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In Los Angeles County, California, 142 cases of human listeriosis were reported from January 1 through August 15, 1985. Ninety-three cases (65.5 percent) occurred in pregnant women or their offspring, and 49 (34.5 percent) in nonpregnant adults. There were 48 deaths: 20 fetuses, 10 neonates, and 18 nonpregnant adults. Of the nonpregnant adults, 98 percent (48 of 49) had a known predisposing condition. Eighty-seven percent (81 of 93) of the maternal/neonatal cases were Hispanic. Of the Listeria monocytogenes isolates available for study, 82 percent (86 of 105) were serotype 4b, of which 63 of 86 (73 percent) were the same phage type. A case-control study implicated Mexican-style soft cheese (odds ratio, 5.5; 95 percent confidence interval, 1.2 to 24.8) as the vehicle of infection; a second case-control study showed an association with one brand (Brand A) of Mexican-style soft cheese (odds ratio, 8.5; 95 percent confidence interval, 2.4 to 26.2). Laboratory study confirmed the presence of L. monocytogenes serogroup 4b of the epidemic phage type in Brand A Mexican-style cheese. In mid-June, all Brand A cheese was recalled and the factory was closed. An investigation of the cheese plant suggested that the cheese was commonly contaminated with unpasteurized milk. We conclude that the epidemic of listeriosis was caused by ingestion of Brand A cheese contaminated by one phage type of L. monocytogenes serotype 4b.

We report the broad spectrum of clinical manifestations in 23 infants with positive cultures for Listeria monocytogenes who were treated in our hospital during a recent epidemic. The majority of infants (70%) were preterm and none was small for gestational age. Thirteen (56%) had respiratory distress at birth with evidence of congenital pneumonia. Four of the 5 deaths occurred among these infants. Four infants considered healthy after resuscitation developed fever and lethargy within 36 hours after birth. Only one of these infants had evidence of pneumonia. We conclude that congenital pneumonia with respiratory distress at birth is the major cause of mortality and morbidity from L. monocytogenes infection in the neonate.

Seven cases of listeriosis identified at perinatal autopsy are described. The cases occurred during the time of a 1985 Los Angeles, California, epidemic of listeriosis from suspected food contamination by Listeria monocytogenes. In only one of seven cases were gross pathologic lesions encountered. Microscopic lesions in six cases consisted of rare, localized microabscesses or granuloma-like lesions in multiple organs and contained histiocytes, monocytes, lymphocytes, and polymorphonuclear leukocytes with variable necrosis. One case had no gross or microscopic findings. Organomegaly was uncommon. The diagnosis was confirmed in three cases by postmortem blood culture. Complete perinatal autopsy is important for confirmation of listeriosis when microbiologic, gross, or microscopic findings alone may not yield characteristic features.

Listeria monocytogenes is an underdiagnosed and underreported cause of congenital sepsis. Twenty mother/infant pairs from whom Listeria was isolated were studied at the University of Southern California School of Medicine and Women's Hospital during the last ten years to delineate antepartum factors indicative of a fetus at high risk for perinatal Listeria sepsis. The combination of high maternal leukocyte count, fetal tachycardia, decreased fetal heart rate variability, and, especially, the absence of intrapartum fetal heart rate accelerations was associated with a complicated course for the neonate with congenital Listeria sepsis. Intrapartum administration of antibiotics decreased fetal morbidity and mortality but did not impair recovery of the organism.