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Leo, M., Haque, R., Kabir, M., Roy, S., Lahlou, R.M., Mondal, D., Tannich, E. and Petri, W.A., 2006. Evaluation of Entamoeba histolytica antigen and antibody point-of-care tests for the rapid diagnosis of amebiasis. Journal of clinical microbiology, 44(12), pp.4569-4571.

(A) Scolex of D. latum from a dog from Russia (scanning electron microscopy photomicrograph). (B) Scolex of D. nihonkaiense from a brown bear from Kamchatka, Russia. (C) Segment of D. pacificum from a man from Lima, Peru. Abbreviations: cs, cirrus sac; ov, ovary; t, testes; u, uterus; up, uterine pore; v, vitellaria.

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In the first part of the study, physicians, veterinarians, and medical laboratories were invited to collect samples of Diphyllobothrium diagnosed in their routine practice. After standard morphological identification, they were asked to preserve a part of fresh stool samples containing eggs, as well as tapeworm segments, in 96% ethanol for further investigations. When possible, a questionnaire reporting clinical data, type of fish eaten, and cooking habits was completed for each patient. In the successive phase, parasites were analyzed using molecular techniques. The partial nucleotide sequence of the cytochrome c oxidase subunit I (cox1 or COI) gene was obtained and compared with reference sequences available in GenBank. The survey allowed us to identify three cases caused by exotic species of Diphyllobothrium locally acquired from imported fish (166, 167). According to anamnestic data, the other patients were infected with D. latum acquired mainly from perch fished in local lakes.

Samples to be identified with molecular techniques (eggs, larval stages, and adult parasites) should be preserved in pure ethanol, whereas DNA extraction from native fecal samples should be performed immediately. Fixatives containing formalin, widely used for the storage of clinical samples, as well as denatured alcohol should be avoided because they damage DNA. It is possible, in some cases, to amplify short DNA regions from parasites already fixed in such solutions (20, 89).

Prolonged or heavy D. latum infection may cause megaloblastic anemia due to a parasite-mediated dissociation of the vitamin B12-intrinsic factor complex within the gut lumen, making B12 unavailable to the host (162). Approximately 80% of the B12 intake is absorbed by the worm, with a differential absorption rate of 100:1 in relation to the absorption by the host. About 40% of D. latum-infected individuals may show low B12 levels, but only 2% or less develop clinical anemia, which is hyperchromic and macrocytic and may be associated with low platelets or low white blood cell counts. Severity of the disease is known to be directly associated with worm burden and by-products produced by tapeworms (60). This deficiency may produce damage to the nervous system, including peripheral neuropathy or central nervous system degenerative lesions. Diphyllobothrium-associated pernicious anemia is rarely reported nowadays (43), and anemia is also rare or nonexistent in the small D. pacificum tapeworm. After successful treatment, B12 levels come back to normal ranges in a period of several months.

The species-specific identification of clinical samples is not essential for the effective treatment of most human infections by Diphyllobothrium. However, it is important from an epidemiological perspective, because there is an urgent need to detect the most important sources of plerocercoids, in particular those of D. pacificum and other marine taxa transmitted by yet-unknown sea fish. Molecular methods have been proven to be a powerful tool for the specific identification of causative agents of human disease, but a fast, cheap, and simple molecular-based diagnostic method for the routine laboratory evaluation of clinical samples is still unavailable.

We are indebted to numerous persons who kindly provided valuable information as well as those who sent clinical samples of tapeworms for molecular evaluation. Special thanks are due to Manuel Tantaleán, Universidad Peruana de Cayetano Heredia, Lima, Peru, for providing valuable information on D. pacificum and Andrea Gustinelli, University of Bologna, Bologna, Italy, for material. Helpful suggestions and critical remarks of anonymous reviewers are also greatly appreciated.

