123 Flashcards
(398 cards)
1
Q
what are protozoa (protists) and worms (helminths)
A
parasites
2
Q
symbiosis
A
interaction between 2 different organism living in close physical association
basically living together
3
Q
mutualism
A
both organisms benefit
e.g bacteria in human colon
4
Q
commensalism
A
1 organism benefits
the other neither benefits or harmed
e.g. staphylococcus
5
Q
parasitism
A
1 organism benefits
the other is harmed
e.g. tb bacteria in human lung
6
Q
4 stages of infectious disease- (symptoms appearance)
A
incubation
prodromal
illness
convalescence
7
Q
incubation period
A
time between infection and the occurance of first symptoms or signs of disease
8
Q
prodromal period
A
short time of generalised, mild symptoms not all infectious diseases have this stage
9
Q
illness stage of infectious disease
A
most severe stage when symotoms are most evident and host immune system not yet fully responded
10
Q
convalescence
A
body gradually returns to normal
variable time depending on pathogen and damage
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
12
Q
stages of infectious disease
A
invasion
multiplication
spread
pathogenesis
13
Q
ways of infectious disease invasion
A
inhalation
oral transmission
intra-uterine
sexual transmission
direct inoculation
direct skin contact
14
Q
invasion stage definition
A
involves entry into the host and transmission from 1 host to another
15
Q
multiplication of infectious disease definition
A
some pathogens can multiply within body whereas others can’t
protists can
helminths cant
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
17
Q
helminths multiplication
A
most cant multiply
so disease severity dependent on number of infectious stages acquired by host over time
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
19
Q
pathogenesis
A
causation and development of clinical disease
20
Q
what is pathogenesis influenced by
A
- number of pathogenic organisms present
- the virulence of the organism
- reaction of the host- degree of resistance
21
Q
incidence
A
number of new cases of infection occurring in a population in a defined period of time
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
23
Q
mortality
A
total number of deaths from disease in a population in a defined period of time
24
Q
leading causes of disease in USA in 1900
A
pneumonia
tb
diarrhoea and enteritis
25
leading causes of disease in USA in 1997
heart disease
cancer
stroke
lung disease
26
in HICs what % deaths are of people 70+
70%
27
in HICs what % of deaths are among people under 15
1%
28
in LICs what % of death are of people under 15
40%
29
in LICs what % of deaths are of people aged 70+
20%
30
what DALY
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
31
how is DALY calculated
adding years of life lost to premature mortality + years lost to (lived with) disability
DALY= YLL + YLD
32
what comparisons does DALY allow
comparisons across range of health problems - quantitative basis for deciding health policies and evaluating cost-effectiveness of control programmes
33
what does DALY no considr
economic loss from disease
direct cost of treatment
social stigma associated with disease
34
skin as a mechanical barrier
top layer is dead cells making it dry preventing bacterial growth
sebaceous glands with fatty acids, lactic acids and low pH (3-5)
35
tight junctions as mechanical barriers
they stop ingested antigens passing into body
36
mechanical barriers for stopping pathogens
tight junctions
skin
mucosal surfaces
37
mucosal surfaces as a mechanical barrier
mucus is slippery
it also traps microorganisms which ae then shed from the body
38
physiological barriers for pathogen entry
low pH in stomach
outcompeting commensal microbiota
anti-microbial peptides (defensins)
lysozymes in tears
cytokines (interferons)
complement (MAC lyses bacteria)
39
immunis
if you recover you never get it again
40
who discouvered/defined vaccination
jenner in the 18th century
41
is adaptive immune response learned or inherent
learned
42
granulocytes
neutrophils
eosinophils
mast cells
basophils
43
phagocyte list
neutrophils
macrophages
dendritic cells
44
lymphocytes list
innate lymphoid cells (ILCs)
natural killer cells
45
neutrophil trap
extracellular traps
nets
can trap bacteria during appendicitis
46
4 signs of inflammation
heat (calor)
redness (rubor)
swelling (tumor)
pain (dolar)
47
local inflammatory response stages
1. chemokine release
2.clotting and complement cascade
3.neutrophils secrete chemokines
4. phagocytosis
5. macrophages migrate into tissue and recruit lympocytes, monocytes and neutrophils
48
chemokine response in local inflammatory response
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
49
systemic acute-phase response
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
50
how many proteins in complement system
about >35
51
where are most complement proteins made
in liver
