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114 Cards in this Set
- Front
- Back
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What are the 5 stages of the infectious process?
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1- entry, with evasion of primary defenses 2- adhesion to host cells 3- propogation 4- damage to host by toxins or inflammatory response 5- evasion of host secondary defenses.
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Synonym for pathogenecity?
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virulence
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What does virulence depend on?
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success in completing some or all of the listed stages
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how can virulence be quantified?
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by ID50, dose requrie to kill 50% of test animals
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Virulence factors (general)
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characteristics of a bacterium that enhance its ability to cause disease
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Points of entry
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respiratory tract, GI, urogenital, skin puncture, cut or burn.
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What must pathogens overcome upon entry?
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phagocytosis, acidic environments of stomach and urogenital tract, hydrolytic and proteolytic enzymes in saliva, stomach and small intestine.
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What characteristic gives bacteria a better chance of surviving primary host defenses?
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an outer polysaccharide capsule
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How does adherence increase virulence?
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prevents the bacteria from being swept away by mucus or fluid flow. Also allows for the formation of a microcolony.
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Example of the importance of adhesion?
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Strains of Neisseria gonorrhoeae that lack pili are not pathogenic
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What bacterial enzymes facilitate invasiveness?
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hyaluronidase and collagenase (degrade ECM to allow easier access to cell surfaces.
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pyogenic
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involves pus formation
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granulomatous
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having nodular imflammatory lesions
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Invasion is followed by _________
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inflammation
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The pus of pyogenic inflammations contains mostly _________
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neutrophils
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granulomatous lesions contain _________
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fibroblasts, lymphocytes, and macrophages
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exotoxin
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proteins that are secreted by both gram + and - bacteria.
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endotoxin
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lipopolysaccharides that are not secreted but are simply part of the integral components of the cell wall of gram -
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as little as _______ can kill a human
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1 ug
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what are the 2 polypeptide components of exotoxins
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one binds the protein to the host cell, the other causes the toxic effect.
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how does diptheria toxin act?
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blocks portein synthesis by attaching an ADP-ribosyl group to human protein elongation factor EF-2.
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Are most exotoxins inactivated by heating?
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Yes at 60 C
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What are exceptions to heat inactivation?
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staphylococcal enterotoxin and E Coli heat-stable toxin.
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What does treatment with formaldehyde do?
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destroys the toxic effect, but does not affect their antigenicity
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toxoids
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formaldehyde-inactivated toxins
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Exotoxin are encoded where in many cases?
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by genes carried on plasmids or temperate bacteriophages
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Are endotoxins heat stable?
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Yes
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At what point are they released into host circulation?
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cell lysis
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What are LPS made of?
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polysaccharide O (somatic region), a core polysaccharide, and a lipid component called lipid A that faces the cell interior
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Which portion of LPS is toxic?
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the lipid A moiety
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what are the main physiologic effects of LPS?
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fever, shock, hypotension, thrombosis, collectively referred to as septic shock
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What problem arises when elinination of the causative bacteria by antibiotics occurs?
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it can intially exacerbate the symptoms by causing sudden massive release of endotoxin into circulation
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How are the effects of LPS produced?
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by activation of the immune system
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What are the two mechanisms of antigenic switching?
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phase variation and antigenic variation
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phase variatoin
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genetically reversible ability of certain bacteria to turn on and off expression of certain surface antigens
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antigenic variation
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modification of the gene for an expressed surface antigen by genetic recombiantion with one of many variable unexpressed DNA sequences. The surface antigen can assume many different antigenic structures
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What are the main groups of medically important gram-positive cocci?
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streptococci and staphylococci
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Streptococci are gram positive, motile/nonmotile, and catalase-negative/positve.
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nonmotile, catalase-negative
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Clinically important genera of streptococci
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streptococcus and enterococcus
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Most streptococci are __________ (energy derivation)
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facultative anaerobes, but can grow fermentatively
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What type of medium is usually used for isolation of streptococci?
