key: cord-017622-aqhyt7jg authors: Robertson, Lucy J.; Björkman, Camilla; Axén, Charlotte; Fayer, Ronald title: Cryptosporidiosis in Farmed Animals date: 2013-08-17 journal: Cryptosporidium: parasite and disease DOI: 10.1007/978-3-7091-1562-6_4 sha: doc_id: 17622 cord_uid: aqhyt7jg Cryptosporidiosis was first identified as a disease of veterinary, rather than human medical, importance, and infection of farmed animals with different species of Cryptosporidium continues to be of veterinary clinical concern. This chapter provides insights into Cryptosporidium infection in a range of farmed animals – cattle, sheep, goats, pigs, cervids, camelids, rabbits, water buffalo and poultry – presenting not only an updated overview of the infection in these animals, but also information on clinical disease, infection dynamics and zoonotic potential. Although extensive data have been accrued on, for example, Cryptosporidium parvum infection in calves, and calf cryptosporidiosis continues to be a major veterinary concern especially in temperate regions, there remains a paucity of data for other farmed animals, despite Cryptosporidium infection causing significant clinical disease and also, for some species, with the potential for transmission of infection to people, either directly or indirectly. significant clinical disease and also, for some species, with the potential for transmission of infection to people, either directly or indirectly. Farmed Animals: Overview Farmed animals, also commonly referred to as livestock or domesticated animals, are those animals that are reared in an agricultural setting in order to produce various commodities -usually food (meat, organs, eggs, dairy products), and/or hair or wool. In some settings farmed animals are also used to supply labour, and the manure of domesticated animals is often used as fertilizer. Animals were probably first farmed, that is their breeding and living conditions controlled by their human owners, around 7000-8000 BC during the first transitions from huntergatherer lifestyles to more settled agricultural living. The physiologies, behaviours, lifecycles of farmed animals generally differ quite substantially from those characteristics of the equivalent wild animals, and this difference impacts the interactions of these farmed animals with their parasites. Farmed animals are exposed to different stresses than wild animals, are kept at different densities, and their lifecycles regulated to such an extent that a parasite-host interaction in a farmed animal may differ significantly from that in a wild animal. Additionally, for infections that are of significant clinical importance, farmers may implement control measures (including treatment or prophylaxis) that alter the infection dynamics. With respect to Cryptosporidium infection, for which a satisfactory chemotherapeutic cure or prophylaxis is not yet available, different species infect different species of farmed animal, and may or may not be of clinical relevance. Table 4 .1 provides an overview of the farmed animals included in this chapter, the species of Cryptosporidium to which they are susceptible and brief notes on the clinical relevance. Greater details are provided in the appropriate chapter sections. Various categories of animals that are 'farmed', including mink, foxes, guinea pigs etc. are not included, largely because of a lack of information on Cryptosporidium in these animals in the domesticated setting. Additionally, farmed fish are not included in this chapter. C. parvum a Common in pre-weaned calves -acute onset diarrhoea. Intestinal location C. bovis Common in post-weaned calves -less pathogenic than C. parvum C. andersoni Older post-weaned calves, yearlings and adults-some failure to thrive. Infects the gastric glands of the abomasum C. ryanae Common in post-weaned calves A range of other species has been reported from cattle and other bovines. These seem to be unusual and are apparently of minor clinical significance Small ruminants, including sheep (Ovis aries) and goats (Capra aegagrus hircus) C. parvum a Relatively common in pre-weaned lambs, associated with diarrhoea C. xiaoi Common in older lambs and sheep, often apparently asymptomatic C. ubiquitum a Common in older lambs and sheep, often apparently asymptomatic Pigs (Sus scrofa domesticus) C. parvum a Less common than in bovines and small ruminants; diarrhoea and vomiting C. suis Relatively common, mild symptoms C. scrofarum Relatively common, mild symptoms Deer (cervids), including red deer (Cervus elaphus) fallow deer (Dama dama), elk/wapiti (Cervus canadensis), white-tailed deer (Odocoileus virginianus), and reindeer (Rangifer tarandus) C. parvum a Information on species detected amongst farmed deer is lacking; diarrhoea in young calves, possibly severe, but can also be asymptomatic C. meleagridis a Appears to have a wide host range, including farmed poultry (and mammals). Mostly infects the intestines and has been associated with generally mild clinical symptoms C. baileyi a A wide avian host range reported, including various farmed poultry species. Detected in many different anatomical sites including digestive tract, respiratory tract, and urinary tract. Has been associated with high morbidity and mortality (continued) of various Cryptosporidium species (see Table 4 .1) means that public health may also be affected by infections in farmed animals. Infection may be direct, from animal to human, or indirect, via a transmission vehicle. A large number of small outbreaks associated with C. parvum in calves and in veterinarians or veterinary students that have been exposed to calf faeces are documented in the literature (e.g. Grinberg et al. 2011; Gait et al. 2008; Robertson et al. 2006) . In addition, a number of outbreaks have been documented associated with children visiting 'petting farms' or similar venues, where interaction with young animals such as lambs or calves is encouraged. Less commonly, transmission between animals such as camels or alpacas and their carers has also been reported. Drinking water, and less often food, has been associated with transmission of Cryptosporidium infection from animals to human populations, with C. parvum from grazing cattle contaminating water supplies particularly implicated. The high densities of farmed animals in water catchment areas mean that implementation of catchment control measures, including preventing defecation into water courses, may have a significant effect on minimising the risk from this potential transmission pathway. There are various species of farmed bovines, with cattle and zebu (Bos taurus and Bos indicus, respectively) amongst the most important livestock worldwide. Both provide meat, milk and other dairy products, and are also used as draught animals, with an estimated 1.5 billion head globally (3 cattle for every 14 people). A comprehensive overview of Cryptosporidium infection in cattle has been published by and the information presented here is largely an update built on this solid basis. Domesticated water buffalo (Bubalus bubalis) is also important domestic livestock in the bovinae sub-family. Domesticated buffalo consist of swamp buffalo and river buffalo. In 2011, the world population of buffalo was estimated to approximately 195 million animals, of which 97 % were in Asia (FAOSTAT 2012). The first report on bovine cryptosporidiosis was published in 1971, when parasites were identified in an 8-month-old heifer with chronic diarrhoea (Panciera et al. 1971) . Since then, Cryptosporidium infection in cattle has been documented in most countries worldwide. Four major Cryptosporidium species infect cattle: C. parvum, C. bovis, C. ryanae and C. andersoni (Table 4 .2; Fayer et al. 2007; Feng et al. 2007; Santín et al. 2004; Langkjaer et al. 2007) . Cryptosporidium parvum has a broad host range and apparently has the ability to infect most mammals, including humans and cattle. In contrast, the other three species have almost exclusively been found in cattle. In addition to these four common species, sporadic natural infections with C. felis, C. hominis, C. scrofarum, C. serpentis, C. suis and C. suis-like genotype have been detected in cattle (Bornay-Llinares et al. 1999; Geurden et al. 2006; Langkjaer et al. 2007; Santín et al. 2004; Smith et al. 2005; Chen and Huang 2012) . The extent to which these findings reflect true infections or accidental carriage, i.e. ingested oocysts that pass intact through the gastrointestinal tract, remains to be clarified. Cattle have also been experimentally infected with C. canis, but natural infection has not been reported ). Many reports on Cryptosporidium in cattle in different countries and settings have been published over the years, showing that Cryptosporidium spp. infections are common worldwide. Both dairy and beef cattle are infected and the prevalence estimates vary considerably among studies. Reported herd level prevalences range from 0 to 100 % (Olson et al. 1997; Chang'a et al. 2011; Maddox-Hyttel et al. 2006; Santín et al. 2004 ). Infected animals have been reported from all age groups but infection is most common in preweaned calves. When calves up to 2 months of age have been investigated in point prevalence surveys, 5-93 % of the calves shed oocysts (Table 4.2; Maddox-Hyttel et al. 2006; Santín et al. 2004; Uga et al. 2000) . Longitudinal studies performed in infected dairy herds showed that all calves in such herds shed oocysts at some time during their first months of life (O'Handley et al. 1999; . The overall picture is that there is an age-related pattern in the species distribution. C. parvum is mostly found in preweaned, monogastric calves up to 2 months of age where it is often the most prevalent species, responsible for more than 80 % of Cryptosporidium infections (Brook et al. 2009; Fayer et al. 2007; Plutzer and Karanis 2007; Santín et al. 2004 Trotz-Williams et al. 2006) . In some areas, however, C. bovis is the dominating species found in preweaned calves (Budu-Amoako et al. 2012a; Wang et al. 2011a; Silverlås et al. 2010b ). The prevalence of C. parvum is considerably lower in older calves and young stock, and there are few reports of C. parvum infection in adult cows Langkjaer et al. 2007; Silverlås et al. 2010b; Castro-Hermida et al. 2011a; Khan et al. 2010; Ondrácková et al. 2009; Muhid et al. 2011; Budu-Amoako et al. 2012a, b In older calves and young stock, C. bovis and C. ryanae are the most commonly found species Fayer et al. 2007; Muhid et al. 2011; Langkjaer et al. 2007; Silverlås et al. 2010b) . C. andersoni is mainly found in young stock and adult cattle (Enemark et al. 2002; Wade et al. 2000; Fayer et al. 2007; Ralston et al. 2003) . Older studies, based on microscopy alone, overestimated the C. parvum prevalence in weaned animals because the similarity in oocyst size makes it impossible to differentiate between C. parvum (~5.0 Â 4.5 μm), C. bovis (~4.9 Â 4.6 μm) and C. ryanae (~3.7 Â 3.2 μm). Molecular studies have revealed different genetic subtypes within the C. parvum and C. hominis species and DNA sequence analysis of the 60 kDa glycoprotein gene is commonly used to further characterize the isolates. A number of C. parvum GP60 subtype families, designated IIa-IIo, have been described. Of these, IIc and IIe are considered anthroponotic, whereas IIa and IId are commonly found in both humans and animals. The other subtype families are uncommon and their zoonotic potential has not been determined. In cattle, C. parvum of the IIa subtype family is especially common. In addition to IIa, IId and occasionally IIl (sometimes named IIj) subtypes are found (Table 4 .3; Xiao 2010). Whether there is a difference in pathogenicity between subtypes is currently unknown, as most genotyping studies to date have focused on herds with a history of calf diarrhoea. It has been suggested that herd management strategies affect subtype distribution. Studies from areas with closed herd management (limited animal movements between herds) have shown a high number of subtypes in the calf population, but only one subtype in each herd (Brook et al. 2009; Mišic and Abe 2007; Soba and Logar 2008; ). It has also been shown that a unique GP60 subtype can persist over time in a closed dairy herd (Björkman and Mattsson 2006) . In contrast, only a few subtypes have been identified in areas with more animal movements between herds, but several subtypes could be present in a herd (Brook et al. 2009; Peng et al. 2003; Trotz-Williams et al. 2006 ). The information on the distribution of Cryptosporidium infection in water buffalo is rather fragmentary. Reported prevalences vary between 3 % and 38 % (Table 4.4 ). An association between prevalence of infection and age of the animals, with the highest prevalence in young calves, has been found (Helmy et al. 2013; Maurya et al. 2013; Nasir et al. 2009; Bhat et al. 2012; Díaz de Ramírez et al. 2012 ). The first report on Cryptosporidium species identification in water buffalo was published in 2005, in which Gómez-Couso et al. (2005) used molecular tools to characterize Cryptosporidium oocysts from an asymptomatic neonatal calf in a dairy buffalo farm in Spain. Sequence analysis of a fragment of the oocyst wall protein (COWP) gene revealed that the isolate was closely related to the Cryptosporidium 'pig' genotype. A few years later, C. parvum was identified in water buffalo calves from Italy (Cacciò et al. 2007 ) and today C. ryanae, C. bovis and (Table 4 .4). Most molecular investigations have been done in calves and thus it is not known if the species distribution differs between animals of different age. One of the few studies that include faecal samples from both calves and older animals was done in Egyptian smallholder herds (Helmy et al. 2013) . C. parvum was most common in calves younger than 3 months but was detected in animals up to 2 years of age. In another study, also from Egypt but from another part of the country, C. parvum was only found in calves, whereas none of the sampled cows shed any Cryptosporidium oocysts (Amer et al. 2013) . When the C. parvum isolates were subtyped by sequence analysis of the GP60 gene, subtype families IId and IIa were found, with a majority of IId in both studies. Subtype IId is the dominating subtype family also in cattle in Egypt (Amer et al. 2010; Helmy et al. 2013 ). Cryptosporidium parvum and C. andersoni are the two species that have been associated with clinical disease in cattle. C. parvum infection is considered a major cause of diarrhoea in young calves (Blanchard 2012; Radostits et al. 2007 ). Calves are often already infected during the first week of life (Uga et al. 2000) and clinical cryptosporidiosis is mostly seen in calves up to 6 weeks of age. The most prominent finding is pasty to watery diarrhoea, sometimes accompanied by lethargy, inappetence, fever, dehydration and/or poor condition. The calf most often recovers spontaneously within 1-2 weeks, but there is a large variation between individuals in how they respond to, and recover from, infection. In some cases the infection may be fatal (Tzipori et al. 1983; Fayer et al. 1998) . A decrease in growth rate may be seen in the weeks after the calves have recovered from the acute phase of the disease (Klein et al. 2008 ), but no long-term effects on growth and performance have been reported. The pathogenesis of bovine cryptosporidiosis is not fully understood but the clinical signs are attributed to both malabsorption and an increase in fluid secretion in the ileum and proximal portions of the large intestine. For references and a brief overview see O'Handley and Olson (2006) . Cryptosporidiosis may be seen in individual calves, but frequently it soon develops among the calves into a herd problem. Concomitant infection with other pathogens, e.g. rotavirus, coronavirus and enteropathogenic Escherichia coli (E. coli F5+) can worsen the clinical signs and prolong the duration of illness (Blanchard 2012) . A number of studies have reported an association between C. parvum infection and diarrhoea in young calves. Many of these were published at the time when all Cryptosporidium oocysts of around 3-5 μm in diameter were considered to be C. parvum. More recent investigations, applying molecular methods to analyse faecal samples from diarrhoeic calves, corroborate these earlier findings. When samples from young calves with diarrhoea were analysed, C. parvum is found to be the dominant species (Quílez et al. 2008b; Imre et al. 2011; Karanis et al. 2010; Soba and Logar 2008; Plutzer and Karanis 2007) . Interestingly, this dominance of C. parvum in diarrheic calves was also seen in a recent Swedish investigation of diarrheic calves ), although C. bovis is the predominant species in randomly selected calves in Sweden. Only one experimental trial has been performed with C. bovis (Fayer et al. 2005 ). Three calves under 1-8 weeks of age were orally inoculated with oocysts. This resulted in subclinical infection in 2 of 3 calves. Both animals had, however, previously been infected with C. parvum and cross-protective immunity could not be excluded. Calves with diarrhoea are significantly more likely to be infected with C. parvum than with C. bovis Starkey et al. 2006; Kváč et al. 2011) . Based on these findings, and based on the fact that C. bovis is not common in calves, but is a widespread subclinical infection in older animals in most countries, C. bovis is commonly considered to be apathogenic to cattle. However, the pathogenic potential deserves further attention as high numbers of C. bovis oocysts in samples from diarrhoeic calves have been reported, even in the absence of C. parvum or other diarrhoeal agents (Silverlås et al. 2010a (Silverlås et al. , b, 2013 . Cryptosporidium ryanae was first described as a separate species by Fayer et al. (2008) , and until then it was known as Cryptosporidium deer-like genotype. An experimental trial was performed in two colostrum-deprived calves 17-18 days old. Both calves started excreting oocysts 11 days after inoculation, but neither of them showed any clinical signs ). There are several reports of the distribution of Cryptosporidium deer-like genotype and C. ryanae. Most studies found a predominance of the parasite in older calves and young stock. So far no association with clinical disease has been reported. In contrast to the other species, C. andersoni infects the abomasum. It does not cause diarrhoea, but C. andersoni infections have been associated with maldigestion. The infection may cause moderate to severe weight gain impairment in young stock and reduced milk production in cows (Anderson 1998; Esteban and Anderson 1995; Lindsay et al. 2000) . A major obstacle from a disease control perspective is the lack of effective means to control Cryptosporidium infection and decrease the level of contamination of the environment with oocysts. Preventive hygiene measures and good management are currently the most important tools to control cryptosporidiosis. Reducing the number of oocysts ingested by neonatal calves may reduce the severity of infection and allow immunity to develop. A common recommendation is to ensure good hygiene in calf facilities and ascertain that all newborn calves ingest an adequate amount of colostrum during their first 24 h of life. Sick calves should be housed in a clean, warm, and dry environment and isolated to prevent spreading of the infection to other calves. Acutely infected animals may need supportive care with fluid and electrolytes, and milk should be given in small quantities several times daily to optimise digestion and minimise weight loss. Over the years, several substances have been tested for potential anticryptosporidial effects with limited success . Halofuginone lactate has shown some beneficial effects such as milder clinical signs and reduced oocyst output when used as prophylactic treatment (De Waele et al. 2010; Silverlås et al. 2009a ). This drug is approved in Europe to treat calf cryptosporidiosis. However, the safety margin is narrow and the substance is toxic at only twice the therapeutic dose, so careful dosage is necessary. Halofuginone lactate treatment should only be considered in herds with severe diarrhoeal problems strongly associated with C. parvum. When treatment is used, it should always be in conjunction with applying measures to reduce environmental contamination and risk of infection. A recent study investigated if an antibody-biocide fusion consisting of a monoclonal antibody "armed" with membrane-disruptive peptides (biocides) could be used for treatment of cryptosporidiosis in calves (Imboden et al. 2012) . Calves 36-48 h of age were challenged once with C. parvum oocysts and were simultaneously administered the antibody-biocide fusion mixed with milk replacer. The antibody-biocide fusion treatment was repeated 5-8 times. Control calves were given milk replacer with placebo. Calves receiving the antibody-biocide fusion had a significantly higher health score and shed fewer oocysts than control calves. These results suggest that this concept might be effective in cattle, but further testing is necessary (Imboden et al. 2012) . Vaccination is successfully used to control many infectious diseases in livestock. However, it takes weeks for a protective immune response to develop after a vaccine has been administered, and as calves may be exposed to Cryptosporidium oocysts immediately after birth, vaccination of newborn calves is unlikely to be successful in preventing cryptosporidiosis. Thus it has been suggested that the most feasible approach is likely to involve passive immunisation (Innes et al. 2011) . Dams are immunised in late gestation and their colostrum is fed to the calves. A recent study investigated antibody responses in calves fed colostrum from heifers vaccinated with a recombinant C. parvum oocyst surface protein (rCP15/60). The calves had measurable quantities of the specific antibody in their serum. However, as the calves were not subsequently challenged with oocysts it remains to be seen whether this immunisation scheme can also prevent symptomatic infection and eliminate oocyst shedding (Burton et al. 2011) . An association between Cryptosporidium oocyst shedding and diarrhoea in buffalo calves has been reported from investigations performed in Egypt, India and Venezuela (Mohanty and Panda 2012; Bhat et al. 2012; Maurya et al. 2013; El-Khodery and Osman 2008; Díaz de Ramírez et al. 2012) suggesting the Cryptosporidium infection is part of the calf diarrhoea syndrome in water buffalo, as it is in cattle. Species identification was only performed in one of these studies, and C. parvum was the only species that was found (Maurya et al. 2013 ). Calves begin shedding C. parvum oocysts 2-6 days after infection and shedding continues for 1-13 days Tzipori et al. 1983) . During the first 2 weeks an infected calf can shed millions of oocysts Uga et al. 2000) resulting in heavy environmental contamination, and efficient dissemination of the parasite within the herd and to the environment. In faecal samples obtained from symptomatic calves naturally infected with C. parvum 10 6 -10 8 oocysts per gram faeces (OPG) are often seen ). In herds with established C. parvum infection, most calves are excreting oocysts between 2 and 4 weeks of age (O'Handley et al. 1999; Uga et al. 2000) . When repeatedly sampled the same 30 calves in a dairy herd from birth to 2 years of age they found C. parvum oocysts in faeces of all individuals before they were 3 weeks old, i.e. a cumulative prevalence of 100 %. C. parvum oocysts were also found in samples collected from a calf at 16 weeks of age and from another at 6 months of age, indicating that oocysts can be shed intermittently over a long period after the initial infection. Alternatively, these late-shedding individuals might not have developed a fully protective immunity after the first infection, and rather than this being a sign of prolonged infection, they had acquired new infections. In this study, molecular analyses indicated the same sub-genotype at the GP60 locus. However, this does not necessarily indicate prolonged infection, as re-infection with the same genotype in the environment may occur if the immunity is not protective. It has been suggested that an increase in C. parvum oocyst shedding may occur in adult cows around calving (so called periparturient rise), but to date there have been few reports to support this. In a recent study, however, dams in a suckler beef herd were found to shed low levels of C. parvum oocysts around the time of calving (De Waele et al. 2012) . Only one experimental infection for each of C. bovis and C. ryanae has been reported so far. Regarding C. bovis, one calf shed oocysts from 10 to 28 days after infection and the other only for 1 day (day 12) (Fayer et al. 2005 ). For C. ryanae, oocyst shedding started 11 days after inoculation. Both infected calves excreted oocysts during 15 and 17 consecutive days, respectively . Shorter prepatent periods have been seen for both C. bovis and C. ryanae in natural infections (Silverlås et al. 2010b; Silverlås and Blanco-Penedo 2013) . No oocyst excretion rate values were determined from the experimental infections, but in naturally infected calves 300 to 8 Â 10 6 OPG and 100-835,000 OPG have been reported for C. bovis and C. ryanae, respectively (Silverlås and Blanco-Penedo 2013) . Young stock and adults may also be infected by the larger C. andersoni (oocyst size~7.4 Â 5.5 μm) and may shed oocysts intermittently for many years (Olson et al. 2004; Ralston et al. 2003) . A periparturient rise in C. andersoni oocyst shedding, seen both as increase in prevalence and in number of oocysts in faeces, has been reported (Ralston et al. 2003) . Several studies have shown that age is associated with Cryptosporidium infection and that young calves have the highest risk of being infected (Maddox-Hyttel et al. 2006; Santín et al. 2004; Sturdee et al. 2003; Fayer et al. 2007 ). This is also the age group that is most often infected with C. parvum and suffers from clinical cryptosporidiosis. Thus, from clinical and zoonotic perspective, knowledge on the epidemiology of cryptosporidiosis in young calves is highly valuable. When potential risk factors for Cryptosporidium infection in pre-weaned calves have been explored, the results differ between studies. One factor that recurs in several studies is the type of flooring in the calf housing area. In Spain, Castro-Hermida et al. (2002) found that straw on the floor or earth floors in the calf pens increased the risk for infection compared with cement flooring, and in Malaysia calves kept in pens with slatted floors and sand floors had an increased risk compared with those in pens with cement floors (Muhid et al. 2011) . A protective effect of cement floors was also reported from the USA (Trotz-Williams et al. 2008) . It was suggested that the reason for this protective effect of cement floors is that they facilitate thorough cleaning. This assumption corroborates the finding that a low frequency of cleaning of the calf pens increased the risk for infection (Castro-Hermida et al. 2002) . It is also consistent with the finding that the use of an empty period in the calf pen between introductions of calves was associated with a lower risk for infection in Danish dairy herds (Maddox-Hyttel et al. 2006) . When cows as a cause of infection were investigated, a higher risk of infection was identified in calves that were housed separately from their dams (Duranti et al. 2009 ), and a lower risk of infection in dairy calves kept with the cow for more than 6 h after birth (Silverlås et al. 2009b) . In one of the few reports to investigate risk factors for infection with different Cryptosporidium species in pre-weaned dairy calves to date (Szonyi et al. 2012) , risk of infection with C. parvum differed to some extent from that of C. bovis. Both C. parvum and C. bovis were more common in the younger calves, but herd size and hay bedding were associated with an increased risk for C. parvum infection, whereas Jersey breed was a risk factor for C. bovis infection. Experimental Cryptosporidium infections in water buffalo have not been reported. However, oocyst shedding dynamics were investigated in naturally infected buffalo calves in a farm located in a tropical dry forest area in Venezuela. Twenty-five calves were sampled from birth to 12 weeks of age. Oocysts were detected from day 5 and 72 % of the calves shed oocysts before they were 30 days (Díaz de Ramírez et al. 2012) . Regarding risk factors for infection, there are some reports of seasonal variations in prevalence (Bhat et al. 2012 There are numerous reports of cryptosporidiosis outbreaks in humans after contact with infected calves. These have often involved veterinary students and students at farm schools (see, e.g., Gait et al. 2008; Grinberg et al. 2011; Pohjola et al. 1986; Robertson et al. 2006; Kiang et al. 2006 ), but also young children have fallen ill after visiting petting zoos or open farms (Gormley et al. 2011; Smith