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yr 1 uni work > 123 > Flashcards

123 Flashcards

1
Q

what are protozoa (protists) and worms (helminths)

A

parasites

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2
Q

symbiosis

A

interaction between 2 different organism living in close physical association

basically living together

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3
Q

mutualism

A

both organisms benefit
e.g bacteria in human colon

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4
Q

commensalism

A

1 organism benefits
the other neither benefits or harmed
e.g. staphylococcus

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5
Q

parasitism

A

1 organism benefits
the other is harmed
e.g. tb bacteria in human lung

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6
Q

4 stages of infectious disease- (symptoms appearance)

A

incubation
prodromal
illness
convalescence

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7
Q

incubation period

A

time between infection and the occurance of first symptoms or signs of disease

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8
Q

prodromal period

A

short time of generalised, mild symptoms not all infectious diseases have this stage

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9
Q

illness stage of infectious disease

A

most severe stage when symotoms are most evident and host immune system not yet fully responded

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10
Q

convalescence

A

body gradually returns to normal
variable time depending on pathogen and damage

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11
Q

severity of disease is dependent on a range of factors including:

A

dose of infection
age
sex
genetics
nutritional status
co-infection with other pathogens

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12
Q

stages of infectious disease

A

invasion
multiplication
spread
pathogenesis

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13
Q

ways of infectious disease invasion

A

inhalation
oral transmission
intra-uterine
sexual transmission
direct inoculation
direct skin contact

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14
Q

invasion stage definition

A

involves entry into the host and transmission from 1 host to another

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15
Q

multiplication of infectious disease definition

A

some pathogens can multiply within body whereas others can’t
protists can
helminths cant

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16
Q

protists multiplication

A

can cause disease after inoculation of only a few infectious stages as they can multiply within body.
disease severity dependent on how quick they multiply

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17
Q

helminths multiplication

A

most cant multiply
so disease severity dependent on number of infectious stages acquired by host over time

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18
Q

spread definition

A

the ability of the organism to move from the initial site of infection to infect other areas of the body
also movement between body systems
some also undergo developmental changes

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19
Q

pathogenesis

A

causation and development of clinical disease

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20
Q

what is pathogenesis influenced by

A
  1. number of pathogenic organisms present
  2. the virulence of the organism
  3. reaction of the host- degree of resistance
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21
Q

incidence

A

number of new cases of infection occurring in a population in a defined period of time

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22
Q

prevalence

A

total number of infected individuals in a population at a given point in time
e.g. number of old and new cases

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23
Q

mortality

A

total number of deaths from disease in a population in a defined period of time

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24
Q

leading causes of disease in USA in 1900

A

pneumonia
tb
diarrhoea and enteritis

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25
Q

leading causes of disease in USA in 1997

A

heart disease
cancer
stroke
lung disease

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26
Q

in HICs what % deaths are of people 70+

A

70%

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27
Q

in HICs what % of deaths are among people under 15

A

1%

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28
Q

in LICs what % of death are of people under 15

A

40%

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29
Q

in LICs what % of deaths are of people aged 70+

A

20%

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30
Q

what DALY

A

disability adjusted life year. the measure used to give an indication of overall burden of disease- measures life years lost due to premature mortality and equivalent years lost because of morbidity

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31
Q

how is DALY calculated

A

adding years of life lost to premature mortality + years lost to (lived with) disability
DALY= YLL + YLD

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32
Q

what comparisons does DALY allow

A

comparisons across range of health problems - quantitative basis for deciding health policies and evaluating cost-effectiveness of control programmes

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33
Q

what does DALY no considr

A

economic loss from disease
direct cost of treatment
social stigma associated with disease

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34
Q

skin as a mechanical barrier

A

top layer is dead cells making it dry preventing bacterial growth
sebaceous glands with fatty acids, lactic acids and low pH (3-5)

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35
Q

tight junctions as mechanical barriers

A

they stop ingested antigens passing into body

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36
Q

mechanical barriers for stopping pathogens

A

tight junctions
skin
mucosal surfaces

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37
Q

mucosal surfaces as a mechanical barrier

A

mucus is slippery
it also traps microorganisms which ae then shed from the body

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38
Q

physiological barriers for pathogen entry

A

low pH in stomach
outcompeting commensal microbiota
anti-microbial peptides (defensins)
lysozymes in tears
cytokines (interferons)
complement (MAC lyses bacteria)

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39
Q

immunis

A

if you recover you never get it again

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40
Q

who discouvered/defined vaccination

A

jenner in the 18th century

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41
Q

is adaptive immune response learned or inherent

A

learned

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42
Q

granulocytes

A

neutrophils
eosinophils
mast cells
basophils

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43
Q

phagocyte list

A

neutrophils
macrophages
dendritic cells

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44
Q

lymphocytes list

A

innate lymphoid cells (ILCs)
natural killer cells

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45
Q

neutrophil trap

A

extracellular traps
nets
can trap bacteria during appendicitis

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46
Q

4 signs of inflammation

A

heat (calor)
redness (rubor)
swelling (tumor)
pain (dolar)

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47
Q

local inflammatory response stages

A
  1. chemokine release
    2.clotting and complement cascade
    3.neutrophils secrete chemokines
  2. phagocytosis
  3. macrophages migrate into tissue and recruit lympocytes, monocytes and neutrophils
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48
Q

chemokine response in local inflammatory response

A

CXCL8/IL8 released from damage endothelial cells and TNF-a release from macrophages
help recruit neutrophils
allow migration from blood
histamines release from mast cells
vasodilation and increased blood vessel permeability

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49
Q

systemic acute-phase response

A

fever- speed up phagocytosis but is costly
leukocytes-WBCs production^
acute phase protein production in liver- CRP binds microbes, activates complement, aids phagocytosis. type 1 interferons, IL-6, CXCL8

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50
Q

how many proteins in complement system

A

about >35

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51
Q

where are most complement proteins made

A

in liver
some are from acute phase response stimulated by cytokines IL-6 and TNF-a

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52
Q

what stimulates acute phase response

A

by cytokines IL-6 and TNF-a

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53
Q

is complement system linked to innate or adaptive immunity

A

both
innate- phagocytosis
adaptive- antibodies

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54
Q

what is teh complement system

A

group of serum proteins in blood that perform defence against pathogens and especially extracellular bacteria

