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Microbial Pathogens > Environments > Flashcards

Environments Flashcards

1
Q

pathogen

A

MO able to cause disease in plant/animal/insect

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2
Q

pathogenicity

A

ability to produce disease in host

virulence in microbes (genetic,biochemical,structural)

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3
Q

outcome of pathogen + host depends on…

A

virulence and resistance/susceptibility of host

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4
Q

mechanisms of pathogenicity

A

invade
colonise
toxins

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5
Q

invasiveness

A

colonisation, bypass defence mechanisms, substances that facilitate invasion

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6
Q

toxigenesis

A

exotoxins released from bacteria and act away from bacteria

endotoxins are cell -associated like part of cell walls of Gram -ve (capsule, LPS)

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7
Q

opportunistic pathogen

A

part of normal flora

infection in compromised host

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8
Q

primary pathogens

A

cause disease as a result of their presence or activity within the normal, healthy host

regardless of microbiota/immune system

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9
Q

how does the environment affect pathogens?

A

ability to survive in diff environments affect ability to transmit to us and determines reservoirs and modes of transmission
can change physiology if in undesirable env. (like Gram +ve spores) so improve survival

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10
Q

3 constraints of env.

A

temperature
pH
anaerobiosis

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11
Q

psychrophile

A

best at low temperature

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12
Q

psychotroph

A

best at moderate temperature but can live at low temp

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13
Q

phile vs troph

A

phile loves while troph tolerates

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14
Q

mesophile

A

most bacteria

in warm-blooded animals

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15
Q

thermophile

A

wide variation, not pathogens

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16
Q

what temperature range do most microbes grow at?

A

over range of 30 degrees with diff mins maxs and optimums

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17
Q

relationship between growth rate and temperature

A

steady linear increase from min to opt
not linear at optimum
rapid plunge of growth after optimum

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18
Q

cold shock adaptation

A

e.g. E.coli
downshift in temperature so inhibition of protein synthesis and modified ribosomes
growth lag, acclimation phase and cold shock proteins (Csp) induced so adapt ribosomes to cold and resume growth

chaperones are used so ribosomes don’t damage

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19
Q

types of cold shock proteins

A

Class I = >10 fold induction
Class II = <10 fold induction

on word

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20
Q

Listeria

A

non-spore forming Gram +ve bacilli

Listeriosis is quite rare and only in pregnants and immunocompromised

widespread in environment

from contaminated food

can grow in low temps of fridge

invade intestinal mucosa and systemic spread from macrophages to liver

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21
Q

Legionella pneumophila

A

motile, aerobic, Gram -ve rod
disrupt IS in phagocytic cells and avoid destruction
forms biofilm in air-conditioning but not in humans
causes bacterial pneumonia

temp affects motility, piliation, virulence
most physiological attributes like flagella are better at lower temp
adhesion more effective at 25 degrees but more virulent at 37 degrees
dominant role for aquatic env so humans accidental host maybe from heat shock response

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22
Q

pH of natural environment

A

0.5 acidic soils to 10.5 alkaline lakes

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23
Q

pH range for most free-living prokaryotes

A

grow over 3 pH units

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24
Q

pH growth changes are…

A

symmetrical

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25
Q

acidophile

A

optimum below neutral
usually archaea, many fungi
for membrane stability
some obligate acidophiles need low pH because membrane dissolves otherwise

some Thiobacillus species

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26
Q

neutrophils

A

grow best at neutral

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27
Q

alkaliphiles

A

grows best at alkaline like soda lakes, high carbonate soils

abligate alkaliphiles grow around pH10

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28
Q

Bacillus - alkaliphile

A

has sodium gradient not pmf (pH proton) gradient because high pH

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29
Q

intracellular pH

A

optimal pH of organism refers to external pH of env. because intracellular needs neutrality

some can vary internal pH in extreme acidophiles/alkaliphiles

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30
Q

why are buffers used in cultures?

