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Listeria monocytogenes infection remains clinically significant because delayed recognition can lead to meningitis, sepsis, fetal loss, neonatal infection, and other severe complications. An important practice gap exists in the early identification and empiric treatment of listeriosis, particularly in older adults, pregnant women, immunocompromised patients, and patients with atypical presentations or negative initial cultures. This activity addresses that gap by reviewing risk-based diagnostic evaluation, interpretation of cerebrospinal fluid and microbiologic findings, appropriate empiric and targeted antimicrobial therapy, and prevention strategies. Participants are expected to gain improved diagnostic accuracy, stronger risk assessment, updated management strategies, and enhanced ability to collaborate with interprofessional team members to reduce complications and improve patient-centered outcomes. Objectives: Identify the epidemiological and clinical relevance of Listeria monocytogenes infection, including its morbidity and mortality when not treated quickly. Assess the risk factors for Listeria monocytogenes acquisition and infection, including individual patient susceptibility and food-consumption behavior, and provide appropriate counseling to selected patients. Compare the clinical, laboratory, and radiological features of meningoencephalitis and meningitis caused by Listeria monocytogenes with those of other etiologies that cause similar disease. Collaborate with other healthcare professionals to determine which patients presenting with central nervous system infections should have proper and timely diagnostic tests and antibiotic coverage for Listeria monocytogenes. Access free multiple choice questions on this topic.

Listeria monocytogenes is a gram-positive, facultative anaerobic, intracellular rod with widespread environmental distribution, commonly found in soil, water, and vegetation, and capable of transient colonization of the human and animal gastrointestinal tract.[1] Human infection typically occurs through ingestion of contaminated foods, particularly raw or inadequately processed products.[1] While infection in the general population is usually asymptomatic or mildly symptomatic, vulnerable hosts, including pregnant individuals, older adults, and immunocompromised patients, are at increased risk for invasive disease, such as antepartum and vertically transmitted infection and central nervous system involvement, which are associated with substantial morbidity and mortality. Please see StatPearls' companion resources, "Bacterial Meningitis, Neonatal Meningitis, Bacterial Diarrhea, Vertical Transplacental Infections, and Antepartum Infections," for further information.

Listeria monocytogenes is a motile, non–spore-forming, facultative anaerobic, gram-positive rod that can grow at refrigeration temperatures (4°C). The organism was named in honor of Joseph Lister after investigators isolated it from a patient with meningitis in 1919, although they first formally described it in 1926 as a zoonotic pathogen affecting rabbits. Listeriosis was recognized as a foodborne disease in 1981 and is now considered a major biohazard in the food industry. Phylogenetically, Listeria monocytogenes is divided into 4 major lineages (I–IV); serotypes within lineage I (1/2a, 3b, and 4b) are most frequently associated with human disease, whereas serotypes within lineage II (1/2c and 3a) are more commonly isolated from food and food-processing environments. Lineages III and IV are primarily animal-associated. The organism’s ability to survive at low temperatures, high salt concentrations, and low pH, as well as to form biofilms, contributes to its persistence in food and food-processing settings.[2]

Listeria infection is the third leading cause of death from foodborne illness in the United States. The Centers for Disease Control and Prevention (CDC) estimates that each year in the United States, 1250 people are infected with Listeria, and 172 people die from the infection.[CDC. Listeria Outbreaks] L monocytogenes is ubiquitous and is found in soil, water, and decaying vegetation. The bacterium can also be found in the human and animal digestive tracts. Foods associated with the highest rates of L monocytogenes–related infections include: Raw sprouts Unpasteurized milk Soft cheeses, especially Mexican-style Cold deli meats Cold hot dogs Smoked seafood

