2266 staph

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Staphylococcus

Skin infection, osteomyelitis, food poisoning,

foreign body infections, MRSA (Methicillin-

resistant Staphylococcus aureus)

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General Characteristics of

the Staphylococci• Common inhabitant of the skin and mucous

membranes

• Spherical cells arranged in irregular clusters

• Gram-positive

• Lack spores and flagella

• May have capsules• 31 species

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S. aureus morphology

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Staphylococcus aureus

Food Poisoning

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St. aureus and food poisoning

• St. aureus causes gastro-enteritis

• Food poisoning is not caused by the organism

but by the toxin that the organism secretes

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Properties of St. aureus that make it

persistent in nature

• Relatively heat resistant

• Resistant to high concentrations of salt

• Can survive long periods on dry inanimateobjects

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Staphylococcus aureus

• Grows in large, round, opaque colonies

• Optimum temperature of 37oC

• Facultative anaerobe

• Withstands high salt, extremes in pH, and

high temperatures

• Produces many virulence factors

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Blood agar plate, S. aureus

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How did the chef get a staph infection?

• Staph is found on any inanimate surface

• Staph is often found associated with the external nasalpassages of 30% of the human population

• Staph is often found on skin surfaces because they can tolerate

the low moisture and high salt content of skin• Staph can easily spread from person to person via hand tohand contact

• Staph can penetrate the deep tissues of skin damaged by

burns

cutsinsect bites

skin diseases — acne, eczema

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What happens when Staph enters a

wound and how does this relate to food

poisoning ?

• Localized staph infection leading to an

abscess (collection of pus)

boils=abscesses in the skin

carbuncle=interconnected abscesses

• Rupture of the abscess leads to therelease of live bacteria and associated

toxin

boils

carbuncle



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How do abscesses and boils form?

• Chef cuts arm and Staph enters deeper skin layer

• St. aureus is surrounded by a capsule thick slime layer

that prevents an immediate immune response

• Bacteria multiply at the site surrounded by the capsule

• St. aureus establishes intimate contact with skin cells

via bacterial techoic acids and fibronectin skin cell

receptors

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Abscess and boil formation (cont’d)

• St. aureus produces coagulase which convertssoluble fibrinogen in plasma to insolublematrix fibrin

• There are two types of coagulasebound coagulase on the surface of the

bacteria causes the bacteria to clump together

free coagulasesecreted from thebacteria into the environment

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Why produce coagulase

• Bound coagulase causes bacteria to clump together.

Why?

the more bacteria in a given location the more effective they are in

1. shielding each other from an immune response and in

2. excreting toxic factors in high quantities

• Free coagulase causes a protective fibrin clot to form

around bacteria. Why?bacteria can grow and divide in protective environment; most immune

cells have been denied entry to the region

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Pus formation is due to an immune

response inside the fibrin clot• Many bacteria are found in fibrin clot

• Also some immune cells did gettrapped in fibrin clot

• Immune cells want to kill St. aureus

• St. aureus wants to kill immune cells

• The war that ensues leads to pusformation

• Pus consists of dead and living St.aureus, dead neutophils and plasmainside a fibrin clot

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Pus formation continued

• The immune cells killing St. aureus

neutrophils surround bacteria, ingest them and produce lysosomal enzymes that killbacteria.

This releases bacterial components that lead to a greater inflammatory responsewhich kills host cells.

• St. aureus killing immune cellswhen neutrophils ingest bacteria the lysosome fuses with the phagosome

St. aureus produces catalase that converts hydrogen peroxide into water and oxygen

St. aureus produces cytotoxins that kill the neutorphils

The dead neutrophils release lysosomal campartment enzymes that will may kill St.aureus but will kill adjacent host cells

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St. aureus and food

• Staph grows and divides in food and produces

an enterotoxin (A-E, G, H, I and J)

• The Staph doesn’t cause food poisoning, the

enterotoxin does

• Enterotoxin is stable to heating at 100oC for 30

minutes.

• Enterotoxin is resistant to degradation by

stomach gastric acids

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Staph enterotoxin causes gastro-

enteritis in two ways

• VOMITINGtoxin works on the vomiting controlcenter of the brain this leads to reversal of peristalsisand vomiting

• DIARRHEAenterotoxin is a superantigen andelicits a strong immune response in the region wherethe toxin is most concentrated. Immune response

causes a loss of brush borders in intestinal epithelialcells; these cells cannot absorb water from the gut.

