Irregular non-spore forming rods part 1, L. Monocytogenes and Erysipelothrix rhusiopathiae Flashcards

1
Q

What are the Pyogenic Cocci

A

Pyogenic – Pus forming

Staphylococcus

S. aureus

Streptococcus

S. pyogenes (Lancefield Group A)

S agalactiae (LG B)

S. pneumoniae

Enterococcus viridant group (LG D)

Neisseria Moraxella Kingella

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2
Q

What are the irregular non-spore forming rods?

A

Listeria genus

Corynebacteria genus

Lactobacillus genus

Erysipelothrix rusiopathiae

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3
Q

Main difference between:

L. monocytogenes

and

L ivanovii

A

L. monocytogenes -> human pathogen, animals can be carriers but it is not pathogenic in them.

L. ivanovii –> animal pahtogen

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4
Q

Listeria monocytogenes physical and culture characteristics, habitat, and transmission

A

Small Gram-positive rod (2uM long), with a single flagella, uniform shape

cultured on agar or blood agar

Facultative anaerobic and Facultative intracellular

Beta-hemolyzing

Catalase positive

CAMP positive

Cold and Salt tolerant

Tolerant to proteolytic eznymes, stomach acid, and bile salts

Serologic classification: Ia, Ib, IVb

Found in animals GI and in some human GI

Zoonotic transmission by eating contaminated food or soil, or getting it into an open wound (common in butchers or animal workers)

Can reporduce in cold temps and is salt resistant, so it can be in contaminated milk or other foods

Human to human transmission is oral or transplacental

Infects patients with impaired cell-mediated immunity (it is intracellular so humoral immunity is not important), elderly, and infants, Transplant patients AND Pregnant Women who are often asymptomatic

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5
Q

What is unique about L. monocytogenes motility?

A

Non-motile by flagella at 37C

At 20C (room temperature or refridgerated) it is motile by flagella and can also reproduce

Flagella based movement is oxygen dependen t, as demonstrated by the picture

Within the body at 37C It moves within the cells by causing actin polymerization, mediated by the ActA protein Comet tails, or Actin rockets.

During this process, it can pass from cell-to-cell while remaining intracellular the entire time.

It can survive phagocytosis, and once inside of an endo-lysosome, the low pH activates pore-forming enzymes, releasing the bacteria into the cytosol.

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6
Q

The normal treatment for L. monocytogenes

Prevention

A

Ampicillin and Gentamycin,

Broad spectrum penicillin and aminoglycoside a classic synergistic treatment Ampicillin damages the cell wall, allowing better penetration for the Gentamycin to inhibit RNA transcription

Alternative treatment, Erythromycin

Resistant to: Cephalosporins

Prevention: Don’t eat raw or partially cooked foods, soft cheese

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7
Q

L. monocytogenes

Antigens

Virulence factors

A

Antigens:

H-antigen-> Flagella

Hemolysin

Virulence Factors:

Flagella

Hemolysins

Listeriolysin (phagosome lysis)

Phospholipase (phagosome lysis)

ActA (Actin polymerization, rocket polymerization)

Internalins (internalin A and B allow it to attach to epithelial cells, eterocytes, and M-cells)

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8
Q

L. monocytogenes clinical diseases

A

Neonatal early onset disease:

Infection occurs in utero or transplacentally. Usually causes abortion or stillbirth.

Or premature birth with Granulomatosis Infantiseptica, severe infection with absecess and granulomas in multiple organs. High mortality

Neonatal late onset disease:

Acquired during birth or soon after.

Presents 2-3 weeks after birth as meningitis or meningoencephalitis with septicemia

Infections in pregnant women

Pregnant women are considered somewhat immunocompromise.

Cell-mediated immunity is worst in the 3rd trimester.

May be asymptomatic, or with non-specific flu/cold symptoms.

OR

Meningitis

Immunocompromised patients:

Meningitis

In healthy adults:

Asymptomatic or mild flu/cold

OR

Acute, self-limited gastroenteritis: fever, nasuea, headache, myalgia, arthralgia (muscle and joint pain)

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9
Q

Laboratory diagnosis of L. monocytogenes

A

CSF is usually negative for bacteria

Gram-positive intracellular rods, and in blood

Serology types Ia, Ib, and IVb are pathogenic

Catalase positive

Beta-hemolysing

CAMP positive (side note, Strep group B are also CAMP positive)

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10
Q

Erysipelothrix rhusiopathiae

Morphology, cultivation

A

Gram positive rods.

non-spore forming.

Irregularly shaped, some curved or squigly and some straight, some in chains.

Culture:

On blood agar, forms small transparent (clear/very pale whitish) colonies

No hemolysis

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11
Q

Breakdown the name Ersipelothrix rhusiopathiae

A

Erysipelo - Ersipeloid - similar to the Erysipelas lesions in pigs. In humans it means a painful violet/purple/red lesion of the hand. Does not form pus.

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12
Q

Erysipelothrix rhusiopathiae

Epedimiology and clinical disease

Diagnosis

Treatment and prevention

A

Found in many animals as hosts, but causes erysipelas in swine

Transmitted strictly from animals to humans, zoonotic, by direct innoculation into open cuts. Butchers, Fishers.

Diagnosis: Biopsy or aspirates from the lesion, staining and cultivation

Symptoms:Erysipeloid lesions, usually of the hands

In rare widespread infections causes endocarditis or septisemia

Treatment and prevention:

Is usually self resolving in a few weeks, but is faster with Peniccilin. Prevention is to vaccinate the swine or animals that the patient is working with, and to use gloves.

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13
Q
A
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