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 Md jaman, B-110605006 

 Listeria (pronounced liss-STEER-ē-uh) is a gram-positive rod-shaped bacterium that can grow

under either anaerobic (without oxygen) or aerobic (with oxygen) conditions. ut ! the six

species o! Listeria" only L. monocytogenes(pronounced maw-#-site-aw-$%&-nee') causesdisease in humans.These bacteria multiply best at -*. degrees + (,-, degrees /)" but also

multiply better than all other bacteria at re!rigerator temperatures" something that allowstemperature to be used as a means o! di!!erentiating Listeria !rom other contaminating bacteria.

Properties of the organism:

 Listeria is the genus o! pathogenic bacteria that causes the in!ection listeriosis. 0t is a !acultative

anaerobic bacteria" capable o! surviving in the presence or absence o! oxygen. They can grow andreproduce inside the host1s cells and is one o! the most virulent !oodborne pathogens" with 2 to

,3 o! clinical in!ections resulting in death. Responsible !or an estimated 4" illnesses and

2 deaths in the %nited States (%.S.) annually" listeriosis is the third-leading cause o! deathamong !oodborne bacterial pathogens" with !atality rates exceeding

even Salmonella and Clostridium botulinum. 5isteriosis mortality rates in the E% higher than !or

other !ood-borne pathogens.

 Listeria monocytogenes is a 6ram-positive  bacterium" in the division +irmicutes" nameda!ter $oseph 5ister . 0ts ability to grow at temperatures as low as 7/ permits multiplication at

typical re!rigeration temperatures" greatly increasing its ability to evade control in human

!oodstu!!s. 8otile via !lagella at , 7/ and below" but usually not at , 7/"9:;  L.

monocytogenes can instead move within eu

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  Listeria welshimeri

  Listeria ivanovii

 Listeria grayi

Md Mahbub Ul Alam (1106050!"

#ondition for gro$th % produ&tion:

1. Temperature: Listeria pre!er temperatures between ,/ and :/ but grow in the range

4:>/. Listeria will grow at normal re!rigeration temperatures" with numbers increasing.

 2. PH:  Listeria pre!er to grow at p& - but they will grow in the range p& >-4. Recent studies

have shown that Listeria may survive and grow in material with a p& as low as :.:. &owever" itseems that the type o! acid used to acidi!y the material and the storage temperature have a

mar

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. #ater activity: The minimum water activity !or the growth o! L. monocytogenes is .*2. 0t can

tolerate high sodium chloride levels and is able to grow in environments o! up to 43 salt" and to

survive in concentrations o! 2 ? ,3. L. monocytogenes is also able to survive !or some time in

low water activity environments" and may survive !ood drying processes. Survival times areextended at chilled temperatures'

Toin Produ&tion:

 Listeria monocytogenes  produce a hemolysin called )isteriolysin O (55)" Listeria ivanovii

 produce *+anolysin O, sphingomyelinase, and le&ithinase

Property of )isteriolysin O

4) 0t has been shown to be highly homologous to streptolysin (S5) and pneumolysin

(@5).

2) 0t has been puri!ied and shown to have a molecular weight o! " daltons

,) 0t consists o! >: amino acids.

:) 0t is produced mainly during the exponential growth phase" with maximum levels a!ter

-4 hours o! growth.

>) 5ess 55 is synthesi'ed at 27/ than at ,7/ with high glucose" and synthesis was

!ound to be best with .23 glucose at ,7/.

) Sorbate at a level o! 23 inhibited 55 synthesis at ,>7/ under aerobic or anaerobic

conditions.

) 55 is active at a p& o! >.> but not at p& ."

$% 55 has been detected in all strains o!  L. monocytogenes& including some that were

nonhemolytic" but not in L. welshimeri or L.  grayi.

'% The gene that encodes its production is chromosomal and has been designated hly

4) 0ts 5A> !or mice is about . ug

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 @uri!ied 55 has been shown to share in common with S5 and @5 the !ollowing propertiesB

4) activated by S&-compounds such as cysteine"

2) inhibited by low Cuantities o! cholesterol"

,) and common antigenic sites as evidenced by immunological cross-reactivity. %nli

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Me&hanism of Pathogenesis:

