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African Health Sciences
Makerere University Medical School
ISSN: 1680-6905 EISSN: 1729-0503
Vol. 7, Num. 2, 2007, pp. 62 - 67

African Health Sciences, Vol. 7, No. 2, June, 2007, pp. 62 - 67

Cyclosporiasis: an emerging public health concern around the world and in Africa

Robert M. Karanja 1, Wangeci Gatei2* and Njeri Wamae2

1Centre for Biotechnology Research & Development (CBRD), Kenya Medical Research Institute, P.O. Box 54840 City Square,
Nairobi, Kenya;
2Centre for Microbiology Research (CMR), Kenya Medical Research Institute, P.O. Box 19464-00200, Nairobi, Kenya;
Correspondence: Robert M. Karanja Centre for Biotechnology Research & Development (CBRD), Kenya Medical Research Institute, P.O. Box 54840, Nairobi, Kenya Email:

Code Number: hs07014

Background: Cyclosporiasis is an emerging gastro-enteric disease caused by the coccidia protozoan Cyclospora cayetanensis. It isassociated with diarrhoea among children in developing countries, in the Americas where C. cayetanensis is endemic, traveller’s diarrhoeaand/or food and waterborne outbreaks in the developed countries.
Objectives:The aim of this review is to highlight cyclosporiasis and its relevance to public health in East Africa and Africa at large.
Methods: All literature on Cyclospora, C. cayetanensis,cyclosporiasis in Africa, and endemic cyclosporiasis was searched from libraries,colleagues and internet but only literature on its history, clinical presentation, epidemiology in endemic settings, and occurrence inAfrica were scrutinised.
Results: In Sub Saharan Africa, cyclosporiasis has been reported in at least 3 countries, including Tanzania, in East Africa, occurring inboth immunocompromised and immunocompetent patients. Zoonotic species of Cyclospora have also been identified in East Africanprimates, indicating likely endemicity of this little reported disease in the region. This can be attributed to lack of awareness in thepublic and medical profession concerning the disease, and therefore not routinely checked at the health centres. Cyclosporiasis ischaracterized by intermittent diarrhoea, and secondary conditions or sequelae such as reactive arthritis syndrome (Reiter’s syndrome),have been associated with progression of the disease. Its management is based on antibiotics, an unusual scenario for a protozoa.
Conclusions: Although many aspects of this disease and its transmission remain an enigma, the situation has been rapidly changing since the disease first came to medical attention in the 1970s.


Cyclosporiasis and Africa – should we be concerned?

Cyclosporiasis is a diarrhoeal disease caused by the protozoan pathogen Cyclospora cayetanensis1 . It is considered an emerging disease of public health concern primarily in the developed countries where it has been identified as the cause of several outbreaks in North America and Europe, and with traveller’s diarrhoea2-6 . In these countries, cyclosporiasis transmission has primarily been linked to foods imported from developing countries adding impetus to the review of food import regulations with far reaching implications on developing country economies that depend on North-South trade in agricultural produce4-9 . The transmission of the disease in the developing South where C. cayetanensis is endemic, remains little understood but has been associated with water and sanitation in Nepal, Guatemala, Nigeria and Egypt7, 10, 11 .

Ashford is credited with having first identified C. cayetanensis as a human pathogen in 1979 in Papua New Guinea 12 . Thereafter, the parasite remained largely uninvestigated and it was not until 1994, when the first detailed morphological description and naming of Cyclospora cayetanensis was done 1 . Few studies have been carried out since then to determine the transmission and epidemiology of cyclosporiasis in Africa and its public health impact on the continent. The disease has been reported in Nigeria, Tanzania and Egypt 13-15 . Although it is thought to be self-limiting in immuno-competent individuals, cyclosporiasis can cause prolonged diarrhoea that could be life threatening in immuno-compromised patients. Moreover, like other coccidian parasites, C. cayetanensis has been associated with various sequelae including biliary disease, aculculous cholecystitis, Guillain-Barré syndrome and reactive arthritis syndrome following prolonged infection 16-19.