Listeria infection is the third leading cause of death from foodborne illness in the United States. The Centers for Disease Control and Prevention (CDC) estimates that each year in the United States, 1250 people are infected with Listeria, and 172 people die from the infection.[CDC. Listeria Outbreaks] L monocytogenes is ubiquitous and is found in soil, water, and decaying vegetation. The bacterium can also be found in the human and animal digestive tracts. Foods associated with the highest rates of L monocytogenes–related infections include: Raw sprouts Unpasteurized milk Soft cheeses, especially Mexican-style Cold deli meats Cold hot dogs Smoked seafood Several notable foodborne Listeria monocytogenes outbreaks have been documented historically. In 1981, L monocytogenes was definitively established as a foodborne pathogen following investigations linking infections to contaminated foods. In 1985, a large outbreak associated with soft cheese resulted in 142 cases, 28 deaths, and 20 fetal losses, highlighting the organism’s severe impact on vulnerable populations. In the United States, the CDC continues to monitor and lead investigations of multistate Listeria outbreaks. Recent outbreaks reported in 2025 include those linked to prepared pasta meals (27 cases, 6 deaths), ready-to-eat foods (10 cases, 1 death), and supplement shakes (42 cases, 14 deaths). [CDC, Listeria Outbreaks] Surveillance data from 10 US sites between 2008 and 2023 demonstrated that, unlike vaccine-preventable causes of bacterial meningitis, the incidence of L monocytogenes meningitis has remained unchanged over time, with a persistently high case-fatality rate of approximately 8%.[3] In Europe, listeriosis is increasing, with the highest number of reported cases recorded in 2023. A consistent upward trend was observed across all member states between 2019 and 2023, with a total of 2993 cases, and no country showed a declining incidence.[ECDC, Annual Epidemiological Report for Listeriosis for 2023]. Furthermore, Listeria monocytogenes represents the causative etiology in approximately 3% of all bacterial meningitis in the US,[3] but its relevance as a cause of bacterial meningitis is greater in subpopulations with specific risk factors, accounting for 4% to 7% of cases in early neonatal meningitis,[4][5] 6% in patients with diabetes mellitus,[6] 8% in patients with alcohol use disorder,[7] 17% in pregnant women,[8] 33% in patients with solid organ transplant,[9] and 40% in patients taking immunosuppressive medication.[10]

Several notable foodborne Listeria monocytogenes outbreaks have been documented historically. In 1981, L monocytogenes was definitively established as a foodborne pathogen following investigations linking infections to contaminated foods. In 1985, a large outbreak associated with soft cheese resulted in 142 cases, 28 deaths, and 20 fetal losses, highlighting the organism’s severe impact on vulnerable populations. In the United States, the CDC continues to monitor and lead investigations of multistate Listeria outbreaks. Recent outbreaks reported in 2025 include those linked to prepared pasta meals (27 cases, 6 deaths), ready-to-eat foods (10 cases, 1 death), and supplement shakes (42 cases, 14 deaths). [CDC, Listeria Outbreaks] Surveillance data from 10 US sites between 2008 and 2023 demonstrated that, unlike vaccine-preventable causes of bacterial meningitis, the incidence of L monocytogenes meningitis has remained unchanged over time, with a persistently high case-fatality rate of approximately 8%.[3] In Europe, listeriosis is increasing, with the highest number of reported cases recorded in 2023. A consistent upward trend was observed across all member states between 2019 and 2023, with a total of 2993 cases, and no country showed a declining incidence.[ECDC, Annual Epidemiological Report for Listeriosis for 2023]. Furthermore, Listeria monocytogenes represents the causative etiology in approximately 3% of all bacterial meningitis in the US,[3] but its relevance as a cause of bacterial meningitis is greater in subpopulations with specific risk factors, accounting for 4% to 7% of cases in early neonatal meningitis,[4][5] 6% in patients with diabetes mellitus,[6] 8% in patients with alcohol use disorder,[7] 17% in pregnant women,[8] 33% in patients with solid organ transplant,[9] and 40% in patients taking immunosuppressive medication.[10] Pregnancy is a major risk factor for listeriosis, with a crude incidence estimated to be 10 to 100 times higher in this group than in the general population. The incidence of maternal–neonatal listeriosis, defined as the presence of Listeria in any maternal, fetal, or neonatal sample, is estimated at 4 to 10 per 100,000 pregnant women in Europe and North America and can account for 11% to 20% of hospitalizations for invasive listeriosis. Maternal–neonatal listeriosis remains one of the infections associated with the highest fetal and neonatal morbidity, leading to fetal losses in at least 25% of cases. A prospective study of 189 neonates born to mothers who tested positive for Listeria monocytogenes infection showed that 76% of neonates born alive to mothers with microbiologically proven maternal–neonatal listeriosis developed infection.[11] One of the largest listeriosis outbreaks occurred in South Africa in late 2017, involving nearly 1000 cases. Among reported cases, approximately 42% involved infected fetuses and neonates.[12]

Current knowledge of the pathophysiology of listeriosis derives largely from results from studies using mouse infection models. Following ingestion, the organism crosses the intestinal epithelium through internalin-dependent interactions (InlA and InlB) with host receptors such as E-cadherin and Met, enabling invasion of nonphagocytic epithelial cells. The liver is thought to be the first target organ after intestinal translocation, where Listeria spp actively multiply until a cell-mediated immune response controls the infection.[13][14] After internalization, the bacterium escapes the phagolysosome via listeriolysin O and phospholipases, replicates within the host cell cytosol, and spreads directly from cell to cell using ActA-dependent actin polymerization, thereby avoiding extracellular exposure and antibody-mediated immune clearance.[14]