et al. 2004) . Contact with cattle has been identified as a risk factor for disease also in casecontrol studies of sporadic human cryptosporidiosis (Hunter et al. 2004; Robertson et al. 2002; Roy et al. 2004) . Altogether, there is plenty of evidence to conclude that Cryptosporidium can be transmitted from calves to humans by direct contact or by contaminated equipment. The risk for zoonotic transmission is likely to be highest in herds with Cryptosporidium associated calf diarrhoeal problems, where oocyst contamination in the barn can reach high levels and where contact with naïve individuals is most likely to occur. Key measures to prevent visitors becoming infected are to ensure good hygiene in the visitor area, providing suitable handwashing facilities and ensure that they are used when workers and visitors leave the premises. C. bovis infections have recently been detected in a few persons living or working on cattle farms (Khan et al. 2010; Ng et al. 2012) . It is not known if these were active infections and the implication of these findings is thus unclear. As molecular typing methods become more accessible, epidemiological studies can investigate C. parvum GP60 subtype distribution in cattle and human populations in different regions. The reports so far indicate that in many areas the subtypes that are most common in cattle are those most often found in humans. For example, C. parvum IIaA15G2R1 was the predominant subtype in both bovine and human infections in Slovenia and Portugal (Soba and Logar 2008; Alves et al. 2006) . In New South Wales, Australia C. parvum IIaA18G3R1 dominated in both calves and people living on cattle farms (Ng et al. 2012) , whereas IIaA16G2R1 was the predominant genotype identified in beef cattle and humans in Prince Edward Island, Canada (Budu-Amoako et al. 2012c). Further information is provided in the review by Xiao (2010) . That the same subtypes are found in cattle and humans might be taken as an indication of zoonotic transmission. However, it is important to note that even when zoonotic C. parvum subtypes are identified in humans, cattle are not necessarily the source of the infection. These zoonotic subtypes can circulate and propagate in the human population in addition to the anthroponotic subtypes. The occasional finding of C. hominis Chen and Huang 2012) in cattle highlights the fact that cryptosporidiosis may be transmitted not only from cattle to humans, but also from humans to cattle. Food-related cryptosporidiosis outbreaks have sometimes been associated with cattle. Foodborne transmission was implicated in cases of children who had drunk unpasteurized milk (Harper et al. 2002) or cider, made from apples collected in an orchard where calves from an infected herd had grazed (Millard et al. 1994 ). Other outbreaks in which cattle were suspected as the source involved vegetables that had been sprayed with water that could have been contaminated with cattle faeces. Often there was only circumstantial evidence that cattle were the source of contamination, and it was not possible to exclude other potential sources (see e.g. CDC 2011; Robertson and Chalmers 2013) . Outbreaks of cryptosporidiosis associated with drinking water have often been attributed to contamination of water catchments by cattle manure. The evidence implicating cattle has sometimes been substantial (Bridgman et al. 1995; Smith et al. 1989 ), but for others the evidence was not conclusive. Grazing cattle or slaughterhouse effluent contaminating Lake Michigan were mentioned as two possible sources of Cryptosporidium oocysts in the large outbreak in Milwaukee, Wisconsin in 1993 (Mac Kenzie et al 1994 , but retrospective analysis of clinical isolates revealed that it was caused by the anthroponotic species C. hominis . This was also the case in the most recent outbreaks in UK (compiled by Chalmers 2012) and a large drinking waterborne outbreak in Sweden in 2010 (Anonymous 2011) . Given that pre-weaned calves are the most likely age group to shed C. parvum oocysts, any measure to prevent waterborne zoonotic transmission should be directed towards this age group. Protective measures could be to prevent young ruminants from accessing water catchments, and compost or spread calf manure on fields where runoff cannot occur. The manure of older ruminants is generally not a zoonotic concern with respect to Cryptosporidium. The seemingly common occurrence of C. parvum in buffalo calves highlights the potential role of water buffalo in zoonotic transmission. Thus the same precautions to prevent transmission of the parasite to humans, by direct contact or through food or water, are also applicable to water buffalo. Sheep (Ovis aries) and goats (Capra aegagrus hircus) are important in the global agricultural economy -producing meat, milk and wool -both in developing countries such as India and Iran, and industrialised countries such as Australia and The United Kingdom (de Graaf et al. 1999; Noordeen et al. 2000; Robertson 2009 ). In 2010, the world stocks were approximately one billion sheep and 910 million goats (FAOSTAT 2013a). Asia has the largest populations of both species, with 42 % and 60 % of the total world populations, followed by Africa (FAOSTAT 2013a). According to a FAO report, over 90 % of the goat population can be found in developing countries (FAO 2012) . Sheep and goats tend to be managed differently to cattle, with flocks grazing large enclosures rather than being kept indoors. There have been fewer studies on Cryptosporidium infection in sheep than in cattle, and even fewer studies have been performed on goats. Nevertheless, it is known that these protozoans are economically important parasites in both ruminant species (Noordeen et al. 2000; Robertson 2009 ). Infection and disease was first described in 1974 for sheep (Barker and Carbonell 1974) and in 1981 for goats (Mason et al. 1981) . Younger animals are more susceptible to infection than older ones, reflected in high shedding rates and diarrhoeal prevalences in lambs and kids up to 1 month of age, whereas infection in older animals is usually subclinical with lower shedding rates (Vieira et al. 1997 ). As for other animals, ovine and caprine Cryptosporidium infection can be found throughout the world. The prevalence varies widely between studies, from 0 % to 77 % in sheep and from 0 % to 100 % in goats. All age groups are susceptible, but infection is more common in lambs and kids than in older animals (Tables 4.5 and 4.6). Study design factors other than age of sampled animals, such as whether only diarrhoeal animals were sampled or not, if a point prevalence study or a longitudinal study was performed and the diagnostic method(s) used, also can affect prevalence data. The effect of using different diagnostic methods is evident in, for example, Giadinis et al. (2012; see also Tables 4.5 and 4.6) and Ryan et al. (2005) , where microscopy resulted in lower prevalences than detected by ELISA and PCR, respectively. Prevalence and species distribution for studies conducted on sheep dating back to 2007 are summarised in Table 4 .5. Specific data for studies on sheep published before 2007 can be found in "Cryptosporidium and Cryptosporidiosis" ; Tables 18.9 and 18.10). Prevalence rates and species distribution for all identified surveys of goats are summarised in Table 4 .6. Several species and genotypes have been identified in sheep, and the species distribution varies between studies and with age of the animals. Cryptosporidium parvum, C. ubiquitum (previously Cryptosporidium cervine/cervid genotype) and C. xiaoi (previously C. bovis-like genotype) are the most common species. Sporadic infection with C. hominis, C. suis, C. andersoni, C. fayeri (previously marsupial genotype I), C. scrofarum (previously pig genotype II), sheep genotype I, and unknown/novel genotypes have been identified (Chalmers et al. 2005; Giles et al. 2009; Karanis et al. 2007; Ryan et al. 2005 Sweeny et al. 2011b; Wang et al. 2010c) . Species distribution differs between studies and between age groups within studies. For instance, C. parvum is commonly found in lambs in Italy, Romania, Spain and the UK (Díaz et al. 2010a; Imre et al. 2013; Mueller-Doblies et al. 2008; Paoletti et al. 2009 ). In other studies, C. ubiquitum or C. xiaoi is the most common species (Fiuza et al. 2011a; Geurden et al. 2008; Robertson et al. 2010; Sweeny et al. 2011b) . For example, Wang et al. (2010c) identified C. ubiquitum in 90 % of all analysed samples, and the species dominated in all age groups, whereas Sweeny et al. (2011b) found C. xiaoi to be the most common (Table 4 .5). Cryptosporidium bovis has also been reported in sheep (Mueller-Doblies et al. 2008; Soltane et al. 2007; Wang et al. 2010c ). Whether C. bovis has actually been identified in sheep, or if it is the closely related species C. xiaoi is uncertain. For instance, Soltane et al. (2007) reported isolates similar to C. bovis, and Mueller-Doblies et al. (2008) reported C. bovis, but a BLAST search of the GenBank accession numbers identified these isolates as C. xiaoi. For the isolates reported as C. bovis by Yang et al. (2009) , no GenBank accession numbers are available, so the true identity of those isolates is uncertain. Similarly, no GenBank records are available from the study of Ryan et al. (2005) reporting the "New bovine B genotype" in sheep. Since C. bovis was first identified as the bovine B genotype, this could actually be the "C. bovis-like genotype", i.e. C. xiaoi. Cryptosporidium andersoni has been identified in a few naturally infected adult sheep (Wang et al. 2010c ), but experimental infection in 4-month-old lambs failed (Kváč et al. 2004) . A couple of apparently related surveys from Mexico have been published, but because of lack of clarity in the data, they will not be reviewed in this text. Two studies from Brazil (Sevá et al. 2010) and Mongolia (Burenbaatar et al. 2008 ) failed to identify Cryptosporidium in any of the collected samples, but the number of sampled sheep was small -11 and 5 animals, respectively. Because of the small number of studies and isolates analysed, it is hard to draw any conclusion about the species distribution in goats. Cryptosporidium parvum, C. xiaoi and a novel genotype have been identified in naturally infected goats (Table 4 .5). In addition, one report of natural infection with C. hominis is also available (Giles et al. 2009 ). The identification of C. xiaoi in a number of samples is in contrast with a failed attempt to infect 36-week-old goats to determine the host range of C. xiaoi (Fayer and Santín 2009 ). Because there is only scant information about cryptosporidiosis in goats, we do not know if an age-related resistance or immunity from a previous Cryptosporidium infection could have affected this experiment, as natural infections indicate that C. xiaoi is infectious to goats. Two studies from Mongolia (Burenbaatar et al. 2008 ) and the United Kingdom failed to identify Cryptosporidium in any of the collected samples, but the number of sampled goats was small -16 and 15 animals, respectively. Cryptosporidiosis has been associated with high morbidity and mortality rates in both lambs and goat kids (Cacciò et al. 2013; Chartier et al. 1995; de Graaf et al. 1999; Giadinis et al. 2007 Giadinis et al. , 2012 Johnson et al. 1999; Munoz et al. 1996; Paraud et al. 2011; Vieira et al. 1997) . High mortality has been described both from natural infection and from experimental studies, where infection doses are generally high (Chartier et al. 1995; Giadinis et al. 2007; Paraud et al. 2010) . In fact, it has been stated to be one of the most important pathogens associated with diarrhoeal disease and mortality in neonatal lambs and kids (Quílez et al. 2008a) . Anorexia and apathy/depression are common symptoms, accompanied by abdominal pain and pasty to watery, yellow and foul-smelling diarrhoea (de Graaf et al. 1999; Snodgrass et al. 1984) . Diarrhoea can last from a few days up to 2 weeks (de Graaf et al. 1999) . Faecal consistency is correlated with oocyst excretion (de Graaf et al. 1999; Paraud et al. 2010 Paraud et al. , 2011 , and a longer duration of diarrhoea is potentially associated with infection early in life (Paraud et al. 2010) . Body condition score and growth are affected (de Graaf et al. 1999) , probably due to both anorexia and the intestinal damage, that can reduce nutrient uptake for weeks (de Graaf et al. 1999; Klein et al. 2008) . Infection in animals older than 1 month is usually subclinical, and even younger animals can be subclinically infected. However, the infection can still affect production, with reduced body condition score (Sweeny et al. 2011a (Sweeny et al. , 2012 , reduced growth rate, and reduced carcass weight and dressing percentage at slaughter (Sweeny et al. 2011a ). As discussed above for cattle, before molecular methods were developed C. parvum was the only species considered to infect and cause disease in sheep and goats (Chartier et al. 1995; de Graaf et al. 1999; Munoz et al. 1996) . Cryptosporidium parvum infection has since been associated with diarrhoea in studies using molecular methods (Caccio et al. 2013; Díaz et al. 2010a; Drumo et al. 2012; Imre et al. 2013; Mueller-Doblies et al. 2008) . However, C. xiaoi has also been associated with mild to severe diarrhoea and mortality (Díaz et al. 2010b; Navarro-i-Martinez et al. 2007; Rieux et al. 2013) , and C. ubiquitum too has been found in a few diarrhoeal samples from lambs (Díaz et al. 2010a) , indicating that C. parvum is not the only pathogenic species in small ruminants. The prepatent period is 3-4 days in goat kids (Paraud et al. 2010 ) and 2-7 days in lambs (de Graaf et al. 1999 ). The patent period can last for at least 13 days (Paraud et al. 2010 ). Shedding peaks a few days to a week into the patent period, and maximum shedding can be as high as 2 Â 10 7 OPG (Rieux et al. 2013) . The length of the patent period and shedding intensity are determined by age, immune status and infection dose (de Graaf et al. 1999) . A natural age-related resistance to infection seems to be present. In one study, the prepatent period increased and intensity of shedding decreased in lambs with increasing age at infection (Ortega-Mora and Wright 1994). In another study, one naturally infected group of goat kids started shedding at 17 days of age and excretion peaked at a mean of 23 Â 10 4 OPG 5-11 days later (Rieux et al. 2013) , whereas another group of animals studied by the same authors started shedding at the