Microbiology 208

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What is the Ziehl-Neelson stain?: -stains for mycobacterium -mycobacterium don't gram stain because of lipid and wax in cell envelope -everything that's not mycobacterium gets stained blue -mycobacterium get stained by carbol fuschin
What colors are gram positive stain and gram negative stain?: Gram positive= blue Gram negative = red
What accounts for the difference in gram staining?: Gram positive organisms have thick cell wall that inhibits decolarization/hold the gram stain
What does the gram stain tell you?: 1. the shape -cocci or rod 2 whether the organism is gram positive or gram negative
How does the M protein cause molecular mimicry?: -There is sufficient amino acid homology between M protein of group A strep and mammalian proteins that form an alpha helix -myosin, tropomyosin, keratin, laminin, sarcolemmal proteins -IgG made against M protein of group A strep can cross-react and bind to host proteins in heart with similar epitopes -> inflammation and acute rheumatic fever -but no direct evidence that it's the antibodies that cause irreversible damage to the heart
Name the features common to all prokaryotes.: 1. Nucleoid 2. 70s ribosomes 3. Absence of membrane bound organelles 4. A cell envelope 5. Rigid cell wall 6.Absence of sterols in their membranes 7. cytoplasmic membrane 8. mesosomes 9. introns virtually absent 10. transcription is coupled to translation
All prokaryotes lack sterols in their cell membrane EXCEPT: mycoplasma
What are the features of the cell wall of prokaryotes?: -made up of petidoglycan -backbone sugars connected by beta1-4 linkage -parallel chains of PDG are cross-linked
What structural feature of prokaryotes does lysozyme target?: lysozyme= enzyme present in tears, saliva -cleaves beta(1-4) linkages of backbone sugars of the peptioglycans that make up the cell wall
What structural feature of prokaryotes does Beta lactam anti-biotics target?: =transpeptidase -this is the enzyme responsible for cross-linking parallel chains of peptidoglycans in the cell wall
What are the functions of the prokaryotic cell wall?: 1. provides shape to cell 2. prevents cell lysis 3. block entry of hydrophobic compounds
What are some features of the cytoplasmic membrane of prokaryotes?: Unique features: 1. DNA attachment site for nucleoid, plasmid 2. mediates iron uptake via siderophores 3. fxn in protein export 4. site of electron transport chain 5. site of PDG synthesis
What is a mesosome?: =Invagination of cytoplasmic membrane of a prokaryote -found in gram-positive bacteria
List of features found in some prokaryotes that can be used in classification.: 1. Unique metabolic capacities 2. capsule 3. flagella 4. glycocalyx 5. storage granules 6. presence of electron transport chain 7. spores
What is a capsule on a prokaryote?: =layer of acidic sugars surround organism -fxn: defend organism against phagocytosis -usually has 2-3 sugars characteristic of organism -can use Quellung rxn to differentiate for S. pneumoniae
What is a Quellung rxn?: =lab test to type S. pneumoniae by its capsule -mix test tube of S. pneumoniae with unknown capsule type with a known Antibody against a certain capsule -positive result: capsule swells
What are the 2 types of flagella?: 1. Peritrichous flagella 2. Polar flagella Note: you can use the flagella stain to distinguish among bacteria
What is peritrichous flagella?: =flagella are all over the organism -Example: Eubcateriales
What is polar flagella?: =flagellum located at one end of organism -Example: Pseudomonadales
What are the functions of the glycocalyx?: 1. inhibit phagocytosis 2. help organism stick to surfaces
What are 3 types of storage granules and what do they store?: 1. Poly-beta-hydoxybutyrate -stores lipids 2. Glycogen or starch -store sugars 3. polymetaphosphate -store phosphate
What are spores?: =cryptobiotic -dormant form of organism -no metabolic activity -resistant to environmental conditions
What are 2 types of gram positive bacteria that produce spores?: 1. Bacillus (ex. B. anthracis) 2. Clostridium
What are the structural components of a spore, from outside to inside?: 1. Coat 2. Cortex -2 layers of PDG -inner more cross-linked 3. Germ cell membrane 4. Core -high concentrations dipicolinic acid and Ca -materials for resuming growth
What are the features of gram positive bacteria?: 1. Cell envelope -different components vs gram negative 2. Lipoteichoic acid 3. No sex pili 4. Permeases -in cytoplasmic membrane -involved in active transport of nutrients
How does the cell envelope of gram positive and gram negative bacteria differ?: Gram Positive 1.PDG layer -very thick cell wall 2. Plasma membrane Gram Negative 1. Outer membrane 2. PDG layer -very thin 3. Plasma membran
All of the following are found in the outer membrane of a gram negative bacteria EXCEPT 1. lipoprotein 2. permeases 3. porin 4. LPS: permeases -these are found in the cytoplasmic membrane in both gram negative AND gram positive
Define LTA: =Lipoteichoic acid -characteristic of gram positive bacteria -fxn: anchoring and adhesion -glycerol or ribitol anchored to glycolipid in membrane
Define LPS: =lipopolysaccharide =endotoxin -feature of gram negative bacteria -located in outer membrane
What are the components of LPS: 1. Lipid A -responsible for endotoxic symptoms 2.Core 3. oligosaccharide side chain -group specific
What are some of the features of gram negative bacteria?: 1. cell membrane differences 2. LPS 3. Nutrient binding proteins 4. adhesions/evasions 5. lipoprotein 6. periplasmic space 7. membrane derived oligosaccharide 8. porins 9. permeases
Define Teichoic acid: =polysaccharides linked by phosphodiester bonds -found on some gram positive bacteria -fxn: 1. anchoring 2. antigen specificity
How do gram positive and gram negative bacteria adhere to stuff? Are they different?: Gram positive -have a surface layers of polysaccharides to provide adhesion Gram negative -have common pili/fimbriae for adhesion -also have sex pili for genetic exchange
What is the catalase test?: -use to tell you if gram positive cocci is: 1. staphylococcus or 2. streptococcus -drop hydrogen peroxide on step --> nothing happens -drop hydrogen peroxide on staph --> bubbles
What is the coagulase test?: -use to distinguish Staphylococcus aureus and non-pathogenic staph (both will turn positive on catalase test) -if a clot forms -> S. aureus -no clot form -> non-pathogenic staph -coagulase enzyme allows organism to clot plasma around it -> allows it to resist phagocytosis
What is the optochin test?: -used to identify steptococcus pneumoniae (will have negative catalase test) -if S. pneumoniae will get zone of inhibition around P disk where bacteria have lysed
What is the Bacitracin test?: -Test to identify group A streptococcus -group A strep sensitive to antibiotic bacitracin -if group A strep-> will see zone of inhibition around A disk
What is the oxidase test?: -test for pseudomonas and neisseria -these have cytochrome c oxidase in their electron transport chanin -if oxidase positive -> color change to dark purple -if no color change, just means it does not have oxidase, it does not mean it doesn't have an electron transport chain!
What are the 4 phases of the bacterial growth curve?: 1. Lag Phase ~incubation period 2. Log Phase 3. Stationary Phase 4. Death Phase
What happens during the log phase of the growth curve?: 1. unrestricted growth by division -diff. bacteria have characteristic growth/doubling times
What happens during the stationary phase?: 1. no net growth 2. environmental conditions not as good as log phase -diff. bacteria respond differently (could have long or short stationary phase) 3. turn on virulence genes to try to change conditions
What are 3 requirements for bacteria growth?: 1. Nutrients -ex. iron 2. Energy source -can be derived from fermentation (does NOT require O2 or an electron acceptor) OR respiration (requires those things) 3. Removal of toxic metaolites -ex. superoxide
How is iron an important nutrient for bacteria?: 1. Required nutrient for bacterial growth 2. Also impt for virulence of bacteria -hosts will try to restrict free iron in the body as a way to control bacterial growth -so bacteria have to have a way to get their iron
What are 3 mechanisms that bacteria use to capture iron?: 1. Produce siderphores to compete with iron binding proteins -ex. some strains of E. coli 2. Direct uptake by stealing from transferrin/lactoferrin -ex. Neisseria 3. Use of heme from breakdown tissues -Bacteroides
How do humans and bacteria differ in regards to fermentation?: -humans: fermentation generates an oxygen "debt" that must be made up -bacteria: don't run up oxygen debt; can directly release fermentatin end products into the environment
What are some fermentation end products released by bacteria?: -Fermentation end products can be used to classify bacteria 1. Ethanol 2. Lactic Acid 3. Propionic Acid 4. Mixed Acid -ex. formic acid 5. Butanediol 6. Butyric Acid and CO2
Which prokaryotes make ETHANOL as a fermentation end product?: =yeasts
Which bacteria make LACTIC ACID as a fermentation end product?: =streptococcus
Which bacteria make PROPIONIC ACID as a fermentation end product?: 1. Propionbacterium =common skin bacteria that cause acne
Which bacteria make MIXED ACID as a fermentation end product?: =E. coli family of enterobacteriaceae -mixed acid= lactic acid, formic acid, acetic acid
How do some Enterobacteriaceace make gas from formic acid?: =have enzyme formic hydrogenlysase that breaks formic acid down to CO2 and H2 ->pH drops -ex: E. coli -Shigella doesn't have this enzyme
Which bacteria make BUTANEDIOL as a fermentation end product?: =Klebsiella (enterobacteriaceace family)
Which bacteria make BUTYRIC ACID and CO2 GAS as fermentation end product?: =Clostridium
Why is superoxide ion important?: =Metabolic byproduct produced by all organisms when they are exposed to O2 -some bacteria differ in ability to detoxify/get rid of enough superoxide ion
What is the enzyme that detoxifies superoxide ion?: =superoxide dismutase -breaks down superoxide to hydrogen peroxidase -most bacteria have either catalase or peroxidase to break down the hydrogen peroxide
Define obligate anaerobes: =bacteria that die when exposed to oxygen -b/c lack superoxide dismutase or don't make enough to get rid of superoxide ion
Define obligate aerobes.: =organisms that lack ability to ferment -must have O2 to survive -have electron transport chain -produce superoxide dismutase and catalase/peroxidase -ex. Mycobacterium tuberculosis
Define facultative organism.: =an organism that can grow with or without oxygen -E. coli, streptococcus, pseudomonas aeruginosa -have superoxide dismutase and catalase/peroxidase -have an electron transport chain
How is streptococcus a unique facultative organism?: -lacks electron transport chain b/c can't make heme groups -but contains superoxide dismutase so can tolerate being in oxygen and considered facultative
Why is pseudomonas aeruginosa considered a facultative organism?: -most pseudomonas are considered obligate aerobes (respire only) -under anaerobic conditions, P. aeruginosa can use nitrate as terminal electron acceptor
How do obligate anaerobes make ATP?: 1. ferments only -clostridium 2. ferments and respires -b. fragillis -has terminal electron acceptor other than oxygen
How do obligate aerobes make ATP?: 1. Respiration ONLY -b/c don't have the enzymes for fermentation
How do facultative organisms make ATP?: 1. Ferments ONLY -no electron transport chain -have superoxide dismutase -ex. streptococci 2. Ferments & respires -use electron transport chain -ex. E. coli 3. Respires ONLY -no enzymes for fermentation -under anaerobic conditions can use terminal electron acceptor other than O2 -ex. P. aeruginosa
Define Plasmids: =accessory circular DNA molecules found in some bacteria -# and type of plasmids can vary between individual strains -> creates genetic diversity -plasmids can contain: 1. virulence genes 2. anti-biotic resistance genes