some are from acute phase response stimulated by cytokines IL-6 and TNF-a
52
what stimulates acute phase response
by cytokines IL-6 and TNF-a
53
is complement system linked to innate or adaptive immunity
both
innate- phagocytosis
adaptive- antibodies
54
what is teh complement system
group of serum proteins in blood that perform defence against pathogens and especially extracellular bacteria
55
the 7functional catagories of complement system
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
7. regulatory proteins- limit complement activation
56
how does innate immune system sense infection
detects molecules from pathogens - pathogen associated molecules patterns (PAMPS)
57
how does body sense infection
PAMPS
PRRs- pattern recognition receptors
58
phagocytosis - oxygen-dependent killing
oxidative burst
superoxide and other toxic oxidants are generated
acts as an anti-microbial
59
oxygen-independent killing
lysozyme- hydrolytic enzyme
defensins- peptides kill bacteria
60
why are parasites effective pathogens
evade innate immune response
hook to avoid flushing
vectors
burrow straight through skin
too big to be phagocytosed
61
is innate or adaptive specific
innate= non-specific
adaptive= specific
62
is innate lifelong
yes
63
is innate present in all animal species
yes
64
innate isn't effective against a wide range of pathogens t/f
false
it is
65
is innate elements present at birth
yes
66
how longs the delay for adaptive effectiveness
delay of 5-6 days before effective response
67
is adaptive immunity gained
yes after exposure to foreign material not from birth
68
adaptive immunity memory
faster respinse to subsequent exposure to same pathogen
69
wheres adaptive immunity carried out
carried out by lymphatic system
70
adaptive immunity is only in vertebrates t/f
true
71
is adaptive immunity lifelong
once aquired its mostly lifelong
72
cells that make up innate system
innate lymphoid cells(ILCs)
natural killer cells
mast cells
eosinophils
neutrophils
macrophages
dendritic cells
73
cells that are part of adaptive immunity
lymphocytes
CD4+ t helper cells
CD8+ cytotoxic t cell
b cells
dendritic cells
74
lymphocyte diameter
6 micrometres
75
lymphocyte life span
3days-8weeks
76
what are lymphocytes activated by
antigen
77
where do t lymphocytes and b cells originate from
bone marrow
b cells then mature in bone marrow
t-cell then move to thymus and mature there
78
how do immune cells find pathogens and each pther
1. interstitial fluid
2. lymph flows through vessel
3. within LNs
4. lymphatic vessels return lymph to blood
79
where do lympocytes function
secondary lymphoid organs: lymph nodes
spleen
80
what do lymph nodes contain
b cells, macrophages, dendritic cells
antibody screting plasma b cells and macrophages in centre
lymph enters afferent end and exists efferent
lymph filter
81
wheres spleen
behind spleen
82
how long is spleen and what does it do
filters blood
12cm long
83
parts of the spleen
red pulp-remove dead RBCs
white pulp-b+T cells, macrophages
germinal centre- proliferating b lymphocytes
84
does lymph have a similar compositon to interstitial fluid
yes
85
antigen presenting cells (APC)
dendritic cells
macrophages
b cells
86
humoral immunity
adaptive
defend against pathogens and toxins in extracellular tissue
b cell/antibody mediated
87
cell mediated immunity
adaptive
cytotoxic t cell mediated
defend against infected cells. cancer cells and transplanted cells
88
whats an antigen
any foregin molecule which is specifically recognised by lymphocytes and elicits a response from them
89
epitopes
antigenic determinant
90
do b and t cells have receptors embedded in plasma membrane
yes
91
each b or t cell is specific for multiple antigen epitope t/f
false
specific for 1 antigen epitope
92
whats the antibody diversity possible
>10^10
93
the b cell receptor is a membrane bound antibody t/f
true
94
all the antiboy subclasses
igM
igE
igA
IgD
IgG
95
igM
first ig to be formed after antigen exposure
pentameric
5 thingys on a circle
96
igE
allergic reactions
97
igA
in secretions
2 of them connected by j-chain
98
igD
membrane bound
99
igG
highest amounts
100
how do t cells develop
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
101
how do t cells get activated
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
102
what does MHC stand for
major histo-compatibility
103
what do APC do
phagocytes
migrate form infection to lymphoid tissues
display processed antigen naive helper t cells
important in triggering primary immune response
104
macrophages can present antigen but are less able to activate naïve t cells than DCs
t/f
true
105
b cells as APC
-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.
106
humoral immunity is... mediated
b cell mediated
antibody-antigen mediated
phagocytosis and complement-mediated killing
107
clonal selection
antigen-driven cloning of lymphocytes
108
all humoral immunity steps
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.
