YA_GIT_2024 PDF

GIT Module: Parasites of the GI BY: Yonas Alemu MSc., Asst prof of medical parasitology DMIP, CHS, AAU – 2024 1 Contents Nematodes Ascariasis, Trichiuriasis, Strongyloidiasis, Ancylostomiasis, Enterobiasis...

GIT Module: Parasites of the GI BY: Yonas Alemu MSc., Asst prof of medical parasitology DMIP, CHS, AAU – 2024 1 Contents Nematodes Ascariasis, Trichiuriasis, Strongyloidiasis, Ancylostomiasis, Enterobiasis Cestodes Taeniasis, Hymenolepiasis, Trematodes Fascioliasis, Fasciolopsiasis 2 ✓ Learning objectives At the end of this session, the students will be able to: Describe the general features, transmission, life cycle, pathogenesis, clinical features, laboratory diagnosis, treatment, prevention and control measures of parasites causing gastro- intestinal tract infection. 3 ✓ General features of Nematodes Round, cylindrical and non segmented body Possess a shiny cuticle (smooth/spined/striated) Dioecious in sex, male smaller with curved tail Females are oviparous/ ovoviviparous/ viviparous Ovoviviparous: Eggs develop internally, hatch within the female's body. E.g. S. stercoralis Oviparous: Egg → Larva (L1 → L2 → L3 → L4) → Adult Viviparous: Larva (L1 → L2 → L3 → L4) → Adult (Bd/Tis Nema..) 4  ✓ General features…. Digestive system is complete, possess mouth, oesophagus & anus Resides in gastro-intestinal tract (small or large intestine) Spread by poor personal hygiene related to feces Humans are the only or major host of intestinal nematodes (direct or simple life cycle) A. lumbricoides,T. trichiura and Hook worm sps are the big three common nematodes. Also known as the geo-helminths (soil transmitted helminths) 5  Transmission: Ingestion of infective egg or feco-oral (the most common) Larva penetrating skin (Hook worm sps and S. stercoralis) Auto/Retro-infection (E. vermicularis), Auto- infection S. stercoralis Rarely: inhalation, trans mammary, transplacental Laboratory diagnosis: Egg in feces ( most often), Larva in feces (S. stercoralis) Recovering egg in the skin around the anus (E. vermicularis) Occasional adult worms: A. lumricoudes, E. vermicularies 6  Ascariasis o A disease caused by Ascaris lumbricoides (large intestinal round worm) o Ascaris suum (a pig ascariasis similar to human A. lumbricoides) o The most prevalent parasite and occur in highest rate in children o Occurs globally with prevalence of 25% (> 0.8 - 1.22 billion people) infected worldwide and 60,000 death annually o In Ethiopia (prevalence ranges from 6 – 77%) o Distributions affected by altitude and climate 7  Habitat and morphology o Adult: o Reside in the small intestine, lifespan of 1 – 2 yrs Capable of producing 200, 000 eggs per day oEgg oFertilized and unfertilized eggs in the feces excreted to soil env’t oRemains viable in soil and dust for up to ~ 10 years oExtremely resistant to adverse Env'tal condition & chemicals i ii 8 i. Fertilized Egg o Consists of ascaroside, chitinous layer, fertilizing membrane and smooth mamillated albuminous coat o Thick, rough, lumpy external shell, round shape, bile stained ii. Unfertilized Egg o Produced by unmated female or before fertilization occurs, do not develop to infective stage o Without ascaroside and fertilizing membrane oBrown, puffy external & thin internal shell, bile stained, elongated 9  Transmission Human host acquire infection by: o Ingestion infective stage with contaminated food or water o Putting finger or toys contaminated with infective egg in to mouth o Eating fecally polluted soil (Geophagia) frequently seen in children, few pregnant women o Rarely by inhalation of eggs carried in blown air Infective stage: Embryonated ova or ova containing 2nd stage larva, infective dose 10-50 eggs 10  Life cycle o Fully embryonated eggs are swallowed & L2 hatches in the stomach & penetrate stomach or duodenal mucosa o L2 enter blood stream – heart & leave through alveoli into lung – then molt twice in the lungs to L3/L4 o Then L4 move up – swallowed back - then reaches small intestine o Develop to adult worm, start mating & lay eggs after 2-3 months o About 200,000 eggs/day are shed with the feces o Embryonate within 2-3 wks in the environment 11  Pathogenic stages L2/3/4, Adult worms 12  Pathogenesis and clinical features