Giardia lamblia is an intestinal parasite with two stages - the trophozoite stage which inhabits the small intestine, and the cyst stage which is excreted and can contaminate water and food. It causes giardiasis through the fecal-oral route. Symptoms include diarrhea, abdominal pain and cramps. Diagnosis involves examining stool samples microscopically for trophozoites or cysts. Treatment typically involves metronidazole antibiotics for 5-10 days to eradicate the parasite in over 85% of cases. Prevention focuses on proper hygiene and water treatment to avoid contamination.
2. INTRODUCTION Protozoan parasite Worldwide distribution Giardia lamblia is a single-celled, bi-nucleated intestinal parasite Has trophozoite and cyst phases Lives in duodenum and jejunum Typically found in lakes, streams, or ponds that have been contaminated by human and other animals It causes giardiasis
5. BODY Bilaterally symmetrical AXOSTYLES Two in numbers, seen in midline as vertical lines NUCLEI Two, one on each side of body
6. FLAGELLAE 8 flagellae (2 anterior, 2 posterior, 2 ventral, and 2 caudal) - all arise from kinetosome SUCKING DISCS 2, Circular in shape Situated on ventral surface
7. Cyst SHAPE Oval or ellipsoid SIZE Length 12um Width 8um NUCLEI Two nuclei in immature cyst Four nuclei in mature cyst FLAGELLAE AND SUCKING DISCS May be seen in cytoplasm Mature cyst
8. LIFE CYCLE of Giardia lamblia Trophozoites Trophozoites Cysts Mature Cysts Duodenum, upper ileum, gall bladder The lower portion of ileum or colon Contaminated water and food Stool Multiplied by binary fission Diarrhea Outside Outside
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10. HABITAT AND TRANSMISSION Trophozoites Colonizes in the intestines of mammals, birds, reptiles and amphibians Definitive host is human intestine Duodenum and Jejunum Cyst Contaminated material Human colon Sigmoid colon TRANSMISSION Via fecal-oral route As few as 10 cysts can cause disease and up to 900 million cysts can be released by an infected individual in one day
11. Trophozoites are attached to the mucosal surface by sucker, reproduced by binary fission Diarrhea, abdominal pain, bloating, nausea, and vomiting Mechanical blockage of the intestinal mucosa, competition for nutrients, inflammation Histology: shortening of microvilli, elongation of crypts, and damaging the brush border of the absorptive cells G. lamblia inhabits the duodenum, jejunum and upper ileum PATHOGENESIS
12. PATHOGENESIS AND PATHOLOGY Fat/CHO digestion decreases and causes malabsorption and maldigestion Absorption decreases due to villus blunting causing malabsorption Malabsorption and maldigestion causes diarrhea Physical damage: clubbing of villi; decreases villus-to-crypt ratio; brush borders of cells are irregular
13. Feeds on mucous that forms in response to irritation Also absorbs vitamins and amino acids Giardia can also interfere with vitamin/nutrient absorption Vitamin A vision Vitamin D Rickets Both of these are due to long standing infections
14. CLINICAL FEATURES Incubation is 1- 2 weeks Onset is gradual Symptoms are nausea, vomiting, diarrhea, dehydration, malaise, flatulence, bloating, cramping, low grade fever and steatorrhea Sequelae are malabsorption, lactase deficiency, weight loss, fatigue, depression and rarely reactive arthritis
15. DIAGNOSIS PATHOLOGICAL EXAMINATION Fecal examination Water-like feces Trophozoites Formed feces Cysts Duodenal fluid or bile examination String test Trophozoites
17. TREATMENT The most common treatment for giardiasis is Metronidazole (Flagyl) for 5-10 days It eradicates Giardia in more than 85% of cases Furazolidone (Furoxone) for 7-10 days Quinacrine is also very effective for treating giardiasis Combination therapy also may be effective Quinacrine and Metronidazole Tinidazole, Secnidazole and Albendazole
18. PREVENTION Avoid water and food that might be contaminated Boil water before drinking, even after filtration Do not brush teeth with tap water that may be contaminated Do not use ice or drink beverages made from tap water Wash hands before eating food