A

maintain pH so not changed by MO growth and waste

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31
Q

pH of most pathogenic bacteria

A

narrow pH range, most pH7

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32
Q

acidic conditions

A

need neutral pH inside - cytoplasmic homeostasis to protect proteins and DNA,
affect capacity for nutrient acquisition and energy generation,
chaperones and aklalisation of periplasm stops denature

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33
Q

Helicobacter pylori (detail on word)

A

gastric and duodenal ulcers
lining of stomach

virulence factors: flagella, urease, adhesins, vacuolating toxin

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34
Q

H.pylori urease

A

neutralise acidic pH of stomach

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35
Q

Koch’s postulates

A

how we know H.pylori causes ulcers
organism from animal put in culture and to another animal from this - should be same as original organism

no animal model for evidence so Marshall drank it himself and got lesions

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36
Q

how does H.pylori survive the acidic pH of the stomach? (what does it colonise, motility, VacA, BabA, UreI)

A

colonise mucin layer not lumen - mucus resists diffusion of protons from stomach acid because composed of negatively charged sulphated polysaccharides which act as buffer so alkaline pH

motility important to reach mucin, but requires short term protection with urease - hydrolyses urea secreted by gastric cells (ammonia + Co2 = neutralise)

VacA - vacuolating cytotoxin produces large vacuoles in mammalian cells

BabA - adhesin recognising LewisB antigen, binds sulphated mucin sugars on epithelial cells

UreI pH sensor - inner membrane protein facilitates urea entry only when acidic pH

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37
Q

Salmonella typhimurium virulence factors

A

adhesins
invasion of mucosal cells of small intestine
type III secretion system (contact dependent)

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38
Q

type II secretion system on Salmonella t

A

acid tolerance and virulence factor
contact dependent - only when contact target cell,
secrete molecules and change cell physiology,
only induced in acidified phagosomes of macrophages

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39
Q

Salmonella acid tolerance

A

grows at neutral pH but survives well till pH 4/5 only if gradual changes

can survive at pH3 if allowed to adapt before exposed, in next generation

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40
Q

Salmonella Fur protein

A

2 regulatory domains, 1 senses iron and 1 senses pH (sensed separately)

iron important virulence factor - hard to get from host, haem full of iron so major toxins haemolysin lyse RBCs for iron

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41
Q

Gram +ve proton pumps

A

F1Fo-ATPases (tolerant bacteria) less sensitive to low pH

GAD consumes protons via glutamate decarboxylation - GABA release

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42
Q

Gram +ve pH tolerance

A 
regulator
cell density - quorum sensing and biofilm growth
altered metabolism
envelope alterations
production of alkali like urease
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43
Q

obligate aerobes

A

require O2 for final electron acceptor in aerobic respiration

a lot of bacteria

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44
Q

obligate anaerobe

A

aerophobes so don’t need O2 and it is toxic,

live by fermentation, anaerobic respiration, bacterial photosynthesis, methanogenesis,

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45
Q

facultative anaerobes/aerobes (+ e.g.)

A

can switch between anaerobic/aerobic metabolism

e.g. E.coli

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46
Q

aerotolerant anaerobes

A

anaerobic metabolism but insensitive to O2 so don’t care

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47
Q

microaerophile

A

obligate aerobe

require O2 but can grow at low levels like below 2 atm

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48
Q

effect of O2 on growth

A

O2 radicals can damage enzymes (H2O2 peroxide or O2- superoxide)

chlorophyll react with O2 in light to produce singlet oxygen radical

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49
Q

how MOs deal with oxygen?

A

aerobes and aerotolerants solve radical accumulation by superoxide dismutase (SOD) which detoxifies radicals)
also catalase - decompose H2O2, almost all have this
and those w/o catalase have peroxidase to decompose H2O2 - electrons from NADH2 reduce peroxide to H2O

obligate anaerobes don’t have these enzymes

photosynthetic MOs protected by carotenoid pigments which react with singlet O2 radicals and lower to non-toxic ground state so detoxify

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50
Q

which MOs contain superoxide dismutase, peroxidase and catalase?

A

SOD: obligate aerobes, most facultative, most aerotolerant

peroxidase: only most aerotolerant
catalase: only obligate aerobes, most facultative

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51
Q

clostridium species are… so…

A

obligate anaerobic pathogens
lack respiratory chain cytochromes, catalase, peroxidase, superoxide dismutase
ATP by substrate-level phosphorylation

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52
Q

substrate-level phosphorylation

A

high energy phosphate bonds from organic intermediates transferred to ADP to form ATP (phosphorylated intermediate not Pi)

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53
Q

lysogenic bacteriophage in C.botulinum

A

virus infects bacteria and remains dormant in DNA, some toxins encoded by these and alter phenotype - lysogenic conversion

