How m/os cause disease

Question 1

Pathogenicity

Answer 1

The ability to cause a disease by overcomeing the defenses of the host

Question 2

Virulence

Answer 2

Virulent (cause disease) vs avirulent (Do not cause problems)
Degree of pathogenicity

Question 3

Portals of entry for a pthogen

Answer 3

Resp, GU, GI,
Skin (Hair follicles, sweat glands i.e. S. aureus)
Parental route
- M/o deposited beneath skin via injectionsm bites, cuts, surgeyr etc.

Question 4

How is virulence often expressed

Answer 4

ID50 (infectious does) (A certain number of microbes that will cause an infection in 50% of the population)

Question 5

LD50 =

Answer 5

a dose that would be lethal for 50% of the population (does not consider how many people will get sick)

Question 6

Portal of entry for anthrax

Answer 6

Skin anthrax: 10-50 spores (skin anthrax is more potent)
inhalation: 10,0000- 20,000
Ingestion: 250, 0000- 1,000,000

Cutaneous anthrax is significantly easier to acquire than inhalation or ingestion forms

Question 7

How potent is the botulism toxin at LD50?

Answer 7

0.03 ng/kg

Question 8

Means that a microbe uses to atttach to host cell at portal of entry

Answer 8

Adhesions or ligands (glycoproteins or lipoproteins) on microbes bind to receptors (carbs) on host cells altering one can block adherence
Capsules and cell wall components
Glycocalyx of streptococcus mutans (surface of teeth - tooth decauy)
Fimbriae of enteropathogenic E. coi: specific cells in small intestine
Fimbriae of Neiseeria gonorrhoeae cells in GU tract
Tapered end as a hook: Treponem pallidum (non proteobacteria, spirochete causing syphillis)

Question 9

How do microorgaisms penetrate the cell

Answer 9

M/Os attach to host cells by adhesion/invasins
Invasins reaarrange nearby host cell cytoskeleton induce ruffling (Ripples help bacteria burry itself into plasma membrane)
M/Os sink into the ruffles and are engulgfed by the host cell, use cytoskeleton to move through bw cells (Lysteria)

Question 10

Virulence of some bacteria is aided by:

Answer 10

Capsule: Impair phagocytosis
Streptococcus pnemonieae
Waxy layer: resist digestion by phagocytes
Mycobacterium tuberculosis
Coagulase: Coagulate the fibrinogen in blood
S. aureus
Kinase: digest fibrin clots
Streptococcus pyogenes, S. aureus.
Hyaluronidase: Hydrolyses hyarulonic acid that holds together some cells in the body (adjacent cells have glue inbw them) Creates space in bw cells for m/os to grow
Collaginase: Hydrolyses collagen
Clostridum
IgA proteases: Destroy iGA antibodies (found in secretions i.e breast milk, and in mucous layers)
Neisseria gonnorrhoeae

Question 11

How does antigen variation work?

Answer 11

M/os alter surface proteins to evade host’s immune system
By the time the body mounts an immune response, the m/o has altered it’s antigens and is unaffected by the antibodies

Question 12

What are antigen proteins

Answer 12

The part of them that illicits an antibody response, each pathogen can change it’s respective surface proteins to avoid detection

Question 13

Siderophores

Answer 13

Take iron from host cells/proteins (transferrin), if not enough, will begin lysing red blood cells

Question 14

How do pathogens cause direct damage to host cells?

Answer 14

Some pathogens grow inside host cells
Viruses
Salmonella
N. gonorrhoeae

Question 15

Exotoxins

Answer 15

Proteins produced inside pathogenic bacteria, mostly Gram +ve, as part of their growth & metabolism; secreted in surrounding medium during log phase

LD50 very small (toxic) - can be neutralized by antitoxin (antibodies produced against these toxins)

Question 16

3 major types of exotoxins

Answer 16

A-B toxin
Membrane disrupting toxins
Superantigens

Question 17

A-B toxin

Answer 17

Active/binding components (binding components causes damage) (diptheria toxin, botulinum toxin etc.)

Question 18

Membrane disrupting toxin

Answer 18

Hemolysins production (streptococcus and staphylococcus)

Question 19

Superantigens

Answer 19

Cause an intense immune response due to release of cytokines from host cells (t cells)
Fever, nausea, vomiting, diarrhea, shock and death
Enterotoxin of s. Aureus

Question 20

Endotoxins

Answer 20

Part of ccell wall of Gram - bacteria

Symptoms similar for different bacteria
Released when bacteria dies or during multiplication
Actiates blood clotting factors that may obstruct capillaries

Composed of lipid
Present in LPS of outer membrane
Not neutralized by antibodies
Relatively large LD50 (not too toxic)
Better for body to deal with on it;s own as to not release endotoxins by treating with antibiotics

Question 21

Plasmids

Answer 21

small, circular DNA molecules that are not connected to bacterial chromosome

Bacteria with plasmids is likely antibiotic resistant or something special bc of the extra genes
Encode gene for resistance to antibiotics, exotosins and other virulence factors

Question 22

Lysogeny

Answer 22

Bacteriophages that can incorporate DNA into bacteriophage becoming prophage

Question 23

Microevolution

Answer 23

: a way to increase the number of pathogenic bacteria
Actibiotic reissitance
Pseudomonoas is well known to be generous at passing on antibiotic resistance

Question 24

Portals of exit

Answer 24

Via secretions, excretions, discharges, or tissues that have been shed by the infected host
Most microorganisms use the same proal of entry for portal of exit
End goal = spread through the population