Lister Ios Is

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Listeriosis

Klara M. Posfay-Barbe a,*, Ellen R. Wald b

a Department of Pediatrics, Childrens Hospital of Geneva, University Hospitals of Geneva, 6 rue Willy-Donze, 1211 Geneva 14, Switzerlandb Department of Pediatrics, University of WisconsinMadison, School of Medicine and Public Health, 600 Highland Avenue, Box 4108, Madison, WI 53792, USA

Keywords:

Early-onset sepsis

Late-onset sepsis

Listeriosis

Neonates

Perinatal infection

s u m m a r y

Listeria monocytogenes, a small, facultative anaerobic, Gram-positive motile bacillus, is an important

cause of foodborne illness which disproportionately affects pregnant women and their newborns. Lis-teria infects many types of animals and contaminates numerous foods including vegetables, milk,

chicken and beef. This organism has a unique proclivity to infect the fetoplacental unit with the ability to

invade cells, multiply intracellularly and be transmitted cell-to-cell. The organism possesses several

virulence factors, including internalin A and internalin B, which facilitate the direct invasion of cells. Cell-

to-cell transmission is promoted by the bacterial surface protein ActA which is regulated by a tran-

scriptional activator known as positive regulatory factor A. Both innate and adaptive immune responses

enable the host to eliminate this pathogen. Clinical manifestations of infection in the newborn fall into

the traditional categories of early- and late-onset sepsis. Therapeutic recommendations include ampi-

cillin and gentamicin for 1421 days.

2009 Elsevier Ltd. All rights reserved.

1. Microbiology

Listeria monocytogenesis a small, facultatively anaerobic, Gram-

positive, motile bacillus. It grows well in broth and on blood agar;

some species produce a narrow zone of beta-hemolysis.1 In clinical

specimens, the organism may be Gram-variable and look like cocci,

diplococci, or diphtheroids, thereby misleading the laboratory

technician. The organism tolerates low temperatures as well as

high pH and high salt concentrations, which allow it to replicate in

soil, water, sewage, manure, animal feed, and contaminated

refrigerated foods. It can survive many months in soil and 2030

days in tap water. Although persisting on environmental surfaces,

pasteurization and most disinfecting agents eliminateListeria.

Only four of the seven species ofListeria infect humans. Most

diseases are due to three primary serotypes: 1a, 1b and 4b. The last

is responsible for almost all outbreaks of listeriosis.2

2. Epidemiology

Listeria spp. are distributed worldwide, but human illness is

reported most frequently in developed countries. Listeria spp. are

an important cause of zoonoses, infecting many types of animals

(domestic pets, livestock, other mammals, rodents, amphibians,

fish, and arthropods) and more than 17 avian species. In

mammals,L. monocytogenes can cause spontaneous abortions and

is the cause of circling disease, a manifestation of basilar

meningitis in which animals move incessantly in a circle. Fecal

oral transmission is the probable means by which organisms are

spread in animals. The pathogen can be transmitted directly from

animals to humans and has been documented in veterinarians,

farmers, and abattoir workers. Vertical transmission from mother

to neonate occurs transplacentally or through an infected birth

canal. Cross-infection in a neonatal unit through contact with

contaminated mineral oil used to bathe infants led to one noso-

comial outbreak.3

Most cases of listeriosis appear to be foodborne, including those

acquired during pregnancy. Many foods can be contaminated by L.

monocytogenes, including raw vegetables, raw milk, fish, poultry,

processed chicken, and beef. Approximately 1570% of hot dogs are

reported to be contaminated withListeriaspp.Listeriaspp. also are

found in the stools ofw5% of healthy adults.4 The infectious dose isestimated to be 104106 organisms per gram of ingested product

but may be lower in immunocompromised hosts and patients who

have diminished gastric acidity or have undergone ulcer surgery.5

The incubation period has not been well-established, but is esti-

mated to be three weeks.

The first clearly documented foodborne (coleslaw) outbreak

was in Nova Scotia in 1981.5 It was associated with a case fatality

of 27%. In other sporadic outbreaks, 11% of all food samples

retrieved from the refrigerator were contaminated, and 64% of the

refrigerators of patients contained at least one contaminated food

item.2* Corresponding author. Tel.: 41 22 382 5462; fax: 41 22 382 5490.

