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GIARDIASIS

Dr. Stéfano Gonçalves Jorge CRM-SP 88.173 Dr. Ademar Yamanaka Publicado em: Yamanaka, A., Jorge, S.G., Soares, E.C., Almeida, J.R.S., Mesquita, M.A., Zeitune, J.M.R., Sakamoto, T, Tanaka, M.: Giardiasis. Endoscopia Digestiva (Japão) 11(3): 469-71, 1999 HISTORY    Giardia lamblia is the most commom protozoan isolated from the gastrointestinal tract in humans. It was first observed and  described in 1681, by Anton Van Leeuwenhoek1, being the first intestinal protozoa identified. In 1859, Vilem Lambl published the  first drawings of the trophozoite and the cyst forms of the parasite. Being so commom in the gastrointestinal tract, with ou  without diarrhea, the discussion about the true nature of the parasite last for decades: “Is it a enteropathogen or a simple  comensal ?” Finally, some studies demonstrating the development of diarrhea in humans and animals after the exposion to  Giardia cleared the question2. It is now considered a true enteropathogen by the World Health Organization3.  MICROBIOLOGY    There are three species of Giardia: agilis (amphibians), muris (rodents, birds and reptiles) and intestinalis (mammals, birds  and reptiles)4. The name Giardia lamblia is not correct, but its use is universaly accept among health care workers. Giardia is a  flagellated protozoa whose life cicle can be divided in two stages: a motile and multiplying form, the trophozoite and the  resistent form, the cyst. The cyst can survive in water and food, and is relatively resistant to chlorination procedures5, difficulting  erradication and prevention of the disease. In fact, the cysts were detected in 81% of raw water6 and in 17% of filtered water7   samples.    Giardiasis occurs after ingestion of contaminated water or food, or by person-to-person transmission. Only 10 to 100 cysts are  necessary8. When ingested, the cyst passes through the acid environment of the stomach, which triggers excystation. Into the  proximal intestine, after exposure to pancreatic secretions, the excystation begins. Usually two trophozoites emerges from each  cyst.    The trophozoite has four flagella simmetrically placed and a concave ventral surface that contains the atachment organelle,  called the ventral disk. After excystation, the trophozoites moves close to the epitelium, generally in the proximal intestine, often  deep in the crypts. It multiplies by binary fission, depending of nutrients. The exposion to high concentrations of bile salts can  promote encystation. The cysts are eliminated with feces, contaminates water or food and can be ingested for another  individual. Those cysts may be ingested by domestic and wild animals, which are considered reservoir of human infection9.  EPIDEMIOLOGY    Giardiasis occurs worldwide. Its prevalence rises in developing contries , especially in children10. It can reach from 20% to  30% in the developing world, and from 2% to 5% in the industrialized countries9. Groups at high risk of giardiasis are: children  and infants (especially those at day care facilities11-12), homosexuals13-15, institutionalized individuals, campers16, travelers17 and immunocompromised18 (common variable immunodeficiency is the most commonly reported). PATHOLOGY    Giardia is found predominantly in the proximal small intestine, but can be found in stomach19, terminal ileum, colon20 and  gallbladder21. There are several hypothesis about the pathogenesis of chronic diarrhea in giardiasis. It is accepted that diarrhea  occurs by the colnization and multiplication of the trophozoites in the lumen of small intestine. Despite it, the very majority of  individual infected is asymptomatic. It can be explained by host factors, parasite load and variable virulence of specific Giardia   isolates9, 22.    The light microscopic features of giardiasis in the proximal small intestine are commonly mild to moderate parcial villous  atrophy, with a mild to moderate increase in crypt depth8. It can be found increase in inflamatory cells in the lamina propria and  in the epithelium, shortening and disruption of microvilli and lymphangiectasia23. The histological changes observed in giardiasis  are, in fact, inespecific24.    