The study of cyclosporiasis is rife with difficulties that have largely contributed to its underreporting in Africa and little public awareness 20 . A key contributor to this is the specialised staining methods for diagnosis that are not routinely carried out in clinicallaboratories 20-22 . Additionally, efforts to elucidate its transmission and biology in endemic areas is impeded by lack of sensitive and specific methods for Cyclospora detection in the environment, agricultural produce and water bodies and further compounded by the lack of a suitable animal-model 23-26 . Cyclosporiasis has therefore remained a little known disease albeit with potentially far reaching impact on the health and economy of developing countries due to its impact on the horticulture industry as a food borne pathogen. Several publications pertaining to the methods of diagnosis and detection exist and have been ably reviewed by others 9 . Our aim is to bring this disease to the attention of African health researchers and to highlight potential areas of study in our likely endemic setting.

History of Cyclosporiasis

According to Lainson 27 , it was Eimer who as early as 1870 first described an organism in intestines of the mole Talpa europaea that was eventually characterized and named Cyclospora caryolytica by Schaudinn in 1902 28 . But C. glomericola, observed in the millipede, was the first species to be classified as Cyclospora by Schneider who established the genus in 1881 29 . So far C. glomericola is the only species out of a total of 19 Cyclospora species identified to date to be encountered in an invertebrate host, the rest being found in reptiles (snakes) and mammals (rodents and non-human primates) 27 .

It was not until the 1970s that cyclosporiasis first came to medical attention when an un-described coccidian was associated with diarrhoea in Papua New Guinea 4, 12 . Thereafter, endemic cases were also reported in Haiti, Nepal, Peru and linked to Travellers Diarrhoea in the 1980s, where it was reported variously as Cryptosporidium muris-like, a flagellate, an unsporulated coccidian, a large Cryptosporidium, a blue-green alga (cyanobacterium-like body), or a coccidian-like body 4, 30 . By 1990 the new pathogen was associated with chronic diarrhoea in acquired immunodeficiency syndrome patients 31 . Nevertheless, it was not until the 1990s that food and water-borne outbreaks in North America grabbed public and scientific attention to the emergence of the disease, after a food or waterborne outbreak of 21 was reported in a Chicago teaching hospital in 1990 32 .

This fuelled efforts to definitively identify and characterise the pathogen, with the first breakthrough occurring in 1992 when Ortega et al., reported they had sporulated and excysted the oocysts, thus ending speculation on the classification of the parasite and placing it in the genus Cyclospora 33 . The same group finally identified and characterised the causative agent as the coccidian Cyclospora cayetanensis (Apicomplexa: Eimeriidae) using classical morphological methods 1, 30 . However, molecular techniques have placed the pathogen closer to Eimeria species, suggesting its classification as such 34, 35 . Today, C. cayetanensis transmission in developed countries through food and water borne outbreaks has been well documented and understood, however the modes of transmission and risk factors in endemic areas remain poorly understood 4, 36, 37 .

Life cycle and Biology

Cyclospora cayetanensis is an obligate intracellular parasite that is normally found in the jejunum. Oocysts found in the stool can be mistaken for the common Cryptosporidium spp. infecting humans, but can easily be distinguished by their larger size (8-10 μm) using an ocular micrometer 38 . The life cycle begins with the ingestion of the sporulated oocyst in contaminated water or food. Unlike Cryptosporidium, this oocyst when freshly passed in the stool is not sporulated and therefore not infective 1, 30 . Oocysts require a few days to weeks, depending on climatic factors, to develop and mature in the environment into the infective sporulated oocyst, thus precluding direct fecal-oral transmission 1, 38 . Temperatures ranging between 25-30ºC are most suitable for sporulation. Upon being ingested, the oocysts excyst in the gut, releasing the sporozoites, which proceed to invade the epithelial cells of the small intestine 39, 40 . The sporozoites undergo two generations of asexual reproduction in the cell, whereby they form meronts that contain numerous merozoites 40 . The first generation meronts have 8-12 merozoites, whilst the second have only 4 merozoites, which penetrate new cells to form gametes. Some of these gametes enlarge to form the female macrogametes and some microgametes that undergo meiosis to form numerous flagellated spermlike microgametes. The mature microgametes leave the microgametocyte and migrate to fertilize the macrogamete. The development of a resilient oocyst wall around the zygote, which contains 2 sporocysts or small oocysts, makes up the unsporulated oocyst. Eventually the oocyst is passed out with stool to begin the process of sporulation. Sporogyny commences in the presence of higher atmospheric oxygen concentrations and is complete between 7-12 days 40-43 .

