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Micro_Test1

QuestionAnswer
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
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