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55
Q

the 7functional catagories of complement system

A
  1. inhibitors- bind pathogens
  2. enzymes
    3.opsonins- ^ phagocytosis
    4.anaphylaxins- inflammation
    5.memebrane attach proteins- lyse pathogens
    6.complement receptors on phagocytes or neutrophils
  3. regulatory proteins- limit complement activation
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56
Q

how does innate immune system sense infection

A

detects molecules from pathogens - pathogen associated molecules patterns (PAMPS)

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57
Q

how does body sense infection

A

PAMPS
PRRs- pattern recognition receptors

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58
Q

phagocytosis - oxygen-dependent killing

A

oxidative burst
superoxide and other toxic oxidants are generated
acts as an anti-microbial

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59
Q

oxygen-independent killing

A

lysozyme- hydrolytic enzyme
defensins- peptides kill bacteria

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60
Q

why are parasites effective pathogens

A

evade innate immune response
hook to avoid flushing
vectors
burrow straight through skin
too big to be phagocytosed

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61
Q

is innate or adaptive specific

A

innate= non-specific
adaptive= specific

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62
Q

is innate lifelong

A

yes

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63
Q

is innate present in all animal species

A

yes

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64
Q

innate isn’t effective against a wide range of pathogens t/f

A

false
it is

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65
Q

is innate elements present at birth

A

yes

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66
Q

how longs the delay for adaptive effectiveness

A

delay of 5-6 days before effective response

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67
Q

is adaptive immunity gained

A

yes after exposure to foreign material not from birth

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68
Q

adaptive immunity memory

A

faster respinse to subsequent exposure to same pathogen

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69
Q

wheres adaptive immunity carried out

A

carried out by lymphatic system

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70
Q

adaptive immunity is only in vertebrates t/f

A

true

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71
Q

is adaptive immunity lifelong

A

once aquired its mostly lifelong

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72
Q

cells that make up innate system

A

innate lymphoid cells(ILCs)
natural killer cells
mast cells
eosinophils
neutrophils
macrophages
dendritic cells

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73
Q

cells that are part of adaptive immunity

A

lymphocytes
CD4+ t helper cells
CD8+ cytotoxic t cell
b cells
dendritic cells

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74
Q

lymphocyte diameter

A

6 micrometres

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75
Q

lymphocyte life span

A

3days-8weeks

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76
Q

what are lymphocytes activated by

A

antigen

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77
Q

where do t lymphocytes and b cells originate from

A

bone marrow
b cells then mature in bone marrow
t-cell then move to thymus and mature there

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78
Q

how do immune cells find pathogens and each pther

A
  1. interstitial fluid
  2. lymph flows through vessel
  3. within LNs
  4. lymphatic vessels return lymph to blood
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79
Q

where do lympocytes function

A

secondary lymphoid organs: lymph nodes
spleen

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80
Q

what do lymph nodes contain

A

b cells, macrophages, dendritic cells
antibody screting plasma b cells and macrophages in centre
lymph enters afferent end and exists efferent
lymph filter

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81
Q

wheres spleen

A

behind spleen

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82
Q

how long is spleen and what does it do

A

filters blood
12cm long

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83
Q

parts of the spleen

A

red pulp-remove dead RBCs
white pulp-b+T cells, macrophages
germinal centre- proliferating b lymphocytes

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84
Q

does lymph have a similar compositon to interstitial fluid

A

yes

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85
Q

antigen presenting cells (APC)

A

dendritic cells
macrophages
b cells

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86
Q

humoral immunity

A

adaptive
defend against pathogens and toxins in extracellular tissue
b cell/antibody mediated

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87
Q

cell mediated immunity

A

adaptive
cytotoxic t cell mediated
defend against infected cells. cancer cells and transplanted cells

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88
Q

whats an antigen

A

any foregin molecule which is specifically recognised by lymphocytes and elicits a response from them

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89
Q

epitopes

A

antigenic determinant

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90
Q

do b and t cells have receptors embedded in plasma membrane

A

yes

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91
Q

each b or t cell is specific for multiple antigen epitope t/f

A

false
specific for 1 antigen epitope

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92
Q

whats the antibody diversity possible

A

> 10^10

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93
Q

the b cell receptor is a membrane bound antibody t/f

A

true

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94
Q

all the antiboy subclasses

A

igM
igE
igA
IgD
IgG

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95
Q

igM

A

first ig to be formed after antigen exposure
pentameric
5 thingys on a circle

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96
Q

igE

A

allergic reactions

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97
Q

igA

A

in secretions
2 of them connected by j-chain

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98
Q

igD

A

membrane bound

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99
Q

igG

A

highest amounts

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100
Q

how do t cells develop

A

undergo 2 selecton processes, positive and negative
1. cell death fro cells that do not recognise self MHC
2. cell death for those that recognise self too strongly

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101
Q

how do t cells get activated

A

by recognition of antigen presented on MHC molecules
TCR on CD8 cell binds to MHC-1

TCR on CD4 cell binds to MHC-11 on antigen

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102
Q

what does MHC stand for

A

major histo-compatibility

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103
Q

what do APC do

A

phagocytes
migrate form infection to lymphoid tissues
display processed antigen naive helper t cells
important in triggering primary immune response

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104
Q

macrophages can present antigen but are less able to activate naïve t cells than DCs
t/f

A

true

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105
Q

b cells as APC

A

-B cells bind antigen via B cell receptor
-Receptor & antigen endocytosed
-B cells present antigens via MHC II to helper T cells with same epitope recognition
-Activated helper T cell secretes cytokines
-Cytokines activate B cell to produce memory B cells and plasma cells.

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106
Q

humoral immunity is… mediated

A

b cell mediated
antibody-antigen mediated
phagocytosis and complement-mediated killing

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107
Q

clonal selection

A

antigen-driven cloning of lymphocytes

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108
Q

all humoral immunity steps

A

Macrophage or dendritic cell phagocytoses pathogen

Antigen processed in macrophage or DC & presented on surface via MHC II

Specific helper T cell recognises processed antigen and binds (aided by CD4 binding to MHC II)

Helper T cell activated

B-cell phagocytoses BCR & antigen, presents antigen on MHC-II

Helper T cell recognises antigen presented by B cell

Cytokines from activated helper T cell fully activate B cell.