109
how do antibodies mediate antigen elimination
b cell binds to antigen and differentiates
requires activation by t helper cell too
110
binding of antibodies to antigens inactivates antigens by
neutralisation-block binding sites= phagocytosis
agglutination- phagocytosis
precipitation of soluble antigens= phagocytosis
complement - cell lysis
111
3 pathways of complement activation
classical
lectin
alternative
112
whats teh antibody-activated complement pathway
classical
113
what does complement bind to
antigen-antibody complexes on cell surface
114
what does opsonisation enhance
phagocytosis
115
perforin
forms pores in target cell membrane
116
granzymes
initiates apoptosis in target cell
117
helper t cells trigger the humoral response and supply cytokines to CTL
t/f
true
118
not all nucleated cells express MHC-1 t/f
false
they all do express it
119
general symptoms of influenza virus
fever
cough
sore throat
120
structure of influenza A virion
mainly spherical
envelope
ssRNA-
replication in the nucleus
segmented genome (8)
121
haemagglutinin (HA)
binds sialic acid receptors --> viral entry
agglutinates RBCs
antigenic (neutralizing)
122
neuraminidase (NA)
cleaves sialic acid to release virus
degrades mucin
antigenic (non-neutralising)
123
matrix protein 2 (M2)
forms proton channel that facilitates uncoating and assembly
stabilizes the virus budding
antigenic (neutralising)
influenza A surface protein
124
the 3 influenza A surface proteins
haemagglutinin (HA)
neuraminidase (NA)
matrix protein 2 (M2)
125
the outer lipid envelope of infulenza
lipid bilayer from plasma membrane of infected host cell
supported by the M1 protein which plays a role in virion assemb;y
126
nucleocapsid of influenza A virus
each of the 8 different single strands of RNA + nucleoprotein (NP) + RNA polymerase (PB1, PB2, PA)
127
epidemic
rapid spread of infection in a city state or country over a short period of time
128
pandemic
an epidemic that spreads across boarders and worldwide, affecting large numbers
129
what level does influenza A causes
most capable of unleashing epidemics and pandemics
130
severest type of influenza
A
then b,c,d
131
what animals does influenza A infect
human
swine
horse
birds
bats
dogs
132
what animals oes influenza B infect
humans
seals
133
what animals does influenza c infect
HUMANS
SWINE
DOGS
134
what animals does influenza D infect
swine
cattle
135
serotypes of influenza
A, B, C, D
according to internal structure proteins (nucleocapsid and matrix)
-these proteins cant cross react
136
how are influenza subtypes names
2 surface glycoproteins
named by specfic HA and NA subtypes
18 HA types
11 NA types
198 different combos
137
what subtypes of influenza have caused human epi/pandemics
H1N1, H2N2, H3N2, H5N1, H7N8
138
the stages of influenza replication
attachment
uncoating
transcription
replication
assembly
budding
139
attachemnt step of influenza replication
HA-Sialic Acid on host cell – virus endocytosed; vesicle membrane and transferred to endosome
140
uncoating step of influenza replication
Endosome acidification - M2 increased H+ -> uncoating
141
transcription step of influenza replication
Nucleocapsid goes to the nucleus and transcribed mRNA are translated into proteins in cytoplasm
142
replication step of influenza replication
The vRNP (-s) converts to cRNP (+s), then trough replication generates vRNP (-s) -> cytoplasm
143
assembly and budding steps of influenza replication
Assembly: HA/NA transported to cell surface with M1 and genome segments
Budding: Virus buds off by NA
144
does haemagglutinin exist as a trimer in influenza virion
yes
145
the 2 sites on each monomer of HA
receptors binding site- host-specificity
cleavage site- single chains is cut to 2, at n-terminus it is fusion peptide which critical for infectivity
146
what do human viruses prefer to bind to
N-acetylneuraminic acid-a,2,6 linked glalactose
147
what do avian viruses prefer to bind to
N-acetylneuraminic acid-a2,3 linked galactose
148
why do we continue to have influenza epidemics/pandemic
antigenic drift- A,B,C types
antigenic shift- just A
149
antigenic drift- influenza virus
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
150
antigenic shift- influenza virus
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
151
treatment of influenza - adamantanes
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
152
treatment of influenza - neuraminidase inhibitors
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)
153
Influenza virus replicates in cytoplasm. (True/False)
false
154
Influenza virus is a positive sense single stranded RNA (+ssRNA) virus with non-segmented genome. (True/False)
false
155
Neuraminidase enables the influenza virus to attach to the host cell. (True/False)
false
156
The influenza RNA polymerase does not have proofreading activity. (True/False)
true
157
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)
fase
158
