Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Micro_Test1
| Question | Answer |
|---|---|
| Using biochemical markers to ID bacteria | Biotyping (Phenotypic classification) |
| Phenotypic Classifications | Biotyping, Serotyping, Susceptibility |
| Staph Aureus biotyping shows | Coagulase |
| Proteus Mirabilis biotyping shows | Urease |
| Detect unique bacterial surface antigens for rapid ID | Serotyping (Phenotypic Classification) |
| Interaction of GAS w/Strep pyogenes CW carbohydrate for this dx. Grp A antigen reacts w/specific Ab. | Pharyngitis |
| Kirby Bauer Technique: standardized growth medium, bacteria, abx on disks for zone of inhibition | Abx Susceptibility Testing |
| Cumulative report of abx susceptibilities | Antibiogram |
| MOST precise method of classification | Genotypic |
| Utilizes characteristics detected by molecular techniques that show DNA/RNA of virus. Used for rapid results. Example: PCR | Genotypic Classification (MOST precise method ID) |
| Size of Bacteria | .2 to 2.0um (.2um is the smallest can see on light microscopy) |
| Spherical/Round bacteria | Coccus |
| Rod shaped bacteria | Bacillus |
| Curved rod shaped bacteria | Vibrio (Spiral) |
| Rigid, Spiral-Shaped rod | Spirillum (spiral) |
| Flexible, thin spiral-shaped bacteria | Spirochete (spiral) |
| SHORT rod bacteria | Coccobacillus |
| Variety of shapes in ONE species | Pleomorphic |
| Planes of division for diplo | Pair |
| Planes of division for strepto | chain |
| Planes of division for staphylo | grapelike cluster |
| Planes of division for tetrad | packet of 4 cells |
| What is the difference between the lipid bilayer in bacteria vs other organisms | NO Sterols in membrane UNLESS Mycoplasma or Ureaplasma(respiratory/urogenital infections) which have NO cell walls. |
| Site of cellular respiration and ATP production Regulate Transport Attachment site for chromosome cell-division Protein secretion Synthesis of cell wall components Anchoring Flagella | Cell membrane |
| Prevention of cell lysis, semi-rigid & shape maintainer by this | Cell wall |
| What is the MAIN structural component of the cell wall | Murein (a peptidoglycan) |
| What comprises the backbone of the cell wall | Repeating disaccharides NAG (N-acetylglucosamine) and NAM (N-acetylmuramic acid) |
| What links glycan backbones of cell wall | transglycosylation via glucosidases |
| What cross-links glycan backbones of cell wall | Transpeptidation via transpeptidase forming tetrapeptides from pentapeptides |
| Thick G+ cells will retain what and stain which color? | Retain crystal violet and are blue |
| Thin G- cells will retain what and stain which color? | Retain safarnin and are red |
| G+ cells have how many layers, how thick? | several layers (25) and 15-80nm thick |
| G- cells have how many layers, how thick? | 1-2 layers(few) and 10nm thick |
| G+ or G-: Bacillus Anthracis | G+ |
| G+ or G-: Staph Aureus | G+ |
| G+ or G-: Strep Pyogenes | G+ |
| G+ or G-: E Coli | G- |
| G+ or G-: Haemophilus influenzae | G- |
| G+ or G-: N. Gonrrhea | G- |
| Comprised of cell membrane, periplasm and outer membrane | G- cell envelope |
| What structures are found in a G- envelope that is NOT found in a G+? | Periplasmic space & outer membrane |
| This contains a thin peptidoglycan layer, transport proteins, hydrolytic enzymes and is space btwn cell membrane & outer membrane | Periplasmic space of G- cell envelope |
| External to periplasmic space has a functional bilayer (inner identical to PM) and outer composed of LPS | Outer membrane of G- cell envelope |
| LPS is at risk when dealing with this organism | G- |
| This virulence factor (embedded in outer membrane of G- cell) leads to toxic response. Is ENDOTOXIN of LPS | Lipid A |
| Links Lipid A (from G- bacteria) to O Antigen | Branched polysaccharide of LPS |
| This highly variable long, linear repeating unit of carbs in LPS is used to identify bacterial strains | O Antigen of LPS |
| Systemic Inflammatory Response Syndrome which releases cytokines can be caused by this | LPS (or endotoxin)-must have lysed cell |
| Fever, Tachycardia >100bpm, Tachypnea >20 breaths/min, Leukocytosis >12000 or Leukopenia <4000 are signs of this when have 2 or more. | Systemic Inflammatory Response Syndrome caused by LPS/Endotoxin (must have lysed bacteria) |
| This can lead to septic shock or MODS | Systemic Inflammatory Response Syndrome caused by LPS/Endotoxin (must have lysed cell) |
| In order to release Lipid A (LPS) what MUST happen to cells? | They MUST lyse therefore be careful during bacteria tx to NOT lyse cells |
| Porins in G- cell envelope do what? | Control diffusion of small metab like sugar, aa, ions |
| Cell membrane & peptidoglycan compose this | G+ cell envelope |
| Teichoic/Lipoteichoic acids within peptiodglycans (virulence factors) are only found in these organisms and can initiate endotoxin-like activity | G+ NOT G- cell wall. |
| An adhesin found in G+ cell, attaches bacteria to other cells | Wall Teichoic (WTA) |
| An adhesin found in G+ cell, anchored to bacterial cell membrane that if shed can release cytokines-->endotoxicity | Lipoteichoic Acids (LTA) |
| Penicillins, cephalosporins and Vancomycin all do this | Disrupt cell wall by interrupting synthesis of peptidoglycan (transpeptidation) |
| Bacitracin & cycloserine are examples of this | Cell wall targets |
| Fill active site of transpeptidase preventing transpeptidation | Beta Lactams |
| Degrades glycan backbone, is an innate lytic enzyme (part of innate immune system) and is found in tears, saliva, mucus & lysosomes of WBCs | Lysozyme |
| Peptidoglycan cell membrane w/mycolic acid layer (covalently linked to G+) creating a "waxy coat" | Acid-fast bacteria cell envelope |
| This waxy coat found on G+ allows cells to resist desiccation, some abx & phagocytosis. | Acid-fast bacterial cell envelope _Composed of Mycolic acid |
| Acid-Fast staining identifies this | Mycolic acids present in acid-fast bacterial cell envelope |
| Acid-fast stain RED | Carbol stain (primary) which means cell is acid-fast |
| Acid-fast stain BLUE | Methylene blue stain (counterstain) which means cell is NON acid-fast |
| Mycobacterium TB is an example of this type of bacteria | Acid-Fast bacteria |
| What has the THICKEST membrane: G+, G- or acid-fast | Acid-Fast |
| Present outside the cell wall comprised of polysaccharide w/glycoproteins. On G+ and G- and is source of K antigen | Glycocalyx _2 Forms: Slime layer & Capsule |
| This source of K antigen protects against desiccation, acts as a barrier to toxic hydrophobic molecules (abx), inhibits phagocytosis & promotes adherence to host cells/other bacteria/surfaces by forming a biofilm | Glycocalyx _2 Forms: Slime layer & Capsule |
| Strep Pneumo uses this as a virulence factor (is NOT virulent=avirulent if doesn't have) | Glycocalyx _Source of K antigen _2 Forms: Slime layer & Capsule |
| This form of wall component is loose, non-uniform, more diffuse and forms a biofilm (on catheters, surface of teeth & mucous membrane of GI tract) | Glycocalyx (Slime layer) |
| This form of wall component is rigid, uniform & closely surrounds cell. ID w/Quellung test which forms an Ab/Antigen rxn leading to swelling | Capsule Glycocalyx _Found on Strep, Haemophilus, Klebsiella & Neisseria |
