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243 medical microbiology Flashcards

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1
Q

the nucleoid

A

irregularly shaped region
location of chromosome
usually 1 per cell
contain all essential genes
double stranded dna in a big circle

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2
Q

plasmid structure

A

small closed circular DNA molecule
can be linear
vary in copy number (1-50)
vary in length (2.3-1354kbp)

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3
Q

do plasmids replicate independently of chromosme

A

yes

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4
Q

plasmids arent required for growth and reproduction
true or false

A

true

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5
Q

plasmids dont carry genes that confer selective advantage
true or false

A

false
e.g. drug resistance

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6
Q

how much room does nucleoid take up

A

can take up alot of space in a cell dependent on how many mbp there are

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7
Q

whats an inclusion

A

granules of organic and inorganic material

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8
Q

do plasmids contian genes required for the cell

A

no
just extra fun add on genes

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9
Q

if low copy number in plasmids

A

not as big of metabolic burden
but daughter cell less likely to get fun extra gene

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10
Q

can plasmids be moved between bacteria

A

yes
drug resistance- conjugation between bacterial strains
but can be used as a benifit as we can insert plasmids into cells on purpose

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11
Q

function of inclusion

A

storage product

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12
Q

when are inclusion mainly formed

A

when bacterial cell goes into stationary phase the amount of inclusions increase

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13
Q

storage products for inclusions examples

A

glycogen- glucose polymer-
poly-b-hydroxybutyrate (PHB)- lipids- is a biodegradable plastic used in suturing
polyphosphate granules- phosphate- difficult to breakdown like glycogen but doesn’t matter as metabolic rate is low- just to keep bacterial cell just about alive
sulphur granules- electron doner for respiration in stationary phase

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14
Q

where are inclusions contained

A

cytoplasm

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15
Q

cytoplasmicmembrane

A

phospholipid bilayer
permeable
integral and peripheral membranes

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16
Q

integral proteins

A

go right through the membrane

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17
Q

peripheral membrane proteins

A

dont go all the way through membranes
just pop out abit

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18
Q

gram test

A

smear of bacterial stuff
fix with flame
crystal violet- binds to peptidoglycan (more gram +)
wash with alchol
counterstain with soemthing pink

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19
Q

what colour is gram +

A

purple
as 90% peptidoglycan stained by crystal vioelt

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20
Q

what colour is gram-

A

pink
as not stained that much by crystal violet

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21
Q

peptidoglycan structure

A

G then M then g then M etc
G= N-acetylglucosamine (NAG) GlcNAc
M= N-acetylmuramic acid (NAM) ManNAc

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22
Q

what MG (NAM-NAG) in peptidoglycan

A

polyerm cahins linked via peptide bridges

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23
Q

teichoic acid locaton

A

in gram positive cell wall
pops pout cell wall- detected by predators- phagocytes detects
lipoteichoic if goes all the way through
made up of GM