The pathogenic mechanism o! L. monocytogenes is a complex process and it can be subdividedinto two phasesB intestinal and systemic. The intestinal phase o! in!ection involves bacterial

coloni'ation in the intestine and conseCuent translocation through the mucosal barrier to blood

circulation or to the lymphatic system !or systemic dissemination. Auring systemic spread" the

organism is transported by dendritic cells or macrophages to the liver" spleen" lymph nodes"

 brain" and to the placenta (in pregnant women). 8any sur!ace associated and secreted proteins

have been recogni'ed as important virulence !actors which are critical !or bacterial persistence in

the intestinal tract" to enter the host cells !or intracellular movement and cell-tocell spread" and to

evade immune system.The maDority o! virulence genes are clustered in a *-

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!urthermore" !ood particles neutrali'e p& to ensure sa!e passage to the small intestine. ile salt

hydrolase (S&) and the bile exclusion system (ilE) protect bacteria against bile salts and

pu/ provides osmotolerance. The organism pierces through the mucosal layer and interacts

with and breaches the intestinal epithelial barrier by three possible pathwaysB through 8-cells

overlying @eyerFs patches" through epithelial cells" and through dendritic cells sampling the

lumen o! intestine Aendritic cells andGor macrophages located beneath the epithelial cell lining

in lamina propria can process and present antigen to helper T-cells (/A:H) or cytotoxic T-cells

(/AH) cells !or immune response or can transport bacteria to extraintestinal sites such as liver"

spleen" lymph nodes" the brain and the !etoplacental Dunction in pregnant women. acterial

translocation through naturally phagocytic 8-cells is a passive process" while translocation

through enterocytes is an active process where bacterial interaction with host cell receptors

initiates a cascade o! signaling events that modi!y cellular architecture to promote bacterial

 passage through cells.

The cellular mechanism o! Listeria pathogenesis involves !our maDor steps

 (4) attachment and entry"

 (2) lysis o! vacuole (phagosome)"

FIGURE: L. monocytogenes translocation pathway through intestinal celllining. Three possible pathways are proposed; (1)translocation through M-

 

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 (,) intracellular growth" and

 (:) cell-to-cell spread (+ig. *.>).

1" Atta&hment and ntry:22 =dhesion is critical in the initial phase o! in!ection. Several

adhesion !actors have been identi!ied to be involved in this process (+ig. *.:). 0nternalin = (0nl=)interacts with epithelial cadherin (E-cadherin) to promote bacterial entry into cells and is

important during intestinal and uteroplacental in!ection. 0nternalin (0nl) interacts with 8et"

g/4C-R" and proteoglycan receptors" and aids in Listeria invasion in hepatocytes and endothelial

cells. Synergistic action o! both 0nl= and 0nl may be needed to achieve cell invasion to various

target sites o! bacterial tropism. The mannose--phosphate li

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5isteriolysin (55) is a sul!hydryl (S&)-activated" pore-!orming hemolysin with a molecular

mass o! >?

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=ctin polymeri'ation protein (=ct=) initiates actin polymeri'ation to aid bacterial movement

inside the cytoplasm. =ct= is a ,* amino acid containing cell sur!ace protein o! K*

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 phosphatidylcholine-speci!ic @5/ (@/-@5/) and 55

Phosphatidyl&holine2-pe&ifi& P)#

@/-@5/ is a 2*-

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RE+ERE#/EB

 =run M. hunia (auth.)-+oodborne 8icrobial @athogensN 8echanisms and @athogenesis-

Springer-Ierlag #ew Oor< (2)

afsan Abir (7 110605008"

oods in+ol+ed:

Ready-to-eat deli meats and hot dogs

• Re!rigerated pPtQs or meat spreads

• %npasteuri'ed (raw) mil< and dairy products

• So!t cheese made with unpasteuri'ed mil

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ales. The prevalence o! 5. monocytogenes in bul< mil< tan< internationally is 4?3 (+S=#L

2*). The presence o! 5. monocytogenes in ready-to-eat products is probably due to

contamination occurring a!ter the product has been processed. This contamination may occur

during additional handling steps such as peeling" slicing and repac

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 Anamul abir (1106050;"

Treatment for )isteriosis

5isteriosis is mainly a !ood-borne illness caused by L. monocytogenesJ people most prone to the

disease are pregnant women" newborns" elderly" and those with &0I or other diseases

compromising immunity. 5isteria in!ections are associated with a high mortality rate" and thuse!!ective antibiotic treatment is essential. =lthough a variety o! antibiotics have activity against

the organism" ampicillin alone or in combination with gentamicin remains the treatment o!

choice. Some patients may reCuire alternative therapies due to allergies or certain disease states.

Second-line agents !or these cases include trimethoprimGsul!amethoxa'ole" erythromycin"vancomycin" and the !luoroCuinolones. /ephalosporins are not active against 5isteria. =mpicillin

is currently the drug o! choice !or treating 5. monocytogenes in!ections. 8any antibiotics have

 been shown to be e!!ective and are used as second-line agents. &owever" !urther study is reCuired!or some o! the most recently introduced antibiotics" such as the !luoroCuinolones" to determine

their place in the treatment o! 5isteria in!ections.

Pre+ention:

Epidemiologic investigations have demonstrated that nearly all types o! !ood can transmit

 Listeria. 8ost sporadic cases and all large outbrea

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5isteriosis is a rare disease that causes mild maternal illness" but can be devastating to the !etus.

 ListeriaFs rare microbiologic !eatures ma

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