Clinical aspects of C. cayetanensis infection


The clinical presentation of C. cayetanensis may include gastrointestinal (GI) symptoms such as loose or watery diarrhoea, nausea, vomiting, abdominal cramps, loss of appetite, or unintentional weight loss; or constitutional symptoms such as fever, chills, muscleaches, joint aches, generalized body aches, headache, or fatigue 8 . Although asymptomatic infections are known to occur, the onset of symptoms in naïve populations observed in outbreaks is 1-14 days post exposure and is often accompanied by a characteristic waxing and waning of symptoms 6, 40, 41, 44 . In endemic countries, symptoms begin approximately 5-8 days after and may persist for a month or more. However, infection without watery diarrhoea is a common occurrence and has been observed in Haiti among other areas 45 .


Detection is based on the identification of oocysts in stool specimens using modified acid fast staining, or hot safranin test 21 . Where cyclosporiasis is suspected, up to 3 stool specimens taken 2 days apart should be tested to rule out the parasite. A rapid method of identification is possible on wet mounts using fluorescent microscopy employing a filter with a wavelength in the range of 340-380 nm, which reveals the bright, pale blue oocysts glow 30 . Polymerase chain methods (PCR) have also been developed for diagnosis and detection in the environment, but the primers appears to cross react with Eimeria spp. 26, 35, 46 .

Differential diagnosis of cyclosporiasis includes all other causes of diarrhoea. Infections with Giardia, Cryptosporidium, Isospora, Toxoplasma and Microsporidia should be suspected in cases of persistent diarrhoea that does not respond to the usual treatment (6, 20, 31, 36, 41, 47). Cyclosporiasis can also present symptoms closely resembling celiac disease and irritable bowel syndrome 48.


Like cryptosporidiosis, C. cayetanensis infection has also been associated with the onset of various extraintestinal complications that may accompany prolonged infection, especially in the HIV immunocompromised patients. These include acalculous cholecystitis 19 ; biliary disease 18 , Guillian-Barré syndrome 17 , and Reiter or reactive arthritis syndrome 16 . One case of C. cayetanensis oocysts found in the sputum of 60-year-old HIV negative male with a history of successfully treated TB has been reported in Argentina 49 , and a similar case has also been reported in Egypt where a 45 year-old HIV negative male with TB history also presented oocysts in the sputum accompanied with active TB infection 50 . The latter has prompted calls for the inclusion of cyclosporiasis as a new causative agent of respiratory disease and as a differential diagnosis for TB. In both TB negative and positive cases, the patients presented with loss of weight, cough with expectoration of purulent sputum and dyspnea. The implications of pulmonary infection to the biology, life cycle and transmission of C. cayetanensis remains to be evaluated, as does its interaction with TB, a disease currently on the increase in Africa due to the HIV/AIDS pandemic 51 .


Symptoms resolve with the administration of Trimethoprim-Sulfamethoxazole, the standard treatment for cyclosporiasis at 160/800 mg oral dose taken twice a day for 7 days or 160/800 mg oral dose taken 4 times a day for 10 days in immunocompromised patients with AIDS often with symptoms resolving and passage of oocysts in the stool ceasing within 24-48 hr 52, 53 .

Epidemiology in endemic setting

The first epidemiological studies conducted in an area endemic for C. cayetanensis, were carried out in 1997-1998 in Guatemala where raspberry exports to USA were linked to cyclosporiasis outbreaks 10 . Children of age groups 1.5 to 4 years and 5 to 9 years were found to be 5 times more likely to be positive for C. cayetanensis in stool samples than adults. Overall infection did not differ significantly by sex. The infection rates were also found to fluctuate seasonally, with prevalence peaking in the rainy season (6.7%) and falling to undetectable levels in the dry seasons. Drinking of untreated water or swimming in rivers or springs, having a septic tank as opposed to municipal sewage, direct contact with the soil and ownership of dogs, chicken or other fowls, were all found to significantly increase risk of infection although cats and pigs did not 10 .

