Micro Exam 1 Fall 2011

Front 1

What does "sarcina" mean?

Back 1

bacteria that arrange in packets of 8 cells

Front 2

Name one exception to the rule that bacteria do not contain sterols in their cell membranes.

Back 2

mycoplasma pneumoniae
-it lacks a cell wall so sterols in the cell membrane are necessary to provide rigidity and support, also provide flexibility

Front 3

What are the functions of the cell wall in bacteria?

Back 3

-maintenance of cell shape
-prevent osmotic lysis
-environmental protection
-anchor for external structures like flagella, etc

Front 4

What molecule is contained in virtually all cell walls?

Back 4

peptidoglycan
-repeating disaccharide cross-linked by tetrapeptides
-backbone is alternating NAG/NAM which are then crosslinked by chains of 4 AAs

Front 5

What are some ways that humans use the ability to target peptidoglycan to our advantage?

Back 5

-peptidoglycan is important for bacterial cell support so we can interfere with the structure/synthesis of this molecule to target bacteria (known as cell wall inhibitors and only affect actively growing cells)
-we can use the following methods:
1)secretion of various antimicrobial compounds (taken from bacteria that naturally produce antimicrobial compounds)
2)secretion of lysozyme (found in egg whites and in granules of PMNs), tears, saliva, and mucus

Front 6

What is the significance of lysozyme as an antimicrobial mechanism?

Back 6

it is found in tears, saliva, and mucus and degrades the glycan backbone of peptidoglycan in bacterial cell walls
-it weakens the integrity of cell wall, even in bacteria that are not actively growing
-

Front 7

What is the main difference between gram positive and gram negative cells (what differentiates them)?

Back 7

Gram Positive=thick peptidoglycan layer and retain the primary stain, crystal violet

Gram Negative=thin PG layer, retain the counterstain, safranin

Front 8

Describe the composition of the cell wall of gram negative bacteria.

Back 8

-they contain 1-2 layers of peptidoglycan plus:
-outer membrane with LPS, trimeric porins and lipoprotein (external to the PG layer), it is a bilayer where inner layer is identical to cell membrane and outer is mostly LPS
-perisplasmic space

Front 9

What is the "O" antigen?

Back 9

the outer portion of LPS found in gram negative bacteria
-they are long linear repeating units of carbs
-serves as attachment sites and has been shown to inhibit phagocytosis
-this portion is highly variable and immunogenic

Front 10

What is the structure of LPS?

Back 10

1)O antigen on outer portion
2)core polysaccharide: connects lipid A to the O antigen
3)lipid A-embedded in the outer membrane has toxin activity, responsible for bacterial sepsis, heat stable and is a B cell mitogen, induces production of cytokines

Front 11

What is the significance of LPS in bacterial septic shock?

Back 11

-LPS directly activates the alternative complement pathway
-binds to receptors and causes release of cytokines leading to symptoms of septic shock

Front 12

What is the function of lipoproteins in the outer membrane of gram negative cells?

Back 12

the most abundant protein of gram-negative cells
-functions to stabilize the outer membrane and anchors the outer membrane to the PG layer

Front 13

Describe the periplasmic space found in gram negative organisms.

Back 13

-located btwn. the outer membrane and the cell membrane
-contains the PG layer, transport proteins, and a variety of hydrolytic enzymes
(some bacteria can concentrate antibiotic hydrolases which lends to resistance so important to do antibiotic susceptibility tests)

Front 14

Describe the structure of gram positive bacteria cell walls.

Back 14

-contain a thick PG layer along with one or both of the following:
-Wall teichoic acids anchored to PG
-Lipoteichoic acids anchored to cell membrane
-both provide elasticity and stability

Front 15

What is the clinical relevance of wall teichoic acids and lipoteichoic acids found in gram positive bacteria?

Back 15

they have 2 main functions that increase the virulence of gram-positive organisms:
-they function as adhesins (structures for adherence, the first step in the invasion process)
-they can initiate endotoxin-like activities when released

Front 16

Describe the composition of acid fast cell walls.

Back 16

they usually contain an intermediate thickness of PG along with the following:
-mycolic acid layer-covalently linked to PG, gives organism a waxy coat to resist dessication, resistance to antibiotics and inhibits phagocytosis
-tetrameric porins-allow passage of small hydrophilic molecules

Front 17

What are the 3 major components of a flagellum?

Back 17

1)filament-contains the H antigen
2)Hook-attaches filament to the cell surface, links to basal body
3)basal body-anchors flagellum in the cell wall and cell membrane
-they allow for motility

Front 18

What are pili?

Back 18

hairlike structures with adhesins at the tips
-they promote adherence to other bacteria or to host cells
-2 types are common pili (fimbriae, contains tips with adhesins usually lectins that bind to sugars) and sex pili
-can target these for antimicrobial therapy to inhibit bacterial colonization

Front 19

What are sex pili (conjugation pili)?

Back 19

-produced by some gram negative bacteria
-adherence btwn. 2 cells for exchange of DNA

Front 20

What is the glycocalyx?

Back 20

-polysaccharide layer outside of the cell wall
-source of K antigen
-commonly referred to as a capsule or slime layer
-can contribute to increased virulence, has many other functions as well including induces abscess formation
-glycocalyx of strep mutans allows for adherence to the tooth enamel

Front 21

What is the Quellung reaction?

Back 21

-a diagnostic test for Strep. pneumoniae
-used to detect the presence of a capsule in respiratory infections when S. pneumoniae is suspected
-test has anticapsular abs that cause the capsule to swell, aiding visualization

Front 22

What are plasmids?

Back 22

they encode for ancillary (non-essential) information
-includes genes that encode antibiotics, resistance, heave metal resistance, toxins, etc...

Front 23

What ribosomal subunits do bacteria have?

Back 23

30s
50s
=70s
-also, transcription and translation are coupled
-the ribosomes are the target of our protein synthesis inhibitors

Front 24

What are some different types of inclusion bodies?

Back 24

-all of the following function as storage depots
-volutin granules-polymers of
inorganic phosphate
-glycogen granules-polymers of alpha-D-glucose
-PHB granules-chains of beta-hydroxybutyric acid

Front 25

What is an endospore?

Back 25

-a resting stage that allows an organism to survive harsh environmental conditions
-conversion from a vegetative state to an endospore often triggered by nutrient depletion
-each endospore contains one chromosome, high concentrations of Ca bound to dipicolinic acid (gives increased resistance to heat), low amounts of essential proteins and ribosomes, and a keratin spore coat
-resistant to many chemicals and toxins (can persist for months to years in this state)

Front 26

What are the 2 clinically relevant genera of bacteria that produce endospores?

Back 26

1)bacillus
2)clostridium
-both gram positive
-the location and size of the spore varies for different species and aids identification

Front 27

Does the optical density measure viable or non-viable cells?

Back 27

both
-the more cells, the more absorption occurs or the light

Front 28

What does a colony forming unit measure?

Back 28

only VIABLE cells
-from diluting and culture and plating it, each colony is from one cell

Front 29

Does the optical density measure viable or non-viable cells?

