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MB 414 > Host-Parasite Interaction > Flashcards

Host-Parasite Interaction Flashcards

1
Q

commensal

A

benefit microbe, harmless to the host

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2
Q

symbiotic

A

mutual benefit to both and microbe

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3
Q

parasitic

A

benefit to the microbe, harm to the host

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4
Q

pathogenicity factors

A
  • in order for a microbe to be pathogenic, it must enter the host, maintain a population, and cause damage to the host.
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5
Q

Type I secretion

A
  • Enterohemorrhagic E. Coli
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6
Q

Type II secretion

A
  • Vibrio cholera
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7
Q

Type III secretion

A
  • Enteropathogenic E. Coli
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8
Q

Type IV secretion

A
  • Agrobacterium tumefacians
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9
Q

Adherence

A
  • proteins
  • Fimbriae
  • Glycocalyx
  • sometimes interactions are specific, sometimes not
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10
Q

proteins:

A
  • N. gonorrhea

- Opa protein binds receptors in urogenital epithelium

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11
Q

Fimbriae

A
  • Salmonella

- fimbriae bind to epithelium of small intestine

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12
Q

Glycocalyx

A
  • help streptococcus mutant bind to tooth surfaces
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13
Q

Toxins

A
  • exotoxins

- endotoxins

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14
Q

endotoxins

A
  • made up of LPS
  • the presence of LPS in an animal is always indicative of an infection, and the innate immune system will kick in any time LPS is detected (pyrogenicity)
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15
Q

exotoxins

A
  • specifically made by the microbe in response to host invasion
  • exported from the cell and have specific targets in or on the host cells.
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16
Q

types of exotoxins

A
  • cytotoxins
  • neurotoxins
  • enterotoxins
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17
Q

cytotoxins

A
  • cause damage to host cell structure and activities
  • protein synthesis inhibitors - diphtheria toxin
  • hemolysins - attack RBC
  • leukocidin - attack WBC
    • do so by inserting pore forming proteins into target cell membranes
18
Q

neurotoxins

A
  • cause damage to neural tissues and disrupt nerve conduction
  • botulism toxin - prevents release of acetyl choline which prevents muscle contraction
  • tetanus toxin - blocks release of gaba which prevents muscle relaxation
19
Q

enterotoxins

A
  • mainly act on tissues in intestines

- cholera toxin - massive diarrhea and water loss

20
Q

A-B exotoxins

A
  • A subunit is the toxin

- B subunit binds to the host cell

21
Q

How AB toxin works

A
  • B subunit (bound to A) will recognize a receptor on the host cell surface and bind to it.
  • The host cell will be signaled to take up the bound AB toxin via endocytosis.
  • upon entry, the A and B will dissociate and the toxin will interact with the target
22
Q

A toxins

A
  • many but not all are enzymes called ADP ribosyltransferases, which transfer the ADP-ribose from a NAD nucleotide to its target protein
  • once target protein has been ADP ribosylated, it becomes inactive
23
Q

targets of ADP-ribosylation

A
  • elongation factor 2 - diphtheria toxin
  • adenylate cyclase - cholera, pertussis toxin
  • G-actin - clostridium toxA
24
Q

Toxin Delivery (Secretion Systems)

A
  • The type I-IV secretion systems are used by Gram-negative bacteria to get virulence factors past both membrane and out of the cell.
  • I and II deliver the secreted protein into the environment around the cell, but are not specific for toxin delivery.
  • III and IV deliver the toxins directly into the cytoplasm of host cells.
25
Q

Type I secretion system

A
  • consists of an outer membrane channel
    • always TolC
  • and an inner membrane ABC transporter
    • depends on the protein
    • each protein requires a unique ABC transporter
26
Q

ABC transporter

A
  • identified by the presence of a protein motif called ATP Binding Casette
  • casette binds and hydrolyzes ATP, providing energy to transport the protein.
  • the rest of the transporter specific for the protein being transported.
27
Q