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blood enriched
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Diseases caused by Group A strep?
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infection of the throat and skin caused by group A Strep
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Group B?
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female genital tract colonization, resulting in sepsis
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streptococcus pneumoniae?
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pneumonia, otitis media, meningitis
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viridans group?
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endocarditis
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a-hemolytic streptococci on blood agar
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cause a change in hemoglobin that results in the appearance of a green pigment that forms a ring around the colony
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B-hemolytic strep on blood agar
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fross lysis of red blood cells, resulting in a clear ring around the colony
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y-hemolytic on blood agar
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cause no change or lysis
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What is the first step in classification of strep?
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blood agar tests
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WhAT is the polysaccharide in the cell wall known as?
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C-carbohydrate
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Is C-carbohydrate antigenic/.
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Yes
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How is C-carb extracted
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with acid
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What is the Lancefield scheme?
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classifies B-hemolytic strep into groups A through U on the basis of C-carb.
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What are the clinically most important groups of B-hemolytic strep?
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types and and B
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What is the most clinically imporant and common pathogen member of the Group A B-hemolytic streptococci?
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S. pyogenes
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Can S.. Pyogenes invade apparently intact skin?
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yes
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Does S. Pyogenes survive well in the environment?
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no, its habitat is infected patients, and normal human carriers
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Side note: Do staphylococcal species survive well in the environment?
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Yes
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Capsule of S. pyogenes
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contains hyaluronic identical to that found in human connective tissue, so the capsule is not recognized as foreign
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Cell wall of S. pyogenes includes fimbriae, group A-specific carb, and protein F
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fimbriae
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pilus like structures. Contain the major virulence factor, the M protein.
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Is the M protein highly variable?
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Yes, meaning a person may have S. pyogenes infections multiple times and encounter a new M protein for which they have no antibodiesw each time
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What is the grou-A carb composed of?
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rhamnose and ?N-acetyl glucosamine
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What is the function of protein F
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mediates attachment to fibronectin in the pharyngeal epithelium
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Does S. pyogenes secrete exotoxins/.
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yes
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What is the only known reservoir in nature for S. pyogenes in nature?
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skin and mucous membranes of the host.
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How is it spread?
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respiratory droplets or skin contact
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Path of S. pyogenes
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attaches to pharyngeal mucosa via protein F, lipotichoic acid, and M protein.
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Can a person be colonized and not be infected?
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Yes
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What is infection of the pharynyx by S. pyogenes called?
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streptococcal pharyngitis.
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What else can infection lead to?
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spread in blood to distant sites, causing cellulitis, fascitis, or myonecrosis
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what is cellulitis?
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acute inflammation of subcutaneous tissue
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what is fasciitis?
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inflammation of the tissue under the skin that covers a surface of underlying tissue
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what is myonecrosis/.
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death of muscle cells
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What is the most common type of S. pyogenes infection
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Pharyngitis
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Synonym for S. phyogenes pharyngitis
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strep throat
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Impetigo
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caused by S. pyogenes (most commonly). Begins on any exposed surface. Treated with a topical agent such as mupiricin, or systemically with with penicillin or cephalosporin
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erysipelas
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firey red advandinc erythema, especially on face and lower limbs
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puerperal sepsis
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initiated during or just after delivery. Causes a disease of the uterine endometrium.
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GAS
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invasive Group A Streptococcal disease
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acute rheumatic fever
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autoimmune disease that occurs 2-3 weeks after the initiation of pharyngitis. Caused by cross reactions between antigens of the heart and joint tissues and the streptococcal angiterh (M protein). Preventable if treated within 10 days of initiation of acute pharyngitis
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acute glomerulonephtitis
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rare. Postinfectious sequela occurs 1 week after impetigo or pharyngitis ensues, due to a few nephritogenic strains of group A strep. Antigen-antibody compleses on the basement membrane initiate the disease.
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Streptococcal toxic shock syndrome
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isolation of group A B-hemolytic strep from blood or another normally sterile body site in the presence of shock and multiorgan failure.
