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78 Cards in this Set
- Front
- Back
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What are the 3 staphylococcus species?
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S.aureus
S.epidermitis S.saprophyticus |
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What clinical diseases are caused by S.aureus?
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scalded skin syndrome
food poisoning toxic shock syndrome cutaneous infections bacteremia endocarditis osteomylitis septic arthritis |
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General characteristics of Staphylococcus spp.
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Gram-positive cocci
grow in grape-like clusters |
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What environment does S.aureus grow in?
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facultative anaerobe - can grow in both aerobic and anaerobic environments
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How does S.aureus protect itself from phagocytosis?
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polymorphonuclear leukocytes (PMNs) located on its capsule
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How does S.aureus protect itself from an immune response?
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Protein A binds the Fc receptor on the immunoglobulin, blocking immunoglobulin from binding to antigen
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What is the role of teichoic acid in the pathogenicity of S.aureus
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mediate binding to fibronectin
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What is the role of peptidoglycan in the pathogenicity of S.aureus
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endotoxin-like activity
peptidoglycan binds to TLR2 to activate inflammatory host response overstimulation of the immune system can lead to septic shock |
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What mechanism accounts for S.aureus being coagulase positive?
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Coagulase enzyme converts fibrinogen on cell surfaces to insoluble fibrin, causing S.aureus to clump
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What toxin in S.aureus is responsible for forming a pore in host cells eventually causing lysis of the host cell?
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alpha hemolysin
forms a 1-2nm pore causing efflux of K+ and influx of Na+ and Ca2+ this changes the osmotic gradient, resulting in the cell being hypertonic to the environment water enters the cell, leading to osmotic swelling and eventual lysis of the cell |
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Desquamation of skin tissue due to action of exfoliating toxins is characteristic of what clinical disease?
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scalded skin syndrome due to S.aureus infection
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What are the characteristics of staphylococcal food poisoning?
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caused by S.aureus
due to action of enterotoxins A-E and G-I produced by 30-50% of S.aureus strains acts directly on neural receptors to stimulate vomiting 2-5 hrs after ingestion resistant to boiling for 30 minutes and digestive enzymes usually self-limiting |
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What causes toxic shock syndrome?
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S.aureus colonizes vagina and produces the toxin TSST-1
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What are the symptoms of toxic shock syndrome?
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high fever
vomiting diarrhea sore throat muscle pain rash hypotension organ failure |
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What is the mechanism of pathogenicity of TSST-1?
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TSST-1 is a superantigen that promotes the release of cytokines
at low concentration, TSST-1 causes leakage of endothelial cells at high concentration, TSST-1 causes cell death TSST-1 can cross mucous membranes to exit site of initial infection and cause systemic disease |
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What cutaneous infections are caused by S.aureus?
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furuncles (boils) - blockage of hair follicle or sweat gland that eventually becomes infected
carbuncle - spread of furuncle infection causing abscesses on adjacent tissues impetigo - small macule enlarges, fills with pus, then ruptures folliculitis - hair follicle is reddened and raised with pus, known as a stye if it occurs on the eyelid |
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How is S.aureus diagnosed?
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Gram stain - gram positive cocci in clusters
Culture on blood agar plates - colonies are gold in color with a zone of hemolysis catalase test - catalase positive coagulase test - coagulase positive |
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What is MRSA and how would you treat it?
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methicillin resistant staph aureus
resistance occurs due to acquisition of a new gene mecA that encodes for a new PBP called PBP2' treat with vancomycin |
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What is the leading cause of nosocomial infections?
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Staphylococcus spp.
Staph epidermidus causes 50% of all catheter and shunt infections |
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What are general characteristics of S.saprophyticus?
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Gram-positive cocci in urine
causes urinary tract infections in young sexually active women symptoms include pain on urination and pus in urine usually successfully treated with antibiotics |
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What are general characteristics of Streptococcus?
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Gram-positive cocci arranged in chains or pairs
Catalase negative |
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What are general characteristics of S.pyogenes?
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beta-hemolytic streptococcus in Lancefield group A
causes purulent infections |
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What is M protein and what bacteria is it associated with?
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cell surface exposed protein composed of 2 alpha helices
functions as an adhesin and antiphagocytic protein in S.pyogenes |
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What are two pore-forming toxins associated with S.pyogenes and what are their pathogenic effects?
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Streptolysin O - forms pores in human cell plasma membrane, lyses erythrocytes and is responsible for beta hemolysis
Streptolysin S - forms pores in plasma membranes of human cells and erythrocytes, serum antibody production against SLS used to diagnose recent Streptococcal infection |
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What enzymes promote spreading of S.pyogenes bacteria in infected tissues?
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Streptokinase A and B - cleave plasminogen setting off a signal cascade resulting in lysis of fibrin clots
DNase A and D - break down DNA present in pus causing reduction in viscosity in abscesses |
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What is the mechanism of C5a peptidase's pathogenicity?
