Assessment of listing and categorisation of animal diseases within the framework of the Animal Health Law (Regulation (EU) No 2016/429): Salmonella infection in poultry with serotypes of animal health relevance (S. Pullorum, S. Gallinarum and S. arizonae)
2017; Wiley; Volume: 15; Issue: 8 Linguagem: Inglês
10.2903/j.efsa.2017.4954
ISSN1831-4732
AutoresSimon J. More, Anette Bøtner, Andrew Butterworth, Paolo Calistri, Klaus Depner, S.A. Edwards, Bruno Garin‐Bastuji, Margaret Good, Christian Gortázar, Virginie Michel, Miguel Ángel Miranda Chueca, Søren Saxmose Nielsen, Mohan Raj, Liisa Sihvonen, Hans Spoolder, Arjan Stegeman, Hans‐Hermann Thulke, Antonio Velarde, Preben Willeberg, Christoph Winckler, Francesca Baldinelli, Alessandro Broglia, Beatriz Beltrán‐Beck, Lisa Kohnle, Dominique Bicout,
Tópico(s)Identification and Quantification in Food
ResumoEFSA JournalVolume 15, Issue 8 e04954 Scientific OpinionOpen Access Assessment of listing and categorisation of animal diseases within the framework of the Animal Health Law (Regulation (EU) No 2016/429): Salmonella infection in poultry with serotypes of animal health relevance (S. Pullorum, S. Gallinarum and S. arizonae) EFSA Panel on Animal Health and Welfare (AHAW), EFSA Panel on Animal Health and Welfare (AHAW)Search for more papers by this authorSimon More, Simon MoreSearch for more papers by this authorAnette Bøtner, Anette BøtnerSearch for more papers by this authorAndrew Butterworth, Andrew ButterworthSearch for more papers by this authorPaolo Calistri, Paolo CalistriSearch for more papers by this authorKlaus Depner, Klaus DepnerSearch for more papers by this authorSandra Edwards, Sandra EdwardsSearch for more papers by this authorBruno Garin-Bastuji, Bruno Garin-BastujiSearch for more papers by this authorMargaret Good, Margaret GoodSearch for more papers by this authorChristian Gortázar Schmidt, Christian Gortázar SchmidtSearch for more papers by this authorVirginie Michel, Virginie MichelSearch for more papers by this authorMiguel Angel Miranda, Miguel Angel MirandaSearch for more papers by this authorSøren Saxmose Nielsen, Søren Saxmose NielsenSearch for more papers by this authorMohan Raj, Mohan RajSearch for more papers by this authorLiisa Sihvonen, Liisa SihvonenSearch for more papers by this authorHans Spoolder, Hans SpoolderSearch for more papers by this authorJan Arend Stegeman, Jan Arend StegemanSearch for more papers by this authorHans-Hermann Thulke, Hans-Hermann ThulkeSearch for more papers by this authorAntonio Velarde, Antonio VelardeSearch for more papers by this authorPreben Willeberg, Preben WillebergSearch for more papers by this authorChristoph Winckler, Christoph WincklerSearch for more papers by this authorFrancesca Baldinelli, Francesca BaldinelliSearch for more papers by this authorAlessandro Broglia, Alessandro BrogliaSearch for more papers by this authorBeatriz Beltrán-Beck, Beatriz Beltrán-BeckSearch for more papers by this authorLisa Kohnle, Lisa KohnleSearch for more papers by this authorDominique Bicout, Dominique BicoutSearch for more papers by this author EFSA Panel on Animal Health and Welfare (AHAW), EFSA Panel on Animal Health and Welfare (AHAW)Search for more papers by this authorSimon More, Simon MoreSearch for more papers by this authorAnette Bøtner, Anette BøtnerSearch for more papers by this authorAndrew Butterworth, Andrew ButterworthSearch for more papers by this authorPaolo Calistri, Paolo CalistriSearch for more papers by this authorKlaus Depner, Klaus DepnerSearch for more papers by this authorSandra Edwards, Sandra EdwardsSearch for more papers by this authorBruno Garin-Bastuji, Bruno Garin-BastujiSearch for more papers by this authorMargaret Good, Margaret GoodSearch for more papers by this authorChristian Gortázar Schmidt, Christian Gortázar SchmidtSearch for more papers by this authorVirginie Michel, Virginie MichelSearch for more papers by this authorMiguel Angel Miranda, Miguel Angel MirandaSearch for more papers by this authorSøren Saxmose Nielsen, Søren Saxmose NielsenSearch for more papers by this authorMohan Raj, Mohan RajSearch for more papers by this authorLiisa Sihvonen, Liisa SihvonenSearch for more papers by this authorHans Spoolder, Hans SpoolderSearch for more papers by this authorJan Arend Stegeman, Jan