Exam V Flashcards

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1
Q

Anton van Leeuwenhoek

A

Skilled at grinding special lenses
Drew the things he viewed: called them animalcules
Did not know where they came from; thought spontaneous generation

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2
Q

Dr. Jenner

A

Small pox was a huge concern
He experimented with cow pox from milk maids and exposed boy to this and then exposed him to someone who had small pox – vaccination found!

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3
Q

Semmelweis

A

Savor of the mothers – ran the maternity ward; strict rule of washing your hands but no one would listen to him at first
Those dissecting cadavers would deliver babies and expose the mothers to the diseases from these dead people

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4
Q

Oliver Holmes

A

well rounded and was able to prove contagions passing from person to person

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5
Q

Lister

A

people in battle were dying from medical treatments more than on the battle field; used phenol on instruments and air in surgery rooms to keep things clean; everyone didn’t believe him at first, but then they saw the changes in survival rates

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6
Q

Pasteur

A

wine makers wanted wine to be consistent, so he made the association between the microbes growing on the grapes and figured out by heating the wine it would be always good; same with milk, apple cider, etc.; well known person who could solve things

Parasitic disease: silkworms that were not infected and kept them isolated and clean, and as long as silkworms infected didn’t come into contact with healthy ones they could do their work

Spontaneous generation: proved that things didn’t spontaneously come to be; used S shaped flasks and when that was cooked nothing would grow, but if you tipped the flask to let fluid out and sat it back up = growth because contamination with dust and bacteria within the peripheral part of the S

Vaccination for chicken cholera: attenuation = injecting the weakened microbe into the chicken so body can make Ab to fight the disease

developed the Rabies vaccine; took the spinal column of infected rabbits and grinded it down

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7
Q

Koch

A

Proved one organism caused one disease; did this with anthrax and TB
Once he saw the pattern, he started checking the major diseases for which organism caused it; made so many connections = golden age of microbiology
Everything had a cause
Developed postulates that are still in use today
Won Nobel Prize
Present in every case of disease, absent in healthy organisms
Isolate and grow organism
Inoculate new host and get same disease
Re-isolate same organism from new host

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8
Q

Molecular Postulates

A

Gene or product in virulent strains but not avirulent ones
Disruption of gene disrupts virulence
Introduction of gene into avirulent strain induces virulence
Gene is expressed while in host
Antibodies to gene product are protective

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9
Q

Paul Ehrlich

A
Syphilis Treatment
Researcher in Koch’s lab
Tried 606 compounds
Arsenic derivative
Took to London, Fleming used
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10
Q

Alexander Fleming

A

Plates he left out – nothing growing around it
Found the mold penicillin that went into the agar dish
In 1940s - mass production of antibiotics leading to the Antibiotics Era
Won the Nobel Prize for Medicine or Physiology

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11
Q

Penicillin

A

1929 – published results
1932 – former student used filtrate on eyes of newborns with gonorrhea and/or staphylococcal infections – did not publish
1939 – Oxford group decided to study
No money in Britian
Rockefeller Foundation in America funded
during this time the war was going on and used the antibiotics for wounded soldiers (USA)
Resistance started in June 1941 - very rapid
Gram negative are more resistant than gram positive

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12
Q

Chemotherapy

A

Sulfonamides discovered– 1932
End of Golden Age of Microbiology
Thought that they had found the medicine for everything…but they were wrong

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13
Q

Emerging Infectious Disease Mechanisms

A

Environmental changes
Mutations to more virulent forms
New manifestations of known organisms
Antibiotic resistant strains

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14
Q

Legionnaire’s Disease

Legionella pneumophilia

A

Can get it in water sources- legionella; legionnaires convention with elderly veterans that drink and smoke – so people in that demographic are prone to having pneumonia; several had the illness and died;
Environmental changes – air conditioning, vegetable water spray, hospitals outbreaks
Adding air conditioning made this a more prominent disease

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15
Q

Lyme Disease

A

Borrelia burgdorferi
Found in Lyme, CN – build houses in deer’s domain; we moved into a territory that had this disease; same with probably ebola
Don’t infect deer, but infect mice and people
Hefty portion of ticks on peninsula carry lyme disease

