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INF: Infections > Block I: General > Flashcards

Block I: General Flashcards

1
Q

sterile areas in the body (no association with bacteria)

A

-CSF, blood, lung, deep tissue

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2
Q

general mechanisms of antibiotic resistance

A
  • de novo mutations causing antibioitc resistant traits
  • transfer of preexisting resistant genes from the environment
  • transver between bacteria (mobile DNA elements & horizontal DNA transfer)
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3
Q

Peptidoglycan

A

major feature of cell walls of bacteria

  • gram-positives: thick peptidoglycan layers
  • gram-negatives: thin peptidoglycan layers

**target for many abx because humans do not have peptidoglycans

  • gives osmostic stability to cell (when acted on by abx, cells lose osmotic stability & lyse)
  • consists of polysaccarhide chains crosslinked by peptide bridges
  • subunit: disaccharide with peptide tail; peptide crossbridge attaches to peptide tail
  • synthesized in cytoplasm, then transferred to membrane to rane, then to the cell wall
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4
Q

bacteria classification: presence of specific enzymes

A
  • ex) catalase: if a bacteria has catalase, it will create bubbles when treated with peroxide (as it detoxifies reactive oxygen species)
  • can also look for presence of: oxidase, urease, coagulase, hemolysin

**enzyme presence is diagnostic/identifying for a bacteria (but not used to classify virulence)

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5
Q

nomenclature of bacteria

A

genus species

(genus then species in italics)

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6
Q

Gram-negative rods

A

pseudomonas

vibrio

enteric: escherichia coli

obligate intracellular parasites: rickettsia, chlamydia

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7
Q

characteristics of the “perfect antibiotic”

A
  • selective (for bacteria)
  • specific
  • lethal
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8
Q

AB Toxins

A

(exotoxins that act intracellularly)

  • A subunit: active subunit that is responsible for enzymatic activity that affects host physiology
  • B subunit: binding subunit that delivers the A subunit & determines which cell types are affected (binds to cell surface receptors)

Ways to distinguish AB toxins:

  • potency (very toxic)
  • ability to mimic infection
    ex) Anthrax toxin is a model of AB toxin translocation
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9
Q

gram stain

A

1- stain with crystal violet (purple)

2- fix stain with potassium iodide

3-decolorize with alcohol (gram positives remain purple)

4- counterstain with safranin (gram negatives become pink)

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10
Q

benefits of the normal flora

A
  • provide nutrients
  • stimulate the immune system (espeically in the gut)
  • compete with pathogens

(germ-free animals are much more susceptible to colonization by intestinal pathogens)

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11
Q

How do macrophages recognize LPS?

A
  • LPS receptor complex (CD14, Toll-like receptor 4, MD2)
  • -CD14= LPS binding portion (protein on surface, grabs LPS out o fsystem)*
  • **if antibodies to CD14 inhibit inflammation induced by LPS and gram-negative bacteria*
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12
Q

(immune mediated tissue disease) acute local tissue damage

A
  • local inflammation impairs tissue function
  • edema
  • neutrophil recruitment & activation

-

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13
Q

exotoxins that act on ECM

A

(extracellular)

  • attack/bind to ECM rather than to host cell itself
  • Staphylococcal scalded skin syndrome (SSSS)– toxin disrupts epithelial tight junctions by degrading desmosome components
  • also: collagenases, elastases, hyaluronidases, DNAses, streptokinase
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14
Q

transpeptidation of peptidoglycan in bacterial cell wall

A
  • when glycan chains are crosslinkjed to each other, losing the terminal D-alanine
  • transpeptidation occurs in both gram positives and negatives, although the gram negative peptidoglycan structure differes soemwhat

**B-Lactam abx inhibit transpeptidation

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15
Q

synergy

A

when 2 antibiotics work better together than separately

(often bactericidal)

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16
Q

current therapy for sepsis

A
  • immediate stabilization (ABCs)
  • obtain initial database
  • obtain appropriate cultures
  • prompt use of antimicrobial agents (consider drainage/surgical drainage)
  • idtenify & manage organ dysfunction

