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PARASITIC CAUSES OF DIARRHOEA.pptx

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PARASITIC CAUSES OF DIARRHOEA.pptx

  1. 1. PARASITIC CAUSES OF DIARRHOEA Dr Arpitta Sarkar Assistant Professor Department of Microbiology JIMSH Budge Budge
  2. 2. Common Parasites causing Diarrhoea • Giardia lamblia • Balantidium coli • Cryptosporidium • Isospora • Cyclospora • Taenia saginata • Taenia solium • Trichuris trichuria
  3. 3. Giardia lamblia Intestinal flagellates
  4. 4. It is the most common flagellate of the intestinal tract. considered as one of the most common cause of infectious diarrhea throughout the world Geog. Dist: Worldwide (tropical and subtropical region) It is more common in warm climates Humans are the only important reservoir of the infection Also known as(Giardia duodenalis ) Causes Giardiasis, also called “traveler’s diarrhea”
  5. 5. Giardia life cycle Giardia has one of the simplest life cycles of all human parasites The life cycle is composed of 2 stages: • The trophozoite which exists freely in the human small intestine • The cyst, which is passed into the environment • No intermediate hosts are required
  6. 6. The trophozoite form of G lamblia
  7. 7. Measures 9-21 micrometers long by 5-15 micrometers wide Teardrop-shaped
  8. 8. GIARDIA CYST
  9. 9. Cyst Ovoidal/ellipsoidal – shaped thick wall Size 8-12um L X 7 - 10um Contains 2-4 nuclei Mature cyst is the infective stage, at least 10 cysts are required to cause infection Habitat: duodenum and jejunum
  10. 10. TRANSMISSION • Only the cyst form is infectious by the oral route • trophozoites are destroyed by gastric acidity • Most infections are sporadic, resulting from cysts transmitted as a result of fecal contamination of water or food, by person-to- person contact
  11. 11. Symptoms • Watery diarrhea that may alternate with soft, greasy stools • Fatigue • Abdominal cramps and bloating • flatulence • Nausea • Weight loss • failure to absorb fat, lactose, vitamin A and vitamin B12 • Signs and symptoms of giardia infection usually improve in two to six weeks, but in some people they last longer or recur
  12. 12. Diagnosis • Stool microscopy • Stool Ag detection • Duodenal content examination • Duodenal biopsy • Serodiagnosis • Molecular diagnosis
  13. 13. Pathogenesis • Infection resulted in crypt hyperplasia associated with an increased enterocyte migration rate • Villus height was decreased in the duodenum, unchanged in the jejunum, and increased in the ileum of infected animals • Epithelial microvilli were markedly shortened, and brush border surface area decreased in the jejunum and ileum of infected animals • Thymidine kinase activity was increased in isolated duodenal villus enterocytes but did not differ in the jejunum and ileum
  14. 14. Stool examination • 3 stools taken at 2-day intervals, are examined for ova and parasites. The cysts are detected 50–70% of the time in the first stool specimen examined, and 90% of the time the cysts are detected after 3 stool specimen examinations • Trophozoites disintegrate rapidly outside of the body but may be found in fresh, watery stools • Cysts are found in soft and (semi)formed stools • Cyst passage is variable and not related to clinical symptoms • If not fresh, stool should be preserved in polyvinyl alcohol or formalin
  15. 15. String test • String test (entero-test) involves a gelatin capsule connected to a weighted nylon string • The patient tapes one end of the string to his cheek and then swallows the capsule • After the gelatin is dissolved in the stomach, the weight carries the string into the duodenum • The string is left there for 4–6 hours or overnight while the patient fasts • After removal, the string is examined for bilious staining, which identifies successful passage into the duodenum • The mucus from the string is examined for trophozoites in iodine or saline
  16. 16. Treatment • Metronidazole • Paramomycin • Quinacrine hydrochloride • Furazolidone • Tinidazole • Albendazole
  17. 17. BALANTIDIUM COLI
  18. 18. BALANTIDIUM COLI • It is largest protozoan • Only ciliated parasites of humans • Causes Balantidiasis
