A rabbit model was established for Chlamydia pneumoniae infection that
may be helpful to understand the pathogenesis of disease in humans, T
welve, pathogen-free, I-month-old New Zealand White rabbits were inocu
lated with 1.0 x 10(7) to 5.0 x 10(7) CFU of purified C. pneumoniae (A
TCC strain VR 1310) via the nasopharynx (1 rabbit died immediately pos
tinoculation, and 11 were available for study), Five controls were ino
culated with the carrier buffer, Ten of the II study rabbits demonstra
ted serological evidence of acute infection (immunoglobulin G antibodi
es, 1:8 to >1:16), with the weakest response at 7 days and the stronge
st response at 28 days, whereas none of the controls showed any seroco
nversion. Study animals were sacrificed in batches of three, on days 7
, 14, 21, and 28, but controls were sacrificed on days 7 and 28, Two-t
hirds of the animals demonstrated evidence of bronchiolitis and pneumo
nia on days 7 and 14 and resolution by day 21, Two study rabbits demon
strated, on histology, early and intermediate lesions of atheroscleros
is: one animal (day 7) showed the accumulation of foamy macrophages (f
atty streak) in the arch of the aorta, and the other animal (day 14) s
howed spindle cell proliferation of smooth muscle cells (intermediate
lesion), Focal periaortitis was seen in the same animal (day 7), C. pn
eumoniae elementary bodies were demonstrated by immunocytochemical sta
in in the lungs (n = 2), liver (n = 3), spleen (n = 5), and aorta (n =
12), one of which corresponded to the intermediate lesion, C. pneumon
iae was cultured from the lungs (n = 2), liver (n = 2), spleen (n = 2)
, and aortic arch (n = 1), All histopathological, immunocytochemical,
and cultural studies were negative in the controls, Hence, the rabbit
provides a useful animal model for the study of C. pneumoniae infectio
n and its complications, particularly atherosclerosis.