E-mail address: [email protected](K.M. Posfay-Barbe).

Contents lists available atScienceDirect

Seminars in Fetal & Neonatal Medicine

j o u r n a l h o m e p a g e : w w w . e l s e v i e r . c o m / l o c a t e / s i n y

1744-165X/$ see front matter 2009 Elsevier Ltd. All rights reserved.

doi:10.1016/j.siny.2009.01.006

Seminars in Fetal & Neonatal Medicine 14 (2009) 228233
mailto:[email protected]://www.sciencedirect.com/science/journal/1744165Xhttp://www.elsevier.com/locate/sinyhttp://www.elsevier.com/locate/sinyhttp://www.sciencedirect.com/science/journal/1744165Xmailto:[email protected]


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was the first identified virulence factor ofL. monocytogenesand is

required for bacterial escape from endocytic vacuoles. LLO-defec-

tive strains are five to 10 times less invasive than wild-type

strains.22 LLO is required in vivo for bacterial growth in tropho-

blastic cells, and for subsequent fetal invasion.8 It is also known as

a modulator of the innate immune response by inducing new

cytokine synthesis in different immune cells and activating

different immune-response-associated pathways, such as the NF-

kappaB pathway.23 The mechanisms behind this activation process

are, however, still unclear.

3.3. Cell-to-cell transmission

Once in the cytoplasm, listeria multiplies rapidly, migrates to the

host cell periphery and into cell-wall protrusions, which will be

taken up and ingested by neighboring cells where a new cycle will

start again (Fig. 1). This migration to the surface of the hosts cell

depends on ActA, a bacterial surface protein.

3.3.1. ActA

ActA is a virulence factor required for cell-to-cell spread of lis-

teria. It uses components of the host cells actin cytoskeleton to

generate a comet-tail which is rich in actin, enabling bacterialpropulsion in the cytosol leading to the infection of uninfected

neighbor cells.24 Strains lacking ActA retain the ability to grow in

the placenta although at a lower rate than wild-type strains but

arestronglycurtailed in their ability to spread from cell to cell.8 This

was demonstrated in an animal model, in which neonatal mice

injected with an isolate ofL. monocytogenes lacking ActA induced

a strong primary and secondary Th1 CD4 and CD8 T-cell response,

but were protected against death from infection with listeria.

Interestingly, motility can be conferred upon other non-motile

micro-organisms (such asL. innocua) by adding ActA.25

3.3.2. Positive regulatory factor A

The expression of nearly all bacterial gene products that

contribute to the survival and virulence of L. monocytogenes,including LLO and ActA, are regulated by a transcriptional activator

known as positive regulatory factor A (PrfA). Strains lacking func-

tional PrfA are not virulent. The effect of PrfA seems to be reduced

at low temperature, but increased at low pH, probably explaining

the increased virulence of strains in a warm, acidic environment

after oral ingestion.26,27 Post-transcriptional mechanisms control-

ling PrfA expression have also been described and contribute to the

synthesis of Int1A, Int1B, and LLO.11

In summary, it is currently believed that: In1A (especially) and

In1B play a key role in the entry of listeria into host cells; LLO

punches holes to allow the organism to multiply inside the cyto-

plasm of the host cell; ActA produces a rocket-like mechanism to

penetrate into neighboring cells; and that all these mechanisms are

co-ordinated by PrfA. New virulence factors forL. monocytogenesaswell as genes involved in virulence or stress-response are described

regularly, increasing the complexity of the bacteriums pathoge-

nicity and its regulatory mechanisms.28

4. Immunology

4.1. Innate and adaptive immune response

L. monocytogenes has been used for decades as a model

organism to study innate and adaptive immune responses against

intracellular pathogens. The innate immune response is immediate

and involves multiple cellular types, cytokines, and bactericidal

effector mechanisms. Monocytes and resident macrophages,

Kupffer cells for example, are known to ingest and destroy listeria.

