Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide







  • Last modified
  • 14 July 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • listeriosis
  • Overview
  • L. monocytogenes, as the reference species for members of the genus Listeria, is a Gram-positive, rod-shaped, non-sporulating bacterium which may be isolated from natural environments, foodstuffs and human...

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Preferred Scientific Name

  • listeriosis

International Common Names

  • English: circling disease; listerellosis; listeria abortion of ruminants; listeria eye disease in sheep; listeria mastitis in cows; Listeria mastitis in ewes; listeria, listeric myelitis in sheep; listeric myelitis in cattle; listeric myelitis in sheep; listeriosis of the brain stem, encephalitic listeriosis in ruminants, listeria; listeriosis, listeria, in birds; pulmonary listeriosis, listeria, in cattle; septicemia listeriosis, listeria, in pigs; septicemic listeriosis, listeria, in sheep


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L. monocytogenes, as the reference species for members of the genus Listeria, is a Gram-positive, rod-shaped, non-sporulating bacterium which may be isolated from natural environments, foodstuffs and humans (Farber and Peterkin, 1991). In 1926 a bacterium was recognized which caused monocytosis in laboratory rabbits (Murray et al., 1926). The first isolation of this bacterium from human communities and their livestock was given by Gill and Nyfeldt who isolated this organism from an ovine and a human case of listeriosis (Gill, 1933; Nyfeldt, 1929). Apart from L. monocytogenes, the genus Listeria spp. consists of five more species. Listeriaivanovii, which was established as an individual species by Seeliger et al. (1984), is the second pathogenic species in the genus Listeria (Boerlin et al., 1992). It may cause clinical listeriosis mainly in small ruminants and cattle. Listeria ivanovii is usually not isolated from foodstuffs and food processing environments. Four more species have been described within recent decades. Listeria innocua got its name due to a complete lack in virulence and pathogenicity. It is the most common listerial species isolated in the food area. L. innocua was taxonomically distinguished from L. monocytogenes not earlier than 1977 (Seeliger, 1981). Rarely found listerial species such as Listeria welshimeri, Listeria seeligeri and Listeria grayi are non-pathogenic although Listeriaseeligeri contains some of the virulence arrangement of the pathogenic species (Gouin et al., 1994). L. seeligeri has been implicated in a small number of cases of sporadic listeriosis of unusual clinical progress (Rocourt and Seeliger, 1985). L. seeligeri and L. welshimeri which were established as listerial species in 1983 by Rocourt and Grimont (Rocourt and Grimont, 1983) are rarely isolated from food processing environments.

The varying origin of listerial species was compared in an expanded panel of Listeria strains from a wide geographical distribution (Rocourt and Seeliger, 1985). All listerial species are detectable in the environment which is the natural reservoir for all bacteria of the genus Listeria spp. Isolates of the species L. monocytogenes, L. innocua and L. ivanovii were obtained from faeces samples therefore indicating adaptability of these species to the mammalian body. The comparison of the presence of Listeria species in samples derived from cases of listeriosis showed that only L. monocytogenes and L. ivanovii were detected in clinical specimens.

Hosts/Species Affected

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The natural reservoirs of L. monocytogenes appear to be soil and mammalian gastrointestinal tracts, both of which contaminate vegetation. Grazing animals ingest the organism and further contaminate vegetation and soil. Animal-to-animal transmission occurs via the faecal-oral route.

Listeriosis is primarily, but not exclusively, a winter-spring disease of housed ruminants. The less acidic pH of spoiled silage (pH >5.0) enhances multiplication of L. monocytogenes. Outbreaks may occur within 10 days of feeding poor-quality silage. Removal or change of silage in the ration often halts the appearance of listeriosis but cases can still occur for 2 weeks or so.

Some reports have suspected late summer and autumn as a prime time of infection in human listeriosis (Niels and Walters, 1981). This, however, has not been further substantiated.


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Generally it is accepted that listeriosis occurs worldwide. Most reports have not surveyed the overall prevalence for a geographical area or a country. They are mainly case reports from sporadic cases or even outbreaks, which were firstly detected in hospitals, health care centres or by public health authorities. These reports are included in the reference list as they confirm the occurrence of listeriosis in a particular region.

Due to the saprophytic origin of listeriae, there are various ways of infecting either animals or humans. L. monocytogenes survives in natural habitats for months and even years (Mitscherlich and Marth, 1984). Therefore, it is likely that a hazard for contamination of food, feed and processing environments is given throughout the year without any obvious changes of frequency in particular seasons. When studying the prevalence and distribution of listeriosis in the clinical area, it has to be considered that the detection of listeriosis is sometimes ambiguous due to the sporadic nature of occurrence, the multi-causal epidemiology and the broad range of symptoms that might appear. For these reasons the incidence of L. monocytogenes infections is probably underestimated. This is especially true in cases where an infection by L. monocytogenes causes uncharacteristic symptoms such as diarrhoea, fever and nausea. In such cases the reason for infection might be suspected as more frequently occurring alternative foodborne pathogens rather than L. monocytogenes.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes


AfghanistanPresentModjadedy and Seraj, 1970
AzerbaijanNo information availableAnnagiev et al., 1978; OIE Handistatus, 2005
BahrainDisease never reportedOIE Handistatus, 2005
BhutanNo information availableOIE Handistatus, 2005
Brunei DarussalamNo information availableOIE Handistatus, 2005
-Hong KongNo information availableLeung et al., 1994; OIE Handistatus, 2005
Georgia (Republic of)Last reported1993OIE Handistatus, 2005
IndiaGugnani, 1999; OIE Handistatus, 2005
IndonesiaDisease not reportedOIE Handistatus, 2005
IranReported present or known to be presentOIE Handistatus, 2005
IraqNo information availableYousif et al., 1984; OIE Handistatus, 2005
IsraelNo information availableOIE Handistatus, 2005
JapanNo information availableYoshida et al., 2000; OIE Handistatus, 2005
JordanCAB Abstracts data miningOIE Handistatus, 2005
KazakhstanDisease not reportedOIE Handistatus, 2005
Korea, DPRDisease not reportedOIE Handistatus, 2005
Korea, Republic ofReported present or known to be presentOIE Handistatus, 2005
KuwaitDisease not reportedSethi et al., 1989; Zaki et al., 1990; OIE Handistatus, 2005
LebanonNo information availableOIE Handistatus, 2005
MalaysiaWidespreadArumugaswamy et al., 1994
-Peninsular MalaysiaDisease not reportedOIE Handistatus, 2005
-SabahDisease never reportedOIE Handistatus, 2005
-SarawakDisease never reportedOIE Handistatus, 2005
MongoliaNo information availableOIE Handistatus, 2005
MyanmarLast reported1997OIE Handistatus, 2005
NepalNo information availableShrestha et al., 1993; OIE Handistatus, 2005
OmanDisease not reportedOIE Handistatus, 2005
PhilippinesDisease not reportedOIE Handistatus, 2005
QatarNo information availableOIE Handistatus, 2005
Saudi ArabiaDisease not reportedOIE Handistatus, 2005
SingaporeDisease never reportedOIE Handistatus, 2005
Sri LankaDisease never reportedOIE Handistatus, 2005
SyriaDisease not reportedOIE Handistatus, 2005
TaiwanLast reported1998Fang CT et al., 2000; OIE Handistatus, 2005
TajikistanNo information availableOIE Handistatus, 2005
ThailandDisease not reportedOIE Handistatus, 2005
TurkeyNo information availableUraz and Yucel, 1999; OIE Handistatus, 2005
TurkmenistanLast reported1997OIE Handistatus, 2005
United Arab EmiratesDisease not reportedOIE Handistatus, 2005
UzbekistanDisease not reportedOIE Handistatus, 2005
VietnamNo information availableOIE Handistatus, 2005
YemenNo information availableOIE Handistatus, 2005


