A 34-year-old Brazilian man presented with a 24-year history of prominent, progressively dilating superficial veins. The veins of the lower limbs dilated first, gradually becoming discolored and indurated (Panel A). After 5 years, varicosities appeared on the anterior chest and abdominal wall (Panel B). Gynecomastia, splenomegaly, and bilateral varicoceles also developed. Jaundice, spider angiomata, and testicular atrophy were not seen. There was no evidence of liver failure; however, a platelet count of 20,000 per cubic millimeter indicated thrombocytopenia. Duplex Doppler ultrasonography of the abdomen showed periportal fibrosis, splenomegaly, and high portal flow. Esophagogastroduodenoscopy confirmed the presence of esophageal varices. Viable eggs ofSchistosoma mansoni were found in stool specimens, which confirmed the diagnosis of intestinal schistosomiasis leading to portal hypertension and splenic sequestration. He was treated with praziquantel and cleared the S. mansoni infection. Despite evidence of profound portal hypertension, he has done well. More than 200 million people worldwide are infected with schistosomes. Of these, approximately 120 million have symptoms and 20 million are severely ill. During the past decade, targeted interventions combining snail control, improved water quality, and the treatment of infected persons have contributed to diminishing the burden of disease.
Trematodes chapter 55 General characteristics Trematodes are commonly called flukes Are leaf shape worms which are generally flat and fleshy Are hemophrodite except for schistosoma, which have separate male and female Have complicated life cycle occuring in two or more host have operculated eggs( except for schistosoma) which contaminated water, perpetuating the life cylce and which are also used to diagnose infections. The first intermediate hosts are snails.
Trematodes The most important trematodes are: Schistosoma species (blood flukes) Clonorchis (liver fluke) Paragonimus (lung fluke). Schistosomes have by far the greatest impact in terms of the number of people infected, morbidity, and mortality.
SCHISTOSOMA Disease: Schistosomiasis. Schistosoma mansoni, Schistosoma japonicum affect the gastrointestinal tract. Schistosoma haematobium affects the urinary tract.
Epidemiology: Approximately 250 million people are infected with schistosomes and 600 million are at risk
SCHISTOSOMA Characteristics: Trematode (blood fluke). Adults exist as two sexes but are attached to each other. Eggs are distinguished by spines: - Schistosoma mansoni has large lateral spine. - Schistosoma japonicum has small lateral spine - Schistosoma haematobium has terminal spine
Life cycle of SCHISTOSOMA In the venous site, the female lays fertilizing eggs which penetrate the gut or bladder wall. The eggs are excreted in the stool or urine and must enter fresh water to hatch. Once hatched, the ciliated larvae (miracidia) penetrate snails and undergo further development into sporocysts and multiplication occurs to produce many free- swimming cercariae Humans are infected by free-swimming forked tail cercariae that penetrate the skin. Cercariae form larvae ‘schistosomula’ that penetrate blood vessels and are carried to the lung and the liver, where they become adults flukes.
Schistosoma Pathogenesis: Eggs in tissue induce inflammation, granulomas, fibrosis, and obstruction, especially in liver and spleen hepatosplenomegaly. S. mansoni damages the colon (inferior mesenteric venules) S. japonicum damages the small intestine (superior mesenteric venules) S. haematobium damages the bladder venules which can lead to carcinoma of the bladder
Schistosoma Transmission: Transmitted by penetration of skin by cercariae. Humans are definitive hosts; snails are intermediate hosts. Endemic in tropical areas: S mansoni in Africa and Latin America, S haematobium in Africa and Middle East, S japonicum in Asia
Schistosoma haematobium eggs in section of bladder
Portal obstruction, in liver and spleen (hepatosplenomegaly)
Schistosoma Laboratory Diagnosis: Eggs visible in feces or urine. Treatment:Praziquantel. Prevention: Proper disposal of human waste. Swimming in endemic areas should be avoided.
Immunity: IL-4 and IL-5 induces B cells to class- switch to produces IgE. IL-5, which induces bone marrow precursors to differentiate into eosinophils IL-3 (along with IL-4), which stimulates mast-cell growth. Ag / Ab activate complement.
Clonorchis sinensis Disease: Clonorchiasis (chinese liver fluke) Characteristics: Trematode (liver fluke). Life cycle: Humans ingest undercooked fish containing encysted larvae (metacercariae) In duodenum, immature flukes enter biliary duct, become adults, and release eggs that are passed in feces. Eggs are eaten by snails; the eggs hatch and form larvae. These multiply through generations and then produce many free- swimming cercariae, which encyst under scales of fish and are eaten by humans
Clonorchis sinensis Transmission: eating raw or undercooked freshwater fish. Humans are definitive hosts; snails and fish are first and second intermediate hosts, respectively. Endemic in Asia. Pathogenesis: Inflammation of biliary tract. Laboratory Diagnosis: Brownish, small, operculated eggs visible in feces. Treatment:Praziquantel. Prevention:Adequate cooking of fish. Proper disposal of human waste.
Symptoms: irritation of the bile ducts which become dilated and deviated. The liver may enlarge, become necrotic and tender and its function may be impaired. Modest infections results in indigestion, weakness and loss of weight. Heavier infections produce anemia, liver enlargement, slight jaundice, edema, and diarrhea.
Clonorchis sinensis operculated, brownish, Small egg
LIFE CYCLE Humans ingest undercooked freshwater crab meat containing encysted larvae (metacercariae). In gut, immature flukes enter peritoneal cavity, burrow through diaphragm into lung parenchyma, and become adults and produce eggs that enter bronchioles and are coughed up or swallowed. Eggs in either sputum or feces that reach fresh water hatch into miracidia that enter snails, multiply through generations into larvae, and then form many free- swimming cercariae that infect and encyst in crabs.
Paragonimus Westermani Transmission: Transmitted by eating raw or undercooked crab meat. Humans are definitive hosts; snails and crabs are first and second intermediate hosts, respectively. Endemic in Asia and India.
Paragonimus Westermani Pathogenesis: Inflammation and secondary bacterial infection of lung. Laboratory Diagnosis: Eggs visible in sputum or feces. Treatment:Praziquantel. Prevention:Adequate cooking of crabs. Proper disposal of human waste.
Serum creatinine concentration is used clinically as a convenient index of kidney function, but it is important to remember that even a minimal elevation in creatinine can reflect significantly decreased rate of glomerular filtration. Hematocrit (varies with altitude): Male: 40.7-50.3% Female: 36.1-44.3%
Increased eosinophils (eosinophilia) is most often associated with allergic diseases and parasites (such as worms). Possible disorders include: eczema leukemia autoimmune diseases asthma hay fever Medications that may cause an increase in eosinophils include: amphetamines (appetite suppressants) tranquilizers bulk-type laxatives containing psyllium certain antibiotics
Other minor parasite Fasciola Hepatica ( sheep liver fluke) Acquisition Ingestion of aquatic plants, water cress Reserviour: sheep, cattle, humans Dz: subclical- fever, nightsweats, malaise Rx: praziquantel
Fasciolopsis buski (giant intestinal fluke) Acquisition Ingestion of acquatic plants, water chestnuts. Reserviour Host: pigs, dogs, rabbits and humans Progression in humans Asymptomatic- abd pain and diarrhea Dx: eggs in feces Rx: Praziquantel