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23 Cards in this Set
- Front
- Back
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Describe Streptococcus pneumonia (pneumococcus)
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grows as pairs of lancet-shaped diplococci (may grow as short chains; present in upper respiratory tract of healthy individuals; most common cause of community-acquired pneumonia (CAP)
also causes bacterial meningitis, otitis media (children), sinusitis (adults) endocarditis, conjunctivitis produces relatively few toxins; ability to cause disease depends upon ability to avoid host defenses and multiply in host tissues, there inducing strong inflammatory reactions |
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Describe the epidemiology of S. pneumonia
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common inhabitant of throat and nasopharynx of healthy individuals (more common in children)
serotypes of pneumococci carried are same serotype associated w/ disease; infection involves new strain not previously carried colonized nasopharynx provides source of organisms for spread to other tissues or individuals |
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Describe the morphology and growth requirements of S. pneumonia
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colonies are alpha-hemolytic; exist in both smooth (encapsulated) and rough (non-encapsulated) varieties; smooth strains are larger, mucoid, and moist-looking
As colony ages, center collapses due to autolysis; aging cultures often stain Gram-negative or Gram-variable organism is fermentative and produces lactic acid; facultative, but doesn't use O2 during aerobic growth relatively fastidious; viability of specimens is reduced by drying; rich culture medium necessary for isolation |
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Describe the identification of S. pneumonia
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1. Optochin sensitivity-paper disks (P disks) impregnated with optochin (ethylhydrocupreine hydrochloride) are placed on blood agar plate on which pure culture of α-hemolytic organism has been inoculated, and plate is incubated overnight
pneumococcus grows zone of inhibition (no bacterial growth and no hemolysis) surrounding optochin disk 2. Bile solubility-performed after bacterial culture has been grown; based upon presence of autolytic enzyme in cell wall; enzyme is activated by detergents (bile and bile salts) test is performed by mixing solution of deoxycholate w/ viable α-hemolytic streptococcus; pneumococcus suspension becomes clear; viridans streptococcus remains turbid |
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Describe the capsule of S. pneumonia
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capsules composed of complex polysaccharides, which are antigenic; 85 distinct serotypes (differ in sugars and their linkages in polysaccharide that forms capsule)
each capsule is antigenically different; isolates serotyped according to immunologic reactivity w/ Ab capsule is most important virulence factor (allows avoidance of phagocytosis by PMN's); non-encapsulated (rough) strains are non-virulent homologous Abs against capsular polysaccharide will opsonize-->phagocytosis (protective against infection and essential for recovery); although Abs provide long-lasting immunity, it's strictly type-specific |
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Describe the vaccines for S. pneumonia
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Certain serotypes are particularly virulent (23 serotypes account for majority of infections); capsular polysaccharides from most prevalent serotypes incorporated into anti-pneumococcal vaccine (Pneumovax) for adults
Another vaccine (Prevnar) prevents invasive disease (sepsis and meningitis) in young children; 7 capsular polysaccharides conjugated to immunogenic protein to improve Ab production against them |
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Describe the extracellular products of S. pneumonia
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1. Pneumolysin O-hemolysin; contributes to virulence
2. Purpura-producing principle-causes purpura and dermal hemorrhage; derived from peptidoglycan 3. Lipoteichoic Acid (LTA)-activates complement and induces inflammatory cytokine production by activating Toll-like receptors 4. IgA protease-cleaves secretory immunoglobulin IgA at hinge region, preparing it for further degradation by other proteases; virulence factor 5. Amidase-autolysin; when cell lyses, releases components that induce inflammation (important part of pathogenic process) |
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Describe corynebacterium diphtheriae
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Gram-positive rod-shaped bacteria; resides in pharynx; spread via respiratory droplets
cause local, somewhat-invasive infection-->systemic illness by production of protein exotoxin that spreads via circulation obligate aerobes, non-motile, grow in clusters (palisades or Chinese characters) |
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Describe the diptheria toxin
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key virulence factor; synthesis induced by iron limitation and is secreted from cell