Arend StegemanSearch for more papers by this authorHans-Hermann Thulke, Hans-Hermann ThulkeSearch for more papers by this authorAntonio Velarde, Antonio VelardeSearch for more papers by this authorPreben Willeberg, Preben WillebergSearch for more papers by this authorChristoph Winckler, Christoph WincklerSearch for more papers by this authorFrancesca Baldinelli, Francesca BaldinelliSearch for more papers by this authorAlessandro Broglia, Alessandro BrogliaSearch for more papers by this authorBeatriz Beltrán-Beck, Beatriz Beltrán-BeckSearch for more papers by this authorLisa Kohnle, Lisa KohnleSearch for more papers by this authorDominique Bicout, Dominique BicoutSearch for more papers by this author First published: 09 August 2017 https://doi.org/10.2903/j.efsa.2017.4954Citations: 3 Correspondence: alpha@efsa.europa.eu Requestor: European Commission Question number: EFSA-Q-2016-00601 Panel members: Dominique Bicout, Anette Bøtner, Andrew Butterworth, Paolo Calistri, Klaus Depner, Sandra Edwards, Bruno Garin-Bastuji, Margaret Good, Christian Gortázar Schmidt, Virginie Michel, Miguel Angel Miranda, Simon More, Søren Saxmose Nielsen, Mohan Raj, Liisa Sihvonen, Hans Spoolder, Jan Arend Stegeman, Hans-Hermann Thulke, Antonio Velarde, Preben Willeberg and Christoph Winckler. Acknowledgements: The Panel wishes to thank Andy Wales and Rob Davies for the support provided to this scientific output. Adopted: 30 June 2017 AboutSectionsPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Abstract Salmonella infection in poultry (Salmonella Pullorum, Salmonella Gallinarum and Salmonella arizonae) has been assessed according to the criteria of the Animal Health Law (AHL), in particular criteria of Article 7 on disease profile and impacts, Article 5 on the eligibility of Salmonella to be listed, Article 9 for the categorisation of Salmonella according to disease prevention and control rules as in Annex IV and Article 8 on the list of animal species related to Salmonella. The assessment has been performed following a methodology composed of information collection and compilation, expert judgement on each criterion at individual and, if no consensus was reached before, also at collective level. The output is composed of the categorical answer, and for the questions where no consensus was reached, the different supporting views are reported. Details on the methodology used for this assessment are explained in a separate opinion. According to the assessment performed, Salmonella can be considered eligible to be listed for Union intervention as laid down in Article 5(3) of the AHL. The disease would comply with the criteria as in Sections 4 and 5 of Annex IV of the AHL, for the application of the disease prevention and control rules referred to in points (d) and (e) of Article 9(1). The assessment here performed on compliance with the criteria as in Section 1 of Annex IV referred to in point (a) of Article 9(1) is inconclusive. The main animal species to be listed for Salmonella according to Article 8(3) criteria are all species of domestic poultry and wild species of mainly Anseriformes and Galliformes, as indicated in the present opinion. 1 Introduction 1.1 Background and Terms of Reference as provided by the requestor The background and Terms of Reference (ToR) as provided by the European Commission for the present document are reported in Section 1.2 of the scientific opinion on the ad hoc methodology followed for the assessment of the disease to be listed and categorised according to the criteria of Article 5, Annex IV according to Article 9, and 8 within the Animal Health Law (AHL) framework (EFSA AHAW Panel, 2017). 1.2 Interpretation of the Terms of Reference The interpretation of the ToR is as in Section 1.2 of the scientific opinion on the ad hoc methodology followed for the assessment of the disease to be listed and categorised according to the criteria of Article 5, Annex IV according to Article 9, and 8 within the AHL framework (EFSA AHAW Panel, 2017). The present document reports the results of assessment on Salmonella infection in poultry with serotypes of animal health relevance (Salmonella Pullorum, Salmonella Gallinarum and Salmonella arizonae) according to the criteria of the AHL articles as follows: Article 7: Salmonella profile and impacts Article 5: eligibility of Salmonella to be listed Article 9: categorisation of Salmonella according to disease prevention and control rules as in Annex IV Article 8: list of animal species related to Salmonella. 