Exam 1 Flashcards

Ch. 1-2, 4, 6-9

1
Q

Characteristics of microbes

A

microscopic (usually)
single-celled (usually)
most are beneficial (i.e. gut, skin, probiotics such as yogurt & cheese) & essential

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2
Q

5 types of microbes

A
  1. bacteria
  2. viruses (subcellular)
  3. protozoa
  4. fungi
  5. algae (unicellular)
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3
Q

prions

A
  • 6th type of microbe
  • Acellular
  • no DNA or RNA genome
  • infectious protein particles
  • submicroscopic
  • reproduction: infectious prion physically interacts with normal protein & converts it to infectious form
  • examples: mad cow disease, scrapie (can only detect prion disease via autopsy)
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4
Q

“The time has come to close the book on infectious diseases. We have basically wiped out infection in the United States.” - Surgeon General in 1967. Why did he say this? Why was he wrong? what is the challenge?

A

1940s: Penicillin, other bacterial vaccines, and pesticides
1960s: more chronic diseases started to appear (i.e. obesity, lung cancer)
The challenge: In the past three decades, 40 previously unknown infectious diseases have emerged or reemerged (present day number is higher)

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5
Q

Five leading causes of death

A
  1. cardiovascular disease
  2. INFECTIOUS DISEASE
  3. cancer
  4. liver & kidney disease
  5. diabetes
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6
Q

6 factors responsible for emerging infections

A
  1. world population growth
  2. urbanization
  3. ecological disturbances
  4. technological advances
  5. microbial evolution & adaptation
  6. human behavior & attitudes
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7
Q

how much of the human population lives in less developed countries? (world population growth)

A

80%

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8
Q

what will the population be by 2050? (world population growth)

A

over 9 billion

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9
Q

Thomas Malthus

A

late 1700s to early 1800s
preacher who warned 200 years ago that unchecked population growth would lead to famine; THE LARGEST PROBLEM WITH POPULATION GROWTH IS INCREASED TRANSMISSION OF INFECTIOUS DISEASES

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10
Q

why does Tokyo, Japan have a reduced level of infectious disease despite high population density? (world population growth)

A

serious public health control

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11
Q

3 types of transmission (facilitated by overpopulation)

A
  1. person-to-person
  2. biological vector (mosquito, tick, fly to human) by taking in bacteria & releasing it to the next host (mosquitoes) or by feces on food (flies)
  3. zoonotic (animal to human) - i.e. rabies, consumption, swine flu
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12
Q

effect urbanization has on emerging infections

A

more of the world’s population is becoming concentrated in cities
poverty => less sanitation & hygiene, safe drinking water, public health infrastructure

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13
Q

what place is home to 68% of the worl’d people living with HIV?

A

Sub-Saharan Africa

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14
Q

what kind of ecological disturbances are responsible for increase in infectious diseases?

A

DEFORESTATION (i.e. Limes disease)
CLIMACTIC CHANGE (i.e. malaria, dengue)
NATURAL DISASTERS
- floods in Southern Africa => more mosquitoes carrying malaria & increase in cholera bc lack of safe drinking water
- drought in Eastern Africa => famine & malnutrition weaken immune system)

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15
Q

what kind of technological advances are responsible for increase in infectious diseases?

A
  • travel means arriving at destination before showing symptoms
  • NOSOCOMIAL INFECTION (from blood products, organ transplants, invasive medical procedures, immunosuppressive therapy or disease)
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16
Q

how does microbial evolution and adaptation play a role in increasing infectious disease?

A
  • resistance to antibiotics & antimicrobials due to adaptation & selection that is accelerated by misuse:
    1) overprescription
    2) failure to complete drug regimen
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17
Q

what kind of human behaviors/attitudes contribute to increasing infectious disease?

