THE SPOROZOA Plasmodium spp. (Malaria Parasites) Malaria parasites belong to Class Sporozoa, Genus Plasmodium. The rtant species affecting man include: P. vivax (p.v.) causes tertian malaria P. falciparum (p.f.) causes malignant tertian malaria P. malariae (p.m.) causes quartan malaria P. ovale (p.o.) causes tertian malaria. P.v. and P.f. are widely prevalent all over the world; P.m. and P.o. only prevalent in the local areas. malaria is one of the five major parasitic disease in China and also one of the six major tropical diseases to which paid attention by WHO. Only P.v. and P.f. are prevalent in our country. Life cycle of P.vivax 1. Final host : Anopheles mosquito; 2. intermediate host: man; 3. infective stage: sporozoite in the salivary gland of mosquito; 4. infective route: mosquito bits the skin; 5. site of inhabitation: in RBC (erythrocytic stage) and liver cells (pre-erythrocytic stage); 6. alternation of generation: schizogony in the liver 8 days; schizogony in RBC 48hrs; sexual reproduction in mosquito; 7. incubation: 14~17days. Penetrate stomach wall fertilization ---------------------------------Ookinete-------Zygote--------------♀♂gametes body cavity oocyst in final host mosquito 9~10 days ♂exflagellation ♀maturation sporozoites stomach invade salivary gland ♀Anopheles mosquito mosquito sucking blood again sucking blood -------------------------------------------------------------------------------------------get into liver via circulation ♀♂gametocytes tachy-sporozoite---8 days brady-sporozoite--- 6 months normal RBC------ring form large trophozoite pre-erythrocytic merozoites erythrocytic merozoite immature schizont mature schizont pathogenesis and Symptoms malarial parasites massively multiply in RBC the involved RBCs rupture noxious and antigenicity materials p.f. infection plug capillaries anemia hypertrophy of host responses liver & spleen ischemia of brain and adrenal nerve & body fluid adjustment allergy blood re-distribution metabolism disorder critical malaria nephritis (allergyu III) chill (skin capillaries contract) fevere (heat loss↓,heat gain↑) cerebral coma sweat (skin capillaries dilation) brings down a fever adrenal shock abdominal form clinical manefestation 1. incubation terian malaria 14~17 days; malignant malaria 8~12 days; quartan malaria 27~40 days 2. typical attack: paroxysms attacks occurs once every other day, malignant malaria occours once every 36 hrs. , quartan malaria occour once every 72 hours. Each paroxysm shows a succession of three stages: (1) cold stage the attack begains with a sudden shaking chill, lasting for 30 minutes to oone hour. (2) fever is generally over 39℃,lasting 3~4 hrs. (3) sweat stage: sweating brings down the fever. (4) anemia: the involved RBCs are destroyded. (5) hepetomagly and splenomagly. 3. Atypical attack: the symptoms are irragular, which occurs due to the recently repeated infection of the same plasmodium; infection with various plasmodium species; infection with variational plasmodium parasite; the initial stage of malaria or attack in a very weak patient. 4. ?? Relapse: after the first malarial symptoms subsided 6~12months, the secondary malarial attack results from the multiplication of the brady-sporozoites harbored in the hepatic cells. 5. ?? Recrudescence(relapse in a short time): after original malarial attack 2~3 months the remainders of erythrocytic parasites , which avoid the host I immunith and massively multiply ,cause malarial attack again. 6. critical malaria is mainly caused by P.f. and occasionally by P.v. the capillaries are pluged by RBC involved by P.F. the ischemia take place in the cerebrum and adrenal causing the metabolism disordere and manifesting cerebrum coma, adrenal shock, abdominal pain. Died of DIC. 7. hemoglobinuria (black watwe fever): this manifestation may occur in the case who with G-6-PD defect was treated by primaquine or quinine, manifesting acute respiratory distress syndrome, renal failure, even cause death. tn this case primaquine and quinine should be replaced by pyrimethamine and choloroquine. 8. malarial nephritis is due to allergy III Diagnosis Refer to the clinical symptoms, signs and history of exposing to the malaria and mosquitoes. The confirmative diagnosis depends on the detection of malarial parasites in the blood film under the microscope. Method: check up the slice specimen with both thin and thick blood smears. Radical cure: chloroquine and primaquine, Chloroquine eliminate the erythrocytic parasites to stop malarial attacking Primaquine eliminate the exo-erythrocytic parasites and the gametocytes to prevent malarial relapse and transmission. Prevention chemoprophlaxis 1. Pyrimethamine should be adminstrereted to whole populations at risk in July to October (mosquito season) 2. chemotherapy