  19. 19. MORPHOLOGY • Trophozoite – in dysenteric stool • Cyst: - in carriers and chronic cases • Both forms: binucleated - large macronucleus and small micronucleus
  20. 20. TROPHOZOITE Cytoplasm- outer clear ectoplasm and inner granular endoplasm Endoplasm contains two nuclei: large kidney shaped macronucleus in center and a small micronucleus in the concavity of the macronucleus Two contractile vacuoles: lie side by side or one above the other maintain the proper osmotic pressure inside cell Numerous food vacuole: contains food particles like debris from host gut, bacteria, starch grains, fat droplets and occasional RBCs, etc. where digestion of food particles takes place
  21. 21. TROPHOZOITE • Whole body covered with a row of tiny delicate cilia – organ of locomotion • Cilia present near the mouth part – longer called “adoral cilia” • Anterior end- narrow • Bears a groove (peristome) that leads to a mouth (cytostome) • followed by a short funnel shaped gullet (cytopharynx) extending up to one-third of the body • Posterior end- broad, round • Bears an excretory opening (cytopyge)
  22. 22. TROPHOZOITE
  23. 23. CYST • Shape: round • Size: 40-60 µm • Immobile and dominant • Surrounded by a thick transparent cyst wall allows the cysts to resist degradation in the acidic environment of the stomach and the basic environment of the small intestine • Contains two nuclei- macronucleus and micronucleus and vacuoles • Cilia- seen in younger cyst but is absorbed on maturity movement ceases
  24. 24. CYST
  25. 25. CYST
  26. 26. Risk factors • Pig’s faeces carrying vast volumes of Balantidium coli contaminates water sources • Humans who work with pigs exposed to Balantidium coli.
  27. 27. Clinical features Chronic disease • Have periods of increased bowel movements (mucous or rarely bloody) • Alternate periods of constipations • Organism load is less and requires repeated stool examination Complications • Seen in immunocompromised and malnourished people • Perforation of large intestine, involvement of appendix, peritonitis, severe dehydration leading to renal failure • Extra intestinal manifestations- rare: liver abscess, pleuritis and pneumonia
  28. 28. LABORATORY DIAGNOSIS • Stool examination-detects trophozoites and cysts • Histopathology • Culture • serology
  29. 29. • Media used: Boeck and Drbohlav egg serum media and Balamuth’s media • Culture rarely necessary as parasites are easily detected by stool microscopy or histopathology
  30. 30. Serology • scrapings of colonic and ceacal mucosa can be stained with H&E
  31. 31. TREATMENT • DOC: Tetracycline- 500 mg four times a day for 10 days • Alternatively Metronidazole- 750 mg three times a day for 5-7 days • Treatment of carriers- preventing spread of the disease. • No relapse or drug resistance reported
  32. 32. Acid fast Intestinal parasites - size Cyclospora – 40-50µm Isospora belli - 20-30 µm Cryptosporidium – 4-6µm
  33. 33. CRYPTOSPORIDIUM
  34. 34. Cryptosporidiosis Disease of birds, reptiles and fishes and also man Cryptosporidium parvum Acid fast - MZN
  35. 35. Transmission • Fecal-oral route • Fomites • Water – Drinking water (even after treatment) – Swimming pools • Unpasteurized Apple Cider • Animal contact • Food
  36. 36. Infectivity • C. parvum has a low ID50 (9-1000 oocysts) • Can be infected by just one oocyst • 10 billion oocysts per gram infected feces
  37. 37. Clinical Characteristics • Secretory diarrhea (some mucous, but no blood) • Slight fever, fatigue, myalgia • Oocysts may infect the lungs and trachea, resulting in cough • Dehydration and extreme weight loss in immunocompromised
  38. 38. Detection • Acid-fast stain of infected feces • Direct immunofluorescence antibody stain using monoclonal antibody to oocyst wall
  39. 39. Treatment • Nitazoxanide – Interferes with folate production • Immunocompetent – C. parvum will usually pass on its own • Immunocompromised – AIDS patients: treat with antiretrovirals and strengthen immune system, no cure – Others: would not benefit from antiretrovirals; keep hydrated
  40. 40. Prevention Water filtration – Filters must be <1 um to filter oocyst Swimming pools – Must be drained if infected fecal accident Pasteurization Hand washing – Particularly in daycares
  41. 41. ISOSPORA & CYCLOSPORA
  42. 42. Isospora
  43. 43. Oocysts