A
  • COMPLACENCY (false assumption that prevention & control are unnecessary; examples include threatened resurgence of AIDS & decreased immunizations)
  • HUMAN MIGRATION (Internally Displaced Persons lack water, shelter, food, & hygiene; Refugees transmit disease in refugee camps)
  • SOCIETAL FACTORS (increased day care use, increased population of elderly, globalization & centralization of food supply, increased tattooing & body piercings)
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18
Q

cell first coined by who & when?

A

Robert Hooke (monk) in 1665

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19
Q

what is the cell theory and who were the three people behind it?

A
  • the cell is the fundamental unit of all organisms
  • all organisms are unicellular or multicellular
  • all cells are fundamentally alike in structure and metabolism
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20
Q

what makes a microbe?

A

1) size
2) metabolic diversity - cells obtain energy from metabolism (heterotrophs vs autotrophs)
3) requirement for oxygen
4) prokaryote vs eukaryote

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21
Q

heterotrophs

A
  • metabolize complex ORGANIC molecules (food) as a source of energy & carbon
  • depend on autotrophs for organic molecules
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22
Q

autotrophs

A
  • use INORGANIC carbon as an energy source (CO2)

- two types: 1) photosynthetic 2) chemosynthetic

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23
Q

photosynthetic autotrophs

A

obtain energy directly from sun; produce oxygen

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24
Q

chemosynthetic autotrophs

A

obtain energy from inorganic compounds

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25
Q

microbes requirement for oxygen - aerobes vs anaerobes vs facultative anaerobes

A
  • AEROBES require O2 for metabolism (breaks down sugars to make energy available)
  • ANAEROBES do not use O2. some can tolerate it but others are killed by it
  • FACULTATIVE ANAEROBES grow better with O2, but can grow w/o it
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26
Q

what is metabolic diversity important for?

A
  • preventing harmful microorganisms from getting nutrients
  • diagnosing
  • note: viruses have no metabolism & are neither aerobes nor anaerobes
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27
Q

prokaryote vs eukaryote

A
  • prokaryotes have no internal components (bound by membranes) & no nucleus
  • eukaryotes have membrane-bound compartments
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28
Q

viruses

A
  • examples: HIV/AIDS, measles, rabies
  • Acellular
  • genome RNA or DNA
  • obligate intracellular parasite (need living cell to replicate)
  • submicroscopic
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29
Q

bacteria

A
  • unicellular
  • prokaryotic
  • microscopic
  • DNA genome, replicate by binary fission (asexual)
  • cell wall (except mycoplasmas)
  • motile by flagella
  • metabolism: heterotrophs & autotrophs
  • important human pathogens, most beneficial or harmless
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30
Q

protozoans

A
  • examples: malaria, leishmaniasis
  • unicellular
  • eukaryotic
  • microscopic
  • DNA genome, asexual or sexual replication
  • No cell wall
  • motile by flagella, cilia, or pseudopods
  • important human pathogens, most harmless
  • Not an intracellular parasite
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31
Q

algae

A
  • examples: dinoflagellates, diatoms
  • unicellular or multicellular
  • eukaryotic
  • microscopic (unicellular only)
  • DNA genome, asexual replication
  • cell wall
  • metabolism: photoautotrophs
  • not infectious; some produce neurotoxin harmful to marine life or humans eating toxin-containing fish or shellfish
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32
Q

fungi

A
  • examples: yeast or molds
  • unicellular (yeast) or multicellular (molds)
  • eukaryotic
  • microscopic (yeast only)
  • DNA genome, asexual or sexual replication
  • cell wall
  • non-motile
  • metabolism: heterotrophs
  • usually harmless or even beneficial; few are pathogenic for humans
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33
Q

symbiosis & types of symbiosis

A
  • “living together”; association between two or more species
  • types:
    1) mutualism
    2) commensalism
    3) parasitism
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34
Q

mutualism

A

both species benefit (i.e. lichens)

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35
Q

commensalism

A

one species benefits

the other neither benefits nor is harmed (i.e. normal flora)

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36
Q

parasitism

A

parasite lives at expense of the host (i.e. all microbial pathogens)

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37
Q

Koch’s postulates

A

1) ASSOCIATION - causative agent must be present in every case of specific disease
2) ISOLATION - causative agent must be isolated in every case of disease & grown in pure culture
3) CAUSATION - causative agent in pure culture must cause disease when inoculated into a healthy & susceptible animal
4) REISOLATION- the causative agent must be reisolated from the lab animal & be identical to the original causative agent

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38
Q

issues with Koch’s postulates?

