State University of New York at BuffaloSchool of Medicine and Biomedical SciencesDepartment of Microbiology and ImmunologyMicrobiology 301February 13, 2015 D. Dombroski [email protected] 829-2355StaphylococcusFamily: MicrococcaceaeGenus: Staphylococcus (large gram +)Species: Staphylococcus aureus (True pathogen) (have capsule)Staphylococcus epidermidisStaphylococcus saprophyticus (opportunistic or nosocomial infection)Microscopic Morphological AppearanceGram positive cocciarrangement – irregular clustersnon-spore formersnon-motileusually no capsule (only aureus has capsule)Virulence FactorsI. Extracellular ProductsA. Protein toxinsHemolysin – lyses red blood cells by disrupting cell membrane Leukocidin – lyses white blood cells by disrupting cell membrane (incapacity host immune response)Enterotoxin – food poisoning (of the gut or GI tract)Toxic Shock Syndrome (TSST-1) – stimulates production of interleukin (IL-1) by macrophages resulting in fever inductionB. EnzymesCoagulase – plasma clotting protein; converts fibrinogen to fibrina. coats bacteria with fibrin and prevents phagocytosisb. aids in attachment Fibrinolysin – digests fibrinogen (fibrin clots) Hyaluronidase (“spreading factor”) – digests hyaluronic acid around host cells promotes invasion Lipase – degrades lipids – allows bacteria to colonize oily skin Penicillinase – hydrolyzes penicillin; drug resistance Catalase – degrades H2O2 – a toxic metabolic end product Exfoliatin or epidermolytic toxin – protease that causes peeling of superficial skin layers by dissolving intracellular bridges1II. Structural Surface Component (aureus)Protein A – surface component linked to peptidoglycan layer of cell wall; inhibits antibody-mediated clearance of bacteria by binding to IgG. Lipoteichoic acid – binds to tissue components; cell adhesionStaphylococcus aureus – major pathogen of genus (nonspore)Carriage location – anterior nares, nasopharynx and skinCarriage rate – 30 to 50% of healthy adultsVirulence Factors/Species Identification of Staphylococcus aureuscoagulase positivehemolysin (alpha toxin)leukocidinprotein Acapsule (inhibits phagocytosis)Toxins of Staphylococcus aureusI. Blood cell toxinshemolysinsleukocidinII. Intestinal toxinsenterotoxinsIII. Epithelial toxinsexfoliatin or epidermolytic toxinInfectious Diseases caused by Staphylococcus aureusI. Superficial infections – localized cutaneous infectionsII. Toxigenic infectionsA. Staphylococcal Scalded Skin Syndrome (SSSS)B. Toxic Shock Syndrome (TSS)C. Gastrointestinal Disease (enterotoxin)III. Systemic (localized) Infections enter blood stream or lymphatic system (infect other organs)I. Superficial Cutaneous InfectionsPyodermic infections – pimples, boils, carbuncles and impetigoCharacteristic symptom – pus formation – Staphylococcus – pyogenic cocciMode of infection (Staph aureus invade the skin, infec site abscess)Staphylococci invade skin at: a. sebaceous gland opening (skin gland)b. hair folliclec. wound- Infection site – abscessPrimary infection sites – face, back of neck, buttocksSymptoms – edema, erythema, pain, pusRisk groups – elderly and young children with poor personal hygiene2Treatment – minor lesions self resolve (Get better with time) surgical incision and drainage chemotherapy – topical antibioticsII. Toxigenic InfectionsA. Staphylococcal Scalded Skin Syndrome (SSSS) (superficial skin)Virulent feature: exfolatin or epidermolytic toxinseparates epidermal layer from the dermis blistering and peeling of the skin exposes red under layergeneral appearance – burned skinMode of infection - syndrome begins as an erythema around the mouth and nose- spreads rapidly to infect skin of the neck, trunk and extremitiesRisk group – infants and young children < 4 years (neonatal infection)Primary infected sites – umbilical cord and eyes – low mortality rateDeath – secondary infection of the denuded skin by other bacterial pathogensTreatment – topical antibiotic – mupirocinB. Toxic Shock Syndrome (TSS)Incidence of Infection – usage of super absorbent vaginal tampons (ultra absorbent tampons make low concentration of Mg which initiate growth of bacteria and produces toxin and the toxin result endothelial death then result fever spike )Virulent feature – toxic shock syndrome toxin -1 (TSST-1) stimulates t lymphocyteMode of infection- super absorbent brands strongly bind Mg++ ions- low concentration of Mg++ triggers TSST-1 production which is absorbed into the bloodstream- TSST-1 (superantigen) that stimulates T-lymphocytes to produce cytokines intravascularly resulting in endothelial cell damage – shock and multisystem organ failureInitial symptoms - high fever, vomiting, diarrhea and muscle cramps (myalgia)Ten days later – hands and soles of feet develop a sunburn-like rash which results in a peeling of the skinSevere symptoms – shock and multi-organ failureDeath – 2 – 5% respiratory failureHigh risk group/high risk factormenstruating women – usage high absorbancy tamponsnon-menstruating groups – postpartum women with surgical wound infections (hysterectomies)nasal surgery and packingPrevention/Control - removal of cellulose based superabsorbent tampons from market in 1980CDC recommends that tampons are not used continuously during a menstrual cycleTreatment – fluid replacement and chemotherapy3C. Toxigenic Gastrointestinal Disease – Food poisoning (food intoxication)Source contamination – food handlerStaphylococcal lesions of skin (hands and nasopharyngeal carriers) contaminate food food unrefrigerated room temperature growth of Staphylococcus aureus production of enterotoxin (exotoxin)Virulent feature – enterotoxin (exotoxin) heat stable - not inactivated by digestive enzymes -toxin production does not alter food taste or smellAction of enterotoxin - disrupts gastrointestinal liningSymptoms – start in 4 – 6 hours – vomiting, cramps, diarrhea, nauseaRecovery –