Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Infection & Immunity > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What is the difference between bactericidal and bacteriostatic agents?

A

Bactericidal agents kill microorganisms rapidly, while bacteriostatic agents only inhibit their growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name three factors that limit the efficacy of antibiotics

A

The speed of action, the sensitivity of the target, and side effects of the antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why are antibiotics selective?

A

Targets are usually metabolites, and they are either impacted in bacteria at doses that do not impact humans, or the target does not exist in the host human cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are five ways that bacteria can become resistant to antibiotics?

A
  • synthesis of drug breakdown enzymes
  • chemical modification of the drug
  • modification of target site
    -prevention of access to target site by increasing export of the drug out of the cell
    -prevention of access to target site through uptake inhibition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does the B-lactam ring in B-lactam antibiotics do?

A

It penetrates the outer membrane of gram-negative bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the mechanism of action of penicillins? Name three aspects

A

It inhibits synthesis of the bacterial cell wall, it binds to penicillin binding proteins, and it is bactericidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which four steps are required for bacteridical action of B-lactam antibiotics?

A
  • association with the bacteria
  • penetration thorugh the outer membrane and periplasmic space in gram-negative bacteria
  • interaction with penicillin-binding proteins
  • activation of autolysin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does autolysin do?

A

It degrades the murein in bacterial cell walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does bacterial antibiotic synthesis lead to resistance?

A

In certain bacteria with drug addition, there is more synthesis of degrading enzymes, so the more drug is added, the more breakdown enzyme there is

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the mechanisms of resistance against penicillins (and other B-lactams antibiotics)? Name three

A
  • Alteration of penicillin binding proteins (PBPs) -production of B-lactamases by the bacteria (lyse the antibiotic)
    -decreases penetration or increased efflux of antibiotic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is antibiotic tolerance?

A

When there is inhibition of a bacterium but not killing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the difference between broad and narrow spectrum antibiotics? And what are limited spectrum antibiotics?

A

Broad spectrum antibiotics are against a wide range of bacteria, while narrow spectrum are only against certain types of bacteria, like gram-positive or gram-negative. Limited spectrum antibiotics only work against a single organism/disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What would you give with a B-lactam antibiotic to decrease resistance risk?

A

You would also give beta-lactamase inhibitors, to prevent the bacterium from killing the antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some adverse effects of penicillins?

A

Includes allergy, diarrhea, rashes, sodium overload, or seizure and renal dysfunction with high dose antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are four mechansims of action of antibiotics against bacteria?

A

Inhibit the synthesis of the bacterial cell wall, lysis of the cell membrane, inhibition of bacterial protein synthesis, affect bacterial metabolism and growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why is vancomycin an important antibiotic?

A

It is often used against gram-positive bacteria that are resistant, also for MRSA, And C. diff, and is often a last-resort antibiotic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name several side effects of vancomycin

A

-rash, renal toxicity, ototoxicity, leukopenia, red man’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the three outcomes of co-therapy with different antibiotics?

A
  • synergism, there is increased drug effectiveness
  • antagonism, the action of one is reduced by the other
  • indifference, there is no change in effectiveness of either drug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why is there a lack of new antibiotic discovery?

A

Because the time-frame of discovery is too long compared to the time-frame of antibiotic resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are four elements considered in choosing antibiotics?

A

Microbiological activity
concentration of bacteria at site of infection
how long bacteria remains at the site of infection
the Minimum Inhibitory Concentration (MIC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do tetracyclines work?

A

They inhibit the bacterial protein synthesis and are bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do sulfonamides work?

A

They inhibit folic acid synthesis and are bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are adverse effects of sulfonamides?

A

Hypersensitivity, hematologic and renal toxicity, photosensitivtiy, drug interactions, and hematopoeitic effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are adverse effects of tetracycline?

A

food drug interactions, GI irritiation, hepatic and renal toxicity, photosensitivity, discoloration of the teeth, and vertigo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are a few strategies for micro-organisms to survive in the body?