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Virulence factors of S. aureusEnzymes:

• Coagulase – coagulates plasma and blood; produced

by 97% of human isolates; diagnostic

• Hyaluronidase – digests connective tissue

• Staphylokinase – digests blood clots• DNase – digests DNA

• Lipases – digest oils; enhances colonization on skin

• Penicillinase – inactivates penicillin

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Virulence factors of S. aureus

Toxins:

• Hemolysins (α, β, γ, δ) – lyse red blood cells

• Leukocidin – lyses neutrophils and macrophages

• Enterotoxin – induce gastrointestinal distress• Exfoliative toxin – separates the epidermis from the dermis

• Toxic shock syndrome toxin (TSST) – induces fever,

vomiting, shock, systemic organ damage

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Epidemiology and Pathogenesis

• Present in most environments frequented by humans• Readily isolated from fomites

• Carriage rate for healthy adults is 20-60%

• Carriage is mostly in anterior nares, skin,nasopharynx, intestine

• Predisposition to infection include: poor hygiene and

nutrition, tissue injury, preexisting primary infection,

diabetes, immunodeficiency

• Increase in community acquired methicillin resistance

- MRSA

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Staphylococcal Disease

Range from localized to systemic• Localized cutaneous infections – invade skin through

wounds, follicles, or glands

– Folliculitis – superficial inflammation of hair follicle; usually

resolved with no complications but can progress

– Furuncle – boil; inflammation of hair follicle or sebaceous

gland progresses into abscess or pustule

– Carbuncle – larger and deeper lesion created by aggregation

and interconnection of a cluster of furuncles

– Impetigo – bubble-like swellings that can break and peel

away; most common in newborns

Cutaneous lesions of S aureus

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Cutaneous lesions of S. aureus

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• Systemic infections

– Osteomyelitis – infection is established in the

metaphysis; abscess forms

– Bacteremia – primary origin is bacteria fromanother infected site or medical devices;

endocarditis possible

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Staphylococcal osteomyelitis in a long bone

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• Toxigenic disease

– Food intoxication – ingestion of heat stable

enterotoxins; gastrointestinal distress

– Staphylococcal scalded skin syndrome – toxin induces bright red flush, blisters, then

desquamation of the epidermis

– Toxic shock syndrome – toxemia leading to

shock and organ failure

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Effects of

staphyloco

ccal toxinson skin

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Toxic Shock Syndrome Toxin

• Superantigen

• Non-specificbinding of toxin to

receptors triggers

excessive immuneresponse

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TSS Symptoms

• 8-12 h post infection

• Fever

• Susceptibility to Endotoxins• Hypotension

• Diarrhea

• Multiple Organ System Failure• Erythroderma (rash)

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TSS Treatment

• Clean any obvious wounds and remove any foreign

bodies

• Prescription of appropriate antibiotics to eliminate

bacteria• Monitor and manage all other symptoms, e.g.

administer IV fluids

• For severe cases, administer methylprednisone, acorticosteriod inhibitor of TNF-a synthesis

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Coagulase-negative Staphylococci

Coagulase-negative staphylococcus; frequently involvedin nosocomial and opportunistic infections

• S. epidermidis – lives on skin and mucous membranes;

endocarditis, bacteremia, UTI

• S. hominis – lives around apocrine sweat glands

• S. capitis – live on scalp, face, external ear

• All 3 may cause wound infections by penetrating

through broken skin

• S. saprophyticus – infrequently lives on skin, intestine,

vagina; UTI

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Identification of Staphylococcus in

Samples

• Frequently isolated from pus, tissue exudates,

sputum, urine, and blood

• Cultivation, catalase, biochemical testing,coagulase

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Catalase test

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Clinical Concerns and Treatment

• 95% have penicillinase and are resistant topenicillin and ampicillin

• MRSA – methicillin-resistant S. aureus –

carry multiple resistance – Some strains have resistance to all major drug

groups except vancomycin

• Abscesses have to be surgically perforated• Systemic infections require intensive

lengthy therapy

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Prevention of Staphylococcal Infections

• Universal precautions by healthcare providers

to prevent nosocomial infections

• Hygiene and cleansing

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