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Vet Micro > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

what are chemotherapeutic agents?

A

chemical agents used to treat disease
destroy pathogenic microbes or inhibit their growth within host.
most are antibiotics

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2
Q

what are antibiotics?

A

microbial products or their derivatives that kill susceptible microbes or inhibit their growth.

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3
Q

how was penicillin discovered?

A

accidentally by Alexander Fleming in 1928
He observed penicillin activity on a contaminated plate

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4
Q

penicillin’s effectiveness demonstrated by

A

Florey, Chain, and Heatley in 1939
they received the nobel prize in 1945 for the discovery and production

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5
Q

selective toxicity

A

the ability of a drug to kill or inhibit pathogen while damaging host as little as possible.

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6
Q

theraputic dose

A

drug level required for clinical treatment

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7
Q

toxic dose

A

drug level at which the drug becomes too toxic for the patient

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8
Q

therapeutic index

A

ratio of toxic dose to therapeutic dose

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9
Q

narrow spectrum drugs

A

attack only a few different pathogens

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10
Q

broad spectrum drugs

A

attack many different kinds of bacteria

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11
Q

cidal agent

A

kills the target pathogen

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12
Q

static agent

A

reversibly inhibits growth of microbes

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13
Q

how is antimicrobial drug effectiveness expressed?

A
  • minimal inhibitory concentration (MIC) - lowest concentration of drug that prevents growth of the pathogen
  • minimal lethal concentration (MLC) - lowest concentration of drug that kills pathogen
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14
Q

main modes of action of antimicrobial drugs

A
  • inhibit cell wall synthesis
  • inhibit protein synthesis
  • inhibit nucleic acid synthesis
  • metabolic antagonists
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15
Q

cytokinesis

A

septation - formation of cross wall between two daughter cells

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16
Q

cell wall synthesis

A
  1. bactoprenol flips NAM and NAG across plasma membrane
  2. glycosyltransferase attach sugars
  3. transpeptidase join amino acids (form bridge of layers)
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17
Q

what is the most crutial feature of penicillins?

A

beta-lactam ring
it is essential for bioactivity
blocks transpeptidase

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18
Q

what can we include in penicillins to increase efficiency?

A

beta lactamase inhibitors with the antibiotic

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19
Q

cephalosporins

A

similar to penicillins
broad spectrum antibiotics that can be used by most patients that are allergic to penicillin
four categories based on their spectrum of activity

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20
Q

vancomycin

A

antibiotic
inhibit cell wall synthesis

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21
Q

many antibiotics bind specifically to the

A

bacterial ribosome

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22
Q

aminoglycosides

A

bind to 30S ribosomal subunit, interfere with protein synthesis by directly inhibiting the process and by causing misreading of the messenger RNA

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23
Q

tetracyclines

A

target the 30S subunit of the ribosome inhibiting protein synthesis

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24
Q

Macrolides

A

binds to 50S ribosomal subunit to inhibit bacterial protein elongation

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25
Q

what are metabolic antagonists?

A
  • they act as antimetabolites - block functioning of metabolic pathways by competitively inhibiting the use of metabolites by key enzymes
  • are structural analogs - structurally similar to and compete with naturally occurring metabolic intermediates to block normal cellular metabolism.
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26
Q

sulfa drugs

A

competitive inhibition of folic acid synthesis enzymes

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27
Q

trimethoprim

A

synthetic antibiotic that also interferes with folic acid production

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28
Q

nucleic acid synthesis inhibition drugs are not as selectively toxic as other antibiotics because

A

bacteria and eukaryotes do not differ greatly in the way they synthesize nucleic acids

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29
Q

fluoroquinolones

A

inhibit bacterial DNA gyrase and topoisomerase II

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30
Q

main mode of action for antibiotics used in lab

A

bacitracin - inhibit dephosphoylation
penicillin
furazolidone - block DNA transcription
optochin - interfere with metabolic processes

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31
Q

HANDOUT - who is associated with the disease and what are the characteristics and which medicine to use

A
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32
Q

antiviral drugs

A

limit the duration of the illness or its severity

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33
Q

antiviral drug for influenza is _____. what does it do?

