Shiga-toxin-producing Escherichia coli (STEC) are a group of enteric pathogens that cause foodborne human infections worldwide. The global incidence of STEC infections is estimated between 0.6 and 136 cases per 100 000 patient years with Germany and the United Kingdom having the highest infection rates in Europe (Chase-Topping et al. 2023). Symptoms range from mild, self-limiting gastroenteritis and diarrhoea to more severe complications, such as haemorrhagic colitis and life-threatening haemolytic uremic syndrome (HUS) (Chase-Topping et al. 2023). Broadly, STEC strains are divided into different serogroups based on their lipopolysaccharide O-antigens, a major component of the bacterial outer surface. STEC serogroup O157 (STEC O157) strains cause the most severe sequalae in humans and account for one-third of all STEC cases (Chase-Topping et al. 2023). However, other non-O157 serogroups, particularly those of the ‘big six’ (O26, O45, O103, O111, O121 and O145) are a threat to human health and the incidence of non-O157 human infections resulting in hospitalisation has steadily increased in recent years (Fitzgerald et al. 2023; Kalalah et al. 2024). Disease severity in humans is strongly correlated with both the type and amount of Shiga toxin (Stx) produced by STEC strains (Dallman et al. 2015; Melton-Celsa 2014). Stx are divided into two antigenically distinct types, Stx1 and Stx2, with further subtypes Stx1a−d and Stx2a−k (Chase-Topping et al. 2023; Melton-Celsa 2014). STEC strains can encode one or multiple Stx subtypes with Stx2a considered the most potent and most frequently associated with severe clinical disease.

Ruminants, particularly cattle, are the primary reservoir of STEC and colonisation is typically asymptomatic (Ferens and Hovde 2011). STEC O157 strains in cattle preferentially colonise at the terminal rectum, whereas non-O157 STEC strains colonise at various locations throughout the gut (Naylor et al. 2003; Menge 2020). The situation is less clear in other ruminant species, with little information on the sites of STEC colonisation in deer; however, experimental challenge studies have shown that STEC O157 primarily colonises the distal intestinal tract of sheep and goats (Best et al. 2009; La Ragione et al. 2009). Transmission of STEC strains to humans is incidental through the consumption of contaminated meat or produce or via direct contact with ruminant faecal matter (Chase-Topping et al. 2023; Fitzgerald et al. 2023). Although non-O157 human infections are increasing, most prevalence, epidemiology and intervention research has focused on STEC O157 in cattle. The herd-level prevalence of STEC O157 in Scottish cattle has been stable at ~20% for the past 30 years and an equivalent prevalence was also determined for English and Welsh herds in the most recent UK-wide survey (Henry et al. 2017; Pearce et al. 2009). On STEC O157-positive farms, <20% of animals account for most of the environmental STEC O157 contamination and >80% of all inter-animal transmission (Chase-Topping et al. 2008). These few animals are considered ‘super-shedders’ that shed >10⁴ colony-forming units per gram of faeces (CFU/g; Chase-Topping et al. 2008).

Although ruminant livestock are recognised as the primary reservoir of STEC, the incidence of human STEC infections from wildlife species is increasing globally. Studies investigating deer as a reservoir species have accounted for 42% of all studies in recent years (Espinosa et al. 2018), highlighting deer as an important species in the STEC transmission cycle.

Prevalence studies conducted in the United Kingdom, Europe, America and Asia consistently estimate a low prevalence of STEC O157 in wild deer populations (0–3%) (Fitzgerald et al. 2023; Szczerba-Turek et al. 2023; Lauzi et al. 2022; Kabeya et al. 2017). Species sampled across these studies included red deer (Cervus elaphus), fallow deer (Dama dama), roe deer (Capreolus capreolus), sika deer (Cervus nippon) and white-tailed deer (Odocoileus virginianus) with no bias between species and carriage of STEC O157 observed. In the United Kingdom, a survey of Scottish wild deer in which 1087 faecal samples were collected estimated a STEC O157 prevalence of 0.28% however, comparable studies aimed at estimating STEC O157 prevalence in England and Wales are lacking (Fitzgerald et al. 2023). Despite the low global prevalence of STEC O157 in wild deer, significant human outbreaks have occurred in Scotland (Smith-Palmer et al. 2018), the United States (Laidler et al. 2013) and Japan (Nagano et al. 2004), where epidemiological investigations concluded that the consumption or handling of contaminated wild deer products or faecal contaminated produce was the cause. Genetic characterisation of isolates from each outbreak found that they encoded both the stx2 Shiga toxin variant and eae genes, a genotype associated with high human pathogenic potential.