Name some features of the bacteria genome.: 1. single circular DNA chromosome 2. about 2-5 thousand genes 3. genes clustered according to biochem fxn and transcribed as a unit (form operon) 4. little non-coding DNA 5. introns are absent
What are some sources of genetic diversity among individual bacterial strains?: 1. plasmids (# & type) 2. phage and phage remnants 3. insertions and deletions of DNA segments (large and small)
What are some genetic differences between E. coli 0157:H7 and E. coli K12?: 1. O157:H7 has 1400 genes not found in K12 2. K12 has 500 genes not found in O157:H7 3. BP differences in genes shared by K12 and O157:H7 4. O157:H7 has plasmid with virulence genes 5. O157:H7 has lysogenic phage encoding Shiga-like toxin
Define wild type: =fxn form of a gene found in nature
Define prototroph: =organism with wild type genes -able to grow with simple requirement for nutrients
Define auxotroph: =a mutant unable to synthesize a required small molecule -must obtain molecule from environment -compared to prototroph requires 1-2 additional nutrients for growth
Define fastidious organism.: =wild type bacteria that have complicated growth requirements -may be tough to grow in culture
Can plasmids replicated themselves?: yes
Define episome: =a nonessential genetic element that can exist 2 ways in bacterial cell 1. integrated into bacterial chromosome 2. free in cytoplasm -ex F plasmid
Define conjugative plasmid: =plasmid capable of transmitting itself between bacteria
Define nonconjugative or mobilizable plasmid: =plasmid that needs help of a conjugative plasmid to transmit itself to other bacteria
Compare broad host range plasmid vs narrow host range: broad=plasmid capable of replication in many unrelated hosts narrow=plasmid that can only replicate in single or couple of closely related host species
Define copy number: =number of plasmids per cell
True or False: bacteria can acquire new DNA: True. this is one method of genetic change in bacteria other method is mutation of existing DNA -mutation rates can vary by environmental conditions
Define bacteriophage: = a virus that infects bacteria -phage genome can be DNA or RNA -2 types of infection: 1. lytic 2. lysogenic (only some bacteriophage capable)
compare lytic and lysogenic infections: =2 types of infections by bacteriophage Lytic= inject DNA, viral DNA takes over metabolic process -> make daughter phages -> daughter phages accumulate -> cell lyses and release progeny Lysongenic =viral dna can integrate into host chromosome or replicate as plasmid, viral dna gets passed on when bacteria divide ->when environmental conditions right, phage excises from host dna-> enters lytic infection
Define insertion sequences: =short pieces of dna that can insert into chromosome but not capable of autonomous replication (unlike plasmid)
What do insertion sequences contain: 1. inverted repeats at the end 2. the gene for transpose =enzyme that allows insertion sequences to jump in and out of pieces of dna -do not need homology with host dna
define transposons: =sequence that behave like insertion sequences flanking other genes -can flank anti-biotic resistance genes -don't need homology with host dna
True or false: anti-biotic resistance can be conferred from a single base pair change.: true
What are the 3 mechanisms of genetic exchange between bacteria?: 1. phage-mediated transfer (transduction) 2. conjugation 3. transformation
True or false: all plasmids are circular: false. -Borrelia species have linear plasmids
Describe phage mediated transfer: -bacterial chromosome gets cut up into pieces and packaged into phage capsules -capsules released w/cell lysis ->float around until infect new cell -bacterial dna gets injected into host -if sufficient homology ->recombination -> bacterial dna from phage incorporated into host
What are the characteristics of generalized transduction?: 1. any gene can be passed to new host bacteria 2. generalized transduction occurs at low frequency 3. no viral dna passed to new host 4. donor & recipient must be closely related to be sensitive to same phage
When does specialized transduction occur?: -when lysogenic phage does sloppy job excising from bacterial dna, takes piece of host dna with it
What are the characteristics of specialized transduction?: 1. transfer of bacterial DNA done by mutant bacteriophage carrying bacterial dna 2. occurs at higher freq. than generalized transduction 3. usu. only few specific genes are excised b/c bateriophage can integrate into host chromosome in few specific places 4. new host can have 2 copies of transduced gene
Which of the following undergo specialized transduction a. streptococcus pneumoniae b. mycobacterium c. C. Diptheriae: =C. diptheriae
Define conjugation: =sex in bacteria -most common mechanism of genetic exchange -very efficient -occurs in both gram negative and gram positive bacteria -requires physical contact between donor and recipient cells -donor cells keep copy of a plasmid
True or false: plasmid carrying antibiotic resistance can spread to different bacterial populations via conjgation: true
True or false: in specialized transduction all progeny phages carry same gene: true
True or false: Hfrs transfer entire chromosome during conjugation: False. -only part gets transferred b/c bacteria can't sustain mating for time it takes to transfer everything
Define F factor: =plasmid found in E. coli impt for conjugation "F" = fertility -bacteria with an F factor can produce sex pili
Describe the process of conjugation: 1. sex pili anchor donor (F+) cell to recipient (F-) 2. F plasmid transfers linear strand of its dna to recipient and donor keeps circular F plasmid 3. single-strand F plasmid in recipient replicates missing strand and circularizes 4. now both donor and recipient are F+
Define transformation: =method of genetic exchange where free dna released by dying bacteria into the environment is taken up by other bacteria and incorporated into their chromosomes
What does transformation require?: Must be sufficient homology between foreign and host dna for recombination event to incorporate foreign dna into host chromosome
What is the name of a gram positive that can undergo transformation?: streptococcus pneumoniae
Name 3 gram negative bacteria that can undergo transformation.: 1. neisseria gonorrhea 2. haemophilus influenzae 3. heliobacter pylori
Can transformation be artifically induced?: yes. -in labratory with heat shock or electrical shock
What are some factors that help bacteria adapt to environmental changes?: 1. Sigma factors 2. Type III secretions systems 3. 2 component regulators
Define Sigma factors: =proteins that must bind in order for RNA polymerase to recognize promoters -changing sigma factors changes which genes get expressed -in stressful conditions can switch sigma factors
What 2 sigma factors can be made during infection in response to stressful conditions in host?: 1. Heat shock sigma factor 2. Stress or stationary phase sigma factor -tied to virulence genes
Define Type III secretions systems: =mechanism to secrete specific proteins into host cells -used by gram negative bacteria like enterobacteriaceae -induced by signals from host cells or specific environmental signals
How do Type III secretions systems: -it forms a channel between inner and outer membranes of bacteria and host membranes -bacterial virulence proteins delievered directly to host cell -impt for many diseases caused by many gram-negative pathogens
Define two component regulators: =mechanisms bacteria use to sense the environment and respond -one component fixed on outer membrane senses environment conditions -under certain conditions, phosphorylate transcription factors -> produce virulence genes
Define pathogenicity island.: =island of dna (several genes to over 100) that contains virulence genes
What diseases are associated with E. coli O157:H7?: 1. hemorrhagic colitis 2. Hemolytic uremic syndrome 3. death in children
How did E. coli O157:H7 acquire its virulence factors?: 1. pathogenicity island -genes for type III secretion system, adherence to intestinal muscosa, way to efface epithelial cells 2. plasmid -genes for: adherence, hemolysin, protease that degrades coag factor V 3. lambda-like phage encoding shiga toxin
Name some features found in all staphylococci.: 1.Gram positive bacteria that grow in clusters 2. divide perpendicular to last plane of division 3. catalase POSITIVE 4. Facultative organisms 5. Electron transport chain 6. Non-motile
Define staphylococcus aureus: =main pathogen of genus staphylococcus (gram positive bacteria)
Name some features unique to S. aureus.: 1. Coagulase positive 2. Thermostable nuclease positive 3. High salt tolerance 4. Ferments mannitol 5. Ribitol in teichoic acid 6. Produces golden pigment from carotenoids -may not always be seen 7. hemolysis seen on blood agar after 24-36 hours
What are features that identify other forms of staphyloccocus than S. aureus?: 1. coagulase negative 2. mannitol fermentation negative 3. thermostable nuclease negative
Define Staphylococcus saprophyticus: =gram positive bacteria 1. coagulase negative (differs from S. aureus) 2. Novobiocin resistant 3. Glycerol in teichoic acid
Define staphylococcus epidermis: =gram positive bacteria 1. coagulase negative (differs from S. aureus) 2. Novobiocin sensitive 3. Glycerol in teichoic acid 4.Slime is its virulence fator
A positive catalase test tells you...: =staphylococcus -add hydrogen peroxide-> bubbles b/c staph able to break it into O2 gas and H20 -able to break down (vs strep) b/c can make heme groups, including one needed for catalase
What disease does S. epidermis cause?: =coagulase negative staphylococci -pathogen originating in hospital -forms biofilm that can cling to foreign bodies like IV catheters and prostethic devices
What disease does S. saprophyticus cause?: =coagulase negative staphylococci -10-20% of UTIs in young women
What are some general features of S. aureus: =gram positive, coagulase positive staphylococci -very hardy pathogen -diseases caused tend to be: 1. localized 2. toxin mediated -makes enzymes leukocidic and hemolysin 1. able to kill neutrophils 2. contribute to inflammation
Describe the carrier state for S. aureus: NOT normal flora -can transiently colonize nasopharynx -Colonization can occur in: 1. nasopharynx 2. skin 3. vagina -increased chances of being colonized occur in 1. medical personnel 2. diabetics 3. IV drug users
What kinds of infections can S. aureus cause?: 1. Direction infection -skin -deep (post-trauma, surgery: osteomyelitis) 2. Bloodstream infections 3. Toxin mediated disease
What kinds of skin infections can S. aureus cause?: 1. Folliculitis 2. Furuncles 3. carbuncles 4. abscesses 5. cellulitis 6. wound infection
Name some bloodstream infections caused by S. aureus: -usu. secondary to direct infections (ex. skin or deep) - +/- metastatic infections 1. osteomyelitis 2. endocarditis 3. lung abcess 4. septic arthritis
Name some toxin mediated diseases caused by S. aureus.: 1. food poisoning 2. scalded skin syndrome, bullous impetigo 3. toxic shock syndrome
All of the following are major shapes of bacteria except: 1. conical 2. Bacilli 3. spiral forms 4. cocci 5. pleomorphic: =conical -cocci = spherical -bacilli = rods -spiral forms = comma-shaped, S-shaped, or spiral shaped -pleiomorphic= lacking a distinct shape
Name 6 gram positive bugs that cause disease in humans: 2 cocci, 4 bacilli 1. Streptococcus 2. Staphylococcus 3. Bacillus (makes spores) 4. Clostridium (makes spores) 5. Corynebacterium 6. Listeria
Name the one group of gram-negative cocci: =Neisseria -diplococci
Name the one group of gram-negative spiral shaped: =spirochetes -too small to be seen with light microscope -surrounded by additional phospholipid rich membrane layer to hid from immune recognition -periplasmic flagella
