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Volume 3, Number 1—March 1997

Cryptosporidiosis: An Emerging, Highly Infectious Threat

Richard L. Guerrant
Author affiliation: University of Virginia School of Medicine, Charlottesville, Virginia, USA

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Cryptosporidium parvum, a leading cause of persistent diarrhea in developing countries, is a major threat to the U.S. water supply. Able to infect with as few as 30 microscopic oocysts, Cryptosporidium is found in untreated surface water, as well as in swimming and wade pools, day-care centers, and hospitals. The organism can cause illnesses lasting longer than 1 to 2 weeks in previously healthy persons or indefinitely in immunocompromised patients; furthermore, in young children in developing countries, cryptosporidiosis predisposes to substantially increased diarrheal illnesses. Recent increased awareness of the threat of cryptosporidiosis should improve detection in patients with diarrhea. New methods such as those using polymerase chain reaction may help with detection of Cryptosporidium in water supplies or in asymptomatic carriers. Although treatment is very limited, new approaches that may reduce secretion or enhance repair of the damaged intestinal mucosa are under study.

An emerging infection comes to our attention because it involves a newly recognized organism, a known organism that newly started to cause disease, or an organism whose transmission has increased. Although Cryptosporidium is not new, evidence suggests that it is newly spread (in increasingly used day-care centers and possibly in widely distributed water supplies, public pools, and institutions such as hospitals and extended-care facilities for the elderly); it is newly able to cause potentially life-threatening disease in the growing number of immunocompromised patients; and in humans, it is newly recognized, largely since 1982 with the AIDS epidemic. Cryptosporidium is a most highly infectious enteric pathogen, and because it is resistant to chlorine, small and difficult to filter, and ubiquitous in many animals, it has become a major threat to the U.S. water supply. This article will focus on the recognition and magnitude of cryptosporidiosis, the causative organism and the ease with which it is spread, outbreaks of cryptosporidiosis infection, and its pathogenesis, diagnosis, and treatment.

Recognition and Magnitude of Cryptosporidiosis

First recognized by Clarke and Tyzzer (1) at the turn of the century and well known to veterinarians, Cryptosporidium was reported as a human pathogen in 1976 by Nime (2). From 1976 until 1982, seven cases of cryptosporidiosis were reported in humans, five of which were in immunosuppressed patients. Since 1982, cryptosporidiosis has been increasingly recognized as a cause of severe, life-threatening diarrhea in patients with AIDS as well as in previously healthy persons (3). Of the first 58 cases of cryptosporidiosis described in humans by 1984, 40 (69%) were in immunocompromised patients who contracted severe, often irreversible, diarrhea (lasting longer than 4 months in 65%); of these 40 patients, 33 (83%) had AIDS (4-6); 55% of the 40 immunocompromised patients died.


Thumbnail of Prevalence of IgG antibodies to Cryptosporidium parvum, by age, in Brazil, China, and the United States.

Figure. Prevalence of IgG antibodies to Cryptosporidium parvum, by age, in Brazil, China, and the United States.

A review of 78 reports of more than 131,000 patients and more than 6,000 controls showed Cryptosporidium infection in 2.1% to 6.1% of immunocompetent persons in industrialized and developing countries, respectively, vs. 0.2% to 1.5% in controls (Table 1). A review of an additional 22 reports of nearly 2,000 human immunodeficiency virus (HIV)-infected persons showed Cryptosporidium infection in 14% to 24% of HIV-infected persons with diarrhea vs. 0% to 5% of HIV-infected controls without diarrhea (7). Seroepidemiologic studies suggest that 17% to 32% of nonimmunocompromised persons in Virginia, Texas, and Wisconsin, as well as nonimmunocompromised Peace Corps volunteers (before travel), have serologic evidence of Cryptosporidium infection by young adulthood. In contrast, more than half of the children in rural Anhui, China, had serologic evidence of cryptosporidial infection by 5 years of age, and more than 90% of children living in an impoverished area of Fortaleza, Brazil, had serologic evidence of cryptosporidial infection in their first year of life (Figure) (8-11).