Dogs from 15 locations having previously reported a high prevalence of heartworm infection were included in the survey according to defined criteria, including the absence of treatment with a macrocyclic lactone for at least 1 year. Blood samples from 1531 dogs were evaluated by an in-clinic immunochromatography test kit (Witness Heartworm, Zoetis, USA) for detection of Dirofilaria immitis antigen. At each location, epidemiologic data, including physical characteristics and clinical signs reported by owners or observed by veterinarians, were recorded on prepared forms for tabulation of results by location, clinical signs, and physical characteristics.

The damage promoted over time to pulmonary arteries, right ventricle, and to all vascular structures near the lungs by the adult worms often leads to severe disease [14], generally recognized by clinical signs, such as coughing, dyspnea, and exercise intolerance [15],[16]. Although the disease is well known in the literature, many times it is difficult to be identified by owners and veterinarians; thus, infected dogs may not receive prompt treatment for heartworm infection. Therefore, there is an urgent need to convince small animal practitioners to include heartworm testing as a routine examination for their dogs even when owners report the absence of any clinical signs that could suggest D. immitis infection.

Overall, presence of clinical signs reported by owners was not predictive of positive tests results for D. immitis (Table 3). However, when associating clinical signs with age or size, without regard for the test result, some correlation could be detected (Table 3): Age was correlated with frequency of coughing (χ2 = 52.2; df = 3; P < 0.001), exercise intolerance (χ2 = 60.5; df = 3; P < 0.001), and weight loss (χ2 = 33.3; df = 3; P < 0.001). Size of the animals was predictive of the presence of coughing (χ2 = 8.33; df = 3; P = 0.040) and weight loss (χ2 = 10.1; df = 3; P = 0.018); however, it was not predictive of exercise intolerance.

Independent of D. immitis antigen test results, testing of various characteristic variables against the reported clinical signs reported by owners indicated that older dogs presented a higher prevalence of exercise intolerance, cough, and weight loss than younger dogs. With regard to size, smaller dogs were more inclined to have a cough and lose weight more frequently, possibly due to heart or respiratory diseases associated with other etiologies [38],[39].

Giardia lamblia colonises the lumen of the upper small intestine of vertebrates4. Its life cycle includes environmentally resistant cysts and proliferating trophozoites, which attach to the gut surface and cause the clinical manifestations of giardiasis4. Unlike other protozoan parasites, AV in Giardia was discovered as a phenomenon occurring in vitro5 (i.e., in the absence of any immune pressure) before being found to occur during animal infections6, suggesting that spontaneous antigenic switching is an inherent characteristic of this parasite7.

Updated: 31 October 2001
E-mail: Steve J. Upton Division of Biology, Kansas State University, Manhattan, KS 66506
Main menu: CryptosporidiumhomepageHistory: The first published report ofCyclospora cayetanensis in humansappearsto be by Ashford (1979), who found unidentified Isospora-like coccidia in the fecesof 3individuals in Papua, New Guinea. At least the photomicrographs in the paper reveal an organism morphologically identical to that we see now. Later, Narango et al. (1989) reported what may be the same organism fromseveral Peruvians with chronic diarrhea and termed the organismCryptosporidium muris-like. Other investigators thought the unsporulated oocysts appeared more similartocyanobacteria, and the name "cyanobacterium-like body" or CLB became prevalent in theliterature (occasionally, authors also used the term "coccidian-likebody" for CLB). Eventually, Ortega et al. (1992) published an abstract reporting that they had sporulatedand excysted the oocysts, resulting in placement of the parasite in the genusCyclospora. They also created the name Cyclospora cayetanensis at this time. However, sincenomorphologic information was presented in the abstract, C. cayetanensis technically becamea nomen nudum (a named species without a description). Although Ortega et al.