Listeriosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

Listeriosis is a heterogeneous group of infectious diseases caused by Listeria spp. (commonly Listeria monocytogenes), a flagellated, catalase-positive, facultatively intracellular, anaerobic, gram-positive bacillus. Listeriosis is a relatively uncommon infection with an annual incidence of listeriosis in the United States ranging between 0.2 to 0.3 cases per 100,000 individuals. Listeria is commonly transmitted via contaminated food or via vertical transmission from mother to fetus. Following transmission, Listeria encodes thermoregulated virulence factor in the human host, invades the intestinal epithelium, and multiplies intracellularly within phagocytic phagolysosomes. Following transmission, Listeria may cause any the following syndromes: neonatal listeriosis, genitourinary infection, gastroenteritis, central nervous system infection, endocarditis, bacteremia, and localized infection. Risk factors in the development of listeriosis include ingestion of uncooked meats and vegetables, unpasteurized (raw) milk and cheeses, processed (or ready-to-eat) meats and smoked seafood.^[1] Populations at higher risk of developing listeriosis include immunosuppressed patients (e.g. transplant recipients, patients with history of splenectomy, patients receiving immunosuppressive therapy, or patients with advanced diabetes, kidney/ liver disease, or active malignancy), neonates, pregnant women, and elderly patients.^[2] The majority of healthy patients do not develop clinical manifestations or may develop a mild, transient bacteremia. Early clinical manifestations (usually fever) typically develop early within 24 hours of transmission. If left untreated, patients typically progress within 1-90 days to develop Listeria-associated complications, including bacteremia, abscess formation, pneumonia, ARDS, acute kidney injury, and CNS impairment. Among healthy children and young adults, the prognosis of listeriosis is generally good. Prognosis is poorer among high-risk populations, who are more likely to develop complications and death even with prompt management. For symptomatic patients, diagnosis of listeriosis is confirmed following the isolation of Listeria monocytogenes from a normally sterile site, such as blood, spinal fluid (in the setting of nervous system involvement), or amniotic fluid/placenta (in the setting of pregnancy). Nonetheless, the diagnosis of listeriosis requires a high pre-test probability, given the organism’s morphological similarity to other organisms, variability in clinical manifestations, and low rates of Gram-staining. All patients with listeriosis require antibiotic therapy. Ampicillin, with or without gentamicin, is the antibiotic of choice for the treatment of listeriosis. Patients intolerant to penicillins may be managed with trimethoprim-sulfamethoxazole. Duration of therapy depends on the clinical syndrome and may range from several days in non-complicated gastroenteritis to 6 weeks in endocarditis or encephalitis. Listerial gastroenteritis is frequently self-limited among healthy adults, but a short course of oral ampicillin may be considered among immunocompromised or pregnant individuals or those who have ingested food implicated in outbreaks. Non-gastroenteritis listeriosis often requires hospitalization and intravenous (IV) antibiotic therapy. Surgery may be required among patients who develop complications, such as abscess formation or advanced endocarditis. General recommendations for the primary prevention of infection with Listeria include appropriately washing and handling of food, maintaining a clean and safe kitchen and environment, cooking meat and poultry thoroughly, safely storing foods, and choosing safe foods. There are no vaccines against listeriosis, and pharmacologic prophylaxis is not recommended.

Listeria monocytogenes (formerly Bacterium monocytogenes) was first isolated in 1926 by Everitt Murray. The organism was renamed Listeria monocytogenes in 1940 in honor of Joseph Lister. Initially described as a bacteria of laboratory animals, the first human cases were described in 1929 by Nyfeldt in Denmark.

Listeriosis may be classified according to the clinical syndrome into the following: neonatal listeriosis, genitourinary infection, gastroenteritis, central nervous system infection, endocarditis, bacteremia, and localized infection.