A
  • trying to isolate only one microbe

- ethical issues (polio only infects humans but can’t inoculate humans with polio)

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39
Q

what three factors does acquiring an infection depend on?

A
  • (n) dose, the number of microbes encountered
  • (v) virulence
  • (R) resistance, host immunity
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40
Q

severity of infection formula

A

D = nV/R

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41
Q

infective dose (ID)

A
  • minimal number of microbes necessary for infection

- more virulent organism usually have smaller IDs

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42
Q

LD50

A
  • lethal dose

- number of microbes necessary to kill 50% of the animals infected

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43
Q

virulence & two types of virulence factors

A
  • severity of the disease
  • measured by # symptomatic/# infected
  • more virulent usually means low ID and high LD
  • virulence factors:
    1) DEFENSIVE STRATEGIES - allow microbes to escape destruction by the host immune system
    2) OFFENSIVE STRATEGIES - result in damage to the host
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44
Q

infectivity

A
  • capacity of agent to produce infection or disease

- measured by # infected/# exposed

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45
Q

pathogenicity

A
  • the capacity of the agent to cause disease in the infected host
  • measured by # symptomatic/# exposed
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46
Q

what is the single most important infectious disease that causes death worldwide?

A

Tuberculosis

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47
Q

toxigenicity

A
  • the capacity of the agent to produce a toxin or poison

- measured by # affected/# exposed

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48
Q

examples of defensive strategies in virulence

A

1) ADHESINS - enable adherence of pathogens to cell receptors at portal of entry
2) M PROTEIN - capsules prevent phagocytosis
3) WAXY COAT
4) ANTIGENIC VARIATION - trypanosomes can change surface antigens (coat) to avoid antibodies (don’t fit)
- Helicobacter pylori (causes peptic ulcers) secretes enzyme urease to survive in highly acidic stomach

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49
Q

examples of virulence offensive strategies

A

1) EXOENZYMES - enzymes are proteins that allow invading bacteria to spread throughout tissues & cause damage)
2) TOXINS (endotoxins, exotoxins, toxoids)

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50
Q

endotoxin

A
  • part of Lipopolysaccharide in outer membrane of gram-negative cells; released when cell disintegrates
  • causes shock, chills, fever, weakness, small blood clots, & possibly death
  • general activity
  • minimal toxicity
  • heat stable
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51
Q

exotoxin

A
  • proteins synthesized by the microbe & secreted into host’s tissues
  • examples include cytotoxin, neurotoxin, enterotoxins
  • activity specific for each toxin
  • high toxicity
  • heat unstable
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52
Q

toxoid

A

detoxified toxin that retains antigenicity

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53
Q

botulinum toxin vs tetanus toxin

A
  • botulinum toxin causes flaccid muscle paralysis by blocking contraction pathways
  • tetanus toxin causes stiffness by blocking relaxation pathways
  • both are exotoxins
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54
Q

virulence mechanisms of viruses (defensive & offensive)

A
  • defensive: antigenic variation (i.e. new vaccine every year for influenza)
  • offensive: death (lysis) of host cell from:
    large numbers of replicating viruses
    inhibit host protein synthesis
    damage plasma membrane
    inhibit host cell metabolism
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55
Q

virulence mechanisms for eukaryotic microbes

A

combination of offensive & defensive strategies for bacteria (adhesins, toxins, antigenic variation)