Name an organism that is neither gram positive or gram negative: =mycoplasma -b/c doesn't have a cell wall
What is special about the staining of mycobacteria?: -weakly gram positive -stain better with acid-fast stain -cause: 1. TB 2. leprosy
How can you differentiate staph and strep?: -both = gram + cocci 1. appearance on gram stain -strep = strips -staph = clusters 2. catalase test -staph bubbles when add hydrogen peroxide (catalase +)
How can different species of strep be classified?: 1. Completeness of hemolysis of RBCs 2. Lancefield Antigens Others 1. biochemical rxns 2. Growth characteristics 3. Genetic studies
Name 5 significant forms of strep that cause disease in humans.: 1. Strep A (strep pyogenes) 2. Strep B (strep agalactiae) 3. Strep D (enterococci and nonenterococci) No Lancefield Antigens 4. Strep pneumoniae 5. Strep Viridans (big group)
Explain hemolysis classification of strep: -incubated overnight on agar plate -based on completeness of hemolysis of RBCs 1. Alpha= only partial hemolysis -green color due to metabolite of hemoglobin 2. Beta=complete hemolysis -clear zone surrounding colony 3. Gamma= no hemolysis
Define Lancefield Antigens: =way to classify different species of strep -based on antigenic characteristics of C carbohydrate (found on cell wall) -Can be: A,B,C,D,E...S
Name features of group A strep: =strep pyogenes 1. Beta hemolytic 2.Lancefield Antigen A 3. M protein -virulence factor -inhibits activation of complement; protects organism against phagocytosis 3. Enyzmes (streptolysin O, streptolysin S, pyrogenic exotoxin, streptokinase, hyaluronidase, DNAases, anti-C5a peptidase)
Define M protein: =major virulence factor for group A strep -fxns: 1. inhibits activation of complement 2. protects against phagocytosis -B cells can make antibodies against it -how much on surface basis of classification for group A strep -M protein adheres to epithelial cells -M protein binds fibrinogen -> can then bind plasminogen -M protein contributes to rheumatic fever pathogenesis -alpha helical structure and is attached to PDG
Define streptolysin O: O=oxygen labile (gets inactivated by oxygen) =enzyme seen in group A strep -destroys RBCs and WBCs -why group A is beta hemolytic -antigenic -antibodies will be made against it
Name 6 diseases caused by group A strep: 4 by local invasion +/- exotoxin release 1. Strep pharyngitis 2. Strep skin infections 3. Scarlet fever 4. Strep toxic shock syndrome 2 delayed antibody mediated diseases 1. rheumatic fever 2. glomerulonephritis
What are the symptoms of strep pharyngitis: 1. red, swollen and pharynx 2. purulent exudate on tonsils 3. high temp 4. swollen lymph nodes
Name some skin infections caused by group A strep: 1. Folliculitis 2. pyoderma 3. erysipelas 3. cellutis 4. impetigo -these infections can also be caused by staph aureus also 1. Necrotizing fascitis and fournier's gangrene
Describe necrotizing fascitis: =caused by group A strep -m proteins block phagocytosis so bacteria can move rapidly thru tissue -trauma -> break in skin -> strep A gets in -> infection along fascia -high mortality rate even when treated
What are the symptoms of necrotizing fascitis?: 1. Swelling, heat, redness at site of infection 2. skin changes color and dies 3. bullae (blisters) tx: 1. surgically remove fascitis 2. penicillin G
What other bugs besides strep group A can cause necrotizing fascitis?: 1. staph 2. clostridium 3. gram negative enterics 4. mixed species
Define fournier's gangrene: =necrotizing fascitis of male genital area and perineum causes: 1. mixed organisms 2. group A strep
How does group A step cause scarlet fever?: 1. by producing pyrogenic toxin (exotoxin) -produces fever and scarlet-red rash
Define streptococcal toxic shock syndrome: -caused by group A strep (similar syndrome caused by S. aureus) -b/c of release of pyrogenic toxin
Describe the characteristics of group B strep: 1. beta hemolytic 2. Think B for baby -cause diseases in: 1. babies 2. immunocompromised
How does group B strep cause diseases in babies?: -some women carry group B strep vaginally -baby acquires during delivery -can cause 1. meningitis 2. pneumonia 3. sepsis
All of the following are important causes of meningitis in neonates except: 1. group B strep 2. neisseria menigitis 3. E.coli 4. Listeria monocytogenes: =neisseria meningitides -major pathogen for meningitis later in life but not in newborn period
Describe main features of strep group viridans.: 1. Big group 2. Alpha hemolytic 3. Normal GI flora 4. Also found in 1. nasopharynx 2. gingival crevices
Name 3 types of infections strep viridans causes: 1. Dental infections 2. endocarditis 3. abscesses
Define Group D strep: 1. alpha hemolytic 2. can be classified as 1. enterococcus 2. non-enterococcus
Characterize S. enterococcus: =group D strep 1. normal bowel flora 2. alpha hemolytic 3. grow in high bile, high NaCl conditions 4. common cause of hospital acquired infections 5. resistant to ampicillin and vancomycin
What diseases do group D strep enterococci cause?: 1. UTIs 2. biliary tract infections 3. bacteremia 4. subacute endocarditis in hospital can also cause: 1. wound infections 2. sepsis 3. heart valve endocarditis
Describe group D strep non-enterococci: =S. bovis 1. alpha hemolytic 2. can grow in high bile amounts 3. lives in GI tract 4. cause similar diseases to enterococci 5. Bovis in blood: better beware cancer in bowel (S. Bovis can be marker for colon cancer)
Define S. pneumoniae: 1. no lancefield antigen 2. lancet-shaped gram positive cocci arranged in pairs 3. Polysaccharide capsule is virulence factor 1. protects from phagocytosis 4. 84 diff. serotypes (based on capsule) 5. Some strains resistant to penicillins
What diseases does S. pneumoniae commonly cause?: 1. Bacterial pneumonia (adults) 2. Bacterial meningitis (adults) 3. otitis media (kids)
What 2 important lab tests identify S. pneumoniae: 1. Quellung rxn -mix w/ serum that contains Ab and stain-> S. pneumonia capsule swells 2. Optochin sensitivity -differentiates S. viridans from S. pneumoniae -S. pneumoniae growth will be inhibited on plate with optochin
What's in pneumovax and who should get it?: =vaccine against S. pneumoniae 1. Contains 25 most common capsular polysaccharide antigens 3. Good for: 1. elderly 2. immunocompromised (HIV, no spleen) -not good for kids
Name some features found in all steptococci: 1. gram positive cocci that grow in chains or pairs -cell division in single plane resulting in chains 2. unable to synthesize heme -no etc; ferment glucose to lactic acid ALWAYS -catalase negative 3. auxotrophic 4. grouped by hemolysis on blood agar plates
Define enterobacteriaceae: =gram negative rods 1. Found in: 1. normal GI flora 2. soil and water 3. plant or insect pathogens 2. All members of this family look alike on gram stain so use special tests to differentiate
Describe characteristics shared by all members of the family enterobacteriaceae: 1. gram negative rods 2. do NOT produced spores 3. Peritrichous flagella -except: Klebsiella, Shigella 4. Oxidase negative 5. facultative organisms -can ferment or respire 6. can reduce nitrate to nitrite
All enterobacteriaceae have peritrichous flagella EXCEPT:: 1. Klebsiella 2. Shigella -non-motile
Name 3 outer-membrane antigens in enterobacteriaceae: 1. K -capsule 2. O -polysaccharide chain of endotoxin or LPS 3. H -flagella
What is the function of the K antigen in enterobacteriaceae?: K=capsule 1. Anti-phagocytic 2. Adhesion -in E.coli helps adhere to GU epithelium in nephroitogenic strains
How do enterobacteriaceae adhere to host cells?: 1. K antigen -capsule 2. O antigen -some promote adherence 3. pili/fimbriae
Compare type 1 vs type 2 pili in enterobacteriaceae: Type 1=mannose sensitive -bind to same site on host cells as mannose -if add mannose first to tissue culture, mannose will bind to all available binding sites and block enterobact. from binding Type 2=mannose resistant -bind at different site on host cell than mannose -adding mannose first to culture will NOT prevent binding -impt virulence factor to help cause disease outside of niche
Name 3 types of fimbriae in enterobacteriaceae: 1. P fimbriae -bind to glycolipids on human P blood group -nephritogenic E.coli 2. X adhesiins -bind diff. globosides -nephritogenic E. coli 3. BFP -bundle forming pili -attach pathogenic E.coli to epithelial host cells
Which 2 forms of strep can cause subacute endocarditis?: 1. strep viridans 2. group D strep -eat at heart valve slowly (vs. staph) -Helped out by strep pyogenes 1. S. pyogenes -> rheumatic fever ->heart damage -> easier for group D and viridans to adhere to valve and cause SBE
All enterobacteriaceae can ferment lactose to gas and acid EXCEPT:: 1. Salmonella 2. Shigella 3. Yersinia -Note: Pseudomonas also non-lactose fermenter Note: most enterobacteriaceae normally found in gut can ferment lactose; most pathogenic ones cannot -can use this in a lab test to check stool for pathogenic enterobact. based on inability to ferment lactose
Compare selective vs differential media: Selective media =growth media made with bile, antibiotics, etc that will inhibit growth of unwanted organisms Differential media =allows similar organisms to be distinguished based upon a metabolic property (ex. lactose fermentation)
Name 2 tests for lactose fermentation applied to enterobacteriaceae: 1. EMB test -eosin methylene blue agar 2. MacConkey Agar
Describe EMB agar: -tests for lactose fermentation 1. eosin inhibits growth gram positive species 2. only sugar on plate is lactose. If able to ferment lactose, will cause drop in pH (produce acid) -> colony appears colored 3. Colonies that cannot ferment lactose will be colorless/color of agar
Describe MacConkey agar: 1. High bile content in plate inhibits growth gram positives 2. if lactose fermented, acid produced, pH drops, colony appears colorled 3. non-fermenter, colony appears colorless
Define methyl red test: -test to see if organism is enterobacteriaceae that uses mixed acid pathways to break down pyruvate -positive 1. E. coli 2. citrobacter
Define VP test: =test to see if organism uses 2,3-butanediol pathway to break down pyruvate -if acetoin (intermediate in pathway) is detected -> color change -VP positive 1. Klebsiella 2. Enterobacter 3. Serratia
Describe colony characteristics of E. coli: 1.grows with green sheen on EMB agar 2. can be primary pathogen or opportunistic pathogen 3. commensal in GI tract -synthesizes vit K -deconjugates bile salts, sex hormones -protects against pathogens by occupying Rcs -make colicins -stimulates anti-microbial peptide synthesis by epithelia cells
Describe colony characteristics of Klebsiella: =enterobacteriaceae 1. produces large, goopy capsule in high glucose 2. non-motile (no H antigen) 3. does NOT cause enteric infections -can cause infections outside of enteric system in hospitalized system 4. can be primary or opportunistic pathogen
Describe colony characteristics of Shigella: 1. non-motile (lacks H antigen) 2. does NOT make gas from formic acid 3. Primary pathogen -usu. not invasive outside colon 4. all species obligate human pathogens 5. most virulence factors plasmid encoded
Describe colony characteristics of Salmonella: 1. All make H2S -EXCEPT: S. typhi 2. primary pathogen 3. S. typhi and S. paratyphi are obligate human pathogens
Describe colony characteristics of Proteus: =enterobacteriaceae 1. Swarms on agar plates -EMB: looks like ripples 2. has urease that helps it to cause UTIs -if urine pH>8, suspect proteus 3. opportunistic pathogen
Compare primary pathogens vs opportunistic pathogens: primary pathogens =capable of causing disease in anyone opportunistic pathogens -only cause disease in certain conditions or certain hosts -some pathogens can be both
All of the following are opportunistic enterobacteriaceae EXCEPT: a. proteus b. enterobacter c. E. coli d. Klebsiella e. salmonella: =salmonella Note; E.coli, Klebsiella can be both primary pathogen and opportunistic