should start I week before entry into the endemic area and be contined for 4 weeks after returning from an endemic area. Mosquito control 1. Eliminate mosquito breeding place 2. Spray insecticides 3. Use mosquito net, screen and repellents to protect the person from mosquito bites. Malaria vaccines have been studying under the grant from WHO. An experimental malarial vaccine has been established only by some scientists in the laboratory and is not available for general use. Toxoplasma gondii T. gondii was first discovered by Nicolle and Manseaux in 1908 in a small rodent, gondi ( 北 非 刚 地 梳 趾 鼠 ), in North Africa. It is world wide distribution and causes toxoplasmosis, which is a zoonosis. Morphology and Life cycle There five stages in its life cycle. They are trophzoite (tachyzoite is free or in the pseudocyst and bradyzoite in the cyst), cyst, shizont, gametocyst and oocyst. The trophzoite is crescent, about 4~7×2~4μm. The cyst is round , about 5~100 in diameter, containing several bradyzoites. The oocyst is oval in shape, about 11×12.5μm, containin two sporangia each of which contains 4 newmoon-shaped sporozoites. The life cycle of T. gondii includes intestinal-epithelial and extraintestinal stage in cats (felines 猫科动物). The sexual reproduction occurs while in the cat. Only asexual reproduction is known in while in other hosts. infective stage is all stages in its life cycle; infective route: (1) mouth, (2) wound, (3) blood transfusion, (4) placenta, (5) organ grafting (transplanting); site of inhabitation: nucleate cells; intermediate host: man, mammals, bird and etc; final host: cat (feline 猫科动物) several maturation schizongny cycle -------------♀♂gametocytes -------------- ♀♂gametes fertilization in final host (feline) zygote int. mucosa immature oocyst invade int.epicilia cat eats the mature oocyst discharded in feces or raw meat with the parasite -------------------------------------------------------------------------------------------environment out side of the body -------------------------------------------------------------------------------------------man eat the oocyst or raw meat with T.gondii infected reservoir host the other parasites invade nucleite cells via placenta wound bloob transfusion asexual reproduction(endodyogeny)------------------------daughter parasites Pathogenesis The material base of pathogenesis Toxotoxin(弓形虫毒素)is a fatal toxin; toxoplasmin(弓形虫素)is the factor leading to congenital mal formation; toxofactor(弓形虫因子)is tissue poison; penetration enhancing factor(穿透增强因子)helps the parasite invade the host’s cells. Congenital infection: this type is most important (1) malformation of fetus (birth defect) such as hydrocephalus, microcephaly, , mental retardation, chorioretinopathy (脉络膜视网膜炎), vision retardation, cleft palate(腭裂), harelip(兔唇) (2) abortion, premature delivery and stillbirth postnatal (acquired) infection: acute stage: parasitemia leads to the pain and swollen of lymph nodes, enlargement of liver, spleen and lymph nodes(. heptomegly, splenomaglyy), fever, fitigue, headache, muscular pain and rare death. Sub-acute stage: the tachyzoites continue to destroy tissues,causing extensive lesions in the lung, liver, heart, brain and eyes. Acute symptoms subside. the enlargement of liver, spleen and lymph nodes, visual disturbence and systemic discomfort still exist. Chronic stage: cysts form in tissues. The encephalitis, myocarditis, chorioretinopathy (脉络膜视网膜炎),and the changes of psychology and emotion may occur. Diagnosis: Necropsy or biopsy of the liver, spleen and lymph node Examination of peritoneal cavity fluid, thoracic fluid and 脑脊液 Xenodiagnosis of patient’s biopsy specimen. Inoculating the biopsy tissue (of liver, spleen and lymph node) into mice peritoneal cavity. Molecular biology test: PCR Immunological test: ELISA(enzyme-linked immunosorbent assay Epidemiology This disease is widespread and clinically important throughout the world. Human infections result from eating raw meat. It is worldwide distribution. Lots of mammals can serve as reservoir hosts. The natural spread of trichinosis is due to mammals kill each other. Humans get the infection by eating raw meat. Toxoplasmiasis is naturally transmitted by animals killing each other. Domestic and wild mammals and birds are all reservoir hosts. Human gets infection by eating raw meat or oocyst, placenta and blood transfusion. It Treatment and prevention *The compatibility of pyrimethamine 乙胺嘧啶 and sulphadiazine 磺 胺嘧啶 is effective but not very well. acetylspiramycini 乙酰螺旋霉素 Quarantine (检疫) of blood donator is also recommended for toxoplasmiasis. Avoid eating raw meat and raising a pet cat. Pregnant woman should avoid contact with cats. Before becoming pregnant the examination of the infection of T.plasma gondii should be done.