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54
Q

exotoxins from C.botulinum

A

released in inactive form, proteolytic cleavage activates it
2 subunits light/heavy linked by disulphide bridge

type A most potent

block release of ACh NT

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55
Q

botulinum toxin mode of action

A

heavy chain (HC) binds toxin to presynaptic receptor so take in by vesicle,
disulphide bond cleaves so chains separate,
LC to cytoplasm and endosomal compartment,
affect proteins for vesicle fusion so can’t release ACh,

zinc endopeptidase LC cleaves synaptosomal-associated protein (SNAP), and vesicle-associated membrane protein (VAMP) and syntaxin

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56
Q

clostridium tetani

A

tetanus - lockjaw
on rust

release antigenic exotoxin which circulates blood, adheres to neuronal receptors and fixes to gangliosides to block glycine NT and GABA release so can’t stop ACh release and causes muscle spasms

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57
Q

C.tetani mode of action

A

HC for cell entry,
C-terminal of HC binds gangliosides, N-terminal allows LC to cross cytoplasm,
LC is a zinc metalloprotease so cleaves synaptobrevin2 (SNARE protein) so vesicles with GABA/glycine can’t dock,
so respiratory paralysis

death so cause anaerobic env for growth

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58
Q

Clostridium difficile

A

antibiotics disturb gut microbiome and reduce conc. of difficile so overgrows and produce toxins A and B

diarrhoea, lesions on colon surface

rapidly fatal because toxins modify host G proteins (glucosyl group added to specific threonine on G protein) and alter actin cytoskeleton

antibiotics not effective so faecal transplantation restores normal microflora

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59
Q

Chagas disease

A

American trypanosoma cruzi

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60
Q

trypanosome types

A

American - cruzi (chagas disease)

African - brucei

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61
Q

mechanical vs biological vectors

A

mechanical - no development in vector e.g. trachoma in bazaar fly

biological - important in life cycle, needs vector, e.g. malaria mosquito, trypanosomiasis tsetse fly

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62
Q

structure of trypanosoma (diagram on paper lecture 4-5 first page)

A

kinetoplastids - flagellated forms, have kinetoplast (modified mitochondria, DNA-containing structure) and nucleus

African tryp. longer and more wavy

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63
Q

trypanosoma life cycle

A

morphological changes in hemoflagellates inside vector and humans

amastigote (circle, almost no flagella) in vertebrate host

paramastigote (more round, flagella begins) in invertebrate hosts

promastigote (longer body and flagella) in invertebrate host

epimastigote invertebrate

trypomastigote in vertebrate host, diff position of nucleus and kinetoplast, important in transmission to and from vector

all stages not infectious until metacyclic trypomastigote in invertebrates and trypomastigote in humans

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64
Q

development for transmission of T.brucei and T.cruzi

A

T.brucei: salivary gland transmission, metacyclic trypanosome only in gland, development then migrate to gland

T.cruzi: in gut, through faecal contamination

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65
Q

Chagas disease vectors

A

reduviid or Triatominae bugs (kissing bugs)

no larvae stage

every stage needs blood

1 meal can be enough for 1 stage

can be long lived - 12 months of starvation

take up to 1ml of blood

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66
Q

Chagas disease transmission cycle

A

in bug faeces - scratch bite and get everywhere

1) metacyclic trypomastigote penetrate various cells
invade IS when invade macrophages, not affected by lysosomes

2) transform to amastigote, to cytoplasm to divide
3) transform to trypomastigotes - movement so bursts out cell to blood to infect more

8 days from infected to infectious
0.6% contact cause infections so contact must be v high for high infections

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67
Q

Chagas disease route of transmission

A

vector-borne kissing bugs (80%)

transfusion of infected blood (<4%-20%)

congenital - regionally high

ingestion of infected sources

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68
Q

2 phases of Chagas disease pathology

A

acute and chronic

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69
Q

acute phase of Chagas

A

symptomatic, 4-8 weeks
usually children or 1st exposure because adults will have chronic if already exposed

fever, gland swell, liver/spleen enlarge, mostly mild but some mortality and severe symptoms

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70
Q

chronic phase of Chagas

A

life long
clinically silent
can progress after 10-20yrs to 20-30% cardiac disease and 8-10% gastrointestinal

genetic variation so diff geographical diff in cardiac/gastro

parasitaemia (levels in blood) drops so harder to detect, not circulating but in cardiac muscle/macrophages

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71
Q

treatment of Chagas?

A

not effective so need prevention

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72
Q

how do you prevent Chagas?

A

vector control

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73
Q

why is vector control hard for Chagas?