| Strep, Haemophilus, Klebsiella & Neisseria all have this in their cell wall | Capsule Glycocalyx _Positive Quellung test |
| This external structure is filamentous, provides motility, source of H antigen | Flagella |
| One or more arising from one or both ends | Polar Flagella |
| Lateral structures over entire surface of cell | Peritrichous Flagella |
| Hair like protein structures that promote adherence to bacteria/host cells. Arranged peritrichously | Fimbria |
| Attaches to/brings bacterial cells together for DNa transfer | Pilus: _Sex Pilus _F pilus _Conjugation pilus |
| 70S structure (30S and 50S subunits): ODD numbers | Bacteria |
| 80S structure (40S and 60S subunits): EVEN | Eukaryotes=EVEN subunits |
| Multiple ribosomes + 1 strand mRNA or multiple copies of a single protein | Polysomes |
| Abx that target the 70S subunit | Aminoglycosides (streptomycin) Macrolides(erythromycin) |
| Area in prokaryotic cell that contains chromosomal DNA+RNA+proteins with NO nuclear membrane | Nucleoid |
| Allows for coupled transcription & translation-->faster protein synthesis. | Nucleoid region because lacks nuclear membrane |
| Both coupled T&T plus polysomes leading to quick response w/enzymes & structural proteins is good for | Changing environment (O2, temp, pH) |
| A dormant "protective stage" (NOT in reproductive stage) that allows a bacteria to survive harsh environment changes (heat, desiccation, disinfectants, acids) by forming a tight membrane around nucleoid | Endospores |
| In favorable conditions this dormant form of some bacteria germinates to make a vegetative cell | Endospore |
| What are 2 G+ that make spores? | Clostridium AND Bacillus (Anthrax) |
| Most bacteria reproduce by this process where one parent divides into 2 daughters. | Binary Fission _Asexual reproduction |
| In vitro w/liquid medium good to make | Batch culture of bacteria |
| During 4 Phases of Bacteria Growth. Stage where: cells not dividing but are metabolically active | Lag Phase |
| During 4 Phases of Bacteria Growth. Stage where: rapid division @constant rate. Generation/Doubling Time ranges from 8min-33hrs depending. | LOG phase (Exponential growth) |
| During 4 Phases of Bacteria Growth. Stage where: rate of cells dividing=dying. Number of live cells is constant | Stationary Phase |
| This external structure is filamentous, provides motility, source of H antigen | Flagella |
| One or more arising from one or both ends | Polar Flagella |
| Lateral structures over entire surface of cell | Peritrichous Flagella |
| Hair like protein structures that promote adherence to bacteria/host cells. Arranged peritrichously | Fimbria |
| Attaches to/brings bacterial cells together for DNa transfer | Pilus: _Sex Pilus _F pilus _Conjugation pilus |
| 70S structure (30S and 50S subunits): ODD numbers | Bacteria |
| 80S structure (40S and 60S subunits): EVEN | Eukaryotes=EVEN subunits |
| Multiple ribosomes + 1 strand mRNA or multiple copies of a single protein | Polysomes |
| Abx that target the 70S subunit | Aminoglycosides (streptomycin) Macrolides(erythromycin) |
| Area in prokaryotic cell that contains chromosomal DNA+RNA+proteins with NO nuclear membrane | Nucleoid |
| Allows for coupled transcription & translation-->faster protein synthesis. | Nucleoid region because lacks nuclear membrane |
| Both coupled T&T plus polysomes leading to quick response w/enzymes & structural proteins is good for | Changing environment (O2, temp, pH) |
| A dormant "protective stage" (NOT in reproductive stage) that allows a bacteria to survive harsh environment changes (heat, desiccation, disinfectants, acids) by forming a tight membrane around nucleoid | Endospores |
| In favorable conditions this dormant form of some bacteria germinates to make a vegetative cell | Endospore |
| What are 2 G+ that make spores? | Clostridium AND Bacillus (Anthrax) |
| Most bacteria reproduce by this process where one parent divides into 2 daughters. | Binary Fission _Asexual reproduction |
| In vitro w/liquid medium good to make | Batch culture of bacteria |
| During 4 Phases of Bacteria Growth. Stage where: cells not dividing but are metabolically active | Lag Phase |
| During 4 Phases of Bacteria Growth. Stage where: rapid division @constant rate. Generation/Doubling Time ranges from 8min-33hrs depending. | LOG phase (Exponential growth) |
| During 4 Phases of Bacteria Growth. Stage where: rate of cells dividing=dying. Number of live cells is constant | Stationary Phase |
| During 4 Phases of Bacteria Growth. Stage where: cells die at log rate & decline of growth conditions because of lack of nutrients, oxygen. See increase in waste products | Decline/death phase |
| There is short term/doubling time during this | Acute infections (sudden onset, short course) Can have Short-term treatment |
| There is long term doubling during this | Chronic infections(slow progressive onset, indefinite duration) Must have Long-term treatment |
| This bacterium has a short generation time (25mins) therefore you should treat it for a relatively short time (10days) | Streptococcus (G+) |
| This bacterium has a long generation time (22hrs) therefore you should treat it for a relatively long time (6-12mos) | Mycobacterium TB (Acid-Fast) |
| These bacteria grow optimally at pH<5.4 | Acidophiles |
| These bacteria grow optimally at pH 5.4-8.5. Is MOST pathogenic bacteria | Neutralophiles |
| These bacteria grow optimally at pH >8.5 | Alkaliphiles |
| These bacteria grow optimally at 15-20'C | Psychrophiles |
| These bacteria grow optimally at 25-40'C. Is MOST pathogenic bacteria | Mesophiles |
| These bacteria grow optimally at 50-60'C. Some can tolerate >100'C | Thermophiles |
| These organisms are physically & biochemically limited to ONE specific habitat | Obligated pathogens |
| These can adapt to specific environmental conditions/can survive under other conditions. MORE than one habitat | Facultative pathogen |
| The five groups of bacteria | Obligate Aerobes Obligate Anaerobes Facultative Anaerobes Microaerophiles Aerotolerant Aerobes |
| Mycobacterium TB(Acid-Fast) is an example of this type of organism which need oxygen present | Obligate aerobes |
| Clostridium(G+) is an example of this type of organism which must live without oxygen | Obligate anaerobe |
| E. Coli (G-) is an example of this type of organism which can grow in the presence/absence of oxygen but PREFERS aerobic metabolism. Under anaerobic conditions will ferment. | Facultative Anaerobes |
| What are the two products of bacterial fermentation? | Lactic Acid and H2 gas formation |
| This byproduct of fermentation causes dental caries. Can happen w/streptococcus mutans (G+) | Lactic Acid Fermentation |
| Damage from production of insoluble H2 causes gas to accumulate & rips tissue apart causing a collapse of blood vessels and reducing O2 supply (making the region anaerobes). Caused by fermentation. Give an example of an organism which does this | Clostridium Perfringens (G+) |
| Treponema is an example of an organism which grows best in small amts of O2. Many types of this organism are capnophiles (INC CO2 is better for growth) | Microaerophiles |
| Capnophile | Increased CO2 is better for growth _Many microaerophiles |