E. Coli O157:H7 secretion system

A
  • causes hemolytic uremic syndrome
  • the disease is caused by production of hemolysin secreted by type I secretion
  • lysed blood cells clog glomerulus in kidneys and waste products accumulate in the blood
  • bacteria almost never found in the blood.
28
Q

Hemolysin action

A
  • hemolysin is secreted as a monomer but assembles as an oligomer in the RBC membrane, and then insert as an octomer into and through the membrane.
29
Q

Type II secretion

A
  • method of getting proteins past the outer membrane, but proteins secreted must be in the periplasm to begin with.
  • use Sec system to transport proteins into the periplasm
  • once in periplasm, push protein past outer membrane by type II
  • homology to type IV pilus
30
Q

Cholera toxin secretion system

A
  • when large numbers of it are ingested, they will make and secrete the cholera toxin. Outbreaks correlated to the sea surface temperatures
  • since 1817 there have been 7 (or *) major pandemics
  • AB toxin that is active against the epithelial cells of the intestines
  • once inside cell, A subunit will modify adenylate (through ribosylation) to make it always activated
    • increases cAMP levels which triggers massive losses fluid, severe diarrhea, dehydrates, and could result in death (from hypovolemic shock)
31
Q

Type III secretion

A
  • they deliver the toxin directly to the cytoplasm of the host cell.
  • The TTSS passes through three membranes.
32
Q

Enteropathogenic E. Coli secretion system (EPEC)

A
  • first attaches to host cell via fimbriae and protein intimin
  • once cell close enough the use the TTSS, the Tir proteins are injected
  • TSSS will inject toxin identified as EspF
33
Q

Tir proteins

A
  • serve as attachment sites for EPEC as well as nucleation sites for actin polymerization.
  • actin pushes the host cell membrane up, creating the pedestal on which EPEC will sit on.
  • basically make their own adherence molecule.
34
Q

EspF

A
  • directed to the mitochondria and causes leaks
  • mitochondria release cytochrome C which signal signal apoptosis.
  • epithelial death causes breakdown of mucosal barrier and diarrhea
35
Q

Type IV secretion

A
  • powered by ATP, also resembles type IV pili (conjugatation pilus)
  • directly inject DNA and protein into the cell.
  • transport occurs all the way from the cytoplasm of the bacteria to the cytoplasm of the host
36
Q

Agrobacterium tumefaciens secretion system

A
  • a gall (plant cancer) caused by insertion of proteins and oncogenic DNA via a type IV secretion apparatus
  • bacteria capable of causing the tumors contain a tumor inducing plasmid (Ti) plasmid
  • must enter through a wound
37
Q

Ti plasmid

A
  • contains a small portion of DNA (T-DNA) that is transferred to the plant to cause the tumor, the opine permeate and opine catabolism proteins, and Vir proteins.
  • contains genes that encode a type 4 secretion system that will transfer T-DNA and the VirD2.
38
Q

VirD2

A
  • site-specific DNA recombinase that will help transport the T-DNA into the nucleus and insert it directly into the plant chromosome.
39
Q

T-DNA

A
  • contains genes that will make the plant produce auxins (plant hormones) and cytokines, plant steroids that will cause the cell to reproduce rapidly and form the gall.
  • also present are the genes that cause the plant to produce opines and nopaline.
40
Q

opines

A
  • rare amino acids that will be excreted by the plant cells to feed the bacteria.
  • argenine and lysine residues lined up
  • A. tumefaciens use the opines as food, but only if they are carrying the Ti plasmid, as it contains the genes required for opine catabolism.
  • bacteria that do not have the plasmid do not have the ability to break down opines.
41
Q

Difference between endotoxin and exotoxin

A 
EXOTOXIN
- protein
- high potency
- high specificity
- enzymatic activity
ENDOTOXIN
- LPS
- low potency
- low specificity
- no enzymatic activity

MB 414 (26 decks)

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