eMedicine Specialties > Infectious Diseases > Bacterial Infections

Listeria Monocytogenes

Karen B Weinstein, MD, FACP, Clinical Assistant Professor, Department of Internal Medicine, Loyola University; Assistant Attending, Department of Internal Medicine, Rush Medical College; Associate Program Director, West Suburban Medical Center
Joanna Ortiz, MD, Infectious Disease Attending Physician, Clinical Instructor, Department of Internal Medicine, West Suburban Medical Center

Updated: Jun 23, 2008

Introduction

Background

Listeria monocytogenes, although an uncommon cause of illness in the general population, is an important pathogen in pregnant patients, neonates, elderly individuals, and immunocompromised individuals. It is typically a food-borne organism. Listeria is also a common veterinary pathogen, being associated with abortion and encephalitis in sheep and cattle. It can be isolated from soil, water, and decaying vegetation.

The most common clinical manifestation is diarrhea. A mild presentation of fever, nausea, vomiting, and diarrhea may resemble a gastrointestinal illness.¹ The microorganism has gained recognition because of its association with epidemic gastroenteritis. In 1997, an outbreak of noninvasive gastroenteritis occurred in 2 schools in northern Italy, involving more than 1500 children and adults.²

Bacteremia and meningitis are more serious manifestations of disease that can affect individuals at high risk. Unless recognized and treated, Listeria infections can result in significant morbidity and mortality.

Pathophysiology

L monocytogenes is a motile, non–spore-forming, gram-positive bacillus that has aerobic and facultatively anaerobic characteristics. It grows best at neutral to slightly alkaline pH and is capable of growth at a wide range of temperatures, from 1-45°C. It is beta-hemolytic and has a blue-green sheen on blood-free agar. It exhibits characteristic tumbling motility when viewed with light microscopy and is difficult to isolate in mixed cultures. It may be mistaken for streptococci or contaminants such as corynebacteria.

Most infections occur after oral ingestion, with access to the systemic circulation after intestinal penetration. Protection against Listeria is mediated via lymphokine activation of T cells on macrophages and by interleukin-18.

CNS infection may manifest as meningitis, meningoencephalitis, or abscess. Endocarditis is another possible presentation. Localized infection may manifest as septic arthritis, osteomyelitis, and, rarely, pneumonia.

Frequency

United States

The frequency of L monocytogenes infection is 9.7 cases per million population. Annually, 2500 cases are reported, with higher incidence rates during the summer months.³ Pregnant women account for 27% of all cases, and most occur during the third trimester. Seventy percent of all nonperinatal infections occur in immunocompromised patients. Corticosteroid therapy is the most important predisposing association in patients who are not pregnant.

Mortality/Morbidity

• The overall mortality rate of L monocytogenes infection is 20-30%.
• Of all pregnancy-related cases, 22% resulted in fetal loss or neonatal death, but mothers usually survive.

Sex

• With the exception of pregnant women, no sex predilection is recognized.

Age

• Women of childbearing age are commonly affected.
• Neonates and elderly individuals are at risk.

Clinical

History

Disease may be a self-limited gastrointestinal tract illness or a more severe CNS infection or bacteremia.

Physical

Examination depends on the organ system involved.

• Infection in pregnancy^4,5
  • Listeria may proliferate in the placenta and cause infection due to impaired cell-mediated immunity during pregnancy.
  • CNS infection is very rare during pregnancy, although it is observed frequently in other compromised hosts.
  • Fever, myalgias, arthralgias, back pain, and headache are classic symptoms of bacteremia. Symptoms may mimic those of a flulike illness. The infection may be mild and self-limited.
  • Listeriosis during pregnancy usually occurs during the third trimester, when cell-mediated immunity is at its lowest.
  • Preterm labor and/or delivery is common. Abortion, stillbirth, and intrauterine infection are possible.
• Neonatal infection (granulomatosis infantisepticum): Two forms are described.⁴
  • Early-onset sepsis, with Listeria acquired in utero via transplacental transmission, results in premature birth. Listeria can be isolated in the placenta, blood, meconium, nose, ears, and throat, among other sites, and manifests as abscesses and/or granulomas.
  • Late-onset meningitis is acquired through vaginal transmission, although it also has been reported with cesarean deliveries.
• CNS infection⁶
  • Listeria has a predilection for the brain parenchyma, especially the brain stem, and the meninges.
  • Mental status changes are common.
  • Seizures, both focal and generalized, occur in at least 25% of patients.
  • Cranial nerve deficits may be present.
  • Strokelike syndromes with hemiplegia may occur.
  • Nuchal rigidity is less common.
  • Movement disorders may include tremor, myoclonus, and ataxia.
  • Patients may present with encephalitis, especially of the brainstem.⁷
  • Meningitis is possible.
  • Ventriculitis, particularly of the fourth ventricle, may develop.
  • Cervical myelitis has been reported.⁸
  • Brain abscess occurs in 10% of CNS infections, often located in the thalamus, pons, and medulla. This uncommon complication is associated with high mortality.⁹
• Febrile gastroenteritis¹
  • L monocytogenes can produce food-borne diarrheal disease, which is typically noninvasive.
  • The median incubation period is 1-2 days, with diarrhea lasting anywhere from 1-3 days.
  • The prevalence of diarrheal illness is high in individuals exposed to inocula of Listeria.
  • Patients present with fever, myalgias, and diarrhea and recover with supportive care.