age of 10 days, with a mean peak of 3 Â 10 6 OPG 0-4 days later, indicating higher virulence, infection pressure or an age-related higher sensitivity in the latter group. Factors such as hygienic conditions, milking practices, herd size (population density), season, climatic zone (within a country), and lambing/kidding season are factors that have been associated with prevalence of infection, prevalence of clinical cryptosporidiosis and intensity of oocyst shedding (Alonso-Fresan et al. 2009; Bomfim et al. 2005; Craig et al. 2007; Delafosse et al. 2006; Giadinis et al. 2012; Maurya et al. 2013; Noordeen et al. 2000 Noordeen et al. , 2001 . However, factors associated with infection and shedding intensity are also impacted by different management systems and climatic conditions; results from small farms in, for example, India cannot be extrapolated to large-scale farming in, for example, the United Kingdom. The significance of sheep and goats as reservoirs for zoonotic cryptosporidiosis is unclear (Robertson 2009 ). The first case of suspected zoonotic transmission from sheep was described in 1989 (Casemore 1989 ), but at that time diagnosis was based solely on microscopy and thus zoonotic transmission cannot be confirmed. However, since the introduction of molecular tools in diagnostics, a number of cases and outbreaks with suspected or confirmed zoonotic transfer from sheep have been described (Cacciò et al. 2013; Gormley et al. 2011 ). In the UK, where sheep farming is an important industry, a seasonal pattern with spring and autumn peaks of human cryptosporidiosis cases is observed, with the spring peak concurring with the lambing season (Anonymous 2002; Gormley et al. 2011; McLauchlin et al. 2000; Nichols et al. 2006) . Lambs in petting zoos seem to be a common infection source (Chalmers et al. 2005; Elwin et al. 2001; Gormley et al. 2011; Pritchard et al. 2007 ). The incidence of human cryptosporidiosis, especially due to C. parvum, dropped significantly during the foot-and-mouth outbreak in the spring and summer 2001 (Hunter et al. 2003) when >6 million livestock animals (~4.9 million sheep; Anonymous 2001) were slaughtered and there were restrictions in animal movements and farm visits, providing further evidence of the importance of zoonotic transmission in this region. In 2012, an outbreak occurred in Norwegian schoolchildren visiting a farm raising several animal species. Cryptosporidium parvum oocysts of an identical and unusual GP60 subtype were identified in faecal samples from six human patients, two lambs and one goat kid. Another human outbreak with the same C. parvum subtype had occurred at the same farm 3 years previously, but at that time very few oocysts were detected in animal faecal samples and molecular analyses were not conducted (Lange et al. submitted) . Cacciò et al. (2013) described a case where a farmer's son fell ill with cryptosporidiosis, being infected with the same and unusual C. parvum subtype that caused high morbidity and mortality in the farm's lambs (Table 4.7) . Studies on C. parvum GP60 subtypes have been performed with sheep and goat isolates, and all isolates were found to belong to the IIa and IId families (Table 4.7) . Several studies using multi-locus genotyping (MLG) have found evidence of specific host associated C. parvum populations (Drumo et al. 2012; Mallon et al. 2003a, b; Morrison et al. 2008 ). In the United Kingdom, sheep MLGs clustered with human and bovine isolates (Mallon et al. 2003a, b) , indicating frequent zoonotic transmission, whereas only one of the 34 MLGs identified in sheep/goats in Italy was also identified in human samples (Drumo et al. 2012) , indicating a low rate of zoonotic transmission. However, the latter study included very few human isolates. Zoonotic transmission is commonly observed with C. parvum, but C. ubiquitum has also been identified in a number of sporadic human cases (Cieloszyk et al. 2012; Elwin et al. 2012; Feltus et al. 2006; Leoni et al. 2006; Ong et al. 2002; Soba et al. 2006; Trotz-Williams et al. 2006 ). Oocysts of this species have been identified in storm water, wastewater, raw water and drinking water (Jiang et al. 2005; Liu et al. 2011; Nichols et al. 2010; Van Dyke et al. 2012) . In Scotland, C. ubiquitum was the third most common species in raw water and the most common species identified in drinking water (Nichols et al. 2010) . Thus, in areas where C. ubiquitum is common in sheep and goats, this species could be a more important cause of zoonotic infection than C. parvum. In addition, the relatively common presence of this species in water indicates a potential for waterborne outbreaks. Natural infection with C. hominis has been reported in one goat and two sheep (Giles et al. 2009; Ryan et al. 2005 ) and in three lambs following experimental infection (Ebeid et al. 2003; Giles et al. 2001 ), but since animals are not natural hosts for this species, risk of zoonotic transmission with this species should be negligible compared with the risk of human-to-human transmission. It is important to note that because Cryptosporidium infection can be subclinical, the zoonotic potential is not restricted to contact with diarrhoeic Cryptosporidium-infected animals (Pritchard et al. 2007 ). Since domestication around 4900 BC in China, the pig has been an important food source (Moeller and Crespo 2009) . Pigs are farmed worldwide, with the global swine inventory estimated at over 800 million in 2002. Because Asian countries are major consumers but do not produce sufficient pigs for their needs, there is a significant international trade in live and slaughtered pigs. China has the world's largest pig population, mostly small herds consisting of only a few animals, and is a net importer of pigs. The United States, European Union, and Canada are major exporters with relatively few but very large production units (Moeller and Crespo 2009) . The global trend is for fewer producers responsible for larger numbers of pigs, and more concentration within the swine industry. Pigs are the primary host for C. suis ) formerly identified as Cryptosporidium pig genotype I and for C. scrofarum (Kváč et al. 2013 ) formerly identified as Cryptosporidium pig genotype II. Farm pigs have also been found infected with C. parvum, C. muris, on one occasion with C. tyzzeri, a species common to mice, and with the novel genotype isolate Eire 65.5 (Kváč et al. 2013) . Cryptosporidiosis occurs in pigs of all ages in 21 countries on 6 continents (Table 4 .8). Before molecular methods were developed C. parvum was thought to infect 152 species of mammals and to consist of several genotypes. Consequently some early studies erroneously reported C. parvum infection in pigs based on the identification of oocysts in faeces by microscopy. Subsequent use of molecular methods provided the necessary tools to identify and distinguish species. Overall, prevalence data for locations, herds and age groups vary greatly and are not directly comparable because some data represent pooled samples (some from litters, others from fecal slurry), some data originate from single farms while other data come from multiple farms. Some surveys have studied individual pigs at various ages, or only those pigs with diarrhoea, or simply specimens submitted to diagnostic laboratories from unspecified locations (Table 4 .8). Even in comparable populations, such as preweaned pigs in the same country or indifferent countries, data differences are too great to draw any conclusions on prevalence. For example: in Australia-reports of 32.7 % versus 6.0 % prevalence (Johnston et al. 2008 vs. Ryan et al. 2003a ; in the Czech Republic-reports of 21.8 % versus 5.7 % prevalence (Kváč et al. 2009a vs. Vitovec et al. 2006 ; or between Serbia and Spain -reports of 32 versus 0 % prevalence (Mišić et al. 2003 vs. Quílez et al. 1996a ). Some studies found significant association between the presence of a particular species and the pigs' age, with C. suis prominent in piglets and C. scrofarum prominent in weaners (Enemark et al. 2003) . In contrast, others found no significant association between species and age or housing conditions (Featherstone et al. 2010b ). These prevalence data reflect vast differences in management practices from location to location with too many unknown factors to draw valid conclusions on cause and effect or location within the 49 cited studies in Table 4 .8 that reported a prevalence of infection between 0.1 % and 100 %. The only variable repeatedly associated with detection of Cryptosporidium is age. Most positive samples were from weaners and growers (Table 4 .8). Generally, prevalence increased until pigs were 10 weeks of age, then gradually declined. The first reports of cryptosporidiosis in pigs found one piglet among 81 herds of nursing piglets with necrotic enteritis, but the significance of this finding was described as unknown (Bergeland 1977) and Cryptosporidium was found at necropsy in three pigs without clinical signs (Kennedy et al. 1977) . Although a higher prevalence of diarrhoea was found in Cryptosporidium-infected pigs than in uninfected pigs (Hamnes et al. 2007) , others found no significant relationship between infection and diarrhoea (Quílez et al. 1996b; Guselle et al. 2003; Maddox-Hyttel et al. 2006; Vitovec et al. 2006; Suárez-Luengas et al. 2007 ). Cryptosporidium was detected histologically in the microvillus brush border of 5.3 % of 3,491 pigs from 133 farms examined for routine diagnostic evaluation (Sanford 1987) . Most infected pigs were 6-12 weeks old. Organisms were detected in the jejunum, ileum, caecum, and colon, but primarily in microvilli of dome epithelium in the ileum. Twenty six percent of Cryptosporidium-infected pigs had diarrhoea but most of these also had other primary agents capable of causing diarrhoea. Similar observations have been made by others. Whereas most infections are asymptomatic or cause only mild, non-specific colitis (Higgins 1999) , pigs known to be naturally infected with C. suis or C. scrofarum have not been found with clinical signs of infection while pigs infected with C. parvum or co-infected other enteropathogens such as rotavirus, Salmonella, or Isospora have had associated diarrhoea and some have died (Enemark et al. 2003; Núñez et al. 2003; Hamnes et al. 2007) . Experimental infections with different species have helped to clarify the relationship of species with clinical disease. Pigs experimentally infected with C. suis (Enemark et al. 2003) or C. scrofarum (Kváč et al. 2013) showed no clinical signs. The pathogenicity of C. parvum isolated from calves was demonstrated in early transmission studies to pigs (Moon and Bemrick 1981; Tzipori et al. 1981b Tzipori et al. , 1982 Argenzio et al. 1990; Vitovec and Koudela 1992; Pereira et al. 2002) . Experimental infection with the avian species, C. meleagridis, obtained from a human infection, consistently resulted in oocyst excretion and diarrhoea in pigs, although mucosal changes were milder than those described for C. parvum (Akiyoshi et al. 2003) . Piglets infected with C. suis had mild or no clinical signs despite excreting large numbers of oocysts, in contrast to those infected with C. parvum that had diarrhoea for a mean duration of 3.5 days and developed inappetence, depression and vomiting (Enemark et al. 2003) . Developmental stages of Cryptosporidium have been observed throughout the intestinal tract. Villous atrophy, villous fusion, crypt hyperplasia, and cellular infiltration of the lamina propria have been observed (Kennedy et al. 1977; Moon and Bemrick 1981; Tzipori et al. 1982 Tzipori et al. , 1994 Sanford 1987; Vitovec and Koudela 1992; Argenzio et al. 1990; Pereira et al. 2002; Enemark et al. 2003; Núñez et al. 2003; Vitovec et al. 2006) . Lesions caused by C. parvum were the most severe, as were clinical signs associated with that species. Changes in the location of stages have been noted. In the first days of infection more stages were found in the proximal intestine, but later more stages were found in distal locations (Tzipori et al. 1982; Vitovec and Koudela 1992) . Extra-intestinal infections also have been reported in pigs. In two naturally infected piglets, the gall bladder was infected (Fleta et al. 1995) . In experimentally immunosuppressed piglets, the gall bladder, bile ducts, and pancreatic ducts were found infected (Healey et al. 1997) . Infections in the trachea and conjunctiva were detected in experimentally infected normal piglets (Heine et al. 1984 ). A survey of faecal slurry from swine finishing operations in Ireland found C. suis, C. scrofarum and C. muris and concluded that Cryptosporidium oocysts can persist in treated slurry and potentially contaminate surface water through improper discharge or uncontrolled runoff . Hamnes et al. (2007) reported C. suis and C. scrofarum in faeces of suckling pigs in Norway and reasoned that farrowing operations were sources of these parasites. Additional data on oocyst concentrations, numbers of oocysts excreted, how long oocysts remain infectious under environmental condition, and modes of transmission of Cryptosporidium species and genotypes are rare or non-existent. A year-long investigation was conducted at four types of swine operations (finishing, farrowing, nursery and gestation) in Georgia, USA (Jenkins et al. 2010) . Mean oocyst concentrations ranged from 11 to 354 oocysts per ml of lagoon effluent; the nursery had the highest concentration of oocysts and the greatest percentage of viable oocysts (24.2 %), C. suis and C. scrofarum were the dominant species with some C. muris and C. parvum. Experimental attempts to transmit C. scrofarum to adult SCID mice, adult BALB/c mice, Mongolian gerbils, southern multimammate mice, yellow-necked mice, and guinea pigs were unsuccessful, suggesting that rodents are an unlikely source of transmission of this species under natural conditions (Kváč et al. 2013 ). Cryptosporidium suis was detected by immunofluorescence microscopy and RFLP analysis of PCR products in stools from an HIV patient in Peru (Xiao et al. 2002a ). The patient was not severely immunosuppressed and was asymptomatic. He had a dog but reported no contact with other animals or animal faeces, including pigs and pig faeces, so the source and method of transmission are unknown. Many countries, including Australia, Canada, China, Korea, Norway, Russia, Sweden, UK, USA and Vietnam, have thriving deer farming industries. New Zealand, a country where deer are not native, has the world's largest and most