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phase 2a mine > microbiology > Flashcards

microbiology Flashcards

1
Q

6 main bacterial causes of meningitis (and age groups for some)

A

streptococcus pneumoniae
neisseria meningitidis
heamophilus influenzae (infants - but vaccine)
listeria (neonates and elderly)
group B streptococcus -agalacticae (neonates)
e.coli (neonates)
but the age allocations are not strict

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2
Q

what does streptococcus pneumoniae look like in microscope

A

gram + diplococci

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3
Q

what is streptococcus pneumoniae like on blood agar

A

alpha hemolytic (partially hemolytic – green)

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4
Q

what is the relation between streptococcus pneumoniae and optochin discs

A

step. pneu is optochin sensitive

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5
Q

what does neisseria meningitidis look like in microscope

A

gram - diplococci

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6
Q

gram - diplococci =

A

neisseria meningitidis

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7
Q

gram + diplococci =

A

streptococcus pneumoniae

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8
Q

gram - cocci-bacillus

A

haemophilus influenzae

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9
Q

what does haemophilus influenzae look like in microscop

A

gram - cocci-bacillus

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10
Q

e. coli in microscope

A

gram negative bacilli

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11
Q

litseria in microscope

A

gram + bacilli

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12
Q

haemophilus influenzae on blood and choc agar?

A

doesnt grow on blood but does on choc (it is fussy and choc gives it better stoof)

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13
Q

can both bacteria and virus causes meningitis

A

yes

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14
Q

can both baceria and virus cause encephalitis

A

no. only virus

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15
Q

list 3 viruses that causes meningitis

A

mumps
enterovirus
herpes simplex virus

polio
echo

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16
Q

list 3 viruses that cause encephalitis

A

herpes simplex virus = most common
varicella zoster = 2nd most common

parvovirus
HIV
mumps
measles
CMV
EBV
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17
Q

CSF is used for meningitis (/ encephalitis) investigation as this is a CNS infection. how is this obtained? what is the macroscopic appearance? then what?

A

lumbar puncture
should be gin-clear. cloudy = white blood cells and already –> memingitis!
then cultured + gram film

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18
Q

what are the treatments for meningitis

A

main= antibiotic from cephlasporin group (from beta lactan group) – cefotaxime or ceftriaxone
also - amoxicllin (a penicillin ) for listeria
they can both cross the blood brain barrier

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19
Q

what are the signs in CSF analysis (not microscope) of bacterial infection

A

neutrophils

raised protein and low glucose (due to bacteria and neutrophils)

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20
Q

meningitis triad of symptoms

A

photophobia
neck stiffness
headache

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21
Q

what other non-antibiotic treatment is given with meningitis

A

anti inflammatories – corticosteroids (dexamethosone) and NSAIDs. these dampen immune system so decrease risk of nerve damage

also analgesia
also fluids

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22
Q

blood agar hemolysis

when would this be useful to identify bacteria?

A

alpha hemolysis - partial hemolysis, - not fully transparant, green/grey (due to hydrogen peroxide produced by bacteria)

beta hemolysis - full hemolysis (rbc burst open) - transparent/ clear

non hemolytic

this is useful to distinguish gram + cocci chains (all catalase negative. all streptococci)

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23
Q

lancefield test

how is it done
what does it distinguish between

A

colonies in water + some antibody coated latex beads from a kit

between B hemolytic bacteria in streptococci group (gram + clusters - = all catalase negative)

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24
Q

two types of neisseria and their effect

A

gonococcal –> urethritis

meningococcus –> meningitis

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25
Q

neisseria in blood and choc agar

A

blood- no haemolysis

choc - grows!

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26
Q

what clinical feature in addition to meningitis symptoms points to meisseria meningitidis as a cause

A

peticheal rash

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27
Q

should you perform a lumbar puncture with neisseria meningitis

A

no. no need - rash + present in blood cultures is enough to diagnose. plus it is dangerous (something to do with coagulation)

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28
Q

what should you do with a diagnosis of neisseria meningitidis

A

treatment = cefotaxime or ceftriaxone (3rd generation cephlasporin group)
notify public health england

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29
Q

appearnace of lymphocytes and neutrophils in gram stain microscope

A 
lymphocytes = purple cells
neutrophils = pink
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30
Q

route of transmittion for group B strep (agalactiae) and e.coli

A

mothers birth canal –> baby skin

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31
Q

X+ V discs ?