A

20 species with diff niches but main 3 in human transmission

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74
Q

Southern Cone Initiative 1991

A

improve housing to reduce vectors and introduce blood screening before transfusions

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75
Q

housing and Chagas disease

A

poorly constructed and deforestation and colonisation means more blood source and habitat
re-infection rates high because of peridomestic vectors (just outside house)

76
Q

white washing (Chagas)

A

plastering walls so no gaps in bricks reduces risk because change vector niche and easier to spot

77
Q

why might insecticide spraying homes not work?

A

have to move all belongings out but might live in there,

lack expertise

might be in farm as well

78
Q

insecticides for Chagas disease

A

DDT not effective and bad
Formulations for walls
paints in development but may be hard to apply

insecticide impregnated materials (ITNs)

79
Q

what is the water droplet in the tsetse fly photo?

A

water droplet so blood more concentrated

80
Q

disease of T.brucei

A

sleeping sickness

81
Q

T. brucei vector

A

Tsetse fly (Glossina spp)

large blood meal

K-strategists - lots effort into producing young and not a lot of them

good vision but need light

salivarian transmitters - multiply in blood stream and migrate and can cross blood brain barrier

82
Q

tsetse fly life cycle

A

don’t lay eggs

larvae develop in females and lay developed larva into soil

83
Q

tsetse transmission cycle

A

morphological changes in vector

procyclic trypomastigote multiplies
epimastigote multiply in salivary gland
blood meal by tsetse so trasmit to humans

3 weeks from infection to infectious and live 6-14 weeks (can reduce transmission if reduce life expectancy of vector)

84
Q

T.brucei diagnosis

A

diagnose later stages with cerebral spinal fluid

chancre circle blisters

85
Q

pathology of HAT (brucei) - early and late stage

A

early stage (haemolymphatic): chancre in 50% rhodesian, through lymphatic system and blood, swollen glands and spleen, local oedema, cardiac abnormalities, headache, fever

late stage (encephalitic): crossed blood brain barrier, sleeping sickness, invade CNS, headache, sleeping pattern, personality, mental function, weight loss, coma and death
acute haemorrhagic leucoencephalopathy (AHL) - brain inflammation and necrosis from O2 starved vessels
86
Q

chancre

A

circle blister from T. brucei

heal to altered pigmentation

87
Q

T. brucie Gambiense vs Rhodesiense

A

phases slightly different

G: long asymptomatic and advanced disease, need early diagnosis

R: acute infection, 1-4 weeks incubation, quickly detectable

88
Q

VSG

A

variable surface glycoprotein on surface of T. brucei

produces strong Ab response

stage-specific: only in trypomastigotes

switch proteins so the ones not detected will proliferate and be selected for

after IS, parasite levels decrease but switches VSG so increased number again (waves)

89
Q

T. brucei treatment

A

4 licensed drugs (on word)

90
Q

morsitans group flies

A

savannah
highly motile
visual and olfactory (smell) cues

91
Q

Palpalis group flies

A

riverine woodlands
less mobile
visual cues

92
Q

Nagana disease in cattle

A

from 3 trypanosomes:
T.b.brucei (chronic to mild)
T.congolense (severe)
T.vivax (less pathogenic) - severe emaciation (blood cells reduced), infertility, reduced milk, weight loss

93
Q

Gambiense control

A

vector control not cost effective

case detection and treatment needed to reduce transmission

94
Q

Rhodesiense control

A

vector control, cattle treatment, so reduce transmission from zoonotic reservoirs, treat to reduce circulation

95
Q

vector control rationale for T. brucei

A

tsetse flies are K-strategists so get rid of few female to to have big impact

96
Q

vector control options for T. brucei

A

destroy larvae sites - not long term

tsetse traps - attracted to dark shapes, electrified, impractical over large areas

insecticide - on traps/animals, effective in open areas

SLT (sterile insect technique) - in Zanzibar, release sterile males but can store sperm so useless if already mated, expensive + intensive

97
Q

problem with using insecticides on cattle to reduce T. brucei (problem, breed selection, solution)

A

would kill tsetse but ticks as well (involved in babesiosis disease) but TBD (tick borne diseases) more severe in older cattle so need to keep exposure to ticks when young so insecticide not helping this

breed selection - Bos tauras susceptible to Babesia but trypanotolerant
Bos indicus resistant to Babesia but susceptible to trypanosomiasis

95% ticks on upperside/bum so diff site from tsetse on legs so only spray legs,
target big ones (at risk - blood meals increase with cattle weight) so leaves young exposed to ticks

98
Q

tiny target traps

A

fly target with mesh with deltamethrin

significantly reduced tsetse population but need combination with case detection and treatment