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24
Q

gram neg cell wall peptidogylcan %

A

peptidoglycan - 10% in periplasm

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25
wheres periplasm located
between inner cytoplasmic membrane and outer memrbanes
26
porins
only in gram neg not + little drainpipes water-filled allow low molecular weight substance in and waste products to leave bacterial cell free-flowing normally some are gated have become a target for antibiotic- porin inhibitor helps the antibiotic
27
lipopolysaccharides (LPS) components
lipid A- embed into membrane core polysaccharide o-polysaccharides- vary's a lot between bacterial species and strains -phagocytes can detect it bacteria -can cahnge sugar compostion making it undetectable to phagocytes (stealthy)
28
do lesspathogenic strains have a capsule
no its normally more pathogenic strains that have capsule
29
bacterial capsule made up of
extracellular polysaccharides (EPS)
30
why do bacteria have capsule
anti predator device
31
is the capsule hydrated
yes can survive in dry conditions as the cell can then just use water from capsule
32
does capsule help bacteria stick
yes upregulate genes for sugar production to make a slime to attach to surfaces
33
s-layer
not all bacteria have monolayer of proteins or glycoproteins functions are a site for adhesion and anti-phagocytic
34
flagella use
forswimming and attachment to surface
35
structure of flagella
9+ 2 dynein motor
36
monotrichious flagella
1 flagellum
37
fimbriae
proteins NOT FLAGELLA up to 1000 short thin hair like proteinaceous recognition and surface attachemtn function
38
pili
similar to fimbriae just longer and thicker less numerous 1-10per cell required for mating and for attachment to surface
39
whats the natural state for the majority of bacteria
attached to surface which isnt that easy as bacteria negatively charged and most surface negative =repulsion must overcome this by using flagella pili fimbriae maybe s-layer
40
the natural human flora
attached majorty to overcome flushing mechanism biofilms large SA bacterial pathogens will also colonise loads of diff surfaces present- soft tissue enamel etc communities- mixed species so important - 90% of human cells are bacterial
41
ways bacteria are identified
16S rRNA sequence comparisons classical taxonomy use of differential and selective media
42
why identify bacteria
sense of order enhance communication between scientists for discussion provide means for accurate id for diagnosis of infection to ensure effective treatment
43
how to identify bacteria
molecule methods classical culture methods
44
comaprison of rRNA sequences in bacteria id
s is sedimentation rate 50S has 2 forms of rRNA (5s and 23s) + 30s (16s rRNA) which is more variable = prokaryotic 70s ribosome draw phytogenic trees to compare
45
what are the 2 domains of bacteria
bacteria (sometimes called eubacteria) archaea (sometimes called archaebacteria)
46
do eukarya have 16s rRNA
no they have 18s rRNA but they call it 16s
47
amphitrichous
1 flagellum at each end of cell
48
lophotrichous flagella
cluster of flagella at one end or both ends
49
peritrichous flagella
spread over entire surface of cell
50
commensalism definition
a form of symbiosis in which one organism derives a benefit while the other is unaffected
51
how many different species of gut bacteria
500 rods rounds spiral tails/flagella
52
is gut microbiota fixed
no changes in numbers and types dependent on things such as diet,antibiotics and age
53
why dont the bacteria in gut hurt us
immune tolerance as immune system knows of the bacterias presence
54
what makes up a community
multiple species of bacteria
55
how many microorganisms are on the epithelial surface of intestine
10-100^12
56
surface area of intestine and si
30-40m2 SI alone= 28-38m2
57
how much do villi increase sa of intestine by
10fold
58
how much do microvilli increase sa by
20fold
59
how much do both villi and microvilli/brush border increase the sa by together
600fold
60
how many layers between contents of gut lumen and mucosa and how thick is it
1 30microns
61
enterocytes?
si epithelial cell terminology
62
where are stem cells found in si
in the crypts they replicate and move up to the villi (but paneth cells go down)
63
what are enterocytes held together by
tight junctions ensures permeability
64
where are crypts of lieberkuhn found
in human colon LI
65
how often is the epithelial lining regenerated inintestines
every 4 to 6 days
66
does the large intestine have villi ?
no
67
what do goblet cells secrete
mucus protecting mucosa from gi secretion and lubricates food and aids removingpathogens
68
what do paneth cells secrete
antimicrobial peptides like defensins and lysozymes, growth factors, enzymes and cytokines
69
what do enteroendocrine secrete
scattered throughout si mainly in crypts secrete various hormones like cholecystokinin, secretin, gastric inhibitory peptide glucafon like peptide 1
70
m cells
unique epithelial cells in the follicle-associated epithelium covering Peyer patches. These cells function as antigen-sampling cells, transporting luminal antigens and microorganisms across the epithelium to initiate lymphoid immune responses
71
peyers patch
aggregate in Peyer patches, the lymph nodules scattered throughout the small intestine but are most abundant in the ileum. These cells are essential to the gut's immune function.
72
tuft cells
(brush cells) are epithelial cells found in the small intestinal villi. These cells have apical microvilli, giving them a "tufted" appearance. Tuft cells are chemosensory cells, sense luminal contents and can secrete various signaling molecules, including cytokines and neurotransmitters, in response to stimuli. Tuft cells help regulate immune responses, mucosal defense, and epithelial repair.
73
what does GALT stand for
gut-associated lymphoid tissue
74
what does galt do
maintain homeostasis of microbiota and immune system controls immune response so theres no autoimmune problems
75
how do cells in the gut communicate with one another
toll-like receptors (TLR) NOD-like receptors (NLR)
76
where are PaaS patches found and what are they
found in scattered along intestinal mucosa dome like enriched in lymphoid tissue key sites for coordinating immune responses to pathogens
77
the 4 dominant phyla of gut microbiome
bacteriodetes firmicutes actinobacteria proteobacteria
78
how are the dominant phyla mainly identified
cant grow in lab so dont know much about id by 16s rRNA sequencing
79
as you age which phyla in gut microbiome becomes more dominant
firmicutes > bacteriodetes > others
80
in babys which gut microbiome phyla is the most present and does it differ if bottle or breast fed
breast fed and bottle fed do differ but are the same when on solid foods mainly firmicutes and bacteriodetes and proteobacteria
81
how is the health of gut microbiome determined
birth/early colonisation environmental factors life style hygiene drug use
82
pros for microbiota living in gut
readily available food source occupy a relatively safe/protected niche
83
pros for the host on having bacteria in gut
keep pathogens at bay aid derivation of nutrients intestinal repair response- influence immune system to go into anti inflammatory state train immune system- stimulate system so more likely to respond to harmful pathogen
84
factors that affect microbiome
environment- household members, pets, travel lifestyle- diet, fitness, stress early colonisation- hospital birth, delivery method, breast fed medical practices- long term antibiotic use and hygiene
85
when some factors outweigh other factors when shaping microbiome what occurs
dysbiosis
86
how does exercise affect microbiome
stimulates gut movement, blood flow, o2 levels, affecting ability of gut bacteria to be cleared and their beneficial products to be circulated
87
probiotics
live organisms intended to provide health benefits when consumed by restoring gut microbiotic
88
prebiotics
the compounds in food that induce growth or activity of beneficial microorganisms and improve digestion
89
synbiotics
mixture of pro and prebiotics maintain good health reduce risks associated with disease
90
how affected are probiotics
yakult and actimel will go straight through u if your healthy dont colonise your gut biofilm
91
prebiotic and butyrate
found in fresh unpasteurised no preservatives fibres in fresh fruit and veg butyrate promotes stem cell proliferation and help regulate oxidative phosphorylation
92
inulin
natural prebiotic extract of chicory root added to processed food controversial studies regarding benefit
93
vit k and vit b on how microbiota benefit host
Vit K: blood clotting, bone metabolism and heart health. Vit B: releasing energy from carbohydrates and fat to breaking down amino acids and transporting oxygen and energy-containing nutrients around the body.
94
short chain fatty acids and how microbiota benefit host
e.g.acetate, proprionate and butyrate Variety of cellular and immune functions. Aid removal of abnormal cells and promote cellular renewal. Alters secretion of immune mediators.
95
how do neuro modulator microbiota benefit host
e.g. GABA , norepinephrine Essential for functioning nervous system and mental health
96
how does butyrate modulate colonic macrophages
through inhibiton of histone deacetylases immunological tolerance modulates generation of t-regulatory cells
97
what approved foruse in recurrent c difficle
faeces collected from a healthy donor and transferred to unhelathy recpient via enema in clinical trial for ibd 90% of c difficle cured
98
dysbiosis is classified as..
a decrease in number of symbionts a loss of diversity an unwarranted growth of pathobionts
99
what diseases are assocaited with dysbiosis
proliferation higher than apoptosis=mucosal hyperplasia = inflammation,cancer or decrease proliferation leads to mucosal atrophy = mucosal atrophy= ulcerative colitis
100
diseases where some evidence of dysbiosis is evident
crohns alzheimers diabetes obesity allergies depression and anxiety
101
what is put in italics when naming bacteria
genus species
102
taxonomic hierarchies titles
domain phylum class order family genus species strain
103
in written exams how are italics written
underlined
104
how many classes does proteobacteria have
5 (α) Alpha-proteobacteria (β) Beta-proteobacteria (γ) Gamma-proteobacteria (δ) Delta-proteobacteria (ε) Epsilon-proteobacteria
105
how many orders does proteobacteria have
14 including Enterobacteriales Legionellales Pseudomonadales Alteromonadales Vibrionales Aeromonadales
106
what class and order is ecoli part of
gamma proteobacteria- class enterbacteriales -order
107
how manyf amilies does enterobacteria have
7 Enterobacteriaceae Erwinaceae Pectobacteriaceae Yersiniaceae Hafniaceae Morganellaceae Budvicaceae
108
the family and genera name for ecoli
family- enterobateriaceae genus- escherichia
109
3 main bacteria collection services
amerian type culture collection (ATCC) national collection of type cultures (NCTC) national collection of industrial food and marine bacteria (NCIMB) each place has different strains of species can have same strain as long as they cross-reference
110
do bacterial strains within a single species behave differently
yes e.g. humans are all homo sapiens but we all behave differently- the same with bacteria some are nice and some are mean
111
class 1 of strain hazard group
very timid strain if accidently ingested no disease would occur no virulent factors very safe
112
class 2 strain haazard group
may get a disease but less safe treat abit more carefully gloves - aseptic techniques
113
class 3 hazard group strain
if ingested definitely get disease multiple virulence factors wont die as treatment for it be very careful kept in cabinet through rubber gloves toxigenic
114
class 4 hazard group strain
would get disease and probably die suit up no known class 4 bacterial species currently at the moment all bacteria can be killed but highly likely for some to appear as antibiotic resistance increase only done in government facilitys
115
why do we care about bacteria strains
tells us whether its hazardous but species can be misreprsented e.g. household cleaning products must kill 4 strains of bacteria - but they usually only test on very timid strains - so wont kill the strains actually found in houses
116
can u get down to strain level in classical taxonomy
no
117
classical taxonomy
ask a bunch of questions/tests in a tree diagram to discover down to the genus level
118
what does classical taxonomy rely on
phenotypic analyses
119
what things do you look at in classical taxonomy
morphology G+C content of DNA physiology and metabolism- like nutreint sources, relationsuip to pH, temp, salinity, products formed, presence of enzyme activity
120
how much help is morphology in bacteria id
not very helpful
121
oxygen tolerance responses
obligate aerobe- all at top anaerobe- at bottom no o2 faculative aerobe- spread out but more at top microaerophile- near top aerotolerant anaerobe- spread out
122
does presence of endospores help id of bacteria
endospore- survival mechanism, yes as not all gram + have endospores
123
endospore
survival mechanism in bad conditions 100s to 1000s survival rate heat resistant, drying, radiation, chemicals very low water content made up of calcium dipicolinate special proteins protect DNA
124
cell motility in bacteria id
useful drop in coverslip with water and see if they are swimming motility test agar also good- growth medium with less agar then normal- makes sloppy so bacteria has chance to move- with die and stains bacteria- just put bacteria on needle into middle- in test tube