Influenza viruses cannot replicate in embryonated chicken eggs. (True/False)
false
159
what family is SARS-CoV-2 belong to
coronaviridae
160
MERS cases and deaths
2521 cases
866 total deaths
161
is SARS-CoV-2 genome single or double stranded
single
162
is SARS-CoV-2 genome segmented
no its non-segmented
163
how long is SARS-CoV-2 geonome
around 30kb long genome
164
how many genes does SARS-COV-2 encode fro
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
functions of S protien in corona virion
-entry of SARS-COV-2 into cells
-host tropism
- protective immune responses
- virulence- severity of disease
166
functions of N protein in corona virion
-component of nucleocapsid
- virus transcription efficiency
- protective immune responses (vaccines)
167
function of M protein in corona virion
- most abundant amongst structural proteins
- assembly of virus particle
168
functions of E protein in corona virion
-smallest amongst all the structural protein
virus assembly and release
169
what do mutations in the RBD of spike proteins determine
-new varients
-transmissibility
-virulence
-vaccine escape
170
steps of SARS-COV-2 replication cycle
1.fusion
2. replication
3. assembly
4.release
171
does delta or omicron varient of covid go deeper in the lungs
delta
172
what cells are found in local immunity in lungs nose etc in adaptive immunity against covid
CD8 t cells, CD4 t cells, IgG, IgA
173
transmission of SARS-COV-2
dropplets
aerosoles
smear infection
174
what does monoclonal antibody/convalescent plasma for ace-2 prevent (covid treatment)
prevent the virus into the host cell
175
how does camostat mesylate prevent covid
prevent SARS-COV-2 into the cell by acting on TMPRSS2
176
lopinavir-ritonavir (HIV) as a covid treatment strategy
inhibition of protease activity of SARS-COV-2
177
ribavirin (HCV) as a covid treatment strategie
may inhibit mRNA capping
178
RNA synthesis inhibitors as covid treatmetn strategies
inhibits SARS-COV-2 RNA synthesis and replication
179
chloroquine group as a covid treatment strategy
interfere with the release of progeny from infected host cells
180
what shape is yersinia pestis
rod-shaped
181
are yersinia pestis gram - or +
gram negative
182
yersinia pestis are not facultative anaerobes t/f
false
183
the 2 main habitats of Y. pestis
flea gut
blood/tissue of a mammalian host
184
how many species of insects have been found to be infected with y. pestis
around 80
185
physical mechanisms accoutning for difference in plague vector efficiency
insect immunity
pathogen must evade digestive enzymes
frequency of feeding/defecation
pathogen must not kill vector too quick
186
does Y. pestis adhere to/ invade the midgut epithelium
no so suceptable to elimination in flea feaces
187
how does y. pestis stay in flea
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
what is about y. pestis that causes the most harm
the toxins produced - lead to endothelial damage and necrosis leading to vascular destruction and local haemorrhaging
189
neutrophils in y. pestis
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
can macrophages kill y. pestis
no
they can phagocytose them but not kill
the bacterial toxins can destroy macrophages and other phagocytic cells
191
is y. pestis an extracellular protein
yes
192
why do lesions occur in y. pestis
from destruction of tissue and effects of endotoxins- peripheral vascular collapse and disseminated intravascular coagulation (DIC)
193
the 3 major plague pandemic
541- the justinianic plague
1347- black death
1894- modern plague
194
between 210-2015 how many cases of the plague were there
3248 cases
584 deaths
195
why is plague a concern for biological weapon
widespread availabilty
mass production and aerosol dissemination
high fatality rate
rapid secondary spread
196
incubation period of the plague
2-4 days but can be as long as 10 days
197
symptoms of the plague
flu like- fever, chill, aches, weakness, vomiting/nausea
198
the 3 forms of plague
bubonic
septicemic
pneumonic
199
the most common form of the plague
bubnic
200
how does the bubonic plague spread in body
multiply and enter in skin then spread via the lymphatic system to lymph nodes
201
advanced stages of bubonic plague
buboes may suppurate- burst to form open sores
202
mortality rate of bubonic plague if untreated
50-60% - but if infected person recovers they are immune
203
whats septicaemia
blood poisening when plague infection spreads to bloodstream
204
can bubonic plague develop into secondary septicaemic plague
yes
205
can septicaemic plague be primary
yes - can be from flea bite or direct contact with infective material
206
DIC
systemic activation of blood coagulation leads to gangrene of the extremities and multi-organ failure
207
mortality of septicaemic plague
100% if left untreated
208
whats the least common type of plague
pneumonic plague
209
whats the most virulent form of the disease
pneumonic
210
what happens in lungs of pneumonic plague
acute pulmonary insufficiency, sepsis, toxic shock
