The respiratory and pericardial lesions in turkeys infected with avian and mammalian strains of Chlamydia psittaci were quantitated to determine if chlamydial strains from different restriction endonuclease groups cause distinct disease syndromes. Immunohistochemistry and light microscopy were used to quantify lesions. Three groups of turkeys were inoculated with chlamydial strains (TT3, VS1, B577) from 3 different restriction endonuclease groups and were necropsied at 15 times through post-inoculation day 70. Only mild, transient, peribronchial pneumonia was seen in turkeys inoculated with the mammalian (B577) strain. No chlamydial antigen was detected in these birds. Pericarditis was the most severe lesion in birds infected with the turkey (TT3) strain of C. psittaci; airsacculitis and bronchopneumonia were the most severe lesions in turkeys infected with the psittacine (VS1) strain. Lateral nasal adenitis was in turkeys from both groups. Chlamydial antigen was seen from post-inoculation days 9 through 50 in the lateral nasal gland and at earlier times in other tissue from VS1- and TT3- infected turkeys;In a second study, transmission electron microscopy, immunogold labeling, and image analysis were used to test the hypothesis that chlamydiae inhibit endosomal acidification. Live and heat-killed elementary bodies (EBs), of an ovine abortion strain of Chlamydia psittaci (strain B577), were inoculated onto monolayers of J774 mouse macrophages and the acidity of endosomes containing EBs was measured. The uptake of 3-(2,4-Dinitroanilino)-3[superscript]'amino-N-methyldipropylamine (DAMP) (a measure of endosomal acidity), at 0.5, 2, 10, and 30 minutes after initiation of elementary body endocytosis, was determined;The acidification of endosomes containing live, but not heat-killed, EBs was inhibited. Inhibition was seen as early as 0.5 minute, and up to 30 minutes, after EB uptake was initiated. The mean pH of endosomes containing heat-killed EBs (30 minutes after phagocytosis) was 5; endosomes with live EBs had a mean pH of 5.8. These findings indicate that inhibition of endosomal acidification is a mechanism whereby chlamydiae evade antigen processing and inhibit phagolysosomal fusion.