99
Q

tiny target traps edge effect

A

much stronger effect in centre than edge so re-invasion into centre after removal

100
Q

apicomplexan parasite structure

A

apical complex with secretory organelles

apical organelles expressed during invade/attachment to host cells

101
Q

life cycle of apicomplexan parasites in humans (e.g. malaria)

A

secrete proteins at apical pole to invade (triggered by free Ca in parasite cytoplasm)

conoid in centre of polar rings protrudes so sensitive to Ca

rhoptries (club shaped) near apical end is secreted during invasion

102
Q

3 processes of apicomplexan parasites (development, life cycle)

A

1) SPOROGONY: after sexual phase comes asexual reproduction forming sporozoites
2) MEROGONY: another asexual reproduction to form merozoites, can have many cycles
3) GAMETOGONY: merozoites become gametes by asexual R then sexual R to zygote and differentiate to sporozoites

103
Q

4 distinct Plasmodium species in humans

A

P. falciparum (most virulent, most morbidity + mortality)

P. vivax (concurrent infection, most morbidity in under 10s)

P. malariae

P. ovale

104
Q

malaria vector

A

FEMALE Anopheles mosquito (only females take blood meals)

105
Q

where is malaria mostly?

A

African and South America

106
Q

malaria mechanism

A

1) infected female takes blood meal
2) sporozoites into blood and then infect liver cells
3) to merazoites, buds to merasome to blood
4) merazoites released from marosome to infect RBCs
5) consumes Hb and multiplies to produce symptoms (2 days)
6) RBCs adhere to walls so block flow so affect brain and kidney and avade IS
7) RBCs burst so merazoites infect new cells
8) some into gametocytes (10-12 days) to another mosquito to develop to gametes and zygote, fertilisation and develop to ookinete which invades gut wall of mosquito and form oocyst, mature and divide to sporozoites to salivary gland (survive 59 days)

107
Q

symptoms in malaria are due to?

A

asexual erythrocytic stage

108
Q

P. falciparum

A

cerebral malaria
often fatal

treatment as cost effective as measles vaccine

109
Q

insecticide bednets (ITNs) for malaria

A

reduced mortality by 20%
low mammalian toxicity
high residual effect

LLINs - preffered form, long lasting

110
Q

how does P. falciparum evade host immunity?

A

60 var genes encode hypervariable erythrocyte membrane protein 1
express 1 at a time in erythrocyte stage so evade is switch var during infection

111
Q

why are vaccines not effective for P. falciparum?

A

protective immunity only as long as residual population of parasites present, if curved then susceptibility returns

112
Q

who is immune to P. vivax?

A

it enters through RBC receptor in people with Duffy blood groups
West Africa evolved without this receptor so immune

113
Q

sickle cell anaemia and malaria?

A

protective against malaria because glutamic acid in Hb replaced with valine so reduces O2 carrying capacity and 80-95% protection against P. vivax

114
Q

malaria drug treatments

A

work in 3 ways: kill in liver, kill asexual parasites in RBCs, kill sexual in RBCs

115
Q

antifolates - malaria drug

A

target folate metabolism so reduces folates which are co-factor for biosynthesis of AAs/nucleotides important for malaria to make DNA

116
Q

why does malaria treatment fail?

A

self-treatment - lower doses to save money and stop when feel better
poor compliance
long drug 1/2 life, don’t clear from system
re-infection
expensive

117
Q

sterile insect technique for malaria

A

GM spermless males

ethics of releasing GM

118
Q

cryptosporidium oocytes resistant to what?

why?

A

water treatment e.g. in filtration of pools
because so small
resistant to chlorine and bleach

have double layer protein-lipid-carb matrix

119
Q

filtration of cryptosporidium oocytes

A

can’t remove with sedimentation: small and low density oocytes have low rate of settling

flocculation: surface charge low so clump from chemicals then can use sedimentation

rapid filtration: after flocculation and sedimentation

slow sand filtration: aerobic bacteria on top produce extracellular polymers for natural biological filter

membrane filtration: final, not often in public water supplies

120
Q

disinfection of cryptosporidium oocytes

A

resistant to chlorination and survive bleach for hours

Uv light no evidence

ozonisation

121
Q

cryptosporidium life cycle

A

trophozoite to merogony to meront I to meront II to microgamont to macrogamont to microgametes to zygote to oocyte (infective stage) to faeces to thick walled oocyte to thin oocyte to sporozoites to released and attach to epithelial wall to become merazoite

feeds off host

some form gametes and zygote and oocyte which goes ti faeces

122
Q

invasion by C. parvum

A

free parasite enter intestinal lumen and attach to epithelium surface among microvilli,
microvilli elongate along surface of parasite to form dense band in cytoplasm of host cell, parasite covered by microvilli

where feeding happens

123
Q

therapy for cryptosporidium

A

no safe or effective

supportive care for immuno-competent

some antibiotics (on word)