125
what 2 enzymes are looked for in classical taxonomy
catalase oxidase
126
catalase test
slide with drop of h2o2 mix with loop of bacteria if catalase present o2 is produced = bubbles if no catalase no bubble formed
127
oxidase activity test
detects presence of cytochrome c (wont get in anaerobic bacteria as dont respire) kovacs reagent: colourless when reduced and purple when oxidised if no colour change= oxidase negative if colour change= oxidase positive
128
do some bacteria have more GC DNA than AT
yes
129
G + C content equation
G +C / G+C+A+T x 100
130
GC content id for bacteria
seperate strands more GC= higher temperatures to split DNA into single strands then measure absorbance as single and double stranded dna have different absorbances then measure melting temp - where 50% of DNA has split into single strands then look on table and look up TM value to see proportion of GC
131
how to test for metabolism when id bacteria
bacteria use carbon source from carbohydrate - dont use all available too them (picky) test whether the bacteria will grow on different carbohydrate medium e.g. on lactose medium with pH indicator - production of acid makes pH change and colour reaction can measure o2 as a product too= air bubbles e.g. 2- hydrogen sulphide - H2S production - forms ferrous sulphide wich is insoluble
132
macconkey agar
specific for enterobacteriacae no growth of gram positive as dont do well in bile salt presence can the bacteria ferment on lactose ? - used as a negative control turns red if it can ferment on lactose
133
blood agar
clear the plate if beta haemolytic stuff as its breaking up erythrocytes
134
what chocolate agar
blood added to boiling hot agar so denatures turns brown only haemophilus and neisseria grow on this media
135
how to differentiate between genera on chocolate agar
need to be more selective add something that only one can use or add something that kills one of them e.g. antibiotics now a selective medium
136
selective media colours for brilliance E.colicoliform
chromogenic coliforms are pink e.coli is purple
137
listeria selective agar
only listeria grows here and can tell level of virulence highly virulent produces halo surrounding colony s it degrades the agar
138
staphylococcus selective media
staphylococcus grows on really salty environemtns so only this will grow also add mannitol to see fermentation for control
139
what % of all bacteria strains can be cultured in a lab
3% leaving 97% unculturable
140
whats a functional guild
bacteria that do the same job in the environment
141
what key elements do bacteria need
carbon nitrogen phospherus
142
2 ways bacteria get carbon
autotroph hetertroph
143
autotroph
make own sugars fixation of inorganic carbon e.g. cyanobacteria- produce neuro toxins , green and purple sulpher bacteria
144
heterotroph
assimilation of organic carbon cant photosynthesise or use inorganic carbon must use preformed sugars most use simple sugars some like actinomycetes and gliding bacteria can use complex sugars like cellulose
145
assimilation
acquisition of nitrogen nh4 no3 organic n most bacteria
146
nitrogen fixation
N2 some cyanobacteria and actinomycetes
147
how do bacteria get nitrogen
assimilation nitrogen fixation
148
how do bacteria get phosphorus
assimilation of PO4
149
what other things do bacteria need for growth excluding n,p, c
H, O, S, Na, K, Cl, Mg, Fe Trace elements e.g. Cu, Mn, Zn Appropriate temp, pH, salinity etc. Electron Donor Energy Source
150
how you catagorise bacteria by growth requirements
soruce of energy electrons carbon
151
how is bacteria catagroised by energy source
phototroph- light chemotroph- chemical reactions
152
how is bacteria catagorised by electron source
organotroph (organic matter) lithotroph- inorganic compounds
153
how to categorise bacteria by carbon source
autotroph - inorganic c hetertrophy- organic c
154
photosynthetic bacteria
photolithoautotrophs: phototroph lithotroph autotroph combo
155
functional guild
A guild is a group of species that exploit the same class of environmental resources in a similar way – regardless of taxonomic position each guild is represented by a core genus a comunity of metabolically related microorganisms kinda like a compromise for ecologists and scientists looking really deep at chemistry and genetics of bacteria
156
hwo many guilds are there
A-G
157
what is guild A
aerobic decomposers (but kinda mineralisators and not really decomposing) use simple sugars - dissolved organic carbon chemoorganoheterotrophs core genus- pseudomonas waste is gas co2 and h20
158
what guild is the biggest group of bacteria
guild A- aerobic decomposers
159
what does guild A utilise for energy carbon and electron source
DOC
160
what is guild B
gliding bacteria chemoorganoheterotrophs core genus- cytophaga true decomposers - POC to DOC- this DOC forms food source for guild A mineralsiers - DOC to CO2 e.g. cellulose, chitin, pectin no flagella similar to A but dont use simple sugars
161
whats guild E
sulphate reducing bacteria chemoorganoheterotrophs core genus= desulfovibrio second largest guild SO4 - H2S dissimilatory sulphate reduction (sulphate respiration) anaerobic respiration
162
whats guild F
purple and green sulpher bacteria photolithoautotrophs core genus= chromatium anoxygenic photosynthesis sulphide as electron source use infra-red tofix co2 purple sulpher granules in cells - chromatium, thiospirillum green sulpher granules outside cell- prosthecochloris, pelodictyon up to 10um long
163
what do guild F use to fix co2
infra-red light energy
164
whats the electron source for guild F
sulphide
165
is guild F anaerobic or aerobic
anaerobic
166
is guild A aerobic or anaerobic
aerobic
167
is guild E aerobic or anaerobic
anaerobic
168
is guild b anaeobic or aerobic
aerobic
169
purple and green non-sulpher bacteria
anaerobic photolithoautotrophic and chemolithoautotrophic complicated chloroflexus (green) rhospirillum (purple) mainly thermophillic
170
guild D
colourless sulpher bacteria chemolithoautotrophs core genus- thiobacillus sits on border of aerobic and anaerobic electron donor abundant in anaerobic anvironment acid tolerant -extreme environements oxidises iron, leach metals
171
guild d waste product
so4+ H2O
172
does guild E oxidise iron
no guild D does
173
is guild d anaerobic or aerobic
sits on the border
174
what guilds is the sulpher cycle made up of
guild E guild D guild F guild E turns SO4 to H2S then guild d and f turns H2S into SO$
175
guild C
nitrifying bacteria chemolithoautotrophs core genus = nitrosomonas guild c is nitrification NH4+ + O = NO2- + H2O NO2- + O = NO3-
176
what are the2 types of nitrifying bacteria in guild c
nitrosomonas- NH4+ to NO2 nitrobacter - NO2 to NO3
177
denitrification
NO3 to NO2 to N2 dissimilatory nitrogenous oxide reduction microaerophilicspecies end product gaseous N (N2, N2O)
178
what fixes nitrogen in nitrogen fixation
diazotrophs
179
what happens to N2 in nitrogen fixation
reduced to NH4 catalysed by nitrogenase
180
is nitrogen anaerobic or aerobic
anaerobic very o2 sensitive aerobic fixation requires specific adaptations
181
nitrogen cycle main steps
NH4 to NO2 by nitrosomas NO2 to NO3 by nitrobacter NO3 to N2 N2 to NH4 additional route of NO3 to NH4 via organic-N (assimilatory nitrate reduction
182
assimilatorynitrate reduction
the route of NO3 to NH4 in the nitrogen cycle
183
which guilds are aerobic
a b
184
which guilds are border anaerobic/aerobic
c d
185
anaerobic guilds
e f g
186
guild g
methanogenic bacteria archaea domain carrys out methanogenesis- forms methane chemolithoautotrops like c and d
187
chemical equatiosn for guild g methane formation
CO2 + 4H2 = CH4 + 2H2o CH3COOH = CH4 +CO2 (slower)
188
what do methanotrophs utilise
methane produced in guild G
189
methanotrophy
use of CH4 as sole C source CH4- methanol- formaldehyde- formate- co2 formate accumulates in biomass co2 is the electron acceptor for methanogens
190
what gasses released flatulence
CO2- odourless, non flamm N2- odourless, non flamm - some members of gut can fix no guilds for H2S and CH4 H2S-rotten eggs and flamm CH4- odourless and flamm
191
whats VOC
volatile organic compounds
192
can you identify genus of bacteria by genus
yes on agar plates bacterial VOCs contribute to our distinctive odour
193
how can your odour change
age diet environment can also change with medical disorders/disease e.g. non-microbial- cancer, diabetes microbial
194
pathogen definition
A pathogen is an organism that causes disease, by impairing or interfering with the normal physiological activities of the host
195
disease definition
a pathological condition of a part, organ, or system of an organism resulting from various causes, such as infection, genetic defect, or environmental stress, and characterized by an identifiable group of signs or symptoms
196
infection definition
the invasion of a host’s bodily tissues by disease- causing organisms (pathogens), their multiplication, and the reaction of host tissues to these organisms and the toxins they produce.
197
pathogenicity definition
the ability to cause disease
198
virulence definition
the degree/intensity of pathogenicity
199
infective dose
the number of bacterial cells required to establish an infection (not L50) the lower the ID the more virulent the pathogen
200
what does spp not in italics mean
numerous species
201
where are virulence factors found
some on chromosomes- not that many as metabolic burden on plasmids- low copy number can reduce the burden on the cell
202
primary pathogens
live their lives just wanting to infect host the microorganisms that cause disease in healthy people
203
opportunistic pathogens
microorganisms that are normally in contact with the host and cause disease when the hosts resistance is low
204
are most pathogens pathogenic
no most are never pathogenic some are opportunistic and very few are primary
205
what must the pathogen have to invade host (6)
- natural reservoir - successfully transmitted to host - penetrate the hosts barriers - colonise sterile surface - over colonise existing surface - colonise a pre-existing natural biofilms
206
non human reservoirs - environment
soil , water fomites- bedding, surgical instruments- e.g. staphylococcus aureus (MRSA)
207
animals as non-human reservoirs
not technically infected - there but not causing disease in animal zoonosis -10^10 cell/g faeces e.g. bacillus anthracis (anthrax) many different viruses vector borne disease like flees on rats are very common
208
can humans be reservoirs
yes
209
typhoid mary
asymptomatic cook poor hygiene linked to 10 outbreaks of typhoid fever (1896- 1906) 51 cases and 3 deaths quarantined for 3 years started cheffing again then they put her back on island for 23yrs
210
why are symptomatic reservoirs better than non symptomatics
because you can actively see and avoid it coughing sneezing experienced in covid
211
what STDs are on the rise
herpes syphilis chlamydia
212
are STDs symptomatic or asymptomatic
can be both can takes weeks show symptoms and by then its too late
213
transmission of bacteria
aerosol- cough, sneeze, shower head direct contact- touch, sec vector-borne- ticks, fleas, body lice
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what happens if bacteria can enter the body
have to overcome flushing mechanisms so mt usattach to epithelium cells and form a biofilm
215
whats teh best plast for pathogen to infect
sterile surface as no competition like bladder or lungs
216
how many bacteria live on and within our body
>10^14
217
4 steps of biofilm formation
conditioning film arrival of bacteria to a surface attachment of bacteria to a surface biosynthesis of the biofilm matrix
218
can pathogens easily get through a biofilm
no
219
conditioning film
basically covered inorganic and organic particles that attracks bacteria
220
how do non motilebacteria get to biofilm
diffusion in turbulant water- increases chances of non motile cell crashing into surface
221
how do motile cells get to bacteria
swim there can detect it chemotaxis
222
what 2 ways do fluids flow
laminar flow turbulant flow
223
if non motile cell what flow do you want to be in
close to edge of laminar flow so can drop out to surface
224
boundary flow
no flow of water
225
is there a boundary layer in laminar flow
yes big boundary layer does mean less chance for nonmotile cells to attach
226
does turbulant flow have boundary layer
can do but normally alot smaller
227
rough surface of water and bacteria
Rough surface-increased vaginations – more of a chance for bacteria to reach and attach surface
228
reversibly bound bacteria
bacteria is negative charge and so is surface normally repulsion (tiny amount) 30-100nmfromsurface so bacteria hovering above the surface will just wash of But heat and drying out and passing through a flame will remove repulsive barrier (only in lab conditions really)
229
how do hovering bacteria attach to the surface
long projecting bridging structures flagella pilli fimbriae stalks teichoic acids goes accross repulsive barrier and pulls cell to surface
230
where are generic adhesions encoded
the nucleoid essential for growth
231
how do generic adhesions adhere to abiotic surfaces
non-living wont have receptors for bacteria to attach to so bind by electrostatic forces
232
how do generic adhesions bind to biotic surface
mainly by glycoprotein receptors some non-pathogenic bacteria all pathogenic bacteria
233
whats a generic adhesion
e.g. pili, fimbriae, flagella, lipoteichoic acid
234
what receptor do teichoic and lipoteichoic acids bind to
fibronectin will bind to glycoprtien specifically mannose
235
waht receptor does flagella bind to
