Bacteria Pathogenicity Ability to Cause Infection.
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Transcript of Bacteria Pathogenicity Ability to Cause Infection.
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Bacteria Pathogenicity
Ability to Cause Infection
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Infectious Diseases
• Encounter-bug meets host (reservoir)
• Bug adheres to host
• Entry-bug enters host
• Multiplication- bug multiplies in host–
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Infectious Diseases
• Damage to host– Virulence of bug or host response
• Outcome- bug or host wins or
• Coexist- chronic infection
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Reservoir
• Exposure to microbe– Humans– Animals – Environment
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Virulence Factors
• Enhance colonization & growth
• # of cells required to establish infection
• Measure of pathogenicity
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Adherence (Virulence Factor)
• Attachment to host cells
• Adhesins on pathogen (proteins)– Bind to complimentary surface receptor
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Adherence
• Prevent infection
• Influenza changes adhesions over time
• Neisseria gonorrhoeae -variety of adhesions
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Portals of Entry
• Mucous membranes– Respiratory
– GI– Genitourinary
• Conjunctiva
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Portals of Entry
• Skin
• Bugs have preferred portal
• C. tetani spores in soil --- anaerobic wound
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Inoculum
• Number of microbes-dose
• Greater dose, more chance infection will occur
• ID50 or LD50 expresses virulence
– Infectious or lethal dose for 50% of population
– LD50 used for toxins
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ID50
• ID50 for B.anthracis via skin is 10 to 50 endospores
• Via which route is infection more likely?
• Via which route is infection more lethal?
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Invasins
• Adherence of microbe to surface
• Activates factors that let microbe in-penetration
• Microbes produce invasins (proteins)
• Endocytosis
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Colonization
• Requires multiplication
• Compete with normal flora for space & nutrients
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Colonization
• Overcome local host defenses– IgA (mucosal surfaces)
• Avoid IgA– Rapid turnover of fimbriae/pili– Antigenic variation in type of pili– IgA proteases (enzymes) destroy IgA
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Multiplication
• Need Fe to multiply– Most is bound in host– Have own iron-binding molecules that compete
for Fe-siderophores• \
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Avoid Phagocytosis
• Avoid recognition & attachment
• Capsule– Impairs phagocytosis DT negative charges– Produce antibodies to capsule– \
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Avoiding Phagocytosis
• Components of cell wall –virulence
– Mycolic acids in M. tuberculosis
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Surviving Within Phagocyte
• Escape from phagosome, vesicle, before
fuses with lysosome
• Prevent fusion with lysosome
• Grow inside phagocyte protected from host
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Tuberculosis
• Ancient disease
• 1/3 of world population infected
• 8 million develop active TB each year
• 2 million die each year
• AIDs increases activation of latent TB
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Tuberculosis
• Dependent upon virulence of strain & host resistance
• Produces cell mediated immunity which prevents active disease in many people
• Multi drug resistance has developed
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S & S of Pulmonary TB
• Chronic disease
• Progressive weight loss
• Night sweats
• Chronic cough
• Hemoptysis
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Mycobacterium tuberculosis
• Acid fast bacillus (AFB)
• Resistant to drying
• Aerobic, slow growth
• Airborne transmission
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Mycobacterium tuberculosis
• Inhale airborne droplets
• Ingested by alveolar macrophages
• Multiply in macrophages even with ongoing immune response
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TB Response
• Host immune response-delayed type hypersensitivity reaction
• Tissue damage DT Inflammatory response
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TB Conversion
• TST skin reaction is positive
• Occurs within 24 – 48 hours after exposure to TB antigens
• Purified protein derivative of bacillus
• Cell mediated immunity
• Sensitized T cells react with proteins
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QuantiferonGold
• Blood test
• Detects interferon gamma
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How to Confirm Diagnosis
• Sputum cultures for AFB smear & culture
• Chest xray
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Pathogenesis
• LTBI (latent TB infection)– Immune defenses contain organism– Formation of tubercle – TB converter– No S&S of disease
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Active Disease
• Low resistance – Disease not controlled– Cytokines damage lung– Acute pulmonary infection– Can spread & cause death
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TB Outcomes
• Primary infection- positive skin test– 90% immune system controls infection via
cellular immunity• TB germs isolated within tubercles( Activated
macrophages)
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TB Outcomes
• 10% progressive primary infection-not controlled– Illness or death if not treated– Cavities in lungs– Spread throughout body
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Secondary or Reactivation Infection
• Reinfection-2nd exposure or
• Bacteria escape immune system-reactivation
• Activated macrophages release cytokines
• Delayed hypersensitivity reaction
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Prevention of Transmission
• Negative pressure rooms
• Respirator masks-fit tested
• Admit staff aware of symptoms of TB
• Yearly TST of staff
• Conversions treated with 6-9 months of INH
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Treatment