  44. 44. Laboratory Diagnosis – Fresh feces – Duodenal contents
  45. 45. Life Cycle
  46. 46. • An oocyst with one sporoblast is released in stool of infected person • After the oocyst has been released, the sporoblast matures further and divides into two • After the sporoblasts divide they create a cyst wall and become sporocysts • The sporocysts each divide twice, resulting in four sporozoites • Transmission occurs when these mature oocysts are ingested • The sporocysts excyst in the small intestine where sporozoites are released • The sporozoites then invade epithelial cells and schizogony is initiated • When the schizonts rupture, merozoites are released and continue to invade more epithelial cells • Trophozoites develop into schizonts, containing many merozoites • After about one week, development of male and female gametocytes begin in the merozoites • Fertilization results in the development of oocysts, which are released in the stool
  47. 47. Pathogenesis • Marked villous atrophy • Crypt hyperplasia in the small intestine
  48. 48. Treatment Bland diet Plenty of rest Combination of trimethoprim and sulfamethoxazole + Perimethamine and sulfadiazine
  49. 49. Prevention and Control • Proper personal hygiene • Adequate sanitation practices • Protected sex
  50. 50. CYCLOSPORA
  51. 51. What is Cyclospora? • Cyclospora cayetanensis is a parasite composed of one microscopic cell • When humans become exposed to this parasite, they become ill with an infection in the digestive tract and intestines called cyclosporiasis
  52. 52. What are the Symptoms of Cyclosporiasis? • Watery diarrhea • Frequent, sometimes 'explosive', bowel movements • Other symptoms may include: – weight loss – stomach cramps/pain – bloating – increased gas • fatigue
  53. 53. Cyclospora life cycle
  54. 54. Cyclospora cayatenesis
  55. 55. Cyclospora cayatenesis – Treatment: – Co-trimoxazole 160/800mg BD for 7 days
  56. 56. Take home message & Summary – Acid fast Intestinal parasites – Persistent diarrhoea – HIV/AIDS – Cryptosporidium spp., - Oocyst – Cyclospora spp., - Oocyst – Isospora spp., - Oocyst – Balantidium coli- Largest intestinal ciliated protozoan
  57. 57. Taenia infestations • Helminths • Parasitic worms • Multicellular • B/L symmetrical • elongated, flat or round animals
  58. 58. TAENIA SAGINATA
  59. 59. TAENIA SAGINATA • Taenia saginata, commonly known as the beef tapeworm, is a zoonotic tapeworm • It is an intestinal parasite in humans causing taeniasis and cysticercosis in cattle
  60. 60. TAENIA SAGINATA • Cattle are intermediate hosts for T. saginata • Humans are infected by eating cysticerci (larval form) in raw or undercooked beef • The larvae mature in about 2 months to adult worms that can live for several years • Adult T. saginata tapeworms are usually 4 to 12 meters in length, but can be as long as 25 meters • T. saginata infection occurs worldwide
  61. 61. HABITAT • Adult worms lives in the small intestine , commonly in Jejunum • Moves against the peristaltic movement
  62. 62. Basics • Complex two-host life cycle • Human beings are the only definitive host (small intestines - 2-4 meters long -800-1000 segments) • Both humans and pigs can act as intermediate hosts (larvae or cysticerci) • Most common in Latin America, Africa and India • 400,000 people have symptomatic neurocysticercosis in Latin America
  63. 63. Tapeworms They are flat in cross section Hermaprhoditic Live in the intestines with feces Life cycles are complex and can include multiple intermediate hosts No mouth, no digestive system They have suckers and teeth that grasp the host Behind a short neck are repeated parts of the worm, each containing reproductive structures with eggs and sperm, which can be released with the host's feces The pieces give the worm a ribbon-like structure, beneficial for absorbing nutrients from the intestine
  64. 64. Differences between T. solium and T. saginata
  65. 65. The scolex The scolex is the part of the worm that anchors it to the intestinal epithelium and prevents that the worm is passed with the digested food Taenia solium has similar muscular SUCKERS and a ROSTELLUM with rows of chitinous hooks Taenia saginata has four muscular SUCKERS
  66. 66. Scolex
  67. 67. Scolex of Diphyllobothrium latum.