A

-finding a nutritional niche,
survive host defense
transfer to a new host
avoid being washed away

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Where are bacterial adhesins located in gram-negative bacteria? and gram-positive bacteria?

A

On the pili/fimbriae, surface proteins, and capsules on gramnegative, surface proteins a fibronectin and capsules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How can microorganisms avoid phagocytosis?

A

-inhibition of phagocyte recruitment and functioning
-microbial killing of phagocytes through exotoxins (leukocidins)
-avoiding NETS
-Escaping ingestion
- poor adherence of the phagocyte to the bacterium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How do microbes avoid complement?

A

-masking of surface components
-incorporation of body’s own materials to avoid complement activation
-binding of complement factors inhibiting the pathways
-hinder access to the target with long-chain smooth LPS to limit access of the MAC to the surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is opsonization?

A

Opsonization is the process of tagging a microbe with surface proteins for phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the four startegies of microbial survival inside phagocytes?

A

-inhibition of lysosome function with phagosomes
- escape into the cytoplasm
- resistance to lysosomal enzymes
- inhibition of the phagocytes’ oxidative pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How do superantigens work?

A

Superantigens lead to non-specific T-cell response, leading to lack of response and unleashing of a toxic cytokine cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the problem with adaptation through antigenic variation or antigenic coat changing?

A

Certain bacteria adapt their surface antigens or have variable surface glycoproteins, allowing evasion when a new antigenic type is on the surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the difference betwen antigenic drift and antigenic shift?

A

Antigenic drift is minor changes in the viral antigen and antigenic shifts are major antigenic changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Explain the concept of fabulation

A

Fabulation is when an organisms cleaves IgA, but the antigen-binding fragment (Fab) remains attached, precenting antigen access for other antibodies

35
Q

What is the difference between latency and chronic infection?

A

Latency is when a microbe avoids host cell response but remains in the body, while chronic infecion is when the microbe is actively infectious but at a low level

36
Q

What is ADCC and when is it used?

A

It is antibody dependent cellular cytotoxicity, which happens when an opsonized organisms is too large to be engulfed by a phagocyte. The antibody-coated target is killed by an Fc-receptor with leukocyte

37
Q

What are the steps of ADCC?

A
  • antibodies bind the antigens on the surface of target cells
  • NK cells CD16 Fc-receptors recognise cell-bound antibodies
  • there is cross-linking of CD16, which triggers degranulation into a lytic synapse
  • tumour cells die by apoptosis
38
Q

What are the microbial strategies before and after phagocytosis for immune system evasion?

A

Before: diversion, humiliation, paralysis, ‘playing hard to get’,
after: murder, indifference, disablement (of phagosome-lysosome) and escape

39
Q

Explain bacterial toxins and their domains

A

Bacterial toxins impact intracellular components and can be used to target the host cell
They have an A-domain and a B-domain. The A-domain is catalytic, with enzyme activity specific to the toxin,
the B-domain binds the cell memrbane and delivers the A-domain into the host cell

40
Q

How do the diphtheria, cholera, and botulinum and tetanus toxin act?

A

Diphtheria –> blocks host cell protein synthesis
Cholera –> elevates intracellular cAMP changing cellular function
Botulinum and tetanus –> target neuron-specific host proteins

41
Q

What is endotoxin and how does it work?

A

LPS on the outer membrane of gram-negative bacteria. It is a massive trigger of inflammation through fever, activation of complement, macrophages, and B-lymphocytes

42
Q

What is bacterial sepsis and its manifestations?

A

Bacterial spesis is an overwhelm of bacteria in the body, causing endotoxic shock, hypotension, and DIC.

43
Q

Endotoxin leads to activation of which four primary signals? What are they doing?

A

C5a from complement
TNF-alpha
IL-1
IL-6.
IL-1 and TNF-alpha lead to acute phase response,
C5a is from complement activation and leads to increase capillary permeability and release of lysosomal enzymes

44
Q

What type of reaction are superantigens associated with?

