Download as pdf or txt
Download as pdf or txt
You are on page 1of 1

Parasitology: Malaria

PLASMODIA Clinical Manifestations:


>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
———————————————————————————————————

PJMC- 2A

You might also like