Malaria Dept. Infectious Disease 2nd Affiliated Hospital CMU.

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Presentation transcript:

Malaria Dept. Infectious Disease 2nd Affiliated Hospital CMU

Definition  Malaria is a parasitosis caused by plasmodia.  It is transmitted to human by the bite of mosquito.  Clinical feature: cyclic chill, high fever & profuse sweating. In chronic illness, there are anemia & splenomegaly.

Etiology  Causative organism: Plasmodia  P. Vivax: tertian malaria  P. Malariae: quartan malaria  P. Falciparum: malignant malaria  P. Ovale: tertian malaria  Pathogenicity: merozoite, malarial pigment &  products of metabolism

Etiology  Tachysporozoite  Bradysporozoite  Merozoite  Sporozoite  Parasitemia

Etiology  Tow period:  human - whole asexual reproduction  mosquito - sexual parasitic stage  Two host:  human - intermediate host  mosquito - final host  notes:  clinical symptoms: erythrocytic stage  relapse: exerythrocytic stage  infectivity: sporozoite

Life cycle of the malaria parasite mosquito microgametocyte zygote oocyst sporozoite Blood stream tachysporozoite merozoite maturerupture Bradysporozoite Blood stream reenter phagocyte merozoite trophzoite shizont mature release merozoite gametocyte Erythrocytic phase Exoerythrocytic stage human

Epidemiology  Source of infection Patient, parasite carrier  Route of transmission  female mosquito biting person  blood transfusion  Susceptibility:  universal susceptibility  no-cross-immunity  re-infection  Epidemic features:  sporadic or endemic, tropic or subtropic

Pathogenesis  Mechanism of attack  merozoite  RBC rupture malaria pigment  products of metabolism   blood stream allergy  P. Faciparam: produce microvascular disease  magnitude of the parasitemia & age of patient  no specific Ab or cell -mediated response

Pathology  Anemia:  P. Vivax - retiform RBC  P. Malariae - mature RBC  P. Falciparum - every RBC  Prolifeation of mononuclear phagocyte  hepatomegaly  splenomegaly  Cerebral edema & congestion

Clinical manifestation Incubation period: quartan malaria: day tertian malaria: 13~15 day malignant malaria: 7~12 day

Clinical manifestation  Typical attack  Chill: abrupt onset, shivering, pale face,cyanosis. Last 10 min or 1~2hr.  High fever: T rise to 40 o C with malaise, myalgia, thirsty. Last 2~6 Hr.  Sweating: profuse sweating with restlessness  regular 48 hr. or 72 hr. Cycle

Clinical manifestation  Sings  anemia  splenomegaly  hepatomegaly, ALT elevate

Clinical manifestation  Perniciouse attack: cause by P. Falciparum  cerebral malaria  high fever, headache, vomiting, convulsion delirum, respiratory failure  hyperpyrexia type  T> 42 0 C, convulsion, delirium  Relapse: early relapse - <3m,  later relapse - >6m

Clinical manifestation  Malaria caused by transfusion  incubation period: 7~10 day  no exerythrogenic phase, no relapse

Complications  Black- water- fever:  cause: 1/inadequate G-6-PD  2/The toxin release by malarial parasite  3/Allergic reaction to anti-malarial drugs  feature:1/chill & fever  2/dark red or black urine  3/severe hemolytic anemia  Acute glomerulonephritis

Laboratory Findings  Blood picture: decrease in RBC & Hb  blood film for parasite  serological examination  ELISA for P. antigen  DNA hybridization

Diagnosis  Epidemiological data  endemic zone  blood transfusion  Clinical manifestation  Laboratory findings  Diagnostic treatment:  chloroqunine for 3 days

Differential Diagnosis  Typhoid fever  Septicemia  Leptospirosis  Encephalitis B

Treatment  Anti-malarial drugs  Chloroquine-susceptable infection  chloroquine : 1g /d, for 3 day, p.o.  primaquine: for 8day, p.o.  Chloroquine-resistant infection  mefloguine:  artemisinine

Treatment  Pernicious attack  Chloroquine: 10mg/kg iv drop in 4 hr. Then 5mg/kg, iv drop in 2 hr.  Quinine: 500mg iv drop in 4 hr.  Radical therapy Chloroquine (3 day) + primaquine ( 8 day )

Prevention  Drug prophylaxis  chloroquine: 0.3g once a week  doxycycline  Kill mosquito  Vaccination