Malaria Flashcards
Sporogony
asexual multiplication, mosquito –>sporozoites (INFECTIVE)
Schizogony
asexual multiplication in the man (Schizonts which burst merozoites)
Malaria life cycle
Mosquito injects sporozoites into the human (infection). The sporozoites travel to the liver for hepatocyte invasion. The sporozoites burst and release merozoites and enter into a blood cell. They form a ring trophozit and undergo a sexual reproduction into gametocytes. The mosquito gets the gametocytes and it forms into a zygote–>ookinete->oocyst–>and travels to the midgut of the mosquito. Int heh midgut of the mosquito, it gbecomes sporozoites and goes into the salivary gland.
Schuffners dots
P vivax and P ovale -enlarge the RBC
Ziemann’s stippling
P malariae
Sinton and Mulligan’s stippling
P knowlesi
Maurers clefts
P falciparum
What is cytoadherence
Happens in P falciparum. PfEMP-1 (Pf Erythrocyte membrane protein 1) Helps sequester parasite in visceral capillaries and venules. Causes endothelial injury and avoids parasite clearance in the spleen
Quotidian Fever
q24 hours schizogony: P knowlesi
Tertian Fever
q48 hours schizogony, P falciparum, P vivax, P ovale
Patent parasitemia
parasitemia detected by optic microscopy (>50p/uL)
sub-patent parasitemia
parasites present in the blood but not detected by optic microscopy <50p/uL
Pre-patent period
Time between infection and detection b y optic microscopy
Incubation period
time between infection and the onset of symptoms
Recrudescence
renewed detection of parasitemia arising from survival of undetectable erythrocytic parasites
Relapse
renewed detection of parasitemia arising from survival of exo-erythrocytic parasites (hypnozoites): Vivax and Ovale
Reinfection
Renewed detection of parasitemia arising from a NEW mosquito bite
Pyrogenic density
level of parasitemia at which fever occurs. Lower in nonimmunes <10,000 pf/uL
Plasmodium Vivax
Tx: Chloroquine + Primaquine
Enlarges the RBC
Uncomplicated Malaria
A patient who presents with symptoms of malaria and a positive parasitological test but NO features of severe malaria
Uncomplicated Hyperparasitemia
Patients who have >4% parasitemia but no signs of severity. They are at risk for severe malaria and resistance and treatment failure
What is severe malaria
Defined as 1 or more of the following:
-Impaired consciousness GCS<11
-Prostration (weakness)
-Convulsions (>2 in 24 hours)
-Pulmonary Edema
-Significant Bleeding
-Shock
-Acidosis
-Hypoglycemia
-Hgb <5
-Cr>3
-Tbili>3 or jaundice
-Hyperparasitemia >5%
Definitions of hyperparasitemia
> 4% without signs of severe malaria
2% in non-immune (i.e. travelers)
4% in endemic regions (i.e. “immune”
10% in all settings
What is the most common ACT that is also safe in pregnancy
artemether-Lumefantrine (AL)
Explain why you need ACT
Artemisin is rapidly acting, short half life, will kill parasite in the blood and gametocytes
You need a partner drug to be longer acting and clear the remaining parasite. Also will help reduce resistance
What is the definition of chloroquine resistance
treatment failure at day 28 >10%
What happens to malaria parasitemia in HIV+?
2-3 fold increase in parasitemia in HIV+ as compared to non HIV patients. (Inversely corelated with CD4 count)
True or false-HIV + patients that are infected with malaria are at higher risk for developing severe malaria
True -increased prevalence of clinical malaria; increased prevelenace of parasitemia, increased parasite density
In HIV +Children with malaria, what do you expect to see?
