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CRP
acute phase protein produced by liver
rises within hours and disappears in days
ESR/BSE
dependent on conc of plasma proteins vs RBC'
fibrinogen = acute phase protein
Ig’s
rises and disappears more slowly
bacterial physiology - 5
one chromosome (usually circular/ball in cytoplasma) → nucleoide
divide by binary fission
geen celkern, mito, ER en golgi
wel DNA, RNA, ribosomes en inclusion bodies
heeft altijd pl mem en meestal celwand
cell wall Gram + → 7
purple
plasma membrane
thick peptidoglycan layer
teichoic acid
no outer membrane → bc no LPS
more resis to environmental conditions (drying)
harder to kill with detergents
cell wall Gram- → 6
pink
plasma membrane
thin peptidoglycan layer
outer membrane with LPS
more susceptible to environmental conditions
easier to kill with lipophillic detergentia → sensi to ethanol etc.
bac cell wall role in pathogenesis - 3
mediates adherence to host tissues
immunostimulatory
cytotoxic properties
virulence peptidoglycan - 2
proinflamma genes → proinfla cytokines prod
peptidoglycan fragment will bind tot TLR-2 on cell mem → act the NF-kB → proinfla gene transcription
virulence LPS - 3
proinflamma genes → proinfla cytokines prod
mostly recognized by TLR4
activates NF-kB even more
bacterial spores - 4
some gram+ can do it
dehydrated structure with thick wall
survival in extreme conditions
soort slaapstand
capsulated bac = virulence factor - 4
composition = polysaccharides
surrounds cell wall
can be present in Gram - or +
more pathogenic than non-encapsulated → bc prevents complement binding
intracellular survival by bacteria = virulence factors 3
what are the fac intracell bacs
what kind of test
invade, survive and replicate within host cells
facultative intracellular → can live inside or outside → salmonella, listeria, mycobac
evade immune system → they dont get killed, bc they hide
the inhib fusion of fagosoom en lysosoom
PCR needed → culture not possible
acid-fast cell wall 3
mycobacterium have thick, waxy cell wall → rich in mycolic acids
wall slows nutrient uptake → long doubling time m. TB
hard to phagocytose/kill
diagnostic tests for acid fast cell walls
ZN stain = ziehl neelsen
appear red
auramine stain
fluor yellow/greenish
which test measures host immune response = serology (4)
IgM → vroeg, acute infectie
IgG → later, doorgemaakte infectie
enzyme immuno-assay
complement fixation test
which test measures host inflammation (3)
CRP
ESR
leukocyte count = aspecific
MALDI-TOF
from culture to name of mo = identifying species
based on proteins
PCR
from body fluid to direct detection of mo
based on DNA/RNA
structure of virus = 2
capsid → protein structure surrounding nucleic acid
around capsid there can be a lipid membrane → envelope
nucleocapsid
capsid + nucleic acid
capsomere
subunit of capsid
naked capsid virus → 3
more resistant to environmental conditions (drying)
more difficult to kill with detergent → chloride and iodine can
entry of host cell → virus-induced endocytosis
enveloped viruses
more susceptible to environmental conditions
easier to kill with lipophilic detergentia
entry host cell → membrane fusion or virus-induced endocytosis
classification DNA
single stranded
double stranded
circular
classification RNA
+/-
single segmented
double segmented
what kind of virus is cytomegalovirus
enveloped double stranded DNA
what kind of virus is enterovirus
non-enveloped positive-sense single stranded RNA virus
DNA virus = 4
DNA resembles host cell DNA
relatively stable within cell → can persist easily
chronic infection/latency
processing in host cell nucleus
low frequency mutations
RNA viruses = 5
RNA labile and intended to be transient = gemaakt om tijdelijk te zijn
persisting infections = unusual
processing in cytoplasm
RNA virues must encode RNA polymerase = own
host cell could never
high freq of mutations → antigenic drift
what kind of virus is mpox
enveloped double stranded DNA virus
what kind of virus is measles
enveloped single stranded RNA virus
steps in viral replication = 6
attachement/absorption which happens before entry even
then viral entry → can be mem fusion/endocytosis
uncoating → viral cpasid is removed and nucleic acid is released
viral replication starts
assembly → new viral particles are now put together
viral exit
viral replication
viral genome is replicated and viral proteins are synthesized
bot host and viral enzymes involved
viral exit → env vs non-env
enveloped viruses → budding
non enveloped → cell lysis
shingles → 4
caused by VZV
herpesvirus family → DNA virus
primary infection = chickenpox (varicella)
always followed by latency in neurons → shingles
prokaryote = 1
bacterium → single cell
eukaryote = 3
protozoa → single cell, can be parasite, post primary pathogens
fungi → multicellular, opportunistic pathogen
helminths → multicellular, can be parasite
types fungi
yeast cell
filamentous fungi with real hyphae → arms with big/a lot of circles
yeast with pseudohyphae → couple arms with no/little circles
structure of fungi
outer cell wall compounds
mannan
glucan
chitin
inner cell membrane → ergosterol
reproduction of yeast = fungi
budding
yeast = unicellular fungi
reproduction of molds = fungi + door wie bestreden (3)
are filamentous fungi → so grow as multicellular hyphal networs
sexual → spores
asexual → conidia
macrofagen, granulocyten, TC
aspergillus fumigatus → what, def disorder
filamentous fungi
if pt doesnt have neutrophils → dangerous = granulocytopenia
invasive aspergillosis → pneumonia/dissemination
candida albicans
lives on skin
disrupted barrier/immune system → vaginitis or stromatitis
trichophyton mentagrophytes
between the toes or on skin → dermatitis
ringworm
direct life cycle
parasite needs only 1 host
complex/indirect life cycle
parasite requires multiple hosts
types of hosts
definitive host → where para reaches sexual maturity, reprod there
mosquito
intermediate host → where larval.asexual stages develop
human
resevoir host → another host that maintains prasite in nature
classidication of parasites
ecto → scbies mite
endo
protozoa → e. histolytica
helminths → s. stercoralis
liofecycle and reprodc giardia lamblia → 5
infective stage → para transmitted via ingestion of mature cysts
in host → excystation
cysts go to duo → stomach acids triggers excy → release throphozoites
tropho → metabolically act stage → stick to intestine wall
reproduction → asex via long binary fission
encystation → in colon thropho goes back to c
hosts of plasmodium
human → intermediate host
anopheles → def host
toxoplasma gondii life cycle → 3 hosts
cysts from cat/rodents → def host
into animals that give eatable meat → int host
into human → dead end host
toxoplasmosis
asymptomatic infection or mild disease in healthy host
impaired TC immunity → risk of severe course of react
helminths types
roundwormes = nematodes → s. stercoralis
tapeworms = cestodes → taenia saginata
flukes = trematodes → schistosoma mansoni
helminths charecteristics → 4
have organs
female or male → also hermaphrodite
production → eggs, sometimes larvae
no replication in host → worms get in by infection (ONE EXCEPTION)
the one exception how worms get in → 4
larvae are excreted peri anal → contact with skin → auto-infection
strongyloides stercoralis
percutaneous infection (nakes feet) → visceral migration → eggs in duo → excrete in feces
TC imapired → severe react