1. Schistosoma

2. Six species affecting human：
Schistosoma haematobium (埃及血吸虫) , found first in an autopsy in Egypt, named in 1858，the life cycle was clarified in 1915~1918
widely spreads in Africa, chiefly in Nile River valley. The adults live in the vesical and pelvic plexus causing painless terminal haematuria, renal failure complicated by the ureter obstruction.
S.japonicum 1883, found first in Japan，named in 1904，the first Chinese case was reported in Changsha, the mainland of China by Logan in 1905

3. S.intercalatum 间插血吸虫 , named in 1934
S.mansoni 曼氏血吸虫 , found first in India by Manson in 1902 ，named in 1907
mainly distributed in Africa and focal area in Latin America. Lives in the portal and hemorrhoidal vein plexus, causing stool with fresh blood, liver cirrhosis and portal vein hypertension.
S.intercalatum 间插血吸虫 , named in 1934
S.mekongi 湄公血吸虫 ,named in 1978
merely distributed in Mekong River Valley, resembles S. japonicum except intermediate host
S.malayensis 马来血吸虫, named in 1988

4. In 1909, proved the mode of infection is by skin on experimental animals
In 1974, proved the schistosomiais is the egg granuloma mediated disease on animal mode
In 1975, Praziquantel was synthesized to try to treat cestode

5. Schistosoma japonicum
The adults live in the mesenteric vein of man etc causing Schitosomiasis

6. 1. Morphology
(1) Adult：
The schistosomes differ in a number of ways from other trematodes.They are diecious,and the two sexes are dissimilar in appearance.

7. ♂： Shorter and thicker, sickle-like，1  1.8 cm in length
Oral sucker at top near by ventral sucker
The esophagus is divided into two branches in front of the
ventral sucker, and then unite to form a cecum at the posterior
third part of the body
Groove-gynecophoral canal, in which the female worm is held
Seven testes are situated one by one

8. oral sucker
ventral sucker
groove gynecophoral canal
Male Schistosome

9. Oral sucker
Testes
Gynecophoral canal
Ventral sucker
Testes
Cecum
Male

10. ♀： Longer and slender，1.3  2 cm ×0.4mm
Dark grey color because of the metabolic RBC in the digestive duct
Oval ovary lies in the mid-portion of the body
The vitellaria are located behind ovary, in the posterior part of the body surrounding the cecum
♀&♂are often copulate together, i.e. copulation (may be pheromone(性信息素) from the male is necessary for the development of female worms)

11. copulation Female Ventral sucker Uterus Uterus Cecum Ovary Vitellaria

12. Paired male and female adult worms
Paired male and female adult worms. The female schistosome is the darker, curled worm within the male's gynecophoric canal.

13. clasp

15. (2) Egg Thin shell The content is a miracidium No operculum,
lateral spine
is often seen
Mature egg is oval in shape, slight yellow in color, 89 x 67µ in size, shell is thin without an operculum but with a lateral spine. The content is a miracidium.

16. The small spine is generally not visible as the egg surface is often covered with faecal debris.
Electron microscope

17. Under the electron microscope there are many micro-tubules on the shell, through which the soluble egg antigen (SEA) secreted by a miracidium.

18. (3) Miracidium
A ciliated , swimming larva， with glands (1 top gland, 2 head glands)
Top gland
Head gland
miracidium

19. (4) Cercaria body cercaria with a forked tail tail stem tail fork
Cercaria is infective stage. It is composed of the body and forked tail (including tail stem and fork) and has 5 pairs of penetrating glands in the body:2 pairs of acidophilic glands，3 pairs of basophilic glands.

20. Forked cercaria of
S. japonicum

22. 2. Life cycle
1. Site of inhabitation: the portal vein system, mainly in the inferior mesenteric vein.
2.  Infective stage: cercaria
3.  Infective route: by skin
4.  Intermediate hosts: Oncomelania snail (钉螺)

23. 5. Reservoir hosts: mammals such as buffalo, cattle, wild rodents, goat, monkey, pig, fox.
6.Eggs are main pathogenic factor: (They are inlaid in the liver and intestinal wall. Some of them are discharged in feces to complete its life cycle).
7. The development in human body requires days. Cercaria can live 1-3 days. Life span of the adults is about years.

