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39 Cards in this Set
- Front
- Back
Beneficial role of normal flora: keep out invaders
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Keep out invaders
Compete for space and nutrients that could be used by pathogens Produce substances that inhibit or kill pathogens -skin bacteria:fatty acids -gut bacteria: bacteriocins, colicins, and other metabolic waste products -vaginal lactobacilli: acidic pH |
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Gnotobiotic
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Known population of bacteria in animals
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Beneficial role of normal flora: immune system
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Constant stimulation
-cross reactivity: antibodies in bowel can cross react against polysaccharide capsule of meningococci -fight opportunistic infection |
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Beneficial role of normal flora: gut morphology
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Bacteria affect gut morphology
-degrade mucus: lack of bacteria=more mucous and longer villi Bacteria affect gut motility -germ free=slower intestines |
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More disease due to normal flora than agents outside the body
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true
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Most common site for infection by pathogens
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Respiratory tract
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Nasal cavity defense mechanisms of respiratory tract
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Mucociliary lining
Hairs Turbinate bones covered with mucus All trap particles 5-10microns |
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Sinus and airway defense mechanism of respiratory tract
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Change in direction from sinus to pharynx
-organisms trapped on back of throat -adenoids and tonsils: immune response Layers of mucus and ciliated cells -antimicrobial compounds: lysozyme lactoferrin, secretory IgA, and antimicrobial peptides -ciliary elevator |
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Aleveoli defense mechanism of respiratory tract
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IgA
Complement Macrophages Glottic closure and cough reflex |
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When can organisms become respiratory tract pathogens
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Inhaled in sufficient number
Airborne Viable and alive in air Deposited in susceptible host tissue |
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2 main obstacles a respiratory tract pathogen must overcome to initiate infection
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Avoid being caught in physical defense mechanisms
Colonize respiratory tract surfaces -avoid phagocytosis -survive and multiply in phagocytic cells |
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Mechanisms of respiratory tract pathogens that initiate disease
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Adherence factors
-Bordetella:FHA, pertactin, fimbriae -S. pyogenes: F and M proteins Extracellular toxins: -Bordetella: pertussis toxin -Diptheria: diptheria toxin Replication in tissues -Chlamydia Evasion of host immunity -capsules (inhibit phagocytosis) Interfere with ciliary activity |
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Bordetella overview
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Very small Gram negative coccobacilli
Non fermentable but can oxidize AA as energy source Strict aerobe Growth in vitro requires prolonged incubation in media supplemented with charcoal, starch, blood, or albumin |
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Bordetella growth and metabolism
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Extremely delicate, fastidious
Survives only a few hours in nasal secretions Grows on blood or blood products supplemented with: -albumin and charcoal -starch -anion exchange resins to bind up fatty acids Forms narrow zones of hemolysis, changes with phase (virulent=hemolytic) |
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Bordetella diagnosis
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Nasopharyngeal swab in place during cough (resides on ciliated cells)
Cuture on Bordet-Gengou (supplemented blood agar) -contaminants inhibited by penicillin Serology for confirmation Direct fluorescein labeled antibiotic on smear: high -many false positives PCR with culture is current diagnostic approach |
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Pertussis incidence
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Vaccine preventable but incidence increasing
20-30% of adults w/ chronic cough >1wk have disease |
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Clinical presentation of B. pertussis
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Incubation: 7-10 days, no symptoms
Catarrhal: 1-2 wks, rhinorrhea, malaise, fever, sneezing, anorexia; largest bacterial culture Paroxysmal: 2-4 wks, repetitive cough with whoops, vomiting, leukocytosis Convalescent: 3-4 wks or longer, decreased cough, secondary complications (pneumonia, seizures, encephalopathy) |
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Bordetella virulence factors
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Attach via filamentous hemaglutinin, fimbriae
Pertussis toxin: A-B toxin, 5 non identical subunits, B subunit binds, A subunit has ADP ribosyltransferase activity, targets phagocytotic cells and increases cAMP levels, impairs chemotaxis and oxidative burst via ACase, stimulates release of T and B cells, induces lymphocytosis Tracheal cytotoxin (Tc): kills ciliated tracheal cells, is a fragment of bacterial cell wall murein Adenylate cyclase: secreted by bacteria and enterse host cell, targets phagocytic cells, increases cAMP and inhibits phagocytic activity LPS: two distinct molecules, standard lipid A and lipid X, both stimulate cytokine release, local damage via inflammation |
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Pertussis treatment
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Supportive in mild disease