Listeria is commonly transmitted via contaminated food or via vertical transmission from mother to fetus. Following transmission, Listeria encodes thermoregulated virulence factor in the human host, invades the intestinal epithelium, and multiplies intracellularly within phagocytic phagolysosomes. It is able to escape lysosomal destruction by secreting phospholipases and listeriolysin O, a hemolysin that is responsible for lysis the vacuole‘s membrane. Listeria then migrates between cells by forming protrusions called filopods or “rockets” using polymerized actin and Gelsolin, an actin-binding protein. Microscopically, tissue infected with Listeria monocytogenes often demonstrates microscopic features of inflammation, exudate formation, and neutrophilia. In prolonged infections, macrophages may be abundantly present in tissue specimens, and granuloma formation may occur.

Listeriosis is caused by the bacterium Listeria monocytogenes, a flagellated, catalase-positive, facultative intracellular, anaerobic, nonsporulating, Gram-positive bacillus. Listeria is commonly found in soil, water, vegetation and fecal material.

Listeriosis is associated with more than one clinical syndrome. It must be differentiated from other infections that cause fever and systemic/localized symptoms (either CNS disease, gastroenteritis, genitourinary disease, endocarditis, or bacteremia), such as E. coli, Neisseria spp., Streptococcus spp., Staphylococcus spp., Shigella, Salmonella, Campylobacter, Serratia spp., or Haemophilus spp., mononucleosis, or tuberculosis. Listeria monocytogenes must also be differentiated from other organisms that are morphologically similar, such as pneumococci, diphtheroids, or Haemophilus spp. Differential diagnosis of listeriosis additionally includes hematologic malignancies (such as leukemia or lymphoma), thyroid disease, drug fever, vasculitides, or rheumatologic diseases.

The annual incidence of listeriosis in the United States is approximately 0.2-0.3 cases per 100,000 individuals.^[3] The incidence of listeriosis is higher among females (especially pregnant women), neonates, elderly individuals, and Hispanic individuals. Listeriosis has a worldwide distribution in both developed and developing countries.^[4]

Risk factors in the development of listeriosis include ingestion of uncooked meats and vegetables, unpasteurized (raw) milk and cheeses, processed (or ready-to-eat) meats, and smoked seafood.^[1] Populations at higher risk of developing listeriosis include immunosuppressed patients (e.g. transplant recipients, patients with history of splenectomy, patients receiving immunosuppressive therapy, or patients with advanced diabetes, kidney/ liver disease, or active malignancy), neonates, pregnant women, and elderly patients.^[2]

Following transmission, the majority of healthy patients do not develop clinical manifestations or may develop a mild, transient bacteremia. Early clinical manifestations (usually fever) typically develop early within 24 hours of transmission. If left untreated, patients typically progress within 1-90 days to develop Listeria-associated complications, including bacteremia, abscess formation, pneumonia, ARDS, acute kidney injury, and CNS impairment. Among healthy children and young adults, the prognosis of listeriosis is generally good. Prognosis is poorer among high-risk populations, who are more likely to develop complications and death even with prompt management.

Fever is the most common symptom of listeriosis. Other symptoms develop on location of the infection: Patients with gastroenteritis may develop watery diarrhea, abdominal pain, vomiting, and headache. Patients with CNS infection may develop symptoms of meningitis, encephalitis, cerebritis, rhombencephalitis, or spinal cord infection, such as headache, back pain, neck pain, photophobia, phonophobia, deafness, confusion, ataxia, seizures, and neurological impairment.

The findings on the physical examination depend on the clinical manifestation of listeriosis. Common findings include fever, tachycardia, pallor, and abdominal tenderness. Signs of neurological involvement may include altered mental state, paralysis, respiratory failure, and coma.

For symptomatic patients, diagnosis of listeriosis is confirmed following the isolation of Listeria monocytogenes from a normally sterile site, such as blood, spinal fluid (in the setting of nervous system involvement), or amniotic fluid/placenta (in the setting of pregnancy). Cultures from non-sterile sites, such as stool samples, are not recommended (1-15% carriage rate) but may still be useful in gastroenteritis with high suspicion of listeriosis. Listeria monocytogenes may be isolated readily on routine media. Since Listeria is an intracellular organism, only 1/3 of cultures yield positive Gram-stains. Selective enrichment media improve rates of isolation from contaminated specimens. The cultures typically require 1-2 days for growth. A negative culture does not rule out infection in the presence of strong clinical suspicion. Cerebrospinal fluid (CSF) analysis may confirm the diagnosis among patients with CNS listeriosis. Serological tests (e.g. listeriolysin O titers) have been used, but their use remains controversial and are currently not recommended. Polymerase chain reaction for the detection of the HLY gene may be diagnostic, but it is not yet widely available for commercial use. Laboratory testing on asymptomatic patients (including high-risk asymptomatic patients) is not recommended.^[4]

