L. monocytogenes is a short, non-spore-forming, gram-positive bacillus. In log phase of growth and in cerebrospinal fluid (CSF), organisms may appear predominantly coccoid and may form short chains that may be mistaken on Gram stain for pneumococci or group B streptococci. Older cultures may stain Gram variable, and they can be confused morphologically with Haemophilus influenzae. L. monocytogenes grows well on most laboratory media. On sheep-blood agar, the colonies are 1 to 2 mm in diameter, gray-white, and translucent, with a narrow zone of alpha-hemolysis that may be most evident on lifting a colony from the plate. Almost all strains of L. monocytogenes are motile, a feature most pronounced at room temperature in a semisolid motility medium. The organism is catalase-positive and oxidase-negative, and it hydrolyzes esculin. Optimal temperatures for growth range from 20° to 37°C, and although growth is faster at 30° to 37°C, the organism’s capacity to replicate at low temperatures is a helpful differentiating feature. L. monocytogenes may be confused in the laboratory with corynebacteria, group B streptococci, enterococci, and diphtheroids.

Somatic and flagellar antigens have been used to classify L. monocytogenes into serotypes, designated numerically. Currently, at least 17 have been identified, with types 1/2a, 1/2b, and 4b accounting for 90% of cases of listeriosis.

L. monocytogenes is widespread in nature. The organism is found in dust, soil, water, sewage, and vegetation. It has caused naturally acquired infection in more than 50 species of animals, including mammals, birds, rodents, crustaceans, and fish. It has been isolated from insects, but they are not considered an important vector of infection. The organism’s capacity to withstand dry, alkaline conditions may account for its persistence in soil and its widespread distribution in nature. Between 1% and 5% of asymptomatic adults harbor this organism in the gastrointestinal tract.

The incidence of human infection is highest in the spring and summer months, but infection in animals occurs more frequently during the winter. Infection in humans is a sporadic occurrence and usually cannot be traced to animal contacts. Most cases probably result from soilborne infection. The acquisition of L. monocytogenes beyond the neonatal period likely results in asymptomatic colonization or infection of the mucous membranes of the throat or gastrointestinal tract, with transient or persistent fecal shedding. Infection may be acquired transplacentally or perinatally after delivery through the birth canal of a colonized parturient. Listeria may be transmitted genitally from person to person, but transmission by the respiratory route has not been documented. Epidemic neonatal listeriosis may be transmitted among infants by contact with the hands of hospital personnel. A nosocomial outbreak was associated with contaminated mineral oil used for infant bathing. Clusters of infections with no evident source also have been described in newborn nurseries and among hospitalized immunocompromised hosts.

Numerous foodborne outbreaks have been documented. In one of them, cabbage used in coleslaw was contaminated, presumably from the manure of a flock of sheep, one of which had died of listeriosis. Pasteurized milk was the source in another outbreak. The milk came from dairy cows that had suffered from Listeria encephalitis. Mexican-style cheese contaminated with L. monocytogenes serotype 4b was implicated in an outbreak in which 58 of 86 cases occurred in mother and infant pairs.

Fecal carriage rates and serologic assessment indicate that many people are exposed to L. monocytogenes, although few develop invasive infection. Most infections are observed in neonates and older persons, a finding suggesting a host-associated immune defect. Also predisposed are persons with reticuloendothelial dysfunction caused by diabetes or cirrhosis, those requiring immunosuppressive or corticosteroid therapy, and patients with malignancy, particularly lymphoma or Hodgkin disease, solid organ transplantation, pregnancy, or human immunodeficiency virus infection. The propensity for listeriosis in persons with T-cell dysfunction demonstrates the important role of thymus-derived lymphocytes and mononuclear phagocytes in host response to this intracellular pathogen. Listeria replicates within the cytoplasm of host cells and usurps their actin-based contractile mechanism to form filopods that are ingested by adjacent cells. This cell-to-cell spread avoids direct contact with the extracellular environment. Thus, cell-mediated immunity is highly important in listeriosis. Immune globulins and complement also function in host defense, but only limited protection is conferred by these T-cell-independent mechanisms.

L. monocytogenes can invade the eyes and skin of humans by direct exposure or inoculation, but invasion of the bloodstream from a gastrointestinal tract source is the most likely route. The organism has tropism for the central nervous system (CNS), particularly the meninges. Hematogenous maternal infection is presumed to seed the placenta and to cause fetal infection through the umbilical vein, with dissemination to multiple organs. Human listeriosis is characterized by the
formation of nodular granulomas that vary in site and number according to the mode of infection, the dose of organisms, and the age and resistance of the host. In neonates, the liver usually is involved diffusely, and granulomas also are observed in the lungs, spleen, adrenal glands, and lymph nodes. The organisms cause necrosis followed by proliferative activity of cells of the reticuloendothelial system. The granulomas undergo central necrosis. At the periphery of the necrotic focus, chronic inflammatory cells and organisms may be seen.

Listeria infections affecting children can be divided into three broad categories: maternal infections, neonatal infections, and infections beyond the neonatal period in children with or without predisposing conditions.