Back 29

both
-the more cells, the more absorption occurs or the light

Front 30

What does a colony forming unit measure?

Back 30

only VIABLE cells
-from diluting and culture and plating it, each colony is from one cell

Front 31

What is biomass?

Back 31

-measures bacterial growth
-sample is washed, dried, and weighed, dry weight is taken
-measures all cells in culture (viable and non-viable)

Front 32

Describe the lag phase of the bacterial growth curve.

Back 32

-there is no cell division here
-increase in biomass from synthesis of macromolecules
-the length depends on form and availability of nutrients and the condition of the inoculum

Front 33

What is biomass?

Back 33

-measures bacterial growth
-sample is washed, dried, and weighed, dry weight is taken
-measures all cells in culture (viable and non-viable)

Front 34

Describe the lag phase of the bacterial growth curve.

Back 34

-there is no cell division here
-increase in biomass from synthesis of macromolecules
-the length depends on form and availability of nutrients and the condition of the inoculum

Front 35

Describe the log phase of the bacterial growth curve.

Back 35

-exponential growth occurs in this phase, rapid cell division
-slope reflects doubling/generation time (determined by the rate of cell division and varies with the microbe)
-pathogens often produce virulence factors at this time
-primary metabolites

Front 36

Describe the late log phase of bacterial growth curve.

Back 36

-transition to stationary
-secondary metabolites (antibiotics, pigments)

Front 37

Describe the log phase of the bacterial growth curve.

Back 37

-exponential growth occurs in this phase, rapid cell division
-slope reflects doubling/generation time (determined by the rate of cell division and varies with the microbe)
-pathogens often produce virulence factors at this time
-primary metabolites

Front 38

Does the optical density measure viable or non-viable cells?

Back 38

both
-the more cells, the more absorption occurs or the light

Front 39

Describe the stationary phase of the bacterial growth curve.

Back 39

-supplies of energy and nutrients exhausted
-resources are then renewed by cell death (release peptides and nucleic acids)
-zero population growth (no change in CFU/mL, OD, biomass)

Front 40

What does a colony forming unit measure?

Back 40

only VIABLE cells
-from diluting and culture and plating it, each colony is from one cell

Front 41

What is biomass?

Back 41

-measures bacterial growth
-sample is washed, dried, and weighed, dry weight is taken
-measures all cells in culture (viable and non-viable)

Front 42

Describe the late log phase of bacterial growth curve.

Back 42

-transition to stationary
-secondary metabolites (antibiotics, pigments)

Front 43

Describe the death/decline phase of the bacterial growth curve.

Back 43

-insufficient resources for growth
-exponential cell death (but still less than the growth rate in log phase)
-determined only by CFU/mL not OD or biomass

Front 44

Describe the lag phase of the bacterial growth curve.

Back 44

-there is no cell division here
-increase in biomass from synthesis of macromolecules
-the length depends on form and availability of nutrients and the condition of the inoculum

Front 45

Describe the stationary phase of the bacterial growth curve.

Back 45

-supplies of energy and nutrients exhausted
-resources are then renewed by cell death (release peptides and nucleic acids)
-zero population growth (no change in CFU/mL, OD, biomass)

Front 46

Describe the death/decline phase of the bacterial growth curve.

Back 46

-insufficient resources for growth
-exponential cell death (but still less than the growth rate in log phase)
-determined only by CFU/mL not OD or biomass

Front 47

Describe the log phase of the bacterial growth curve.

Back 47

-exponential growth occurs in this phase, rapid cell division
-slope reflects doubling/generation time (determined by the rate of cell division and varies with the microbe)
-pathogens often produce virulence factors at this time
-primary metabolites

Front 48

Describe the late log phase of bacterial growth curve.

Back 48

-transition to stationary
-secondary metabolites (antibiotics, pigments)

Front 49

Describe the stationary phase of the bacterial growth curve.

Back 49

-supplies of energy and nutrients exhausted
-resources are then renewed by cell death (release peptides and nucleic acids)
-zero population growth (no change in CFU/mL, OD, biomass)

Front 50

Describe the death/decline phase of the bacterial growth curve.

Back 50

-insufficient resources for growth
-exponential cell death (but still less than the growth rate in log phase)
-determined only by CFU/mL not OD or biomass

Front 51

Describe the death/decline phase of the bacterial growth curve.

Back 51

-insufficient resources for growth
-exponential cell death (but still less than the growth rate in log phase)
-determined only by CFU/mL not OD or biomass

Front 52

Describe the stationary phase of the bacterial growth curve.

Back 52

-supplies of energy and nutrients exhausted
-resources are then renewed by cell death (release peptides and nucleic acids)
-zero population growth (no change in CFU/mL, OD, biomass)

Front 53

Describe the late log phase of bacterial growth curve.

Back 53

-transition to stationary
-secondary metabolites (antibiotics, pigments)

Front 54

Describe the log phase of the bacterial growth curve.

Back 54

-exponential growth occurs in this phase, rapid cell division
-slope reflects doubling/generation time (determined by the rate of cell division and varies with the microbe)
-pathogens often produce virulence factors at this time
-primary metabolites

Front 55

Describe the death/decline phase of the bacterial growth curve.

Back 55

-insufficient resources for growth
-exponential cell death (but still less than the growth rate in log phase)
-determined only by CFU/mL not OD or biomass

Front 56

Describe the lag phase of the bacterial growth curve.

Back 56

-there is no cell division here
-increase in biomass from synthesis of macromolecules
-the length depends on form and availability of nutrients and the condition of the inoculum

Front 57

Describe the stationary phase of the bacterial growth curve.

Back 57

-supplies of energy and nutrients exhausted
-resources are then renewed by cell death (release peptides and nucleic acids)
-zero population growth (no change in CFU/mL, OD, biomass)

Front 58

What is biomass?

Back 58

-measures bacterial growth
-sample is washed, dried, and weighed, dry weight is taken
-measures all cells in culture (viable and non-viable)

Front 59

Describe the late log phase of bacterial growth curve.

Back 59

-transition to stationary
-secondary metabolites (antibiotics, pigments)

Front 60

What does a colony forming unit measure?

Back 60

only VIABLE cells
-from diluting and culture and plating it, each colony is from one cell

Front 61

Describe the log phase of the bacterial growth curve.

Back 61

-exponential growth occurs in this phase, rapid cell division
-slope reflects doubling/generation time (determined by the rate of cell division and varies with the microbe)
-pathogens often produce virulence factors at this time
-primary metabolites

Front 62

Does the optical density measure viable or non-viable cells?

Back 62

both
-the more cells, the more absorption occurs or the light

Front 63

Describe the lag phase of the bacterial growth curve.

Back 63

-there is no cell division here
-increase in biomass from synthesis of macromolecules
-the length depends on form and availability of nutrients and the condition of the inoculum

Front 64

What is biomass?

Back 64

-measures bacterial growth
-sample is washed, dried, and weighed, dry weight is taken
-measures all cells in culture (viable and non-viable)

Front 65

What does a colony forming unit measure?