Brain MRI may be helpful in the diagnosis of Listeria monocytogenes brain lesions. Findings on MRI suggestive of listeriosis include lesions in the cerebellum, brainstem, and cortex.^[5] High-signal lesions on T2-weighted images and enhancing lesions on T1-weighted images can be identified in the cerebral parenchyma on MRI following administration of IV contrast. With a high pre-test probability, brainstem involvement on MRI is strongly suggestive of listeriosis. Contrast MRI is recommended among all patients presenting with listerial meningitis, listerial bacteremia, suggestive CNS signs and symptoms or upon suspicion of intracranial listeriosis.

Additional studies for the diagnosis of listeriosis are not recommended.

All patients with listeriosis require antibiotic therapy. Ampicillin, with or without gentamicin, is the antibiotic of choice for the treatment of listeriosis. Patients intolerant to penicillins may be managed with trimethoprim-sulfamethoxazole. Duration of therapy depends on the clinical syndrome and may range from several days in non-complicated gastroenteritis to 6 weeks in endocarditis or encephalitis. Listerial gastroenteritis is frequently self-limited among healthy adults, but a short course of oral ampicillin may be considered among immunocompromised or pregnant individuals or those who have ingested food implicated in outbreaks. Non-gastroenteritis listeriosis often requires hospitalization and intravenous (IV) antibiotic therapy.

Surgery is not usually recommended among patients with listeriosis. Surgery may be indicated in cases of Listeria-associated complications, such as abscess formation requiring abscess drainage or advanced endocarditis require valve repair.

General recommendations for the primary prevention of infection with Listeria include appropriately washing and handling of food, maintaining a clean and safe kitchen and environment, cooking meat and poultry thoroughly, safely storing foods, and choosing safe foods. In addition to the general recommendations on how to prevent an infection with Listeria, there are additional recommendations specifically for persons who are at higher risk, such as pregnant women, elderly, and individuals with compromised immune status. There is no vaccine against listeriosis. Pharmacologic prophylactic measures against listeriosis are not helpful.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2] Yazan Daaboul, M.D. Serge Korjian M.D.

Listeria monocytogenes (formerly Bacterium monocytogenes) was first isolated in 1926 by Everitt Murray. The organism was renamed Listeria monocytogenes in 1940 in honor of Joseph Lister. Initially described as a bacteria of laboratory animals, the first human cases were described in 1929 by Nyfeldt in Denmark.

• Listeria monocytogenes is thought to had been identified by Hulphers in histologic sections before World War I in Sweden.^[2]
• In 1926, Listeria monocytogenes was first isolated from rabbits by the bacteriologist Everitt George Dunne Murray following an outbreak in laboratory animals.^[3][4]
• Murray named the organism Bacterium monocytogenes. Murray’s culture is the oldest well-preserved culture of the bacteria and is kept at the Pasteur Institute in Paris.^[3][4]
• In 1929, the first human cases of Listeria infection were reported in Denmark by Nyfeldt. At the time, he associated infectious mononucleosis to listeriosis, claiming that the bacteria was the causative agent of infectious mononucleosis. However, this hypothesis was not proven.^[2][3]
• Listeria was later renamed Listerlla monocytogenes and finally Listeria monocytogenes in 1940 to honor Joseph Lister, the British scientist who discovered that sterilizing surgical instruments before operations is associated with reduced risk of infections.^[5]
• In 1934, Burn first established a connection between Listeria monocytogenes and neonatal granulomatous septicemia.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Listeriosis may be classified according to the clinical syndrome into the following: neonatal listeriosis, genitourinary infection, gastroenteritis, central nervous system infection, endocarditis, bacteremia, and localized infection.

