Cryptosporidiosis is a highly prevalent GI parasitic disease caused by species of the protozoal genus Cryptosporidium that infect a wide range of animals, including humans, throughout the world. Cryptosporidiosis is very important in neonatal ruminants, in which it is characterized by mild to severe diarrhea, lethargy, and poor growth rates. In infected individuals, Cryptosporidium oocysts can be detected in fecal smears or fecal flotation sediments stained with an acid-fast stain. Treatment is supportive, consisting of antidiarrheal remedies and replacement of fluids and electrolytes. Strict hygiene is cardinal to preventing infections.
Cryptosporidiosis is a common GI parasitic disease of great importance in neonatal calves, lambs, goat kids, and children, for which no completely effective treatment exists (see cryptosporidiosis video). It is caused by ubiquitous protozoa (Cryptosporidium spp) that contaminate water and food and are difficult to eliminate from the environment.
Etiology and Epidemiology of Cryptosporidiosis
Nineteen species and 40 genotypes of Cryptosporidium have been identified. C hominis (formerly C parvum type I) is a specific human pathogen. C parvum (formerly C parvum type II) is zoonotic and infective to many animals, including humans and calves.
Four cryptosporidial species have been isolated from cattle: C parvum, C andersoni, C bovis, and C ryanae. C andersoni infects the abomasum of older cattle; C bovis and C ryanae are found in weaned calves.
C parvum is a common cause of diarrhea in neonatal calves, and cryptosporidial oocysts have been detected in the feces of 28–80% of dairy calves 1–3 weeks old (1). Infection can be detected as early as 5 days old, and most calves excrete organisms between days 5 and 12 after infection. Diarrhea in calves 5–15 days old is often a result of cryptosporidial infection.
C parvum, C ubiquitum, and C xiaoi frequently infect young lambs and goats. Diarrhea can result from a monoinfection; however, it is more commonly associated with mixed infections. Infection can result in severe outbreaks of diarrhea, with high case fatality rates in lambs 4–10 days old and in goat kids 5–21 days old.
C parvum, C suis, and C scrofarum are commonly reported in pigs from 1 week old through market age—a wider age range than in ruminants. Most infections are subclinical, and the organism does not appear to be an important enteric pathogen in pigs; however, it can contribute to malabsorptive diarrhea in nursing and postweaning piglets.
Cryptosporidial infection in foals appears less prevalent and occurs at a later age than in ruminants, with excretion rates peaking at 5–8 weeks old. Infection is not usually detected in yearlings or adult horses. Most studies indicate that cryptosporidiosis is not common in foals; infections in immunocompetent foals are usually subclinical. Persistent clinical infections occur in Arabian foals with inherited combined immunodeficiency.
Cryptosporidiosis is also recorded in young deer and can be a cause of diarrhea in artificially reared orphans.
Transmission of Cryptosporidiosis
The source of cryptosporidial infection is oocysts that are fully sporulated and infective when excreted in feces. Large numbers (104–108 oocysts/gram feces) are excreted during the patent period, resulting in heavy environmental contamination. Infection can be transmitted directly from calf to calf, indirectly via fomite or human transmission, via contamination in the environment, or via fecal contamination of the feed or water supply.
Ingestion of as few as 17 cryptosporidial oocysts can lead to infection. Oocyst shedding during the patent phase of infection can be intermittent. A periparturient rise in the excretion of oocysts can occur in ewes. Cryptosporidium parvum is not host specific, and infection from other species (eg, rodents, farm cats) via contamination of feed is also possible.
Cryptosporidial oocysts are resistant to most disinfectants and can survive for several months in cool, moist conditions. Oocyst infectivity can be destroyed by freeze-drying and exposure to temperatures < –20°C (–4°F) or > 65°C (149°F). Ammonium hydroxide (5%) and hydrogen peroxide (10%) are effective at destroying oocyst infectivity after approximately 30 minutes of exposure (2, 3). Infectivity of oocysts in calf feces decreases after 1–4 days of drying.
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Concurrent infections with other enteric pathogens, especially rotavirus and coronavirus, are common in cryptosporidiosis cases, and epidemiological studies suggest that diarrhea is more severe in mixed infections. Immunocompromised animals are more susceptible to disease than are immunocompetent animals; however, the relationship between disease and failure of passive transfer of colostral immunoglobulins is not clear.
Age-related resistance to Cryptosporidium infection, unrelated to prior exposure, occurs in lambs but not in calves. Infection results in the production of parasite-specific antibodies; however, both cell-mediated and humoral antibodies, as well as local antibodies in the gut of neonates, are important in protection.
Case fatality rates in cryptosporidiosis are generally low, unless the condition is complicated by other factors (eg, concurrent infections, energy deficits from inadequate intake of colostrum and milk, or chilling due to adverse weather conditions).
