Experimental Infection of Rhipicephalus sanguineus Ticks with the Bacterium Rickettsia rickettsii, Using Experimentally Infected Dogs

Author(s)

Piranda, Eliane M. ^[1] ; Faccini, Joao Luiz H. ^[2] ; Pinter, Adriano ^[3] ; Pacheco, Richard C. ^[4] ; Cancado, Paulo H. D. ^[1] ; Labruna, Marcelo B. ^[5]

Affiliation

^[1] ESBAM, Curso Med Vet, Manaus, Amazonas - Brazil

^[2] Univ Fed Rural Rio de Janeiro, Inst Vet, Rio De Janeiro - Brazil

^[3] SUCEN, Sao Paulo - Brazil

^[4] Univ Fed Mato Grosso, Fac Vet Med, Cuiaba, MG - Brazil

^[5] Univ Sao Paulo, Fac Vet Med, Dept Vet Prevent Med, BR-05508270 Sao Paulo - Brazil

• Document type: Journal article
• Source: VECTOR-BORNE AND ZOONOTIC DISEASES; v. 11, n. 1, p. 29-36, JAN 2011.
• Web of Science Citations: 31

Abstract

We evaluated if Rickettsia rickettsii-experimentally infected dogs could serve as amplifier hosts for Rhipicephalus sanguineus ticks. In addition, we checked if Rh. sanguineus ticks that acquired Ri. rickettsii from dogs could transmit the bacterium to susceptible hosts (vector competence), and if these ticks could maintain the bacterium by transstadial and transovarial transmissions. Uninfected larvae, nymphs, and adults of Rh. sanguineus were allowed to feed upon three groups of dogs: groups 1 (G1) and 2 (G2) composed of Ri. rickettsii-infected dogs, infected intraperitoneally and via tick bites, respectively, and group 3 composed of uninfected dogs. After larval and nymphal feeding on rickettsemic dogs, 7.1-15.2% and 35.8-37.9% of the molted nymphs and adults, respectively, were shown by polymerase chain reaction (PCR) to be infected by Ri. rickettsii, confirming that both G1 and G2 dogs were efficient sources of rickettsial infection (amplifier host), resulting in transstadial transmission of the agent. These infected nymphs and adults successfully transmitted Ri. rickettsii to guinea pigs, confirming vector competence after acquisition of the infection from rickettsemic dogs. Transovarial transmission of Ri. rickettsii was observed in engorged females that had been infected as nymphs by feeding on both G1 and G2 dogs, but not in engorged females that acquired the infection during adult feeding on these same dogs. In the first case, filial infection rates were generally <50%. No tick exposed to G3 dogs was infected by rickettsiae in this study. No substantial mortality difference was observed between Ri. rickettsii-infected tick groups (G1 and G2) and uninfected tick group (G3). Our results indicate that dogs can be amplifier hosts of Ri. rickettsii for Rh. sanguineus, although only a minority of immature ticks (<45%) should become infected. It appears that Rh. sanguineus, in the absence of horizontal transmission, would not maintain Ri. rickettsii through successive generations, possibly because of low filial infection rates. (AU)