A

Toxic shock syndrome and cytokine storms are often from superantigens

45
Q

The S. aureus genome is built up of what?

A

A core genome and mobile genetic elements

46
Q

What is a plasmid?

A

Plasmid is small circular DNA in bacteria that can replicate independently

47
Q

What are the five types of plasmids?

A

F-plasmids -> set pili
resistance plasmids
col plasmids -> bacteriocins (kill other bacteria)
degradative plasmids –> digest unusual substance
virulence plasmids -> make bacterium pathogenic

48
Q

What are transposons?

A

Repetitive DNA sequences that have the capability to move on the genome, causing mutations or altered gene expression

49
Q

What are pathogenicity islands?

A

They are distinct genetic elements encoding virulence factors which are transferred through plasmids or transposons

50
Q

What are bacteriophages?

A

They are a virus whcih infects a bacterium, leading to bacterium killing.

51
Q

Name a few ways S. aureus evades the immune system

A
  • It secretes phenol-soluble modulins (PSM), which bind to formyl-receptor 2 (FPR2), which leads to neutrophil killing. The neutrophil secretes neutrophil serine proteases (NSPs) which will degrade the PSMs.
  • s. aureus secretes protein A (SpA) which protects from phagocytosis and inhibits complement activation
  • S. aureus secretes leukocidins such as PVL or HLgAB which promote NETosis and nucleases that degrade NET-DNA
52
Q

What are five routes of entry for respiratory infectious agents?

A
  • inhalation
    aspiration of upper airway contents
    spreading along the mucous membrane surface
    through the blood circulation
    direct penetration
53
Q

Why is epiglottitis such a serious infection?

A

With epiglottitis, the epiglottis is inflamed and becomes swollen, which obstructs the airway and impacts breathing negatively. It could cause suffocation if swelling is severe enough

54
Q

What is the most common strain causing epiglottitis in children?

A

Haemophilus influenza

55
Q

What is bronchititis and the main cause? What type of viruses or bacteria can cause bronchitis?

A

Bronchitis is inflammation of the bronchi, mostly caused by infection but can also be irrititants. Viruses include rhinovirus, coronaviruses, RSV, influenzas, adenoviruses.
Bacteria include m. pneumoniae, c. pneumoniae, and bordetella pertussis (pertussis causing, kinkhoest)

56
Q

Why is it called staphylococcus aureus?

A

It looks golden when cultured on a plate, or a golden grape-like cluster

57
Q

What determines whether staphylococci are pathogenic or not?

A

Possession of the enzyme coagulase. Coagulase positive are pathogenic, while coagulase negative are less invasive/non-pathogenic

58
Q

What is toxic shock syndrome? what is the main symptom causer?

A

When there is an overload of bacteria such as s. aureus (gram+) which causes a cytokine storm due to its superantigen(s). The symptoms come from TSST1, toxic shock syndrome toxin 1. It can be fatal.

59
Q

How is toxic shock syndrome treated?

A

Intensive care with fluids, ventilation, and renal therapy
removal of the source of infection/bacterial spread
antibiotics

60
Q

What causes scalded skin syndrome?

A

The toxin of a specific s. aureus strain, know as exfoliatin

61
Q

What are the three different types of hemolysis organisms?

A

alpha hemolysis organism: excretes hemolysins causing partial rbc breakdown (incomplete hemolysis)
beta hemolysis organism: excretes potent hemolysins, leading to complete hemolysis
gamma organism: do not hemolyse

62
Q

What are five types of diseases caused by S. pyogenes

A

strep throat, impetigo, erysipelas, cellulitis, invasisve strep A infections (necrotizing fasciitis, myositis, toxic shock-like syndrome)

63
Q

How is strep throat diagnosed? What is the preffered treatment?