Subsequent epidemiological studies in endemics areas of Haiti, Nepal and Peru have corroborated higher infection rates in children, seasonal fluctuation of prevalence, and risk associated with water source and ownership of domestic animals, particularly fowl, guinea pigs and rabbits 37, 54 . However no oocysts were detected in a survey for C. cayetanensis in domestic animals carried out for 1.5 years in an endemic area in Haiti, ruling out domestic animals as a reservoir 24 . Studies in Peru have also shown that previous infection offers significant protection against subsequent exposures 54 . This consolation is however short lived as clinical sequale may still be linked with asymptomatic infection. Humans are therefore the only known host for C. cayetanensis, but the eating of raw or insufficiently cooked bivalves, which are filter feeders that concentrate pathogens from waters, has been shown to be a risk factor 55 .

Reports of Cyclospora spp. infecting non-human primates in the East African countries of Uganda, Kenya, Tanzania and Ethiopia have led to efforts to conduct studies of non-human primates in order to better understand the epidemiology and ecology of endemic cyclosporiasis 25, 56-59 . Host specificity of Cyclospora species in the different non-human primates, geographic overlaps of both monkey and parasite species notwithstanding, corroborated the likelihood of humans as the sole definitive host of C. cayetanensis 58 . However the collection of oocyst positive stools from the studied troops of vervet monkeys, baboons and colobus monkeys at all times of the year in Kenya, which is notable for extreme weather patterns, demonstrated a lack of seasonality in infection contrary to expectations 58 .

Cyclospora the enigma

It is clear that the epidemiology of cyclosporiasis as we know it today is a study in contradictions, as the causative agent itself remains shrouded in mystery. How can a pathogen incapable of direct faecaloral infection and lacking a zoonotic reservoir or ubiquitous presence in the environment 38 , be responsible for so many widespread outbreaks of gastroenteritis all over the world? Trace amounts of oocyst contamination in food products indicate that the infective dose of C. cayetanensis is likely to be very low 38 . However attempts at experimental infection in both humans and animals have all proved futile 25, 60 . The lack of an animal model has therefore made it hard to determine the viability of oocyst exposed to varying environment conditions that may impact its transmission 38 . While most outbreaks have been linked to food sources, just as many unexplained sporadic cases linked to water/sewage transmission have been reported in the developed countries 32, 38, 61 . These cases may signify ubiquitous endemicity, remaining undetected due to seasonality of infection, but by what means the parasite survives from one infection season to the next remains unknown.

Even more puzzling is the dearth of C. cayetanensis reports in African populations and as a cause of traveller’s diarrhoea in visitors returning from the continent. The screening of over 4,800 samples using modified acid fast staining, and other concerted efforts in previous years have all failed to determine the presence of C. cayetanensis in Kenya 62 . In addition to economic restraints for effective routine diagnosis in health centres and national/regional surveillance, it has been postulated that the amount of sulpha drugs administered in sub Saharan Africa as drugs of choice for malaria and other infectious diseases may suppress the parasite, humans being the only reservoir 36 . Could sulfadoxinepyrimethamine (SP), the now largely ineffective but still affordable treatment of malaria, be our unlikely saviour? Or is it the use of trimethoprim (Septrin), which is widely used as a first line of antibiotics and in management of HIV before ARVs? Significantly higher HIV and malaria prevalence in sub-Saharan Africa may account for a higher drug pressure than other parts of the world, however, the withdrawal of SP as a first line antimalarial due to resistance and similar use of Septrin in C. cayetanensis endemic Peru and Haiti where 5-11% HIV prevalence have been documented, makes the dearth of reported African cyclosporiasis all the more mysterious.

