Neonatal listeriosis is acquired transplacentally or during or after delivery. Symptoms are those of sepsis. Diagnosis is by culture of mother and infant. Treatment is antibiotics, initially ampicillin plus an aminoglycoside.
In utero infection with Listeria monocytogenes can result in fetal dissemination with granuloma formation (eg, in the skin, liver, adrenal glands, lymphatic tissue, lungs, and brain). If a rash is present, it is referred to as granulomatosis infantisepticum. Aspiration or swallowing of amniotic fluid or vaginal secretions can lead to in utero or perinatal infection of the lungs, manifesting in the first several days of life with respiratory distress, shock, and a fulminant course.
Symptoms and Signs
Infections in pregnant women may be asymptomatic or characterized by a primary bacteremia manifesting first as a nonspecific flu-like illness.
In the fetus and neonate, clinical presentation depends on the timing and route of infection. Abortion, premature delivery with amnionitis (with a characteristic brown, murky amniotic fluid), stillbirth, or neonatal sepsis (see Symptoms and Signs) is common. Infection may be apparent within hours or days of birth (early onset) or it may be delayed up to several weeks. Neonates with early-onset disease frequently are of low birth weight, have associated obstetric complications, and show evidence of sepsis soon after birth with circulatory or respiratory insufficiency or both. Neonates with the delayed-onset form are usually full-term, previously healthy neonates presenting with meningitis or sepsis.
Blood and cervix specimens should be obtained from any pregnant woman with an unexplained febrile disease and cultured for L. monocytogenes. A sick neonate whose mother has listeriosis should be evaluated for sepsis (see Neonatal Sepsis), including cultures of either umbilical cord or peripheral blood, CSF, gastric aspirate, meconium, any potentially infected tissue, the mother's lochia and exudates from cervix and vagina, grossly diseased parts of the placenta, and amniotic fluid (if available). CSF examination may show a predominance of mononuclear cells, but usually polymorphonuclear cells predominate. Gram-stained smears frequently are negative but may show pleomorphic, gram-variable coccobacillary forms, which should not be disregarded as diphtheroid contaminants. Laboratory confirmation of the organism involves biochemical testing and observation of motility using a slide test or showing motility in semisolid media. To do the slide test, colonies of the organism that have grown on solid media are mixed with saline and examined under a microscope. L. monocytogenes exhibits a distinctive end-over-end “tumbling” motility due to the presence of flagella at both ends. Serologic tests are not useful. Molecular detection via PCR appears to be sensitive and specific but remains a research tool at present.
Mortality, ranging from 10 to 50%, is higher in neonates with early-onset disease.
Treatment of the newborn is with ampicillin plus an aminoglycoside (see also Aminoglycosides). A 14-day course is usually satisfactory (21 days for meningitis), but the optimal duration is unknown. Other possible drugs include ampicillin or penicillin with rifampin or trimethoprim/sulfamethoxazole, trimethoprim/sulfamethoxazole alone, and meropenem, but they have not been well evaluated.
Neonates with sepsis require other measures (see Treatment). In heavy infection, drainage/secretion precautions may be considered.
Food products that may be contaminated by L. monocytogenes (eg, unpasteurized dairy products, soft cheeses, raw vegetables, prepared deli meats and salads, refrigerated meat spreads or smoked seafood) should be avoided by pregnant women. If infection during pregnancy is recognized, treatment may then be given before delivery or intrapartum to prevent vertical transmission, but the usefulness of such treatment is unproved.
Last full review/revision May 2013 by Mary T. Caserta, MD
Content last modified July 2013