211
case-fatality of pneumonic plague
100%
212
how is pneumonic plague spread
cough droplets
diect and close contact
213
where can specimens be obtained for diagnosis of the plague
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
if caught early- treatment for the plague
antiobiotics in large doses- streptomycin, tetracycline, chloramphenicol
for 10-14 days
supportive therapy- rehydration and blood pressure maintanence
215
how quick can pneumonic plague kill
18-24hr
216
prevention/ control methods of the plague
quarantine
vaccines- formaldehyde inactivated whole-cells and only partial protection
avoid direct contact
rodent control
education
217
how many species on yersinia genus
up to 17
218
yersinia pseudotuberculosis
mild
self-limiting disease
transmitted by faecal-oral route
219
did y.pestis diverge from y. pseudotuberculosis
yes within the last 10000 years
220
transmission of Yersinia pestis by fleas is - dependent on both gene acquisition and loss of function mutations
t/f
true
221
what protein does yersinia murine toxin gene encode for
phospholipase D whcih protects y. pestis within the flea gut
222
The ymt gene was acquired through horizontal gene transfer - enabled a bacterium previously found in the gut to use an arthropod vector (survives insect gut)
t/f
true
223
can y. pseudotuberculosis form a biofilm in some environments t/f
yes
but not within fleas
224
Homologues of >100 Y. pseudotuberculosis genes are present as non-functional pseudogenes in Y. pestis
t/f
false
its 200
225
rcsA is functional in Y. pseudotuberculosis but not in Y. pestis
t/f
true
226
whats the breeding ground for mosquito
swamps
227
what causes malaria
a protozoan parasite- genus plasmodium
228
chance of gettin maaleria
>1/1000
>1 billion at high risk
229
in 2015 how many cases and deaths of malaria
211 milllion cases
429 000 deaths
230
where do most malaria deths occur
african region
90% all deaths occur here
231
malaria is not a acute febrile illness t/f
false it is
shows signs of fever
232
malaria is a periodic fever caused by erythrocyte destruction t/f
true
233
are types of malaira defined by the periodicity of fever
yes
234
is malaira transmitted by male or female mosquitoes
female anopheles mosquito
235
where can anopheles mosquitos survive
latitudes 60 N and 40 S
below 2000 metres
236
how can malaria be transmitted
introduced - biting local
airport-acquire malaria without travelling
transfusion- blood
mainline- needles
congenital- pregnancy to baby
237
sporozoites
into skin by mosquito
circulate in blood for 30mins
penetrate hepatocytes
undergoes schizogony(asexual reproduction)
forms 30 000-40 000 merozoites
238
sprozoites to merozoites
sporozoites invade liver cells and nucleus divides to form a schizont
the schizont ruptures and releases merozoites which infect RBCs
239
merozoites
apical organelles which contain proteins for parasite invasion
must invade RBCs
multiple asexually
disease causing stage
240
trophozoite
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
gametocyte
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
zygote- malaria
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
ookinete
5-10hr the zygote differentiates to cigar shaped invasive ookinete
motile penetrates intestinal wall of mosquito
differentiates to oocyst attached to mosquito midgut
244
oocyst
grow rapid and divide into sporozoites
longest phase- 8-35d
temp dependent - high temp=fast mature
245
how many sporozoites are produced from 1 oocyst
1000
246
what happens when oocyst bursts
sporozoites release into body cavity of mosquito
migrate to salivary ducts
mosquito then bites host and injects sporozoite saliva
247
what do toxins release when schzonts burst stimulate
t cells to produce cytokines like TNFa which mediate fever bone marrow depression and erythrophagocytosis
248
can you get anaemia from malaria
yes loss of RBCs due to parasite growth, depression of erythrpoiesis and erythrophagocytosis lead to anaemia
249
can clotting defects occur in malaria
yes
250
clinical features of malaria
periodic fever
anaemia
acute respiratory distress
hypoglycaemia(low sugar)
hepatomegaly/splenomegaly (big liver/spleen)
haemoglobinaemia
haemoglobinuria
capillary blocakge
251
haemoglobinaemia
haemaglobing in blood plasma
252
haemoglobinurea
haemoglobin in the urine (blackwater fever)
253
iRBC
infected red blood cell protein on surface cause cytoadhesion of rbc to endothelial cells
254
diagnosis of p. falciparum
blood smear- giesma stain
rapid diagnostic test- finger prick
nucleic acid amplification-based diagnostic- sensitive detection of low density malaria infections
255
chemotherapy for malaria treatment
quinine - orginaly bark
was replaced with chloroquine as its safer, more effective, easier to make and fewer side effects
replaced after WW11
256
Intracellular parasite (trophozoite stage) digests haemoglobin - generates free haem which is toxic
t/f
true
257
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
true
258
Chloroquine (CQ) is a strong base, uncharged at neutral pH but carries a positive charge at acidic pH
t/f
false its a weak base
259
charged CQ diffuses through parasite plasma membrane and food vacuole (FV) membrane
t/f
false its uncharged chloroquine
260
Food vacuole (FV) is acidified – so chloroquine becomes charged and concentrates up to several 1000-fold within the FV
t/f
true
261
how does chloroquine kill parasite
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
why is chloroquine being resisted
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
body plan of a neamtode
alimentary canal extends from mouth at anterior to anus at posterior
264
preadaptation
an adaptation that serves a different purpose from the one for which it evolved
parasitic nematodes exhibit this
265
how is nematodes biochem/physiology adapted
survive lots of conditions including both anaerobic and aerobic
eat wide range of food
tough outer cuticle to withstand envi insults
266
are there always 4 larval stages and 2 moults
no there are 4 moults not 2
267
do nematodes undergo asexual reproduction
no
268
how mant times has parasitism arisen in nematodes
9 times
269
what % of world population harbour at least 1 GI nematode
20%
270
is the intensity or prevalence important in nematode infections
intensity
271
what does overdispersed distribution of nematodes mean
>70% of worms are found in <15% of hosts
272
why do soil transmitted helminths (STHs) like the GI
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
reasons fro high prevalence of STH infections
widespread distribution of nematodes
resilience of eggs to harsh environment
lots of eggs per parasite
poor socioeconomic conditions
lack of education
274
ascariasis
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
how long can ascariasis worms get
males- 10-30cm
females-20-35cm
276
where do adult ascariasis worms live
in small intestines
277
what happens when ascariasis eggs are swallowed
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
how long can adult worms live - ascariasis
1-2 yrs
279
what % of ascariasis infections are asymptomatic
85%
280
how do ascariasis cause pathology
with ingestion and migration of larvae- haemorrhagic pneumonia, asthema due to allergins
adult parasites in intestine
wandering adults outside intestine
281
adult worms in the intestine problems - ascaraisis
abdominal discomfort
nausea
malnutrition
intestinal blockage
85% of obstructions occur in children
282
wandering adults worms outside intestine- ascariasis
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
diagnosis of ascariasis
coprological-eggs in poo
serological-antigens/bodies
molecular- PCR of parasite DNA from eggs in poo
image based diagnostics
284
image based diagnostics in ascariasis
after barium meal reveals worms as elongated filling defects
high ultrasound shows the worms
285
what is filariasis caused by
an infection with Wuchereria bancrofti
infection with nematodes of the family filarioidea
286
3 types of filariasis
lymphatic- lymphatic system
subcutaneous- skin layer
serous cavity- peritoneal, pleural or pericardial cavity
287
how are filarial worms transmitted
mosquitoes and black flys
288
how is wuchereria bancrofti transmitted
by a mosquito bite and causes elephantiasis
289
how long are elephantiasis worms
females- 80-100mm
males- 40mm
290
wuchereria bancrofti life cycle
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
clinical presentations of wuchereria bancrofti
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
consequences of lymphatic elephantiasis
social stigma and bad mental health
loss of income earning opportunties
increased medical expenses for patients
isolation
poverty
293
preventiaon of lymphatic filariasis
avoid mosquito bites
nets
long sleeves
repellent
mass drug treatment of entire communities
294
mebendazole- ascaris treatment
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
ivermectin
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
what shape are cestodes
dorso-ventrally flattened ribbon like bodies
can be very long
297
scolex
anterior attachment organ on cestode
posses either hooks + suckers or only suckers to attach host tissue
298
strobila
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
does cestodes have a gut
no as theres a degeneration of non-essential systems like sensory systems, muscles and locomotory systems
300
whats the body wall of the cestode called
the tegument
301
the body wall (tegument) of cestodes
metabolically active layer through which nutrients are absorbed and secretions and waste materials exported
302
proglottids
grow continuously from neck and new ones replace old
303
scolex of t. solium - pork tapeworm
4 large suckers and rostellum containing double row of hooks
304
scolex of t. saginata - beef tapeworm
4 large suckers
no rostellum and restellar hooks
305
are proglottids monoecious
yes they contain both male and female sex organs
306
Fertilisation can't occur between
proglottids of the same or a different
tapeworm
t/f
false it can occur
307
what happens after proglottids are fertilised
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
how do cestodes absorb nutrients
from the host intestine directly through tegument
not passive
tegument has microvillus to increase SA
309
whats teh functional units of cestodes
protonephridium
310
excretion in cestodes
cilia generate current- excess water with nitrogenous waste forced into tubules and out of worm via excretory pores
311
how do tapeworms get into intermediate host
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
cysticercus
when an embryophore(thick memebrane or wall) forms around oncosphere
313
cysticerci
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
inspection of meat with cysticerci
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
where is taenia saginata geogrpahical distribution
worldwide
common in africa east europe, phillipines, latin america. not in india as hindus dont eat beef
316
taenia solium distribution
most prevelent where humans live in areas of close contact with pigs and eat undercooked pork
rare in muslim countries
317
sympotms of tape worm
rare intestinal/appendix blockage
penetrate gut wall
psychological distress
abdominal pain
nausea
weight loss
318
how long can adult tapeworms live
several years
319
how are humans infected with eggs in t. solium
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
are cysticercosis acquired by eating undercooked pork
no
by ingesting solium eggs excreted in human faeces
321
how many people does cysticercosis affect worldwide
50 million
322
pathogenesis of cysticercisis
muscles- lump under skin
eyes- rare but can caused disturbed vision or detached retina
neurocysticercosis
323
neurocysticerosis
seizures and headaches causing confusion balance problems and brain swelling
leading cause of acquired epilepsy in developing world
324
treatment of neurocysticercosis
depends on number and stage of infection
mangement of symptoms
praziquantel- kills viable cysts
325
echinococcus granulosus
dog tape worm
326
are humans definitive or intermediate hosts of echinococcus granulosus
intermediate hosts
327
how long are adult dog tapeworm
3-6mm
328
how large are hydatid cysts
1-20cm long
329
germinal layer of hydatid cysts
(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
protoscoleces of hydatid cysts
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
laminated layer in hydatid cyst
is a thick (several mm), non-living, carbohydrate-rich matrix, secreted by the GL.
332
where do most of hydatid cysts develop
95% develop in lungs or liver but can form in brain
333
diagnosis of dog tapeworm
CT
MRI
usually seen in autopsy or surgery as is normally asympotmatic
334
treatmetn of dog tape worm
PAIR- puncture, aspiration, injection, re-aspiration
surgery
drug treatment- albendazole
watch and wait
335
are schistosomes nematodes, cestodes or trematodes
trematodes
336
how many countries are endemic to trematodes and how many people infected
>70 countrys
200 million infected
337
schistosomiasis is classified as neglected tropical disease
t/f
true
338
where do 85% of schistosomiasis cases occur
africa
339
the 3 major factors responsible for maintaining schistosome transmission
1. pollution of water with excreta containg eggs
2. preseence of suitable snail hosts
3. human contact with water infected with cercariae
340
life cycle of schistiomiasis
1. break barrier
2. migrate in circulation
3. mature
4. pair up
5. find a home
6. reproduce (lay eggs)
341
cercariae in s. mansoni
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
when carcariae shed their tails what do they become
schistosomula
343
where do schistosomula migrate
from skin to liver via lungs in the vasculature and lymphatics
344
where do schistosomula matuer into adult worms
in the liver
345
adult trematode worms pairing up
females live within the males gynaecophoric canal
live about 5 yrs
live in venous system
are dioecious and sexually dimorphic
346
how many eggs do paired female trematode worms release per day
300-3000 /day
347
life cycle of trematode in snail host
hatch becoming motile
infect snail
non-motile
copies
release cercariae
infect human host
348
miracidia
eggs release miracidia
ciliated larval stage
free living and motile
infective for 6-8hrs
locate snails using light and sail derived chemicals
349
sporocysts
inside snail tissue miracidium turn into non-motile sporocyst
produce cercariae
cercariae from snails infect human host
350
cercarial dermatitis from schistosomiasis
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
parasite maturation of schistosomiasis
katayama syndrome
2- weeks after infection
usually mild
cough
hepatosplenomegaly
pyrexia- fever
weight loss
giant urticaria- hives
352
s. haematobium symptoms
haematuria - blood in urine