2 Data and methodologies The methodology applied in this opinion is described in detail in a dedicated document about the ad hoc method developed for assessing any animal disease for the listing and categorisation of diseases within the AHL framework (EFSA AHAW Panel, 2017). 3 Assessment 3.1 Assessment according to Article 7 criteria This section presents the assessment of Salmonella infection in poultry with serotypes of animal health relevance (S. Pullorum, S. Gallinarum and S. arizonae) according to the Article 7 criteria of the AHL and related parameters (see table 2 of the opinion on methodology (EFSA AHAW Panel, 2017)), based on the information contained in the factsheet as drafted by the selected disease scientist (see Section 2.1 of the scientific opinion on the ad hoc methodology) and amended by the AHAW Panel. 3.1.1 Article 7(a) Disease Profile It is important to note that only two serovars of Salmonella enterica subspecies arizonae are considered to be of commercial significance, and only in turkeys because of their ability to be transmitted vertically from infected breeding flocks. These closely related serovars are thought to have been eradicated from all major turkey breeding nations, but their occurrence in low income countries or wild turkey populations is uncertain. 3.1.1.1 Article 7(a)(i) Animal species concerned by the disease Susceptible animal species Parameter 1 – Naturally susceptible wildlife species (or family/orders) S . arizonae Salmonella enterica subsp. arizonae includes around 100 serovars (Grimont and Weill, 2007) and has a broad host range. It can potentially cause infection, which is usually subclinical, in many species of birds, such as domestic fowl (Gallus gallus), ducks (Anas platyrhynchos), turkeys (Meleagris gallapavo), geese (Anser anser), quail (Coturnix japonica), guinea fowl (Numida meleagris) and pheasants (Phasianus colchicus) (Oros et al., 1998; Shivaprasad, 2008), and reptiles (Köbölkuti et al., 2008; Clancy et al., 2016). It should be noted that many 'Arizona' group isolates from reptiles and birds may be of the biphasic diarizonae subspecies of Salmonella enterica (Hall and Rowe, 1992; Köbölkuti et al., 2008; Yong et al., 2008; Lukac et al., 2015; Clancy et al., 2016). S . Gallinarum Order Galliformes (Chappell et al., 2009); natural outbreaks of fowl typhoid (FT; S. Gallinarum) have been reported in sparrows, parrots, ring-necked doves, ostriches and peafowl (Harbourne, 1955). Clinical outbreaks among species other than chickens and turkeys are uncommon (Shivaprasad, 2000). Individual cases of disease have occasionally been reported in free-ranging game birds, such as partridges (Shivaprasad and Barrow, 2008). S . Pullorum Order Galliformes (Chappell et al., 2009); there are reports of naturally occurring infection in many bird species, although most cases are traced to some contact with chickens (Bullis, 1977). Natural outbreaks of Pullorum disease have been reported in quail, sparrows, parrots, canaries and bullfinch (Shivaprasad and Barrow, 2008), although clinical disease is unusual among species other than chickens, turkey and pheasants (Spickler, 2009). Parameter 2 – Naturally susceptible domestic species (or family/orders) S . arizonae Turkey (Meleagridis gallopavo) is the principal species for infection with serovars O18:Z4,Z23 and O18:Z4,Z32 (Weiss et al., 1986; Hall and Rowe, 1992; Hafez, 2013). Other domestic poultry, including chickens (Gallus gallus) and ducks may occasionally show disease (Bigland and Quon, 1958; Silva et al., 1980), but economic effects are minor other than in turkey production. Arizonae serovars may be found in animal feed that has been contaminated by reptile faeces and may thereby be occasionally transmitted to domestic animals, especially laying hens that are fed on non-heat-treated feed, usually causing a transient subclinical infection. S . Gallinarum Order Galliformes; principal clinically affected species are chickens (Gallus gallus) (Bullis, 1977; Shivaprasad et al., 2013) and turkeys (Meleagris