ABSTRACT
The ability of the sand fly Phlebotomus papatasi to transmit Leishmania major, the etiologic agent of zoonotic cutaneous leishmaniasis, to Meriones shawi, the natural reservoir host of this parasite, was studied under laboratory conditions. Sand flies became infected with L. major after feeding on a lesion of needle-inoculated M. shawi. Moreover, P. papatasi, previously infected with L. major, transmitted the parasite to M. shawi by bite during a second bloodmeal. Two months after the blood-meal, the animal developed a lesion on its ears. Xenodiagnosis was performed on the infected animal. The infectivity of M. shawi to P. papatasi lasted for five months, period corresponding to winter season in North Africa. We have thus demonstrated the transmission of L. major by P. papatasi to M. shawi under laboratory conditions. Our results show that reservoir hosts surviving winter time are the main source of infection for P. papatasi during the following season, and subsequently they play a major role in the persistence and transmission of L. major between transmission cycles.
Subject(s)
Gerbillinae/parasitology , Leishmania major/pathogenicity , Leishmaniasis, Cutaneous/parasitology , Leishmaniasis, Cutaneous/transmission , Phlebotomus/parasitology , Animals , Disease Reservoirs/parasitology , Female , Insect Vectors/growth & development , Insect Vectors/parasitology , Leishmania major/isolation & purification , Leishmania major/physiology , Leishmaniasis, Cutaneous/veterinary , Meals , Phlebotomus/growth & development , Rodent Diseases/parasitology , Seasons , TunisiaABSTRACT
Preimmunization of mice with salivary gland homogenate (SGH) of long-term colonized (F29) female Phlebotomus papatasi Scopoli (Diptera: Psychodidae) induced protection against Leishmania major Yakimoff & Schokhor (Kinetoplastida: Trypanosomatidae) co-inoculated with the same type of SGH. In contrast, preimmunization of mice with SGH of wild-caught female P. papatasi did not confer protection against L. major co-inoculated with the same type of SGH. Similarly, SGH from recently colonized (F1) female P. papatasi did not protect mice against L. major. These results suggest that when developing a sand fly saliva-based vaccine, the natural vector populations should be considered.
Subject(s)
Leishmaniasis, Cutaneous/physiopathology , Phlebotomus Fever/transmission , Phlebotomus/pathogenicity , Animals , Female , Leishmaniasis, Cutaneous/transmission , Mice , Mice, Inbred BALB C , Salivary Glands/parasitology , Zoonoses/parasitologyABSTRACT
Dogs are the main reservoir host of Leishmania infantum, etiologic agent of human visceral leishmaniasis (HVL) and canine visceral leishmaniasis (CVL). Transmission of L. infantum to humans and dogs is mainly through the bite of infected sand flies. In the Western Mediterranean basin, Phlebotomus perniciosus is the main vector of L. infantum. However, occasional vertical transmission of L. infantum has been reported. This study investigated L. infantum vertical transmission in offspring of experimentally infected dogs. Among 14 surviving puppies from three female beagle dogs that developed CVL following an experimental infection with L. infantum, one was tested positive by indirect immunofluorescence antibody test, by PCR and by xenodiagnosis with a high parasite burden in the spleen at 14 months old. None of the remaining puppies were tested positive for L. infantum. These findings strongly suggest that infected puppies following vertical transmission can sustain infection and contribute in infecting sand flies with L. infantum. Any strategy for controlling CVL should take into consideration the vertical transmission of L. infantum.