Listeriosis may be classified according to the clinical syndrome. Clinical syndromes are shown in the following table:^[1][2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Yazan Daaboul, M.D.

Listeria is commonly transmitted via contaminated food or via vertical transmission from mother to fetus. Following transmission, Listeria encodes thermoregulated virulence factor in the human host, invades the intestinal epithelium, and multiplies intracellularly within phagocytic phagolysosomes. It is able to escape lysosomal destruction by secreting phospholipases and listeriolysin O, a hemolysin that is responsible for lysis the vacuole‘s membrane. Listeria then migrates between cells by forming protrusions called filopods or “rockets” using polymerized actin and Gelsolin, an actin-binding protein. Microscopically, tissue infected with Listeria monocytogenes often demonstrates microscopic features of inflammation, exudate formation, and neutrophilia. In prolonged infections, macrophages may be abundantly present in tissue specimens, and granuloma formation may occur.

• In adults, Listeria is usually found in soil, water, vegetation and fecal material. It is commonly transmitted via contaminated food.

• Uncooked meats and vegetables (including refrigerated foods)
• Unpasteurized (raw) milk and cheeses, as well as other foods made from unpasteurized milk
• Cooked or processed foods, including certain soft cheeses, processed (or ready-to-eat) meats, and smoked seafood

• In neonates, Listeria is usually transmitted by vertical transmission from mother to fetus.

• Listeria monocytogenes genes encodes thermoregulated virulence factor.
• The expression of virulence factors is optimal at 37 ºC and is controlled by a transcriptional activator, PrfA, whose expression is thermoregulated by the PrfA thermoregulator UTR element.
• At low temperatures, the PrfA transcript is not translated due to structural elements near the ribosome binding site.
• As Listeria infects the human host, the translation of the virulent genes is initiated.

• The primary site of infection is the intestinal epithelium, where the bacteria invade non-phagocytic cells via the “zipper” mechanism:

• Uptake is stimulated by the binding of listerial internalins (Inl) to host cell adhesion factors such as E-cadherin or Met.
• This binding activates certain Rho-GTPases which subsequently bind and stabilize the Wiskott-Aldrich syndrome protein (WASp).
• WASp can then bind the Arp2/3 complex and serve as an actin nucleation point.
• Subsequent actin polymerization extends the cell membrane around the bacterium, eventually engulfing it.
• The net effect of internalin binding is to exploit the junction forming-apparatus of the host into internalizing the bacterium.

• Listeria’s ability to penetrate the gastrointestinal lining depends on the following factors:^[1]

• Number of ingested organisms
• Host’s susceptibility
• Virulence of the organism

• Listeria may also cross the blood-brain barrier, and fetoplacental barrier, and cause meningoencephalitis, and mother-to-fetus infections.

• The majority of bacteria are targeted by the immune system prior to proliferation and development of clinical manifestations. Organisms that escape the initial immune response avoid the immune system by spreading though intracellular mechanisms within phagocytes.

• Listeria expresses D-galactose receptors on its surface. D-galactose binds to the macrophage‘s polysaccharide receptors and induces phagocytosis.
• Once phagocytosed, Listeria is encapsulated by the host cell‘s acidic phagolysosome.
• Listeria escapes lysosomal destruction by secreting phospholipases (encoded by PLCB gene) and listeriolysin O (encoded by HLY gene), a hemolysin that is responsible for lysis the vacuole‘s membrane.^[2]
• Listeria then replicates intracellularly within the host cytoplasm.

