-Q fever endocarditis and valvular degeneration. We also studied the presence of C. burnetii in valves by immunohistochemical analysis, culture, and polymerase chain reaction (PCR). Histologically, Q fever endocarditis was characterized by significant fibrosis and calcifications, slight inflammation and vascularization, and small or absent vegetations. Despite antibiotic treatment, non-statistically significant variations at the histologic level were observed. These pathologic features could be confused with noninfectious valvular degenerative damage. We found that the detection of C. burnetii in cardiac valves by immunohistochemical analysis, culture, and PCR decreased significantly only after 1 year of antibiotic treatment, which emphasizes the long persistence of this organism in valve tissues. Pathologic and immunohistochemical analyses may contribute to the diagnosis of Q fever endocarditis.

Adult↗

Correlation between ratio of serum doxycycline concentration to MIC and rapid decline of antibody levels during treatment of Q fever endocarditis.

Endocarditis is the major clinical manifestation of chronic Q fever. Although doxycycline along with hydroxychloroquine remains the mainstay of medical therapy for Q fever endocarditis, there are wide variations in the rapidity of the patient's decline of antibody levels during such therapy. We undertook a retrospective examination of whether there was any correlation between the ratio of serum concentration to MIC of doxycycline and response to treatment in patients with Q fever endocarditis. Included herein are 16 patients from whom Coxiella burnetii was isolated from cardiac valve materials. Serology and measurement of doxycycline and hydroxychloroquine serum levels were performed and recorded after 1 year of treatment. The MIC of doxycycline for C. burnetii isolates was determined using the shell vial assay in a real-time quantitative PCR assay. At the completion of a year-long therapy with doxycycline-hydroxychloroquine, all those that showed a low decline of antibody levels (n = 6) (i.e., <2-fold decrease in antibody titer to phase I C. burnetii antigen) had a ratio of serum doxycycline concentration to MIC between 0.5 and 1. In contrast, those having a ratio of > or =1 showed a rapid decline of phase I antibody levels (n = 9; P < 0.05). The only patient who died had a serum doxycycline-to-MIC ratio of <0.5, and the isolate of C. burnetii cultured from this patient was resistant to doxycycline (MIC = 8 microg/ml). The ratio of serum doxycycline concentration to MIC should be monitored during the course of therapy in patients with Q fever endocarditis.

Adult↗