24. ----invading the intermediate host（ Oncomelania snail ）
passed in feces
Egg
Development in fresh water
Enter to water
----invading the intermediate host（ Oncomelania snail ）
Miracidium hatching out
Mother sporocyst
1mon
Daughter sporocyst
By skin
----invading the final host (humans etc )
Cercaria hatching out
Schistosomula
blood & lymphatic vessels ---- pulmonary A ---- right heart- ----Lung ---- left heart---- systemic circulation ---- varies parts of whole　body ---- abdominal cavity A、mesenteric A---- stomach V,
mesenteric V---- hepatic portal V---- mesenteric V
1mon
Adult

27. How do the cercairae invade the skin of the host?
To attach to host’s skin by the head organ of the cercaria
By the mechanical function of muscles of cercaria
By the function of secretions of penetration glands of cercaria
Cercaria can enter the host’s skin in 10seconds
– several min

28. 1. Penetration of the skin by cercariae
2. Migration and maturation of immature worms

29. How do the parasites become mature?
♀♂schistosomes must clasp each other to be sexually mature ,this may be associated with the exchange of sexual pheromone
Penetration of the skin by cercaria to laying egg days
How do the parasites lay the eggs?
The ♀ gets separated from the male and migrates against blood stream to the small veins in the submucosa of intestine then lays her eggs， eggs /per female/ daily

30. What is the life of the eggs?
Where do the eggs go?
① Deposited in the intestinal wall (50 ~ 60% of eggs)
② The eggs are carried to liver by the blood
stream， deposited in liver along the branches
of hepatic portal veins (23% of eggs)
③ Passed in feces
What is the life of the eggs?
Eggs in tissues may mature in 10 ~ 11d after laid down
Eggs are alive for 10 ~ 11d and then die --- calcify

31. How do the eggs be passed in feces?
The inflammation and necrosis of the intestinal mucosa resulting from the SEA and other secretions by the mature eggs deposited in intestinal wall
The intestinal motility becomes rapid
The pressure of abdominal cavity and blood pressure become higher
The factors above make the eggs pass into the lumen of intestine along with the necrotic tissues and then pass in feces
Eggs can be found in stool days

32. How long is the life span of adult?
Most of them can survive for 3~10 years，some for more than 20 years
Infective stage：
The mode of infection：
Parasitic site：
Final host：
Reservoir host:
Intermediate host：
Cercaria
By skin
Mesenteric V of man and other mammalians
Man
Water buffalo, cattle, pig, dog, cat, goat,
rabbit, mouse, etc
Oncomelania snail （Oncomelania hupensis）

33. (2) Two sexes are separate.
Blood fluke is a special kind of flukes because of following characters:
(1) The adult worms look like nematodes, elongated
cylindrical in shape.
(2) Two sexes are separate.
(3) Egg without operculum, but with a lateral spine.
(4) Only one intermediate host required.
(5) Lack of metacercaria stage, no redia but two
generations of sporocyst
(6) The infective stage is cercaria.
(7) The infective route is by skin.
(8) The eggs are main pathogenic stage.

34. mechanical damage + immuno-pathological damage
3. Pathogenesis
mechanical damage + immuno-pathological damage
(1) Cercaria
— cercarial dermatitis (type Ⅰ, Ⅳ hypersensitivity)
urticaria(荨麻疹)， itching
(2) Schistosomula
-- pass through lungs etc, appear
venulitis, lymphangitis, hemorrhages, giant cell reaction
and eosinophils infiltration
--- fever, cough (with bloody ) and eosinophilosis etc
(3) Adult
-- doesn't cause pathological changes significantly, but the waste products, secretions, metabolic products and toxins products of worm can induce to form immuno-complex, which damages host (type III hypersensitivity)
-- egg granuloma
(4) Egg