oLung tissue damage due to migratory larvae oIntestinal obstruction - too many adult worms, mechanical damage oAberrant migration of adult worms during fever and when seeking mates to; common duct, Liver, Pharynx, Peritoneum cause obstruction & inflammation oParasite secretes trypsin inhibitor, interfere with proper digestion, absorption of food (protein-energy and vitamin A deficiency) oToxic effects due to hypersensitivity to the worm antigens 13 o Clinical features depends upon worm burden & sensitization Lung phase of Juvenile worm: 5-6 days after exposure oPneumonitis (Loeffler’s Pneumonia), hemorrhage due to penetration of lung capillaries “Verminous pneumonia” oAn irritating nonproductive cough & burning substernal discomfort aggravated by coughing or deep inspiration oLess commonly, dyspnea and blood-tinged sputum oEosinophilia subsides slowly after symptomatic phase 14  Intestinal phase adults: 2-3 months after infection oAbdominal pain, fever, diarrhea, malabsorption of nutrient, Stunted growth, cognitive impairment, intestinal obstruction oWandering worm and heavy worm burden oMigration of an adult worm up the esophagus provokes coughing & oral expulsion of the worm oIntestinal perforation, peritonitis, blockage of bile ducts, obstruction of respiratory tract, liver abscess 15  Laboratory Diagnosis oMacroscopically look for adult worms that may occasionally passed in the stool or through the mouth or nose oMicroscopic examination of stool for egg (Intestinal Ascariasis) oDirect wet mount is adequate in moderate to heavy infection oConcentration techniques may be used in light infection o Larvae can be identified in sputum or gastric aspirate during the pulmonary migration phase 16  Treatment o Albendazole: A single dose of 400 mg or o Mebendazole: 100 mg BID for 3 days or single dose of 500mg o Ivermectin: 150-200mg/kg once is effective o Pyrantel pamoate: 11mg/kg once, max 1g is safe in pregnancy o In partial intestinal obstruction: nasogastric suction, IV fluid & instillation of piperazine through nasogastric tube o For complete obstruction and its severe complications require immediate surgical intervention 17  Prevention and Control oPrevention of human exposure by oWashing hands before eating & after defecation, trimming finger, avoid eating uncooked foods such as vegetables oPreventing soil become polluted with feces by: oSanitary disposal of feces in latrines, avoid use of night soil as fertilizer oHealth information provision and treating infected individuals o MDA programmes repeated at 3-6 month intervals (high burden) 18  Trichiuriasis o Caused by Trichuris trichiura (Whipworm – due to the whip- like body form) o Trichuris suis (pigs), Trichuris vulpis (dogs) o Infections more frequent among children and in tropical areas where poor sanitation practices are common o ~ 1 billion people are infected annually, prevalence of 11.6% in SSA countries oIn Ethiopia: Prevalence varies in localities, 25% are infected 19  Habitat and morphology Adult o Resides in large intestine (caecum) and appendix o Whip-like in shape, anterior 3/5th of the worm resembles a whip & the posterior 2/5th are thick o Male: Size 30-45 mm, coiled tail, Female: 35-50mm, straight thick tail 20 Egg / Ova o Passed in the feces to the env’t, not infective immediately o Shell: fairly thick and smooth, with two layers o Shape: "tea tray eggs” or barrel - shaped with a colorless protruding mucoid hyaline plug at each end o Size and Color: 50-54m, yellow brown & bile stained o Content: un segmented central granular mass ovum 21  Transmission and life cycle o Ingestion of infective stage (embryonated egg) with contaminated water, food or from contaminated hand (infective dose10-100 eggs) o Eggs are swallowed, intestinal microflora stimulate egg hatching and larvae released into the upper duodenum o Then larvae attach themselves to the villi of small intestine or invade the intestinal walls o After 3-10 days they move down to the caecum & ascending colon where they mature into adult worms 22 oThe adult worms become threaded into the mucosa fixed with the anterior portions (life span of the adults is about 1-5 years) oThe females begin to oviposit un embryonated eggs 60 - 70 days