Brainscape's Knowledge GenomeTM

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


See full index

life protection > week 3 > Flashcards

week 3 Flashcards

1
Q

Define the terms: Normal flora; Opportunistic pathogen; pathogen; pathogenesis; virulence; colonisation and normal flora; asymptomatic carriage; infection.

A

pathogen- a bacterium, virus, or other microorganism that can cause disease.

pathogenesis- the origination and development of a disease

virulence- the severity

look the rest up if dont know

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

List the natural defence mechanisms of the host that protect against bacterial infection

A

macrophages, lymphocytes.
barriers, ciliary elevators, mucous membranes, hair etc.

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

List examples of bacterial virulence determinants: - e.g. adhesins, capsules, exotoxins

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

Describe the main stages of a bacterial infection from adherence, immune evasion, transmission to clearance

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

Describe the direct and indirect effects of bacterial infection that cause tissue damage

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

Explain mechanism of action of type 1 bacterial toxins and how this results in disease

A

act at cell membrane but not transported in.

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

Define Koch’s postulates

A

be present in every case of the infection
be cultured from cases in vitro
reproduce disease in an animal
be isolated from the infected animal.

bit out of date.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Explain their mechanism of action of type 2 bacterial toxins and how this results in disease

A

forms pores in the membrane or facilitates enzymatic disruption.

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

Explain their mechanism of action of type 3 toxins and how this results in disease

A

translocated into the cell.

e.g cholera causes ATP-cAMP–> GTP-> cGTP which opens Cl channels and electrolyte loss.

dysentery cleaves r28s from ribosome- prevents protein formation

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

Describe mechanisms of disease pathogenesis as a consequence of bacterial infections

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the role of acute inflammatory changes in disease pathogenesis as a consequence of bacterial infections

A

inflammation is the weapon of the host.
it accumulates phagocytes + white blood cells
can cause a pyogenic infection if met by certain bacteria - leukocidin from staphylococci

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

Identify the role of bacterial enzymes, bacterial exotoxins.
what secreted exotoxins?

A

exotoxins are secreted by bacteria
can enact enzymatic lysis/ pore formation/ inhibition of protein synthesis.

exotoxins are made by gram + and -.

endotoxins only made by gram -ve.

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

Describe the mechanism of disease in Toxic Shock Syndrome- SUPERANTIGENS

A

toxins produced by staphlococcus aureius and streptococcus pyogenes.

able to act simultaneously on MHC2 and T lymphocites.

causes IL-1,6, TNF-a, inteferon gamma.

results in approx 20-30% of all cells being recruited- very large amounts of inflammation generated.

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

Outline immunopathology as a consequence of infection including immune complex related disease, molecular mimicry, autoimmunity and infection.

A

type 3 hypersensitivity reaction-
immune complexes formed by interaction of antibody and antigen.

antibodies can cross react with host cell as they are simalar

e.g rheumatic fever group A carb on strep + structural glycoprotein on heart valve.

or M protein of strep and cardiac muscle

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

discuss the actions of endotoxins.

A

part of the cell wall of gram -ve bacteria

activate macophage/ monocite cells. they release IL-1,6,8 TNF-A
cytokines act variously- including liver, clotting cascade, endothelium

activate compliment via alternate path.

can trigger clotting cascade.

results in inc vasc permeability, hypotension, fever, disseminated intravascular coagulation, multiple organ failure.

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

discuss type IV hypersensitivity reactions

A

T helper cells bind to specific antigens - release cytokines (inc TNF-a- activates macrophages)

can cause tissue damage greater than the pathogen would.

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

Define the term antibiotic, and discuss their microbiological origins and natural functions

A

Antibiotic- natural product of fungi and bacteria, kill or inhibit other microorganism. aid in natural selection and selective advantage.

mostly derived from fermentation, and altered chemically by us to change properties.

18
Q

Describe the considerations for the choice of an antibiotic

A

spectrum of activity- broad vs narrow

bacteriocidal vs bacteriostatic (immune suppression etc)

route of administration

microbial antagonism

active dose vs toxic effect.

age/ renal capacity/ excretion

cost

clinical condition

19
Q

Explain the microbiological principles of the following terms: therapeutic index, selective toxicity, spectrum of activity.

A

therapeutic index- active dose vs toxic effects. avoid damage whilst doing rx, no safe drug.

selective toxicity- have effects on microbes but not on humans- i.g folic acid metabolism.

spectrum of activity- how many microorganisms that antibiotic is sensitive to

20
Q

Outline the main sites of action of antibiotics in the bacteria

A

focus on cell wall action

21
Q

Outline the components of the bacteria cell wall and describe their roles in antibiotic action

A

peptidoglycan found in gram +/-. much more in gram +ve.

penicillin prevent wall development.

