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Diarrhea > The Microbial World > Flashcards

The Microbial World Flashcards

1
Q

Koch’s Postulates

A

Koch first demonstrated that a microorganism causes disease (anthrax)

  1. The organism is regularly found in the lesions of the disease
  2. Isolated in pure culture
  3. When inoculated, culture should produce similar disease in experimental animals
  4. Organism should be able to be recovered from lesions in these animals
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2
Q

Discovery of Antiobiotic

A

Caused by unkempt lab

Left plates with bacteria on them, came back to find that mold was growing and the area around the mold did not have any bacteria

The mold secreted penicillin which inhibited growth of bacteria

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3
Q

Origins of Microbiology

A

1674: discovered microorganisms
1870: Germ theory
Cause contamination, cause disease
Late 1800s: Agents of diseases discovered; vaccination
Early 1900s: Viruses discovered; antiobiotics discovered
1900s: Threat of ID declines due to sanitation and hygiene, chlorination, antibiotics, vaccines, animal and pest control
Today: Re-emergence of IDs because we were treating patients with antibiotics (comeback diseases) and new diseases

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4
Q

Why are some diseases re-emerging?

A
  1. Increased globalization and trade
  2. Misuse of antibiotics
  3. Evolution of microorganisms
  4. Decline in public health (war zones)
  5. Inc in IC people (transplants, chemotherapy)
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5
Q

Prokaryotic vs. Eukaryotic

A

Divide by binary fission

Prokaryotic: (Bacteria!)
Small
Rigid peptidoglycan cell wall

Eukaryotic:
Evolved from fusion of prokaryotic cells
Membrane bound organelles
No cell wall in animals
Larger
Nucleus and mito contain DNA
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6
Q

Sizes of Microorganisms and How we see them

A

Viruses < Bacteria < Protozoa and Fungi

Electron microscope < Light microscope < Human eye

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7
Q

Taxonomy

A

Escherichia coli

Genus, species

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8
Q

Definition of a species

A

Eukaryotes: Members can mate and have fertile offspring

Prokaryotes: Look at the 16S rRNA. If it is more than 97% different, they are not in the same species

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9
Q

Bacterial Shapes

A 
Bacillus: rod
Coccus: circular
Streptococcus: chain
Staphylococcus: clump
Spirochete: snake-like; predestined to penetrate tissues
Club shaped

Can also have appendages (flagella)
Spores: formed under bad environment as a way for the bacterium to stay alive (dry, nutrient deficient environment)

Capsule: Often anti-phagocytic; leads to more chronic infection that tends to disseminate further than if it were not capsular

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10
Q

Gram - membrane

A

Second outer membrane
Porins allow nutrients in and out of the cell
Thin peptidoglycan layer in periplasmic space
Outer leaflet has lipopolysaccharides linked to membrane by acyl chain
When washed with ethanol, can extract lipids and increase porosity, thus removing the crystal violet-iodine complex

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11
Q

Gram + membrane

A

Thick peptidoglycan layer

Permeability layer; Preventing loss of crystal violet-iodine, appearing purple

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12
Q

Gram Stain Test

A
  1. Fresh sample dried on plate
  2. Stained with crystal violet, all cells appear purple
  3. Add iodine, decreases solubility within cell, cells still appear purple
  4. Cells decolonized by washing with ethanol
    * DIFFERENTIAL step*
    Gram+ retain purple
    Gram- do not (colorless)
  5. Cells rinsed with counter stain safarin which stains Gram- PINK
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13
Q

Virulence

A

ID and LD (lethal)
ID50: number of microorganisms needed to infect 50% of host population

If you have a 10^5 bacteria and inject into ten mice, half will come infected

Virulence is opposite of ID

Ex. Shigella has a LOW ID, in the 10s. Takes a very small amount of organisms to infect 50% of hosts. Would be considered very virulent

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14
Q

Sterile areas in the body

A
  1. Lower respiratory tract
  2. Upper genitourinary tract

Intestine is LOADED with bacteria (large)

Skin has no Gram-

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15
Q

Lyme disease transmission

A

Zoonotic
Vector-borne

Reservoir is a mouse, transmitted to humans with the help of a tic

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16
Q

Preventive Measures

A

Standard: Hand hygiene, procedure appropriate

Contact: Gloves, gowns, private room
ex. diarrhea from norovirus or C. diff

Droplet precautions: If pathogens don’t travel more than 3 feet; masks/respirators, closed room
ex. influenza, N. meningitidis

Airborne precautions: Travel more than 3 feet; PARP respirators, airborne infection, All air leaving room going through HEPA filter
ex. Measles, Mycobacterium tuberculosis

Full barrier precautions: airborne + contact plus eye protection
ex. avian/pandemic influenza, SARS

17
Q

Types of pathogens (3)

A
  1. Nonpathogens: present in microbiome; normal flora; occupy niches and prevent pathogens from coming in and causing the disease
  2. Opportunistic: present as normal flora; if it gets into the wrong tissues it can cause problems, or if it is given the opportunity of an IC patient
  3. Primary pathogens: if you see this in the sample, you know it is causing the disease
    Immunizations common
18
Q

Stages of Bacteria Pathogenesis

A
  1. Transmission
  2. Adhesion
  3. Colonization
  4. Spread
  5. Damage (directly- toxins or enzymes by bacterial products; indirectly- inflammation (immune responses))
  6. Evasion of host immunity (in host survival)
  7. Transmission to a new naive host
19
Q

Virulence factors

A

Help bacteria invade the host, cause disease, evade host defenses

Some are targeted by vaccines and detected by specific tests

Adhesins: Allow bacteria to adhere to tissues

Invasins: Allow bacteria to get inside a host cell; evade humoral inflammation; now relying on cell-mediated inflammatory response to clear infection; nutrient rich cytoplasm and safe from host defense responses