gene encoding DT located on genome of lysogenic bacteriophage integrated into bacterial chromosome (lysogenic conversion); strains w/out phage don't produce DT toxin has 2 subunits, A (active) and B (binding); B subunit binds to receptor on target cell membrane and delivers A subunit into cytoplasm A subunit becomes enzymatically active ADP ribosyltransferase which consumes NAD and transfers ADP ribose onto essential component of protein synthesis machinery, inhibiting protein synthesis and killing intoxicated cell local damage to pharyngeal mucosa causes formation of a grayish pseudomembrane that can cause suffocation; circulating DT can damage heart, peripheral nerves and kidneys <5 cases per year in US recently due to universal use of vaccine based on diphtheria toxoid (inactivated form of DT that retains its immunogenic activity) |
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Describe influenzaviridae
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orthomyxoviridae; negative sense single stranded RNA viruses (Baltimore Class V)
RNA alone is not infectious; capsid core contains RNA-dependent RNA polymerase (RNA transcriptase) to make (+) strand RNA messenger from (–) ssRNA genome segmented; have multiple strands of genome (8 segments) helical nucleocapsids surrounding RNA segments w/ lipid envelope added at cell membrane; outer surface of envelope has glycoprotein spikess-hemagglutinin (H) and neuraminidase (N) viral proteins of membrane are glycosylated by cellular mechanisms; early synthesis of viral messenger RNA takes place in nucleus (needs host cell factors as primer for replication) |
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Describe influenza pathogenesis and virulence
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hemagglutinin spikes important in attachment of virus to cell and infection; neuraminidase spikes are enzymes which help free newly synthesized virus from cells
Influenza types A (pandemics), B (epidemics), and C (mild) cause acute respiratory disease; route of infection is via aerosol droplets, (90% attack rate in close quarters) virus replicates in superficial respiratory cells, and destroys ciliated columnar epithelium in bronchi 3 major human influenza A hemagglutinins (H1, H2, H3) and 2 neuraminidase (N1, N2); different strains have different combinations and different minor Ags |
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contrast antigenic drift and antigenic shift
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A. drift-chance mutations; result in minor changes in virus
B. shift-reassortment b/t strains; results in major changes in surface Ags (causes severe pandemics) source of Ags for new strains are birds (ducks) pig supports replication of both human and avian influenza viruses; 2 viruses in same porcine cell results in segments from both viruses being present; when nascent nucleocapsids are packed and bud from cell membrane, avian and human segments are both incorporated |
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Describe influenza vaccines
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because influenzavirus strains change quickly, health authorities conduct surveillance of influenza outbreaks to predict which strains will be dominant epidemics in coming year to decide which strains will be used in upcoming vaccine (not always correctly predicted)
Influenza vaccines contain 2 strains of Type A and 1 strain of type B traditional vaccine against influenzavirus is killed (split) virus vaccine, propagated in embryonated chicken eggs prior to viral inactivation; provides short-lived immunity new live vaccine (FluMist)administered as nasal spray vaccines are effective only against specific strains of influenzavirus they contain |
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Describe the pathogenesis of coccidioides (C. immitis or C. posadasii)
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dimorphic, soil-dwelling fungi; causes coccidiomycosis (valley fever); results from inhaling spores (arthroconidia); acquired in southwestern US
organisms exist as filamentous moulds; individual filaments (hyphae) elongate and branch alternating cells w/in hyphae degenerate, leaving barrel-shaped viable elements (arthroconidia) arthroconidia become airborne for extended periods; small size allows them to evade initial mechanical mucosal defenses and reach deep into the bronchial tree, where infection is initiated in nonimmune host |
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Describe the life cycle of coccidioides
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Once in susceptible host, arthroconidia enlarge, become rounded, and develop internal septations (spherules); septations encompass uninuclear elements (endospores); spherules rupture and release packets of endospores that develop into spherules, thus propagating infection locally
if returned to artificial media or the soil, the fungus reverts to its mycelial stage |
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Describe the host immune response and clinical presentation of coccidioides
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immune response plays critical role in control of infection; necrotizing granulomas containing spherules identified in patients w/ resolved pulmonary infection
in disseminated disease, granulomas are poorly formed or not developed, creating PMN response in asymptomatic resolved infection, delayed-type hypersensitivity is common 1/2-2/3 are subclinical infections; patients protected from 2nd primary infection most common clinical presentation is self- limited CAP 1–3 weeks after infection (indistinguishable from bacterial or other infections w/out lab tests); symptoms (especially fatigue) last for weeks-months |
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Describe complication of coccidioides