Production of cytokines, such as interleukin (IL)-1, IL-6, and tumor

necrosis factor (TNF)-a are central in decreasing susceptibility to

disease by recruiting neutrophils. On the other hand, the adaptive

immune response against infection induced by L. monocytogenes

peaks about one week after infection, and is mainly a CD8 T-cell

response. This response has twomain functions: the specific lysis of

infected cells and rapidproduction of IFN-g in response to IL-12 and

IL-18.29 It is now hypothesized that early IFN-gproduction leads to

an accelerated formation of granulomas at sites of infection,

thereby walling off the infection. In mouse strains of listeria that

do not elicit an early IFN-gresponse, acute inflammation continues

and listeria spreads between cells. Clearance ofL. monocytogenesis

believed to be mediated through a Th1 immune response. IFN-gis

a crucial contributor to the Th1 response by activating macro-

phages, increasing antigen presentation via the MHC class I and II

pathways, and by inhibiting the expansion of Th2 cells.30

A number of research groups have been focused on describing

the cells which produce IFN-g in infections caused by L. mono-

cytogenes. It seems likely that several cells, including natural killer

(NK) cells, dendritic cells during the early phase of innate immu-

nity, antigen-specific CD4 TH1 cells,and effector and memory CD8

T-cells during the later phase of adaptive immunity, produce IFN-g

during infection.29,31 Tocomplicate ourunderstanding of the role ofIFN-gin listerial infection, it appears that IFN-gboth promotes the

control of bacterial replication and also induces (paradoxically), the

erosion of CD8 T-cell memory during infection, thereby impairing

subsequent protective mechanisms.32 In summary, IFN-g plays

a critical role in both innate and adaptive immune responses to L.

monocytogenes.

4.2. Toll-like receptors and autophagy

Toll-like receptor (TLR) 2 and TLR5 have been reported to

recognize L. monocytogenes.33 TLR recognition of listerias lip-

oteichoic acid, lipoproteins, peptidoglycans and flagellin leads to

the production of cytokines which inturn directly activate innate

effectors and recruit other cells.34,35 Interestingly, however, ina murine model in which animals lack myeloid differentiation

factor 88 (MyD88), an adaptor molecule downstream from TLRs, it

was shown that the animals are highly susceptible to infectionwith

listeria and that a MyD88-independent innate and adaptive

immune response exists.36

Macro-autophagy, also referred to as autophagy, is a recently

described mechanism involved in the immune response of

mammals to micro-organisms.37 Briefly, through autophagy, an

infected cell can target an invading micro-organism and restrict its

growth by destroying it in the lysosome. It then induces an adaptive

immune response via presenting peptides on MHC Class I and II

molecules. Recent studies have shown that autophagy targets L.

monocytogenes before bacterial escape into the cytosol. However,

listeria is capable of using alternate strategies, including ActA-dependent polymerization mentioned earlier, to avoid

destruction.38

4.3. Specific relation to immunology of pregnant woman and child

The maternal immune system faces an important challenge

during pregnancy, i.e. to prevent rejection of the semi-allogenic

fetus and to protect itself and also the fetus from infection. Many

observations suggest that pregnancy is associated with a shift from

Th1 to Th2 cellular response and that the maternal immune system

is biased toward humoral immunity and away from cell-mediated

immunity (that could be harmful to the fetus). However, these

changes appear mostly to occur locally, as there is no strong

evidence suggesting that the maternal immune system is

K.M. Posfay-Barbe, E.R. Wald / Seminars in Fetal & Neonatal Medicine 14 (2009) 228233230


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compromised overall during pregnancy. New immunomodulating

mechanisms, not specific to L. monocytogenes, have been studied

extensively and are reviewed elsewhere.39,40 L. monocytogenes, on

the other hand, has to develop different strategies against the

defence mechanisms of the host to survive. While some of these

defences are not specific to pregnancy, such as gastric acidity, lis-

teria has mastered manipulating the differences related to the

immaturity of the immune system of the fetus. Neonatal immunity

is reported to be Th2-biased. This avoids maternal rejection of fetal

antigens induced by Th1-type inflammation that may result in

spontaneous abortion or premature delivery.41 Furthermore, it

appears that (murine) neonates have a lower expression of

mannose-binding lectins and certain TLRs than adults.42 These

mediators are necessary to develop Th1 immune responses and

might explainwhy neonates are highly susceptible to infectionwith

listeria. This fact has been questioned by others who believe that it

is not a decreased expression of TLRs, but instead a TLR-induced

TNF-a production which is significantly decreased in neonates.43

Interestingly, the same authors acknowledge that neonates are

capable of a robust IL-6 production, indicating that the intrinsic TLR

pathway is functional at birth, and suggesting an abnormal, still

unclear, TLR defect related to Th2.