56
Q

5 stages of microbial disease

A

1) INCUBATION - period between initial infection & symptoms
2) PRODROMAL - period of early symptoms
3) ILLNESS - disease is most acute
4) DECLINE - symptoms subsiding
5) COVALESCENCE - symptoms disappear & recovery

57
Q

epidemiology

A

branch of medicine that deals with the source, cause, & control of infectious disease & other public health problems

58
Q

epidemiologists

A
  • determine why disease outbreaks occur at a particular time and/or place
  • population-based disease control
59
Q

leading causes of mortality in 1900 vs 2015 (epidemiology & quantification)

A
1900:
respiratory infectious diseases
heart diseases
diarrhea & enteritis
2015:
#1 is chronic diseases
infectious diseases at the bottom
60
Q

zika virus

A
  • spread through mosquitos
  • affects pregnant women & leads to lack of cranial development in baby
  • considered an STD as well bc it can be passed to a pregnant woman by her infected husband
61
Q

Hippocrates

A

460 - 377 B.C.

  • linked malaria, yellow fever, & swamps
  • Father of Medicine
  • movement away from supernatural with no knowledge of the germ theory
62
Q

Edward Jenner

A
  • late 1700s

- observations regarding cowpox lead to smallpox vaccine (1st vaccine)

63
Q

Ignaz Semmelweis

A
  • mid 1800s
  • “savior of mothers”
  • early pioneer of antiseptic procedures (lemon-lime handwashing)
  • idea: wash hands to prevent childbed fever
  • ideas were disregarded until Louis Pasteur & germ theory
64
Q

John Snow

A
  • 1849

- Broad Street Pump –> cholera outbreaks in London from water supply

65
Q

4 classifications of disease

A

1) SPORADIC- occasionally & unpredictable (i.e. tetanus)
2) ENDEMIC - regularly at steady level in particular location (i.e. common cold)
3) EPIDEMIC - sudden increase in morbidity & mortality above norm (i.e. plague)
4) PANDEMIC - epidemics that spread across continents (i.e. 1918 influenza, HIV/AIDS)

66
Q

2 types of epidemic

A

1) COMMON-SOURCE - contact w a single contamination source

2) PROPAGATED - person-to-person contact

67
Q

herd immunity (group immunity)

A
  • proportion of immunized individuals in population

- smaller number of susceptible individuals = less opportunity for contact between them & infected individuals

68
Q

reproduction rate (R-nought)

A
  • measure of potential for transmission
  • mean number of secondary cases, occurring in nonimmunized population in wake of infection
  • R-nought must be greater than 1 to spread; if less, it will die out
69
Q

how do epidemiologists predict time for spread of disease?

A

by looking at southern vs northern hemispheres

70
Q

synthetic opioid

A

fentanyl

71
Q

why must the vaccine for influenza be adjusted each year?

A

influenza is an RNA virus which means that more mutations occur = constantly changing

72
Q

cycle of microbial disease

A

pathogen –> reservoir (source) of pathogen –> transmission to susceptible host –> portal of entry –> portal of exit

73
Q

reservoir of infection

A
  • site in which microbes survive & multiply & from which they are transmitted
  • all pathogens must have one or more reservoirs to survive
  • targets to prevent or stop epidemics
  • humans are the only known reservoir for smallpox, gonorrhea, measles, polio, etc.
74
Q

active carriers

A

individuals who have a microbial disease

75
Q

healthy carriers

A
  • have no symptoms & transmit disease
  • harbor microbe after recovery indefinitely
  • example: Typhoid Mary (Mary Mallon) carrier of pathogen that causes typhoid fever (fecal oral transmission); west nile virus
76
Q

chronic carriers

A
  • harbor pathogen after recovery, but don’t become ill again

- nontransmittable

77
Q

zoonoses

A
  • diseases of animals that can affect humans; animals serve as reservoirs & carriers of pathogen
  • i.e. west nile virus - active transmission between birds & mosquitos but occasionally travels to dead end host such as horses (high mortality rate) in which the virus cannot get at a high enough amount to be transmittable
78
Q

nonliving reservoirs

A
  • some organisms can survive & multiply in nonliving environments, such as water & soil
  • example: spore formers like Clostridium bacteria can survive in soil
79
Q

transmission

A

mechanism for spreading infectious agent to susceptible person

80
Q

horizontal transmission (direct)