Current knowledge of the pathophysiology of listeriosis derives largely from results from studies using mouse infection models. Following ingestion, the organism crosses the intestinal epithelium through internalin-dependent interactions (InlA and InlB) with host receptors such as E-cadherin and Met, enabling invasion of nonphagocytic epithelial cells. The liver is thought to be the first target organ after intestinal translocation, where Listeria spp actively multiply until a cell-mediated immune response controls the infection.[13][14] After internalization, the bacterium escapes the phagolysosome via listeriolysin O and phospholipases, replicates within the host cell cytosol, and spreads directly from cell to cell using ActA-dependent actin polymerization, thereby avoiding extracellular exposure and antibody-mediated immune clearance.[14] The predominantly intracellular life cycle explains the often prolonged incubation period of listeriosis, ranging from days to several weeks, compared with the rapid onset typical of extracellular bacterial meningitides, such as Streptococcus pneumoniae infection or Neisseria meningitidis infection.[14] Systemic dissemination, with invasion of the preferred secondary target organs (the brain and the gravid uterus) and progression to overt clinical disease, occurs via intermittent bacteremia following replication in the liver and spleen, with effective containment largely dependent on intact cell-mediated immunity, particularly CD8 T lymphocytes and activated macrophages.[13] Additionally, central nervous system involvement reflects both hematogenous spread and retrograde neural invasion, and Listeria monocytogenes has a characteristic predilection for the brainstem, leading to rhombencephalitis. This pattern distinguishes it from most other causes of acute bacterial meningitis. The organism’s brainstem tropism is thought to be related to bacterial migration along cranial nerves and preferential invasion of specific neuronal populations, resulting pathologically in microabscesses, perivascular inflammation, and necrotizing lesions in the pons and medulla. Unlike classic acute bacterial meningitis, listerial central nervous system infection often presents subacutely with focal neurologic deficits, cranial nerve palsies, and fluctuating consciousness, reflecting its intracellular spread and localized parenchymal invasion rather than overwhelming meningeal inflammation.[15]

The predominantly intracellular life cycle explains the often prolonged incubation period of listeriosis, ranging from days to several weeks, compared with the rapid onset typical of extracellular bacterial meningitides, such as Streptococcus pneumoniae infection or Neisseria meningitidis infection.[14] Systemic dissemination, with invasion of the preferred secondary target organs (the brain and the gravid uterus) and progression to overt clinical disease, occurs via intermittent bacteremia following replication in the liver and spleen, with effective containment largely dependent on intact cell-mediated immunity, particularly CD8 T lymphocytes and activated macrophages.[13] Additionally, central nervous system involvement reflects both hematogenous spread and retrograde neural invasion, and Listeria monocytogenes has a characteristic predilection for the brainstem, leading to rhombencephalitis. This pattern distinguishes it from most other causes of acute bacterial meningitis. The organism’s brainstem tropism is thought to be related to bacterial migration along cranial nerves and preferential invasion of specific neuronal populations, resulting pathologically in microabscesses, perivascular inflammation, and necrotizing lesions in the pons and medulla. Unlike classic acute bacterial meningitis, listerial central nervous system infection often presents subacutely with focal neurologic deficits, cranial nerve palsies, and fluctuating consciousness, reflecting its intracellular spread and localized parenchymal invasion rather than overwhelming meningeal inflammation.[15] Pregnancy is a major risk factor for listeriosis because physiologic downregulation of cell-mediated immunity, particularly type 1 helper T-cell responses, helps maintain fetal tolerance but also impairs the host’s ability to control intracellular pathogens such as Listeria monocytogenes. The placenta constitutes a unique immunologic niche, and Listeria monocytogenes efficiently invades syncytiotrophoblasts and cytotrophoblasts via internalin-dependent mechanisms, leading to placentitis with intense local bacterial replication.[13] Placental infection compromises maternal–fetal circulation and facilitates transplacental spread to the fetus, frequently resulting in miscarriage, stillbirth, or severe neonatal sepsis, often despite mild or nonspecific maternal symptoms.[16]