Causes

• Most infections are due to food-borne transmission.
• A substantial minority of infections are transmitted by other modes.
  • Transmission can occur transplacentally or via an infected birth canal.
  • Isolated incidences of cross-infection in neonatal nurseries have been reported.

Differential Diagnoses

Other Problems to Be Considered

Meningeal carcinomatosis
Lymphomatous meningitis
Multiple sclerosis
Vasculitis
Viral encephalitis or meningitis
Fungal meningitis
Brain abscess
Bacterial meningitis
Septic abortion
Pyelonephritis in pregnancy

Workup

Laboratory Studies

• Blood cultures should be performed. Blood culture results are positive in 60-75% of patients with CNS infections.
• Listeria demonstrates "tumbling motility" in wet mounts of cerebrospinal fluid (CSF). Listeria organisms are motile in wet mounts of CSF.
• CSF Gram stain results are positive in less than 50% of patients. CSF analysis reveals pleocytosis, and CSF protein levels are moderately elevated. CSF glucose levels may be low, and if so, are associated with a poor prognosis.
• Laboratory results that show diphtheroids should prompt heightened awareness for the possibility of Listeria infection, particularly in immunocompromised patients.
• CSF culture findings are positive in nearly 100% of patients.
• Serologic testing is not reliable.
• Stool cultures are neither sensitive nor specific.

Imaging Studies

• MRI is superior to CT scan for demonstrating CNS disease, especially in the brainstem.¹⁰
• Transesophageal echocardiography should be performed if endocarditis is suspected.

Procedures

• Lumbar puncture should be performed if CSF infection is suspected.

Treatment

Medical Care

• Intravenous antibiotics must be started immediately when the diagnosis is suspected or confirmed.
• Diagnosis is established by culture of the organism from blood, CSF, or other sterile body fluid.
• Person-to-person transmission does not occur; therefore, isolation precautions are not necessary.

Consultations

Listeriosis may be sporadic or may be part of a larger epidemic. The table below lists some of the most recent epidemics. Consultation with an infectious disease specialist or an epidemiologist is important when epidemic listeriosis is suspected.

Epidemic Listeriosis

Medication

Antibiotic therapy is the treatment of choice. Bacteremia should be treated for 2 weeks if the patient is immunocompetent. Longer courses may be required in the immunocompromised patient. Meningitis should be treated for 3 weeks; endocarditis, for 4-6 weeks; and brain abscess, for at least 6 weeks. Ampicillin is generally considered the preferred agent, but other agents may be acceptable. Gentamicin is added frequently for synergy, but it may be discontinued after 1 week of clinical improvement in order to decrease the chance of renal toxicity or ototoxicity.¹⁹

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Ampicillin (Omnipen, Marcillin)

DOC. Interferes with bacterial cell wall synthesis during active multiplication, causing bactericidal activity against susceptible organisms.

Dosing

Adult

2 g IV q4h

Pediatric

200-400 mg/kg/d IV divided q4h

Interactions

Probenecid and disulfiram decrease renal excretion of ampicillin, causing an increase in levels; conversely, allopurinol increases excretion and has an additive effect on ampicillin rash; may decrease effect of oral contraceptives

Contraindications

Documented hypersensitivity (also to other penicillins)

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Dose adjustments may be necessary in renal failure; appearance of rash should be carefully evaluated to differentiate a nonallergic ampicillin rash from a hypersensitivity reaction

Trimethoprim-sulfamethoxazole (Bactrim)

Indicated for patients unable to take penicillin antibiotics. Inhibits bacterial synthesis of dihydrofolic acid by competing with paraaminobenzoic acid, which results in inhibition of bacterial growth.

