Staph.Lecture 1 Flashcards
What are the key characteristics of staphylococci
- gram + arranged in single cells , pairs, tetrads, and short chains, but appear predominantly in grape-like clusters
- non-motile
- non-spore-forming
**4. catalase POSITIVE (very useful to separate strep from staph!)
- facultative anaerobes (except: S. aureus, subsp. anaerobius and S. saccharolyticus–these two are also catalase NEGATIVE).
4 important staphylococci species
- S. aureus (ohreeus)
- S. epidermidis (ehpeedurmiss)
- S. saprophyticus (saprofitikus)
- S. lugdunensis (lugdone.eesis)
S. aureus KEY characteristics
- grape like clusters
- uniform, equal size
- round
- gram POSITIVE
- on blood agar plates: grow large, 48hrs, off white, cream, sometimes gold.
- clearing zone=beta hemolysis
S. aureus HABITAT
- external environments
- skin and mucous membranes
- anterior nares (20-40% adults)
- intertriginous skin folds
- perinuem
- axillae
- vagina
- significant opportunistic pathogen under appropriate conditions
S. aureus FACTORS predisposing to SERIOUS INFECTION (8)
- defects in leukocyte chemotaxis
- congenital: Wiskott-Aldrich syndrome, Down’s syndrome, Job’s syndrome, Chediak-Higashi syndrome)
- acquired: DM, RA
- defects in opsonization by antibodies secondary to congenital or acquired hypogammaglobulinemias or complement component
- defects in intracellular killing of bacteria following phagocytosis due to inability to activate the membrane bound oxidase system (CGD-chronic granulomar disease, lymphoblastic leukemia, acute and chronic myelogenous leukemia)
- skin injuries (*burns, surgical incisions, eczema, sports injuries-falling on turf)
- presence of foreign bodies (sutures, IV lines, prosthetic devices)
- infections with other agents, particularly viruses (eg influenza, measles)
- -sometimes with influenza wont die from virus, die from secondary pneumonia infection.
- chronic underlying diseases (e.g. malignancy, alcoholism, heart disease)
- use of antibiotics to which the infecting S. aureus is not susceptible (MRSA staph…)
OBJECTIVE 2: S. aureus VIRULENCE FACTORS-Components that interfere with phagocytosis (1/4)–CPPC
- Components that interfere with phagocytosis
- CAPSULES-interfere with phagocytosis, prevent ingestion of organism by PMNs
- PROTEIN A-binds Fc region of IgG, interfering with opsonization an dingestion of organism by PMNs
- PANTON-VALENTINE LEUKOCIDIN (PVL)-an enzyme that alters cation permeability of rabbit an human leukocytes resulting in white cell destruction
- COAGULASE-forms a clot; binds to prothrombin catalyzing conversion of fibrinogen to fibrin, which in turn acts to coat bacterial cells with fibrin, rendering them ore resistant to opsonization and phagocytosis
S. aureus-serious infection sites
usually those in which the organism is part of normal flora.
