ars.els-cdn.com · web viewregarding ph, many strains grow over the range 5.5-8.0 but generally not...

Supplementary materialAppendix A. List of the 121 hazard after the duplicates removal and the result of the eligibiligy assessment. In the columns there are the references in which are based the decision to keep the hazard in the model.

N Hazard Presence in studied population in the last 20

years

Considered as a pork-borne disease to

humans

Is this hazard

relevant?1 Actinobacillus

actinomycetemcomitansNot reported in BR last 20

yearsNot considered a pork-

borne hazardNo

2 Actinobacillus pleuropneumoniae (Abilleira et al., 2010)

Not considered a pork-borne hazard

No

3Actinobacillus suis

Not reported in BR last 20 years


No

4Adenovirus (Garcia, 2011)


No

5Aerococcus sp. (Matajira et al., 2015)


No

6Aeromonas spp.

(Lucena, 2007) (Igbinosa et al., 2012; Praveen et al., 2016)

Yes

7 African Swine Fever Virus (ASFV)



No

8Alaria alata


(Djurković-Djaković et al., 2013)

No

9Anaplasma sp.



No

10 Arcobacter spp. (Oliveira et al., 2010) (Collado et al., 2009) Yes11

Ascaris suunNot reported in BR last 20


borne hazardNo

12Ascarops strongylina



No

13Aujesky Virus (AV)



No

14Bacillus anthracis

Not reported in BR last 20 years (Fosse et al., 2008)

No

15Balantidium coli (Nishi et al., 2000)


No

16 Bordetella bronchiseptica (Coutinho et al., 2009)


No

17 Bovine Malignant Catarrhal Fever Vírus (BMCFV)



No

18Brachyspira hampsonii



No

19 Brachyspira hyodysenteriae

(Barcellos and Sobestiansky, 2012)


No

20Brachyspira innocens



No

21Brachyspira pilosicoli (Barcellos et al., 2000)


No

22 Brucella suis (Poester et al., 2002) (Fosse et al., 2008) Yes23 C. cellulosae/Taenia

solium(Coldebella et al., 2017) (Fosse et al., 2008) Yes

24Chlamydia suis



No

25 Circovírus (Soares, 2011) Not considered a pork- No

borne hazard26 Classical Swine Fever

Virus (CSFV)Not reported in BR last 20


borne hazardNo

27Clostridium botulinum

* (Acha and Szyfres, 2003a)

Yes

28Clostridium difficile *


No

29 Clostridium perfringens * (Fosse et al., 2008) Yes30

Clostridium tetaniNot reported in BR last 20


borne hazardNo

31

Coronavirus

(Brentano, L.; Zanella, J.R.C.; Mores, N.; Piffer,

2002)


No

32Cryptosporidium suis



No

33Cyclospora sp.

Not reported in BR last 20 years (Dixon, 2015)

No

34Cytomegalovirus (Dutra et al., 2016)


No

35Demodex spp. (Santarém et al., 2005)


No

36 Dicrocoelium dendriticum



No

37 E. coli [ETEC, EPEC] * (Fosse et al., 2008) Yes38 E. coli [STEC] (Martins et al. 2011) (Fosse et al., 2008) Yes39

Encefalite japonesaNot reported in BR last 20


borne hazardNo

40 Encephalomielitis Virus (EV)



No

41Entamoeba polecki



No

42Enterococcus sp. (Filsner, 2013)


No

43Enterovirus



No

44 Erysipelothrix rhusiopathiae (Coutinho et al., 2011)


No

45Escherichia fergusonii



No

46Stephanurus dentatus



No

47Fasciola hepática



No

48 Foot and Mouth Disease Vírus (FMDV)


No

49Francisella tularensis


(Uddin Khan et al., 2013)

No

50 Fusarium spp. (Fumonis) (Oldoni and Teixeira, 2012)


No

51Giardia sp.



