Malaria Flashcards
what is the most common cause of fever in a returned traveler?
malaria
how do many docs misdiagnose malaria?
forget to get a travel history!
mosquitoes carry malaria- where do they store it?
salivary gland
vector for malaria?
anopheles mosquito
non human reservoir for malaria?
none except for macaques with P. knowlesi
“hidden plasmodia” dilemma
after infection, the sporozoites circulated free for only about half an hour, and then vanished for several days they hide/go to liver cells!!!
sporozoites
come from mosquito
tiny thread like
short lived in the blood –> travel to the hepatocytes
schizont
in liver
asymptomatic
contains merozoites (the merozoites are infective for RBCs)
merozoites
how many in Pv? Pf?
merozoites are infective daughter cells that invade RBCs
10,000 in Pv
30,000 in Pf
what form is transmitted by mosquito saliva?
sporozoites
after merozoites infect the RBCs, what do they form?
ring-stage trophozoites
ring stage trophozoites turn into …
which do what?
schizonts
schizonts rupture and release merozoites which infect more RBCs
hypnozoite
- Dormant liver stage in P. vivax and P. ovale -> can have recurrent infxns
- Release blood stage parasites weeks to months after primary infection
which two malaria types can have recurrent infections due to a dormant stage?
P vivax and P ovale
1 - mosquito bites and injects sporozoites
2 - sporozoites go to liver and form schizonts which rupture and release merozoites (exo-erythrocytc cycle)
3 - merozoites go to blood and for primary ringed trophozoites
–they can either become gametocyte or mature trohpzoite
4 - mature trophozoite becomes schizont which ruptures and releases more merozoites into blood (erythrocytic cycle)
5 - gametocytes form new gametocytes which can infect new mosquito if an uninfected mosquito bites person
6) sporogenic cycle = gametocytes inside new mosquito create macrogametocyte and then an oocyst which creates new sporozoites
how long does it take for malaria symptoms to appear?
P falciparum
P ovale
P vivax
P malariae
Pf 8-11 days
Po/Pv 10-17
Pm 18-40
onset of symptoms of malaria coincides with….
the start of the erythrocytic cycle
incubation with ______can be up to 20 years due to chronic subclinical erythrocytic stage
P. malariae
3 evolutionary defenses against malaria
Duffy antigen negative (P viva uses duffy agent to enter RBCs)
sickle cell trait (selective sickling of falciparum infected RBCs)
G6PD deficiency (malaria parasites grow poorly in G6PD deficient rbcs d/t increased ROS in rbcs)
classic triad of symptoms for malaria
fever, chills, headache
three clinical types of malaria
acute uncomplicated
severe malaria
hyperreactive malarial syndrome (tropical splenomegaly)
uncomplicated (mild) malaria
Occurs with all Plasmodium species
—–sudden episodes of: fevers, chills, and sweats
- cold stage with shaking – 2. hot stage with high temperature (>104°F) – 3. sweating stage with resolution of fever
episodes last 6-10 hours, and then recur
every 2 days with P. vivax and P. ovale (tertian fever)
and for P. falciparum (malignant tertian fever)
every 3 days with P. malariae (quartan fever)
complicated/severe malaria
Can cause any of these:
• Cerebral malaria (change in mental status, coma)
• Respiratory distress
• Severe anemia (hct <15%)
• Renal failure
• Hypoglycemia
- Circulatory collapse (shock) and lactic acidosis
- Bleeding disorder (spontaneous bleeding or evidence of DIC)
******complications primarily occur with P falciparum, usually when parasitemia >2% (% of rbcs infected).
complicated malaria is usually with what species?
falciparum
why are falciparum infections the most severe?
because it will infect ANY rbcs
asexual blood stage parasites of P. falcip. can develop in erythrocytes of all ages there is
NO LIMIT ON THE DEGREE OF PARASITEMIA
What is the mechanism for tissue harm in malaria?
tissue hypoxia and lactic acidosis
RBCs become “sticky” and clog up vasculature
SEQUESTRATION! –> Erythrocytes containing mature P. falcip. parasites develop “knobs” and express adhesion molecules that bind to endothelium of capillaries/venules.
Also there is decreased deformability of infected AND non-infected RBCs, contributing to sludging, aggregation, and blockage of vessels.
This causes tissue hypoxia and organ failure.
cerebral malaria
•acute encephalopathy not attributable to other causes in a patient with malaria
decreased consciousness + delirium + seizures
brain has increased mass (swollen)
cerebral malaria is driven by sequestered RBC in brain blood vessels
cerebral malaria untreated Px and treated Px
untreated - 100% die
treated - 20% die
cerebral malaria is diven by what process?
RBCs accumulation in brain parenchyma
malaria diagnosis - 3 methods
blood smear - thick and thin
antigen testing
PCR
BinaxNow
malaria card test - antigen capture
Control line + T1 and T2
- all three lines Pf or combined
- just C and T1 –> Pf
- C and T2 –> Px, Pm, Po
enlarged cells + schuffners dots
which species?
vivax or ovale
vivax or ovale
enlarged infected RBCs and schuffners dots
TOP vivax - schizont with 12-24 merozoites
BOTTOM ovale - schizont that is oval and fewer merozoites (6-12)
what species makes band forms?
malariae
P malariae
P malariae
owl eye trophozoite, infected cells are smaller, has yellow/brown pigment
features of P malariae
owl eye trohpozoites
smaller infected cells
yellow/brown pigment
P falciparum
multiple ringed trophozoites and banana shaped gametocyte
multiple ringed trophozoites and banana gametocyte?
p falciparum
if malaria smear is negative, keep what?
repeating smears/Ag tests every so often until better
prevention of malaria
PPE
chemotherapy =
–doxycycline
–atovaquone/proguanil
–mefloquine
–Primaquine
–Chloroquine (in chloroquine-sensitive areas)
admit all patients with ___
falciparum
Patients with P. vivax and P. ovale should receive therapy (primaquine) to
eradicate any remaining hypnozoites after treatment for intraerythrocytic stage.