FLUIDS

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17
Q

monoclonal

A

cultured bacteria that consist of genetically identical individuals descended from a single ancestor

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18
Q

minimum bactericidal concentration (MBC)

A

minimum concentration of drug that kills the bacteria

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19
Q

Bacteria Capsule Histo

A
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20
Q

major factors that contribute to antimicrobial resistance epidemic in bacteria

A

1-non-prescription antibiotic use (creates strong environmental selection pressure)

-animal feeds, easy access to abx in developing countries, antibacterials present in household cleaners

2- misuse of abx

-lack of stewardship, noncompiance in patients

3-poor santiation (puts bacteria into environment)

4-lack of new abx in drug development pipeline

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21
Q

how bacteria overcome the innate defense of phagocytosis

A
  • thick polysaccharide capsules
  • resist lysosomal killing by growing within the phagolysosome
  • prevent phagolysosome fusion, so that can’t be degraded
  • escape from phagosome

-

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22
Q

transposition

A

(process of gene transfer within an organism)

  • via transposons: small DNA elements that can cut themselves out of sequence and add themselves in elswehere
  • transposons often carry additional genes to ensure their survivial– leading to abx resistance
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23
Q

critical microbial products involved in sepsis

A

gram negative: LPS, DNA

gram positive: protein toxins, lipotheichoic acid, lipoproteins, peptidoglycan

**gram positive and gram negative sepsis can not be distinguished clinically

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24
Q

elements of antimicrobial therapy

A
  • selective toxicity of the agent
  • susceptibility of the pathogen to the agent
  • effective concentration at the site of infection
  • maintenance of effective concentration for sufficient time
  • side effects
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25
Q

phagocytosis as an innate defense in deep tissue/blood

A
  • neturophils, monocytes, macrophages are all involved in phagocytosis
  • phagocytes are recrutied during the inflammatory response
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26
Q

influx and efflux of gram negative bacteria

A
  • in gram negatives, there is the inner membrane and outer membrane (serving as 2 checkpoints for any influx or efflux_
  • outer membrane has porins: semi-selective energy-independent channels
  • inner membrane has transporters/pumps

**these checkpoints control drug uptake & efflux into bacteria (effectiveness of abx)

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27
Q

chemotaxis

A
  • important function of motility
  • movement in response to chemical stimulus (attractants are bacteria that swim up concentration gradients, repellents swim down gradients)
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28
Q

Superantigens

A

(exotoxins that work extracellularly)

  • bind to TCR and MHC outside of peptide-binding grooves, resulting in activation of all T-cells with a certain domain –> causing massive release of cytokines
    ex) staphylococcal TSS
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29
Q

macrophage vs monocyte

A
  • both are phagocytes
  • longer-lived than neutrophils
  • macrophages: in tissues
  • monocytes: in circulation
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30
Q

(immune mediated tissue disease) chronic local tissue damage

A

-chronic inflammation eventually results in displacement of tissue cells with leukocytes & fibrin

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31
Q

what is a bacterium?

A
  • microscopic
  • haploid
  • anucleate
  • prokaryotic
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32
Q

mechanisms of bacterial pathogen damage to host

A

-either immune-mediated (collateral damage resulting from immune activation by bacteria; can be due to either innate or adaptive immune responses)

OR

-toxin-mediated damage (damage resulting from product of bacteria)

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33
Q

the human microbiome(s)

A
  • composition of microbiome varies in different areas of the body
  • mouth, skin, colon, esophagus, stomach, vagina
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34
Q

selective toxicity of an antimicrobial

A

STRATEGIES:

  • lack of target in human host
  • difference in target sensitivity
  • differential concentration of antibiotic by bacterial & human cells
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35
Q

steps required of a bacterium to cause disease

A

1- encounter & enter host

2-establish an infectious niche

3- multiply, cause tissue damage

4-spread to other tissues, hosts, or both

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36
Q

blood agar

A
  • medium containing RBCs
  • frequently used for throat cultures
  • hemolysins present (lyse RBCs) in host, and type of hemolysis seen in the blood agar is useful for distinguishing different species of streptococci
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37
Q

minimum inhibitory concentration (MIC)