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Lab identification of GAS- latex test
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positive = latex particles bead together. Negative = separate
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How can group-A carb be identified?
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by the precipitin rxn
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What is the antibiotic of choice for acute streptococcal disease?
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penicillin G - S. Pyogenes has not acquired resistance
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What if pt is penicillin allergic?
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macrolide is the preferred drug
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How are necrotizing fascitis and streptococcal toxic shock syndrome treated?
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Penicillin G + clindamycin
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How is rheumatic fever prevented?
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rapid eradication of the infecting organism
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When is prolonged prophylactic antibiotic therapy recommended?
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after an episode of autoimmune diseaes rheumatic fever, because having it once is a major risk factor for having it again.
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What are the top 4 bacterial suspects?
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streptococcus pyogenes, corynebacterium diphtheriae, Neisseria gonorrhoeae, Mycoplasma pneumoniae
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What would be the likely population to have sore throat caused by Neisseria Gonorrhoeae?
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Sexually active oral to genital contact
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What bacterial molecules associated with gram + bacteria cause an acute phase inflammation?
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teichoic acid
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What are pathogenecity islands? Ex?
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"Groups of genes that are physically linked and are expressed in a coordinate fashion. Streptococcal M protein , which confers anti-phagocytic properties, exist on large pathogenicity island. Pseudomonas Biofilm Production is coordinated on a pathogenicity island ( quorum sensing)
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What are examples of adhesins
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pili, P fimbriae, slime or capsular material
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Streptococcus pyogenes adhesin qualitites that contribute to antigenicity
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Fimbriae with M protein which adheres to host cells and is the main antigenic component ( highly variable). F protein binds to fibronectin in the pharyngeal epithelium. Lipotechoic acid ( LTA) also contributes to adhesion
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What is ciliostasis and ciliated cell killing?
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killing cilia that make up the mucous elevator for example.
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Examples of Ciliostasis and ciliated cell killing bacterium:
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Pseudomonas aeruginosa, Bordetella sp, Chlamydia pneumoniae all defeat the hosts ciliated epithelium
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Example of metabolic byproduct that cause tissue damage:
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lactic acid
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Streptolysin S & O
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cause cell lysis and disrupt lysosomal membrane after engulfment causing release of lysosomal contents
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Protein synthesis inhibiting toxins
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Diphtheria toxin, Exotoxin A of Pseudomonas, Shiga toxin, Verotoxin of E. coli
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Toxins that increase cAMP
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Cholera toxin, E. coli enterotoxin, Anthrax toxin
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What do toxins that increase cAMP do?
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Cause loss of water out of cells- diarhea
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Streptolysin S and O
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lyse erythrocytes, leukocytes and platelets.
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Streptokinase A and B
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activate a host-blood factor plasminogen by cleavage. This dissolves blood clots.
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DNAse
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Reduces viscosity (caused by loose DNA strands) of abscess material and facilitates spread.
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What are anti-streptolysin O-antibodies useful?
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anti-streptolysin O anti-bodies are useful for documenting recent Streptococcus infection
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How does Streptococcus avoid activation of phagocytic cells?
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production of C%a peptidase
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How does strep avoid recognition by cells of the innate immune system?
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The M protein of Strep pyogenes binds factor H which degrades complement factor C3b, which is an important mediator of opsonization and phagocytosis.
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How does strep avoid ingestion by the process of phagocytosis?
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Streptococcus avoids phagocytosis by having a hyaluronic capsule. Become internalized to maintain persistent infections
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Super antigens
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stimulate T cells by simultaneously binding TCR and class 2 MHC directly and non specifically, causing the release of a large amount of interleukins and a life threatening immune response. Leads to T cell death by stimulating them but not being a target for them due to masking????
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S. pyogenes can avoid phagocytosis by
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stimulating release of lysosomal contents
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Are viruses responsive to antibiotics?
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No
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Cough
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not bacterial.
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