Beruflich Dokumente
Kultur Dokumente
Department of Infectious Diseases Third Affiliated Hospital Sun Yat-sen University Lin Yang
Definition
A parasitic diseases caused by plasmodium species. Transmitted by the bite of infected female anopheline mosquitoes. Characterized by periodic paroxysm with shaking chills, high fever, heavy sweating. Anemia and splenomegaly in cases suffering from several attack of paroxysm.
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P. vivax and P.ovale-caused malaria often relapse. P.falcipraum-caused malaria often shows irregular fever, and may occur cerebral malaria.
History
and now
Be epidemic in 92 countries and area New cases of malaria a year: 300 to 500 millions About two millions cases die a year About one million children die of malaria a year In China: In 2000:
Etiology
Four species of plasmodium cause malaria in human. P. vivax, P. ovale. P. malariae P. falciparum
Each species has its own morphologic, biologic, pathogenic, and clinical characteristics.
P.vivax is the most common. P. falciparum--- the most strong pathogenicity causes the cerebral malaria, causes the chief mortality, presents the therapeutic problem of chloroquine resistance.
Two hosts : Two types of reproduction: asexual reproduction in human Humans as intermediate host sexual reproduction in female anopheles Female anopheles as final host
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Infective sporozoite in female anopheles Schizont containing merozoites in human liver cells (reproduce asexualy)
(intraerythrocytic phase) (exoerythrocytic phase)
RBC rupture
release merozoites
parasite debris, pigments and metabolites
(reproduce sexualy)
anopheles
paroxysm
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Life
(In female anopheles) infective sporozoite blood circulation of human human liver cells : schizont containing merozoites (tachysporozoites for 1-2 weeks, bradysporozoites for 3- 6 months relapse, exoerythrocytic phase) pour into blood circulation by liver cell rupture invade RBC: merozoite ring form trophozoite schizont containing merozoites (intraerythrocytic phase) Periodic paroxysm gametocytes female anopheles RBC rupture , release merozoites parasite debris, pigments and metabolites 11 clinical paroxysm human body
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life cycle in RBC and periodic paroxysm Clinical periodic paroxysm depend on life cycle of plasmodium in erythrocytes . Different plasmodium, the length of life cycle in RBC is different, so the interval of periodic paroxysm is different. P. vivax, and P. ovale: 48hour P. malariae: 72hour P. falciparum: 36-48hrs, and irregular
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Anopheles mosquito
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Anopheles mosquito
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Immunity
species specific, strain specific, last for a short time only. No across protective immunity, For example: immunity to P. falciparum does not protect from P.vivax. Immunity usually does not prevent from reinfection, but reduce the severity of the
Distribution
geographic distribution
and in China.
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Seasonality
Generally, malaria occurs in autumn and summer, but no seasonality,and malaria occur whole year in tropics and subtropics.
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Hepato-splenomegaly
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Mechanism of paroxysm
Erythrocytes rupture (hemolysis), release parasite debris, pigments and metabolites induce periodic paroxysm with shaking chill, high fever and heavy sweating.
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Clinical manifestations
1. Incubation period 2. Prodromal period 3. Clinical forms Typical form, Mild form, Cerebral malaria, Recrudescence, Relapse.
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Incubation period
P. vivax and P. ovale 13~15 days P. malariae 24~30 days P. falciparum 7~12 days
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Prodromal period
many patients experience a prodromal
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Clinical forms
1> Typical form
Periodic attack of paroxysm with shaking chills-- high fever--heavy sweating. Shaking chills last for 20 min to 1 hrs, high fever: T rise to or over 40C for 2 to 6 h,
with severe headache, myalgia, and skin becomes warm and dry.
heavy sweating:
last for 30 min to 1 h, anemia and moderate splenomegaly in cases with several paroxysms.
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Intermittent period
fatigue or being asymptomatic Intermittent period (interval of attack) is determined by the length of asexual erythrocytic cycle: P. vivax and P. ovale , about 48 hrs--paroxysm attack every other day; P. malariae, about 72 hours paroxysm attack every three days P. falciparum , 36-48 hours; paroxysm attack every 36 to 48 hrs
In early stage of paroxysm, intermittent period may irregular.
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Physical examination:
Anemia and splenomegaly in patients after
several paroxysms. Tender hepatomegaly in less frequently. Other physical findings: Jaundice, urticaria, petechial, rash, etc. may be seen in less frequently.
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2>.Mild form
Often seen in patients living in endemic
region of malaria.
Clinical manifestations of paroxysm are not
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3>.Cerebral malaria
The most serious type of malaria.
4>.Recrudescence
Appear clinic signs of malaria a short time after primary paroxysm.