(1993)later published additional details about this coccidian, it wasn't until 1994 that a completemorphologic description was published to validate the name (Ortega et al., 1994). Thus, the correct name for this parasite is Cyclospora cayetanensis Ortega, Gilman, & Sterling, 1994, and the etymology of the nomen triviale is derived from Cayetano Heredia University in Lima, Peru. Duringthis 2-year period when C. cayetanensis was a nomen nudum, anyonewishing to publisha complete morphologic description and change the name would have been free to do so. But, we are now doomed forever in our struggle to spell and pronounce "cayetanensis."Life-cycle and basic biology: The life-cycleof Cyclospora cayetanensis begins,like all enteric coccidia, with ingestion of a sporulated "oocyst" (the environmentally resistent cyst stage). This sporulated oocyst contains 2 "sporocysts" (smaller cysts within the oocyst), each enclosing 2 "sporozoites" (the infective stages; each oocyst contains a total of 4 sporozoites). Once inside the gut, these sporozoites exit from the sporocysts and oocyst, eventually penetrating epithelial cellsalong the small intestine. The preferred site is the jejunum. Sporozoites undergo multiple fission inside cells to form "meronts,"which contain numerous "merozoites." Ortega et al. (1997a) has described two asexual generations: the first having 8-12 merozoites and thesecond as having 4 merozoites. The finalgeneration of merozoites penetrate new cells to formgametes, which can also be found in the jejunum. Most gametes simply enlarge to form the female gamete, or "macrogamete." Somebecome "microgametocytes," which undergo multiple fission to form numerous flagellatedsperm-like "microgametes." Mature microgametes exit the microgametocyte, fertilize themacrogametes, and a resistent oocyst wall is layed down around the zygote. In time, theunsporulated oocyst is sloughed from the intestinal wall along with the host cell and passesintothe external environment with the feces. Further development of sporocysts and sporozoitesistermed "sporogony" or "sporulation" and occurs only in the presence of the higheratmosphericoxygen concentrations. Sporulation is complete in 7-12 days at a "warm" room temperature, for instance at 30 C. Hosts: Humans may be the only true hostsfor this coccidian. Although the parasite has been reportedfrom chimpanzees, Pan troglodytes from Uganda (Ashford et al.,1993), and baboons and chimpanzees from Tanzania (Smith et al.,1996), these may actually represent one or more morphologicallysimilar species. Eberhard et al. (1999,Emerg. Inf. Dis. 5: 651-658) described 3 new species from primates although both the morphologic and molecular data suggested little difference between the three and with that found in humans. Nonetheless,a more recent follow up study suggests that oocysts derived from humans may not be infectious to non-human primates (although no positive controls, humans, could be used in the study) (Eberhard et al. 2000). There arealsoreports of the parasite in dogs (Yai etal. 1997) and poultry (Garcia-Lopez et al. 1996; Sherchand et al. 1999),but it is likely that the former is either Hammondia heydorni orNeospora caninum and the latter either