A

There is usually slight fever with sore throat and pus in the back of the red throat
Diagnosis confirmation is with throat swab and culturing on blood agar. penicillin or erythromycin are preferred treatment

64
Q

What is scarlet fever?

A

A specific s. pyogenes infection with lysogenic activity against erythrogenic toxins, leading to a rash and a strawberry color tongue

65
Q

What is erysipales and how is it treated?

A

It is an acute infection and inflammation of the dermal layer of skin, leading to painful patches that enlarge and thicken. Treatment with penicillin or erythromycin

66
Q

Why treat strep infections when they are self-limiting?

A

To avoid post-strep complications like rheumatic fever and acute glomerulonephritis

67
Q

How do pneumococci spread and multiply?

A

pneumococci resist phagocytic clearance by expressing of a polysaccharide capsule

68
Q

What types of disease/damage can pneumococcal infection cause?

A

otitis media, sinusitis, chronic bronchitis, pneumonia, bacteremia, meningitis

69
Q

Why is it easy to diagnose bacteremia and meningitis from pneumococcal infection, but hard to diagnose pneumonia and otitis media?

A

Because for bacteremia and meningitis pneumococci can be measured in the blood or csf, while from the lungs or ears it is difficult to measure what bacteria have caused the problem as these areas are not sterile otherwise

70
Q

What are predisposing factors of pneumococcal pneumonia?

A

Age (the extremes), upper respiratory viral infection that has already caused damage, diabetes, alcoholism, and smoking

71
Q

What is the cause of streptococcal pneumonia?

A

the virulence factor capsular polysaccharide which protects against phagocytosis, and rapid growth of the bacteria in the alveolar spaces

72
Q

What are symptoms of strep. pneumonia and how is it diagnosed?

A

There is abrupt onset of chest pains, chills, and labored breathing. It is diagnosed with a chest x-ray to see if there is new infiltrate, and through bacterial culture and staining (although untelling because lungs are not sterile)

73
Q

What are the four phases of pneumonia?

A

Congestion: there is entry and contact with alveolar walls, causing increased blood flow and dilatation resulting in congestion
red hepatization: congestion leads to extravasation of rbcs and hemorrhage into alveoli, making the lung very red
grey hepatization: macrophages phagocytose the neutrophils, rbcs and inflammatory debris
resolution: alveolar exudate is removed, lung returns to normal

74
Q

What are some complications of pneumonia?

A

pulmonary fibrosis, lung abscess, empyema (pus in pleural space), ARDS, bacteremia, lung collapse

75
Q

What are treatment options for strep pneumonia?

A

penicillin, cefotaxime, oflaxacin

76
Q

What are the three systems of pneumonia classification?

A

By the cause (e.g. viral, bacterial, rickettsial)
by the place where infection took place (CAP, HAP, Ventilator associated pneumonia)
By site of pneumonia in the lung (lobar, interstitial, bronchal)

77
Q

What are common causes of CAP?

A

Strep pneumoniae
Haemophilus influenzae
Moraxella catarrhalis

78
Q

What is characterized as hospital-acquired pneumonia?

A

pneumonia arising after being admitted for >48 hours, or occuring <7 days after discharge from the hospital

79
Q

What are the common signs of croup?

A

Laryngotracheitits (inflammation of larynx and trachea) with sudden barking cough and difficult respiration

80
Q

What are symptoms of whooping cough? What is it caused by?

A

Whooping cough is caused by B. pertussis, very contagious, which leads to coughing

81
Q

What is the main difference between gram-negative bacteria and gram-positive bacteria?

A

Gram-negative have an outer membrane, while gram-positive bacteria have a thick murein wall layer

82
Q

What is SSSS?

A

Staphylococcal scalded skin syndrome, causes excessive sloughing of the skin by exfoliative toxins

83
Q

Why do pneumococci express autolysin?

A

It degrades their own cell wall, which contributes to the release of inflammatory mediators leading to immune response

Infection & Immunity (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions