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Plasmodium

-causes malariatransmitted by Anopheles mosquito

-sexual and asexual phasessexual phase occurs in mosquitoes, asexual phase in

host RBCseventually burst from RBCs and cause periodic fever, anemia

-4 main species: Plasmodium malariae, vivax, ovale, falciparum

-each species has different appearanceallows for differentiation in stainedsmears

RBCs in Vivax and Ovale are pale and enlarged and contain granules

RBCs in Malariae are not enlarged and do not contain granules

RBCs in Plasmodium contain small rings

-Life Cycle is VERY IMPORTANT!

-sexual cycle begins when anopheles mosquito ingests gametocytes from

infected human

-in mosquito, gametocytes mature into zygotepenetrates gut wallforms

oocystwithin this 1000s of sporozoites---cyst ruptures and sporozoites released

into body cavity and salivary glands

-asexual cycle begins when infected mosquito bites human and sporozoitesare injected into bloodcirculate to liver and infect hepatocytesform 1000s of

merozoites (note: in Vivax and Ovale, some sporozoites become dormant and form

hypozoites)hepatocytes rupture and merozoites released into blood to infect

RBCs

-erythrocytic stage begins with merozoite attaches to and invades RBC

becomes a ring shaped trophozoitemultiply and form new merozoitesafter 48-

72 hrs RBC ruptures and merozoites released to infect more RBCs and repeat cycle;

some merozoites become gametocytes and can be taken up by mosquito if bitten

and start sexual cycle

-RBC rupture cycle recurs until immune response develops and stops

erythrocytic cycle-hypnozoites in Vivax and Ovale avoid immune destructioncan reactivate

and start cycle again at a later timeleads to second release of merozoites to infect

RBCs= relapse

Physiology

-Vivax and Ovale infect reticulocytes

-Malariae infects senescent RBCs

-Falciparum infects all stages of RBCs, produce high levels of parasitemiamost

severe disease

-RBC Duffy Antigen and glycoprotein A are receptors for PlasmodiumDuffy-

negative people are resistant to Vivax

-Sickle cell trait limits intensity of Falciparumthese people are resistant toFalciparum (sickle cell gene is very common in high malaria places)

-similar protective effect in thalassemia, G6PD Deficiency

-once infect RBCs, parasites induce changes in RBC membranechanges in lipid

concentration, incorporation of parasite antigens

Pathogenesis

-Fever

-irregular fever hallmark

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-occurs when RBCs rupture and merozoites are released (either parasite

releases pyrogens, or macrophages induced to release TNF and IL-1)

-when all the RBCs become synchronizedrupture at the same time

results in cyclical fever (either every 48 hrs or 72 hrs)

-Anemia

-RBCs destroyed by rupture or phagocytosis-when hemolysis is massivecan result in hemoglobinuriacauses dark

urine= blackwater fever

-Circulatory changes

-high fever causes vasodilationhypotension

-Falciparum can cause RBCs to stick to endotheliumcan lead to hypoxia,

lactic acidosis, hypoglycemia (if affects the braincalled cerebral malaria)

-Cytokines

-pts have elevated TNF alpha and IL-1

-high levels of TNF can cause up-regulation of endothelial adhesion

moleculesprecipitate tissue hypoxia and cerebral malaria

-Other phenomena-thrombocytopenia

-acute glomerulonephritis, progressive renal disease

Immunity

-host quickly develops immune response that limits parasite replication and

manifestations without eliminating parasite= premonition

-prolonged recovery period with recurrent exacerbationsbecome less severe and

less frequenteventually stop

-T and B cells involved

Manifestations

-incubation period is about 2 weekscan be prolonged if pts on antimalarial agents

(may be months)-fever, chills, splenomegaly, anemia

-hallmark is malaria paroxysm: cold stage/chills for 1 hras body temp increase

chills stop and get vasodilationbody temp rises to 41 degrees C and severe

fevereventually fever decreases and get profuse sweatingpt is very exhausted

at the end but fine until next cycle (paroxysms occur when parasite sporulation

becomes synchronized and RBCs ruptureat same time; in Falciparum, may never

get synchronizationfevers are irregular)

-paroxysms become less frequent/severeeventually stop

-Cerebral malaria: delirium, seizures, coma, rapid death

-Acute renal failure, jaundice

Diagnosis-via stained blood smears to see parasites

Treatment

-Chloroquineinhibits degradation of hemoglobin, thus limiting availability of

amino acids for parasite growth----falciparum can be resistant

-others include mefloquine, quinine

-add primaquine of Vivax or Ovale to kils hypnozoites!!

-no vaccine

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Arenaviruses

-zoonotic infectionsrodents are reservoir

Arenaviruses associated with hemorrhagic fever

-Lassa virus and Junin virus cause hemorrhagic feverfever, hemorrhagic

manifestations, shock, neurologic symptoms, bradycardia

-Lassa virus can also cause myocarditis, hepatitis, deafness-dx suggested via recent travel history and clinical syndrome

-pts suspected of having infxn should be isolated

-tx: IV ribavirin helps in Lassa fever

Lymphocytic Choriomeningitis Virus

-reservoirs are hamsters and mice

-fever, headache, myalgias, sometimes meningoencephalitis

-dx via history of rodent contact

Marburg and Ebola Virus

-filoviruses

-reservoir is monkeys

-can cause fulminant, lethal hemorrhagic disease and shock in humans-dx via recent travel history

-no specific therapy

Hantavirus

-hanta hemorrhagic fever with varying degrees of acute renal failure

-possible reservoir is rodents

-other species can cause hantavirus pulmonary syndromefulminant respiratory

diseasetransmitted via inhalation or direct contact with skin breaks

Henipavirus

-pneumonia and encephalitis

-reservoir is Pteropus fruit bat

-transmitted via aerosolsVesicular stomatitis virus

-outbreaks in cattle and horses that can be transmitted to humans with contact with

infected animals

-fever, vesicular lesions on lips and in mouth

-self limiting

Coxiella Burnetti

-causes Q fever

-transmitted via inhalation of aerosolized droplets from cattle, sheep, goat placentas

**(NO arthropod vector!!!)

-coxiella grows well in placental tissue-common in farmers, vets, animal researchers, slaughterhouse workers

-fever, chills, headache, dry cough, patchy interstitial pneumonia

-chronic infection sometimes causes endocarditis

***(NO rash)

-no rash and no arthropod vector distinguish it from Rickettsial diseases

-Dx: serology

-tx: doxycycline shortens the course

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