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id & micro - fungi & parasites - pathophysiology

id & micro - fungi & parasites - pathophysiology

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Published by: jmosser on Jan 19, 2010
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03/26/2013

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2
Malaria
Global Burden
 
Was formerly prevalent in US; eradicated via infection controls & social improvement
 
1
st
 
global push (‘50s) to eradi
cate based on DDT+chloroquine; success in some areas, partial in others
o
 
No serious attempt in Africa
o
 
Failed: unrealistic expectations, no integration with existing infrastructure
 
 
Chloroquine-resistant
P. falciparum
& DDT-resistant Anapholes
 
Global distribution today
: Africa
biggest,
SE Asia
drug resistant, also other parts of world
o
 
Very different distribution in different countries within Africa
 –
some much higher than others
Epidemiology 
 
Parasitic, mosquitos
; 247M cases/yr, 891K deaths, 85% in
sub-saharan Africa
(
YOUNG KIDS & PREGNANT)
 
o
 
Resurgence
: drug resistance, other factors,
no vaccine
 
 
Four species
of 
 
malaria:
 
o
 
Plasmodium falciparum:
90% infection; almost all death in Africa, MDR, vaccine efforts
 
o
 
P. vivax 
:
 
big contributor in
SE Asia
morbidity (& mortality)
 
o
 
P. ovale
(Africa only),
P. malariae
too
 
Highly variable
around world &
within
 
countries
with
different presentation
 
o
 
Related to
intensity
of burden,
duration of transmission
 
o
 
Classic definitions: Spleen rate:
hypo
endemic <
meso
<
hyper
<
holo
 
 
Acquired immunity
:
o
 
Stable
malaria: heavy, perennial transmission;
endemic
 
Generally
protected from severe dz
after age 5 (except for in pregnancy
 
o
 
Unstable
malaria: less intense transmission;
epidemics / outbreaks
 
Protective immunity: later age or
not at all
;
all ages vulnerable
Immunity 
 
Humoral & Cellular;
Initially:
innate
+
spleen
 
 
Maternal Ab
last 3-
6 mo (don’t see severe dz in children < 6mo
)
Protection:
slow, need
 prolonged, repeated 
exposure;
protection from infection is not achieved
 
 
Immunity
lost
if 
exposure stops:
very common to see expat visit old country & get malaria
 
Diminished immunity in
pregnancy
:
increased risk of disease & complications, incl. still birth/miscarriage/low birth wt)
 
Limited interaction with HIV
:
 
co-infection, not opportunist
o
 
Viral load increases in acute phase; lost protection against malaria
o
 
Biggest interactions in
HIV+ pregnant women
 
Innate immunity
:
 
Malaria hypothesis
: red cell polymorphisms distributed geographically because of selective pressure of malaria
 
o
 
Hb structure, thalassemias
(Hb synth)
, G6P deficiency
(RBC enzyme),
Duffy negative blood
(PM of cell)
 
o
 
HLA types
? May protect against severe malaria
 
Duffy receptor
and
vivax 
malaria
 
Chemoine receptor; spans PM, present in endothelial cells,
only
P. vivax 
binds for entry to RBC
 
Duffy negative: primarily present in Africans (
no vivax)
 
 
3
Life Cycle
A.
 
Mosquito bite
(
femaleanopheles mosquito atnight)
Sporozoites
 injected; clinically Asx
B.
 
Hepatic
stage: multiplestages,
6d-weeks
of 
“incubation”, results in
hepatic schizont
filled with
merozoites
(still Asx)
(
P. vivax & P. ovale
canarrest here as
hypnozoites
inliver &
relapse
months toyear after primary infection)
C.
 
Schizont ruptures
andreleases
merozoites
intoblood stream, which
infect erythrocytes
.
D.
 
Erythrocytic schizonts
filled with
merozoites
 
rupture
; more red cellsreleased:
periodicity
(via
asexual
reproduction)
 E.
 
Some
merozoites
 
differentiate
into
gametocytes
 
F.
 
Gametocytes
taken up by female anapholes mosquito;
sexual
 reproduction takes place in her, infects other host
 Note: SEXUAL forms responsible for transmissionASEXUAL for periodicity of symptoms
Invasion of erythrocytes leads to
knobs
forming (
“sticky” RBC)
 Species-specific characteristics:
 
P. falciparum
:
 
~5.5d incubation in
liver
 
48 hr
erythrocytic cycle (
fever periodicity)
 
Tons
of merozoites per schizont
 
 
Infects ALL KINDS of RBC
(
HIGH
parasitemia)
 
 
Need
HIGH
burden for fever
(even more if immune)
 
P. vivax 
 
 
8 day incubation
 
48h periodicity
 
Fewer merozoites /schizont
 
Invades
mostly
RETICULOCYTES
(
LOW
parasitemia)
 
Need
lower
burden for fever
 
Can form
hypnozoites
(dormancy!)
P. malariae:
 
 
72h periodicity
 
P. ovale
:
 
Similar to
P. vivax 
 
 
Can form
hypnozoites
(dormancy!)
 
Clinical presentation & Diagnosis
 
Complex; many vital systems involved;
Asx
in
hepatic
&
sporozoite
stages
 
Disease from
red blood cell stage
: stimulates
host immune response
 
 
Periodic fever
(chill
rigors
high fever
sweating
release),
non-specific
 
o
 
Can also have cough, H/A, body ache, malaise, weakness, diarrhea
o
 
Signs: fever,
anemia
, jaundice,
enlarged spleen
/liver
 
If patient has Sx post-
Tx, what’s up?
 Recrudesence:
 
P. falciparum & P.malariae,
reappearance
of parasites inthe blood (e.g. after being pushed downbelow detectable threshold.
Relapse
:
P. vivax & P. ovale
,
revival of hypnozoites
in the liver.
Re-infection
: new infection for patient

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