Dosing

Adult

20 mg/kg/d of trimethoprim IV divided q6h

Pediatric

Administer as in adults

Interactions

May increase prothrombin time of warfarin, monitor coagulation tests and adjust dose prn; serum levels of dapsone and TMP may increase when administered concomitantly; incidence of thrombocytopenia purpura may increase when used concurrently with diuretics in elderly patients; hepatic clearance of phenytoin may be decreased and half-life prolonged when administered concurrently; sulfonamides can displace methotrexate (MTX) from plasma protein-binding sites, thus increasing free MTX concentrations; this may potentiate MTX effects in bone marrow depression; hypoglycemic response of sulfonylureas may be increased with concurrent administration of both medications; may decrease renal clearance of zidovudine, causing an increase in zidovudine levels

Contraindications

Documented hypersensitivity; megaloblastic anemia due to folate deficiency; infants <2 mo

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBCs CBC count frequently; if significant reduction of any formed blood element is noted, discontinue therapy; goiter production, diuresis, and hypoglycemia may occur; high IV doses or prolonged infusions may cause bone marrow depression manifested as thrombocytopenia, leukopenia, or megaloblastic anemia
Exercise caution in patients with possible folate deficiency (eg, chronic alcoholism, elderly, anticonvulsant therapy, malabsorption syndrome)
Hemolysis may occur in G-6-PD deficiency; if signs of bone marrow depression occur, give leucovorin prn to restore normal hematopoiesis; oral leucovorin (5-15 mg/d) has been recommended; because of their unique immune dysfunction, patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment; administer adequate fluid to prevent crystalluria and stone formation; perform urinalyses and renal function tests during therapy

Chloramphenicol (Chloromycetin)

Binds to 50 S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria.

Dosing

Adult

50-100 mg/kg/d PO/IV divided q6h for 10 d; not to exceed 4 g/d

Pediatric

50-75 mg/kg/d PO/IV divided q6h

Interactions

Administered concurrently with barbiturates, levels may decrease while barbiturate levels may increase, causing toxicity; manifestations of hypoglycemia may occur with sulfonylureas; rifampin may reduce levels, presumably through hepatic enzyme induction; may increase effects of anticoagulants; may increase serum hydantoin levels, possibly resulting in toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use only for indicated infections or as prophylaxis for bacterial infections; serious and fatal blood dyscrasias (eg, aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) can occur; evaluate baseline and perform periodic blood studies approximately every 2 d while in therapy; discontinue upon appearance of reticulocytopenia, leukopenia, thrombocytopenia, anemia, or findings attributable to chloramphenicol; adjust dose in liver or kidney dysfunction; caution in pregnancy at term or during labor because of potential toxic effects on fetus (gray syndrome)

Follow-up

Deterrence/Prevention

• Cook all raw food thoroughly.
• Wash raw vegetables.
• Avoid consumption of raw (unpasteurized) milk or milk products.
• Wash hands, knives, and cutting boards after handling uncooked foods.
• Pregnant or immunocompromised patients should avoid soft cheeses (eg, feta, Brie, Camembert, bleu). Cream cheese, yogurt, and cottage cheese are allowed.
• Reheat leftover or ready-to-eat foods (eg, hot dogs) until steaming hot.
• Avoid delicatessen foods unless they are thoroughly reheated.
• Cook food to a safe internal temperature.

Miscellaneous

Medicolegal Pitfalls

• US regulatory agencies recommend a recall when L monocytogenes is detected in processed foods that are eaten without cooking.
  • The United States Department of Agriculture's Food Safety and Inspection Service has issued new regulations for ready-to-eat meat and poultry processing plants by outlining a program to control and test for L monocytogenes.¹¹
  • Systems have not been perfected; therefore, patient education is most effective in prevention.

References

1. Ooi ST, Lorber B. Gastroenteritis due to Listeria monocytogenes. Clin Infect Dis. May 1 2005;40(9):1327-32. [Medline].