B cell activated to produce clones of plasma cells and memory B cells

Antibody production from plasma cells.

Elimination of pathogen.

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109
Q

how do antibodies mediate antigen elimination

A

b cell binds to antigen and differentiates
requires activation by t helper cell too

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110
Q

binding of antibodies to antigens inactivates antigens by

A

neutralisation-block binding sites= phagocytosis
agglutination- phagocytosis
precipitation of soluble antigens= phagocytosis
complement - cell lysis

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111
Q

3 pathways of complement activation

A

classical
lectin
alternative

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112
Q

whats teh antibody-activated complement pathway

A

classical

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113
Q

what does complement bind to

A

antigen-antibody complexes on cell surface

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114
Q

what does opsonisation enhance

A

phagocytosis

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115
Q

perforin

A

forms pores in target cell membrane

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116
Q

granzymes

A

initiates apoptosis in target cell

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117
Q

helper t cells trigger the humoral response and supply cytokines to CTL
t/f

A

true

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118
Q

not all nucleated cells express MHC-1 t/f

A

false
they all do express it

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119
Q

general symptoms of influenza virus

A

fever
cough
sore throat

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120
Q

structure of influenza A virion

A

mainly spherical
envelope
ssRNA-
replication in the nucleus
segmented genome (8)

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121
Q

haemagglutinin (HA)

A

binds sialic acid receptors –> viral entry
agglutinates RBCs
antigenic (neutralizing)

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122
Q

neuraminidase (NA)

A

cleaves sialic acid to release virus
degrades mucin
antigenic (non-neutralising)

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123
Q

matrix protein 2 (M2)

A

forms proton channel that facilitates uncoating and assembly
stabilizes the virus budding
antigenic (neutralising)
influenza A surface protein

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124
Q

the 3 influenza A surface proteins

A

haemagglutinin (HA)
neuraminidase (NA)
matrix protein 2 (M2)

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125
Q

the outer lipid envelope of infulenza

A

lipid bilayer from plasma membrane of infected host cell
supported by the M1 protein which plays a role in virion assemb;y

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126
Q

nucleocapsid of influenza A virus

A

each of the 8 different single strands of RNA + nucleoprotein (NP) + RNA polymerase (PB1, PB2, PA)

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127
Q

epidemic

A

rapid spread of infection in a city state or country over a short period of time

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128
Q

pandemic

A

an epidemic that spreads across boarders and worldwide, affecting large numbers

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129
Q

what level does influenza A causes

A

most capable of unleashing epidemics and pandemics

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130
Q

severest type of influenza

A

A
then b,c,d

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131
Q

what animals does influenza A infect

A

human
swine
horse
birds
bats
dogs

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132
Q

what animals oes influenza B infect

A

humans
seals

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133
Q

what animals does influenza c infect

A

HUMANS
SWINE
DOGS

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134
Q

what animals does influenza D infect

A

swine
cattle

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135
Q

serotypes of influenza

A

A, B, C, D
according to internal structure proteins (nucleocapsid and matrix)
-these proteins cant cross react

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136
Q

how are influenza subtypes names

A

2 surface glycoproteins
named by specfic HA and NA subtypes
18 HA types
11 NA types
198 different combos

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137
Q

what subtypes of influenza have caused human epi/pandemics

A

H1N1, H2N2, H3N2, H5N1, H7N8

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138
Q

the stages of influenza replication

A

attachment
uncoating
transcription
replication
assembly
budding

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139
Q

attachemnt step of influenza replication

A

HA-Sialic Acid on host cell – virus endocytosed; vesicle membrane and transferred to endosome

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140
Q

uncoating step of influenza replication

A

Endosome acidification - M2 increased H+ -> uncoating

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141
Q

transcription step of influenza replication

A

Nucleocapsid goes to the nucleus and transcribed mRNA are translated into proteins in cytoplasm

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142
Q

replication step of influenza replication

A

The vRNP (-s) converts to cRNP (+s), then trough replication generates vRNP (-s) -> cytoplasm

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143
Q

assembly and budding steps of influenza replication

A

Assembly: HA/NA transported to cell surface with M1 and genome segments

Budding: Virus buds off by NA

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144
Q

does haemagglutinin exist as a trimer in influenza virion

A

yes

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145
Q

the 2 sites on each monomer of HA

A

receptors binding site- host-specificity
cleavage site- single chains is cut to 2, at n-terminus it is fusion peptide which critical for infectivity

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146
Q

what do human viruses prefer to bind to

A

N-acetylneuraminic acid-a,2,6 linked glalactose

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147
Q

what do avian viruses prefer to bind to

A

N-acetylneuraminic acid-a2,3 linked galactose

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148
Q

why do we continue to have influenza epidemics/pandemic

A

antigenic drift- A,B,C types
antigenic shift- just A

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149
Q

antigenic drift- influenza virus

A

minor changes in antigenic sites of the HA and NA due to error prone replication and no proofreading
selective advantage- seasonal
influenza A,B,C

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150
Q

antigenic shift- influenza virus

A

major changes due to the reasortment of genes when 2 diff influenza infect same host
occurs due to segmented genome, wide host range
complete change of HA, NA or both
only in influenza A
usually need non-human intermediate

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151
Q

treatment of influenza - adamantanes

A

adamantanes and rimantadien are M2-ion channel inhibitors
block uncoating
influenza A only
CNS+ anticholinergic effect, teratogenic
M2 mutates alot so strains are developing resistance

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152
Q

treatment of influenza - neuraminidase inhibitors

A

oseltamivir and zanamavir
influenza A and B
well tolerated some vomit
effective within 48h onset
releif from symptoms 1-2 days
treatment or prophylaix (oseltamivir
oral or inhaled (zanamavir)

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153
Q

Influenza virus replicates in cytoplasm. (True/False)

A

false

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154
Q

Influenza virus is a positive sense single stranded RNA (+ssRNA) virus with non-segmented genome. (True/False)

A

false

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155
Q

Neuraminidase enables the influenza virus to attach to the host cell. (True/False)