22
Q

Outline the role of penicillin binding proteins (transpeptidases) in the synthesis of peptidoglycan and the action of penicillin’s and cephalosporins

A

both beta Lactam antibiotics.

PBP usually forms peptidoglycan dimers, which then form the wall.

betalactams bond to PBP and prevent wall maturation

23
Q
  1. Explain the microbiological principles and clinical relevance of the following terms: disc diffusion test; MIC; serum bactericidal test
A

disc diffusion test- diameter of zone of exclusion measured- categorised as resistant/ intermediate/ susceptible

minimum inhibitory concentration- exact concentration of antibiotic needed to inhibit growth. can guide treatment dose/ length.

24
Q
  1. Discuss why antibiotic blood levels sometimes need to be measured and how this might be accomplished
A

ensure has gotten concentrations higher than the minimum inhibitory concentration.
can guide more effective treatment strategies- spiking high can cause more effectivenss in some abs.

measure at the peak (1-2hrs post administration) and at the trough (immediately before next dose)

25
Q
  1. Distinguish between a bactericidal and a bacteriostatic antibiotic. Explain why both types of antibiotics are useful
A

bacteriocidal antibiotics- kill bacteria- used in serious infection.
bacteriostatic- cause a stasis of the bacteria. - relies on host mechanisms, not good in immuno suppressed.

26
Q
  1. Explain how to detect drug resistant bacteria
A

take sample of bacteria

expose to different types of drug, if continues to grow then resistant.

may take 16-20 hours

27
Q

Recognize the cardinal signs and symptoms of meningitis and meningococcal septicaemia, relating each to the underlying pathophysiological mechanisms

A

headache- swelling and possibly increased CSF

non-blanching rash- small bleeds around the skin

neck pain (arched back and extended neck posture)- inflamed meninges

dislike of lights- inflamed meninges

high temperature- sign of infection

reduced feeding in infants/ babies

floppy baby

Brudzinskis sign.

28
Q

Demonstrate an understanding of the importance of early intervention in a case of suspected bacterial meningitis

A

it can quickly cause sepsis and cause irreparable damage to the brain and spinal cord.

29
Q

List the tests performed on blood and CSF in a case of suspected meningitis

A

blood cultures
glucose csf
csf cell count- lymphocytes/ neutrophils etc.
csf pcr
csf fluid culture
csf gram stain

30
Q

Describe which tests are most useful in the immediate management of a suspected case of meningitis

A

blood cultures
lumber puncture- facilitate CSF cell count. CSF glucose testing
PCR amplification of cultures

swabs (throat, nasopharngeal, faeces) to detect for enteroviruses

31
Q

Name 4 bacteria that cause meningitis

A

Neisseria meningitidis
haemofolous influenzae type b
streptococcus pneumoniae

group B beta-haemolytic streptococcus

32
Q

Describe the changes in the CSF glucose, protein and white cell count in the cases of bacterial and viral meningitis

A
33
Q

Explain why and when antigen detection assays are useful

A

detects bacteria specific DNA - can then facilitate accurate antibiotic therapy.

can take a longer time than latex agglutination asseys

34
Q

Explain the value of serotyping of meningococci in terms of Public Health

A

can monitor the effectiveness of vaccine campaigns.
can monitor levels within the community and its spread.

35
Q

Give an example of each of the following mechanisms of drug resistance: Antibiotic inactivating enzymes, altered target, by-pass metabolic routes, altered transport of drug

A
36
Q

List 3 ways Gram negative bacteria may be penicillin resistant

A

alteration of porins
Beta lactamase
alternative forms/ mutations in efflux pumps
Penicillin binding protein mutates and so is no longer a fit for the molecule

37
Q

Discuss the role of bacterial plasmids in drug resistance

A

exchange of genetic material between bacteria (plasmids) can transfer the information for antibiotic resistance.

38
Q

Demonstrate recognition of the role of antibiotic misuse in the emergence of bacterial resistance

A

most resistance occurs in countries where use is heaviest.

resistance increases with use.

39
Q

Explain the concepts behind antibiotic treatment strategies to prevent bacterial drug resistance

A

stop feeding it routinely to animals
complete course of ABx + directly observed therapy in TB

combination therapy

infection prevention measures (ward, society, personal)

40
Q

Describe the history of methicillin resistant Staphylococcus aureus (MRSA)

A
41
Q

Explain why Gram positive and Gram negative bacteria have different sensitivities to antibiotics

A

different structures of the cell wall mean different binding sites and molecules available.

gram +ve membrane is highly porous and lets things in

gram -ve much more barrier resistance.

need different mechanisms to target the different physiologies.

life protection (5 decks)

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