Listeriosis due to Listeria monocytogenes typically presents with nonspecific systemic symptoms such as fever, malaise, and headache but may progress to severe invasive disease affecting the central nervous system or, in pregnant women, the maternal–fetal unit.[12][17] Meningitis and meningoencephalitis account for the majority of central nervous system infections caused by L monocytogenes in humans (70% to 97%),[15] but the spectrum of central nervous system syndromes also includes brain abscesses and, particularly, rhombencephalitis (brainstem involvement). L monocytogenes meningitis and meningoencephalitis can present in half of patients with the classic triad of fever, neck stiffness, and altered mental status. Other clinical signs, such as focal neurologic deficits, cranial nerve palsies, and ataxia, can differ from those seen with rapid infections caused by Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae.[18] Central nervous system infection due to L monocytogenes may evolve subacutely over days to weeks, and meningismus can be less pronounced, whereas focal brainstem signs (eg, ataxia and cranial neuropathies) are more suggestive of rhombencephalitis, which is not typical of acute bacterial meningitis caused by encapsulated organisms.[19] In pregnant women, maternal infection most often presents with flu-like symptoms and fever and may be subtle or absent. Listeria spp sepsis may masquerade as pyelonephritis or influenza. Placental infection leads to high rates of fetal loss, preterm labor, or neonatal systemic disease, reflecting hematogenous placental seeding rather than overt maternal central nervous system involvement. Placental infection can occur without severe maternal disease, underscoring the need for high clinical suspicion in pregnant patients with fever and gastrointestinal prodromes.[12][17] The diagnosis is often established in retrospect following delivery of an infected infant. Neonatal infection due to Listeria spp can cause pneumonia, sepsis, or meningitis. Most neonates present with respiratory distress, fever, rash, jaundice, or lethargy. A pathognomonic, although rare, finding in neonatal infection due to Listeria spp is granulomatosis infantiseptica, a disease characterized by widespread microabscesses and granulomas.[12][20]

In pregnant women, maternal infection most often presents with flu-like symptoms and fever and may be subtle or absent. Listeria spp sepsis may masquerade as pyelonephritis or influenza. Placental infection leads to high rates of fetal loss, preterm labor, or neonatal systemic disease, reflecting hematogenous placental seeding rather than overt maternal central nervous system involvement. Placental infection can occur without severe maternal disease, underscoring the need for high clinical suspicion in pregnant patients with fever and gastrointestinal prodromes.[12][17] The diagnosis is often established in retrospect following delivery of an infected infant. Neonatal infection due to Listeria spp can cause pneumonia, sepsis, or meningitis. Most neonates present with respiratory distress, fever, rash, jaundice, or lethargy. A pathognomonic, although rare, finding in neonatal infection due to Listeria spp is granulomatosis infantiseptica, a disease characterized by widespread microabscesses and granulomas.[12][20] Listeriosis with L monocytogenes sepsis, or bacteremia without central nervous system involvement, accounts for one-third of all adult cases of invasive listeriosis. In nonpregnant adults, L monocytogenes sepsis almost always occurs in patients with malignant neoplasms, organ transplants, or other immunocompromised states. In these settings, the presentation is also nonspecific and mimics sepsis caused by other gram-positive and gram-negative pathogens.[1]

Listeriosis with L monocytogenes sepsis, or bacteremia without central nervous system involvement, accounts for one-third of all adult cases of invasive listeriosis. In nonpregnant adults, L monocytogenes sepsis almost always occurs in patients with malignant neoplasms, organ transplants, or other immunocompromised states. In these settings, the presentation is also nonspecific and mimics sepsis caused by other gram-positive and gram-negative pathogens.[1] Listeria monocytogenes can also cause a range of less common invasive syndromes, including infective endocarditis, osteoarticular infections (osteomyelitis and septic arthritis), focal abscesses (hepatic and splenic), peritonitis, and, rarely, endophthalmitis or cutaneous infection, predominantly in immunocompromised hosts.[1] These atypical focal infections account for a small minority of invasive listeriosis cases (generally <10%) but are associated with significant morbidity, often presenting subacutely and requiring prolonged antimicrobial therapy and, in some cases, surgical intervention.[1] Despite being acquired through ingestion of contaminated food, severe Listeria monocytogenes infection typically lacks prominent gastrointestinal tract symptoms because the organism does not produce enterotoxins and instead rapidly translocates across the intestinal epithelium with minimal local inflammation, favoring intracellular invasion and systemic dissemination to sanctuaries, rather than toxin-mediated enteritis.