The gastric giardiasis is strongly correllated with chronic atrophic gastritis, often showing intestinal metaplasia and H. pylori   infection19, 34. It is believed that a decrease in gastric acidity is essential for the colonization of Giardia into the stomach. SYMPTOMS The incubation period for acute giardiasis is between 1 to 2 weeks. Diarrhea occurs in more than 90% of individuals17, 25. It usually begins with abdominal discomfort, nausea, anorexia and flatulence. Those are followed by explosive and watery  diarrhea, with abdominal cramps. Usually, is self-limited within 2 to 4 weeks.   The cronic giardiasis can present with diarrhea, loose stools, constipation, fatigue, weight loss, eructation, bloatedness,  flatulence, nausea, vomiting and epigastric pain26. It can mimic a inflamatory bowel disease27. There is no evidence of a role of  giardiasis in nonulcer dyspepsia28. The nutrition insufficiency is the major complication of giardiasis. In adults, it produces minor consequences, with  symptoms that can completely revert with treatment. In children, however, the nutricional insuficiency can produce growth and  development impairment.  DIAGNOSIS    The search for trophozoites and cysts of Giardia in fresh stool is still the most used method. As the trophozoites can survive  only for a brief period in feces, he is only found in examinations of fresh stool from watery diarrheas. For a more sensitive  screening, it is necessary five or six stools, because cyst excretion varies in intensity day to day29. Trophozoites can be identified by endoscopic brush biopsy of the proximal small intestine30 or by histopathologic samples. Those can also be detected in duodenal juice.   The enzyme immunoassay for copro-antigen detection reveals to be almost as sensitive as microscopy of stool31, and can become less expensive32. However, the complaints of a patient with giardiasis are usually inespecific. The direct examination of  stools can provide not only the diagnosis of giardiasis – it can demonstrate the presence or not of other parasites.   DNA-based detection methods of Giardia in stools has some difficulties due the large amount of other DNA and inibitory  substances, as the difficult of lysing cysts. The results shows sensitivity and specificity below the microscopic detection33. TREATMENT    Three major classes of drugs are used for giardiasis: nitroimidazole derivatives, acridine dyes such as mepacrine and  nitrofurans such as furazolidone. Metronidazole and tinidazole are the drugs of Choice because the short treatmente period. In  treatment failures, a second-line drug may be required9.  PREVENTION There are several reasons why giardiasis will never erradicate. Giardia is widely distributed through mammals and others,  the cysts can survive even in the absence of animals resevoir and the vast majority of humans infected are asymptomatic. All  efforts in prevent giardiasis must focus on hygiene education, detection of parasites in drinking water and a search for a  vaccine. As the most parasitary infections, the most profound symptom of the disease is felt in the development countries:  children without access to clean water and education, who can not grow or develop as they could.  REFERENCES 1.      Dobell CA: The discovery of intestinal protozoa in man. Proc R Soc Med 13:1-15, 1920; 2.      Fantham HB, Porter A: The pathogenicity of Giardia ( lamblia ) intestinalis to men and to experimental animals. BMJ 2:139-141, 1916; 3.      WHO Expert Committee. Intestinal protozoan and helmintic infections. WHO Technical Report Series 666. Geneva: World Health Organization, 1981; 4.      Bingham AK, Meyer EA: Giardia excystation can be induced in vitro in acid solutions. Nature 277:301-302, 1979; 5.      Filice FP. Studies on the citology and life history of a Giardia from the laboratory rat. Univ Calif Publ Zool, 57:53-146, 1952; 6.      