A

-mimimum concentration of a drug that inhibits a bacteria

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38
Q

SOS response

A
  • if a cell is exposed to DNA damage, it triggers RecA protein to be active, which induces mutations (under stress)
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39
Q

AB toxins that modulate cAMP levels intracellularly

A
  • cholera & pertussis toxins: ADP-ribosylate G proteins–> actiavtion of adenylate cyclase
  • anthrax EF toxin & pertuss AC toxins: adenylate cyclase enzymes
  • increase cAMP: increases fluid secretion from epithelial cells, inhibits phagocyte chemotaxis & effector functions
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40
Q

Gram negative cocci

A

neisseria

& others

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41
Q

How to categorize microbes?

A
  • phylogeny (based on 16S RNA)
  • structure (shape & stain)
  • nature of interaction with host (symbiosis, commensalism, parasitism)
  • pathogenic strategies
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42
Q

sedementation coefficients (refers to molecular weight) of bacteria bacterial ribosomes

A

70S

-made of 2 subunits; in bacteria: 30S and 50S

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43
Q

direct detection method of diagnosing infection

A
  • DNA or microbial antigen detection
  • very specific & sensitive
  • tests not always available
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44
Q

replisome

A

origin of DNA replication in bacteria

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45
Q

Phase Variation

A

-phase variation results in phenotypic heterogeneity in an organism

**important to vary antigens in host

-evade host defenses, adapt to different niches

mechanisms:

slipped strand mispairing

site-specific recombination

epigenetic regulation mediated by DNA methylation

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46
Q

therpeautic index

A
  • ratio of the minimum toxic dose to the minimum effective dose
  • this ratio must be >1 for an abx to be of use

**high therapeutic index= not generally toxic to patients

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47
Q

Gram-Negative Bacteria (structure)

A
  • inner membrane (inside cell wall, consists of phospholipid)
  • outer membrane (outside cell wall, consists of phospholipis & lipopolysaccharide LPS)
  • LPS is the endotoxin of gram negative baceria (pathogenesis)
  • 2 types of protein in outer membrane: porin & lipoprotein
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48
Q

how many toll-like receptors do humans have?

A

10

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49
Q

gram-positive cocci

A

staphylococcus

streptococcus

enterococcus

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50
Q

epidemiology of sepsis

A
  • more common among men
  • more common among nonwhite
  • gram-positive more positive than gram-negative
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51
Q

colloquial name for streptococcus pneumoniae

A

pneumococcus

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52
Q

sepsis

A

formal definition: alterations in physiology (fever, respiratory rate, blood pressure, organ function)

accompanied by an infection

-life-threatening condition that arises when the body’s response to an infection injures its own tissues & organs

(local infection with profound systemic response)

-sepsis can be mimicked by other non-infectious disorders

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53
Q

transduction

A

(process of horizontal gene transfer between organisms)

  • agent: phage (viruses that infect bacteria)
  • virulent phages: replicate within host cell, then destory host, releasing infectioius virions
  • temperate phages: replicate lytically or go latent

generalized transduction: phages with nonspecific DNA encapsulation package host DNA instead of phage DNA during lytic growth– then can inject DNA into new cell

specialized transduction: when bacterial genes transferred from one cell to another by becoming incorporated into a phage chromosome (phage uses SOS response to induce replication, then find a new host after excising itself)

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54
Q

teichoic acid

A
  • polymer of ribitol-phosphate or glyercol-phosphate
  • part of gram positive cell walls, confers stability of the peptidoglycan
  • not yet used as target for abx
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55
Q

what kind of growth is characteristic of microbial growth?