toll-like receptor 5 non a glycoprotein
236
extra adhesions
pathogens only- want to be very secure when binding- the generic adhesions aid the initial attachment only pathogens dock with membrane adhesion proteins using attachment proteins
237
attachment proteins
dock the bacterial cell onto host cell sugar-binding proteins encoded by plasmid bind to surgar residues in host receptor- glycan- mainly glycoproteins
238
what are attachment proteins encoded by
the plasmid
239
gram neg attachment protein
trimeric autotransporter adhesions (TAAs) also known as typeIV secretion system
240
gram postiive attachment protein eg
groupA strep -protein M staph-proteinA c diff- CbpA
241
what happens once a bacteria is attached to surface
makes a capsule whether the bacteria had one already or not only when high number of cells will the capsule/slime is made so requires more than 1 cell
242
where is the capsule slime encoded
alg gene - for alginate production cementes bacteria to surface
243
why are more than1 cell needed to attach to surface for capsule slime to form
they communicate with each other and upregulate certain genes the alg gene over-secrete alginate to form slime and cement to surface biofilm now grows via in house divisions to produce mature biofilm
244
how do gram negative and pos cells communicate with each other
gram postalk to each other by cell signalling via oligopeptides recognition on another cell then response with turning on virulent factor gram neg- acyl-homoserine lactones (AHL,HSL)
245
N-acyl-homoserine lactones (HSLs) how do they produce signals
Every length of carbon cahin you can have a c and oc and a hc All variants behave differently when they talk to each other most studied is pseudomonas aeruginosa
246
low conc of HSLs vs high conc
if below threshold theres no co-ordinated response bit once above threshold they can do something constructive and co-ordinated
247
what does quorum mean
its the density threshold of the amount of bacteria cells needed for a co-ordinated response product starts to be made at this point no point in product production in low conc
248
what bacteria was quorum sensing discouvered in
aliivibrio fischeri-bioluminescence no bioluminescence in low density of bacteria cells but was in high conc had a LuxIR regulon
249
LuxIR regulon strucutre
regulatory genes encoding for HSL i and activator protein R, promotors for both operons then further downstream theres structural gens that encode for light production
250
what happens with LuIR regulon at a high conc of cell
theres enough high level of autoinducer to re-enter the cell and turn on the bioluminescent gene
251
why would bacteria communicate to down regulate genes
to decrease expression of flagella as they wont be swimming anywhere now as they are attached to surface
252
composition of a mature biofilm matric
cells- 2-5% water- around 98%
253
what are exopolymeric substance (EPS)
cellular cement forms matrix framework provides structure and integrity gives biofilms a defined architecture
254
how is the biofilm structured
layers stack upon each other unfair amounts of nutrients so top layer grows faster so produce more matrix becomes top heavy and mushroom shaped
255
if healthy what will biofilms look like
very compact slow growth impenitrible to bacteria
256
what does an unhealthy persons biofilm look like
lots of gaps between biofilm stacks easier for pathogens to exploit
257
is there a max height for biofilms to reach
yes its an equilibrium between birth and death
258
how are cells removed from biofilm in sloughing
turbulence scouring grazing- little impact on human body - if small enough can be phagocytosed 1/3 of stool is gut microflora
259
programmed detachment for bacteria in biofilms
synchronised liberation of daughter cells more hydrophillic daughter cells change in lipopolysaccharides down reg of high mwt LPS leaves low mwt LPS shot out biofilm where attachment elsewhere is possible
260
why is life within biofilm good
protected from desiccation, starvation, poisening, predation, colonisation of other bacteria pooled extracellular enzymes antimicrobial compounds -embedded
261
are biofilms more difficult to kill
can require x1000 fold higher conc of antimicobial agent to kill cells are embedded in a matrix -less diffusion upregulation of stress tolerance
262
pseudomonas aeruginosa genes and what autoinducer do they produce
Lasl-LasR - OdDHL (OC12) RhII-RhIR- BHL (C4)
263
primary and secondary attachment of pathogen colonisation
- preliminary with generic antigens- non specific=to matric and specific=to receptor -secondary- to host adhesion proteins - immediate if no biofilm. if biofilmmust dissolve matrix to avoid dislodgement
264
are pathogen adhesions and extracellular enzymes controlled by QS
no they are virulence factors but not controlled by QS
265
once the pathogen has docked what does it become
an infection
266
how does pathogen infection lead to a disease
cell division --> quorum upregulates or expresses new virulence factors QS controlled leads to disease- when the body starts showing symptoms
267
virulence definition
Virulence refers to the degree of damage caused by a microbe to its host.
268
pathogenicity definition
The pathogenicity of an organism - its ability to cause disease - is determined by its virulence factors.
269
whats an invasin
extracellular protein (enzyme) that some bacteria have that are able to penetrate into or between cells act to break down host cells in the immediate vicinity of bacterial growth (short range)
270
hyaluronidase invasin
produced by strep, staph, clos attacks interstitial cement of connective tissue by depolarising hyaluronic acid can use the hyaluronic acid as a c source
271
neuraminidase invasin
produced by intestinal pathogens like vibrio cholerae and shigella dysenteriae degrades neuraminic acid (sialic acid) , an intercellular cement of the epithelial cells of the intestinal mucosa
272
the invasins streptokinase and staphylokinase
produced by strepto/staphlococci convert inactive plasminogen to plasmin which digests fibrin and prevents clotting of the blood allowing more rapid diffusion of the infectious bacteria can dissolve clots so effective/inexpensice thrombolysis medication in some MI
273
coagulase invasin
produced by staphlococcus aureus makes more collagen so pathogen stays localised
274
collagenase invasin
produced by clostridium histolyticum/ perfringens break down collagen which facilitates gas gangrene in tissue
275
when are endotoxins released
when bacteria lyse
276
are endotoxins direct or indirect
indirect activates many host systems that cause damage
277
are exotoxins specific or unspecific
they act on specific targets
278
What are invasins?
Extracellular enzymes that help bacteria penetrate or break down host tissues.
279
What is the role of hyaluronidase?
It degrades hyaluronic acid in connective tissue, helping bacteria spread.
280
Which bacteria produce hyaluronidase?
Streptococci, Staphylococci, Clostridia.
281
What does neuraminidase do?
It degrades neuraminic (sialic) acid in epithelial cells, aiding bacterial invasion.
282
Which bacteria produce neuraminidase?
Vibrio cholerae, Shigella dysenteriae.
283
How do streptokinase and staphylokinase aid bacterial spread?
They convert plasminogen to plasmin, breaking down blood clots and allowing bacteria to spread.
284
What is the function of coagulase?
it induces blood clot formation to localize the infection, protecting bacteria from the immune system.
285
What bacteria produce coagulase?
Staphylococcus aureus.
286
What is the role of collagenase?
it degrades collagen, facilitating tissue destruction and bacterial invasion.
287
What are the two major types of bacterial toxins?
Endotoxins and Exotoxins.
288
what is an endotoxin?
A lipopolysaccharide (LPS) component of the outer membrane of Gram-negative bacteria, released when the bacteria lyse.
289
How do endotoxins cause damage?
they indirectly activate immune responses, leading to fever, shock, inflammation, and coagulation disorders.
290
What is the toxic component of LPS?
Lipid A.
291
How do endotoxins affect the pharmaceutical industry?
They contaminate drugs, requiring strict removal processes (e.g., LAL assay for detection).
292
What are exotoxins?
Actively secreted proteins that act on specific cellular targets
293
are exotoxins heat-stable?
No, they are usually heat-labile (except some like Staphylococcal enterotoxins).
294
How do endotoxins and exotoxins differ in terms of immunogenicity?
Exotoxins are highly immunogenic and can be made into vaccines (toxoids), while endotoxins are weakly immunogenic and cannot be modified into toxoids
295
What are the three main types of exotoxins?
Cytolytic toxins, A-B toxins, and Superantigens.
296
How do cytolytic toxins work?
They disrupt the host cell membrane by: -Forming pores in the membrane. -Enzymatically degrading phospholipids.
297
What is the function of hemolysins?
They lyse red blood cells (beta-hemolysis) to release nutrients
298
What bacteria produce hemolysins?
Streptococcus pyogenes, Staphylococcus aureus.
299
What are leukocidins?
Cytolytic toxins that specifically kill white blood cells.
300
What are examples of phospholipase cytotoxins?
Clostridium perfringens alpha-toxin and Staphylococcus aureus beta-toxin.
301
What are A-B toxins?
Two-subunit toxins where: B-subunit binds to host cell receptors. A-subunit enters the cytoplasm and disrupts cellular function.
302
What is the function of the B-subunit in A-B toxins?
It binds to glycan receptors on host cells.
303
What is the function of the A-subunit?
It disrupts protein synthesis or signal transduction inside the host cell.
304
What bacterial infections are caused by A-B toxins?
Botulism (Clostridium botulinum). Tetanus (Clostridium tetani). Diphtheria (Corynebacterium diphtheriae). Cholera (Vibrio cholerae).
305
What is the role of Diphtheria toxin?
it inhibits protein synthesis by ADP-ribosylating elongation factor-2 (EF-2).
306
What is unique about the diphtheria toxin gene
It is encoded by a β-phage (lysogenic bacteriophage).
307
How does botulinum toxin cause paralysis?
It blocks acetylcholine release at neuromuscular junctions, preventing muscle contraction.
308
How does tetanus toxin cause muscle spasms?
It blocks inhibitory neurotransmitters (GABA & glycine) in motor neurons, leading to continuous muscle contractions.
309
What is Botox®?
A commercial preparation of botulinum toxin used to relax muscles and reduce wrinkles.
310
What are superantigens?
Exotoxins that hyperactivate the immune system, causing excessive inflammation.
311
How do superantigens differ from regular antigens?
They bypass antigen processing, directly activating T-cells at massive levels, leading to immune system damage.
312
What conditions are associated with superantigens?
Toxic Shock Syndrome (TSS) caused by Staphylococcus aureus and Streptococcus pyogenes.
313
Name some bacteria that produce A-B toxins and their diseases:
e.coli, toxin type A-5B disease gastroenteritis salmonella spp A-B salmonellosis/typhoid fever
314
What are the two types of bacterial attachment to host surfaces?
Non-specific attachment (to the extracellular matrix) and specific attachment (to host receptors).
315
What extracellular enzymes help bacteria penetrate biofilms?
Glycosidases, proteases, and DNase
316
Why do bacteria use Quorum Sensing (QS) before launching an attack?
To ensure they have reached a sufficient population density to overwhelm the host defenses.
317
What are virulence factors?
Molecules that enhance bacterial survival, colonization, immune evasion, and damage to the host.
318
What are the main categories of virulence factors?
Adhesins, Invasins, Toxins, and Siderophores.
319
What are invasins?
Extracellular enzymes that break down host tissues to allow bacterial penetration and spread.
320
What is the function of streptokinase and staphylokinase?
They convert plasminogen to plasmin, breaking down fibrin clots and allowing bacteria to spread.
321
What is the function of neuraminidase?
It degrades neuraminic acid (sialic acid), which is essential for the integrity of epithelial cell junctions.
322
What is the role of coagulase in bacterial infections?
It promotes clot formation, allowing bacteria to hide from immune cells within fibrin deposits.
323
What is the function of collagenase?
It breaks down collagen, facilitating tissue destruction and bacterial invasion.
324
What are endotoxins?
Lipopolysaccharides (LPS) found in the outer membrane of Gram-negative bacteria.
325
How do endotoxins cause fever and inflammation?
They trigger the release of endogenous pyrogens that act on the hypothalamus to raise body temperature.
326
What are some effects of endotoxins on the host?
Fever, shock, inflammation, diarrhea, vomiting, blood coagulation, and weakness.
327
Why are endotoxins a problem in pharmaceuticals?
Even small amounts of endotoxin contamination can trigger severe immune responses in patients.
328
What is the LAL (Limulus Amoebocyte Lysate) assay used for?
Detecting endotoxin contamination in medical products.
329
How do exotoxins differ from endotoxins?
Exotoxins are secreted proteins, while endotoxins are part of the outer membrane. Exotoxins act on specific targets, while endotoxins have systemic effects.
330
How do cytolytic toxins work?
Inserting into the membrane and forming pores. Enzymatic degradation of phospholipids in the membrane.
331
What are hemolysins?
Cytolytic toxins that destroy red blood cells.
332
What bacteria produce hemolysins?
Streptococcus pyogenes, Staphylococcus aureus.
333
What are leukocidins?
Cytolytic toxins that specifically kill white blood cells (leukocytes).