2. Aureli P, Fiorucci GC, Caroli D, Marchiaro G, Novara O, Leone L, et al. An outbreak of febrile gastroenteritis associated with corn contaminated by Listeria monocytogenes. N Engl J Med. Apr 27 2000;342(17):1236-41. [Medline].

3. Pappas G, Panagopoulou P, Christou L, Akritidis N. Category B potential bioterrorism agents: bacteria, viruses, toxins, and foodborne and waterborne pathogens. Infect Dis Clin North Am. Jun 2006;20(2):395-421, x. [Medline].

4. Mylonakis E, Paliou M, Hohmann EL, Calderwood SB, Wing EJ. Listeriosis during pregnancy: a case series and review of 222 cases. Medicine (Baltimore). Jul 2002;81(4):260-9. [Medline].

5. Sheffield JS. Sepsis and septic shock in pregnancy. Crit Care Clin. Oct 2004;20(4):651-60; viii. [Medline].

6. Mylonakis E, Hohmann EL, Calderwood SB. Central nervous system infection with Listeria monocytogenes. 33 years' experience at a general hospital and review of 776 episodes from the literature. Medicine (Baltimore). Sep 1998;77(5):313-36. [Medline].

7. Armstrong RW, Fung PC. Brainstem encephalitis (rhombencephalitis) due to Listeria monocytogenes: case report and review. Clin Infect Dis. May 1993;16(5):689-702. [Medline].

8. Josephson SA, Pillai DR, Phillips JJ, Chou D. Neurolisteriosis presenting as cervical myelitis in an immunocompetent patient. Neurology. Apr 11 2006;66(7):1122-3. [Medline].

9. Dee RR, Lorber B. Brain abscess due to Listeria monocytogenes: case report and literature review. Rev Infect Dis. Nov-Dec 1986;8(6):968-77. [Medline].

10. Faidas A, Shepard DL, Lim J, Nelson JE, Baddour LM. Magnetic resonance imaging in listerial brain stem encephalitis. Clin Infect Dis. Jan 1993;16(1):186-7. [Medline].

11. Gottlieb SL, Newbern EC, Griffin PM, Graves LM, Hoekstra RM, Baker NL, et al. Multistate outbreak of Listeriosis linked to turkey deli meat and subsequent changes in US regulatory policy. Clin Infect Dis. Jan 1 2006;42(1):29-36. [Medline].

12. Ericsson H, Eklöw A, Danielsson-Tham ML, Loncarevic S, Mentzing LO, et al. An outbreak of listeriosis suspected to have been caused by rainbow trout. J Clin Microbiol. Nov 1997;35(11):2904-7. [Medline].

13. Büla CJ, Bille J, Glauser MP. An epidemic of food-borne listeriosis in western Switzerland: description of 57 cases involving adults. Clin Infect Dis. Jan 1995;20(1):66-72. [Medline].

14. Dalton CB, Austin CC, Sobel J, Hayes PS, Bibb WF, Graves LM, et al. An outbreak of gastroenteritis and fever due to Listeria monocytogenes in milk. N Engl J Med. Jan 9 1997;336(2):100-5. [Medline].

15. Goulet V, Rocourt J, Rebiere I, Jacquet C, Moyse C, Dehaumont P, et al. Listeriosis outbreak associated with the consumption of rillettes in France in 1993. J Infect Dis. Jan 1998;177(1):155-60. [Medline].

16. Linnan MJ, Mascola L, Lou XD, Goulet V, May S, Salminen C, et al. Epidemic listeriosis associated with Mexican-style cheese. N Engl J Med. Sep 29 1988;319(13):823-8. [Medline].

17. Schlech WF 3rd, Lavigne PM, Bortolussi RA, Allen AC, Haldane EV, Wort AJ, et al. Epidemic listeriosis--evidence for transmission by food. N Engl J Med. Jan 27 1983;308(4):203-6. [Medline].

18. Evans JR, Allen AC, Stinson DA, Bortolussi R, Peddle LJ. Perinatal listeriosis: report of an outbreak. Pediatr Infect Dis. May-Jun 1985;4(3):237-41. [Medline].