A
  • exponential growth: every cell takes the same amount of time to complete a binary fission event
  • a limitation of exponential growth is having enough nutrition for this growth
  • log phase cells show most consistent physiological parameter (so are the standard for most experiments in microbio)
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56
Q

why are bacitracin and vancomycin’s mechanisms unique?

A

they both bind to microbial metabolites rather than inhibiting an enzyme

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57
Q

gyrase & topoisomerase

A
  • maintain the supercoiling of bacterial DNA
  • recognize improperly coiled DNA and fix it

**protein-bound DNA is good target for antibioics (quinolones & fluoroquinolones)

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58
Q

EARLY GOAL-DIRECTED THERAPY (EGDT) for sepsis

A

-administration of IV fluids within the first 6 hours of presentation

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59
Q

bacteria classification: interaction with oxygen

A
  • anaerobic: grow in oxygen-free environment
  • obligate anaerobe: killed by oxygen (often form spores so that they can spread in environment)
  • facultative anaerobe: can live in aerobic or anaerobic environment
  • aerobic: grow in oxygen-containing environment
  • obligate aerobe: need oxygen to grow
  • some are “microaerophilic”- they ferment (metabolism without oxygen) for energy, but can grow in contact with oxygen at less than atmospheric pressure
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60
Q

4 categories of Immune-mediated tissue disease after bacterial infection

A

1- acute local damage

2-chronic local damage

3-acute systemic disease

4-chronic systemic disease

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61
Q

How do bacteria resist B-lactam antibiotics?

A

-they produce beta lactamase, which breaks down the B-lactam ring in the abx, making it ineffective

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62
Q

Spirochetes

A

treponema

borrelia

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63
Q

shapes of bacteria

A
  • bacillus: rod
  • coccus: sphere
  • coccobacillus (oval)
  • comma (vibrio)
  • helical (spirochete)
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64
Q

autoclave

A

procedure for sterilizing solutons (especially those that form spores)

  • invovles a chmaber into which high pressure steam is injected
  • kills spores
65
Q

Bacterial Flagella

A
  • promote motility
  • variable between bacteria
  • not essential for growth, but important for infection
66
Q

Sulfonoamides mechanism of action

A
  • interfere with folate synthesis
  • block the action of dihydropteroate synthase (DPS) (competitive inhibition)
  • DPS not found in humans
67
Q

(immune mediated tissue disease) chronic systemic disease examples

A

Reactive Arthritis: chronic inflammation secondary to many bacterial infections

-doesn’t require direct infection of joints (symtpoms are due to immunological response & persist after abx treatment)

Cachexia (wasting): can result from chronic inflammation

Immune Complex Disease: circulating antigen-antibody complexes become depositied in glomeruli or joints, triggering local complement activation & inflammation

68
Q

fastidious bacteria

A

-bacteria with many growth requirements

(have evolved in nutrient-rich environments so have lost many biosynthetic pathways required for growth on a simple media)

also called obligate pathogens/non-culturable

69
Q

6 general mechanisms for antibiotic resistance in bacteria

A

1- target site absent

2-enzymatic inactivation (*most common mechanism of transmissable resistance)

3-target site modification (high level resistance)

4-drug efflux (low level resistance)

5- altered cell wall permeability

6- bacteria present excessive binding sites that are decoys

70
Q

Innate defenses in deep tissue & blood

A
  • iron starvation
  • complement
  • phagocytosis
  • confinement of infection (abscess or granuloma)
71
Q

differential media

A

-lab media that permits visual distinction of different types of bacteria due to differences in coloring or colony morphology

72
Q

adjusting drug dosing based on pharmacokinetic parameters

A
  • clearance is most important parameter
  • loading dose will be the same for all patients, but following doses have to be adjusted based on weight & other factors
73
Q

Classes of Exotoxins

A

(secreted by bacteria)