A

false

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156
Q

The influenza RNA polymerase does not have proofreading activity. (True/False)

A

true

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157
Q

In the replication cycle of the influenza virus, the viral RNA is copied into DNA before integration into the genome of the host cell. (True/False)

A

fase

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158
Q

Influenza viruses cannot replicate in embryonated chicken eggs. (True/False)

A

false

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159
Q

what family is SARS-CoV-2 belong to

A

coronaviridae

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160
Q

MERS cases and deaths

A

2521 cases
866 total deaths

161
Q

is SARS-CoV-2 genome single or double stranded

162
Q

is SARS-CoV-2 genome segmented

A

no its non-segmented

163
Q

how long is SARS-CoV-2 geonome

A

around 30kb long genome

164
Q

how many genes does SARS-COV-2 encode fro

A

27 genes
which are either
structural-constitute the virion and include S,E,M,N
- non structural- not components of virion, include NSP1,NSP2,NSP3,NSP14
-accessory proteins- only in infected cells, include ORF3b, ORF6, ORF7a

165
Q

functions of S protien in corona virion

A

-entry of SARS-COV-2 into cells
-host tropism
- protective immune responses
- virulence- severity of disease

166
Q

functions of N protein in corona virion

A

-component of nucleocapsid
- virus transcription efficiency
- protective immune responses (vaccines)

167
Q

function of M protein in corona virion

A
  • most abundant amongst structural proteins
  • assembly of virus particle
168
Q

functions of E protein in corona virion

A

-smallest amongst all the structural protein
virus assembly and release

169
Q

what do mutations in the RBD of spike proteins determine

A

-new varients
-transmissibility
-virulence
-vaccine escape

170
Q

steps of SARS-COV-2 replication cycle

A

1.fusion
2. replication
3. assembly
4.release

171
Q

does delta or omicron varient of covid go deeper in the lungs

172
Q

what cells are found in local immunity in lungs nose etc in adaptive immunity against covid

A

CD8 t cells, CD4 t cells, IgG, IgA

173
Q

transmission of SARS-COV-2

A

dropplets
aerosoles
smear infection

174
Q

what does monoclonal antibody/convalescent plasma for ace-2 prevent (covid treatment)

A

prevent the virus into the host cell

175
Q

how does camostat mesylate prevent covid

A

prevent SARS-COV-2 into the cell by acting on TMPRSS2

176
Q

lopinavir-ritonavir (HIV) as a covid treatment strategy

A

inhibition of protease activity of SARS-COV-2

177
Q

ribavirin (HCV) as a covid treatment strategie

A

may inhibit mRNA capping

178
Q

RNA synthesis inhibitors as covid treatmetn strategies

A

inhibits SARS-COV-2 RNA synthesis and replication

179
Q

chloroquine group as a covid treatment strategy

A

interfere with the release of progeny from infected host cells

180
Q

what shape is yersinia pestis

A

rod-shaped

181
Q

are yersinia pestis gram - or +

A

gram negative

182
Q

yersinia pestis are not facultative anaerobes t/f

183
Q

the 2 main habitats of Y. pestis

A

flea gut
blood/tissue of a mammalian host

184
Q

how many species of insects have been found to be infected with y. pestis

185
Q

physical mechanisms accoutning for difference in plague vector efficiency

A

insect immunity
pathogen must evade digestive enzymes
frequency of feeding/defecation
pathogen must not kill vector too quick

186
Q

does Y. pestis adhere to/ invade the midgut epithelium

A

no so suceptable to elimination in flea feaces

187
Q

how does y. pestis stay in flea

A

forms large multicellular aggregates too big to excrete
also biofilm creates blockage in the proventriculus (a valve connecting oesophagus and midgut - it grows and stops blood flow to midgut

188
Q

what is about y. pestis that causes the most harm

A

the toxins produced - lead to endothelial damage and necrosis leading to vascular destruction and local haemorrhaging

189
Q

neutrophils in y. pestis

A

early stage- accumulation of neutrophils
however as Yp is surrounded by the F1 capsule protein, phagocytosis by neutrophils is prevented.
later Yp injects effector proteins into neutrophils killing/disabling them

190
Q

can macrophages kill y. pestis

A

no
they can phagocytose them but not kill
the bacterial toxins can destroy macrophages and other phagocytic cells

191
Q

is y. pestis an extracellular protein

192
Q

why do lesions occur in y. pestis

A

from destruction of tissue and effects of endotoxins- peripheral vascular collapse and disseminated intravascular coagulation (DIC)

193
Q

the 3 major plague pandemic

A

541- the justinianic plague
1347- black death
1894- modern plague

194
Q

between 210-2015 how many cases of the plague were there

A

3248 cases
584 deaths

195
Q

why is plague a concern for biological weapon

A

widespread availabilty
mass production and aerosol dissemination
high fatality rate
rapid secondary spread

196
Q

incubation period of the plague

A

2-4 days but can be as long as 10 days

197
Q

symptoms of the plague

A

flu like- fever, chill, aches, weakness, vomiting/nausea

198
Q

the 3 forms of plague

A

bubonic
septicemic
pneumonic

199
Q

the most common form of the plague

200
Q

how does the bubonic plague spread in body

A

multiply and enter in skin then spread via the lymphatic system to lymph nodes

201
Q

advanced stages of bubonic plague

A

buboes may suppurate- burst to form open sores

202
Q

mortality rate of bubonic plague if untreated

A

50-60% - but if infected person recovers they are immune

203
Q

whats septicaemia

A

blood poisening when plague infection spreads to bloodstream

204
Q

can bubonic plague develop into secondary septicaemic plague

205
Q

can septicaemic plague be primary

A

yes - can be from flea bite or direct contact with infective material

206
Q

DIC

A

systemic activation of blood coagulation leads to gangrene of the extremities and multi-organ failure

207
Q

mortality of septicaemic plague

A

100% if left untreated

208
Q

whats the least common type of plague

A

pneumonic plague

209
Q

whats the most virulent form of the disease

210
Q

what happens in lungs of pneumonic plague

A

acute pulmonary insufficiency, sepsis, toxic shock

211
Q

case-fatality of pneumonic plague

212
Q

how is pneumonic plague spread

A

cough droplets
diect and close contact

213
Q

where can specimens be obtained for diagnosis of the plague

A

lymph nodes
blood if septicaemic
sputum- pneumonic
bronchial/tracheal washin- not ideal as they contain other bacteria
PCR
radiology used for progresson not diagnosis