334
How do A-B toxins enter cells?
B-subunit binds to a receptor on the host cell. The toxin is endocytosed. A-subunit enters the cytoplasm, disrupting cell function.
335
What is the mechanism of Diphtheria toxin?
It inhibits protein synthesis by ADP-ribosylating EF-2, preventing translation.
336
How do superantigens affect the immune system?
They bind directly to MHC-II and T-cell receptors, bypassing normal antigen presentation, leading to excessive cytokine release.
337
who developed first antibiotic
Alexander flemming in 1928 penicillin
338
when did chemists start working on synthesising antibiotic instead of naturally occuring bacteria
1960
339
antibiotic definition
substances that are selectively toxic to microorganisms they kill or inhibit microorganisms without harming the patient
340
how are antibiotics selectively toxic
because of the differences between prokaryotic and eukaryotic cells
341
examples of ways antibiotics can be delivered to humans and anumals
humans- pills, injections, iv, meats that have been given antibiotics animals- food, water, excretion from both - environment becomes sink - natural bacteria starts becoming resistant
342
what layer does penicillin target
peptidoglycan layer
343
why doesnt penicillin go for human cells
as it target peptidoglycan layer wich is only found in bacterial cell walls
344
how are antibiotics classified
based on chemical structure, spectrum of activity and mode of action etc
345
do bactericidal agents kill bacteria
yes- inhibit the cell wall formation of bacteria and irreversible
346
do bacteriostatic agents kill bacteria
no but they prevent growth of bacteria - arresting growht reversible - dont complete course it will come back inhibit dna replication and protein synthesis work with the immune system- let it catch up and remove threat
347
wahts minimal bactericidal concentration
MBC refers to the conc of drug required to kill 99.99% od bacterial population
348
class of penicillins
beta-lactam group of antibiotics
349
mechanism of action of penicillin
They are cidal ( kill bacteria) by binding to and destroying bacteria cell walls thereby resulting in bacterial death.
350
penicillin spectrum of activity/clinical units
Skin soft tissues, chest infection, pneumococcal, meningococcal and staphylococcal infections ( fluclox) but there are major problems with resistance.
351
side effects of penicillins
allergic reactions- rash or anaphylactic reactions
352
peptidoglycan structure
repeating polymer MG(NAM-NAG) polymer chains cross linked via peptide bridges G= N-acetylglucosamine (NAG) M= N-Acetylmuramic acid (NAM)
353
how does penicillin affectbacterial cell wall
interferes with linking enzymes and NAM cells burst from osmotic pressure because the integrity of peptidogylcan cant be maintained
354
mechanism of action of aminoglycosides
binds to ribosomes and prevents protein synthesis
355
spectrum of activity of aminoglycosides
Broad spectrum against mainly Gram negative bacteria such as E coli, pseudomonas, klebsiella , proteus. They have limited activity against Gram positive bacteria often used in combination with Beta-lactam antibiotics to treat Gram positives such as streptococcal and staphylococcal infections.
356
clinical uses of aminoglycosides
Used for UTIs, intra-abdominal infections, gynaecological infections, used in combination with penicillins to treat endocarditis.
357
sides effects of aminoglycosides
hearing loss- ototoxicity renal impairment - nephrotoxicity
358
examples of aminoglycosides
gentamicin streptomycin
359
ecamplesof tetracyclines
tetracyclcine doxycycline
360
mechanism of action of tetrcycline
prevent bacterial protein synthesis and bacteriostatic rather than cidal
361
spectrumof activity and clinical uses of tetracycline
broad spectrum against gram + some gram - treat skin soft tissue infections chest infections lyme disease rickettsial infections
362
metabolism of tetracyclines
Tetracyclines are well absorbed after oral administration. Penetration is good into bone, skin, lung and kidneys. It is inactivated by the liver and excreted into faeces and urine. They bind to calcium and magnesium to form an insoluble complex. Their absorption is therefore inhibited by dairy produce.
363
contraindicition / side effects of tetracyclines
not forpregnant women and children -affects skeletal development teeth discolouration photosensitivity
364
tetracycline binds to what
bind to A site of 30s ribosomal subunit
365
what does tetracycline prevent
binding to trna to a site prevents protein synthesis bacteriostatic
366
tetracycline efflux
limit access of tetracylcin to ribosomes - intracellular conc reduced by pumping it out the cell efflux resistance genes found on plasmids resisitance gene product is cytoplasmic membrane protein thats energy dependent tetracycline transporter efflux genes found on gram+ and -
367
questions that need asking before prescribing antibiotics
Have they got an infection? What type of infection do they have? - fungal, bacterial, viral ? Can I wait for culture results or do they need empiric antibiotics? - how sick is person? Aim to give targeted antibiotics whenever possible. Not all positive microbiology needs antimicrobial treatment.
368
examples of factors to consider when choosing antibitoic
organism related factors- site of infection/ likely pthogen, sensitivity patient related- immune status, renal/hepatic function, tolerability, side effects, pregnancy, children antibiotic related- absorption, half life, protein bidning, metabolism, eliminations, active metabolites,drug interactions
369
mechanism of resistance for strptomycin
ribosome and streptomycin bind very tightly ribosomes loose conformation from mutation streptomycin can no longer bind
370
inhibitors of protein synthesis
aminoglycosides tetracycline and some aminoglycosides chloramphenicol
371
how many ribosomal protection proteins are there
9 tet(M), tet(O), tet(S), tet(W) tet(Q), tet(T) otr(A), tetP(B) and tetC
372
what do ribosomal protection proteins do
they are cytoplasmic proteins that protect the ribosomes from the action of tetracycline:
373
how do ribosomal protection proteins protect ribosomes from tetracycline(4)
- interact/associate with ribosome- making insensitive to tetracycline inhibition - they bind to ribosome causing alteration conformation preventing tetracycline from binding to the ribosome - stopping protein synthesis - genes for ribosomal protection found on plasmids and self-transmissible chromosomal elements -tet(X) gene is example of tetracycline resistance due to enzymatic alteration- tet(X) is 44-kDa cytoplasmic protein that chemically modifies tetracycline in presence of oxygen and NADPH
374
example reason for increasing antimicrobial resistance
-inappropriate use of antibiotics like animal husbandry and agriculture (pig farming) -weak antimicrobial resistance surveillance -poor infection prevention (prevention better than cure) -insufficient diagnostic, prevention and therapeutic tools -overuse of them -disruption of commensal microflora, natural protection from -pathogens- increased antibiotic use -antibiotics in water supply?
375
why is antimicrobial resistance a problem
treatment failure increased mortality increased health care cost resistance spread in the community spread of resistance from acute to primary care and country to country
376
whats intrinsic resistance
naturally occuring due to normal genetic, structural or physiological state of the organism - antiobiotic sensitivity- no site for antibiotic to do its thing
377
whats acquired antibiotic resistance
results from altered genetic structural or physiological state of organism 1-induced genetic mutation (after pressure from antibiotics) 2- acquired-by transfer of genetic material from one bacteria to another
378
examples of ways microorganisms can be antibiotic resistance
no binding site/ altered efflux pump enzyme production that inactivates antibiotic alternate metabolic pathway decreased permeability or loss of porin channel biofilm formation
379
how does alternative metabolic pathways create antibiotic resistant bacteria
This is when an antibiotic acts by inhibiting a metabolic pathway in the microorganism but the cell reverts to using an alternative pathway to evade the action of the antibiotic
380
are genes that confer antibiotic resistance carried on chromosome or plasmids
either
381
how do plasmids move between bacteria
horizontal gene transfer trasnduction conjugation transformation
382
transduction for HGT
This is when an antibiotic acts by inhibiting a metabolic pathway in the microorganism but the cell reverts to using an alternative pathway to evade the action of the antibiotic
383
2 cycles for transduction for HGT
lytic cycle lysogenic cycle
384
conjugation fro HGT
uses plasmids recipient cell has no plasmids cell comes together and attach plasmid doesn't transfer as whole entity sends a strand in which re-circularises requires proximity so biofilms are ideal
385
transformation in HGT
free-dna is picked up from the environment recombination occurs between donor dna and recipient dna
386
how do eukaryotes effect recombination
the sexual cycle and meiosis
387
how do prokaryotes achieve genetic exchange (3)
transformation - uptake naked dna conjugation- utilise plasmids transduction - utilises bacteriophages
388
True Pathogen (obligate)
an organism that can cause infection in individuals with normal host defences. e.g. Vibrio cholerae , Chlamydia trachomatis, Yersinia pestis
389
Opportunistic pathogen ('opportunist') + examples
an organism that can cause infection in individuals with abnormal host defences. Commensals may be opportunistic pathogens e.g. Staphylococcus aureus, Pseudomonas aeruginosa
390
pathogenicity defintion
capacity of an organism to cause disease will it wont it
391
how do you know that a given pathogen causes a specific disease
kochs postulates: - pathogen present in every case - pathogen isolated from diseased host and grown in pure culture (viruses?????) -specific disease must reproduce when pure culture of pathogen is inoculated into health susceptible host - pathogen must be recouverable from experimentaly infected host
392
limitations of Kochs postulates
Viruses (2nd postulate) Host effects (3rd postulate) Polymicrobial infections Infectious doses
393
how can we exploite virulence factors
toxins- diphtheria- toxoid immunisatiom. tetanus- antitoxin capsule- strep pneumoniae- vaccine adhesions - uropathogenic e.coli= nothing yet
394
commensal microbial load in cm^2 in large intestine
10^14
395
ratio of aerobes to anaerobes in skin and colon
skin = 1:1 colon= 1:1000
396
what sort of things change normal flora
changes in hormonal physiology/development antibiotics can select for resistant flora- candida overgrowth in mouth. c diff new organisms can be acquires- neonate from maternal genital tract during birth. gram - colonoistaion of gut and urinary tract in hospital patient. cross-infection with c.diff, MRSA, VRE
397
cholecystitis and cholangitis
gall bladder swelling and inflammation of bile duct system
398
harmfull effects of gut bacteria
normal flora escapes- e.g. burst appendix leading to peritonitis cholecystits and cholangitis- often mixed infection, e.coli and enterococci uti
399
how do you treat opportunistic infection
address host factor more than using antibiotics
400
ways in which you can get opportunistic infection
immunosuppression-cancer, transplant breach defences- iv, catheter, wound foreign body- prosthesis, splinter debility- malnutrition, ill, old age
401
c diff symptoms
diarrhoea fever loss of appitate nausea pain
402
c diff shape and gram stain
rod-shaped gram +
403
does c diff form spores
yes
404
is c diff anaerobic or aerobic
anaerobic - strictly
405
whos vulnerable to c diff
antibiotics PPI- reduce stomach acid hospital setting 65+ IBD,cancer,kidney problems (underlying condition) weakend immune system surgery on digestive system
406
c diff virulence factors
resistant to lysozymes adhesins- cwp famproteins, fibronectin, collagen,lipoprotein, HSP invasins - proteases, flagellae
407
what does c diff do togut
24hrs after exposure- normal 30+ hrs-toxins damage cells = inflamm and fluid build up 36+- inflamm cells burs, spores leave colon and spread
408
whats mucormycosis caused by
fungus in order mucorales
409
mucormycosis characterised by what
hyphae growing in and around vlood vessels life threatening in diabetic or severly immunocompromised
410
how does gram stain shift in immunosuppressed patients
gram+ to gram - opens up person for infection
411
whats latent pathogen mean simply
when you think the pathogen is gone it hasnt and comes back to haunt
412
whats the spleen do
filterp main antibody production site efficient clearance of bacteria
413
post splenectomy sepsis
only got houts severity assessed organ failure high mortality (50-70%) mainly caused by s.pneumoniae
414
how is post splenectomy sepsis prevented
immunisation anitimicrobial prophylaxis - long term penicillin, probs not indefinate
415
how to prevent infections
-Immunization -Appropriate infection control -Engineering controls (filters etc) -Selected screening for latent infection with appropriate treatment and/or suppression -Prophylaxis
416
hows aspergillus prevented
Aspergillus prevention Filtered hospital air Barrier protection during renovation or construction Protective isolation (HEPA filtered) for hematopoietic stem cell transplants Provide respiratory protection when patients must leave protected environment
417
hows legionella prevented
Prohibit showers (use sponge baths) Implement surveillance for Legionella cases Monitor water supply: if Legionella present initiate decontamination (controversial)