19. Lorber B. Listeriosis. Clin Infect Dis. Jan 1997;24(1):1-9; quiz 10-1. [Medline].

20. Cunha BA. Antibiotic Essentials. 7^th ed. Royal Oak, MI: Physicians Press; 2008.

21. Armstrong D, Cohen J, eds. Listeria Monocytogenes. In: Infectious Diseases. London, UK: Mosby; 1999:8.15.1-8.15.20.

22. Berenguer J, Solera J, Diaz MD, Moreno S, Lopez-Herce JA, Bouza E. Listeriosis in patients infected with human immunodeficiency virus. Rev Infect Dis. Jan-Feb 1991;13(1):115-9. [Medline].

23. Blatt SP, Zajac RA. Treatment of Listeria bacteremia with vancomycin. Rev Infect Dis. Jan-Feb 1991;13(1):181-2. [Medline].

24. Broome CV. Listeriosis: Can we prevent it?. ASM News. 1993;59:444-6.

25. Calubiran OV, Horiuchi J, Klein NC, Cunha BA. Listeria monocytogenes meningitis in a human immunodeficiency virus-positive patient undergoing hemodialysis. Heart Lung. Jan 1990;19(1):21-3. [Medline].

26. Chang J, Powles R, Mehta J, Paton N, Treleaven J, Jameson B. Listeriosis in bone marrow transplant recipients: incidence, clinical features, and treatment. Clin Infect Dis. Nov 1995;21(5):1289-90. [Medline].

27. Charpentier E, Gerbaud G, Jacquet C, Rocourt J, Courvalin P. Incidence of antibiotic resistance in Listeria species. J Infect Dis. Jul 1995;172(1):277-81. [Medline].

28. Cherubin CE, Appleman MD, Heseltine PN, Khayr W, Stratton CW. Epidemiological spectrum and current treatment of listeriosis. Rev Infect Dis. Nov-Dec 1991;13(6):1108-14. [Medline].

29. Cunha BA. Central nervous system infections in the compromised host: a diagnostic approach. Infect Dis Clin North Am. Jun 2001;15(2):567-90. [Medline].

30. Cunha BA, Fatehpuria R, Eisenstein LE. Listeria monocytogenes encephalitis mimicking Herpes Simplex virus encephalitis: the differential diagnostic importance of cerebrospinal fluid lactic acid levels. Heart Lung. May-Jun 2007;36(3):226-31. [Medline].

31. Cunha BA, Filozov A, Remé P. Listeria monocytogenes encephalitis mimicking West Nile encephalitis. Heart Lung. Jan-Feb 2004;33(1):61-4. [Medline].

32. Decker CF, Simon GL, DiGioia RA, Tuazon CU. Listeria monocytogenes infections in patients with AIDS: report of five cases and review. Rev Infect Dis. May-Jun 1991;13(3):413-7. [Medline].

33. Farber JM, Peterkin PI. Listeria monocytogenes, a food-borne pathogen. Microbiol Rev. Sep 1991;55(3):476-511. [Medline].

34. Gellin BG, Broome CV, Bibb WF, Weaver RE, Gaventa S, Mascola L. The epidemiology of listeriosis in the United States--1986. Listeriosis Study Group. Am J Epidemiol. Feb 15 1991;133(4):392-401. [Medline].

35. Gorbach SL, Bartlett JB, Blacklow NR, eds. Listeria Monocytogenes. In: Infectious Diseases. 2^nd ed. Philadelphia, Pa: WB Saunders; 1998:1750-5.

36. Gross E, Slauson S. Update on emerging infections: news from the Centers for Disease Control and Prevention. Preliminary FoodNet Data on the incidence of infection with pathogens transmitted commonly through food--selected sites, United States, 2003. Ann Emerg Med. Nov 2004;44(5):532-6. [Medline].

37. Hof H, Nichterlein T, Kretschmar M. Management of listeriosis. Clin Microbiol Rev. Apr 1997;10(2):345-57. [Medline].

38. John JF. Listeria Monocytogenes. In: Vinken PJ, Bruyn GW, eds. Handbook of ClinicalNeurology. Vol 8. New York, NY: Elsevier Science; 1988:89-101.

39. Klein NC, Schoch PE, Cunha BA. Listeria. Infect Control Hosp Epidemiol. May 1991;12(5):311-4. [Medline].

40. Latcha S, Cunha BA. Listeria monocytogenes meningoencephalitis: the diagnostic importance of the CSF lactic acid. Heart Lung. Mar-Apr 1994;23(2):177-9. [Medline].

41. Lorber B. Listeria Monocytogenes. In: Mandell GL, Bennett GE, Dolin R, eds. Principles and Practices of Infectious Diseases. 6^th ed. Pennsylvania, PA: Churchill and Livingstone; 2005:2478.