  68. 68. Strobila • In most cestodes the scolex is tiny when compared to the strobila which makes up most of the actual “worm” • The strobila consists of a linear series of proglottids • Tape worms are hermaphrodites and each proglottid carries a set of female and male reproductive organs • These segments are released and are eliminated with the feces of the host
  69. 69. Strobila
  70. 70. Strobila
  71. 71. Egg • Spherical, brown in colour • 31-43µm in diameter • Surrounded by embryophore • Inside the emryophore is the hexacanth embryo(oncosphere) with three pairs of hooklets • Does not float on saturated salt solution • Infective only to cattles
  72. 72. Cysticercus cellulose • It is a semitransparent and elliptic bladder, like a white pomegranate seed, about 0.6-1cm. • There is fluid and a white scolex with 4 suckers and hooklets in the bladder
  73. 73. Cysticercus cellulose
  74. 74. Cysticercus cellulose in pork
  75. 75. Life cycle
  76. 76. Life cycle
  77. 77. Target tissue • Predilection for migration to eyes, CNS and striated muscles • CNS involvement is termed as Neurocysticercosis
  78. 78. Types of cysts • Cysticercus cellulosae Larva form of T. solium in host tissue Small (<2cm), round, thin walled Lodges in the parenchyma or the subarachnoid space Provokes only a minor inflammation Often remain silent
  79. 79. Cysticercus racemose • Large lobulated cysts with predilection for basal cisterns • Causes cysticercotic arachnoiditis and presents as meningitis • Causes obstruction of 4th ventricle and resultant raised ICP and hydrocephalus • Can cause occlusion of vessels and vasculits resulting in stroke • Causes intense inflammatory reaction and seizures
  80. 80. Mode of infection • Humans are both intermediate and definitive hosts. • Cysticercosis develops when humans become intermediate hosts by ingesting the embryonated eggs of the tapeworm, which release oncospheres that penetrate the intestinal wall, enter the bloodstream, and disseminate into the tissue
  81. 81. • HETEROINOCULATION eggs may come from the environment • INTERNAL AUTOINOCULATION regurgitated from proglottids into the stomach • EXTERNAL AUTOINOCULATION from the fingers of an infected person
  82. 82. Classification • Anatomical classification • Sotelo et al classification • Carpio et al classification • Chorobski Classification
  83. 83. Anatomical Classification • Parenchymal NC • Intraventricular NC • Meningeal NC • Spinal NC • Ocular NC
  84. 84. Parenchymal NC • Seizures • Headache, nausea and vomiting • Stroke • Frontal lobe involvement • Cerebellar Ataxia • Fulminant encephalitis in massive initial infection
  85. 85. CT image
  86. 86. Intraventricular NC • 5- 10% of all cases • 4th ventricle most common site for obstruction • Cysts in lateral ventricles less likely to cause obstruction • Hydrocephalus and acute, sub acute or intermittent signs of raised ICP without localizing signs
  87. 87. Meningeal NC • Meningeal irritation resembling TBM • Raised ICP from oedema, inflammation and presence of cyst obstructing flow of CSF
  88. 88. Spinal NC • Spinal cord compression • Nerve root pain • Transverse myelitis • Arachnoiditis
  89. 89. Ocular NC • Visual impairment (decreased visual acquity) • Scotoma, retinal detachment, iridocyclitis
  90. 90. Investigations • Stool Routine and Microscopy • Fundoscopy • Biopsy and histopathology • CT with contrast • MRI • Serology EITB sensitivity of 98% specificity of 100% ELISA in CSF sensitivity of 87% specificity of 95
  91. 91. Tuberculoma Versus Cysticercus Granuloma Cysticercus Granuloma •Round in shape •Cystic •20mm or less with ring enhancement or visible scolex •Cerebral edema not enough to produce midline shift or focal neurological deficit
  92. 92. Tuberculoma • Irregular in shape • Solid • Greater than 20mm • Associated with severe perifocal edema and focal neurological deficit
  93. 93. Natural course • Rate of spontaneous resolution of a solitary cysticercus granuloma in patients with seizures • 3 months - 18.8% • 6 months - 36.4% • 1 year - 62.5%
  94. 94. Treatment • Antiepileptic therapy • corticosteroids (dexamethasone) • albendazole (15 mg/kg per day for 8–28 days) or praziquantel (50–100 mg/kg daily in three divided doses for 15–30 days)