214
Q

if caught early- treatment for the plague

A

antiobiotics in large doses- streptomycin, tetracycline, chloramphenicol
for 10-14 days
supportive therapy- rehydration and blood pressure maintanence

215
Q

how quick can pneumonic plague kill

216
Q

prevention/ control methods of the plague

A

quarantine
vaccines- formaldehyde inactivated whole-cells and only partial protection
avoid direct contact
rodent control
education

217
Q

how many species on yersinia genus

218
Q

yersinia pseudotuberculosis

A

mild
self-limiting disease
transmitted by faecal-oral route

219
Q

did y.pestis diverge from y. pseudotuberculosis

A

yes within the last 10000 years

220
Q

transmission of Yersinia pestis by fleas is - dependent on both gene acquisition and loss of function mutations
t/f

221
Q

what protein does yersinia murine toxin gene encode for

A

phospholipase D whcih protects y. pestis within the flea gut

222
Q

The ymtgene was acquired through horizontal gene transfer - enabled a bacterium previously found in the gut touse an arthropod vector (survives insect gut)
t/f

223
Q

can y. pseudotuberculosis form a biofilm in some environments t/f

A

yes
but not within fleas

224
Q

Homologues of >100Y. pseudotuberculosisgenes are present as non-functional pseudogenes in Y. pestis
t/f

A

false
its 200

225
Q

rcsA is functional inY. pseudotuberculosisbut not inY. pestis
t/f

226
Q

whats the breeding ground for mosquito

227
Q

what causes malaria

A

a protozoan parasite- genus plasmodium

228
Q

chance of gettin maaleria

A

> 1/1000
1 billion at high risk

229
Q

in 2015 how many cases and deaths of malaria

A

211 milllion cases
429 000 deaths

230
Q

where do most malaria deths occur

A

african region
90% all deaths occur here

231
Q

malaria is not a acute febrile illness t/f

A

false it is
shows signs of fever

232
Q

malaria is a periodic fever caused by erythrocyte destruction t/f

233
Q

are types of malaira defined by the periodicity of fever

234
Q

is malaira transmitted by male or female mosquitoes

A

female anopheles mosquito

235
Q

where can anopheles mosquitos survive

A

latitudes 60 N and 40 S
below 2000 metres

236
Q

how can malaria be transmitted

A

introduced - biting local
airport-acquire malaria without travelling
transfusion- blood
mainline- needles
congenital- pregnancy to baby

237
Q

sporozoites

A

into skin by mosquito
circulate in blood for 30mins
penetrate hepatocytes
undergoes schizogony(asexual reproduction)
forms 30 000-40 000 merozoites

238
Q

sprozoites to merozoites

A

sporozoites invade liver cells and nucleus divides to form a schizont
the schizont ruptures and releases merozoites which infect RBCs

239
Q

merozoites

A

apical organelles which contain proteins for parasite invasion
must invade RBCs
multiple asexually
disease causing stage

240
Q

trophozoite

A

single-celled nucleated mass of protoplasm
high metabolic active
ingest haemoglobin- brake down to haemozoin which accumulates in food vacuole
plasmodium also modifies RBCs membrane to take up nutrients
divide to give merozoites

241
Q

gametocyte

A

After several erythrocyte cycles some trophozoites develop to gametocytes
4 days to mature
nothing happens to these unless they are taken up by a mozquito

242
Q

zygote- malaria

A

when mosquito drink the male and female gametocytes burst out of RBC
male produces 8 microgametes which fuse with female macrogamete to form zygote
diploid stage

243
Q

ookinete

A

5-10hr the zygote differentiates to cigar shaped invasive ookinete
motile penetrates intestinal wall of mosquito
differentiates to oocyst attached to mosquito midgut

244
Q

oocyst

A

grow rapid and divide into sporozoites
longest phase- 8-35d
temp dependent - high temp=fast mature

245
Q

how many sporozoites are produced from 1 oocyst

246
Q

what happens when oocyst bursts

A

sporozoites release into body cavity of mosquito
migrate to salivary ducts
mosquito then bites host and injects sporozoite saliva

247
Q

what do toxins release when schzonts burst stimulate

A

t cells to produce cytokines like TNFa which mediate fever bone marrow depression and erythrophagocytosis

248
Q

can you get anaemia from malaria

A

yes loss of RBCs due to parasite growth, depression of erythrpoiesis and erythrophagocytosis lead to anaemia

249
Q

can clotting defects occur in malaria

250
Q

clinical features of malaria

A

periodic fever
anaemia
acute respiratory distress
hypoglycaemia(low sugar)
hepatomegaly/splenomegaly (big liver/spleen)
haemoglobinaemia
haemoglobinuria
capillary blocakge

251
Q

haemoglobinaemia

A

haemaglobing in blood plasma

252
Q

haemoglobinurea

A

haemoglobin in the urine (blackwater fever)

253
Q

iRBC

A

infected red blood cell protein on surface cause cytoadhesion of rbc to endothelial cells

254
Q

diagnosis of p. falciparum

A

blood smear- giesma stain
rapid diagnostic test- finger prick
nucleic acid amplification-based diagnostic- sensitive detection of low density malaria infections

255
Q

chemotherapy for malaria treatment

A

quinine - orginaly bark
was replaced with chloroquine as its safer, more effective, easier to make and fewer side effects
replaced after WW11

256
Q

Intracellular parasite (trophozoite stage) digests haemoglobin - generates free haem which is toxic
t/f

257
Q

Digestion takes place inside Plasmodium food vacuole – contains lipid bodies that take up haem which is polymerised into a black non-toxic pigment (haemozoin)
Digestion takes place inside Plasmodium food vacuole – contains lipid bodies that take up haem which is polymerised into a black non-toxic pigment (haemozoin)
t/f

258
Q

Chloroquine (CQ) is a strong base, uncharged at neutral pH but carries a positive charge at acidic pH
t/f

A

false its a weak base

259
Q

charged CQ diffuses through parasite plasma membrane and food vacuole (FV) membrane
t/f

