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169 Cards in this Set
- Front
- Back
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FLAGELLA
- force - arrangement |
ION motive force
- rotates like a windmill Arrange: - monotrichous (P. aeruginosa), amphi, lopho (h. pylori), bilopho -rare , peri (E. coli) Growth is from the tip (center is porous) chemotaxis is moving up a [gradient] |
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Pili / Fimbriae
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GRAM NEGATIVE
- involved in adherence/binding - F/ sex pili = gene transfer (conjugation) - Can be virulence factors - used in initial stages of biofilm formation (gross- catheters) |
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Capsules
+ capsule = S-type colony - capsule = R-type |
glycocalyx = mucus layer
- makes it resistant to osmotic changes & phagocytosis (pushed around instead of engulted) |
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CELL WALL / PEPTIDOGLYCAN
(murein or mucopeptide) - structure - unique - mollicules |
NAM / NAG glycan sheets w/ 2 tetrapeptide crosslinks
- D-amino acids - Gram + has lysine exc: steph aureus has a pentapeptide glycine linkage - Gram - has diaminopimelic acid Mollicutes do not have cell wall (but not affected by penicillin) ex// x-plasmas |
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GRAM POSITIVE BACTERIA
**virulence is mostly linked with their exotoxins** (not as much for gram negative |
- no OM
- no periplasmic space - no LPS --> NO ENDOTOXIN (but lipoteichoic acid can sometimes be) - no lipids/Lipoproteins - THICK peptidoglycan layer - Lysine peptidoglycan cell layer - Pentapeptide cross-linkage - + teichoic & teichuronic acids on cell wall --> bind protons, lowering pH, and decreasing autolysin degradation |
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GRAM NEGATIVE BACTERIA
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- No Teichoic or Teichuronic acids
- + LPS, OM, Periplasmic space, Lipoproteins (A) - Thin Peptidoglycan - Diaminopimelate in tetrapeptide crosslink - Direct bonding of peptidoglycan crosslinkage. |
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OUTER MEMBRANE
**receptor for bacteriophages & antigenic determinant** |
LIMITS HYDROPHOBIC & AMPHIPATHIC DRUGS
- quite permeable to most small molecules (2' porins) = molecular sieve - Outer leaflet of OM has LPS attached to it. - Inner leaflet has lipoproteins crosslinking it to peptidoglycan = STABILITY Made up of LPS & phospholipids |
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LPS
**O-Ag is variable** |
UNIQUE to Gram negative bacteria
ENDOTOXIN - VERY VIRULENT 3 PARTS: - Lipid A - Core oligosacchardie - Unique hydrophilic O-Ag = virulence factor required for escaping phagocytosis. NEGATIVELY CHARGED: bind divalent cations - prevents hydrophobic molecules form crossing OM **LPS ALONE CAN CAUSE DEATH** Lipid A is the toxic part |
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Periplasm
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Between IM & OM
Highly viscous contents: binding proteins (4 chemotaxis), protective enzymes (exotoxins), and ETC |
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PENICILLIN
LYSOZYME AUTOLYSIN |
Penicillin: binds transpeptidase & prevents peptide crosslinks in peptidoglycan/cell wall
--> unstable Lysozyme: BREAKS glycan bonds (backbone of cell wall) - B-1-4 bonds * spheroplast --> protoplast (no cell wall) AUTOLYSIN: "restructuring enzyme" breaking cross-linked bonds - reason why penicilin works - works great on Gram+ strains (staph & strep) |
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ENDOSPORE
ex// Bacillus and Clostridium |
resistant to extreme heat, etc.
*heat to 120degrees* - complex, multi-layered peptidoglycan coat - Calcium dipicolinate stabilizes core |
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BACTERIA TYPES BASED ON OXYGEN NEED
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1. Obligate aerobe: O2 is terminal e- acceptor
2. Facultative anaerobes 3. Microaerophiles: like low [O2] 4. Obligate anaerobes: O2 is toxic 5. Aerotolerant anaerobes: can live in it, but can't use O2 |
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Anaerobic respiration
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electron acceptor is something other than oxygen.
Fermentation: goal is to RE-OXIDIZE NADH for use in glycolysis |
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2 major non-digestible carbs in legumes
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Stachyose & Raffinose
- alpha-galactosyl linkages |
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DEFENSINS
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Part of innate immunity (nonspecific)
- cysteine-rich peptides produced by epithelia & PMNs - broad-spectrum defense antibiotics |
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TERMS OF HOST/PARASITE RELATIONSHIPS
- commensalism - syngerism - opportunism - nosomoial - pathogen - virulence |
1. Commensalims: transient, neutral relationship
- parasite usually benefits (host unharmed) 2. Synergism: 2+ things work together to produce an end result that 1 alone couldn't ex// viral influenza + bacterial pneumonia 3. Opportunism: only capable of dz when host is immune deficient ex// p. jiroveci (fungus) = pcp 4. Nosocomial: acquired at a health facility - usually opportunistic infxn (bacteria) Pathogen = microbe capable of dz Virulence = DEGREE of pathogenicity |
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TISSUE TROPISM
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Microbe's PREFERRED body site
- you can tell by the presence of tissue specific-R (Toll-like R) |
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NORMAL FLORA
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Population of microbes that are in/on humans iN THE ABSENCE OF DISEASE
aka INDIGENOUS FLORA - opportunistic pathogens. |
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BENEFITS OF NORMAL FLORA
**colon has the most normal flora = Bacteroides & fusobacterium** |
1. TRIGGER THE IMMUNE RESPONSE:
- gut flora "primes" T/B cells --> memory pools - "tweaks" immune system (GALT) 2. Bacterial antagonism ex// Lactobacillus in vagina (microaerophilic) 3. Produce nutrients - VIT B & K |
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EFFECTOR LYMPHOID TISSUE
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forms protective immunity at the site of entry
ex// epithelium over GALT has M cells that transport bacteria/Ags from lumen --> lymphoid tissues - Plasma cells in the lamina propria secrete IgA - APCs secrete TGFb to activate CD4 cells - Tregs secrete IL-10 & TGFb to suppress CD4 cells |
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CROHN'S DZ
CELIAC DZ |
CROHN'S:
- genetic predisposition - breakdown of strict regulation of the mucosal immue system's response 2 flora CELIAC: - gluten - immune mediated changes in the villous structure = decreased absorption of nutrients |
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FACTORS DETERMINING HOST/PARASITE RELATIONSHIPS
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1. Availability of oxygen
2. Surface colonization - Adhesins (pili) ,Invasin (integrin-R) = Gram NEGATIVE - Fibronectin (mucosal epith) = GRAM POSITIVE 3. Survival Mechanism: - Masking - Subvert Phagocytosis: capsule, Protein A, inhibit phagocyte recruitment - Survival within phagocytes: inhibit fusion into lysosome or resist enzymes 4. Subvert Immune Responses - Immunosuppression - superantigens - Masquerading (change Ag coats, variable glycoproteins) 5. Proteolysis of Abs: exoenzymes inactivating IgA dimers |
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EXOENZYMES
- coagulase - hyaluronidase - streptokinase - hemolysins |