AlgeriaNo information availableBelouni and Rahal, 1992; OIE Handistatus, 2005
AngolaNo information availableOIE Handistatus, 2005
BeninNo information availableOIE Handistatus, 2005
BotswanaNo information availableOIE Handistatus, 2005
Burkina FasoNo information availableOIE Handistatus, 2005
BurundiNo information availableOIE Handistatus, 2005
CameroonNo information availableMalesieux, 1969; OIE Handistatus, 2005
Cape VerdeDisease not reportedOIE Handistatus, 2005
Central African RepublicDisease not reportedOIE Handistatus, 2005
ChadNo information availableOIE Handistatus, 2005
Congo Democratic RepublicNo information availableOIE Handistatus, 2005
Côte d'IvoireDisease not reportedOIE Handistatus, 2005
DjiboutiDisease not reportedOIE Handistatus, 2005
EgyptNo information availableHaberberger et al., 1990; OIE Handistatus, 2005
EritreaDisease not reportedOIE Handistatus, 2005
GhanaNo information availableOIE Handistatus, 2005
GuineaDisease never reportedOIE Handistatus, 2005
Guinea-BissauNo information availableOIE Handistatus, 2005
KenyaCAB Abstracts data miningGossler and Hunermund, 1973; OIE Handistatus, 2005
LibyaDisease not reportedOIE Handistatus, 2005
MadagascarDisease not reportedVoelckel J et al., 1968; OIE Handistatus, 2005
MalawiNo information availableOIE Handistatus, 2005
MaliNo information availableOIE Handistatus, 2005
MauritiusDisease not reportedOIE Handistatus, 2005
MoroccoNo information availableOIE Handistatus, 2005
MozambiqueNo information availableOIE Handistatus, 2005
NamibiaDisease not reportedOIE Handistatus, 2005
NigeriaNo information availableEyo et al., 1969; Ako-Nai et al., 1999; OIE Handistatus, 2005
RéunionNo information availableOIE Handistatus, 2005
RwandaNo information availableOIE Handistatus, 2005
Sao Tome and PrincipeDisease not reportedOIE Handistatus, 2005
SenegalNo information availableLafaix et al., 1967; OIE Handistatus, 2005
SeychellesNo information availableOIE Handistatus, 2005
SomaliaNo information availableOIE Handistatus, 2005
South AfricaNo information availableAdams and Toxopeus, 1978; Jacobs MR et al., 1978; OIE Handistatus, 2005
SudanLast reported2001Shigidi, 1979; OIE Handistatus, 2005
SwazilandNo information availableOIE Handistatus, 2005
TanzaniaNo information availableOIE Handistatus, 2005
TogoDisease never reportedOIE Handistatus, 2005
TunisiaDisease not reportedBoukadida J et al., 1993; OIE Handistatus, 2005
UgandaDisease not reportedOIE Handistatus, 2005
ZambiaNo information availableChintu and Bathirunathan, 1975; OIE Handistatus, 2005
ZimbabweDisease not reportedOIE Handistatus, 2005

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaReported present or known to be presentSchlech et al., 1983; Davies et al., 1984; Farber and Peterkin, 1991; OIE Handistatus, 2005
-Nova ScotiaLocalisedEmbil et al., 1984; Evans JR et al., 1985
MexicoReported present or known to be presentVictoria et al., 1967; OIE Handistatus, 2005
USAReported present or known to be presentFarber and Peterkin, 1991; Schuchat A et al., 1991; Schuchat et al., 1991; OIE Handistatus, 2005

Central America and Caribbean

BarbadosOIE Handistatus, 2005
BelizeNo information availableOIE Handistatus, 2005
British Virgin IslandsDisease not reportedOIE Handistatus, 2005
Cayman IslandsNo information availableOIE Handistatus, 2005
Costa RicaNo information availableSchuchat A et al., 1991; Schuchat et al., 1991; OIE Handistatus, 2005
CubaLast reported2001OIE Handistatus, 2005
CuraçaoDisease not reportedOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicDisease never reportedOIE Handistatus, 2005
El SalvadorLast reported2001OIE Handistatus, 2005
GuadeloupeNo information availableOIE Handistatus, 2005
GuatemalaNo information availableOIE Handistatus, 2005
HaitiDisease never reportedOIE Handistatus, 2005
JamaicaReported present or known to be presentOIE Handistatus, 2005
MartiniqueReported present or known to be presentOIE Handistatus, 2005
NicaraguaNo information availableOIE Handistatus, 2005
PanamaNo information availableOIE Handistatus, 2005
Saint Kitts and NevisDisease never reportedOIE Handistatus, 2005
Saint Vincent and the GrenadinesDisease not reportedOIE Handistatus, 2005
Trinidad and TobagoDisease never reportedAshiru and Bratt, 1998; OIE Handistatus, 2005

South America

ArgentinaCAB Abstracts data miningOIE Handistatus, 2005
BoliviaDisease not reportedOIE Handistatus, 2005
BrazilLast reported2003OIE Handistatus, 2005
ChileReported present or known to be presentOIE Handistatus, 2005
ColombiaLast reported2002OIE Handistatus, 2005
EcuadorDisease never reportedOIE Handistatus, 2005
Falkland IslandsReported present or known to be presentOIE Handistatus, 2005
French GuianaDisease not reportedOIE Handistatus, 2005
GuyanaDisease not reportedOIE Handistatus, 2005
ParaguayNo information availableOIE Handistatus, 2005
PeruNo information availableOIE Handistatus, 2005
UruguayReported present or known to be presentOIE Handistatus, 2005
VenezuelaDisease not reportedOIE Handistatus, 2005


AndorraDisease not reportedOIE Handistatus, 2005
AustriaNo information availableAllerberger, 1999; OIE Handistatus, 2005
BelarusReported present or known to be presentOIE Handistatus, 2005
BelgiumNo information availableArt and André, 1991; OIE Handistatus, 2005
Bosnia-HercegovinaNo information availableOIE Handistatus, 2005
BulgariaReported present or known to be presentOIE Handistatus, 2005
CroatiaCAB Abstracts data miningOIE Handistatus, 2005
CyprusLast reported1995OIE Handistatus, 2005
Czech RepublicLast reported1999OIE Handistatus, 2005
DenmarkNo information availableFrederiksen and Samuelsson, 1992; OIE Handistatus, 2005
EstoniaSerological evidence and/or isolation of the agentOIE Handistatus, 2005
FinlandReported present or known to be presentLyytikainen O et al., 2000; OIE Handistatus, 2005
FranceReported present or known to be presentGoulet and Marchetti, 1996; OIE Handistatus, 2005
GermanyReported present or known to be presentSchwarze et al., 1989; OIE Handistatus, 2005
GreeceChryssanthopoulos C et al., 1982; OIE Handistatus, 2005
HungaryRalovich and Domján-Kovács, 1996; OIE Handistatus, 2005
IcelandReported present or known to be presentOIE Handistatus, 2005
IrelandReported present or known to be presentOIE Handistatus, 2005
Isle of Man (UK)Reported present or known to be presentOIE Handistatus, 2005
ItalyNo information availableSalamina et al., 1996; OIE Handistatus, 2005
JerseyDisease never reportedOIE Handistatus, 2005
LatviaLast reported2002OIE Handistatus, 2005
LiechtensteinReported present or known to be presentOIE Handistatus, 2005
LithuaniaDisease not reportedOIE Handistatus, 2005
LuxembourgNo information availableOIE Handistatus, 2005
MacedoniaOIE Handistatus, 2005
MaltaLast reported2001OIE Handistatus, 2005
MoldovaDisease not reportedOIE Handistatus, 2005
NetherlandsReported present or known to be presentMulder and Zanen, 1986; OIE Handistatus, 2005
NorwayReported present or known to be presentOIE Handistatus, 2005
PolandReported present or known to be presentOIE Handistatus, 2005
PortugalReported present or known to be presentOIE Handistatus, 2005
RomaniaOIE Handistatus, 2005
Russian FederationReported present or known to be presentOIE Handistatus, 2005
SlovakiaReported present or known to be presentOIE Handistatus, 2005
SloveniaReported present or known to be presentOIE Handistatus, 2005
SpainReported present or known to be presentVazquez-Boland et al., 1991; Nolas-Salas J et al., 1998; OIE Handistatus, 2005
SwedenReported present or known to be presentEricsson et al., 1997; OIE Handistatus, 2005
SwitzerlandReported present or known to be presentBüla et al., 1995; OIE Handistatus, 2005
UKReported present or known to be presentLow and Donachie, 1997; OIE Handistatus, 2005
-Northern IrelandReported present or known to be presentOIE Handistatus, 2005
UkraineLast reported2003OIE Handistatus, 2005
Yugoslavia (former)No information availableOIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)Reported present or known to be presentOIE Handistatus, 2005