L. monocytogenes can also gain access to the neonate via oralexposure during the passage through the birth canal. Enteric anti-

microbial peptides derived from Paneth cells provide protection

from intestinal infection. However, these cells are not present

during the first weeks of life. Recently, Menard et al. described an

antimicrobially active form of peptide, called CRAMP (cathelin-

related antimicrobial peptide), in the epithelium of neonatal mice,

which is expressed constitutively during the first weeks of life

only.44 CRAMP provides significant protection against bacterial

growth in the gut. This developmental switch in innate immune

effector expression (i.e. CRAMP being functional only while Paneth

cells are lacking) is a newly described mechanism in the early

protection against infection with listeria. Enhanced understanding

of the specificity of the immune system in neonates may lead to

novel treatment strategies in years to come.

5. Neonatal disease

Worldwide,L. monocytogenesis one of the three major causes of

meningitis in neonates. Clinical manifestations may be very similar

to those seen with group B streptococcal disease, and there is a high

fatality rate (350%). There are two forms of neonatal listeriosis.

5.1. Early onset

The mothers of affected children often have a flu-like illness

a few days before delivery, which may be preterm. Listeria

bacteremia presents with an acute febrile illness, which is often

accompanied by myalgias, arthralgias, backache and headache.Maternal illness is observed most often in the third trimester.

Neonatal death and stillbirth occur in approximately one-fifth of

maternal infections. Two-thirds of the infants who survive delivery

to a woman who experiences listeriosis in pregnancy will develop

neonatal infection. The infants are believed to be infected in utero

because of the bacteremic phase of their mothers, but ascending

infections have been described. The highest concentrations of L.

monocytogenes are found in the lung and gut, suggesting that

infection also can be acquired in utero via inhalation and ingestion

of infected amniotic fluid as well as via the hematogenous route.

During labor, brown-stained amniotic fluid is seen and maternal

fever may be present. Serotypes 1a and 1b are most common.

The mean onset of symptomsis 1.5 days after birth. A sepsis-like

picture predominates, but other common manifestations are acute

respiratory distress, pneumonia, and more rarely, meningitis or

myocarditis. Strategies implemented to prevent group B strepto-

coccal sepsis in the newborn may have secondarily decreased the

rate of early-onset listerial infection.

Granulomatosis infantisepticum is a widely disseminated

granuloma characteristic of severe listerial disease. The lesions are

more common in the liver, skin and placenta, but also appear in the

brain, adrenal glands, spleen, kidney, lungs and gastrointestinal

tract. Aspiration of infected fluid can contribute to acute respiratory

failure and hemodynamic compromise in the neonate.

5.2. Late onset

This form of neonatal listeriosis is less common than the early-

onset form, but it occurs more frequently in term infants who are

the products of uncomplicated pregnancies. The babies are healthy

at birth, and the maternal history is usually normal. The first

manifestations of infection appear several days to weeks after birth,

with a mean onset of illness at 14.3 days after birth. The clinical

manifestation in this group is more likely to be meningitis than

sepsis, but it can be subtle, with fever, irritability, anorexia, diar-

rhea, and lethargy. Postpartum transmission is assumed to occur

either during delivery or nosocomially. Serotype 4b is mostfrequent in late-onset disease.