COAG: microbe can clog/coag plasma even in presence of anti-coag
- fibrinogen --> fibrin HYAL = SPREADING FACTOR - breaks down hyaluronic acid in CT - causes cellulitis STREP = FIBRINOLYSIN - breaks down fibrin clot - used clinically - plasminogen --> plasmin (fibrinolytic) HEMO: rbc cytolysis |
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VIRULENT MICROBIAL TOXINS
- where do they act? - examples |
1. ACT ON HOST CELL SURFACE (landing strip):
- Pattern Recognition-R: Lipoteichoic acid, LPS, Flagella --> bind to TLRs - Pore-forming toxins - Super-Ags: bind outside the cleft 2. MODIFY INTRACELLULAR PROTEINS - Exotoxin AB --> bind to R, endocytose, "A domain" enters cytosol = toxic ex// Gram+ C. dificile toxin A - Type III Cytotoxins: module actin cytoskeleton 3. Exotoxins - mostly GRAM POSITIVE (STILL ALIVE) - used in vaccines (good Ags even when dead) - NO FEVER 4. ENDOTOXINS - from DEAD GRAM NEGATIVE - LIPID A (less toxic than exotoxin) - NOT used in vaccines 5. ENTEROTOXINS - exotoxins working on GI tract - food poisoning = dead bact ex// Staphylococcus |
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SPECIFIC EXOTOXINS
- anthrax - diphtheria - botlism - tetanus |
1. ANTHRAX TOXIN: Bacillus anthracis
- 3pt toxin: protective Ag, edema factor (--> adrenaline overload), lethal factor - inhaled is worst 2. Diphtheria toxin: Corynebacterium diphtheriae - inhibits protein synthesis in euk cells 3. Botulism: Clostridium botulinum - neurotoxin @ NMJ 4. Tetanus Toxin: Clostridium tetani (looks like a racket) - neurotoxin = tetanospasmin: inhibits release of inhibitory NTs - loackjaw/tetanus - SPORES! **EXOTOXINS DON'T ELICIT FEVER** SPORES OF GRAM+ BACILLI ARE SO TOXIC!! |
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endotoxin symptoms
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1. FEVER (not in exotoxins)
2. chills 3. weakness generalized aches shock = extreme cases GRAM NEG SEPTICEMIA = MICROBES IN BLOOD --> CLINICAL SYMPTOMS |
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MICROBIAL ESCAPE TECHNIQUES: AVOIDING HOST DEFENSES
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1. Encapsulation
2. antigenic masking 3. antigenic drift 4. anticomplement strategies 5. subverting phagocytosis 6. subverting the immune response 7. Proteolysis of IgA Abs --> intracellular growth |
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endotoxin symptoms
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1. FEVER (not in exotoxins)
2. chills 3. weakness generalized aches shock = extreme cases GRAM NEG SEPTICEMIA = MICROBES IN BLOOD --> CLINICAL SYMPTOMS |
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MICROBIAL ESCAPE TECHNIQUES: AVOIDING HOST DEFENSES
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1. Encapsulation
2. antigenic masking 3. antigenic drift 4. anticomplement strategies 5. subverting phagocytosis 6. subverting the immune response 7. Proteolysis of IgA Abs --> intracellular growth |
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Prototroph vs. Autotroph
- fermentation mutants |
Prototroph: FEWEST nutritional requirements (usually wt)
Auxotrophs: mutants that require one or more metabolites as supplements not required by the wt to grow - Fermentation mutants: genetic variants that lost their ability to utilize individual sugars |
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Antigenic mutants
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- change the antigens on bacterial envelopes
- "phase variations": some bacteria periodically change their coats |
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Antibiotic resistance
- how do bacteria get it? |
- Resistance is most often acquired as a new genetic trait from another microorganism
- CONJUGATION = #1 Mtts are NOT the most common mechanism - other ways: transduction, transformation |
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POINT MUTATIONS
- transition vs. transversion - Missense: neutral vs. silent - Nonsense - frameshift |
Point mtts are reversible (?)
Transition: Pur --> pur or Pyr --> pyr - caused by UV radiation Transversion: Pur --> pyr - caused by oxidative stress Missense: Diff AA - neutral = new AA is chemically equiv to original - same protein fxn - silent = base change = same aa Nonsense = Stop codon Frameshift = deletion or insertion |
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Suppressor mutations
- intra vs extra - genis |
Additional mutation at a secondary site = restores original phenotype
Intragenic: within the same gene, but not same site at original mtt Extragenic: usually occurs in tRNA gene |
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SPONTANEOUS MUTATIONS
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1. Base mispairing due to tuatomeric shifts & ionizations
--> transitional mtts 2. Strand slippage --> deletions or insertions 3. Spontaneous (chemical changes) - Depurination --> random base sub - Deamination --> transitional |
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Induced Mtts
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1. RADIATION
- xray (ionizing) --> point mtts - UV (non-ionizing) --> thymine dimers 2. Base aNALOGS: EX// 5-bromouracil 3. Base modifying agents: - deaminate, hydroxylate, alkylate, etc. 4. Intercalation - deletion --> frameshirt ex// acridine oragne, ethidium bromide. |
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Mtts with more than a single base
- recombination is carried out by rec genes in bacteria |
Deletions: maybe 2' recombo (usually not reversible
- usually direct repeats Inversions: caused by recombo - invert repeats Insertions: transposons = insertion sequences; usually cause gene inactivation |
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BACTERIAL TRANSFORMATION
- requirements - discovery **ONLY horizontal gene transfer mechanism to use ONLY genes intrinsic to bacterial chromosomes* |
Only COMPETENT cells can use dsDNA (only 1 strand enters cell)
--> cuts it up and recombines with DNA ex// Strep, Bacillus, Neisseria, Hemophilus Artificial transformation: Ca2+ shock, electroporation - but the dsDNA enters whole through spaces in cell envelope Griffith's Pneumonococcus exp: rough colonies took up smooth colony DNA from dead bacteria --> virulent |
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TRANSDUCTION
- GENERAL *temperate phages can reproduce w/o killing host* |
TEMPERATE BACTERIOPHAGES CARRY DNA FROM ONE BACTERIA TO ANOTHER
- generalized: any gene - only bacterial - Specialized: specific genes - both prophage & bacterial genes (next to prophage insertion site) |
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GENERALIZED TRANSDUCTION
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- transducing viruses are made during the LYTIC cycle of a temperate virus
- transducin particles = ONLY bacterial dna (NOT PHAGE GENES) - host DNA = any region of donor genome VIRUS REQUIREMENTS: - phage can't destroy host DNA completely during lytic cycle - phage uses indiscriminate head-filling mechnaism for dsDNA packaging *transduced DNA must recombine w/ host genome (part of a replicon) |
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SPECIALIZED TRANSDUCTION
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- Produced by induction of a lysogen
- Only genes next to insertion site can be transferred - Phage + bacterial genes (not used for mapping) - Specific insertion site for temperate phage - aberrant excision |
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PHAGE CONVERSION
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Normally, only genes needed to maintain repression are expressed during lysogeny
Some phages carry genes that remain active during lysogeny --> gives lysogenic cells new traits ** genes are a PERMANENT PART of the viral genome ** --> bacteria become VIRULENT 2' prophage genes |