  95. 95. Steroids • Corticosteroids represent the primary form of therapy for cysticercal encephalitis and arachnoiditis causing hydrocephalus and progressive entrapment of cranial nerves • High doses of iv Dexamethasone can be followed by oral therapy with Prednisolone 1mg/kg/day or Dexamethasone 0.1mg/kg/day administered 3 times a week
  96. 96. • Glucocorticoids induce first-pass metabolism of praziquantel and may decrease its antiparasitic effect • Cimetidine should be co-administered to inhibit praziquantel metabolism • For this reason albendazole is preferred
  97. 97. Surgery restricted to • Placement of ventriculo-peritoneal shunts for hydrocephalus • Excision of single big cysts causing mass effect • Endoscopical excision of intra ventricular parasites
  98. 98. • Proglottids morphlogy and structure are used to differentiate between the two type of taenia • Scolex structure can also be used
  99. 99. Treatment of T. saginata • Single dose of praziquentel 10mg/kg is highly effective • Niclosamide single 2gm single dose is also effective
  100. 100. Prophylaxis • Inspection of all beef / pork for cysticerci • Thorough cooking • Proper disposal of faeces • Infected people should be treated to break parasitic life cycle
  101. 101. Treatment of T.solium • Praziquentel 10mg/kg single dose is the drug of choice • Niclosamide single 2gm single • Vomiting should be avoided to prevent cysticercosis • Puragtives may be given 1-2 hr after antihelminthic treatment • Instructed for carefull washing of both hands after defecation
  102. 102. Trichuris trichiura
  103. 103. Chronic Trichuriasis are often marked bY • Frequent blood-streaked diarrheal stools • Abdominal pain and tenderness • Nausea • Vomiting • Anemia • Weight loss
  104. 104. • The worms has thin anterior and thick posterior part • They attach to intestinal mucosa by embedding their anterior part. • They feed on tissue fluid (not blood)
  105. 105. Geographical distribution • Worldwide distribution • It is more common in Asia • Less in Africa and South America • Rare in the United states
  106. 106. How man become infected? • Infection to man is by ingestion of the infective eggs (contain larva) that may be in contaminated food or drink, hands with soil • The larva hatch in the human small intestine then migrate to large intestine • They attach to mucosa of the large intestine. • Then develop into mature worms with in three months • After mating female produce 2,000–10,000 single-celled eggs per day • which come out with feces. • Worms can live up to five years
  107. 107. Life cycle
  108. 108. Eggs of Trichuris trichiura • Shape: oval (barrel- shaped) has polar hyaline mucoid blugs • Size: 60 x40 µm • Color: honey brown • Shell: Thick • Contents: Mass of granules (Unembryonated)
  109. 109. Development of T. trichura eggs Eggs are single celled when passed with human feces The develop into 2 cell, 4 cell, morula, egg contain larva (in soil ) 3-Thelarvated egg (infective to human) The development of infective eggs in soil takes about 2-3weeks
  110. 110. Complications • Colonic obstruction because of the tangle of worms • Ulceration of large intestine which result in blood loss. • Iron deficiency anemia • Rectal prolapse
  111. 111. Rectal prolapse
  112. 112. Laboratory Diagnosis • T. trichuria worm inhabit human large intestine • The female produces large number of eggs 2,000–10,000 per day • The worms are not found stool because they attach to the mucosa of large intestine
  113. 113. • Stool sample is suitable for the diagnosis. suitable diagnostic technique: • A- direct wet examination for feces (heavy infection) • B-Concentration by sedimentation or by floatation to detect (very light infection) • Diagnostic stages: eggs
  114. 114. Quality control C. Philippensis egg T.trichiura egg
  115. 115. Treatment Several anthelmintics drugs of choice: • Albindazole • Mebendozle
  116. 116. Prevention & control • Prevent contamination of soil with human feces • Construction of latrines • Washing hands before eating (children, soil worker) • Washing vegetables & fruits • Do not use the night soil as fertilizer
  117. 117. • Contraindication for albendazole is pregnancy • Contraindication for mebendazole are hypersensitivity and early pregnancy

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