Da. Jobe et al., ABILITY OF CANINE LYME-DISEASE VACCINE TO PROTECT HAMSTERS AGAINST INFECTION WITH SEVERAL ISOLATES OF BORRELIA-BURGDORFERI, Journal of clinical microbiology, 32(3), 1994, pp. 618-622
We used flow cytometry to determine levels of borreliacidal antibodies
in hamsters after vaccination with a commercially available canine Ly
me disease vaccine. In addition, we evaluated the ability of vaccinate
d hamsters to resist infection with several isolates of Borrelia burgd
orferi. Borreliacidal antibodies could be detected 1 week after a prim
ary vaccination, peaked at weeks 3 to 5, and then rapidly declined. On
e week after a booster vaccination, borreliacidal activity was detecte
d at a dilution of 1:10,240, and it decreased fourfold by week 10 afte
r the booster vaccination. Vaccinated hamsters were protected against
infection with less than or equal to 10(6) B. burgdorferi 297 organism
s during the peak borreliacidal response (5 weeks after primary vaccin
ation or 2 weeks after booster vaccination). However, hamsters were no
t fully protected from development of Lyme arthritis when the titer of
borreliacidal antibodies was <1:5,120. In addition, no significant bo
rreliacidal activity was induced against B. burgdorferi C-1-11, LV4, o
r BV1, which belong to three other seroprotective groups. These studie
s demonstrate that vaccination with the canine Lyme disease vaccine in
duces protective antibodies against B. burgdorferi 297. However, signi
ficant levels of borreliacidal antibodies are not produced until 5 wee
ks after vaccination, and protection is short-lived. In addition, no b
orreliacidal activity was induced against other isolates of B. burgdor
feri. Because of this, the incorporation of multiple isolates or prote
in subunits may be necessary to increase the effectiveness of future v
accines.