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examples of virulent bacteria 2' phage conversion
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1. C. diphtheriae: b-phage has tox gene
2. V. Cholerae: 2 phages --> pili & filaments = diarrhea 3. E. coli: 3 phages --> stx & hemolysin genes 4. toxic shock syndrome - neurotoxins in staph aureus & botulinum, tetanus |
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CONJUGATION
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BACTERIA SEX
- MOST EFFICIENT; majority of horizontal gene transfer 1. F+ x F- conjugation - F plasmid can integrate into bacterial chromosome --> Hfr 2. Hfr x F- conjugation - recipient cell stays F- - unidirectional 3. Mobilizable plasmids - small R-plasmids use conjugation bridges set up f plasmid in the same cell 4. Conjugative transposons - nonhomologous recombo |
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PLASMID CLASSES
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1. Resistance plasmids
2. Virulence: ex// bacillus anthracis 3. Genetic transfer fxn: f plasmid 4. Bacteriocins 5. Degradative: esp soil microbes |
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F+ x F- conjugation
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F pilin --> conjugation bridge
- Single-stranded nick at oriT - transferred 5' --> 3' - recipient cell only gets ssDNA - plasmid is a complete replicon - recipient cell = F+ super fast and efficent |
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CHROMOSOMAL INTEGRATION OF F PLASMID
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- NOT site specific (unlike phages)
- infrequent = Hfr cell (high frequency of recombo) |
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Hfr x F- conjugation
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1. plasmid nuclease nicks 1 strand at oriT
2. Rolling replication starts at 3' end of nick 3. Sequential, unidirectional, 5' --> 3' gene transfer 4. Rarely complete transfer - F- cell only gets a few bacterial genes from donor 5. DNA fragments must recombine (homologous recombo) |
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CONJUGATIVE TRANSPOSONS
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- COVALENTLY CLOSED CIRCULAR INTERMEDIATES
= NONHOMOLOGOUS RECOMBO - intracellular or intercellular transposition (via conjugation) ex// tetracycline resistance |
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GRAM POSITIVE BACILLI (RODS)
- types |
ENDOSPORE FORMING:
1. BACILLUS: aerobic - bacillus anthracis - bacillus cereus 2. CLOSTRIDIUM: anaerobe - c. perfringens (gas gangrene) - c. tetani - c. botulinum - c. dificile NON-ENDOSPORE FORMING RODS: 1. CORYNEBACTERIUM: - c. diphtheriae 2. Listeria: - listeria monocytogenes |
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BACILLUS
- morphology & culture |
AEROBE
- or facultative anaerobe - gram POSITIVE - grow well on ORDINARY MEDIA |
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BACILLUS ANTHRACIS
- INCIDENCE, EPIDEMIOLOGY, TRANSMISSION |
SOIL, VEGETATION
- ZOO-NOSIS: anthrax is mainly a herbivore dz - we eat these animals and get sick **bioterrorism*8 |
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B. ANTHRACIS
- VIRULENCE FACTORS |
1. POLY-D-GLUTAMIC ACID CAPSULE
- not polysacc - antiphag 2. ANTHRAX TOXIN: - from a plasmid - NOT hemolytic - 3 distinct Ags --> 2 toxic molecules: PA, EF, LF *Acts exotoxin AB* Protective Ag is binding domain & EF or LF is the Active (A) domain - edema factor = ^ cAMP intracell = cell loses water --> edema - Letal factor: zinc metalloprotease cleaving MAPK --> cell death |
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B. ANTHRACIS AND HUMAN DISEASE
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1. CUTANEOUS: malignant pustule
- vesicular / bullous lesion w/ PERIPHERAL NONPITTING EDEMA - BLACK PAINLESS CENTRAL ESCHAR 2. GI ANTHRAX: - bad GI syptoms 3. INHALATION (woolsorter's) - spores are inhaled & carried to lymph nodes **WIDENED MEDIASTINUM*** - feels like cold, but no runny nose or sputum - pleural effusions |
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b. anthracis
- dx & tx **there is a vaccine** - nonencapsulated strain |
dx:
- establish animal exposure = GI - cutaneous: painless black center - inhalataion = WIDENED mediastinum ( not always ) *microscope: BIG, GRAM+ BACILLI WITHOUT ENDOSPORES* - don't sporulate in tissues *PCR or y phage lysis = confirms culture tx: cipro or doxy |
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B. CEREUS
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food poisoning (starchy foods like rice)
- enterotoxins - acute: within a few hours - emetic form vs. diarrhea form. ( Heat stable toxin (made outside body) vs. heat-labile toxin(made in intestines)) *also has bacteriocins* |
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CLOSTRIDIUM
- MORPHOLOGY - CULTURE - DISEASES |
- GRAM POSITIVE
- ENDOSPORE FORMING BACILLI - STRICT ANAEROBES (some are aerotolerant) *diseases* - tetanus - botulism -gas gangrene -psuedomembranous colitis (abx-assc'd) |
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c. dificile
- Physio & stricture - virulence factors |
gram +, spore forming bacilli
- strict anaerobe virulence: toxinA: ENTEROTOXIN: INTESTINAL FLUID SECRETION, mucosal injury, hemorrhagic necrosis toxinb: cytotoxin: depolymerization of actin --> no cell cytoskeleton |
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CDAD
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endog or environmental
- Abx can change normal enteric flora --> c. dificile OVERGROWS & RELEASES TOXINS--> inflamed colon --> exudative plagues (pseudomembrane) --> pseudomembranous (abx-assc'd) colitis, toxic megacolon - colon perf - sepsis - death **watery diarrhea = big symptom |
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c. dificile
- EPIDEMIOLOGY **becoming almost as bad as MRSA (ca-cdi) - TRANSMISSION |
- part of NORMAL enteric microbiota (< 5% people): "colonized" people
**IATROGENIC & NOSOCOMIAL** (from oral abx) - CA-CDI = Community acquired: MORE FREQUENT, more serious, less tx'able TRANSMISSION: - shed in fecs - anything can be storage depot for SPORES - Transferred via hands (alcohol gel doesn't kill spores!) |
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c. dificile
- diagnosis |
Isolate bacteria or detect Toxin A or b in pt's feces
- EIA = toxin A - New membrane test: c. DIFF Ag & toxin - colonoscopy = NASTY YELLOW BUMPS ON COLON EW. |
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CLOSTRIDIUM TETANI
- structure - epidemiology |
SMALL, motile, endospore+, gram+
(commonly stains gram NEGATIVE) - strict anaerobe *loosk like a drumstick - terminal endospore* bacteria is everywhere - many neonates die from it |
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c. tetani
- disease **local toxin --> systemic reaction |
Incubation: days --> weeks (tetanospasm travels via retrograde axonal transport)
- tetanus works on presynaptic terminals of INHIBITORY neurons (prevents release): Gly & GABA = SPASTIC PARALYSIS - trismus - risus sardonicus - dysphagia (can't swallow) - cardiac arrythmias |
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c. botulinum
- structure - epidemiology |
gram+, OBLIGATE ANAEROBE, endospore+
- super potent toxins - bacteria is everywhere: home canned oods - classic/foodborne botulism - infant - wound |
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C. BOTULINUM
- disease - classical - dx |
toxin is released in inactive form & cleaved
- affects axon terminals of efferent motor neurons = FLACCID paralysis * food poisoning & predominantly MOTOR/NEURO symptoms dx: - clinical dx b/c lab culture takes too long - isolate the bacteria/toxin from food or feces - mouse biassay |