A

false its uncharged chloroquine

260
Q

Food vacuole (FV) is acidified – so chloroquine becomes charged and concentrates up to several 1000-fold within the FV
t/f

261
Q

how does chloroquine kill parasite

A

positive charge at acidic pH
uncharged CQ goes through plasma membrane and food vacuole membrane of the parasite
becomes charged
interferes with haemozoin formation and haem remains which is highly toxic so kills parasite

262
Q

why is chloroquine being resisted

A

exposure of parasites to sub-therapeutic dose of drug
sharing drug or not completing course
parasites aren’t killed and have opportunity to become resistant

263
Q

body plan of a neamtode

A

alimentary canal extends from mouth at anterior to anus at posterior

264
Q

preadaptation

A

an adaptation that serves a different purpose from the one for which it evolved
parasitic nematodes exhibit this

265
Q

how is nematodes biochem/physiology adapted

A

survive lots of conditions including both anaerobic and aerobic
eat wide range of food
tough outer cuticle to withstand envi insults

266
Q

are there always 4 larval stages and 2 moults

A

no there are 4 moults not 2

267
Q

do nematodes undergo asexual reproduction

268
Q

how mant times has parasitism arisen in nematodes

269
Q

what % of world population harbour at least 1 GI nematode

270
Q

is the intensity or prevalence important in nematode infections

271
Q

what does overdispersed distribution of nematodes mean

A

> 70% of worms are found in <15% of hosts

272
Q

why do soil transmitted helminths (STHs) like the GI

A

acces to host easy through ingestion
nutrients in gut
transmission ensured by ease of exit to world
GI nematodes are commonest but not most pathogenic

273
Q

reasons fro high prevalence of STH infections

A

widespread distribution of nematodes
resilience of eggs to harsh environment
lots of eggs per parasite
poor socioeconomic conditions
lack of education

274
Q

ascariasis

A

Ascaris lumbricoides
STH
thick shell eggs
egg production 2 moths post-infection
eggs shed in unembryonated state and embryonate in warm moist soil
time form ingestion to larval migration=10-14 days
lay 200 000 eggs/d

275
Q

how long can ascariasis worms get

A

males- 10-30cm
females-20-35cm

276
Q

where do adult ascariasis worms live

A

in small intestines

277
Q

what happens when ascariasis eggs are swallowed

A

hatch
invade intestinal mucosa
carried via portal then systemic circulation to lungs
mature in lungs then penetrate alveolar walls to throat and are swallowd
develop to big worms in SI

278
Q

how long can adult worms live - ascariasis

279
Q

what % of ascariasis infections are asymptomatic

280
Q

how do ascariasis cause pathology

A

with ingestion and migration of larvae- haemorrhagic pneumonia, asthema due to allergins
adult parasites in intestine
wandering adults outside intestine

281
Q

adult worms in the intestine problems - ascaraisis

A

abdominal discomfort
nausea
malnutrition
intestinal blockage
85% of obstructions occur in children

282
Q

wandering adults worms outside intestine- ascariasis

A

enter other organs
bile duct- jaundice, fat metabolism interfered
break through appendix or intestine wall- fatal peritonitis
vomited up or come through nose
suffocation if in trachea

283
Q

diagnosis of ascariasis

A

coprological-eggs in poo
serological-antigens/bodies
molecular- PCR of parasite DNA from eggs in poo
image based diagnostics

284
Q

image based diagnostics in ascariasis

A

after barium meal reveals worms as elongated filling defects
high ultrasound shows the worms

285
Q

what is filariasis caused by

A

an infection with Wuchereria bancrofti
infection with nematodes of the family filarioidea

286
Q

3 types of filariasis

A

lymphatic- lymphatic system
subcutaneous- skin layer
serous cavity- peritoneal, pleural or pericardial cavity

287
Q

how are filarial worms transmitted

A

mosquitoes and black flys

288
Q

how is wuchereria bancrofti transmitted

A

by a mosquito bite and causes elephantiasis

289
Q

how long are elephantiasis worms

A

females- 80-100mm
males- 40mm

290
Q

wuchereria bancrofti life cycle

A

filarial larvae go into bite wound
develop into adults that reside in lymphatics
a mosquito ingests the microfilariae when eating
loose sheaths and go to mosquitos thoracic muscles
develop to third stage larvae and go to prosboscis to infect another human after bitng

291
Q

clinical presentations of wuchereria bancrofti

A

most asymptomatic
lymphoedema- swelling from fluid collection in arms and legs breasts and genitalia
difficult to fight infection
bacterial infection causes hardening of skin- elephantiasis
tropical pulmonary eosinophilia syndrome-cough, wheezing

292
Q

consequences of lymphatic elephantiasis

A

social stigma and bad mental health
loss of income earning opportunties
increased medical expenses for patients
isolation
poverty

293
Q

preventiaon of lymphatic filariasis

A

avoid mosquito bites
nets
long sleeves
repellent
mass drug treatment of entire communities

294
Q

mebendazole- ascaris treatment

A

binds to b-tubulin and inhibits microtubule assembly
impaired glucose uptake
reduced energy production
good for GI but not tissue nematodes as poorly absorbed from gut

295
Q

ivermectin

A

binds with glutamate-gated chloride channels in invertebrate nerve and muscle cells
causes increased cell membrane permeability to cl- ad hyperpolarisation of nerve/muscle cell
results in paralysis and death

296
Q

what shape are cestodes

A

dorso-ventrally flattened ribbon like bodies
can be very long

297
Q

scolex

A

anterior attachment organ on cestode
posses either hooks + suckers or only suckers to attach host tissue

298
Q

strobila

A

the segmented part of the body of a tapeworm that consists of a long chain of proglottids
on cestodes
can grow 15-30cm/d

299
Q

does cestodes have a gut

A

no as theres a degeneration of non-essential systems like sensory systems, muscles and locomotory systems

300
Q

whats the body wall of the cestode called

A

the tegument

301
Q

the body wall (tegument) of cestodes

A

metabolically active layer through which nutrients are absorbed and secretions and waste materials exported