• INH for LTBI or TB conversion
• TB disease-active TB– 4 drugs till drug sensitivities return– DOT
• 9- 12 months of treatment– Slow growing– Impedes abx entering cell wall
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Resistant TB
• MDR TB– Resistant to INH, & 1 other TB drug
• XDR TB– Resistant to all 1st line drugs– Use 2nd line drugs for several years– Often leads to death
• DT improper treatment
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BCG
• Live culture of M. bovis– Attenuated strain– Used in other countries to protect children from
miliary disease– Can cause positive reaction on TST
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Latent vs Active
• Latent TB– Infected but no S&S– Not infectious
• Active TB– S&S of disease– Infectious if pulmonary TB
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Leprosy
• Hanson’s disease- discovered in 1873
• Seen in tropics and underserved countries
• U.S.-150 new cases per year
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Leprosy
• Infection of nervous system
• Infects the peripheral nerves within skin
• 2 forms of disease dependent upon immune response
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M. leprae
• Tuberculoid form– Regions of skin, lost sensation surrounded by
nodules– Lose pigmentation– Causes strong cell mediated response– Activated macrophages keep microbe under
control
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Lepromatous Form
• Weak immune response & microbe spreads
• Skin & nerve cells infected
• Shed large #s in nasal secretions and oozing sores-more infectious
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Invasion via Enzymes
• Exoenzymes- excreted to outside
• Coagulases-clot fibrinogen in blood
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Kinases
• Breakdown fibrin– Produced by strep– Invades tissues & spreads– Used to isolate infections
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Enzymes
• Hyaluronidases – hydrolyzes hyaluronic acid (polysaccharide)
• IgA proteases– Destroys IgA antibodies in secretions
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Enzymes
• Leukocidins– Kill neutrophils
• Hemolysins-staph & strep– Dissolve RBCs– Able to obtain Fe
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Invasion via Toxins
• Toxins– Poisonous substances damage tissues– Cause shock, fever, inhibit protein synthesis
• Two types– Exotoxins– Endotoxins
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Exotoxins
• Produced inside cell
• Mostly proteins, kill in low concentrations
• Mainly gram positive
• Gene on plasmids or phages– Not bacterial genes
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Exotoxins
• Destroy part of cell or inhibit metabolic processes– Specific for each exotoxin
• Toxin responsible for S &S of disease
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Exotoxins
• Antitoxins– Antibodies to toxin
• Toxoid– Inactivated exotoxin– Use to induce immunity to toxins– Vaccines
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A-B Toxins
• 2 parts-polypeptides
• A-active or enzyme component
• B-binding component
• B binds toxin to host cell
• A-B toxin enters
• Components separate & A kills host– Disrupts protein synthesis
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Superantigens
• Bacterial toxins provoke intense response
• Stimulate nonspecifically T cells
• T cells release cytokines– Fever, N & V, diarrhea
– System wide effect with organ failure
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Naming of Exotoxins
• Neurotoxins attack nerve cells
• Cardiotoxins-heart cells
• Hepatoxins-liver cells
• Leukotoxins-WBCs
• Enterotoxins-release of fluids-nausea, vomiting & diarrhea
• Cytotoxins-variety of cells
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Endotoxin
• Lipid A
• Stimulates macrophages to release cytokines– High levels are toxic
• Activate complement & immune defenses
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S & S
• Chills, fever, weakness, aches
• Later shock and death
• Activate blood clotting– Clots obstruct capillaries– Death of tissues-DIC
• Endotoxin shock sepsis
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Shock
• Loss of blood pressure
• Gram negatives-endotoxin shock
• Cytokine-tumor necrosis factor (TNF)
• Damages blood vessels -leaky
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Endotoxins
• Do not promote antitoxins ( abs to Lipid A)
• Antibodies produced to bug don’t affect toxin
• Assay to detect minute amounts of endotoxins in drugs & body fluids
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Staphylococci
• Staph divided based upon coagulase
• S. aureus is coagulase positive
• S. epidermidis (CNS)
• Found on humans and animals
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S. aureus
• Named for yellow pigmented colonies
• Facultative anaerobe, catalase positive
• Grows well in nares-colonization
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S. aureus
• If infected, shed high numbers– Don’t work around food or patients
• Survives well in environment-resists drying
• Now resistant to most antibiotics
• MRSA
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Epidemiology
• Nasal carriers have 2-7 times greater risk of infection than non carriers
• Screening of high risk pts
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Successful Pathogen
• Biofilm
• Capsule
• Exoenzymes
• Toxins
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Biofilm
• Protective growth medium for microorganisms– WBCs, antibodies, antibiotics
• ET & trach tubes-PNA
• IV catheters-BSIs
• Implants- SSIs
• Facilitates transfer of resistant genes
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Capsule
• Protection from phagocytes
• Attachment
• Prevents dehydration
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Enzymes
• Proteases– Degrade fibrous protein in collagen
• Hyaluronidase– Degrades cement between cells
• Promote spread in tissues
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Enzymes
• Lipases– Colonize hair follicles– Breaks down sebum
• Leukocidins– Kill WBCs– Pus formation (pyogenic)
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Skin Infections
• Pimples, boils, abscesses– Impetigo of newborn, blisters– Infection of insect bites, burns, scrapes etc.