• Extracellularly, Listeria has flagellar-driven motility. However, at 37°C, flagella cease to develop, and the bacteria has uses the host cell‘s cytoskeleton to migrate.
• Listeria polymerizes an actin tail or “comet” using virulence factor ActA.^[3][4]
• The tail is formed in a polar manner. Its function is to aid the bacteria in migrating towards the host cell’s outer membrane.^[5]
• Gelsolin is an actin-binding protein that is located at the tail of Listeria. Gelsolin accelerates the bacterium‘s motility.
• Once at the cell‘s inner surface, the actin-propelled Listeria pushes against the cell membrane to form protrusions called filopods or “rockets”.
• The protrusions are guided by the cell‘s leading edge to contact with adjacent cells, which subsequently engulf the “Listeria rocket”.^[6]

• Tissue infected with Listeria monocytogenes often demonstrates microscopic features of inflammation, exudate formation, and neutrophilia.^[7] Occasionally, focal abscesses and yellow nodular formation may be present, suggestive of tissue necrosis.
• Commonly infected tissues include:

• Lungs
• Spleen
• Liver
• Lymph nodes
• Maternal placenta

• Meningeal listeriosis cannot be distinguished from other causes of meningitis by microscopy alone. However, identification of intracellular gram-positive bacilli in the CSF is highly suggestive of the diagnosis.^[8]
• In prolonged infections, macrophages may be abundantly present in tissue specimens, and granuloma formation may occur.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Listeriosis is caused by the bacterium Listeria monocytogenes, a flagellated, catalase-positive, facultative intracellular, anaerobic, nonsporulating, Gram-positive bacillus. Listeria is commonly found in soil, water, vegetation and fecal material.^[1]

• Listeriosis is caused by the bacterium Listeria spp.
• Listeria monocytogenes is the most common species associated with development of listeriosis.
• The genus Listeria contains ten species:

• L. fleischmannii
• L. grayi
• L. innocua
• L. ivanovii
• L. marthii
• L. monocytogenes
• L. rocourtiae
• L. seeligeri
• L. weihenstephanensis
• L. welshimeri

• Of note, Listeria dinitrificans was previously thought to be part of the Listeria genus, but it has been reclassified into the new genus Jonesia.^[2]

Bacteria; Firmicutes; Bacilli; Bacillales; Listeriaceae; Listeria; Listeria monocytogenes.

• Listeria monocytogenes is a flagellated, catalase-positive, facultative intracellular, anaerobic, nonsporulating, Gram-positive bacillus.

• In the environment, Listeria monocytogenes is commonly found in soil, water, vegetation and fecal material.
• Animals may be asymptomatic carriers of Listeria.^[1]
• L. monocytogenes has been associated with foods such as raw milk, pasteurized fluid milk, cheeses (particularly soft-ripened varieties), ice cream, raw vegetables, fermented raw-meat sausages, raw and cooked poultry, raw meats, and raw and smoked fish.^[3]
• Listeria has the ability to grow at temperatures as low as 0°C, allows its multiplication in refrigerated foods. At refrigerated temperature such as 4°C, the amount of ferric iron in the environment promotes the growth of L. monocytogenes.^[4]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Yazan Daaboul, M.D.

Listeriosis is associated with more than one clinical syndrome. It must be differentiated from other infections that cause fever and systemic/localized symptoms (either CNS disease, gastroenteritis, genitourinary disease, endocarditis, or bacteremia), such as E. coli, Neisseria spp., Streptococcus spp., Staphylococcus spp., Shigella, Salmonella, Campylobacter, Serratia spp., or Haemophilus spp., mononucleosis, or tuberculosis. Listeria monocytogenes must also be differentiated from other organisms that are morphologically similar, such as pneumococci, diphtheroids, or Haemophilus spp. Differential diagnosis of listeriosis additionally includes hematologic malignancies (such as leukemia or lymphoma), thyroid disease, drug fever, vasculitides, or rheumatologic diseases.

The differential diagnosis of listeriosis includes the following:

• Infectious causes of gastroenteritis, such as E. coli, Shigella, Salmonella, or Campylobacter
• Infectious causes of neonatal meningitis, such as E. coli or Group B Streptococcus
• Infectious causes of CNS disease, such as N. meningitidis, Streptococcus spp., or abscess formation
• Infectious causes of genitourinary diseases, such as Candida infections, E. coli, Staphylococcus spp., enterobacteriaceae, Serratia spp., or Hemophilus spp.
• Infectious causes of endocarditis, such as Staphylococcus or enterobacteriaceae
• Other organisms that have morphological resemblance to Listeria, such as pneumococci, diphtheroids, or Haemophilus spp.
• Hematological malignancies
• Tuberculosis
• Infectious mononucleosis
• Sarcoidosis
• Drug fever
• Thyroid disease
• Rheumatologic disease
• Vasculitis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

