Corynebacterium, Pseudomonas & Listeria

Front 1

describe the basic structure and Gram reaction of Corynebacterium diphtheriae (6)

Back 1

-Gram-Positive
-Club-Shaped pleomorphic rods

-Red metachromatic granules
-Aerobic

-non-motile

-catalase-positive

Front 2

explain how humans become infected with Corynebacterium diphtheriae

Back 2

Humans are the only reservoir. Minor componenet of skin, nose, vag, urethre

person-to-person contact or respiratory droplets

Front 3

describe populations at risk for infection and disease with Corynebacterium diphtheriae

Back 3

Unvaccinated or (old) person whose vaccine was long enough ago to lose immunity

Old person traveling or young immigrant = think diphtheriae

Front 4

list the disease(s) caused by Corynebacterium diphtheriae

Back 4

Respiratory Diphtheria

Cutaneous Diphtheria

Front 5

describe the clinical findings of Respiratory Diphtheria

Back 5

1. attachment, replication, & release of exotoxin in pharynx
2. 2-4 day incubation period

3. Sudden onset pharyngitis with exudate, low-grade fever

4. Gray Pseudomembrane develops
5. In severe cases: neck swelling,
systemic complications = myocarditis and neuropathy

Front 6

describe the clinical findings of Cutaneous Diphtheria

Back 6

1. Entry through skin breaks
2. Papule develops into chronic non-healing ulcer; may see grayish membrane

Front 7

explain the basic mechanism(s) of pathogenesis of Corynebacterium diphtheriae

Back 7

Disease caused by toxigenic strains of organism lysogenized with phage carrying tox gene.

Non-toxogenic straings can cause other disease (that's all she said).

Front 8

virulence factors of Corynebacterium diphtheriae

Back 8

Diphtheria toxin is an A-B exotoxin produced when Fe is low

the “active” toxin inhibits protein synthesis by inactivating elongation factor 2 (EF-2); results in cell death

Front 9

describe how Corynebacterium diphtheriae is prevented.

Back 9

Prevention with vaccine:

a. DTaP
b. Td*
c. Tdap

Front 10

describe the basic structure and Gram reaction of Pseudomonas aeruginosa

Back 10

1. Gram-negative rod, typically in pairs
2. Usually motile
3. Obligate aerobe
4. Oxidase-positive
5. Non-lactose fermenter

6. Some strains produce a capsule.
7. Very resistant to disinfectants (can grow in some soaps!).
8. Can grow in water containing only trace amounts of nutrients (e.g. tap water).

Front 11

explain how humans become infected with Pseudomonas aeruginosa

Back 11

ubiquitous in envrionment; Not in normal flora

Huge problem in hospitals

opportunistic pathogen

Front 12

describe populations at risk for infection and disease with Pseudomonas aeruginosa

Back 12

opportunistic pathogen:

-burn patients

-chronic respiratory disease

-indwelling catheters

-immunosuppression

-chronic antibiotic use

-lengthy hospital stay

Front 13

list the disease(s) caused by Pseudomonas aeruginosa

Back 13

P. aeruginosa can infect and cause disease in almost all body sites, including:

Pulmonary infections

Skin infections

Urinary tract infections

Ear infections

Eye infections

Bacteremia

Front 14

Pulmonary infections with Pseudomonas aeruginosa are most common in what type of patients?

Back 14

Chronic infection of LRT is common among patients with cystic fibrosis who may present with chronic productive cough, anorexia & weight loss, wheezing and tachypnea.

Front 15

Infection of hair follicles with Pseudomonas aeruginosa is usually due to exposure to __________, aka “_________”

In bacteremic patients, P. aeruginosa can produce characteristic skin lesions
referred to as _______

Back 15

Infection of hair follicles with Pseudomonas aeruginosa is usually due to exposure to contaminated water, aka “hot tub
folliculitis”

In bacteremic patients, P. aeruginosa can produce characteristic skin lesions
referred to as ecthyma gangrenosum.

Front 16

Ear infections with Pseudomonas aeruginosa can result in

Back 16

mild infection of external ear (“swimmer’s ear”), to chronic otitis media, to more invasive infection which can affect the temporal bone and result in osteomyelitis, and even spread to CNS.

Front 17

explain the basic mechanism(s) of pathogenesis of Pseudomonas aeruginosa

Back 17

usually as an opportunistic pathogen in immunocompromised and/or diabetic hosts, and i.v. drug users.