advanced deer farming industry. Although it is difficult to find estimates on the numbers of deer farmed worldwide, more than one million deer were being farmed in New Zealand in 2011 (Sources: Statistics New Zealand and Deer Industry New Zealand http://www.deernz.org/about-deer-industry/nz-deer-industry) -compared with five million dairy cows -and there are over 2,800 deer farmers. More than 90 % of the New Zealand deer industry's products are exported, with approximately half of the export going to Germany and Benelux. Species of deer which are commercially farmed varies regionally, but the following species are now being farmed in various parts of the world: red deer (Cervus elaphus), wapiti or elk (Cervus canadensis), fallow deer (Dama dama), sika (Cervus nippon), rusa deer (Rusa timorensis), and reindeer (Rangifer tarandus) (FAO http://www.fao.org/docrep/004/X6529E/X6529E02.htm). Although farmed deer are an important resource in many countries, much of the published information on Cryptosporidium in deer refers to studies on wild or free-ranging cervids (e.g. white-tailed deer in USA, roe deer in Spain, caribou in Canada, and moose, red deer, roe deer and reindeer in Norway; Rickard et al. 1999; Castro-Hermida et al. 2011b; Johnson et al 2010; Hamnes et al. 2002) . While these studies on free-ranging cervids may give useful information regarding the species or genotype of Cryptosporidium that might infect farmed deer (C. ubiquitum, C. parvum), as farmed deer probably differ quite substantially from their wild counterparts regarding exposures and stresses, extrapolation of prevalence data from wild to farmed deer may give an incorrect picture. Indeed, a study in Poland found that the prevalence of Cryptosporidium was significantly higher in wild red deer than farmed red deer (27 % compared with 4.5 %), and mean oocyst concentration was also five times higher in faecal samples from wild red deer (Paziewska et al 2007) . However as the sample size was relatively small (52 wild deer, 66 farmed deer) and from only single locations and as age and symptoms were not indicated, it is not possible to determine the reason for these differences. The few studies on the prevalence of Cryptosporidium infection in different farmed or domesticated cervids are summarised in Table 4 .9. The lack of surveys for Cryptosporidium infection in farmed deer is surprising, given the clear association of infection with clinical disease in farmed cervids. Some of the first published studies on Cryptosporidium infection in cervids are case reports of severe (high mortality) outbreaks among farmed red deer calves. In one outbreak in Scotland, UK among 82 artificially reared red deer calves, 56 developed cryptosporidiosis and 20 subsequently died; 80 % of the calves with diarrhoea and 50 % of apparently asymptomatic calves excreted oocysts and post mortem histopathological examination of the intestines demonstrated lesions similar to those seen in other species (Tzipori et al. 1981a) . Another outbreak among new-born red deer calves in the UK also resulted in high mortality, with calves dying at 24-72 h of age. However, this outbreak was not characterized by diarrhoea, and terminal uraemia was proposed as the symptom leading to death (Simpson 1992) . Outbreaks of cryptosporidiosis in red deer calves have also been reported from New Zealand, again with relatively high mortality (10 out of 10 calves dying within a few days of illness onset in one outbreak, and 7 out of 10 calves dying within 3 days of illness in another outbreak) (Orr et al. 1985) . Severe subactute enteritis in the small and large intestine were reported in both outbreaks. Information from other species of farmed deer is more scanty, but a retrospective study of neonatal mortality in farmed elk (Pople et al 2001) identified Cryptosporidium infection as one of the most important causes of enteritis leading to death (7 cases out of 11 of infectious enteritis from a total of 111 cases in which 46 had no specific cause of death identified). Among these 7 cases, 4 were associated with an outbreak on a single farm (Pople et al 2001) . Unfortunately, information on the species of Cryptosporidium infection associated with clinical disease in deer and Cryptosporidium associated with asymptomatic infection is lacking. One outbreak on a Scottish farm occurred when deer were put to graze on a pasture that had previously been grazed by a Cryptosporidium-infected herd of cattle (Angus 1988) , and therefore it seems probable that this might indicate infection with C. parvum; it might be speculated that infection of deer with deer-adapted C. ubiquitum is less likely to cause severe symptoms. Published information about infection dynamics in farmed deer is minimal. However, a longitudinal study in asymptomatic farmed red deer in Ireland (Skerrett and Holland 2001) provides some interesting data. Asymptomatic low-level (<10 OPG) oocyst shedding from adult hinds appeared to continue throughout the year, except during the calving season (May -June), when there was a 2-log increase in oocyst excretion rate; the highest level recorded was 67,590 OPG. The authors speculate that this may be related to hormonal or immunological changes, or perhaps alterations in stress levels. The authors note that this preparturient rise in oocyst shedding results in contamination of the environment for the new born calves. However, in this study, although calves became infected, oocyst excretion was low (not exceeding 150 OPG, and usually less), and clinical disease was not observed. Again, the species of Cryptosporidium in these infections is unknown. Both C. parvum and C. ubiquitum have zoonotic potential, but there appear to be no documented cases of proven zoonotic transmission from/to deer. Those studies (USA and Australia) that have investigated deer as sources of contamination in watersheds, have focused on wild deer only and provided contrasting results (Cinque et al 2008; Jellison et al 2009 Camelids are members of the family Camelidae, and include the tribe Camelini (including dromedaries and Bactrian camels), and the tribe Lamini (llamas, alpacas, vicuñas, and guanacos). There are two species of camel. Approximately 14 million domesticated onehumped dromedaries (Camelus dromedarius) are found in Middle Eastern countries including the Sahel and Horn of Africa, as well as parts of Southern Asia where they provide people with milk, food, and transportation. Nearly two million domesticated two-humped bactrians (Camelus bactrianus) are native to the steppes of central Asia the Gobi and Taklamakan Deserts in Mongolia and China. Alpacas (Vicugna pacos) and llamas (Lama glama) exist only in the domesticated state and are found worldwide. However, both are native to South America and are raised primarily for fibre production although llamas were once used extensively as work animals. The young of both are called crias. Camels and dromedaries: In the relatively few studies of dromedaries in Northern Africa and the Middle East, the prevalence of cryptosporidiosis varied greatly (Table 4 .10). None of 23 camels from Iraq (Mahdi and Ali 1992) and none of 110 camels on farms in Tunisia were found positive for Cryptosporidium (Soltane et al. 2007) . Cryptosporidium was detected in one of four camel calves in Egypt (Abou-Eisha 1994). However, in an abattoir in Yazd Province in Iran, microscopic examination of 300 faecal specimens detected 61 (20.3 %) positive for Cryptosporidium and 12 (12 %) positive abomasal mucosa specimens. At an abattoir in Isfahan Province in central Iran, of 63 adult male and 40 adult female dromedary camels examined, 39 (37.9 %) were Cryptosporidium-positive (Razawi et al. 2009 ). In northwestern Iran, of 170 faecal samples from camels 17 (10 %) were positive for Cryptosporidium-like oocysts (Yakhchali and Moradi 2012) . The prevalence was significantly higher (20 %) in calves less than a year old. Oocysts have also been recovered from wild and zoo-housed camels. Faeces from a 3-year-old Bactrian camel in the Wild Animals Rescue Centre of Henan Province in China were found positive for C. andersoni (Wang et al. 2008b) . Oocysts from a zoo-housed Bactrian camel (Fayer et al. 1991) were infectious for mice (Anderson 1991) and were identified as C. muris (Xiao et al. 1999; Morgan et al. 2000) ; those from camels in the Czech Republic were identified as C. andersoni. Other zoo-housed camels have been found to be infected with Cryptosporidium (Abou-Eisha 1994; Gomez et al. 2000; Gracenea et al. 2002) . Alpacas and llamas Cryptosporidium oocysts have been detected in both these species. However, in California none of 354 llamas from 33 facilities were found positive (Rulofson et al. 2001 ) nor were 61 alpacas on two farms in Maryland . Elsewhere in North America, Europe, and Australia small numbers of alpacas, llamas and guanacos have been examined and a few have been found positive for Cryptosporidium (Table 4 .11). Most examinations were conducted by microscopy, but those that utilized molecular methods identified only C. parvum (Morgan et al. 1998; Starkey et al. 2007; O'Brien et al. 2008; Twomey et al. 2008) . The exception is a study in which a cria was found infected with C. ubiquitum (Gomez-Couso et al. 2012) . A national survey of 5,163 1-15-day-old alpacas in 105 Andean herds in Peru, the natural habitat for nearly 80 % of the world's alpacas, found 2 % of the youngest alpacas increasing to 20 % of the oldest alpacas, infected with Cryptosporidium spp., with an overall prevalence of 13 % (Lopez-Urbina et al. 2009 ). More recently in Peru, 4.4 % of 274 alpacas from 12 herds were found positive for Cryptosporidium spp. (Gomez-Couso et al. 2012) . Herd prevalence was 58.3 % (7/12 herds) for Cryptosporidium. The highest prevalence (20 %) was found in the 8-week-old group (Gomez-Couso et al. 2012) . Camels and dromedaries Few data are available on the subject of clinical illness associated with cryptosporidiosis in camels. Of 170 faecal samples, 17 camels (10 %) were positive for Cryptosporidium-like organisms (Yakchali and Moradi 2012). The prevalence was significantly higher in camel calves (<1 years old) (20 %) than other age groups, in which the diarrhoeic calves had a prevalence of 16 %. Alpacas and llamas Not all alpacas and llamas infected with Cryptosporidium show clinical signs of infection. Of 110 healthy crias and their 110 dams 7 % and 8 %, respectively, were found excreting oocysts (Burton et al. 2012) . Oocysts of C. parvum were detected in 4 of 14 faecal samples from healthy crias and in one sample from a cria with diarrhoea (Twomey et al. 2008) . Cryptosporidium was observed in a post-operative neonatal llama with diarrhoea, cachexia, dehydration and electrolyte abnormalities (Hovda et al. 1990 ). During 8 days that intravenous fluids and nutritional support were provided, these signs were not observed. Of 20 Cryptosporidium-infected alpaca crias with diarrhoea, 15 exhibited weight loss and 5 had a poor appetite (Waitt et al. 2008 ). Most were 8-18 days old when examined. Additional potential gastrointestinal pathogens were found in 7 of these crias. Sixteen crias recovered after supportive therapy that included intravenous rehydration, with partial parenteral administration of nutrients, antimicrobials, oral nutrients, plasma, insulin and other palliative treatments. Additional reports of diarrhoea associated with cryptosporidiosis have been reported in alpaca and llama crias (Cebra et al. 2003; Shapiro et al. 2005; Whitehead and Anderson 2006; Starkey et al. 2007 ). Three fatal cases (2 with diarrhoea) of cryptosporidiosis were reported in alpaca crias less than 30 days of age (Bidewell and Cantell 1998) . At necropsy, intestinal congestion and distension were noted, oocysts were detected in Ziehl-Neelsen stained smears, and no other significant organisms or toxins were detected. In South America, llama and alpaca husbandry is a vital economic activity and neonatal diarrhoea syndrome (NDS) is the most common and costly enteric disease in newborn llamas and alpacas (Lopez-Urbina et al. 2009 ). However, the role of cryptosporidiosis in NDS has not been clearly identified. Camels and dromedaries Only rare circumstantial data of zoonoses are available and the link is very tenuous. In Yazd Province in Iran, 24 of 100 people in long-term contact with camels were found infected with Cryptosporidium spp. (Sazmand et al. 2012) . Infection was higher in winter than summer (16/50 compared with 8/50). Alpacas and llamas In New York, Cryptosporidium parvum infection was identified in 5 crias, 3 of their caretakers were confirmed to have cryptosporidiosis, and three others were suspected to have cryptosporidiosis, suggesting zoonotic transmission (Starkey et al. 2007 ). Rabbit farming (cuniculture) for meat, wool, and fur production occurs in a variety of settings around the world, and mostly involves the European (or common) rabbit (Oryctolagus cuniculus). Small-scale backyard cuniculture is common in many countries (especially in Africa and South America), but commercial operations on a larger scale are found in Europe (particularly Italy, Spain and France) and Asia (particularly China and Indonesia). In the EU, rabbit meat production was estimated to be around 520,000 tonnes carcass-weight equivalent in 2005 (EFSA-AHAW 2005). In addition, rabbits continue to be bred for biomedical purposes -but this type of rabbit breeding will not be considered further in this chapter. Production and consumption of rabbit meat is relatively low in North America. Different rabbit breeds are used for meat, wool, and fur -with the most commonly used meat breeds being New Zealand, Californian, Florida White and Altex, all having good growth rates and desirable reproductive characteristics. Much of the information presented in this section is derived from a comprehensive review article from 2010 (Robinson and Chalmers 2010) . The majority of published prevalence information on Cryptosporidium in rabbits refers to studies on wild rabbits. Nevertheless, there have been several studies on the occurrence of infection in farmed rabbits and also in laboratory rabbits. The majority of these studies (involving both wild and domestic rabbits) are summarised in Robinson and Chalmers (2010) . In Table 4 .12, selected prevalence studies (rather than case reports) from farmed rabbits only are summarized, including two recent studies from China. Additionally, a further three studies from China and referenced in Zhang et al. (2012) are not