AustraliaReported present or known to be presentFrancis and Gilbert, 1992; Paul et al., 1994; OIE Handistatus, 2005
-Western AustraliaPresentNiels and Walters, 1981
French PolynesiaDisease not reportedOIE Handistatus, 2005
New CaledoniaNo information availableOIE Handistatus, 2005
New ZealandReported present or known to be presentBrett et al., 1998; OIE Handistatus, 2005
SamoaNo information availableOIE Handistatus, 2005
VanuatuDisease never reportedOIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE Handistatus, 2005


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Viceral listeriosis in neonates and young animals is signified by multiple spots of micro-abcesses in most of the inner organs especially the liver and spleen. In elder animals, histopathological findings depend on the organs infected and might not be rather distinctive. Histopathology of the encephalitic form of listeriosis presents as perivascular cuffing and micro-abcesses in the brainstem. Gram-staining and use of fluorescent antibodies might help to confirm clinical suspicions in a more sensitive manner (see pictures).


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Clinical and laboratory diagnosis

The isolation of the pathogen from blood is frequently unsuccessful due to the unknown course of infection during the septicaemic phase. Additionally, there is a gap in time between the onset of the septicaemic phase and appearance of clinical symptoms (usually the time-point of the first clinical interventions).

The encephalitic form is presumptively diagnosed with respect to the range of symptoms recorded during the clinical investigation. Each presumptive diagnosis must be confirmed by a microbiological investigation using specimens such as blood, cerebrospinal fluid, brain tissue or similar. Histopathological findings are usually pathognostic.

Samples of lumbar cerebrospinal fluid (CSF) can readily be collected under local anaesthesia (Scott, 1992). Cases of listeriosis present with an elevated CSF protein concentration, 0.8-2.0 g/l (normal 0.3 g/l), and a mild pleocytosis comprised of large mononuclear cells (Scott, 1992; Scott, 1993a,b).

Clinical and laboratory diagnosis of the gastroenteritic listeriosis may be ambiguous due to the circumstance that the pathogen may be a commensal of the normal microbial flora of the gut. In the case of suspecting listerial mastitis, confirmation of the listerial etiology is usually simple as the pathogen is persistently shed into the raw milk. Only mammary tissue was found positive by microbiological examination in two cases of mastitis in Austrian cattle. Microbiology as well as PCR-examination of regularly drawn blood samples revealed repeated detection of listerial DNA by PCR but no isolation of the microbes from the blood. Inner organs such as the liver, spleen, kidneys, local lymph nodes and brain were neither positive by microbiology nor by PCR (Wagner et al., 2000).

Abortions in cattle, sheep and humans frequently occur in the last third of gestation. Microscopic examination of the placenta as well of the amnion fluid is reliable due to the high number of L. monocytogenes being present.

A variety of reference methods for the detection of L. monocytogenes by conventional microbiology have been implemented into the food hygiene area (International Standardization Organisation ISO 11290 -1:1998; International Dairy Federation IDF 143A:1995; Association of American Analytical Chemists-AOAC-recommended method as recommended by the Food and Drug Administration; Nordic Committee on Food Analysis NMKL 136:1990). Strategies for identification of listeriae from food are usually based on selective enrichment of Listeria spp. from foodstuffs followed by isolation of presumptive colonies on selective solid media. Species confirmation using the CAMP reaction, catalase and oxidase reaction, microscopy and biotyping terminates the investigation. Direct plating is used for Listeria enumeration and in samples and specimens where either no or a low number of background flora is expected (e.g. cerebrospinal fluid, blood, water).

It has to be considered that food samples contain chemical substances and competing flora which may inhibit multiplication of the Listeria spp. Therefore, the enrichment step is rather crucial in food microbiology. An appropriate enrichment protocol should combine a high productivity with respect to listerial growth and a high selectivity against competing microorganisms. However, the properties of different enrichment protocols vary regarding selectivity and productivity (Asperger et al., 1999). The International Standardization Organisation (ISO) proposes an enrichment procedure which consists of a 24 hour first-step enrichment in half-Fraser broth and 48 hour second-step enrichment in full-Fraser broth (ISO, 1998; Fraser and Sperber, 1988). After enrichment, an aliquot is streaked onto selective agar plates (either Palcam or Oxford agar). This procedure requires for a sequential discrimination among pathogenic and non-pathogenic listerial species as neither Palcam nor Oxford plates indicate the pathogenic species. Using the CAMP reaction, the pathogenic and haemolytic species L. monocytogenes (CAMP + with Staphylococcus aureus) and L. ivanovii (CAMP + with Rhodococcus equi) are separated from the non-pathogenic and non-or weakly haemolytic other Listeria species. Reliability of confirmation may vary as L. monocytogenes isolates may be marked by weak or even negative haemolysis (Allerberger et al., 1997), catalase reactions (Bubert et al., 1997) and variability in sugar fermentation. Therefore identification of field isolates may lead to unclear species-specific discrimination.

The broths and the selective agar plates are offered by many suppliers either as non-supplemented basis formulae which have to be supplemented in an individual working step, or in ready to use-formats. A significant improvement of Listeria microbiology was given with the development of a biotyping scheme based on sugar fermentation patterns in ready to use- strip formats (Bille et al., 1992). As a more recent improvement, chromogenic selective media were introduced into the market (Rapid L. mono®, ALOA®) which allow rapid differentiation of L. monocytogenes from other non-pathogenic Listeria species directly by both a colour and an enzymatic reaction on the plate. Both chromogenic media were found equally reliable or even superior in comparison to selective plates used in the traditional ISO method (Vlaemynck et al., 2000; Karpiskova et al., 2000). This procedure speeds up the overall investigation time. A similar strategy was followed by the development of the L. monocytogenes blood agar (LMBA, Johansson et al., 2000). The LMBA medium enhances the appearance of haemolysis of presumptive L. monocytogenes clones thus improving interpretability of haemolytic activity.

Apart from conventional microbiology, there have been described a variety of immunoassays (Wagner and Bubert, 1999), DNA hybridization assays (Hitchins, 1999) or other DNA-based amplification assays (Polymerase Chain reaction: PCR, Ligase Chain Reaction: LCR, Nucleic Acid Sequence-Based Amplification: NASBA). A recently published multiplex PCR format allows the species-specific detection and discrimination of the most important listerial species in a single tube reaction (Bubert et al., 1999). A powerful and highly automated strategy is the combination of DNA amplification and fluorogenic on-line detection of the amplified product (Bassler et al., 1995; Nogva et al., 2000; Norton and Batt, 1999; Wang and Hong, 1999).

There are some general shortcomings using DNA-based detection principles. Foodstuffs display a variety of chemically complex liquid and solid matrices thus making reliable sample preparation difficult. DNA-based techniques do not merely detect viable cells as they detect DNA from dead cell material. Most molecular techniques require for a prior enrichment step to multiply the listerial targets to numbers which are detectable in the sequential nucleic acids amplification. Conclusively, though new molecular strategies have initiated a lot of research activities, there is a striking lack for standardization and quality assurance in the field (More than 200 hits are listed when search items L. monocytogenes and PCR are combined in a PubMed search).