| Lactobacillus acidophilus(G+) is an example of an organism which can survive in oxygen but does NOT use oxygen | Aerotolerant Anaerobes _Can survive in esophagus & stomach |
| This is dependent on the ability to produce enzymes which breakdown/neutralize O2 & ROS generated by cells. | Oxygen sensitivity |
| In order to breakdown O2 and ROS must produce what? | SOD: superoxide dismutase which converts O2 Peroxidase or Catalase: decomposes H2O2 |
| Converts oxygen | SOD: Superoxide Dismutase |
| Decomposes H2O2 | Peroxidase Catalase |
| To treat anaerobe infections would use this | Hyperbaric Oxygen (HBO) Therapy since obligate anaerobes will lack SOD/catalase/peroxidase and therefore will undergo lethal oxidations when exposed to O2 |
| How does high osmotic environments (hypertonic soln) effect bacteria | Lethal by causing excess loss of water from cell |
| These bacteria are adapted to high salt content. Examples are Vibrio cholerae & S Aureus | Halophiles |
| Grow on standard media in lab. Example: Pseudomonas(G-) | Nonfastidious |
| Require specific nutrients for survival. Example: N. Gonorrhea(G-), Treponema Pallidum(G-) | Fastidious |
| Bacterial DNA has what components? | One Copy of dsDNA, CCC(covalently closed circle), supercoiled. _Haploid organisms |
| Are bacteria haploid or diploid? | Haploid |
| Extrachromosomal DNA not essential for survival in bacteria. Majority are covalently closed circle (CCC) dsDNA, but can be linear. Codes for beneficial zuxiliary info. Replicates autonomously | Plasmid |
| What codes for auxiliary info such as abx resistance, toxins & useful enzymes | Plasmid |
| What causes a plasmid to replicate? | Replicates autonomously |
| Uptake of naked DNA from lysed cell by acompetent bacteria | Transformation |
| This cell receives DNA that encodes for a USEFUL protein after transformation | Recipient cell |
| Receiving a beneficial form of a gene post acquistion called | Positive Result |
| Receiving a inactive form of a gene post acquistion called | Negative Result |
| Receiving a NO change in form of a gene post acquistion called | Null Result |
| One way transfer of DNA from one to another w/direct contact of sex or F pilus. Larger pieces of DNA is transferred | Conjugation |
| This organism transfers F plasmid from F+/donor to F-/Recipient using conjugation | E. Coli (G-) |
| This is transferred as ssDNA & replicates in D & R cells | F Plasmid |
| This joins cells NOT for DNA transfer | Conjugation Pilus |
| Which pili are involved in conjugation: F pilus, Sex pilus, conjugation pilus | F Pilus AND Sex Pilus NOT conjugation pilus |
| Transfer of bacterial chromosomal DNA using a bacteriophage(virus which infects bacteria) | Transduction |
| Virulent phage replicates within bacterial host & fragmented bacterial DNA packaged into capsid of newly formed phage. A defective phage able to transduct will infect the bacterial cell injecting bacterial DNA which will recombine with the genome. | Example of virulent phage w/generalized transduction & lytic cycle. _Transduction will cause the cell to burst and release many copies(lytic) |
| Temperate phage injects viral DNA & lysogenic conversion occurs(viral DNA inserts into bacterial chrom) & phage-->Prophage. If viral DNA carries a virulence factor then bacteria converted to a pathogenic microbe | Temperate phage with specialized transduction and lysogenic cycle |
| Viral DNA insertion into bacterial chromosome | Lysogeny (occurs during lysogenic conversion) |
| Prophage | What a phage becomes after lysogeny (viral DNA insertion) occurs |
| Corynebacterium Diphtheria has virally encoded diphtheria toxin. Would be an example of this type of transduction | Specialized transduction: Lysogenic conversion where viral DNA carries virulence factor-->pathogenesis |
| Strep Pyo has virally encoded scarlet fever toxin. Would be an example of this type of transduction | Specialized transduction: Lysogenic conversion where viral DNA carries virulence factor-->pathogenesis |
| Vibrio Cholera(G-)has virally encoded cholera toxin. Would be an example of this | Specialized transduction: Lysogenic conversion where viral DNA carries virulence factor-->pathogenesis |
| Mobile genetic element responsible for most genetic variability in bacterial populations & spread of abx resistance genes | Transposons |
| Microbes found at certain sites in healthy individuals in complete absence of disease | Normal flora |
| Makeup of microbial populations dependent on | Physiology, age, habitat, diet |
| Occupy site in/on body & prevent colonization by pathogens | Beneficial microbes |
| Induce cross-reacting ab's & stimulate immune response | Beneficial microbes _E Coli ab will react w/H influenzae type B |
| Synthesize Vitamins K & B complex & compete with pathogens for limiting nutrients. Make substances which inhibit/kill microbes(bacteriocins, lactic acid) | Beneficial microbes |
| Response to local phys/environ factors which impose selection for or against specific flora. | Tissue tropism |
| 1)Specialized habitats provide certain growth factors 2)Microbes attach to specific receptor sites on tissues | Tissue tropism _Impose selection for certain flora |
| Lipids in sebaceous glands and nutrient substrates in GI tract help do what | Provide specialized habitats which provide certain growth factors |
| Tooth enamel w/slime layer and microvilli in small intestine w/fimbriae do this | Allow microbes to attach to specific receptor sites on tissues |
| Strep Salivarius on tongue example of this | Tissue tropism |
| E Coli on Epithelium of small intestine epithelium example of this | Tissue tropism |
| Staph Aureus on nasal membranes example of this | Tissue tropism |
| Staph epidermidis on skin example of this | Tissue tropism |
| Variation in composition/numbers from birth to old age of flora in oral cavity, vagina, large intestine, skin | Ecological succession of bacteria |
| Resident flora | Always present @characteristic sites |
| Transient flor | Establish then are eliminated through competition w/other microbes. Host factors impt. |
| Resident & transient flora impt for this | Homeostasis |
| Normal flora create disease when inoculated into sterile site. Example includes endocarditis & UTI | Displaced organisms |
| Oral bacteria into bloodstream | Endocarditis _Displaced organism |
| Intestinal bacteria into urinary tract | UTI _Displaced organism |
| Oral thrush & vulvovaginal candidiasis can be caused by this occuring w/candida albicans(G-) | Overgrowth of a species due to prolonged use of broad spectrum abx |
| Pseudomembranous colitis by Clostridium Difficile(G+,Bacillus,Obligate Anaerobe) can be caused by this | Overgrowth of a species due to prolonged use of broad spectrum abx |
| Quinolones and beta lactams can cause this with prolonged use | overgrowth of species such as candida albicans & c difficile leading to thrush, candidiasis, pseudomembranous colitis |
| Secreted enzyme which starts biochem rxns in plasma by converting fibrinogen to fibrin. Forms clots by blocking WBC access to bacteria & preventing phagocytosis | Coagulase |
| Staph Aureus (G+) is positive or negative for coagulase | Coagulase Positive |
| S epidermidis is positive or negative for coagulase | Coagulase Negative: CNS-CoNS |
| S Saprophyticus | Coagulase Negative: CNS-CoNS |
