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39 Cards in this Set

  • Front
  • Back
Beneficial role of normal flora: keep out invaders
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
Gnotobiotic
Known population of bacteria in animals
Beneficial role of normal flora: immune system
Constant stimulation
-cross reactivity: antibodies in bowel can cross react against polysaccharide capsule of meningococci
-fight opportunistic infection
Beneficial role of normal flora: gut morphology
Bacteria affect gut morphology
-degrade mucus: lack of bacteria=more mucous and longer villi
Bacteria affect gut motility
-germ free=slower intestines
More disease due to normal flora than agents outside the body
true
Most common site for infection by pathogens
Respiratory tract
Nasal cavity defense mechanisms of respiratory tract
Mucociliary lining
Hairs
Turbinate bones covered with mucus

All trap particles 5-10microns
Sinus and airway defense mechanism of respiratory tract
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
Aleveoli defense mechanism of respiratory tract
IgA
Complement
Macrophages
Glottic closure and cough reflex
When can organisms become respiratory tract pathogens
Inhaled in sufficient number
Airborne
Viable and alive in air
Deposited in susceptible host tissue
2 main obstacles a respiratory tract pathogen must overcome to initiate infection
Avoid being caught in physical defense mechanisms
Colonize respiratory tract surfaces
-avoid phagocytosis
-survive and multiply in phagocytic cells
Mechanisms of respiratory tract pathogens that initiate disease
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
Bordetella overview
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
Bordetella growth and metabolism
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)
Bordetella diagnosis
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
Pertussis incidence
Vaccine preventable but incidence increasing
20-30% of adults w/ chronic cough >1wk have disease
Clinical presentation of B. pertussis
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)
Bordetella virulence factors
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
Pertussis treatment
Supportive in mild disease
Erythromycin, tetracycline, or chloramphenicol in sever disease

Ampicillin is NOT effective
Legionella physiology and structure
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
Legionella reservoir
Lakes, humidifiers, hot tubs, protozoa
Algae blooms enhance growth
Person to person transmission not documented
Legionella virulence
Capable of replication in alveolar macrophages
Prevent phagolysosome fusion: DOT/Icm
Legionnaires disease
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
Pontiac fever
Legionella
Self limiting illness
Fever, chills, myalgia, malaise, headache
No pneumonia
2-5 day incubation
No antibiotic treatment
Pneumonia epidemiology
Most common infection related death in US and Europe
Children - mainly viral
Adults - mainly bacterial
Neonates - chlamydia from birth
Pseudomonas aeruginosa overview
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
P. aeruginosa Epidemiology
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
P. aeruginosa infections
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
P. aeruginosa virulence factors
Many!
LPS - endotoxin
Exotoxin A - ADP ribosylation of EF2
Elastase - destroys elastin
P. aeruginosa treatment
Resistant to most antibiotics
Susceptible only to aminoglycosides and some cephalosporins
Usually treated with two or more antibiotics for synergistic effects
Moraxella catarrhalis overview
AKA Brahamella and Neisseria
Gram negative, oxidase positive, identical to Neisseria on Gram stain
Major cause of upper respiratory and lower respiratory infections
Moraxella catarrhalis epidemiology
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
Moraxella catarrhalis prevention and treatment
No vaccine
90% b-lactamase positive
Corynebacterium diptheriae overview
Gram positive
Non-capsulated
Non-sporing
Non-motile
Rods
"Chinese letters"
Diptheria prevention
DTaP (diptheria, tetanus, and acellular pertussis) vaccine
1 to 4 components
-pertussis toxin, FHA, fim, pertactin
5 doses
Diptheria epidemiology
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
Diptheria toxin
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
Diptheria diagnosis
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
Diptheria treatment
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