35. The developmental processes of the egg granuloma
At early stage
--- eosinophilic abscess ( Eos↑, lymphocytes, macrophages )
Ag-Ab complex around the eggs, named Hoeppli
phenomenon
At chronic stage
--- pseudotubercle (macrophages,
lymphocytes, fibroblasts, multynucleated giant cells)
At late stage
--- fibrous granuloma (nodule结节 )
(the eggs die and become calcified, fibroblasts –fibrous
tissues ↑↑)

36. Destructing the eggs and limiting the antigens of the eggs
The consequence results caused by
the egg granuloma
Destructing the eggs and limiting the antigens of the eggs
Damages on the tissues
egg granulomas causing obstruction of blood vessels ----fibrosis of hepatic periportal tissue （pipestem fibrosis）--- presinusoidal obstruction to blood flow --- portal hypertension --- hepatosplenomegaly, ascites ，abdominal collateral vein dilatation and esophagogastric varices，upper gastrointestinal bleeding

37. The main pathogenic factor is the egg
The main pathological change is the formation
of egg granuloma
The essential reason of chronic schistosomiasis
is also the formation of the egg granuloma

38. Eggs inlaid in the portal areas and intestinal wall
SEA type IV allergy
Local tissues necrosis, proliferation and fibrosis
intestinal ulcers,
Liver cirrhosis stool with blood,
Pus and eggs
Spleen Portal vein hypertension syndrome
Enlargement
Function failure
Immunity Anemia Collateral circulation
between portal vein and ascites, albumin,
secondary infection vena cava are established emaciation
Esophageal Umbilicus Hemorrhoid
varicosity varicosity varicosity
Hemorrhage of superior digestive tract
Die of hepatic coma, superior digestive
tract bleeding and infective complication

39. 1) Acute schistosomiasis (Katayama fever)
Clinical manifestation：
1) Acute schistosomiasis (Katayama fever)
Usually seen in persons who first exposure to schistosome
Incubation period ： 40d in average （14 ~ 84d）
Symptoms and sings ：
Fever：intermittent or remittent fever
Gastrointestinal symptoms：diarrhea（with mucus and
bloody stool）,poor appetite, nausea
Cough ：
Enlargement of liver and spleen：liver pain
Examinations in lab：WBC↑, Eos↑， albumin↓,
globulin↑，eggs in stool test（+）,COPT（+）

40. 2) Chronic schistosomiasis：
Usually seen in persons who contact infested water repeatedly in endemic area
or the acute cases who have light infection or not been treated appropriately (is 90% of the cases in endemic areas)
Asymptomatic type--is common
Symptomatic type
-- chronic diarrhea
-- hepatosplenomegaly
-- egg examination repeatedly（+），COPT（+） 90%

41. 3) Advanced schistosomiasis
Due to repeated or heavy exposure to the cercariae, or no
effective treatment, clinical types ---
Megalosplenia type：the weight of spleen can be up to ~ 4000g, Hyperspleno functionism--- blood cell count falls down
Ascites type：decompensation of liver function，last for a long time顽固
Colonic polyposis: left lower abdominal pain and abdominal mass, diarrhea with blood,
Dwarfism： due to repeated or heavy exposure to the cercariae in childhood儿童

42. In late stage, the patients with schistosomiasis often die of secondary syndrome并发症（ e.g abdominal collateral vein dilatation and esophagogastric varices，upper gastrointestinal bleeding, hepatic coma, canceration of colonic polypi, etc.）

43. 4) Ectopic schistosomiasis
Commonly involving sites ：
lungs：pulmonary hypertension, right
ventricular failure, cough
Central nervous system：brain, spinal cord,
monoplegia, hemiplegia
Rarely involving sites：
myocardium, pancreas, thyroid gland, etc

44. 4. Immunity
(1) Antigen, circulating antigen,
circulating immune complex
Antigens of schistosomula, adult and egg are very
complicated
CAg (circulating antigen)：Secretions, waste
products, metabolic products,
integument shed of the worm etc e.g.
① GAA（gut associated antigens ）
② MAA（membrane associated antigens ）
③ SEA（soluble egg antigens ）

45. CIC （ circulating immune complex）
deposition on tissue -----typeⅢ hypersensitivity，
e.g. schistosome nephropathy
Some are diagnostic Ag
Some are immuno-pathological Ag
Some are protective Ag

46. (2) Concomitant immunity
It is an incomplete immunity or non-sterilizing immunity .It can not eliminate the schistosomes completely from the host when it happened.It is conferred by a still existing infection,does not destory the parasites of the infection already present. If living schistosomes are completely eliminated by drug,the resistance will disappear.