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C. PERFRINGENS
- Structure - virulence -epidemiology |
STRUCTURE: big, rectangular, gram+,
- makes endospores, but it's not seen in clinical specimens - aerotolerant anaerobes - ALPHA TOXIN: lecithinase, hemolysin, increases vascular perm *bacteria is everywhere - endog or exog exposure |
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c. perfringens
- diseases & dx gram stain & cx: spores usually not seen |
- GAS GANGRENE & other soft tissue infxns
- food poison - speticemia - myonecrosis * can cause shock & death * |
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CORYNEBACTERIUM
- morph & culture - epidem |
SMALL, PLEOMORPHIC, GRAM+ RODS, NO SPORES
- CLUB SHAPES (CORYNE) - ANGULAR PAIRS (V & Y forms): chinese letters - METACHROMATIC granules - methylene blue COLONIZE skin & mucus membranes - C. diphtheria: poor people disease of the projects/old people - transferred via resp. droplets & skin |
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C. DIPTHERIAE
- DISEASE LOCALIZED DISEASE W/ GENERALIZED TOXEMIA |
RESP:
- 2-6 incubation while bacteria multiply locally on pharynx - Bull-necked: edema 2' exotoxin - Exudative phayngitis: thick pseudomembrane (can't remove w/o bleeding) --> can obstruct airway = suffocate * cytotoxin is released & disseminated via lymph & blood * - bacteria stay in epithelium - exotoxin AB --> inactivates elongation factor --> no protein synth **toxins are from lysogenic bacteriophage** --> heart & liver damage |
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C. DIPHTHERIA
- DX |
CULTURE:
- nasopharynx & throat samples - culture on loeffler's serum medium & tinsdale telurate agar - test for exotoxin TOXIGENICITY TEST: - in vivo: mouse - in vitro: elek plate - test for precipitation of toxin & anti-toxin * microscope sucks bc there are nonpathogenic diphtheroids in resp tract that look like c. dipht |
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DIPHTHEROIDS
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NON-TOXIGENIC CORYNEBACTERIUM SPECIES
- morpho same - same locations - opportuinstic pathogens - abx-resistnat |
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LISTERIA MONOCYTOGENES
- morpho, culture -epidem **don't confuse w/ streptococci **affects people w/ crappy cell-mediated immunity** |
NO SPORES, short, gram+, rods (coccobacilli)
- tumbling motility - FACULTATIVE ANAEROBES: like acidic, salty, wide temperature ranges (survive in fridge - low temps) * food-borne pathogen --> bacteremia & meningoencephalitis w/ FEW GI - Listeria's LIST: Preggers, neonates, elderly & immunocompromised * don't eat milk, soft cheese, & deli meat INTRACELLULAR PARASITES: listeriolysin O & phospholipases prevent phagolysosome fusion |
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L. MONOCYTOGENES
- VIRULENCE & DISEASE |
facultative INTRACELL pathogens
- ActA protein (internalin) can mediate actin-directed motiligy 1. enters SI 2. E-cadherin receptors induce uptake 3. Pore forming hemolysin escapes phagolysosome 4. Multiplies in cytosol 5. Uses ActA to polymerize actin at one of its cells 6. propels itself into another cell (cell-cell transmission) *most are asymptomatic* - MENINGITIS= most common - only super immunocomprised are at risk of primary bacteremia |
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L. MONOCYTOGENES
- DX |
CULTURE #1
- microscope sucks bc CSF gram stain usually lack visible bacteria (intracell) |
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PYOGENIC COCCI
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1.Staph
2. Strep 3. Enterococcus (fecal strep) 4. Neisseria |
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STAPHYLOCOCCI
- morph - growth - epidem |
GRAM+, spherical, clustered (staphule = grape bunch)
- facultative anaerobe - may appear singly or small clusters *NOT fastidious *MOST resistant of non-spore forming pathogens: - withstand salty, dry, hot, abx EPIDEM: - SKIN & Mucous membranes - fibronectin-R + teichoic acids. **STAPH = #1 CAUSE OF NOSOCOMIAL INFXN |
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Distinguinshing bw STAPHYLOCOCCI
- s. aureus vs. others |
S. AUREUS = PRIMARY PATHOGEN
- others are opportunists **COAGULASE TEST IS THE MOST IMPORTANT** - aureus = POSITIVE - other staph = NEGATIVE - Staph aureus also has +DNase production and +Mannitol fermentation, +Total hemolysis.. **other staph = CoNS - CoNS: opportunistic pathogen, make thick capsules, biofilms, and major cause of endocarditis of artificial valves. |
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STAPHYLOCOCCUS AUREUS
- VIRULENCE FACTORS |
1. surface proteins: adhesins, fibronectin binding proteins
2. Invasin: leukocidin, kinases (fibrinolysis), hyaluronidase 3. Escape phagocytosis: Capsule, Protein A (binds Fc), Coagulase (pro-clot) 4. Survive phagocytosis: Catalase 5. Imm. Disguises: Protein A, Coagulase 6. Membrane-damaging toxins: Alpha toxin (porin), Hemolysin, leukotoxin/cidin 7. Exotoxin: Toxic shock, Epidermolytic/Exfoliatin, Staph enterotoxins - TSST, ET, SE 8. Acquired resistance to antimicrobial agents |
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STAPH AUREUS EPIDEM
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LIVES IN ANTERIOR NARES
-community-acquired infxns = auto-infxns *CA strains of staph are tx-able with most Abx (except beta-lactams) *BUT, CA-MRSA is more virulent & infxns are more invasive **spread is assc'd with poor hygiene& |
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S. AUREUS DISEASES
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PYOGENIC:
- folliculitis - furuncles (boils) - carbuncles -impetigo - wound infxn SYSTEMIC: - Pneumonia - septicemia - empyema - septic arthritis - osteomyelitis - acute endocarditis TOXIGENIC - TSS - Food poisoning - scalded skin syn |
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PYOGENIC INFXN OF S. AUREUS
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Folliculitis: most common, small
Stye: folliculitis at base of eyelid Furuncle = boil folliculitis --> furuncle --> Carbuncle (interconnecting furuncles deeper in SC tissue) *impetigo: not confined to hair follicle - spread throughout epidermis **these infxns are common in kids** - face & limbs |
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SYSTEMIC INFXNS:
*FOCAL PATTERN: spreading from a local cutaneous infxn to other sites (esp bone) |
1. osteomyelitis: metaphysis
2. Pneumonia: aspirated from nose - usu. when carrier is already fighting 1 infxn - or from hematogenous spread *50% fatality* 3. Bacteremia - Insulin-dept diabetes & vascular graft - indwelling intravasc catheter 4. Endocarditis: 50% die - s. aureus & CoNS infxn can occur |
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TOXIGENIC STAPH AUREUS DISEASE
- TOXIC SHOCK SYNDROME |
1. TSS: TSST-1 growing in vag or wound
- DIFFUSE MACULAR ERYTHEMATOUS RASH (flat, red) - desquamation of skin **staph enterotoxins B & C are also super-Ags SHOCK, BLANCHING RASH, FEVER - DON'T develop protective Abs STAPH TSS: minor/surface colonization, +rash, NO bacteremia tx: clinda & erythromycin & vanc - add 3rd gen cephalosporin to cover gram NEG bact |
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TOXIGENIC STAPH AUREUS DISEASE
- scalded skin syndrome - infects who? where? |
- Kid (<4 yo)
- infection of umbilicus or eyes EXFOLIATIN (exotoxin AB) *ABRUPT onset of localized perioral erythema --> covers body w/in 2 days - large bullae (cut. blisters) --> desquamation - recovers when protective Abs appear in a week |
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TOXIGENIC STAPH AUREUS DISEASE
- STPAH FOOD POISONING *infection type: eat living bacteria, which release toxins once they're inside you (typhoid & cholera) |
Enterotoxin is made BEFORE you eat it (intoxication type - like botulism)