Pathogenesis of Cryptosporidiosis
The life cycle of Cryptosporidium consists of six major developmental events. Ingestion of the oocyst is followed by excystation (release of infective sporozoites), merogony (asexual multiplication), gametogony (gamete formation), fertilization, oocyst wall formation, and sporogony (sporozoite formation).
Oocysts of Cryptosporidium spp can sporulate within host cells and are infective when passed in the feces. Infection persists until the host’s immune response eliminates the parasite.
In natural and experimentally produced cases of cryptosporidiosis in calves, cryptosporidia are most numerous in the lower part of the small intestine and less common in the cecum and colon. Prepatent periods are 2–7 days in calves and 2–5 days in lambs. Oocysts are usually passed in the feces of calves for 3–12 days.
Clinical Findings of Cryptosporidiosis
Calves with cryptosporidiosis usually have mild to moderate diarrhea that persists for several days, regardless of treatment. The age at onset is later and the duration of diarrhea tends to be a few days longer than in cases of diarrhea caused by rotavirus, coronavirus, or enterotoxigenic Escherichia coli. Feces are yellow or pale and watery, and they contain mucus (see diarrhea and fecal matting images).
Courtesy of Dr. William Harold Witola.
Courtesy of Dr. William Harold Witola.
Persistent diarrhea can result in marked weight loss and emaciation. In most cases of cryptosporidiosis, diarrhea is self-limiting after several days. Varying degrees of listlessness, anorexia, and dehydration are present. Only rarely do severe dehydration, weakness, and collapse occur, in contrast to findings with other causes of acute diarrhea in neonatal calves.
Case fatality rates can be high in herds with cryptosporidiosis when the calf feeder withholds milk and feeds only electrolyte solutions during the episode of diarrhea. The persistent nature of the diarrhea leads to a marked energy deficit in these circumstances, and the calves often die of inanition at 3–4 weeks old.
Lesions of Cryptosporidiosis
The small intestine in cases of cryptosporidiosis shows villous atrophy. Histologically, large numbers of the parasite are embedded in the microvilli of the absorptive enterocytes. In low-grade infections, only a few parasites are present, with no apparent histopathological changes in the intestine. The villi are shorter than normal, with crypt hyperplasia and a mixed inflammatory cell infiltrate.
Diagnosis of Cryptosporidiosis
Clinical signs
Detection of Cryptosporidium oocysts in fecal smears
Diagnosis of cryptosporidiosis is based on the detection of cryptosporidial oocysts by microscopic examination of fecal smears stained with acid-fast stain (Ziehl-Neelsen or modified Kinyoun), fecal flotation, ELISA, immunochromatographic lateral flow assay, direct immunofluorescence assay, and PCR assay. Fecal flotation (using Sheather's solution) is the most sensitive (67–92%) and specific (88–100%) of these techniques, with a relatively low cost per test.
Fecal flotation requires centrifuging a homogenized fecal sample suspension in saturated sucrose or sodium chloride solution, aspirating the top layer and diluting it in distilled water (5-times dilution or more), centrifuging, placing the sediment on a slide, and performing acid-fast staining to look for cryptosporidial oocysts that appear as red spherical to ovoid structures (4–6 mcm in diameter) by light microscopy (see fecal smear image).
Courtesy of Dr. William Harold Witola.
Generally, if diarrhea is caused by cryptosporidia, there should be 104–108 oocysts/gram of feces. In unstained fresh fecal smears, the oocysts are difficult to detect by normal light microscopy, but they are readily detected by phase-contrast microscopy as small (4–6 mcm in diameter), nonrefractile spherules.
Treatment of Cryptosporidiosis
Supportive care
Nutritional support
Antidiarrheal remedies
No licensed drugs are available in the US to treat Cryptosporidium parvum infection in food animals. Anecdotal reports of success with extralabel use of various compounds have not been replicated in controlled trials. However, various experimental drugs are being investigated:
Halofuginone (registered in several countries but not in the US), when administered at 4 mg/kg, PO, every 24 hours for 7 days, has been found to decrease disease severity and oocyst shedding in calves (4).
Paromomycin (not registered in the US), when administered at 100 mg/kg, PO, every 24 hours for 11 days, has proved successful in suppressing oocyst shedding and disease in lambs and goat kids (4).
A phytocomplex feed supplement (combination of green tea, cinnamon oil, and pomegranate extracts), given at 400–1,200 g/tonne of feed, has been found to markedly suppress oocyst shedding and ameliorate disease progression in calves (5, 6).
Calves with cryptosporidiosis should receive supportive treatment with fluids and electrolytes, both orally and parenterally, as needed until recovery is complete. Whole milk from cows should be given in small quantities several times daily (to the full requirement) to optimize digestion and minimize weight loss.