| Toxin which lyses rbc membrane. Detect with isolation streak of bacteria on BAP. Used to differentiate Streptococci | Hemolysin |
| Complete streptococci infection will show this w/Hemolysin | =Beta White colony & clear halo |
| Partial streptococci infection will show this w/Hemolysin | =Alpha Gray/green colony & partial halo |
| No streptococci infection will show this w/Hemolysin | =Gamma White colony & NO halo |
| S. pyogenes & S agalactiae show white colony & clear halo. Type of strep? | Beta |
| S. mutans shows gray/green colony & partial halo. Type of strep? | Alpha |
| Enterococcus faecalis if put on a hemolysin test would show this | White colony with no halo |
| Fatty acid (sebaceous glands) & salt(sweat glands) do what to most bacteria/molds | Inhibit growth |
| Where are microbes more present? | Moist areas _axilla, perineum, head _intertriginous areas |
| On dry skin what type of organism predominates | G+ _S epidermidis(CNS, facultative anaerobe/halophile) _Propionbacterium acnes(anaerobic, pleomorphic) _Diphtheroids:Corynebacterium(facultative anaerobic bacilli) |
| Responsible for acne, present on dry skin | Propionibacterium acnes |
| Must grow on mannitol salt agar, present on dry skin | Staph epidermidis |
| What's present on moist skin | Normal dry skin G+ and G- like E. coli and Acinetobacter |
| Motile facultative anaerobe with O, H, K antigens. Must grow on MacConkey's agar to isolate enteric bacteria. Present on moist skin | E Coli |
| Unlike E coli, also G- present on moist skin, this bacteria is NOT motile & is obligate aerobic | Acinetobacter |
| Staph Aureus | Gram Positive |
| E Coli | Gram Negative |
| Fungi and parasites | Eukaryotes |
| Established microbe w/NO interference w/normal body function | Colonization |
| Established microbe that INVADES host tissues & multiplies. May or not manifest disease | Infection |
| Abnormal condition of body that occurs when interaction leads to pathogenesis & damage to host | Disease |
| Any objective evidence of disease noted by an observer (changes caused by disease, seen by provider) | Signs |
| Any subjective evidence of disease noted by an observer (changes caused by disease, felt by patient) | Symptoms |
| Indicator of disease, sensed and observed. Both a sign and symptom | Fever |
| Generalized Aches and Pains | Damaged tissue releases mediators stimulating pain receptors in joints & mm |
| Localized Pain | Pathogen or wbc release mediators which stimulate pain receptors |
| Yeast | Unicellular |
| Molds | Multicellular |
| Headache | Blood vessels in brain dilate as result of mediators released by damaged tissue |
| Fever | Endogenous & exogenous pyrogenes released which effect hypothalamus |
| Sore Throat | Pathogens & WBC release inflammatory cytokines cause swollen pharynx lymphatic tissue |
| Nausea | Ingested toxins stimulate neural center |
| Opportunistic Pathogens | Part of normal flora that establish disease when move to UNprotected site _Staph Aureus(G+) _E Coli(G-) _Candida Albicans(Acid Fast) _C Difficile (G+) |
| Anterior nares/nostrils & perianal region. Coagulase + cocci. Ferment mannitol | S. Aureus(G+) |
| Around perineum & thighs of DM. Obligate anaerobe bacilli that forms endospores. Associated w/gas gangrene & food borne disease | Clostridium Perfringens(G+) |
| Bifidobacterium | Bifurcated bacteria _G+ |
| In Eye, microbes from skin | S epidermidis(G+)-CoNS S Aureus(G+)-rare, catalase-positive |
| In Eye, microbes from nasopharynx | Strep Pneumo(G+): alpha hemolytic, lancet shaped diplococci Neisseria(G-) Nonmotile, Aerobe Moraxella Catarrhalis(G-) Nonmotile, Aerobe |
| Strep Pneumo(G+) | alpha hemolytic, lancet shaped diplococci |
| Predominant flora in mouth | G+ cocci Alpha hemolytic viridans streptococci _S mutans |
| Responsible for dental caries & plaque. Deposit polymers of glucose(glucans) & forms biofilms. Lowers pH by fermentation & demineralizes enamel(caries) | S mutans(G+) |
| Can seed bacteria into bloodstream causing endocarditis | S mutans(G+) |
| Found in the mouth, a yeast which causes oral thrush & dental stomatitis. G+ w/no peptidoglycan | Candida Albicans (Acid-Fast) |
| Upper respiratory tract | nares, sinus, nasopharynx, oropharynx, larynx |
| Lower respiratory tract | trachea, bronchi, bronchioles, alveoli |
| Primary carriage site for S. Aureus(G+) in 30% of pop | Nares(nostrils) |
| Healthy sinuses | Sterile _Mucociliary escalator |
| Predominant flora in naso & oro pharynx. | G+ Cocci 4 alpha hemolytic viridans Strep _Strep pneumo |
| Potentially pathogenic, found in naso & oropharynx. G+ | Strep Pneumo |
| Gram Negative Diplococci found in upper respiratory tract | Moraxella Catarrhalis N. Meningitidis |
| Gram Negative Bacilli(rods) found in upper respiratory tract | E coli Klebsiella Proteus |
| Motile, encapsulated(mucoid colony) found in upper respiratory tract | Klebsiella (G-) |
| Highly motile (swarms on agar plate) found in upper respiratory tract | Proteus (G-) |
| Gram - Pleomorph found in upper respiratory tract | H Influenzae (Pleomorph) _Nonmotile _Fastidious _Encapsulated |
| Normal flora continues to level of where in upper respiratory tract | Larynx |
| Virtually free of microbes(cleansing action of ciliated epithelium). Any microbes/bacteria reaching here swept out (mucociliary blanket). | Lower Respiratory Tract: trachea, bronchi, bronchioles, alveoli |
| PCR | Rapid method for identifying & culturing bacteria that cannot otherwise be grown |
| Mucociliary escalator | Action mucociliary blanket which removes bacteria by cough, sneeze etc (move outward) |
| What controls the # and population of bacteria in the GI | Acidic pH and bile |
| Few to no normal flora in this section of GI tract | Esophagus & stomach _Must be acid tolerant to live here |
| Stomach flora | Lactobacillus(G+) Helicobacter Pylori(G-): motile vibrio |
| Urease producer(localized pH INC) responsible for gastric ulcers. | Helicobacter Pylori(G-): motile vibrio |
| Duodenum & jejunum flora | Lactobacillus(G+) Enterococcus Faecalis(G+): Group D streptococcus. Alpha, beta, gamma hemolysis |
| Ileum flora | Pop & diversity increase. Similar to colon(bacteriodes-G- and Bifidobacterium-G+) |
| Colon flora are numerous & complex. 500-1000 taxa. Anaerobes predominate! | Bacteriodes_encapsulated bacilli, obligate anaerobes Bifidobacterium_pleomorph obligate anaerobe |
| What predominates in the colon? | Anaerobes |
| Encapsulated bacilli, obligate anaerobe found in colon | Bacteriodes(G-) _Higher in meat-lovers compared to vegans |
| Pleomorph, obligate anaerobe found in colon | Bifidobacterium(G+) _>90% total bacteria |
| What controls species composition & numbers in colon? | Diet |
| Undergoes eco succession from birth through life | Vagina |
| During child-bearing years this is the predominant microbe. Metabolizes glycogen, produced by vaginal epithelium, induced by estrogen production | Lactobacillus Acidophilus(G+) _Low pH-Lactic Acid production _Prevents establishment of other bacteria |
| Clue cells | Bacterial vaginosis |
| Potentially pathogenic vaginal bacteria | Candida Albicans(Acid-Fast) |
| Responsible for neonatal meningitis. 1/4 women have this beta-hemolytic. Found in vagina | Streptococcus Agalactiae OR Group B Strep |