124
Q

toxoplasmosis

A

T. gondii chronic infection in 1/3 humans and animals

mild in healthy,
life threatening in immunocompromised and foetus

complex life cycle: intestinal/tissue phases
intestinal only in felines, merogony and gamogony,
sexual cycle produce oocytes excreted in faeces

125
Q

toxoplasmosis life cycle

A

feline host

cats eat rodents so tachyzoites ingested and oocyst in cat faeces not infectious but sporozoites later released which infects people and penetrates intestinal epithelium and invades macrophages where binary fission occurs to produce tachyzoites causing host cell rupture and release

cats only infected once so need fresh host

126
Q

toxoplasmosis human infection

A

congenital/blood transfusion/from cats liver tray/other meat

127
Q

dormant/resting toxoplasmosis

A

slow replication, host cells encapsulated (tissue cysts),
bradyzoites secrete chitin and other to form cyst wall to hide from IS

reactivation from waning IS
starts tachyzoite fast stage so tissue damage and inflammation

128
Q

toxoplasmosis and rodent psychology

A

less cautious of cats, reduce fear to complete life cycle

129
Q

toxoplasmosis and human psychology

A

increased risk traffic accidents because prolong reaction times
suicide attempts - personality type increase chance

130
Q

toxoplasmosis and schizophrenia

A

details in notes
42% Sch were T.gondii +ve
some Sch meds inhibit replication

131
Q

toxoplasmosis vaccine

A

for sheep not humans because could become pathogenic

cat vaccine would be useful

132
Q

small colony variants (SCV) of mycobacteria

A

mutations
variant phenotype of S.aureus, normally fast growing but slow in biofilms so hard to kill with antibiotics

get SCvs with other like E.coli., P.aeruginosa, salmonella, gonorrhoea etc.

133
Q

antibiotics for SCV

A

normally target growth but biofilm-mediated infections and TB are slow growing/dormant so hard to treat

134
Q

ionophores (mycobacteria)

A

reversibly bind ions,
chemical structures of various membrane-active agents,
molecules perturb membrane and vary in size/chemical structure - determine if bactericidal and how rapid

high lipophilic content interact with hydrophobic membrane
(clofazimine exception - kills latent mycobacteria but all others have anti-biofilm properties)

135
Q

intracellular pathogens

A

protected from IS/antibiotics,
s. aureus is extra/intracellular,
uptake by non-professional phagocytes,

SCV internalisation mediated by fibronectin bridging between FnBPs and alpha5beta1-integrin receptor

136
Q

leprosy

A

can’t catch easily
chronic disease of skin/nerves - lose sensation

prefers 30 degrees but extremeties like cool nose

migrate to Schwann

facial deformity, ears curl, lose fingertip feeling

high infection dose - 1 cell to infect

cause chronic granulomatous (inside macrophages)

137
Q

leprosy treatment

A

MDT (multidrug therapy) - Clofazimine, Rifampicin, Dapsone, early diagnosis prevents permanent disability, some side effects

138
Q

leprosy structure

A

unique cell wall - capsule like material, mycolic acids up to 20 carbon lengths like wax, peptidoglycan linked to mycolic acids with Arabinan Galactan polymers

139
Q

leprosy diagnosis

A

Ziehl Neelsen stain (red)

140
Q

leprosy mechanism

A

1) inhalation and migration to macrophages
2) can subvert infection with cellular immunity
3) humoural response (Ab) not effective because of wax and because intracellular
4) tuberculoid pole - aggregation of macrophages, cells break out to nerve cells, to Schwann, cause ischemia so die
5) bacteria has laminin like projections (LBP21) that bind laminin (LAMA2) on schwann outer membrane
6) Tol receptors 1/2 important in resistance, not work so stimulate infection and don’t trigger T cells properly

141
Q

TLR1 (leprosy)

A

wild type 6021
mutant TLR1 I602S to resistant to leprosy
so TLR1 involved in pathogenesis

