To study the possibility of immunization against Cryptosporidium baileyi Current, Upton et Haynes, 1986 with the attenuated anticoccidial vaccine, Paracox™ and oocysts of C. parvum Tyzzer, 1912, chickens were inoculated orally with either 3 x 10’ vaccine oocysts or 8 x I O5 C, baileyi or C. parvum oocysts at 1 week of age. The inoculation with Paracox™ vaccine and C. parvum oocysts was repeated at 2 and 3 weeks of age. Uninfected birds served as controls. All animals with the exception of one uninfected group were challenged orally with either 8 x 105 C. baileyi or 3 x 10s Eimeria tenella Railliet et Lucet, 1891 oocysts at 4 weeks of age. Sera were collected at 4 weeks of age, and were examined by ELISA using C. baileyi antigens. Birds inoculated with C. parvum oocysts did not shed C. parvum oocysts in their faeces, but anticryptosporidial antibodies could be detected in the sera. The total oocyst output of C. parvum inoculated chickens was 17% of that of previously uninfected birds after the oral challenge with C. baileyi. Considering that antibodies play no or only a minor role in resistance to C. baileyi, these results suggest that inoculation of chickens with C. parvum oocysts stimulated also cellular immune response. Based on the relative body weight gain, faecal scores, oocyst output, mortality, and caecal lesions in the birds immunized with Paracox™ vaccine and challenged with E. tenella, the vaccination induced only a moderate protection against the reinfection. The results of crossimmunization of chickens with Eimeria spp. and C. baileyi suggest that attenuated anti-eimerian vaccines do not induce any protection against cryptosporidial infection.
Fleas (95 Pulex irritans, 50 Ctenocephalides felis, 45 Ctenocephalides canis) and ixodid ticks (223 Ixodes ricinus, 231 Dermacentor reticulatus, 204 Haemaphysalis concinna) were collected in Hungary and tested, in assays based on PCR, for Bartonella infection. Low percentages of P. irritans (4.2%) and C. felis (4.0%) were found to be infected. The groEL sequences of the four isolates from P. irritans were different from all the homologous sequences for bartonellae previously stored in GenBank but closest to those of Bartonella sp. SE-Bart-B (sharing 96% identities). The groEL sequences of the two isolates from C. felis were identical with those of the causative agents of cat scratch disease, Bartonella henselae and Bartonella clarridgeiae, respectively. The pap31 sequences of B. henselae amplified from Hungarian fleas were identical with that of Marseille strain. No Bartonella-specific amplification products were detected in C. canis, I. ricinus, D. reticulatus and H. concinna pools.