The Organism

Among protozoa, C. parvum is the major human pathogen that is also found in numerous mammals. It is slightly smaller than the murine Cryptosporidium, C. muris, and is also distinguished from the other Cryptosporidium species commonly seen in birds, turkeys, snakes, and fish. Infection begins when a person ingests chlorine-resistant, thick-walled oocysts (7). These hardy oocysts appear to be infectious, with an estimated ID50 (from studies in humans) of one isolate containing only 132 oocysts (12). Infections may occur with ingestion of as few as 30 oocysts; some infections have occurred with just one oocyst (13).

When the oocysts reach the upper small bowel, the proteolytic enzymes and bile salts enhance the excystation of four infectious sporozoites, which enter the brush border surface epithelium and develop into merozoites capable of replicating either asexually or sexually beneath the cell membrane (but extracytoplasmically) in the brush border epithelial cell surface. Sexual stages combine to form new oocysts, some of which (perhaps 20% as thin-walled oocysts) may sporulate and continue infection in the same person, while others (thick-walled oocysts) are excreted. Although few organisms may enter through M cells, systemic infection essentially does not occur; the occasional biliary tract or respiratory tract infections in immunocompromised patients probably reached these sites through the lumenal surface.

Cryptosporidiosis Outbreaks

Numerous well-documented outbreaks of cryptosporidiosis have occurred. Most of these often waterborne outbreaks have involved subtle problems in the flocculation and/or filtration process (17-21). These outbreaks culminated in the huge waterborne outbreak in Milwaukee, which was initially thought to be viral gastroenteritis, reported to the State Health Department on April 5, 1993, diagnosed on April 7, and followed by an advisory note that evening to the public to boil all drinking water (Table 2). This became the largest waterborne outbreak in U.S. history and affected an estimated 403,000 persons, thus constituting a 52% attack rate among those served by the South Milwaukee water works plant. Several immunocompromised patients died, and many previously healthy persons became ill. The mean duration of illness was 12 days with a range of 1 to 55 days, and the average maximum number of watery diarrheal stools was 19 per day at the peak of illness. While watery diarrhea was the predominant symptom among 93% of confirmed cases, other symptoms such as abdominal pain, low-grade fever, and vomiting were not infrequent; 75% of infected nonimmunocompromised persons had an average 10-lb weight loss.

Additional outbreaks involving public swimming pools and wade pools have further documented the ability of Cryptosporidium to cause infection even when ingested in relatively small amounts of fully chlorinated water (22-26). While the leading causes of 129 drinking and recreational water outbreaks in the United States from 1991 through 1994 were Giardia and Cryptosporidium, cryptosporidiosis accounted for substantially more cases (even if the Milwaukee outbreak were excluded) (23,24,26). In addition, although Cryptosporidium oocysts cannot multiply in the environment, an outbreak of foodborne cryptosporidiosis, affecting 54% of those ingesting incriminated freshly pressed apple cider, has been reported (27). In this outbreak, Cryptosporidium oocysts were found in the cider press, as well as in a calf on the farm from which the apples were obtained. There was also a 15% secondary attack rate in households involved in this outbreak. The apparent person-to-person spread in households and institutions such as day-care centers and hospitals further documents the highly infectious nature of Cryptosporidium. In an urban slum area in northeastern Brazil, secondary household infections occurred in 58% of households with an infected child (index case) despite the 95% prevalence of antibody in children more than 2 years of age (28).