In L monocytogenes central nervous system infection, routine blood investigations are nonspecific and typically reveal leukocytosis and elevated inflammatory markers, such as C-reactive protein. At least 2 sets of blood cultures should be obtained, because they have positive results in up to 50% of invasive listeriosis cases, including those with central nervous system involvement. Lumbar puncture is indicated in patients with suspected central nervous system infection unless contraindicated by focal neurologic deficits, severe immunosuppression, or neuroimaging findings suggestive of a space-occupying lesion with mass effect and risk of herniation, although such features are uncommon in typical listerial meningitis. Cerebrospinal fluid analysis commonly demonstrates pleocytosis (90 to 8900 cells/µL) with a mononuclear-predominant differential, elevated protein levels, and mild hypoglycorrhachia. Microbiologic identification of L monocytogenes in cerebrospinal fluid provides a definitive diagnosis; however, up to 50% of cerebrospinal fluid cultures may be negative, particularly following prior antibiotic exposure.[21] Classic cerebrospinal fluid features predictive of bacterial meningitis are frequently absent; In L monocytogenes infection, up to 23% of patients lack cerebrospinal fluid abnormalities suggestive of bacterial meningitis, compared with 12% in other bacterial etiologies. In addition, Gram stain sensitivity is low (24%) compared with approximately 80% in nonlisterial bacterial meningitis.[15] Given the limited sensitivity of conventional cerebrospinal fluid diagnostics, molecular methods are increasingly important. Polymerase chain reaction assays targeting L monocytogenes in cerebrospinal fluid demonstrate sensitivities ranging from 82% to 100% and specificities exceeding 90%, including multiplex polymerase chain reaction panels used in routine clinical practice.[22] Metagenomic next-generation sequencing of cerebrospinal fluid is an emerging complementary diagnostic tool, particularly in culture-negative cases; results from recent case series demonstrated identification of L monocytogenes by next-generation sequencing in 10 of 15 patients, including 5 with negative cerebrospinal fluid cultures.[21][23]

Given the limited sensitivity of conventional cerebrospinal fluid diagnostics, molecular methods are increasingly important. Polymerase chain reaction assays targeting L monocytogenes in cerebrospinal fluid demonstrate sensitivities ranging from 82% to 100% and specificities exceeding 90%, including multiplex polymerase chain reaction panels used in routine clinical practice.[22] Metagenomic next-generation sequencing of cerebrospinal fluid is an emerging complementary diagnostic tool, particularly in culture-negative cases; results from recent case series demonstrated identification of L monocytogenes by next-generation sequencing in 10 of 15 patients, including 5 with negative cerebrospinal fluid cultures.[21][23] In routine clinical practice, L monocytogenes is isolated by culture from sterile sites, and antimicrobial susceptibility testing is widely available and highly reproducible when performed using standardized reference methods, such as broth microdilution or gradient diffusion, in accordance with the European Committee on Antimicrobial Susceptibility Testing and the Clinical and Laboratory Standards Institute CLSI guidelines.[EUCAST. Clinical Breakpoint Tables; CLSI M45] The organism exhibits a predictable susceptibility profile, with reliable activity of ampicillin and penicillin and intrinsic resistance to cephalosporins, making extensive resistance testing unnecessary in most cases.[17] Clinically significant acquired resistance remains rare.[1] While molecular diagnostics provide rapid pathogen identification, they do not replace phenotypic antimicrobial susceptibility testing, because they cannot reliably predict antimicrobial susceptibility beyond known intrinsic resistance mechanisms.[12][17][24]

In routine clinical practice, L monocytogenes is isolated by culture from sterile sites, and antimicrobial susceptibility testing is widely available and highly reproducible when performed using standardized reference methods, such as broth microdilution or gradient diffusion, in accordance with the European Committee on Antimicrobial Susceptibility Testing and the Clinical and Laboratory Standards Institute CLSI guidelines.[EUCAST. Clinical Breakpoint Tables; CLSI M45] The organism exhibits a predictable susceptibility profile, with reliable activity of ampicillin and penicillin and intrinsic resistance to cephalosporins, making extensive resistance testing unnecessary in most cases.[17] Clinically significant acquired resistance remains rare.[1] While molecular diagnostics provide rapid pathogen identification, they do not replace phenotypic antimicrobial susceptibility testing, because they cannot reliably predict antimicrobial susceptibility beyond known intrinsic resistance mechanisms.[12][17][24] Neuroimaging is an important adjunct in the evaluation of listerial central nervous system infection, particularly in atypical presentations. Computed tomography may be normal or show nonspecific findings, whereas MRI is more sensitive, revealing meningeal enhancement, parenchymal involvement, or characteristic brainstem lesions in cases of rhombencephalitis.[15] L monocytogenes demonstrates a predilection for the pons, medulla, cerebellum, and cerebellar peduncles, often presenting as asymmetric T2-weighted and fluid-attenuated inversion recovery hyperintensities associated with cranial nerve deficits.[15][19] In up to 10% of central nervous system infections, particularly among immunocompromised patients, macroscopic brain abscesses occur without meningeal involvement and are preferentially located in subcortical regions, the thalamus, the pons, or the medulla, reflecting the organism’s intracellular and hematogenous spread.[15][17]