Serology and Typing

A serological typing scheme, which is comprehensive and reliable has been reviewed by Seeliger and Höhne (1979). Typing by serology employs antigenic reactions with 15 somatic (O-antigenic factors) and 5 flagellar antigens (H-factors). The typing scheme currently used comprises 6 serotypes including 16 serovars (Bannermann, 1995). The pathogenic species L. monocytogenes and L. ivanovii can be distinguished into four serogroups (1/2, 3, 4 and 7) and one serogroup (5), respectively. Although serotyping has been the most important epidemiological tool for years, it lost some of its importance due to the insufficient discriminatory capacity (Bannermann, 1995). This was emphasized by the fact that approximately 91% of the clinical L. monocytogenes isolates tested were assigned to serovars 1/2a, 1/2b and 4b (McLauchlin, 1987). Furthermore standardization and quality assurance of antigenic sera production is difficult thus restricting the use of serotyping to highly specialized expert laboratories. However, serotyping still remains the basis of Listeria typing as it allows the assignment of isolates to a limited and clearly characterized number of types. Detailed epidemiological investigations are nowadays performed using phage-typing, enzyme typing, restriction fragment analysis or other mostly DNA-based typing schemes (Selander et al., 1986; Loessner and Busse, 1990; Wesley and Ashton, 1991; Bille and Rocourt, 1996)

Differential diagnosis

Listeriosis can be differentiated from pregnancy toxaemia in ewes or ketosis in cattle by careful clinical examination, cerebrospinal fluid (CSF) changes, and 3-OH butyrate concentrations below 3.0 mmol/l. Furthermore, in pregnancy toxaemia or ketosis, facial and ear paralysis are absent. Hypocalcaemia can be differentiated from listeriosis by absence of cranial nerve dysfunction and rapid response to the intravenous infusion of calcium borogluconate solution. Scrapie has a much more insidious onset than listeriosis, leading to emaciation and behavioural changes with hyperaesthesia to tactile and auditory stimuli. Brain abscesses and coenurosis present with circling, contralateral blindness and proprioceptive deficits, and no cranial nerve deficits.

In cattle, the unilateral signs of trigeminal and facial paralysis, when present, help to differentiate listeriosis from:

  • Peripheral vestibular lesions
  • Basillar empyema (pituitary gland abscess)
  • Bovine spongiform encephalopathy
  • Thromboembolic encephalitis
  • Polioencephalomalacia
  • Sporadic bovine encephalomyelitis
  • Lead poisoning

Rabies must always be considered in the differential diagnosis of listeriosis in cattle.

In lambs, listeriosis should be differentiated from brain abscess and nephrosis. Peripheral vestibular lesions are common in growing lambs and can be differentiated from listeriosis by lack of depression and normal trigeminal nerve function.

Abortion can be caused by a variety of bacteria such as Brucellaabortus Bang, Campylobacter fetus, Neospora spp., and Leptospira spp. (Radostits et al., 1999).

List of Symptoms/Signs

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SignLife StagesType
Acoustic Signs / Deafness Sign
Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Digestive Signs / Diarrhoea Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Digestive Signs / Difficulty in prehending or chewing food Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Digestive Signs / Dysphagia, difficulty swallowing Sign
Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Diagnosis
Digestive Signs / Grinding teeth, bruxism, odontoprisis Sign
Digestive Signs / Hepatosplenomegaly, splenomegaly, hepatomegaly Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Digestive Signs / Inability to open (trismus) and / or close jaw, mouth Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Diagnosis
Digestive Signs / Rumen hypomotility or atony, decreased rate, motility, strength Sign
Digestive Signs / Tongue protrusion Sign
Digestive Signs / Tongue weakness, paresis, paralysis Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Digestive Signs / Vomiting or regurgitation, emesis Sign
General Signs / Abnormal proprioceptive positioning, knuckling Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
General Signs / Ataxia, incoordination, staggering, falling Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Diagnosis
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Fever, pyrexia, hyperthermia Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
General Signs / Forelimb weakness, paresis, paralysis front leg Sign
General Signs / Generalized lameness or stiffness, limping Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
General Signs / Generalized weakness, paresis, paralysis Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Diagnosis
General Signs / Head, face, ears, jaw weakness, droop, paresis, paralysis Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Diagnosis
General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass Sign
General Signs / Hemiparesis Sign
General Signs / Hypothermia, low temperature Sign
General Signs / Inability to stand, downer, prostration Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
General Signs / Increased mortality in flocks of birds Poultry:All Stages Sign
General Signs / Intraocular mass, swelling interior of eye Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia Sign
General Signs / Neck weakness, paresis, paralysis, limp, ventroflexion Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Diagnosis
General Signs / Opisthotonus Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
General Signs / Oral cavity, tongue swelling, mass in mouth Sign
General Signs / Paraparesis, weakness, paralysis both hind limbs Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
General Signs / Reluctant to move, refusal to move Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
General Signs / Stiffness or extended neck Sign
General Signs / Sudden death, found dead Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
General Signs / Tetraparesis, weakness, paralysis all four limbs Sign
General Signs / Torticollis, twisted neck Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sign
General Signs / Weakness of one hindlimb, paresis paralysis rear leg Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
General Signs / Weakness, paresis, paralysis of the legs, limbs in birds Sign
General Signs / Weight loss Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Nervous Signs / Abnormal behavior, aggression, changing habits Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Nervous Signs / Circling Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Diagnosis
Nervous Signs / Coma, stupor Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Nervous Signs / Constant or increased vocalization Sign
Nervous Signs / Disoriented, memory loss Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Nervous Signs / Excitement, delirium, mania Sign
Nervous Signs / Excitement, delirium, mania Sign
Nervous Signs / Head pressing Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Nervous Signs / Head tilt Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Diagnosis
Nervous Signs / Head, face, neck, tongue hypoesthesia, anesthesia Sign
Nervous Signs / Hyperesthesia, irritable, hyperactive Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Nervous Signs / Propulsion, aimless wandering Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Diagnosis
Nervous Signs / Seizures or syncope, convulsions, fits, collapse Sign
Nervous Signs / Tremor Sign
Nervous Signs / Tremor Sign
Nervous Signs / Tremor Sign
Ophthalmology Signs / Abnormal corneal pigmentation Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Ophthalmology Signs / Abnormal pupillary response to light Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Ophthalmology Signs / Abnormal pupillary shape or defect in the iris Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Diagnosis
Ophthalmology Signs / Anisocoria Sign
Ophthalmology Signs / Blindness Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling Sign
Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature Sign
Ophthalmology Signs / Conjunctival, scleral, redness Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Ophthalmology Signs / Corneal edema, opacity Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Ophthalmology Signs / Corneal neovascularization, pannus Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Ophthalmology Signs / Corneal ulcer, erosion Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Ophthalmology Signs / Decreased or absent menace response but not blind Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Ophthalmology Signs / Hypopyon, lipid, or fibrin, flare, of anterior chamber Sign
Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes Sign
Ophthalmology Signs / Mydriasis, dilated pupil Sign
Ophthalmology Signs / Nystagmus Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Ophthalmology Signs / Ptosis, lid droop Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Diagnosis
Ophthalmology Signs / Purulent discharge from eye Sign
Ophthalmology Signs / Strabismus Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Reproductive Signs / Abortion or weak newborns, stillbirth Cattle & Buffaloes:Cow,Other:Adult Female,Pigs:Sow,Sheep & Goats:Mature female Diagnosis
Reproductive Signs / Agalactia, decreased, absent milk production Sign
Reproductive Signs / Agalactia, decreased, absent milk production Sign
Reproductive Signs / Cold mammary gland, cool udder Cattle & Buffaloes:Cow,Other:Adult Female,Pigs:Sow,Sheep & Goats:Mature female Sign
Reproductive Signs / Decreased, dropping, egg production Poultry:Mature female
Reproductive Signs / Firm mammary gland, hard udder Cattle & Buffaloes:Cow,Other:Adult Female,Pigs:Sow,Sheep & Goats:Mature female Sign
Reproductive Signs / Mastitis, abnormal milk Cattle & Buffaloes:Cow,Other:Adult Female,Pigs:Sow,Sheep & Goats:Mature female Sign
Reproductive Signs / Purulent or mucoid discharge, cervix or uterus Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
Reproductive Signs / Retained placenta, fetal membranes Cattle & Buffaloes:Cow,Other:Adult Female,Pigs:Sow,Sheep & Goats:Mature female Diagnosis
Respiratory Signs / Coughing, coughs Sign
Respiratory Signs / Decreased respiratory rate Cattle & Buffaloes:Calf,Pigs:Piglet,Sheep & Goats:Lamb Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Sign
Respiratory Signs / Ingesta in nasal passage Sign
Skin / Integumentary Signs / Rough hair coat, dull, standing on end Sign
Skin / Integumentary Signs / Skin edema Cattle & Buffaloes:Calf,Pigs:Piglet,Sheep & Goats:Lamb Sign

Disease Course

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The facultative intracellular parasitism and strategy of L. monocytogenes to spread within the host are unique (Portnoy et al., 1992). This bacterium is characterized by the ability to adhere to host cells by membrane-bound internalins. The receptors for adherence have recently been reported (Braun et al., 2000, Gaillard et al., 1991). After cell invasion, microbial cells are located within a phagolysosome. Escape from the phagolysosome is dependent on listerolysin (LLO) and mediated by a phosphatidylinositol-specific-phospholipase-C and a metalloprotease (Portnoy et al., 1992).