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C5a peptidase cleaves C5a of the complement system
C5a is responsible for recruiting neutrophils and macrophages to the site of infection Thus, C5a peptidase prevents recruitment of immune system cells in S.pyogenes infection |
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What clinical diseases are caused by S.pyogenes infection?
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pharyngitis (strep throat)
scarlett fever skin infections necrotizing fasciitis streptococcal toxic shock syndrome bacteremia |
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What causes scarlett fever?
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Strains of S.pyogenes that produce streptococcal pyrogenic exotoxins (SpeA, SpeB, SpeC, SpeD)
toxins act as superantigens, leading to release of cytokines and resulting in inflammation |
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What skin infections are associated with S.pyogenes?
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impetigo
cellulitis |
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How is S.pyogenes diagnosed?
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Gram stain - Gram positive cocci in chains
Blood Agar culture - causes beta-hemolysis and is catalase negative rapid strep test to diagnose pharyngitis |
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How is S.pyogenes treated?
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Penicillin
Erythromycin if Penicillin allergy exists treat severe infections with Penicillin + Clindamycin |
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What are the general characteristics of Streptococcus agalactiae?
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Gram positive cocci in chains
beta-hemolytic Group B causes neonatal sepsis and meningitis can colonize the vagina and be passed to infant through delivery |
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What are some important species of Viridans Streptococci?
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S.bovis - correlated with colon malignancies
S.pneumoniae - leading cause of community-acquired pneumonia |
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What are some general characteristics of the Enterococci spp?
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normally inhabit GI tract
second most common cause of nosocomial infections gamma-hemolytic |
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What are the medically important species of Enterococci?
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E.faecalis
E.faecium |
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What clinical diseases are caused by Enterococci infection?
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surgical wound infection
urinary tract infection biliary tract infection intraabdominal infections bacteremia |
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How are Enterococci infections treated
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Penicillin or Ampicillin - resistance is a problem
Vancomycin |
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What are general characteristics of Bacillus Anthracis?
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Gram positive rods in chains
spore forming aerobic |
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What diseases are caused by Bacillus Anthracis?
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Cutaneous Anthrax
Inhalation Anthrax Gastrointestinal Anthrax |
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What are the symptoms of cutaneous anthrax?
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spores are introduced into the skin
small red macule forms macule enlarges to form an ulcer usually resolves spontaneously 20% mortality rate |
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What are the symptoms of inhalation anthrax?
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spores are inhaled
symptoms similar to severe respiratory infection: fever shortness of breath hypotension shock death within 3 days |
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What are the symptoms of gastrointestinal anthrax?
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ingested from contaminated meat
mortality rate approaches 100% |
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Describe the structure of the anthrax toxin.
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A-B subunit toxin
A = activity Edema factor (EF) - adenylate cyclase activity causes inflammation and inhibits neutrophil activity Lethal factor (LF) - zinc metalloprotease that cleaves host cell kinases and causes lysis or inactivation of macrophages, dendritic cells, and suppressor T cells B = binding Protective antigen (PA) binds to cells and facilitates entry of EF and LF |
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How is bacillus anthracis diagnosed?
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Gram stain - gram negative in chains
Growth on blood agar plates streaked with pus or sputum serologic tests |
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What are general characteristics of Listeria monocytogenes?
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Gram positive bacillus
Metabolically facultative - grows in aerobic and anaerobic conditions foodbourne transmission beta-hemolytic catalase positive |
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What clinical diseases are caused by Listeria monocytogenes?
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meningitis
fetal infections neonatal infections |
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What virulence factors enable Listeria monocytogenes to travel from cell to cell without entering the extracellular environment?
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internalin
listeriolysin O phospholipases C enzymes ActA - polymerization of actin into a comet tail that allows bacteria to invade neighboring cell |
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Why is a Gram stain not used to diagnose Listeria monocytogenes?
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Listeria monocytogenes is present in too low a number to be detected via Gram stain of the CSF
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How is Listeria monocytogenes diagnosed?
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Growth of organism on blood agar plate from CSF, blood, or amniotic fluid
Small smooth colonies surrounded by rim of beta-hemolysis catalase positive |
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How is Listeria monocytogenes treated?
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Ampicillin
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What are the general characteristics of Corynebacterium?
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aerobic Gram positive bacilli
irregular swelling on one end causes club-shape non-spore forming |
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What are the medically important species of Corynebacterium?
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C.diphtheriae
C.ulcerans C.jeikeium |
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Describe the clinical disease caused by C.diphtheriae.
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Diphtheria
spread by person-to-person direct contact or droplets symptoms include sore throat, fever, difficulty swallowing, cough, hoarseness, rhinorrhea Pseudomembrane composed of necrotic cell debris, fibrin, and blood cells form on oropharynx, palate, nasopharynx, nose, or larynx |
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What toxin is associated with C.diphtheriae?
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Diphtheria toxin (DT)
heat labile gene carried on phage A-B toxin A inhibits peptide elongation by ADP-ribosylating EF-2 inhibition of protein synthesis in pharyngeal epithelium --> necrosis |
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What toxin are ADP-ribosylating toxins and what is its mechanism of action?
