Studies examining the prevalence of Cryptosporidium in deer are not as abundant as they are for other ruminants, and the majority focus on wild deer rather than farmed deer. However, one systematic review of the literature estimated the overall global prevalence of Cryptosporidium in deer to be 7.8% (484/9480; Lv et al. 2021). This prevalence varies greatly and depends on many factors, including method of detection, species of deer, farmed or wild deer, age of animal, country of origin, time of year of sampling and number of samples collected. In a study of wild deer in Scotland, Cryptosporidium was detected in 12.3% of samples (122/991), with the highest incidence detected in sika deer (24.2%; 23/95) and lower incidences in roe deer (13.2%; 52/394) and red deer (10.2%; 47/463), although there were fewer samples from sika deer, which may have impacted the result (Bartley et al. manuscript in preparation). Of the Cryptosporidium-positive samples, 18% (22/122) were C. parvum, the main zoonotic species, 10.7% were Cryptosporidium ubiquitum (previously known as deer-like genotype which also has zoonotic potential) and the majority (63%) were Cryptosporidium ryanae (not zoonotic and commonly detected in post-weaned bovine calves; Bartley et al. manuscript in preparation). The detection result was lower than a previous study in Scotland, which reported an overall Cryptosporidium prevalence of 80% in wild red deer (the majority of which were the zoonotic species C. parvum), although the sample size was much smaller (20 deer) and they were collected in an area with a known Cryptosporidium problem (Wells et al. 2015). Another study detected Cryptosporidium in 3 out of 46 (6.5%) roe deer faecal samples collected in a single water catchment in Cumbria (north-west England), and these were demonstrated to be C. ubiquitum and deer genotype (Robinson et al. 2011).

A study in Ireland examining the shedding pattern of Cryptosporidium in 40 farmed red deer hinds and calves over a one-year period reported detecting oocysts in 39.3% (114/290) of hinds and 60% of calves (21/35; Skerrett and Holland 2001). Unfortunately, no molecular analysis was carried out on the positive samples, so the species of Cryptosporidium being carried by these deer are unknown. Interestingly, the largest number of positive samples detected in hinds occurred in May and June, which coincides with calving and could therefore potentially represent a source of oocysts for neonatal deer calves. Indeed, the periparturient transmission of Cryptosporidium has been reported in sheep (Ye et al. 2013) and cows (De Waele et al. 2012) and reports of a periparturient rise in the shedding of other parasites are well documented (Fthenakis et al. 2015) and hypothesised to be due to hormonal changes in the dam, changes in immunity or due to the stress of giving birth.

Despite there being evidence for Cryptosporidium causing neonatal diarrhoea in deer calves/fawns, there is a significant lack of data available, highlighting the requirement for research in this area. Of the few reports that exist, the earliest is from 1980 and describes an outbreak of diarrhoea in red deer calves artificially reared on premises in Scotland that had experienced a Cryptosporidium outbreak in their beef suckler calves a few months earlier (Tzipori et al. 1981). Of the 82 deer calves, which were housed at the research unit, 68% developed diarrhoea within two weeks of arriving at the unit and 24% of calves died. At the same time, two deer calves that were being reared naturally outside also died. Cryptosporidium oocysts were detected in 80% of faecal samples collected from diarrhoeic deer calves and 50% of samples from non-diarrhoeic calves. Ileal and caecal contents of the two deer calves reared naturally were examined and found to contain large numbers of Cryptosporidium oocysts. Histopathological examination of the intestines demonstrated Cryptosporidium oocysts present in the microvillar borders of the small and large intestines. Oocysts were most commonly found in the caecum and colon, with few detected in the jejunum and upper ileum. Haematoxylin and eosin staining of the intestine demonstrated total atrophy of the villi and elongation of crypts in the ileum and infiltration of the lamina propria with mononuclear cells.

Outbreaks of Cryptosporidium involving artificially reared red deer calves in the 1980s were also described in New Zealand (Orr et al. 1985). In the first, a group of 10 red deer calves reared in small pens on cow’s colostrum and ewe’s milk substitute went on to develop yellow scour and died within a few days of illness onset, despite treatment with electrolytes and antibiotics. The second case involved 10 red deer calves that had been removed from their dams at two days old and reared on ewe’s milk substitute; eight of the calves went on to develop a pasty yellow scour 7–13 days later. Despite treatment with antibiotics, electrolytes and kaolin preparations, seven of the eight scouring calves died within three days of illness onset. Histopathological examination of the small intestine of calves in both outbreaks revealed moderately severe subacute enteritis with stunted villi, with infiltration of immune cells to the lamina propria and numerous. Cryptosporidia were detected on the epithelial surface of the villi.

