Mouse fibroblasts (L cells) infected with the 6BC strain of
Chlamydia psittaci
released potassium ion (K
+
) into the extracellular milieu in a way that depended on size of inoculum and time after infection. When the multiplicity of infection was 500 to 1,000 50% infectious units (ID
50
) per L cell, loss of intracellular K
+
was first apparent 4 to 10 h after infection and was nearly complete at 6 to 20 h. Magnesium ion and inorganic phosphate (P
i
) were also released. Similar multiplicities of ultraviolet-inactivated
C. psittaci
also caused release of K
+
. Leakage of inorganic ions probably resulted from immediate damage to the host-cell plasma membrane during ingestion of large numbers of chlamydiae. With multiplicities of 1 to 50 ID
50
per L cell, ingestion of
C. psittaci
was not by itself enough to cause release of K
+
and P
i
from infected L cells. There was a delay of 36 to 72 h between infection and massive leakage of intracellular ions during which time the chlamydiae multiplied extensively. Fifty ID
50
of ultraviolet-inactivated
C. psittaci
per L cell did not bring about significant leakage of K
+
, even after 72 h. The mechanism whereby these multiplicities of infection destroy the ability of host cells to retain intracellular molecules is not known. HeLa 229 cells also released K
+
and P
i
after infection, but these losses occurred more slowly than in comparably infected L cells, possibly because
C. psittaci
did not multiply as extensively in HeLa cells as it did in L cells. The significance of the inability of chlamydiae-infected cells to regulate the flow of molecules through their plasma membranes is discussed.
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