The spread of cryptosporidiosis in day-care centers is well documented, with 14 outbreaks reported in the United States, as well as others in the United Kingdom, France, Portugal, Australia, Chile, and South Africa (29). Illnesses usually occurred in the summer and early fall, especially during August and September in the United States and Portugal. Attack rates were 13% to 90%, with the highest rates found among nontoilet-trained toddlers and staff caring for children in diapers. Overall prevalence rates were usually in the 1.8% to 3.8% range; however, rates as high as 30% in day-care homes were reported (30). During outbreaks, 3.7% to 22.9% of infected children may not have diarrhea; infectious oocysts may be excreted for up to 5 weeks after diarrheal illness ends (31). In addition, numerous nosocomial outbreaks of cryptosporidiosis have occurred among healthcare workers as well as patients in bone marrow transplant units, pediatric hospitals, and patient wards with HIV-infected patients (32-37). Furthermore, elderly hospitalized patients may also be at risk for Cryptosporidium infection (38). In one Pennsylvania hospital, 45% of nurses, medical students, and house staff caring for an HIV-positive patient with cryptosporidiosis seroconverted (39).

Numerous potential animal and water sources have been found to be infected with Cryptosporidium. In the Gonçalves Dias slum in Fortaleza, Brazil, 10% of animals (including dogs, pigs, donkeys, and goats), 6.3% during the dry season to 14.3% during the wet season, had Cryptosporidium in their stool specimens. In addition, 22% of drinking water sources studied were infected with Cryptosporidium oocysts (40). Furthermore, LeChavalier et al. have documented that Cryptosporidium oocysts were present in 27% of 66 drinking water samples obtained from 14 states and one Canadian province (mean of 0.18 NTU) (41,42).

Pathogenesis and Impact

C. parvum does not infect tissue beyond the most superficial surface of the intestinal epithelium; however, it can derange intestinal function. Although a parasite enterotoxin has been extensively sought and some reports have suggested that one may exist (43), this issue remains controversial, and the source of substances in the stools of infected animals and patients that induce secretion remains unclear (44). Extensive studies in a piglet model of cryptosporidiosis by Argenzio and colleagues demonstrate the loss of vacuolated villus tip epithelium (approximately two-thirds of the villus surface area), accompanied by an approximate 50% reduction in glucose-coupled sodium cotransport. What remains is a predominance of transitional junctional epithelium, in which increased glutamine metabolism drives a sodium-hydrogen exchange, to which is coupled chloride transport. Thus, glutamine drives neutral sodium chloride absorption in an apparent prostaglandin-inhibitable manner in Cryptosporidium-infected piglet epithelium (45). Furthermore, Argenzio and colleagues have demonstrated increased macrophages that produce increased tumor necrosis factor (TNF) in the lamina propria of Cryptosporidium-infected piglets (46). Although TNF did not directly affect epithelial transport, when a fibroblast monolayer was added, an indomethacin-inhibitable secretory effect was noted with TNF (46). Consequently, the researchers propose a prostaglandin-dependent secretory effect, which occurs 1) through a bumetanide-inhibitable chloride secretory pathway, predominantly from crypt cells; and 2) through the inhibition of neutral sodium chloride absorption through the amiloride-sensitive sodium:hydrogen exchanger, predominantly in the junctional or transitional epithelium during active cryptosporidial infection. Reduced xylose and B-12 absorption are among the effects described in humans and animals with cryptosporidiosis (47-49). Disruption of intestinal barrier function with strikingly increased lactulose to mannitol permeability and absorption has been documented during active symptomatic cryptosporidial infection in children and in HIV-infected adults (Lima et al., unpublished observations) (50).

Cryptosporidium appears to be one of the leading causes of diarrhea, especially persistent diarrhea, among children in northeastern Brazil (51,52). In addition, the incidence of diarrhea has been nearly double for many months in young children after symptomatic cryptosporidial infections, suggesting that the disrupted barrier function in infected children leaves residual damage resulting in increased susceptibility of injured epithelium to additional diarrheal illnesses (Agnew et al., unpub. obs.).

Recognition and Diagnosis

The diagnosis of C. parvum in patients with diarrhea is usually made by using acid-fast or immunofluorescence staining on unconcentrated fecal smears. Appropriate concentration methods may enhance detection when small numbers of oocysts are present, but some methods such as formalin-ethyl acetate concentration may result in loss of many oocysts (52,53). While several enzyme-linked immunosorbent assay methods are available for detection of fecal cryptosporidial antigen with 83% to 95% sensitivity in diarrheal specimens, these methods are less sensitive in formed specimens and require more time. Microscopy using immunofluorescence antibody is slightly more sensitive and may be faster (54,55).