High mortality due to suspected Cryptosporidium infection in neonatal farmed red deer calves was reported in the United Kingdom in an unusual situation where calves died very young and diarrhoea was not present (Simpson 1992). In this outbreak, the calves were born to hinds that had been wild-caught in Scotland and moved to a farm in Cornwall two to three months before calving and held on ground previously grazed by sheep. Twenty-five out of 30 calves (83%) became weak and lethargic and died within 24–48 hours of birth, despite treatment with electrolytes and antibiotics. Diarrhoea was absent in the majority of calves, but large numbers of Cryptosporidium oocysts were detected in the duodenum, ileum and colon at postmortem examination (PME). The calves were also severely uraemic, which was thought to contribute to the cause of death.

Although cryptosporidiosis was initially only believed to be a disease of artificially reared deer, the reports above of suckled deer calves also succumbing to the disease (Tzipori et al. 1981; Simpson 1992) suggest that this is an important disease in all deer. Studies have demonstrated the long-term production effects of Cryptosporidium infection in beef calves (Shaw et al. 2020) but whether infection impacts the live weight gains of deer calves remains to be determined.

Diagnosis is based on the detection of tiny (4–5 mm) Cryptosporidium oocysts in faecal samples by microscopy, as well as clinical observations (watery yellow diarrhoea, lethargy, reduced appetite, loss of condition), although not all infected deer develop diarrhoea. Molecular analysis of oocysts can further differentiate the species, which allows for the identification of any zoonotic threat. At PME, histopathological examination can reveal atrophy of the villi with congestion and haemorrhage, as well as mononuclear cell infiltration of the lamina propria. Haematoxylin and eosin staining can also be used to demonstrate Cryptosporidium life cycle stages in gut tissue.

There are very few treatment options available for Cryptosporidium infection and none licenced for use in deer, so treatment relies on supportive therapy and, unfortunately, is not always successful. The use of electrolyte solutions to replace fluids is crucial in acutely infected deer calves and oral colostrum and intravenous infusion of deer serum have been reported to aid recovery. A report from New Zealand details some success using toltrazuril at 40 mg/kg, given orally as a 1.25% solution in water, to treat deer fawns (Hicks 1994). Broad-spectrum antibiotics may be given to help control secondary infections (e.g. ceftiofur hydrochloride or procaine benzylpenicillin).

Halofuginone lactate can be used as a preventative treatment in dairy and beef calves and has been shown to reduce diarrhoea and oocyst shedding when used for seven consecutive days; however, it is toxic if overdosed and there are no studies detailing its effectiveness for treating cryptosporidiosis in deer.

Prevention of infection can be difficult and relies on a combination of factors involving animal management and reducing exposure to environmental contamination. Quality and quantity of colostrum are important, so good, balanced nutrition in hinds pre-calving is important and adequate uptake of colostrum by deer calves is essential within the first six hours of life – although this is very difficult to manage in an outdoor environment where calving often takes place out of sight. Where deer calves are born indoors, any calves showing signs of scour should be quarantined until one week after scouring stops. Deep and regular straw bedding can help keep animals clean and away from potentially contaminated faeces. Oocyst contamination can be reduced by steam cleaning pens/sheds or using an appropriate disinfectant. Most of the common farm disinfectants are not effective at killing Cryptosporidium oocysts at the manufacturer’s recommended concentrations; however, 3% hydrogen peroxide can reduce oocyst infectivity after four minutes of contact time (Wells et al. 2019). Other effective disinfectants include 2% Keno™ cox (two hours contact time), 2.5% Neopredisan^® 135-1 (two hours contact time) and 10% OX-VIRIN^® (one hour contact time; Wells et al. 2019). Management of hinds at mating and calving may also help reduce transmission of Cryptosporidium. For example, hinds can be organised into smaller mating groups so that timings of calving can be worked out and hinds grouped accordingly (so that young calves and older calves are kept separated). First calvers should be kept separate from older hinds as they will have less immunity and the density of hinds can be kept low to try to reduce the spread of disease.

Cryptosporidium parvum

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