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HMS Immunology and Microbiology > Microbiology Introduction > Flashcards

Flashcards in Microbiology Introduction Deck (36)
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1
Q

Vertical transmission

A

from mother to child before, during or shortly after birth.

2
Q

fomite

A

An object that transmits an infection

3
Q

Horizontal transmission

A

From one person to another

4
Q

Zoonoses

A

infections acquired from vertebrates. They can occur by direct contact or in animal products

5
Q

vector

A

an arthropod that transmits an infection

6
Q

Adhesion to Host

A

Large parasites (e.g. worms) adhere by mechanical means, e.g. biting mouth parts. •

Microscopic organisms bind to host through receptor-ligand interactions. Ligands are normal host structures. Binding to a cell surface is the first step in entering host cell for intracellular pathogens

7
Q

Intoxication

A

Due to ingestion of a toxin that bacteria have produced in food. None of the microbe need be ingested or invasive in order to be intoxicated.

8
Q

Surface infection

A

Infection of the skin or mucosal surfaces

9
Q

Invasive infection

A

Extend into normally sterile spaces in the body.

Routes of spread of pathogens in the body include along the axons of nerves, within the blood or lymphatics, and by direct extension within tissues.

10
Q

antigenic variation

A

When a species of pathogen exists with different surface antigens (and expresses only some or one at a time) or when individuals within that species can change their surface antigens over time.

An effective immune response against one antigenic type does not prevent subsequent or prolonged infection with another antigenic type of that pathogen.

11
Q

Opportunistic pathogens

A

Cause infections in hosts with compromised defenses. Most opportunistic pathogens are environmental organisms that have not evolved to evade the immune response.

12
Q

virulence

A

The ability of a pathogen to cause damage

13
Q

Ways by which a pathogen may damage the host

A
  • Killing host cells by intracellular microbes. This usually happens after the microbe replicates and lyses the host cell.
  • Secreted toxins
  • Effector molecules injected into host cells
  • The host immune system
  • Transformation of host cells
  • Mechanical impairment of host organs
  • Malnutrition
14
Q

The presence of such organisms at sites where they are part of the microbiota. . .

A

does NOT indicate an infection

15
Q

Most bacteria can devide every ___.

A

Most bacteria can devide every 20-30 minutes.

At least, during the logarithmic growth phase

16
Q

Role of peptidoglycan in bacterial cell walls

A

There is a high concentration of solutes within the bacterial cell, so water tends to move into the bacterial cell when they are in a hypotonic environment. This could lyse (pop) the bacteria. Bacteria must protect themselves from this osmotic stress.

17
Q

Mycobacterium

A

Has a thick waxy layer surrounding the cell instead of a conventional layer of peptidoglycan.

This includes Mycobacterium tuberculosis, the cause of tuberculosis. Mycobacteria are the only “acid-fast” bacteria, meaning they retain stains even when decolorized with strong acids. This is due to the thick waxy coating. Another characteristic of mycobacteria is that they replicate more slowly than most other bacteria.

18
Q

The Gram Stain

A
19
Q

Outer Membrane of Gram-Negative Bacteria

A

Have second membrane surrounding the cell, in addition to the cytoplasmic membrane. The outer membrane encircles the peptidoglycan. This gives rise to a periplasmic space.

The outer membrane contains a unique molecule called lipopolysaccharide or LPS.

Usually contains porins to facilitate diffusion of imporant molecules. Loss of porin expression is an important mechanism of development of antibiotic resistance, as antibiotics utilize porins to enter the cell.

20
Q

LPS

A
21
Q

Porins

A

Trimeric proteins that form a pore in the outer membrane. The inside of the pore is lined with charged amino acids, which facilitates small, charged molecules moving across the outer membrane. Charged molecules ~700 Daltons, or about the size of a tripeptide, can cross this membrane via porins.

Most antibiotics act on Gram negative bacteria in the periplasmic space or in the cytosol. Loss of porin expression is an important mechanism of development of antibiotic resistance.

22
Q

How hosts get around bacterial capsules

A

Antibodies!

But a few kinds of bacteria produce capsules that are identical to host molecules, and the body will not produce antibodies against such capsules. This may be considered another mechanism of immune evasion.

23
Q

How capsules enable immune evasion

A

First, capsules are charged, making them difficult for phagocytes to engulf. Second, some capsules downregulate activation of complement, reducing opsonization of bacteria.

24
Q

mechanisms of horizontal gene transfer in bacteria

A

conjugation, transformation and transduction.

25
Q

“Competent” bacteria

A

Capable of taking up DNA via transformation

26
Q

Conjugation

A
27
Q

temperate phages

A

Can take one of two pathways of growth in bacteria:

Lysogenic growth

Lytic growth

28
Q

Types of transposable elements

A

insertion sequence: Carries only the genetic information necessary for its own reproduction

transposon: Carries additional extraneous information

29
Q

C. difficile

A

Clostridium are anaerobic spore-forming Gram-positive rods responsible for several unrelated diseases with various clinical manifestations. C. difficile is harbored in the large intestine of a small percentage of healthy humans, where it tends to remain in low numbers. Most commonly colonizes children <1 y.o. and residents of nursing homes. The mode of transmission is via the spore form.

30
Q

C. difficile-mediated disease

A

Exposure to antibiotics establishes susceptibility to C. difficile infection. The most common antimicrobial drugs associated with C. difficile diarrhea are cephalosporins, ampicillin, and clindamycin. During or after antibiotic administration, spores germinate and the C. difficile grows in large numbers, producing its toxins. • When toxin production achieves a critical level in the large bowel, illness begins.

Results in diarrhea, fever and abdominal pain. Severe cases result in “pseudomembranous colitis” in which dead white blood cells and debris form a whitish yellow pseudomembrane on the surface of the colon.

31
Q

C. difficile-derived toxins

A

The organism produces two toxins (toxin A and toxin B) in the intestinal lumen, and the toxins damage the epithelial lining of the bowel wall.

These toxins dysregulate the cytoskeletal structure of the intestinal epithelial cells, which results in the breakdown of tight junctions between epithelial cells and resulting loss of epithelial integrity. There is a strong host inflammatory response as well.

32
Q
A

Pseudomembranous Colitis

33
Q

Diagnosis of C. difficile infection

A

Detection of the toxin in stool is highly specific but insensitive for disease.

Polymerase chain reaction (PCR) is highly sensitive for detection of C. difficile disease but it cannot distinguish between colonization and disease.

Detection of a non-toxin protein produced by C. difficile, called glutamate dehydrogenase or GDH, is sometimes used as a screening test for C. difficile, but confirmation of toxin production is needed to make a firm diagnosis after screening.

34
Q

C. difficile infection treatment and prevention

A

Oral antibiotics (metronidazole or vancomycin) can be used to successfully treat the overgrowth of C. difficile in the intestine.

Prevention: The antibiotics most commonly associated with the disease should not be used on susceptible populations of patients (e.g., those in nursing homes) if other antibiotics are available. Proper education in the methods of transmission of the disease, hand hygiene and appropriate use of gloves and gowns can reduce the spread of the organism.

35
Q

What determines gram positivity vs negativity?

A

Thickness of peptidoglycan wall!

NOT the membrane!

36
Q

Penicillin vs Ampicillin

A

Ampicillin is just penicillin with an extra amide.

Ampicillin’s extra group gives it an extra charge and makes it appear more like a tripeptide, making it easier to be picked up by porins.