dysuria- painful urination
abdominal pain
bladder inflammation
353
is human schistosomiasis a immunopathological disease
yyes
354
granuloma formation
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
fibrosis
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
hepatosplenic disease
hepatosplenomegaly
portal hypertension - pressure in vein connecting intestines and live due to cirrhosis and ascites(fluid in abdominal cavity)
357
epidemiology of schistosomiasis
infection rises throughout childhood
peaks in older children/young adults at low transmission rates
declines into older ages
358
diagnosis of schistosomiasis
eggs in stool/urine
worm antigen CCA in urine
ultrasound
bladder/rectal biopsy
serological testing
359
prazaquantil trematodes
single oral dose
well absorbed from GI tract
few side effects
few contra-indications
increasing reports of resistance
360
is reinenfection common after chemotherapy- trematodes
yes very common as there is a snail host Prescence
chemotherapy dosnt always kill adults just suppress eggs production
361
schistosomiasis prevention
no vaccine
no drugs to prevent
avoid swimming in endemic countrys
drink ;safe; water
362
principle of immunisation
vaccines contain antigens found on pathogens causing disease but exposure to the antigens in a vaccines does not cause disease
363
vaccination vs immunisation
vaccination refers to getting the injection
immunisation means receiving a vaccine and becoming immune disease as a result of the vaccine
364
how do vaccines work
induce active immunity
immunological memory
365
requirments for good vaccine
doesnt cause disease
safe
stability- easy storage
cost
administration ease
long term protection
interrupt spread of infection
366
types of vaccines
live
inactivated
subunit
passive immunotherapy
367
live vaccines
whole pathogen for which virulence has been artificially reduced = attenuation
368
inactivated vaccines
whole 'killed' organisms
369
subunit vaccines
certain components of pathogens can be purified usually with recombinant DNA tech
- toxoid
- surface protein
viral vector
DNA and RNA
370
what age group does polio afect mainly
<5
371
in polio how many cases result in paralysis
1 in 200
372
since 1988 polio cases decreased by how much
99.9%
373
the 3 countrys that were still polio endemic in 2017
afghanistan
nigeria
pakistan
374
3 serotypes of poliovirus
type 1- brunhilde
type 11- lansing
type 111- leon
375
live attenuated oral vaccine (OPV or sabin)
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
advantages of live attenuated vaccine
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
disadvantages of live attenuated vaccine for polio
may give subclinical or mild form of infection
cant be given to immunosuppressed or pregnant
may revert back to virulent form
378
killed organisms inactivated polio vaccine (Salk)
3 serotypes
cant cause circulating vaccine derived polio virus
antibodies-prevent polio to CNS
SUBCUTANEOUS INJECTION
379
Advantages of inactive vaccines
cannot cause infection
can be given to immunosuppressed and pregnant people
380
disadvantages of inactive vaccines
less immunogenic and requires addition of adjuvants and booster doses
381
role of an adjuvant
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
what bacteria is tetanus caused by
clostridium tetani
produces a neurotoxin when it grows in anaerobic conditions
383
tetanus symptoms
muscle spasms
lock jaw
seizures
eventually death
384
example of a toxoid vaccine
tetanus vaccine
385
example of a surface protein vaccine
hepatitis B virus vaccine
386
what surface protein is used in hep B vaccine
HBsAg - produced using recombinant DNA
used to be dont by purifying blood of carrier which was unsafe and expensive
387
example of a viral vectory vaccine
astrazeneca/oxford SARS-CoV-2 vaccine
388
what do you inject in DNA vaccines
nucleic acids encoding antigens
389
concerns around DNA vaccines
possible genomic incorporation of immunising DNA might activate oncogenes
doesn happen in RNA vaccines
390
what were the first mRNA vaccines to be deployed for mass immunisation of human
moderna and pfizer covid19 vaccines
391
do mRNA vaccines encode full length or the receptor binding domain of the SARS-CoV-2 viral spike protein
t/f
true
392
is RNA or DNA more labile in vaccines
RNA so care must be taken for long term storage
393
primary failure of vaccines
fails to make an adequate immune response to vaccine so infection still possible anytime
394
secondary failure for vaccines
makes adequate immune response initially but immunity wanes overtime
most inactivated vaccines ae like this so booster needed
395
why is there no HIV vaccines
high mutation rate with lots of varients
396
why arent there parasite vaccines
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
was there a measles outbreak due to lower uptake of MMR vaccine
yes- andrew wakefeild published a report linking autism and MMR vaccine which has been since discredited
398
