The Q fever epidemic in The Netherlands: history, onset, response and reflection. Epidemiol Infect

Department of Bacteriology and TSEs, Central Veterinary Institute of Wageningen UR, Lelystad, The Netherlands.
Epidemiology and Infection (Impact Factor: 2.54). 10/2010; 139(1):1-12. DOI: 10.1017/S0950268810002268
Source: PubMed


The 2007-2009 human Q fever epidemic in The Netherlands attracted attention due to its magnitude and duration. The current epidemic and the historical background of Q fever in The Netherlands are reviewed according to national and international publications. Seroprevalence studies suggest that Q fever was endemic in The Netherlands several decades before the disease was diagnosed in dairy goats and dairy sheep. This was in 2005 and the increase in humans started in 2007. Q fever abortions were registered on 30 dairy goat and dairy sheep farms between 2005 and 2009. A total of 3523 human cases were notified between 2007 and 2009. Proximity to aborting small ruminants and high numbers of susceptible humans are probably the main causes of the human Q fever outbreak in The Netherlands. In general good monitoring and surveillance systems are necessary to assess the real magnitude of Q fever.

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Available from: Hendrik-Jan Roest, Aug 08, 2014
    • "Inhalation of aerosolised C. burnetii bacteria is the most probable route of introduction of the organism in a farm (Welsh et al., 1958; Berri et al., 2005; Roest et al., 2012). Depending on factors as immune status of the animals, flock/herd size and virulence of C. burnetii, eventually, introduction of C. burnetii in a farm leads to spreading of the infection within the flock/herd and, possibly, results in abortion storms, as has occurred in the Netherlands between 2005 and 2009 (Wouda and Dercksen, 2007; Van den Brom and Vellema, 2009; Roest et al., 2011). "
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    ABSTRACT: Q fever is an almost ubiquitous zoonosis caused by Coxiella burnetii, which is able to infect several animal species, as well as humans. Cattle, sheep and goats are the primary animal reservoirs. In small ruminants, infections are mostly without clinical symptoms, however, abortions and stillbirths can occur, mainly during late pregnancy. Shedding of C. burnetii occurs in feces, milk and, mostly, in placental membranes and birth fluids. During parturition of infected small ruminants, bacteria from birth products become aerosolized. Transmission to humans mainly happens through inhalation of contaminated aerosols. In the last decade, there have been several, sometimes large, human Q fever outbreaks related to sheep and goats. In this review, we describe C. burnetii infections in sheep and goats, including both advantages and disadvantages of available laboratory techniques, as pathology, different serological tests, PCR and culture to detect C. burnetii. Moreover, worldwide prevalences of C. burnetii in small ruminants are described, as well as possibilities for treatment and prevention. Prevention of shedding and subsequent environmental contamination by vaccination of sheep and goats with a phase I vaccine are possible. In addition, compulsory surveillance of C. burnetii in small ruminant farms raises awareness and hygiene measures in farms help to decrease exposure of people to the organism. Finally, this review challenges how to contain an infection of C. burnetii in small ruminants, bearing in mind possible consequences for the human population and probable interference of veterinary strategies, human risk perception and political considerations. Copyright © 2015 Elsevier B.V. All rights reserved.
    Veterinary Microbiology 07/2015; DOI:10.1016/j.vetmic.2015.07.011 · 2.51 Impact Factor
    • "The partly closed status of some herds to prevent infectious diseases like paratuberculosis and caseous lymphadenitis could have made a herd more susceptible for C. burnetii or new strains of this bacterium. Secondly the new introduction of a more virulent strain or a genetic shift to a more virulent strain could have contributed to the cause of the outbreak (Roest et al. 2011b). "
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    ABSTRACT: About 80 years ago, Q fever research began due to human outbreaks of unknown origin, associated with domestic animals. Since then, some but not all characteristics of this “query” disease, caused by the intracellular bacterium Coxiella burnetii were revealed. In this chapter the bacteriology of the bacterium, clinical presentation, epidemiology and transmission of the disease in humans and animals are presented. Domestic small ruminants are the main source of human Q fever. Although Q fever is considered to be an occupational disease, outbreaks have a major public health impact and attract most attention. The Dutch Q fever outbreak, involving 4000 human cases over the years 2007–2010, is an example of how Q fever can re-emerge from an endemic state into an outbreak of unforeseen dimension. In this outbreak the epidemiological link between dairy goats and human cases was confirmed by genotyping for the first time. This was possible due to the previous development of genotyping assays that are applicable on clinical material. Although Q fever seems to be a blue print for outbreaks it is not known yet what factors are essential to cause outbreaks and how they interact. To prevent outbreaks, a better understanding of these factors and their interaction is necessary and research should therefore focus on this.
    Zoonoses - Infections Affecting Humans and Animals, 01/2015: pages 317-334; , ISBN: 978-94-017-9456-5
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    • "Numbers of chronic Q fever increased thereafter, amounting to over 200 cases identified until 2011 with a 13% lethality [10] [11]. From 2009 onwards, consecutive measures to curtail the livestock epidemic included mandatory vaccination and culling of carrying animals on infected farms [8]. Some preventive measures, like avoiding human proximity to infected farms, were not feasible due to the dense population. "
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    ABSTRACT: Background: Following a large Q fever outbreak in the Netherlands, patients at risk for chronic Q fever received a whole-cell Q fever vaccine. Sensitized people were excluded based on pre-vaccination screening with skin test (ST) and serology. An investigational IFN-γ-production assay was added. No previous experience existed for Q fever vaccination in this patient risk-group with predefined cardiac valvular anomalies or aortic aneurysm/prosthesis and many co-morbidities. We studied the adverse events (AE) and their association with patient characteristics and immunological parameters. Methods: AE registration covered the week after skin test and 90 days following vaccination, with the use of diaries, interviews and spontaneous reports. Serious (S)AE were assessed immediately to ensure safety. We coded AE according to reported severity. Univariate and multivariate analysis addressed associations. Results: Pre-vaccination screening led to exclusion of 182 patients with positive serology and 207 patients with positive skin test-reading. The skin test did not lead to any causally related SAE. Subsequent vaccination of 1370 patients did not reveal unexpected AE; however, 80% of vaccinees reported local AE (in 26% of these pronounced or extensive). The two causally related SAE (0.1%) both concerned a persistent subcutaneous injection site mass. AE were more frequent in women, younger patients, and those without immunosuppressive co-morbidity/medication. The occurrence of local AE after skin test was associated with pre-vaccination positive serology and high IFN-γ production. This was also true for local AE following vaccination, with a strong association with local AE after skin test as well. The proportion of vaccinees with positive serology and positive IFN-γ values 6 months after vaccination was higher in those with local AE after skin test or after vaccination (non-significant, probably due to small numbers). Conclusion: Q fever vaccination was safe but reactogenic in this high-risk patient-group. Rates of local AE were higher in women, younger age groups and in those with positive immunological parameters. Vaccinees with local AE after skin test or after vaccination appear to have more pronounced post-vaccination immune responses.
    Vaccine 10/2014; 32(49). DOI:10.1016/j.vaccine.2014.09.061 · 3.62 Impact Factor
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