Ancylostomiasis ( hook worm ) ◼ It is cased by Ancylostoma duodenale or Necator americanus. ◼ The adult hookworm is 1 cm length and lives in the duodenum and upper jejunum. eggs are passed in the feces and in the moist soil, the larvae develop into the filariform larvae which is the infective stage which penetrates the human skin and carried to the lungs where they ascend to the bronchi are swallowed and mature in the small intestine within 4 – 7 weeks. Pathology: ◼ The larvae may cause allergic inflammation at the site of entry into the skin. ◼ Heavy infection may cause pulmonary eosinophilia. ◼ The worms attach to the small bowel mucosa and withdraw blood ( 0.15 ml/worm/day for A. duodenale). ◼ The degree of anaemia is variable and it deepened on :- ✓ 1)worm load, 2)nutritional status, 3)iron store. Clinical features 1)dermatitis usually on the feet (( ground itch )).2)paroxysmal cough with blood-stained sputum associated with patchy pulmonary consolidation. (( pulmonary phase )).3)Vomiting and epigastric pain may occur.4)Iron deficiency anemia, protein-losing enteropathy, and hypoproteinemia.5)Cardiac failure may result from chronic iron deficiency Investigations 1)Eosinophilia, 2) the characteristic ovum can be recognized in the stool. 3) fecal occult blood test will be positive. Management ◼ mebendazole 100 mg/12 hr. for 3 days or single dose albendazole 400mg.oral iron for treatment of anemia. Ascaris lumbericoides ( round worm ) ◼ Pale yellow nematode 20 – 35 cm length. Human are infected by eating food contaminated with ova. Ova will hatch in the duodenum to larvae which migrate through the lungs, and ascend the bronchial tree, from which they may be swallowed and mature in the small intestine. Clinical features ◼ variable symptoms from vague abdominal pain to malnutrition ◼ obstructive complications: intestinal complications mainly in the terminal ileum or bile duct obstruction. Investigations ◼ Diagnosis by:1) Eosinophilia, 2)demonstration the ova in the feces, 3) Adult warm may be expelled orally or rectally, 4)Ba. Meal may demonstrate the adult warm. Treatment Mebendazole 100 mg/12 hr. for 3 days OR, Albendazole 400 mg single dose OR, Piperazine 4 gm as a single dose. For obstructive complications: i.v fluid, nasogastric suction and piprazine. Prevention: ✓ Community chemotherapy regimen OR Treating school age group. Enterobius vermicularis ( Thread worm ) ( Pin worm ) ◼ It is common world wide, mainly children, after swallowing of the ova, development take place in the small intestine but the adult worms are found chiefly in the colon. Clinical features ◼ The gravid female worm lays ova around the anus causing intense itching especially at night, the ova carried to the mouth by the fingers ( auto Re-infection ) ◼ Adult worm may be seen moving on the buttocks or in the stool. Investigations: ◼ Adhesive cellophane tap to the perianal skin in the morning to detect the ova. ◼ Perianal swab moistened with saline Treatment ◼ Single dose mebendazole 100 mg OR, Albendazole 400mg OR, Piperazine 4 gm ◼ Treatment may be repeated after 2 weeks. All the family members should be treated.Clothes, bed liven, nail cutting
2-Trematodes ( FLUKES ) Leaf-shaped
Schistosomiasis ◼ There are 3 species of the genus Schistosoma causing the disease in human: S. haematobium, S. mansoni & S. japonicum. ◼ The ovum is passed in the urine or faeces of the infected individual and gains an access to fresh where the ciliated miracidium inside it will be liberated into the water where it enters the intermediate host ( fresh water snail ) in which it multiplies and a large number of (fork-tailed cercaria) are liberated to the water, where they can penetrate the skin or the mucous membrane of the mouth of the human.They transform into schistosomula and pass through the lungs and by the bloodstream to the liver and so to the portal vein where they mature. Within 4 – 6 weeks, adult worms migrate to the venules draining the pelvic viscera where the females deposit ova. Pathogenesis stage time S. haematobium S. mansoni S. japanicum Cercarial Days Papular dermatitis at site of penetration As for S.haematobium penetration Larval migration & Weeks Pneumonitis, myositis, hepatitis, fever, As for S. haematobium maturation eosinophilia & seroconversion Early egg deposition Months Cystitis, haematuria Colitis, Hepatitis ,Portal ectopic granuloma in the skin, CNS,… hypertension, Ectopic Immune complex GN granuloma, GN Late egg deposition Years Fibrosis & calcification of ureters and Colonic polyposis & bladder Bacterial infection,Calculi, stricture,Periportal fibrosis, Hydronephrosis Carcinoma,Pulmonary Portal hypertension, granuloma & pulmonary hypertension Pulmonary granuloma & pulmonary hypertension Clinical features ◼ Itching lasting 1 – 2 days at the site of cercarial penetration. ◼ After a symptom-free – period of 3 – 5 weeks, acute Schistosomiasis (Katayama syndrome) such as urticaria, fever, muscle aches, abdominal pain, headache, cough, sweating, hepatosplenomegaly, lymphadenopathy and pneumonia may be present and there is eosinophilia.Katayama syndrome seen in severe S.mansoni and S. japanicum but rare in S. haematobium. ◼ Acute Schistosomiasis subsides after 1 – 2 weeks. Chronic Schistosomiasis due to egg deposition depends upon the intensity of the infection and the species S. Haematobium ◼ Painless terminal haematuria.Frequency due to bladder calcification.Frequent UTI.Bladder or ureteric stone formation.Hydronephrosis.Renal impairment & renal failure with contracted calcified bladder. Loin pain radiated to the groin. Haemospermia.Intestinal symptoms may follow