Eimeria mitis or apseudoparasite. Diagnosis: Oocysts of Cyclospora arespherical, measure 9.0 micrometers in diameter, and are passed in thefeces unsporulated. They are passed in low tomoderate numbers, and are easily recognized using conventional microscopy(tryhere). Fluorescent microscopy employing a filter with a wavelength inthe range of 340-380 nm reveals the oocysts to glow a bright, pale blue.Clinical signs and pathogenesis: Individualsinfected with Cyclospora mayexperience prolonged watery diarrhea, abdominal cramping, weight loss, anorexia, myalgia, and occasionally vomiting and/or fever. Symptoms generally begin approximately 1 week (5-8 days) after ingestionof oocysts and these may persist for a month or more. The small intestine becomes inflammed, and theparasite causes mucosal changes that include villous atropy and crypt hyperplasia. Mild infections may produce few or no clinical signs. Epidemiology: With the exception of someoutbreaks, the overall prevalence ofCyclospora in North America appears to be farless than 1%. Outbreaks seem to occur most frequently in late spring and summer, and these warmer temperatures are clearly needed to get oocysts to sporulate with any rapidity. In addition, this time of year correlates with increased import of fruits and vegetables into the US from our more southern neighbors. Individuals becomeinfected when they ingest contaminated food or water containing viable, sporulated oocysts. Because so many of the foods we consume are shipped over long distances and involvecontact bymany individuals, transportation of pathogens such as Cyclospora between statesandcountries has become unavoidable. However, the odds of becoming infected withCyclospora, and many other foodborne pathogens, can be greatly diminished bysimplywashing fruits and vegetables well prior to consumption. However,it should be noted that simply washing foods does not removed 100% of theoocysts (see Ortega et al., 1997b). Treatment: Some success has been achievedtreating patients with co-trimoxazole(160mg trimethoprim, 800 mg sulfamethoxazole) twice daily for 7 days. Children should receive trimethoprim at 5 mg/kg body weight plus sulfamethoxazole at 25 mg/kg body weight twice a day for 7 days. For morespecific information on treatment, see the papers below marked with anasterisk (*). Other: An informal survey by the AmericanSociety of Parasitologists a few years ago found that the averagephysician in medical school now receives only about 6 total hours of parasitologic training during medical school. Considering that over 400 different species of parasites are known to infect humans (see Ashford andCrewe, 1998, The parasites of Homo sapiens. Liverpool School ofTropicalMedicine, 128 pp. ISBN 0-9508756-9-4), excludingmost arthropods such as mosquitos, flies, and ticks, this training isnothingless than dismal. Few physicians will initially suspect cyclosporiasis,and few have even heard of it, which collectively results in lackof specific testing for this organism (see 2000,Emerg. Inf. Dis. 6: 200-203). It appears likely that most infectionsgo undiagnosed.Cyclospora cayetanensis: additional links CDC information for health care providers
Differentiation of Cyclospora from Eimeria by PCR
FDA public announcement
Outbreaks in 1996 (MMWR 45: 549-551, June 1996)
Protocol for preparation of oocysts for PCR following extraction from produce
Cyclospora cayetanensis: select citationsNote: This is not a complete list of publications on Cyclospora cayetanensis, but it does contain most papers through 2001. If there are papers missing that you feel should be added, please send me a copy and I'll post them as soon as I have time. I do not plan to update this page beyond 2001 as I only work on this parasite occasionally and have a lot of other webpages to maintain.
