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Staphylococcus

Skin infection, osteomyelitis, food poisoning, foreign body infections, MRSA (Methicillinresistant 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 burns cuts insect bites skin diseasesacne, 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
boils

Rupture of the abscess leads to the release of live bacteria and associated toxin

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 (contd)


St. aureus produces coagulase which converts soluble fibrinogen in plasma to insoluble matrix fibrin There are two types of coagulase bound 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. 2. shielding each other from an immune response and in 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. aureus
neutrophils 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 cells


when 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

St. aureus and food


Staph grows and divides in food and produces an enterotoxin (A-E, G, H, I and J) The Staph doesnt 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 gastroenteritis 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. aureus


Enzymes: 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 (, , , ) 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 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

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 staphyloco ccal 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

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
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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