gallopavo) (Hafez, 2013), also pheasants, quail, guinea fowl, peafowl (Moore, 1946; AHVLA, 2008; Ravishankar et al., 2008; Macovei et al., 2010; Casagrande et al., 2014). Significant clinical outbreaks are uncommon apart from among chickens, turkeys and pheasants (Shivaprasad, 2000). S . Pullorum Order Galliformes; the principal host species is domestic chickens (Gallus gallus). Infection of turkeys (Meleagris gallopavo) is reported to follow contact with chickens in many cases (Shivaprasad and Barrow, 2008). Outbreaks in pheasants and guinea fowl are also reported (Hafez, 2013). Parameter 3 – Experimentally susceptible wildlife species (or family/orders) S . arizonae Experimental infection of wildlife species with the turkey-associated O18 serovars is not reported. S . Gallinarum Corvids (rooks and jackdaws) manifested clinical disease with mortality following exposure by various routes (Harbourne, 1955). Pigeons appeared resistant to clinical disease following oral or parenteral exposure (Aydin et al., 1978). S . Pullorum S. Pullorum shows low virulence via the oral route in mice, and is cleared rapidly from systemic tissues after parenteral inoculation (Barrow, 1994). Parameter 4 – Experimentally susceptible domestic species (or family/orders) S . arizonae Experimental infection of chicks with the turkey-associated O18 serovars has been reported (Youssef and Geissler, 1979; Silva et al., 1980), demonstrating clinical signs similar to neonatally infected turkey poults in a proportion of individuals. Crop inoculation of turkey poults and chicks with similar doses of turkey Arizona group isolates resulted in more severe disease and mortality in the turkeys than in the chicks (Hinshaw and McNeil, 1946). S . Gallinarum Rabbits showed minor intestinal pathology following oral inoculation, whilst there was systemic persistence in mice of the same S. Gallinarum strain for over 2 weeks following intravenous inoculation (Barrow, 1994). However, clinical signs were not seen. Rats orally infected with a high dose (109 colony forming units (CFU)) of S. Gallinarum shed the organism in faeces for up to 121 days (Badi et al., 1992a). Experimental inoculation of chickens produces outcomes consistent with natural disease (Barrow, 1994; Berchieri et al., 2001). S . pullorum Natural or experimental disease has been reported in various mammalian species: chimpanzee, rabbit, guinea pig, chinchilla, pig, kitten, fox, dog, pig, mink, cow, rat (Bullis, 1977; Shivaprasad and Barrow, 2008), although details are sparse. Oral inoculation studies (Barrow et al., 1994) in rabbits, rats, guinea pigs and mice did not show clinical effects with doses (in the range 107 to 109 cfu) that caused clinical disease in chicks. Reservoir animal species Parameter 5 – Wild reservoir species (or family/orders) S . arizonae The relevant serovars are closely associated with turkeys. Wild turkeys are the likely principal wild reservoir species for turkey-specific serovars. S. arizonae is primarily carried by reptiles in warm countries, and these free-living animals can be considered reservoir hosts. Infection of poultry is often associated with contamination of feed or the production environment by reptile faeces (Köbölkuti et al., 2008; Clancy et al., 2016). Rodents may be an effective short-term reservoir or vector species on infected premises to facilitate persistence of infection between flocks (Goetz, 1962). S . Gallinarum The agent has been isolated from free-living corvids, pigeons, psittacine birds, ducks (Harbourne, 1955; Georgiades and Iordanidis, 2002; Spickler, 2009), chicken-house rats (Aydin et al., 1978; Badi et al., 1992b), and there is serological evidence of serovar Gallinarum in doves (Espinosa-Arguelles et al., 2010). Many avian species may be carriers (Barrow et al., 1994; Javed et al., 1994). Shedding by pigeons appeared to be transient following experimental oral exposure (Aydin et al., 1978). Rats from area of poultry houses harboured S. Gallinarum in intestines, while experimentally inoculated wild rats shed S. Gallinarum for 3 months following oral inoculation (Badi et al., 1992a). Red poultry mite (Dermanyssus gallinae) from infected poultry houses can harbour S. Gallinarum for months, and is the main route for carry-over between