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LISTERIA MONOCYTOGENES

PATHOGEN SAFETY DATA SHEET - INFECTIOUS SUBSTANCES

SECTION I - INFECTIOUS AGENT

NAME: Listeria monocytogenes.

SYNONYM OR CROSS REFERENCE: Listeria, listeriosis, listeriasis, listerellosis, and circling disease (in animals) Footnote 1-Footnote 13.

CHARACTERISTICS: Listeria monocytogenes is a facultatively anaerobic, gram-positive, rod-shaped coccobacillus, typically measuring 0.5 to 2μm long and 0.5μm in diameter Footnote 1, Footnote 3, Footnote 4, Footnote 9. L. monocytogenes has the ability to grow at low temperature, a range of pH values (between 4.3 and 9.6), and can reproduce at temperatures between 1 and 45°C Footnote 1, Footnote 3.

L. monocytogenes is divided into 11 serovars; however, most human and animal cases are caused by serovars 4b, 1/2b, and 1/2a Footnote 1, Footnote 3.

SECTION II - HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: L. monocytogenes was first described as a human pathogen in the 1920s Footnote 1, Footnote 5. Although relatively rare, human listeriosis is often severe and mortality rates can approach 50% Footnote 1, Footnote 3. Certain factors predispose individuals to infection with L. monocytogenes, such as neonates, pregnancy, leukemia, Hodgkin’s disease, diabetes mellitus, alcoholism or cirrhosis and immunosuppressive or cytostatic therapy Footnote 10. Most commonly, listeria causes a mild febrile illness however, several types of listeriosis disease manifestations are recognised; for instance, listeriosis in pregnancy, listeriosis of the central nervous system (CNS), febrile gastroenteritis, glandular listeriosis, local listeriosis, typhoid listeriosis, and atypical listeriosis Footnote 10.

Listeriosis in pregnancy: Occurs mostly during the third trimester, and is characterised by a “flu like” illness with symptoms such as fever, chills, malaise, arthralgia, back pain, and diarrhoea Footnote 3, Footnote 6, Footnote 10, Footnote 12. In many cases the infection is subclinical or inapparent; however, intrauterine infection of the foetus can lead to foetal death, spontaneous abortion, premature delivery, or the birth of a foetus that dies shortly after birth Footnote 5, Footnote 6, Footnote 10. Surviving newborns with listeriosis are often classified as “early onset” or “late onset”. Early onset neonatal listeriosis due to transplacental infection often presents as pneumonia and/or sepsis Footnote 9, Footnote 12. Severe disease can result in widespread granulomas (granulomatosis infantisepticum) Footnote 9, Footnote 12. Late onset neonatal listeriosis is said to occur from infection during birth, with neonates showing symptoms of meningitis one to several weeks after birth Footnote 3, Footnote 9. In both early and late onset neonatal listeriosis, the mortality rate ranges from 20 to 30% Footnote 9.

Listeriosis of the CNS: Meningitis is the most frequently recognised listerial infection Footnote 6. Common symptoms of listeriosis of the CNS include high fever, nuchal rigidity, tremor and/or ataxia, and seizures Footnote 6. The most common form of non-meningitic form of CNS listeriosis is encephalitis involving the brainstem (rhombencephalitis) Footnote 6.

Febrile gastroenteritis: A non-invasive form of listeriosis that manifests as symptoms typical of gastroenteritis, for example, fever, diarrhoea, and vomiting Footnote 6, Footnote 9, Footnote 10.

Glandular listeriosis: Resembles infectious mononucleosis with swelling of the salivary glands and nuchal lymph nodes Footnote 10.

Local listeriosis: Can manifest as papules and pustules on the hands and arms following direct contact with infectious material, and can be accompanied by constitutional symptoms (fever, myalgia, and/or headache) Footnote 13.

Typhoid listeriosis: Characterised by high fever and is particularly frequent in immunocompromised individuals Footnote 10.

Atypical listeriosis: Rare cases of have been described with symptoms such as endocarditis, purulent (mononuclear) pleural exudates, pneumonia, urethritis, and abscesses Footnote 10.

EPIDEMIOLOGY: Listeriosis occurs worldwide, but is seen mostly in industrialised countries Footnote 3, Footnote 4. Although L. monocytogenes was described as a human pathogen in the 1920s (mistakenly thought to be the cause of infectious mononucleosis), the first documented outbreak of food-borne listeriosis was in 1979 in 23 patients in a Boston hospital Footnote 3, Footnote 5. The first confirmed outbreak in Canada, and first definitive link of listeriosis cases to food, was in 1981 in the Maritime Provinces and was due to consumption of contaminated cabbage in coleslaw Footnote 5. Further outbreaks occurred during subsequent years and were often associated with a particular food type, from vegetable products in the early 1980s, to dairy products in the mid 1980s and early 1990s, to ready-to-eat meat and poultry products in the late 1990s to early 2000s Footnote 2, Footnote 5. Indeed, ready-to-eat meat and poultry products were responsible for a multi-state outbreak in the United States in 1999 that resulted in 101 cases of illness and 21 fatalities, and more recently in Canada (originating in North York, Ontario) in August 2008, resulting in 57 confirmed cases (mostly in Ontario) and 22 confirmed deaths Footnote 2, Footnote 7.

