Listeriosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathogenesis
L monocytogenes is ubiquitous in the environment. The main route of acquisition of Listeria is through the ingestion of contaminated food products. Listeria has been isolated from raw meat, dairy products, vegetables, and seafood. Soft cheeses and unpasteurized milk are potential dangers, however post-pasteurization outbreaks of infection from dairy have been from pasteurized milk.
There are four distinct clinical syndromes:
- Infection in pregnancy: Listeria can proliferate asymptomatically in the vagina and uterus. If the mother becomes symptomatic, it is usually in the third trimester. Symptoms include fever, myalgias, arthralgias and headache. Abortion, stillbirth and preterm labor are complications of GU infection.
- Neonatal infection (granulomatosis infantisepticum): There are two forms. One, an early-onset sepsis, with Listeria acquired in utero, results in premature birth. Listeria can be isolated in the placenta, blood, meconium, nose, ears, and throat. Another, late-onset meningitis is acquired through vaginal transmission, although it also has been reported with caesarean deliveries.
- CNS infection: Listeria has a predilection for the brain parenchyma, especially the brain stem, and the meninges. Mental status changes are common. Seizures occur in at least 25% of patients. Cranial nerve palsies, encephalitis, meningitis, meningoencephalitis and abscesses can all occur.
- Gastroenteritis: L monocytogenes can produce food-borne diarrheal disease, which typically is noninvasive. The median incubation period is 1-2 days, with diarrhea lasting anywhere from 1-3 days. Patients present with fever, muscle aches, gastrointestinal nausea or diarrhea, headache, stiff neck, confusion, loss of balance, or convulsions.