Back 65

only VIABLE cells
-from diluting and culture and plating it, each colony is from one cell

Front 66

Does the optical density measure viable or non-viable cells?

Back 66

both
-the more cells, the more absorption occurs or the light

Front 67

Define sterilization.

Back 67

a physical or chemical process that destroys or removes all microbial life, including spores

Front 68

Define disinfection.

Back 68

a physical or chemical process that eliminates nearly all microbial life, but some forms may persist (ex. spores)

Front 69

Define decontamination.

Back 69

a physical or chemical process that reduces microbes to an acceptable level (not able to cause disease)

Front 70

What is antigenic drift?

Back 70

-the accumulation of mutations which alters protein product
-over time leads to variability in population and forms antigenically distinct strains
-can produce an unlimited number of strains in a spp.
-

Front 71

Describe the example of antigenic drift relating to the influenza virus.

Back 71

hemagluttinin (glycoprotein spike that aids in attachment to host) and neuraminidase (enzyme on spike, allows virus to release from host)
-these 2 molecules undergo drift over time and can change from year to year
-this is responsible for the yearly flu vaccine

Front 72

Describe the example of influenza A and antigenic shift.

Back 72

-reassortment of viral genome when cell (pig) is infected by 2 different strains of the flu A virus
-this can produce a new subtype and lead to possible pandemic b/c there is no immunity to the new flu A strain
-this happens quickly and is drastic

Front 73

What is phase variation and what is it an example of?

Back 73

-one type of antigenic switching
-it refers to the genetic reversible ability to turn off and turn on something
-usually happens to genes coding for surface antigens (capsule, pili, flagella, LPS), these genes are always part of genome
-can be regulated by site specific inversion of DNA sequence by recombinase or posttranscriptionally by stability of mRNA

Front 74

Describe a clinical application of phase variation.

Back 74

uropathogenic E. coli (UPEC)
-uses fimbriae to attach to host tissue during colonization of bladder
-during phase ON it produces fimbriae and attaches to uroepithel.
-during phase OFF it does not produce fimbriae and remains free floating in urine

Front 75

What is gene conversion/cassette mechanism of antigenic switching?

Back 75

-it is due to recombination within specific group of genes
-results in alteration of surface antigen characteristics but maintains biological function
-also known as "gene shuffling"
-a surface antigen expresses different antigenic structures
example: N. gonorrhoeae has 20 genes that code for pilin, majority are not expressed but shuffling and recombining chromosomal regions leads to multiple antigenically different pilin with different AA sequences

Front 76

What is relapsing fever?

Back 76

disease caused by Borrelia recurrentis (a spirochete)
-it expresses variant surface ags
-due to gene conversion/cassette mechanism
-body responds with a fever each time the organism "gene shuffles" and expresses a new variant of its own epitope on the surface ag

Front 77

Describe the example of Plasmodium falciparum using the cassette mechanism.

Back 77

it is a protozoa which causes malaria
-spread through the anopheles mosquito
-this organism generates variable surface glycoproteins (VSG) which is a detectable ag on surface of RBC-->hides from immune system

Front 78

Describe the example of Trypanosoma brucei using gene conversion/cassette mechanism.

Back 78

it is a protozoan that causes African sleeping sickness
-vector is the tsetse fly
-produces VSG which leads to it hiding from the immune system

Front 79

What is homologous recombination?

Back 79

-sequence similarity
-transformation, transduction, and conjugation are some types
-newly obtained DNA replaces homologous DNA on chromosome
example: "naked DNA" codes for a lipase gene which is taken up by a host cell from environment, new lipase ssDNA aligns with resident lipase and rec proteins carry out recombination
-the old chromosomal DNA is replaced by NEW homologous DNA

Front 80

What is nonhomologous recombination?

Back 80

-site directed recombination, NO rec proteins involved as in homologous
-results in addition to NOT replacement of chromosomal DNA
-can disrupt a gene, if insert into the promoter or coding sequene of gene (NULL mutation)

Front 81

What are the 3 mobile genetic elements?

Back 81

1)insertion sequence
2)composite transposon
3)pathogenicity island
-does NOT mean they replicate on their own, they don't!
-all undergo nonhomologous recombination
-they can transfer DNA within a cell from one position to another or transport DNA from one cell to another

Front 82

Describe an insertion sequence.

Back 82

-the simplest form of mobile genetic element
-made of 150-1500 bp of DNA
-requires transposase gene integration into replicon
-has inverted repeats at end of molecule, does not carry additional coding regions/genes
-inserts in specific sequence and creates direct repeats upon insertion

Front 83

What is a transposon?

Back 83

-has 2 insertion sequence sequences at either end of the molecule
-found in prok. and euk.
-can carry genes for antibiotic resistance, toxins,
-each gene=promoter + coding sequence
-can insert into and inactivate a gene (including chromosomes or plasmids) and if that gene was essential =cell death

Front 84

What is a pathogenicity island?

Back 84

-distinct genome segments of pathogens which encode virulence factors
-unusual clusters of genes (10-200 kb in length) inserts in tRNA and tRNA like genes
-has direct repeat DNA motifs at boundaries as other MGEs do, and insertion elements within sequence
-genes carried in PAI have a different %G+C than parent cDNA
-overtime unstable and is lost, these are not found on nonpathogenic forms of the same spp.
ex: can create different pathogens of same bacterial spp. as in Enterotoxic E. coli and uropathogenic E. coli

Front 85

What are plasmids?

Back 85

-small genetic elements which replicate independently of chromosome
-supercoiled CCC ds DNA which vary in size
-carry information that may not be essential but can confer a selective advantage such as antibiotic resistance, heavy metal and toxin resistance, virulence factors, etc.
-

Front 86

What is an "R plasmid"?

Back 86

-AKA representative plasmid
-carries 1 or more antibiotic resistance and contains resistance transfer factor genes that mediate the transfer of the plasmid from 1 cell to another

Front 87

What are episomes?

Back 87

plasmids that can integrate into the hosts chromosome

Front 88

What is the exception to plasmid and chromosome structure?

Back 88

borrelia burgdorferi-causative agent Lyme disease
-has linear and circular plasmids, linear chromosomal DNA

Front 89

What are the plasmid encoded virulence factors that we discussed in class (3)?

Back 89

1)tetanus neurotoxin-clostridium tetani
2)exfoliative toxin-staph aureus
3)enterotoxins-E. coli

TET, EET, SET

Front 90

What is a bacteriophage?

Back 90

-species specific and utilizes host cell machinery to complete replication of vDNA, assemble viral particles
-uses a lytic or lysogenic cycle to produce new virions

Front 91

What are the 3 ways in which gentic exchange of DNA can occur among bacteria?

Back 91

1)transformation
2)conjugation
3)transduction

Front 92

What is transformation?

Back 92

-acquisition of genetic information
-incorporation of exogenous/naked DNA into cytoplasm (plasmid) or chromosome of recipient cell by homologous recombination
-usually develops a log phase during lab cell culture b/c takes time to occur

-

Front 93

What is conjugation?