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16
Q

Necrotizing fasciitis

A

Streptococcus pyogenes
Strep infection; can cause scarlet fever with prickly rash; back in the day this was a dangerous disease; now our immune systems can better fight this
Same toxin that causes prickly outbreak, it also causes necrotizing fasciitis: very fast – 24 hours
The microbe changed over time – deadly; we don’t know what caused the switch

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17
Q

Cat Scratch Disease

A

Bartonella henselae
cats scratch causing swelling in lymph nodes
Bacillary Angiomatosis – HIV patients get this; looks like blood vessel wart
The child must have a better immune system – can fight this; but HIV immune compromised patients cause the warts
Same organism with two different presentations

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18
Q

Vancomycin Resistant Entercocci

A

Big problem in hospitals
Antibiotic testing to measure resistance
Different resistance patterns
Vancomycin is the last resort antibiotic – some strains have become resistant to it = extremely bad; must be extremely cautious of not passing it to other people in the hospital
Must treat the person with multiple antibiotics and this is not as effective but only resort
Must clean EVERYTHING to keep spread under control

Mechanism: will not allow the binding of the D ala residues on the termini so cross linking cannot occur in peptidoglycan and this destroys the cell wall; resistant stains put D lactate instead of D ala

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19
Q

Acid Fast Stain

A

Mycobacterium sp.
Nocardia sp.
Waxes in cell wall
Does not gram stain because no cell wall and has wax like structure instead
Organism with heat fixation; use carbol fuchsin and phenol then rinsed with water, then acid, then rinsed; if redish color = positive
Not acid fast: takes blue counter stain

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20
Q

Fluorescent Staining

A
Use Ab (primary and secondary)
Very helpful, can see organism when low concentration is present, quick to get results (especially when you don’t have the time aka patient is dying)
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21
Q

Blood Agar

A

When an organism has hemolytic properties – key clue
Alpha – green color
Beta – yellow looking, but actually clear because killed all RBCs – extremely important if beta hemolysis
Gamma – no hemolysis and not used
Alpha and beta are what matters

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22
Q

Chocolate Agar

A

Fastidious organisms- picky about where they grow
Haemophilus influenzae
Neisseria gonorrhoeae

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23
Q

MacConkey Agar

A

Enterics grow in GI tract
ALL GRAM NEGATIVE grow, but the agar inhibits gram + organisms from growing
Lac + = E. coli – turns pink and is a lactose fermenter (easier to treat)
Lac - = P. aeruginosa – stays yellow/no color and is a non fermenter (hard to treat)

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24
Q

Buffered Charcoal Yeast

A

Legionella

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25
Q

Sabouraud Dextrose

A

Candida albicans (fungus)

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26
Q

Lowenstein Jensen

A

Mycobacterium tuberculosis

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27
Q

Klebsiella pneumoniae

A

mucoidal growth - encapsulated

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28
Q

Mycobacterium

A

Pigmented Growth

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29
Q

Proteus

A

swarming/wave-like

30
Q

Catalase Test

A

Differentiates Staphylococci (+) from Streptococci (-)
Detects presence of catalase enzyme – breaks down peroxide
+ = bubbling/fizzing
- = no reaction

31
Q

Coagulase Test

A

Conversion of fibrinogen to fibrin
Differentiates Staphylococcus aureus (+) from other Staphylococci (-)
+ = forms a clot
- = no reaction

32
Q

Indole Test

A

One test used to differentiate Escherichia coli (+) from other enterics
+ = magenta
- = yellow

33
Q

Oxidase Test

A

Tests for presence of enzyme cytochrome oxidase c
Pseudomonas aeruginosa (+)
+ = purple
- = no change

34
Q

Drugs that Inhibit Prokaryotic Protein Synthesis

A

Chloramphenicol, Erythromycin, Tetracycline, and Streptomycin

35
Q

Quinolones (gram - vs. gram +)

A

Action - gram negative bacteria
inhibition of DNA gyrase, unable to pack DNA into cell
Specific for bacterial DNA gyrase

