Blood Parasites

Vocabulary flashcards covering core terms, organisms, life-cycle stages, vectors, clinical manifestations, diagnostics, and treatments related to blood-borne protozoan parasites discussed in the lecture.

malaria

mosquito borne disease caused by Plasmodium sp.; fever/chills/flu like illness; untreated=severe complications, possibly death; most affected children in sub-Saharan Africa; prevent via bed nets, insecticide, antimalarial drugs; most common thing in US from travel

malaria geography

depends on climate-tropical/sub tropical; Anopheles mosquito

malaria life cycle

female mosquito sucks blood, injects sporozoites; sporozoites go into liver cells, infect liver, form schizont (sac) w/parasites inside (merozoites) (exoerythrocytic); dormant state = hypnozoites (erythrocytic); schizont ruptures, merozoities infect RBCs (immature trophozoite); mature trophozoites repeat schizont cycle (asexual) or mature into gametocyte (sexual), wait for mosquito, become macrogametocyte and micro gametocyte, together form oocyst and rupture into sporozoites

malaria incubation period

typically 7 to 30 days after infection, depending on the Plasmodium species. Shorter=falciparum, longer=malariae; antimalarial drugs can delay appearance esp with vivax and ovale

exoerythrocytic

doesn’t occur in bloodstreambut in liver cells during malaria life cycle.

uncomplicated malaria

primary attack (paroxysm): cold stage (cold, shivering), hot stage (fever, headache, vomiting, seizures young children), sweating (return to normal temp, sweats, tiredness); fever/chills=rupture of erythrocytic schizont; every 2nd day with tertian (falcifarum, vivax, ovale), every 3rd day with quartan (malariae)

severe malaria

in people who have no immunity to malaria or immunity decreased; P. falciparum complicated by serious organ failure/blood abnormalities/metabolism (cerebral, severe anemia, pulmonary adema/ARDS, black water fever)

malaria transmission routes

organ donation, blood transfusion, needles, baby from infected mother

malaria resistant conditions

sickle cell anemia (abnormal hemoglobin can’t be ingested, low conc of potassium); Duffy antigen negative RBCs (vivax can’t bind); prior infection

malaria clinical

symptoms/physical findings; first symptoms not specific; severe-more striking; confirm via lab test

Plasmodium falciparum

Most lethal human malaria species; infects all RBC stages, shows multiple rings and banana-shaped gametocytes; troph has Maurer’s clefts; schizont 8-24 merozoites; makes RBCs sticky

Plasmodium vivax

all stages in blood; reticulocytes; troph ameboid-spread out; schizont has Schüffner’s dots, 12-24 merozoites, yellow-brown; gametocyte stretches out, very round

Plasmodium ovale

all stages in blood; reticulocytes; troph fimbriated (spikes), Schuffner’s dots, dark brown; schizont Schuffner’s dots, 6-14 merozoites

Plasmodium malariae

all stages in blood; old RBCs; band or basket or birds eye trophozoites; schizont Ziemann’s stippling (rare), 6-12 merozoites, dark brown, occasional rosettes

Ring Stage

Early intra-erythrocytic trophozoite of Plasmodium, seen as delicate ring in RBC cytoplasm. “headphones”

Schizont

Asexual stage of Plasmodium containing multiple merozoites produced by nuclear division.

Merozoite

Daughter parasite released from schizont that invades new red blood cells.

Gametocyte

Sexual stage of Plasmodium taken up by mosquito (e.g., crescent forms in P. falciparum).

Hypnozoite

Dormant liver stage of P. vivax and P. ovale responsible for malaria relapses.

Maurer’s clefts

Staining dots in P. falciparum-infected RBCs associated with protein export.

Schüffner’s dots

Fine red stippling in RBCs infected by P. vivax or P. ovale.

Ziemann’s stippling

Coarse dots sometimes seen in P. malariae-infected erythrocytes.

Anopheles mosquito

Female vector that transmits malaria parasites to humans.

Malaria Paroxysm

Cyclic attack of chills, fever, and sweating caused by synchronous RBC rupture.

Tertian Malaria

Fever cycle every 48 h (P. falciparum, P. vivax, P. ovale).

Quartan Malaria

Fever cycle every 72 h (P. malariae).

Recrudescence

Recurrence of malaria symptoms from surviving blood parasites after incomplete clearance-from immune system or treatment failure; all species bur most common falciparum, malariae

Relapse

Return of malaria months or years later owing to liver hypnozoites (vivax, ovale).

Cerebral Malaria

Severe P. falciparum complication with neurologic dysfunction from microvascular blockage.

Blackwater Fever

Hemoglobinuria and renal failure from massive hemolysis in falciparum malaria, often with G6PD deficiency + quinine.

G6PD Deficiency

Enzymatic defect predisposing to hemolysis; affects choice of antimalarials (contra-indicates primaquine).

Duffy Antigen Negativity

Absence of Fy blood group receptor on RBCs conferring resistance to P. vivax invasion.

Chloroquine

Traditional antimalarial effective against blood stages of sensitive Plasmodium species.

Primaquine

Drug that eradicates hypnozoites and gametocytes; requires prior G6PD testing.