2001 papersAlakpa, G.E. 2001. Studies on Cyclospora cayetanensis as an emerging human diarrhoeal pathogen in Lagos, Nigeria. PhD dissertation, University of Lagos, Nigeria. Barta, J.R. et al. 2001. Molecular phylogeny of the other tissue coccidia: Lankesterella and Caryospora. J. Parasitol. 87: 121-127.Chokephaibulkit, K. et al. 2001. A report case of Cyclospora and Cryptosporidium mixed infection in a HIV-negative child in Thailand. J. Med. Assoc. Thailand. 84: 589-592. Clark, S.C. and McIntyre, M. 2001. Acid-fast bodies in faecal smears stained by the modified Ziehl-Neelsen technique. Br. J. Biomed. Sci. 58: 7-10. Connor, B.A. et al. 2001. Reiter syndrome following protracted symptoms of Cyclospora infection. Emerg. Inf. Dis. 7: 453-454.Dalton, C. et al. 2001. Viability of Giardia intestinalis cysts andviability and sporulation state of Cyclospora cayetanensis oocystsdetermined by electrorotation. Appl. Environment. Microbiol. 67: 586-590.Egloff, N. et al. 2001. Chronic watery diarrhea due to co-infection with Cryptosporidium spp. and Cyclospora cayetanensis in Swiss AIDS patient traveling in Thailand. J. Travel Med. 8: 143-145. Gascon, J. et al. 2001. Cyclosporiasis: a clinical and epidemiological study in travellers with imported Cyclospora cayetanensis infection. Med. Clin. (Barcelona) 116: 461-464. de Gorgolas, M. et al. 2001. Cyclospora cayetanensis cholecystitis in apatient with AIDS. Ann. Intern. Med. 134: 166.Katz, D.E. and Taylor, D.N. 2001. Parasitic infections of the gastrointestinal tract. Gastroent. Clin. North Amer. 30: 797-815.Khalifa, A.M. et al. 2001. Effect of ozone on the viability of some protozoa in drinking water. J. Egypt. Soc. Parasitol. 31: 603-616.Klein, N.C. and Cunha, B.A. 2001. New uses of olderantibiotics. Med. Clin. North Amer. 85: 125-132.Lopez, A.S. et al. 2001. Outbreak of cyclosporiasis associated with basil in Missouri in 1999. Clin. Inf. Dis. 32: 1010-1017.Nunez, F.A. and Finlay, C.M. 2001. Training for diagnosis of intestinal parasitic diseases in the national laboratory system of Cuba. Cad. Saude Publica 17: 719-724. Pinel C. et al. 2001. Cyclosporiasis: an emerging intestinal protozoaninfection. Presse Med. 30: 23.Pratdesaba, R.A. et al. 2001. Cyclospora cayetanensis in three populations at risk in Guatemala. J. Clin. Microbiol. 39: 2951-2953.Okhuysen, P.C. 2001. Traveler's diarrhea due to intestinal protozoa. Clin. Inf. Dis. 33: 110-114.Oliver, C. et al. 2001. Sequence variability in the first internal transcribed spacer region within and among Cyclospora species is consistent with polyparasitism. Int. J. Parasitol. 31: 1475-1487. Sanders, J.W. and Tribble, D.R. 2001. Diarrhea in the returned traveler. Curr. Gastroenterol. Rep. 3: 304-314.
2000 papersAdam, R.D. et al. 2000. Intervening transcribed spacer region 1variability in Cyclosporacayetanensis. J. Clin. Microbiol. 38: 2339-2343. Alakpa, G.E. et al. 2000. Cyclospora cayetanensis infection in Lagos, Nigeria: a preliminary report. Proceedings of the annual meeting of the American Society for Microbiology, 21-25 May 2000, Washington, D.C. American Society for Microbiology. p. 603. (abstract). Alakpa, G.E. et al. 2000. Cyclospora cayetanensis in watery-diarrhoeal stools in Lagos, Nigeria. Specialist Doctor 7: 5-9.Ali, M.S. et al. 2000. Intestinal spore-forming protozoa among patientssuffering from chronic renalfailure. J. Egypt. Soc. Parasitol. 30: 93-100. Arcay, L. 2000. Elagua como ruto para infecciones de protozoarios especialmente de enteropatogeos emergentes: Cryptosporidium parvum, Cyclospora cayetanensis y microspora. Arch Hosp. Vargas 42: 107-116. Arcay, L. et al. 2000. Structures of the life cycle of Cyclospora cayetanensis (Protozoa, Coccidia) in the feces of patients with diarreic syndrome. Acta Biol. Venez. 