22. CLASSIFICATION Superclass Rhizopoda Subphylum Sarcodina Family Entamoebidae Order Amoebida Class Labosea Species Entamoeba
23. SPECIES Entamoeba histolytica Pathogenic Entamoeba dispar Non pathogenic group E. hartmanni E. polecki E. coli E. gingivalis
24. MORPHOLOGY TROPHOZOITES Size 20-40 µm Nucleus Single (4-7 µm) Cytoplasm Ingested red cells Rich in glycogen Chromatoid bodies Locomotion Rapid, gliding, explosive with single pseudopodium
25. MORPHOLOGY CYSTS Shape Spherical Size 10-16 µm Nuclei Four Glycogen vacuole Chromatoid bodies Killed by desiccation or boiling
26. EPIDEMIOLOGY Geographic distribution is worldwide Second to malaria as cause of death due to parasitic protozoa Transmission is Fecal-Oral Hosts are humans, cats, dogs and rats ~10% world population infected Prevalence in tropical countries is >30%
27. 10% of infected persons develop invasive disease 40,000-100,000 deaths annually High prevalence in low socio-economic status, overcrowding, poor personal hygiene, no indoor plumbing, immigrants from endemic areas, mentally retarded, promiscuous male homosexuals Increased severity in children especially neonates, pregnancy and post-partum states, corticosteroid use, malignancy, malnutrition
28. LIFE CYCLE CYST Ingestion by humans Excystation in small intestine Encystation in colon Excretion in faeces TROPHOZOITE Asymptomatic colonization Amoebic colitis Liver abscess
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30. VIRULENCE FACTORS GIAP Adherence Amebapore Cytolytic Proteases Necrosis Resistance to complement mediated lysis Trophozoites in liver abscess and colonic lesions are resistant
32. HOST IMMUNITY High titers of anti-amoebic antibodies occur by 7th day of illness Serum of patients with high titers of anti-amoebic antibodies causes lysis of trophozoites Recurrence does not occur after liver abscess and colitis Amoebas recovered from liver abscess and colonic lesions are resistant to complement mediated lesions
39. MICROSCOPY Multiple samples are required Saline preparation has very low yield Endoscopic biopsy/ulcer edge scrapings has high yield Stool for hematophagous amoebas/Nuclear morphology Trichrome stain Iron Hematoxylin stain Concentration techniques (Formal-acetate) Iodine staining for cysts
40. CULTURE Sensitive but time consuming Multiple samples are not required NNN medium Does not differentiate between E. histolytica and E. dispar Helpful in asymptomatic or chronic infections with low levels of cyst passage Useful to evaluate efficacy of cure or existence of infection when the presence or absence of antibodies is not definitive
41. SEROLOGY Anti-amoebic Antibodies (IgG and IgM) Develop only in E. histolytica infections High levels occur in 80% acute cases and 90% convalescent cases Titers remain high for years, not useful in endemic areas ELISA stool antigen Rapid and simple High sensitivity and specificity Can distinguish between E. histolytica and E. dispar ELISA serum antigen IHA Useful in liver abscess and colitis
42. MOLECULAR DIAGNOSIS PCR High sensitivity and specificity Can also detect trophozoites by detecting rRNA genes
44. TREATMENT E. dispar carriage does not require treatment Asymptomatic E. histolytica carriage should be treated Intraluminal Infection Diloxanide furoate 500mg TDS for 10 days Paromomycin Iodoquinol Symptomatic Amoebiasis Metronidazole 750mg TDS for 5-10 days Tinidazole, Secnidazole and Albendazole
45. Extra-intestinal Amoebiasis Metronidazole + Paromomycin/Diloxanide furoate + Emetine Needle Aspiration For large abscess Open Surgical Drainage If needle aspiration is not possible Perforation/Peritonitis Anti-protozoal drugs + Antibacterial drugs + Peritoneal drainage
46. PREVENTION Adequate water purification Low levels of chlorine does not kill cysts Boiling of drinking water Treating vegetables and fruits with strong detergent soap and then soaking in acetic acid for 5-10 minutes Proper waste disposal Immunization Under trial