Microbiology Ch. 15 Pathogenicity

Front 1

Three portals of entry

Back 1

-Mucous Membranes
-Skin
-The Parenteral Route

Front 2

Mucous Membranes

Back 2

Access through respiratory tract,
GI tract, Genitourinary tract, and conjunctiva

Front 3

Skin

Back 3

Protective barrier, Some enter through hair follicles/ sweat glands.
Larvae and Fungi contact skin

Front 4

Parenteral Route

Back 4

Through split/ open membranes or skin

Front 5

LD50

Back 5

Lethal dose for 50% of a sample population (potency of toxin)

Front 6

The LD50 of botulinum toxin is 0.03 ng/kg; the LD50 of Salmonella toxin is 12 mg/kg. Which is the more potent toxin?

Back 6

Botulinum toxin more potent than salmonella

Front 7

How would a drug that binds mannose (a sugar receptor) on human cells affect a pathogenic bacterium?

Back 7

The adhesins/ ligands would be unable to bind to receptors on the host cell

Front 8

Common function of capsules and M proteins

Back 8

Both resist phagocytosis
Capsules: glycocalyx increase virulence
M Proteins: heat-resistance, acid-resistance, mediates attachment to host epithelial cells

Front 9

Expect bacteria to make coagulase and kinase simultaneously?

Back 9

No:
Coagulase- enzymes coagulate fibrinogen in blood (clot)
Kinases- break down fibrin (digest clots)

Front 10

Why doesn’t the influenza vaccine offer more than a few months of protection?

Back 10

It alters it surface antigens, by a process called "antigenic variation"- By the time the body mounts an immune response, the pathogen has already altered its antigens and is unaffected by the antibodies

Front 11

How does E. coli cause membrane ruffling?ill

Back 11

Change plasma membrane at point of contact; Microbes produce invasins (surface proteins) that rearrange nearby actin filaments of the cytoskeleton; ruffling allows microbe to be engulfed by the cell

Front 12

Siderophores

Back 12

Bacterial iron-binding proteins secreted by pathogens when they need iron; take iron away from iron-transport proteins, binding and forming a complex

Front 13

How does toxigenicity differ from direct damage?

Back 13

Direct: Rupture host cell, releasing and spreading pathogen
Toxin: inhibit protein synthesis, destroy blood cells, disrupt nervous system, cause fever

Front 14

Exotoxin V. Endotoxin.

Back 14

Ex: produced within bacteria and secreted into surroundings or released by lysis
En: lipid portions of the LPS in the outer membrane of g(-) cell wall; are released when the bacteria die and cell wall breaks apart

Front 15

Difference between food infection and intoxication

Back 15

Infection: Bacteria present grows and produces illness
Intoxication: Bacteria produces toxins which cause illness

Front 16

Washwater containing Pseudomonas was sterilized and used to wash cardiac catheters. Three patients developed fever, chills, and hypotension following cardiac catheterization. The water and catheters were sterile. Why did the patients show these reactions? How should the water have been tested?

Back 16

The bacteria was killed but the toxin was still present

Front 17

How can lysogeny turn the normally harmless E. coli into a pathogen?

Back 17

It can undergo lysogenic conversion, change in the characteristics of the microbe due to a prophage (DNA of bacteriophage incorporated into bacterial chromosome); bacteria immune to infection by same phage and prophage can cause pathogenesis

Front 18

Define cytopathic effects

Back 18

Visible signs of viral infections

Front 19

Examples of Cytopathic effects

Back 19

-mitosis prevention
-lysis
-form inclusion bodies
-cell fusion
-antigenic changes
-chromosomal changes
-transformation

Front 20

Cytocidal Effects

Back 20

Viruses cause cell death

Front 21

Noncytocidal Effects

Back 21

Viruses damage cells, but do not cause death

Front 22

Syncytium (a CPE)

Back 22

aggregates of giant multinucleate cells- diagnostic of measles, mumps, common cold

Front 23

Transformation (a CPE)

Back 23

Results in immortal cells b/c of no contact inhibition

Front 24

Virulence factor (contributes to the pathogenicity) of fungi

Back 24

-Tichothecene toxins inhibit protein synthesis (Fusarium)
-Proteases (Candida)
-Capsule prevents phagocytosis (Cryptococcus)

Front 25

Virulence factor (contributes to the pathogenicity) of protozoan

Back 25

Antigenic variation (trypanosoma) stays one step ahead of host’s immune response

Front 26

Virulence factor (contributes to the pathogenicity) of helminthic

Back 26

Parasitically use host tissue for their growth

Front 27

Virulence factor (contributes to the pathogenicity) algal

Back 27

Produce paralytic neurotoxins (saxitoxin)

Front 28

List microbial portals of exit

Back 28

Respiratory: coughing/ sneezing
GI Tract: Saliva/ Feces
Genitourinary: genital secretions
(Blood or Wound infections)