A

if a clearing around them- this means the bacteria have munched the nutrient that has spilled out of the discs

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32
Q

how to apply gram stain

A 
heat fixate bacteria
apply crystal violet
iodine treatment
remove stain
counterstain
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33
Q

blue/purple colour gram stain

A

gram +

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34
Q

red/pink colour gram stain

A

gram -

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35
Q

coagulase test

done how
used when
different results
meaning

A

colonies in tube with saline and rabbit plasma

used to differentiate gram + cocci that are clusters (aka staphylococcus, aka catalase +)

positivie = yes coagulase produced by bacteria. clumping like precipitate looks like. if tilted doesnt move like normal liquid
– staph aureus

negative = no coagulase produced
no clumping. tilts as normal. may be more yellow
– staph epidermidis
– staph saprophiticus

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36
Q

staphylococcys vs streptococcus

A

both are gram + cocci

staphylococcus = clusters
streptococcus = chains
staph = catalase +
strep= catalase -
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37
Q

staphylococcus under microscop

A

gram + cocci clusters

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38
Q

streptococci under microscope

A

gram + cocci chains

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39
Q

catalase test

done how
results

A

hydrogen peroxidase + colonies.

catalase + looks like white, foamy, bubbles of Oxygen
– staphylococcus

catalse - looks like clear flat liquid droplet
– streptococcus

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40
Q

what are the possible bacteria of alpha hemolytic blood agar observation

how would you distinguish them?

A
  • strep viridans (think endocarditis)
  • streptococci pneumoniae (think meningitis, and pneumonia)

distinguish them with an optochin disc. strep viridans is not sensitive. strep pneumoniae is

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41
Q

macconkey agar

A

distinguishes gram - rods

lactose fermenting = red- pink
– e.coli, klebsiela

non-lactose fermenting = yellow/white (normal colour)
– shigella, salmonella, pseudomonas, proteus

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42
Q

CLED agar

A

normally blue
can distinguishes gram - rods:

lactose fermenting- yellow
– ecoli, klebsiella

lactose non fermenting- blue (normal colour)
– shigella, salmonella, pseudomonas, proteus

grows UTI pathogens well

doesn’t let proteus swarm

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43
Q

sp and spp meaning

A 
sp= species singular
spp = species plural
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44
Q

where are the sterile sites of the body? name 5

A 
1 blood
2 CSF
3 pleural fluid
4 joints
5 lower resp tract
6 urinary tract
7 peritoneal cavity
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45
Q

where are the areas in the body naturally colonised by bacteria? name 3

A 
1 mouth
2 skin
3 vagina
4 urethra
5 large intestines
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46
Q

what colour is CCDA agar

A

black

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47
Q

chocolate agar

A

brown

allows organisms to grow that dont grow easily on blood agar because they are fussy

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48
Q

XLD agar colour

- good for?

A

bright red/pink/orange
v selecitve
good for shigella, salmonella

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49
Q

optochin disc

A

whether bacteria are sensitive to optochin

yes= strep pneumoniae

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50
Q

is blood agar selective

A

no. many can grow here

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51
Q

name two examples of enteroviruses

A

rhinovirus

echovirus

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52
Q

name 3 examples of respiratory viruses

A 
1 influenza
2 coronavirus
3 rhinovirus
4 measles
5 mumps
6 rubella
7 parvovirus
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53
Q

viral vs bacteria swab

A

viral swab = green
then PCRed

bacterial swab = charcoal
then cultured

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54
Q

what test is used to identify viruses

A

PCR

- specific primers detect

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55
Q

when is PCR available to view

A

next day

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56
Q

PCR pros and cons

A

fast
sensitive
identifies specific viral cause

expensive

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57
Q

blood film time

A

get results in hours

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58
Q

glandular fever treatment

A

supportive

avoid contact sport for 6w+ to avoid splenic rupture

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59
Q

ELISA test

A

viral antibody binds to enzyme in assay (grid thing)

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60
Q

clotted (yellow top) serum sample to serology?

A

looks for evidence of past/ present infection and immunity (eg rubella, HIV, HBV)

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61
Q

neonate with rubella IgG

adult with CMV igG

traveller rabies immunoglobulin

A

passive antibody but not infected

protective antibody from prior infection

passive antibody from injection

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62
Q

HIV tests

3

A

antibody
antigen
HIV RNA

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63
Q

why do you need to retest a HIV test

A

if reported negative : repeat after 4 w (could be early stage so not detectable yet/ test error/ mic up)

if reported positive: repeat straight away (2xpos = pos, 1 pos and 1 neg = do a third test)

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64
Q

which antibiotics can you give if someone is allergic to penicillin

A

clindamycin
erythromycin
vancomycin

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65
Q

name an antibiotic that is good for MRSA

A

vancomycin

a glycopeptide

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66
Q

c diff down microscope

A

gram + rods

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67
Q

c diff
aquired when
symptoms

A

squired after antibiotic use - replace gut flora
old patients, hospitals
collitis

symptoms -
diarrhea

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68
Q

E.coli related diseases

A

UTIs inc pyelonephritis etc
Gastroenteritis
meningitis
bloody diarhea, abdom cramps

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69
Q

staph aureus related diseases

A

osteomyelitis
septic arthritis
UTI

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70
Q

do helicobacter pylori have flagellae?