ACT INSIDE HOST CELLS

-AB toxins

ACT EXTRACELLULARLY

  • membrane-disrupting toxins
  • superantigens
  • extracellular matrix degrading enzymes
74
Q

enzymes that lead to lysis of peptidoglycan in cell wall

A

lysozyme

endopeptidase

amidase

75
Q

drugs that target peptidoglycan vs drugs that target membranes of bacteria

A

=drugs that target the membranes are less selective

76
Q

McConkey Agar

A
  • classified as both selective and differential media
  • selective media designed specifically for selective growth of gram negative enteropathogens
  • made with crystal violet & bile salts (preventing the growth of gram positives)
  • lactose & pH indicator used to identify if lactose-utilizing organisms are present

–> result: selective identification of gram negative enteric organisms

77
Q

(immune mediated tissue disease) acute systemic responses

A
  • septic shock= most dramatic
  • caused by overwhelming systemic innate immune response to bacteria
  • symptoms: result from systemic stimulation of innate immunity & cytokine release
78
Q

what is the effect of the vast majority of bacteria on humans?

A

-either beneficial or non-harmful (normal flora/microbiome)

*only a small minority are pathogens (causing disease)

79
Q

which bacteria can undergo transformation to incorporate other DNA into their genome?

A

(horizontal gene transfer)

-naturally competent bacteria: streptococcus, hemophilus, neisseria

80
Q

immunologic assays for diagnosis of infection

A
  • presence of antibodies or T cells specific for a microbial antigen
  • diagnosiing active infection requires seroconversion, increase in titerm or IgM test
81
Q

heavily colonized ares of the body

A

-large bowel, mouth, skin, vagina

82
Q

what is the toxic moiety of endotoxin?

A
  • Lipid A (lipid A inserts LPS onto the outer membrane of gram negative bacteria)
  • LPS administration into humans mimics sepsis
83
Q

c. difficile

A
  • most common cause of pseudomembranous colitis in humans
  • most commonly seen after normal flora is eradicated by antibioitcs (shows importance of normal microbiome)
84
Q

bacterial secretion systems, to establish infection in host

A
  • type III & IV secretion systems
  • span from bacterial cytosol to host cytosol
  • bacteria inject effector proteins that alter host physiology

**only occurs in gram negative bacteria

85
Q

culture method of diagnosing infection

A
  • must be followed by additional microscopic/biochemical/molecular or immunological assays
  • common
  • can be difficult/impossible for some pathogens
86
Q

what is an antibiotic?

A

antimicrobial agent of microbial origin

87
Q

Bacteria Capsule

A
  • loosely-associated polysaccaride; gel-like layer of polymers that surround some bacteria
  • not essential for bacterial growht
  • variable (not seen in all bacteria)
  • important for resisting immunity (inhibit phagocytosis by host cells)
88
Q

common diagnostic methods of infections

A

-microscopic, culture, direct detection of microbial products, immunologic assays

89
Q

Therapeutic Inhibition of Exotoxins

A
  • active immunization: vaccines containing inactivated toxin protein (toxoid); producing protective antibodies
    ex) diphtheria, tetanus, botulism

-passive immunization: therapeutic administartion of anti-toxin antibodies raised in animals

-small molecule inhibitors (being developed)

90
Q

where is DNA located in bacteria?

A

condensed in the nucleoid

91
Q

microscopic method of diagnosing infection

A
  • i.e. gram stain, acid fast stain
  • useful & quick, but not specific
92
Q

why do people with sepsis sometimes present with normal vital signs?

A
  • elderly/malnourished patients may not have fever: don’t have normal cytokine release
  • people on beta-blockers may not show tachycardia
  • WBC may be changing and could appear in normal range when lab work done
93
Q

features of bacteria that can be used to identify a bacterium

A
  • size, shape, staining
  • interactions with oxygen
  • nutritional requirements
  • presence of particular enzymes
  • antigens
  • molecular methods
94
Q

complement system

A
  • innate defense in deep tissue/blood
  • microbe recognized, induces proteolytic signaling cascade, which leads to covalent deposition of complement components on the surface of the microbe & the generation of pro-inflammatory peptides
95
Q

cultivation of bacteria

A

-can be cultured on liquid and semisolid media (agar)

