“…Thirty-seven studies reported ReA following Campylobacter ( n = 19) and NTS infections ( n = 26) (Buxton et al, 2002, Bremell et al, 1991, Dworkin et al, 2001, Eastmond, 1983, Ekman et al, 2000, Gumpel et al, 1981, Hakansson et al, 1976, Hannu et al, 2002a, Hannu et al, 2002b, Helms et al, 2006, Pitkanen et al, 1981, Lee et al, 2005, Locht et al, 1993, Locht and Krogfelt, 2002, Locht et al, 2002, Mattila et al, 1994, Mattila et al, 1998, McColl et al, 2000, Petersen et al, 1996, Pitkanen et al, 1983, Ponka et al, 1984, Rohekar et al, 2008, Rudwaleit et al, 2001, Samuel et al, 1995, Schiellerup et al, 2008, Schoenberg-Norio et al, 2010, Short et al, 1982, Ternhag et al, 2008, Thomson et al, 1992, Thomson et al, 1994, Townes et al, 2008a, Tuompo et al, 2013, Uotila et al, 2014, Urfer et al, 2000, Doorduyn et al, 2008, Arnedo-Pena et al, 2010, Eastmond et al, 1983, Melby et al, 1990) in up to 63% of patients with either infection (Supplementary Table 4). The majority of studies reported ReA triggered by Campylobacter ( n = 14) or NTS infection ( n = 18) in < 10% of patients with gastroenteritis.…”