Back 93

mating or quasisexual exchange of genetic information
-one bacterium to another
-occurs with most if not all eubacteria, usually bacteria of same spp. or closely related
-requires contact btwn. 2 bacteria
-results in the ONE way transfer of DNA from donor to recipient
-genes that direct conjugation are carried on conjugative plasmids which may also carry antibiotic resistance (carries genes for transfer of plasmid, ability to make sex pilus, and initiate DNA synthesis)
-transfer of conjugative plasmid as linear ssDNA, rolling circle replication produces dsDNA plasmid in recipient

Front 94

What is transduction?

Back 94

transfer of bacterial DNA from one bacterium to another by a bacteriophage (virus)
-phage picks up fragments of bDNA and packages it into phage particles/virions
-the bDNA is then delivered to infected cell and incorporated into bacterial genome
-

Front 95

What type of secretory system does conjugation use?

Back 95

type IV
-carries out process of DNA transfer
-identified in gram pos and neg bacteria

Front 96

Describe rolling circle replication.

Back 96

mobilization begins with plasmid-endoded protein makes single-stranded site specific cleavage at oriT
-Nick initiates rolling circle replication
-the dislaced linear strand is then directed to the recipient
-transferred DNA recircularizes and replicates

Front 97

Describe conjugative gram negative bacteria.

Back 97

have a specialized sex pilus-conjugative pilus
-example: E. coli where pilus is produced by donor

Front 98

Describe conjugative gram-positive bacteria.

Back 98

no sex pilus
-adhesin molecules on surface of donor aid in contact establishment

Front 99

Describe the structure of bacteriophages.

Back 99

capsid-protein shell
tail with/without tail fibers
nucleic acid core (RNA or DNA)

Front 100

Describe the lytic cycle of virulent phages.

Back 100

-lytic cycle is key to generalized transduction
-during phage assembly of lytic cycle DNA packaging does not discriminate (bDNA vs. viral DNA)
-capsid filled bDNA (defective phage), does not contain vDNA
-the phage then attaches and injects bDNA, after injection generalized transduction completed and bDNA recombines with host chromosomal DNA
-the phages are host cell specific and therefore carry out homologous recomb.

Front 101

Describe the lysogenic cycle of the temperate phage.

Back 101

-this cycle is the key to specialized transduction
-the phage attaches, injects/pentrates, lysogeny then occurs in which there is integration of vDNA into bDNA/chromosome in site directed nonhomologous recombination-->latent prophage formed vDNA (lysogenic conversion of bacterial cell turns it into a lysogen)
-viral DNA replicates w/bacterial host DNA and it is passed to bacterial daughter cells
-until stress activates prophage and the lytic cycle occurs

Front 102

Describe specialized transduction.

Back 102

lysogenic cycle is key to this
-during phage assembly of stress-induced lytic cycle the prophage is incorrectly excised from bDNA which incorporates bDNA located next to integration site of vDNA
-defective phages are produced when the capsids are packed which includes vDNA and bDNA, lysis releases the phages and they infect new host cells -->specialized transduction occurs of the bDNA
-if the prophage carries a virulent gene then a pathogenic lysogen is produced

Front 103

What is mutualism?

Back 103

each member provides benefits for other

Front 104

What is commensalism?

Back 104

one member benefits and the other is not harmed
example: strep pneumo
neisseria meningitidis
-virulence in these 2 not normally turned on

Front 105

What are some benefits of normal microbiota?

Back 105

1)synthesize and excrete vit. K and B12 (enteric bacteria)
2)prevent colonization by pathogens (competition for resources)
3)antagonize pathogens (produce substances to inhibit or kill)
4)stimulate development of tissues
5)stim. prod. of cross-reactive abs (behave as ags, induce Ab-mediated immunity, ex:E. coli ab cross reacts with H.influenzae type B to prevent infection)

Front 106

What gram staining group predominates skin colonization?

Back 106

gram positive
-gram negative predominate mucous membranes, lower intestine, and colon

Front 107

What is a sign?

Back 107

any objective evidence of disease as noted by an observer (changes due to disease, observed by a clinician)

Front 108

What is a symptom?

Back 108

the subjective evidence of disease as sensed by the patient (changes due to disease, experienced by the patient)

Front 109

What entity is both a sign and a symptom?

Back 109

fever!

Front 110

What microbe causes strep throat?

Back 110

strep pyogenes

Front 111

What microbe causes dental caries?

Back 111

strep mutans

Front 112

What are the 5 stages of disease?

Back 112

incubation
prodromal
acute
decline
covalescent

Front 113

Describe stage 1 of disease-Incubation (preclinical stage).

Back 113

-the pathogen has entered the body through the "portal of entry"
-NO signs or sx
-innate immune system has NOT been activated
-the pathogen must be an infectious dose/inoculum to gain entry and inititate growth
-the person is NOT infectious under most circumstances in this stage

Front 114

What does inoculum mean?

Back 114

the number of microbes required for disease

Front 115

Describe stage 2 of disease-prodromal (warning stage).

Back 115

-appearance of signs and sx of an illness, pathogens generate early signs and sx such as rashes, headaches, etc (general malaise)
-activation of the innate immune system
-numbers have increased since incubation stage
-easily transmitted even before host realizes they have the pathogen

Front 116

Describe stage 3 of disease-acute stage. (also called clinical illness)

Back 116

-most severe during this period = ACME of the illness
-signs and sx characteristic for the disease
-balance btwn host immune system and pathogen virulence, either tipped to recovery or death, acquired immune system has been activated
-pathogen numbers are stationary and may increase or decrease
-communicable disease are easily transmitted in this stage

Front 117

Describe stage 4a of a disease-decline stage.

Back 117

-the illness is still apparent but the signs and sx dwindle
-immune system activity is reduced
-pathogen is cleared from the host
-the disease is contagious if the individual becomes a carrier (ex. S aureus in nasal passages)

Front 118

Describe stage 4b of a disease (alternative decline stage in which the pathogen is not cleared from the host).

Back 118

-the pathogen is not cleared and instead does one of the following:
1)becomes dormant-mycobacterium tb results in latent infection
2)undergoes antigenic variation-presents immune system with unknown ag such as borrelia recurrentis-results in relapse of infection
3)resists antimicrobial tx-staph aureus (MRSA)-results in recurrent infection
-the individual is communicable is they re-enter the prodromal stage

Front 119

Describe stage 5 of a disease-convalescent.

Back 119

-pt. is now returning to full health
-see end of signs and sx
-no activity by immune system toward pathogen
-pathogen cleared from host
-not communicable since NO presence of pathogen (unless that person becomes a carrier)

Front 120

What are opportunistic pathogens?

Back 120

organisms that can be members of pts. normal flora and do not produce disease in normal setting but can establish disease when introduced to an unprotected site (such as blood tissues, etc)
-pt.subject to trauma, w/defective immune system, or preexisting condition more susceptible

ex: E. coli, S. aureus, C. difficile

Front 121

What are some of the most notable examples of opportunistic pathogens?