- SKIN: folliculitis, impetigo, furuncles and carbuncles, post-surgical wound infections
- NOSE AND THROAT-sinusitis, peritonsillar abscesses, mastoiditis, bronchitis and **STAPHYLOCOCCAL PNEUMONIA (usually involving infection with influenza)
- GI TRACT, URETHRA, VAGINA-enterocolitis, cystitis, prostatitis, cervicitis, salpingitis, pelvic abscess
S. aureus-serious infection-child with pyoderma
PYODERMA=pyogenic (pus forming) skin dz. causes may be infectious, such as staphylococcal infections, or possible AUTOIMMUNE (pyoderma gangrenosum)
S. aureus-serious infection-furuncle (or boil)
- skin dz caused by infection of hair follicles, resulting in localized accumulation of pus and dead tissue
- red, pus-filled lumps that are tender, warm, extremely painful
- a yellow or white point at center of lump can be seen when boil is ready to drain
S. aureus-serious infection-carbuncle (foruncle gone wild)
- abscess larger than a boil, usually with one or more openings draining pus onto the skin
- may develop anywhere, but they are most common on the back and the nape of the neck
S. aureus-serious infection-Toxin-mediated Infections
- scalded skin syndrome: neonates and children under 4
- Toxic-shock syndrome
- food poisoning
S. aureus-serious infection-Disseminated infections
During localized infection metastasis via blood (to other distant sites) may result in:
- pneumonia
- bacteremia
- endocarditis
- osteomyelitis
- septic arthritis
- septic embolization
- metastatic infections
OBJECTIVE 2: S. aureus VIRULENCE FACTORS-Hemolysins (2/4)
- HEMOLYSINS (LYSINS, TOXINS)
–LYSINS–
ALPHA HEMOLYSIN
-lyses RBCs of several animals
-dermonecrotic (causes necrosis of the skin) on subcutaneous injection
BETA HEMOLYSIN
-sphingomyelinase will cause varying lysis of RBCs from different animals due to difference in membrane sphingomyelin content (test with sheep blood)
-produces “hot-cold” lysis (hemolysis enhance at low temp after 35 C incubation)
DELTA HEMOLYSIN
-produced by 97% of S. aureus and 50-70% of coagulase negative Staph
-acts as surfactant that disrupts the cell membrane, interacts with membrane to form channels that increase in size over time resulting in leakage of cellular contents
-some coagulase-negative staphylococci produce enough delta toxin to cause NEC (necrotizing enterocolitis) in neonates
GAMMA HEMOLYSIN
-found in some S. aureus strains, also causes lysis of variety o cells
–TOXINS–
EXFOLIATINS or EPIDERMOLYTIC TOXINS
-responsbile for “STAPHYLOCOCCAL SCALDED SKIN SYNDROME”
-toxin dissolves the mucopolysaccharide matrix of epidermis, causing separation of skin layers; rare in adults
ENTEROTOXINS
-heat-stable molecules responsible for clinical features of STAPHYLOCOCCAL FOOD POISONING
-most common cause of food poisoning in the US
-toxin produced in contaminated food by toxigenic strains, vomiting with or without diarrhea (2-8hrs-because you are ingesting the toxin itself when you eat the food) + quick recovery (24-48 hrs)
{salmonella or shigella will show up a day or two later. avoid giving AB, should let it pass by itself}
OBJECTIVE 2: S. aureus VIRULENCE FACTORS-Enzymes (3/4)
- ENZYMES
FIBRINOLYSINS
-break down fibrin clots and facilitate spread of infection to contiguous tissues
HYALURONIDASE
-hydrolyze intercellular matrix of acid mucopolysaccharides in tissue acting to spread organisms to adjacent tissue
PHOSPHOLIPASE C
-described in patients with ARDS (acute respiratory distress syndrome) and DIC (disseminated intravascular coagulation-rare life threatening condition prevents blood from clotting normally)
-tissues affected by the E become ore susceptible to damage and destruction by bioactive complement components and products during complement activation
OBJECTIVE 2: S. aureus VIRULENCE FACTORS-
- SUPERANTIGENS
Group of toxins known as pyrogenic toxin superantigens, these include:
-toxic shock syndrome toxin-1 (TSST-1) of S. aureus
-streptococcal pyrogenic exotoxins (SPE)-toxic-shock-LIKE-syndrome
-streptococcal superantigens
All posses THREE biologic characteristics: - pyrogenicity
- superantigenicity
- enhance lethal effects of minute amounts of endotoxin
All induce polyclonal T-cell proliferation
S. aureus-Lab Identification-COAGULASE (VIRULENT FACTOR)
Tube coagulase-free coagulase reacts with substance in plasma called coagulase-reacting factor that converts fibrinogen–> fibrin. (rare S. aureus ma be coagulase-NEG and some animal isolate {S. intermedius, S. hyicus, S. delphini, S. schleiferi, subsp. coagulans} may be tube coagulase-POSITIVE. COAGULASE POSITIVE = STAPH AUREUS