Neuroimaging is an important adjunct in the evaluation of listerial central nervous system infection, particularly in atypical presentations. Computed tomography may be normal or show nonspecific findings, whereas MRI is more sensitive, revealing meningeal enhancement, parenchymal involvement, or characteristic brainstem lesions in cases of rhombencephalitis.[15] L monocytogenes demonstrates a predilection for the pons, medulla, cerebellum, and cerebellar peduncles, often presenting as asymmetric T2-weighted and fluid-attenuated inversion recovery hyperintensities associated with cranial nerve deficits.[15][19] In up to 10% of central nervous system infections, particularly among immunocompromised patients, macroscopic brain abscesses occur without meningeal involvement and are preferentially located in subcortical regions, the thalamus, the pons, or the medulla, reflecting the organism’s intracellular and hematogenous spread.[15][17] In suspected antepartum L monocytogenes infection, diagnosis relies primarily on maternal laboratory testing and microbiologic confirmation. Blood cultures are the mainstay because maternal bacteremia is frequently present even in mild or nonspecific febrile illness.[20] Molecular methods, such as polymerase chain reaction targeting L monocytogenes DNA in maternal blood, can provide rapid adjunctive confirmation, particularly when cultures may be negative or after antibiotic exposure.[12][25] Routine amniotic fluid or placental sampling is not performed antepartum due to procedural risk and limited clinical indications. Fetal ultrasonography is used to detect indirect signs of intrauterine infection, such as fetal hydrops, growth restriction, or oligohydramnios, which may prompt closer monitoring or empiric therapy.[26]

In suspected antepartum L monocytogenes infection, diagnosis relies primarily on maternal laboratory testing and microbiologic confirmation. Blood cultures are the mainstay because maternal bacteremia is frequently present even in mild or nonspecific febrile illness.[20] Molecular methods, such as polymerase chain reaction targeting L monocytogenes DNA in maternal blood, can provide rapid adjunctive confirmation, particularly when cultures may be negative or after antibiotic exposure.[12][25] Routine amniotic fluid or placental sampling is not performed antepartum due to procedural risk and limited clinical indications. Fetal ultrasonography is used to detect indirect signs of intrauterine infection, such as fetal hydrops, growth restriction, or oligohydramnios, which may prompt closer monitoring or empiric therapy.[26] In the setting of fetal loss or stillbirth, placental and amniotic fluid cultures, as well as polymerase chain reaction, provide definitive confirmation of vertical transmission, demonstrating that L monocytogenes can directly infect the placenta and fetus. For example, findings from studies showed that in cases of miscarriage or stillbirth, placental cultures had positive results for Listeria spp in a substantial proportion of cases, even when maternal blood cultures were negative, confirming the pathogen’s tropism for the placenta and its role in adverse fetal outcomes.[25] These results complement antepartum clinical evaluation by illustrating the pathophysiology of vertical transmission, though clinicians primarily use these methods for retrospective diagnosis rather than routine antepartum testing.

In most cases, treatment for L monocytogenes central nervous system infection is initiated empirically in patients with suspected meningitis or meningoencephalitis who have specific risk factors. The presence of the following conditions should prompt the medical team to include empirical coverage for L monocytogenes: Age 50 years or older (60 years or older per World Health Organization criteria) [27] Pregnancy Immunosuppressive therapy Solid organ transplant Malignant neoplasm Advanced human immunodeficiency virus infection Diabetes mellitus End-stage kidney disease Liver cirrhosis Alcohol use disorder Treatment is usually intravenous ampicillin or amoxicillin (2 grams every 4 hours). Because L monocytogenes is intrinsically resistant to cephalosporins, most clinical guidelines recommend adding a cephalosporin to standard empirical regimens for bacterial meningitis in at-risk patients. Once L monocytogenes is definitively identified by culture or molecular methods (polymerase chain reaction), antimicrobial therapy should be continued for at least 21 days.[27][28] A frequent clinical challenge arises in patients with risk factors for L monocytogenes meningitis in whom no causative pathogen is identified despite appropriate diagnostic evaluation with culture and molecular testing. In such cases, completion of empirical anti-listerial therapy should be considered.