Polymerase chain reaction (PCR) provides a new method that may help detect Cryptosporidium in water supplies or asymptomatic carriers. A genomic DNA library has been constructed in the plasmid pUC18 for propagation in Escherichia coli. After sequencing a 2.3 kilobase C. parvum-specific fragment, a 400-base sequence with a unique Sty I site has been amplified by using primers of 26 nucleotides each (56). Laxer et al. then used a 20-base probe labeled with digoxigenin-11-dUTP to detect C. parvum DNA in fixed, paraffin-embedded tissue (57). In addition, primers for a 556 BP Cryptosporidium-specific region of the small subunit 18s ribosomal RNA gene have been used to produce a PCR product with unique Mae 1 sites that distinguish C. parvum from C. baileyi and C. muris (58). Available methods for detection of viable oocysts in environmental samples are relatively insensitive and under active investigation.

Treatment and Prevention

Despite numerous attempts at examining transfer factor, hyperimmune colostral antibody, and more than 100 antiparasitic and antimicrobial agents, few agents have shown modest benefit in controlled studies; paromomycin is one of them. Although this agent does not eradicate the parasite in immunocompromised patients, it slightly reduces parasite numbers (from 314 x 106 to 109 x 106 oocysts shed per day) and decreases stool frequency, with a tendency toward improved Karnofsky scores and reduced stool weight (59). In view of its effectiveness in driving sodium cotransport (60) and its success in studies of experimental animals, we are examining a new approach to speeding repair of disrupted intestinal barrier function by using glutamine and its derivatives.

The ability of the thick-walled oocysts to persist and spread in the environment and their well-documented resistance to chlorine are responsible for the spread of Cryptosporidium even in fully chlorinated water supplies that meet existing turbidity standards in drinking water and swimming pools. Although some scientists have noted that 9,600 parts per million (mg/l) of chlorine for one minute of exposure are required to decontaminate water (14), others have noted that even after exposure to full-strength household bleach (5.25% sodium hypochlorite; 50,000 parts per million) for 2 hours, the oocysts still remained infectious for experimental animals (15). While Giardia are 14 to 30 times more susceptible to chlorine dioxide or ozone, respectively, ozone is probably the most effective chemical means of inactivating Cryptosporidium oocysts (16). Consequently, eradication of the organism from drinking water supplies depends on adequate flocculation and filtration, rather than chlorination. Although previous turbidity requirements were based on the removal of larger parasite cysts such as those of Giardia lamblia or Entamoeba histolytica, the smaller C. parvum oocysts are more difficult to remove. Several waterborne outbreaks, including the recent outbreak in Milwaukee, have occurred with turbidity levels in the 0.45 to 1.7 nephelometry turbidity units (NTU) range. In a study of waterborne cryptosporidiosis, predominantly among HIV-positive adults in Clark County, Nevada, Goldstein et al. (1996) report that the outbreak was associated with a substantial number of deaths and that the turbidity of the implicated water never exceeded 0.17 NTU (much lower than the new standard of 0.5 NTU required for 95% of measurements each month, with no spikes over 1.0 NTU) (5).

New approaches to the eradication of infectious oocysts from water supplies are needed, possibly using reverse osmosis, membrane filtration, or electronic or radiation methods, instead of the ineffective chemical or difficult filtration techniques currently used. Ideally, these new methods would provide low cost, effective treatment that could be applied in developing areas as well. Meanwhile, an improved understanding of the pathogenesis and impact of Cryptosporidium infections should aid the development of improved treatment and control of this ubiquitous, highly infectious threat to the water supply and to the people it serves, especially malnourished children and immunocompromised patients around the world.

Dr. Guerrant is Thomas H. Hunter Professor of International Medicine and director, Office of International Health, University of Virginia School of Medicine. He holds several patents on innovative approaches to the diagnosis and treatment of common gastrointestinal illnesses. In addition to his many other contributions, Dr. Guerrant is instrumental in shaping tropical medicine training in the United States.