A
  • person-to-person
  • touch & sex
  • droplets (don’t remain airborne)
  • animal bites
81
Q

vertical transmission (direct)

A
  • transplacental

- mother to child (breast milk, birth canal)

82
Q

indirect transmission & types

A
  • microbes pass from reservoir to intermediate agent then to host
  • types:
    ~ VEHICLEBORNE - via food, water, biological products, & fomites (inanimate objects)
    ~ AIRBORNE - aerosols of water or dust particles smaller than droplets; remain airborne for long time
    ~ VECTORBORNE - arthropods or insects
83
Q

mechanical passive transmission (vectorborne indirect transmission)

A

microbes do not invade, multiply, or develop in vector; transmission on feet, etc.

84
Q

what is happening with vector borne diseases?

A
  • lack of resources for vector control
    1980s & 90s DDT (insecticide) became illegal (can bioaccumulate & become resistant) –> emergence of almost eradicated diseases
  • lack of political will
85
Q

nosocomial infection distribution

A

1) urinary tract infections
2) surgical site infections
3) lower respiratory infections
4) other
5) cutaneous
6) IV catheterizations

86
Q

naming bacteria

A
  • names using Linnaeus’s binomial classification system
  • genus name capitalized (usually named after someone)
  • species name not capitalized (indicated habitat)
87
Q

broad spectrum antibiotics vs narrow spectrum antibiotics

A
  • broad spectrum antibiotics work against gram + AND gram - (i.e. Amoxicillin, Tetracycline)
  • narrow spectrum antibiotics work against gram + OR gram - (i.e. Z-pak - Azithromycin)
88
Q

nucleoid

A
  • region of cytoplasm containing chromosomal dsDNA (one or more circular &/or linear chromosomes)
89
Q

plasmids

A
  • small, circular, independently replicating, dsDNA
  • encode limited number of genes
  • expand genetic capability of host cell (may encode virulence genes; R FACTORS => plasmids encoding antibiotic resistance genes)
  • infectious nature
90
Q

spores

A
  • viable for long periods (centuries or longer)
  • resistant to heat, boiling, drying, radiation & chemical compounds
  • important pathogens include ‘Bacillus anthracis’ & ‘Clostridium’
91
Q

DNA structure

A
  • Deoxyribonucleic Acid => polymer of repeated nucleotides
  • nucleotide => a nitrogenous base, deoxyribose, & 1-3 phosphates
  • nitrogenous bases: purines (A & G), pyrimidines (C & T)
92
Q

DNA replication

A
  • “parental” dsDNA separates into single strands
  • single strand is template for new “daughter” strand following Chargaff’s rule (A-T; G-C)
  • bidirectional
93
Q

transcription: DNA to mRNA

A
  • RNA polymerase uses one strand of DNA as template for transcribing mRNA copy (complementary)
  • begins with promoter. ends with terminator
94
Q

translation: mRNA to protein

A
  • mRNA is translated by ribosomes into 20 amino acid language of proteins
95
Q

amino acid structure

A
  • central carbon w one of 20 side chains
  • amino group
  • carboxyl group
96
Q

characteristics of genetic code (codons)

A
  • mRNA reads in blocks of three letter codons
  • each codon hydrogen bonds with complementary anticodon of tRNA
  • 64 possible codons in genetic code:
    ~ only one start codon
    ~ 3 stop codons (no tRNA)
    ~ redundant (most amino acids encoded by two or more codons)
    ~ 3rd nucleotide may not be significant to specify amino acid identity (“wobble”)
97
Q

constitutive gene

A

always expressed (turned on)