included in Table 4 .12 due to inaccessibility of the original publications. Zhang et al. (2012) do not provide any details on these studies and it is not certain that they refer to farmed rabbits. Although some surveys refer to Cryptosporidium parvum, all those studies in which genotyping has been used (including from wild rabbits; e.g. Nolan et al. 2010) suggest that the majority of natural infections in rabbits, if not all, are caused by C. cuniculus. Nevertheless, experimental infections with other species of Cryptosporidium have been established in rabbits, as summarised by Robinson and Chalmers (2010) . Although the majority of surveys do not report symptoms associated with cryptosporidiosis in rabbits, experimental infections in preweaned rabbits have been associated with diarrhoea and high mortality (e.g. as reported by Robinson and Chalmers 2010; Mosier et al 1997) and also as described by Pavlásek et al. (1996) in farmed rabbits. However, even asymptomatic infection may result in some pathology, as noted by Inman and Takeuchi (1979) , who reported blunted villi, a decrease in villus-crypt ratio, and mild oedema in the lamina propria in an apparently asymptomatic adult rabbit. Thus, even asymptomatic infection may reduce stock productivity. Although no outbreaks of cryptosporidiosis in rabbit farms have been documented in the literature, acute outbreaks of diarrhoea with high mortality rates are frequently observed in rabbits (Banerjee et al 1987) . Although bacterial agents are frequently considered to be the aetiological agent, it seems probable that some may be due to undiagnosed cryptosporidiosis. For example, the parasitological techniques (direct microscopy and flotation) used for investigating epizootic outbreaks of diarrhoea, characterized by a high morbidity and mortality, in different commercial rabbit farms in Mexico (Rodríguez-De Lara et al 2008) may have been insufficient for detecting Cryptosporidium infection, particularly if the operators had little experience in diagnosing this infection. Information on the dynamics of Cryptosporidium infection in farmed rabbits is mostly lacking, although low oocyst excretion rates were reported in the majority of studies on rabbits in general (not just farmed rabbits). The studies from the Czech Republic provide some data, but, as the animals were not sampled individually, the data are difficult to interpret, and suggest that the source of infection for young rabbits may be low-level excretion of oocysts from mother rabbits at around parturition (Pavlásek et al. 1996) . C. cuniculus is rarely, but sporadically, identified in human infections. In 3030 Cryptosporidium-positive faecal samples submitted for routine typing in UK between 2007 and 2008, 37 (1.2 %) were identified as C. cuniculus, with both GP60 Va and Vb subtype families detected . However, the greatest evidence for C. cuniculus from rabbits having a significant zoonotic potential came from a waterborne outbreak of cryptosporidiosis in England in 2008 affecting 29 people; C. cuniculus, subtype VaA18 was identified in eight patients, a water sample from the implicated supply, and from the colon of a carcass of a rabbit (presumably wild) that was found in a tank at the water treatment works . Nevertheless, transmission of Cryptosporidium to humans from farmed rabbits has not been recorded, and an investigation exploring associations between farm animals and human patients with cryptosporidiosis did not implicate rabbits as a source of infection . The world stock of birds in production in 2011 was estimated to 22 Â 10 9 animals (FAOSTAT 2013b). Approximately 56 % of the world stock was found in Asia, whereas Europe, North America and South America had approximately 10-11 % each of the population. The largest group was chickens, with 90 % of the total stock. Ducks, turkeys and geese/guinea fowls constituted 6.1 %, 2.1 % and 1.7 % respectively, and other birds (ratites, pigeons etc.) only constituted 0.1 % of the world stock. The main chicken, duck and goose/guinea fowl production is in Asia (54 %, 90 % and 91 % within each group respectively), and most of the turkey production in North America (54 %), followed by Europe (23 %). For other birds, 50 % of the reported production was located in Asia, 41 % in Africa and 9 % in Europe. Chickens (Gallus gallus domesticus) are descendants of the Red jungle fowl (Gallus gallus), with some hybridization with the Grey junglefowl (G. sonneratii). Broilers are usually kept in intense systems and reach slaughter size at about 6 weeks of age. Organically bred broilers and broilers kept on free range grow a bit more slowly. Laying hens can produce over 300 eggs in their first production year, but after that production declines rapidly. Domesticated ducks (Anas platyrhynchos domesticus) are, except for the Moscovy duck (Cairina moschata), descendants of the Mallard (Anas platyrhynchos). The majority of domesticated geese (Anser anser domesticus) descend from the Greylag goose (Anser anser), but the breeds Chinese goose and African goose are derived from the Swan goose (Anser cygnoides). Ducks and geese are bred for meat, eggs and down, and ducks, to a lesser degree, also for the production of foie gras. The domestic turkey (Meleagris gallopavo) is a progeny of the wild turkey, which is found in the wild in the United States http://www.turkeyfed.com.au/Turkey_Info. php. Turkeys are bred for meat production. The breed used is the white broad breasted turkey, introduced into commercial production in the 1950s http://bizfil.com/turkeyraising-primer. As with commercial chicken broiler farming, turkey farming is intense. The poults are extremely fast-growing, and reach approximately 6 kg at 10 weeks of age if given proper nutrition http://bizfil.com/turkey-raising-primer/. The United States has the highest consumption of turkey meat per person, and they are also the largest turkey producer, with 7.32 billion pounds of turkey meat produced in 2011 http://www.agmrc.org/commodities__products/livestock/poultry/turkey. Among ratites, mainly ostriches (Struthio camelus) are farmed, but rheas (Rhea americana) and emus (Dromaius novaehollandiae) are also kept for production. Ratites are bred for meat, egg, and feather and leather production. Farming for feather production began already in the nineteenth century. Partridges, such as the Grey or English partridge (Perdix perdix) and red-legged partridge (Alectoris rufa), are gallinaceous birds used as game, and have been introduced in different parts of the world for this purpose. Another gallinaceous bird is the helmeted guinea fowl (Numida meleagris). They are used for pest control, eating ticks and other insects, and can be kept as an alarm system among other domesticated birds due to their loud and shrieking warning call. The meat is considered a delicacy. The Japanese quail (Coturnix japonica) is bred for meat and eggs. Domestic pigeons (Columba livia domestica) are the progeny of the world's oldest domesticated bird, the Rock pigeon. Pigeons are bred for meat, sporting competitions, homing, as exhibition birds or pets. Cryptosporidium infection has been associated with large morbidity and mortality in different bird species (Bezuidenhout et al. 1993; Hoerr et al. 1986; Pages-Mante et al. 2007; Penrith et al. 1994; Ritter et al. 1986; Santos et al. 2005 ) and can thus be of great economic importance. Avian cryptosporidiosis was first described in chickens (Tyzzer 1929) . The infection was subclinical and situated in the caecum. Invasive stages looked identical to those of C. parvum, but no oocyst description was made, and no name was proposed. Today, three valid species have been identified in poultry. In addition, five genotypes have been identified in wild ducks and geese, and five additional genotypes have been described from other birds. The Cryptosporidium oocysts identified by Slavin in 1955 were morphologically similar to C. parvum, described in mice in 1912 (Tyzzer 1912) , and the infection site was the distal ileum. Slavin identified this bird Cryptosporidium as a unique species, C. meleagridis. When molecular methods were introduced as a means of species determination, it was verified that C. parvum and C. meleagridis were indeed different species (Sreter et al. 2000) . A species with a larger oocyst, first identified in chickens, and infecting the intestine, bursa and cloaca, was described and named C. baileyi ). This species is also involved in respiratory cryptosporidiosis, infecting the epithelium of sinuses, air sacs, nasopharynx, trachea and bronchi (Itakura et al. 1984; Lindsay et al. 1987) . Infection of the conjunctiva (Chvala et al. 2006 ) and urinary tract, including the kidneys has also been shown Trampel et al. 2000) . A third species, C. galli, infecting the proventriculus of chickens, was described by Pavlásek in 1999 , and re-described in 2003 (Pavlásek 1999 Ryan et al. 2003b) . The species was probably described in finches already in 1990 (Blagburn et al. 1990 ) and later the name C. blagburni was proposed ). However, molecular analyses have shown that C. blagburni is the same species already described as C. galli, and thus the latter is considered to be the valid species name. In addition, isolates referred to as goose genotypes I-IV have been identified in Canada geese and a duck genotype has been described in a Black duck and Canada geese. Of the other genotypes described in birds (avian genotypes I-IV and the Eurasian woodcock genotype), avian genotype II has been detected in ostriches. Two proposed species are today considered as nomen nudum due to lack of sufficient data. Cryptosporidium tyzzeri in chickens was described in 1961 (Levine 1961 ) and later C. anserinum, found in the large intestine of geese was described (Proctor and Kemp 1974) . Based on 18S rDNA phylogeny, C. galli and the woodcock genotype belong to the clade of gastric cryptosporidia together with C. andersoni, C. muris and C. serpentis, whereas C. meleagridis, C. baileyi, goose genotypes I and II and the duck genotype belong to the intestinal clade . Cryptosporidium meleagridis is closely related to the group including C. parvum and C. hominis; C. baileyi is closely related to the snake genotype, goose genotypes I, II and the duck genotype cluster together and are closely related to C. scrofarum, C. bovis, C. ryanae and the deer genotype. Goose genotypes III-IV and avian genotypes I-IV were not included in the phylogenetic tree. In another publication, goose genotypes I (goose #1, 2, 3, 6 and 8), II (goose #9) and the duck genotype (goose #5) are closely related, whereas goose genotypes III (goose #3b) and IV (goose #7) are more distant (Jellison et al. 2004) . The avian genotypes are more scattered. Avian genotypes I and II belong to the intestinal clade and are closely related to C. baileyi. Genotypes III and IV belong to the gastric clade, where genotype III is closely related to the Eurasian woodcock genotype and C. serpentis, and genotype IV is closely related to C. galli (Ng et al. 2006) . Prevalence data based on fecal examination could be affected by the time from sampling to analysis. This has been observed when oocyst numbers in chicken faeces dropped to approximately one third in samples stored for a week from first to second analysis, and where first analysis was performed on the day after sampling (C. Axén, unpublished data). It is possible that oocysts die and are quickly degraded by detrimental effects (extreme pH) due to the high ammonium content of bird droppings. A flock prevalence of 41 % (23/56), with 10-60 % within-flock prevalence, was reported for C. baileyi respiratory infection in broilers in the USA (Goodwin et al. 1996) . In Morocco, Cryptosporidium sp. were found in 14 (37 %) of 38 investigated flocks. Within-flock prevalence ranged from 14 % to 100 %, and the highest prevalence (52 %) was identified in broilers aged 36-45 days, with no infection prior to 25 days of age (Kichou et al. 1996) . Diagnosis was based on histopathology. An overall Cryptosporidium prevalence of 10.6 % for layer chickens and 3.4 % for broiler chickens was shown in a study of faecal samples from 2015 birds in China (Wang et al. 2010a ). The highest prevalence (24.6 %) was found in 31-60-day old laying chickens, whereas prevalences in broiler chickens never exceeded 5 %. DNA analysis identified C. baileyi as the major species, with 92/95 investigated samples, and only 3 samples were positive for C. meleagridis (Wang et al. 2010a) . In contrast, another recent study identified C. meleagridis as the major species in chickens (Baroudi et al. 2013) . The overall Cryptosporidium prevalence was 34.4 % by histopathology, and the highest prevalence (46.2 %) was identified in 16-30-day-old chickens, which is in line with the results from Kichou et al. (1996) and Wang et al. (2010a) . The majority of the birds were infected with C. meleagridis only (n ¼ 25). Cryptosporidium baileyi only was detected in four birds and a mixed C. meleagridis/C. baileyi infection was found in one bird. However, these chickens had died from diarrhoea, which could affect the outcome regarding Cryptosporidium sp. A morbidity of 5-10 % due to sinusitis was reported for a flock where Cryptosporidium sp. could be isolated from diseased poults (Glisson et al. 1984) . It was stated that macroscopic post mortem examination of the infraorbital sinuses of healthy birds was normal compared with those of diseased birds, but it was not clearly stated whether Cryptosporidium sp. was also identified in the healthy birds and thus the infection prevalence cannot be estimated. Goodwin et al (1988b) identified invasive Cryptosporidium stages in turkey poults form a farm where the poults suffered from self-limiting diarrheal of unknown aetiology, but no prevalence estimation was given. Prevalences of 80 % in 17-day-old poults, 38 % in 24-day-old and 0 % in !60-day-old poults was found by Woodmansee et al. (1988) . Oocysts were identified as C. meleagridis based on morphology and infection site. A 35.5 % (17/60) prevalence in diarrhoeic or just unthrifty poults was reported in Iran (Gharagozlou et al. 2006) . Prevalence was based on histological examination of intestinal, bursal and cloacal tissues. Examination of faeces revealed that only 29 % of the infected birds shed oocysts. Infection was identified in 1-7-week-old poults, whereas the 43 uninfected poults all were older than 7 weeks. DNA analysis was not performed and oocyst size was not stated in the publication, but based on infection