- transferred from PEOPLE SYMPTOMS: - FAST GI SYMPTOMS - SHORT (<24 hr) *staph can grow in salty/sugary foods (osmotolerant bacteria)* - heat stable enterotoxin **POTLUCK POTATO SALAD** |
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TREATMENT OF STAPH INFXN
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1. Pencillinase-resistant penicillins for MSSA
- ex// flucloxacillin, cloxacillin, oxacillin 2. or 1st Gen cephalosporins & beta-lactam inhbitior combos ex// augmentin **staph is super abx-resistant** + beta-lactamase: penicillin & amp resistant +MRSA **ALWAYS INCLUDE VANC IN INITIAL ABX REGIMEN FOR LIFE THREATENING INFXNS** |
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streptococcus
- morpho - physio - culture **use catalase to distinguish b/w staph & strept |
PYOGENIC
- GRAM+ spherical - +capsule (virulent) - non-endospore - non-motile - AEROTOLERANT anaerobe - LACK CATALASE & oxidase *catalase splits H2O2 & releases O2* --> requires enriched media (like blood agar) - small, nonpigmented colonies - kinda fragile |
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STREPTOCOCCUS CLASSIFICATION
for serology: used C carb antigens on cell wall |
1. Hemolytic Pattern:
- beta: complete, clear zone around colonies - alpha: incomplete (green zone) - gamma: NO hemolysis 2. Clinical: pyogenic, oral, enteric 3. Serological: - GROUPA: Pyogenes - primary human pathogen - GROUPB: strep. agalactiae - neonatal infxns - GROUPC: animal pathogen mostly - GROUPD: enterococcus faecalis (UTIs) |
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STREP VIRULENCE FACTORS
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1. EXTRACELLULAR STUFF (EXOTOXINS)
- STREPTOKINASE (fibrinolysis) - Streptodornase (DNase) - Hyaluronidase - pyrogenic (rash, superAgs, TS-likeS & necrotizing fasciitis *strawberry tongue of scarlet fever* - Hemolysins: Streptolysin O & S 2. CELL SURFACE: - M protein: colonization & resist phag * rheumatogenic --> autoimmune rheumatic carditis - Capsular polysacc (C-substance) - Fibronectin-binding protein (f protein) - Lipoteichoic acid (adherence) |
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STREP
- SOURCES, MODES OF INFXN |
HUMANS STORE DZ
1. S. pyogenes= children - S. pneumoniae: kids (adults) - S. agalactiae & enterococcus faecalis = colon |
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STREPTOCOCCUS PYOGENES
(GAS) - diseases **staph TSS usu DOESN'T have bacteremia - desc |
GROUP A, BETA HEMOLYTIC
- most virulent (95% of dz caused by strept) - CARRIED BY KIDS 1. Streptococcal pharyngitis: strep throat 2. Pyodrema (impetigo): young kids - purulent infxn: vesicle --> pustule 3. Scarlet Fever: throat infxn --> erythrogenic toxin - red, diffuse rash (strawberry tongue) - make Abs; no recurrent rash 4. Erysipelas: skin --> dermis & sc tissues - vesicular eruptions 5. NECROTIZING FASCIITIS - cellulitis --> bullae --> gangrene/massive tissue necrosis --> multiorgan fail & sytemic problems 7. strep TSS: - assc'd with bacteremia, soft-tissue infxn, shock, multiorgan fail - hx of minor trauma, recent sx, varicella infxn |
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NONSUPPURATIVE SEQUELLAE TO STREP PYOGENES INFXN
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1. Rheumatic Fever
- 2-3 AFTER infxn - inflamm changes in heart, joints, vasc - Cross-reactivity of Abs to M proteins 2. ACUTE GLOMERULONEPHRITIS: IC dep. - days-weeks post-infxn - mostly in kids |
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DIAGNOSIS & TX OF GAS INFXN
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DX: CULTURE OR RAPID STREPT TEST
- culture takes 2 days - strep test has high false negative TX: aMOX + CLAVULANATE, oral cephalosporin, or clinda |
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STREP PNEUMONIAE
- DESC - EPIDEM |
Alpha hemolysis
- dplococcal - +capsule ( MAJOR virulence factor ) - bile solubility: autolysin activated by bile salts HUMANS CARRY IT IN NASOPHARYNX **daycare, prisons, etc** most common agent in community-acquired pneumonia |
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PNEUMOCOCCAL DISEASES
- mech - dx -tx **PREVNAR VACCINE** - QUELLUNG REACTION USED TO TYPE THE PENUMOCOCCAL STRAIN (capsule Ag) |
anything that impairs mucociliary motion/cough reflex can cause s. pneumoniae to travel down --> LRI
Mech: Cell wall & pneumolysin = INTENSE INFLAMM (activates C') --> LEUKOCYTES come --> ^ exudative fluid --> consolidation, radioopacity, poor gas exchange = pneumonia DX: - CHEST XRAY REQUIRED - distinguish b/w strep pneumo & strep viridans *s. pneumo is inhibited by OPTOCHIN --> zone of inhibition TX: - DOXY, any cephalosporin (if MDRSP isn't suspected <-- quinolone or telithromycin) |
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OTHER S. PNEUMO DISEASES
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1. MENINGITIS
- S. Pneumo is most common cause of bact. meningitis (used to be h. influenzae <--Hib vacc) 2. Acute otitis media - most common cause - via eustachian tube - amox = #1 abx |
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ENTEROCOCCUS FAECALIS
- DESC - EPIDEM |
GROUP D STREP, LIVE IN LARGE INTESTINE
- facultative anaerobes - grow anywhere - super RESISTANT; SURVIVORS - salty, high temps, bile *most infxns are endogenous* at risk: - long hospitalization or long abx course of broad spectrum abx |
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ENTEROCOCCUS FAECALIS
- diseases - tx |
- Nosocomial infxn (catheters)
- UTIs - bacteremia & ednocarditis (like others) - wound infxns (esp intraabd) TX: - COMBO of aminoglycosides w/ cell wall-active abx *>20% are vanc resist (VRE) = tx w/ lanezolid - resistance is plasmid mediated --> transfer to other bacteria (dif. species) |
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STREPTOCOCCUS AGALACTIAE
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GBS
- septicemia, pneumonia, meningitis in NEONATES - GRAM+ cocci chains, BETA hemolytic - catalase negative + capsule colonize LOWER GI & GU TRACT (babies get it from mom) in adults: skin, soft tissue infxn, bacteremia, UTI, pneumonia |
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GBS
- DX -TX * ALL pregnant women need to be screened for colonization @35 wks and treated* - IV penicilin G before delivery |
dx:
- hydrolyze hippurate & + cAMP test - yellow color, narrow zone of beta hemolysis tx: penicillin G. (benzylpenicillin) - |
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VIRIDANS STREP.
(green = viridans) |
ALPHA HEMOLYSIS - GREEN, INCOMPLETE
- oral cavity normal flora - opportunistic bitches *abx are prophylactically prescribed to dental pts w/ damaged heart valves (previous rheumatic fever) - eat up the valve slowly unlike staph |
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LACTOCOCCUS LACTIS
(LACTOCOCCI) |
NON-hemolytic, non-pathogenic
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GRAM NEGATIVE ENTERICS
- MAJOR GROUPS * = BELONG IN ENTEROBACTERIACAEAE FAILY |
ALL ARE GRAM NEGATIVE RODS
- mainly diarrhea, UTI, & bacteremia MAJOR GROUPS: 1. COLIFORMS: *E. coli, *enterobacter, *Klebsiella 2. Pathogens: *Salmonella, *sHIGELA 3. OPPORTUNISTS: *SERRATIA, *PROTEUS-MORGANELLA-PROVIDENCIA, PSEUDOMONAS 4. VIBRIOS & related: vibrio, campylobacter, helicobacter |
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ENTEROBACTERIACEAE FAMILY
- commons - Ag structure |
short, gram- rods
- normal flora - facultative anaerobes - nonfastidious - genetic xchange can occur across different genera common: 1. ferment glucose w/ acid production 2. Reduce nitrates to nitrites 3. Don't make oxidase Somatic Ags: R (nonspecific polysacc) & O (very specific) Flagellar: H Ags (phase variation - flip flop) Capsular: K & Vi Ags (pathogenic) Pili Ags |
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ESCHERICHIA COLI