98
Q

regulated genes

A
  • INDUCIBLE GENE expressed only when an inducer is present

- REPRESSED GENE is “turned off” when repressor is present

99
Q

operons

A

group of functionally related genes that are controlled by same regulatory sequences (promoter)

100
Q

mutations

A
  • cause change in nucleotide sequence of DNA
  • consequences:
    1) harmful
    2) beneficial (rare)
    3) silent
  • cause:
    ~ unrepaired error in DNA replication
    ~ mutagens (chemical agents or physical agents)
    ~ transposons “jumping genes”
101
Q

types of recombination

A
  • VERTICAL: sexual reproduction passes on genetic change from parents to offspring
  • HORIZONTAL (lateral): recombination occurs between donor cell & recipient (not reproduction)
    ~ three examples: transduction, conjugation, & transformation
102
Q

bacterial conjugation

A
  • requires cell-to-cell contact (transfer of ssDNA)
  • donor requires F factor
  • donors are F+ (have F plasmid and produce sex pilus)
  • recipient is F-
  • transfer of ssDNA makes recipient F+
103
Q

abiotic bacterial growth

A

temperature, oxygen, water

104
Q

biotic bacterial growth

A

disease, competition, predation

105
Q

bacterial growth - four major growth phases

A

1) LAG - adaptation to new conditions
2) EXPONENTIAL/LOGARITHMIC - the cell population doubles with each generation
3) STATIONARY - rate of cell division=rate of death (nutrients depleted & toxins accumulate)
4) DEATH - cells dying>rate of cell division

106
Q

culturing bacteria: diagnostics

A
  • CLINICAL SPECIMEN obtained to grow in culture to identify cause of infection (throat swab, urine or blood culture –> growth medium –> streak across agar plate)
  • METABOLIC TESTS
  • RAPID STREP ANTIGEN TESTS (identify ‘Streptococcus pyogenes’)
    ~ type of diagnostic test depends on source
    ~ can also detect anti-bacterial antibodies in blood or amplify pathogen’s DNA
107
Q

determining which antibiotic a bacterial isolate is sensitive to

A

done by:

  • spread isolate onto agar plate
  • apply antibiotic-containing disks to plate surface
  • “ZONES OF INHIBITION” (no growth) form around any disks that inhibit the bacterium’s growth
108
Q

API-20E test

A
  • multitest procedure

- 20 tests to differentiate bacteria belonging to Enterobacteriaceae family (cause UTIs or diarrhea)

109
Q

Atypical bacteria

A
- MYCOPLASMAS
~ no cell wall, no shape
~ very small; special media for growth
~ disease: walking pneumonia
- CHLAMYDIAE
~ obligate intracellular parasites
~ disease: urethritis, trachoma, lymphogranuloma venereum
- RICKETTSIAE
~ obligate intracellular parasites
~ transmitted by arthropods (except for Q fever)
110
Q

antibiotics

A

produced by microbes

111
Q

sulfonamide (sulfa) drugs

A
  • first “wonder” drugs
  • antimicrobials bc they are synthetic
  • inhibitor of enzyme involved in folate synthesis (inhibit growth of bacteria but doesn’t kill)
  • saved millions in WWII
112
Q

penicillin

A
  • first antibiotic used in 1941
  • discovered by Alexander Fleming (staphylococci in petri dish contaminated with penicillium mold after 2 wk vacation)
  • semisynthetic penicillin derivatives include methicillin, ampicillin, & penicillin V
113
Q

broad-spectrum antibiotics

A
  • inhibit gram + and gram -
  • used when bacterium is unknown
  • may kill normal flora, allowing non-susceptiable organisms to flourish and antibiotic resistance
  • examples: amoxicillin, carbapenems, streptomycin, tetracycline, chloramphenicol
  • treats bacteremia, sepsis, pneumonia
114
Q