flocks (Zeman et al., 1982; Parmar and Davies, 2007; Ivanics et al., 2008). Infected red mites can be carried between farms on equipment or the clothing of workers or visitors, as well as being carried by wild birds moving between farms. Ticks (Argas spp.) also can harbour the agent but their role in epidemiology is uncertain (Stefanov et al., 1975). S . Pullorum The agent has been isolated from several free-living or semiwild avian species, including parrots, sparrows, quail, peacock, doves, pheasants and pigeons (Javed et al., 1994; Akhter et al., 2010; Hua et al., 2012), and has been isolated from the intestine of rats on affected fowl premises (Anderson et al., 2006). In many countries in which S. Pullorum has been eradicated from commercial scale poultry breeding and production, there remains a reservoir in wild and commercially bred game birds that are released into the wild for shooting. The regular, sporadic occurrence of Pullorum disease in hobbyist flocks in developed countries reflects the likely persistent presence of a wildlife reservoir (Shivaprasad and Barrow, 2008; Barrow and Freitas Neto, 2011; OIE, 2012). Parameter 6 – Domestic reservoir species (or family/orders) S . arizonae Adult turkeys exhibit asymptomatic intestinal carriage and faecal shedding for extended periods (Shivaprasad, 2008). Historically, small numbers of isolates of the relevant serovars have been reported from other species, including dogs and sheep in the USA (Weiss et al., 1986), although the significance of this in respect of reservoir status is unknown and there are no recent supporting reports. S . Gallinarum Domestic waterfowl (ducks, geese) appear to be largely resistant to clinical disease (Moore, 1946; Barrow et al., 1999; Shivaprasad, 2000), but can harbour the agent (Adzitey et al., 2012). It is thought that small backyard flocks of domestic fowl, which may never be subject to diagnostic investigations, represent an important reservoir of infection. Isolation of the agent has been reported from apparently asymptomatic commercially farmed chickens (4% of cloacal swab or faeces samples) in Bangladesh (Parvej et al., 2016). S . Pullorum Domestic waterfowl (ducks, geese) appear to be largely resistant to clinical disease (Shivaprasad and Barrow, 2008), but can harbour the agent (Anderson et al., 2006; Hua et al., 2012). Isolation of the agent has been reported from apparently asymptomatic commercially farmed chickens (3.3% of cloacal swab or faeces samples) in Bangladesh (Parvej et al., 2016). 3.1.1.2 Article 7(a)(ii) The morbidity and mortality rates of the disease in animal populations Morbidity Parameter 1 – Prevalence/incidence S . arizonae Disease in turkeys is confined to the first few weeks of life and morbidity is highly variable, reflected in quoted mortality figures of 3.5–90% (Hafez, 2013). Nineteen serotypes of S. arizonae were isolated from 6,577 samples collected from 371 different poultry houses of broilers in north-western Spain between 2011 and 2015 and prevalence in the sample was 0.29% (Lamas et al., 2016). S . Gallinarum Morbidity and mortality are highly variable owing to effects of age, flock management, nutrition, stressors such as travel, other diseases, and variation between breeds of the primary (chicken) host (Shivaprasad, 2000; Freitas Neto et al., 2007; Chappell et al., 2009; Barrow and Freitas Neto, 2011). In respect of the last point, median parenteral lethal dose varies over a 107-fold range between inbred resistant and susceptible chicken breeds, likely mediated by features of the host's reticuloendothelial system (Barrow et al., 1994; Barrow and Freitas Neto, 2011). Brown egg-layers are known to be more susceptible than white egg-layers (Barrow and Freitas Neto, 2011). Experimentally, 60% morbidity was reported in outbred chickens (Chappell et al., 2009). Among Indian broiler flocks, there was a morbidity of approximately 10–15% in recent reports (Arora et al., 2015). S . Pullorum Morbidity (and mortality) are highly variable owing to effects of age (younger birds are more susceptible, unlike fowl typhoid), flock management, nutrition, stressors such as travel, other diseases, and variation between breeds of the primary (chicken) host (Freitas Neto et al., 2007; Shivaprasad and Barrow, 