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Chapter 14
Pathogenic gram-positive bacteria
| Question | Answer |
|---|---|
| What are the main gram positive pathogenic genera | Staphylococcus, streptococcus, enterococcus, bacillus, listeria, Corynebacterium, clostridium |
| What mycolic acid bacteria also have a gram positive cell wall | mycobacterium and nocardia |
| What bacteria is grouped with positive gram because of genetics but has no cell wall | mycoplasma |
| What will be used to differentiate gram positive pathogenic genera | cell morphology and division arrangement (macro/microscopic), biochemical properties (catalase test), osmotic requirements (halotolerant test), O2 classification, acid fast stain, endospore formers, and special motility) |
| What bacteria are grouped together bc they are gram positive cocci | staphylococcus, streptococcus, and enterococcus |
| What bacteria are gram positive bacilli | bacillus, listeria, Corynebacterium, clostridium |
| What bacteria are gram positive acid fast bacilli | mycobacterium and nocardia |
| What bacteria are gram positive pleomorphic no cell wall | mycoplasma |
| What is the structure of staphylococcus | grows in clusters of cocci |
| What is the physiology of staphylococcus | Facultative anaerobe, nonmotile, catalase positive, halotolerant, tolerant of desiccation, radiation, and heat |
| What does staphylococcus halotolerance help it with? its tolerance for desiccation radiation and heat? | to tolerate salt on human skin. to survive on environmental surfaces |
| What are the pathogenic staphylococcus | s. aureus, and s, epidermis |
| S. aureus | pathogenic staphylococcus that is more virulent strain, and have a variety of conditions depending on the site of infection |
| S. epidermis | pathogenic staphylococcus, a part of normal microbiota of human skin but can be opportunistic |
| Properties of S. aureus | has protein A, coagulase, slime layer, catalase, hyaluronidase, staphylokinase, lipase, beta lactamase, toxins |
| properties of S. epidermidis | slime layer, catalase, and lipase only |
| What is the epidemiology of S. aureus | found in normal human microbiota usually on moist skin (arm pits, groin, skin folds) and mucous membranes (nasal passage, GI tract, and UGI tract) |
| What is prevention of S. aureus | handwashing and aseptic techniques |
| How is S. aureus transmitted | direct contact or fomites |
| What is the pathogenesis of S. aureus | infections occur when S breach physical barriers, few hundred can result in disease |
| what features give S. aureus is pathogenicity | structures that help it evade phagocytosis, production of enzymes, and production of toxins |
| What structural defenses help S. aureus defend against phagocytosis | protein A coat on the cell surface, bound coagulase, and synthesize polysaccharide slime layer |
| Protein A | coats the cell surface, bind to IgG, inhibits opsonization and complement cascade |
| Bound coagulase | converts fibrinogen into fibrin molecules, fibrin clots hide the bacteria from phagocytic cells |
| Synthesize polysaccharide slime layers/ capsule | inhibit leukocyte chemotaxis and phagocytosis, and facilitates attachment of staphylococcus to surface |
| Enzymes of S. aureus | a part of pathogenesis, enzymes include: cell-free coagulase, hyaluronidase, staphylokinase |
| cell-free coagulase | enzyme that triggers clotting |
| hyaluronidase | breaks down hyaluronic acid, and enables bacteria to spread between cells |
| staphylokinase | dissolves fibrin threads in blood clots and allows s. aureus to free itself from clots |
| S. aureus extracellular enzymes | lipases and beta-lactamase |
| lipase | an extracellular enzyme that digests lipids and allows staphylococcus to grow on the skin and in oil glands |
| beta-lactamase | breaks down penicillin and allows bacteria to survive treatment with b-lactam antimicrobial drugs |
| Toxins produced by S. aureus | cytolytic, exfoliative, toxic-shock syndrome, enterotoxins |
| Enterotoxins | stimulate symptoms associated with food poisoning |
| Toxic shock syndrome toxins do what | cause TSS |
| Exfoliative toxins do what | cause skin cells to separate and slough off |
| cytolytic toxins do what | disrupt the cytoplasmic membrane of variety of cells and leucocidins can lyse leukocytes specifically |
| What are the categories of diseases caused by S. aureus | non-invasive, cutaneous, systemic |
| What are non-invasive disease caused by S. aureus | food poisoning, caused by ingestion of enterotoxin-contaminated foods |
| What are cutaneous diseases caused by S. aureus | various skin conditions, scalded skin syndrome, impetigo, folliculitis |
| systemic diseases caused by S. aureus | toxic-shock syndrome, bacteremia, endocarditis, pneumonia. and osteomyelitis |
| toxic shock syndrome is what and what is it caused by | a S. aureus systemic disease, non-streptococcal, some s. bacteria produce TSS toxin, which absorbs into the blood and produced fever, vomiting, rash, and low blood pressure |
| bacteremia | the presence of bacteria in the blood, a systemic S. aureus disease, |
| endocarditis | A systemic S. aureus disease, damage to the lining of the heart |
| Pneumonia | A systemic S. aureus disease, inflammation of the lungs and empyema occurs when pus fills the lungs |
| osteomyelitis | inflammation of the bone marrow, a systemic disease caused by S. aureus |
| Diagnosis of S. aureus | detection of gram positive cocci in grapelike clusters that coagulase positive |
| treatment of S. aureus | methicillin, vancomycin used to treat methicillin resistent MRSA infections |
| Prevention of S. aureus | hand antisepsis, important to prevent HAIs |
| What is the epidemiology of S. epidermidis | it is found in the human microbiota, found everywhere on the skin but especially in the UR, GI and UGI of humans |
| How is S. epidermidis transmitted | by direct contact and fomites |
| what can prevent S. epidermidis | handwashing and aseptic technique |
| What are the pathogenesis component of S. epidermidis | slime layer (form biofilms) and extracellular enzymes: lipase only |
| What are the diseases caused by S. epidermidis | opportunistic nosocomial infections, and catheter associated infections |
| How can S. epidermidis be diagnosed | detection of gram positive, cluster of coagulase negative and sensitive to novobiocin |
| How are S. epidermidis treated | with antibiotics |
| How are S. epidermidis prevented | antisepsis prior to catheterization |
Created by:
Acrob89
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