- desc - classes of pathogenic e. coli (7) **E. coli is friends w vibrio & shigella - can look like either (ETEC & EHEC/EIEC) |
small, STRaight, gram- rods, single
- normal / motile / maybe capsule 1. NPEC: #1 cause - UTIs, hemolysin, capsule, P pilus 2. ETEC: Traveler's diarrhea, LT (ac) & ST (gc) exotoxins - similar to cholera toxin (^cAMP & cGMP) - rice water poo 3. EPEC: infantile watery diarrhea, bundle-forming pili, O Ags 4. EHEC: Hemorrhagic colitis & hemolytic uremic syndrome (kids) - 0157:H7 serotype (ground beef); verotoxin/Shiga-like = kills kidney cells Developing countries: EIEC (enteroinvasive - like shigella) & EAEC (enteroaggregative) 7. E. coli causing neonatal meningitis: K1 Ag on capsule |
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E. COLI
- DX *coliforms = normal inhabitors of colon* |
SPECIMENS: urine, stool, csf
blood agar = hemolytic colonies macConkey's agar = pink colonies (lactose+) EMB agar = iridescent *these media inhibit gram+ bacteria & select for lactose fermenters |
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KLEBSIELLA PNEUMONIAE
- live in? - virulence - diseases |
- intestinal & resp tract
Virulence: - big, jello capsule (large halos) - K1 & K2 Ags Diseases: - acute bacterial pneumonia: lobar (bloody, necrotizing, consolidation) pneumonia, currant jelly sputum, fatal - UTI dx: mucoid colonies, lactose+, nonmotile K. ozenae & K. rhinoscleromatis also cause URI dz |
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SALMONELLA
- characteristics - diseases - classification |
Lactose negative
H2S positive = black media Motile Typhoid fever: s. typhi Bacteremia: s. enteritidis Enterocolitis: s. typhimurium Kauffmann-White scheme of classification: O, H, & Vi antigens are used. |
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SALMONELLA
- bacteremia - enterocolitis tx |
Bacteremia:
- usually only in pts w/ chronic underlying disease - early invasion of blood after ingestion - spiking fever, FOCAL LESIONS, NO DIARRHEA ENTEROCOLITIS: - MOST COMMON result of infxn - 12-72 hours incubation - diarrhea & GI symptoms, low fever - self limiting tx: cipro *sepsis danger is always there* |
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SALMONELLA TYPHI
- symptoms - dx / tx *facultative intracell parasite* |
Human feces: LOTS needs to be ingested
SI --> peyer's, lymph, blood --> organs (gallbladder) *loves to grow in bile* Incubation 1-2 weeks (variable) symptoms: - super high fever, - constipation --> BLOODY diarrhea - rose spots - delirious, hepatosplenomegaly * MULTIPLY in macros (not killed by them)* Anti-Vi Ab in serum = diagnostic tx: cipro |
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SHIGELLA
- dysentery |
enterobacteriaceae family
- gram negative - lactose negative - DON'T produce sulfur - NONmotile - S. dysenteriae - transmitted via Flies, Fingers, Feces, Food & water BACILLARY DYSENTERY: - inflamm & sloughing of intestinal wall - dz of institutions (daycare) - SUPER infectious (don't need a lot) - NEVER invade blood - Virulence: LPS, shiga neurotoxin = enterotox & neurotox (meningismus) - HALLMARK: BLOOD & PUS IN STOOL - also: watery diarrhea, rectal spasms - self-limiting w/in 4-8 days (multiple drug resistance is very common) |
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SERRATIA MARCESCENS
- OPPORTUNISTIC BITCH - DESC - CLINICAL - TX |
COLON
- LACTOSE NEGATIVE - Exotoxin: DNase - bright red pigment (but humans = achromogenic) OPPORTUNIST - septicemia,local cllulitis, catheters infxns, burns, pulm, - high ABX resistance (like other opportunists) |
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PROTEUS-MORGANELLA-PROVIDENCIA GROUP
- OPPORTUNISTS |
ALL LACTOSE NEGATIVE
ALL UREASE + (except maybe prov. H2S + : Proteus (Salmonella is only other enterobacteria) H2S - : Morganella & providencia *Frequent cause of UTI & kidney stones |
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PSEUDOMONAS AERUGINOSA
- OPPORTUNISTIC enteric - infxns - virulence |
small, gram negative rods
- SUPER HARDY & everywhere - motile - NON-fermenter (obligate aerobe) - Oxidase+ - pigments: pyocyanin & pyoverdin - smells fruity burn infections = green pus Ecthyma gangrenosum: assc'd w/ bacteremia Virulence - pili (epithelia), adhesins (mucins) - capsule (alginate polysacc) - exotoxin A (same mech as c. diptheriae - inhibit protein synth) - LPS - many exoenzymes - efflux pumps: pump out Abx infect 2/3 of super sick pts - combo of many Abx - ^ fatality rate |
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VIBRIOS
general |
curved, comma gram negative rods
- salty (halophilic): except for v. cholerae - OXIDASE+, Motile |
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VIBRIO CHOLERAE
*other vibrios are related to contaminated seafood (diarrhea or skin lesions) |
waters & people (developing countries)
- like high alkaline pH O1 serogroup: ALL cholera - classic: more severe - El Tor: more prevalent, not as bad Choleragen: enterotoxin like LT of e. coli ( ^cAMP = MASSIVE fluid loss) - die after 12-18 hours - rapid dehydration - RICE WATER STOOLS: water, NON-BLOODY diarrhea w/ mucus flecks tx: self limiting - give lotsa fluids |
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CAMPYLOBACTER JEJUNI
enteric |
small, gram negative, CURVED rod (vibrio-ish; S shaped)
- motile - birds & animals, oral-anal activity MAJOR human pathogen - enterocolitis (~ dysentery) - enteric fever (if in blood) - cholera-like enterotoxin - self limiting in 2-7 days isolationg requires minimal o2 & Abx+ media - easily treated w/ abx |
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HELICOBACTER PYLORI
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Curved, spiral gram negative rod
- motile - urease + hides deep in mucous layer of stomach (in healthy pts too) - urease breaks down urea --> ammonia protective cloud - mucinase - rapid motility * gastritis & ulcers - no bacteremia tests: - same media as campylobacter, - urease breath test - gastric biopsies |
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NEISSERIA
butthead (N. meningitidis & N. gonorrhoeae) |
GRAM NEG DIPLOCOCCI
- fastidious: chocolate agar / Thayer-Martin - 5% CO2 (capnophilic), NONhemolytic - use ferment carbs to differentiate species. - non-motile microscope: INTRACELLULAR diplococci *use nucleic acid amp & genetic probes to dx* |
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N. gonorrhoeae
culture & physio **all microscope negatives must be confirmed w/ culture** |
gram neg diplococci
- fastidious: choc agar & thayer-marin - capnophilic (5% co2) oxidase+, catalase+, IgA protease - ferment carbs: differentiate species *ferments glucose ONLY (not maltose or sucrose) |
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n. gonorrhoeae
- virulence - epidem *only ferments glucose (for Gonorrhea) |
virulence: (NO exotoxins)
LPS - lipid A = major virulence adhesins: pili Invasins: Opa, Por (OM) IgA protease b-lactamase #2 STD (50% women are asympt) |
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n. gonorrhoeae
- clinical dz - symptoms in men/women/infant |
DZ:
Pili: long dist attch Por: close attch to mucosal columnar cells Endocytosis: Por prevents fusion 2 lysosome LPS: stimulates inflamm, TNF-a, cytotoxic Male: 2-7 day incubation - PURULENT urethral dc, dysuria women: cervix - vag dc, dysuria, abd pain SCARRING --> PID, salpingitis, infertile, ectopic preg infant: Purulent conjunctivitis --> blindness |
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n. gonorrhoeae
- tx |
ceftriaxone or cEFIXIME
plus tx for chlamydia (azithro or doxy) |
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NEISSERIA meningitidis
- culture (virulence) - epidem/transmission |
GRAM NEG DIPLOCOCCI
transparent, nonpigmented, nonhemolytic, colonies; fastidious Virulence: Polysacc capsule & LPS (IgA Protease & pili) Incidence: Kids <5 yo & 12-24 yo Transmission: resp droplets |