HOST RANGE: L. monocytogenes has been isolated from many organisms, including humans and other mammals, fish, crustaceans, and insects Footnote 4, Footnote 10.

INFECTIOUS DOSE: The approximate infective dose of L. monocytogenes is estimated to be 10 to 100 million colony forming units (CFU) in healthy hosts, and only 0.1 to 10 million CFU in individuals at high risk of infection Footnote 11.

MODE OF TRANSMISSION: The predominant mode of L. monocytogenes transmission is by ingestion of contaminated food Footnote 1-Footnote 5, Footnote 10, Footnote 11. L. monocytogenes can also be transmitted transplacentally from mother to child during pregnancy and via the birth canal during birth Footnote 3, Footnote 9, Footnote 10, Footnote 12.

Direct contact with diseased animals may lead to transmission to farmers and veterinarians during the birthing of domestic farm animals Footnote 13.

Nosocomial infections and person-to-person transmission (excluding vertical) are recognised but rare Footnote 1.

INCUBATION PERIOD: Can vary depending on the mode of transmission and dose received, but typically ranges from 1 to 4 weeks, and can be as high as several months Footnote 4, Footnote 10. Febrile gastroenteritis as a result of L. monocytogenes has a short incubation period, typically 18 to 20 hours Footnote 2, Footnote 9.

COMMUNICABILITY: L. monocytogenes can be transmitted from mother to child during pregnancy and childbirth Footnote 3, Footnote 9, Footnote 10, Footnote 12.

SECTION III - DISSEMINATION

RESERVOIR: Soil, manure, decaying vegetable matter, silage, water, animal feed, fresh and frozen poultry, fresh and processed meats, raw milk, cheese, slaughterhouse waste, and asymptomatic human and animal carriers Footnote 4.

ZOONOSIS: Yes, through consumption of foodstuffs containing infected animal products, manure contaminated vegetables, and by direct contact with animal tissues during birthing and butchering Footnote 1-Footnote 5, Footnote 9, Footnote 10, Footnote 13.

VECTORS: None.

SECTION IV - STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: Susceptible to most broad spectrum and gram-positive spectrum antibiotics, except the cephalosporins are active against L. monocytogenes in vitro Footnote 8. In vivo, the most active are ampicillin and amoxicillin Footnote 8.

SUSCEPTIBILITY TO DISINFECTANTS: At room temperature, L. monocytogenes is susceptible to sodium hypochlorite, iodophor compounds, and quaternary ammonium compounds Footnote 14. Five to 10-fold higher concentrations of the above compounds are required at 4°C Footnote 14.

PHYSICAL INACTIVATION: L. monocytogenes can be inactivated by ozone, high pressure (500MPa), and high temperatures (at least 70°C for 2 minutes) Footnote 14, Footnote 15.

SURVIVAL OUTSIDE HOST: L. monocytogenes is commonly found in nature, particularly in association with soil, is relatively heat resistant, can tolerate cold temperature environments well, and can survive at low pH Footnote 9, Footnote 15.

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. Listeriosis can be diagnosed in the laboratory by cultivation of the organism, and demonstration of the infectious agent or its products in tissues or body fluids Footnote 1, Footnote 10.

Several commercially available kits exist for the detection of L. monocytogenes. These rapid procedures are based on ELISA and PCR technology; however, none have been validated for use as a diagnostic tool Footnote 2, Footnote 4.

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: Treatment for human listeriosis with ampicillin or amoxicillin together with gentamicin is the primary choice of therapy Footnote 8. The recommended course of treatment is ampicillin for 2 to 4 weeks Footnote 10. The addition of gentamicin for 2 weeks should be considered for immunocompromised patients Footnote 10.

An alternative therapy for individuals allergic to β-lactams is intravenous co-trimoxazole Footnote 10.

IMMUNIZATION: None currently available.

PROPHYLAXIS: No chemoprophylaxis exists; however, precautions for individuals who are immunocompromised or pregnant women include the avoidance of raw food and vegetables, undercooked meat, soft cheeses, and cheeses prepared from unpasteurised milk Footnote 10.

SECTION VI - LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: A particularly rare laboratory-acquired infection with some suspected cases, none of which have been confirmed Footnote 16.

SOURCES/SPECIMENS: Blood, cerebrospinal fluid, faeces, placenta, skin lesions, pus, amniotic fluid, menstrual blood, lochia, respiratory secretions, meconium, gastric aspirate, animal tissues/specimens, and infected organs such as brain and liver Footnote 2-Footnote 4, Footnote 10.

PRIMARY HAZARDS: Accidental autoinoculation, exposure to the tissues of experimentally infected animals, and L. monocytogenes cultures Footnote 17.