after infection o Sheds 3,000 - 20,000 eggs per day in stool to the soil env’t oEmbryonate within 3wks in soil (needs a warm, moist, plenty of oxygen) oThe embryonated eggs are extremely resistant to environment, stay for 1-2 years or even 7 years 23  Pathogenic stages L2/3, Adult worms 24  Pathogenesis and Clinical features Are largely determined by the adult worm burden o 100 million cases o Favors warmer tropical and subtropical climate 28  Common to see in immunocompromised individuals Human is the definitive host, but can infect primates and dogs In Ethiopia: It is not highly prevalent in most areas is found in the same geographical areas with hookworm The infection is rare or absent in many arid lowland areas like Ogaden and pastoral areas in the Awash Valley 29  Worms has both free living and parasitic generations Can develop in to free living generation in the soil out side the human host, adults live for 2 weeks, L3 for several wks Parasitic females produce eggs asexually by maternal gene derived parthenogenesis mechanism to produce identical offspring b/c there is no parasitic males Females can reside in the small intestine for several years 30  Habitat and morphology Free living male and female: on external soil environment Parasitic adult females: buried in the mucosal epithelium of the small intestine of human Egg: hatch larvae in the sub mucosa of small intestine Rhabditiform larvae: Passed in the feces and external L1 environments, non infective, motile diagnostic stage Filariform larvae: soil and water, the, infective and pathogenic stage pointed vs notched tail end… L3 31  Transmission Skin penetration of filariform larva: L3 (infective stage) Autoinfection, the rhabditiform larva become infective filariform larva while on the same infected host, ✓Penetrating intestinal mucosa (internal autoinfection) or perianal area (external autoinfection) Ingestion of filariform larva thru contaminated food or water Transmamary & organ transplantation: rarely 32  Life Cycle ▪ Complex, Two types of cycles exist: ✓Free-living (indirect) cycle Rhabditiform larvae in stool molts 4x free living adult males and females produce eggs rhabditiform molts 4x to free living adult males or females larvae or Rhabditiform larvae molts 2x Filariform larvae develop filariform larvae may initiate parasitic life cycle 33 ✓Parasitic (direct) cycle Filariform larvae penetrate skin heart lung molt 2x Alveolar space bronchial tree pharynx swallowed develop to adult female in small intestine produce egg by parthenogenesis which yield rhabditiform larvae Rhabditiform larvae in stool molt 2x develop to filariform rhabditiform may molts 4x to free living adult males or females larvae to initiate the free living cycle 34 Free living cycle Pathogenic stages L3, Adult female 35  Pathogenesis and Clinical features It is usually asymptomatic People with weaker immune systems are more susceptible Cutaneous phase ✓Large number of larva produce itching and erythema at the site of infection within 24 hours of invasion Pulmonary phase ✓The migratory larva in the lung producing bronchopneumonia and full blown pneumonitis 36  Intestinal phase ✓Adult worms invasion causes abdominal pain, sloughing of the intestinal mucosa; mucoid diarrhea, nausea, vomiting, anemia Hyper-infection syndromes due to hyper infection ✓Occurs when the immune status of the host suppressed by either drugs, malnutrition or the concurrent diseases ✓Characterized by massive larval invasion of the lung or any other organ including CNS, which is fatal 37  Laboratory Diagnosis Microscopic finding of the larvae in faeces or in duodenal aspirates using direct or concentration methods Serological techniques Nematode Larva culture techniques (harada-mori filter paper, agar plate) Examination of serial samples may be necessary because direct stool examination is relatively insensitive 38 Harada mori filter paper culture technique 39  Treatment o Ivermectin oral 200µg/kg daily for 2 days o Albendazole 400 mg daily for seven days Prevention and Control o Proper disposal of feces in latrine o Avoid use of night soil as a fertilizer o Wearing protective footwear o Treating infected individual o Health information provision 40  Ancylostomiasis