A

tamiflu
neuraminidase inhibitor - facilitates the release of virus
- shorten the course of illness

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34
Q

anti HIV drugs

A
  • nucleoside reverse transcriptase inhibitors (NRTI’s) - target and interfere with the critical steps in viral replication process
  • nonnucleoside reverse transciptase inhibitors (NNRTI’s) - prevent HIV DNA synthesis by selectively binding to and inhibiting the viral reverse transcriptase enzyme
  • protease inhibitors (PI’s) - block activity of HIV protease
  • integrase inhibitors - prevent incorporation of HIV genome into hosts chromosomes
  • fusion inhibitors - prevent HIV entry into cells
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35
Q

what are the most successful at anti HIV?

A

drug cocktails to curtail resistance

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36
Q

treating superficial mycoses

A

topical and oral
disrupt membrane permeability and inhibit sterol synthesis
disrupts mitotic spindle - may inhibit protein and DNA synthesis.

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37
Q

treating systemic mycoses (in the bloodstream)

A

difficult to control and treatments can be fatal

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38
Q

antiprotozoan drug mechanism is

A

not precisely known.

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39
Q

types of drug resistance

A
  • intrinsic - part of structural/born with it. mycoplasma resistance to beta lactam antibiotics and other cell wall inhibitors and other cell wall inhibitors simply because they lack a cell wall
  • acquired - occurs when there is a change in the genome of a bacterium that converts it from one that is sensitive to an antibiotic to one that is resistant.
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40
Q

drug tolerant bacteria (persisters) lack the mechanisms for _____ ______ and ignore the presence of antibiotics.

A

antibiotic resistance

41
Q

mechanisms of drug resistance

A
  • modify the target of the antibiotic - change the plasma membrane and alter enzymes so it can be targeted
  • drug inactivation - enzyme from plasmid break up antibiotics
  • minimize the concentration of antibiotic in the cell - antiporter kicks out antibiotic
  • bypass the biochemical reaction inhibited by the agent or increase the production of the target metabolite. - bacteria make their own or they are producing enough of their own that they have enough to function.
42
Q

overcoming drug resistance

A
  • give drug in appropriate concentrations to destroy susceptible microbes and most spontaneous mutants
  • give 2 or more drugs at same time - maybe it didn’t change target for one of the drugs so it might work
  • use drugs only when necessary and take the full dosage so there arent any that create resistance
43
Q

possible future solutions to overcoming drug resistance

A

use of bacteriophages to treat bacterial disease

44
Q

immune system

A

composed of widely distributed cells, tissues, and organs
recognizes foreign substances or microbes and acts to neutralize or destroy them

45
Q

nonspecific immune response (innate)

A

first line of defense
offers resistance to any microbe or foreign material
lacks immunological memory

46
Q

specific immune response (adaptive)

A

resistance to a particular foreign agent
has “memory”
effectiveness increases on repeated exposure to agent

47
Q

physical barriers of nonspecific (innate) resistance (direct and indirect factors)

A

direct factors - nutrition, physiology, fever, age, genetics
indirect factors - personal hygiene, socioeconomic status, living conditions

48
Q

along with host’s secretions (flushing), barriers are the __ __ _ _ against microbes.

A

first line of defense

49
Q

skin - innate characteristics

A
  • strong mechanical barrier to microbial invasion
  • inhospitable environment for microbes
  • shedding of outer skin cells, slightly acidic, high NaCl conc., subject to periodic drying
50
Q

mucous membranes

A
  • resists penetration and traps many microbes
  • antimicrobial secretions
  • lysozyme - hydrolyzes bond connecting sugars in peptidoglycan
  • lactoferrin - secreted by certain immune cells and sequesters iron from plasma
  • lactoperoxidase - produces superoxide radicals
51
Q

respiratory system

A
  • mucociliary blanket traps microbes and once they are trapped they are transported away from the lungs by coughing or sneezing or salvation washing the microbes to the stomach
52
Q

GI tract

A

stomach - gastric acid
small intestine - pancreatic enzymes, bile, intestinal enzymes, peristalsis
large intestine - shedding of columnar epithelial cells, secretory IgA, normal microbiota

53
Q

Genitourinary tract

A

unfavorable environment - low pH, lactobacilli, urea and other toxic metabolic end products in urine
- flushing urine and mucus
- distance barrier of male urethra

54
Q

what is the secretion of the eye and what is in the secretions?

