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When mouse fibroblasts (L cells) were infected in suspension or in monolayer with 10 to 100 50% infectious doses (ID(50)) of Chlamydia psittaci (6BC) per host cell, they showed signs of damage 24 to 48 h later. Host-cell injuries were termed multiplication dependent when both the ingestion and subsequent reproduction of C. psittaci were required; when only ingestion but not replication was needed, the injuries were considered to be multiplication independent. The time that the injury was first apparent, as well as its final magnitude, was proportional to the multiplicity of infection. When L cells ingested infectious or ultraviolet-inactivated C. psittaci, damage was manifested by failure to exclude trypan blue, by leakage of lactic dehydrogenase, by inhibition of reproduction as measured by ability to form colonies, by inhibition of protein and deoxyribonucleic acid synthesis, and eventually by cell disintegration. Infectious, but not ultraviolet-killed, chlamydiae stimulated host-cell glycolysis. Heat-killed chlamydiae were without measurable toxicity. The time of appearance of host-cell injury was always earlier, and its terminal magnitude always greater, with infectious inocula than with ultraviolet-inactivated ones. The multiplication-independent toxicity of ultraviolet-killed C. psittaci disappeared with inocula of less than 10 ID(50) per L cell, but an inoculum of only a single ID(50) of infectious chlamydiae per host cell injured most of the cells it infected, as evidenced by increased trypan blue staining and decreased efficiency of colony formation. The toxicity of multiplicities of infection between 10 and 100 ID(50) of infectious C. psittaci per host cell was the sum of both multiplication-dependent and -independent components. The effects of chloramphenicol and isoleucine deficiency on the ability of C. psittaci to injure L cells suggested that some synthesis of protein by both parasite and host may be essential for expression of multiplication-independent chlamydial toxicity. The failure of infectious chlamydiae to stimulate host-cell glycolysis in the presence of cycloheximide suggested that this multiplication-dependent consequence of chlamydial infection was also dependent on protein synthesis by the host.
K R Kellogg, and
K D Horoschak, and
J W Moulder
July 1976,
Infection and immunity,
K R Kellogg, and
K D Horoschak, and
J W Moulder
September 1976,
Infection and immunity,
K R Kellogg, and
K D Horoschak, and
J W Moulder
September 1982,
Infection and immunity,
K R Kellogg, and
K D Horoschak, and
J W Moulder
October 1981,
Infection and immunity,
K R Kellogg, and
K D Horoschak, and
J W Moulder
December 1980,
Infection and immunity,
K R Kellogg, and
K D Horoschak, and
J W Moulder
July 1979,
Infection and immunity,
K R Kellogg, and
K D Horoschak, and
J W Moulder
February 1983,
Infection and immunity,
K R Kellogg, and
K D Horoschak, and
J W Moulder
February 1978,
Infection and immunity,
K R Kellogg, and
K D Horoschak, and
J W Moulder
November 1970,
Canadian journal of microbiology,
K R Kellogg, and
K D Horoschak, and
J W Moulder
March 1982,
Infection and immunity,