Induced by non-standard pathogenic therapy or drug resistant plasmodium (merozoites ).
5>.Relapse
appear clinic signs of malaria about three to six months or longer after primary attack. caused by bradysporozoites of P. vivax and P. ovale.
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Relapse
Recrudescence
three to six months or longer short time after primary attack after primary attack Caused by bradysporozoites non-eradicated parasite P. vivax and P. ovale. Four species of plasmodium non-standard therapy or drug resistance
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Complications
Hemolytic urinemic syndrome
failure.
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Nephropathic syndrome
usually occurs in cases of p. malariae infection. Patients with hypertension, edema, massive protein in urine, etc.
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Diagnosis
Epidemiological data Clinical manifestations Laboratory findings
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Epidemiological data
History of living in or traveling to epidemic areas. History of blood transfusion. Neonates was born by malaria mothers.
Clinical manifestations
Periodic paroxysms with shaking chills, high fever, sweating. Anemia and splenomegaly may present.
Fever patterns may be irregular in some cases
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Laboratory findings
WBC, RBC, Hb.
Normal white blood cell count, decreased red blood cell count and hemoglobin level.
Thick
Plasmodium species are found in thick and thin blood smear, or bone marrow smear. --------Definitive diagnosis Thick and thin blood smear are very simple and important
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Differential diagnosis
septicemia leptospirosis typhoid fever bile duct infection Japanese encephalitis toxic form of shigellosis
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Typhoid fever:
Insidious onset, sustained fever, relative bradycardia, rose spots, positive Widals reaction and positive blood culture for salmonella typhi.
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Prognosis
Good in ordinary cases. Poor in cerebral malaria and Black Water Fever.
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Treatment
1. Symptomatic and supportive treatment
2. Etiologic treatment:
A.Control paroxysm treatment
B. Prevent relapse
C. Prevent transmission
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Etiologic treatment
Treatment principle:
1.Combination anti-paroxysm treatment with preventing from relapse and transmission treatment
Anti-paroxysm
kill reproducting plasmodia in RBC
Prevent relapse:
kill bradysporozoite
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It is necessary to examine G-6-PD before giving primaquine because primaquine may induce acute intravascular hemolysis in patients with G-6-PD deficiency.
primaquine only is given in these patients without G-6-PD deficiency.
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pyromaridine phosphate()
mefloquine() quinine sulfate () arteflene() benflumethtolum()
naphthoquine phosphate()
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Artemisinine ()
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b>.artesunate
100mg bid orally for the first day, 100mg qd for the next 4 days, total amount is 600mg.
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chloroquine (sensitive plasmodia) pyromaridine phosphate quinine slowly intravenous drip, then given orally
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Another drug: tafenoquine shows to kill bradysporozoite and gametocyte. 0.3 /day for 7 days.
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plasmodia to control paroxysm, then, examining G-6-PD. If G-6-PD is normal, the drug primaquine killing bradysporozoite and gametocyte must be given to prevent relapse and transmission.
primaguine is given in these patients without
G-6-PD deficiency .
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Prophylaxis
1.Treatment of patients and carriers
pyrimethamine 0.25 qw
doxycycline() 0.2 qw
No vaccine is available
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Summary
Malaria is a parasitic diseases caused by plasmodium species, and transmitted by the bite of infected female anopheline mosquitoes. Be caused by four species of plasmodium: P. vivax, P. ovale. P. malariae P. falciparum Occur major in tropic and subtropic area All person are susceptible, and no last immunity Life cycle of plasmodium: two hosts, two types of reproduction
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The clinical features periodic paroxysm with shaking chills, high fever, heavy sweating. Anemia and splenomegaly in some of cases . Cerebral malaria. Relapse and Recrudescence Definite diagnosis: Plasmodium species is found in thick and thin blood smear, or bone marrow smear.
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Etiologic treatment principle: 1.Combination anti-paroxysm with prevent replase and transmission treatment 2. Examining G-6-PD before giving primaquine. Control paroxysm treatment, 1.chloroquine-sensitive plasmodia first choice :chloroquine 2.chloroquine -resistant plasmodia 3. Control paroxysm for cerebral malaria artesunate, first choice chloroquine (sensitive plasmodia) slowly intravenous drip ,then orally
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Prevent relapse: kill bradysporozoite: primaquine, for 8 days Prevent transmission: kill gametocyte: primaquine for 3days primaguine only is given in these patients without G-6-PD deficiency . Prophylaxis No vaccine is available 1.Treatment of patients and carriers 2.Control mosquito vectors 3. Individual protection: Avoid mosquito bite chemoprophylaxis
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