| Normal flora in urinary tract(similar to skin) | Staph Epidermidis(G+) Diphtheroids(G+) Enteric Bacteria: E Coli(G-) & Proteus(G-) |
| Micturition(urination) | Limits/prevents colonization of urethra. Microbes flushed from urethra. |
| Bladder urine | Normally sterile because of midstream catch |
| Midstream catch | Reduces normal flora contamination in urethra |
| Microbes isolated from where represent infection w/potential for disease | Bodily fluids, tissues, upper urinary tract |
| Normal flora in kidneys & bladder | There are NO normal flora here |
| Patient subject to trauma, with defective immune system or preexisting condition. More susceptible to opportunistic microbe. | Opportunistic Pathogens _Pseudomonas A _Nocardia Asteroides |
| Skin of burn victim or lungs of CF patient | Pseudomonas A opportunistic pathogen |
| Respiratory infection in immunosuppressed or immunocompromised | Nocardia asteroides opportunistic pathogen |
| Always associated w/disease. Signs & Sx caused by damage to or loss of tissues/organs. Host inflammatory response. | Mycobacterium TB(Acid-Fast) N. Gonorrhea(G-) |
| Acid, gases, byproducts of metabolism formed during growth | Tissue damaging metabolites _Strep mutans(lactic acid-->dental caries) |
| Proteins, enzymes act locally to damage host cells. Affect tissue matrices & intracellular spaces. Help spread & growth of pathogen. Damages to host cell can be pathologic | Invasins or "Spreading factors" _Hyaluronidase _Collagenase _Neuraminidase _Streptokinase & Staphylokinase |
| Attacks interstitial cement of connective tissue. Depolymerizes hyaluronic acid | Hyaluronidase _Invasin/Spreading Factor |
| Breaks down collagen, framework of mm | Collagenase _Invasin/Spreading Factor |
| Degrades neuraminic acid(sialic) which is intercellular cement | Neuraminidase _Invasin/Spreading Factor |
| Activate plasminogen. Breakdown blood clots. | Fibrinolysins: Streptokinase & Staphylokinase _Invasin/Spreading Factor |
| Binds to receptors on host cells/tissues and binds to carbohydrate moieties-glycoproteins | Adhesins _Vibrio Cholerae(G-) _E coli(G-) |
| Capsule w/slime layers and biofilms which comprised of this. Helps w/adhesins | Glycocalyx |
| Lead to colonization of inert & organic materials. Becomes continual or intermittent infection source. | Biofilms _Strep mutans _Staph Epidermidis |
| Forms biofilms on IV catheters. Skin flora | Staph Epidermidis |
| Forms glucan & binds to tooth enamel. Secretes glucosyltransferase | Strep Mutans |
| Attach to specific host molecules for "tissue tropism" part of adhesin mechanism | Fimbriae/Pili _N Gonorrhea(G-) |
| Attaches to conjunctiva | N Gonorrhea(g-) with its pili |
| NOT fimbriae/pili are proteins associated w/cell ENVELOPE(wall/membrane) mediate binding specificity. Part of adhesins | Afimbrial adhesins _Staph Aureus (G+) _Strep Pyogenes (G+) _Can lead to endocarditis/pharyngitis |
| Look like enzymes, heat labile, high activity & specificity | Toxins |
| Toxic to cells, usually by direct action. Secreted into ECF or associated w/bacterial cell surface. Have components which bind host receptors. Can be both G+ and G- | Exotoxins |
| Toxic to cells, usually by direct action. Secreted into ECF or associated w/bacterial cell surface. Have components which bind host receptors. Can be both G+ and G-. Causes GI Sx (vomit, diarrhea, nausea) | Enterotoxins _Shigella dysenteriea(G-) _Staph aureus(G+) |
| Bloody diarrhea & abdominal cramping w/this G- enterotoxin | Shigella dysenteriae |
| Vomiting and diarrhea with this G+ enterotoxin | Staph aureus |
| Enzymatic component of A-B Exotoxin | A Subunit: Attack Cell |
| Binding subunit of A-B Exotoxin. Binds toxin to host cell Receptor | B Subunit: Binds toxin to cells |
| After binding (B subunit), attacking enzyme(A subunit) enters | A-B Exotoxins _Diphtheria _Shigella dysenteriae _C botulinum _C tetani |
| Causes flaccid paralysis | C botulinum (lysogenic conversion) |
| Causes spastic paralysis | C tetani |
| Lysogenic conversion | Virus=Bacteriophage |
| Plasmid | Extrachromosomal DNA |
| Immunogenic & deadly at extremely low concentrations | Functional exotoxin |
| Denatured toxins, still immunogenic, in vaccines | Toxoids _Diphtheria toxoid vaccine _Teatnus toxoid vaccine |
| Attack host cell membrane | Membrane-active Exotoxins _Proteases(Pseudomonas) & Lipasis(C Perfringens) & Hemolysis(Strep Pyogenes) |
| Toxins which activate 1/5 T cells in absence of antigen(usually normal 1/10000) causing release of LARGE amt of cytokines. Possible life-threatening response & T cell death | Superantigens _Staph Aureus in Toxic Shock Syndrome _Strep Pyo in pyrogenic exotoxin A-SpeA |
| Toxic Shock syndrom toxin(TSST-1) | Staph Aureus _Superantigen |
| LPS of gram negative bacteria. Toxicity in lipid component(Lipid A). Immunogenicity is in the polysaccharide part | Endotoxin |
| Remains associated w/cell wall until cell disintegrates by autolysis, lysozymes or phagocytosis. Causes inflammation, activates complement. Leads to fever, HTN, shock & possible death | LPS _Endotoxin |
| Extracellular, diffusible. Denatured by boiling. Forms toxoid. High potency. High specificity. Often enzymatic activity. | Exotoxin |
| LPS, part of outer membrane, cannot dentaure by boiling, does NOT form toxoid, low potency, low specificity, no enzymatic activity. Pyrogenic | Endotoxin |
| Spread from primary site of infection(toxins & antigenic molecules). Cytotoxic effects remote from focus of infections. | Circulation via blood & lymph _Staph Aureus |
| Exfoliative toxin (desquamation of upper epidermis). Focus on the conjunctiva. | Staph Aureus causing Scalded Skin Syndrome |
| With poorly antigenic polysaccharide, deters phagocytosis & protects against degradation in phagolysosome. (Strep Pneumo) | Evasion of immune response via Encapsulation |
| Intracellular growth & escape detection (Mycobacterium TB) | Evasion of immune response via Intracellular growth |
| Chelate available iron & transport into cell. Scavenge from host iron-binding proteins Lactoferrin & transferrin | Siderophores _Iron Capture by Microbes |
| Body's immune response to infection can result in signs & sx of disease | Antibacterial immunopathogenesis |
| Bacteria can induce tissue damaging immune responses | Treponema Pallidum-Syphilis _Organ & nerve destruction. Induced by binding of WBC to endothelium |
| Cross-reacting antibacterial antibodies | Strep Pyogenes _Rheumatic Fever, sequela to infection. _Ab's to cell wall M protein. Cross-react w/& damage to heart valves & mm. |
| Stage 1 of Disease | Incubation _Pathogen has entered thru "Portal of Entry" via entry/shedding |
| Stage 2 of Disease | Prodromal |
| Stage 3 of Disease | Acute |
| Stage 4 of Disease | Decline |
| Stage 5 of Disease | Covalescent |
| NO signs/sx. Innate immune system NOT activated. Must be an INFECTIOUS dose/INOCULUM to gain entry, start growth. NOT infectious. | Stage 1 of Disease: Incubation _Preclinical |
| Number of microbes needed for disease | Inoculum _Shigella 200 CFU _Vibrio Cholerae 1e8 CFU |
| (# colonies) x (Dilution Factor) | CFU |
| Appearance of signs/sx in "illness." Pathogens generate early signs/sx (nonspecific). Activation of the innate immune system.Numbers have INC since incubation stage. Easily transmitted even before host realizes has bug. | Stage 2 of Disease: Prodromal _Warning |
