Download THE SPOROZOA

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.