418
what % of hospitalised patietn acquire infection
5-10%
419
HAI
hospital acquired infection they are notpresent in incubation at admission does count if you get ill after discharge
420
most common HAI
surgical site infections(30-35%) UTI- 20% pneumonia <20% sepsis 3-5% other <20%
421
exogenous sources of HAI
direct inoculation into patient without colonisiaiton in ICU - hygienic measures - easy to prevernt
422
endogenous HAI sources
infections caused by already colonising microorganisms
423
difference between early and late endogenous
early- colonizing flora which patient had before hospitalization (S.pneumoniae, E.coli) late- hospital flora which which firstly colonizes patient’s body, and then can cause infection flora (MRSA, P.aeruginosa)
424
the 3 tyoes of HAI possibilitys
commensal nosocomially colonised patient infected patient
425
susceptible populations exampls
surgical patients ICU patients burn patients immunocompromised patients elderly age in general
426
symptoms of necrotizing fasciitis
fever, swelling, pain skin changes similartocellulitis or abscess hardening of skin redness skin shiny and tense
427
signs of later stages ofnecrotizing fasciitis
bullae bleeding into skin gas in the tissue reduced sensation over skin - nerve damage
428
risk factors necrotizing fasciitis
poor immune function cancer obesity alcoholism IV drug use peripheral artery disease trauma surgery
429
type 1 necrotizing fasciitis
70-80% cases mixture bacterial types normally abdominal or groin areas gram+ = staph aureus, strep pyogenes, enterococci gram- = e.coli, pseudonomias aeruginosa and anaerobes
430
whats clostridial infection
accounts for 10% of type 1 necrotizing fasciitis infectio
431
what clostridium species caused clostridial infections
Clostridium perfringens, Clostridium septicum, and Clostridium sordelli (which typically cause gas gangrene
432
what toxins does clostridium perfingens produce in clostriial infection
a-toxins- excess platelt aggregation, acidic o2 deficient envi for bacteria. can inhibit migration of WBC a-toxin and gamma-toxin = destruction of RBC. damage blood vessel integrity. suppress heart function
433
type II necrotizing fasciitis
20-30% cases extremities strep pyogenes bacteria alone or with staph affects young healthy adult with aninjury
434
type III necrotizing fasciitis
vibrio vulnificus found in saltwater break in the skin
435
type VI necrotizing fasciitis
possibily fungal in nature
436
different risk areas in hospital
high= operating theatre, incubators, sterile units moderate= patient room, exam rooms, wating rooms low = corridors, cafes
437
what HAI pathogens are transmitted through air
staph acinetobacter aspergillus
438
What are the two main pathways for repairing DNA double-strand breaks (DSBs)?
Non-homologous end joining (NHEJ) and homology-directed repair (HDR).
439
What are the four steps of homology-directed repair?
1) Presynapsis: Generation of single-stranded DNA (ssDNA). 2) Synapsis: Pairing of ssDNA with an intact homologous duplex to form a heteroduplex. 3) Postsynapsis: DNA synthesis using homologous DNA as a template. 4) Resolution: Separation of two DNA duplexes.
440
What role does the RecBCD complex play in homology-directed repair?
It generates single-stranded tails at DSBs by helicase and nuclease activity, with modulation by Chi sequences.
441
whats the global bacteria cells number
5x10^30
442
examples of emerging bacteria threats
yersinia pestis- plague legionellapneumophila camplobacter spp helicobactr pylori chlamydia staph aureus (MRSA)
443
types of yersinia pestis infections
pneumonic plague bubonic plague septicemic plague
444
whats the most serious bioterrorism threat to humans
the plague aerosols/low infective does spreads easily availability in nature fatal if not treated
445
is legionella pneumophila always a threat
no not a threat in natural envi only in human areas like air conditioning systems and warm areas created by humans
446
are biofilsm a threat
yes on gums catheters implantations harbour infections can spread through body causing septicaemia
447
antibiotic alternatives
use less- selectivity develop new ones use poo
448
why use poo as a antiobitoc alternative
full of bacteriophage these infect bacteria they are ubiquitous and have a huge diversity
449
how much of marine bacteria can be infected by phage
70%
450
is sea water a good sources fro phages
yes dense natural source for phage and other viruses 9x10^8 virions per ml-1
451
phage structure
genetic material- ssRNA, dsRNA, ssDNA, dsDNA. in circular or linear forms capsid potion and then tail portion that varies in legth or can be absent - has tail spikes, helical sheath,core, collar
452
is phage therapy lytic or lysogenic therapt
lytic
453
will phage replace antiobiotics
no but promising role in situations where antibiotics arent sufficient alone
454
where to source bacteriphages
collect local water samples like effluent outlets or sewage corpses
455
why are phages better than antibiotics
effective when super bacteria appears teh super phage already attacks it localised use stop reproducing once bacteria destroyed
456
why are antibiotics better than phages
phage must be refrigerated doctors need special training difficult to treat multiple infection IV phage applucatoon- human antibiodies produced different cocktails of phages needed region to region or even person to person viruses cant alwasy reach site of bacteria negative public perception
457
how to deliver phages
Intramuscular, SC, intraperitoneal oral for GI infections localy- topical for wounds, ear for P.aeruginosa
458
manuka honey use
effective against 80 microorganisms Affects osmolarity Peroxide activity Methylglyoxal is the major antibacterial component Targets include: stress and membrane proteins Decreases: quorum sensing, Siderophores (access to Fe) surface adhesion Biofilms Inhibits formation Disrupts established biofilms Inhibits adhesion to epithelial cells Binding to humans cells
459
teixobactin
a new antibiotic active against c.diff,bacillus anthracis, MRSA, m.tuberculosis ineffective against most gram - effective at low dose not commercially available as haven't figured out how to deliver into the body
460
whats a parasite
eukaryotic organism that live in or on another organism and causes harm to the host they cause harm to the host
461
is there such thing as a good parasite which doesnt cause harm to its host
no all parasites causes some level of harm
462
what are the 2 main groups of parasites
protozoa helminths (worms)
463
how many cell organisms are protozoa
single cell
464
how many cells do helminth organisms have
they are multicellular vary from from small to very large often have small eggs
465
which parasite species causes malaria
plasmodium spcies parasite
466
what is a giardia and where does it live
a parasite and lives in gut
467
where do cryptosporidium parasite live
in the gut
468
the 2 examples of helminth parasite that need to know
schistosomes (Schistosoma species) roundworms (Ascaris lumbricoides)
469
what parasite species cause hookworms
Ancylostom and necator
470
what parasite causes liver flukes helminths
Fasciola
471
what parasites causes filarial nematodes helminth
brugia and wuchereria (Elaphantiasis)
472
what parasites cause tapeworms
Taenia and echinococcus (live in gut but dont cause major harm to host)
473
whats the direct methods of diagnosis of parasites
visulalisation of the parasite (Classical parasitological diagnosis) detection of some specific component of the parasite like DNA or antigen detection tests
474
what are the 3 methods of diagnosis of a parasite
direct method indirect method sample type
475
indirect methods of parasite
involve detection of the effects of parasite like clinical diangosis from symptoms biochem test like change in blood metabolites serological tests like antibodies against parasites
476
how are sample types used to diagnose parasites
blood and stool samples urine, sputum, tissue biopsy less used which sample is taken is dependent on the parasite thats suspected
477
how do you find the prevelence of a parasite from population including false neg and pos results
prevelance = total positives (including false ones) / total population (All results even false neg and pos)
478
sensitivity in terms of parasite diagnostic tests
sensitivity= proportion of true positives identified true positives / true positives + false negatives if the sensitivity is high then small number of false negatives
479
specificity in terms of parasite diagnosis
proportion of true negatives identified true negatives / true negatives false positives high specificity = small number of false positives
480
sensitivity definiton (in parasites)
measures how often a test correctly identifies a person who has the condition (true positive rate)
481
specificity definition (parasites)
measures how often a test correctly identifies people who do not have the condition that being tested for (true negative rate)
482
is the diagnostic tests for parasites perfect
no you get false negs and pos and we dont know actual prevalence of disease in the population - only have a sample taken from the population theres normally a trade of between specificity and sensitivity (if ones increased it can lead to the other being decreased)
483
when is the sensitivity more important than the specificity of a paraste test
when its a life threatening infection (as its more important to get who has the condition correct rather than the correct id of who doesnt)
484
when is the specificity more important than the sensitivity in tests for parasites
extent of treatment side effect if serious side effects its better to know specificity than sensitivty
485
what 5 species are known to cause malaria
Plasmodium falciparum Plasmodium vivax Plasmodium malariae Plasmodium ovale Plasmodium knowlesi
486
whats the transmission malaria overview
bit by femail mosquitoes Anopheles spp (> 100 species)
487
whats the best known vector of p.falciparum malaria in africa
Anopheles Gambiae
488
what are the known animal reservours of malaria
no significant animal reservoirs except P.Knowlesi in macaque
489
what are the diagnostic stages inmalaria
in the blood stream in forms rings trophozoites schizonts gametocytes
490
how many cases of malaria per year
247million 620 000 deaths
491
where are the majority if malaria ifections
90% in africa
492
between the 5 types of malaria whats the frequency of each compared to one another
P. falciparum > P. vivax >> P. malariae > P. ovale >> P. knowlesi
493
how many cases of malaria is p.falciparum responsible for
around 50%
494
how mant cases of malaria is p.vivax responsible for
43%
495
when do you use antibody detection for malaria
not for diagnosis use ELISA (Enzyme-Linked Immunosorbent Assay) IFAT (Indirect Fluorescent Antibody Technique) The IFA technique can be used to determine if a patient has been infected with Plasmodium. Because of the time required for development of antibody and also the persistence of antibodies, serologic testing is not practical for routine diagnosis of acute malaria. also useful for: Screening blood donors involved in cases of transfusion-induced malaria when the donor’s parasitemia may be below the detectable level of blood film examination Testing a patient, usually from an endemic area, who has had repeated or chronic malaria infections for a condition known as tropical splenomegaly syndrome Testing a patient who has been recently treated for malaria but in whom the diagnosis is questioned.
496
classic symptoms of malaria
cold stage- shivering, temp rise hot stage - peripheral vasodilation (flushed), high pulse, high temp(41c) sweating stage - copious sweating, fall in temp
497
common symptoms of malaria
anaemia splenomegaly jaundice
498
what is cerebral malaria
a serious complication of p.falciparum infection results in coma
499
examples of direct parasitological tests
microscopy- thick and thin blood filsm (current gold standard) quantitatve buffy coat (QBC) - acridine orange
500
molecular biologu method of testing for malaria
PCR
501
detection of specific malaria antigens tests
(immunochromatographic malaria rapid diagnostic tests (mRDTs) -Paracheck-Pf - histidine-rich protein 2 (HRP2) -Binax (ICT) – HRP2 + aldolase (a pan-malarial antigen common to all four malaria species) -OptiMal – detects a species-specific enzyme, parasite lactate dehydrogenase (pLDH), produced by live malaria parasites
502
what do the thick and thin films of malaria show us
thick - sensitivity - detects parasitaemia as lowas 0.0001% thin-specificity - speciesid, counting of parasites stained with giesma, leishmans, feilds or similar
503
positive sample of QBC malaria psotive
 -Crescent-shaped gametocytes will appear near the interface of the lymphocyte/monocyte and platelet layers.  -schizonts and mature trophozoites may appear in the granulocyte layer. -Ring-shaped immature trophozoites will appear throughout the red blood cell layer, with a concentration near the interface with the granulocyte layer.
504
what are the 3 main types of leishmaniasis
visceral (or kala-azar) cutaneous (or oriental sore) mucocutaneous (or espundia)
505
how is leishmaniasis transmitted
bite from infected female sand flies specifically phlembotomus and lutzomyia species
506
whats the main diagnostic stage for leishmaniasis
amastigote stage these multiply in cells such as macrophages
507
how many people are at risk of leishmaniasis
350 million in 98 countires
508
how many cases of leishmaniasis /yr
visceral (VL) 200 - 400K cases/yr (fatal) cutaneous (CL) 0.7 - 1.2M cases/yr (disfiguring)