20: 35-42. Bern, C. et al. 2000. The contrasting epidemiology of Cyclospora and Cryptosporidium among outpatients in Guatemala. Am. J. Trop. Med. Hyg. 63: 231-235. Cann, K.J. et al. 2000. Cyclospora infections in England and Wales: 1993to 1998. Commun. Dis. Publ. Health 3: 46-49.Chalmers, R.M. et al. 2000. Foodborne outbreaks of cyclosporiasis havearisen in North America. Is the United Kingdom atrisk? Commun. Dis. Publ. Health 3: 50-55. De Carli, G.A. 2000. Infeccoes oportunistas por protozoariosparasitos: uma revisao sobre Cryptosporidium parvum, Cyclosporacayetanensis, Isospora belli e microsporidios. Rev. Bras. Anal. Clin. 32: 205-214.De Carli, G.A. 2000. Parasitologia Clinica. Diagnostico de Laboratoriodos coccidiios e microsporidios intestinais. Cadernos EPIPUCRS 14, SerieFarmacia 1, Analises Clinicas-Parasitologia, Porto Alegre. 73 pp.Deodhar, L. et al. 2000. Cyclospora infection in acquired immunodeficiency syndrome. J. Assoc. Phys. India 48: 404-406.Di Giullo, A.B. et al. 2000. Cyclospora cayetanensis in sputum and stoolsamples. Rev Inst. Med. Trop. Sao Paulo 42: 115-117.Eberhard, M.L. et al. 2000. Attempts to establish experimental Cyclosporacayetanensis infection in laboratory animals. J. Parasitol. 86: 577-582.Ferreira, M.S. 2000. Infections by protozoa in immunocompromisedhosts. Mem. Inst. Oswaldo Cruz 95: 159-162.Franzen, C. et al. 2000. Taxonomic position of the human intestinalprotozoan parasite Isospora belli as based on ribosomal RNAsequences. Parasitol. Res. 86: 669-676. Green, S.T. et al. 2000. Two simultaneous cases of Cyclospora cayetanensisenteritis returning from the Dominican Republic. J. Travel Med. 7: 41-42.Hermandez-Mora, M.G. et al. 2000. Cyclosporiasis. Med. Clin. (Barcelona) 115: 431-444.Herwaldt, B.L. 2000. Cyclospora cayetanensis: a review, focusing on theoutbreaks of cyclosporiasis in the 1990s. Clin. Inf. Dis. 31: 1040-1057.Mohle-Boetani, J.C. et al. 2000. The impact of health communication andenhanced laboratory-based surveillance on detection of cyclosporiasisoutbreaks in California. Emerg. Inf. Dis. 6: 200-203. Mota, P. et al. 2000. Microsporidia and Cyclospora: epidemiology andassessment of risk from the environment. Crit. Rev. Microbiol. 26: 69-90.Nichols, G.L. 2000. Food-borne protozoa. Br. Med. Bull. 56: 209-235.Orlandi, P.A. and Lampel, K.A. 2000. Extraction-free, filter-basedtemplate preparation for rapid and sensitive PCR detection of pathogenicparasitic protozoa. J. Clin. Microbiol. 38: 2271-2277. Parija, S.C. and Bhattacharya, S. 2000. Pictorial CME. Isospora belli and Cyclospoa cayetanensis in a case of chronic diarrhea in an immunocompromosed host. J. Assoc. Phys. India 48: 1192. Robertson, L.J. and Gjerde, B. 2000. Isolation of Cyclospora oocysts fromfruits and vegetables using lectin-coated paramagnetic beads. J. FoodProt. 63: 1410-1414. Santana, A.M. et al. 2000. Emergence of a new pathogen: Cyclospora cayetanensis in patients infected with human immunodeficiency virus. Rev. Cubana Med. Trop. 52: 66-69. Thomas, R.E. 2000. Preparing patients to travel abroad safely. Part4: Reducing risk of accidents, diarrhea, and sexually transmitteddiseases. Can. Fam. Physician 46: 1634-1638. Vasquez Tsuji, O. et al. 2000. Cyclospora cayetanensisinfection. Laboratory diagnosis. Rev. Latinoam. Microbiol. 42: 45-52.*Verdier, R.I. et al. 2000. Trimethoprim-sulfamethoxazole compared withciprofloxacin for treatment and prophylaxis of Isospora belli andCyclospora cayetanensis infection in HIV-infected patients. A randomized,controlled trial. Ann. Int. Med. 132: 885-888. Wallace, D.J. et al. 2000. Incidence of foodborne illnesses reported bythe foodborne diseases active surveillance network (FoodNet)-1997. FoodNetworking group. J. Food Prot. 63: 807-809.
