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exam revision > micro pracs > Flashcards

micro pracs Flashcards

1
Q

shape of H influenzae type b

A

cocobacilli

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2
Q

treatment of H influenzae b

A

cefotaxime steroids

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3
Q

prevention of h influenzae type b

A

conjugate vaccine

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4
Q

what do neisseria meningitidis grp b look like

A

GN diplococci

small white colonies

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5
Q

what is characteristic clinical sign of meningococcal type b

A

fine petechial rash

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6
Q

what do strep pneumoniae look like

A

GP diplococci

alpha haemolysis

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7
Q

treatment for strep pneumoniae

A

vancomycin (lots are pen resistant)

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8
Q

what does grp B strep look like on gram stain and plate

A

GPC in chains

beta haemolysis

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9
Q

is it significant if we find virus in blood or another sample if testing for meningitis

A

not necessarily - can carry viruses with us asymptomatically

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10
Q

name of fungi that can cause meningitis

A

cryptococcus neoformans

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11
Q

clinical findings on fungal menintitis

A

raised protein
low glucose
high lymphocytes

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12
Q

anergy

A

when lymphocyte not fully stimulated, becomes unresponsive - switches off autoreactive T cells

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13
Q

ignorance

A

lymphocyte never encounters antigen even if has self-reactive R

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14
Q

regulation

A

Tregs - can suppress activity of CD4 adn CD8

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15
Q

epitope spreading

A

complex antigen encountered
at least 3 epitopes that B cells can bind
B cells specific to different epitopes, but through processing end up presenting same antigen on MHC
so one T cell can drive 3 different B cells
so might need only one autoreactive T cell to drive different autoreactive B cells

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16
Q

what is ASCOT

A

anti-streptolysin O test - to see if previously exposed to strep pyogenes

17
Q

coeliac have abs against

A

transglutaminase and deamidated gliadin

18
Q

what disease has eg of epitope spreading

A 
coeliac autoreactive B cell with specificity to TTG will take up whole complex of TTG adn gliadin
presents gliadin (Bc peptide) and activates T cell 
T cell then drives B cell response to TTG and gliadin
19
Q

what is CIN

A

selective media for yersinia

20
Q

yersinia gram stain

A

GPR

21
Q

are salmonella and shigella lactose fermenting?

A

no

22
Q

is e coli lactose fermenting

A

yes

23
Q

what is CAMP for

A

campylobacter

24
Q

what is selenite broth for

A

salmonella

25
Q

malaria form in blood

A

trophozoytes

26
Q

what characterises falciporum in RBCs

A

multiple early signet ring formations

27
Q

what is more severe, falciporum or vivax

A

falciporum

28
Q

malaria lifecycle

A

sporozoites infect hepatocytes
hepatocytes rupture and release merozoites
merozoites infect RBCs
RBCs rupture and release schizont

29
Q

how to tell falciporum and vivax apart in thin film

A

falciparaum - infected cells same size, signet ring, more than one trophozoite in RBC
vivax - infected cells larger, single trophozoite in RBC

30
Q

ramdidiform larvae

A

strongyloides

31
Q

rose spots

A

sign of untreated severe bacterial infection

32
Q

salmonella typhi lifecycle

A

ingested (doesnt initially cause gastro), moves through lymphatics to mesenteric lymph nodes, primary bacteraemia, multiplication in liver, spleen, macs, bone marrow, secondarysepticaemia - fever
then to gall bladder - cholescystasis
bile to SI - gastro

33
Q

what is GC media

A

lysed blood media, antimicrobials on one side

34
Q

treatment for gonorrhoea

A

high dose ceftriaxone + azythromycin for chlamidia

35
Q

elementary body of chlam

A

infectious non-replicating, hardy

36
Q

reticulate body of chlam

A

intracellular, replicating

37
Q

chlam lifecycle

A

EB entry into mucosal epithelium via adhesniosn and R mediated endocytosis
EB encorporated into endosome, but doesnt fuse with lysosome
EB becomes metabolically active RB
RB converted to EB
release of EB

38
Q

parvovirus B19 2nd or 3rd trimester infection

A

foetal anaemia - could lead to fetal hydrops - treat with intrauterine transfusion

39
Q

treatment for syphilis

A

penicillin

exam revision (15 decks)

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