2008; Chappell et al., 2009; Barrow and Freitas Neto, 2011). Brown egg-layers are known to be more susceptible than white egg-layers (Barrow and Freitas Neto, 2011). There is a clear age effect, with older growing and mature fowl often not exhibiting clinical signs, although (depending on other factors including breed susceptibility) acute disease may be seen in older fowl on some occasions and egg production and hatchability of eggs is usually affected (Shivaprasad and Barrow, 2008; OIE, 2012). Infected adult turkeys usually show no clinical signs (Hafez, 2013). Parameter 2 – Case-morbidity rate (% clinically diseased animals out of infected ones) S . arizonae Accurate figures are not available for this. S . Gallinarum Accurate figures are not available for this. Given the breed-associated variation in susceptibility, the case-morbidity rate is likely to vary substantially. S . Pullorum Accurate figures are not available for this. Given the breed- and age-associated variation in susceptibility, the case-morbidity rate is likely to vary substantially (OIE, 2012). Mortality Parameter 3 – Case-fatality rate S . arizonae Mortality among poultry is variable. Although mortality may reach 90%, more commonly mortality is up to 15%, being highest in the first three weeks and continuing up to five weeks of age (Shivaprasad, 2008; Hafez, 2013). S . Gallinarum Classically, a high mortality is described for fowl typhoid (Shivaprasad et al., 2013), with a reported range of 10–93% of chicks infected at or around hatching (Shivaprasad and Barrow, 2008), although most outbreaks of severe clinical disease occur in adult laying or breeding birds, during the laying period. The case-fatality rate was consistently around 70% in recent outbreaks (2005–2013) among broiler chicks in India (Arora et al., 2015). However, again management, age, etc., affect outcomes and the morbidity rate is often much higher than mortality (Shivaprasad and Barrow, 2008). In a typical outbreak in a large cage laying flock, mortality can eventually reach 90%, with only isolated birds that carry genetic resistance remaining alive (Davies, 2016). In naturally infected birds, the outcome of the infection is marked by high morbidity and up to 80% mortality (Shivaprasad, 2000). In affected turkey flocks, initial mortality is usually substantial, up to about 25%, and there is a tendency for intermittent recurrence of clinical disease over 2–3 weeks, with lower mortality during this phase (Hafez, 2013). Losses typically are lower on premises after the first outbreak of disease (Shivaprasad and Barrow, 2008). Experimentally, the speed and degree of mortality was highly dose-dependent among 4-day-old chicks, ranging from 4% to 84% over 28 days post-inoculation (Berchieri et al., 2001). Oral median lethal doses for chickens of 104 and 105.2 CFU have been claimed (Berchieri et al., 2001; Barrow and Freitas Neto, 2011). S . Pullorum Classically, a high mortality is described for Pullorum disease in young chickens and turkeys (Hafez, 2013; Shivaprasad et al., 2013), with up to 100% of chicks, and poults dying when infected at or around hatching (Shivaprasad and Barrow, 2008). Highest losses usually occur during the second week after hatching, with a rapid decline in case mortality between the third and fourth weeks of age. However, again management, age, etc., affect outcomes and the morbidity rate under commercial conditions is often much higher than mortality, which can be as low as 0% (Shivaprasad and Barrow, 2008). Experimentally, oral inoculation of 1-day-old chicks and turkey poults with a virulent turkey-associated S. Pullorum strain resulted in mortality among turkey groups of 42–78%, peaking at 6–11 days post-inoculation; among chicken groups mortality was 66–75%, peaking at 13–22 days post-inoculation (Gwatkin, 1948). By contrast, oral inoculation of slightly older (4-day-old) layer chicks with 109 cfu of an unrelated S. Pullorum strain resulted in no acute disease or mortality (Berchieri et al., 2001). AHVLA received intestinal swabs were from 10-day-old pheasant poults of which 100 had died out of 1,000 birds placed. (http://www.thepoultrysite.com/search/?cat=0&q=Salmonella+pullorum&x=9&y=8 Accessed 15/06/2017, AHVLA: Salmonella Pullorum in Gamebirds 29 July 2011). 