Presentation is loading. Please wait.

Presentation is loading. Please wait.

The Trematodes. CLASSIFICATION OF PARASITES PROTOZOAHELMINTHS Unicellular Single cell for all functions Multicellular Specialized cells 1:Aoebae: move.

Similar presentations


Presentation on theme: "The Trematodes. CLASSIFICATION OF PARASITES PROTOZOAHELMINTHS Unicellular Single cell for all functions Multicellular Specialized cells 1:Aoebae: move."— Presentation transcript:

1 The Trematodes

2 CLASSIFICATION OF PARASITES PROTOZOAHELMINTHS Unicellular Single cell for all functions Multicellular Specialized cells 1:Aoebae: move by pseudopodia. 2:Flagellates: move by flagella. 3:Ciliates: move by cilia 4:Apicomplexa(Sporozoa) tissue parasites Round worms (Nematodes): - elongated, cylindrical, unsegmented. Flat worms : - Trematodes: leaf-like, unsegmented. - Cestodes: tape-like, segmented.

3 Schistosomiasis Schistosomiasis is a disease caused by infection with parasitic blood flukes. It is also known as "bilharziasis" after Theodor Bilharz, who first identified the parasite in 1852. The parasites that cause schistosomiasis live in certain types of freshwater snails. Emergence of cercariae (the infectious form of the parasite) from the snail leads to contamination of the water. Individuals can become infected when skin comes in contact with contaminated water and is penetrated by cercariae. There are three major species Schistosoma mansoni (Africa and South America), S. japonicum (East Asia) cause intestinal tract disease), and S. haematobium (Africa and Middle East) causes genitourinary tract disease. Infection tends to occur in rural areas; urban areas usually lack the freshwater conditions needed for the snail intermediate host to thrive. Wet rice culture is an important source of exposure in East Asia and parts of Africa. Children and adult acquire the infection by bathing in freshwater ponds, lakes, and rivers contaminated with cercariae, Most individuals have a mild to moderate parasite load with limited morbidity ; heavy infection with significant consequence for disease occurs among relatively few individuals in a population..

4

5 Lifecycle of schstosoma The lifecycle of schistosomiasis is complex and requires both intermediate and definitive hosts, Human contact with fresh water is required for transmission of schistosomiasis. The lifecycle begins with seeding of eggs into fresh water through feces (S. mansoni andS. japonicum) or urine (S. haematobium) from infected humans or animal reservoirs. The eggs hatch and release miracidia, which are viable for up to seven days until they penetrate snail intermediate hosts, followed by production of cercariae, which are released from the snail into the water after four to six weeks. Cercariae can survive up to two days in the water,Cercariae penetrate human skin (definitive host), shed their tails, and become schistosomulae, which migrate through the circulation until they reach the liver where they mature into adults over two to four weeks. The adult worms migrate against portal blood flow to the mesenteric venules of the small and large intestine (S. japonicum ), the mesenteric venules of the colon (S. mansoni) or the vesical venous plexus (S. haematobium). The male schistosome forms a groove in which the female resides. After one to three months, the females worms deposit eggs in the small venules of the mesenteric or perivesical systems. The eggs move toward the lumen of the intestine (S. mansoni and S. japonicum) or bladder and ureters (S. haematobium) and are eliminated in feces or urine, respectively. The adult worms usually survive for five to seven years but can persist for up to 30 years

6

7 Developing schistosom e in liver The left liver lobe is enlarged with a sharp edge, and splenomegaly may extend below the umbilicus and into the pelvis in some cases. The occlusion of the portal veins, portal hypertension with splenomegaly, portocaval shunting, and gastrointestinal varices

8 PATHOGENESIS & CLINICAL MANIFESTATIONS OF SCHIStOSOMIASIS In general, clinical disease is caused by the host immune response to migrating eggs. Adult worms absorb host proteins and coat themselves with host antigens, allowing prolonged residence in the bloodstream with evasion of immune attack, Migration of eggs through tissues can be associated with inflammation, and subsequent fibrosis, In the bowel, inflammation can result in ulceration, blood loss, and scarring. In the liver, can lead to portal hypertension and subsequent esophageal varices In the bladder, the eggs cause granulomatous inflammation, ulcerations, and development of pseudopolyps in the vesical and ureteral walls, which may mimic malignancy. In addition, chronic inflammation due to schistosomiasis has been associated with bladder cancer. CLINICAL MANIFESTATIONS:Acute infection (Swimmer's itch, sudden onset of fever, urticaria and,chills, myalgias, arthralgias, dry cough, diarrhea, abdominal pain, and headache.) Chronic infection : (Intestinal schistosomiasisHepatosplenic schistosomiasis, Pulmonary complications, Genitourinary schistosomiasis)