A

yes

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71
Q

which layer of the stomach do helicobacter pylori live in?

pathophysiology

A

mucin layer.

they then damage the gastric cells below –> ulceration

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72
Q

what do neisseria gonnorhea look like down microscope in discharge/smear

A

gram - diplococci within cytoplasm of polymorphs

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73
Q

proteus effect on agar

A

swarms agar, tide marks
eg blood agar, MacConkey
but not CLED
- so CLED is good for urine microorganisms

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74
Q

lower UTI vs upper UTI symptoms

A

lower- dysuria, frequency, urgency

upper - loin pain,fever, rigors, haematuria

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75
Q

causes of UTI

A 
KEEPPSS
Klebsiella
e coli
enterococci
proteus
pseudomonas
staph epideermis
staph saprophyticus
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76
Q

what is looked at in microscopy for UTIs (whats the sample)

A

mid stream urine (this avoids contamination from perineum / vagina)

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77
Q

what does MSU stand for

A

mid stream urine

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78
Q

what does pure growth mean?

A

only 1 bacteria growing there

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79
Q

lactose fermenting vs non lactose fermintnig gram - bacilli

A

lactose fermenting

  • e.coli
  • klebsiella

non-lactose fermenting

  • shigella
  • salmonella
  • proteus
  • psuedomonas
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80
Q

how might pseudomonas be differentiated from non-lactose fermenting gram - rods

A

pseudomonas is oxidase +ve

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81
Q

what does CSU stand for? what is important to note about it

A

catheter sample urine

can not perform dipstick urinalysis / microscopy. on catheter bag

because urinary catheter bag may produce inflam response with no infection present

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82
Q

what happens if epithelial cells are found in the microscopy of a urine sample

A

poorly taken sample. it is contaminated. needs to be repeated. can not be analysed

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83
Q

what is the point of using a CLED plate with a LUTS patient

A
  1. promotes growth of urinary tract pathogens
  2. differentaites between lactose and non-lactose fermenting bacteria
  3. doesnt let proteus swarm
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84
Q

why is urine analysed at antenatal visits

A

looking for blood/protein
screening for pre-eclampsia
and for asymptomatic bacteriuria (Ascending UTI–> pyelonephritis –> miscarriage)

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85
Q

what does multiple bacteria growing on agar suggest in respect to UTIs?

A

mixed culture suggests contamination (from vagina/perineum)

may not be a correct MSU sample

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86
Q

what is the most common site for soft tissue skin infection/

A

lower leg

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87
Q

abscesses signs

A

few

tender

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88
Q

deep skin infection signs/symptoms

A

erythema

marked pain

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89
Q

causes of soft tissue infection

A

group A beta hemoltic streptococcus (s.pyogenes)
staphylococcus aureus

atypical causes seen in needle drug users/ immunocomprimised

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90
Q

types of soft tissue infection

  • erysipelas = where
  • cellulitis = where
A

erysipelas – intradermal
cellulitis – sub-cut
both same bacterial causes

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91
Q

is skin soft tissue infection more commonly caused by local breach of body defences (…eg?) or blood stream spread?

A

local breach

  • ulcer
  • eczema
  • insect bite
  • athletes foot
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92
Q

sampling for soft tissue infection

A
  • blood culture
  • pus from abscess if poss
  • swab skin at site of entry if skin breached (eg athletes foot)
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93
Q

impetigo

  • presentation
  • affects who
A
  • itchy, red, growing lesion which is weeping/ crusty

- infants/kids

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94
Q

what antibiotics can most gram + be treated with

A

flucoxycillin

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95
Q

what antibiotic can most gram - be treated with

A

cefotaxime (A cephlasporin)

96
Q

would staph and strep grow better on aerobic or anaerobic blood agar

A

both - aerobic

anaerobic= peptostreptococcus

97
Q

what antibiotc is used to treat group a lancefield strep (strep pyogenes)

A

pencillin

98
Q

empirical antimicrobials=?

A

initial antibiotics regimen given within 24h of admission. started just after sample specimens are collected

99
Q

what does MRSA stand for

what is it resistant to

A

methicillin resistant staph aureus

this is resistant to flucloxicillin

100
Q

how is MRSA carriage identified

A

swab –> chromogenic MRSA plate

if resistant to cefoxitin, then = MRSA

101
Q

encephalitis symtpoms

A 
fever
lethargy, fatigue
decreased conciousness, drowsy
maybe fits
associated with meningitis (= meningo-encephalitis)
102
Q

pnuemonia features

A

plueritic chest pain
rusty/green sputum coughed up
cough
breathless ness

asympotmatic pneumonia if these symptoms predominate:
myalgia
arthralgia
headache

signs:
fever
consolidation (dullness to percussion, bronchial breathing)