Treatment is usually intravenous ampicillin or amoxicillin (2 grams every 4 hours). Because L monocytogenes is intrinsically resistant to cephalosporins, most clinical guidelines recommend adding a cephalosporin to standard empirical regimens for bacterial meningitis in at-risk patients. Once L monocytogenes is definitively identified by culture or molecular methods (polymerase chain reaction), antimicrobial therapy should be continued for at least 21 days.[27][28] A frequent clinical challenge arises in patients with risk factors for L monocytogenes meningitis in whom no causative pathogen is identified despite appropriate diagnostic evaluation with culture and molecular testing. In such cases, completion of empirical anti-listerial therapy should be considered. The addition of an aminoglycoside to β-lactam therapy in L monocytogenes meningitis remains controversial. Historically, clinicians have recommended this approach in cases of localized disease, such as brain abscess, endocarditis, and bone infection.[29] Some guidelines recommend individualizing this decision based on clinical severity. The rationale for adding gentamicin is to achieve synergistic bactericidal activity because β-lactams alone are often bacteriostatic against Listeria spp. However, results from retrospective studies of invasive listeriosis, including meningitis, have not demonstrated improved clinical outcomes with aminoglycoside combination therapy.[30][31] In patients with penicillin allergy, trimethoprim–sulfamethoxazole is considered the preferred alternative therapy to ampicillin or amoxicillin. If dexamethasone is initiated empirically while awaiting confirmation of the cause of bacterial meningitis, the European Society of Clinical Microbiology and Infectious Diseases guidelines recommend discontinuation if the identified pathogen is not Haemophilus influenzae or Streptococcus pneumoniae. Nevertheless, some experts still advocate continuing adjunctive corticosteroid therapy regardless of the causative organism.[27] L monocytogenes coverage should also be considered in the treatment of immunosuppressed patients presenting with brain abscess without meningitis, with guidelines recommending trimethoprim–sulfamethoxazole as part of the empirical antibiotic combination.[27]

The addition of an aminoglycoside to β-lactam therapy in L monocytogenes meningitis remains controversial. Historically, clinicians have recommended this approach in cases of localized disease, such as brain abscess, endocarditis, and bone infection.[29] Some guidelines recommend individualizing this decision based on clinical severity. The rationale for adding gentamicin is to achieve synergistic bactericidal activity because β-lactams alone are often bacteriostatic against Listeria spp. However, results from retrospective studies of invasive listeriosis, including meningitis, have not demonstrated improved clinical outcomes with aminoglycoside combination therapy.[30][31] In patients with penicillin allergy, trimethoprim–sulfamethoxazole is considered the preferred alternative therapy to ampicillin or amoxicillin. If dexamethasone is initiated empirically while awaiting confirmation of the cause of bacterial meningitis, the European Society of Clinical Microbiology and Infectious Diseases guidelines recommend discontinuation if the identified pathogen is not Haemophilus influenzae or Streptococcus pneumoniae. Nevertheless, some experts still advocate continuing adjunctive corticosteroid therapy regardless of the causative organism.[27] L monocytogenes coverage should also be considered in the treatment of immunosuppressed patients presenting with brain abscess without meningitis, with guidelines recommending trimethoprim–sulfamethoxazole as part of the empirical antibiotic combination.[27] In pregnant women with suspected placental or vertical Listeria monocytogenes infection, early initiation of targeted antimicrobial therapy is critical, as maternal antimicrobial treatment administered 1 or more days before delivery is associated with a significant reduction in neonatal disease severity. Recommended therapy consists of high-dose intravenous ampicillin 2 g every 4 hours or amoxicillin 2 g every 4 to 6 hours to ensure adequate maternal and placental exposure. In patients with β-lactam allergy, trimethoprim–sulfamethoxazole is the preferred alternative when the benefits outweigh potential fetal risks, with treatment typically lasting at least 14 days, tailored to maternal response and obstetric evolution.[32]