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transfer ADP-ribose from NAD to host cell proteins, causing altered activity of host cell proteins
ADP-ribosylating toxins: exotoxin A of P.aeruginosa cholera toxin of Vibrio cholerae heat labile toxin of E.coli Pertussis toxin of Bordetella pertussis |
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What are the treatments for Corynebacterium diphtheriae?
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horse antisera against dyphtheria toxin
antibiotics - do not increase rate of healing, but do prevent spread of organism close monitoring for respiratory or cardiac failure |
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What is a toxoid?
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chemically treated toxin that is no longer toxic but retains immunogenicity
useful as a vaccine |
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What are the general characteristics of the Clostridia spp. of bacteria?
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gram positive rods
spore-forming strictly anaerobic |
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What are the medically important species of Clostridia?
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C.tetani
C.botulinum C.perfringens C.difficile |
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What bacteria causes tetanus?
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Clostridium tetani
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What are the mechanisms of pathogenicity of C.tetani?
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Tetanus toxin (tetanospasmin)
A-B toxin A chain consists of a protease that cleaves proteins in neuronal synapses, resulting in blockage of neurotransmitter release B chain mediates binding of cell receptors of inhibitory motor neurons in spinal cord |
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How does Tetanus toxin cause Tetanus?
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toxin released from C.tetani binds to peripheral motor neuron terminals
peripheral motor neurons --> axons --> neuron cell bodies in CNS in neuron cell bodies, Tetanus toxin blocks release of presynaptic inhibitory neurotransmitters reduction in inhibition causes increased resting firing rate of motor neurons |
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What are the symptoms of Tetanus?
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increased masseter muscle tone (lockjaw)
increased tone of neck, shoulder, and back muscles increased tone of abdominal and leg muscles spasms sympathetic nervous system symptoms: hypertension, tachycardia, arrhythmia, sweating, vasoconstriction neonatal tetanus |
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What are treatment and prevention techniques of C.tetani infections?
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Treatment: penicillin, tetanus immunoglobulin
Prevention: tetanus toxoid vaccine |
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What is the mechanism of pathogenicity of C.botulinum?
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Botulinum toxin
A-B toxin A subunit - protease that cleaves components of neuroexocytosis apparatus, blocking release of ACh B subunit - mediates binding to cell receptors of neurons in neuromuscular junction net result is decreased motor neuron activity due to blocked transmission of nerve impulses botulinum toxin variants encoded by genes carried on bacteriophages |
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What are the clinical diseases caused by C.botulinum?
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Food-borne botulism - ingestion of toxin leads to symmetric descending paralysis, cranial nerve involvement (diplopia, dysarthria, dysphagia, resp. failure), nausea, vomiting, abdominal pain
Wound botulism - wound contamination with C.botulinum spores causes symptoms similar to food-borne botulism but without the GI findings Infant botulism - C.botulinum colonizes the infant intestine causing paralysis; can be prevented by avoiding honey for infants less than 12 months of age |
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What is the treatment for C.botulinum infection?
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respiratory support
trivalent equine antitoxin |
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What clinical illnesses are caused by C.perfringens?
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food-poisoning
gangrene |
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What clinical diseases are caused by C.difficile?
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diarrhea associated with antibiotic use
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What are general characteristics of Actinomycetes?
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G+ rods
resemble fungi 2 medically important genera: Actinomyces spp. Nocardia spp. |
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What are the general characteristics of Nocardia spp.
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Belong to the Actinomycetes family
G+ bacilli in elongated chains or filaments with branches aerobic 2 medically important species: N.asteroides N.brasilliensis |
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What are the mechanisms of Nocardia's pathogenicity?
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neutralize oxidants
prevent phagosome acidification inhibit phagosome-lysosome fusion lesions infiltrated with neutrophils but neutrophils are unable to kill the bacteria |
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What clinical diseases are caused by Nocardia infection?
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Pulmonary nocardiosis - subacute pneumonia with nodules, cavitation, and empyema; dissemination to CNS, skin, soft tissue, and other organs can lead to abscess formation
Transcutaneous inoculation (actinomycetoma) - caused by inoculation of organism into tissues of the foot, fistula formation, serous or purulent discharge, lesions |
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How are Nocardia infections treated?
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Trimethoprim/sulfamethoxazole and other sulfa drugs
Minocycline and amikacin are alternatives treatment must be continued for 6-12 months to prevent relapse drainage of brain abscesses |
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What are general characteristics of Actinomyces spp.?
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part of the Actinomycetes family
G+ bacilli facultative anaerobes, but grow best anaerobically non-spore forming found in normal flora of mouth, GI tract, and female genital tract |
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What clinical diseases are caused by Actinomyces infection?
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Actinomycosis
oral-cervicofacial disease abdominal or pelvic disease |
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What is a diagnostic feature of Actinomyces in Gram staining?
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sulfur granules
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How is Actinomyces infection treated?
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Penicillin for up to 12 months
Tetracycline/doxycycline is an alternative |
