#10 drug resistant pathogens: concepts and applications Flashcards

1
Q

Antibiotic resistance has rapidly evolved every time a new antibiotic has been introduced. Explain.

A

Antibiotic resistance evolves because every time one is administered it weeds out all of the week bacteria selecting for the resistant ones so now only strong ones live and replicate and they can mutate to make further modifications to resist antibiotics.

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2
Q

What are antibiotics, and how do they work?

A

Antibiotics are injections of a heterogeneous class of molecules that interfere with the growth, survival, and reproduction of bacteria. Many antibiotics occur naturally and are isolated from bacteria and fungi but some antibiotics are entirely synthetic.
Antibiotics work by targeting essential bacterial physiology, causing microbial cell death or reduced growth. There are five major antibiotic targets: the cell wall, the cell membrane, protein synthesis, DNA and RNA synthesis, and folic acid metabolism

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3
Q

What are some differences between prokaryotic and eukaryotic cells?

A

Prokaryote: circular DNA molecule, 1 chromosome, cell wall, folic acid metabolism
Eukaryote: linear DNA molecules, 2 chromosomes, no cell wall

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4
Q

When resistance has evolved in natural ecosystem, resistance genes can move into human bacterial pathogens through any of three mechanisms. Describe these three mechanisms (Note: be specific here).

A

Transformation: uptake of naked DNA that is used as a source of genetic material
Transduction: viruses (bacteriophage) bring along a piece of the genome from their last bacterial host when they infect a new bacterial host
Conjugation: a bridge is built between 2 bacterial cells letting plasmids and sometimes chromosomes cross over and recombine.

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5
Q

Misuse and overuse is making antibiotics less effective. Describe three scenarios where this statement is true (hint: watch the video and be specific in your answer; this question is worth a lot).

A
  • 40-50% of AB use in hospitals is unnecessary so we are overusing them which increases resistance
  • Misuses with intensive farming practices where they use AB for animals that are packed together and spreading bacteria across all of them easily makes a great environment for AB resistance to spread
  • Horses have an adapted form of MRSA from humans and the horses spread MRSA back to humans that can spread among humans again
  • Meat consumed contained resistant strains and then those resistant strains sit in the intestinal microbiota of humans like for the traveler who had the superbug when he consumed food overseas and then later it attacked him
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6
Q

Pathogens can potentially hide from the immune system inside cells. How does the adaptive immune system deal with this situation?

A

The adaptive immune system can detect that the cell is deformed or wrong when they are filtered through the spleen and then excreted from the body. One example is the plasmodium infects RBC which makes them more rigid which is recognized when they are filtered through the spleen which filters them out but plasmodium counters by inserting proteins that helps them bind to capillaries thus delaying entry to spleen.

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7
Q

Describe the steps involved in the production of antibodies?

A

A specific immune response is triggered by an antigen that’s associated with a specific pathogen then the body produces antibodies to match the antigen. The antibody and antigen bind and attract cells to engulf and destroy the pathogen.

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8
Q

Define virulence. What is the virulence-transmission trade-off? Describe an example of this trade-off?

A

Virulence is the portion of the damage that the infection causes (to the host) that is due to properties intrinsic to the pathogen.
Virulence transmission trade off: is the level of virulence balance with the need for transmission
Example: rabbit population in Australia was controlled by myxoma virus which originally had a 100% mortality rate so it was a highly virulent strain that morphed into a less virulent strains but stabilized at strain III with a virulence level of 3 that had a fatality rate of 75-95%. This happened because if the virus killed the host before it could infect other rabbits its not being very effective so it reduced its virulence in favor of a higher transmission rate.

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9
Q

When pathogens move from one host species to another species, it might be more virulent in the new host. Briefly explain why.

A

It could be more virulent to the new host because the host has never encountered anything like it so it has no defenses and it can easily kill the new host like the bubonic plague or Ebola whose primary host wasn’t humans and those hosts were asymptomatic.

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10
Q

Many of the commensal microbes provide essential benefits to the host. Name five of them.

A
  • Break down food compounds
  • biosynthesis of vitamins and amino acids
  • resistance to pathogens,
  • protect against epithelial injury
  • development and training of immune system
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11
Q

What are the two roles of skin?

A

A defensive barrier and because they are colonized by microbiota they are an important for interaction with the immune system

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12
Q

What is one consequence of imperfect vaccines?

A

Imperfect or leaky vaccines: protect individuals to a certain degree but continues to allow or the forward transmission of the disease
Widespread use of imperfect vaccine can drive the evolution of increased virulence in pathogens by allowing the patent to live longer

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13
Q

What is intrinsic virulence? What is extrinsic virulence?

A

Extrinsic virulence: when a pathogen is virulent in one host but not another
Intrinsic virulence: how virulent a pathogen is within the host

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14
Q

Pathogens can also disrupt immune function in several ways. Please list them. Then, describe an example in detail of how pathogens disrupt immune function. Be specific here

A

 Block intercellular signaling or intracellular defenses
Example: Viruses in the herpes family can also block antigen processing by inhibiting gene expression and peptide transport (preventing the presentation of MHC class I molecules).
 Slow the recruitment of immune cells
 Some viruses disrupt signaling and cell adhesion, inhibiting inflammation.
 Kill immune cells directly
 Vary surface proteins to confuse the immune system
Many bacteria, including those causing bubonic plague, whooping cough, and stomach ulcers, vary their surface properties, by frameshift mutations that cause amino acid substitutions.

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15
Q

Plasmodium confronts and solves problems in two hosts. Please describe how Plasmodium counters the immune system in two hosts.

A

Plasmodium, must deal with the immune system of its definitive host species (its mosquito vector). In mosquitoes, where the Plasmodium parasite is attacked by phagocytosis, the parasite mimics the surface of mosquito cells, suppressing immune response.
The plasmodium avoids detection in humans by presenting highly polymorphic antigens which change a bunch so the immune system cant identify it as a pathogen.

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