It has multiple virulence factors, which may be differentially expressed by different strains, and in response to environmental signals.

Front 18

virulence factors of Pseudomonas aeruginosa

Back 18

1. LPS, pili, flagella, capsule

2. exotoxin A = which inhibits protein synthesis resulting in cell death and tissue necrosis.

3. pyocyanin, a blue-green pigment which promotes tissue damage and recruitment of neutrophils.

4. Type III secretion system which “injects” cytotoxins into host cells

Front 19

describe how Pseudomonas aeruginosa is prevented.

Back 19

Infection control practices to prevent contamination of sterile equipment and fluids,
e.g. ventilators, dialysis machines, nebulizer fluid.

Hand washing by hospital personnel.

Prophylactic use of antibiotics is NOT recommended—promotes emergence of antibiotic-resistant strains!

Front 20

What does Pseudomonas aeruginosa smell like?

Back 20

grape kool aid

pyocyanin with grape like odor

Front 21

describe the basic structure and Gram reaction of Listeria monocytogenes (5)

Back 21

1. Gram-positive coccobacilli/short rods, often in pairs or short chains.

2. Motile at room temperature; characteristic end-over-end tumbling.

3. Facultative anaerobe.
4. Facultative intracellular pathogen.
5. Can grow at broad temperature range

Front 22

explain how humans become infected with Listeria monocytogenes

Back 22

-Ubiquitous in environment
-Transient colonization of humans common

-Large outbreaks & sporadic cases occur in association with contaminated food

-Can be transmitted from infected mother to fetus transplacentally or perinatally.

Front 23

describe populations at risk for infection and disease with Listeria monocytogenes

Back 23

only causes serious disease in certain high-risk populations:

extremes of age, pregnant women, persons with severe cell-mediated immune deficiency (e.g. transplant recipients, lymphoma patients, patients with AIDS), cancer, diabetes, alcoholism, liver or kidney disease.

Front 24

list the disease(s) caused by Listeria monocytogenes

Back 24

Listerosis - occurs in:

1. Healthy adults

2. Pregnant women

3. Neonates (Early and Late Onset)

4. immunocompromised and elderly adults

Front 25

describe the clinical findings of Listerosis in:

1. Healthy adults

2. Pregnant women

Back 25

1. Healthy adults = asymptomatic or flu-like

2. Pregnant women = non-specific flu-like illness; CNS involvement is rare. However, infection can lead to fetal death, premature birth, or infected newborns, so blood cultures are recommended for pregnant women with fever of unknown origin

Front 26

describe the clinical findings of Listerosis in:

1. Neonates Early Onset

2. Neonates Late Onset

Back 26

1. Early-onset (granulomatosis infantiseptica) due to transplacental infection of fetus and characterized by disseminated abscesses and granulomas in multiple organs. Most affected infants are stillborn or die shortly after birth.

2. Late onset due to perinatal infection during or shortly after birth; presents as meningitis or meningoencephalitis after ~ 3 days after birth.

Front 27

In immunocompromised and elderly adults, listeriosis most commonly presents as ____________ which can range from a mild illness with fever and mental status changes to fulminant with coma.

Back 27

In immunocompromised and elderly adults, listeriosis most commonly presents as meningoencephalitis which can range from a mild illness with fever and mental status changes to fulminant with coma.

Front 28

explain the basic mechanism(s) of pathogenesis of Listeria monocytogenes

Back 28

1. Attachment to receptors on enterocytes, M cells, Peyer’s patches in GI tract
2. Phagocytosed, but escapes phagolysosome using exotoxin, Listeriolysin O and enzymes
3. Replicates in cell cytoplasm
4. Forms actin tail to invade neighboring cells.
5. Invades intestinal lining &
disseminates.

Front 29

describe the following virulence factors of Listeria monocytogenes:

1. listeriolysin O and Phospholipase C

2. Bacterial protein, ActA

Back 29

1. activated by acidic pH of phagolysosome - enable bacteria to escape into the cell cytoplasm where they replicate.

2. assembles actin forming an actin tail that moves the bacterium to cell membrane. A filopod is formed that pushes the bacterium into an adjacent cell; this cell-to-cell movement evades humoral immune response.

Front 30

describe how Listeria monocytogenes is prevented.

Back 30

Prevent by safe food handling and consumption (ie dont drink unpasteurized milk)

No vaccine