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Staphylococcus

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

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Staphylococcus

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  1. Staphylococcus Skin infection, osteomyelitis, food poisoning, foreign body infections, MRSA (Methicillin-resistant Staphylococcus aureus)

  2. 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

  3. S. aureus morphology

  4. Staphylococcus aureus Food Poisoning

  5. 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

  6. 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

  7. 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

  8. Blood agar plate, S. aureus

  9. 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 diseases—acne, eczema

  10. 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

  11. 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

  12. 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 coagulase bound coagulase on the surface of the bacteria causes the bacteria to clump together free coagulasesecreted from the bacteria into the environment

  13. Why produce coagulase • Bound coagulase causes bacteria to clump together. Why? the more bacteria in a given location the more effective they are in • 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

  14. 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

  15. 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

  16. 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

  17. Staph enterotoxin causes gastro-enteritis in two ways • VOMITINGtoxin works on the vomiting control center of the brain this leads to reversal of peristalsis and vomiting • DIARRHEAenterotoxin 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.

  18. 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

  19. Virulence factors of S. aureus Toxins: • Hemolysins (α, β, γ, δ) – lyse red blood cells • Leukocidin – lyses neutrophils and macrophages • Enterotoxin – induce gastrointestinal distress • Exfoliativetoxin – separates the epidermis from the dermis • Toxic shock syndrome toxin (TSST) – induces fever, vomiting, shock, systemic organ damage

  20. 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

  21. StaphylococcalDisease 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

  22. Cutaneous lesions of S. aureus

  23. StaphylococcalDisease • 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

  24. Staphylococcal osteomyelitis in a long bone

  25. StaphylococcalDisease • 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

  26. Effects of staphylococcal toxins on skin

  27. Toxic Shock Syndrome Toxin • Superantigen • Non-specific binding of toxin to receptors triggers excessive immune response

  28. TSS Symptoms • 8-12 h post infection • Fever • Susceptibility to Endotoxins • Hypotension • Diarrhea • Multiple Organ System Failure • Erythroderma (rash)

  29. 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

  30. 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

  31. Identification of Staphylococcus in Samples • Frequently isolated from pus, tissue exudates, sputum, urine, and blood • Cultivation, catalase, biochemical testing, coagulase

  32. Catalase test

  33. 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

  34. Prevention of Staphylococcal Infections • Universal precautions by healthcare providers to prevent nosocomial infections • Hygiene and cleansing

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