| Acute stage most severe during this time. Characteristic for the dz, signs & sx. Balance btwn host immune system & pathogen virulence tipped to recovery or death. Acquired-immune system active. Pathogen numbers are stationary(inc or dec). | Stage 3 of Disease: Acute _Clinical Illness |
| Acquired-immune system active & can easily transmit | Stage 3 of Disease: Acute _Clinical Illness |
| Rapid developing signs & sx w/peak in intensity. Recede as pt moves to Decline stage | Acute stage in acute disease |
| Signs and sx persist for an intermediate-->indeterminate period of time, slow move to Decline stage | Acute stage in chronic disease |
| Illness is still apparent but signs/sx dwindle. Immune activity is decreased. Ab's have been formed. Communicable if individual becomes Carrier | Stage 4 of Disease: Decline Stage _Typhoid Fever: Salmonella Typhi |
| Pt is now returning to full health. Signs & sx ending. No activity twd pathogen & pathogen is cleared from host. Not communicable since NO presence of pathogen | Convalescent Stage |
| Chem substance w/ability to inhibit growth or kill BACTERIAL cell | Abx |
| Can you use abx on bacterial or viruses? | Bacteria |
| Inhibits growth of target organisms | Bacteriostatic _Do NOT use w/immunocompromised pt's or for infections in privileged sites |
| Effective against a limited array of microorganisms | Narrow-spectrum abx |
| Effective against a wider array of microorganisms | Broad spectrum abx |
| More harmful to the bacterial cell than to the host cell. Often, differences btwn eukaryotes & prokaryotes are exploited. | Selective Toxicity _Cell wall inhibitors, 70s protein synthesis inhibitors |
| beta lactams, abx, vancomycin, cycloserine, bacitracin | Inhibit peptidoglycan synthesis _Cell wall inhibitor |
| Penicillin + Penicillin analog(Clavulinic acid) | Extend spectrum of activity |
| 1st generation cephalosporins | G+ cocci, G- enterics |
| 2nd generation cephalosporins | Extended Spectrum: more G-, less G+ than previous gen |
| 3rd generation cephalosporins | Broad Spectrum: more G- (inc resistance to beta-lactamase) some can cross BBB |
| 4th generation cephalosporins | Extended spectrum to P aeruginosa & some G+. Use in meningitis cases _INC resistance to beta-lactamase |
| Act as cationic detergents by disrupting lipid bilayer of G- cell walls. Toxic to host, used externally | Polymyxins |
| Aminoglycoside | Protein synthesis inhibitor _bactericidal |
| Tetracycline | Protein synthesis inhibitor _bacteriostatic |
| Chloramphenicol | 50S unite inhibitor _LIMITED use bc causes aplastic anemia _bacteriostatic |
| Macrolides | 50S unite inhibitor _bacteriostatic |
| Can cause aplastic anemia | Chloramphenicol |
| Intereferes w/DNA or RNA synthesis | Rifampin & Fluoroquinolones |
| Inhibits DNA-DEPENDENT RNA polymerase(transcription) | Rifampin _bactericidal |
| Inhibits DNA GYRASE activity | Fluoroquinolones _bactericidal |
| Analogs of PABA that interfere w/folic acid synthesis by competing for dihydropteroate synthase. Often given w/TMP-SXT | Sulfa drugs(Sulfonamides) _Bacteriostatic _Broad Spectrum |
| Analog of pteridine portion of dihydrofolic acid that interfere w/folic acid synthesis by inhibiting DHF reductase. Often given w/TMP-SXT | Trimethoprim _Bacteriostatic |
| Why does a bacteria need folic acid? | Essential for nucleic acid synthesis |
| Random mutations in DNA that allow resistance to occur | Chromosomal resistance |
| Transfer of gene/plasmids that allow resistance | Acquisition of chromosomal or extrachromosomal DNA |
| Referred to as RTFs or R Factors | Resistance Factors where genes can be found on the plasmid conferring resistance: _Chromosomal _Acquisition of chromosomal/extrachromosomal DNA |
| Alteration of drug targets (like ribosomal mutation) would cause what? | Resistance _ex: Resistance to erythromycin & rifamycin |
| Alteration of PM permeability and/or INC drug transport would cause what? | Resistance |
| Synthesis of enzymes that inactivate abx would cause what? | Resistance |
| Alteration of a metabolic pathway would cause what? | Resistance |
| Resistance to erythromycin & rifamycin occured thru this mechanism | Alteration of drug target by changing the bacterial ribosome |
| Resistance to erythromycin & tetracycline occured thru this mechanism | Alteration of PM permeability and/or INC drug transport |
| Resistance to beta lactams, chloramphenicol, aminoglycosides, tetracycline occured thru this mechanism | Synthesis of enzymes that inactivate abx |
| Resistance to sulfonamides, trimethroprim occured thru this mechanism | Alteration of a metabolic pathway |
| Enterococcus faecalis, Mycobacterium TB, Pseudomonas can have clinical variations which are this | Resistant to ALL |
| Abx use in animals, social factors, innapropiate pt use, collateral damage & not washing hands | Factors contributing to resistance |
| How do animals contribute to abx resistance? | They consume/excrete abx Can transmit resistant bacteria in food Genetic transfer to human specific organisms |
| How do social factors fuel resistance? | Poverty encourages devo of resistance thru under-use of drugs. Resistance is emerging from overuse of drugs in wealthy countries. Globalization, INC travel & trade ensure that resistant strains quickly move elsewhere. |
| How many unneccessary Rx are used in the US? | 60million/150million. _For viral sinusitis |
| Factor that helps resistance in GI? | Abx disrupt normal flora |
| Why may abx fail when NOT caused resistance | Not able to reach microorganisms: cannot cross BBB Be too toxic at doses required to be effective against targeted microorganisms |
| All these organisms are OBLIGATE INTRACELLULAR PARASITES | Viruses _ONLY reproduce in living cells _NO independent metabolism! |
| Viruses are filterable agents, what does this mean? | Passage through fine pore filters is possible (viruses are small in size) |
| Replicate in a pattern that is fundamentally difft from ALL other living cellular organisms. Progeny made in assembly line fashion. | Viruses |
| Are viruses made through binary fission or in assembly line fashion? | Assembly line fashion |
| Central goal of ALL viruses | Rapidly replicate new virions at expense of host cell. _Could lead to lysis/cell death though non-lethal strategies may also be used |
| Virus remains assoc w/host but genes are largely UNexpressed. Does NOT cause death to host but lies dormant | Prophage(bacterial lysogens) or provirus _Stable & long-term but can be terminated by environment |
| Infection without cell death; unusual virus-host interaction in which virus is found in a long-term association w/the host | Persistent Infection |
| Intermittent acute episodes of a virus production btwn which there's almost a total absence of virus particles & very limited viral macromolecular synthesis. | Latent Infections _Herpes Simplex |
| Nonlytic production of virus, continued presence of substantial #'s of virus particles during periods in which clinical dz absent | Hepatitis B virus |
| Infected host cells are "immortalized" and properties altered (transformed) to those of cancer cells | Transforming Infections _HPV |