SPECIAL HAZARDS: Those at greater risk of infection (pregnant women or immunocompromised individuals) should take extra care when working in a laboratory where L. monocytogenes is propagated or handled Footnote 3.

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2 Footnote 18.

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious material, animals, or cultures.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable Footnote 17. Eye protection must be used where there is a known or potential risk of exposure to splashes.

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC) Footnote 17. The use of needles, syringes, and other sharp objects should be strictly limited. Additional precautions should be considered with work involving animals or large scale activities.

SECTION VIII – HANDLING AND STORAGE

SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply an appropriate disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up Footnote 17.

DISPOSAL: Decontaminate all wastes that contain or have come in contact with the infectious organism before disposing by autoclave, chemical disinfection, gamma irradiation, or incineration.Footnote 17.

STORAGE: The infectious agent should be stored in leak-proof containers that are appropriately labelled.Footnote 17.

SECTION IX - REGULATORY AND OTHER INFORMATION

REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: December 2011

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada.

Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright ©
Public Health Agency of Canada, 2011
Canada

REFERENCES:

Footnote 1
Low, J. C., & Donachie, W. (1997). A review of Listeria monocytogenes and listeriosis. Veterinary Journal, 153(1), 9-29.

Footnote 2
Donnelly, C. W. (2001). Listeria monocytogenes: A continuing challenge. Nutrition Reviews, 59(6), 183-194.

Footnote 3
Acha, P. N., & Szyfres, B. (2003). Listeriosis. Zoonoses and Communicable Diseases Common to Man and Animals (3rd ed., pp. 168-179). Washington D.C.: Pan American Health Organization.

Footnote 4
Bille, J., Rocourt, J., & Swaminathan, B. (2003). Listeria and Erysipelothrix. In P. R. Murray, E. J. Baron, J. H. Jorgensen, M. A. Pfaller & R. H. Yolken (Eds.), Manual of Clinical Microbiology (8th ed., pp. 461-471). Washington, D.C.: ASM Press.

Footnote 5
Gahan, C. G. M., & Hill, C. (2005). Gastrointestinal phase of Listeria monocytogenes infection. Journal of Applied Microbiology, 98(6), 1345-1353.

Footnote 6
Doganay, M. (2003). Listeriosis: Clinical presentation. FEMS Immunology and Medical Microbiology, 35(3), 173-175.

Footnote 7
Public Health Agency of Canada. (2008). Listeria monocytogenes outbreak.http://www.phac-aspc.gc.ca/alert-alerte/listeria/listeria_2008-eng.php

Footnote 8
Hof, H. (1991). Therapeutic activities of antibiotics in Listeriosis. Infection, 19(SUPPL. 4), S229-S233.

Footnote 9
Roberts, A. J., & Wiedmann, M. (2003). Pathogen, host and environmental factors contributing to the pathogenesis of listeriosis. Cellular and Molecular Life Sciences, 60(5), 904-918.

Footnote 10
Krauss, H., Schiefer, H. G., Weber, A., Slenczka, W., Appel, M., von Graevenitz, A., Enders, B., Zahner, H., & Isenberg, H. D. (2003). Bacterial Zoonoses. Zoonoses: Infectious Diseases Transmissible from Animals to Humans (3rd ed., pp. 205-208). Washington, D.C.: ASM Press.

Footnote 11
Farber, J. M., Ross, W. H., & Harwig, J. (1996). Health risk assessment of Listeria monocytogenes in Canada. International Journal of Food Microbiology, 30(1-2), 145-156.

Footnote 12
Mylonakis, E., Paliou, M., Hohmann, E. L., Calderwood, S. B., & Wing, E. J. (2002). Listeriosis during pregnancy: A case series and review of 222 cases. Medicine, 81(4), 260-269.

Footnote 13
Regan, E. J., Harrison, G. A. J., Butler, S., McLauchlin, J., Thomas, M., & Mitchell, S. (2005). Primary cutaneous listeriosis in a veterinarian [2]. Veterinary Record, 157(7), 207.

Footnote 14
Mafu, A. A., Roy, D., Goulet, J., Savoie, L., & Roy, R. (1990). Efficiency of sanitizing agents for destroying Listeria monocytogenes on contaminated surfaces. Journal of Dairy Science, 73(12), 3428-3432.

Footnote 15
Gaze, J. E., Brown, G. D., Gaskell, D. E., & Banks, J. G. (1989). Heat resistance of Listeria monocytogenes in homogenates of chicken, beef steak and carrot. Food Microbiology, 6(4), 251-259.

Footnote 16
Collins, C. H., & Kennedy, D. A. (1999). Laboratory acquired infections. Laboratory acquired infections: History, incidence, causes and preventions (4th ed., pp. 1-37). Woburn, MA: Butterworth-Heinemann.

Footnote 17
Public Health Agency of Canada. (2004). In Best B., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.

Footnote 18
Human pathogens and toxins act. S.C. 2009, c. 24, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009. (2009).