1999 papersAbou el Naga, I.F. 1999. Studies on a newly emerged protozoalpathogen: Cyclospora cayetanensis. J. Egypt. Soc. Parasitol. 29: 575-586.Ajisawa, A. 1999. Cryptosporidium, Cyclopsora, Microsporidia. RyoikibetsuShokogun Shirizy 1999: 97-99. Alakpa, G.E. et al. 1999. Preliminary studies on Cyclospora cayetanensis, an emerging diarrhoeal pathogen: are physicians in Nigeria aware? Specialist Doctor 6: 9-12. Albert, M.J. et al. 1999. Case-control study of enteropathogens associatedwith childhood diarrhea in Dhaka,Bangladesh. J. Clin. Microbiol. 37: 3458-3464. Bern, C. et al. 1999. Epidemiologic studies of Cyclospora cayetanensis inGuatemala. Emerg. Inf. Dis. 5: 766-774.Brown, G.H., & Rotschafer, J.C. 1999. Cyclopospora: a review of anemerging parasite. Pharmacotherapy 19: 70-75.Casemore, D.P. 1999. Cyclospora species as a cause of diarrhoea in humans.Br. J. Biomed. Sci. 56: 78-79.Cegielski, J.P. et al. 1999. Cryptosporidium, Enterocytozoon, andCyclospora infections in pediatric and adult patients with diarrhea inTanzania. Clin. Inf. Dis. 28: 314-321.Connor, B.A. et al. 1999. Cyclosporiasis: clinical and histopathologiccorrelates. Clin. Inf. Dis. 28: 1216-1222.De Carli, G.A. 1999. Diagnostico laboratorial da Cyclosporacayetanensis. Revista Brasileira de Analises Clinicas 31(3): 143-150.Duszynski, D.W. et al. 1999. Coccidia (Apicomplexa: Eimeriidae) in theprimates and the scandentia. Int. J. Primatol. 20: 761-797.Eberhard, M.L. et al. 1999. Morphologic and molecular characterization ofnew Cyclospora species from Ethiopian monkeys: C. cercopitheci sp. n., C.colobi sp. n., and C. papionis sp. n. Emrg. Inf. Dis. 5: 651-658.Eberhard, M.L. et al. 1999. Survey for Cyclospora cayetanensis in domesticanimals in endemic area of Haiti. J. Parasitol. 85: 562-563.Eberhard, M.L. et al. 1999. Cyclospora cayetanensis infections in Haiti: acommon occurrence in the absence of watery diarrhea. Am. J. Trop. Med.Hyg. 60: 584-586. Escobedo, A.A., & Nunez, F.A. 1999. Prevalence of intestinal parasites inCuban acquired immunodeficiency syndrome (AIDS) patients. Acta Trop. 72:125-130. Fryauff, D.J. et al. 1999. Cyclospora cayetanensis among expatriate andindigenous populations of west Java, Indonesia. Emerg. Inf. Dis. 5:585-588. Gumbo, T. et al. 1999. Intestinal parasites in patients with diarrhea andhuman immunodeficiency virus infection in Zimbabwe. AIDS 13: 819-821.Herwaldt, B.L. et al. 1999. The return of Cyclospora in 1997: anotheroutbreak of cyclosporiasis in North America associated with importedraspberries. Ann. Int. Med. 130: 210-220. Jinneman, K.C. et al. 1999. An oligonucleotide-ligation assay for thedifferentiation between Cyclospora and Eimeria spp. polymerase chainreaction amplification products. J. Food Protect. 62: 682-685. Katz, D. et al. 1999. Cyclosporiasis associated with imported rapberries,Florida, 1996. Publ. Health Rep. 114: 427-438.Lopez, F.A. et al. 1999. Molecular characterization of Cyclospora-likeorganisms from baboons. J. Inf. Dis. 179: 670-676.Mezzari, A. et al. 1999. Cyclospora cayetanensis, um novo protozoario aser pesquisado. Rev. Assoc. Med. Brasil. 