Microbes Review

Front 1

Koch’s postulates

Back 1

he organism must always be found in the diseased animal, but not healthy ones.
b. The organism must be isolated from diseased animals and grown in pure culture outside of the animal.
c. The organisms isolated in pure culture must initiate and reproduce the disease when inoculated into susceptible animals.
d. The organisms should be reisolated from the experimentally infected animals.

Front 2

LD50

Back 2

a. The experimental dose of microbes needed to kills 50% of test subjects

Front 3

ID50

Back 3

a. The experimental dose of microbes needed to infect 50% of test subject

Front 4

What are the main components of the innate immune system?

Back 4

a. Skin/epithelia, pH of stomach, design of upper respiratory tract, secretions, inflammation (complement), cellular barriers (macrophages, Neutrophils)

Front 5

What are the main 4 categories of microbes? What makes them different?

Back 5

a. Bacteria = prokaryotes, no internal membranes, one circular chromosome, divide via binary fission
b. Virus = obligate intracellular pathogen, no energy-making capability (use host)
c. Fungi = eukaryotic, heterotrophic, thick cell wall (chitin, mannan, glucan)
d. Parasite = eukaryotic invertebrates, complicated life-cycle with morphogenesis
e. Prion = infectious protein, not an organism

Front 6

What are the steps common to all infectious disease?

Back 6

a. Encounter: Agent meets the host
b. Entry: Agent contacts a tissue within the host
c. Spread: Agent spreads from the site of infection
d. Multiplication: The agent multiplies in the host
e. Damage: The agent, the host response, or both cause damage
f. Outcome: The infection resolves in favor of the host or pathogen, or a mutualistic relationship occurs.

Front 7

Criteria for choosing antibiotic therapy

Back 7

a. Gram positive versus Gram negative, presence/absence of capsule, metabolic pathways utilized, resistance

Front 8

a. Host

Back 8

organism with which a microorganism (MO) is associated

Front 9

b. Normal (Commensal) Flora

Back 9

MO associated with a healthy host

Front 10

c. Pathogen

Back 10

MO with the capability to cause infectious disease (ID)

Front 11

d. Opportunist

Back 11

can cause ID in a damaged host (rarely in healthy hosts)

Front 12

e. Nosocomial pathogen

Back 12

agent of ID acquired via a medical environment

Front 13

f. Infection

Back 13

MO growing on a host (clinically = disease)

Front 14

g. Virulence Factor

Back 14

substance which allows a MO to cause ID

Front 15

h. Pathogenesis

Back 15

process by which the MO causes ID

Front 16

i. Zoonosis

Back 16

an ID communicable from animals to humans

Front 17

conjugative pilli

Back 17

exchange of genetic material

Front 18

adhesive pilli

Back 18

important for attachment via adhesins which dictate tropism/mediate internalization into epithelial cells and macrophages

Front 19

General Assembly of pilli

Back 19

c. generally assembled by adding subunits to the bottom; allows twitching motility; aids in biofilm formation

Front 20

Capsule: role in disease.

Back 20

a. Mucopolysaccharide/peptide layer of protective material; may be on either gram+ or gram- bacteria
b. resists phagocytosis by innate immune cells; causes pyogenic infection

Front 21

Flagella: basic structure and function

Back 21

a. Organelles of locomotion, rotates like a propeller (CW = random tumbling, CCW = forward)
b. comprised of basal body, hook, and filament (assembled from the tip, with subunits being sent down the flagella tube)
c. allows chemotaxis

Front 22

LPS (Endotoxin): structure and function in disease

Back 22

a. Outer leaflet of outer membrane of Gram- bacteria; has O antigen (repeating pentasaccharides, used to identify MO’s), core (attaches O Ag to lipid A), and lipid A (glycophospholipid, responsible for sepsis)

Front 23

Bacterial Cell membrane functions

Back 23

a. Act as an osmotic barrier, be selectively permeable, allow carrier-mediated transport, site of cytochrome activity / proton motive force generation (energy for ATP synthesis)

Front 24

Cell Wall: structure, function and role in disease.

Back 24

a. Made of peptidoglycan (disaccharide units of GlcNAc and MurNAc connected by glycosidic bonds, cross-linked by peptide bonds made by transpeptidase, which makes the cell wall rigid)

Front 25

General antibiotic targets

Back 25

a. Penicillin Binding Proteins (Transpeptidase): inhibition prevents cross-linking, cell wall weakens, and cell lyses by osmotic pressure [Resistance via production of β-Lactamase]

Front 26

Tropism

Back 26

a. The location that a MO preferentially targets for infection

Front 27

II. Mechanisms to subvert host defenses or cause infection:

Back 27

a. capsule production
b. biofilm production – UTI / Pseudomonas; resists antibiotics, phagocytosis
c. Type 3 Secretion
d. Invasion
e. Subversion of neutrophils
i. UPEC invades bladder epithelial cells, Salmonella invades gastroepithelial cells
f. Adhesins (UPEC = FimH, EHEC = intimin)

Front 28

III. How are EHEC and UPEC different? What makes them different?

Back 28

a. UPEC: Causes UTI (dysuria, frequency), has Type I pilli, forms biofilms
b. EHEC: Causes gastroenteritis, has Type III secretion (injects effector proteins [Tir] that aid binding and prevents phagolysosomal fusion)
i. associated with HUS

Front 29

IV. Who gets UTIs? Why?

Back 29

a. Females, due to close proximity of the urinary tract and anus

Front 30

V. What are some important virulence factors involved? (UTIs)

Back 30

a. FimH adhesins (allows adherence to uroplakins on facet cells) at the tip of Type 1 pilli [allows bacteria to withstand flow of urine]
i. also important in invasion and establishment of Intracellular Bacterial Colonies
b. Flagella (allow Uropathogenic E.coli (UPEC) to flux in/out of cells, avoiding apoptotic defense mechanisms)

Front 31

VI. What is HUS?

Back 31

a. Hemolytic Uremic Syndrome

Front 32

VII. How do you get it? (HUS)

Back 32

a. Lysis of EHEC (via antibiotic use, usually) releases Shiga toxin that causes bleeding, renal failure, and (rarely) death

Front 33

VIII. How does H. influenzae cause otitis?

Back 33

a. Colonizes nasopharynx, expresses Hap, forms microcolonies/biofilm in middle ear

Front 34

IX. What virulence factors does H. influenzae use?

Back 34

a. Hap: non-pillus adhesin that promotes formation of microcolonies in the presence of SLPI (otherwise it’s cleaved)
i. SLPI is present in inflammatory situations (i.e. viral infection)

Front 35

X. Where is H. influenzae normally found and what else does it cause?

Back 35

a. Human respiratory tract; can cause pneumonia

Front 36

XI. How do E. coli and Salmonella use TTSS (Type III Secretion System) differently?

Back 36

a. EHEC injects effector proteins after binding, including Tir, which binds Initimin and allows pedestal formation beneath the EHEC
b. Salmonella use TTSS to initiate take-up into epithelial cells into endosomes and to prevent lysosomal destruction inside macrophages.