oA parasitic disease caused by two major hook worm species oAncylostoma duodenale (Old world Hook worm) oNecator americanus (New world Hook worm) oWidely distributed throughout the tropics and subtropics oMore than 1 billion people are infected world-wide oChildren, agricultural workers and miners are mostly infected o Are hematophagous or are the voracious blood feeders of all the nematodes 41  Habitat and morphology oAdult: resides in small intestine: Jejunum, duodenum of man (D.H) oEggs: excreted in the feces to the env’t; not infective to human oTwo forms of larva: (Rhabditiform & filariform larvae) free in soil and water env’t oAdults organ of attachment to host tissue: oTeeth in their buccal cavity enable their attachment to intestinal mucosa from where they suck their host's blood oHead is slightly bend (hook) A. duod N.amer 42  Egg o A. duodenale produce 20,000 egg/day which is twice than N. americanus oShape: oval, Size : 65-40m oShell: very thin and appears as black line oColour: the cells inside are pale gray oContent: contains an ovum which appears segmented of about 4-8 blastomeres 43  Transmission and life cycle o Infective stage: filariform larvae L3, MID 10-50 larvae o Route of entry: mainly penetration of the skin, but also ingestion, transmammary (A. duodenale), and rarely transplacental o On contact of host, filariform larvae penetrate the skin and carried through the veins to the heart and then to the lungs o Penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx and swallowed reaching the small intestine 44 oMature into adults, reside and attach to the intestinal wall with resultant blood loss of the host oEggs passed in the feces & rhabditiform larva hatch in 1-2 days under favorable conditions (shade, moisture, warmth) oAfter 5 to 10 days (molts twice) and they become filariform L3 oLarva can survive 3 to 4 wks in favorable environmental conditions oThe worm's mean life span is: 15 years for A. duodenale and 3-7 years for N. americanus 45  Pathogenic stages L3/4 Adult 46 47  Pathogenesis and clinical features oMost infections are asymptomatic (90%) oComplications arise from a combination of intestinal inflammation and progressive iron/protein-deficiency anemia Dermal: Cutaneous invasion and subcutaneous migration of larva oDermatitis known as ground itch; papule with itching and burning sensation, allergic reaction, Local erythema, oScratching leads to secondary infection 48  Oral Ingestion: of filariform larva (A.duodenale) oKnown as Wanaka syndrome; Nausea, vomiting, pharyngeal irritation, cough, dyspnea Pulmonary phase: Migration of larvae through lung, bronchi, and trachea oLoffler's syndrome, Pneumonitis (allergic reaction), Bronchitis, cough, asthma, low fever, oHemoptysis, chest-pain, eosinophilia 49  Intestinal phase: Adult worms attachment & injury to upper intestinal mucosa oWeakness and fatigue in adults, stunt growth & development in children oAnorexia, epigastric pain & gastro-intestinal hemorrhage, hypoproteinemia 50  Hematologic: continuously move to new places to feed on blood o0.03 ml for N. americanus & 0.26 ml A. duodenale, up to 200 ml per day in heavy infections oAnemia, edema, iron deficiency, chronic inflammation and immune response leads to cardiac failure 51  Laboratory Diagnosis oMicroscopic examination of feces for eggs o Fresh feces by saline wet mount and/or with formalin-ethyl concentration technique o A. duodenale & N. americanus eggs are indistinguishable morphologically, reported as hook worm species seen o If feces is >12 hours old, a larva may be seen inside the egg and the larva may hatch o PCR, immunological or serological tests (IgE), Eosinophilia 52  Treatment oAlbendazole, Pyrantel pamoate, Mebendazole, Thiabendazole oIf anemic: high protein diet supplemented with ferrous sulphate, folic acid and vitamin B12 Prevention and control oCultivate personal and environmental hygienic habits oIndividual protection (shoe wearing), glove for hand exposure oSanitary disposal of feces, avoid use of night soil as fertilizer oHealth information and treat the patients and carriers. 