142
Q

M.leprae genome

A

reduced genome, lost key genes but still have all essential ones and pseudogenes

143
Q

Clofazimine for mycobacteria

A

membrane-disrupting agent, bad side effects,
impact healthy cells but prefer bacterial cell walls,
aggregation of antimicrobial bends lipid bilayer of mycobacteria to form Toroidal pore

1) barrel-stave pore: hydrophobic part of antimicrobial align with membrane lipids and hydrophilic face in
2) carpet-like pore: coating of bilayer, micelle formation, membrane dissolution

so leaky membrane and cells die

144
Q

treatment for mycobacteria

A

clofazimine
rifampicin
sulphones and sulphonamides

145
Q

mycobacterium tuberculosis

A

disease of immunocompromised
burden in poor countries
aerosol - spreads by inhalation of 1-3 bacilli
1/3 population has dormant/latent TB that can reactivate

146
Q

mycobacterium tuberculosis genome

A

reductive evolution so reducing genome because don’t need,

evolutionary tree useful for diagnostics

147
Q

mycobacterium tuberculosis life cycle (similar to leprosy)

A

1) macrophages eat it, signals attract monocytes, forms big pus granuloma (aggregation of infected macrophages, producing lipids so foamy macrophages)
2) macrophages respond to infected macrophages, lymphocytes surround structure as well
3) vascularisation, more vessels around granuloma
4) fibrous cuff if cells not cleared, can’t get antibiotics in granuloma
5) macrophage in middle dissolved by TB to form caseum (impenetrable)
6) loss vascularisation, TB multiplication, opens up, to lymph and blood to infect more macrophages

148
Q

immune response to TB

A

5% massive progression and proliferation
90% have elimination and latent and 5-10% of these will re-activate

suppression of T cell activation and toll cell activation
pH tolerant so survive macrophages

149
Q

BCG vaccine

A

widely used but controversial

80-90% efficacy

no new vaccine since this one, had to stick with live attenuated (expensive)

northern hemisphere has low IFN-gamma response before vaccine so it significantly increases it

southern hemisphere has high IFN-gamma before so not much response after vaccine

can’t treat during latency

150
Q

TB diagnosis

A

biomarkers in peripheral blood
signals from transcription
metabolites in urine/breath/sputum
x-ray/scan
Zhiel Neelson stain (resists acid rinse so stays coloured)
smear microscopy (only works 5 months with TB but infectious by 3rd month so can’t early diagnose)

hard to diagnose because feels like bad cold

151
Q

TB treatment

A

5 antibiotics

152
Q

environmental mycobacteria (EM)

A

opportunistic pathogen

risk to immunocompromised (HIV) and with pre-existing lung disease and Helminth infections

153
Q

EM and BCG

A

EM may interfere with BCG vaccine - by blocking (immunity restricts BCG growth) or masking (can’t give additional immunity to already induced by EM)

154
Q

diseases by EM

A 
pulmonary
disseminated
lymphadenitis - enlargement of nodes
cutaneous disease - skin
nosocomial
155
Q

evolution of EM

A

M. marinum (amphibia/fish pathogen) closely related to M. ulcerans (human pathogen) - both produce mycolactone toxin

high G and C content (bases), need to survive outside host and adapt to many diff env.

156
Q

mycolactone toxin

A

large gene cluster on large plasmid, came in before split into marinum/ulcerans

immunosuppressive and analgesic - don’t feel infection

induce apoptosis, inhibit inflammatory cytokine, inhibit T from skin to lymphoid organs, damage nerve cells

157
Q

cutaneous disease (EM)

A

Buruli ulcer by M. ulcerans
necrotising, subcutaneous
3rd most common human mycobacteria (after TB & leprosy) and least understood

subverts IS, kills pains, develops in bone so irreversible deformity

mostly Africa, some Australia

maybe possums

low prevalence but bad where prevalent

158
Q

similarities of M. ulcerans to mycobacteria

A

subvert macrophage response

IFN-g protect (from non-tuberculous)

mycolactone unique to ulcerans

target scaffolding proteins

MHC reduced so no T cell response

ulcerans no tropism for schwann but diffuses into them

BCG against TB + leprosy + buruli ulcer

159
Q

buruli ulcer pathology

A

primary infection turns to latency - lesion in immunocompromised

disseminated - spread so worse, or localised

clearance and self-healing can happen depending on mycolactone

can progress to osteomyelitic - bone, permanent damage because bone stays in that position

160
Q

buruli ulcer pathogenesis

A

low optimal temp
mycolactone high cytotoxicity
BCG against osteomyelitis

161
Q

mycolactone biosynthesis (BU)

A

like fat synthesis but without reduction

repeating units of polyketide causes necrosis
build up fat but keto groups not reduced but cyclise,
polyketide secondary metabolism

162
Q

BU in possums in Australia

A

found in faeces

1) possums ingest from env/insect vector
2) amplify and shed
3) insect contaminated
4) transmit to humans via insect or direct from env.

