Report On Epidimiology,pathogenesis And Treatment Principles Of Parasitic Invations

pg-1 Report on Epidemiology , pathogenesis , clinic, the treatment principles of the parasitic invasions ascariasis,toxocariosis,enterobiasis,taeniasis). 1) Ascariasis- Ascaris lumbricoides (roundworm, nematode infection) A) Epidemiology- worldwide prevalence, mostly common in poor rural communities where there is heavy fecal contamination of the immediate environment. Widely distributed in tropical & subtropical and humid areas. One billion people are infected worldwide. Transmission occurs via feacally contaminated soil, which will cause the hand to mouth fecal carriage. So the disease is spread to humans passively by ingesting infective eggs. Main location in adults – small intestines B) Pathogenesis- ingesting eggs initiates infection. Eggs hatch in the duodenum resulting larvae penetrate the wall of the small intestines & migrate via the circulationheart & lungsascends the bronchial tree into the oropharynxswallowedreturn to the small intestinedevelop into adult worms. Life cycle is completed in about 2 months. Adult worms may live 6-12 months in jejunal lumen. Adult worms-white or reddish colour,15-35 cm long. Egg production. ~200,000/day. C) Clinical features- infection can be entirely asymptomatic. Although heavy infection can cause nausea, vomiting, abdominal discomfort, anorexia. Lung phase of larval migration about 9-12 days after egg ingestion. Pt may develop an irritating nonproductive cough and burning substernal discomfort that is aggravated by coughing or deep inspiration. Fever is usually reported sometimes exceeding38.5c. Eosinophilia develops during this symptomatic phase & subsides slowly over weeks. Chest X rays may reveal evidence of eosinophilic pneumonitis. (Loeffler s syndrome) with round or oval infiltrates. Adult worms in the small intestines usually cause no symptoms. Heavy infection in children may cause pain , small bowel obstruction, sometimes complicated by perforation, intussuseption or volvulus. Can lead to malabsorption, malnourishment may occur in children. Most common site for the worm to obstruct in the intestine is the ileocaecal junction. Worms occasionally invade the appendixacute appendicitis or bile duct biliary obstruction & suppurative cholangitis can also cause pancreatitis. D) Diagnosis*Microscopic detection of eggs in stools . Occasionally adults worms are passed in the stools or vomited & larvae are sometimes found in sputum during pulmonary phase. *Eosinophilia can be marked in migratory phase & decrease when adult worms settle in the small intestines. *Bilirubin increases when liver damage. E)TreatmentMebendazole 100mg 2 times daily.-3 days. Or single dose of piperazine 100mg/kg or pyrantel pamaoate 10mg/kg.Surgical intervention if obstruction occurs.( Piperazine & pyrantel pamoate has antagonistic mode of action. so must not administer together.) 2) Toxocariosis A) Epidemiology worldwide. Caused by Toxoara canis or T .cati. (known also as visceral or occular larva migrans) T canis or T cati mature in soil & usually infect dogs.& cats. Puppies are the most important natural hosts & infection is seen most commonly in children between 1-4 yrs of age. These are animal nematodes.(roundworms) B)Pathogenesis-adult worms in soil infect dogs & cats eggs passed by these animals  may be accidental ingestion by humans.--> Eggs hatch in the intestine  larvae penetrate the intestinal wall & migrate through through liver , lungs, CNS, eyes & all other tissues via circulation. C)Clinical features1. Visceral larvae migrans syndrome (LVM) Consists of fever , anorexia, hepatospleenomegaly, skin rashes, pneumonitis & asthmatic attacks depending on the affected organs. Mostly occurs in 2-5 yr old children. Self limiting in 6-8 monthsif eggs intake ceases . Death can occur due to invasion of brain & heart.(rarely) 2. Ocular larvae migrans syndrome.(OLM) With none or mild systemic manifestations. OLM lesions consist mostly of granulomatous reactions in the retina that may cause visual impairment. Mostly in older children.

pg -2 D) Diagnosis1Marked eosinophilia, hepatomegaly 2 Elevated plasma IgG,IgM, IgE 3.Identification of foreign body eosinophilic granulomas in histological sections. 4.Specific antibody detection by elisa 5. If liver damage increase ALAT. E)TreatmentDiethylcarbamazine(DEC) 2-6mg/kg daily in divided doses for 3 weeks or Thiabendazole 25mg/kg 2 times daily for 5 days.(prednisolone 20-40mg/d po) 3) Enterobiasis (threadworm infection) A)Epidemiology- occurs worldwide but more prevalent in temperate & cold climates . Childrenare most commonly infected, but it may effect whole families , inhabitants of residential institutions & people living in over crowded conditions. B) Pathogenesis- infestation usually results from finger transfer of ova from the perianal area to fomites( clothing,bedding, furniture,rugs,toys) from which the ova is transmitted to the mouth & swallowed Reinfestation or auto infestation easily occurs through finger transfer of ova from perianal area to the mouth. Threadworm reach maturity in the lower GIT /colon female worm migrates to the perianal region (usually at night) deposits eggs within the skin folds transmission by hands(also called dirty finger disease) eggs can remain infective at room temp for 2-3 weeks.-->eggs hatch & larvae migrate back within the rectum& lower intestine(retroinfestation) Superficial damage to the colonic mucosa occuring heavy infection, 2 yr bacterial infection can occur. C)Clinical features – intensive priritis ani is usually the only symptom which is related to egg laying in the perianal region by female worm at night. Perianal excoriations from persistent scratching , vaginitis in young girls may occur. Abdominal pain ,insomnia, convulsions can occur.( occasionally migration into peritoneum & viscera may occur) D) Diagnosis- Feces does not contain eggs. Diagnosed by applying a piece of clear adhesive tape to the perianal region. Then the tape is examined microscopically of adherent eggs. Adult worms may be seen leaving the anus. C)Treatment-single dose of Mebendazole 100mg followed by a2nd dose 2 weeks later. Alternative Pyrantel pamoate or Piperazine. Family members should be treated prophylactically. Anti pruritic ointments creams used on perianal region topically may help. 4) Taeniasis. Taenia saginatta (beef tape worm), / Taenia solium(pork tape worm) Belongs to the subclass Cestoda. Adults live in the intestinal tract of vertebrates. They are hermaphrodites & cross fertilization between proglottids is frequent. The larvae exist in the tissues of vertebrates & invertebrates. Infection is transmitted to humans by ingestion of meats infected with larval forms. Structurally they consist of a head that is adorned with suckers & hooks (T.solium) & suckers alone(T.saginatta). the head is attached via a short slender neck to several segments or proglottids that form a chain like structure . the terminal proglottid is the most mature . the entire worm is covered with a continuous elastic cuticle. Nutrients are absorbed directly through the cuticle.