3.1.1.3 Article 7(a)(iii) The zoonotic character of the disease Presence Parameter 1 – Report of zoonotic human cases (anywhere) S . arizonae Human disease associated with turkey serovars (O18:Z4,Z23 and O18:Z4,Z32) does not appear to have been reported in any detail (Shivaprasad, 2008). Isolates of these serovars have been reported from humans in the USA (Weiss et al., 1986), including 222 between 2003 and 2013 (CDC, 2016); these are unexpectedly high numbers and it is not clear whether these were associated with disease. It seems likely, given the data source, that at least some of these isolates were from individuals showing symptoms of illness warranting sampling and culture. Human infections with O18:Z4,Z23 and O18:Z4,Z32 were described among Latin Americans in California in the 1980s, and in the same report a link was identified between human arizonosis associated with other serovars and the consumption of reptile-associated folk medicines (Waterman et al., 1990). It is possible the O18 serovars are acquired in many cases by a similar route. There are numerous reports of human arizonosis, caused by other serovars, typically in association with reptiles or travel (Hall and Rowe, 1992; Shivaprasad, 2008; Di Bella et al., 2011; Gunal and Erdem, 2014). Gastroenteritis and systemic infections have been reported. S . Gallinarum Being avian host-adapted, S. Gallinarum poses minimal zoonotic risk (Eswarappa et al., 2009; OIE, 2012). Just 13 of around 391,000 human Salmonella isolations from the US Centers for Disease Control and Prevention between 1996 and 2006 were reported as S. Gallinarum/Pullorum (CDC, 2008); in the period 2003–2013 the equivalent proportion was zero, from 462,000. S . Pullorum Being avian host-adapted, S. Pullorum poses a very low zoonotic risk (Shivaprasad, 2000; OIE, 2012). Historical case reports in the literature indicate S. Pullorum can induce an acute, self-limiting enteritis after consuming highly contaminated food, typically infected eggs (Mitchell et al., 1946; Shivaprasad, 2000). More prolonged gastroenteritis was attributed to S. Pullorum in one case, but the immune status of the patient is unclear (Judefind, 1947). 3.1.1.4 Article 7(a)(iv) The resistance to treatments, including antimicrobial resistance Parameter 1 – Resistant strain to any treatment even at laboratory level S . arizonae The agent is not known to be resistant to antibiotics, but data on incidence and trends in resistance is scarce as the organism has not been reported in recent years. S . Gallinarum/ S . Pullorum Clinical disease and losses can be suppressed by antibiotic treatment (Ravishankar et al., 2008; Barrow and Freitas Neto, 2011). Infection cannot be eliminated from flocks by use of antimicrobials (Georgiades and Iordanidis, 2002; Ravishankar et al., 2008; Barrow and Freitas Neto, 2011). Antibiotic resistances appear to reflect prevailing regional patterns of antibiotic usage and clonal dissemination of strains and reflects trends amongst Salmonella enterica isolates from poultry more generally (Javed et al., 1994; Georgiades and Iordanidis, 2002; Kumar et al., 2012; Agada et al., 2014). There is evidence, from survey and surveillance data, of increasing antimicrobial resistance over time (Zeman et al., 1982; Lee et al., 2003; Ivanics et al., 2008; Ravishankar et al., 2008; Barrow and Freitas Neto, 2011; Filho et al., 2016). 3.1.1.5 Article 7(a)(v) The persistence of the disease in an animal population or the environment Animal population Parameter 1 – Duration of infectious period in animals S . arizonae Acute disease with mortality in young turkeys has a duration typically of 3–5 weeks, but older animals may carry the agent in the intestinal tract and shed it chronically (Shivaprasad, 2008). S . Gallinarum Shedding in the faeces was reported during clinical disease 'and into the stage of convalescence' (Gauger, 1937). A more recent oral inoculation study, using relatively susceptible 18-week brown laying hens, showed a minority of hens to have positive caecal contents at each of 3, 7, 14 and 21 days post-inoculation (Oliveira et al., 2005). In the same report, other studies showed shedding usually occurred in the days shortly before death, from 7 to 28 days
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