When considering the differential diagnosis of Listeria monocytogenes infection of the central nervous system, clinicians should evaluate other infectious causes of meningitis, including: Viral etiologies Neisseria meningitidis infection Haemophilus influenzae infection Streptococcus pneumoniae infection. In immunocompromised patients, additional pathogens such as: Herpesviruses Mycobacterium tuberculosis infection Cryptococcus spp infection Lumbar puncture is critical for distinguishing bacterial from viral meningitis, while neuroimaging is essential for identifying noninfectious conditions that may mimic meningeal syndromes, such as subarachnoid hemorrhage. In cases of brain abscess, the differential diagnosis includes: Bacteria from the oral flora Streptococcus pneumoniae infection Staphylococcus aureus infection In immunosuppressed patients, Mycobacterium tuberculosis infection Nocardia spp infection Fungi (eg, Cryptococcus) Toxoplasma gondii infection. In pregnant patients with suspected Listeria spp infection, the differential diagnosis should also include other causes of maternal febrile illness and adverse pregnancy outcomes, such as: Intraamniotic infection due to Escherichia coli infection Group B Streptococcus infection Viral infections (eg, cytomegalovirus and parvovirus B19) Noninfectious causes of fetal distress or pregnancy loss

Listeria  monocytogenes infection represents approximately 3% of all cases of bacterial meningitis in the US, with a high case-fatality ratio, surpassed only by that associated with Streptococcus pneumoniae.[3] The mortality rate increases in patients with more comorbidities.[33] A patient without coexisting disease has an approximately 10.7% mortality rate, whereas a patient with several comorbidities, including diabetes mellitus and cardiac disease, has a mortality rate of near 24%.[34] Immunocompetence also plays a large role in overall mortality among patients. Mortality in pregnant patients with L monocytogenes meningitis is also substantial (29%), higher than the 17% described in nonpregnant adults with L monocytogenes meningitis. The rate of fetal loss is also high, up to 57% of reported neonatal death.[8]

Prevention Education for immunosuppressed patients and pregnant women should address the risks of consuming ready-to-eat foods and dairy products that lack high-temperature disinfection. Specific examples of foods to avoid include unheated queso fresco-type cheeses, whether made with pasteurized or unpasteurized milk; unheated deli meats, cold cuts, hot dogs, and fermented or dry sausages; premade deli salads, such as coleslaw and potato, tuna, or chicken salad; refrigerated pâté or meat spreads; smoked fish; raw or lightly cooked sprouts; and cut melon left outside refrigeration. Patients also need education on avoiding cross-infection by keeping tableware and food-preparation surfaces, including the tabletop used for food preparation, clean. Furthermore, nurses and clinicians should educate immunosuppressed patients and pregnant women about symptoms of listeriosis. [CDC. People at Increased Risk for Listeria Infection] Patient leaflets designed by the CDC are available to educate pregnant women.[CDC. Protect Your Pregnancy from Listeria]

Clinical pearls regarding L monocytogenes include: Always consider L monocytogenes as an infectious agent in neonates, older adults, and immunocompromised patients. Transmission involves the fecal-oral route. L monocytogenes is a foodborne illness that can replicate at refrigerator temperatures. Ampicillin or trimethoprim-sulfamethoxazole is the treatment of choice, together with other broad-spectrum antibiotics, until the causative pathogen is identified. Early recognition in adults with central nervous system infection is key to increasing the chance of survival and, in pregnant women, to improving neonatal prognosis. L monocytogenes is uniformly resistant to cephalosporin antibiotics.

L monocytogenes is a foodborne illness that has the propensity to cause meningitis or fetal demise in unborn infants and, as such, requires treatment from an interprofessional health care team. Primary care clinics and emergency departments are the first line of defense in diagnosing meningitis and initiating appropriate therapy. Intake nurses and triage staff play an important role in recognizing unstable vital signs that might meet criteria for systemic inflammatory response syndrome and should alert the clinician to these findings. Clinicians must maintain a high index of suspicion for meningitis, perform diagnostic testing, and initiate broad-spectrum antibiotics in the emergency department to cover the most likely pathogens based on patient risk factors. Early detection and diagnosis of meningitis are critical for good outcomes. A diagnosis of meningitis requires admission to the hospitalist team and consultation with an infectious disease clinician to help narrow the spectrum of antibiotic coverage by analyzing cerebrospinal fluid and blood cultures. Infectious disease clinicians and hospitalists should work closely with pharmacists to select appropriate antibiotics for patients based on the most up-to-date antibiogram data. After recovery and discharge, the patient should establish care with or continue treatment from their primary care clinician. Nursing staff need to be fully apprised of the patient's condition, monitor patients at all follow-up visits to ensure no regression occurs, and promptly report any concerns to the treating clinician. Finally, hospitals should have committees in place and protocols for treating L monocytogenes–associated infections.[34]