53  Enterobiasis o Is a parasitic disease caused by Entrobius vermicularis (Pin Worm or Thread worm or Seat worm) o E. gregorii (primates), E. muris (mice), E. anthropopitheci (apes) oOccurs worldwide but common among people living together oChildren 13 main, 15-30 lateral uterine branches ✓Taenia solium: Grey-blue & translucent, 13mmX8mm 3 to 13 lateral compound uterine branches Small chains of 4-6 rectangular segments found in the feces 76  ✓ Egg / Ova stage characteristics ✓Taenia saginata / Taenia solium Round, dark shell, thick, radially straited (embryophore), yellowish-brown, bile stained, 30-40 m in size Content enclosed by a fine membrane with six hooklets Egg of T. solium infective immediately 77 ✓ Larval stage characteristics ✓Taenia saginata / Taenia solium Larval stage known as cysticercus Cysticercus bovis – T. saginata Cysticercus cellulose – T. solium Has invaginated scolex in fluid filled cystic body 78  Transmission and life cycle Ingestion of cysticercus larvae in infected raw or undercooked beef meat (saginata) or pork meat (solium) T. solium Ingesting ova or proglotids accidentally or autoinfection Internal auto-infections while eggs develops to larvae by reverse peristalsis parasite Definitive Hosts Intermediate Hosts T. saginata Human Cattle & Other herbivores T. solium Human Pigs, Human 79 80 81  Pathogenesis and clinical manifestation Intestinal Taeniasis (as a result of adult) Mostly asymptomatic but depends on host status and burden of infection Symptoms: abdominal discomfort, loss of appetite, indigestion, vomiting, nausea, weight loss, diarrhea, intestinal obstruction 82 Cysticercosis (extra intestinal): larvae Encyst in any organ or tissue but commonly in subcutaneous tissue, brain and eye Symptoms depend on location and number of larva Subcutaneous nodules,, headache, Neurocysticercosis, Epilepsy, Meningitis, encephalitis, Blurred or loss of vision Degenerating larvae evoke cellular reaction, Fibrosis, Necrosis 83 Laboratory Diagnosis 84  Treatment ✓Intestinal taeniasis: Single dose of praziquantel is the drug of choice Niclosamide in a single-dose is an alternative drug ✓Cysticercosis: ▪Excision is the best method if the cysts are accessible ▪Praziquantel and/or albendazole with Corticosteroids to reduce the inflammatory reactions 85  Prevention and control Proper cooking of beef and pork meat before eating. Proper sanitation and personal hygiene to prevent the occurrence of eggs in the environment Avoid eating raw vegetables grown in polluted soil to prevent from acquiring cysticercosis Treatment of cases with taeniasis solium as they can develop cysticercosis due to autoinfection 86  Hymenolepiasis Is parasitic disease caused by Hymenolepis nana (Dwarf Tapeworm), Hymenolepis dimunita (Rat tapeworm) Hymenolepis nana Widely distributed in countries with warm climates than in cold Fairly common in Ethiopia, children are more commonly infected than adults The only cestode infecting humans (DH) without requiring an IH But optionally, larval and adult beetles serve as IH 87  Habitat and morphology Adult: oHabitat is the small intestine of the definitive hosts o Adult worm 1- 4.5cm long and 0.5 – 1mm wide o Neck is long and slender o Scolex has 4 suckers & rostellum with a single row of 20–30 hooks o Proglottids are wider than long with lateral genital pore 88  ✓ Egg stage Round to oval, double thin external membrane & internal membrane Colorless or very pale gray with hexacanth oncosphere, 35-50m diameter Thread like polar filaments that lie between the eggshell & the oncosphere Eggs are infective when passed in feces 89  Transmission and life cycle Mode of Transmission Ingestion of egg with contaminated food, drink or finger Accidental ingestion of larva stage cysticercoid from insects Autoinfection Life Cycle Ingestion of embryonated egg or cysticercoid infected arthropods 90  The egg hatches and releases oncosphere which develops into cysticercoid in the intestinal villus The larva breaks out of the villus and grows into an adult worm The scolex of the adult worm attaches to small intestine and eggs are released out in feces The eggs are ingested by human or insects (flea, beetle) that develop into cysticercoid larvae 91  Pathogenic stages Larvae, adult stages 92  Pathogenesis and Clinical symptoms ▪ Most cases are asymptomatic, but with heavy infection: ▪ Abdominal