Exotoxins: (Enterotoxins); secreted from a bacterial cell; bacteria mediated pathogenesis

Endotoxins: Released when cell is lysed; potent toxin that signals immune response; host mediated pathogenesis; GRAM- ONLY

Degradative enzymes: Break down tissues; allow bacteria to spread in tsisues

20
Q

Adhesins

A

Allow bacteria to adhere to tissues
Pili (fimbriae) on E. coli
Protein adhesins: pull bacteria closer so they stick better to tissues and allow colonization
Biofilms: bacteria stick together and attach to a surface (plaque, catheter causes UTI)

21
Q

Intracellular (bacterium growth)

A

Obligate: always need a host cell to replicate in
Facultative: can work intracellularly or extracellularly; life to replicate outside of the cell but then go into the cell to escape humoral immune responses and have access to more nutrients

22
Q

Systemic disease (bacterial spread)

A

Vs. localized

Destruction of tissue barrier by tissue damaging enzymes
Penetration of cell membrane (invasion)

23
Q

Types of Invasion of pathogens

A
  1. Passive uptake: immune cells that uptake bacteria (phagocytosis)
  2. Active invasion: Invasins on cell surface induce uptake by non-phagocytic cells; OR make virulence factors that allow them to invade non-phagocytic cells
    Salmonella, Yersinia
  3. Transcytosis: Intracellular motility by actin polymerization; go through cells
    Shigella, Listeria
24
Q

Syringe secretion systems

A

T3SS
Type 3 and 4 are syringe mechanisms
Multi-protein complex expressed by bacteria cell
Can inject effector proteins from bacterium into the cell
1. Mess with actin
2. Cleave rRNA, blocking protein synthesis, killing the cell

Make a complex stretching from bacteria cytosol into the host cell cytosol; effector proteins never encounter extracellular environment

25
Q

Types of exotoxins

A
  1. Enzymes
    Act on extracellular matrix
    Collagenase, hyaluronidase
2. AB type toxins
Two components (subunits)
Cholera, diphtheria, shiga, pertussis, tetanus, anthrax, botulinum, E. coli heat labile toxin
  1. Membrane damaging toxins:
    Phospholipases ex. Perfringens alpha toxin
    Pore forming toxins ex. Listeriolysin
    Cause hemolysis
  2. Superantigens:
    Enterotoxins of S. aureus
26
Q

AB toxins

A

Intracellular acting toxin

B: Binds to cell surface receptor; determines host cell specificity of toxin; forms pore
A: disulfide bonds are broken and A becomes Active enzymatically and is transported to cell interior; toxic activity

Targets of A subunits:
1. ADP ribosylating toxins
Diptheria toxin: inactivates elongation factor (translation, protein synthesis)
Cholera toxin, pertussis: Activates adenylate cyclase (increasing cAMP levels)

  1. Others
    Shiga, EHEC: cleaves rRNA (translation, protein synthesis)
    Tetanus, botulinum: Blocks release of neurotransmitter

Examples of AB

  1. Shiga toxin
  2. E coli LT1
  3. Petussis toxin

Single A subunit with multiple B (A1B5)

*B subunit good target because it will affect all things downstream

27
Q

Superantigens

A

Causes nonspecific binding of T cells
Produced by some pathogenic viruses and bacteria most likely as a defense mechanism against the immune system
Temporary interaction where the APC will just present the peptides of pathogens to the T lymphocyte
VERSUS SUPERANTIGEN which locks the presenting state APC to T lymphocyte

28
Q

Endotoxin: LPS

A

Released by cell lysis, not secreted

Toxicity due to lipid A component (fatty acids, disaccharide, diphosphate)
Also has O-antigen component

Causes septic shock

Binds to LPS binding protein and interacts with host receptor CD14

Signals through toll-like recepor

29
Q

How do pathogens evade host immune responses?

A
  1. Defensive
    Capsule: protects from being phagocytksed
    Serum resistance due to modification of LPS preventing C5b-9 complex
  2. Offensive
    Produce toxins which degrade immune components (C5a, IgA proteases)
    Killing of phagocytes
  3. Stealth
    Antigenic variation
30
Q

Antigenic variation

A
  1. A pathogen expresses an immunodominant surface antigen (largely recognized by immune system)
  2. Shut down expression of antigen and start expressing another type of antigen unrecognizable by antibodies
  3. Bacteria buys itself time to replicate until host develops a new set of antibodies that will recognize the new coat and try to kill the cells
31
Q

Iron acquisition

A

Most bacteria need iron for growth

-bactin

Bacteria produce siderophores which bind to iron and then bind to a receptor on the bacteria to be taken up
Main way to acquire iron for growth

32
Q

Virulence factors are encoded on:

A
  1. Chromosome: stable
  2. Pathogenicity island: Region of DNA that has all the genes coding for a specific set of virulence genes (ex. all components of T3SS: effector proteins and needle
  3. Plasmid: dispensable, can be transferred to another bacteria; extrachromosomal smaller DNA replicon
  4. Bacteriophage: spread DNA between bacteria (transduction) - bacterial viruses
  5. Transposon: highly motile; can accelerate spread of genetic material
33
Q

Complentation

A

Reintroduction of a functional gene into mutant bacterium should restore the invasive wild type if the mutant is responsible

34
Q

Type I toxin

A

Bypass cell membranes by activating signaling molecules on the cell surface

35
Q

Type II

A

Directly attack the host cell membrane resulting in increased permeability

Diarrhea (3 decks)

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