The annual incidence of listeriosis in the United States is approximately 0.2-0.3 cases per 100,000 individuals.^[1] The incidence of listeriosis is higher among females (especially pregnant women), neonates, elderly individuals, and Hispanic individuals. Listeriosis has a worldwide distribution in both developed and developing countries.^[2]

• The annual incidence of listeriosis in the United States is approximately 0.2-0.3 cases per 100,000 individuals.^[1]
• The CDC estimates that approximately 1600 illnesses and 260 deaths due to listeriosis occur annually in the United States.^[2]
• Compared with the 1980s, the incidence of listeriosis significantly declined by 42% in the past 10 years. The incidence of listeriosis is thought to have plateaued.^[3]
• The global annual incidence of listeriosis is estimated at 0.7 per 100,00 cases.^[4]
• The global incidence of listeriosis among those >70 years of age is 2.1 per 100,00 cases.^[4]
• The incidence among pregnant women is 12.0 per 100,000 cases.^[4]

Listeriosis occurs more frequently in neonates and in the elderly.

• Since listeriosis affects pregnant women (approximately 25% to 30% of all cases), women are more likely to develop listeriosis compared with men.
• There is no predilection to listeriosis when men and non-pregnant women are compared.

• Racial predilection to the development of listeriosis is unconfirmed.
• Pregnant Hispanic women are thought to be at higher risk of developing listeriosis, but the association with the disease may be due to pregnancy or due to ethnicity.^[5]

• Listeriosis has a worldwide distribution in both developed and developing countries.^[6]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [3]

Risk factors in the development of listeriosis include ingestion of uncooked meats and vegetables, unpasteurized (raw) milk and cheeses, processed (or ready-to-eat) meats, and smoked seafood.^[1] Populations at higher risk of developing listeriosis include immunosuppressed patients (e.g. transplant recipients, patients with history of splenectomy, patients receiving immunosuppressive therapy, or patients with advanced diabetes, kidney/ liver disease, or active malignancy), neonates, pregnant women, and elderly patients.^[2]

The following foods may be associated with higher risk of developing listeriosis:^[1]

• Uncooked meats and vegetables
• Unpasteurized (raw) milk and cheeses as well as other foods made from unpasteurized milk
• Cooked or processed foods, including certain soft cheeses
• Processed eady-to-eat meats, such as hot dogs and deli meats (contamination may occur after factory cooking but before packaging or even at the deli counter)
• Smoked seafood
• Mexican-style cheeses (such as queso fresco)

Shown below is a table summarizing low and high risk cheese types.^[3]

The following are considered populations at high risk of developing listeria bacteremia and neurolisteriosis:^[4][5]

• Pregnant women are approximately 10-24 times more likely than the general population to develop listeriosis.^[6]
• Approximately 25% to 30% of all Listeria infections occur among pregnant women.

• Pregnant Hispanic women are approximately 24 times more likely than the general population to develop listeriosis.^[6]
• The association between Hispanic ethnicity and listeriosis is unconfirmed and may be confounded by pregnancy.

• Neonates are at high risk of developing listeriosis.
• Transmission of Listeria to neonates occurs either in-utero or during delivery.

• More than half (58%) of all Listeria infections occur among adults older than 65 years of age.
• Adults 65 years and older are approximately 4 times more likely than the general population to develop listeriosis.^[6]

• Immunosuppressed individuals have a higher risk of developing listeriosis.
• Immunosuppressed conditions include organ transplantation, history of splenectomy, active malignancy, administration of either steroids, chemotherapy, radiation, or monoclonal antibodies, advanced liver or kidney disease, diabetes mellitus, or HIV/AIDS.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Following transmission, the majority of healthy patients do not develop clinical manifestations or may develop a mild, transient bacteremia. Early clinical manifestations (usually fever) typically develop early within 24 hours of transmission. If left untreated, patients typically progress within 1-90 days to develop Listeria-associated complications, including bacteremia, abscess formation, pneumonia, ARDS, acute kidney injury, and CNS impairment. Among healthy children and young adults, the prognosis of listeriosis is generally good. Prognosis is poorer among high-risk populations, who are more likely to develop complications and death even with prompt management.

