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At least 19 recordsLinked to original sources
PubMed2001

Abattoir-associated Q fever: a Q fever outbreak during a Q fever vaccination program.

OBJECTIVES: To investigate an abattoir outbreak of Q fever in southem New South Wales with reference to the protective effect and safety of the formalin-inactivated Q fever vaccine (Q Vax) administered before and during the outbreak. METHODS: In September 1998, after notification of four Q fever cases in the abattoir, a cohort investigation of 103 workers was undertaken. Data on age, sex, immune status, vaccination status and main work area were obtained from the medical officer administering the vaccination program and abattoir records. Symptoms and occupational risk factors for illness were obtained from interview of 63 (61%) employees. RESULTS: Of 103 abattoir employees, 16 (16%) had immunity from previous Q fever exposure and 19 (18 %) had been vaccinated at least six weeks before the first case of Q fever exposure in the abattoir. Of the remaining 68 workers who were susceptible to primary infection, 29 (43%) had laboratory confirmed acute primary Q fever and eight were suspected cases. No workers vaccinated before the likely period of exposure developed Q fever. Of 32 workers vaccinated post-exposure, four developed laboratory-confirmed Q fever within eight days of vaccination. Vaccination administered 10 or more days after the likely period of exposure showed no significant protective effect (RR=0.57; 95% CI 0.13-2.57; p=0.60). CONCLUSIONS: Q-Vax was highly effective when administered in advance of the likely period of Q fever exposure. Post exposure vaccination was not shown to be protective. IMPLICATIONS: This study reinforces meat industry vaccination guidelines for abattoir employees. The optimal time to vaccinate workers is before they are put at occupational risk.

Abattoirs↗
PubMed2005

Immune response genes in the post-Q-fever fatigue syndrome, Q fever endocarditis and uncomplicated acute primary Q fever.

BACKGROUND: The influence of immune response gene variations on the development of chronic complications of Q fever is presently unclear. AIM: To compare the frequencies of allelic polymorphisms in immune response genes in different Q fever patient groups. DESIGN: Genetic association study. METHODS: We measured the frequencies of immune response gene variants in: (i) an expanded group of 31 post-Q-fever fatigue patients (QFS); (ii) 22 Q fever endocarditis patients (QFE); and (iii) 22 patients who made an uncomplicated recovery from their initial attack of primary acute Q fever, comparing them with various standard control panels from the general population. RESULTS: There were significant differences between the three Q fever groups. QFS patients differed from both QFE and uncomplicated patients and controls in the frequency of carriage of HLA-DRB1*11 and of the 2/2 genotype of the interferon-gamma intron1 microsatellite. Carriage of the HLA DRB1*11 allele was associated with reduced interferon-gamma and IL-2 responses from PBMC stimulated with ligand in short-term culture. QFE showed differences in the IL-10 promoter microsatellites R and G and had higher frequencies of the TNF-alpha receptor II 196R polymorphism. Q fever patients who had made an uncomplicated recovery differed from those with QFS or QFE, but were not significantly different in allelic frequencies to the control panels. DISCUSSION: These immunogenetic differences support the concept of different immune states in chronic Q fever, determined by genetic variations in host immune responses, rather than by solely properties of Coxiella burnetii.

Coxiella burnetii↗
PubMed2003

SCID mouse model for lethal Q fever.

Q fever, a worldwide zoonosis caused by Coxiella burnetii, has many manifestations in humans. Endocarditis is the most serious complication of Q fever. Animal models are limited to acute pulmonary or hepatic disease and reproductive disorders. An appropriate experimental animal model for Q fever endocarditis does not yet exist. In this study, severe combined immunodeficient (SCID) mice infected with C. burnetii showed persistent clinical symptoms and died, whereas immunocompetent mice similarly infected became asymptomatic and survived. The SCID mice examined in this study had severe chronic lesions in their primary organs: the heart, lung, spleen, liver, and kidney. The heart lesions of the SCID mice were similar to those in humans with chronic Q fever endocarditis: they had focal calcification and expanded macrophages containing C. burnetii. The 50% lethal dose of C. burnetii in SCID mice was at least 10(8) times less than that in immunocompetent mice. The SCID mouse is highly susceptible to C. burnetii, and the immunodeficiency of the host enhances the severity of Q fever. This animal model could provide a new tool for the study of chronic Q fever and Q fever in immunodeficient hosts.

Animals↗
PubMed1992

Spontaneous splenic rupture complicating acute Q fever.

