Biology and intracellular pathogenesis of high or low virulent Chlamydophila psittaci strains in chicken macrophages.

Within a few days post infection of SPF turkeys, highly pathogenic Chlamydophila (Cp.) psittaci genotype A and D strains can be found in blood monocytes/macrophages, while this effect is less pronounced for infection with a milder genotype B strain. To elucidate on the observed difference, we studied the developmental cycle of avian Cp. psittaci strains of varying virulence in a matched avian monocyte/macrophage cell line (HD11) by electron microscopy and immunofluorescence and determined the gene transcription of 26 Type III secretion related genes and six control genes upon infection of HD11 cells. The genotype A (84/55) and D (92/1293) strains (1) clearly induced actin recruitment to the site of entry, (2) initiated host cell degeneration at earlier time points, and (3) survived and proliferated better when compared to the milder CP3 strain. Strain 84/2334, genetically intermediate between Cp. psittaci and Cp. abortus, did not induce actin recruitment. Limited mRNA transcripts for the cell division genes ftsW and ftsK were in agreement with the observed low replication of Cp. psittaci in these host cells. The results also indicated that genes coding for the structural components of the Type III secretion system were transcribed earlier compared to an infection in epithelial cells. Based on the presented results, we postulate that upon infection of blood monocytes/macrophages, Cp. psittaci deliberately limits its replication and immediately arms itself to infect other cells elsewhere in the host, whilst using the monocytes/macrophages as a quick transport vehicle.