302
Q

proglottids

A

grow continuously from neck and new ones replace old

303
Q

scolex of t. solium - pork tapeworm

A

4 large suckers and rostellum containing double row of hooks

304
Q

scolex of t. saginata - beef tapeworm

A

4 large suckers
no rostellum and restellar hooks

305
Q

are proglottids monoecious

A

yes they contain both male and female sex organs

306
Q

Fertilisation can’t occur between
proglottids of the same or a different
tapeworm
t/f

A

false it can occur

307
Q

what happens after proglottids are fertilised

A

fill with
eggs and gravid proglottids break off
the chain and pass out in faeces
OR can crawl ‘caterpillar-like” through
the anal sphincter

308
Q

how do cestodes absorb nutrients

A

from the host intestine directly through tegument
not passive
tegument has microvillus to increase SA

309
Q

whats teh functional units of cestodes

A

protonephridium

310
Q

excretion in cestodes

A

cilia generate current- excess water with nitrogenous waste forced into tubules and out of worm via excretory pores

311
Q

how do tapeworms get into intermediate host

A

larval stage oncosphere penetrates through gut wall through mucosa of duodenum and tehn goes into blood and encysts within tissues
embryophore (thick membrane) forms structure around oncosphere
called cysticerus

312
Q

cysticercus

A

when an embryophore(thick memebrane or wall) forms around oncosphere

313
Q

cysticerci

A

measly prok/beef infective within 7-10weeks and remains viable for several months
when eaten attaches to intestine wall and develops into adult tapeworm

314
Q

inspection of meat with cysticerci

A

if only a few detected meat frozen for 20 days then safe
can withstand freezing for 70 days
if big infection carcass is destroyed

315
Q

where is taenia saginata geogrpahical distribution

A

worldwide
common in africa east europe, phillipines, latin america. not in india as hindus dont eat beef

316
Q

taenia solium distribution

A

most prevelent where humans live in areas of close contact with pigs and eat undercooked pork
rare in muslim countries

317
Q

sympotms of tape worm

A

rare intestinal/appendix blockage
penetrate gut wall
psychological distress
abdominal pain
nausea
weight loss

318
Q

how long can adult tapeworms live

A

several years

319
Q

how are humans infected with eggs in t. solium

A

with eggs ingested by contaminated with faeces or autoinfection
=can ingest eggs through faecal contamination from proglottids being carried back into the stomach by reverse peristalsis

320
Q

are cysticercosis acquired by eating undercooked pork

A

no
by ingesting solium eggs excreted in human faeces

321
Q

how many people does cysticercosis affect worldwide

A

50 million

322
Q

pathogenesis of cysticercisis

A

muscles- lump under skin
eyes- rare but can caused disturbed vision or detached retina
neurocysticercosis

323
Q

neurocysticerosis

A

seizures and headaches causing confusion balance problems and brain swelling
leading cause of acquired epilepsy in developing world

324
Q

treatment of neurocysticercosis

A

depends on number and stage of infection
mangement of symptoms
praziquantel- kills viable cysts

325
Q

echinococcus granulosus

A

dog tape worm

326
Q

are humans definitive or intermediate hosts of echinococcus granulosus

A

intermediate hosts

327
Q

how long are adult dog tapeworm

328
Q

how large are hydatid cysts

A

1-20cm long

329
Q

germinal layer of hydatid cysts

A

(20µm thick) is a living, syncytial tissue, within which developing (D) and mature brood capsules (MBC) form (<1mm); these produce protoscoleces (P, 100µm), (equivalent to cysitcerci).

330
Q

protoscoleces of hydatid cysts

A

can either be retained in brood capsules or burst out into cyst fluid (CF) – each protoscolex has potential to differentiate into another hydatid cyst

331
Q

laminated layer in hydatid cyst

A

is a thick (several mm), non-living, carbohydrate-rich matrix, secreted by the GL.

332
Q

where do most of hydatid cysts develop

A

95% develop in lungs or liver but can form in brain

333
Q

diagnosis of dog tapeworm

A

CT
MRI
usually seen in autopsy or surgery as is normally asympotmatic

334
Q

treatmetn of dog tape worm

A

PAIR- puncture, aspiration, injection, re-aspiration
surgery
drug treatment- albendazole
watch and wait

335
Q

are schistosomes nematodes, cestodes or trematodes

A

trematodes

336
Q

how many countries are endemic to trematodes and how many people infected

A

> 70 countrys
200 million infected

337
Q

schistosomiasis is classified as neglected tropical disease
t/f

338
Q

where do 85% of schistosomiasis cases occur

339
Q

the 3 major factors responsible for maintaining schistosome transmission

A
  1. pollution of water with excreta containg eggs
  2. preseence of suitable snail hosts
  3. human contact with water infected with cercariae
340
Q

life cycle of schistiomiasis

A
  1. break barrier
  2. migrate in circulation
  3. mature
  4. pair up
  5. find a home
  6. reproduce (lay eggs)
341
Q

cercariae in s. mansoni

A

photo-tropic
shed intermediate snail
survive 12-48h
attach to skin and use proteases to break through the epidermis
use forked tail to swim
use water turbulence and skin derived fatty acids to locate human host

342
Q

when carcariae shed their tails what do they become

A

schistosomula

343
Q

where do schistosomula migrate

A

from skin to liver via lungs in the vasculature and lymphatics

344
Q

where do schistosomula matuer into adult worms

A

in the liver

345
Q

adult trematode worms pairing up

A

females live within the males gynaecophoric canal
live about 5 yrs
live in venous system
are dioecious and sexually dimorphic

346
Q

how many eggs do paired female trematode worms release per day

A

300-3000 /day

347
Q

life cycle of trematode in snail host

A

hatch becoming motile
infect snail
non-motile
copies
release cercariae
infect human host

348
Q

miracidia

A

eggs release miracidia
ciliated larval stage
free living and motile
infective for 6-8hrs
locate snails using light and sail derived chemicals

349
Q

sporocysts

A

inside snail tissue miracidium turn into non-motile sporocyst
produce cercariae
cercariae from snails infect human host

350
Q

cercarial dermatitis from schistosomiasis

A

cercariae burrrowing through the skin causing reaction
secondary exposure to infection
15 mins after exposure
develop for 2-3 days
resolves within 5 days