Prevalence estimates of non-O157 STEC in deer vary greatly. In the United Kingdom, the prevalence of non-O157 STEC in wild deer has been estimated at ~69% based on faecal sample positivity for stx1 and/or stx2 genes (Pearce et al. 2023). Compared with wild deer, significantly lower levels of non-O157 STEC were found in deer sampled from parks, zoos and farms (Pearce et al. 2023). It is unclear whether certain deer species are more likely to carry non-O157 STEC than others. Several studies in Europe and America reported no difference in the prevalence of non-O157 STEC between red deer (18–22%) and roe deer (17–24%), whereas others have reported a higher prevalence in red deer (Soare et al. 2021; Szczerba-Turek et al. 2020, 2023; Lauzi et al. 2022). In a survey conducted in Poland, prevalence in fallow deer (9.65%) was significantly lower than in red and roe deer, although this finding needs to be confirmed by other studies to assess true interspecies prevalence. Population densities greater than 15 wild deer per square kilometre have also been associated with increased prevalence and increased gut colonisation by non-O157 STEC (Soare et al. 2021). This is supported by one study (Pearce et al. 2023) that found a higher prevalence of stx genes present in farmed deer samples compared with those collected from deer in zoos and parks but not wild deer or abattoir samples.

Non-O157 STEC strains with a wide variety of O-types have been isolated from deer but isolation of strains from the ‘big six’ O-types causing human infections is rare. STEC O128:H2, O22:H16 and O146:H21 were the dominant strain types in Scottish wild deer, whereas STEC O146:H28 strains were dominant in several European studies and STEC O22:H16 and O10:H45 were dominant in Japan (Szczerba-Turek et al. 2020, 2023; Lauzi et al. 2022; Kabeya et al. 2017). Several Shiga toxin subtypes have been identified in non-O157 STEC deer isolates, with Stx2b being the most frequently encoded, either alone or in combination with Stx1c. Both Stx2b and Stx1c are also less pathogenic than Stx2a and, interestingly, several studies failed to detect the eae gene, which is associated with severe human disease, in non-O157 STEC deer isolates. The highly pathogenic genotype, stx2a⁺ eae⁺, is also rare in deer suggesting that non-O157 STEC deer isolates are less pathogenic than those isolated from other animal reservoirs. Nonetheless, non-O157 STEC deer isolates still pose a significant human health risk because clinical cases have been associated with several non-O157 deer genotypes including STEC O146:H28 strains. Stx2a can be found in a small number of deer isolates and common deer toxin subtypes Stx2b and Stx1c can still cause severe disease in humans (EFSA BioHaz Panel 2020).

Colonisation by STEC in ruminants is considered asymptomatic, although few studies have investigated signs in host species outside cattle. In a single study in which white-tailed deer were experimentally infected with a high dose of STEC O157, deer did not experience any lethargy or anorexia and there was no evidence of attaching and effacing lesions, characteristic of STEC O157 colonisation, at postmortem examination (Fischer et al. 2001). Two of the six infected deer experienced mild non-haemorrhagic diarrhoea although it was unclear if this was due to STEC O157 infection (Fischer et al. 2001). Although Stx is the key virulence factor in humans, there is no pathogenesis associated with Stx in ruminants. For STEC O157, Stx has been shown to promote colonisation at the terminal rectum through various mechanisms, but does not cause intestinal damage or other complications observed in humans (Fitzgerald et al. 2019). These differences in Stx pathogenesis between ruminants and humans are thought to arise due to interspecies differences in the distribution of the Stx receptor, Gb3, on host cells (Sapountzis et al. 2020). In humans, most studies have focused on STEC O157, which intimately adheres to and colonises the gut using an array of adhesion proteins and secretion systems (Farfan and Torres 2012). Once colonised, Stx toxins are expressed and released at the site of infection, which target local Gb3-positive cells and can cross the gut barrier to spread systemically (Joseph et al. 2020). STEC typically causes diarrhoeal infections ranging from mild, watery diarrhoea to haemorrhagic colitis; however, 6–25% of cases develop life-threatening HUS characterised by kidney cell damage, haemolytic anaemia, thrombocytopenia and renal failure (Joseph et al. 2020).

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