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Microbiology-1 > Bacterial Pathogenesis > Flashcards

Bacterial Pathogenesis Flashcards

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1
Q

Pathogenic bacteria are clonal or non clonal?

A
  1. clonal (virulence genes, isolated in pure culture)
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2
Q

Can strains of the same species can have distinct phenotypes? Examples?

A

Yes, through selection (mutations present at low frequency, mutants selected bc growth advantage in particular conditions.

ex. tissue tropism: enteropathogenic vs. uropathogenic E. coli

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3
Q

Immune selection

A

host immune response in relapsing fever is the driving force for antigenic variation Borrelia hermsii

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4
Q

antibiotic resistance

A
  • more commonly selected in population rather than individual
  • inappropriate use of antibiotics in humans, or overuse of antibiotics in livestock
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5
Q

What are Koch’s postulates for establishing the cause of an infectious disease?

A
  1. Microorganisms found in all cases of the disease and in appropriate location
  2. micro can be grown outside the hosr (in pure culture in vitro) for several generations
  3. reinoculation of cultivated micro causes the disease
  4. microor can be isolated from experimentally produced disease
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6
Q

koch’s postulates requires culture and an experimental model. Which do not statisfy the postulates?

A
  1. growth in vitro: some cannot be cultured
    - treponema pallidum (syphillis): use animal model
    - tropheryma whipplei (Whipple’s disease): identify by PCR

experimental infection: absence of animal model

  1. neisseria gonorrhoeae: use human experimental model
  2. polymicrobial infection

-

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7
Q

Pathogenicity

A
  1. transmissibility
  2. production of toxins and enzymes
  3. adherence to host cells
  4. secretion of bacterial proteins into host cells
  5. invasion of host tissue
  6. survival inside host cells
  7. evasion of host immune response
  8. tissue damage from host immune response
  9. requirement for iron
  10. regulation of virulence factors
  11. antibiotic resistance
  12. mobile genetic elements
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8
Q

Transmissibility: Why have clinical symptoms?

A

advantage of mild disease: survival of host enhnaces change of trnasmission

  1. non-adapted host/pathogen: incidental infection of humans, often by zoonotic bacteria (ex. salmonella in poultry)
  2. clinical symptoms that produce transmission (ex. vibro cholerae)
  3. disease manifestatino that are due to host response to pathogen (ex. tissue scarring- chlamydia trachomatis)
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9
Q

What are some clinical symptoms that promot transmission?

A

respiratory route: coughing, sneezing

Gastrointestinal: diarrhea

STI: genital dischare and genital ulcer

person-to-person transmissoin by direct contact: skin discharge

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10
Q

Transmissibility: portal of entry

A

via mucous membrane

normal skin is good barrier vs abnormal skin (wounds, nbites, burns) & mucous membrane (chemotheraphy)

arthropod vectors

injection drug use

medial intervention: surgery, catheters

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11
Q

Transmissibility: spread within the body

A

direct tissue spread

vascular

lymphatics

carriage w/in MO

ascending/descending spread within a tract

ex. respiratory intection- upper (bronchitis)–>lower (pneumonia) (Descending)

urinary tract infect- bladder (cystitis)–>kidney (pyelonephritis) (ascending)

genital tract infection- lower (cervicities)–>upper (pelvic inflammatory dx)(ascending)

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12
Q

how do Extracellular bacteria cause disease?

A

cause disease via the effect of toxins and enzymes

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13
Q

How do intraellular bacteria cause disease?

A

invade host cells. often cause of chronic infection

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14
Q

Exotoxins

A

highly toxic proteins secreted by bacteria into extracellular envirn.

  1. in a few cases performed toxin is ingested, but usually an active bacterial infection is required
  2. may act locally or distant site.
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15
Q

What are the subunits in exotoxins?

A

A: active subunit w/ specific toxin activity

B: binds to specific host cell receptor; involved in entry of exotoxin into cell

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16
Q

Example of 2 subunit exotoxin?