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n. meningitidis
- pathogenesis *ferments maltose & glucose* |
1. Pili: colonize non-ciliated epithilium of nasopharynx
2. virulence factors do their thing 3. CROSS mucosal barrier --> bloodstream (septicemia) 4. Type IV pili+ (PilC): breach BBB --> meningitis |
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N. MENINGITIDIS
- DISEASES |
1. MENINGOCOCCEMIA
septicemia w/ or w/o meningitis + petechiae or purpura w/in 1-3 days 2. Meningococca meningitis - fatal if untreated - stiff neck, headache, nausea, FEVER 3. penumonia 4. arthritis, urethritis |
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N. MENINGITIDIS
- TX |
Penicillin G or cEFTRIAXONE
* abx prophylaxis for those exposed (military)* |
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Moraxella catarrhalis
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LOOKS LIKE NEISSERIA (diplococci)
- makes beta-lactamase - gram negative causes LRIs & #3 cause of Otitis media in healthy kids |
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KINGELLA KINGAE
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OXIDASE+, nonmotile, gram- coccobacillus (looks diplococcus like neisseria)
- HEMOLYTIC (unlike neiss). - in MOUTH, causes bone/joint/tendon infxns |
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Haemophilus
- culture needs - morpho - epidem |
FASTIDIOUS GRAM NEGATIVE COCCOBACILLUS
only humans - nasopharynx - most LACK a capsule (except influenzae & parainfluenzae) Need x factor (hgb) & V factor (NAD - yeast extract) - grows on chocolate agar (not blood) **only encapsulated strains are invasive** |
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Haemophilus
- culture needs - morpho - epidem |
FASTIDIOUS GRAM NEGATIVE COCCOBACILLUS
only humans - nasopharynx - most LACK a capsule (except influenzae & parainfluenzae) Need x factor (hgb) & V factor (NAD - yeast extract) - grows on chocolate agar (not blood) **only encapsulated strains are invasive** |
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H. INFLUENZAE
fastidious gram negative coccobacillus - strain types - clinical interest - Virulence factors |
2 Strain types: encapsulated (Polyribitol phosphate) vs not (nontypeable)
Type b strain = encapsulated, invasive infxns (meningitis, epiglottitis), vaccine exists CHILDREN = SOME - Sinusitis, OM, Meningitis, acute Epiglottitis Virulence: - PRP Capsule = MAJOR *Opsonin = Ab against tybe b - IgA Protease (mucosa) - OM proteins & LPS (ciliostasis) - Pili - |
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H. INFLUENZAE
- meningitis features (compare w/ neisseria & strep) - adult diseases - lab dx. |
6mo-3yo: MENINGITIS
- low mortality & sequelae - subacute (1-2 days) - children <5 *N. meningitidis: + rash *S. pneumoniae: <2 yo, high mortality, follows pneumonia/septicemia ADULTS: - Pneumonia in crappy immunity (copd, etc) *NONTYPEABLE H. flu is responsible for these infxns* Labs: -Gram stain NEGATIVE -Culture on chocolate agar & satellite phenomenon (Staph strip) -Immuneoelectrophoresis |
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H. Influenzae
- tx / prevention |
cephalosporins
rifampin prophylaxis for active carriers Hib conjugate vaccine (type B polysacc) |
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H. parainfluenzae
H. aegyptius H.ducreyi |
h.p = subacute bacterial endocarditis
h.a: pink eye (contagious conjuncitivits) h. ducreyi: Venereal dz (chancre) |
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BORDETELLA PERTUSSIS
(WHOOPING COUGH) - morpho - culture needs -epidem |
FASTIDIOUS GRAM NEGATIVE COCCOBACILLUS
virulent strains = cap'd - Bordet-Gengou medium / Regan-Lowe medium Pts: young infants w/o vaccine & 5-10 yrs post-vaccine Air-borne droplets - only for humans |
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BORDETELLA PERTUSSIS
- VIRULENCE FACTORS |
1. Pertussis Toxin: Adhesin & toxin
- binds ciliated resp cells - Inactivate Gprotein (adenylate cyclase still on, ^cAMP) = mucus production ^ - Inhibits phag, monocyte - LYMPHOCYTOSIS in blood 2. Adenylyl cyclase/hemolysin toxin - ^ intracellular adenylate cyclase & ^ cAMP - same as pertussis kind of (^ mucus) 3. .TRACHEAL TOXIN: peptidoglycan - kills ciliated resp cells - IL-1 Released --> ^ NO? **Prolonged cough of whooping cough is due to tracheal toxin (KILLS cells; need to grow new ones) |
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B. PERTUSSIS
- DX - tx |
- CLASSIC; ^ WBC = 15-30 X 10^3
(apparent lymphocytosis - trapped & cant get to lymphoid tissue) *pertussis toxin* - Serologic dx: IgG or IgA to PToxin - PCR - Culture - DFA TX: - supportive care: most seek tx in paroxysmal stage (2-4 wk) when bacteria are dying - Macrolide = erythromycin (prevent spread) - DTaP: acellular vaccines |
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b. pertussis
- stages - bact growth |
Incubation: 7-10 days
- no symptoms - exponential growth Catarrhal: 1-2 wks - "meh" symptoms - MAX bacterial growth (express autolysin now) Paroxysmal: 2-4 wks - AWFUL symptoms: vomiting post cough, leukocytosis - bact growth dying down - abx here won't help get rid of bacteria Convalescent: 3-4+ weeks - no bacteria - secondary complications: pneumo, seizures, encephalopathy |
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ANAEROBIC BACTERIA
- cause of abscess formation - where are they? - clues tx: surgical I & D, debridement, and abx |
OPPORTUNISTIC BITCHES
- mucosal flora Capsule = abscess CLUES: - foul smelling bacteria - infxn site close to mucosa or 2' animal bite - Necrosis/gas - nothing seen in gram stain of original exudate (anaerobic) - AMINOGLYCOSIDES DON'T WORK |
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BACTEROIDES FRAGILIS
- morpho - assc'd site of infxn |
ANAEROBIC GRAM NEGATIVE BACILLI
- MAJOR OPPORTUNIST (normal UR & GI tract) - intraabdominal infxns, gyn, skin/soft tissue etc *spontaneous peritonitis |
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B. FRAGILIS
- VIRULENCE - LABS - TX |
1. Adherence: fimbria, hemaggluttin
2. O2 tox & phag: - capsule (abscess), IgA/M/G proteases, beta-lactamase **OXYGEN TOLERANCE** - Superoxide dismutase & catalse (aerotolerant anaerobes are rare) LABS: - kanamycin, vancomycin, colistin- R - 20% bile - O2 free transport system TX: - Sx : drain & remove necrosis - long term & prophylactic ABX (b4 sx) |
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MYCOPLASMA & UREAPLASMA
- desc - assc'd infxns - important species - transmission/incubation |
NO CELL WALL; tiny tiny tiny
- extra & intra-cellular M. pneumoniae: Walking/atypical pneumoniae M. genitalum: GU infxns (PID) U. urealyticum: GU infxns (urease+) Transmission: resp droplets & sex 2-3 weeks incubation |
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MYCOPLASMA & UREAPLASMA
- DX, TX |
DX:
- NEEDS STEROLS IN MEDIA - pcr, dna, ELISA - SLOW GROWTH on cx TX: NO BETA LACTAMS (no cell wall) - erythromycin/azithromycin/tetracycline |
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Mycoplasma
- virulence |
1. MAJOR = ADHERENCE FACTORS:
- Adhesin: binds sialic acid = no mucociliary axn = dry cough 2. toxic metabolites: H2O2 & Superoxide = INHIBITS host catalase 3. Immunopathogenesis: superantigens - M. pneumonia (5-15 yo) |
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Mycoplasma pneumonia
- Epidemiology - Clinical *differentiate from other atypical pneumonia (Legionella & chlamydia)* |
NOT seasonal
Clinical: - tracheobronchitis - primary atypical pneumonia - incubation 2-3 weeks - persisent nonproductive hacking cough - xray shows pneumonia before symptoms appear |
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M. PNEUMONIA
- LABS - TX |
Serology:
- Cold agglutinins = IgM (50% pts) - ELISA/PCR Culture: sterol-rich media 2-3 weeks to grow Microscope is uselss: no gram stain TREATMENT: ERYTHROMYCIN & TETRACYCLINE - NO cell wall (penicillins & cephalosporins ineffictive) **LONG DURATION** |
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M. genitalium vs. U. urealyticum
- epidem - clinical - labs tx |
GU TRACT
- m. genitalium = most = urethritis - both assc'd with chorioamnionitis & postpartum fever labs: - slow growth on culture - ureaplasma = urease+ on acidic media - PCR/DNA probes *treat w/ tetracycline (also active against chlamydia) - or azithro / quinolone |
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Primary symptoms assc'd with mycoplasmal infxns
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Night sweats, intermittent fevers, malaise, skin rashes, joint/muscle pain
*linked to several chornic diseases (RA, Fibromyalgia, gulf war syndrome* **GROWS IN CELLS WITHOUT KILLING THEM*** |
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Primary symptoms assc'd with mycoplasmal infxns
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Night sweats, intermittent fevers, malaise, skin rashes, joint/muscle pain
*linked to several chornic diseases (RA, Fibromyalgia, gulf war syndrome* **GROWS IN CELLS WITHOUT KILLING THEM*** |
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SPIROCHETES (ORDER)
- morpho - stain - main families/genus & dz |
GRAM NEGATIVE SPIRALS
- ALL MOTILE: endoflagella Borrelia is only one to easily stain gram negative S. - Treponema: Syphilis S. - Borrelia: Lyme dz L. - Leptospirosis |
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TREPONEMA & ASSC'D DISEASES
(GRAM NEGATIVE SPIROCHETES) |
T. perteneu: yaws in tropics
T. carateum: pinta - tropical diseases: chronic skin lesions - non-venereal (just dirties) + syphilitic serology *tx w/ penicillin T. denticola: periodontal dz T. pallidum: SYPHILIS (systemic dz) |
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SYPHILIS
- primary - secondary - tertiary/late |
PRIMARY: host mucocutaneous areas
chancre: papule --> painless ulcer (heals 2 mos) - TONS of spirochetes --> blood/lymph - most transfer occurs NOW *punched out lesion (swimming pool) SECONDARY: flu - infectious, nonpruritic rash (palms & soles too) - Condylomata lata: gray papular lesions in moist areas TERTIARY: rare - chronic inflamm: organ/system damage - Gummatous dz: granulomatous-like lesions of bone/skin |
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CONGENITAL SYPHILIS
- SYMPTOMS **diff dx: cmv, TOXOPLASMOSIS, RUBELLE, Hsv, hep b. |
Transplacental dissemination of T. pallidum after 16th week of gestation
- higher risk during mom's early stage of syphilis symptoms: 2wk-8mo - osteochondritis/periostitis - hepatosplenomeg - rhinitis - FTT - maculopapular rash (hands/feet) - anemia - nephritic syn LATE: - Bone malformations - dental malformations (hutchinson's incisors?) - keratitis = blindness - deaf |
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SYPHILIS VIRULENCE
(T. pallidum) *cell surface is kinda non-antigenic - small # of antigenic targets |
NO RECOGNIZED VIRULENCE FACTORS
= CHRONIC INFLAMM RESPONSE - Endoflagella: rapid invasion of many tissues - Slow metabolism: doesn't trigger immunity - Evades host iron-sequestration - Adhesion: neutrophil damage to tissue - MMP-1: collagen breakdown - Treponemal lipopetides: induce IL-6, IL-2, TNF-a *Induce T & B cell = IgM & IgG |
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SYPHILIS DX
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#1 Treponemal Ag tests:
- FTA-ABS: indirect Ab test - TP-PA: agglutination 2. Microscopy: dark-field/silver staining - exudates from skin lesions (other areas have good spirochetes) - spirochetes don't live long 3. Serological tests: initial detection - Reagin Abs: IgG & IgM - Cardiolipin - VDRL & RPR * measures lipid release during tissue damage* - high false positive possible 4. cultures suck cuz it doesn't grow in artificial cultures |
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SYPHILIS TX
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1. PENICILLIN
- benzathine penicillin G: early / late / congenital - Aqueous crystalline penicillin & procaine penicillin = neurosyphilis - doxy or tetracycline |
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BORRELIA
- MORPHO - TYPES OF RELAPSING FEVER |
BIGGEST spirochetes, gram negative
- slow growth in BSK medium RELAPSING FEVER: - Louse born: B. recurrentis (fluid-transmission) *poor* - Tick borne: B. dudonii (tick bite) *endemic/summer* |
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PHASES OF RELAPSING FEVER ("TICK FEVER")
- acute - relapsing |
ACUTE: incubation = days-2 wks
- acute fever & chilld - rash - headache - maylgias - cough - vomit - conjunctival infxn - hepatosplenomegaly Relapsing: - LBRF: SINGLE relapse - TBRF: MULTIPLE relapse |
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Relalpsing fever
- dx - tx |
DX:
- wRIGHT/GIEMSA stain - acridine orange staining *periph blood smear* don't culture looking for borrelia recurrentis or b. duodonii tx: - single dose of erythromycin or tetracycline: LBRF - 10DAY COURSE TBRF |
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LYME DZ
- ORG - TRANSMISSION - VIRULENCE |
B. burgdorferi (USA) - LONGEST
B. afzelli/garinii = europe Tick bites: white mice, deer Virulence: no known, chronic inflamm ( like syphilis) - MMps, apoptosis of monocytes, - Tick proteins (OspA & OspC) = suppress t cell - Inhibit C': lipoprotein binds to plasma FHL - changes lipoprotein coats - endoflagella |
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LYME DZ
- CLINICAL & DX - TX |
CLINICAL:
- eRYTHEMA MIGRANS: 3-30 DAYS post bite - AV block - Sudden onset arthritis intense join inflamm - ophtho - CNS stuff: face palsy, meningitis DX: - em RASH - HX - labs: serology (late stage) - culture EM rash in BSK medium (early stage) - PCR, SILVER STAINING tx: oral doxy & IV penicillin g, CEFTRIAXONE OR CEFOTAXIME |
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leptospira
- desc |
gram negative spirochetes
- hooked ends - obligate aerobe - mOTILE, - L. interrogans = leptospirosis |
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LEPTOSPIROSIS
- transmission - pathogenesis - clinical |
transmission:
- indirect contact w/ urine from infected animals - occupational dz * natural disasters - hurricans* PATHOGENESIS: - ENTRY: cuts, mucosa, aerosal, eat - incubate: 1-2 wks - SYSTEMIC *Acute vs. Severe* Clinical: acute = septic phase (flu) severe: impaired liver & renal fxn - JAUNDICE - hemorrhagic pneumonitis & acute pulm distress - chf |
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leptospirosis
(weil's dz, infectious jaundice) |
LABS:
- Direct exam of blood/csf (1ST WEEK) - URINE (after 1st week) - Serology: IHA, MAT, ELISA tx: IV penicillin G or doxy = late oral tetra, amox, amp, dox = early |
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FACULTATIVE INTRACELLULAR ORGANISMS
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1. Listeria monocytogenes
2. Salmonella typhi 3. Legionella 4. Mycobacterium 5. Yersinia 6. Brucella 7. Francisella tularensis *inhibit phagosome-lysosome fusion* |
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bacteria w/ exotoxin AB
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- bACILLU SNATHRACIS
- CLSTRIDIUM BOTULINUM - C. TETANI - C. DIPHTHERIAE - V. CHOLERAE |
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4 BACTERIA THAT & cAMP via exotoxins
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1. Cholera
2. anthrax 3. Monteczuma's revenge = enterotoxigenic e. coli 4. Pertussis. |
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TOP 3 Causes of bact. meningitis in newborns (<3 mo)
- other 2 after 3 mo? |
GBS, E. coli, Listeria monocytogenes
- after 3 mo (no more maternal Abs): H. flu & n. meningitides. |