Action – gram positive bacteria
Inhibition of topoisomerase IV

36
Q

Beta Lactams

A

family that includes penicillin

attacks the cell wall

37
Q

Sterols in Membrane

A

Only in mycoplasm

38
Q

Mesosome

A

Invagination in cytoplasmic membrane where DNA binds to replicate
Segregation of chromosomal DNA into daughter cells

39
Q

Peptidoglycan

A

composed of alternating NAG NAM NAG NAM
In gram +: peptidoglycan is thick, hydrophilic Gly cross bridges that hold the cell together by trans or carboxypeptidases kicking off the terminal D-Ala amino acid to form the Lys - Gly bridge
In gram -: doesn’t need the Gly bridge because only one layer think peptidoglycan, and so close that the molecules can directly link

Lysozyme: breaks the NAG NAM bonds = bactericidal; use when you want to kill the bacteria completely ex. in cases of necrotizing fasciitis or meningitis; gram positive are sensitive to it, but gram negative are resistant because the outer membrane provides protection

40
Q

Penicillin Binding Proteins (PBPs)

A

Enzymes that cross-link amino acids
Transpeptidases
Carboxypeptidases
Known as Penicillin Binding Proteins (PBP’s) because they are targets for action of penicillins and other beta-lactams (bactericidal because won’t allow the cross bridge linkages within peptidoglycans)

41
Q

Peptidoglycan Synthesis

A
  1. Cytosol- UDP- NAG and UDP-NAM polymers formed
  2. Membrane- UDP-NAM is transferred to a lipid carrier via bactoprenol, UDP is displaced, and NAG added to NAM (bactoprenol transports to a cell wall growth point)
  3. Periplasm/Exterior- autolytic enzymes cut NAM-NAG loose from bactoprenol so it can be added to the cell wall so cross linking can occur; cycle then continues
42
Q

Gram Negative vs. Gram Positive

A

Gram Positive: thick peptidoglycan, contains teichoic/lipoteichoic acids in cell walls (not sure purpose but our immune system can detect them), some strains produce endotoxin

Gram Negative: LPS (endotoxin in some strains), outer and inner membrane, periplasmic space, lipoproteins

43
Q

LPS

A

On gram negative - endotoxin
O antigen: Linear polysaccharide with 50-100 repeating units w/4-7 sugars /unit; Used in serotyping

Core: No associated activities, contains unusual sugars, spacer between O antigen and Lipid A

Lipid A: toxic portion that can cause sepsis; stirs up our immune system and contained in gram negative rods

44
Q

Septic Shock

A

Patient with sepsis and blood infection: start them on antibiotic which causes lysis of bacteria releasing more endotoxin = bad
All we can do is keep the person alive long enough to survive the reaction of the immune system against the bacteria
Research: they are looking at shutting down some components of the immune system to defeat it… must have immune system to correlate with meds, but need to shut it down just a little bit to get over the endotoxins

45
Q

Porins

A

Within the outer membrane of gram negative bacteria
Restrict entry by size
Important in antimicrobial choice
Vancomycin is too large to enter
Permits entry of hydrophilic molecules
May restrict some antiseptics or disinfectants that act on cell membrane
attachment site for bacteriophage

46
Q

Periplasmic Space

A

part of gram negative bacteria
Contains degradative enzymes- “binding proteins” like trans and carboxypeptidases
Enzymes that inactivate antibiotics like beta lactams= Beta-lactamase
If you have a mixed infection and you pick penicillin, if you have an organism (gram positive) breaking down beta lactam into the environment, it is helping the gram negative bacteria; need to pick something that doesn’t allow it to go into the environment

47
Q

Beta Lactasmases

A

produced by gram negative and positive
Numerous enzymes that cleaves beta lactam ring
Penicillinases
Cephalosporinases
ESBLs (extended spectrum beta-lactamases)
More than 200 different beta lactamases

48
Q

Mechanisms of resistance to beta lactam antibiotics

A
  1. Block the drug from entering via the cell membrane
  2. Change PBP
  3. Secrete the beta lactamase to hydrolyze the drug used
    Gram negative- 1-3
    Gram positive- 2 and 3
49
Q