351
Q

parasite maturation of schistosomiasis

A

katayama syndrome
2- weeks after infection
usually mild
cough
hepatosplenomegaly
pyrexia- fever
weight loss
giant urticaria- hives

352
Q

s. haematobium symptoms

A

haematuria - blood in urine
dysuria- painful urination
abdominal pain
bladder inflammation

353
Q

is human schistosomiasis a immunopathological disease

354
Q

granuloma formation

A

concentric layers of cells forming distinct lesion
a response to antigens released by egg/miracidium
immune cells accumulating around egg(miracidia)
the granuloma protects the host from effects of toxins released by dying miracidia

355
Q

fibrosis

A

egg-induced granulomas transformed into permanent fibrous lesion by deposits of fibrous tissue around egg
can cause portal vein branches to resemble sections of clay pipe stems blocking it and development of anastomoses

356
Q

hepatosplenic disease

A

hepatosplenomegaly
portal hypertension - pressure in vein connecting intestines and live due to cirrhosis and ascites(fluid in abdominal cavity)

357
Q

epidemiology of schistosomiasis

A

infection rises throughout childhood
peaks in older children/young adults at low transmission rates
declines into older ages

358
Q

diagnosis of schistosomiasis

A

eggs in stool/urine
worm antigen CCA in urine
ultrasound
bladder/rectal biopsy
serological testing

359
Q

prazaquantil trematodes

A

single oral dose
well absorbed from GI tract
few side effects
few contra-indications
increasing reports of resistance

360
Q

is reinenfection common after chemotherapy- trematodes

A

yes very common as there is a snail host Prescence
chemotherapy dosnt always kill adults just suppress eggs production

361
Q

schistosomiasis prevention

A

no vaccine
no drugs to prevent
avoid swimming in endemic countrys
drink ;safe; water

362
Q

principle of immunisation

A

vaccines contain antigens found on pathogens causing disease but exposure to the antigens in a vaccines does not cause disease

363
Q

vaccination vs immunisation

A

vaccination refers to getting the injection
immunisation means receiving a vaccine and becoming immune disease as a result of the vaccine

364
Q

how do vaccines work

A

induce active immunity
immunological memory

365
Q

requirments for good vaccine

A

doesnt cause disease
safe
stability- easy storage
cost
administration ease
long term protection
interrupt spread of infection

366
Q

types of vaccines

A

live
inactivated
subunit
passive immunotherapy

367
Q

live vaccines

A

whole pathogen for which virulence has been artificially reduced = attenuation

368
Q

inactivated vaccines

A

whole ‘killed’ organisms

369
Q

subunit vaccines

A

certain components of pathogens can be purified usually with recombinant DNA tech
- toxoid
- surface protein
viral vector
DNA and RNA

370
Q

what age group does polio afect mainly

371
Q

in polio how many cases result in paralysis

372
Q

since 1988 polio cases decreased by how much

373
Q

the 3 countrys that were still polio endemic in 2017

A

afghanistan
nigeria
pakistan

374
Q

3 serotypes of poliovirus

A

type 1- brunhilde
type 11- lansing
type 111- leon

375
Q

live attenuated oral vaccine (OPV or sabin)

A

Live attenuated polio vaccine originally produced by allowing polio virus to grow in non-optimal conditions and selecting randomly occurring mutants that had lost neuro-virulence

376
Q

advantages of live attenuated vaccine

A

inexpensive
easily administered
induces systemic and mucosal immunity
probably lifelong
short term shedding in faeces can result in passive immunisation of people in close contact

377
Q

disadvantages of live attenuated vaccine for polio

A

may give subclinical or mild form of infection
cant be given to immunosuppressed or pregnant
may revert back to virulent form

378
Q

killed organisms inactivated polio vaccine (Salk)

A

3 serotypes
cant cause circulating vaccine derived polio virus
antibodies-prevent polio to CNS
SUBCUTANEOUS INJECTION

379
Q

Advantages of inactive vaccines

A

cannot cause infection
can be given to immunosuppressed and pregnant people

380
Q

disadvantages of inactive vaccines

A

less immunogenic and requires addition of adjuvants and booster doses

381
Q

role of an adjuvant

A

enhance immune response to the antigens included in the vaccine
to carry vaccine antigen and slow its release
to provoke a local inflamm response
e.g. aluminium hydroxide

382
Q

what bacteria is tetanus caused by

A

clostridium tetani
produces a neurotoxin when it grows in anaerobic conditions

383
Q

tetanus symptoms

A

muscle spasms
lock jaw
seizures
eventually death

384
Q

example of a toxoid vaccine

A

tetanus vaccine

385
Q

example of a surface protein vaccine

A

hepatitis B virus vaccine

386
Q

what surface protein is used in hep B vaccine

A

HBsAg - produced using recombinant DNA
used to be dont by purifying blood of carrier which was unsafe and expensive

387
Q

example of a viral vectory vaccine

A

astrazeneca/oxford SARS-CoV-2 vaccine

388
Q

what do you inject in DNA vaccines

A

nucleic acids encoding antigens

389
Q

concerns around DNA vaccines

A

possible genomic incorporation of immunising DNA might activate oncogenes
doesn happen in RNA vaccines

390
Q

what were the first mRNA vaccines to be deployed for mass immunisation of human

A

moderna and pfizer covid19 vaccines

391
Q

do mRNA vaccines encode full length or the receptor binding domain of the SARS-CoV-2 viral spike protein
t/f

392
Q

is RNA or DNA more labile in vaccines

A

RNA so care must be taken for long term storage

393
Q

primary failure of vaccines

A

fails to make an adequate immune response to vaccine so infection still possible anytime

394
Q

secondary failure for vaccines

A

makes adequate immune response initially but immunity wanes overtime
most inactivated vaccines ae like this so booster needed

395
Q

why is there no HIV vaccines

A

high mutation rate with lots of varients

396
Q

why arent there parasite vaccines

A

they have ways to evade the immune response - antigenic polymorphisms/ variation, drifts and shift
also most people who experience parasites are in LICs where funding isnt possible

397
Q

was there a measles outbreak due to lower uptake of MMR vaccine

A

yes- andrew wakefeild published a report linking autism and MMR vaccine which has been since discredited

yr 1 uni work (13 decks)

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