A
  1. corynebacterium diphtheriae (inhibition of protein sysnthesis)
  2. vibro cholerae (inducers of cAMP-incresed secretion)
  3. clostridium tetani (neurotoxin- block release of inhibitory transmitters, continuous excitatory)
  4. Clostridium botulinum: (neurotoxin- block ach release)
  5. Anthrax toxin *
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17
Q

What is special about the 2 subunit anthrax toxin?

A
  • 3 proteins make up 2 toxins
  • “protective antigen” is the B subuit of each of the 2 toxins
  • the A subunit for 2 toxins (a. edema factor: adenylate cyclase, b. lethal factor: kills cells)
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18
Q

Superantigens. produced by?

A

some exotoxins are superantigens

produced by bacteria and viruses

  • highly antigenic, heat lablile
  • partially denatured by treatment w/ formalin, acid or heat–>toxoid (non-toxic but still antigenic- used for immunizations- diphtheria, tetanus toxoids
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19
Q

what is the action of superantigens?

A

Polyclonal stimulation of subset of lymphocytes (tcells) to dicide and produce cytokines

ex. TSST-1, stre exotoxins, pyrogenic toxins- cause fever

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20
Q

Endotoxin

A

LPS (in gram- cell wall, liberated when bacteria lyse)

21
Q

what is the mechanism of action for an endotoxin?

A

endotoxin in bloodstream–>binds to R on MO–>cytokine release (IL-1, TNFa)–>inflammatory & coagulation cascades

22
Q

Can gram + cuse septic shock without LPS?

A

yes, probably due to peptidoglycan, less potent than LPS

23
Q

What is the toxic moiety in LPS?

A

Lipid A

24
Q

what is the clinical effect of endotoxin?

A

fever and septic shock

-LPS not as toxic as exotoxin, less antigenic too, relatively heat stable

25
Q

Summary of Exotoxin vs Endotoxin

A
26
Q

What are some examples of enzymes?

A

may not be intrinsically toxic, but can cause tissue damage

  1. hyaluronidase: degrades Hyaluronidase acid
  2. streptokinase: fibriolysin
  3. coagulase: coagualtes plasma
  4. catalase: inhibits oxidative killing
  5. cytolysins kill host cells: streptolysin S & O, Listeriolysin O
27
Q

how is Adherence to host cells mediated?

A

ahesions (bacteria) and host cells (receptors)

-antibodies against the adhesion can block adhesion and protect host from infection

28
Q

How to bacterial cells physically attach?

A

binding by pili (aka fimbriae)- hairlike appendages that extend form bacterial surfaces

29
Q

Type III secretion of bacterial proteins

A

specialized system for secreting bacterial virulence proteins into host cells

only pathogenic Gram -

secreted proteins modulate host cell fxn

30
Q

what are the functions of the secreted bacterial proteins?

A
  1. induce or prevent uptake by mammalian cells
    ex. induce uptake- bacteria invade mammalian cells. salmonella

prevent uptake: prevent phagocytosis MO, yersinia

  1. Induce of prevent death of mammalian cell
    ex. induce apoptosis in MO, yersinia
    ex. prevent apoptosis: intracellular bacteria, chlamydia
31
Q

Invasion of host cell

A
  • Some bacteria can incduce their uptake by normally non-phagocytic cells
  • requires specific interaction btw baterial ligand and host cell receptor
  • involved actin cytoskeleton rearrangements
  • often involves Type III secretion system
32
Q

How do pathogens survive inside host cells?

A

Advantages of intracellular localization

  1. nutrient rich envir
  2. absence of competing microorg.
  3. protected from humoral immune system
    ex. survucal inside phagolyso (coxiella), inhibition of phagolyso (chalmydia), escape into cytosol/actin based motility (listeria)
33
Q

What are some examples of antiphagocytic activity?

