**1. Introduction**

378 A Bird's-Eye View of Veterinary Medicine

Wikse, S.E. (1985). Feedlot cattle pneumonia. *Vet Clin North Am Food Anim Pract,* 1, pp. 289-

Q fever (for query fever) is a zoonosis caused by *Coxiella burnetii,* a small gram-negative (0.2 to 0.4 μm wide, 0.4 to 1 μm long), obligate-intracellular bacterium. Historically, it was considered as *Rickettsia* but gene-sequence analysis classifies *Coxiella* genus in the order *Legionellale*, family *Coxiellaceae* (Seheradi, 2003).

Pleomorphic bacteria are classified in three groups: large cell variants (LCV), small-cell variants (SVC) and small dense cells (SDC). The SCVs and the SDCs are the most frequent forms in the host and certainly (the most) resistant forms in the environment. The LCV form of *Coxiella burnetii,* which shares features common with gram-negative bacteria, diffuse chromatin and process clearly distinguishable outside and cytoplasmic membranes with LPS exposed on the surface. The LCVs are larger, more pleomorphic and metabolically active than the SCVs and the SDCs. The SDCs have been visualised in LCV as endospores, and they may be liberated upon the lysis of LCV or binary transverse fission with unequal cell division. The SDCs alone have never been isolated, free-living amoeba can provide an intra-cellular niche for SDC formation and survival of *Coxiella burnetii* in the environment. Binary transverse fission was observed both in the SCVs and the LCVs in cells cultured. The form changes within lifecycle of *Coxiella burnetii* are strategy to survive (Arricau-Bouvery & Rodolakis, 2005).

*Coxiella burnetii* occurs in two phases. In the culture, it transforms from a virulent phase I type to an avirulent phase II. In the phase II, bacteria have alerted expression of cell wall lipopolysaccharide (LPS), do not occur in nature and are killed by macrophages (Hotta et al., 2002). The survival strategy of the bacteria is based on multiplication in mature phagosomes of monocytes/macrophages. The virulence is connected to the LPS expression. The virulent *Coxiella burnetii* entered into monocytes through αvβ3 integrin and survived inside the cells (Dellacasagrande et al., 2000). Avirulent variants were more easily ingested than virulent bacteria but they were eliminated by monocytes. Their phagocytosis was mediated by αvβ<sup>3</sup> integrin-IAP complex and CR3, suggesting that the efficiency of *Coxiella burnetii*  phagocytosis mainly results from the activation and CR3-dependent phagocytosis, thus

Epidemiology, Zoonotic Aspect and Current Epidemiological Situation of Q Fever in Poland 381

Fig. 1. Life cycle of the bacteria (Arricau-Bouvery & Rodolakis, 2005) (1). Entry of the spore in the eukaryotic cell and acidification of the endosome of the phagosome. (2) Multiplication of small-cell variants (SCV) by transverse binary fission and differentiation to large-cell variants (LCV). (3) Fusion of the endosome with the lysosome, acidification of the phagolysosomal. (4) Multiplication of LCV by transverse binary fission, differentiation of LCV to SCV and development of the polar endospore in LCV. (5) Release of the spore and

In humans, Q fever occurs the most often in direct contact with infected animals in slaughterhouses, as well as fur and veterinarians. Infections from human to human are very rare, and may have place especially in hospitals where patients infect the others through sputum released during coughing. Sporadic human infections of Q fever occurred after contact with infected parturient women, via transplacental transmission resulting in congenital infections, during autopsies, intradermal inoculation or blood transfusion. It has been postulated that transmission of *Coxiella burnetii* among mammals occurs mainly via inhalation of infected dust and aerosols (Maurin & Raoult, 1999). It is very difficult to explain some cases of *Coxiella burnetii* infections. The literature dates showed that there is possibility of sexual transmission of Q fever among mammals. The studies showed that heifers infected intravaginally with a suspension of *Coxiella burnetii* shed bacteria in their urine few days later. Moreover studies on nine Polish patients, who were employed in Spain during sheep shearing season showed occurrence of antibodies to *Coxiella burnetii* antigens in their serum. The antibodies were detected also in their spouses but they did not occur in sera from the other family members. Moreover, scanning electron microscopy of

SCV out of the cell.

**3. Epidemiology 3.1 Zoonotic aspects** 

preventing CR3 engagement. It is possible that *Coxiella burnetii* induced impairment of CR3 function results from uncoupling αvβ3 integrin from IAP (Capo et al., 1999).

The heterogeneity among strains of *Coxiella burnetii* is low degree (Vodkin et al., 1986). However, when DNA from 38 *Coxiella burnetii* isolates was examined by using restriction fragment length polymorphism (RFLP) analysis, six genomic groups (I to VI) were detected (Hendrix et al., 1991). The genome size of *Coxiella burnetii* nine Mile strain amounts to 2.1 Mb. The size of genome is highly variable among different isolates and ranging from 1.5 to 2.4 Mb (Willems et al., 1998). Genomic groups (I, II and III) are associated with animal, tick or acute Q fever in human, whereas group IV and V are isolated from human Q fever endocarditis cases. Group VI isolates were obtained from feral rodents in dungway, and their pathogenicity is unknown (Maurin & Raoult, 1999).

*Coxiella burnetii* is the well-known causative agent of Q fever, but neglected as zoonosis. Q fever has spread worldwide both in humans and in animals (Kruszewska et al., 1996). C*oxiella burnetii* can infect many animal species including mammals, birds and arthropods such as ticks. Generally, Q fever is asymptomatic, but it can lead to abortions and stillbirths in mammals. In these animals, *Coxiella burnetii* can induce pneumonia as well as abortion, stillbirth and delivery of weak lambs, calves or kids, which are the most frequent clinical sings of the disease. *Coxiella burnetii* in humans causes highly variable clinical manifestations ranging from acute to fatal chronic infections. However, about 60% of the infections are asymptomatic seroconversions. Acute Q fever is mainly a flu-like disease, or atypical pneumonia or hepatitis. Q fever is essentially an airborne disease. The infections occur after inhalation of aerosols generated from infected placentas, body fluids or contaminated manure. Transmission of this pathogen is generally associated with abortion of domestic ruminants, particularly sheep (Arricau-Bouvery & Rodolaski, 2005).

Tetracyclines are the best for treating Q fever. Although, Q fever endocarditis has been treated by the use of the combination of doxycyline with chloroquinolone. The time of treatment is very long and it takes for 18 to 36 months in order to cure chronic Q fever (Maurin & Raoult, 1999).