6. Diagnosis

Listeriosis usually presents with leukocytosis, but unlike its

name, rarely with monocytosis. Isolation of Listeria spp. from

a normally sterile site defines the disease. Thirty-six hours of

incubation usually are necessary for sufficient growth for identifi-

cation. The pathogen often is observed on the Gram stain of the

meconium of infected newborns. Carriage in the gastrointestinal

tracts of older children may be common but difficult to demon-

strate because the organism is fastidious and normal flora are

plentiful. Screening of rectal or vaginal cultures is not clinically

useful.Cold enrichment is not as good as selective media to isolate the

organism from specimens containing multiple species (e.g. in food

or stools). Rapid detection tests are based on the use of either

monoclonal antibodies or nucleic acid hybridizations, but they only

identify the genus Listeria.45

When the central nervous system is infected, cerebrospinal fluid

(CSF) is usually purulent, with leukocyte counts of 10010 000/mL

(0.110 109/L). Polymorphonuclear leukocytes predominate in

70% of cases, but the severity of the inflammatory response does

notcorrelate with the prognosis. The Gram stain of CSFis positive in


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L. monocytogenes can multiply within macrophages, several

prerequisites must be fulfilled to inhibit these hidden bacteria.

Antibiotics must penetrate into and distribute within host cells and

remain stable within this environment. Recommmendations are

based on data obtained from in-vitro susceptibility testing, animal

models, and clinical experience with small numbers of patients

who were compared with historic controls.

No controlled trials have established a drug of choice or duration

of therapy for listeriosis. L. monocytogenes is sensitive in vitro to

penicillin G, ampicillin, erythromycin, sulfamethoxazole, trimeth-

oprim, chloramphenicol, rifampin, tetracyclines, and aminoglyco-

sides. Bactericidal antibiotics include sulfamethoxazole,

trimethoprim, and aminoglycosides. Gentamicin and tobramycin

have been reported to have greater in-vitro activity than strepto-

mycin, kanamycin, and amikacin. Listeria always are resistant to

cephalosporins.48 Chloramphenicol should not be used because of

unacceptable failure and relapse rates, and quinolones do not havegood in-vitro activity. Ampicillin, which is superior to penicillin,

and gentamicin have shown synergistic effects in some studies.48

Accordingly, gentamicin with ampicillin is recommended for

treatment of listerial meningitis.

If the patient is allergic to ampicillin or gentamicin, sulfame-

thoxazole-trimethoprim is recommended because it is bactericidal

and reaches adequate levels in the serum and CSF.48 No systematic

study has examined the duration of therapy, but the current

recommendations are 1421 days of treatment for meningitis due

toL. monocytogenes.

8. Prevention

There is no vaccine for listeria infection. Dietary recommenda-

tions for preventing foodborne listeriosis were established by the

Centers for Disease Control and Prevention (CDC) in 1992. They are

similar to those for other foodborne illnesses and include thorough

cooking of raw food from animal sources; washing of raw vegeta-

bles; avoidance of unpasteurized dairy products; keeping uncooked

meats separate from vegetables; washing hands, knives, and

cutting boards after exposure to uncooked food; and regular

cleaning and disinfection of the insides of refrigerators. Persons at

high risk for listeriosis should avoid soft cheeses, reheat (until

steaming hot) leftover and ready-to-eat foods, and avoid cold cuts if

unable to reheat them thoroughly.

TheUS Department of Agriculture began surveillance in 1989 for

L. monocytogenes in ready-to-eat processed meats and enforced

regulations prohibiting the sale of contaminated meats. Since then,

the number of cases of listerial infection has dropped substantially.

The CDCs Division of Foodborne, Bacterial and Mycotic Diseases

tracks the annual incidence of certain foodborne illnesses,

including listeria, in 10 states through Food Net Surveillance.49

Between 1996 and 2006, the incidence of listeria declined by 36%,

although an outbreak in 2002, related to contaminated turkey

meat, resulted in 54 illnesses, eight deaths and three fetal deaths in

nine states (Fig. 2).49

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2.0

1.0

0.5

0.4

1996-1998

1999 2000 2001 2002 2003

Year

Relative

rate(logscale)

2004 2005 2006 2007

0.9

0.8

0.7

0.6

Fig. 2. Relative rates of laboratory-confirmed infections with listeria compared with

19961998 rates, by year (Foodborne Diseases Active Surveillance Network, USA,

19962007).

Research directions

To understand better how this quiet saprophyte

becomes a deadly agent.

To determine the infectious dose of listeria and to define

the extent of human illness by searching for listeria inoutbreaks of febrile gastroenteritis where no other

pathogens are identified.

To identify new bacterial and host effectors.

To examine interaction and activation processes

between bacteria and host, especially in vulnerable

populations, such as neonates.

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