• Cellulitis– Spread of bug through skin and soft tissue
• Wound infections-major cause • Use of antibiotics• Resistant MRSA
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Invasion via Toxins
• Produce many exotoxins
• Secreted to outside– Increase ability to invade tissue and cause
damage
• Exfoliatin toxin-scalded skin syndrome– Occurs in infants
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Toxic shock syndrome
• Superantigen
• Symptoms – High fever, hypotension, vomiting, rash &
death
• Female normal flora– Use of tampons abrade wall
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S. aureus Intoxication
• Enterotoxin causes food poisoning– Restricted to GI tract
• S & S – Vomiting, diarrhea, abdominal cramps
• Prevention-hand hygiene & refrigerate food – Toxin not produced
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Treatment
• Use of antibiotics for infections only
• Over use/misuse
• Resulted in selection of MRSA in hospitals
• Isolate these patients
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CA-MRSA
• MRSA in community
• Patient lacks risk factors for HA-MRSA– Hospitalization– Surgery– Long term care– Dialysis– Indwelling catheters
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Outbreaks in Community
• Sports participants
• Daycare, elementary schools
• Inmates
• Military recruits
• Men having sex with men (MSM)
• Tattoo recipients
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CA-MRSA
• Susceptible to more antibiotics
• Gene for Panton-Valentine leukocidin (PVL)
• Causes skin & soft tissue infections
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PVL Gene
• May be associated with severe necrotizing infections
• HA MRSA & S. aureus strains rarely carry this gene
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Preventing Transmission• Exclude from work, school, sports, etc.
• Dispose of used bandages in trash
• Avoid sharing personal items
• Shower every day with Dial or anti-bacterial soap
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Clostridium botulinum
• Gram positive rod
• Soil and vegetation
• Produces several exotoxins- neurotoxin
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Neurotoxin
• Toxin causes flaccid paralysis of muscles
• Prevents release of neurotransmitter, acetylcholine– Muscles can’t contract
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Botulism-Foodborne Disease
• Disease caused by exposure to toxin– Microbe can’t compete with normal gut flora in adults
• Infant botulism-don’t have protective gut flora– Associated with honey
• Treatment-supportive care– Ventilator
– Antitoxins-trivalent
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Toxin
• 1 pt kills everyone in world• 1 oz kills everyone in US• Botox –type A
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Clostridium tetani
• Gram positive, endospore forming rod
• Found in soil contaminated with animal feces
• Encounter- deep puncture wounds with dirt
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Neurotoxin
• Released by lysis of bacteria
• Binds to nerve cells that control contraction of skeletal muscles
• Toxin blocks relaxing pathway so both muscles contract spasm
• Jaw muscles first, can’t open mouth
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Lockjaw
• Death from spasms of respiratory tract– Pneumonia & regurgitation of stomach contents
• Prevention– DPT -toxoid, inactivated toxin– Anti toxin neutralizes toxin
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Clostridium difficile
• Anaerobe
• Endospore forming rod
• Vegetative cells– Survive for at least 24 hr on inanimate surfaces
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Epidemiology
• Present in soil and water
• Found in gut of humans & animals
• Hospitals are a major reservoir– 20-40% of pts become colonized
• Recently, found in pork
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Range of Disease
• Asymptomatic carriage ( outnumber those with disease)
• Clostridium difficile infection (CDI)
• Pseudomembranous colitis
• Toxic megacolon
• Sepsis
• Death
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Pathogenesis of CDI
• C. difficile ingested either as vegetative form or spores
• Spores germinate in small intestine • Normal flora disrupted by antibiotic
therapy, disease can occur• C. difficile releases toxins causing severe
inflammation of colon
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New Issues
• CDI rates are increasing
• Epidemic strain found in US, Canada, & Europe
• More severe disease– Higher mortality– Higher rates of colectomy
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Treatment
• Stop the inciting antibiotics• 25% recover without further treatment• Flagyl is first line of therapy
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Treatment
• Must monitor response to therapy
• Vanco po for moderate to severe disease
• Both antibiotics disrupt the normal flora– Susceptible to relapses or re-infection
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Transmission
• Fecal-oral route
• Contaminated hands of HCWs
• Contaminated hands of patients
• Contaminated environment
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Environment
• Clean and disinfect surfaces in close proximity of the patient
• Patient care equipment.
• Use bleach for C. difficile
• Privacy drapes