Back 121

1)P. aeruginosa-skin of burn victim or lungs of CF pts.
-gram neg. bacillus, motile, obligate aerobe
2)nocardia asteroides-resp. infections in immunosuppressed or compromised ppl
-gram pos. obligate aerobe, weakly acid fast

Front 122

What are virulent bacteria (strict pathogens)?

Back 122

-always associated with disease
-signs and sx due to damage or loss of tissues and organs, also host inflammatory response
-ex: mycobacterium tb, N. gonorrhoeae

Front 123

Describe how bacteria use tissue damaging metabolites to create pathogenesis.

Back 123

-they use acid, gases, or other byproducts formed during growth to harm their host

ex: Clostridium perfringens-produces hydrogen gas which inflates and separates the tissues so the organism can move through the tissues

Front 124

Describe how bacteria use invasins or spreading factors to create pathogenesis.

Back 124

-can use enzymes/proteins which act locally to damage host cells or affect tissue matrices and intracellular spaces
-these facilitate growth and spread of the pathogen which can lead to a certain pathology
-ex: neuraminidase, collagenase, etc

Front 125

What does hyaluronidase do?

Back 125

used by bacteria, attacks the interstitial cement of CT and depolymerizes hyaluronic acid

Front 126

What does neuraminidase do?

Back 126

used by bacteria, degrades neuraminic acid which is the intercellular cement of epithelial cells of the intestinal mucosa

Front 127

What do streptokinase and staphylokinase do?

Back 127

used by bacteria
-they are fibrinolysins that prevent the clotting of blood

Front 128

What are adhesins?

Back 128

-they allow pathogens to bind to receptors on host cells and tissues (bacterial ligand + host cell receptor)
-most bind to carb moieties like glycoproteins
ex: vibrio cholerae and e.coli attachment to brush border cells of host villi in sm. intestine

Front 129

Describe how strep. mutans adheres to the enamel of teeth.

Back 129

produces a glycocalyx material called dextran (complex-branched chain of glucans) by secreting glucosyltransferase which binds the bacteria to enamel of teeth
-this is a type of adhesin

Front 130

What is a biofilm and describe an example of the organism that can colonize IV catheters.

Back 130

a biofilm is colonization of inert materials and organic materials (like catheters and native heart valves)
ex:staph. epidermidis forms a biofilm on IV catheter, this is continual source of infection

Front 131

Describe an organism that uses fimbriae for attachment to host molecules.

Back 131

uropathogenic strains of E. coli use P fimbriae that bind to epithelium of the kidneys

Front 132

What are afimbrial adhesins and what are some examples of microbes that use these?

Back 132

-they are proteins in the cell envelope of bacteria, have mediated binding specificity, used to adhere to hose organism
-use type V secretory system
examples: Staph. aureus and Strep. pyogenes-use fibronectin binding proteins that recognize the host cell glycoprotein (called MSCRAMMs and are a class of microbial surface components that bind fibronectin)

Front 133

What is an exotoxin?

Back 133

-they are proteins that are toxic to cells, usually by direct action
-they are secreted into the ECF or associated with bacterial cell surface
-have components which bind host cell receptors
-they are produced by both gram pos and neg. cells

Front 134

What is an enterotoxin?

Back 134

an exotoxin that produces GI sx
-example: s. aureus causes vomiting and diarrhea

Front 135

What are functional exotoxins?

Back 135

they are immunogenic and deadly at extremely low concentrations

Front 136

What are toxoids?

Back 136

denatured toxins that are used for immunization
-ex: diphtheria toxoid vaccine
tetanus toxoid vaccine (dTaP)

Front 137

Describe the A-B exotoxins.

Back 137

-have 2 domains called A and B
A is the enzymatic component which attacks and enters cell
B binds the toxin to the host cell receptor
-B binds, then A attacks

Front 138

What is the mechanism of Corynebacterium diphtheriae?

Back 138

lysogenic conversion of host cell, diptheria toxin stops protein synthesis of host cell -->leads to cell death
-uses AB exotoxin

Front 139

Describe the mechanism of action of E. coli relating to exotoxins.

Back 139

uses the AB exotoxin class
-plasmid that acts as an enterotoxin which stim. Adenylate cyclase and causes diarrhea

Front 140

Describe the mechanism of Clostridium botulinum.

Back 140

uses AB exotoxin system
-lysogenic conversion of host cell, the botulinum toxin prevents release of Ach at synapse, no mm.contraction-->flaccid paralysis

Front 141

Decribe the mechanism of Clostridium tetani.

Back 141

uses the AB exotoxin system
-plasmid that contains the tetanus toxin and prevents inhibitory NT release-->no mm. relaxation and spastic paralysis occurs

Front 142

Describe the membrane active toxins (type of exotoxin).

Back 142

they are not as well characterized as AB toxins, they attack host cell membrane and lyse or kill host cell
-examples:
1)proteases-elastase in cell membrane of P. aeruginosa (type II secretory system)
-metalloprotease of legionella pneumophila
2)lipases-C. perfringens-alpha toxin-lecitinase in cell membrane

Front 143

Through what secretory system do shigella and salmonella enter host cells?

Back 143

type III

Front 144

What uses the type I secretory system in bacteria?

Back 144

hemolysins

Front 145

What are superantigens? Give examples.

Back 145

-they activate 1 in 5 T cells in the absence of antigen
-cause release of massive amounts of cytokines which leads to a possible life-threatening response and T cell death
examples: S. aureus toxin TSST-1
S. pyogenes-pyrogenic exotoxin A

Front 146

What are endotoxins?

Back 146

-refers to the LPS of gram-negative bacteria
-heat stable, toxicity associated with lipid A
-immunogenicity associated with polysaccharide components
-elicits variety of inflammatory responses, activates complement (alternative pathway)
-leads to fever, hypotension, shock and possible death
-NO TOXOIDS TAKEN FROM THESE

Front 147

Describe some examples in which common microbes invade normally sterile tissues.

Back 147

1)shigella dysenteriae-resists lysozyme, acid and bile, colonizes GI tract
2)E.coli and Bacteroides fragilis-enter sterile peritoneal cavity by appendix rupture or endoscopic puncture

Front 148

Describe an example of a bacteria that can circulate via blood or other means spreading from primary infection site.

Back 148

-in general, bacterial toxins and other antigenic molecules which are transported by blood and lymph can cause cytotoxic effects at remote sites
example: S. aureus-scalded skin syndrome (SSS), exfoliative toxin from desquamation of upper epidermis which then goes to umbilicus or conjunctiva

Front 149

Describe encapsulation and how bacteria can use this mechanism to evade the host immune response.

Back 149

-the bacteria is covered with poorly antigenic polysaccharide which deters phagocytosis
-this protects it against degradation in phagolysosomes of macrophages
ex: Strep. pneumoniae

Front 150

Describe how some bacteria can use the mechanism of intracellular growth to evade the host immune response.