103
Q

most common cause of pneumonia =

A

Strep pneumoniae

104
Q

pulmonary TB causes

A

mycobacterium tuberculosis and mycobacteium bovis

105
Q

infective endocarditis diagnosis

A

modified duke criteria

definite IE = 2 major crieria, OR 1 major and 3 minor, OR 5 minor

MAJOR

  • positive blood culture with typical IE microorganisms
  • new partial dehiscence (wound seperation) of prosthetic valve
  • new valvular regurgitation

MINOR

  • predisposing factor (cardiac lesion, recreational drug inj)
  • fever >38
  • embolic evidence (arterial emboli, pulmonary infarcts, janeway lesion, conjuntival haemorrhage)
  • immunological problems (glomerulonephritis, osler’s nodes, roth’s spots)
  • rheumatoid factor
  • microbiological evidence (positive blood culture (but not major criteria) or serological evidence of infection )
106
Q

if something is resistant to cefoxitin, what is it resistant to also?

A

methicillin

107
Q

sabaraud’s agar (SAB)

A

promotes griwth of non bacterial pathogens eg fungus

108
Q

what type of organism is candida

A

fungus

109
Q

are enterococcus species streptococcus?

A

yes

110
Q

where do enteric infections refer to?

A

intestines

111
Q

name 3 symptoms of enteric infection

A 
1 stomach ache
2 diarrhae (can be sever/fatal)
3 vomitting
4 fever
5 abdominal cramps
112
Q

c. diff diarrhea treatment

A

stop the causative antibiotic if still taking.

+ vancomycin / metronidazole

113
Q

what does metrondiazole antibiotic treat

A

anaerobic bacteroides (+c.diff)

114
Q

what is an API strip

A

series of biochemical reaction that determine the bacteria based on metabolic and enzymatic qualities

115
Q

name 3 microorganism causes of ascending cholangitis due to impacted gall stone

A 
1 klebsiella pneumoniae
2 e coli
3 enterobacter
4 enterococcus
5 anaerobes
116
Q

is bacterial or viral meningitis more serious

A

bacterial

viral is benign and selflimiting

117
Q

commensal

A

organism colonises part of body but is not disease causing

118
Q

virulence

A

degree of ability to cause disease (eg toxins and how good it is at colonising)

119
Q
  • spores

- name their virulence factor

A
  • store DNA

- resistant to destruction (eg heat, chemicals)

120
Q

ziehl neelson stain detects what

A

mycobacteria

good for when gram stain doesn’t work

121
Q

in to out describe bacteria structure

A 
circular double stranded DNA
membrane(S)
cell wall
capsule
flagella

not all have each thing though

122
Q

gram + /- membranes

A

gram + = 1 membrane (large peptidoglycan)
gram - = outer and inner membrane – with lipoprotein and small peptidoglycan in between. lipopolysacharide attached to outside

123
Q

gram +/- peptidoglycan

A

gram + = large peptidoglycan component (on outside cos only 1 membrane)
gram - = small, in between 2 membranes

124
Q

gram +/- lipopolysaccharide

A

gram + = no

gram - = yes. attached to outer membrane. this is the endotoxin

125
Q

gram +/ - endo and exotoxin

compare features of endo/exotoxins

A

ENDOTOXIN
- only gram - : the lipid A of the lipopolysaccharide on the outer membrane

  • non specific
  • stable in hear
  • weak antigenicity (response in immune system)
  • cannot convert to toxoid

EXOTOXIN
- gram + and - : protein secreted

  • specific
  • unstable in heat
  • strong antigenicity
  • can concert to toxoid
126
Q

how to bacteria swap genetic info (horizontally)

A

plasmid . these replicate autonomously and pass between bacteria (=transformation) picked up naked from enviroment eg after rupture

bacterial conjugation = cell-cell contact via pilus - plasmid exchanged here (=conjugation)

phage ( virus) infects and replicates bacteria, giving it new gene (=transduction)

127
Q

what is transforamtion

A

when plasmids pass from one bacteria to another, picked up naked from environment eg after rupture
new genetic material introduced (horizontal gene transfer)

128
Q

how is staph aureus spread

A

touch and aerosols

129
Q

how can you distinguish staph aureus and staph epidermis on blood agar

A

staph aureus - golden colonies

staph epid - white colonies

130
Q

where is strep pneumoniae commensal?