Motility of L. monocytogenes in the intracellular space is driven by the ActA protein which induces directional actin assembly (Dabiri et al., 1990). Spreading of L. monocytogenes occurs without intercellular passage. Cell wall protrusions of an infected cell containing the pathogen are presented to neighbouring cells for uptake. Cell to cell spread is mediated by a broad range phospholipase-C (Vazquez-Boland et al., 1992). The hly, plcB and actA genes that respectively encode for LLO, phospholipase-C and ActA, are all under the control of PrfA, encoded by prfA, a member of the cyclic AMP receptor protein family of bacterial transcription factors.

The complex cycle of pathogenesis and the striking dependency of the development of the disease on the immune status of the host do not allow narrowing down either the incubation time or the minimal infective dose to exact values. The incubation time averages 30 days (one day to greater than 70 days), the minimal infective dose seems to exceed 103 cfu/ml (McLaughlin, 1995).

General symptoms, if at all, are unspecific and are associated with an attack of fever that might occur at the initial stages of the infection. Further symptoms vary according to the organ tropism of the infection. The incubation is shortest in goat neonates where sudden death might occur, followed by sheep and cattle. Suspected infection of fowl and poultry is usually recorded by an increase of the fatality rate but does not lead to clinical symptoms (Wesley, 1999).

Listeria that are ingested or inhaled tend to cause septicaemia, abortion and latent infection. Those that gain entry to tissues have a predilection to localize in the intestinal wall, medulla oblongata and placenta; or to cause encephalitis via minute wounds in the buccal mucosa.

The visceral or acute septicaemic form of listeriosis is more frequently described in younger animals. Furthermore, the septicaemic form of listeriosis is more frequent in some livestock species such as pigs and horses (Wesley, 1999). Along with a septicaemic phase, depression might be recorded. A gastroenteritic manifestation of listeriosis leads to diarrhoea in humans and animals (mainly weaning animals). In an outbreak of human listeriosis in Italy, the most common symptoms were diarrhoea, fever, nausea, headache, sore throat, arthromyalgias, vomiting and abdominal pain (Salamina et al., 1996). In pregnant individuals, the septicaemial spread of the listerial cells touches the placenta within 24 hours incubation (Radostits et al., 1999). This may lead to the abortion of the embryo within a couple of days after the septicaemic phase. Stillbirth might be seen depending on the time-point of attack during gestation. If the attack is directly before partition the neonate will be born with the disease (early onset listeriosis).

The most frequent course of listeriosis in small ruminants and cattle affects the brain. The penetration of the mucosal barrier by L. monocytogenes takes place within the mouth cavity due to injury and inflammation of the buccal mucosa or tooth disease. The ongoing infection ascends via the cranial nerves into the brain where listeriae usually cause a unilateral infection of the brainstem.

Listeric encephalitis affects sheep, cattle, goats and, occasionally, pigs. It is essentially a localized infection of the brainstem that occurs when L. monocytogenes ascends the trigeminal nerve. Clinical signs vary according to the function of damaged cranial nerve nuclei. Signs also include depression due to involvement of the ascending reticular activating system (ARAS), and circling (vestibulo-cocchlear nucleus). Initially, affected animals are anorexic, depressed, disoriented and may propel themselves into corners or lean against walls. Such a propulsive tendency must be differentiated from head pressing observed with cerebral lesions such as ovine pregnancy toxaemia (also occurring during late gestation). Affected animals may move in a circle towards the affected side but this is by no means pathognomic of listeriosis. Facial paralysis with drooping ear, deviated muzzle, flaccid lip and lowered eyelid on the affected side develops. There is unilateral lack of blink response. There is profuse, almost continuous, salivation with food material impacted in the cheek of the affected side due to trigeminal nerve paralysis which also results in loss of skin sensation of the face. Terminally, affected animals fall, and unable to rise, lie on the same side; involuntary running movements are common.

More rarely the eyes and the mammary glands might be attacked. As cardinal symptoms, conjunctivitis and ophthalmitis occur in the primary case (Welchman et al., 1997). The etiology of listerial ophthalmitis must be differentiated from pathogens causing similar symptoms, for instance Moraxella bovis. With regard to infections affecting the udder, L. monocytogenes probably ascends from the stable environment into the teat cisterns and from there into the gland cistern (Gitter et al., 1980). Listerial mastitis usually causes subclinical or even inapparent symptoms. In two cases of mastitis in Austrian cattle, the only diagnostic hint at an unphysiological process was an unspecific rise of the number of somatic cells secreted into the raw milk. At high lactation, the number of L. monocytogenes cells exceeded 104cfu/ml. From the view of food hygiene, it is remarkable that the excretion of L. monocytogenes into the raw milk can prolong for extended periods (Wagner et al., 2000).


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Encephalitis is the most readily recognized form of listeriosis in ruminants. It affects all ages and both sexes, sometimes as an epidemic in feedlot cattle or sheep. Gimmers (aged 18 to 24 months) are most commonly affected due to teeth eruption facilitating infection of buccal lesions. Outbreaks of listeriosis can be encountered in young lambs (aged 4 to 8 weeks) which have access to silage. Listeriosis is classically seen during late gestation in sheep fed poorly conserved silage. The clinical course in sheep and goats is often rapid; death may occur 24-48 hours after onset of clinical signs. With aggressive antibiotic therapy and supportive care the recovery rate can be up to 30 per cent. In cattle, the disease course is less acute with a higher treatment response approaching 50 per cent. Lesions are localized in the brainstem and the signs indicate dysfunction of the third to seventh cranial nerves, and occasionally other nerve nuclei.

Human listeriosis is a sporadic disease of rather low incidence in the population. The infection is usually transmitted to both animals and humans via contaminated food- and feeding stuffs.

In Austria, the incidence of human listeriosis is approximately 0.15-0.17 cases/100,000 of the population (Allerberger, 1999). Earlier studies performed by the Center for Disease control (CDC) in Atlanta suggested an incidence of 7.1 cases/ million persons/ year in the USA (Gellin and Broome, 1989). More recently, the FoodNet initiative estimated the incidence for human listeriosis in the USA as 0.5 cases/100,000 inhabitants in 1997 with no tendency to a changing pattern (Wallace et al., 2000). This number was ranked in sixth position, as causes of food poisoning, behind campylobacteriosis (24.7), salmonellosis (13.7), shigellosis (7.9), E. coli O157-infections (2.1) and yersiniosis (0.9). In a further study, the incidence of human listeriosis was estimated as ranging from 0.1 to 11.3 cases/ million persons/ year in Europe (Gledel, 1987; Ralovich, 1987).

Rarely, listeriosis appears in an accumulated manner. In such cases, an increase in incidence is caused by the multiple infection of particular groups of humans due to a common source of infection. In some outbreaks, the source of infection has never been confirmed (Niels and Walters, 1981; Allerberger and Guggenbichler, 1989; Farber and Peterkin, 1991). According to the recommendations of the Federal Institute for Health Protection of Consumers and Veterinary Medicine, Berlin (quoted from a comment of the scientific committee on veterinary measures relating to public health, Brussel, 23. 9. 1999), 21 outbreaks of foodborne origin were recorded in the years 1976-1999 worldwide. Outbreaks of human listeriosis have been most frequently detected in the USA (5 times), France (3 times) and Australia (3 times). In 21 epidemics, vegetables including cereals (four cases), seafood (including fish and fish products) (four cases), milk including milk products (seven cases) or meat (including processed meat products) (four cases) were associated with listeriosis as the most probable source of transmission.

