>Sub-order Hemosporina ; Causes Malaria >Incubation period -9 to 14days >Medically significant species: P. falciparum, P. ovale, P. vivax, P. malariae, >fever, headache, chills and shivers, nausea and/or vomiting P. knowlesii, initially found in Southeast Asia(Malaysia), in macaque monkeys >severe forms -vomiting, diarrhea, seizure, coma,death EPIDEMIOLOGY >Common manifestations: Anemia ,Splenomegaly ,Hepatomegaly ,Fever >WHO, in 2020, 241 million cases worldwide >95% in Africa ; 627000 deaths, 98% in Africa, 80% in children <5y/o 1.Fever - When RBC ruptures, release pyrogens >Transmission: Bites of Anopheles; Blood transfusion & placental transfer >Fever pattern specific for each species (must know): WORLD ENDEMIC PLACES ▪Tertian malaria /Every 3 days (48hrs) –P vivax, ovale and falciparum >Africa andAsia ; Central and SouthAmerica ; Haiti and the DominicanRepublic; ▪Quartan malaria / Every 4 days (72hrs) –P malariae some parts of the Middle East ; some of the Pacific Islands >Atypical pattern maybe seen PHILIPPINE DATA >Malarial Paroxysm: Chills ->Fever->Sweating >Philippines,2019: 12M at risk (13%) ;malaria-free in 2030 ; 95% cases –from 2.Anemia Palawan ; 5% -rest of thecountry >Plasmodium requires hemoglobin for nutrition and growth >58 out of 80 provinces are declared malaria-free >Hgb (Hgb F) &blood cell abnormalities(G6PD, sickle cell anemia, thalassemia) >4,870 cases, 4 deaths(2018) =Protective/Resistant of malaria >Endemic places (DOH,2019): Palawan, Sulu , Mindoro Occi , Sultan Kudarat >RBC rupture & loss of iron causes anemia in patients ——————————————————————————————————— >Thus severity of anemia depends on severity of infection VECTOR : Anopheles mosquito >Anemia more often in P. falciparum & less common in P. malariae >Species found in Philippines: Anopheles mangyanus; A. balabacensis; A. 3.Splenomegaly maculatus ; A. litorensis *Abnormalities in the blood may cause splenomegaly >2 most common: A. flavirostris ; A.minimus *Abnormal morphology of RBC, like knobs >Anopheles -Resting : Abdomen points upward; Feeding: Abdomen straighten *Hemozoin may also cause splenomegaly >Aedes, Culex- Resting: Abdomen downward/parallel to surface 4.Hepatomegaly - Secondary to the splenomegaly 5.Blackwater fever - Seen in P. falciparum infections Anopheles >Massive hemolysis= hemoglobinemia, hemoglobinuria & acute renal failure >ONLY females feed on blood -> needs hemoglobin for eggs >Tea colored urine hence the name >Males feed on nectar 6.Cerebral Malaria - Most serious neurological complication >Night feeders(4 pm- 4 am); Eggs laid on shaded slow running, clean,fresh H20 >Severe infection of the CNS ; Seizure, coma and death ——————————————————————————————————— >Long term neuroproblems in survivors ; Pathogenesis poorly understood Life cycle ——————————————————————————————————— >Obligate intracellular parasites Pathogenesis of Malaria >2 stages: Sporogony–sexual phase ; Schizogony–asexual phase >RBC destruction by the spleen and the merozoite plus loss of iron = anemia >2 hosts :Man –intermediate host ; Mosquito –definitive host (sexual phase) >Change in cell morphology, causing increase stickyness of RBC causes vessel >Extrinsic phase aka: Invertebrate phase , Sporogony obstruction and hemorrhage = tissue anoxia >Intrinsic phase aka: Vertebrate phase, Asexual cycle ; Occurs in MAN >Shock and DIC - Severe cases ——————————————————————————————————— INTRINSIC PHASE Lab Diagnosis >Exo-Erythrocytic Schizogony >History (travel, nature of fever) ; PE (S/S, urine color) ; Serology ; PCR ; RDT *Mosquito bites -> Injects sporozoite ->Invades liver cells -> Transforms to (Rapid diagnostic test); Blood film exam (GOLD STANDARD) trophozoite ->Divides into many schizont by binary fission -> Each schizont ——————————————————————————————————— becomes a merozoite -> Liver cell ruptures releasing merozoites -> Some of Blood Smear this merozoite becomes hypnozoite (true for vivax and ovale) >Timing of collection; Prefer 1hr before onset of fever (parasite is still inside *Hypnozoite- source of reinfection in vivid and ovale the RBC; Mature trophozoite form) >Collection sample ; Prefer capillary sample/ fingerprick! (abnormal RBC >Erythrocytic schizogony (ES) accumulate in capillary region) *Merozoite released to blood -> Infect RBC via specific receptors ->Once inside, transforms into young trophozoite with chromatin dot & cytoplasm ring-> *Reporting of Results: Growing trophozoite consumes Hgb ->Uses globin as food and heme as >Degree of Infection pigments ->RBC changes can be seen at this stage + Knobs or stippling seen 1.Thin film = # of infected cells / 1000 RBC x 100 2.Thick film = # of parasite / 100 WBC x 100 >Young schizont– 1 chromatin dot becomes 2 >Report: % infection, Genus and species, Stages of devt >Growing schizont–more than 1 but less than that of mature schizont *Next step after getting the % infection: >Mature schizont–each species hast different number of chromatin: >Absolute count: % infection x RBC ct = infected cells/ mm3 *P. vivax, ovale 12 –24 ; *P. malariae 6 –12 ;*P falciparum 18 -24 ——————————————————————————————————— >Once mature -> RBC ruptures -> Merozoites release to infect other RBC = one Prevention ES cycle >Vector control: Mosquito nets, Insecticides, Insect repellant >Time it takes for 1 ES cycle: P vivax & ovale 48 hrs ; P malariae 72 hrs ; P >Medication: Prophylactic anti-malarial drugs falciparum 36 –48 hrs >Vaccine - WHO recommends RTS vaccine to be given to Children in areas of >After 2 or more ES cycle, some merozoites undergo gametogenesis moderate to severe P. falciparum infections ——————————————————————————————————— Gametogenesis Treatment: Anti malarial drug activity >Macrogametocyte–female ; Microgametocyte –male >Tissue schizonticides ; Blood schizonticides ; Gametocytocides >Infects the mosquito to begin Extrinsic phase/Sporogony/Sexual phase ——————————————————————————————————— Drugs in Malaria Sporogony Cycle >Blood schizonticides kill parasite in the blood >Drop in temp causes gametocyte to transform into macro (has pole) & *Chloroquine, quinine, pyrimethamine, etc. microgametes(has flagella) *Chloroquine is the drug of choice for P. falciparum >They fuse to become a zygote (Macro + Micro = Zygote) >Gametocytocides kill sexual forms of the parasite, preventing transmission >Zygote becomes amoeboid, a ookinete *Chloroquine, quinine are also gametocytocides for P. ovale and vivax but not >Caused outpouching of gut wall to form an oocyst for P. falciparum >Inside oocyst, parasite divide to become sporocysts *Primaquine can be used for P. falciparum >Sporocyst rupture &release sporozoite ->Sporozoite travels to salivary glands ———————————————————————————————————