bowel wall involvement. Strong association with squamous cell carcinoma of the bladder. S. Mansoni ◼ Variable symptoms from malaise, abdominal pain, frequent blood-stained diarrhea & rectal polyps Portal hypertension may cause massive splenomegaly.Fatal haematemesis from esophageal varices or progressive ascites. Liver function is initially preserved because the pathology is fibrotic rather than cirrhotic.S. mansoni infection predisposes to the carriage of salmonella. S. Japanicum ◼ The adult worm infect human, dogs, rats, cats, pigs & sheep.The pathology is similar to that of S. mansoni, but it produces more eggs and extensive & widespread lesions. The clinical features resemble severe infection with S. mansoni with added neurological features. Small as well as large bowel may be affected. Investigations: ◼ 1)Demonstration of eggs or serological evidence of the infection: a) S. haematobium → terminal spined egg. b) S. mansoni → lateral spined egg. c) S. japanicum → lateral rudimentary spined egg. ◼ 2)Ultrasonography may show bladder wall thickening and calcification with or without hydronephrosis ◼ 3)Cystoscopy may show: sandy patches, bleeding mucosa & later distortion. ◼ 4)Sigmoidoscopy may show: inflammation and bleeding with biopsy for ova in S. mansoni and S. japanicum. ◼ 5)Eosinophilia. 6)Serology: via ELISA as a screening test. Treatmant: ◼ Praziquantel 40 mg/kg once is the drug of choice for all forms of Schistosomiasis produce 80% cure & 90% reduction in egg counts in the remaining. S/E: nausea and abdominal pain ◼ Oxamniquine is useful and safe in chronic hepatic forms of S. mansoni. Surgery may be required for residual lesions.Plastic surgery for uretric stricture and fibrotic lesions Removal of rectal papilloma by diathermy. Prevention: ◼ the life cycle is terminated if the ova in urine or faeces are not allowed to contaminate fresh water containing the snail host. Mass treatment of the population. Attack on the intermediate host (the snail). 3-cestodes (tapeworms) ◼ they inhabit intestinal tract,they have no alimentary system and absorb nutrient through there surface.The anterior surface (scolex) has suckers for attachment to the host. From the scolex, a series of progressively developing segments are arises.Larvae are librated from ingested ova. ◼ Human acquired the infection by eating undercooked beef infected with cysticercus bovis (the larval stage of Taenia Saginata – beef tapeworm-).Undercooked pork containing larval stage of T. Solium (pork tapeworm) ◼ Undercooked fresh water fish containg larva of Diphillobothrium latum (fish tapeworm) ◼ Usually only one adult tapeworm is present in the gut but up to ten have been detected. Taenia saginata ◼ Adult worm may be several meters length and produce little or no intestinal upset in human being. ◼ Ova may be found in the stool which is indistinguishable from T. solium ova. ◼ Praziquantel is the drug of choice.Niclosamide is an alternative. ◼ Prevention depend on efficient meat inspection and through good cooking of beef Taenia solium ◼ It is not as large as T. saginata.The adult worm is found only in human following the eating of undercooked pork containing cysticerci Cysticercosis: ◼ It is acquired by ingestion of tapeworm ova from contaminated fingers or by eating contaminated food.The larvae are librated from eggs in the stomach and then penetrate the intestinal mucosa and carried to many parts of the body,where they developed and form cystiserci ( 0.5 – 1 cm cysts that contain the head of a young worm ). They do not grow or migrate & located in subcutaneous tissues, skeletal muscles and brain. Clinical features: ◼ Cysts can be palpated under the skin or mucosa, they may cause few or no symptoms and will die & become calcified.Heavy brain infection may cause features of encephalitis.Cerebral signs do not occur until the larvae die, 5 – 20 years later in form of epilepsy or personality disorders.Abnormal gait or signs of internal hydrocephalus. Investigations ◼ calcified cyst can be recognized radiologicaly.Brain CT or MRI are more sensitive. Epileptic fit starting in adult life in endemic area suggest the diagnosis.Antibody detection by IFAT Treatmant ◼ intestinal infection, Niclosamide followed by mild laxative.For cerebral cystisercosis, praziquantel improve prognosis.Albendazole for parenchymal neurocystisercosis .Prednisolone given 1 day before praziquantel or allbendazole .Antiepileptic drugs should be given. Surgery for hydrocephalus Echinococcus granulosus))taenia echinococcus(( : Hydatid disease ◼ Dogs are the definitive host, the larval stage ( hydatid cyst ) normally occurs in sheep, cattle, camels and other animals.By handling the dog or drinking contaminated water, human may ingest the eggs &the embryo will liberated in the small intestine and then to the blood stream and then to the liver.The resultant cyst will grow very slowly & it may be calcified or rupture giving rise to multiple cysts. Clinical features ◼ It typically acquired during childhood.Usually symptomless.It may cause pressure symptoms ◼ In 75% of patients with hydatid disease, the right lobe of the liver is involved and contain a single cyst.In the others single or multiple cysts may be found in the lungs, liver, bone, brain or elsewhere. Investigations: ◼ 1)Clinical,2)Radiological.3)Ultrasound finding.4)Complement fixation.5)ELISA Treatmant: ◼ hydatid cyst should be excised wherever possible.Albendazole 400mg/12hr for 3 months used for inoperable or multiple cysts and to reduce the infectivity of the cyst preoperatively.praziquantel 20 mg/ kg/12hr. for 14 days kill protoscolices perioperativly.