96
Q

Periplasmic space

A

aqueous compartment between inner and outer membranes in gram-negative bacteria

97
Q

bacterio-static drugs

A

inhibit bacterial growth

98
Q

iron starvation in deep tissue/blood

A
  • innate defense against bacteria
  • transferrin system keeps free iron levels low
  • iron-binding proteins are induced during inflammaition
  • bacteria secre siderophores to try to traph free iron
99
Q

components of outer envelopes of bacteria

A

capsule, pili, flagella –> not essential for growth; important for infection

outer membrane, cell wall, inner membrane –> essential for growth; targets for antibiotics

100
Q

Bacteria fimbriae and pili

A
  • adhesive structures that extend away from surface
  • major antigens
  • variable between bacteria
  • not essential for growth
101
Q

Acid-Fast Bacteria (structure)

A

(primaroly Mycobacteria)

  • structure is basically gram-positive organization (inner membrane, cell wall)
  • differ: large amounts of lipid in outer envelope & mycolic acid

–> thought to be responsible for acid-fast stain

102
Q

septicemia

A

lots of bacteria in the blood

sepsis: speticemia plus evidence of a systemic response

103
Q

bacteria classification: nutritional requirements

A
  • non-culturable (obligate pathogens): have co-evolved with host for so long that they are unable to be cultured in lab
  • auxotroph: able to grow in lab, but need specific pathogens to grow
  • prototroph (facultative pathogens): bacteria can make everything they need to grow; all they need is P, N, C in environment
104
Q

bacteria have some different biochemical pathways than humans

A

-ex) bacteria can provide essential vitamins to humans (ex biotin, vitamin K)

**these unique biochemical pathways are good targets for antibiotics (antimicrobials)

105
Q

gram-negative vs gram-positive bacterial cell envelopes

A

GRAM-NEGATIVES: thin, densely woven cell wall, plus an outer membrane attached to cell wall

GRAM-POSITIVES: thicker, less dense cell wall , with no outer membrane

106
Q

LB media

A
  • most widely used medium in bacteria labs
  • main ingredients; casein, yeast extract, NaCl
107
Q

Koch’s Postulates

A

rigorous way to demonstrate causation between microbe and infection

1-find agent in diseased population/tissue

2-isolate agent & grow it in pure culture

3-cause disease by inoculating purified agent into animals

4-reisolate agent from experimentally infected animals

108
Q

Gram-positive rods

A

spore formers: bacillus, clostridium

corynebacterium

listeria

109
Q

Growth/Division of Bacteria

A
  • bacteria multiply by binary fission
  • extraordinary metabolic efficiency (achieved by tight control & coordination of enzymatic activities & gene expression)

e coli grows by elongation, then septation, then binary fission

110
Q

transformation

A

(process of horizontal gene transfere between organisms)

  • agent: DNA
  • organism takes up naked DNA from its environment & integrates it into its genome

**this only occurs in naturally competent bacteria

111
Q

major routes that bacteria take to encounter/enter a host:

A
  • via contaminated water supplies *fecal/oral transmission)
  • infectious aerosols *from nasal cavity to oral cavity)
  • arthropod vectors
112
Q

Systemic Inflammatory Response Syndrome (SIRS)

A

alteration in pulse, temp, respiratory rate, WBC

SIRS+ infection –> sepsis

113
Q

granuloma

A

confinement of infection initiated by macrophages

114
Q

surface antigens of gram negative enteric bacteria

A
  • K-antigen found in capsule
  • O-antigen
  • H-antigen found in flagellum

**these variable surface structures are helpful for classification of bacteria

115
Q

clinical sequelae of sepsis

A

1-edema: lowers BP, reduces perfusion of heart

2-disseminated IV coagulation, resulting in hemorrhage– reducing blood volume & further contributing to shock

116
Q

how does vancomycin affect bacterial cell walls?

A
  • inhibits the growth of the glycan chain of peptidoglyan in the cell wall
  • rather than inhibiting an enzyme, it binds to the terminal D-alanine and inhibits growth of the bacteria
117
Q

what mechanisms facilitate horizontal gene transfer?

