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Q fever is a zoonosis caused by the intracellular bacterium Coxiella burnetii. Both humoral and cellular immunity are important in the host defence against intracellular bacteria. Little is known about the immune response to C. burnetii infections in domestic ruminants even though these species are the major source of Q fever in humans. To investigate the goat's immune response we inoculated groups of pregnant goats via inhalation with a Dutch outbreak isolate of C. burnetii. All animals were successfully infected. Phase 1 and Phase 2 IgM- and IgG-specific antibodies were measured. Cellular immune responses were investigated by interferon-gamma, enzyme-linked immunosorbent spot test (IFN-γ Elispot), lymphocyte proliferation test (LPT) and systemic cytokines. After two weeks post inoculation (wpi), a strong anti-C. burnetii Phase 2 IgM and IgG antibody response was observed while the increase in IgM anti-Phase 1 antibodies was less pronounced. IgG anti-Phase 1 antibodies started to rise at 6 wpi. Cellular immune responses were observed after parturition. Our results demonstrated humoral and cellular immune responses to C. burnetii infection in pregnant goats. Cell-mediated immune responses did not differ enough to distinguish between Coxiella-infected and non-infected pregnant animals, whereas a strong-phase specific antibody response is detected after 2 wpi. This humoral immune response may be useful in the early detection of C. burnetii-infected pregnant goats.

Coxiella burnetii is the causative agent of the zoonotic disease Q fever. Since its first recognition as a disease in the 1930s, the knowledge about the agent and the disease itself has increased. This review summarizes the current knowledge on C. burnetii and Q fever, its pathogenesis, diagnosis and control. C. burnetii is a bacterium which naturally replicates inside human or animal host cells. The clinical presentation of Q fever varies per host species. C. burnetii infection in animals is mainly asymptomatic except for pregnant ruminants in which abortions and stillbirth can occur. In humans, the disease is also mainly asymptomatic, but clinical presentations include acute and chronic Q fever and the post-Q fever fatigue syndrome. Knowledge of the pathogenesis of Q fever in animals and excretion of C. burnetii in infected animals is crucial in understanding the transmission routes and risks of human infection. Our studies indicated that infected pregnant animals only excrete C. burnetii during and after parturition, independent of abortion, and that C. burnetii phase specific serology can be a useful tool in the early detection of infection. Domestic ruminants are the main reservoir for human Q fever, which has a major public health impact when outbreaks occur. In outbreaks, epidemiological source identification can only be refined by genotypic analysis of the strains involved. To control outbreaks and Q fever in domestic ruminants, vaccination with a phase 1 vaccine is effective. Future challenges are to identify factors for virulence, host susceptibility and protection.

Q fever is a zoonosis caused by the bacterium Coxiella burnetii. One of the largest reported outbreaks of Q fever in humans occurred in the Netherlands starting in 2007; epidemiologic investigations identified small ruminants as the source. To determine the genetic background of C. burnetii in domestic ruminants responsible for the human Q fever outbreak, we genotyped 126 C. burnetii-positive samples from ruminants by using a 10-loci multilocus variable-number tandem-repeat analyses panel and compared them with internationally known genotypes. One unique genotype predominated in dairy goat herds and 1 sheep herd in the human Q fever outbreak area in the south of the Netherlands. On the basis of 4 loci, this genotype is similar to a human genotype from the Netherlands. This finding strengthens the probability that this genotype of C. burnetii is responsible for the human Q fever epidemic in the Netherlands.