narrow-spectrum antibiotics

A
  • treats specific families of bacteria and causes less disruption
  • does not kill many normal flora and less resistance
  • examples: azithromycin, erythromycin, vancomycin
  • treats ear infections, throat infections, UTI, typhoid, pneumonia
115
Q

bactericidial

A

directly kills cell

116
Q

bacteriostatic

A

inhibits growth of cells, immune system eliminates cells

117
Q

mechanisms of antibiotics

A
  • INTERFERENCE W CELL WALL SYNTHESIS (beta-lactam antibiotics interfere with peptidoglycan synthesis)
  • INTERFERENCE WITH PROTEIN SYNTHESIS (70S ribosomes for bacteria vs 80S for eukaryotes)
  • INTERFERENCE WITH CELL MEMBRANE FUNCTION (Polymyxin B is used topically because of toxicity)
  • INTERFERENCE WITH NUCLEIC ACID SYNTHESIS (block DNA replication & RNA polymerase)
  • INTERFERENCE WITH METABOLIC ACTIVITY (antimetabolites bind with enzymes [molecular mimicry] and makes them inactive; sulfa drugs mimic a precursor to folic acid)
118
Q

acquisition of antibiotic resistance

A

results from genetic change such as:

  • CHROMOSOMAL MUTATION (confers resistance to only a single antibiotic)
  • acquisition of R (RESISTANCE) PLASMID from resistant strains (resistance to several antibiotics; 1st report in Japan in 1959 with Shigella)
  • TRANSPOSONS “JUMPING GENES” (carry antibiotic resistance genes)

natural selection favors survival of resistant cells

119
Q

mechanisms of antibiotic resistance

A
  • ENZYMATIC INACTIVATION (beta-lactamase cleaves penicillins; break down antibiotics)
  • ALTER ANTIBIOTIC UPTAKE (membrane pump to expel antibiotics; decrease membrane permeability)
  • MODIFY TARGET OF ANTIBIOTIC (antibiotic receptor site)
  • DEVELOP ALTERNATE METABOLIC PATHWAY (i.e. resistance to sulfonamides)

*bacteria share antibiotic resistance genes by HORIZONTAL GENE TRANSFER

120
Q

consequences of antibiotic misuse

A
  • gonorrhea resistance to quinolones in Hawaii
  • more than 90% of Staphylococcus aureus strains are resistant to penicillin and other antibiotics
  • vancomycin resistance appearing in staphylococci and enterococci
  • drug-resistant TB strains increasing
121
Q

food intoxication (food poisoning)

A
  • ingestion of bacterial toxins (with or without the microbe present)
  • N/V and diarrhea (some can result in numbness and tingling around lips and cause damage to nerves and organs)
  • symptoms appear quickly
122
Q

foodborne infection

A
  • bacteria multiply in intestinal tract, secrete an enterotoxin, and may invade cells of intestinal tract
  • N/V, diarrhea, and possibly bloody stools
  • symptoms can start 1 hour after eating to 10 days later (some parasite infections take months to develop symptoms)
  • symptoms can last from one day to months
123
Q

Botulism

A
  • caused by neurotoxin of Clostridium botulinum (gram + spore-forming bacillus) found in soil
    ~ anerobic symptoms: paralysis, lethargic
    ~ therapy: antitoxin and mechanical ventilation (until body can metabolize toxin out)
    ~ botox
  • Clostridium perfringens food poisoning
124
Q

staphylococcal food poisoning

A
  • caused by staphylococcus aureus (g+ coccus)
  • most common food poisoning (under reported bc its not a notifiable disease)
  • found in nasal passages
  • heat stable enterotoxin
  • symptoms: n/v, abdominal cramps, diarrhea
  • severe symptoms appear within a few hours; quick recovery
  • treatment: rest, fluids, meds to calm stomach (antibiotics not useful)
125
Q

salmonellosis

A
  • caused by several species of Salmonella (g- bacilli)
  • symptoms: (gastroenteritis) n/v, abdominal cramps, diarrhea, possibly fever
  • symptoms develop 12-72 hours after infection; last 5-7 days
  • treatment: manage symptoms, hydrate, antibiotics not necessary unless it spreads from intestines
126
Q

salmonella enteritidis

A
  • in intestinal tracts

- prevention: no vaccine; don’t eat raw or undercooked eggs, poultry, or meat; wash hands and surfaces