9 Eggs of Schistosoma mansoni

10

11 Eggs of Schistosoma mansoni in the liver

12 Cellular reaction around eggs of Schistosoma mansoni

13 Egg of S. haematobium Schistosomaiasis granuloma

14

15 Pathology of Schistosomiasis Schistosoma haematobium Causes urinary schistosomiasis 1.PREPATENT PERIOD 10-12 wks 2.EGG DEPOSITION AND EXTRUSION: 1.painless haematuria 2.Inflammation of bladder and burning micturition 3.CNS involvement 3.TISSUE PROLIFERATION AND REPAIR: Fibrosis, papillomata in the bladder and lower ureter leading to obstructive uropathy. Periportal fibrosis Lung and CNS involvement Schistosoma mansoni Causes intestinal schistosomiasis 1.PREPATENT PERIOD 5-7 wks 2.EGG DEPOSITION AND EXTRUSION: 1.dysentery (blood and mucus in stools), 2.hepatomegaly splenomegaly 3.CNS involvement 3.TISSUE PROLIFERATION AND REPAIR:Fibrosis, Papillomata in intestine, Pperiportal fibrosis,hematemesis Lung and CNS involvement.

16 Schistosome dermatitis, or "swimmers itch” occurs when skin is penetrated by a free-swimming, fork-tailed infective cercaria..

17 Bladder lesions in urinary schistosomiasis

18 Hepatosplenomegaly in chronic schistosomiasis

19 Portal hypertension in chronic schistosomiasis

20

21 Diagnosis of Schistosomiasis Schistosoma haematobium Parasitological: –Examination of urine Immunological –Serological tests Indirect: –Radiological –Cystoscopy Schistosoma mansoni Parasitological –Examination of stools Immunological –Serological tests Indirect: –Radiological –endoscopy

22 Egg of S. haematobium Egg of S. japonicum

23 Egg of S. mansoni

24 Drug of choice for schistosomiasis is Praziquantel

25 Life-cycle of Fasciola hepatica

26 FASCIOLA HEPATICA F. hepatica occurs globally, mainly in sheep-rearing areas of temperate climates. Infection is endemic in Central and South America, Europe, Asia (especially China, Vietnam, Taiwan, Korea, and Thailand), Africa, and the Middle East. Sheep and cattle are the most important definitive hosts of F. hepatica;. Snails are intermediate hosts. Humans are incidental hosts and most often acquire infection by eating watercress grown in sheep-raising areas. Infection may also be transmitted by other freshwater plants, including lettuce, mint, and parsley. Humans can also acquire infection by drinking contaminated water containing viable metacercariae ;. After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, peritoneal cavity, and liver parenchyma into the biliary ducts, where they develop into adults; in humans, this takes three to four months. The adult flukes reside in the large biliary ducts of the host,Migrating metacercariae cause liver destruction, necrosis and fibrosis. In addition, adult flukes can partially obstruct the bile ducts, causing thickening, dilatation, and fibrosis of the proximal biliary tree. The amount of liver damage is correlated with the parasite load; the number of adult flukes that reach the biliary tree.

27

28

29 Snail intermediate host of : Fasciola hepatica

30 Watercress, one means of transmission of fascioliasis

31

32

33

34 Fasciola hepatica

35 Pathology and clinical picture : –True infection causes mainly biliary obstruction and liver damage. –False infection is when eggs are eaten in infected animal liver and passed in stools. Diagnosis: eggs in stools or duodenal aspirate..

36 Fasciola hepatica in bile duct Fasciola hepatica adult

37 Egg of Fasciola hepatica

38 Treatment: Triclabendazole is the drug of choice to treat fascioliasis and is on the WHO list of essential medicines. The correct dosage is calculated based on the person’s weight (10 mg/kg) and the tablets are given at one time. Triclabenda zole

39 Sheep liver infected with Fasciola hepatica

40 Fasciola hepatica: false infection

41 Fasciola hepatica: false infection (eggs in stools)


Download ppt "The Trematodes. CLASSIFICATION OF PARASITES PROTOZOAHELMINTHS Unicellular Single cell for all functions Multicellular Specialized cells 1:Aoebae: move."

Similar presentations


Ads by Google