• Following transmission, the majority of healthy patients do not develop clinical manifestations or may develop a mild, transient bacteremia.^[1]
• The median incubation period for listeriosis-associated gastroenteritis is approximately 24 hours (range from 6 hours to 10 days).
• Systemic manifestations of listeriosis may be slow-occurring, and the duration from transmission to development of systemic manifestations widely varies between 1 day to 90 days following transmission.^[2][3][4]

• Listeria-associated gastroenteritis typically occurs 24 hours following ingestion of contaminated food.
• Patients typically manifest with fever, nausea, vomiting, and watery diarrhea.
• Listeria-associated gastroenteritis is usually self-limited and lasts for a mean of 2 days among healthy individuals.
• In high-risk patients, systemic manifestations of Listeria may occur, and patients are at higher risk of developing Listeria-associated complications.^[1]

• Among pregnant women, listeriosis typically manifests during the third trimester of gestation.^[1]
• Pregnant women typically first present with mild flu-like symptoms, such as fever and chills, that are difficult to diagnose.
• As the disease progresses, pregnant women typically develop Listeria-associated bacteremia (typically without CNS involvement)
• If left untreated, listeriosis among pregnant women typically results in fetal sequelae, including fetal death, premature birth, or neonatal sepsis.^[1]

• Neonates may be infected either in-utero infection, which manifests with neonatal sepsis or during delivery, which manifests with neonatal meningitis.
• Both infections are usually rapid-occurring, and infected neonates appear sick-looking with greyish-bluish discoloration at birth.
• If left untreated, neonates may develop granulomatosis infantiseptica, a severe in-utero infection, and death.^[1]

• L. monocytogenes has tropism for the brain stem and meninges.
• Patients with Listeria-associated CNS infection typically develop fever followed by altered mental status, seizures, cranial nerve palsy, hemiplegia, and ataxia.^[1]
• Patients may either develop rhombencephalitis, cerebritis, spinal cord infection, meningitis alone, encephalitis alone, or both (meningoencephalitis).
• Patients with Listeria-associated rhombencephalitis typically experience a bi-phasic course. First, patients develop worsening headache, fever, vomiting for a 3-5 days, followed by an abrupt-onset of neurological impairment (cranial nerve palsy, ataxia, altered mental status, seizures).^[1]
• If left untreated, brain abscesses may develop. The location of the brain abscesses is typically in the thalamus, pons, and/or medulla.
• The majority of patients with advanced CNS disease develop long-term sequelae.

Listerial endocarditis may affect either native or prosthetic valves.

• If left untreated, the majority of patients with Listeria-associated endocarditis progress to develop bacteremia.^[1]

• Compared with the general population, high-risk patients are more likely to develop invasive disease and Listeria-associated complications.^[5]
• Complications of invasive disease include the following:^[1][6]
• Disseminated intravascular coagulation
• ARDS
• Rhabdomyolysis
• Acute kidney injury
• Septicemia^[7]
• Meningitis^[7]
• Encephalitis^[8]
• Corneal ulcer^[9]
• Pneumonia^[10]
• Intrauterine or cervical infection in pregnant women, may result in:^[11]

• Spontaneous abortion (2nd/3rd trimester)
• Stillbirth
• Preterm birth
• Granulomatosis infantiseptica: pyogenic granulomas distributed over the whole body, and the newborn may suffer from physical retardation

The prognosis of listeriosis depends on the health status of the host:^[12]

• Healthy children and young adults have a good prognosis and are at low-risk of developing Listeria-associated complications and long-term sequelae.
• High-risk populations, including pregnant women, neonates, elderly, and immunosuppressed individuals, have a poorer prognosis with a high death rate (even when treatment is administered promptly).

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]

There are no screening recommendations for listeriosis.^[1]

There are no screening recommendations for listeriosis.^[1]

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