Back 150

-there is no inactivation of host cell so the microbe escapes immune detection
examples: Rickettsia-obligate intracell.
Mycobacterium:facultative intracellular organism

Front 151

Describe an example of a bacterium that can reduce phagocytic cell function to evade the host cell immune response.

Back 151

example: Strep. pyogenes-has streptolysins which are cytotoxins that kill phagocytic cells

Front 152

What are examples of bacteria that can inactivate antibody to evade the host immune response.

Back 152

1)S. pneumoniae-IgA degrading proteases
2)S. aureus-surface protein A which binds Fc portion IgG

Front 153

What are examples of how some bacteria can inhibit complement to evade the host cell immune response?

Back 153

1)O antigen of LPS protects cell from complement mediated lysis
2)antigenic variation

Front 154

What are siderophores and what are their function?

Back 154

-they chelate available iron and transport it into the cell
-scavenge from host iron-binding proteins (lactoferring and transferrin)
-the lack of iron in the host can INDUCE toxin production
examples:
1)corynebacterium diphtheriae
2)P. aeruginosa-exotoxin A
(both are AB toxins-stop protein synthesis)

Front 155

What is a major contraindication for using bacteriostatic drugs?

Back 155

should not be used on immunocompromised patients or for infections in privileged sites (in which immune cells cannot invade and clear infection)
-example: HIV pts, pregnant women

Front 156

What are some examples of narrow spectrum antibiotics?

Back 156

erythromycin, vancomycin, clindamycin

Front 157

What are some examples of broad spectrum antibiotics?

Back 157

amoxicillin, tetracycline, streptomycin, chloramphenicol

Front 158

Describe the difference btwn. euk. and prok. ribosomes.

Back 158

euk=80s, 60+40

prok.=70s, 30+50

Front 159

What is the molecule found in yeast that is structurally very similar to cholesterol?

Back 159

ergosterol

Front 160

What is empirical therapy when talking about antimicrobials?

Back 160

predicts the sensitivity of the organism to antimicrobials

Front 161

What is rational therapy?

Back 161

antimicrobials prescribed against specific known organism

Front 162

Describe the B-lactam antibiotics.

Back 162

they are cell wall synthesis inhibitors (and therefore considered bactericidal)
-penicillins, cephalosporins
-they are all structurally related by possessing a B-lactam ring
-they block the transpeptidation step in bacterial cell wall synthesis (no cross linkage of tetrapeptides)
-

Front 163

What is the function of beta-lactamase?

Back 163

enzyme that inactivates penicillin

Front 164

Describe penicillin G.

Back 164

-narrow spectrum, inactivated by B-lactamase
-often combined with probenecid to decrease tubular excretion rates
-sensitive to acid hydrolysis
-has a very short half-life

Front 165

Describe Penicillin V.

Back 165

-more stable to acids
-rarely used clinically (b/c resistance is common)
-poor bioavailabillity
-little toxicity and short half-life

Front 166

Why were synthetic penicillins developed?

Back 166

-increase stability to acids
-to be resistant to B-lactamase
-to expand the spectrum of activity
3 groups are:
1)penicillinase-resistant penicillins
2)extended spectrum penicillins
3)anti-pseudomonal pens

Front 167

Describe penicillinase resistant penicillins.

Back 167

more toxic than natural penicillins
-resistant to B-lactamase
-still narrow spectrum of activity, used for gram pos. and some staph infections
examples:flucloxacillin and dicloxacillin

Front 168

Describe extended spectrum penicillins.

Back 168

-spectrum of activity expanded to many gram neg, less effective on gram positives
-acid stable
-sensitive to B-lactamase
-examples: ampicillin, amoxicillin

Front 169

Describe the anti-pseudomonal penicillins.

Back 169

-spectrum of activity exapdned
-highly effective ongram neg. rods, less effective on gram pos.
-administered parenterally (not orally)
-sensitive to B-lactamase
-examples: piperacillin, carbenicillin

Front 170

What are combination products and give an example.

Back 170

a penicillin + a penicillin analog
-they expand the spectrum of activity
one example is clavulanic acid which is used in combo with amoxicillin (drug called augmentin)
-the clavulanic acid has a b-lactam ring that serves as a competitive inhibitor and slows breakdown of amoxicillin

Front 171

Describe cephalosporins in general.

Back 171

-they are bactericidal
-usually more resistant to B-lactamase than penicillins
-there are 4 generations

Front 172

Describe 1st generation cephalosporins.

Back 172

-fairly broad spectrum, work on gram pos. cocci except MRSA and enterococci, some gram neg. enterics.
-not often used as first drug of choice!

Front 173

Describe 2nd generation cephalosporins.

Back 173

-extended spectrum, more gram neg. but weaker against gram pos.
-

Front 174

Describe 3rd generation cephalosporins.

Back 174

-broad spectrum, used mainly for gram neg.
-increased resistance to b-lactamase
-some can cross BBB (can be used for meningitis)

Front 175

Describe 4th generation cephalosporins.

Back 175

-extended spectrum: P. aeruginosa and some gram pos. cocci (effective in meningitis cases)
-increased resistance to b-lactamase
-cross BBB, parenterally admin.

Front 176

Describe bacitracin.

Back 176

a cell wall synthesis inhibitor and therefore is bactericidal
-effective on gram pos. and gram neg. cocci
-used topically due to toxicity
-interferes with movement of PG precursors through the cell membrane and so precursors never even reach the cell wall, works upstream of penicillin effects

Front 177

Describe vancomycin.

Back 177

a cell wall synthesis inhibitor
-narrow spectrum, effective on gram pos. cocci, used mainly for methicillin resistant organisms and pts. allergic to B-lactam antibiotics
-has toxicity issues (ototoxicity, nephrotoxicity, red man syndrome from increased histamine release)
-binds to terminal peptides so can't cross link and build cell wall

Front 178

Describe polymyxins.

Back 178

-work by disrupting cell membranes, found in OTC antibiotic topicals
-effective against gram neg. bacteria
-act as cationic detergents and increase water uptake by cell, efflux of ions and cell will lyse
-toxic to host, used on localized, external infections

Front 179

Describe daptomycin.

Back 179

-disrupts bacterial cell membrane function
-irreversible binding to cell membrane results in rapid depolarization, efflux of K+
-inhibits RNA, DNA, and protein synthesis=bacterial cell death
-used for gram pos.
-inactivated by pulmonary surfactants and therefore not used for tx of pneumonia
-toxicity risk in elderly esp.

Front 180

What are the 2 classes of 30s ribosome subunit inhibitors?

Back 180

aminoglycosides and tetracyclines

Front 181

What are the 50s ribosome subunit inhibitors?

Back 181

chloramphenicol, macrolides, clindamycin, streptogramins, linezolid

Front 182

Describe aminoglycosides.

Back 182

-they are bactericidal
-broad spectrum-often used for enterics, used synergistically with b-lactams (ex: streptomycin, gentamicin)
-irreversible binding to 30s subunit, interference with initiation complex leads to misreading of mRNA and aberrant proteins-->premature release of mRNA from ribosomes leads to incomplete protein

Front 183

Describe tetracyclines.