The severity of human listeriosis leads to a high case fatality (³ 30%). This feature is rather uncommon with other foodborne pathogens. Apart from recently described gastro-enteritis associated outbreaks, the clinical course of infection is commonly marked by sepsis, meningo-encephalitis, encephalitis (predominantly rhombencephalitis), and abortions mainly in elderly and pregnant individuals (Dalton et al., 1997; Farber and Peterkin, 1991; Salamina et al., 1996; Slutsker and Schuchat, 1999). In neonates, listeriosis appears as an early onset disease (granulomatosis infantiseptica, infection mainly during pregnancy) leading to a pustulous infection and formation of micro-abscesses mainly in the inner organs (liver, spleen, lung and kidney) or as late onset listeriosis (infection probably during or after birth; Slutsker and Schuchat, 1999). The disease is more frequently observed and diagnosed in humans suffering from underlying diseases however presumptively healthy individuals may also get infected. Infection of non-immunocompromised individuals sometimes leads to mild symptoms comparable to symptoms of a non-severe influenza.

In a study comprising of 84 sporadic cases of listeriosis in the Sydney area, 56% and 41% of all patients showed septicaemia and encephalitis, respectively. The mortality was calculated as 21%.Of all patients interviewed, 86% suffered from underlying diseases (Paul et al., 1994). Listeriosis is a disease of humans, domestic and wild animals. 37 mammal and 20 bird species including cold-blooded animals and ticks were listed as carriers (Gray and Killinger, 1966; Brackett, 1988). The disease has been described in apes, cattle, sheep, goats, horses, fowl, poultry and fish (Jemmi and Keusch, 1994; McClure and Strozier, 1975; Wesley, 1999). Outbreaks in small ruminants such as sheep and goats, poultry and chickens have been repeatedly reported (Chand and Sadana, 1999; Toit, 1977; Meredith and Schneider, 1984; Nagi and Verma, 1967; Yousif et al., 1984; Wiedmann et al., 1999). Furthermore, infections have been described in rabbits and chinchillas (Finley and Long, 1977; Peters and Scheele, 1996).

Healthy humans may carry L. monocytogenes. Whilst a 2-6% isolation rate was stated by Rocourt and Cossart (1997) a recent study performed in a panel of more than 500 healthy Austrians revealed a clearly lower percentage of <0.5% (Grif et al., unpublished results). A similar prevalence of carriage was found for domestic animals in a Japanese study where 1.6% and 0.6 % of the cattle and pigs in a study were confirmed as healthy carriers (Iida et al., 1991). L. monocytogenes was isolated from exotic animals held as pets in Germany such as snakes (1.3%), tortoises (30%) and other exotic amphibians (60%, Weber et al., 1993). Studies on the prevalence of L.monocytogenes carriage in wild animals in Japan, found 13.4% and 6.1% of bird and mammalian faeces and intestinal contents samples contained the pathogen, respectively (Yoshida et al., 2000). A higher prevalence was estimated for rats (up to 77.8%) although this prevalence was dependent on the area where the rats were caught (Inoue et al., 1992).

The investigation of the serum prevalence of antibodies against the most important L. monocytogenes serovars in Nigeria revealed values ranging from approximately 20% and 36% in cattle and pigs, respectively (Oni et al., 1989). These data indicate the frequent contact of livestock animals to the saprophytically living L. monocytogenes isolates. In the same study, serum prevalence of antibodies was statistically higher in chickens, which were not intensively kept and managed.

Rarely, listeriosis is acquired by obscure ways of transmission. There are a few reports in the literature where other vehicles of transmission, rather than foods, were observed, such as mineral oil (Schuchat et al., 1991). Direct transmission to humans by infected animals was reported (predominantly farmers or veterinarians, McLaughlin, 1995). The amnion fluid of infected cows may contain ³ 108 cfu L. monocytogenes/ ml. Usual symptoms are cutaneous lesions on arms which appear about one day post exposure. Human to human transmission by post-parturition exposure was described in cases of late onset listeriosis in neonates through cross-contamination in intensive childcare units (McLaughlin, 1995). However, there is no doubt that the majority of cases of human listeriosis are acquired by ingestion of contaminated food. The exposure frequency of the consumer was calculated with respect to different exposure levels (101 to >106/cfu/ml or g). It was calculated that a person is exposed 35.5 times or 0.8 times to 10 or >106 cfu L. monocytogenes /ml or g/ year, respectively (Notermans et al., 1998). With respect to these data, the low incidence for human listeriosis is surprising. The hypothesis that cross-immunity could be mediated by the exposure of humans to the more frequently found, apathogenic species L. innocua was recently substantiated (Geginat et al., 1999).

As a conclusion of Listeria epidemiology, the possibilities of Listeria spp. entry into the food chain have to be considered. Listeria spp. could be brought into the food chain through uptake by or infection of animals at the farm level or through cross-contamination of milk, meat, fish and vegetables due to poor processing hygiene either at the farm or at the processing level. Post-processing product recontamination during packaging and retailing might be a further reason for Listeria contamination of foodstuffs. For instance, in Costa Rica, a significant correlation was revealed between the incidence of occurrence of L. monocytogenes in fish (65%) and the hygiene conditions at local fish markets (Bianchini et al., 1999).

As a possible source for uptake of Listeria spp. by farm animals, silage feed was identified. Loosely acidified silage exhibits an excellent survival and even multiplication substrate. Listeria might start up with multiplication in the silage when the pH does not drop beneath 5.2-5.6 (Mitscherlich and Marth, 1984). Especially ventilated parts of the silage (outer parts) allow the growth of aerophilic organisms such as moulds, which may shift the pH to higher values. In turn, this boosts Listeria multiplication. It was shown by Amtsberg (1979) that outer parts of the silage may contain up to 3x103cfu/g. Fenlon et al. (1996) reported that cattle fed on hay or manufactured diets do not excrete L. monocytogenes whereas animals fed on silage usually do. However, from the usually sporadic nature of listeriosis in sheep and cattle it can be concluded that shedding of L. monocytogenes into faeces does not mandatorily cause a spreading of the pathogen among other individuals of the herd when these animals are kept in a good condition.

The risk of contamination or infection either of the stable environment, a raw product or the individual (mastitis) is accumulated when the contaminated silage is brought into the stable for feeding purposes. In an Austrian study, Listeria spp. was more frequently isolated from ovine faeces at the end of the winter feeding season when silage feed was required but the quality was poorer. In the same study, the frequency of listerial contamination of ovine raw milk samples was found highest during the silage-feed period (Pless et al., 2000).

With respect to food processing plants, it is obvious that the primary way of contamination regards the plant environment by transmission of Listeria from outside into the facility. Once inside the plant, Listeria spp. are capable of occupying niches from where spreading into the processing lines might persist for years. This is why sanitation of contaminated plants is sometimes highly frustrating and time- and money consuming (Wagner et al., 1996). In the meat industry, contamination of beef and pork seems to occur mainly through recontamination of carcasses during or after slaughter. Data from a Danish study showed a low incidence of Listeria spp. in the faeces of swine (approximately 1.7%) but a higher incidence of contaminated pork carcasses after slaughter (Skovgaard and Norrung, 1989).

Impact: Economic

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Listeriosis occurs sporadically in cattle and sheep; rarely does the prevalence exceed 2 per cent of the population at risk, but the mortality rate, despite intensive antibiotic and supportive therapies, is high. The clinical course in sheep and goats is often rapid; death may occur 24-48 hours after onset of clinical signs. With aggressive antibiotic therapy and supportive care the recovery rate can be up to 30 per cent. In cattle the disease course is less acute with a higher treatment response approaching 50 per cent.