The controversy and questions surrounding C. cayetanensis are no less intriguing. Whereas there is compelling molecular evidence for its reclassification as a mammalian Eimeria species, only C. cayetanensis DNA sequences and C. colobi, C. cercopitheci and C. papionis from East African non-human primates are available 27, 34, 36, 57 . The way forward on the classification of this parasite in the light of these new developments remains uncharted waters. The biology of C. cayetanensis in the host is no less intriguing. The presence of oocysts in HIV negative TB patients strongly suggests the existence of an extraintestinal parasite lifecycle and colonization in humans that is yet unknown 49, 50 . Moreover, more studies are required to determine whether C. cayetanensis interacts with TB or has only been observed in TB patients because it is an acid-fast staining organism like the TB bacillum. Extra-intestinal stages in the life cycle of Cyclospora talpae in European moles have been demonstrated in the liver where sexual stages develop in the bile duct epithelial cells 63, 64 . C. cayetanensis has similarly been shown to cause biliary disease in HIV/AIDS patients suggesting possible colonization of the liver 18, 36 . Unfortunately, the lack of animal/experimental models remains an impediment to resolving these questions.

Conclusions and recommendations

Cyclosporiasis therefore presents an everbroadening frontier cutting across multiple disciplines of research including clinicians, epidemiologists, parasitologists, veterinarians, environmental scientists among others. As a food-borne disease that impacts on horticulture (the backbone of most developing country economies) and primarily infects children and HIV/AIDS patients, routine surveillance in both the population and environment should be carried out. Surveillance in populations should include sputum samples regardless of TB or HIV status. The role of its interaction with TB and/or HIV should also be elucidated. Use of nonpathogen Cyclospora spp. such as non-human primates cyclosporiasis and C. talpae and mole hosts should be developed as alternative animal models for the study of extra-intestinal colonization and disease. Additionally, the possible role of sulphur drugs in control of cyclosporiasis should be evaluated, in order to address the impact of the disease in Africa.


This work was funded by the Centre for Microbiology Research and is published with the permission of Director, Kenya Medical Research Institute.