A

in oro pharynx

131
Q

where is viridans streptococci

A

often oral
also deep organ absesses (brain, liver, lung)
endocarditis

132
Q

name 3 bacterial causes of endocarditis

A 
staph aureus
enterococci
strep viridans
strep pneumoniae
pseudomonas
133
Q

corynebacterium

  • appearance under microscope
  • an/aerobic
  • produced
  • treatment
  • prevention
A

gram + rods
aerobic
produces toxins that inhibit protein synthesis
treatment : anti-toxin, erythromycin
prevention: toxoid vaccination (inactive toxin)

134
Q

do gram negative have a capsule

A

yes

135
Q

proteobacteria
2 types
gram + or -

A

gram -

enterobacteria and non-enterobacterial proteobacteria

136
Q

e coli
where is commensal
what feature
name 3 things it causes

A

commensal in gut
peritrichous flagella (=all over surface)
UTIs, wound infection, gastroenteritis, Travellers diarrhea

137
Q

shigellosis =
cause
symptoms
toxin

A

shigella caused disease
severe bloody diarrhea, >30/day inc pain and cramping, fever
low infective dose
toxin = shiga toxin. binds to receptors and stops translation and protein synthesis, killing the cell

138
Q

salmonellosis =
route
toxins
effect

A

salmonella enterica causes it
ingest contaminated food/water
no toxins
diarrhea (fluid+electroylte loss) and tissue injury

139
Q

salmonella species

A

salmonella enterica = causes salmonellosis

salmonella bongori = rare

140
Q

what are ETEC and EHEC

A

forms of e.coli
additional genes make them more pathogenic
ETEC causes travellers diarrhea

141
Q

vibriocholera virulence factor

A

1 flagellum
pilli
toxin

142
Q

cholera route of transmission

symptoms

treatment

A

undercooked shellfish
drinking contaminated drinking water

diarhea voluminous (litres of lost fluid + electrolyte –> hypovolemic shock)

ORS oral rehydration salts

143
Q

obligates=

eg

A

cannot be cultured on a medium, only in humans

eg chlamydiae

144
Q

fungi cell wall=

fungi membrane=

A

chitin

contains ergosterol rather than cholesterol

145
Q

yeast vs mould

A 
yeast = single celled. divide by budding
mould = multicellular. hyphae and spores
146
Q

when is fungi life threatening

A

immunocomprimised, post surgical

lots cannot grow in humans and most that do are mild

147
Q

fungi treatment (theoretical)

A

inhibit RNA/DNA synthesis
attack membrane (contains ergosterol rather than cholesterol)
– put pores in
– inhibit ergosterol synthesis
target cell wall (humans have no cell walls)

148
Q

fungi detection in blood/fluids/tissues

A

blood cultures are undersensitive

fluid/tissues is better

149
Q

how do viruses replicate

A

intracellular - requires host:

  • attaches to cell receptor
  • enters cell and uncoats – sheds virion
  • does transcription using host cell materials and machinery to create proteins, genome, enzymes etc
  • virion assembled in host cell
  • bursts out/ budding/ exocytosis
150
Q

are viruses DNA or RNA

A

can be either

this is surrounded by protein coat +/- membrane

151
Q

which are bigger viruses or bacteria

A

bacteria

152
Q

do viruses have cell wall
do viruses have membrane
do viruses have organelles

A

no
sometimes
no

153
Q

how do viruses cause disease

A

1 direct destruction of host cells - (lysis)

2 damage through cell proliferation (continuous expression of oncogenes –> dys/nepplasia–>cancer)

3 modification of host cell (eg flattens epithelial cells and villi atrophy so decrease absorption area in the small intestine)

4 ‘over-reactivity’ of immune system

5 evasion of host cells inc immune cells

  • lies latent and can reactivate
  • spreads cell-cell –doesn’t need to leave and re-enter
  • antigenic variability
  • prevents host cell apoptosis as needs it to live
  • downregulation of host defence proteins
  • prevents MHC displaying of antigens
154
Q

protozoa
classes
based on

A

classification based on how they move

  • amoeboids (temporary protrusions = pseudopodia)
  • ciliates (have cilia)
  • sporozoa (non-motile)
  • flagellates (flagella)
155
Q

amoeboids transmission

A

faecal-oral (unsanitary food/water)

156
Q

African trypanosomiasis

aka
vector
microorganisms
symptoms

A

sleeping sickness
tsetse fly
flagellate (protozoa)
systemic infection (fever, fatigue etc) + CNS involvement (drowsy, personality change)

157
Q

american trypanosomiasis

aka
vector
microorganisms

A

Chagas disease
triatome bug
flagellate (protozoa)
systemic infection (fever, headache etc) + cardiac, megaoesophagus and megacolon + eye swell

158
Q

examples of flagellate (protozoa)

A 
american  trypanosomiasis
african trypanosomiasis
leishmaniasis
giardia lambia
trichomoniasis
159
Q

malaria types

microorganism

A 
plasmodium falciparum (most common and most severe)
p malariae
p ovale
p vivax
p knowlesi

protozoa

160
Q

malaria epidemiology

A

sub-S Africa
North of S America
S Asia

rare in UK

161
Q

malaria risk factors

A

Travel to or residency in areas with malarial risk
Poor
young/old
pregnant

162
Q

malaria liver stage

A

Infected mosquito takes a blood meal and injects SPOROZOITES (infected form of plasmodium)