How are some enterobacteriaceae pathogenic: =acquired additional genetic material; virulence factors -genes for various fxns 1. adhesins -type 2 pili 2. invasins 3. capsules 4. toxins 5. anti-oxidants 6. iron transporters
Define invasins.: =proteins that act locally in invasion of host cell -bind beta-1 integrins on cell surface
A capsule can help evade microorganisms by:: 1. prevent phagocytosis 2. cover C3 binding sites on LPS -> reduces efficiency of PMNS, Macrophage from binding with C3R 3. E.coli with K1 capsule is heavily sialylated -prevents activation of alternative complement cascade
Compare LT and ST toxins: =both toxins produced by enterobacteriaceae LT toxin -acts like cholera toxin -constituitive stim. adenylyl cyclase -cell secretes: Cl, Na, H20 ST toxin -elevates intracellular cGMP -cell secretes: Cl
How does Shiga toxin work?: -cleaves adenosine residue in 23S rRNA part of 60s ribosomal subunit -> inhibit protein synthesis -> cell death
Define enteric bacteria: =gram negative bacteria associated with the GI flora or disease
Name the 6 families of enteric bacteria: 1. Enterobacteriaceae 2. Vibrionaceace 3. Pseudomonaceace 4. Camplyobacteraceace 5. Bacteriodaceace 6. Heliobacteraceace
Name 3 primary pathogen enterobacteriaceace: primary pathogen=capable of causing disease in anyone 1. Shigella 2. Salmonella 3. Yersinia
All of the following enterobacteriaceace can be considered opportunistic pathogens EXCEPT: 1. Proteus 2. Klebsiella pneumoniae 3. Yersinia 4. E.coli: =Yersinia (primary pathogen) Klebsiella pneumoniae and E.coli can act as either primary or opportunistic pathogens
Name the 3 major pathogenic species of Staphylococcus: 1. S. aureus 2. S. epidermidis 3. S. saprophyticus
What are Staphylococcus characteristics on: a. gram stain b. catalase test c. culture: Gram stain -gram positive cocci -clusters of grapes Catalase test -positive -have catalase-> can break H202 into gas and water -> bubbles culture -S. aureus has gold pigment on blood agar
How can you differentiate S. aureus from other beta hemolytics on blood agar cultures?: -beta hemolytics=complete hemolysis of RBCs -clear zones on blood agar plate S. aureus -also beta hemolytic -golden pigment on blood agar
How can you differentiate S. aureus from the other 2 pathogenic forms of staphyloccus?: 1. coagulase test -only S. aureus is coagulase positive -it activates coagulase -> causing formation of blood clot
True or false: most staphylococci are resistant to penicillin G: -true -compared with group A strep that can cause many of same diseases as S. aureus but are SENSITIVE to penicillin G
Name some proteins of S. aureus that can disable our immune system: 1. Protein A 2. Coagulase 3. Hemolysins 4. Leukocidins 5. Penicillinase 6. Novel penicillin binding protein
How do the hemolysins and leukocidins of S. aureus affect our immune system?: 1. Hemolysins -destroy RBCs, neutrophils, macrophages, platelets 2. Leukocidins -destroy WBCs
S. aureus is coagulase positive. What role does coagulase play in its pathogenicity?: -coagulase leads to fibrin formation around bacteria--> protects bacteria from phagocytosis
How does Protein A of S. aureus affect our immune system?: -protein A has binding sites that can bind the Fc portion of IgG -can protect S. aureus from opsonization and phagocytosis
How does penicillinase and novel penicillin binding protein affect our immune system?: =S. aureus has both 1. Penicillinase -disrupt beta-lactam portion of penicillin -> inactive 2. Novel penicillin binding protein -confer resistance to some strains against penicilinase-resistant penicillins and cephalosporins
Name 4 enzymes of S. aureus that can tunnel through tissue: 1. hyaluronidase -break down connective tissue 2. staphylokinase -lyses fibrin clots 3. lipase -degrades fats and oils 4. protease -destroy tissue proteins
Name 3 exotoxins from S. aureus.: 1. exfoliatin 2. enterotoxins 3. toxic shock syndrome toxin
Name 3 diseases caused by S. aureus exotoxins and which toxins cause each disease.: 1. Gastroenteritis -enterotoxins 2. Toxic shock syndrome -toxic shock syndrome toxin 3. Scalded skin syndrome -exfolatin
How does the exfolatin cause Scalded skin syndrome?: -exofoliatin= toxin produced by S. aureus -causes skin to slough off
How does toxic shock syndrome toxin cause toxic shock?: -toxic shock syndrome toxin is an exotoxin produced by 20% of S. aureus -pyrogenic toxin -binds to MHC II-> big T cell response -> cytokines -> symptoms
Describe the symptoms of toxic shock syndrome caused by S. aureus.: Sudden onset of: 1. high fever 2. nausea 3. vomitting 4. watery diarrhea followed days later by 1. red rash 2. peeling of skins in palms and soles -can be associated with septic shock (low BP) and organ damage
Name 8 diseases S. aureus causes by direct organ invasion: 1. pneumonia 2. meningitis 3. osteomyelitis 4. acute bacterial endocarditis 5. septic arthritis 6. skin infections 7. bacteremia/sepsis 8. UTI
Name some causes of toxic shock syndrome caused by S. aureus.: 1. tampons 2. infected sutures from surgery 3. cutaneous and subcutaneous infections 4. infections following childbirth or abortions
How do you get toxic shock syndrome from a tampon?: =tampons left in place for a long time stimulate S. aureus to release exotoxin Toxic Shock Syndrome toxin -toxin goes through vaginal mucosa and stimulate TNF and IL-1
True or false: gastroenteritis caused by S. aureus is from people eating food with exotoxin already in it: true -staphylococci can grow in food and then produce exotoxin w/in food
Who is most likely to get Scalded skin syndrome: -skin infection caused by S. aureus -babies and children most likely affected
How do you differentiate endocarditis caused by S. aureus from that caused by strep viridans or group D strep?: 1. rapidness of onset -endocarditis from S. aureus has a very rapid onset -endocarditis from streps has more gradual onset
How do you diagnose septic arthritis?: -examine synovial fluid -yellowish, turbid fluid with lots of neutrophils -cultures positive for bacteria (ex. S. aureus)
Name some skin infections caused by S. aureus: -note: many of same infections caused by group A strep 1. impetigo 2. cellulitis 3. local abcesses, furuncles, carbuncles 4. wound infections
Define methicillin.: =penicillinase-resistant penicillin -is not broken down by penicillinase so able to kill most strains of S. aueus
Define MRSA: =methicillin-resistant Staphylococcus aureus -strain of S. aureus that has acquired multi-drug resistance even to penicillinase resistant penicillins like methicillin and nafcillin -have penicillin binding protein 2A -strains tend to develop in hospitals b/c of broad spectrum antibiotic use
True or false: MRSA can be transferred from patient to patient in hospitals from hand contact with health care workers: -true
Name one antibiotic that can be used in treatment of MRSA infections: -vancomycin
Describe Staphylococcus epidermis: -normal bacterial flora found widely on body -gram positive cocci -catalase positive -coagulase negative -Novobiocin sensitive -Glycerol in teichoic acid -Slime is its virulence factor -one of 3 pathogenic forms of staph -facultative anaerobe
How does Staphyloccous epidermis cause disease: 1. IV lines and foley catheters -gets into bloodstream of comprised hospital patients -can form biofilms -cause bacteremia and sepsis 2. indwelling prostethic devices -most frequent cause of infections in tissues with prosthetic devices
Why is biofilm formation important for S. epidermis to cause disease?: biofilm=extracellular polysaccharide network that forms mechanical scaffold around bacteria fxns: 1. allows to bind to prosthetic devices, IV lines 2. protects from attack with antibiotics, immune system
True or false: staphylococcus is a frequent skin contaminant in blood cultures: true -need to see if S. epidermidis is found in 2 blood cultures suspect bacteremia
Describe Staphylococcus saprophyticus: 1. gram positive cocci 2. catalase positive 3. coagulase negative 4. facultative anaerobe 5. one of 3 forms of staph that can cause disease in humans 6. Novobiocin resistant 7. Glycerol in Teichoic acid
Name a disease caused by Staphylococus saprophyticus.: 1. UTIs in young sexually active women -most common cause
Describe Vibrio Cholera: -curved gram negative rod -single polar flagellum -pathogen factor: cholera toxin -causes cholera
How does Vibrio cholera cause the disease cholera: -bacteria attach to GI epithelial cells but do NOT invade -releases choleragen (toxin) -choleragen gets into cells -> activates G protein -> activate adenylylate cyclase -> increase cAMP ->active secretion of Na into gut lumen -> H20 and CL- follow -> watery diarrhea
Describe cholera. What organism causes it?: =watery (vs inflammatory) diarrheal disease -death from dehydration -transmission by fecal-oral route (usu contaminated H2O) -caused by Vibrio cholera (enteric gram negative bacteria) -disease mediated by actions of choleragen (toxin)
Describe Camplylobacter jejuni: -gram negative bacteria -one of major causes of diarrhea (bloody) -reservoir: poultry, animals, unpasteurized milk -fecal-oral route of transmission
Describe Helicobacter pylori: 1.gram negative enteric bacteria 2.most common cause of duodenal ulcers 3. faint, slender curved gram negative rods 4. oxidase positive 5. sheathed polar flagella 6. fastidous and slow growing 7. urease positive
Why do we care so much about pseudomonas aeruginosa?: =gram negative enteric bacteria 1. colonizes and infects the sick, immunocompromised patients 2. Resistant to nearly every antibiotic
Describe Pseudomonas aeruginosa: =gram negative enteric 1. obligate aerobe -but can survive anaerobically by using nitrate as terminal electron acceptor -non-lactose fermenter 2. produces green fluorescent pigment and blue pigment -> colored colonies 3. grape-like odor 4. infects immunocompromised, sick patients 5. very antibiotic resistant 6. oxidase positive 7. minimal media growth requirements
Name some infections pseudomonas aeruginosa can cause:: 1. Pneumonia 2. Osteomyelitis 3. Burn-wound infections 4. UTIs, pyelonephritis 5. Endocarditis 6. Sepsis 7. Malignant external ottitis 8. Corneal infections
Explain the mneumonic BE PSEUDO: -lists major diseases caused by Pseudomonas aeuruginosa -Burns -Endocarditis -Pneumonia -Sepsis -External Malignant Otitis media -UTI -Diabetic osteomyelitis
Describe the family Bacteriodaceae: =family of enteric gram negative rods -obligate anaerobes -make up 99% of flora in intestines -Also found in mouth, vagina
Name 3 species that are part of the Bacteriodaceae family.: 1. Bacteriodes fragilis 2. Bacteroides melaninogenicus 3. Fusobacterium
Describe bacteriodes fragilis: -gram negative enteric -normal flora of GI -obligate anaerobe -able to form abscesses after trauma to the abdomen -Unique features: 1. no lipid A in outer membrane (no endotoxin)
Describe bacteroides melaninogenicus: =gram negative enteric bacteria -found in mouth, GI (normal flora), vagina -obligate anaerobe -produces black pigment on blood agar -Can cause disease 1. necrotizing anaerobic pneumonias 2. periodontal disease
Describe fusobacterium: =gram negative enteric -NOT part of normal flora of GI -able to cause disease -obligate anaerobe
Name some diseases caused by fusobacterium: 1. periodontal disease 2. aspiration pneumonias 3. abdominal and pelvic abscesses 4. Otitis media
Describe peptostreptococcus: -gram positive cocci -anaerobe -normal flora of mouth, vagina, intestine -can be involved with 1. abscesses 2. aspiration pneumonias
Name some characteristics shared by the family pseudomonadaceae: =gram negative rods 1. Polar flagela -need special stain to visualize 2. Oxidase positive -distinguishes from enterobacteriaceae 3. Respire only (obligate aerobes) 4. Nutritional versatile -can survive on lots of different foods
All pseudomonads are obligate aerobes EXCEPT:: P. aeruginosa -can survive in anaerobic environments by using nitrate as terminal electron acceptor