site, host species and symptoms the authors suggested that C. meleagridis was the species responsible. A 10.0 %, 10.5 % and 2.5 % pre-slaughter prevalence respectively (age 4-9 weeks) was detected upon faecal examination of three flocks from the same farm (McEvoy and Giddings 2009). One of 59 turkeys was positive at post-slaughter examination (age 14 weeks). Upon DNA analysis, all six positive samples were identified as C. parvum. In a recent study, a 43.9 % prevalence of C. meleagridis was shown in deceased turkeys, with the highest prevalence (57.9 %) in poults aged 16-30 days (Baroudi et al. 2013) . In one study, 73 (57 %) of 128 ducklings and 44 (59 %) of goslings aged 8-35 days were infected with Cryptosporidium (Richter et al. 1994) . Infection was present in both intestinal and respiratory tract, but oocyst morphology was not described. In a study on experimental infection with Usutu virus in geese, Cryptosporidium developmental stages in tissue samples were an accidental finding. This was further investigated by in situ-hybridization, and Cryptosporidium infection was detected in 89 % of conjunctival tissue samples and 88 % of bursal tissue samples. DNA analysis revealed presence of C. baileyi (Chvala et al. 2006) . C. baileyi was also identified in two ducks in Rio de Janeiro (Huber et al. 2007 ). Ratites Cryptosporidium infection in ostriches was first described in the early 1990s (Allwright and Wessels 1993; Bezuidenhout et al. 1993; Gajadhar 1993 Gajadhar , 1994 Penrith et al. 1994; Penrith and Burger 1993) . Infection was first identified in faecal samples from 14 (8.5 %) of 165 ostriches imported from Africa to Canada (Gajadhar 1993) . Penrith and Burger (1993) identified invasive stages in a section of the small intestine of a 4-week old chick that has suffered from rectal prolapse, and Allwright and Wessels (1993) identified Cryptosporidium in histology sections of the bursa, intestine and pancreatic ducts. In 1994, Gajadhar et al. characterized the isolated oocysts and investigated host specificity. The oocysts were morphologically similar to those of C. meleagridis, but attempts to infect suckling mice, chickens, turkeys and quail failed, indicating that this was probably another species. In addition, only faecal samples were investigated, so the infection site was not determined (Gajadhar 1994) . As this study was conducted before molecular tools were commonly used for Cryptosporidium species determination, the true identity of this isolate will remain unknown. A low prevalence, with only 2 (0.6 %) of 336 investigated samples from ostriches aged 2 months-5 years being Cryptosporidium positive, was found in Greece (Ponce Gordo et al. 2002) . Oocysts were of two sizes, 3.8 Â 3.8 μm and 5.7 Â 4.8 μm, indicating the presence of two different species. In contrast, in a Spanish study a 60 % Cryptosporidium prevalence in adult rheas and ostriches was found (Ponce Gordo et al. 2002) . The authors reported an oocyst diameter of 3-5 μm, which is similar to the description provided by Gajadhar (1994) . Molecular analysis of the isolates was not performed. Oliveira et al. (2008) found 44 % prevalence in 77 ostriches based on microscopy. Oocysts were generally morphologically similar to C. baileyi and Cryptosporidium avian genotype II . However, the morphometric variation was so large that the authors suggested that more than one species had been identified (Oliveira et al. 2008) , but this was not verified by molecular analysis. An isolate similar to C. baileyi in both oocyst morphology and PCR-RFLP banding pattern was described from Brazilian ostriches (Santos et al. 2005) . The isolate was characterized as a sister taxon to C. baileyi by sequence analysis of the 18S rDNA, HSP70 and actin genes (Meireles et al. 2006) , and was named Cryptosporidium avian genotype II by another research group (Ng et al. 2006) . Experimental infection (oral or intratracheal) with the Brazilian isolate in chickens failed (Meireles et al. 2006) . The avian genotype II has also been identified in Vietnam. On a single ostrich farm 110 (23.7 %) of 464 samples were positive for Cryptosporidium oocysts. The highest prevalence as well as the highest shedding intensity (35.2 %) was found in 2-3 month-old animals. Of 17 samples used for molecular characterization, all were found to be avian genotype II (Nguyen et al. 2013) . Wang et al (2011b) reported Cryptosporidium infection in 53 (11.7 %) of 452 investigated ostrich samples. Prevalence peaked at the age of 4-8 weeks with 16.2 %. No infection was detected in birds younger than 1 week or older than 12 months. Molecular analysis of positive samples identified only C. baileyi. Quails and partridges Enteric cryptosporidiosis in quails, with oocysts similar to C. meleagridis, was first described in 1986 (Hoerr et al. 1986; Ritter et al. 1986) . Early attempts at experimental infection of quail with C. baileyi isolated from chickens failed Lindsay et al. 1986 ), but were later successful (Cardozo et al. 2005) . Natural infection was first documented in 2001 ). Since then, natural C. baileyi infection has been described in two reports (Murakami et al. 2002; Wang et al. 2012) . One large survey of Cryptosporidium infection in quails was performed in China . Out of 1,818 faecal samples, 239 (13.1 %) from 29 (61.7 %) farms were positive. Infection was most common among 72-100-day old quails (23.6 %). DNA analysis revealed C. baileyi in 237 samples and C. meleagridis in two samples. One case of Cryptosporidium infection in partridges was described (Pages-Mante et al. 2007) . Pigeons There are a few reports of cryptosporidiosis in pigeons (Ozkul and Aydin 1994; Qi et al. 2011; Radfar et al. 2012; Rodriguez et al. 1997) . Radfar et al. (2012) describe an overall prevalence of 2.9 % in 102 examined adult and nestling birds, with 3.4 % prevalence in adults and 2.3 % prevalence in nestlings. The other articles are case reports (Ozkul and Aydin 1994; Rodriguez et al. 1997 ) and a study on pet birds in general, where C. meleagridis was found in one pigeon (Qi et al. 2011 ). Respiratory as well as intestinal and bursal Cryptosporidium infections cause disease in chickens, but infection without clinical symptoms has also been observed (Fletcher et al. 1975; Taylor et al. 1994) . In Spain, a 90 % morbidity due to respiratory infection in one flock was caused by Cryptosporidium sp. Weekly mortality rates were 0.9-1.5 % (Fernandez et al. 1990 ). Infection was detected in the trachea and oesophagus. In another flock investigated in the same study, weight loss was the primary symptom, and bursal cryptosporidiosis was diagnosed (Fernandez et al. 1990 ). Goodwin et al. (1996) found a correlation between C. baileyi infection of the trachea and severity of tracheitis symptoms, airsacculitis and condemnation of birds. In respiratory cryptosporidiosis, co-infection with other pathogens has been identified in a number of studies. Cryptosporidium sp. and concurrent adenovirus infection was identified in a large broiler flock with respiratory disease (Dhillon et al. 1981) . In a retrospective study on post mortem diagnoses of respiratory cryptosporidiosis, it was found that co-infection with virus or bacteria was common (Goodwin et al. 1988a) . In another study, Cryptosporidium sp. and Aspergillus or bacteria were detected in the lungs of four layer chickens that died from pneumonia. Cryptosporidium were also found in the ureters and kidneys (Nakamura and Abe 1988) . The effect of Cryptosporidium infection alone on development of clinical symptoms in these cases cannot be estimated, but there is probably a synergistic effect of co-infections, increasing the severity. Such a synergistic effect of co-infection with infectious bronchitis virus or Escherichia coli has been reported (Blagburn et al. 1991) . Respiratory symptoms were reported from chickens that had been experimentally inoculated intra-tracheally with C. baileyi, whereas infection was successful but caused no symptoms in orally inoculated chickens (Lindsay et al. 1988) . C. meleagridis infection was associated with diarrhoea and mortality in one study of Algerian chickens (Baroudi et al. 2013 ). Experimental C. meleagridis infection of chickens has been observed to result in the chickens becoming indolent and having soiled feathers. Growth retardation was reported, but compensatory growth occurred after a few weeks (Tumova et al. 2002) . Turkey was the first animal species in which clinical cryptosporidiosis was described (Slavin 1955) . Infection was associated with diarrhoea at 10-14 days of age, but other parasites (including Histomonas, Trichomonas and Strongylides) were also detected. Experimental infection (crop inoculation) with C. meleagridis produced infection of the ileum, caecum and bursa, but was not associated with clinical symptoms (Bermudez et al. 1988 ). The isolate used was from symptomatic poults; however, these were simultaneously infected with reovirus (causing enteritis and hepatitis). Co-infection with Cryptosporidium and reovirus in turkeys with enteritis and hepatitis, leading to increased mortality, has also been shown in another study (Wages and Ficken 1989) . The presence of other pathogens in these studies could indicate a low to moderate primary pathogenicity of C. meleagridis. Self-limiting diarrhoea (moderate to severe in character), a slower growth rate and growth deformities were reported from one farm where diseased poults were diagnosed with Cryptosporidium infection (Goodwin et al. 1988b ). Other pathogens were not excluded, as was also mentioned by the authors. In dead poults that had suffered from depression and diarrhoea (faeces adhered on the hind part of the body), necropsy revealed lesions in the small intestine. Microscopic investigation identified Cryptosporidium sp. in the respiratory tract and kidneys, as well as in the gastrointestinal tract (Tacconi et al. 2001) . Diarrhoea, emaciation, lethargy and reduced growth associated with natural C. meleagridis infection have been reported from Iran, but the presence of other pathogens was not excluded (Gharagozlou et al. 2006) . Of 60 diarrhoeal and/or unthrifty birds, 17 (35.3 %) were identified as Cryptosporidium positive by histology, and C. meleagridis was reported based on oocyst morphology. Baroudi et al. (2013) identified C. meleagridis in 25 (44 %) of 57 examined turkeys that died from diarrhoea, but infection with other pathogens was not investigated. Respiratory cryptosporidiosis has also been described in turkeys (Ranck and Hoerr 1987; Tarwid et al. 1985) . Tarwid et al. (1985) identified Cryptosporidium sp. in necropsied birds from two outbreaks of colibacillosis. Colibacillosis is, according to the authors, a secondary disease in turkeys, and Cryptosporidium sp. was identified as the primary pathogen. Symptoms were frothy conjunctivitis and increased mortality. Necropsy revealed pathological changes such as pericarditis, peritonitis and air-sacculitis in addition to the conjunctivitis that was observed in live birds. Thirteen birds with respiratory disease were all positive for Cryptosporidium sp. by histology (Ranck and Hoerr 1987) . Microscopy of sinus and/or tracheal exudates revealed oval oocysts in some samples, but oocyst size was not described, and both C. baileyi and C. meleagridis can appear oval (length/width ratios of 1.05-1.79 and 1.00-1.33 respectively ). Symptoms such as coughing, rattling, sneezing, frothy eyes and swollen sinuses were reported. Other pathogens were present in all but two of the examined birds, and it is unclear whether the infection with Cryptosporidium played a primary role in the pathogenesis or not. Studies on cryptosporidiosis in turkeys, including clinical symptoms, are summarised in Table 4 .13. Clinical cryptosporidiosis in ducks and geese seems to be less common and milder (see Table 4 .14) than in other poultry. Only mild respiratory symptoms resulted from experimental C. baileyi infection (both oral and intratracheal inoculation) in ducks (Lindsay et al. 1989 ). Respiratory and intestinal infection occurred for both infection routes, but symptoms (sneezing, rales, mild dyspnea) were only present in animals infected by the intratracheal route. Mason (1986) described a case of conjunctival cryptosporidiosis. However, since only one of 97 affected ducks was Cryptosporidium positive, the author concluded that the parasite was not the cause of the disease. Similarly, no symptoms occurred in geese in which Cryptosporidium infection was detected in the conjunctivas and bursas (Chvala et al. 2006); and Richter et al. (1994) noted that enteritis and upper respiratory tract symptoms were equally present in infected and non-infected ducks and geese. Mortality was not increased in the positive flocks (Richter et al. 1994) . Ratites Cryptosporidium infection in ostrich chicks has been associated with cloacal and phallus prolapse, leading to high mortality (Bezuidenhout et al. 1993; Penrith et al. 1994; Santos et al. 2005) . Bezuidenhout et al (1993) found that prolapsed cloacas were heavily infected, whereas Penrith et al. (1994) described heavy infection of both the bursa and cloaca in affected chicks, but healthy chicks were not infected. Santos et al (2005) also identified Cryptosporidium infection in the rectum, coprodeum, urodeum and bursa of two dead chicks with cloacal prolapse, both originating from a farm with high mortality rates in 7-30-day-old chicks. However, the authors did not associate the problems with the infection, since changed management practices decreased clinical symptoms and mortality, although Cryptosporidium infection was still present on the farm. Enteritis was indicated by the presence of intestinal invasive stages and rectal prolapse in one chick examined by Penrith and Burger (1993) . Because diarrhoea was not reported it is unknown whether the prolapse was caused by intense bowel movements or something else. Cryptosporidium infection has also been associated with pancreatic necrosis (Allwright and Wessels 1993) . Quails and partridges Cryptosporidium infection has been shown in both diarrhoea and respiratory disease in quails (Guy et al. 1987; Hoerr et al. 1986; Murakami et al. 2002; Ritter et al. 1986 ). Hoerr et al. (1986) reported high mortality rates from 5 days of age in quails infected with Cryptosporidium sp., and with no bacterial or viral pathogens detected. Acute fatal diarrhoea with mortality rates of up to 45 % in 0-17-day-old birds was described by Ritter et al (1986) . Reovirus was also