Much of our work on cryptosporidiosis is supported by an International Collaboration in Infectious Diseases Research Grant #2 U01 AI26512 from the National Institute of Allergy and Infectious Diseases, National Institutes of Health. Some of these materials were presented as a part of an American Society for Microbiology symposium on emerging infections at the 95th general meeting in Washington, D.C.



  1. Tyzzer  EE. A sporozoan found in the peptic glands of the common mouse. Proc Soc Exp Biol Med. 1907;5:123.
  2. Nime  FA, Burek  JD, Page  DL, Holscher  MA, Yardley  JH. Acute enterocolitis in a human being infected with the protozoan Cryptosporidium. Gastroenterology. 1976;70:5928.PubMedGoogle Scholar
  3. Current  WL. Human cryptosporidiosis. N Engl J Med. 1983;309:13257.PubMedGoogle Scholar
  4. Navin  TR, Juranek  DD. Cryptosporidiosis: clinical, epidemiologic, and parasitologic review. Rev Infect Dis. 1984;6:31327.PubMedGoogle Scholar
  5. Goldstein  ST, Juranek  DD, Ravenholt  O, Hightower  AW, Martin  DG, Mesnik  JL, Cryptosporidiosis: An outbreak associated with drinking water despite state-of-the-art water treatment. Ann Intern Med. 1996;124:459.PubMedGoogle Scholar
  6. Vakil  NB, Schwartz  SM, Buggy  BP, Brummitt  CF, Kherellah  M, Letzer  DM, Biliary cryptosporidiosis in HIV-infected people after the waterborne outbreak of cryptosporidiosis in Milwaukee. N Engl J Med. 1996;334:1923. DOIPubMedGoogle Scholar
  7. Adal  KA, Sterling  CR, Guerrant  RL. Cryptosporidium and related species. In: Blaser MJ, Smith PD, Ravdin JI, Greenberg HB, Guerrant RL, editors. Infections of the gastrointestinal tract. New York: Raven Press; 1995;72:1107-28.
  8. Zu  S-X, Li  J-F, Barrett  LJ, Fayer  R, Zhu  S-Y, McAuliffe  JF, Seroepidemiologic study of Cryptosporidium infection in children from rural communities of Anhui, China. Am J Trop Med Hyg. 1994;51:110.PubMedGoogle Scholar
  9. Ungar  BLP, Soave  R, Fayer  R, Nash  TE. Enzyme immunoassay detection of immunoglobulin M and G antibodies to Cryptosporidium in immunocompetent and immunocompromised persons. J Infect Dis. 1986;153:5708.PubMedGoogle Scholar
  10. Ungar  BL, Gilman  RH, Lanata  CF, Peres-Schael  I. Seroepidemiology of Cryptosporidium infection in two Latin American populations. J Infect Dis. 1988;157:5516.PubMedGoogle Scholar
  11. Ungar  BL, Mulligan  M, Nutman  TB. Serologic evidence of Cryptosporidium infection in US volunteers before and during Peace Corps service in Africa. Arch Intern Med. 1989;149:8947. DOIPubMedGoogle Scholar
  12. DuPont  HL, Chappell  CL, Sterling  CR, Okhuysen  PC, Rose  JB, Jakubowski  W. The infectivity of Cryptosporidium parvum in healthy volunteers. N Engl J Med. 1995;332:8559. DOIPubMedGoogle Scholar
  13. Haas  CN, Rose  JB. Reconciliation of microbial risk models and outbreak epidemiology: the case of the Milwaukee outbreak. Proceedings of the American Water Works Association 1994;517-23.
  14. Centers for Disease Control. Waterborne disease outbreaks, 1986-1988. MMWR CDC Surveill Summ. 1990;39:113.