Babesia microti

Tick-borne parasite causing babesiosis (Ixodes scapulars) (black-legged/deer ticks)

Babesia divergens

Babesiosis agent in Europe; intraerthrocytic; Ixodes ricinus; bovine babesiosis

babesia geography

worldwide; divergens=Europe, splenecctomized; microti=US

babesia life cycle

femle tick sucks blood, injects sporozoites, mature into troph then merozoite, ruptures and reproduces asexually (mouse or human), gametocyte waits for blood meal, sexual reproduction in tick

babesia clinical

most asymptomatic; usually short incubation period; divergens more severe

babesia diagnosis

pleomorphic; vacuolated; no pigment; tetrads; extracellular

Maltese Cross

Tetrad arrangement of Babesia merozoites in RBCs, pathognomonic but rare.

babesia treatment

clindamycin in combo w/other; maybe transfusion

kinetoplast

mass of mitochondrial DNA, sometimes close to nucleus

undulating membrane

organelle of locomotion in certain flagellate-finlike extension of cytoplasmic membrane w/flagellar sheath

parabasal body

cytoplasmic body closely associated w/kinetoplast in some

Amastigote

Non-flagellated intracellular form

Promastigote

Elongated, flagellated extracellular stage

Epimastigote

kinetoplast anterior to nucleus, undulating membrane

Trypomastigote

kinetoplast completely posterior

Leishmaniasis cause

sandfly transmission; obligate intracellular protozoa from Leishmania; infect mononuclear phagocytic cells

leishmania geography

mostly tropics/subtropics, rainforests to deserts; visceral=india, bangladesh, nepal, sudan, brazil; mexico, S/C America, S Europe, Asia (not SE), middle east, africa

Cutaneous Leishmaniasis

1+ ulcers where sandflies fed; sores can change size/appearance; volcano; scab maybe; sores painless or painful; maybe swollen lymph nodes; sometimes symptoms delayed

mucocutaneous leishmaniasis

1-5 years after ulcers heal; can spread to nose/throat/mouth; mucus membrane destruction; runny/stuffy nose, nose bleeds, difficulty breathing

Visceral Leishmaniasis (Kala-azar)

damages internal organs, bone marrow, immune system; usually fatal untreated; symptoms don’t appear for months

leishmania diagnosis

cutaneous: skin biopsy-look for DNA; visceral: enlarged spleen/liver, bone marrow biopsy or blood sample needed;

leishmania life cycle

female sucks blood, transfers promastigote-phagocytosed by macrophages, loses flagella-becomes amastigote, multiplies in tissues and spreads; sandfly ingests RBCs w/amastigote, transforms to promastigote in insect gut-goes back to mouth parts

leishmania transmission

needles, blood transfusion, or congenital

african trypanosomiasis cause

trypanosoma brucei-small kinteoplast, extracellular, can replicate, other transmission rare

Trypanosoma brucei gambiense

West African sleeping sickness agent; chronic course.

Trypanosoma brucei rhodesiense

East African sleeping sickness agent; acute, rapid progression.

african trypanosomiasis clinical

3 stages: trypanosomal chancre (ulcer), hemolymphatic, meningoencephalitic

african trypanosomiasis life cycle

tsetse fly sucks blood, injects trypano mastigotes (metacyclic trypomastigote), multiplies in blood, goes to lymph/spinal fluid, in blood goes back to fly and becomes procyclic trypomastigote, then back to metacyclic

african trypanomiasis diagnosis

microscopic exam of biopsy, or fluid, late stage CSF; wet prep and Giemsa, maybe conc techniques

african trypanosomiasis transmission

congenital; blood transfusion/sexual contact rare

Trypanosoma cruzi

American trypanosome causing Chagas disease; transmitted blood sucking bugs; big kinetoplast, c shape, intracellular/extracellular but only replicate intracellular, transmitted by other methods

american trypanosomiasis geography

Americas from S US to argentina, mostly poor rural areas of mexico, s/c america; chronic charges disease major problem in latin america

american trypanosomiasis clinical

acute phase: asymptomatic, sometimes nonspecific symptoms, rarely more severe with cardiac/neurologic involvement; chagomas (inflammatory nodules) may develop around bite; most resolve into subclinical chronic form; symptomatic: years/decades later, cardiac/GI, complications can be fatal, amastigote in muscle can lead to megaesophagus/megacolon/dilated cardiomyopathy

american trypanosomiasis life cycle

triatomine bug (kissing bug) bites, transfers metacyclic trypomastigote in feces, allergic reaction causes scratching, transforms into amastigote in cells, then trypomastigote-bursts from cells into blood, picked back up by bug, becomes epimastigote in bug gut, then metacyclic trypomastigote

american trypanosomiasis diagnosis

microscopic exam of fresh uncoagulated blood or buffy coat, thin/thick blood smears (Giemsa)

american trypanosomiasis transmission

feces, blood transfusion, congenital, transplant

Toxoplasma gondii

infects most species of warm blooded animals

toxoplasmosis

a leading cause of death from food borne illness in US-few have symptoms, usually immune system keeps in check; one of the most neglected infections

toxoplasma symptoms

most asymptomatic, some feel like flu; severe from acute or reactivated, damage brain/eyes/other organs, can affect newborns

toxoplasma transmission

undercooked/contaminated meat/shellfish, drinking water, cat feces contact, congenital, organ transplant or blood transfusion

toxoplasma diagnosis

serologic testing, observe specimen in fluid/tissues, molecular techniques for amniotic fluid

toxoplasma life cycle

fecal oocysts ingested, tissue cysts in animals, eat tissue-develop into tachyzoites, develop into tissue cyst bradyzoites

Tachyzoite

Rapidly multiplying crescent-shaped form of T. gondii during acute infection.

Bradyzoite

Slow-growing form of T. gondii within tissue cysts during chronic infection.