Name some of the virulence factors P. aeruginosa uses: -has many tools but no single factor is decisive for virulence -binding proteins and capsules 1. fimbriae 2. alginate (impt for infections in CF) 3. pyochelin -siderophore -Toxins and pigments 1. endotoxin 2. pigments (fluorescein and phenazines) 3. Pyocins 4. Exotoxin A (like diptheria toxin) 5. Exotoxin S -enzymes
Describe how aliginate is a virulence factor for pseudomonas aeruginosa: =exopolysaccharide capsule -strains associated with cystic fibrosis patients constitutively make the capsule fxns 1. inhibits ciliary clearance of bronci 2. allows adhesion of bacteria to each other 3. antiphagocytic 4. causes blocking antibody to be produced in CF patients
How do pigments act as virulence factors for pseudomonas aeruginosa?: -pigments are toxic to WBCs -usu increased production of pigments when environmental conditions not favorable -pigments have antibiotic properties
How does Exotoxin A act as a virulence factor for pseudomonas aeruginosa?: -extraceullar toxin -acts like diptheria toxin but not related -induced by iron limitation -binds to R-> enter host cytoplasm -> catalyzes ADP ribosylation of EFA -> inhibit protein synthesis -> host cell dies
How does elastase act as a virulence factor for pseudomonas aeruginosa?: -destroys blood vessel linings -implicated in hemorrhagic and necrotic lesions of lung -this is what allows P. aeruginosa to cause ecythyma gangrenosum -skin infection caused by damage to blood vessels -> hemorrhage and necrosis
How does Las R and Las I regulate pseudomonas aeruginosa?: -Las R=regulates transcription of proteases, elastase, exotoxin A -Las I coordinates action of Las R -Las I acts as quorum sensor -When Las I produced in high concentrations, it directly affects actions of Las R
Name some mechanisms of antibiotic resistance in pseudomonas aeruginosa: 1. posession of beta lactamases 2. possession of aminoglycoside inactivating enzymes 3. possession of enzymes that acetylate chloramphenicol 4. expulsion of tetracycline 5. possession of altered drug targets (penicillin binding proteins)
Name some host defenses against pseudomonas aeruginosa: 1. normal body surfaces 2. intact normal flora -P. aeruginosa is opportunistic and takes advantage of when normal flora disrupted by antibiotics 3. neutrophils
Define ecthyma gangrenosum: =necrotic skin lesion seen in neutropenics -caused by Pseudomonas aeruginosa -black necrotic tissue and elastase destroys blood vessels
Name 5 other pseudomonads besides P. aeruginosa: 1. Burkholderia mallei 2. Burholderia pseudomallei 3. Burkholderia cepacia 4. Stenotrophomonas maltophilia 5. Pseudomonas flurescens -burkholderia= pseudomonas
Describe Burkholderia mallei: -member of pseduomonas family -only non-motile pseudomonad -causes glanders (disease in horses but humans can acquire from horses) -symptoms of glanders: pneumonia, necrosis of mucus membranes
Describe Burkholderia pseudomallei.: -member of pseudomonas family -found in soil in SE Asia -multitrichous polar flagella -infection can be dormant for years and appear in times of stress -causes melioidosis (chronic lung disease)
Describe Burkholderia cepacia: -member of the pseudomonas family -opportunistic pathogen in CF and CGD patients -very resistant to antibiotics -multitrichous polar flagella
Describe Stenotrophomonas maltophilia: -other pseudomonad -3 most common Gram negative pathogen isolated from sputum of CF patients -spread by contaminated equipment -nosocomial opportunistic pathogen -very resistant to antibiotics
Describe Pseudomonas fluorescens: -member of the pseudomonas family -grows at 4 degrees celsius -can infect blood transfusions and medication stores
Describe the characteristics of acinetobacter in culture: 1. grows on minimal media 2. nonmotile 3. encapsulated 4. unable to reduce nitrate 5. respires only 6. nutrionally versatile
Describe acinetobacter: =gram negative rod 1. during stationary phase looks coccobacillary 2. oxidase negative 3. lacks distinguishing characteristics 4. nosocomial pathogen 5. able to grow at various temps and pHs, can use many energy sources 6. resistant to many antibiotics 7. risk of disease for immunocompromised (opportunistic)
Name the virulence factors of acinetobacter: 1. capsule -inhibits phagocytosis 2. LPS 3. Bacteriocins -can kill other strains of same of related species with these proteins -pseudomonas also has these
Name some of the mechanisms for antiobiotic resistance in acinetobacter: 1. possession of beta lactamases 2. alteration of penicillin binding proteins 3. loss of porins 4. possession of efflux pump
True or false: acinetobacter can be misinterpreted on gram stain: -true 1. sometimes can retain dye and look gram positive 2. can be misinterpreted to be another gram negative organism that is commonly associated with clinical syndrome
Name some diseases caused by acinetobacter.: 1. Pneumonia -ventilator use 2. Bacteremia 3. Meningitis -post neurosurgery 4. Others -cellulitis, lower UTI, burns and wound infections
How do you treat serious Acinetobacter infections?: -with combination antibiotic therapy based on sensitivities of specific isolates
Describe the group characteristics of the Campylobacter species: 1. look like gulf wings on gram stain (thin curved gram negative rods) 2. oxidase positive 3. polar flagella 4. fastidious and slow growing -require special conditions for growth in culture 5. urease test negative
Name important disease causing species of Campylobacter.: 1. Campylobacter jejuni 2. Campylobacter coli 3. Campylobacter fetus
Describe the laboratory characteristics of Campylobacter fetus.: 1. No growth at 42 degrees celsius 2. sensitive to cephalothin 3. resistance to nalidixic acid 4. resistant to complement lysis These 4 characteristics distinguish from Campylobacter jejuni and coli (have opposite on each of the 4)
Describe the transmission of campylobacter: -resevoir in animals -transmitted through 1. direct contact with animals 2. contaminated food -chicken 3. contaminated water -Campylobacters sensitive to gastric acid
Describe Campylobacter jejuni: -gram negative bacteria -leading cause of acute diarrhea worldwide -able to cause both watery and inflammatory diarrhea -some infections are asymptomatic
How does campylobacter jejuni cause diarrhea?: -Campylobacter is invasive: it trasmigrates through epithelial cells by unknown mechanisms -disrupts tight jxns -mikes cytotoxin that is a DNAase that breaks DNA and leades to cell cycle arrest
True or false: campylobacter jejuni is resistant to complement killing: False -C. jejuni is sensitive to complement killing -C. fetus is resistant to complement killing
Name some virulence factors for Campylobacter jejuni: 1. capsule 2. flagella 3. Type III secretion system 4. Glycosylation 5. cytotoxin that causes breaks in DNA
Describe the diarrhea caused by campylobacter jejuni: -can be watery or inflammatory (bloody) -lasts 4-5 days -fever and abdominal cramping -about 20% relapse -may continue to shed bacteria for up to 1 month after
Name 2 major complications of Campylobacter jejuni infections.: 1. Guillan Barre syndrome 2. reactive arthritis
Name 2 types of antibiotics used to treat Campylobacter jejuni infections.: 1. Macrolides (erythromycin) 2. quinolones
What type of antigen receptor on host cells initiates signaling in campylobacter infections?: NOD=intracellular pathogen R -recognizes peptidoglycan 1. NOD1 -recognizes gram negative cell wall 2. NOD 2 -recognizes gram positive cell wall
Describe Campylobacter fetus: -gram negative bacteria -Rare zoonotic infection -mostly affects immunocompromised -if infected when pregnant can result in abortion -can cause systemic disease 1. Bacteremia 2. Thrombosis
Name the virulence factor for Campylobacter fetus: =S protein capsule -protein crystal NOT polysaccharide -prevents C3b binding -enables it to get into bloodstream and cause systemic disease (bacteremia)
True or false: half the world is infected with H. pylori: -true -most infections acquired during childhood -infects last a lifetime -humans are only known reservoir
Describe the pathology caused by H. pylori: -able to colonize gastric mucosa layer and epithelium -no invasive potential -infection always associated with inflammation (gastritis) but this can be asymptomatic
Name some diseases H. pylori can cause.: 1. duodenal ulcers -curable if get rid of H. pylori infection 2. gastric ulcers 3. gastric cancer 4. MALT lymphoma -curable with anti H. pylori therapy 5. chronic and acute antral and corpus gastritis
Name some virulence factors associated with H. pylori: 1. Urease -neutralizes gastric acid so it can survive and colonize 2. Motility -flagella allow to swim through mucus layer to get close to epithelium 3. Adherence -binds to epithelial cells through multiple adhesions 4. Cag pathogenicity island -complex of proteins important for secretion of virulence factors i to epithelial cells -CagA protein itself loosens tight jxns when injected into cells 5. Vac A -cytotoxin that disrupts cellular organelles
How does H. pylori cause gastritis (inflammation)?: -stimulates cells to produce IL-8 -> attracts neutrophils and initiate inflammatory process -> TH1 response -infected gastric tissue also produces IL-1 -> cell activation and atrophy
How do we diagnose H. pylori infection?: Invasively 1. endoscopy and test antral biopsy for urease activity Non-invasive 1. look for IgG antibodies 2. urea breath test
How is an H. pylori infection treated?: -combination 2-3 drugs (single drug tx doesn't work) 1. PPIs 2. antiotics
How does omeprazole help with H. pylori infections?: -direct antimicrobial activity -raises gastric pH and improves activity of antibiotics
Define peptostreptococci.: =gram positive cocci that occur in short chains, pairs, or individual -anaerobes -live in mouth and intestine -can cause disease alone (vs mixed infection) -can cause abscesses in brain, liver, breast, lung
Define Bacteroides fragilis: -major pathogen of Bacteroides family -obligate anaerobe, gram negative rod -normally lives in GI tract +/- vagina -resistant to bile -can survive in O2 but can't grow -able to produce Vit K
Name some virulence factors for Bacteroides fragilis: 1. polysaccharide capsule -antiphagocytic -capsule can induce abscess formation 2. Beta lactamases -provides penicillin resistance 3. Bile resistant -able to deconjugate bile salts
Name some disease caused by Bacteroides fragilis.: 1.diverticulitis 2. septic abortion 3. septic thrombosis 4. GI infections
Name 3 gram negative anaerobes normally found in body that are capable of causing disease.: 1. Bacteroides 2. Prevotella 3. Fusobacterium
Describe the bacteroides family.: -gram negative anaerobes (rods) -nonmotile -indigenous gut flora -have LPS less toxic than LPS pf enterobacteriaceae -most frequent cause of anaerobic infections -B. fragilis is major member
_____ is the drug of choice when treating anaerobic infections: =Metronidazole -anaerobes very sensitive and not much resistance
What are some common features of clinical presentation with anaerobic infection.: 1. Mixed infection -Facultative organisms use up O2 and provide nutrients for anaerobes to thrive 2. Form purulent abscesses 3. Anaerobes tend to cause infections in injuries adjacent to normal habitat
Name 2 host defenses against anaerobic infections: 1. Normal oxygenated tissues -most impt defense 2. Oxidative burst of phagocytes
How do anaerobes cause disease?: =opportunistic pathogens -wait until something is wrong with body (poor perfusion, tissue injury) to get in and cause disease -normally found in oral cavity, vagina, gut
Bacteriodes fragilis are resistant to ____ but sensitive to ____ and ______.: 1. penicillin 2. clindamycin 3. metronidazole
Describe Prevotella melaninogenica: =short small gram negative rods -anaerobes -named b/c grow black on special type of blood agar -usually live in oral pharynx -can also be found in GI and vagina -some penicillin resistant strains