  15. Fayer  R. Effect of sodium hypochlorite exposure on infectivity of Cryptosporidium parvum oocysts for neonatal BALB/c mice. Appl Environ Microbiol. 1995;61:8446.PubMedGoogle Scholar
  16. Korich  DG, Mead  JR, Madore  MS, Sinclair  NA, Sterling  CR. Effects of ozone, chlorine dioxide, chlorine, and monochloramine on Cryptosporidium parvum oocyst viability. Appl Environ Microbiol. 1990;56:14238.PubMedGoogle Scholar
  17. Rush  BA, Chapman  PA, Ineson  RW. Cryptosporidium and drinking water [Letter]. Lancet. 1987;2:6323. DOIPubMedGoogle Scholar
  18. D'Antonio  RG, Winn  RE, Taylor  JP, Gustafson  TL, Current  WL, Rhodes  MM, A waterborne outbreak of cryptosporidiosis in normal hosts. Ann Intern Med. 1985;103:8868.PubMedGoogle Scholar
  19. Smith  HV, Girdwood  RWA, Patterson  WJ, Hardie  R, Green  LA, Benton  C, Waterborne outbreak of cryptosporidiosis. Lancet. 1988;:1484. DOIPubMedGoogle Scholar
  20. Hayes  EB, Matte  TD, O'Brien  TR, McKinley  TW, Logsdon  GS, Rose  JB, Large community outbreak of cryptosporidiosis due to contamination of a filtered public water supply. N Engl J Med. 1989;320:13726.PubMedGoogle Scholar
  21. MacKenzie  WR, Hoxie  NJ, Proctor  ME, Gradus  MS, Blair  KA, Peterson  DE, A massive outbreak in Milwaukee of Cryptosporidium infection transmitted through the public water supply. N Engl J Med. 1994;331:1617. DOIPubMedGoogle Scholar
  22. McAnulty  JM, Fleming  DW, Gonzalez  AH. A community-wide outbreak of cryptosporidiosis associated with swimming at a wave pool. JAMA. 1994;272:1597600. DOIPubMedGoogle Scholar
  23. Moore  AC, Herwaldt  BL, Craun  GF, Calderon  RL, Highsmith  AK, Juranek  DD. Surveillance for water-borne disease outbreaks—United States, 1991-1992. MMWR CDC Surveill Summ. 1993;42:122.PubMedGoogle Scholar
  24. Kramer  MH, Herwaldt  BL, Craun  GF, Calderon  RL, Juranek  DD. Surveillance for waterborne-disease outbreaks—United States, 1993-1994. MMWR Morb Mortal Wkly Rep. 1996;45:133.PubMedGoogle Scholar
  25. Gerba  CP, Gerba  P. Journal of the Swimming Pool and Spa Industry. 1996;1:918.
  26. Steiner  TS, Thielman  NM, Guerrant  RL. Protozoal agents: what are the dangers for the public water supply. Annu Rev Med 1996.
  27. Millard  PS, Gensheimer  KF, Addiss  DG, Sosin  DM, Beckett  GA, Houck-Jankoski  A, An outbreak of cryptosporidiosis from fresh-pressed apple cider [published erratum appears in JAMA 1995 Mar8;273(10):776]. JAMA. 1994;272:15926. DOIPubMedGoogle Scholar
  28. Newman  RD, Zu  S-X, Wuhib  T, Lima  AAM, Guerrant  RL, Sears  CL. Household epidemiology of Cryptosporidium parvum infection. Ann Intern Med. 1994;120:5005.PubMedGoogle Scholar
  29. Cordell  RL, Addiss  DG. Cryptosporidiosis in child care settings: a review of the literature and recommendations for prevention and control. Pediatr Infect Dis J. 1994;13:3117.
  30. Diers  J, McCallister  GL. Occurrence of Cryptosporidium in home day-care centers in west-central Colorado. J Parasitol. 1989;75:6378. DOIPubMedGoogle Scholar
  31. Stehr-Green  JK, McCaig  L, Remson  HM, Raines  CS, Fox  M, Juranek  DD. Shedding of oocysts in immunocompetent individuals infected with Cryptosporidium. Am J Trop Med Hyg. 1987;36:33842.PubMedGoogle Scholar
