Vector Borne Apicomplexans Flashcards
Babesiosis Name Location Definitive host Intermediate host Incidental host Transmission Life cycle Diagnosis Treatment (4) Prevention
- Babesia microti / duncani
- Location: only RBCs (not hepatocytes like plasmodium)
- Definitive host: deer tick (Ixodes scapularis; same as Lyme)
- Intermediate host: mice and small mammals
- Humans are incidental hosts
- Transmission: nymph stage of deer tick. Found in NE and upper Midwest (WI / MN). Also possible to pass congenitally.
- Life cycle: Tick takes mouse blood meal to introduce. Trophozoite –> merozoite (maltese cross) –> gamete –> taken up in tick w/ next blood meal. Fertilization in gut –> sporozoite. Tick bites human to introduce.
- Diagnosis – Babesia form maltese cross inside RBCs. CDC can differentiate spp. Look for hemolytic anemia and thrombocytopenia in acutely ill pxs.
- Treatment – Combo therapy includes atovaquone and azithromycin. Use Clindamycin and quinine for severely ill pxs. Never monotherapy.
- Prevention – stay out of woods or wear DEET.
Babesia Pathology
- Usually asymptomatic
- Hemolytic anemia and nonspecific flu-like sxs (fever, chills, body aches, weakness, fatigue) weeks / months after exposure.
- Some pxs have hepatosplenomegaly or jaundice
What is most common type of malaria in Africa?
Falciparum
Clues to falciparum (4)
Parasitemia >3%
RBC has more than one ring
Banana shaped gametocytes
No trophozoites / shizonts
Which malaria adheres to tissues? What does it do?
Falciparum attaches to endothelia cells –> damage / ischemia
Where is P vivax?
South America
Malaria Location Definitive host Intermediate host / Reservoir (knowlesi) Transmission Pxs at risk Immunity
- Location: hepatocytes and RBCs
- Definitive host: mosquito
- Intermediate host / Reservoir: humans; primates are reservoir for P knowlesi
- Transmission: female Anopheles mosquito, congenital, and needle transfer. Infection is decreasing, largely due to nets.
- Most fatalities occur in kids and prima gravida females
- Immunity – slow to develop, requiring multiple infections. Short-lived if leave endemic area. Need spleen to remove infected RBCs, so asplenia is big risk factor. Antigenic variation of NOD proteins (allow for adhesion to endothelium) prevents sufficient immune attack. In reality, immunity just refers to how high of a parasitic load they can tolerate w/o sxs.
Malaria Life Cycle
- Sporozoites injected and invade hepatocytes. Takes less than 10 min.
- After 7-10 days, it leaves the liver and invades RBCs
- Predictable waves of parasitemia, hemolysis, and fever. Fever occurs w/ erythrocytic shizogany.
- Once they reach a certain level of parasitemia, sexual recombination occurs, which then is picked up by another mosquito.
Fever timing for P vivax, ovale, malariae, falciparum, and knowlesi
- P vivax / ovale: 48 hr spike
- P malariae: 72 hr spike
- P falciparum: 48 hr broad
- P knowlesi: 24 hrs
Who is most at risk for anemia from malaria? Which strains?
Pathophysiology of anemia (4)
Mainly in kids younger than 2 due to weaker immune system.
Falciparum and vivax.
Due to RBC lysis, increased removal of uninfected RBCs, suppression of erythropoiesis, and immune destruction of RBCs coated w/ parasite molecules.
Which strain of malaria causes thrombocytopenia?
Falciparum
Constitutional sxs of malaria (5)
Chills, fever, splenomegaly, myalgia, headache
Which strains of malaria remain dormant / latent in liver?
Vivax / ovale
Which strain of malaria can cause progressive renal disease?
P malariae
Which strain of malaria causes cerebral malaria?
Falciparum