47. Although protection is not complete,the 60%-80% kill rate is highly effective in controlling the intensity of parasitism. This condition,in which adult worms from a primary infection can survive in a host resistant to reinfection ,has been termed Concomitant immunity.

48. (3)Immune evasion
Schistosomal adult can escape the immune attack of host and survive in the immunologically competent host.it is immune evasion. Generally,the Schistosomes can escape the immune attack due to antigenic disguise and mimicry,modification of host immune responses ,and so on.

49. Antigenic disguise
The developing schistosomula have ability to disguise themselves by absorbing host molecules ,including immunoglobulins,blood group glycolipids,and histocompatibility complex antigens. It is called Antigenic disguise.

50. Antigenic mimicry
Schistosomes are incapable of synthesizing fatty acids or cholesterol,they must bind low-density lipoproteins of host onto their surface so as to prevent the host from recognizing these parasites as foreign. these bound low-density lipoproteins may be essential in allowing the parasite to evade the host immune response.It is called Antigenic mimicry.

51. (4) Mechanisms of protective immunity
The major immune responses to schistosome infection mainly associate with cellular immunity, e.g. immunopathologic changes, protective immunity, immunoregulation, and also associate with the humoral immunity.
TH1-derived cytokines are more important in the establishment of protective immunity, whereas the TH2-type responses are associated with tissue damage caused by egg.

52. It has been believed that the mechanism of killing larval schistosomes is primarily antibody-dependent,cell-mediated cytotoxicity(ADCC) .

53. Schistosomula penetrating the skin after the primary infection are coated with specific antibodies,bound to eosinophils,and destroyed before they can reach the portal system. Schistosome-specific IgE antibodies ,when combined with eosinophils,appear to play a major role in the host immune response and resistance to reinfection. IgG antibodies and macrophages , neutrophils,etc,can also kill larval schistosomes via ADCC.

54. ADCC neutrophil eosinophil platelet macrophage IgG/IgE IgG/IgM O2
IgE/IgM
platelet
IgE
macrophage

55. 5. Diagnosis
(1) Parasitic diagnosis
1）Stool examination
① Direct fecal smear
② Kato-katz’s smear method for EPG
③ Water sedimentation method
④ Miracidia hatching method – first choice
2） Rectal biopsy -- for terminal stage

56. COPT（ CircumOval Precipitation Test ）
(2) Immunological test
1）Ab detection
ID (Intradermal test)
COPT（ CircumOval Precipitation Test ）
IEST （ immunoenzymatic staining test ）
Immunoblotting / western blot
DDIA (dipstick dye immunoassay)
IHA, ELISA, IGSS
2）Ag detection：maybe distinguish current & past
infection & evaluating the effect of drug e.g.
dot-ELISA / Sandwich ELISA

57. (3) Ultrasound examination
for advanced case, e.g.
hepatomegaly
& splenomegaly

58. In Asia, Africa, South America, 77 countries
6. Epidemiology
(1) Distribution
In Asia, Africa, South America,
77 countries
200 millions cases , 600 million are at risk
Japan has controlled Schistosomiasis since 1978

60. √ In China 12 provinces in the south part 391(381) endemic counties
79 million people in endemic areas
14.8 billion square meters snail ridden
7 provinces still report new cases yearly

61. Hubei, Hunan, Jiangxi, Anhui, Jiangsu, Sichuan & Yunnan
Shanghai, Guangdong, Fujian,
Guangxi & Zhejiang

62. Still be a public health problem
地区分布（ ）
防治后日本血吸虫感染的

63. (2) The links of transmission
1）The source of infection：patient, carrier,
reservoir host
2）The rout of transmission：
Eggs entering into water
There exist Oncomelania snail in the same
water body
People and reservoir host contact with infested
water (Transmission season: April to Oct )
3）Susceptible population： all of the people,
lower age people，people who come from no-
endemic areas