  32. Baxby  D, Hart  CA, Taylor  C. Human cryptosporidiosis: a possible case of hospital cross infection. BMJ. 1983;287:17601. DOIPubMedGoogle Scholar
  33. Dryjanski  JD, Gold  JWM, Ritchie  MT, Kurt  RC, Lim  SL, Armstrong  D. Cryptosporidiosis. Case report in a health team worker. Am J Med. 1986;80:7512. DOIPubMedGoogle Scholar
  34. Collier  AC, Miller  RA, Meyers  JD. Cryptosporidiosis after marrow transplantation: person-to-person transmission and treatment with spiramycin. Ann Intern Med. 1984;101:2056.PubMedGoogle Scholar
  35. Gentile  G, Venditti  M, Micozzi  A, Caprioli  A, Donelli  G, Tirindelli  C, Cryptosporidiosis in patients with hematologic malignancies. Rev Infect Dis. 1991;13:8426.PubMedGoogle Scholar
  36. Navarrete  S, Stetler  HC, Avila  C, Aranda  JAG, Santos-Preciado  JI. An outbreak of Cryptosporidium diarrhea in a pediatric hospital. Pediatr Infect Dis J. 1991;10:24850. DOIPubMedGoogle Scholar
  37. Ravn  P, Lundgren  JD, Kjaeldgaard  P, Holten-Anderson  W, Hjlyng  N, Nielsen  JO, Nosocomial outbreak of cryptosporidiosis in AIDS patients. BMJ. 1991;302:27780. DOIPubMedGoogle Scholar
  38. Neill  MA, Rice  SK, Ahmad  NV, Flanigan  TP. Cryptosporidiosisan unrecognized cause of diarrhea in elderly hospitalized patients. Clin Infect Dis. 1996;22:16870.PubMedGoogle Scholar
  39. Koch  KL, Phillips  DJ, Aber  RC, Current  WL. Cryptosporidiosis in hospital personnel. Ann Intern Med. 1985;102:5936.PubMedGoogle Scholar
  40. Newman  RD, Wuhib  T, Lima  AA, Guerrant  RL, Sears  CL. Environmental sources of Cryptosporidium in an urban slum in northeastern Brazil. Am J Trop Med Hyg. 1993;49:2705.PubMedGoogle Scholar
  41. LeChevallier  MW, Norton  WD, Lee  RG. Occurrence of Giardia and Cryptosporidium spp. in surface water supplies [published erratum appears in Appl Environ Microbiol 1992 Feb;58:780]. Appl Environ Microbiol. 1991;57:26106.PubMedGoogle Scholar
  42. LeChevallier  MW, Schulz  W, Lee  RG. Bacterial nutrients in drinking water. Appl Environ Microbiol. 1991;57:85762.PubMedGoogle Scholar
  43. Guarino  A, Canani  RB, Casola  A, Pozio  E, Russo  R, Bruzzese  E, Human intestinal cryptosporidiosis: secretory diarrhea and enterotoxic activity in Caco-2 cells. J Infect Dis. 1995;171:97683.PubMedGoogle Scholar
  44. Sears  CL, Guerrant  RL. Cryptosporiodiosis: the complexity of intestinal pathophysiology. Gastroenterology. 1994;106:2524.PubMedGoogle Scholar
  45. Argenzio  RA, Rhoads  JM, Armstrong  M, Gomez  G. Glutamine stimulates prostaglandin-sensitive Na(+)-H+ exchange in experimental porcine cryptosporidiosis [see comments]. Gastroenterology. 1994;106:141828.PubMedGoogle Scholar
  46. Argenzio  RA, Lecce  J, Powell  DW. Prostanoids inhibit intestinal NaCl absorption in experimental porcine cryptosporidiosis. Gastroenterology. 1993;104:4407.PubMedGoogle Scholar
  47. Modigliani  R, Bories  C, LeCharpentier  Y, Salmeron  N, Messing  B, Galian  A. Diarrhea and malabsorption in acquired immune deficiency syndrome: a study of four cases with special emphasis on opportunistic protozoan infestations. Gut. 1985;26:17987. DOIPubMedGoogle Scholar