45: 347-348.Mosimann, M. et al. 1999. Excessive watery diarrhea and pronounced fatiguedue to Cyclospora cayetanensis infection in an HIV infected travelerreturning from the tropics. Schweiz. Med. Wochenschr. 129: 1158-1161. Nace, E.K. et al. 1999. Evaluation of Streck tissue fixative, anonformalin fixative for preservation of stool samples and subsequentparasitologic examinations. J. Clin. Microbiol. 37: 4113-4119. Ponce de Leon et al. 1999. A new trichromic safranin stain for thedetection of Cryptosporidium parvum, Cyclospora cayetanensis, species ofMicrosporidia and Isospora belli in fecalmaterial. Rev. Latinoam. Microbiol. 41: 211-214. Ramakrishna, B.S. 1999. Prevalence of intestinal pathogens in HIV patientswith diarrhea: implications for treatment. Ind. J. Pediatr. 66: 85-91.Ranhitham, M. et al. 1999. Cyclospora cayetanensis - an emerging coccidianparasite. J. Assoc. Physicians India 47: 1198-1199.Ranjitham, M. et al. 1999. Cyclospora cayetanensis, a new emergingcoccidian parasite. J. Commun. Dis. 31: 137-139.Reverand, S. et al. 1999. Cyclospora cayetanensis en ninos asintomaticos del area Metropolitana de Caracas. Rev. Fed. Med. Venez. 7: 26-31.Rose, J.B. and Slifko, T.R. 1999. Giardia, Cryptosporidium, and Cyclosporaand their impact on foods: a review. J. Food Prot. 62: 1059-1070.Serpentini, A. et al. 1999. Cyclospora cayetanensis: review of an emergingintestinal pathogen. Ann. Biol. Clin. (Paris) 57: 677-683.Shellabear, C.K. & Shah, A.J. 1999. Cyclospora cayetanensis: an emergingfood pathogen. Food Australia 51: 30-32.Sherchand, J.B. et al. 1999. Study of Cyclospora cayetanensis in healthcare facilities, sewage water and green leafy vegetables inNepal. S. E. Asian J. Trop. Med. Publ. Health 30: 58-63. Shlim, D.R. et al. 1999. Persistent high risk diarrhea among foreigners inNepal during the first 2 years of residence. Clin. Inf. Dis. 29: 613-616.Sterling, C.R. & Ortega, Y.R. 1999. Cyclospora: an enigma worthunraveling. Emerg. Inf. Dis. 5: 48-53.1998 papersAbou el Naga, I.F. et al. 1998. Preliminary identification of anintestinal coccidian parasite in man. J. Egypt. Soc. Parasitol. 28:807-814. Abreu de Borges, E.B. et al. 1998. Cyclospora cayetanensis y microsporidia en heces de pacientes con sida y sindrome diarreico. Rev. Fed. Med. Venez. 6: 89-96.Arcay, L. et al. 1998. Incidencia de Cyclospora cayetanensis y microspora en pacientes de la poblacion circunvecina del Rio Anare (Venezuela) y su presencia en el agua del Rio. Arch. Hosp. Vargas 40: 157-162. Bellagra, N. et al. 1998. Co-infection with Cryptosporidium sp. andCyclospora sp. in a AIDS stage HIV patient. Ann. Biol. Clin. (Paris) 56:476-478. Berlin, O.G. et al. 1998. Autoflourescence and the detection ofCyclospora oocysts. Emerg. Inf. Dis. 4: 127-128.Caceres, V.M. et al. 1998. A foodborne outbreak of cyclosporiasis causedby imported raspberries. J. Fam. Pract. 47: 231-234.Curry, A. and H.V. Smith. 1998. Emerging pathogens: Isospora, Cyclosporaand microsporida. Parasitology 117: s143-s159.Drenaggi, D. et al. 1998. Cyclosporiasis in a traveler returning fromSouth America. J. Travel Med. 5: 153-155.Fernandes, A.O. et al. 1998. Human cyclosporiasis diagnosis: report of acase in Sa

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