Listeriosis is a disease of high economic importance due to expenses for food monitoring and food control, product recall and sanitation of food plants. Further costs for medical treatment of diseased individuals due to hospitalization must be regarded (Roberts and Pinner, 1990). In a recently published study, contamination with L. monocytogenes (813 recalls) was listed as the most frequent cause for 1370 recalls of food and cosmetic products from the US market from 1993 through 1997. 574 out of the 813 recalls were either due to L. monocytogenes contamination of dairy products (196 recalls), pastries (129 recalls), salads (125 recalls) or sandwiches (124 recalls, Wong et al., 2000). Single episodes of illnesses had been reported in about 19% of all recalls due to microbial contamination. In a further study, it was shown that listeriosis is the foodborne disease which most frequently requires hospitalization of the patients (88% of all patients in comparison to 21% for salmonellosis). In addition the fatality rate is highest in comparison to other more frequently occurring foodborne diseases (Wallace et al., 2000). In a Canadian risk assessment study, the total annual costs with regard to illness and death caused by L. monocytogenes were estimated at 11-12.6 million US$/year (Farber et al., 1996).

Zoonoses and Food Safety

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The problems concerning emergence of foodborne diseases are of pivotal importance for public health concerns. The number for total cases of campylobacteriosis, salmonellosis and shigellosis in the USA were estimated at approximately 2,454,000, 1,412,500 and 448,250 a year. In comparison, listeriosis contributes to the statistics with an estimated number of 2,518 cases (Mead et al., 1999). With respect to the total number of cases, it was calculated that the probability of foodborne origin of human listeriosis is 99%. The hospitalization rate was estimated highest among all other foodborne pathogens and exceeded the number for botulism. The case fatality rate was second to rarely occurring Vibrio vulnificus infections. The probability of underestimation of total cases is rather low in comparison to other foodborne diseases due to the severe course of infection. It was calculated that the true number of human listeriosis might be double the numbers annually recorded (Mead et al., 1999).

Food Hygiene

From the time point of the first description of the phenotype, it took decades to demonstrate the importance of L. monocytogenes as a foodborne pathogen. The foodborne origin of human listeriosis was mandatorily shown in 1981 when an epidemic of human listeriosis was successfully traced back to the consumption of coleslaw in Nova Scotia, Canada (Schlech et al., 1983). Within the following years, three major milk-product-borne outbreaks were recorded, of which two occurred in the USA and one in Switzerland (Fleming et al., 1985; Büla et al., 1995; Linnan et al., 1988; James et al., 1985).

Raw consumed foodstuffs or re-contaminated foodstuffs, if offered in a ready-to-eat condition, are the risk foodstuffs. In the dairy field, the prevalence for L. monocytogenes contamination of raw bulk-tank-milk and dairy milk samples was reported as 1.3% and 0.94% in Canada and Turkey, respectively (Farber et al., 1988, Uraz and Yucel, 1999). However, higher prevalence was reported from milk samples drawn in Northern Ireland (Harvey and Gilmour, 1992). Generally, the examination of the prevalence of L. monocytogenes in bulk-tank-milk is dependent on the detection efficacy of the method used as, contaminated farm milk samples are highly diluted when collected with milk of other suppliers. Microbiological investigations of raw milk which was gained from an udder infected by L. monocytogenes, showed that approximately 4x104 Listerial cells/ml were shed into the raw milk during high lactation (Wagner et al., 2000). According to milk and milk products, pasteurization studies have shown that the heating of raw milk to temperatures above 69°C killed the listerial cells (Farber et al., 1988a). Therefore survival of listerial cells during pasteurization is due to technical problems regarding the pasteurization process. An outbreak of listeriosis was traced and was most likely to an unreliable heat treatment during pasteurization (Fleming et al., 1985).

It is assumed that the initial contamination level of milk and meat products is rather low. Nichols et al. (1998) reported that 0.6% of 3065 patè samples exceeded contamination levels higher than 200cfu/g. In a Japanese study, 12.2 to 37.0% of various minced meat samples of different origin were found positive for L. monocytogenes but in most of them, the contamination level was lower than 100cfu/g. Only 10.9% of minced chicken samples exceeded 100cfu/g. An even lower contamination level was achieved from examination of 92 salmon samples where all samples showed a lower value than 10cfu/g. L. monocytogenes could not be detected in any samples of vegetables (Inoue et al., 2000). These findings are in contrary to a study conducted in Malaysia, where both the contamination rate of meat samples (chicken portions 60%, beef 50%) and vegetables (leafy vegetables 22%, beansprout 85%) were clearly higher (Arumugaswamy et al., 1994).

Although the minimal infective dose for listeriosis is still unclear, it is largely accepted that, in most cases and for most foodstuffs, Listeria have to multiply before they will become a risk for human consumers. Therefore, the intrinsic, foodstuff-specific processing factors and the extrinsic, technology-specific processing factors are of high importance in preventing or reducing listerial growth. Ready-to-eat foodstuffs such as soft cheeses made from raw or pasteurized milk (low alkaline pH on the cheese surface), cold-smoked salmon and fish products (cold-smoking is not sufficient to reduce significantly the number of contaminants), patés and other meat products (‘rillettes’, jellied pork tongue) have been associated with outbreaks of listeriosis (Embarek, 1994; Büla et al., 1995; Ericsson et al., 1997; Goulet et al., 1998; Goulet et al., 1995; James et al., 1985; Linnan et al., 1988; McLauchlin et al., 1991). Therefore it was shown in a study comparing finfish and shellfish samples which were differently processed by either cold-smoke or hot-smoke treatment that the incidence for listerial contamination was clearly higher when cold-smoking (21.3% versus 8.8%) was applied (Heinitz and Johnson, 1998). In soft cheeses made from raw milk, L. monocytogenes was detectable in 42 % of samples. In comparison, only 2% of the cheese samples made from heat treated milk were contaminated (Loncarevic et al., 1995). In a few cases, poultry meat and meat products (‘turkey franks’) and vegetables have been involved in human listeriosis (Ryser, 1999).

However, during recent years there have been outbreaks recorded which do not fit into the common scheme. Lyytikainen (2000), for instance, reported an outbreak of listeriosis where both the implication of the foodstuff (butter) and serovar (3a) were unusual.

Prevention and control

The risk for acquisition of either human or mammalian listeriosis is minimized if the contamination of food and feeding stuffs is prevented. Efforts have to focus on the microbiology of raw materials, prevention of re-contamination at early or advanced processing steps and controls of storing and shelflife of foods as these may restrict or even reduce the listerial multiplication. Zero-tolerance policy as stated by most of the (inter)national food hygiene directives in Europe is a stringent tool to exclude contaminated foodstuffs from the food chain. However, there are other regulations implemented which differentiate among foodstuffs at high risk or low risk . In Canada, ready-to-eat foods (RTE foods) which have been implicated in cases or even outbreaks of listeriosis are considered class I (action is taken when L. monocytogenes is detected in 50g of such foodstuffs). All other RTE foods which may support growth of L. monocytogenes and whose shelflife is more than 10 days are considered class II (action is taken when contamination level exceeds 0/25g). Class III-RTE foods are those which do not support growth or whose shelflife is shorter than 10 days. In such foods, a contamination level of 100cfu/g is tolerated depending on an adequately good manufacturing practice in the food plant (Farber et al., 1996). Such regulations try to find a balance between consumer protection on the one side and economical requirements on the other.

The wide spectrum of possibilities which may lead to the (re)contamination of foodstuffs at various stages of processing, trading and food preparation requires for concerted action by food scientists, food producers and public health authorities if a reliable control of foodborne microbial hazards is desired. Risk analysis models allow the quantification, management and communication of a hazard that is associated with a particular foodborne pathogen. It is the scientific basis for the establishment of directives and national/ international regulations. General requirements for conducting a risk assessment are knowledge concerning the minimal infective doses (MID) of a pathogen, its pathogenicity and virulence features, and the properties of the pathogen interaction with the host immune system. Data on the prevalence of contamination and the initial contamination level of particular foods and on the exposure frequency of a certain population must be collected. Finally the capacity of multiplication under proper or even improper processing and storage conditions including preparation and consumption habits is of importance.