Back 183

-they are bacteriostatic
-broad spectrum used mainly for intracellular bacteria, enterics, some protozoa and UTIs
-NOT given to children (can penetrate bone) or pregnant women
ex: doxycyline, etc.
-reversilby bind to 30s ribosomal subunit
-block binding of aminoacyl tRNA to the acceptor site on the mRNA ribosome complex

Front 184

Describe chloramphenicol.

Back 184

-is bacteriostatic
-broad spectrum antibiotic used only for certain infections (typhoid, meningococcal)
-it is toxic
-binds to 50s ribosomal subunit reversibly and inhibits peptidyl transferase and prevents elongation of peptide chain
-poor selective toxicity

Front 185

Describe macrolides.

Back 185

-are bacteriostatic broad spectrum that are readily used
-ex:erythromycin, azithromycin, etc.
-binds to 50s subunit reversibly
-block formation of the initiation complex and translocation step in protein elongation

Front 186

Describe clindamycin.

Back 186

-mechanism similar to macrolides (binds to 50s), bacteriostatic
-useful against some MRSA strains, anaerobes and some protozoa (malaria)
-used topically for tx of acne
-moderate toxicity issues

Front 187

Describe streptogramins

Back 187

-combo drug
-each drug binds distinct sites on 50s ribosome
-they are bacteriostatic individually, but bacteriostatic in combo
-used in tx of most gram pos. bacteria, resistant E. faecium, some MRSA

Front 188

Describe linezolid.

Back 188

-prevents formation of inititation complex
-can also bind "A" site on ribosome complex if formed
-effective against gram pos., but also used on vancomycin resistant organisms
-relatively safe drug

Front 189

Describe rifamycins (rifampin).

Back 189

-is bactericidal, effective against M. tuberculosis and some gram pos. cocci
-used in combo usually with isoniazid
-inhibits DNA dependent RNA polymerase

Front 190

Describe fluoroquinolones.

Back 190

-synthetic antibiotics initially used primarily for UTIs
-are bactericidal
-broad spectrum against many gram neg. aerobes
-inhibit DNA gyrase
ex:cipro, norfloxacin
-moderate tox. issues, should not be given to kids or preggers women

Front 191

Describe metronidazole.

Back 191

-is bactericidal
-narrow spectrum: used for anaerobes and protozoans
-reduction of metronidazole results in cytotoxic substances formed that disrupt DNA

Front 192

Describe sulfonamides.

Back 192

-they are analogs of PABA (one of precursor to make folic acid in bacteria)
-bacteriostatic, broad spectrum
-compete with PABA for dihydropteroate synthase which inhibits folic acid synthesis, bacteria need this for synthesis of nucleic acids and therefore can't make DNA

Front 193

Describe trimethoprim.

Back 193

-analog of the pteridine portion of dihydrofolic acid
-bacteriostatic
-usually used in combo with sulfa drugs (bactericidal in combo) -CALLED TMPSMZ
-inhibits the enzyme dihydrofolate reductase, inhibits folic acid synthesis =no DNA synthesis

Front 194

Describe dapsone.

Back 194

-mechanism identical to sulfa drugs
-bacteriostatic
-used in tx of leprosy and pneumocystis carinii pneumonia
-toxicity b/c blocks cytochroms p450 function, can result in toxic hepatitis

Front 195

Describe isoniazid.

Back 195

-analog of nicotinamide and pyridoxamine
-bactericidal against growing organisms
-used for tx of TB
-interferes with synthesis of mycolic acids

Front 196

What 2 groups are antifungal agents divided into?

Back 196

polyenes and azoles

Front 197

Describe nystatin.

Back 197

a polyene antifungal
-too toxic for systemic use, not absorbed from alimentary canal
-used for mucosal candidiasis and GI fungal infections
-interact with sterols in the cell membrane to form channels through which small molecules leak from inside of the fungal cell to the outside

Front 198

Describe amphotericin.

Back 198

-polyene antifungal
-can be used IV
-used to tx of systemic candidiasis and exotic mycoses
-similar mode of action to nystatin and can be very toxic to humans

Front 199

Describe miconazole.

Back 199

-antifungal azole
-interferes with cell membrane formation (blocks synthesis of ergosterol)
-dual action against fungi and some gram pos. cocci
-resistance rare

Front 200

Describe fluconazole.

Back 200

-wide spectrum of activity on yeasts and other fungi
-used to prevent Candida infection in HIV pts.
-minor toxicity

Front 201

Describe intraconazole.

Back 201

-similar to fluconazole, with a broader spectrum and increased toxicity
-inhibits the fungal cyt. P450 oxidase mediated synthesis of ergosterol (precursor to Vit. D)
-no penetration in CNS

Front 202

Describe terbinafine.

Back 202

an antifungal, allylamine drug that blocks ergosterol synthesis in fungal cell membrane
-used in dermatophyte infections (parasitic fungal infections)
-used as a topical and tablet, risk of hepatic toxicity with admin. as tablet
ex:lamisil

Front 203

Describe echinocandins.

Back 203

-used in systemic candidiasis and aspergillosis
-inhibits production of glucan in cell wall (targets cell wall directly)
-known as penicillin of antifungals

Front 204

Describe how bacteria can become resistant through altering drug targets. (ex ribosome mutation)

Back 204

the bacterium makes a protein product with an altered binding affinity for the drug
-often modifies the bacterial ribosome
-resistance to erythromycin and rifamycin occurred this way

Front 205

What 3 organisms are becoming resistant to everything?

Back 205

Enterococcus faecalis
mycobacterium TB
pseudomonas aeruginosa

Front 206

What 2 organisms are indicated in otitis media?

Back 206

turicella otitidis (bacillus) and alloiococcus otitis
-both are aerobes found in external auditory canal

Front 207

What organisms are predominantly found in healthy sinuses?

Back 207

healthy sinuses are sterile due to the mucociliary blanket

Front 208

What was historically called doderlein's bacillus?

Back 208

lactobacillus acidophilus (found in vagina)

Front 209

What are the predominant bacteria of the vagina and what is their significance?

Back 209

lactobacillus acidophilus and corynebacterium sp
-they metabolize glycogen to lactic acid or acetic acid
-the resulting low pH of the vagina prevents grwoth of most bacteria (including potentially pathogenic yeast candida)

Front 210

What microbe dominates the oral microbiota from birth until the appearance of teeth?

Back 210

streptococcus salivarius
-makes up 98% of total oral microbiota until appearance of teeth

Front 211

What changes occur in the oral microbiota after the eruption of teeth?

Back 211

-leads to colonization by S. mutans and S. sanguis
-require a nondesquamating/nonepithelial surface in order to colonize
-these organisms will persist as long as teeth enamel remains
-also creation of the gingival crevice area increases habitats for anaerobic spp such as prevotella, fusobacterium, veillonella)

Front 212

What changes occur in the oral microbiota at puberty?