42. Pigrau C, Almirante B, Pahissa A, Gasser I, Martinez Vasquez JM. Clinical presentation and outcome in cases of listeriosis. Clin Infect Dis. Jul 1993;17(1):143-4. [Medline].

43. Pinner RW, Schuchat A, Swaminathan B, Hayes PS, Deaver KA, Weaver RE, et al. Role of foods in sporadic listeriosis. II. Microbiologic and epidemiologic investigation. The Listeria Study Group. JAMA. Apr 15 1992;267(15):2046-50. [Medline].

44. Riedo FX, Pinner RW, Tosca ML, Cartter ML, Graves LM, Reeves MW, et al. A point-source foodborne listeriosis outbreak: documented incubation period and possible mild illness. J Infect Dis. Sep 1994;170(3):693-6. [Medline].

45. Schneider JI. Rapid infectious killers. Emerg Med Clin North Am. Nov 2004;22(4):1099-115. [Medline].

46. Schuchat A, Robinson K, Wenger JD, Harrison LH, Farley M, Reingold AL, et al. Bacterial meningitis in the United States in 1995. Active Surveillance Team. N Engl J Med. Oct 2 1997;337(14):970-6. [Medline].

47. Skogberg K, Syrjanen J, Jahkola M, Renkonen OV, Paavonen J, Ahonen J, et al. Clinical presentation and outcome of listeriosis in patients with and without immunosuppressive therapy. Clin Infect Dis. Apr 1992;14(4):815-21. [Medline].

48. Spitzer PG, Hammer SM, Karchmer AW. Treatment of Listeria monocytogenes infection with trimethoprim-sulfamethoxazole: case report and review of the literature. Rev Infect Dis. May-Jun 1986;8(3):427-30. [Medline].

49. Swaminathan B, Rocourt J, Bille J. Listeria. In: Murray PR, Baron EJ, Pfaller MA, Tenover FC, Yolken RH, eds. Manual of Clinical Microbiology. 6^th ed. Washington, DC: ASM Press; 1995:341-8.

50. Taege AJ. Listeriosis: recognizing it, treating it, preventing it. Cleve Clin J Med. Jun 1999;66(6):375-80. [Medline].

51. Tappero JW, Schuchat A, Deaver KA. Reduction in the incidence of human listeriosis in the United States. Effectiveness of prevention efforts? The Listeriosis Study Group. JAMA. Apr 12 1995;273(14):1118-22. [Medline].

52. Uldry PA, Kuntzer T, Bogousslavsky J, Regli F, Miklossy J, Bille J, et al. Early symptoms and outcome of Listeria monocytogenes rhombencephalitis: 14 adult cases. J Neurol. 1993;240(4):235-42. [Medline].

53. Walsh RD, Gurevich I, Cunha BA. Listeria: A potential cause of febrile transfusion reactions. J Hosp Infect. 1993;18:81-82.

Keywords

Listeria monocytogenes, L monocytogenes, diarrhea, listeriosis, epidemic gastroenteritis, bacteremia, meningitis, CNS infection, meningoencephalitis, endocarditis, septic arthritis, osteomyelitis, pneumonia, corticosteroid therapy

Contributor Information and Disclosures

Author

Karen B Weinstein, MD, FACP, Clinical Assistant Professor, Department of Internal Medicine, Loyola University; Assistant Attending, Department of Internal Medicine, Rush Medical College; Associate Program Director, West Suburban Medical Center
Karen B Weinstein, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Illinois State Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

Joanna Ortiz, MD, Infectious Disease Attending Physician, Clinical Instructor, Department of Internal Medicine, West Suburban Medical Center
Joanna Ortiz, MD is a member of the following medical societies: American College of Physicians, Chicago Medical Society, Illinois State Medical Society, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Medical Editor

Mark Raymond Wallace, MD, Infectious Disease Fellowship Director, Orlando Regional Healthcare; Clinical Professor of Medicine, Florida State University
Mark Raymond Wallace, MD is a member of the following medical societies: American Medical Association, American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Joseph F John Jr, MD, FACP, FIDSA, FSHEA, Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center
Disclosure: BioMerieux Honoraria Review panel membership; Cubist Honoraria Review panel membership; Pfizer Honoraria Speaking and teaching; Merck Stock dividends stock holdings

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)