Sporozoites travel to the liver and infect LIVER CELLS

Liver cells mature into SCHIZONTS

Schizonts grow and RUPTURE, releasing MEROZOITES into the blood

163
Q

what is the dormant stage and which forms of malaria have it

A

In p.vivax and p.ovale there is an additional dormant stage here where HYPNOZOITES can persist in the liver, allowing relapses

164
Q

blood stage malaria cycle

A

Merozoites enter circulation and infect RBC (from liver stage)

Rbc mature into TROPHOZOITES, which mature into SCHIZONTS

Schizonts grow and RUPTURE, releasing more merozoites into blood

Continued cycle, infecting more rbc

Immature trophozoites also go on to differentiate into sexual stage GAMETOCYTES

Gametocytes mature and are picked up by the next mosquito that bites you in their BLOOD MEAL (infecting the mosquito)

165
Q

malaria vector

A

infected female anopheles mosquito

166
Q

vector stage malaria cycle

A

Mosquito takes in blood meal and ingests gametocytes

Gametocytes mature from MICRO –> MACROGAMETOCYTES

MALE AND FEMALE macrogametocytes FUSE to form an OOCYTE

Oocyte grows and ruptures, releasing SPOROZOITES

Sporozoites travel to SALIVARY GLAND - here they will be passed on when the mosquito takes a blood meal

167
Q

which is the most severe form of malaria and why

A

Plasmodium falciparum

1) Rapid replication
2) Cytoadherence
Infected rbc show surface proteins that cause adherence between rbc and endothelial walls
3) Rosetting
Big blobs or rbc - including non-infecting ones
Allows SEQUESTRATION - they hide from the body’s immune system in rosettes, surrounded by non-infected rbc so infiltrate organs
Vascular occlusion → bleeding, leaky vessels

168
Q

is it the liver, blood or vector stage that is responsible for malarial symptoms

A

blood stage

169
Q

malarial symptoms and why

A

merozoites→ trophozoites → schizonts → rbc rupture so this causes waste products and toxic factors as the infected cells lyse. Macrophages and other mediators release inflammatory cytokines in response.

Chills (fever)
Rigors
Cough 
Headache
Muscle ache (myalgia)
Fatigue 
Nausea, vom , diar
Flu-like symptoms

Haemolysis rises big time - to break down infected rbc. This, along with cell lysis of infected cells causes

Anaemia (tired, sob)
Jaundice (pre-hepatic accumulation)
Haemoglobinuria (rbc products in kidney → dark urine)
Severe : hypovolemia, fits, impaired consciousness

170
Q

signs of malaria

A

Fever
Splenomegaly
Hepatomegaly
Severe: fits, hypovolemia

171
Q

diagnosis of malaria

A

Blood film- smear
–Thick blood film
Count parasitic rbc (dark dots)
% parasitemia in rbc indicates severity - 2%+ is severe
–Thin blood film
Determine which type/ strain of malaria
Repeat to ensure no false results form gamete stage of cycle

172
Q

malaria treatment

A

uncomplicated = oral quinine (others)

complicated (has complications) = IV artesunate
(if not possible, IVE quinine and doxycycline)

Primaquine eliminates dormant hypnozoites (p.vivax, p.ovale)

Artemesmin = for uncomplicated, mixed infection type malaria

treat symptoms

173
Q

malarial complications x4

A

Cerebral malaria:

  • Vascular occlusion
  • Hypoglycaemia
  • Leak causes rise in intracranial pressure (ICP)
    • Coma, Drowsy, Seizures

Renal failure

  • Vascular occulsion
  • BP drop
  • Dehydration
  • Overwork
  • Proteinuria, fatigue, haematuria

ARDS = acute respiratory distress syndrome

  • Vascular occlusion
  • Increased vascular permeability
  • Oedema, anaemia, breathless ness, hypoxic

Shock

  • Sepsis
  • Increase in vasc permeability
  • Bleeding
  • Inflammation
  • anaemia
174
Q

primary vs opportunistic pathogen

A

primary pathogen can cause disease in a proportion of exposed individuals irrespective of immunological status. opportunistic only causes disease if immunocompromised

175
Q

how does IgA fight against viruses and bacteria

A

cells are coated with IgA

blocks attachment binding to host cell

176
Q

how do antibodies fight against viruses and bacteria

A

osponisation - attach to pathogen so they are more easily phagocytosed

177
Q

how does IgM fight against viruses

A

agglutinates viruses together in clumps so they are trapped

igM is a large molecule- many attached

178
Q

how do complements fight against viruses and bacteria

A

osponisation and cell lysis

179
Q

how do antibiotics work

+ example of each

A

inhibit cell wall synthesis
- beta lactans inc penicillin and cephalosporins (target peptidoglycan layer so work best on gram +)

impair nucleic acid synthesis
- rifampacin

impair protein synthesis

  • 30S part of ribosome - tetracyclines
  • 50S part of ribosome - macrolides (clarithromycin, erythromycin)

impair folate synthesis
- sulphonamides

180
Q

bacteriostatic antibiotics

bactericidal antibiotics

A

prevent growth of bacteria (and kill most)
- prevent protein synthesis (and so toxin production), metabolism or DNA production

kill majority of bacteria (more)
- inhibit cell synthesis

181
Q

antibiotics MIC and MBC

A

MIC = minimum inhibitory concentration (minimum concentration of antibiotic that inhibits growth)