detected in necropsied birds, but another study reported that experimental infection with reovirus alone did not produce diarrhoea, whereas infection with Cryptosporidium sp., either alone or simultaneously with reovirus, resulted in severe diarrhoea and mortality (Guy et al. 1987) . A synergistic effect of co-infection was, however, shown, since oocyst shedding was higher and reovirus infection became systemic and liver necrosis occurred (Guy et al. 1987) . Muramaki et al. (2002) reported a daily mortality rate of 5.7 % in one farm, where birds suffered from upper respiratory tract disease and decreased egg production. Respiratory symptoms were head swelling, nasal discharge and increased lacrimation, and necropsy revealed sinusitis, airsacculitis and egg peritonitis. Co-infection of Cryptosporidium sp., Mycoplasma gallisepticum and other bacteria was shown. The authors concluded that M. gallisepticum was the primary pathogen, but that the mixed infections in conjunction with high ammonia concentrations in the air worsened the symptoms. The role of Cryptosporidium infection in respiratory disease in quails thus remains unclear. Wang et al. (2012) reported that no clinical symptoms were seen in 1,818 sampled quails, of which 239 were Cryptosporidium positive. C. meleagridis was the only pathogen identified in an outbreak of diarrhoea and cough in red-legged partridge chicks (Pages-Mante et al. 2007) . Morbidity rates were 60-70 % and mortality more than 50 %, indicating high pathogenicity. Invasive stages were identified in both the respiratory and intestinal tract, suggesting that not only C. bailey might be associated with respiratory avian cryptosporidiosis. Pigeons Diarrhoea associated with cryptosporidiosis in pigeons has been described in four birds (Ozkul and Aydin 1994; Rodriguez et al. 1997) . Rodriguez et al. (1997) described a 40 % morbidity of yellow watery diarrhoea, weight loss, dehydration and weakness in a farm with 280 pigeons. Mortality was 5 % and necropsy of three birds revealed invasive stages of Cryptosporidium in the small intestine, caecum, colon, cloaca, and bursa. No viruses or bacteria could be isolated. Ozkul and Aydin (1994) identified invasive stages in the small intestine of a pigeon that had been depressed and had evidence of diarrhoea in the form of faeces in its hind feathers. Isolates of both C. baileyi and C. meleagridis derived from one domestic bird species have been successfully transmitted to other domestic birds Lindsay et al. 1987) . C. galli has not been experimentally transmitted between different domestic birds, but has been shown in finches as well as chickens (Blagburn et al. 1990; Pavlásek 1999 Pavlásek , 2001 Ryan et al. 2003b) , and thus has the potential to infect different bird species. The prepatent period of C. baileyi is approximately 4-8 days (Hornok et al. 1998; Lindsay et al. 1988; Rhee et al. 1991; Tumova et al. 2002) . However, in the first report on C. baileyi infection in chickens, a prepatent period of up to 24 days was described ). Older chicks have a slightly longer prepatent periods than younger ones (Lindsay et al. 1988; Rhee et al. 1991; Taylor et al. 1994; Tumova et al. 2002) . The patent period varies more. At oral inoculation of 2-day-old chicks, a patent period of 26 days was seen, whereas it was 11-15 days in chicks inoculated at 14 days of age, 11-12 days in chicks inoculated at 28 days of age and <7 days in chicks inoculated at 42 days of age (Lindsay et al. 1988 ). With intratracheal inoculation, the same authors described patent periods of 27, 11-19, 10-11 and <7 days in these age groups (Lindsay et al. 1988 ). Rhee et al. (1991) and Tumova et al. (2002) observed a mean patent period of approximately 14 days. Oocyst excretion peaked on day 12 and days 11-17 post inoculation, respectively (Rhee et al. 1991; Tumova et al. 2002) . Taylor et al. (1994) showed shorter patent periods and lower total oocyst output in older than younger chickens. There was also an effect of infection dose, in that oocyst output was higher and declined more slowly with lower infection doses (Taylor et al. 1994) . Similar observations were made for 1-and 9-week old chicks (Sreter et al. 1995) . In that study, the mean patent period for 1-week old chicks was 32 days, but one chicken shed oocysts for 151 days. C. meleagridis was shed in the faeces on days 4-7 post infection in two chickens experimentally infected at 6 weeks of age (Woodmansee et al. 1988 ). Tumova et al. (2002) infected 7-day-old chicks. Oocysts first appeared 3 days later and the patent period lasted for 16-17 days. Shedding rates were significantly lower than in chicks inoculated with the same number of C. baileyi oocysts. The prepatent and patent period of C. galli has been described to be 25 and 6 days respectively (Pavlásek 2001) , but was later reported as unknown when C. galli was redescribed (Ryan et al. 2003b ). The prepatent period of C. meleagridis in turkeys inoculated at 7-11 days of age was 2-4 days (Bermudez et al. 1988; Sreter et al. 2000; Woodmansee et al. 1988) . Woodmansee et al. (1988) reported that oocysts were shed for only 4 days; Sreter et al. (2000) found the patent period to be 8-10 days, whereas Bermudez et al. (1988) reported oocyst shedding and invasive stages still being present at day 21 post inoculation. Oocyst shedding rates were moderate (Sreter et al. 2000) , and low to moderate (Bermudez et al. 1988) . Experimental infection with C. baileyi induced mild infection of the bursa ). Lindsay et al. (1987) inoculated turkey poults via the intratracheal, oral and intracloacal route. All three experiments caused infection, but only poults inoculated via the trachea developed symptoms (Lindsay et al. 1987 ). Lindsay et al (1986) described a prepatent period of 5 days and a possible patent period of 9-10 days in experimentally infected Muscovy ducks, based on investigation of pooled faecal samples (Lindsay et al. 1986 ). Oocyst morphology was not described. The intestine, bursa and cloaca were positive for invasive stages, but these tissues can be infected by both C. baileyi and C. meleagridis (Table 4 .14). For quails, one study describes a prepatent period of 7 days and a patent period of 21 days for C. baileyi (Cardozo et al. 2005) . Otherwise, no data are available. Only one of the species and genotypes commonly infecting birds -Cryptosporidium meleagridis -has, so far, proved to be important in human cryptosporidiosis. This species is the third most common species in human cryptosporidiosis worldwide. In the industrialised world, C. meleagridis infection is usually associated with cryptosporidiosis cases in travellers to Asia or Africa (Elwin et al. 2012; Insulander et al. 2013; Leoni et al. 2006 ), but autochthonous cases have also been described (Elwin et al. 2012; Leoni et al. 2006; Silverlås et al. 2012) . Studies on Cryptosporidium prevalence and species distribution in humans in South America have identified C. meleagridis infection at about the same prevalence as C. parvum (Cama et al. 2003 (Cama et al. , 2008 . Although this is a true zoonotic species, there is only one report in which the bird source has been identified, and in that case, chickens and not turkeys were involved (Silverlås et al. 2012) . It is not known whether anthroponotic transmission occurs with this species, but it has been indicated by the fact that not all C. meleagridis-infected patients in an epidemiological investigation had had bird or animal contact (Elwin et al. 2012) . C. meleagridis has the potential to infect other mammalian species as well, and experimental infection of mice, rats, rabbits, pigs and calves has been reported (Akiyoshi et al. 2003; Darabus and Olariu 2003) . Due to the wide host range and the close relationship of C. meleagridis to C. parvum and C. hominis, it has been proposed that this species originated as a mammalian Cryptosporidium species, and later adapted to birds (Xiao et al. 2002b . One study has identified C. parvum in turkeys (McEvoy and Giddings 2009), indicating that this species could play a role in zoonotic transmission. However, only one of 59 birds post-slaughter was positive compared to 2.5-10.5 % of the 5-10-week younger poults, which means risk of transmission via contaminated meat should be very small. The higher prevalence in poults should not pose a risk as long as the flocks are closed to the public. The shedding intensity was not reported, but prevalence indicates that infection rather than just intestinal passage was present. Some studies have identified C. parvum, C. hominis and C. hominis-like isolates in Canada geese (Jellison et al. 2004 (Jellison et al. , 2009 Zhou et al. 2004 ). The authors conclude that these findings are probably not associated with infection and parasite proliferation, but rather transient carriage. Nevertheless, this indicates that domesticated ducks and geese can potentially act as transmission vehicles for these species. Infection with C. baileyi has been identified in one immunodeficient patient. Diagnosis was based on oocyst morphology and biology -experimental infection of mice failed whereas inoculated chickens developed infection of the intestine, bursa and trachea (Ditrich et al. 1991) . Since this patient was immunodeficient and no other reports exist, this species should not be considered as a true zoonotic agent. Ever since animals were first domesticated, and humans became dependent upon them for the commodities that they supply, particularly food and fibre, the infections that affect the health and productivity of livestock have been a concern. Cryptosporidiosis was first identified as a disease of veterinary significance in the 1950s (in turkeys) and then in the early 1970s in calves, but major interest in cryptosporidiosis only developed with the first report of a human cases later that decade, and the recognition that Cryptosporidium infection was also of medical importance. Since then our knowledge on the veterinary significance of Cryptosporidium infection has expanded enormously -particularly in the livestock sector most impacted by cryptosporidiosis -young calves. However, as demonstrated in this chapter, it should not be forgotten almost all farmed animals may be pathologically affected by at least one species of Cryptosporidium, often causing clinical disease that in some instances may be fatal. For some Cryptosporidium species in some farmed animal species, transmission may be anthropozoonotic. Cryptosporidium is a hugely successful parasite, as demonstrated by its host range and wide geographic distribution, and its control has proved challenging. As long as humans raise and depend on animals, there will be a need to control the transmission of cryptosporidiosis amongst livestock species. 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An outbreak of waterborne cryptosporidiosis caused by posttreatment contamination Outbreaks of enteric infections caused by multiple pathogens associated with calves at a farm day camp Natural Cryptosporidium hominis infections in Scottish cattle Investigation of farms linked to human patients with cryptosporidiosis in England and Wales Experimental cryptosporidiosis in germfree lambs Genetic classification of Cryptosporidium isolates from humans and calves in Slovenia Molecular characterisation of Cryptosporidium isolates from humans in Slovenia Prevalence of Cryptosporidium spp. (Eucoccidiorida: Cryptosporiidae) in seven species of farm animals in Tunisia PCR-RFLP analysis of the Cryptosporidium oocyst wall protein (COWP) gene discriminates between C. wrairi and C. parvum, and between C. parvum isolates of human and animal origin Age-dependent resistance to Cryptosporidium baileyi infection in chickens Morphologic host specificity and molecular characterization of a Hungarian Cryptosporidium meleagridis isolate Risk factors associated with Cryptosporidium infection on dairy farms in a New York State watershed An outbreak of cryptosporidiosis among alpaca crias and their human caregivers Survey of zoonoses recorded in Scotland between Long-term study of Cryptosporidium prevalence on a lowland farm in the United Kingdom Molecular characterization of Cryptosporidium isolates from pigs in Zaragoza, northeastern Spain Differentiating human from animal isolates of Cryptosporidium parvum Cryptosporidium and Giardia associated with reduced lamb carcase productivity Longitudinal investigation of protozoan parasites in meat lamb farms in southern Western Australia Impacts of naturally acquired protozoa and strongylid nematode infections on growth and faecal attributes in lambs Evaluation of factors associated with the risk of infection with Cryptosporidium parvum in dairy calves Cryptosporidium in market pigs in southern California USA Retrospective ultramicroscopic investigation on naturally cryptosporidial-infected commercial turkey poults Cryptosporidiosis in the respiratory tract of turkeys in Saskatchewan Variations in oocyst output associated with Cryptosporidium baileyi infections in chickens Genotypes and subtypes of Cryptosporidium spp. in neonatal calves in Northern Ireland Urinary tract cryptosporidiosis in commercial laying hens Genotype and subtype analyses of Cryptosporidium isolates from dairy calves and humans in Ontario Association between management practices and within-herd prevalence of Cryptosporidium parvum shedding on dairy farms in southern Ontario Detection of assemblage A Giardia duodenalis and eimeria spp Performance and oocyst shedding in broiler chickens orally infected with Cryptosporidium baileyi and Cryptosporidium meleagridis Cryptosporidiosis in two alpaca (Lama pacos) holdings in the South-West of England Cryptosporidium parvum (sp. nov.), a coccidium found in the small intestine of the common mouse Coccidiosis in gallinaceous birds Diarrhea in young red deer associated with infection with Cryptosporidium Experimental infection of piglets with Cryptosporidium Enterocolitis in piglets caused by Cryptosporidium purified from calf faeces Experimental cryptosporidiosis in calves: clinical manifestations and pathological findings Prevalence of Cryptosporidium parvum infection and pattern of oocyst shedding in calves in Japan Identifying host sources, human health risk and indicators of Cryptosporidium and Giardia in a Canadian watershed influenced by urban and rural activities Outbreak of cryptosporidiosis in dairy goats in Brazil Cryptosporidium parvum in cattle, sheep and pigs in Galicia (N.W. 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