pg - 3 Taenia saginata(beef tape worm) A)Epidemiology- measures up to 10 cm in length inhabits in upper jejunum & is prevalent in humans in all beef eating countries. (Africa.Middle east, south America,Mexico mainly) B)Pathogenesis- ribbon like adult worm inhabits the human intestinal tractegg containing proglottids are passed in the stool.& ingested by cattleeggs hatch in the cattle. Liberating larvae (oncospheres) that invade the intestinal wall carried by blood stream to striated muscle where they develop in 2 months to a cysticercarius (small cyst that contains a single inverted scolex) humans are infected by eating the cysts in raw or undercooked beef. The cysticercari attach to intestinal mucosa & mature in about 2 months. Adult worms may live several years. C) clinical features- Majority asymptomatic. Symptoms are mild with vague epigastric & abdominal pain,occasional diarrhea and vomiting ,weakness, fatigue, anaemia.-vit b12 deficiency ,weight loss may occur. Rarely- pancreatitis & appendicitis due to obstruction. D)Diagnosis- Presence of proglittids, which are visible macroscopically or the eggs, which are seen microscopically in faeces (stool) or perianal region. Examining perianal clear adhesive tape swabs for ova in which case the scolex(the head) or proglottids are required to establish the species. E) Treatment – Niclosamide 2g as a single dose. Prasiquantel 10mg/kg as a single dose. F)Prevention- Carefully inspection of beef for cycticerci. (encysted larval forms.) refrigeration of beef at 0C for 5 days or cooking at 57C for few minutes destroy the cysticerci. Taenia solium(pork tape worm) A)Epidemiology – Measures upto 6cm in length. World wide distribution, mostly in Eastern Europe, south east asia and Africa. B)Pathogenesis – Humans get infected by eating pork infected by cysticerci. Humas also act as intermediate hosts and develop cysticercosis by accidental ingestion of T.solium eggs from human excreta or if an adult tape worm is present in the intestine, regurgitation may bring gravid proglottis from the intestine to the stomach. Where oncospheres may hatch & start migration to subcutaneous tissue , muscle,viscera, CNS. Ova can rupture before or after excretion in faeces. If B/f  intermediate larval stage  cysticercus cellulosae  cysticercosis. If A/f  faeces ingested by pig  cysticercus in body tissue/miscles --. Raw or undercooked pork ingested by human maturation in to the adult form which lives in the upper jejunum. C)Clinical features – same as t.saginata D)Treatment – Same as t.saginata. however b/c release of ova can occur during treatment and theoretically could be carried back to the stomach releasing the intermediate larva stage, treatment should be followed by a saline purge. Human cysticercosis Occur by autoinfection or heteroinfection by eggs of t.solium and invasion of tissues by the intermediate larval forms. – cysticercus cellulosae common in Asia, Africa, south America. May develop in any tissue in the body. Most common 3 clinical forms recognized. 1) Cerebral cysticercosis – Present as epilepsy, as a space occupying lesionor as focal neurological defecites. Including hemiplagia and behavioral changes. 2) Ocular cysticercosis – may be present as retinitis, uveitis, conjunctivitis, Choroidal atrophy. Blindness may occur. 3) Subcutaneous cysticercosis – Present as small pea size nodules in sub cutaneous tissue. Diagnosis 1) biopsy of a subcutaneous nodule – characteristic translucent membrane 2) Radiography may show calcified degenerative cysticerci 3) Brain CT should be performed (mainly when there is subcutaneous form.) 4) Indirect haemoaggltination test. Treatment. 1)Involves surgical excision of the cistercerci if possible. 2)praziquantal is the drug of choice 3)Stroids given during therapy to avoid reactions. 4) for cerebral form anti-epileptic drugs.(cerebral cysticercosis in symptoms include headache, nausea, vomiting behavioral changes and hemiplegia.)

Report on Epidemiology , pathogenesis , clinic, the treatment principles of the parasitic invasions ascariasis,toxocariosis,enterobiasis,taeniasis).. Report prepared by 1. Dr. Sajid Mahmood, MD (EU), Accident & Emergency Department, NHS Royal infirmary Liverpool United Kingdom. 2. Dr. Adnan Akram, MD (EU), Department of Infectious Diseases. University Hospital Riga Latvia. 3. Dr. Aftab Ahmed, MD (EU), Infection Control Department, Kaunas Medical University Clinic. Lithuania. Contact: publications [at] infekcijas.eu