A

flushing action of tears
lysozyme, lacterferrin, secretory IgA in tears

55
Q

chemical mediators in nonspecific (innate) resistance

A
  • gastric juices, lysosome, urea
  • variety of defensive chemicals such as defensins and other polypeptides are also found in blood, lymph, and other body fluids
  • defensive proteins found in the blood
56
Q

complement system 3 major activities

A
  • stimulating an inflammatory response by helping to recruit white blood cells
  • lysing microbial cells
  • promoting phagocytosis (opsonization)
57
Q

opsonization

A
  • microbes are coated by serum components (opsonins) in preparation for recognition/ingestion by phagocytic cells
  • bind to microbial cells, coating them for phagocyte recognition - can be antibody, complement, or antibody and complement
58
Q

Functions of complement proteins

A
  • function as chemotactic signals that recruit phagocytes to their activation site
  • puncture cell membranes causes lysis
  • many complement activities unite the innate and adaptive arms of the immune system to destroy and remove invading pathogens
59
Q

complement activation

A
  • activated following enzymatic cleavage
  • must be activate in cascade fashion
  • 3 pathways of activation - alternative, lectin, classical
60
Q

alternative complement pathway

A
  • dependent on interaction of complement with repetitive structures on pathogens
  • begins with activation of C3
  • results in formation of membrane attack complex
61
Q

lectin complement pathway

A
  • also called the mannose binding lectin pathway - mannose is a part of a lot of pathogens
  • activation of C3 and lectin binding
  • dependent on interaction of host mannose-binding protein (MBP) with pathogen surfaces - enhances phagocytosis
62
Q

classical complement pathway

A
  • dependent on antigen-antibody interactions
  • acquired immunity and not as fast as other pathways
  • produces cleavage products that participate in opsonization, chemotaxis, and the membrane attack complex.
63
Q

cytokines are soluble __or _____ that are released by one cell population that act as _______ ______ or _______ ______

A

proteins or glycoproteins
intracellular mediators or signaling molecules

64
Q

3 simplified categories of cytokines

A
  • regulators of innate immunity
  • regulators of adaptive immunity
  • stimulators of hematopoiesis
65
Q

cytokines are divided into 4 functional groups. what are they?

A
  • chemokines - stimulate cell migration
  • interleukins - released from one leukocyte and act on another leukocyte
  • interferons - regulatory cytokines produced in response to infection
  • colony stimulating factors (CSF’s) - stimulate growth and differentiation of immature leukocytes in bone marrow
    additional class - tumor necrosis factors - - (TNF) - stimulates an inflammatory response
66
Q

mast cells

A
  • bone marrow derived cells
  • differentiate in blood and connective tissue
  • contain granules containing vasoactive mediators
  • play important role in development of allergies and hypersensitivities
67
Q

granulocytes

A
  • irregularly shaped nuclei with two to five lobes
  • cytoplasm has granules with reactive substances - kill microbes enhance inflammation
  • three types - basophils, eosinophils, neutrophils
68
Q

neutrophils (type of granulocyte)

A
  • highly phagocytic
  • circulate in blood then migrate to sites of tissue damage
  • kill ingested microbes with lytic enzymes and reactive oxygen metabolites contained in primary and secondary granules
69
Q

monocytes and macrophages

A
  • highly phagocytic cells
  • monocytes - produced in bone marrow and released into blood circulation - after circulating for 8 hours they turn into macrophages
  • macrophages - larger than monocytes, reside in specific tissues, highly phagocytic. release chemokines to recruit neutrophils
70
Q

dendritic cells

A
  • many long cellular projections
  • present in blood, skin, and mucous membranes of the nose, lungs, and intestines
  • contact, phagocytose, and process antigens - display foreign antigens on their surfaces (antigen presentation)
  • capable of eliciting immune response from T-cells activating adaptive immune system
71
Q

lymphocytes

A

major cells of the adaptive immune system
major populations include T cells, B cells, and NK cells

72
Q

innate lymphoid cells

A

NK cells - do not have memory
stimulated same methods as neutrophils, macrophages, and DCs

73
Q

phagocytosis

A

process by which phagocytic cells (monocytes, tissue macrophages, dendritic cells, and neutrophils) recognize, ingest and kill extracellular microbes