Name 2 diseases caused by Prevotella melaninogenica: 1. Lung infections 2. dental infections -normally lives in oral cavity and pharynx
What are the virulence factors for prevotella melaninogenica?: 1. collagenase 2. leukocyte inhibitory factor 3. capsule
Define Fusobacterium: =pale staining, slender, gram negative rods (with tapered ends) -anaerobes -normal flora of oral cavity, GI tract, vagina -no capsule -potent LPS -butyric acid is major metabolic end product -includes: 1. Fusobacterium necrophorum 2. Fusobacterium nucleatum
Define fusobacterium necrophorum: -gram negative rod; anaerobe -on gram stain broad rounded ends with bulges in middle of cells -major cause of liver abscesses -virulence factors 1. leukocidin 2. hemolysin
Describe fusobacterium nucleatum: -gram negative rod; anaerobe -has thin pointed ends -cause of pulmonary infections
Name 3 gram positive anaerobes that can cause disease.: 1. Peptostreptococci 2. Actinomyces israelii 3. Clostridium species
Define Actinomyces israelii.: =gram positive branching rod -anaerobe -flora of mouth, GI, vagina -Not acid fast (used to distinguish from Norcardia) -sulfur granules are seen in pus of abscesses caused by actinomyces -penicillin sensitive
Describe actinomycosis: =chronic destructive abscesses in connective tissue -abscesses expand by burrowing through sinus tracts to skin or internal organs -can get infections in abdomen, cecum, appendix, lung, chest, face, neck, uterus (IUD) -pus contains sulfur granules
What stain can differentiate Actinomyces israelii from another gram positive branching rod?: -Acid Fast stain -actinomyces (anaerobe) does not stain -Norcadia is acid fast (aerobe) -important to distinguish b/c Norcadia is penicillin resistant
Name some characteristics of the clostridium species: =gram positive large, pleomorphic rods -anaerboes -after 48 hours cultures stain gram negative -if motile have peritricous flagella -found in soil -some found in GI tract -Includes: 1. C. perfrigens 2. C. difficile -
Name some enzymes produced by Clostridium species: -known to produce many enzymes 1. collagnase 2. protease 3. hyaluronidase 4. lecithinase 5. DNAase 6. neuraminidase 7. toxins
Describe Clostridium perfrigens: -gram positive large, pleomorphic rod -found in soil and intestine -anaerobe -non-motile -has subterminal spores -forms double zone of hemolysis on blood agar
Name some diseases caused by Clostridium perfrigens.: 1. gas gangrene 2. soft tissue infections 3. food poisoning 4. abdominal infection of biliary tree 5. septic abortions
Describe gas gangrene: =rapid infection of injured muscle -life and limb threatening -forms from fermentation of bacteria in muscle tissue -Clostridium perfrigens causes 90% of cases -particularly seen in diabetics because of poor perfusion
Name some important virulence factors associated with Clostridium perfringens: 1. alpha toxin =lecithinase=Ca dependent phospholipase C -causes lysis of RBCs and other cell 2. Enterotoxin type A -causes acute food poisoning -ex. stuffing in the turkey filled with spores
Define Clostridium difficile: =gram negative large, pleomorphic rod -anaerobe -has subterminal spore -often acquired in hospital and colonizes GI tract
Why do people worry about Clostridium difficile?: -nosocomial infeciton -causes most cases of pseudomembranous colitis -causes 1/4 cases of diarrhea with antibiotic therapy -increase in incidence of infections caused by this anaerobic bacteria
How do the virulence factors of Clostridium difficile cause disease?: 1. Toxin A -enterotoxin 2. Toxin B -cytotoxin -bind to Rs on intestinal cells ->glucosylate Rho proteins and disrupt cell jxns -> massive secretion of fluid (diarrhea) and acute inflammatory infiltrate -exotoxin bad for old, or immunocompromised
True or false: all antibiotics can lead to clostridium difficile diarrhea or colitis.: -true -most likely culprits: broad spectrum 1. penicillins 2. cephalosporins 3. clindamycin
How do you diagnose and treat disease caused by Clostridium difficile?: Diagnose 1. endoscopy 2. toxin assay of stool Treatment 1. metronidazole 2. vancomycin 3. stop offending antibiotic
Define exotoxin: =extracellular proteins with specific enzymatic activities -often sole cause of disease -encoded on accessory genetic elements (plasmids) -major virulence factor -many exotoxins affect cAMP metabolism
Define toxigenic bacteria: =bacteria that make and excrete exotoxins Include: 1. Vibrio cholerae 2. E. coli 3. Bordetella pertussis 4.Corynebacterium diptheriae 5. Clostridium tetani 6. Pseudomonas aeruginosa 7. Bacillus anthracis 8. Clostridium botulinum
Define toxoid.: =a molecule that closely resembles a toxin but lack its biological activity -can be developed into vaccine -will induce protective antibody response against a disease caused by that toxin -ex. tetanus and deptheria vaccines
Describe the general structure of exotoxins.: -2 domains 1. B domain -binding 2. A domain -active
Describe Vibrio cholerae.: =short, curved, motile, gram negative rod -causes cholera -Virulence factor 1. exotoxin= cholera toxin
The symptoms of cholera include...: 1. profuse watery diarrhea (rice water) 2. vomitting 3. nausea -can die from dehydration -caused by Vibrio cholerae
Define cholera toxin: =exotoxin that is the major virulence factor for Vibrio cholerae -toxins 5 B subunits bind GM1 on host membrane ->form pore for A subunit -> A subunit ADP ribosylates alpha subunit of Gs -> Gs loses GTPase activity -> causes adenylylate cyclase to keep producing cAMP -effects: 1. increased cAMP-> Cl- secretion 2. water and Na follow -> watery diarrhea -shows immunologic cross-reactivity w/LT toxin of E. coli
Describe the LT toxin of E.coli.: -plasmid encoded -destroyed by heat -related to cholera toxin -causes: 1. traverler's diarrhea 2. diarrhea in infants -works by same mechanism as cholera toxin to cause diarrhea
Compare and contrast cholera toxin and LT toxin: -both cause diarrhea by disrupting Gs alpha subunit -> continual production of cAMP -evolutionarily related LT diarrhea not as severe as cholera b/c: 1. LT toxin not secreted 2. LT toxin must be cleaved by host protesases.
Define ST toxin of E. coli: =exotoxin that is a major virulence factor -not destroyed by heat (vs LT) -plasmid encoded -Causes diarrhea by different mechanism than LT toxin
How does ST toxin cause diarrhea?: -ST toxin binds guanylate cyclase C on brush border -toxin binding elevates intracellular cGMP -> Cl- secretion
Why is diarrhea caused by ST toxin of E.coli more severe in infants?: -b/c infants have more of the guanylate cyclase C (=guanylin R)
Describe the pertussin toxin: =exotoxin -chromosomally encoded -blocks inhibition of adenylate cyclase by ADP ribsosylation of Gi -> AC uninhibited and continues to make cAMP -infects respiratory epithelium -> whooping cough -toxin is diffusible
True or false: Bordetella pertussis secretes its own adenylyl cyclase: -true: this inhibits inflammatory response b/c it messes up the cAMP cycle in phagocytes -also secretes pertussis toxin that releases inhibition on host AC to increase cAMP levels in respiratory epithelium
Name 4 exotoxins that interfere with the cAMP metabolism to cause disease: 1. cholera toxin -causes cholera (severe diarrhea) 2. LT toxin of E.coli -causes diarrhea 3. ST toxin of E.coli -causes diarrhea 4. pertussis toxin of Bordetella pertusis -causes whooping cough
Define diptheria toxin: =exotoxin that is major virulence factor for Corynebacterium diptheriae -phage encoded (not all strains of the bacteria carry this phage) -toxin is produced in response to iron restriction -exotoxin produces tissue distruction -> increased availability of nutrients (iron) -develop neutralizing antibodies; will have immunity from future infections
Describe the mechanism of action of diptheria toxin: -synthesized as single AA chain, must be cleaved in 2 chains to work -catalyzes ADP ribosylation of EF2 -> knocks out host protein synthesis -cells die and get tissue necrosis -infects: 1. throat 2. skin wounds (sometimes) -if toxin absorbed systemically can produce cardiotoxicity
Describe exotoxin A of Pseudomonas aeruginosa.: =exotoxin that is chromosomally encoded -it is under control of lasR -produced in response to iron restriction -must unfold for activity -catalyzes ADP ribosylation of EF2 ->knock out host protein synthesis -example of convergent evolution with diptheria toxin b/c same fxn but not related toxins -exotoxin A destroys cells during corneal infections
Name 2 exotoxins that disrupt protein synthesis.: 1. diptheria toxin of corynebacterium diptheriae 2. exotoxin A of pseudomonas
Define tetanus toxin: =exotoxin that acts as neurotoxin -produced by Clostridium tetani -plasmid encoded -found in all strains =metalloprotease
How does tetanus toxin work?: -terminal spores get into injury -C. tetani is obligate anaerobe and grows as redox potential drops -metalloprotease that degrades proteins for docking on surface of Neurotransmitter vesicles -> blocks NT release from presynaptic neurons -> disinhibition of motor neurons -> spastic paralysis -able to get into SC by retrograde axonal transport
Once patient has been infected with tetanus, they cannot be reinfected: False. -no immunity if patient survives b/c not enough toxin to raise an immune response
Describe botulism toxin: -exotoxin produced by Clostridium botulinum -neurotoxic -phage encoded -botulism can result from: 1. ingestion of preformed toxin (improper canning) 2. wound infection 3. infant botulism
How does botulism toxin work?: =metalloproteinase -acts on presynaptic neurons at NMJ to prevent ACh release -degrades proteins for docking on surface of NT vesicles -> ACh can't be released -> flaccid paralysis -without treatment, death be respiratory failure -recovery involves sprouting of new neurons (takes time)
Describe floppy baby syndrome: =infant botulism -caused by giving children under 1 year of age honey -syndrome caused by Clostridium botulinum spores that may be present in honey -C. botulinum colonizes GI tract -> botulinism toxin produced -> progressive muscular weakness, poor motor development, flaccid paralysis
Compare and contrast tetanus toxin and botulism toxin.: Compare -both neurotoxins -both metalloproteinases that act on presynaptic cells to prevent NT release -when associated with wound infections, no wound may be apparent sometimes Contrast -tetanus -> spastic paralysis -botulism -> flaccid paralysis
Describe Bacillus anthracas.: =gram positive rod -produces spores -non-motile -grows well on blood agar -grows aerobically -virulence factors encoded on 2 plasmids
Name the 3 major virulence factors associated with B. anthracis.: 1. Edema factor -calmodulin-dependent adenylyl cyclase -causes edema 2. Lethal factor -protease cleave MAP kinases -> inhibition MAP kinase pathway -> cell death 3. Protective antigen -associates w/ EF and LF to promote entry into cells
Name the 3 major anthrax syndromes.: -caused by Bacillus anthracis 1. cutaneous -most common 2. inhalation -most lethal 3. GI
Describe the species Haemophilus: =small gram negative coccobacillus -> pleomorphic rod (size varies) -non-motile -+/- capsule -facultative anaerobe -Major types 1. H. influenzae 2. H. ducreyi
Define Haemophilus influenzae: 1.gram negative coccobacilli - pleomorphic rods 2.fastidious growth -requires X and V for growth 3. facultative anaerobe 4. grows on chocolate agar 5. classified into serotypes based on polysaccharide capsule
Name 4 diseases caused by Haemophilus influenzae type b: -able to cause invasive disease b/c can get into bloodstream 1. meningitis 2. septicemia 3. epiglottitis 4. pneumonia -disease usually seen in kids younger than 5 years who have not been immunized
Name 3 diseases caused by non-typable Haemophilus influenzae: 1. bronchitis/pneumonia 2. otitis media 3. sinusitis -diseases seen mostly in kids younger than 5 not immunized