Examples of Capsulated Organisms

A

Streptococcus pneumoniae
Klebsiella pneumoniae
Haemophilius influenzae type b
Neisseria meningitidis
Escherichia coli K1
prevents dehydration, provides protection from phagocytosis and environment, and adherence
capsule does not provide growth, but virulence

50
Q

Pili/Fimbrae

A

Mostly gram negatives
adherence and sexual conjugation
virulence factor
antigenic variation making it hard for the immune system
ex. Escherichia coli and Neisseria gonorrhoeae

51
Q

Sporulation

A

GRAM POSITIVE ONLY
Bacillus sp.: Aerobic and Gram-positive rod
Clostridium sp.: Anaerobic and Gram-positive rod
Harsh environmental conditions induce
Change from vegetative state to spore
Location of spore may be used in identification
dehydrated
like hibernation metabolically
contains dipicolinic acid
extremely hardy
concern in disinfection, sterilization, etc.

52
Q

Transposons

A

can pick up and move to a different site on a DNA molecule
Actual movement: transposition via transposase
IS- insertion sequences; cut themselves out and insert into another area; two ways of transposition
1. Replicative: make a copy of itself and move somewhere and end up with 10 copies of capsule gene for example because it there is a mutation in one it doesn’t lose its virulence
2. Non-replicative: cuts itself out and moves to another location – no multiple copes; happens a lot from plasmid to chromosome
A transposon can be located on a plasmid move to chromosome so it becomes permanent and part of chromosomal material
We use plasmids in research and rely on these methods so the genes can be introduced into the bacteria and we can study it

53
Q

Competent Cells

A

use specialized buffers that help the cells pick up the DNA; when competent the cells are ready to pick up the DNA during transformation

54
Q

Bacillus thuringiensis

A

Bacillus thuringiensis is a gram positive soil dwelling bacteria, aerobic, capable of producing endospores.
Commonly used as a pesiticide

55
Q

Bacterial Growth: Temperature & pH

A

Psychrophile – very cold
Mesophile – middle temps
Thermophile – slight higher temps
Hyperthermophile – in hot springs – very hot temperatures

Acidophil: acidic conditions
Neutrophile: neutral conditions
Alkaliphile: basic conditions

56
Q

Bacterial Growth: Oxygen Content

A

Obligate aerobes – need O2 to survive
Obligate anaerobe – O2 will kill it and needs to be as far away from O2 as possible
Micro-aerophil – likes lower O2 content but want some
Facultative anaerobe – can grow with or without O2; most successful in the human body because the more flexible

57
Q

Bacterial Growth Curve

A

Take advantage of this to figure out when to harvest the bacterial
All bacteria grow through four phase growth phase
Lag phase – figuring out where it is and what genes do I need to turn on and off; growth is small
Log – starts to replicate via binary fission with rapid growth
Stationary phase: growth = death; plateau because the nutrients are being depleted and wastes are building up and it becomes toxic so then the death phase occurs from the toxic wastes
During each stage of growth genes are constantly changing with which ones are being transcribed and translated or stopped
Prime time to harvest: the stationary/plateau phase

58
Q

Nosocomial

A

hospital acquired/healthcare associated
Endogenous source- from the patient
Exogenous source- anything except the patient (equipment, flowers, etc.)
Cut off: after 48 hours

59
Q

Opportunities Infections

A

an infection caused by a microorganism that does not usually cause a disease in a healthy individual
example: foley catheter

60
Q

Vertical vs. Horizontal Transmission

A

Vertical: parent to child (mother to child, fetus, etc.)
Horizontal: human to human; direct contact (STI’s), human to fomite, and human to respiratory, fecal/oral, and blood (all intermediates to infect another human)

61
Q

Ingestion, Inhalation, Trauma, Needle Stick, Arthropod Bite, and Sexual Transmission