  48. Gardner  AL, Roche  JK, Weikel  CS, Guerrant  RL. Intestinal cryptosporidiosis: pathophysiologic alterations and specific cellular and humoral immune responses in rnu/+ and rnu/rnu (athymic) rats. Am J Trop Med Hyg. 1991;44:4962.PubMedGoogle Scholar
  49. Heine  J, Moon  HW, Woodmansee  DB. Persistent Cryptosporidium infection in congenitally athymic (nude) mice. Infect Immun. 1984;43:8569.PubMedGoogle Scholar
  50. Goodgame  RW, Kimball  K, Ou  CN, White  AC Jr, Genta  RM, Lifschitz  CH, Intestinal function and injury in acquired immunodeficiency syndrome-related cryptosporidiosis. Gastroenterology. 1995;108:107582. DOIPubMedGoogle Scholar
  51. Fang  G, Lima  AAM, Martins  CC, Nataro  JP, Guerrant  RL. Etiology and epidemiology of persistent diarrhea in northeastern Brazil: a hospital-based prospective case control study. J Pediatr Gastroenterol Nutr. 1995;21:13744. DOIPubMedGoogle Scholar
  52. Wuhib  T, Silva  TM, Newman  RD, Garcia  LS, Pereira  ML, Chaves  CS, Cryptosporidial and microsporidial infections in human immunodeficiency virus-infected patients in northeastern Brazil. J Infect Dis. 1994;170:4947.PubMedGoogle Scholar
  53. Weber  R, Bryan  RT, Bishop  HS, Wahlquist  SP, Sullivan  JJ, Juranek  DD. Threshold of detection of Cryptosporidium oocysts in human stool specimens: evidence for low sensitivity of current diagnostic methods. J Clin Microbiol. 1991;29:13237.PubMedGoogle Scholar
  54. Newman  RD, Jaeger  KL, Wuhib  T, Lima  AA, Guerrant  RL, Sears  CL. Evaluation of an antigen capture enzyme-linked immunosorbent assay for detection of Cryptosporidium oocysts. J Clin Microbiol. 1993;31:20804.PubMedGoogle Scholar
  55. Kehl  KS, Cicirello  H, Havens  PL. Comparison of four different methods for detection of Cryptosporidium species. J Clin Microbiol. 1995;33:4168.PubMedGoogle Scholar
  56. Laxer  MA, Timblin  BK, Patel  RJ. DNA sequences for the specific detection of Cryptosporidium parvum by the polymerase chain reaction. Am J Trop Med Hyg. 1991;45:68894.PubMedGoogle Scholar
  57. Laxer  MA, D'Nicuola  ME, Patel  R. Detection of Cryptosporidium parvum DNA in fixed, paraffin-embedded tissue by the polymerase chain reaction. Am J Trop Med Hyg. 1992;47:4505.PubMedGoogle Scholar
  58. Awad-El-Kariem  FM, Warhurst  DC, McDonald  V. Detection and species identification of Cryptosporidium oocysts using a system based on PCR and endonuclease restriction. Parasitology. 1994;109:1922. DOIPubMedGoogle Scholar
  59. White  AC Jr, Chappell  CL, Hayat  CS, Kimball  KT, Flanigan  TP, Goodgame  RW. Paromomycin for cryptosporidiosis in AIDS: a prospective, double-blind trial. J Infect Dis. 1994;170:41924.PubMedGoogle Scholar
  60. Lima  AAM, Soares  AM, Freire  JE Jr, Guerrant  RL. Cotransport of sodium with glutamine, alanine and glucose in the isolated rabbit ileal mucosa. Braz J Med Biol Res. 1992;25:63740.PubMedGoogle Scholar




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DOI: 10.3201/eid0301.970106

Table of Contents – Volume 3, Number 1—March 1997

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