  1. Ortega YR, Gilman RH, Sterling CR. A new coccidian parasite (Apicomplexa: Eimeriidae) from humans. J. Parasitol. 1994;80:625-629.
  2. Curry A, Smith HV. Emerging pathogens: Isospora, Cyclospora and Microsporidia. Parasitol 1998;117:S143-S159.
  3. Drenaggi D, Cirioni O, Giacometti A, Fiorentini A, Scalise G. Cyclosporiasis in a traveler returning from South America. J. Travel Med. 1998;5(3):153-155.
  4. Herwaldt BL. Cyclospora cayetanensis: a review, focusing on the outbreaks of cyclosporiasis in the 1990s. Clin. Infect. Dis. 2000;31(4):1040-1057.
  5. Ho AY, Lopez AS, Eberhart MG, Levenson R, Finkel BS, da Silva AJ, et al. Outbreak of cyclosporiasis associated with imported raspberries, Philadelphia, Pennsylvania, 2000. Emerging Infect. Dis. 2002;8(8):783-786.
  6. Mansfield LS, Gajadhar AA. Cyclospora cayetanensis, a food- and waterborne coccidian parasite. Vet. Parasitol. 2004;126(12):73-90.
  7. Alakpa GE, Clarke SC, Fagbenro-Beyioku AF. Cyclospora cayetanensis infection: vegetables and water as possible vehicles for its transmission in Lagos, Nigeria. Br. J. Biomed. Sci. 2003;60(2):113-114.
  8. Crist A, Morningstar C, Chambers R, Fitzgerald T, Stoops D, Deffley M, et al. Outbreak of cyclosporiasis associated with snow peas — Pennsylvania, 2004. MMWR 2004;53(37):876-878.
  9. Shields JM, Olson BH. Cyclospora cayetanensis: a review of an emerging parasitic coccidian. Int. J. Parasitol. 2003;33(4):371-391.
  10. Bern C, Hernandez B, Lopez MB, Arrowood MJ, de Mejia MA, de Merida AM, et al. Epidemiologic studies of Cyclospora cayetanensis in Guatemala. Emerging Infect. Dis. 1999;5(6):766-774.
  11. El-Karamany EM, Zaher TI, el-Bahnasawy MM. Role of water in the transmission of cyclosporiarsis in Sharkia Governorate, Egypt. J Egypt Soc Parasitol. 2005;35(3):953-962.
  12. Ashford RW. Occurrence of an undescribed coccidian in man in Papua New Guinea. Ann. Trop. Med. Parasitol. 1979;73:497-500.
  13. Alakpa GE, Clarke SC, Fagbenro-Beyioku AF. Cyclospora cayetanensis infection in Lagos, Nigeria. Clin Microbiol Infect. 2003;9(7):731-733.
  14. Cegielski JP, Ortega YR, McKee S, Madden JF, Gaido L, Schwartz DA, et al. Cryptosporidium, enterocytozoon, and cyclospora infections in pediatric and adult patients with diarrhea in Tanzania. Clin. Infect. Dis. 1999;28(2):314-321.
  15. Nassef NE, el-Ahl SA, el-Shafee OK, Nawar M. Cyclospora: a newly identified protozoan pathogen of man. J Egypt Soc Parasitol. 1998;28(1):213-219.
  16. Connor B, Johnson E, Soave R. Reiter syndrome following protracted symptoms of Cyclospora infection. Emerging Infect. Dis. 2001;7(3):453-454.
  17. Richardson RF, Remler BF, Katirji B, Murad MH. Guillian-Barre syndrome after Cyclospora infection. Muscle Nerve 1998(669-671).
  18. Sifuentes-Osornio J, Porras-Cortes G, Bendall RP, Morales-Villarreal F, Reyes-Teran G, Ruiz-Palacios GM. Cyclospora cayetanensis infection in patients with and without AIDS: biliary disease as another clinical manifestation. Clin. Infect. Dis. 1995;29:613-616.
  19. Zar FA, El-Bayoumi E, Yungbluth MM. Histological proof of acalculous cholecystitis due to Cyclospora cayetanensis. Clin. Infect. Dis. 2001;33:e140-e141.
  20. Mohle-Boetani JC, Werner SB, Waterman SH, DJ V. The impact of health communication and enhanced laboratory-based surveillance on detection of cyclosporiasis outbreaks in California. Emerging Infect. Dis. 2000;6(2):200-203.
  21. Eberhard ML, Pieniazek NJ. Laboratory diagnosis of Cyclospora infections. Arch. Pathol. Lab. Med. 1997;121(8):792-797.
  22. Kimura K, Kumar Rai S,Takemasa K, Ishibashi Y, Kawabata M, Belosevic M, et al. Comparison of three microscopic techniques for diagnosis of Cyclospora cayetanensis. FEMS Microbiol Lett. 2004;238(1):263-266.