Erythromycin, tetracycline, or chloramphenicol in sever disease Ampicillin is NOT effective |
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Legionella physiology and structure
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Slender, pleomorphic, Gram negative rods
Stain poorly with common reagents Nutritionally fastidious, require L-cysteine and enhanced growth with iron salts Nonfermentative L. pneumophilia: 85% of all infections -serotypes 1 and 6 most common |
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Legionella reservoir
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Lakes, humidifiers, hot tubs, protozoa
Algae blooms enhance growth Person to person transmission not documented |
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Legionella virulence
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Capable of replication in alveolar macrophages
Prevent phagolysosome fusion: DOT/Icm |
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Legionnaires disease
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Exposure to onset of illness: 2-10 days
Mortality rate: 15-20% Elderly, smokers, chronic lung, immunocompromised more susceptible Symptoms: Fever, chills, cough (dry or mucous), muscle aches, headaches, tiredness, loss of apetite, sometimes diarrhea Difficult to distinguish by symptom and chest xray Antibiotic therapy: erythromycin or erythromycin with rifampin |
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Pontiac fever
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Legionella
Self limiting illness Fever, chills, myalgia, malaise, headache No pneumonia 2-5 day incubation No antibiotic treatment |
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Pneumonia epidemiology
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Most common infection related death in US and Europe
Children - mainly viral Adults - mainly bacterial Neonates - chlamydia from birth |
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Pseudomonas aeruginosa overview
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Obligate aerobe, Gram negative rod
Arranged in pairs Polar flagella Simple nutritional needs Some strains mucoid due to production of polysaccharide alginate Irregular iridiscent colonies Characteristic smell Blue pigment - pyocyanin |
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P. aeruginosa Epidemiology
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Ubiquitous in nature and hospital
Contact with healthy individuals usually insignificant -opportunistic environmental pathogen Cultured from sinks and cleaning solution Respiratory equipment and dialysis tubing susceptible |
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P. aeruginosa infections
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Pulmonary: mild tracheobronchitis to necrotizing bronchopneumonia, cystic fibrosis
Skin: wound patients, hair follicles Urinary: catheters Ear: swimmers ear, inner ear infection, chronic otitis media Bacteremia: dissemination to other organs/tissues |
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P. aeruginosa virulence factors
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Many!
LPS - endotoxin Exotoxin A - ADP ribosylation of EF2 Elastase - destroys elastin |
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P. aeruginosa treatment
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Resistant to most antibiotics
Susceptible only to aminoglycosides and some cephalosporins Usually treated with two or more antibiotics for synergistic effects |
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Moraxella catarrhalis overview
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AKA Brahamella and Neisseria
Gram negative, oxidase positive, identical to Neisseria on Gram stain Major cause of upper respiratory and lower respiratory infections |
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Moraxella catarrhalis epidemiology
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Incidence: children 0-3, older people with COPD, immunocompromised and hospitalized
Human reservoir: 75% of kids <3yo and 1-3% healthy adults Entry through inhalation of aerosols Young children at increased risk due to immature mucosal IgA, eustachian tube orientation, and sinus development Acute otitis media, sinusitis, and conjunctivitis |
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Moraxella catarrhalis prevention and treatment
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No vaccine
90% b-lactamase positive |
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Corynebacterium diptheriae overview
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Gram positive
Non-capsulated Non-sporing Non-motile Rods "Chinese letters" |
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Diptheria prevention
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DTaP (diptheria, tetanus, and acellular pertussis) vaccine
1 to 4 components -pertussis toxin, FHA, fim, pertactin 5 doses |
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Diptheria epidemiology
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Distribution maintained in asymptomatic carriers and unvaccinated host
Humans only known reservoir -oropharynx or skin surface Spread person to person: respiratory droplets or skin contact |
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Diptheria toxin
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dtxR is a tox repressor
-when bound to Fe it binds DNA and blocks tox transcription -in low Fe tox gene expressed A-B exotoxin -ADP ribosylation of EF2 prevents protein growth |
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Diptheria diagnosis
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Microscopy nonspecific: metachromatic granules observed
Culture on nonselective blood agar and selective cysteine-tellurite or serum tellurite agar Important to demonstrate toxigenicity to rule out normal flora ELEK test: immunodiffusion assay nucleic acid amplification test |
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Diptheria treatment
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Urgent supportive therapy to maintain airway is essential
Penicillin or erythromycin kill organisms but has little effect since disease is toxin mediated Antitoxins neutralize toxin 85% vaccination required for herd immunity |