163
Q

BU vector

A

strong evidence of biting amphibious beatles

Notonectidae carry disease in mouth

found M. ulcerans DNA in insects, mainly in July

disease most prevalent when lots notonectidae

164
Q

BU epidemiology

A

endemic where human activity - deforestation etc so not much to bite except humans

no difference with water bugs

165
Q

BU evolution

A

M. ulcerance close to M. tuberculosis but diff disease

166
Q

BU treatment

A

antimycobacterial drugs but no evidence and lack clinical trials and too late for irreversible damage

monotherapy could cause drug resistance so multiple is better to use

167
Q

Crohn’s disease(CD)

EM

A

association with cattle MAP disease
evidence for and against MAP causing Crohn’s: lecture 13 slide 22

pasteurised milk doesn’t kill so MAP pass to milk to humans

MAP detected in Crohn’s patients but also MAP in humans without Crohn’s

humans with MAP animals don’t have higher CD prevalence

168
Q

intracellular vs extracellular mycobacteria, how?

A

free-living amoeba may have conditioned mycobacteria to be intracellular and subvert IS

169
Q

mycology

A

study of fungi

170
Q

fungi characteristics

A

eukaryotic
chemoheterotroph
rigid cell wall, layers of polysaccharides, rigid matrix,
feed: saprophytes (decaying matter) or parasites (living matter),
osmotrophic (absorb food)

disease mostly skin/hair/nails
can hydrolyse keratin

171
Q

lichens

A

fungi

on walls, pollution indicators

172
Q

fungal pathogen mechanisms (3)

A

1) allergic hypersensitivity reactions
2) toxins like mycotoxins
3) infection, growth in/on body = mycosis

173
Q

3 main types of fungal infections

A

1) cutaneous (superficial) mycoses: surface of skin
2) subcutaneous mycoses: beneath skin, localised, spread by mycelial growth
3) systemic mycoses: not common, whole body, can kill

174
Q

why is cutaneous fungi called superficial?

A

where no living cells so no cellular response

175
Q

dermatophytes

A

cutaneous fungi that use keratin as nutrient source so digest it

176
Q

treatment/prevention of cutaneous fungal infections

A

topical therapy - creams

oral antifungals - fluconazole

177
Q

what type of infection is yeast?

A

superficial (cutaneous) or systemic fungi

178
Q

how does yeast affect the IS?

A

body recognises PAMPs, yeast cell wall binds PRRs and causes inflammation, fever, phagocytosis, activates alternative complement pathway and lectin pathway

179
Q

yeast candida albicans

A

produce pseudohyphae
buds elongate - tube like structure - filament (pseudohypha) - help invade deeper tissues after colonises epithelium

dimorphic so diff form in env and body

180
Q

candidiasis infection

A 
from lots diff types of yeasts
some only in immunocompromised
vaginitis
thrush
less commonly infects lungs/blood/heart/brain

10% septicaemia - enters blood

181
Q

diagnosis of superficial fungal infections

A

1) collect sample - where most viable fungus, with blunt scalpel
2) direct microscopy - presence of small, round to oval, thin walled clusters of budding yeast cells and branching pseudohyphae, colonies are white/cream with smooth waxy surface

182
Q

treatment of superficial fungal infections

A

topical imidazole compound
azoles
polyenes
oral fluconazole

prolonged therapy may cause resistance

183
Q

subcutaneous fungal infection examples

more detail on word

A

chromobloastomycosis

sporotrichosis

184
Q

treatment of systemic fungi

A

chemotherapy - difficult

amphotericin B antibiotic - affect cell membrane but side effects

exposure rarely eliminated except with air filtration

185
Q

fungal pathogenicity

A

1) promote fungal colonisation:
adhere to host cells,
capsules resist phagocytosis,
candida albicans - cytokine GM-CSF suppress complement for chemotaxis of phagocytes and acquire iron from RBCs so haemolysins.

2) damage host:
enzymes digest cells - proteases and host cytokines,
mycotoxins - lose muscle coordination, weight loss, tremors, aflatoxins are carcinogenic

186
Q

GM-CSF

A

granulate-macrophage colony-stimulating factor

Microbial Pathogens (1 decks)

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