Experimental Studies on the Virus of "Q" Fever

Freeman, Mavis

doi:10.1093/clinids/5.4.800

Cited by 46 publications

(39 citation statements)

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“…Although psittacosis was first described in Switzerland in 1880 [16], the causative organism was not described until 1930, and then simultaneously in England, Germany and the USA. The influenza virus was discovered in England in 1933 [17] and Coxiella burnetii, the cause of Q fever was discovered in Australia in 1937 [18]. Most recently legionella bacteria (1977) [19] and Chlamydia pneumoniae (1986) [20] were discovered in the USA.…”

Section: Historical Issuesmentioning

confidence: 99%

Community-acquired pneumonia in Europe: causative pathogens and resistance patterns

Woodhead¹

2002

European Respiratory Journal

181

117

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Section: Historical Issuesmentioning

confidence: 99%

Community-acquired pneumonia in Europe: causative pathogens and resistance patterns

Woodhead¹

2002

European Respiratory Journal

181

117

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“…At the end of the 1930s, the "filterpassing agent" responsible for human Q fever was identified as a rickettsial pathogen by Burnet and Freeman after inoculation of infected material in mice, guinea pigs, and monkeys (1,4). Soon after the isolation of the bacterium by Cox and Burnet, the pathogenicity of C. burnetii was studied in mice and guinea pigs, and this investigation was completed and enriched by Sidwell's work in the 1960s (5)(6)(7)(8).…”

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confidence: 99%

Mouse Model of Coxiella burnetii Aerosolization

et al. 2016

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cCoxiella burnetii is mainly transmitted by aerosols and is responsible for multiple-organ lesions. Animal models have shown C. burnetii pathogenicity, but long-term outcomes still need to be clarified. We used a whole-body aerosol inhalation exposure system to mimic the natural route of infection in immunocompetent (BALB/c) and severe combined immunodeficient (SCID) mice. After an initial lung inoculum of 10 4 C. burnetii cells/lung, the outcome, serological response, hematological disorders, and deep organ lesions were described up to 3 months postinfection. C. burnetii-specific PCR, anti-C. burnetii immunohistochemistry, and fluorescent in situ hybridization (FISH) targeting C. burnetii-specific 16S rRNA completed the detection of the bacterium in the tissues. In BALB/c mice, a thrombocytopenia and lymphopenia were first observed, prior to evidence of C. burnetii replication. In all SCID mouse organs, DNA copies increased to higher levels over time than in BALB/c ones. Clinical signs of discomfort appeared in SCID mice, so follow-up had to be shortened to 2 months in this group. At this stage, all animals presented bone, cervical, and heart lesions. The presence of C. burnetii could be attested in situ for all organs sampled using immunohistochemistry and FISH. This mouse model described C. burnetii Nine Mile strain spread using aerosolization in a way that corroborates the pathogenicity of Q fever described in humans and completes previously published data in mouse models. C. burnetii infection occurring after aerosolization in mice thus seems to be a useful tool to compare the pathogenicity of different strains of C. burnetii.

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“…1 Burnet and Freeman subsequently identified the isolates as rickettsia-like. 2 They now constitute a separate genus, Coxiella burnetii, unrelated to rickettsiae and are phylogenetically closer to Legionella sp. 3 C. burnetii is an intracellular bacterium.…”

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Abattoir‐associated Q fever: a Q fever outbreak during a Q fever vaccination program

Gilroy

Formica

Beers

et al. 2001

Australian and New Zealand Journal of Public Health

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Objectives : To investigate an abattoir outbreak of Q fever in southern 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% Cl 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.

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Experimental Studies on the Virus of "Q" Fever

Cited by 46 publications

References 0 publications

Community-acquired pneumonia in Europe: causative pathogens and resistance patterns

Community-acquired pneumonia in Europe: causative pathogens and resistance patterns

Mouse Model of Coxiella burnetii Aerosolization

Abattoir‐associated Q fever: a Q fever outbreak during a Q fever vaccination program

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