| Inflammation of stomach/intestine. Frequent children mortality in devo nations | Gastroenteritis |
| Nausea, diarrhea, vomiting, cramps, malaise, anorexia, myalgia, headache. ACUTE WATERY DIARRHEA. | Viral gastroenteritis |
| Incubation period for replication of virus in small intestine epithelial cells | 15-48hrs _Disease:3-5days_may be shed at low levels for days-->wks post-illness |
| Viral gastroenteritis dx via this: | Antigen detection by Rotazyme(enzyme immunoassay) or latex agglutination test |
| Tx for viral gastroenteritis | Primary=Oral Re-hydration NO abx!!!! |
| 2 main settings for viral gastroenteritis | Infant diarrhea & food outbreaks(fecally contaminated) |
| Rotavirus & enteric adenovirus are examples of viruses active in this main setting | Infant diarrhea _In locations where clean water/food even |
| Prevention of viral gastroenteritis | Vaccines available for Rotavirus(Rotateq/Rotarix) but immunity is short lived. NO primary prevention means. |
| Rotavirus | Endemic SEVERE DIARRHEA of infants _infect small intestine villi enterocytes disrupting osmotic function _5-7day course of fever/vomit |
| Winter vomiting disease_occur every winter | Rotavirus: infant severe diarrhea |
| Which rotavirus vaccine has been recalled bc of links to intussception | Rotasheild |
| Rotavirus vaccines STILL available | Rotateq Rotarix |
| dsDNA virus in endemic diarrhea of infants. Lasts LONGER than rotavirus(5-12days). | Enteric Adenovirus _Identify via Immunoassay |
| Norwald & SRSVs(Norovirus) cause epidemics of diarrhea/vomiting. Usually mild, self-limited(24-48hrs) & seen in older children, adults. | Calciviruses _VERY resistant to inactivation _Associated w/food(shellfish) |
| Spread readily person-to-person & water-borne. Causes short/mild diarrhea in older kids/adults | Norovirus |
| Acute dz caused by Vibrio cholerae infection. Massive human deaht. Frequent attendant of disasters | Cholera |
| Colonizes in small intestine(without changing the physical integrity of the mucosa). Cause ACUTE & MASSIVE watery diarrhea. "RICE WATER" stools. Rapid depletion of fluids-->Hypovolemic shock, metabolic acidosis, death | Cholera _Incubate 1-5days w/abrupt sx onset |
| Rice water diarrhea(1L/hr) w/m cramps, poor turgor, wrinkle skin over fingers(WASHERWOMAN HANDS), sunken eyes, NO pulse in extremities | Cholera _Incubate 1-5days w/abrupt sx onset |
| G- Bent rod shape. NO spore formation. Facultative anaerobe. Motile, polar flagellum | Cholera _Incubate 1-5days w/abrupt sx onset of watery rice diarrhea |
| Cholera serogroups classified by this | O (Somatic) antigens |
| Serogroup O-1 | Classic Epidemic Cholera |
| Serogroup O-139 | New cholera found in India. Until found this thought all was O-1 serogroup. |
| Tx of Cholera | Fluid/electrolyte replacement |
| How is cholera spread? | Contaminated food/drinking water. _Found naturally in marine coastal areas/estuaries |
| 1-20% in endemic regions carriers of this & are asymptomatic | Cholera |
| Primary prevention for cholera | Proper sewage control |
| Gastroenteritis to mild cholera-like illness. Most common cause of food-borne illness in Japan(coastal organism). Endemic in US Gulf Coast. Most frequently associated in US w/mishandling infected seafood | V parahaemolyticus |
| Normal inhabitant of coastal waters. Associated w/OYSTERS. Season: common where WARM. | V Vulnificus |
| Wound infections & contact w/seawater or oysters put you at risk for contracting this | V parahaemolyticus or V Vulnificus |
| Consumption of raw oysters, underlying debilitating pt(alcoholism), bullous skin lesions, shock, liver dysfunction can cause this | Sepsis _high fatality rate |
| Tx of sepsis | Tetracycline |
| Raw oyster consumption may cause this | Acute self-limiting diarrhea |
| Serogroup of E Coli | O Antigen=LPS |
| Serotype of E Coli | H Antigen=Flagella |
| Normal flora E coli this serogroup | O86 |
| Disease carrier serogroup of E Coli | O55 |
| E Coli that looks like cholera disease process. "TRAVELER'S" diarrhea(afebrile, watery). Food poisoning | ETEC =Enterotoxigenic E Coli |
| E Coli that produces diarrhea which becomes bloody after 1-3days with cramps, vomiting. Fever in only ~50% pts. Can be fatal due to HEMOLYTIC UREMIC SYNDROME(HUS) | EHEC O157:H7 =Enterohemorrhagic E Coli |
| Cannot ferment sorbitol so will appear as white colonies on MacConkey's sorbitol agar. | EHEC O157:H7 =Enterohemorrhagic E Coli |
| Complications of EHEC O157:H7 | Hemolytic Uremic Syndrome Acute Renal Failure (8-10%) More common in elderly, young Shiga-like toxin(SLT) key virulence factor |
| Key virulence factor for EHEC O157:H7? =Enterohemorrhagic E Coli | Shiga-like toxin |
| Tx of EHEC O157:H7? =Enterohemorrhagic E Coli | Oral rehydration Avoid Abx Do NOT use Anti-Motility agents in kids/infants |
| EHEC O157:H7 associated with this? =Enterohemorrhagic E Coli | Beef & Raw milk. Person-to-person documented Raw spinach |
| NEW cause of HUS that's traced to alfalfa sprouts. High fatality rate, expressed Shiga toxin | E Coli O104:H4 |
| Microbe widely found in chicken products | Camplyobacter jejuni _incubates 1-7days |
| G- curved rod, motile, microaerophilic, grows well at 42'C | Camplyobacter jejuni _incubates 1-7days _Chicken products |
| Pt has prodrome w/fever, headache, malaise, myalgia 12-24hrs BEFORE diarrhea. See loose stools to frank dysentery, fever, ab cramp. Severe acute Right LQ pain that mimics appendicitis | Camplyobacter jejuni _Improves after several days, self-limiting _Chicken products |
| This diarrhea causing virus is carried & excreted for 2-3 wks after disease. Have severe acute ab pain in Right LQ (mimic appendicitis) because of invasion of mesenteric lymph nodes w/inflammation | Camplyobacter jejuni _Chicken products |
| Found in intestinal tract of birds especially. Transmitted thru food source. mostly. High in young adults, peaks in summer months | Camplyobacter jejuni _Chicken products |
| Complications of Campylobacter jejuni(found in chicken products) | Reiters Syndrome (HLA-B27 individuals) Guillain-Barre Syndrome |
| Chief cause of Guillain-Barre Syndrome? | Camplyobacter jejuni _Chicken products |
| Complication of this causes Reiters syndrome | Camplyobacter jejuni _Chicken products |
| What are signs of Camplyobacter jejuni _Chicken products causing disease? | Fever and prodrome prior to diarrhea |
| Consequence of infection w/Helicobacter Pylori | Chronic active gastritis Peptic ulcers |
| G- curved rods that are HIGHLY motile. Stain best in tissue biopsy w/Giemsa. COPIUS UREASE production | Helicobacter Pylori |
| Primarily targets pylors epithelial cells causing gastritis: cramps, halitosis, nausea, vomiting | Helicobacter Pylori |
| Would eradicating Helicobacter Pylori relieve symptoms | NO correlation |
| Virulence factor for Helicobacter Pylori | Urease _Produces CO2 & NH4 to protect virus(raises pH) and ammonium can be toxic to cells |
| Gastritis caused by this MUST be from large ingestion. Smoking is a risk factor. Associated w/stomach adenocarcinoma | Helicobacter Pylori |
| Dx of Helicobacter Pylori | Histo detection in bio samples+Culture _Microaerophilic environment w/high humidity, 7days incubation, special media _Detect w/CLO test |
| CLO test | Tests for Urease Activity _Helicobacter Pylori DETECTION |