A

transposition

recombination

118
Q

horizontal gene transfer in bacteria

A

-method that antibiotic resistance can arise

processes to move DNA WITHIN an organism

  • homologous recombination
  • transposition

processes to move DNA between organisms

  • transformation
  • conjugation
  • transduction (generalized & specialized)
119
Q

profile of an ideal antibiotic

A
  • high therapeutic index
  • acid-stable (so can take it PO)
  • absorbed in gut
  • penetrates all body compartments
  • not metabolized rapidly
  • slowly excreted
  • no side effects
  • B-lactams are closest to perfect: high therapeutic index, low toxicity
120
Q

what is the first host defense that bacteria encounter?

A

innate immunity

(every pathogen has to overcome innate immunity)

121
Q

how does bacitracin affect bacterial cell walls

A
  • bacitracin inhibits recycling of bactoprenol (lipid carrier) to the monophosphate in peptidoglycan frowth
  • bacitracin binds to the metabolite, inhibiting further bacterial growth
122
Q

lipopolysaccharide (LPS)

A
  • forms the outer leaflet of the outer membrane of gram negative bacteria
  • not found in animal cells
  • aka “endotoxin” because it activates immunity
  • structure: polysaccharide (O-antigen), attached to core oligosaccharide, with Lipid A tails
123
Q

normal flora

A

-microbes which normally colonize healthy humans

(whereas pathogens are microbes which cause disease)

  • some members of normal flora can cause disease
  • most of normal flora bacteria are starved for nutrients at any given time
124
Q

molecular methods used to ID DNA from bacteria

A
  • MALDI-TOF: matrix assisted laser desorption ionization time of flight mass spec (uses presence of small molecule metabolites for identification, can only be used with cultured isolate)
  • PCR: polymerase chain reaction; can identify species, does not require culture, used to amplify nucleic acids
  • deep sequencing (next-gen & others)–looks at DNA sequence of many fragments
125
Q

conjugation

A

(process of horizontal gene transfer between organisms)

  • agent: plasmid
  • plasmids are DNA molecules that replicate separately from bacterial chromosome (often circular)
  • transfer of plasmids between bacteria, which encode functions require for transfer & replication
  • then, transposition or recombination of plasmid occurs, passing the plasmid along
126
Q

septic shock

A

sepsis + shock

(SIRS + infection + shock)

shock: organ hypoperfusion
- systemic manifestation of the local inflammatory response

127
Q

how do mycoplasmas differ from other bacteria?

A

they lack peptidoglycan

-have sterols in cytoplasmic membranes to help strengthen membrane (partially compensating for lack of cell wall)

128
Q
A

Bacteria Capsule Histo

129
Q

sterilization

A

the killing of all organisms and infectious agent s in a preparation

130
Q

important sites of tranlsation in bacteria

A

A site: aminoacyl-tRNA site

P site: peptidyl-tRNA site

E site: exit site

131
Q

pili and fimbriae

A

protein protrusions from the surface of bacteria

-function: adherence, allowing bacterium to adhere to surfaces

132
Q

harmful effects of normal flora

A
  • antibiotic resistance
  • -resistance determinants can be carried on single plasmids or transposons*
  • -enteric bacteria exchange genes continually with each other & environment*
  • -pathogens can acquire resistance determinants via occasional contact with enterics or environment*
  • corrosive metabolic products
  • ptoential to cause disease (opportunistic pathogens that get to a site where they shouldnt be)
133
Q

resistance genes (generally originating in the environemnt) are transferred to pathogesn by three mechanisms…

A

transformation

conjugation

transduction

134
Q

what is the most important factor to beat germs?

A

sanitation

(then vaccination, then antimicrobial therapy)

135
Q

IgA Protease

A

-some bacteria secrete IgA protease, which cleaves IgA that is part of the adaptive immunity in sMALT cells

136
Q

presenting signs of sepsis

A
  • temp greater than 38C or less tahn 36C
  • HR > 90bpm
  • Respiratory Rate >20bpm
  • WBC: >12k or <4k
  • signs of infection
137
Q

what staining procedure is used for visualizing mycobacteria?