LeChevallier MW, Norton WD, Lee RG: Ocurrence of Giardia and Cryptosporidium spp. in surface water supplies. Appl Environ Microbiol 57:2610-2616,  1991; 7.      LeChevallier MW, Norton WD, Lee RG: Giardia and Cryptosporidium spp. in filtered drinking water supplies. Appl Environ Microbiol 57:2617-2621, 1991; 8.      Rendtorff RC. The experimental transmission of human intestinal protozoan parasites: II. Giardia lamblia cysts given in capsules. Am J Hyg 59:209-220,  1954; 9.      Farthing MJG. Giardiasis. Gastroenterol Clin North Am, 25:3, 493-515, 1996;   10.  Bryan RT, Pinner RW, Belkerman RL. Emerging infectious diseases in the United States. Ann N Y Acad Sci 740:346-361, 1994; 11.  Keystone JS, Krajden S, Warren MR. Person-to-person transmission of Giardia lamblia in day-care nurseries. Can Med Assoc J 119:241-248, 1978;   12.  Black RE, Dykes AC, Sinclair SP, Wells JG. Giardiasis in day-care centers: evidence of person-to-person transmission. Pediatrics 60:486-491, 1977;   13.  Laughon BE, Druckman DA, Vernon A, et al. Prevalence of enteric pathogens in homosexual men with and without acquired immunodeficiency syndrome. Gastroenterology 94:984-993, 1988; 14.  Schmerin MJ, Jones TC, Klein H. Giardiasis: association with homosexuality Ann Intern Med 88:801-803, 1978; 15.  Phillips SC, Mildvan D, William DC, et al: Sexual transmission of enteric protozoa and helminths in a venereal disease clinic population. N Engl J Med  305:603-606, 1981; 16.  Barbour AG, Nichols CR, Fukushima T. Na outbreak of giardiasis in a group of campers. Am J Trop Med Hyg 25:384-389, 1976;   17.  Brodsky RE, Spencer HC Jr, Schultz MG. Giardiasis in american travelers to the Soviet Union J Infect Dis 130:319-323, 1974;   18.  Nagura H, Kohler PF, Brown WR. Immunocytochemical characterization of the lymphocites in nodular lymphoid hyperplasia of the Bowel Lab Invest 40:1  66-73, 1979; 19.  Doglioni C, De Boni M, Cielo R, et al. Gastric Giardiasis J Clin Pathol 45:964-967, 1992; 20.  Howard LH, Fink DS, Lubin J, et al. Giardiasis diagnosed by biopsy of the colon and terminal ileum: Unusual sites for a common pathogen Am J  Gastroenterol 90:1011-1013, 1995; 21.  Goldstein F, Thornton JJ, Szydlowski T. Billiary tract dysfunction in giardiasis Am J Dig Dis 23:559-560, 1978; 22.  Nash TE, Herrington DA, Losonsky GA, Levine MM. Experimental human infections with Giardia lamblia J Infec Dis 156:6 974-984, 1987; 23.  Oksüzoğlu G, Aygencel SG, Haznedaroğlu IC, et al. Am J Gastroenterol 91:2 409-410, 1996; 24.  Oberhuber G, Stolte M. Giardiasis: analysis of histological changes in biopsy specimens of 80 patients J Clin Pathol 43:641-643, 1990; 25.  Moore GT, Cross WM, McGuire D, et al. Epidemic giardiasis at a ski resort N Engl J Med 281:402-407, 1969;   26.  Chester AC, MacMurray FG, Restifo MD, Mann O. Giardiasis as a chronic disease. Dig Dis Sci 30(3):215-218, 1985;   27.  Gunasekaran TS, Hassall E. Giardiasis mimicking inflamatory bowel disease J Pediatr 120:424-426, 1992;   28.  Carr MF Jr, Ma J, Green PHR. Giardia lamblia in patients undergoing endoscopy: lack of evidence for a role in nonulcer dyspepsia Gastroenterology  95:972-974, 1988; 29.  Goka AKJ, Rolston DDK, Mathan VI, et al. The relative merits of faecal and duodenal juice microscopy in the diagnosis of giardiasis Trans R Soc Trop  Med Hyg 84:66-67, 1990; 30.  Bendig DW. Diagnosis of giardiasis in infants and children by endoscopic brush cytology J Pediatr Gastroenterol Nutr 8:204-206, 1989;   31.  Mank TG, Zaat JOM, Deelder JTM, et al. Sensitivity of microscopy versus enzyme immunoassay in the laboratory diagnosis of giardiasis Eur J Clin  Microbiol Infect Dis 16:615-619, 1997; 32.  Marshall MM, Naumovitz D, Ortega Y, Sterling CR. Waterborne protozoan pathogens Clin Microbiol Rev 10:67-85, 1997; 33.  Weiss JB. DNA probes and PCR for diagnosis of parasitic infections Clin Microbiol Rev 8:113-130, 1995;   34.  Muñoz E, Carmona T, Chaves F, et al. Identification of Giardia lamblia by gastric brush cytology Acta Cytol 40:1331-1332, 1996;