Bacterial Pathogenesis Flashcards
1
Q
asymptomatic, inapparent, subclinical infection
A
-host defenses clear pathogen before any symptoms of disease are notes
2
Q
communicable infection
A
can be passed from host to host
3
Q
contagious infection
A
highly communicable
4
Q
noncommunicable infection
A
- comes from environment, not a previous host
- botulism, legionnaires
5
Q
latent infection
A
-disease subsides, but microorganisms remain in body and can restart disease later
6
Q
chronic carrier state
A
-host survives disease but continues to shed the pathogen indefinitely
7
Q
parasitism
A
- pathogens are parasites in the sense that they harm the host by taking its resources to reproduce themselves
- all viruses and a few bacteria are obligate intracellular parasites, must enter host cells to reproduce
- more bacteria are facultative intracellular parasites, meaning that they can reproduce outside the host cells when they need to
- be careful of confusion of parasites-protazoa and helminths
8
Q
nonpathogens
A
- very unlikely to cause disease
- most environmental bacterial and normal flora
- very low virulence
- LD50 very high (lethal dose to kill 50% of pop)
- ID50 high (infectious dose to 50% pop)
9
Q
opportunistic pathogen
A
- unlikely to cause disease in a healthy adult
- will take advantage of injury of immunosuppression
- legionella, pseudomonas, enterobacter
- low virulence
- LD50 high
- ID50 med/low
10
Q
pathogen
A
- regularly causes disease in previously healthy hosts
- n. gonorrheae, shigella, norwalk virus
- Mid-high virulence
- LD50 med/low
- ID50 med/low
11
Q
virulence
A
- numerical measure of pathogenicity
- lower ID50 means fewer infecting organisms are needed to cause symptoms of disease
- lower LD50 means fewer infecting organisms needed to kill the host
12
Q
virulence factors
A
- genes found empirically to be determinants of pathogenicity
- can be encoded in pathogenicity islands
- can be plasmids or come from phages
- E coli has an acquisition of virulence that makes it disease causing-uropathogenic gains the ability to attach to respiratory tract
13
Q
survive extreme environments
A
-pH tolerance, siderophores, resistance to drying, resistance to detergents
14
Q
siderophores
A
- bind iron
- need it to grow
- need to steal it from us
15
Q
Adhesion
A
- pili/fimbrae/curli
- slime layer
- adhesins
- biofilm formation
16
Q
Immune evasion
A
- capsule
- IgA proteases
- macrophage apoptosis inducers
- antigenic variation (switching out)
- serum resistance (stops complement)
17
Q
host cell takeover
A
- endosome escape routes
- actin polymerization pathways (use cells actin to make pseudopods to get to neighboring cells)
- type 3 and 4 secretion systems (3-peptides, 4-DNA)
18
Q
poison the host
A
- tissue degrading enzymes (stop oxygen or immune from getting to bacteria-coagulase)
- endotoxins
- exotoxins
19
Q
endotoxins
A
- cell wall/membrane components trigger septic shock
- gram neg- LPS/LOS
- gram pos-teichoic acids
- exposure can lead to overproduction of TNF and IL1, DIC, SIRS, death
- symptoms are immunogenic, antibody is not protective and vaccination is not useful
20
Q
exotoxins
A
- polypeptides
- secreted from cell or injected by T3SS
- most toxic substances known
21
Q
exotoxin themes
A
- often encoded in plasmids or bacteriophages rather than bacterial genome
- common toxic strategies include superantigenicity, interference with signal transduction, depolymerization of actin
- several exotoxins have a similar A-B subunit structure-B delivers A to A’s toxicity site- A can be ADP rybosylase
- almost always heat liable, inactivated toxoids are often useful vaccines
22
Q
superantigens
A
- undermine specificity of immune response (activates up to 25% of T cell repertoire instead of normal .001-.001 %)
- can cause shock and multiple organ failure
- most common are s aureus, strep pyrogens–>TSS
23
Q
Cholera, E coli, B cereus in gut
A
- increase adenylate cyclase activity
- leads to fluid and electrolyte loss (osmotic gradient)
- watery diarrhea to spread bacteria
- heat stable e coli enterotoxin (which is an exotoxin) causes same effect by stim guanylate cyclase
24
Q
diphtheria
A
- tox gene encoded by lysogenic bacteriophage
- A subunit ADP ribosylates TF EF-2- things allowed to cross nuclear membrane and affect gene expression
- makes a pseudomembrane in resp tract
- kills by suffocation
25
C difficile A and B
- glucosylate Rho GTPase
| - leads to depolymerization of actin, apoptosis, and a major inflammatory response in the gut (pseudomembranous colitis)
26
MRSA PV leukocidin
- forms pore in cel membranes and leads to lysis- like our complement system
- PVL genes are phage born
27
Infection
-pathogen defeats innate immunity for successful colonization
28
incubation period
-microbial numbers too low to produce symptoms, most rapid growth
29
prodrome
-non-specific immunogenic symptoms as adaptive immunity is raised:fever/ fatigue
30
specific illness period
-pathogen mediated symptoms emerge as large numbers of pathogens express virulence factors
31
recovery/convalescence
-immune system gains upper hand and dramatically reduces pathogen numbers;patient begins to regain strength
32
ways to be virulent
- surviving extreme conditions
- adhesion
- immune evasion
- host cell takeover (T3,4SS, actin)
- poisoning host-toxins
- other
33
transmission of pathogens
- respiratory droplets
- fecal-oral
- direct contact
- sexual contact
- blood blood
- vertical-transplacental, vaginal delivery, breast milk
- animal reservoir-zoonosis
- fomite (washcloth, countertop)
- vector (tick/mosquito)
34
coagulase
- breaks down fibrinogen to form a fibrin clot around S aureus
- invasion of host tissue
35
collagenase/hyaluronidase
- break down tissue to s pyrogenes can penetrate
| - invasion of host tissue
36
pyrogenic IF response
-pus forming, predominantly neutrophils
37
granulomatous IF response
-macrophages kill most of the bacteria, but some survive inside macrophages within a granuloma
38
facultative intracellular
- mycobacteria, legionella, brucella, listeria
- legionella also inhibits fusion of lysosome with phagosome and inhibits acidification if fusion does occur along with chlamydia
39
obligate intracellular
-chlamydia and rickettsia
40
invasins
-virulence factors recognized by cell-surface integrins, docking leads to cell entry
41
Q fever
-allows lysosome fusion and survives acidification
