Staphylococcus

Skin infection, osteomyelitis, food poisoning, foreign body infections, MRSA (Methicillin-

resistant Staphylococcus aureus)

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

S. aureus morphology

Staphylococcus aureus

Food Poisoning

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

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 inanimate objects

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

Blood agar plate, S. aureus

How did the chef get a staph infection?

• Staph is found on any inanimate surface• Staph is often found associated with the external nasal

passages 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 to

hand contact• Staph can penetrate the deep tissues of skin damaged by

burnscutsinsect bitesskin diseases—acne, eczema

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 the release of live bacteria and associated toxin

boils

carbuncle

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

Abscess and boil formation (cont’d)

• St. aureus produces coagulase which converts soluble fibrinogen in plasma to insoluble matrix fibrin

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

the bacteria causes the bacteria to clump together

free coagulasesecreted from the bacteria into the environment

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

Pus formation is due to an immune response inside the fibrin clot

• Many bacteria are found in fibrin clot• Also some immune cells did get

trapped in fibrin clot• Immune cells want to kill St. aureus• St. aureus wants to kill immune cells• The war that ensues leads to pus

formation• Pus consists of dead and living St.

aureus, dead neutophils and plasma inside a fibrin clot

Pus formation continued

• The immune cells killing St. aureusneutrophils surround bacteria, ingest them and produce lysosomal enzymes that kill bacteria. This releases bacterial components that lead to a greater inflammatory response which kills host cells.

• St. aureus killing immune cellswhen neutrophils ingest bacteria the lysosome fuses with the phagosomeSt. aureus produces catalase that converts hydrogen peroxide into water and oxygenSt. aureus produces cytotoxins that kill the neutorphilsThe dead neutrophils release lysosomal campartment enzymes that will may kill St. aureus but will kill adjacent host cells

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

Staph enterotoxin causes gastro-enteritis in two ways

• VOMITINGtoxin works on the vomiting control center of the brain this leads to reversal of peristalsis and vomiting

• DIARRHEAenterotoxin is a superantigen and elicits a strong immune response in the region where the toxin is most concentrated. Immune response causes a loss of brush borders in intestinal epithelial cells; these cells cannot absorb water from the gut.

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

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

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

Staphylococcal DiseaseRange 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

Staphylococcal Disease

• Systemic infections – Osteomyelitis – infection is established in the

metaphysis; abscess forms– Bacteremia – primary origin is bacteria from

another infected site or medical devices; endocarditis possible

Staphylococcal osteomyelitis in a long bone

Staphylococcal Disease

• 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

Effects of staphylococcal toxins on skin

Toxic Shock Syndrome Toxin

• Superantigen

• Non-specific binding of toxin to receptors triggers excessive immune response

TSS Symptoms

• 8-12 h post infection

• Fever

• Susceptibility to Endotoxins

• Hypotension

• Diarrhea

• Multiple Organ System Failure

• Erythroderma (rash)

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, a corticosteriod inhibitor of TNF-a synthesis

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Coagulase-negative Staphylococci

Coagulase-negative staphylococcus; frequently involved in 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

Identification of Staphylococcus in Samples

• Frequently isolated from pus, tissue exudates, sputum, urine, and blood

• Cultivation, catalase, biochemical testing, coagulase

Catalase test

Clinical Concerns and Treatment

• 95% have penicillinase and are resistant to penicillin 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

Prevention of Staphylococcal Infections

• Universal precautions by healthcare providers to prevent nosocomial infections

• Hygiene and cleansing