127
Q

salmonella typhi

A
  • causes typhoid fever
  • organism invades cells lining of small intestines; causes ulcers, bloody stools, fever, and possibly delirium
  • treatment: antibiotics and wash hands
  • prevention: two vaccines available that require repeated immunization, wash hands, avoid eating raw foods, don’t drink untreated water
128
Q

shigellosis

A
  • caused by several species of Shigella (g- bacillus)
  • symptoms: gastroenteritis and possible dysentery
  • symptoms occur 1-2 days after infection and last 5-7 days
  • treatment: oral or IV rehydration and possibly antibiotics
  • prevention: no vaccine, wash hands
  • threat of antibiotic resistance
129
Q

cholera intoxication

A
  • caused by exotoxin secreted by vibrio cholerae (g- curved rod)
  • symptoms: rice-water diarrhead
  • treatment: oral rehydration therapy, no antibiotics
130
Q

enterotoxigenic E. coli

A
  • lives in intestines; commensal bacteria usually
  • most common cause of traveler’s diarrhea
  • prevention: coliform test
131
Q

E. Coli O157:H7

A
  • symptoms: severe stomach cramps, diarrhea (often bloody), vomiting
  • incubation period 3-4 days; most recover in 5-7 days
  • most cases are mild; Hemolytic uremic syndrome (significant blood loss) may result in death in children under 5
  • treatment: non-specific supportive therapy, hydration, no antibiotics
  • prevention: consumption of contaminated food, water, and feces
132
Q

campylobacteriosis

A
  • caused by campylobacter jejuni (g- bacillus)
  • symptoms: bloody diarrhea, cramping, abdominal pain, fever, n/v 2-5 days after exposure
  • treatment: hydration and occasionally antibiotics
  • prevention: food handling
133
Q

listeriosis

A
  • caused by listeria monocytogenes (g+ bacillus)
  • grows under refrigeration
  • symptoms: fever, muscle aches or stiff neck (similiar to meningitis)
  • prevention: food safety
  • treatment: antibiotics
134
Q

pseudomembranous colitis

A
  • caused by clostridium difficile (g+ spore-forming bacillus)
  • depletion of normal flora by use of antibiotics may allow C. diff to grow out & cause diarrhea
135
Q

4 steps to prevent foodborne illness

A

1) clean
2) separate
3) cook
4) chill (keep fridge below 40F)

136
Q

diphtheria

A
  • airborne bacterial disease
  • caused by exotoxin produced by Corynebacterium diphtheria (g+ bacillus)
  • kills epithelial cells –> forms leathery pseudomembrane
  • symptoms: weakness, sore throat, fever, swollen glands; 2-3 days for thick coating to build in nose and throat (suffocation in children); toxin diffuses into bloodstream and may cause damage to heart
  • treatment: diptheria antitoxin and antibiotics
  • prevention: isolation and vaccination (TDAP)
137
Q

pertussis - whooping cough

A
  • caused by Bordetella pertussis (g- coccobacillus)
  • humans are the only reservoir
  • exotoxin damaged ciliated cells that clear mucous from air passages => “whoop”
  • reemerging disease
  • symptoms develop 5-10 days after being exposed
  • early symptoms: runny nose, low-grade fever, mild cough, apnea
  • later symptoms: 1-2 weeks of progression include paroxysms (fits) of rapid coughs followed by whoop, vomiting, exhaustion (coughing can last for 100 days)
  • treatment: antibiotics, hydrate
  • prevention: VACCINATION (DTaP) [booster q 10 years], good hygiene