Name the major virulence factors of Haemophilus influenzae.: 1. Capsule 2. IgA1 protease 3. Endotoxin (LOS) 4. Outer membrane proteins involved in iron acquisition 5. pili and other adhesins 6. beta lactamases (some)
Why is the capsule important in Haemophilus influenzae?: -composed of polyribosyl ribitol (PRP) -seroytpes of H. influenzae classified by capsule subtype -type b causes most disease -antibody specific for the capsule are protective
Why is Haemophilus influenzae type b the most common cause of meningitis in children less than 3 years old?: -children less than 18 moths do not raise a good response to polysaccharide antigens alone(T independent response) -vaccine produced by conjugating PrP (sugar) to a protein -> induces T dependent antibody response
True or false: the incidence of Haemophilus influenzae type b disease is increasing: -false -b/c we now have a vaccine to protect kids -any disease now seen usually in unvaccinated children -but increase in disease due to type f
What do Haemophilus influenzae and Bordetella pertussis have in common?: 1. causes diseases of childhood 2. gram negative rods 3. fastidious (tough to grow) 4. spread by droplets
Describe Bordetella pertussis.: -gram negative coccobacilli or pleomorphic rods -strict aerobe -fastidious organism -spreads by droplets -causes whooping cough -can be cultured on Bordet-Gengou Agar (has potatoe in it)
Name the virulence factors of Bordetella pertussis.: 4 attachment factors -filamentous hemagglutinin (FHA) -Pertactin (outer membrane protein -pili -pertussin toxin 4 toxins -adenylate cyclase/hemolysin -tracheal cytotoxin -pertussis toxin -LOS
Expression of which of the Bordetella pertussis virulence factors is NOT controlled by the bvg locus? a. FHA b. pertussis toxin c. tracheal cytotoxin d. adenylate cyclase/hemolysin: -tracheal cytotoxin -stops ciliary beating and kills ciliated epithelial cells -> loss of mucociliary elevator
Describe whooping cough: -respiratory disease caused by Bordetella pertussis -babies most susceptible -2 phases; 1. Catarrhal phase -mild resp symptoms -culture + for B. pertussis -caused by local damage from colonization 2. Paroxysmal phase -intense coughing spells, vomitting, convulsions, cyanosis (turn blue) -symptoms caused by pertussis toxin
Describe Haemophilus ducreyi: -gram negative coccobacillus to pleomorphic rod -very fastidious -causes gential ulcers (STD) -risk factor for HIV transmission
How do you distinguish between staphylococcus and streptococcus?: =catalase test -staph: catalase + -strep: catalase -
How do you distinguish between different types of streptococcus?: =pattern of hemolysis 1. Alpha hemolysis (green/partial) -S. pneumoniae -Strep viridans 2. Beta (complete) -Group A strep -Group B strep 3. No hemolysis -Enterococcus -peptostreptococcus
How do we distinguish between S. pneumoniae and strep viridans?: -both are alpha hemolytic strep (incomplete/green) 1. Quellung rxn -S. pneumnoiae has capsule and well have + quellung 2. Optochin -S. pneumoniae is sensitive 3. Bile solubility -S. pneumoniae is bile soluble
How do we distinguish between Group A and B strep?: -both are beta hemolytic strep (complete/clear hemolysis) 1. Bacitracin -Group A is bacitracin sensitive (ex. S. pyogenes)
How do we distinguish among Staphylococcus aureus from other Stapylococci?: 1. Coagulase test -S. aureus is coagulase +
How do we distinguish between Staph epidermis and Staph saprophyticus?: 1. Novobiocin -S. epidermis is Novobiocin sensitive
How do we distinguish between Neisseria meningitidis and Neisseria gonorrhoeae?: =both are gram negative cocci 1. Maltose fermentation -N. meningitidis ferments maltose and N. gonorrhoaeae does not
How do we distinguish among gram negative rods?: 1. Lactose fermentation -Those bacteria that do ferment bacteria can be further subclassified as fast fermenters vs slow fermenters -non-lactose fermenters can be distinguished by the oxidase test
How do we distinguish Pseudomonas from other non-lactose fermenters that are gram negative rods?: 1. Oxidase test -Pseudomonas is oxidase + -Shigella, Salmonella, Proteus are oxidase -
True or false: a vaccine containing various N termini of M proteins may never be feasible for hear of causing autoimmune disease: -true
Define molecular mimicry: =where pathogen produces epitopes similar to host (proteins, sugars) -molecular mimicry can cause disease when adaptive immune responses raise against pathogen cross-react with host epitopes (antibodies, T cells)
Give 3 examples of molecular mimicry diseases and name the bugs involved.: 1. Acute rheumatic fever -group A strep 2. Guillan-Barre disease -Campylobacter jejuni -other viruses and bacteria can also trigger 3. Atherosclerosis -Chlamydia pneumoniae -has weakest evidence of 3 diseases to support a link
Name the major symptoms of rheumatic fever: =no "rheum" for SPECCulation 1. subcutaneous nodules 2. polyarthritis 3. erythema marginatum (skin rash) 4. chorea 5. carditis
Name 4 important predisposing factors to developing acute rheumatic fever.: 1. Magnitude of host response to group A strep -more severe pharyngitis -> more likely to produce high Ab titer -> higher chance to develop ARF 2. Family Hx -increased risk if have 1st degree relative w/ARF 3. Previous episode of ARF -if had once, chances of having again are 30-50% -tx subsequent infections with PCN prophylactically 4. Increased frequency of certain MHC class II alleles
Name some laboratory tests used to confirm acute rheumatic fever: 1. Antibody tests -detect preceding Strep infection -ASO, Anti-DNAse B, etc -need 4x increase in Ab titer 2. Isolation of Group A strep -problematic 3. Acute phase reactants -ESR, C-reactive protein -nonspecific markers of inflammation -aspiring, corticosteroid use screw up levels
Define Guillain-Barre syndrome: =acute post-infectious paralytic illness -rapid onset of symmetrical limb weakness, loss of deep tendon reflexes, absence of fever at onset -sporadic -can be caused by viruses, vaccines (rabies), bacteria -disease with evidence of molecular mimicry
How does Campylobacter jejuni exhibit molecular mimicry?: -Certain strains (019) of Campylobacter jejuni contain neuraminic acid in O side chain of LPS -antibodies raised against C. jejuni cross react with ganglioside on peripheral neurons -> paralysis and G-B syndrome
How could chlamydia exhibit molecular mimicry?: -thought to possibly have a role in developing atherosclerotic plaques of heart disease but not strong evidence -chlamydia from respiratory infections infects macrophages -> infected macrophages travel through blood and interact with endothelial cells -> chronic inflammation -injection myosin fragments with similar homology to chlamydia epitopes into mice also caused inflammation in heart
Name 4 group characteristics of Neisseria: 1. Gram negative diplococci 2. Kidney bean shaped 3. Oxidase positive -have cytochrome c oxidase in their electron transport chain 4. 8 species, 2 pathogenic 1. N. gonorrhoeae 2. N. meningitidis
Describe the growth characteristics of pathogenic Neisseria: -very fastidious!!! 1. Need 4-8% CO2 to grow 2. Will not grow at 22 degrees celsius (unlike non-pathogenic Neisseria species) 3. Susceptible to heart, cold, and drying 4. Highly autolytic in stationary phase 5. Cannot tolerate free fatty acids in growth media Have pili when isolated, which makes transformation possible
Name 2 media types that pathogenic Neisseria will grow on: -very picky! 1. Chocolate agar 2. Thayer Martin media -chocolate agar + bunch of antibiotics that kill other pathogens
True or false: Neisseria produce acids from sugars by fermentation: -false -unlike most other bacteria, they produce acid by an oxidative pathway
Describe the mechanism of invasion of epithelial cells by pathogenic Neisseria: 1. Stick to mucus secreting but NOT ciliated cells using pili and opa proteins. Cause ciliostasis with LOS and PDG. Endocytosis directed by porins 2. Transported through the cell 3. Get spit out into basement membrane ->inflammation 4. Ciliated and non-ciliated host cells are destroyed 5. Organisms resist killing by Ab and complement 5. Attach to endothelial cells 7. Get into bloodstream (if bacteremia)
Name the important virulence factors for Neisseria meningitidis.: 1. Iron binding proteins 2. polysaccharide capsule 3. Pili 4. Porins 5. Surface proteins that block Ab 6. Adherence surface proteins 7. LOS -endotoxin that is side chain of LPS 8. IgA protease
Name 3 species of bacteria that have IgA protease as a virulence factor: -cleaves IgA antibodies 1. Neisseria 2. S. pneumoniae 3. H. influenzae
What are some of the key differences in virulence factors between N. gonorrhoeae and N. meningitidis?: 1. N. gon no capsule 2. Surface proteins that block Abs -N. g: block IgG -N. m: block IgA 3. Adherence surface proteins -N. g has opa protein 4. LOS has different effects
Define opa protein: =opacity protein -protein that promotes adherence to mucosa and PMN -found in Neisseria gonorrhoeae -can exhibit antigenic variation -if present, colony will look opaque (characteristic of local disease) -if colony is clear (no opa) -> suggest disseminated gonococcal infections
Contrast the actions of LOS in N. meningitidis and N. gonorrhoeae.: LOS= endotoxin that is side chain of LPS 1. N. meningitidis -causes cytokine release -> local inflammatin +/- septic sock and DIC -13 different serotypes 2. N. gonorrhoeae -LOS damages epithelial cell cilia -> sloughing -exhibits antigenic variation
Name 4 diseases caused by Neisseria meningitidis.: 1. Meningitis 2. Meningococcemia -low grade fever, skin lesions, arthritis over days to weeks 3. Waterhouse-Friederichsen syndrome -bilateral destruction of adrenal glands -> DIC and shock 4. pneumnoia -rare
Describe meningitis caused by Neisseria: -LOS causes local cytokine release -> damage to brain -systemic cytokine release -> shock and DIC -highly fatal if untreated -mainly affects infants and kids 10-20 yrs -can get residual neurological effects -disease can either be endemic or epidemic -disease is transmitted via nasal droplets from asymptomatic carriers -diagnosis by gram stain of CSF +culture of CSF, skin lesions, or blood
What is the key feature to diagnose meningitis due to N. meningitidis?: 1. skin lesions -start as petechiae and become purpuric and eventually necrotic -due to endotoxin (LPS/LOS) -> vascular necrosis and hemorrhage into surrounding skin
What are some host immune factors that can increase susceptibility to bacteremia from N. meningitidis?: 1. Absence of bacteriocidal antibodies 2. production of blocking antibodies 3. deficiency of terminal complement components (C6,7, 8) 4. Mannose binding lectin deficiency -normally NBL attaches to LOS to initiate MAC formation and opsonizatin of Neisseria 5. PAI-1 (plasminogen activation)
True or false: meningitis vaccine is produced against the capsule of N. meningitidis: -true -several different serotypes based on capsule -vaccine made against capsule of serotypes responsible for most of cases of meningitis
How do we treat meningitis caused by N. meningitidis?: 1. penicillin 2. cephalosporin
Name 2 high risk groups for meningitis due to Neisseria meningitidis.: 1. Infants 6 months- 2 years old -not able to produce own Ab yet 2. Army recruits
Describe the symptoms of meningitis in an infant: -fever -vomitting -irritability -+/- lethargy -bulging fontanelle (neonate) -stiff neck (older infants)
Contrast the diseases caused by Neisseria gonorrhoeae in men and women: Men 1. urethritis 2. epididymitis Women 1. cervicitis 2. salpingitis (infection of fallopian tubes) 3. PID =pelvic inflammatory disease -15-20% of infections N. gonorrhoeae causes disseminated gonococcal infection
Describe the epidemiology of gonorrhea: 1. Infection usually seen in sexually active young adults (teens-30 yrs) 2. venereal infection by N. gonorrhoeae is acquired via the genitourinary epithelium -50% of women are asymptomatic