Several days of intensive care and feeding might be required before recovery is apparent. Parenteral nutrition may be considered for valuable calves.
Control of Cryptosporidiosis
Cryptosporidiosis is difficult to control. Decreasing the number of oocysts ingested can decrease the severity of infection and allow immunity to develop. Calving should take place in a clean environment, and adequate amounts of colostrum should be fed at an early age.
Calves should be kept separate, without calf-to-calf contact, for at least the first 2 weeks of life, with strict hygiene at feeding. Diarrheic calves should be isolated from healthy calves during the course of diarrhea and for several days after recovery. Great care must be taken to avoid mechanical transmission of cryptosporidial infection.
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Calf-rearing houses should be vacated and cleaned out on a regular basis; an all-in all-out management system, with thorough cleaning and several weeks of drying between batches of calves, should be used. Rats, mice, and flies should be controlled when possible, and rodents and pets should not have access to calf grain and milk feed storage areas.
Hyperimmune bovine colostrum can decrease the severity of diarrhea and the period of cryptosporidial oocyst excretion in experimentally infected calves. Protection is not related to circulating levels of specific antibodies but requires a high titer of C parvum antibodies in the gut lumen for prolonged periods. Many research groups have attempted to develop effective vaccines against cryptosporidia; to date, however, vaccinations against Cryptosporidium have not been effective.
Zoonotic Risk of Cryptosporidiosis
Infections of cryptosporidiosis in domestic animals can be a reservoir for infection of susceptible humans. C hominis and C parvum are considered relatively common nonviral causes of self-limiting diarrhea in immunocompetent humans, particularly children. In immunocompromised humans, however, disease can be severe.
In humans, Cryptosporidium infection is transmitted predominantly from person to person; however, direct infection from animals and waterborne infection via contamination of surface water and drinking water by domestic or wild animal feces can also be important.
Animal handlers on a calf farm can be at high risk of developing diarrhea due to cryptosporidiosis transmitted from infected calves. Immunocompromised people should be restricted from access to young animals and possibly from access to farms.
Key Points
Cryptosporidiosis is a GI parasitic disease of vertebrate animals and humans.
The disease is noteworthy in young ruminants, in which it causes mild to severe diarrhea and delayed growth.
Cryptosporidium oocysts can be detected in acid-fast–stained fecal smears of infected animals.
No fully effective drugs exist to treat cryptosporidiosis; supportive care is indicated.
Control involves strict hygiene to eliminate or decrease contamination of the environment by Cryptosporidium oocysts.
For More Information
Rideout H, Cook AJC, Whetton AD. Understanding the Cryptosporidium species and their challenges to animal health and livestock species for informed development of new, specific treatment strategies. Front Parasitol. 2024;3:1448076.
Khan SM, Witola WH. Past, current, and potential treatments for cryptosporidiosis in humans and farm animals: a comprehensive review. Front Cell Infect Microbiol. 2023;13:1115522.
Tomazic ML, Garro C, Schnittger L. Cryptosporidium. In: Florin-Christensen M, Schnittger L (ed.). Parasitic Protozoa of Farm Animals and Pets. Springer; 2018:11–54.
Thomson S, Hamilton CA, Hope JC, et al. Bovine cryptosporidiosis: impact, host-parasite interaction and control strategies. Vet Res. 2017;48:42.
Also see pet owner content regarding GI parasites in horses.
References
Thomson S., Hamilton CA, Hope JC, et al. Bovine cryptosporidiosis: impact, host-parasite interaction and control strategies. Vet Res. 2017;48(1):42. doi:10.1186/s13567-017-0447-0
Weir SC, Pokorny NJ, Carreno RA, Trevors JT, Lee H. Efficacy of common laboratory disinfectants on the infectivity of Cryptosporidium parvum oocysts in cell culture. Appl Environ Microbiol. 2002;68(5):2576-2579. doi:10.1128/AEM.68.5.2576-2579.2002
Robertson LJ, Campbell AT, Smith HV. (1992) Survival of Cryptosporidium parvum oocysts under various environmental pressures. Appl Environ Microbiol 58:3494–3500
Rideout H, Cook AJC, Whetton AD. Understanding the Cryptosporidium species and their challenges to animal health and livestock species for informed development of new, specific treatment strategies. Front Parasitol. 2024;3:1448076. doi:10.3389/fpara.2024.1448076
Park I, Nam H, Wickramasuriya SS, et al. Host-mediated beneficial effects of phytochemicals for prevention of avian coccidiosis. Front Immunol. 2023;14:1145367. doi:10.3389/fimmu.2023.1145367
Witola WH. Efficacy of Trouw Nutrition Phytocompounds Against Cryptosporidiosis in Bovine Calves. Unpublished manuscript. College of Veterinary Medicine, University of Illinois Urbana-Champaign; 2024.