| Tx of Helicobacter Pylori | Tetracycline+Bismuth-containing drugs |
| GI infection prevention | Proper animal excretion control, food handling, hand wash, traveling: boil it, peel it, cook it or forget it. |
| Facultative intracellular enteric bacilli-->inflammatory disease of large bowl. Incubate 3days. | Shigellosis _Normal watery diarrhea-->dysentery(blood, mucuous & PMNs in stool, fever, cramp) |
| Blood, mucuous & PMNs in stool, fever, cramp is a progression from this watery diarrhea | Shigellosis _G Neg, NO spores, Facultative Anaerobe, NONmotile, NonLactose Forming _PMN & RBCs in diarrhea |
| G Neg, NO spores, Facultative Anaerobe, NONmotile, NonLactose Forming that causes dysentery | Shigellosis _Blood & mucous in feces+Acute onset _PMN & RBCs in diarrhea |
| COMPLICATIONS of Shigellosis? _Blood & mucous in feces+Acute onset _PMN & RBCs in diarrhea | Reiter's (Unspecified acute inflamm arthritis) & HUS (Hemolytic Uremic Syndrome) |
| Causes of Reiter's Disease: urethritis, polyarthritis, inflamm eye disease, skin lesions (=nonspecific acute inflamm eye disease) | Campylobacter Jejuni OR Shigellosis |
| Hemolytic Uremic Syndrome seen in these 2 stomach issues because of this toxin production. Causes acute renal failure. | Shigella Toxin: _EHEC (O157:H7) _Shigellosis |
| What is the reservoir for Shigellosis? | Humans! _Therefore highly infectious in kids 1-4 and carrier state can exist ~1-2mos. _Person-to-Person transmission |
| Most severe type of shigella | Group A: _S. Dysenteriae |
| 2nd most severe type of shigella | Group B: (Common in US) _S. Flexneri |
| 3rd most severe type of shigella | Group C: (Common in US) _S. Boydii |
| LEAST severe type of shigella | Group D: _S. Sonnei |
| Prevention of Shigella | Handwashing! |
| Incubate 12-48hrs, sudden onset of sx. 2-3day duration in host (most severe infants/elderly). At risk if cancer, DM, AIDS, person on abx | Salmonellosis _G-, Non-spore form, Facultative anaerobe, Motile, Non-lactose Fermenting |
| How do you determine diarrhea caused by salmonella or shigella. | Won't ferment lactose |
| How you differentiate between salmonella & shigella?? | Both do not ferment lactose, if see: 1)RBC & PMN=Shigella 2)Macs & PMN=INC Leukocytes=Salmonella |
| What do you see when you look at Salmonella in the lab? | Fecal leukocytes: MORE macs than PMNs -Culture: sample food/water/fecal/Blood if have fever _CANNOT ferment lactose! |
| Can use a flourescent Ab test (FA) & serological confirmation for this dx | Salmonella _HIGH dose |
| When should you give abx to treat Salmonella? | Only if disease is systemic (AIDS) |
| Eggs, Beef, Pifs, Dogs, Cat, Reptiles are reservoirs for this | Salmonella _HIGH dose |
| Highest incidence of salmonella | Infants & children 6mos-5yrs (can carry up from 1-2mos to a yr) _Summer/Fall |
| Prevention of salmonella | Change food processing, change animal husbandry, change consumer preferences |
| Owning a pet may carry risk of this if immunocompromised | Salmonella |
| Caused by abx use & interaction with C Difficile (Bacillus, OBLIGATE Anaerobe, G+, forms subterminal spores) | Pseudomembranous Colitis (PMC) |
| Abx which can cause Pseudomembranous Colitis (PMC) by INC C Difficile | Clindamycin, Cephalosporins, Ampicillin, some antineoplastics |
| Why hard to distinguish Pseudomembranous Colitis (PMC) | 1_Diarrhea w/lower ab cramp OR 2_Severe colitis w/o pseudomembrane OR 3_Classic Pseudomembranous Colitis |
| What type of colitis? Profuse diarrhea, pain, FEVER, nausea, malaise, dehydration | Severe colitis w/o pseudomembrane (no dying cells) |
| Severe colitis sx w/ELEVATED YELLOW PLAQUES 2-10mm over mucosa. | Pseudomembranous Colitis (PMC) _See dying cells |
| Fibrin mesh of necrotic cells, PMNs, Monos & RBCs | Pseudomembrane |
| How do you detect Pseudomembranous Colitis (PMC) | Detect toxin in feces (EIA/Latex agglutination assay. Tissue culture assay) _Gram Stain of stool G+ rods w/SUBTERMINAL spores |
| See subterminal spores | Pseudomembranous Colitis (PMC) _Abx-->C Difficile |
| Many hospitals will screen abx-associated diarrhea for this | Pseudomembranous Colitis (PMC) _Abx-->C Difficile |
| Pseudomembranous Colitis (PMC) Tx still may not prevent this | Relapse (20%). Many will suffer multiple relapses. |
| Predisposing factor for Pseudomembranous Colitis (PMC) | Normal gut flora disruption allowing for subsequent colonization by C Difficile |
| Many infants can harbor this organism as normal flora w/o being sick | C. Difficile |
| Increased outbreaks of C. Difficile-->Pseudomembranous Colitis (PMC) here | Nosocomial (hospitals) _ASYMPTOMATIC pts act as reservoir --->Make sure to clean toilets |
| Acute food-borne G+ bacillus (NONmotile). Aerotolerant anaerobe. Spore former | C. Perfringens Type A _SHORT incubation time (complete recovery in 1 day) _Meat/Poultry(cooking does NOT kill spores) _HIGH dose |
| To dx C Perfrigens (G+ bacillus, NONmotile, Aerotolerant anaerobe, spore former) what must you do? | Isolate LARGE #'s of microbe in food/feces since HIGH dose organism |
| G+, Bacillus, AEROBIC MOTILE spore former | Bacillus Cereus Foodborne Dz (No Fever!) 1)Emetic Form=1-5hrs after 2)Diarrgheal form=1-17hrs after _Grain/Rice/Veggies |
| Preformed toxin will cause Upper GI sx 1-5hrs after ingestion of this G+, Bacillus, AEROBIC MOTILE spore former ? | Emetic Form of Bacillus Cereus Foodborne Dz _No fever _Grain/Rice/Veggies |
| Ingestion of INC # of vegetative cells that produce this toxin will cause profuse watery diarrhea 1-17hrs after ingestion | Diarrheal Form of Bacillus Cereus (No fever) _G+, Bacillus, AEROBIC MOTILE spore former _Grain/Rice/Veggies |
| Second ONLY to Salmonella as a cause of foodborne dz. Caused by consumption of HEAT STABLE PREFORMED TOXIN in food | Staphylococcal Foodborne Dz(Enterotoxin A) _Acute emetic/diarrhea 1-6hrs after eating _INC Saliva _Recover 1-4days |
| Acute emetic/diarrhea with INC saliva after 1-6hrs of ingesting food. Self-limiting | Staphylococcal Foodborne Dz(Enterotoxin A) _Eating a HEAT STABLE PREFORMED TOXIN |
| Virulence Factor for Staphylococcal Foodborne Dz(custard filled baked goods, canned foods, processed meats, potato salads) | Enterotoxin A(water sol, heat stable). _Emetic response: stimulate CNS to vomit _Diarrheal: INC transmucosal movement into lumen coupled w/DEC H20 Absorption |
| Toxin absorbed in gut, stimulus reaches CNS impulse to vomiting center | Emetic Response of: Enterotoxin A=Virulence Factor for Staphylococcal Foodborne Dz _(custard filled baked goods, canned foods, processed meats, potato salads) |
| INC fluid transmucosal movement into lumen coupled with DEC water absorption | Diarrheal Response of: Enterotoxin A=Virulence Factor for Staphylococcal Foodborne Dz _(custard filled baked goods, canned foods, processed meats, potato salads) |
| Source of Enterotoxin A=Virulence Factor for Staphylococcal Foodborne Dz | Humans! (Human-to-human interaction) _Warm conditions _Only ~50% link to lesion-carrying individual linked to dz _(custard filled baked goods, canned foods, processed meats, potato salads) |
| Can you use abx on Enterotoxin A=Virulence Factor for Staphylococcal Foodborne Dz | No, this is an intoxication, abx will NOT help |
Created by:
glittershined
Popular Medical sets