How is gonorrhea due to N. gonorrhoeae diagnosed?: Men: seeing GC (gonorrhoeaecocci) in PMNs on a gram stain Women: culture of cervical pus
Neisseria _______ is lysed by IgG to capsule and complement while Neisseria _______ is lysed by IgM to LOS (endotoxin): 1. meningitidis 2. gonorrhoeae
True or false: you can fail to clear a Neisseria gonorrhoeae infection because you produce IgG blocking antibodies that interfere with IgM's ability to lyse.: -true
How do we treat gonorrhoeae?: -single dose of drug b/c poor patient compliance 1. Cepthtriaxone
What are the symptoms of gonorrhea in men?: -symptoms due to urethritis 1. painful urination 2. pus discharge from penis -complications include: 1. epididymitis 2. prostatitis 3. urethral stricutres -in men who have sex with men, you can get gonorrhea infections in the rectum
What are the symptoms of gonorrhea in women?: -many women are asymptomatic 1. painful urination 2. pus filled discharge from: -urethra -cervix 3. lower abdominal pain 4. pain with sexual intercourse -can progress to PID (pelvic inflammatory disease) -infection of upper female organs -abnormal menstrual bleeding -cervical motion tenderness
Describe the group characteristics of Chlamydia: =obligate intracellular parasites (bacteria) -considered gram negative but little/no peptidoglycan -has distinct infectious (EB) and reproductive (RB) forms -cause persistent and recurrent infections
How do chlamydia act as intracellular parasites?: -prevent phagolysosomal fusion and live in phagosome -act as energy parasites b/c can't make own ATP -import nutrients from cytosol of host
Name 3 species of chlamydia that cause disease in humans.: 1. C. trachomatis -blindness -urethritis -cervicitis -salpingitis 2. C. psittaci -pneumonia 3. C. pneumoniae -pneumonia
How do we identify Chlamydia psittaci and Chlamydia trachomatis with lab tests?: C. psittaci -use a complement fixation test to look at LPS, which is genus specific Ag C. trachomatis -direct fluorescent Ab staining of genital exudates with labeled monoclonal Ab against LPS or MOMP -nucleic acid hybridization can detect asymptomatic genital infection in women
How do we treat chlamydia.: 1. Azithromycin -long acting macrolide -good for patients with compliance issues
Describe the life cycle of chlamydia: 1. The extracellular elementary body attaches to a specific host cell R and undergoes parasite-specific endocytosis -stays in phagosome and EB prevents fusion with phagolysosome 2. EB differentiates into RB (reticulate bodies) and multiply and make more EB 3. EBs can be released from cell by cytolysis
What's the difference between EBs and RBs of chlamydia?: -RBs are metabolically active and able to replicate and synthesize proteins EBs are infectious (think like spores) but not metabolically active and can't replicate
Describe Chlamydia trachomatis.: -obligate intracellular parasite -has round EB -divided into biovars based on target host cells 1. Biovar trachoma 2. Biovar lymphogranuloma venereum -Biovars are subdivided into serovars -causes blindness, urethritis, cervicitis, salpingitis
Contrast the biovars of Chlamydia trachomatis.: -based on target host cells 1. Biovar trachoma -infects squamocolumnar epithelial cells of eye and GU tract 2. Biovar LGV -infects inguinal lymph nodes and cause lymphogranuloma venereum
Define trachoma: =preventable blindness caused by infection with Chlamydia trachomatis -chronic follicular conjunctivitis that progresses to conjunctival scarring -> cornea abrasions -> blindness -seen mainly in kids in under-privileged populations
True or false: systemic IgG is protective against Chlamydia infections: -false
Describe Chlamydia psittaci.: -obligate intracellular bacterial parasite -2 biovars: 1. Avian -causes human and bird pneumonias 2. Mammalian -no disease in humans Causes: 1. Psittacosis (parrot fever) 2. endocarditis -disease associated with bird handlers and poultry workers
Describe Chlamydia pneumnoniae: -EB is pear shaped -causes: 1. pneumonia 2. pharyngitis 3. bronchitis -some association with heart disease
Define obligate intracellular parasite: =only can survive by establishing "residence" inside animal cells -2 examples: 1. Chlamydia 2. Rickettsia
Why is chlamydia a unique gram negative organism on gram stain?: -stains red but has no PDG layer and no muramic acid
Why are penicillins ineffective against chlamydia?: -b/c they have no PDG layer (target of penicillins) -this is how you usually differentiate urethritis (STD) caused by N. gonorrhoeae from those caused by Chlamydia trachomatis b/c infections with chlamydia don't respond to penicillins -usu tx urethritis w/antibiotic (ceftriaxone) to cover all 3 bugs known to cause urethritis
Name 2 pathogens that cause PID.: PID= pelvic inflammatory disorder 1. Chlamydia trachomatis 2. Neisseria gonorrhoeae -PID can cause fallopian tube scarring that can result in: 1. infertility 2. ectopic pregnancy 3. chronic pelvic pain -chlamydia can cause asymptomatic PID that leads to fertility
Contrast bacteremia and septicemia: bacteremia= presence of viable bacteria in blood (shown by positive blood culutures) Septicemia -bacteremia with clinical symptoms (tachycardia, hypotension) -suggest host has mounted systemic inflammatory response
True or false: coagulase is the defining virulence factor for staph aureus: -false -no single virulence factor is decisive -staph uses a combo of binding proteins, enzymes, and toxins to cause infection
True or false: once you've have a staph aureus infection, you have immunity against future infections: -false -you can get infections with staph aureus again and again because no protective immune response is made
Describe the surface features of staph aureus that act as virulence factors: 1.Protein A -binds IgG by Fc part so IgG can't bind Fc R on phagocytes -> inhibit phagocytosis 2.Binding proteins -bind to proteins on host surface including fibronectin, fibrinogen, collagen II 3. Capsule -anti-phagocytic
How do the virulence factor enzymes of S. aureus work: 1. clumping factor -binds fibrinogen 2. coagulase -binds prothrombin -> it converts fibriongen -> fibrin -> fibrin polymerizes -> form clots -when S. aureus covered in fibrin, it's resistant to phagocytosis 3. staphylokinase -causes clot dissolution -activates conversion of plasmin -> lyses the clot
Name 5 major types of toxins used by S. aureus.: 1. Hemolysins -form pores in membranes of RBCs, plts, WBCs, allow ion leakage ->cell death 2. Leukocidin -kill WBCs through pores 3. Exfoliative exotin (ET) -mediator of scalded skin syndrome and impetigo -superantigen 4.Toxic Shock Syndrome Toxin (TSST-1) -causes toxic shock -superantigen 5. Enterotoxin (SE) -Heat stable, foot poisoing -superantigen
Define superantigen: =molecule that binds with high affinity to MHC II R of macrophages -does not bind in antigen binding grove -stimulates polyclonal T cell response -can lead to major systemic side effects including fever, hypotension, skin lesions, shock, multiorgan failure, death
Give some examples of superantigens: Staph aureus 1. Toxic shock syndrome toxin 2. Exfoliative exotoxin 3. enterotoxin B Strep pyogenes 1.Exotoxin A 2. Erythorgenic toxin
True or false: virulence genes are constituitively expressed: -false
How is the virulence of staph aureus controlled?: 1. with accessory gene regulation (Agr) -quorum sensing stimulates agr to make RNAIII that regulates the txn of virulence genes -upregulate toxins -downregulate surface proteins
Describe the mechanism of methicillin resistance: -plasmid mediated -mutation in transpeptidase -> decreased affinity for beta lactam antibiotics -MRSA strain of staph aureus are resistant to all 2nd generation penicillins (not just methicillin) -also poorly responsive to cephalosporins
Describe S. pneumoniae: -gram positive cocci -alpha hemolytic -optochin sensitive (bile salt sensitive) -lancet-shaped diplocci -no animal reservoir -autolytic (can destroy itself) -capsule most impt virulence factor -penicillin sensitive
Describe strep viridans: -gram positive cocci -alpha hemolytic -optochin resistant -normal flora -can cause dental carries
Describe S. pyogenes: =group A strep -gram positive cocci, chains -beta hemolytic -Bacitracin sensitive -causes lots of diseases -person-person spread -M protein most important virulence factors
True or false: you can be repeatedly infected with strep pyogenes in one's life: -true -because antibodies against M protein are specific to that M protein type, but not to other M proteins -over 80 types of M protein
Name 2 enzymes that help strep pyogenes spread through tissues.: 1. streptolysin S -potent cytotoxin that can kill a variety of host cells -virulence factor for necrotizing fascitis 2. Streptokinase -can hydrolyze fibrin and other host proteins
Describe strep agalactiae: =group B strep -beta hemolytic -part of normal vaginal and/or intestinal flora in 20-30% of adults -diagnosis by CAMP test -can cause diseases in babies -first days of life: pneumonia and septicemia -1st month of life: bacteremia and meningitis -capsule type III most likely to cause meningitis 1. infections through placenta 2. infections through birth canal
Describe CAMP test: -used to aid in diagnosis of strep agalactiae (group B strep) -by itself, group B strep is weakly beta hemoytic -when incubated with staph aureus -> exaggerated hemolysis -unknown isolate is streaked on blood agar plate perpendicular to staph aureus streak -if group B strep, will get arrowhead pattern of hemolysis
Describe group characteristics of mycoplasma: -prokaryotic cells that resemble gram negative bacteria but lack cell wall -no PDG ->don't gram stain well -also inherently resistant to B lactam antibiotics -grow on artificial media with "fried egg" morphology -facultative organisms -require sterols for growth
Name 3 species of mycoplasma that can cause disease in humans: 1. Mycoplasma pneumoniae -respiratory disease 2. Ureaplasma urealyticum -GU infections urethritis, epididymitis 3. Mycoplasma hominis -GU infections, pyelonephritis, pelvic inflammatory disease, postpartum/postabortal fever
Describe pneumonia caused by mycoplasma pneumoniae: -atypical pneumonia -tracheobronchitis with non-productive cough -seen in young adults and children -transmitted by respiratory droplets -non-culture lab techniques (ELISA, etc) required for mycoplasma pneumonia identification -infection stimulates production of IgM to I antigen on RBCs -> can get intravascular hemolysis -> positive cold agglutinin response
How does Mycoplasma pneumoniae cause infection?: -M. pneumoniae spread by respiratory droplets -attaches to epithelial cells by P1 adhesion -damages mucosa by producing hydrogen peroxide and superoxide -> ciliastasis and epithelial necrosis
How do we distinguish pseduomonas from enterobactericeae?: 1. Flagella -pseudomonas: polar -enterb: peritrichous 2. Oxidase test -pseudo: positive -enterb: negative 3. lactose fermentation -pseudo: non-fermenter -enterb: ferments -note: will not distinguish from salmonella, shigella, yersinia
How do we distinguish Acinetobacter from other bacteria: 1. oxidase negative -vs. Neisseria 2. Respire ONLY -vs enterobacteriaceae 3. Unable to reduce nitrate -vs enterobacteriaceae
How do we distinguish between Campylobacter and helicobacter?: 1. Urease test -both oxidase positive and slender gram negative rods -helicobacter is urease positive
How do you distinguish bacteroides fragilis from fusobacterium nucleatum?: =by gram stain
All of the following are found in the periplasmic space of gram negative bacteria EXCEPT: 1.penicillin binding proteins 2. membrane derived oligosaccharide 3. Beta lactamases 4. petidoglycan 5. lipid A: lipid A
How can the body clear an infection by mycoplasma pneumoniae?: =by making antibodies against them -acquiring of IgG Ab against M. pneumoniae explains decline in incidence of infection after childhood

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