MBC = minimum bactericidal concentration (minimum concentration of antibiotic that kills)

182
Q

two qualities of antibiotics

A

concentration dependant – low MIC - low conc of antibiotic needed. then dose size needs to be above this MIC

time dependant – time antibiotic stays bound to site = long (give doses regularly enough to keep amount above MIC)

183
Q

how do bacteria resist antibiotics

A

antibiotic target on bacteria changed by the bacteria (mutations, covering it)

bacteria destroy/inactivate antibiotics (beta lactamase enzyme breaks down beta lactam antibiotics)

bacteria prevent antibiotic access to it (change porin size/number/selectivity)

remove antibiotic (active pump in bacteria removes antibiotic from bacteria)

184
Q

how do bacteria become resistant

A

some are intrinsically, naturally resistant (=all strains are resistant)
most = acquired . either by spontaneous gene mutation or horizontal gene transfer from another bacteria

185
Q

conjugation

A

plasmids exchanged by pilus –>new genetic material introduced (horizontal gene transfer)

186
Q

transduction

A

new gene inserted by phages (viruses) –> new genetic material introduced (horizontal gene transfer)

187
Q

what are macrolides (clarithromycin, erythromycin) / lincosamides (clindamycin) good for

A

penicllin allergy

188
Q

why are beta lactams better for gram + than gram -

A

inhibit cell wall synthesis by targetting peptidoglycan layer gram + have big peptidoglycan layer but gram - is small (between inner and outer membrane)

189
Q

mycobacteria=

gram stain?
example

A

type of bacteria
they cannot be identified with gram stain due to high molecular weight lipids on cell wall (neither gram +/-). they are identified with ziehl neelson stain.
acid fast bacilli
eg TB

190
Q

mycobacteria qualities

  • an/aerobic
  • mobility
  • spore formation?
  • cell wall?
  • phagocytosis
  • speed of growth and implications of this
  • immune response
A
  • aerobic
  • nonmotile
  • no spore formation
  • cell wall present - has high molecular weight lipids on it. this helps it survive in the environment and against phagocytosis (survives inside macrophage
  • slow growing – so slow onset in disease, slow to grow in cultures and slow to respond to treatment
  • granulomas (with mycobacteria inside)
191
Q

high risk of TB

A 
infant
elderly
malnutrition
intense exposure
immunosuppression
192
Q

tb pathogen

A

mycobacterium tuberculosis

193
Q

primary vs latent TB

A

primary = inhaled to lungs. goes into lymph nodes. cell-mediated immune response (intrinsic)

latent = not unwell. but cell mediated immune response from T cells remains inc skin test positive still

194
Q

HIV stages

A

1 acute primary infection

  • 2-4w after exposure
  • abrupt non specific symptoms
  • transient immunosuppression as HIV causes CD4 count to drop before rising slowly (as HIV replicates in CD4 (Th) cells

2 i) asymptomatic phase / clinically latent

    • long
  • -progressive loss of immunity
    • still infectious despite no symptoms
    ii) early symptomatic HIV

3 AIDS

    • opportunistic infections
    • CD4<200
195
Q

HIV replication

A

replicates in CD4 ( Th )

this causes CD4 count to fall, before gradually rising again (transient immunosuppression)

196
Q

what is normal CD4 count and what is it in AIDS

what is considered a late HIV diagnosis

A

normal = 500-1500
AIDS = less than 200
late diagnosis is when HIV found and CD4<350

197
Q

how is HIV monitored

A 
CD4 count (cell count per microlitre)
HIV viral load  (RNA copies per microlitre)

extension of progression, prognosis, and response to treatment

198
Q

HIV symptoms

A 
abrupt onset of non specific symptoms
 fever
rash
lethargy
depression
weight loss
199
Q

PGL =

A

persistant generalised lymphadenopathy

enlarged lymph nodes at at least 2 non contigous sites

seen in clinally latent/asymptomatic stage of HIV

200
Q

what infections might flare up with HIV, name 3

A 
oral candida 
shingles (in 2+ dermatomes)
thrombocytopenia
toxoplasmosis (ring enhancing lesions in brain)
pneumonia
herpes
201
Q

HIV treatment/ prevention

A

TREATMENT
ART antiretroviral therapy
target diff points in HIV life cycle
once viral load is undetectable, it is untransmittable!