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residual pulmonary sequelae (nodules or peripheral thin-walled cavities) are uncommon; chronic pulmonary or extrapulmonary infections are rare
extrapulmonary complication-African or Filipino ancestry have higher risk; heavily immunosuppressed patients have much higher risk Disseminated infections more frequent in adults than in children (skin, skeletal system, meninges are most common sites) |
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Describe the diagnosis of coccidioides
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A. serology
detects IgM and IgG Abs tube-preciptin (TP) and IgM Abs found in serum soon after infection and persist for weeks (not useful for gauging disease progression) complement-fixation (CF) and IgG Abs occur later in course of disease and persist longer; rising CF titers associated w/ clinical progression; CF Ab in CSF is indicator for coccidioidal meningitis; Abs disappear over time as illness resolves B. culture grows w/in 3–7 days on artificial media (blood agar) C. microscopy spherules identified under direct examination of sputum after Gomori methenamine silver (GMS) staining fixed tissues (biopsies)-spherules w/ surrounding inflammation seen w/ hematoxylin-eosin or GMS |
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Describe legionella pneumophilia
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thin, pleomorphic gram-negative rod; may show elongated, filamentous forms
demonstrated by silver impregnation methods (Dieterle stain) and some simple stains w/t decolorization steps (stains poorly w/ normal gram stains) Polar, subpolar, and lateral flagella present (motile) contains outer membrane, thin peptidoglycan layer, and cytoplasmic membrane; toxicity of lipopolysaccharide (LPS) is significantly < other Gram-negative bacteria LPS side chains (homopolymer of legionaminic acid) render cell surface highly hydrophobic--> increases adherence of bacterial cells to membranes and increased concentration in aerosols can't be grown on ordinary blood agar; requires buffered charcoal-yeast extract (BCYE) supplemented w/ Fe, cysteine and acidic conditions (pH 6.9); growth under aerobic conditions is slow (2-5 days) colonies have distinctive surface resembling ground glass 16 serogroups; Philadelphia strain (serogroup 1) is most common; limited number of serogroups (1 to 4) account for most infections |
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Describe the cause, entry, and microscopic features of L. pneumophilia
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inhaled by aerosols created in manmade water supplies that harbor the organism; propensity to attack lungs, producing necrotizing multifocal pneumonia marked by headache, fever, chills, dry cough, and chest pain
multiple foci in both lungs and extension to pleura (spread outside respiratory tree is rare) process involves alveoli and terminal bronchioles (spares larger bronchioles and bronchi) inflammatory exudate contains fibrin, PMNs, macrophages, and erythrocytes preponderance of bacteria wi/n phagocytes and lytic destruction of inflammatory cells are strking features |
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Describe virulence factors and pathogenesis of L. pneumophilia
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facultative intracellular pathogen; pathogenicity depends on ability to survive and multiply w/in macrophages
attach to alveolar macrophages; pili and outer membrane proteins (OMP) bind complement components; macrophage invasion potentiator (Mip) facilitates early stages of cell entry into endocytotic vacuole Inside vacuole, replicates by preventing phagosome-lysosome fusion and avoiding acidification and enzymatic digestion endosome recruits secretory vesicles from the endoplasmic reticulum (ER) remodeling it into rough ER accomplishes control of phagocyte by secreting proteins that modulate host cell vesicle traffic and prevent transport into lysosome extracts iron from transferrin; peptide toxin inhibits activation of oxidative killing mechanisms of phagocytes Induction of apoptosis and formation of pore-forming toxin-->death of macrophage; lysis of dying macrophages releases new population which repeats infective cycle multiple degradative enzymes released-->destructive lesions in lung and systemic toxicity related to cytokine release |
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Describe the epidemiology of L. pneumophilia
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found in H2O and moist environments; exist as parasites of protozoa (amoebas)-environmental reservoir
transmission to humans occurs when aerosols are created in manmade H2O supplies; outbreaks occur around large buildings w/ cooling towers or air-conditioning system as the spreading vehicle hospital outbreaks-respiratory devices, hot water system (faucets and shower heads) can persist in H2O supply despite standard disinfection procedures (particularly in warm H2O and pipes contain scale or low-flow areas that compromise chlorine access) |
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Describe the lab diagnosis of L. pneumophilia
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Tissue samples stained w/ direct fluorescent Ab (DFA); lung aspirates, bronchoalveolar lavage, or biopsies are preferred samples; not found in sputum
DFA is rapid, but low sensitivity; PCR-rapid, more sensitive antigenuria detection test-sensitive for the most common (serogroup 1); less sensitive for other serogroups |
