Steinhauer Flashcards
P. falciparum
Mostly tropics
30,000 merozoites from hepatic cycle
Like younger cells
Only see multiple ring form and gametocytes (banana shaped)
Only one to do the clumping and rosetting
P. vivax
Tropics but not that much in africa 10,000 merozoites per hepatic cycle Like reticulocytes Can relapse See schizont and macrogametocytes One ring
P. malariae
Cosmopolitan but spotty
Like older RBC
P. ovale
Can relapse
Likes young
P. knowlsi
Southeast asia
Anopheles
Face down, ass up, thats the way it likes to suck
Plasmodium life cycle
Mesquito injects sporozoits into human
Make it to liver by inducing parasitophorous vacuole
The replicate and release merozoites back into blood
Make it to blood cells and make trophozoites
Ring troph
Signet ring trophozoite
Hemozoin with schizont
Can reenter cycle or make micro/macrogametocyte which get picked up by mesquito
How long until you have malaria symptoms
14-35 days
Uncompliccated malaria
Acute fever Paroxysms- chill then sweats Vivax every 48 hours benign tertian Falciparum every 72 hours malignant tertian Due to TNF-a Anemia
Complicated malaria
Organ failure
Cerebral- Neuro problems
Blackwater fever- Dark hemoglobinuria
Hyperparasittemia with 5% RBC infected
Why is P. falciparum more pathogenic
More merozoites, more invasion of RBC
PfEMP1- expression causes cytoadhesions=endothelium adhesions and rosetting and protects parasites from being cleared by spleen
Sticky cells and disease
TNF—iNOS which disrupts neurons- cerebral effects
Malarial relapse
Normally within 3-5 years
Have a dormant state in liver with clearance from RBC
P. vivax and ovale
Recrudescense
Low level in RBC with no hypnozoites
P. Falciparum
Plasmodium dx
Thick blood smear- recognize parasite
Thin blood smear- specific dx
Serological, PCR
Rapid- for falciparum (HRP2) and vivax
Genetic resistance to malaria
Sickle cell (PfEMP1 malformation, microRNA also disrupt parasite, and heme oxygenase 1 inhibits cerebral malaria)
Duffy blood groups (vivax and knowlesi)
Thalassemia
G6PDH
Duffy blood group
Genes common in africa, the reason why vivax doesn’t exist there
Lack of receptors for parasite attachment
Host defense of plasmodium
Spleen clears infected cells
Ab- Premunition: asymptomatic parasitemia (not common with travelers)
Babesia microti
Northeastern and upper midwest
Babesia divergens
Midwest and europe
Babesio duncani
West coast
Babesiosis general
Flu like symptoms unless immunocomprimised
Most via tick (Ixode scapularis and pacificus), some from blood transfusion
Important host- Permyscu leucopis mouse, same as Borrelia
Babesiosis life cycle
After feeding, adult females drop off the third host to lay eggs(1), usually in the fall. Eggs hatch into six-legged larvae(2)and overwinter in the larval stage. In the spring, the larvae seek out and attach to the first host, usually a small rodent(3). Later in the summer, engorged larvae leave the first host(4)and molt into nymphs(5), usually in the fall. The ticks overwinter in this stage. During the following spring, the nymphs seek out and attach to the second host(6), usually another rodent (e.g., a mouse) or lagomorph (e.g., a rabbit). The nymphs feed on the second host and drop off later in the summer(7). Nymphs molt into adults(7a-7b)off the host in the late summer or fall, and overwinter in this stage. The next spring, adults seek out and attach to a third host, which is usually a larger herbivore (including cervids and bovids), carnivore, or human(8). The adults feed and mate on the third host during the summer. Females drop off the host in the fall to continue the cycle. Females may reattach and feed multiple times. The three hosts do not necessarily have to be different species, or even different individuals. Humans may serve as first, second or third hosts.