Q fever is usually a self-limited febrile illness that involves the lungs and the liver. Acute complications are rare. We present the case of a 30-yr-old patient with spontaneous splenic rupture during the course of acute Q fever infection. He was admitted to the hospital with high temperature and the radiological signs of an atypical pneumonia. Forty-eight hours after admission, he developed shock. Because of free intraabdominal liquid, a laparatomy was performed that revealed a tear in the enlarged spleen. A splenectomy was performed. The diagnosis of Q fever was established by a significant titer increase in complement fixation test and IgM-ELISA. Serological investigations into the patient's surroundings revealed evidence of Q fever infection in 10 additional persons. Q fever should be taken into account as a possible differential diagnosis in patients with unexplained febrile illness and symptoms of pneumonia. The acute course of Q fever infection can be complicated by splenic rupture. The diagnosis of an acute infection with Coxiella burnetii often requires serologic testing of a second serum sample obtained at least 10 days after the onset of symptoms. Q fever should be ruled out in cases of unexplained splenic rupture particularly in Q fever endemic areas.

Adult↗
PubMed1999

Q fever.

Q fever is a zoonosis with a worldwide distribution with the exception of New Zealand. The disease is caused by Coxiella burnetii, a strictly intracellular, gram-negative bacterium. Many species of mammals, birds, and ticks are reservoirs of C. burnetii in nature. C. burnetii infection is most often latent in animals, with persistent shedding of bacteria into the environment. However, in females intermittent high-level shedding occurs at the time of parturition, with millions of bacteria being released per gram of placenta. Humans are usually infected by contaminated aerosols from domestic animals, particularly after contact with parturient females and their birth products. Although often asymptomatic, Q fever may manifest in humans as an acute disease (mainly as a self-limited febrile illness, pneumonia, or hepatitis) or as a chronic disease (mainly endocarditis), especially in patients with previous valvulopathy and to a lesser extent in immunocompromised hosts and in pregnant women. Specific diagnosis of Q fever remains based upon serology. Immunoglobulin M (IgM) and IgG antiphase II antibodies are detected 2 to 3 weeks after infection with C. burnetii, whereas the presence of IgG antiphase I C. burnetii antibodies at titers of >/=1:800 by microimmunofluorescence is indicative of chronic Q fever. The tetracyclines are still considered the mainstay of antibiotic therapy of acute Q fever, whereas antibiotic combinations administered over prolonged periods are necessary to prevent relapses in Q fever endocarditis patients. Although the protective role of Q fever vaccination with whole-cell extracts has been established, the population which should be primarily vaccinated remains to be clearly identified. Vaccination should probably be considered in the population at high risk for Q fever endocarditis.

Animals↗
PubMed2004

Link between impaired maturation of phagosomes and defective Coxiella burnetii killing in patients with chronic Q fever.

Q fever is caused by Coxiella burnetii, a bacterium that survives in monocytes/macrophages by resisting their natural microbicidal activity. Because the link between bacterial killing and phagosome maturation has yet to be demonstrated, we evaluated responses in monocytes from both immunologically naive control subjects and patients with various manifestations of Q fever. Monocytes from patients with chronic Q fever in evolution, who do not control the infection, exhibited defective phagosome maturation and impaired C. burnetii killing. Both responses were stimulated in patients recovering from Q fever. Phagosome maturation and C. burnetii killing were significantly correlated. Defective phagosome maturation and impaired C. burnetii killing were induced by adding interleukin (IL)-10 to monocytes from convalescent patients and were restored by IL-10 neutralization in chronic Q fever in evolution. We show that phagosome maturation and microbial killing are linked in Q fever and that IL-10 regulates both features of microbicidal activity.

Adult↗
PubMed1984

Vaccine prophylaxis of abattoir-associated Q fever.

Q fever is an important cause of morbidity in Australian meatworkers; recently there have been sharp outbreaks of Q fever in abattoirs in several states. In an attempt to control Q fever by vaccination, 924 nonimmune volunteers at two South Australian abattoirs were inoculated with one dose of a purified, formalin-inactivated, Coxiella burneti, Henzerling strain, phase 1 vaccine. Some 56% of workers in one abattoir, and 64% in the other, seroconverted after vaccination. In the 18 months after vaccination, no Q fever occurred in fully vaccinated subjects, whereas there were 34 cases in 1349 unvaccinated workers. Transient local reactions were noted in most vaccinated subjects; only a few had mild general reactions. No cases of vaccine-enhanced disease were observed. Vaccination of susceptible individuals with a purified C burneti phase 1 vaccine appears to be safe and effective in preventing Q fever in the abattoir.

Abattoirs↗