A

acid-fast

138
Q

Beta Lactam Antibiotics

A
  • inhibit transpeptidation of peptidoglycan in bacterial cell wall
  • classified because they contain a B-lactam ring
  • irreversible inhibitors by covalently bonding; serve as a substrate mimick
139
Q

how is drug resistance to mycobacterium tuberculosis caused?

A

ALL by mutation (because m. tuberculosis does not acquire DNA from its environment)

-therefore, TB treated with a cocktail of abx

140
Q

predominant mechanism of how antibiotic resistnace occurs

A

spontaneous mutation

-mutation that makes a drug bind less strongly (disrupts the drug binding site but not the activation site)

141
Q

spores

A

formed by sepcies of Clostridium & Bacillus (gram positive rods)

  • single spore produced within parent cell
  • spores have NO metabolic activity
  • resistant to: heat, radiation, toxic chemicals, dessication
142
Q

what mediates transcription in bacteria?

A

RNA polymerase

143
Q

2 generalizations about metabolic requirements of bacteria

A
  • all require reduced carbon & nitrogen for growth
  • all derive energy from organic substrates by fermentation or oxidation with oxygen

(they are chemoheterotrophs)

144
Q

membrane disrupting toxins

A

(exotoxins that act extracellularly)

  • can kill phagocytes
  • used by some intracellular bacteria to escape from phagosome & enter host cytoplasm
  • often obligate anaerobes, trying to create anaerobic environment by digesting tissue
    ex) alpha toxin of c. perfringens (gas gangrene)
145
Q

abscess

A

-confinement of infection initiated by neutrophils

146
Q

selective media

A

-lab media that contains (in addition to nutrients) cmpds that specifically inhibit the growth of one set of organisms, permitting detection of another set)

147
Q

when treating a patient with bacterial infection, what are the 2 main lab science questions ?

A

1- which bacterium is it?

2- to which antibiotics is it susceptible?

148
Q

bacterio-cidal drugs

A

-kills the bacteria (reduces the viability of the culture)

149
Q

bacteremia

A

bacteria in th eblood

150
Q

homologous recombination

A

(process that moves DNA within an organism)

-2 homologous pieces of DNA “cross over”

151
Q

how bacteria overcome mucosa defense

A
  • flagellae: promote motility
  • fimbriae & pilli: adhesive structures so that bacteria can adhere to epithelium
  • sloughing epithelium (bordetella pertussis)
152
Q

chocolate agar

A

-sheep RBCs heat to 56 degree C a+ standard agar

153
Q

areas of the body where some bacteria is present

A

-small bowel, trachea, stomach

154
Q

Gram positive bacteria (structure)

A
  • teichoic acid is principal structural component of layers beyond the cell wall (mostly linked to peptidoglycan)
  • lack of outer membrane makes gram positives more susceptible to many abx (especially glycopeptides and lipopeptides)
155
Q

exotoxin vs endotoxin

A
  • endotoxin: intrinsic bacterial structure that can induce immunopathology (ex LPS)
  • exotoxin: other secreted bacterial products that induce pathology (can cause disease in the absence of infection; symptoms can persist after abx treatment)
156
Q

5 main categories of germs

A

bacteria

viruses

fungi

protozoa

helminths

157
Q

biofilms

A
  • population of bacteria embedded in an adherent layer of glycocalyx (often important to infectious processes)
  • facilitates spread of infection & protects embedded bacteria from antibodies & phagocutes
158
Q

host defenses at epithelial surfaces

A
  • skin: physical barrier, inhospitable environment, salt
  • mucosa: clearance of bacteria by physical flow, barrier, antibacterial secretions, mucosa-associated lymphoid tissue (MALT) produces secretory IgA (part of adaptive immune ressponse)

INF: Infections (5 decks)

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