74
Q

2 mechanisms for recognition of microbe and phagocyte

A
  • opsonin-independent (nonspecific) recognition
  • opsonin-dependent (opsonic) recognition
75
Q

phagocytosis can be greatly increased by

A

opsonization

76
Q

opsonin dependent pathogen recognition

A

recognize serum components attached to pathogens

77
Q

opsonin independent pathogen recognition

A

common pathogen components are nonspecifically recognized to activate phagocytes - signaling mechanism involved
- involves nonspecific/specific receptors on phagocytes

78
Q

intracellular digestion

A

once bound, microbes can be internalized and delivered to a lysosome to become a phagolysosome
- respiratory burst reactions occur once phagolysosome forms
- toxic oxygen products are produced which can kill invading microbes

79
Q

innate immune system host response is

A

inflammation - nonspecific response to tissue injury can be caused by pathogen or physical trauma

80
Q

acute inflammatory response

A
  • release of inflammatory mediators from injured tissue cells initiates a cascade of events which result in the signs of inflammation
  • involves chemical mediators
81
Q

chemical mediators involved in acute inflammatory response

A
  • selectins - cell adhesion molecules on activated capillary endothelial cells
  • integrins - adhesion receptors on neutrophils
  • chemotaxins - chemotactic factors released by injured cells
82
Q

what happens during an acute inflammatory response

A
  • margination
  • diapedesis/extravasion - diapedesis - cell squish through capillary call into tissue - extravasion - get rid of bacteria
  • capillary widening
  • increased permeability
  • attraction of leukocytes
  • systemic response
83
Q

macrophages release chemotaxins that

A

stimulate permeability of cell wall and recruit other cells that perform phagocytosis

84
Q

what processes and or signals initiated immediately after the stick broke through the barriers?

A
  • macrophages on skin and in tissue
  • chemotaxins and mast cells are released - increase membrane permeability and dialate them (increase blood flow)
  • neutrophils stick to selectins and integrins that recruit them to that area. now they can move through the membrane and destory pathogen and recruit others
85
Q

describe the innate immune defenses occurring two days after the skin being punctured by the stick

A
  • cells and signals increase blood flow
  • neutrophils consume bacteria so much to the point that they kill themself (pus)
86
Q

innate immune defenses once the wound has been cleaned

A
  • macrophages and dendritic cells becoming antigen presenting cells
  • what type of antimicrobial drug is prescribed? broad spectrum
87
Q

binary fission process

A
  • a cell prepared for division by enlarging the cell wall, plasma membrane, and overall volume.
  • dna replication starts
  • the septum begins to grow inward as the chromosomes move towards opposite sides of the cell. other cytoplasmic components are distributed to the two developing cells
  • the septum is synthesized completely through the cell center creating 2 separate cell chambers
  • the daughter cells are divided.
88
Q

cytokinesis (septation) steps

A
  • selection of site for septum formation
  • assembly of Z ring (composed of protein FtsZ
  • assembly of cell wall synthesizing machinery
  • constriction of cell and septum formation
89
Q

what are the different things that protein synthesis inhibitors target?

A
  • aminoacyl-tRNA binding
  • peptide bond formation
  • mRNA reading
  • translocation
90
Q

antibacterial drugs that inhibit nucleic acid synthesis functioning by inhibiting

A

DNA polymerase and topoisomerases (fluoroquinolones)
RNA polymerase (rifamycins)

91
Q

antiviral drug development is slower because….

A

it is hard to specifically target viral replication

92
Q

why are there fewer antifungal agents than antibacterial agents?

A

the similarity of eukaryotic fungal cells and human cells.
many have low therapeutic index and are toxic

93
Q

what is phagocytosis?

A

the process by which phagocytic cells (monocytes, tissue macrophages, dendritic cells, and neutrophils) recognize, ingest, and kill extracellular microbes.

94
Q

____ _____ is the immediate response of body to injury or cell death

A

acute inflammation

95
Q

cardinal signs of inflammation

A

-redness
-swelling
-warmth
-pain
-altered function

96
Q

penicillin mode of action

A

blocks the enzyme that catalyzes transpeptidation and prevents the synthesis of complete cell walls leading to lysis of the cell.
acts only on growing bacteria that are synthesizing new peptidoglycan.

97
Q

how are drug tolerant bacteria drug tolerant?

A

embedded in biofilms or are growing too slowly to be inhibited.

98
Q

alveolar macrophages are

A

phagocytic cells in alveoli of lungs

Vet Micro (3 decks)

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