Rabbit model for Chlamydia pneumoniae infection

Abstract

A rabbit model was established for Chlamydia pneumoniae infection that may be helpful to understand the pathogenesis of disease in humans. Twelve, pathogen-free, 1-month-old New Zealand White rabbits were inoculated with 1.0 ؋ 10 7 to 5.0 ؋ 10 7 CFU of purified C. pneumoniae (ATCC strain VR 1310) via the nasopharynx (1 rabbit died immediately postinoculation, and 11 were available for study). Five controls were inoculated with the carrier buffer. Ten of the 11 study rabbits demonstrated serological evidence of acute infection (immunoglobulin G antibodies, 1:8 to >1:16), with the weakest response at 7 days and the strongest response at 28 days, whereas none of the controls showed any seroconversion. 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-thirds of the animals demonstrated evidence of bronchiolitis and pneumonia on days 7 and 14 and resolution by day 21. Two study rabbits demonstrated, on histology, early and intermediate lesions of atherosclerosis: one animal (day 7) showed the accumulation of foamy macrophages (fatty streak) in the arch of the aorta, and the other animal (day 14) showed spindle cell proliferation of smooth muscle cells (intermediate lesion). Focal periaortitis was seen in the same animal (day 7). C. pneumoniae elementary bodies were demonstrated by immunocytochemical stain in the lungs (n ‫؍‬ 2), liver (n ‫؍‬ 3), spleen (n ‫؍‬ 5), and aorta (n ‫؍‬ 2), one of which corresponded to the intermediate lesion. C. pneumoniae 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 infection and its complications, particularly atherosclerosis.

Chlamydia pneumoniae-induced pathological signaling in the vasculature

“…Multiple intranasal inoculation at 8, 10 and 12 weeks of age caused a significant progression of pre-existing atherosclerotic lesions (Campbell et al, 2000), suggesting that Cp infected already predamaged areas and maintained atherosclerotic progression. Similar results were obtained in rabbit models where chlamydial infection led to a progression of pre-existing early atherosclerotic lesion development (Fong et al, 1997;Muhlestein, 2000).…”

Association of raised titres of antibodies to Chlamydia pneumoniae with a history of pre‐eclampsia

“…Epidemics of C. pneumoniae occur every five to seven years with primary infection occurring in teenage years and the prevalence rising with age. 16 Cycles of reinfection are common 28 and serum antibodies do not appear to have a protective effect. The prevalence of serum antibodies starts to rise steadily at school age in Western countries, and it is estimated that between 50% and 70% of adults are seropositive.…”

The role of infectious agents in the pathogenesis of vasculitis

“…In particular, Fong et al 6 demonstrated that intratracheal infection with CP in New Zealand white rabbits fed on a standard diet was able to induce atherosclerotic changes, which in one animal were associated with an adventitial lymphocytic infiltrate. 6 This latter finding suggests a role for CP in inducing adventitial periarteritis. In humans, CP infection has been linked to GCA (giant cell arteritis), which in a minority of cases is characterized histologically by adventitial periarteritis 7 in the absence of the more typical transmural infiltrate.…”