A Portuguese isolate of Borrelia lusitaniae induces disease in C3H/HeN mice

A low-passage, Portuguese isolate of Borrelia lusitaniae, strain PotiB2, wa s inoculated into C3H/HeN mice and disease was monitored by histopathology at 8 weeks after spirochaete challenge. Ear, heart, bladder, femoro-tibial joint, brain and spinal cord were examined. B. lusitaniae strain PotiB2 (6 of 10 mice) and B. burgdorferi sensu stricto strain N40 (9 of 10 mice) indu ced similar lesions in the bladder of infected mice characterised as a mult ifocal, lymphoid, interstitial cystitis. Moreover, both B. lusitaniae PotiB 2 and B. burdorferi N40 induced lesions in the heart of infected mice. The lesions induced by B. lusitaniae PotiB2 (2 of 10 mice) were characterised a s a severe, necrotising endarteritis of the aorta, with a minimal, mixed in flammatory infiltrate (neutrophils, macrophages and lymphoid cells) extendi ng into the adjacent myocardium. In contrast, B. burgdorferi N40 induced a periarteritis of the pulmonary artery (7 of 10 mice), with no involvement o f the endothelium and more extensive inflammation and subsequent necrosis o f the adjacent myocardium. This infiltrate was composed entirely of mononuc lear cells, predominantly mature lymphocytes and plasma cells. No lesions w ere noted in the joints or central nervous system with inoculation of strai ns N40 or PotiB2, and co-inoculation of either strain with Ixodes ricinus s alivary gland lysate did not affect the resulting pathology. Serology, exam ined 8 weeks after inoculation, indicated a different reactivity in mice in fected with B. lusitaniae PotiB2 compared with B. burgdorferi N40. Immunobl ot analysis demonstrated that mice with lesions resulting from infection wi th B. lusitaniae PotiB2 reacted only to the flagellin protein (41 kDa) or t o flagellin and OspC, whereas mice infected with B. burgdorferi N40 reacted with multiple high and low mol. wt proteins, including flagellin, p93, p39 , OspA, OspB and OspC. These results indicate that B. lusitaniae PotiB2 ind uced pathology similar to B. burgdorferi N40 when inoculated into susceptib le mice. Moreover, these results establish the first animal model of diseas e with B. lusitaniae. This mouse model can be used to characterise the immu nopathogenesis of B. lusitaniae infection and to delineate the proteins res ponsible for disease induction in susceptible mice.