Blood Parasites

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schizogony

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multiple fission
one cell – replicates nuclei many times (let’s say 10)
THEN divides into multiple different cells (1 per nuclei)

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schizont

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cell asexually reproducing

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merozoite

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progeny of schizont

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cyst (features)

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protected - somewhat dormant
may see nuclear division w/o cytokinesis -> multiple nuclei

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sporozoite

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infective stage of Sporozoa (Plasmodium)

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trophozoite

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metabolically active/growing stage of protozoans
when getting ready to leave body will form cysts w/ protective coating

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Plasmodium Phylum

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Apicomplexa (formerly Sporozoa)
non-motile (although early development has flagella
MATURE stage NOT motile)

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Plasmodium lifecycle

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"1) Mosquito (Anopheles) inserts proboscis -> injects anti-clotting enzymes & sporozoites
2) Sporozoite -> liver, becomes trophozoite (trophozoite = ONLY in liver for Thrush)
3) Trophozoite starts schizogony = merozoite
4) Single merozoite into RBC: replicate into multiple cells via schizogony

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Plasmodium pathology

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1) bursting RBC -> release "toxins"
2) sticky RBC cause blockage (esp. CNS, lungs, kidney, spleen)

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Plasmodium species

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P. vivax (benign tertiary malaria)
P. falciparum
P. malariae
P. ovale

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Cytokine released and causing malaria paroxysm

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TNF alpha (reduces RBC production)

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Conditions giving resistance to malaria

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1) sickle cell anemia
2) G6PDH deficiency (milder infxn c/o parasite needs enzyme)

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benign tertiary malaria

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p. vivax
43% of all malarias, paroxysms (sx) every 48 hrs
get into RBC by DUFFY BLOOD TYPE (40% Af. Am have resistant blood type, 0.1% Caucasians)
invades RETICULOCYTES; "Vivax = Vivre - alive = weakest"

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mild tertian malaria

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p. ovale

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malignant tertiary malaria

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p. falciparum
most virulent - 50% of all malaria, no true remission
more merozoites/RBC than others, can infect ANY stage RBC

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quartan malaria

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72 hour symptoms, 7% of malarias
enters aging RBC (can relapse 50 yrs later)

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hypnozoite

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dormant P. vivax or P. ovale in Liver
can RELAPSE (different than recrudescence)

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recrudescence

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P. malariae - low level replication w/o symptoms (chronic infxn)

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Malaria pathology

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1) fever c/o RBC waste products AND TNF-alpha
2) paroxysm - sudden appearance of symptoms (chills, then fever, then normal) falciparum = always feel crappy
3) anemia - RBC destruction (cannot recycle iron fast enough), TNF-alpha lowers erythropoeitin, infected RBC stick to normal RBC -> lysis 4) Cerebral malaria - P. falciparum (10% of cases)

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Malaria treatment

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quinine (some p. falciparum has multi-drug resistance)

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PfEMP-1

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P. falciparum Erythrocyte Membrane Protein-1 -> Ag variation (60 variants)
Expressed on surface of infected RBCs
contribute to RBC cytoadherance

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Malaria diagnosis

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Light micro, fluor micro, PCR
Rapid Ag detection: HRP-2 = histidine rich protein 2 (P. falciparum only) and parasite lactate dehydrogenase
Ab to HRP-2

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Maltese cross in RBC smear

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Diagnostic of Babesiosis (max: 4 merozoites per cell)
similar to malaria but NO schizonts or gametocytes
infxn from tick (Ixodes)

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lymph node swelling near eye

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Romana's sign: T. cruzi (when conjuntiva = portal of entry)
fever also common NO PAROXYSMS

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Babesia vector, reservoir, symptoms

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Vector = Ixodes (tick)
Reservoir = animals (cattle)
Symptoms similar to malaria but NO PAROXYSM

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kinetoplasmid

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concentrated area in mitochondria of trypanosoma (dark staining)
used for diagnosis

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kinetosome

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similar to basal body of flagella;
"Kinetosome = S for swimming"

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undulating membrane

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some species of Trypanosoma

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hosts of trypanosoma

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vertebrates and invertebrates (heteroxenous = two hosts)

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trypomastigote

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stage w/ undulating membrane & kinetosome near posterior end of organism
often found in human blood (but NOT in cells)

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amastigote

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very short flagella; Trypanosoma

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T. brucei disease
lives where in insect

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African trypanosomiasis (Salivaria section = salivary of insect digestive tract)

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T. cruzi disease
lives where in insect

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American trypanosomiasis "Chagas disease" (Stercoraria section = hindgut of insects)

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T. brucei subspecies

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T. b. brucei
T. b. gambiense
T.b. rhodesiense
Cannot distinguish morphologically

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T. brucei vector

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Tsetse fly (aka Glossina)

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T. b. brucei infxn

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parasite only of animals (cattle, etc.)

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T. b. gambiense infxn, reservoir

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chronic
human reservoir (although infects animals too) "G shaped like C for Chronic"
invades CNS, salivaria

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T. b. rhodesiense infxn, reservoir

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acute
animal reservoir (although infects humans too)
does NOT get into CNS (immune response does), salivaria; "Rhodesia on East like Rhode island, Vacation on East (don't go to Ivory Coast - West); Vacation for short time = Acute, Head - not long enough to get in"

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Tbg & Tbr pathogenesis

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1) Ag variation (transposon moves gene to end near telomere, knocks out copy of old gene -> expression)
2) replicate in blood and invade organs (Tbr not in CNS - Tbg is)
3) immune response (Abs & C' stim kills host cells -> anemia & CNS problems)
Note: Tbr doesn't get into CNS but immune response does

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Signs of Tbg

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Winterbottom's sign: pain, fever, headache, LN swelling
somnambulism, neuro problems, injury/death c/o sudden fall

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T. brucei Ag variation

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tranposons: moves expressed gene to end near telomere -> knocks out old gene (although orig. copy still around)
roughly 1000 genes for glycoprotein (VSG = variable surface glycoprotein)
changes roughly every week

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T. cruzi appearance
lifecycle

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Stains as C-shape, No Ag variation
Insect (kissing bug) feeds -> poops -> host scratches -> enters
Replicates in phagocytes (amastigote stage w/in cells) -> ruptures and exits as trypomastigote

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T. cruzi vector

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Triatoma (aka "Kissing Bug")
stercoraria = in poop of bug; "Cruzi takes a crap and kisses"

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T. cruzi pathology

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Enters/kills phagocytes in LN -> inflamm
forms pseudocysts (pockets of parasites) in muscle or brain
Acute phase = parasite in heart -> death in 3-4 wks (fever, Romana's sign)
Chronic phase = adults, dmg c/o nerve loss - can be asymptomatic then: heart dmg, megaesophagus, megacolon