509
whats the visceral leishmaniasis fatality rate
95%
510
where is most of visceral leishmaniasis found
90% found in indai, Bangladesh, brazil, sudan
511
wyas visceral leishmaniasis is diagnosed
-clinical (anaemia, leucopenia) -antibody detection (Agglutination -test, ELISA, IFAT,ICT) -parasitological (amastigotes in aspirates from splean, lymph,liver, promastigotes detection) -antigen detection (KAtex urine test) -molecular bio(PCR,NASBA)
512
whats the incubation period for visceral leishmaniasis
1-2mnth to over 10yrs so can be asympotomatic for years
513
symptoms of visceral leishmaniasis
fever, splenomegaly, hepatomegaly, anaemia,wasting, pigmentation, swollen lymph nodes, infections post kala-azar dermal symptoms like skin rash can occur later
514
how is a parasitological splenic aspirate taken for leishmaniasis done
large needle through the abdomen into spleen very invasive high infection risk requires skill hospital setting (not all these are feasible in LICs)
515
how are parasitological samples of leishmaniasis taken for diagnosis for microscopy
remove tissue from CL lesion stain with Giemsa find the amastigotes in smear difficult to find if low infection level is ways to take sample and grow sample to see if promastigotes are present
516
KAtex urine test
direct test latex agglutination test - latex particales coated with antibodies against leishmania antigen non invasive sensitivity 47-95% specificity 82-100% (low false pos)
517
direct agglutination test for leishmaniasis
antibodies produced against surface antigens of parasites DAT detects antibodies to the parasites in blood/serum uses freeze dried trypsin-treated fixed stained L.donovani promastigotes pale blue= pos result
518
DAT for leishmaniasis sensitivity and specificity
96.5%-100% sensitive 91-95% specific does have reproducability problems has problems with false pos but easy to read an no equipemnt required
519
whats an IFAT test for leishmaniasis
indirect fluorescent antibody test leishmania promastigotes on slide human serum diluted and label with dye
520
IFAT pos and neg
very reliable but requires flourescence microscope and is technically demanding sensitive 96% specific 98% not suited for field conditions used for diagnosis of VL since 1970s
521
ELISA test in diagnosing leishmaniasis
VL serological screening 96 wells coated with antigen patient antibodies and antigen quanitifed using enzyme labelled anti-human immunoglobulins large no of samples at same time sensitive and specific but needs lab
522
immunochromatographic strip test for diagnosis of leishmaniasis
rapid serodiagnostic test nitrocellulose strips impregnated with recombinant rK39 antigen dectects antibodies against L.donoani and infantum sensitivity 100% specificity 98% less specific in feild conditions
523
transmission cycle of visceral leishmaniasis in brazil
lutzomyia longipalpis vector of leish infantum dogs sole reservoir humans incidental host vector is abundant in animal sheds
524
Brazilian MoH response to leishmaniasis
100k dog death 6-8k human deaths spray insectiside after human case reservoir dog control - kill infected dogs drugs education
525
what samples are taken from dogs to test for leishmaniasis
hair - 2g of it collected and stored at 4c blood- for PCR- 5-10ml collected in 10ml K2 EDTA-coated tubes by venepuncture of leg or neck
526
electronic noise as a diagnosis tool for leishmaniasis
clear diff between infected and uninfected dogs with sensitivity and specificity >94% needs alot more testing but is promising for future diagnosis
527
how and what is Giardiasis caused by
caused by Giardia duodenalis, flagellated enteric protozoan occurs after ingestion of cysts in water, food or faecal-oral
528
how does Giardiasis develop
after ingestion of cysts in SI excystation releases trophozoites (multiply by longitudinal binary fission can be free or attached in gut using a sucking disk encystation occurs and parasite moves towards colon cysts passed in faeces
529
how many people worldwide are infected with giardiasis
estimated 250million mainly in tropical countries 3000 cases/yr in england 2.5mill in USA
530
hows giardiasis diagnosied (LIST)
clinical diagnosis (symptoms/signs) parasitological diagnosis - trophozoites and cysts in stool- direct immunoflourescence direct antigen tests (Lateralflow, ELISA) molecular methods (real time PCR)
531
symptoms of giardiasis
diarrhoea for >1week eggy belching abdominal distention nausea foul-smelly bulky explosive watery diarrhoea malabsorption/malnutrition if severe diarrhoea chronic - non-blood diarrhoea, cramps, bloating, nausea, weight loss
532
what do direct flourescence assay detect in giardiasis and whats the sens and spec
detects giardia cysts specificity and sensitivity is 96-100%
533
Giardia intestinalis ELISA Ag test
-Detects antigen found in Giardia cysts -Sensitivity 97%; Specificity 100% (cf. microscopy) -Can be used on fresh, frozen or preserved specimens (10% formalin) -Suitable for symptomatic patients with repeated negative stool microscopy -Or where there are no experienced microscopists -Discriminates from Crohn’s disease and ulcerative colitis
534
what is cryptosporidiosis and how do you get it
cryptosporidium spp are coccodian protozoans (distant malaria relative) first diagnosed in 1976 get it from oocysts ingested in water and food
535
what are the reservoirs for cryptosporidiosis
mammals reptiles fish birds
536
cryptosporidiosis life cycle
Following ingestion, excystation occurs, sporozoites are released and parasitize epithelial cells of the small intestine. Two different types of oocysts are produced, the thick-walled, which is commonly excreted from the host, and the thin-walled oocyst , which is primarily involved in autoinfection. Oocysts are infective upon excretion, thus permitting direct and immediate fecal-oral transmission.
537
location of most cryptosporidiosis
worldwide but more common in tropics less common than giardiasis
538
how many cryptosporidiosis cases in uk and africa
3000-6000 in uk 3million infants in Africa
539
diagnosis methods of cryptosporidiosis
Clinical diagnosis: signs and symptoms Parasitological diagnosis: microscopy of stained oocysts; direct immunofluorescence Direct antigen tests: lateral flow and ELISA Molecular biology methods: real-time PCR
540
signs and symptoms of cryptosporidiosis
watery diarrohea nausea vomiting cramps weight loss bloating fever malaise incubation periods of several days
541
parasitological diagnosis of cryptosporidium
Oocysts not recognised in normal saline/iodine methods need to do Ziehl-Neelsen 70% sensitive 80% specific
542
cryptosporidium ELISA Ag test
Detects antigen found Cryptosporidium cysts Sensitivity 97.7%; Specificity 100% (cf. microscopy) Can be used on fresh, frozen or preserved specimens (10% formalin) Suitable for symptomatic patients negative for other infectious agents Or where expertise in specialised staining techniques for Cryptosporidium oocysts is not available Post-treatment test of cure Techlab, USA, Cat.No.PT5014
543
the taxonomy of tigers an example
species Panthera tigris (tigers) genus Panthera (the big cats) subfamily Pantherinae (biggish cats – inc. clouded leopards, marbled cats) family Felidae (all cats) suborder Feliformia (cat-like – inc. civets, mongooses, hyaenas) order Carnivora (carnivorous predators/scavengers)
544
whats the taxonomy of SARS-CoV2 (NCBI)
species Severe acute respiratory syndrome-related coronavirus subgenus Sarbecovirus (SARS, beta coronaviruses) genus Betacoronavirus subfamily Orthocoronavirinae (“straight” coronaviruses) family Coronaviridae suborder Cornidovirineae (coronaviral nidoviruses) order Nidovirales (“nest” viruses)
545
whats the baltimore classification
and older version of taxonomy more simple type I-VI
546
what types of viruses can cause disease in humans (7)
Deltaviruses Double-stranded DNA viruses Single-stranded DNA viruses Double-stranded RNA viruses Single-stranded RNA viruses (positive strand) Single-stranded RNA viruses (negative strand) Retro-transcribing viruses
547
an example of a deltavirus
Hepatitis D
548
Hepatitis D virus
a deltavirus depends on co-infection with hepB enveloped RNA virus 1700bp, ssRNA, circular, smallest animal virus 20% mortality worldwide spread
549
examples of dsDNA viruses
adenoviridae- human adenoviruses A-G (1-57) Herpesviridae -HSV, VZV, CMV, KSHV, EBV, Roseolovirus Mimiviridae Papillomaviridae -HPV 1-170 Polyomaviridae Poxviridae -Smallpox, tanapox, cowpox Human cirrhosis virus
550
how is adenovirus spread
droplet or faecal-oral route
551
adenovirus 14 stats
2006 USA: 140 cases, 53 hospitalised, 24 intensive care 2007 Lackland Airforce Base, TX, USA: 268 cases, 27 hospitalised, 2 deaths
552
adenovirus 36 stats
30% obese, 11% non-obese Ad36+ve average 52 lbs heavier 7% 1992, 20% 2009
553
signs of herpesvirus
cold sores chickenpox shingles genital herpes
554
what type of virus are herpesvirus
dsDNA
555
what typeof virus is papillomavirus
dsDNA
556
examples of papillomaviruses
plantar warts genital warts
557
whats the most common cause of cervical cancer
70% from papillomarvirus HPV 16 and 18 30% is from 11 other papill virus infections
558
when was smallpox eradicated
1977
559
hows rotavirus spread
faecal oralroute
560
what type of virus is reoviridae (rotavirus)
dsRNA virus
561
how many rotavirus deaths a year
453 000 mainly in LICs and mainly children affected
562
examples of ssDNA viruses
anelloviridae - torque teno virus circoviridae- cyclovirus vietnam parvoviridae - erythrovirus B19
563
ss(+)RNA virus examples
astroviridae- human astrovirus caliciviridae - norovirus flaviviridae- flaviviruses (yellow fever, west nile virus), hepc and g hepeviridae - hep E
564
how many caliciviridae (norovirus) deaths a year
200 000
565
what virus is the leading cause of diarrhoeal death in adults
norovirus a ss(+)RNA virus about half of all food poisening in western world
566
examples of flaviviruses and what type of virus causes them
ss(+)RNA viruses west nile dengue virus tick-bourne encephalitits virus yellow fever virus
567
hows west nile virus spread
by Culex mosquitoes has moved from africa to europe and Namerica recently a sporadic disease outbreaks often in dead birds and horses
568
dengue virus
a flaviviruses ss(+)RNA virus 100million cases/yr 12 000 deaths/year can take months to resolve mainlyin tropical regions
569
tick borne encephalitis virus
200 deaths/yr increasing problem Eurasia in but no one knows why
570
how many deaths from yellow fever a year
30 000 its a ss(+)RNA flavivirus was serious problem in NA during slave trade era now eradicated in NA but still problems in south america
571
what tyep of virus causes Hep C E and G
ss(+)RNA c and g = flaviviridae hep E - hepeviridae
572
how many affected and deaths from Hep C
200 mill infected 350 000 deaths/yr
573
574
hep E mortality rate
2% mortality 20% in pregnant women
575
hep G seropositivity
13% relatively benign minor pathology
576
examples of nidovirales viruses
coronavirues,SARS middle east respiratory syndrome 2012
577
examples of picornavirales
human enteroviruses polio hep A seneca valley virus hand-foot-mouth disease bornhol, disease human parechovirus
578
what sympotms does human enteroviruses cause
many common colds and mild diarrhoeal infection
579
hows Hep A spread
faecal-oral non-fatal hep
580
hand-foot-mouth disease
ss(+)RNA virus discovered in new Zealand in 1957 highly contageous flu-like symptoms + diarrhoea rashs on hands feet and mouth a common childhood infection
581
Bornholm disease virus
ss(+)RNA virus picornavirales in norway in 1872 denmark in 1933 severe lower chest pain unusual infection that stimulates heart attack symptoms
582
examples of Togaviridae ss(+)RNA viruses
rubella ross river virus O'nyon'nyong virus Chikungunya virus Semliki forest virus Barmah virus Sindbis virus
583
2 sub catagorys in ss(-)RNA viruses
arenaviridae bunyaviridae
584
arenaviridae
a ss(-)RNA virus rodent faecal-oral transmission lassa viruses tacharibe viruses haemorrhagic fever
585
haemorrhagic fever
500 000 cases/year 5000 deaths ss(-)RNA viruses
586
examples of tacharibe viruses
a ss(-)RNA virus Guanarito virus (Venezuela, 618 cases, 30% fatality) Junin virus (Argentina, since 1958, 30% fatality) Machupo virus (Bolivia, 200 cases, 12 fatal) Sabia virus (Brazil, only 3 cases) Whitewater Arroyo virus (USA, 3 cases ,all fatal)
587
examples of bunyaviridae
a ss(-)RNA viruses crimean-congo haemorrhagic fever hantavirus dugbe bunyamwera rift valley fever
588
how is crimean-congo haemorrhagic fever transmitted
thebite of the tick hyalloma
589
whats the fatality rate of crimean-congo haemorrhagic fever and Dugbe
30% fatal
590
Hantavirus
10-100% fatal cause severe respiratory syndrome worldwide cases the only bunyavirus thats non-arbovirus like the arenavirus in that it is rodent-borne disease
591
Bunyawera and rift valley fever
ss(-)RNA virus african mosquito borne 2% fatal zoonosis from cattle cattle to humans via mosquito bites
592
does bornaviridae increase risk of psychiatric disease
yes
593
are Filoviruses or Haemorrhagic fevers more dangerous
both caused by ss(-)RNA virus and spread person to person. filoviruses are more dangerous eg ebola virus, marburg virus 34-83% fatal
594
Nipah virus, Hendra virus
flu like symptoms respiratory/renal failure 60% fatality ss(-)RNA viruses mononegavirales paramyxoviridae paramyxovirinae #
595
measles
ss(-)RNA virus mononegavirales aramyxoviridae common childhood western disease rash vaccine started to increase due to MMR vaccien rejectionin UK
596
mumps