  23. Dowd SE, John D, Eliopolus J, Gerba CP, Naranjo J, Klein R, et al. Confirmed detection of Cyclospora cayetanensis, Encephalitozoon intestinalis and Cryptosporidium parvum in water for drinking. J. Water Health 2003;1(3):117-123.
  24. Eberhard ML, Nace EK, Freeman AR. Survey for Cyclospora cayetanensis in domestic animals in an endemic area in Haiti. J. Parasitol. 1999;85(3):562-563.
  25. Eberhard ML, Ortega YR, Hanes DE, Nace EK, Do RQ, Robl MG, et al. Attempts to establish experimental Cyclospora cayetanensis infection in laboratory animals. J. Parasitol. 2000;86(3):577-582.
  26. Shields JM, Olson BH. PCR-Restricted Fragment Length Polymorphism method for detection of Cyclospora cayetanensis in environmental waters without microscopic confirmation. Applied and Environmental Microbiology 2003;69(8):4662-4669.
  27. Lainson R.The Genus Cyclospora (Apicomplexa: Eimeriidae), with a description of Cyclospora schneideri n.sp. in the snake Anilius scytale scytale (Aniliidae) from Amazonian Brazil - a review. Mem. Inst. Oswaldo Cruz vol.100 no.2 2005;100(2).
  28. Schaudinn F. Studien über krankheitserregende Protozoen I. Cyclospora caryolitica Shaud., der Erreger der perniciösen Enteritis des Maulwurfs. Arb. K. Gesundheitsamte 1902;18:378-416.
  29. Schneider A. Sur les psorospermies oviformes ou coccidies. Espécies nouvelles ou peu connues. Arch. Zool. Exp. Gen. 1881;9:387-404.
  30. Ortega YR, Sterling CR, Gilman RH, Cama VH, Diaz F. Cyclospora species - a new protozoan pathogen of humans. N. Engl. J. Med. 1993;328:1308-1312.
  31. Hart AS, Ridinger MT, Soundarajan R, Peters CS, Swiatlo AL, FE K. Novel organisms associated with chronic diarrhoea in AIDS. Lancet 1990;335:169-170.
  32. Huang P,Weber JT, Sosin DM, Griffin PM, Long EG, Murphy JJ, et al. The first reported outbreak of a diarrheal disease associated with Cyclospora in the United States. Ann. Intern. Med. 1995;123:409-414.
  33. Ortega YR, Sterling CR, Gilman RH, Carna VA, Diaz F. Cyclospora cayetanensis: a new protozoan pathogen of humans. In: The 41st Annual Meeting of the American Society of Tropical Medicine and Hygiene; 1992: J Am Soc Trop Med Hyg; 1992. p. 210.
  34. Pieniazek NJ, Herwaldt BL. Reevaluating the molecular taxonomy: is human-associated Cyclospora a mammalian Eimeria species? Emerg. Infect. Dis. 1997;3:381-383.
  35. Relman DA, Schmidt TM, Gajadhar A, Sogin M, Cross J, Yoder K, et al. Molecular phylogenetic analysis of Cyclospora, the human intestinal pathogen, suggests that it is closely related to Eimeria species. J. Infect. Dis. 1996;173:440 -445.
  36. Eberhard ML, Arrowood MJ. Cyclospora spp. Curr. Opin. Infect. Dis. 2002;15(5):519-522.
  37. Lopez SL, Bendik JM, Alliance JY, Roberts JM, daSilva AJ, Moura INS, et al. Epidemiology of Cyclospora cayetanensis and other intestinal parasites in a community in Haiti. J. Clin. Microbiol. 2003;41(5):2047-2054.
  38. Sterling CR, Ortega YR. Cyclospora: An Enigma Worth Unraveling. Emerg. Infect. Dis. 1999;5(1):48-53.
  39. Bendall RP, Lucas S, Moody A, Tovey G, Chiodini PL. Diarrhoea associated with cyanobacterium-like bodies: a new coccidian enteritis of man. Lancet 1993;341:590-592.
  40. Ortega Y, Nagle R, Gilman RH, Watanabe J, Miyagui J, Kanugusuku P. Pathologic and clinical findings in patients with cyclosporiasis and a description of intracellular parasite life-cycle stages. J. Infect. Dis. 1997;176:1584-1589.
  41. Connor BA, Reidy J, Soave R. Cyclosporiasis: clinical and histopathological correlates. Clin. Infect. Dis. 1999;28(1216-1222).
  42. Sun T, Ilardi CF, Asnis D, Bresciani AR, Goldenberg S, Roberts B, et al. Light and electronmicroscopic identification of Cyclospora species in the small intestine: evidence of the presence of asexual life cycle in human host. Am. J. Clin. Path. 1996;105:216-220.