The valid food hygiene directives that outline a strict zero-tolerance for the occurrence of L. monocytogenes in foodstuffs at high risk imply that a profound Listeria risk assessment is not yet available in many countries worldwide. This is mainly due to a lack of scientifically proven data.

The production-related quality assurance tools (GMP, GHP, HACCP) intend to avoid the accumulation of a microbial risk at the farm or facility level. All three concepts should work together in a strategic manner. Whereas GMP and GHP display the basis of food manufacturing in general, HACCP refers to particular food type-dependent processing conditions. The functionality of particular preventive quality assurance concepts are supervised by a food surveillance system run by public health authorities. The surveillance should be able to recognize a microbial hazard when the in-house quality assurance has failed to eliminate it. With respect to storage conditions, shelflife properties, preparation habits and consumption of foodstuffs, post-processing hygiene principles must be repeatedly communicated to food handlers, retailers and consumers because they are usually not experts in the hygiene area. To complete the theoretical considerations by a practical example, the Austrian cheese monitoring initiative is briefly described. The initiative was launched by the Institute for Milk Hygiene, Milk Technology and Food Science (IMMF) in 1986 and led to the establishment of an almost nation-wide Listeria monitoring council.

The monitoring is organized in a three-step configuration. According to a sampling plan, the industrial cheese production facilities send dairy environment samples twice a month to the IMMF, preferably wash waters and smear waters (First step: routine control of the processing environment). An examination of sample volumes of 1 litre increases the detection limit of the microbiological analysis and intends an early identification of an ongoing contamination, favourably before the product itself is already contaminated (details in Asperger, 1998). In cases of detection of L. monocytogenes in the dairy environment, the product safety is proven by a second-step intervention phase which leads to an intensified investigation of product lots which are either under processing or ready for packaging and delivery to the market. A final phase is focused on the elimination of the contaminant from the facility via hygiene and sanitation activities. In escorting surveys, the clinical and foodborne L. monocytogenes strains which are isolated/collected by the National Reference Center for Listeriosis or food hygiene inspection and monitoring authorities are sent to the IMMF for typing and epidemiological tracking.

The efficacy of the monitoring is corroborated by the fact that no epidemiological evidence for the implication of milk or milk products in sporadic cases of listeriosis was ever recorded in Austria in about 15 years of surveillance.

Disease Treatment

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The outcome of medical treatment and recovery is sometimes ambiguous though the organism is highly susceptible to a wide array of antibiotics in in vitro testing (Hof, 1997). In vitro susceptibility studies using a broth dilution method or similar can lead to controversial results in comparison to the results of application in the patient. Tamagawa et al. (1996) reported two cases of listeriosis in a new-born and a 48-year-old patient where the outcome was fatal although, the causal strain was highly susceptible to the array of antibiotics used. Cell culture studies which investigated the inhibitory effect of some antibiotics on intracellular stages of Listeria revealed no correlation between the minimal inhibitory concentrations found during extracellular multiplication in culture media and those observed during intracellular growth in HeLa cells (Michelet et al., 1994). One of the reasons is likely the facultative intracellular survival and spreading of L. monocytogenes in blood and other cells. In such stages the pathogens are as they were ‘masked’ for weakly or non-penetrating antibiotics.

The only drugs not being sufficiently effective in in vitro susceptibility testing are newer cephalosporins and fosfomycin. MacGowan et al. (1990) found that cephalothin, chloramphenicol, ciprofloxacin and ofloxacin were less active in comparison to most of the 21 other antimicrobial drugs examined and that cefuroxime, enoxacin, norfloxacin and fosfomycin were the least active in 103 strains tested. Charpentier et al. (1995) showed that no strain was resistant to ampicillin, chloramphenicol, erythromycin, gentamicin, kanamycin and vancomycin.

Resistance of Listeria to antibiotics is rarely detected and usually restricted to some drugs. From a study comparing the in vitro susceptibility of L. monocytogenes to a range of antibiotics in two-test format. It was concluded that the in vitro susceptibility of L. monocytogenes has not changed during recent decades as old reference strains did not differ in their resistance features in comparison to more recently collected isolates (Heger et al., 1997). However, Poyart-Salmeron et al. (1990) described a plasmid that mediated multiple drug resistance to a clinical L. monocytogenes isolate. Generally there is some confusion in literature on the incidence of antibiotic resistance in listeriae. Wesley (1999) stated that L. monocytogenes is resistant to many antimicrobial drugs, however, a review of management of listeriosis emphasized that most Listeria strains are susceptible to the majority of antimicrobial drugs (Hof, 1997). In a French study, the percentage of resistance to tetracycline and minocycline was highest in 1100 Listeria strains tested (Charpentier et al., 1995). Similarly, Wong et al. (1990) reported a resistance of 14.5% of L. monocytogene isolates to methocillin and tetracyclines but almost no resistance to 10 other antimicrobial drugs. Chlorotetracyclines, however, have been mentioned as an effective drug in review articles (Wesley, 1999; Radostits et al., 1999). Radostits at al. (1999) recommend intravenous injection of 10mg/kg body weight for 5 days at early time points of an ongoing infection in cattle but they state that this treatment is less effective in sheep. However, as reported in many other studies, amoxicillin seems to be a highly effective drug and is frequently given in combination with gentamicin. Alternatively penicillin at a concentration of 44 000Units/kg body weight might be intramuscularly administered daily for 7 to 14 days (Radostits et al., 1999). As a general rule it must be said that the prognosis is poor when severe clinical symptoms are overt.

Listeria monocytogenes is susceptible to penicillin, ampicillin, ceftiofur, erythromycin and trimethoprim/sulphonamide; the drug of choice is penicillin (ampicillin is too expensive in most agricultural systems). High doses of penicillin are required because of the difficulty in achieving minimum bactericidal concentrations in the brain. Recovery depends on early aggressive antibiotic treatment. If signs of encephalitis are severe, death usually occurs despite treatment.

Penicillin G should be given with the first dose up to 300,000 iu/kg bodyweight injected intravenously followed by more conventional dose rates (44,000 iu/kg) by intramuscular injection twice daily for 3 days. The high cost of such initial treatment results in the situation whereby sheep are more commonly treated at dose rates around 100,000 iu/kg. There is no advantage in treating sheep for more than 4 to 7 days, certainly not 42 days as recommended in some standard veterinary texts. Intravenous injection of 1.0 mg/kg dexamethasone at first presentation remains controversial but there is clinical evidence that this regimen achieves higher success rates than antibiotic treatment alone. Supportive therapy, including fluids and electrolytes by orogastric tube, is required for animals having difficulty eating and drinking.

Prevention and Control

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There are only few reports in literature where live vaccines have been developed and evaluated in field trials. Linde et al. (1991) used metabolic shift mutations based on the selection of resistant clones against streptomycin and rifampicin. The authors created attenuated mutants that protected 95% of mice when they were challenged with a 100-fold LD50 of a fully virulent strain. In a field study, the vaccine was used in flocks of sheep. The results indicated a lower incidence for listeriosis and higher postnatal body weight in offspring’s from vaccinated rather than unvaccinated ewes (Linde et al., 1995). However, none of these promising vaccine candidates found its way into routine application mainly due to the following reasons: Live attenuated vaccines bear a risk for idiopathic infection in connection with diseases which act by immune depression or are boosted by immune depression. This is the case with listeriosis. Furthermore, vaccination is a cost factor and the occurrence of listeriosis in animals is low. Other strategies using non-pathogenic vectors as shuttles or unspecific stimulation of the immune system were not successful due to the insufficient protection efficacy or observation of side effects (Gentschev et al., 1992, Wirsing et al., 1988).

In countries such as Norway where husbandry of sheep and goats is of high agro-economical value, large vaccination trials have been undertaken. In an estimation of the economical impact of vaccination on husbandry costs, it was calculated that a vaccination is beneficial in flocks of sheep which comprise more than 100 ewes and record 1-2 cases of listeriosis per year (Vagsholm et al., 1991). To the knowledge of the author there is no L. monocytogenes vaccine available on the Austrian veterinary vaccine market. The production and delivery of a German Listeria vaccine was rejected by the Wirtschaftsgenossenschaft deutscher Tierärzte in 1995.


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