ss(-)RNA virus mononegavirales 30% orchitis 15% testicular atrophy/sterility 27% abortion very mild cold symptom dangerous in pregnancy lumps
597
Rhabdoviridae
rabies 97% human cases from dog bites 92% fatal 55 000 deaths/yr
598
examples of retro-transcribing viruses
Hepadnaviridae Hepatitis B Retroviridae Orthoretrovirinae Deltaretrovirus (HTLV-I, HTLV-II) Gammaretrovirus (XMRV, hERVs) Lentivirus (HIV-I, HIV-II) Spumaretrovirinae Spumavirus (Human foamy virus)
599
what type of virus is a risk factor for leukaemia
deltaretroviruses like HTLV-I, HTLV-II
600
what are the top ten global causes of death in 2021
1.Ischaemic heart disease 2.COVID-19 (8.7 million deaths) 3.Stroke Chronic obstructive pulmonary disease Lower respiratory infections Trachea, bronchus, lung cancers Alzheimer disease and other dementias Diabetes mellitus Kidney diseases Tuberculosis NOTE: AIDS no longer in top 10
601
what are the top viral killers
COVID-19 (2021: 8.7 million) AIDS (2008: 2 million; 2012: 1.6 million; 2023: 620,000) Diarrhoea Rotavirus (2004: 527,000; 2013: 215,000) Norovirus (2022: 200,000 - static) Hepatitis B (1.1 million – going up) Pneumonia Influenza (290,000 – 650,000 deaths/year – seasonal; 600,000 to 40 million - pandemic) Measles (1980: 2.6 million; 2000: 548,000; 2011: 158,000; 2023: 107,500) Hepatitis C (2015: 350,000; 2024: 200,000) Rabies (59,000 – going up) Yellow fever (30,000 – 60,000 – fluctuating/static) Dengue fever (2015: 12,000; 2024: 3000) Hepatitis D (5% * 254 million chronic HepB *20% = 2.5 million)
602
what are the clinical categories when diagnosing disease (9)
Jaundice Febrile polyarthritis Haemorrhagic fevers Severe acute respiratory infections (SARI) Encephalitis/meningitis Rash Diarrhoea Arboviruses Rodent faecal-oral
603
viral diseases with jaundice symtpoms
hep A,B,C,D,E,G yellow fever human cirrhosis virus
604
viral diseases that cause febrile polyarthritis as a clinical symptom
Dengue fever (Flaviviridae - Flavivirus) Ross River virus (Togaviridae) O’nyong’nyong virus (Togaviridae) Chikungunya virus (Togaviridae)
605
viral diseases that cause haemorrhagic fevers
Yellow fever (Flaviviridae - Flavivirus) Lassa/Tacharibe viruses (Arenaviridae) Crimean-Congo/Dugbe viruses (Bunyaviridae) Ebola/Marburg virus (Mononegavirales - Filoviridae)
606
viral diseases that cause severe acute respiratory infections (SARI)
Influenza H5N1/H7N9 (Orthomyxoviridae) SARS/MERS (Nidovirales – Coronaviridae) Hantavirus (Bunyaviridae) Adenovirus 14 (Adenoviridae) Nipah/Hendra virus (Mononegavirales - Paramyxoviridae)
607
viral diseases that cause encephalitis/meningitis
Cyclovirus VietNam (Circoviridae) West Nile virus (Flaviviridae - Flavivirus) Tick-borne encephalitis virus (Flaviviridae - Flavivirus) Lymphocytic choriomeningitis virus (Arenaviridae) Rabies (Mononegavirales – Rhabdoviridae) Thogotoviruses (Orthomyxoviridae)
608
examples of viral diseases that cause a rash
Herpes simplex virus (Herpesviridae) Roseolovirus (Herpesviridae) Varicella zoster virus (Herpesviridae) HPV (Papillomaviridae) Smallpox/cowpox (Poxviridae) Erythrovirus (Parvoviridae) Dengue fever (Flaviviridae - Flavivirus) Ross River virus (Togaviridae) O’nyong’nyong virus (Togaviridae) Chikungunya virus (Togaviridae) Rubella (Togaviridae) Measles (Mononegavirales - Paramyxoviridae) Hand-foot-and-mouth disease (Picornavirales
609
viral diseases that cause diarrhoea
noroviruses (caliciviridae) rotaviruses (reoviridae) hand-foot-and-mouth virus (picornavirales)
610
examples of arboviruses
Flaviviridae – Flaviviruses West Nile virus, dengue virus, tick-borne encephalitis virus, yellow fever virus Togaviridae (all except Rubella) Ross River virus, O’nyong’nyong virus, Chikungunya virus, Semliki forest virus, Barmah virus, Sindbis virus Bunyaviridae (all except Hantavirus) Crimean-Congo haemorrhagic fever, Dugbe, Bunyamwera, Rift Valley fever Orthomyxoviridae – Thogotoviruses Dhori virus, Thogoto virus, Quaranfil, Johnston Atoll, Lake Chad see lecture 17, slide 13
611
examples of rodent faecal-oral viral disease
Arenaviridae -Lassa viruses -Tacaribe viruses Bunyaviridae -Hantavirus
612
what does Pfu (plaque forming units) quanitfy
quantifies presence of a virus
613
Haemagglutination inhibtion assay
quantifies the presence of a virus in wells serial dilution when littles/no virus the RBCs settle to a button when there is virus the RBC agglutinate
614
what technique detects viral nucleic acid
diagnostic tests through PCR such as covid 19 pcr tests
615
what technique detects viral proteins
serologic diagnostic test like in covid detection (lateral flow tests)
616
what techniques detect host antibodies to viral proteins
sandwich ELISA antibody-capture ELISA neutralization assay
617
sandwich ELISA
quantifies the presence of virus proteins antigen being tested for on well test sample added wash antibody B added and binds only if antigen was present in sample wash enzyme-conjugated secondary antibody added only binds if AB binds chromogenic substrate added and colour change measured by spectrometry
618
Antibody-capture ELISA
quantifies the presence of antibodies to virus well coated with virus or viral antigen test sample added give time to bind wash any bound will be detected by addition of secondary antibody to which an enzyme is coupled positive result indicated by coloured product
619
whats the biggest viral pandemic
influenza A been around for ages loads of subtypes
620
spanish infleunza A
1918-20 40 million deaths subtype H1H1
621
antigenic drift of influenza A
between pandemics natural selection a response to selection pressures
622
antigenic shift of influenza A
kaunching new pandemics H5N1 H7Nx H9N2 ?? new subtype usually out competes
623
influenza intitially defined by serotypes
if a strain could be neutralized by antibodies raised against another strain (and usually vice versa), those two strains were in the same serotype Serotypes could be defined based on antibodies against H and N proteins A strain could then be defined by its H serotype and N serotype, hence H1N1, H2N2, H3N2 – its subtype
624
is antigenic shift or drift worse news
drift- moderatly bad news- need flu vaccine top up inwinter shift- very bad, new pandemic, current vaccines wont work. probs high death rate
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examples of influenza A reservoirs
wild birds of the sea and shore like seagulls can infect horses and farm animals and humans virus now jumps from all the different reservoirs
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whats the incubation period
the time from contracting the virus to development of symtpoms
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EVD incubation period
Average 11 days – range 2-21 days Average symptoms to hospitalization period – 5 days Average serial interval – 15 days Average time to death – 10 days Average time to recovery – 17 days
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Hep Ab incubation period
almost immediatly theres virus in faeces dont start till about 3rd week
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how long is course of AIDs virus if left untreated
7 years
630
how long is HIV prevalent in a person
the first 9 months the body produces antibpdies for up to 5yrs though
631
where did HIV come from?
HIV-1 appears to have jumped from chimpanzees to humans in central Africa in the late 19th century (estimation by molecular phylogenetics) HIV-1 diversified within central Africa for at least 50 years before achieving a consistent spread outwith that continent by 1970s subtype 1B spread to haiti and then new york, san fran HIV-1C spreadto south africa then india HIV-1A the former soviet bloc
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WNV and where it was first detected and spread
detected in africa but now global in 2000s alarm in USA now spreading in europe expected to arrive in uk
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Zika virus where it started and spread
field survey in uganda 1947 sporadic cases in Africa in 60-80s isolated in malaysia 1966 2007 outbreak on pacific island Yap spread over south east asia reached america in 2015 big outbreak in brazil which then spread brazilian Zika to west africa (serious in pregnancy for child)
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rise in cases of Zika virus
before 2007 only 14 cases confirmed yap island 2007- 183 cases 2013 polynesia outbreak- 32000 by 2015 over 1.3million estimated cases
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what is R
R0= T=0. start of outbreak R begins high then goes down as outbreak progresses R= number of ongoing cases
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how to calculate R
Ps = proportion susceptible Pst = proportion susceptible at time t Rt = R0 x Pst Pr = 1 - proportion susceptible Prt = proportion resistant at time t HET = Herd Immunity threshold = Pr needed for R=1 HET = (R0 -1)/R0 VE = vaccine efficacy = % vaccinated who are resistant Proportion to vaccinate = HET/VE
637
why is Prt always less than R0
proportion and time always less than at beggining g(R0) as people gain immunity
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Zika R values
zika colombia= 3-6.6 zika polynesia = 1.8-2 zika micronesia= 4.3-5.8 zika rio= 2.33
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SARS-CoV2 R number
2.63 new varients about 3.3 omnicrons= 5.5.
640
polio vaccine history
Original vaccine was inactivated (killed) in 1950s 1batchof vaccine which in late 50s has been inaccurately killed- bunch of kids got polio So stopped vaccine (rise in the 60s) And changed to oral vaccine Tenuation vaccine-live virus with mutations – so not virulent Oral vaccine – less hesitancy due to no needles
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attenuation polio vaccine
sequences changes sabin vaccine then reverted to neurovirulent 119 isolate - 6 mutations caused to go back to its virulent form
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how is the yellow fever vaccine made
passage process asibi strain of YFV mouse brain to mouse embryo leads to loss of viscerotropism whole chick to chick embryo tissue without CNS means loss of neurotropism without immune serum
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circulating vaccine derived poliovirus and how itcauses polio
polio spread by faecal oral route in areas with sewage enters water supply individuals can acquire passive immunity cVDPV circulates initially without causing disease can revert back to disease causing form why we dont use oral vaccines for polio in alot of places
644
peptide cocktail vaccine advantages
safe (we think?) wide coverage- no need for new vaccine every year comparatevely cheap
645
peptide cocktail vaccine problems
safety? how to deliver effectivness?
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peptide cocktail vaccine and infleunza
immunise people simulatneouslt to all types of influenza is a possibility autoimmune response can occur if too much protein injected
647
the 5 species that cause human schistosomiasis
Three are widely distributed: Schistosoma mansoni (Africa) S. haematobium (Africa and Middle East) S. japonicum (S.E. Asia and China) Two are more localised: S. intercalatum (Central and W. Africa) S. mekongi (Cambodia and Laos)
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how is schistosomiasis spread
Spread by contact with water containing infective stage (cercariae) that burrow through the skin eggs from female worms shed in faeces and urine so spreads easier in areas of poor sanitation and poverty
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whats the intermediate host for schistosomiasis
snails
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how many people infected and how many at risk of schistosomiasis
240mill infected in 78 tropical and sub-tropical countries 800 mill at risk
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how many deaths per year in africa due to schistosomiasis
300 000
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how is schistosomiasis treated
praziquantel re-infection is very common if water source is still infected and used
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clinical and parasitological diagnosis for schistosomiasis
clinical - signs/symptoms- inflammatory hepatosplenomegaly, fibrosis in portal vein,oesophageal varices, severe chronic fibrotic disease increased portal pressure and ascites parasitologival- eggs in faeces/urine-recommended aproach by WHO
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antigen and antibody detection of schistosomiasis
antibody- ELISA + others antigen - circulating cathodic and anodic antigens - closest to gold standard
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clincial diagnosis of schistosomiasis
cercarial dermatitis (cercaria burrow through skin) Kayatama syndrome S.haematobium causes urinary schistosomiasis- adults paired up in vessels near the bladder and eggs released in urine- causes haematuria, abdominal pain NON of these symptoms are completely diagnostic
656
Kayatama syndroe
dry cough (lung infection) hepatosplenomegaly fever rash weight loss caused by schistosomiasis
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Kato-Katz thick stool smear
used for intestinal schistosomiasis good specificity poor sensitivity for low intensitiy infection widely used
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FLOTAC
a commercially available flotation system to achieve conc of schistosomiasis eggs to increase chances ofseeing them to increase sensitivity
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yr2 (7 decks)

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