Vol. 18(7–8) NSW Public Health Bulletin | 137 Q fever is a zoonotic disease caused by the obligate intra- cellular Gram-negative bacterium Coxiella burnetii. 1 This Bug Breakfast discussed the disease, natural history and issues affecting population control. Background Q fever has been described in most countries of the world; however, it is a notifiable disease in only a few. 1 It has a low infectious dose and survives harsh environmental con- ditions. 2 As a result, it has been classified as a group B bioterrorist agent by the US Centers for Disease Control and Prevention (CDC). Cattle, sheep and goats have been considered the primary human reservoir for C. burnetii; however, many other animals including Australian native species are known to be infected. Although most infected animals exhibit very few clinical signs, they shed C. burnetii in their milk, urine, faeces and particularly in amniotic fluid and placenta. 2 Human transmission occurs through inhalation of aerosols of infected body fluids, the ingestion of unpasteurised milk or dairy products, or by inhalation of dried infectious dusts. Person-to-person transmission is rare. Those most at risk of Q fever are abattoir workers, livestock workers and veterinarians, farmers, shearers and laboratory workers. The Australian annual notification rate peaked at 4.9 per 100 000 persons in 1993 and decreased to 1.7 per 100 000 persons in 2005. 3 The highest incidence of Q fever occurs in south and central-western Queensland and northern NSW areas with men aged 40–44 years having the highest age-specific rate. 4,5 Natural history, diagnosis and treatment The incubation period for Q fever is usually 19–21 days (range one to six weeks). The illness presents with rapid onset of fevers, chills, profuse sweating, headaches, and muscle and joint pain, although the subclinical to clinical ratio is approximately 3:1. Occasionally hepatitis, pneu- monia or neurological manifestations may occur in the acute illness. If C. burnetii persists, it leads to chronic, Bug Breakfast in the Bulletin: Q fever Melissa J. Irwin A , Andrew R. Lloyd B and Peter D. Massey C A NSW Public Health Officer Training Program, NSW Department of Health B School of Medical Sciences, University of NSW C Hunter New England Population Health, Hunter New England Area Health Service localised Q fever infection. Endocarditis (particularly in those with underlying valvular heart disease) is the most common manifestation of chronic, localised infection. In addition, a postinfective fatigue syndrome (in the absence of ongoing infection), termed post-Q fever fatigue syn- drome, is commonly reported. 6 C. burnetii exists in two antigenic phases in laboratory culture systems, Phase I and Phase II. In nature, the organ- ism exists in the Phase I state and is virulent and highly infectious. 1 Antibodies to both appear in a characteristic order in acute Q fever: IgM Phase II, IgM Phase I, IgG Phase II and then IgG Phase I. The appearance of IgG anti- bodies may be delayed up to six to eight weeks following the onset of symptoms. 7 Diagnosis of acute Q fever requires a high index of clini- cal suspicion and relies on acute and convalescent serol- ogy. Although IgM antibody detection from a single serum sample is convenient, this assay is commonly associated with false positive test results. Acute Q fever is treated with doxycycline, although rifampicin and ciprofloxacin are also effective. Chronic Q fever is characterised by ongoing illness, localised tissue injury and high titres of Phase I antibodies (IgG and IgA), and requires prolonged treatment with doxycycline, rifampicin and hydrochloroquine. Population control of Q fever Australia has access to the only licensed vaccine against Q fever available worldwide (QVax, CSL Ltd). Immunis- ation of high-risk occupational groups has been the major population control method; however, significant gaps remain in our knowledge of the optimal immunisation strategy. The vaccine is a purified suspension of formalin- inactivated C. burnetii. This vaccine is highly effective, 8 but its uptake is constrained by the fact that serological and skin testing are required prior to immunisation to prevent hypersensitivity reactions in those who may have been previously exposed. The vaccine produces protection via generation of cellular immunity (rather than antibodies) and is likely to provide lifelong protection. A Federally-sponsored National Q fever Management Program to support screening and immunisation com- menced in 2001 and concluded in NSW in June 2004. 9 The program resulted in most abattoir workers being immu- nised; however, many other at-risk rural populations remain unimmunised and account for the majority of noti- fications in many regions of Australia. Although respira- 10.1071/NB07037 BUG BREAKFAST IN THE BULLETIN