A

Ingestion: Salmonella, Shigella, E. coli
Inhalation: Mycobacterium, Legionella
Trauma: Clostridium tetani
Needle Stick: Staphylococcus epidermidis, S. aureus
Arthropod Bite: Borrelia, Ehrlichia, Rickettsia
Sexual Transmission: Neisseria, Chlamydia

62
Q

Capsule

A
Structure surrounding the cell
Usually composed of polysaccharides; exception: Bacillus anthracis 
Several functions:
   adherence
   prevents dehydration
   avoid phagocytosis
   nutrient sources
Bacteria: 
   Neisseria meningitidis
   Streptococcus pneumoniae
   Klebsiella pneumoniae
   Haemophilus influenzae type b
   Pseudomonas aeruginosa
   Bacillus anthracis
63
Q

Biofilm

A

A community of microorganisms encased within an exopolysaccharide matrix attached to a solid surface or to each other.
attachment, growth, and detachment
cause 65% of nosocomial infections

64
Q

Direct and Indirect Ways Pathogens cause Damage

A

Direct: Invade and disrupt cells, produce degradative enzymes (elastase via pseudomonas) and toxins, gain access to nutrients

Indirect: Trigger an Immune response where the host can damage itself
Superantigen: causes massive immune response resulting in shock and organ failure.

65
Q

Toxins

A

Exotoxins: proteins produced and secreted by the bacterium into the extracellular environment (Gram negative and positive); have varied mechanisms of action, attack different host cells, preformed toxins: food poisoning, ex. S. aureus; superantigen; toxic shock

1. Neurotoxins: interfere with neural transmission; Clostridium tetani tetanus toxin
2. Enterotoxins: Vibrio cholerae cholera toxin

Endotoxin: only LPS on gram negative; septic shock

66
Q

AB toxin example: diphtheria toxin

A

A subunit is the active portion
B subunit binds to the receptor and transports the toxin into the target cell
Need both to work

Mode of Action: 
Same as P. aeruginosa Exotoxin A
ADP-ribosyl transferase
Inactivates elongation factor 2
Inhibits host protein synthesis
67
Q

Cholera

A

ADP ribosylates a protein that regulates adenylate cyclase in intestinal epithelial cells.

irreversibly activates the regulatory protein
activates adenylate cyclase
causing cAMP concentration to rise
triggering the cell to pump water from the bloodstream into the intestinal tract causing diarrhea

68
Q

Superantigen

A

Cross linking of T-cell receptors and MHC II molecules
Stimulates massive cytokine production and inflammatory response
Result can be toxic shock leading to death
Gram positive cocci: TSST 1 Staphylococcus aureus

69
Q

Mechanism of LPS

A

LPS binds to CD14 and toll like receptor 4 (TLR4) on monocytes and macrophages
Induces IL-1 and TNFα production
IL-1 produces fever
TNFα more cytokine production and fever
Activates complement pathway: vasodilation
Stimulates B cells: antibody production
Overall can lead to hypotension and shock

70
Q

Evasion of Host Defenses

A
  1. Prevent phagocytosis
    S. pneumoniae, H. influenzae, and K. pneumoniae, produce a capsule
    S. pyogenes produces M protein
  2. Kill white blood cells
    Staphylococcus & Streptococcus produce leukocidins to destroy leukocytes and macrophages
  3. Confuse the immune system
    Antigenic variation: change structure of surface antigens therefore antibodies do not recognize bacteria
    example: Neisseria gonorrhea
    Molecular mimicry: bacteria camouflage themselves with host proteins example: IgA
  4. Grow intracellularly
    Prevent phagosome/lysosome fusion: Mycobacterium
    Escape the phagosome: Listeria and Rickettsia.
    Break down H2O2: Staphylococci produce catalase
71
Q

Location of Virulence Factor Genes

A

The chromosome: Pathogenicity islands
Plasmids
Bacteriophages
Transposons

72
Q

Virulence Mechanisms

A
Adherence
Invasion
Byproducts of growth (gas, acid)
Toxins
Degradative enzymes
Cytotoxic proteins
Endotoxin
Superantigen
Inflammation
Evasion of phagocytosis
Capsule
Resistance to antibiotics
Intracellular growth