64. √Epidemic factors
Natural factors: environment, temperature, level of water, natural of soil & vegetation
Social factors: economic level, sanitary condition, medical care, way to produce in local & local costumes (water-contacting, e.g. catching fish, planting rice, washing commodes, vegetables and clothes )
So environment modification, development of economy, health education & national program of schistosomiasis control will impact on the transmission significantly

65. (3) Types of endemic areas (in China)
1) Marshy type(江湖洲滩型): still serious
Hubei, Hunan, Jiangxi, Anhui, Jiangsu
82.1% infested snail areas
2) Mountainous and hilly type(山丘型)
Sichuan, Yunnan
3) Water-net type(水网型) controlled
Shanghai(1985), Guangdong(1985), Fujian,
Guangxi & Zhejiang controlled

66. Mountainous and hilly type
Water-net type
Mountainous and hilly type
Marshy type

67. areas infested snails will enlarge
New problems:
areas infested snails will enlarge

68. 7. Prevention and Treatment
The strategy of control of
schistosomiais（WHO ）
Before 1984 – eliminating transmission
Since 1984 – control / reduce morbidity

69. (1) Control of the source of infection
1）Investigate and treat patients & carriers
Praziqantel
①mass chemotherapy
②selective mass chemotherapy
③modified mass chemotherapy
④targeted mass chemotherapy
⑤chemotherapy for the most dangerous population
2）Treat and kill the reservoir hosts

70. (2) Control snail
environment modification
molluscicide to kill the snails
biological methods to control of the snails

71. Detection of Infested
water by mice

72. Control and deal with night soil Protection of water from contaminated
(3)
Health education
Control and deal with night soil
Protection of water from contaminated
Give up some habits of sanitary, life,
production styles
Protection of individuals
---avoid directly contacting with the water
contaminated by cercariae
--- put on protective clothes
--- apply some chemical repellent on the skin
(dibutyl phthalate 邻苯二甲酸二丁酯 或灭蚴宁）
--- use of a vaccine

73. Important words Questions
1.What are the differences in life cycle among S. japonicum and C. sineses , F. buski , P. westermani?
2. What are the differences of infective ways from other flukes?
3. Why does the development of economy will improve the progress of schistosomiasis control?
Important words
copulation, portal-mesenteric venous system, hypersensitivity, granuloma, fibrosis, portal hypertension, splenomegaly, colonic polyposis, ascites, dwarfism, concomitant immunity, immune evasion, Oncomelania hupensis, cercarial dermatitis

74. THANKS A LOT!

75. cercarial dermatitis

76. Reservoir host: water
buffaloes, cattle, pigs 返回

77. 血吸虫病患者

78. Excising the enlarged spleen from and advanced schistosomiasis patient
For late stage case 返回

81. abdomen distention looks like a big drum, emaciation looks like a fire wood.返回

86. A patient of schistosomiasis

87. dwarfism 返回

88. abdomen distention looks like a big drum, emaciation looks like a fire wood. Ascites, emaciation, varicosity, and splenomegaly

89. 脐疝
肝硬化腹水

91. 返回
canceration of colonic polypi

92. 返回

93. The infective inhabitation of Schistosoma japonicum: mesenteric vein返回

94. √Snail:
Oncomelania hupensis is the
only intermediate of S.japonicum.
Females lay eggs in Spring.
Baby snail grows under water, develops to
be adult in Autumn, one year’s life span ,
infected by miracidiae then release cercariae

95. Mountainous
areas
Water-net &
marshy areas
ribbing snail
smooth snail

96. Oncomelania snail

98. The intermediate host of S. japonicum: Oncomelania snail返回

99. Egg-granuloma in liver(inflammatory reaction)
egg were surrounded by eosinophilis

100. eosinophils
egg 返回

101. Egg granuloma in liver
pseudotubercle 返回

103. Fibrous granuloma (nodule)返回

104. 返回

106. 返回

110. Livelihood around water (washing clothes, bathing, etc
Livelihood around water (washing clothes, bathing, etc.) perpetuates schistosomiasis.

114. 返回