PREVENTION
nonpharmacological - condoms, needles, screen blood products for transfusion, diagnosis, partner notiification etc
PreP: pre-exposure prophylaxis (before sex)
PEP: post- exposure prophylacis (within 72h)
circumsision
STI control (ulcerative STIs have enhanced HIV transmission)
microbicides (vaginal gel, not used much)

202
Q

does HIV screening exist

A

yes eg antenatal

venous/salivary

203
Q

what is a retroviridae

A 
enveloped virus (HIV - outer lipid envelope layer is studded with glycoprotein)
RNA is copied into DNA by reverse transcrption then incorporated into the host

hiv

204
Q

what is a lentivirus

A

a type of retrovirus with long incubation period

HIV

205
Q

what is the 90/90/90 target

A

UN AIDS target
90% of HIV =diagnosed
90% of diagnosed HIV = on ART treatment
90% on ART treatment = viral suppression

by 2020

206
Q

what is HIV tropic to

A

to immune cells (esp CD4+ cell, but also macrophages and others)

tropism = where the virus infects and replicates in

207
Q

if HIV infects immune cells , how does the immune system respond?

A

made difficult as if macrophage engulfs, it cannot kill and it allows it to meet other immune cells - spread!

there is partial immune response (vigorous but ineffective) for some years

  • antibodies neutralise
  • CD8 (Tc) kill infected cells
208
Q

how does HIV affect CD4 cells

A

depletes :

  • by direct cytotoxicity as they are infected and taken over
  • decreased production in bone marrow due to HIV (viral reservoir)
209
Q

varicella zoster virus stages

A 
primary infection = chickenpox
dormancy period (lies in dorsal root/ cerebral ganglion)
secondary reactivation = shingles
210
Q

how is chicken pox transmitted

when is it infectious

A

touching rash (via mucous membranes)
infectious from day 0
not infectious when it has crusted

211
Q

when is good/bad to get chicken pox

A 
good= child - usually benign
bad= pregnant (foetus catches it = foetal varicella syndrome), adult, immunocompromised, smokers
212
Q

chicken pox diagnosis

A 
swab lesion (pop if needed)
send for VZV PCR
213
Q

chicken pox vs small pox rash distribution

A

chicken pox =in warmer areas (central)

small pox = more extremeties

214
Q

foetal varicella syndrome (FVS)

A

foetus infected in chickenpox pregnancy
usually transient (rarely there are severe defects eg microcephaly, growth retardation, limb hypoplasia, skin /occular scarring)
shingles in year 1 of life

215
Q

shingles high risk

A

immunocompromised, elderly

216
Q

what does shingles look like

A

skin lesion
blister fluid
v painful

in single dermatome (red flag if multiple)

217
Q

what does parvovirus look like

A

rosy cheek
+ reticular mottling
+ risk of anaemia (due to prevention of rbc maturation)

218
Q

worms categories (helminth categories)

A

nematodes (round worms)
trematodes (flatworms)
cestodes (tapeworms)

219
Q

pre-patent period (Worms)

A

interval between infection and appearance of eggs in the stool

220
Q

dimorphic fungi=

A

fungi that exist as both yeasts and moulds, switching between the two depending on the conditions

221
Q

antigenic drift vs shift

and type of disease prevalence associated

A

spontaneous mutations – gradually minor changes – epidemics

sudden emergency of new subtype – pandemics

222
Q

protozoan infection immune response

A

blood stage = humoral immunity (extrinsic)

tissue stage = cell mediated (intrinsic)

223
Q

worm replication where?

A

not in humans, outside body

224
Q

worm immune response?

A

poor. insufficient to kill

225
Q

worms - diagnosis

A

stool microscopy- look for eggs

or may see macroscopically

226
Q

antibiotic for strep pneumoniae

A

amoxicillin

227
Q

how does an antigen test work

A

antigen of virus/bacteria added. serum added. antigen will stick to IgM or Ig G if present. enzyme causes colour change

228
Q

‘atypical’ causes of pneumonia and their treatment

A

coxiella
chlamidya
legionella
mycoplasma

not susceptible to beta lactams! (amoxicillin) so need macrolide instead - clarithromycin

229
Q

what do X and V nutrient factors allow to grow

A

haemophilus influenzae

230
Q

how can you obtain a sputum sample in someone with dry cough

A

bronchoalveolar lavage - bronchoscopy passed in, fluid deposited and collected

induced sputum - breathe in saline via a nebuliser ,cough

231
Q

sabourdad’s agar

  • colour of agar
  • grows what
A

pale yellow

fungi (inhibits bacteria) - candida

232
Q

fungi grows on what agar

A

sabourdad’s

233
Q

causes of reactive arthritis

A

salmonella shigella yersnia chlamidya

234
Q

warm swollen tender joint = what until proven otherwise

A

reactive arthritis

235
Q

which TB treatment interacts with the oral contraceptivepill

A

Rifampicin

236
Q

malaria investigations

A

blood and other cultures not useful

blood FILM

phase 2a mine (38 decks)

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