pain, nausea, loss of appetite, vomiting, diarrhea, and anemia. ▪ Irritability, anal pruritus may be due to an allergic response Laboratory Diagnosis ▪ Microscopic finding of ova stage in the feces: wet mount or concentration techniques 93  Treatment Praziquantel Prevention and control Rodent control, control of beetles & fleas Cleaning of the areas of food storage Sanitary practices in food handling and personal practices Treating infected individuals and health information provision 94 Hymenolepis diminuta (Rat tapeworm) Is a cestode frequently found in rodents but infrequently seen in humans Prevalent worldwide, but only a few human cases have been reported in Australia, United States, Spain, Italy and Ethiopia The prevalence is higher in countries such as Malaysia, Thailand, Jamaica, Indonesia  Habitat and Morphology Adult: Resides in small intestine Scolex has very small rostellum with no hooks 20 - 60 cm long, mature proglottid similar to H. nana Eggs: Excreted to env’t thru feces Slightly bigger eggs and proglottids than H. nana DH: Rodents, Human, IH: various insects (adults or larvae) 96 Eggs Shape: round or slightly oval, Color:-Yellow-brown or bile pigmented Striated outer and a thin inner membrane The oncosphere has six hooks, no polar filaments Size 70 - 85 µm X 60 - 80 µm, 97  Transmission and life cycle Transmission: Ingestion of cysticercoid larvae (infective stage) directly Ingestion of larvae harboring insects or rodents Life cycle: Ingestion of an insects carrying the cysticercoid larvae directly from the environment or in precooked cereals, raw rodents 98  Adults mature within 20 days & attaches to the small intestine wall Eggs are released in the small intestine from gravid proglottids & expelled to the environment The mature eggs are ingested by an intermediate host (insects, rodents) Oncospheres released, penetrate the intestinal wall and develop into cysticercoid larvae in an IH Ingestion of cysticercoid larvae or raw/under cooked food, rodents Pathogenic stages Larvae, adult  Pathogenesis and clinical presentation Mostly asymptomatic Symptoms occur only with heavy infections. abdominal pain, irritability, itching, eosinophilia, diarrhea Gastrointestinal discomfort, itchy anus, poor appetite Weakness  Laboratory Diagnosis Finding eggs in stool in wet mount or concentration techniques Requires repeated examinations Treatment Praziquantel, adults and children, 25mg/kg in a single-dose therapy Alternatives: Niclosamide, Nitazoxanide  Prevention and control Rodent control Avoid rodent consumption Sanitary practices in food handling and personal practices Control of insect vectors Treating infected individuals and health information provision  General characteristics of trematodes ✓Are generally flat, un segmented, leaf shaped worms (exception, schistosomes- cylindrical) ✓Vary in size from species just visible to the naked eye to large fleshy species 104 ✓Attachment Organ Characteristics- 2 suckers Muscular oral sucker surrounding mouth at anterior end One or more suckers on ventral surface (called “ventral sucker,” “posterior sucker,” or acetabulum.” 105 ✓Digestive tract Digestive tract consists of mouth Y & esophagus divides to “ “ shaped 106 ✓Reproduction Most are monoecious: male & female reproductive organs Schistosomes are dioecious (separate sex) 107 ✓ General life cycle and developmental stages 108 ✓Ova or egg Contains miracidium inside shell Usually have an operculum or spine Many of flukes have very distinctive eggs ✓Adult Found in the definitive host and reproduce sexually Are restricted to specific region of host and even host specific 109  Fascioliasis Is a waterborne and foodborne zoonotic disease caused by two parasites of class Trematoda, genus Fasciola F. hepatica (liver fluke or Sheep liver fluke) F. gigantica (large liver fluke) Other liver flukes species also includes; Clonorchis sinensis, Opisthorchis viverrini 110  Fasciola hepatica Has cosmopolitan distribution with high prevalence in most sheep and cattle raising countries Does not play an important role in human health In Ethiopia Causes serious economic loss throughout the highlands by infecting cattle and sheep Human is not the primary host, but few reported cases of