A
  1. adsorb normal host component to surface of bacteria: staphylococcus aureus protein A binds IgG
  2. Surface factors that inhibit phagocytosis
    - polyysacc capsule
    - m protein- group A strep
    - pili- neisseria gonorrhoeae
  3. type III secreted proteins that prevent phagocytosis
  4. kill phagocytic cell: group A streptococcal steptolysin
34
Q

evasion of host immune response: polysaccharide capsule

A

prevents complement deposistion and is poorly immunigenic

  • polysaccharide induces T cell-independent immune response
    ex. neisseria meningitidis, streptococcus pneumoniae, haemophilus influenzae

poor immune response in children <2yrs

35
Q

Are antibodies against capsular polysaccharide type specific or non specific?

A

specific, do not protect agaisnt diff types

ex. penumococcal vaccine is directed against 23 capsular polysaccahride tyeps

antibodies protect agsinst systemic infect not mucosal colonization

36
Q

What are some ways that pathogens evade host immune responses?

A
  1. antiphagocytic activity
  2. polysacc capsule
  3. antigenic variation
  4. IgA protease
37
Q

How do pathogens escape immune response via antigenic variation?

A

shift in the expression of surface antigens

ex. niesseria gonorrhoeae: 3 surface molecules (lipooligosacc, pili, Opa proteins) can each be sweitch to diff antigenic forms
ex. borrelia hermsii (relapsin fever): repertoire of variant surface antigen that is antigenically distinct

38
Q

How do pathogens evade for immune response via IgA protease?

A

cleaves IgA (mucosal immunity)

ex. enzymes produced by:

Neisseria gonorrhoeae,

neisseria meningitidis,

haemophilus influenzae,

streptococcus pneumonia

39
Q

What are 4 types of tissue damage that is caused by the host immune response?

A
  1. immune complex deposition
    - baterial antigen + Ab complement
    - post-streptococcal acute glomerulonephritis: deposition of immune complezes in glomeruli of kidney
  2. molecular mimicry
    - post-streptococcal rheumatic fever is an autoimmune process w/ Ab against streptococcal antigen cross-rx againt host tissue
  3. tissue damage and scarrying: chlamydis trachomatis
  4. delayed type hypersensitivity: TB
40
Q

Where is most iron in the body?

A

intracellular: Hb and myoglobin

41
Q

Is most iron free?

A

very little iron is free. extracellular iron is bound to transferrin (in plasma) and lactoferrin (in milk and other secretions)

42
Q

What do bacteria use to capture iron?

A

siderophores

ex. E.coli

43
Q

regulation of virulence factors

A

bacteria regulate the expression of virulence factors in response to environmental signals

ex. temperature, ions availability, iron avaiability, etc

44
Q

What are 3 mechanism for antibiotic resistance?

A
  1. inhibition of antibiotic
  2. target side alteration
  3. decreased intrabacterial accumulation of antibiotic
45
Q

explain the inhibition of antibiotic mechanism for ab resistance.

A

often by enzymatic hydrolysis of the ab

ex. enteric gram - bacilli that produce b-lactamases

46
Q

explain target site alteration mech of ab resistance

A

decreases binding affinity of the ab for the target

ex. penicillin-resistant strep penumoniae (altered PBP protein)
ex. MRSA expressing altered PBP protein
ex. Vancomycin resistance enterococcus expressing altered cell wall oligopeptide

47
Q

explain how the decreased intrabacterial accumulation of abs is involved in the mech of ab resistance

A
  • decreased outer membrane permeability
  • changes in porin channels
  • increased drug efflux: often results in multidrug resistance

(pseudomonas aeruginosa uses all 3 of these mech to prevent accumulatin of ab)

48
Q

mobile genetic elements

A

allow acquisitio of genetic infro by horizontal transfer including virulence genes and ab resistance genes

  1. plasmids- passed by conjugation, contain ab resistance genes
  2. phages- bacteria infected by lytic phages or carry prphaes in the bacterial chr. (Ex. v. cholerae)
49
Q

examples of some cases in which only strains that have the prophage and its virulence genes cause specific disease

A

Microbiology-1 (8 decks)

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