Listeria

Front 1

Only listeria sp that infects humans?

Back 1

Listeria monocytogenes

Front 2

Lysteria physiology and structure
gram? shape?
oxygen use?
temp range?
salt tolerance?
motility?
spores?
catalase rxn?
intra/extracellular?

Back 2

gram pos rods (short), often in pairs or short chains
facultative anaerobe
broad temp range (1-45C), relatively heat resistant
can grow at high salt conc.
motile at room temp, but not at 37C, uses tumbling motion
non-spore forming
catalase pos
facultative intracellular

Front 3

Steps of infection

Back 3

ingestion of contaminated food
survives stomach
adheres to cells/penetrates enterocytes or M cells
acid pH of phagolyosome activates Listeriolysin O and 2 phospholipases
bact released into cytosol
bacterial replication
ActA mediates movement of bacteria into the cell membrane
bact pushed into another cell
cycle repeats

Front 4

Listeria can grow in what types of cells?
what mediates entry into non-phagocytic cells?
entry into macs following passage thru intestinal lining results in what?
what is required to clear a listeria infection? why?

Back 4

can grow in macs or epithelial cells
internalins mediate entry into non-phagocytic cells
entry into macrophages carries bacteria to liver and spleen resulting in disseminated disease
cell-mediated immunity is required to clear the infection because bacteria are never exposed to the humoral immune system

Front 5

Entry of listeria into cells
via what proteins?
usually interact with what on host cell?
internalized by what mechanism?

Back 5

listeria surface proteins (internalins) invovled in attachment/entry
interact w/host cell glycoprotein receptors (Internalin A binds to E cadherin)
internalized by zipper mechanism

Front 6

Virulence factors

Back 6

Internalins
Exotoxins (hemolysins)
ActA protein
Internalins
Growth at 4C (in fridge!)
Intracellular growth

Front 7

Listeria exotoxins

Back 7

= hemolysins
lead to release of bact into the cytosol via lysis of vacuoles

1.listeriolysin O
pore forming toxin
essential for pathogenicity (mutants that lack it are avirulent)
optimal activity at acid pH

2. 2 phospholipase Cs

Front 8

ActA protein

Back 8

allows movement and spread
located on cell surface
coordinates assembly of actin
distal end of actin tail is fixed, assembly occurs near end of bacterium
results in double membrane vacuole -- means it's never exposed to outside- not exposed to humoral immune system

(vacuole then cleaved by the hemolysins)

Front 9

Listeria sources of infection

Back 9

soil, water, veggies
animals (asymptomatic carriage)
humans (low level GI carriage in 1-5% of healthy people)

Front 10

Transmission

Back 10

usu occurs w/consumption of contaminated food
cheeses, milk, deli meat, turkey raw veggies (esp cabbage)

processed food can become infected after processing (cold cuts, soft cheeses)

Front 11

High risk groups

mortality rate

Back 11

elderly
defective cellular immunity (transplants, lymphomas, AIDS, glucocorticoids)
diabetes, kidney disease, cancer pts
pregnant women (20x risk of healthy adults)
neonates suffer effects of infection during pregnancy via transplacental transmission

mortality 20-30%

Front 12

Listeriosis in healthy adults

Back 12

usu asymptomatic
may have mild flu-like illness, possible GI symptoms

Front 13

What is unique that results from listeria's ability to pass from cell to cell?

Back 13

can cross:
blood brain barrier (meningitis)
intestinal barrier
placental barrier (abortion)

Front 14

Listeria meningitis in adults
how common?
at risk pts?
sequelae?
mortality?

Back 14

most common symptomatic presentation in adults
suspect listeria in pts w/cancer, organ transplants, or immunocompromised, or pregant women (if any of these have meningitis)
high mortality rate
significant neurological sequelae

Front 15

Listeria- primary bacteremia

Back 15

unremarkable Hx of fever and chills (common in pregnant women)
or acutely- high grade fever and hypotension
only severely immunocompromised and infants of pregnant women are at risk of death

Front 16

Presentation in pregnant women

Back 16

can present w/meningitis, bacteremia, unremarkable fever/chills, or acute high fever/hypotension

high danger to fetus/newborn

Front 17

Neonatal listeria
early onset vs late onset

Back 17

early:
acquired in utero (transplacental)
abortion, stillbirth, premature birth
causes granulomatous infantiseptica:
disseminated abscesses and granulomas in multiple organs
high mortality rate

late onset:
acquired at or soon after birth (2 wks)
meningitis or meningoencephalitis w/septicemia
must rule out other causes of childhood CNS disease (eg, group B strep)

Front 18

Listeria diagnosis

Back 18

microscopy- intracellular and extracellular gram + coccobacilli (hard to differentiate from step pneumo and enterococci)

lab culture: grows on most media, small zone of beta hemolysis
grows well at 4C (cold enrichment)
positive CAMP test (enhanced hemolysis when grown next to S. aureus)
motile

ID serotypes via serological tests (13 described serotypes)

Front 19

Listeria treatment

Back 19

combo of gentamicin and either penicilin or ampicillin

erythromycin for those w/allergies to penicillin

most Abx are only bacteriostatic to listeria
listeria resistant to cephalosporin, macrolides, and tetracyclines