Increased prevalence/severity of anemia
Increased transfusion requirements
increased prevalence of coma, hypoglycemia
increased prevalence of concomittant bacteremia
what happens to hgb in HIV+ Malaria infections
hgb drops fast after malaria infection. slow to recover
What is the 2nd/third cause of severe morbidity in HIV patients
malaria
what is the mean CD4 count decline per year for:
1 malaria episode
2 malaria episodes
3 malaria episodes
5/uL for 1 malaria
84/uL for 2 malaria episodes
142/uL for >3 malaria episodes
Bactrim in HIV + prevents from what
Malaria
PCP
Toxoplasma
What happens to HIV RDTs during malaria episode
Specificity decreases
What happens to viral load of HIV in malaria
it transiently increases
if a child is taking zidovudine-containing regimen and is treated with artesunate/amodiaquine for malaria, what side effect to be aware of?
neutropenia
genetic traits that protect from severe malaria
sickle cell *
alpha thal, b thal, g6pd, blood group O
NEURO: GCS<11 (adults); Children <2 Blantyre
>2 seizures in 24 hours
prostatitis (weakness)
CV: Acidosis Bicarb <15 /kussmaul
BE>8
Lactate>5
SHOCK SBP<70 *children <80 adults
PULM: ARDS , SpO2<92%, RR>30
ABD: Jaundice, Tbili>3 WITH parasitemia>100,000
RENAL: ARF: Cr>3 or BUN>20
ENDO: Hypoglycemia <40
HEME: Bleeding , Hgb <5 in children, <7 in adults together with parasite count >10,000
ID: Hyperparasitemia P falciparum parasitemia >10%
Ruptured spleen can happen in what plasmodium species
P vivax malaria
Children with severe malaria clinical findings
-Prostrated (unable to sit)
-Comatose (unable to localize to pain) (blantyre<2)
-Acidotic breathing with nasal flaring and intercostal muscle use
Cerebral Malaria definitions/clinical features
“Unarousable coma” GCS<11, Blantyre<2 WITH post ictal coma at least 30 minutes after last seizure; confirmed P falciparum
-Coma
-Convulsions (can have non-clonic status in children)
-Symmetrical UMN lesion
-Dysconjugate gaze
-Abnormal posturing, pouting, fontal release
-Retinopathy
malarial retinopathy looks like
-White centered hemorrhages, vessel color change, peri and extra macular whitening
Children with cerebral malaria clinical features
raised ICP, impaired oculo-vestibular reflexes, flaccid muscle tone, convulsions
5-30% fatality of cerebral malaria
10% of survivors have long term neuro-psych deficits
how many children die from cerebral malaria? how many have long term neuro-psych deficits?
5-30% fatality
10% survive
If survived cerebral malaria, what sequelae can you have as a child
cortical blindness, involuntary movements, hemiplegia, spasticity, cognitive and learning defects
why are pregnant women at risk for malaria
lose their innate immunity, placenta chondroitin sulfate A is a good receptor for the parasite to bind to
What is IPTp for pregnant women
Recommended for pregnant women in moderate high malaria transmission areas Africa: 4 antenatal clinic visits, they should get sulfadoxine-pyrimethamine (SP) by DOT and folic acid daily
*If P falciparum mutations are prevalent, Rx dihydroartemisinin-piperaquine and insecticide treated bed nets
What is the treatment of severe malaria in areas with established artemisin resistance ?
Give parenteral artesunate + parenteral quinine, then can switch to Triple artemisinin combination therapy
severe vivax malaria: can see splenic rupture
pLDH RDT
Detects vivax, falciparum, malariae, ovale
Predictors of malaria without parasite demonstration
Splenomegaly, thrombocytopenia, hyerbilirubinemia
false negatives of RDTs
low parasitemia, some other plasmodium, HIGH faclciparum (Prozone effect), MUTATIONS (not with HRP2)
what parasite level is needed for RDTs
500p/uL
highest areas of resistance to chloroquine
indonesia, papa new guinea
child with severe malaria -cerebral signs, what to consider
translocation of gram negatives-cover with ceftriaxone
when do you transfuse a child
4-6 and shock OR below 4 always
what is the maximum parasitemia in a thick film
5+ (100 parasites /field)
4+ parasitemia
10-100 parasites/field
3+ parasitemia
1-10 parasitemia/field
Malaria ppx for SE ASia (Thailand, Cambodia, Lao, Myanmar)
malarone (for lao and myanmar)