Back 212

the complexity of the biota increases with time
-bacteroides and treponemal spirochetes last to colonize

Front 213

What microbe usually plays a dominant role in causing abscesses of alveolar bone, lung, brain or extremities after gaining entrance via surgical wounds through the mouth?

Back 213

prevotella melaninogenicus

-also these wounds can introduce oral strep (like strep. mutans) which adheres to damaged heart valves and initiates bacterial infective endocarditis

Front 214

Describe the microbiota in the GI tract.

Back 214

-differences in composition are influenced by age, diet, and cultural conditions
esophagus: contains only bacteria swallowed with saliva and food
stomach:few bacteria here, too acidic,mainly acid-tolerant lactobacilli (at least 1/2 pop. in US has helicobacter pylori-gastric ulcers)
small intestine:proximal has sparse gram pos. including lactobacilli and enterococcus faecalis, distal portion-more bacteria including coliforms and bacteroides
large intestine:similar to feces, coliforms group, enterococci, clostridia, and lactobacilli found
-predominant spp. are anaerobic bacteroides, anaerobic lactic acid bact. in genus bifidobacterium
-also significant numbers of anaerobic methanogenic (Archaea) bacteria in colon

Front 215

Describe the ecological succession of the GI tract.

Back 215

-at birth, entire tract is sterile until first feeding
breast fed infants: 90% intestinal bacteria are bifidobacteria (human milk contains Growth factor for this), low proportions of enterobacteriaceiae and enterococci
bottle fed: bifidobacteria are NOT predominant
cow's milk or solid food: bifidobacteria joined by enterics, bacteroides, enterococci, lactobacilli, and clostridia

Front 216

What are the normally sterile areas of the body?

Back 216

body fluids, tissues (bone, mm. , blood, CT), upper urinary tract including kidneys and bladder

Front 217

What are coliforms?

Back 217

associated with bacteriologically polluted water and consist of a group of related bacteria
total coliforms: (CEEK) citrobacter, Escherichia, enterobacter, klebsiella

Front 218

What are enterics?

Back 218

gram neg. bacilli
-enterobacteriaceae are C PESSKEY Strains of bacteria
-citrobacter, proteus, escherichia, salmonells, shigella, klebsiella, enterobacter, yersinia, serratia

other pathogenic enterics include: vibrio, campylobacter, helicobacter

Front 219

What 2 methods of moist heat do not reliably kill endospores?

Back 219

boiling and pasteurizing,
autoclaving does kill endospores

Front 220

What type of UV light is used as a germicide?

Back 220

UVC-short
doesn't penetrate the atmosphere, used to sterilizing surfaces, glass/plastic labware, and thin layers of liquid
-damages DNA and creates thymine dimers
-PPE for eyes and skin recommended

Front 221

What is a high level disinfectant?

Back 221

chemical sterilization
-kills all microorganisms but will not effectively kill large numbers of bacterial spores or prions
-used for heat sensitive critical and semi-critical equipment
-standard procedures not effective against prions

Front 222

What is an intermediate level disinfectant?

Back 222

kills mycobacteria, vegetative bacteria, most viruses and fungi, but not spores
-used on some semi-critical and non-critical equipment

Front 223

What are the phenolic compounds?

Back 223

ex: triclosan which is common in antibacterial soaps, also found in deodorant, toothpaste, etc

ex: listerine-4 phenolics +alcohol
-denature proteins and disrupt membranes, surface disinfectant, personal hygiene products, not effective against spores and non-env. viruses

Front 224

Describe Quaternary ammonium compounds.

Back 224

ex: benzalkonium chloride
-antiseptic towelettes and contact lens solutions
-they denature intracell. components
-disinfections of non-critical surfaces
-not effective against spores and viruses

Front 225

What are some compounds you can use when you can't autoclave? (endoscopes, resp. equip., etc)

Back 225

-aldehydes
-ethylene oxide (gas-explosive)-long sterilization times and post-steriliazation aeration required to remove toxic residues
-peroxides-peracetic acid=hydrogen peroxide+acetic acid-stronger biocide than H2O2 alone

Front 226

What can be used to disinfect medical equipment surfaces?

Back 226

alcohols
-hypochlorites
-iodine tinctures/iodophores (antiseptic iodophores not suitable for use a disinfectants)

Front 227

What can be used for disinfection of non-critical surfaces?

Back 227

phenolic compounds (as found in lysol)
-quaternary ammonium compounds
-hypochlorite-.1% chlorine can be used for high level disinfection with contact time of about 20 mins.

Front 228

What are the 2 main functions of wall teichoic and lipoteichoic acids in gram positive bacteria that help to increase the virulence?

Back 228

1)they function as adhesins (for invasion of host cells)
2)can initiate endotoxin like activities when released

Front 229

What are the 2 common acid fast genera?

Back 229

nocardia and mycobacterium

Front 230

What 2 pigments does the acid fast stain process use?

Back 230

carbol fuschin and methylene blue

Front 231

What are the 2 clinically relevant genera that produce endospores?

Back 231

clostridia and bacillus
-both gram positive

Front 232

What is MacConkey agar?

Back 232

it is differential and selective
contains peptone and lactose
-bile salts which inhibit Gram +
-crystal violet inhibits Gram +
neutral red is the pH indicator

Front 233

What are the 3 basic categories of growth factors for bacteria?

Back 233

1)purines and pyrimidines-nucleic acid synthesis
2)AAs-protein synthesis
3)vitamins-act as coenzymes

Front 234

What are mesophiles?

Back 234

most pathogenic bacteria are this type
-optimum temp for survival and growth is 30-37 C
-survive best in moderate temps

Front 235

What are obligate Psychrophiles/cryophiles?

Back 235

survive best in temps under 20 degrees celsius
-deep sea, cold marine environments, etc

Front 236

What are facultative psychrophiles/psychrotrophs?

Back 236

survive best in temps between 0-35 Celsius
-not found in extremely cold condition, can live in fridge

Front 237

What is a microaerophile?

Back 237

requires oxygen, but at reduced levels

Front 238

What is an aerotolerant anaerobe?

Back 238

does not require O2 and does not use O2 but has enzymes for ROS usually

Front 239

What is a facultative anaerobe?

Back 239

does not require O2 but will use it if present

Front 240

What does an organism with a BSL-1 classification signify?

Back 240

these are agents that are not known to consistently cause disease in healthy adults

Front 241

What does BSL2 classification mean?

Back 241

agents associated with human disease
-transmission by ingestion, percutaneous injury, or mucus membrane exposure

Front 242

What does BSL3 classification of microbes mean?

Back 242

indigenous or exotic agents associated with serious to fatal human disease with the potential for aerosol exposure

Front 243

What does BSL4 classification of microbes mean?

Back 243

dangerous/exotic agents with a high potential for causing life-threatening disease, potential aerosol transmission or the risk of infection is unknown, but related to agents with aerosol transmission

Front 244

What are standard precautions?

Back 244

-they protect both pts. and health care workers,
-prevent spread of infectious organisms from pt. to pt., environment to pt., health care worker or pt., pt. to health care worker, environment to health care worker