  43. Tran Van Nhieu J, Nin F, Fleury-Feith J, Chaumette MT, Schaeffer A, Bretagne S. Identification of intracellular stages of Cyclospora species by light microscopy of thick sections using hematoxylin. Hum. Pathol. 1996;27:1107-1109.
  44. Ayala-Gaytan JJ, Diaz-Olachea C, Riojas-Montalvo P, Palacios-Martinez C. Cyclosporidiosis: clinical and diagnostic characteristics of an epidemic outbreak. Rev. Gastroenterol. Mex. 2004;69(4):226-229.
  45. Eberhard ML. Cyclospora cayetanensis infections in Haiti: a common occurence in the absence of watery diarrhea. Am. J. Trop. Med. Hyg. 1999;60(4):584-586.
  46. Pieniazek NJ, Slemenda SB, da SilvaAJ,Alfano EM,Arrowood MJ. PCR confirmation of infection with Cyclospora cayetanensis. Emerg. Infect. Dis. 1996;2:357-359.
  47. Rezk H, el-Shazly AM, Soliman M, el-Nemr HI, Nagaty IM, Fouad MA. Coccidiosis among immuno-competent and compromised adults. J Egypt Soc Parasitol. 2001;31(3):823 -834.
  48. Vidyut Pingé-Suttor, Chris Douglas, Antony Wettstein. Cyclospora infection masquerading as coeliac disease. MJA 2004;180(6):295-296.
  49. Di Gliullo AB,Cribari MS,Bava AJ,Cicconetti JS,Collazos R. Cyclospora cayetanensis in sputum and stool samples. Rev Inst Med Trop Sao Paulo 2000;42(2):115-117.
  50. Hussein EM, Abdul-Manaem AH, el-Attary SL. Cyclospora cayetanensis oocysts in sputum of a patient with active pulmonary tuberculosis, case report in Ismailia, Egypt. J Egypt Soc Parasitol. 2005;35(3):787-793.
  51. World Health Organization. Global Tuberculosis Control: Surveillance, Planning, Financing. WHO Report 2004. Geneva, Switzerland: WHO; 2004. Report No.: WHO/ CDS/TB/2004.331.
  52. Hoge CW, Shlim DR, Ghimire M, Rabold JG, Pandey P, Walch A, et al. Placebo-controlled trial of co-trimoxazole for Cyclospora infections among travellers and foreign residents in Nepal. Lancet 1995;345:691-693.
  53. Madico G, Giman RH, Miranda E, Cabrera L, Sterling CR. Treatment of Cyclospora infections with co-trimoxazole. Lancet 1993;342:122-123.
  54. Bern C, Ortega Y, Checkley W, Roberts JM, Lescano AG, Cabrera L, et al. Epidemiologic differences between cyclosporiasis and cryptosporidiosis in Peruvian children. Emerging Infect. Dis. 2002;8(6):581-585.
  55. Negm AY. Human pathogenic protozoa in bivalves collected from local markets in Alexandria. J Egypt Soc Parasitol. 2003;33(3):991-998.
  56. Ashford RW,Warhurst DC, Reid GD. Human infection with cyanobacterium-like bodies. Lancet 1993;341:1034.
  57. Eberhard ML, da Silva AJ, Lilley BG, Pieniazek NJ. Morphological and molecular characterization of new Cyclospora species from Ethiopian monkeys: C. cercopitheci sp.n., C. colobi sp.n., and C. papioni sp.n. Emerging Infect. Dis. 1999;5(5):651-658.
  58. Eberhard ML, Njenga MN, DaSilva AJ, Owino D, Nace EK, Won KY, et al. A survey for Cyclospora spp. in Kenyan primates, with some notes on its biology. J. Parasitol. 2001;87(6):1394-1397.
  59. Smith HV, Paton CA, Girdwood RW, Mtambo MM. Cyclospora in non-human primates in Gombe, Tanzania. Vet. Rec. 1996;138(21):528.
  60. Alfano-Sobsey EM, Eberhard ML, Seed JR, Weber DJ, Won KY, Nace EK, et al. Human challenge pilot study with Cyclospora cayetanensis. Emerging Infect. Dis. 2004;10(4):726-729.
  61. Wurtz R. Cyclospora: a newly identified intestinal pathogen of humans. Clin Infect Dis 1994;18:620-623.
  62. Gatei W,Wamae CN, Mbae C,WaruruA, Mulinge E,Waithera T, et al. Cryptosporidiosis: prevalence, genotype analysis, and symptoms associated with infections in children in Kenya. Am J Trop Med Hyg 2006;75(1):78-82.
  63. Mohamed HA, Molyneux DH. Developmental stages of Cyclospora talpae in the liver and bile duct of the mole Talpa europaea. Parasitol 1990;101:345-350.
  64. Pellérdy L, Tanyi Z. Cyclospora talpae sp.n. (Protozoa: Sporozoa) from the liver of Talpa europaea. Folia Parasitol (Praha) 15: 275-277 1968;15:275-277.

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