No

52

H1N1

(Brentano, L.; Zanella, J.R.C.; Mores, N.; Piffer,

2002)


No

53H5N1/N7N7


(Uddin Khan et al., 2013)

No

54Haemophilus parasuis (Abilleira et al., 2010)


No

55 Helicobacter spp. (Yamasaki et al., 2009) Not considered a pork- No

borne hazard56 Hepatitis A Virus

(HAV)Not reported in BR last 20


borne hazardNo

57 Hepatitis E virus (HEV) (Bodnar et al., 2010) (Fosse et al., 2008) Yes58

Hyostrongylus sp. (D’Alencar et al., 2011)Not considered a pork-

borne hazardNo

59Isospora suis



No

60Klebsiella pneumoniae (Almeida et al., 2007)


No

61Lawsonia intracellularis (Viott et al., 2013)


No

62Legionella spp.



No

63Leptospira sp.



No

64 Listeria monocytogenes (Pissetti et al., 2012) (Fosse et al., 2008) Yes65 M. tuberculosis/bovis (Coldebella et al., 2017) (Fosse et al., 2008) Yes66 Macracanthoehyncus

sp. (Morés et al., 2007)Not considered a pork-

borne hazardNo

67Menangle Vírus (MV) (Morés et al., 2007)


No

68Metastrongylus spp.



No

69Microsporum spp.



No

70MRSA (Masson, 2011)


No

71Mycobacterium avium (Morés et al., 2007)


No

72 Mycoplasma hyopneumoniae (Takeuti et al., 2017)


No

73Mycoplasma hyorhinis

(Yamaguti et al., 2015) Not considered a pork-borne hazard

No

74Mycoplasma suis



No

75Necator americanus



No

76Nipah Virus (NV)



No

77Norovirus (Cunha et al., 2010)


No

78Ochratoxin A (Kruger et al., 2010)


No

79Oesophagostomum spp.



No

80Pararotavirus



No

81Pasteurella multocida (Oliveira Filho et al., 2018)


No

82PEDV



No

83 Physocephalus sexalatus



No

84Poliovirus type 1 (PV 1)



No

85Proteus spp. (Almeida et al., 2007)


No

86 PRRS Not reported in BR last 20 Not considered a pork- No

years borne hazard87

Pseudomonas spp. (Almeida et al., 2007)Not considered a pork-

borne hazardNo

88Rabies vírus (RV)


No

89Rhodococcus equi (Morés et al., 2007)


No

90Rickettsia spp.



No

91Rotavirus A



No

92 Salmonella [non-typhoidal]

(Kich et al., 2011) (Fosse et al., 2008) Yes

93Sapovirus



No

94 Sarcocystis suihominis (Coldebella et al., 2017) (Fosse et al., 2008) Yes95

Sarcoptes scabiei(Barcellos and

Sobestiansky, 2012)Not considered a pork-

borne hazardNo

96 Schistossoma Japonicum



No

97Shigella spp.



No

98Staphylococcus aureus

* (Bennett et al., 2013; Fosse et al., 2008)

Yes

99Streptococcus porcinus



No

100 Streptococcus suis (Abilleira et al., 2010)


No

101 Strongyloides ransomi



No

102 Swine Parvovirus (SPV) (Gava et al., 2009)


No

103 Taenia suis



No

104 TGEV



No

105

Thermophilic Campylobacter

(Biasi et al., 2011) (OIE, 2008) Yes

106

Torque teno vírus (TTV)



No

107 Toxocara canis

Not reported in BR last 20 years (Taira et al., 2004)

No

108

Toxoplasma gondii

( Valença et al., 2011; Marques-Santos et al.,

2017)

(Dixon, 2015) Yes

109 Trichinella spp.


(Djurković-Djaković et al., 2013)

No

110 Trichomonas buttreyi



No

111 Trichomonas foetus



No

112 Trichomonas rotunda



No

113 Trichuris suis (Viott et al., 2013)


No

114 Tricophyton spp.



No

115 Tritrichomonas suis



No

116 Trypanosoma cruzi



No

117 Trueperella pyogenes

(Ribeiro et al., 2015) Not considered a pork-borne hazard

No

118

Vesicular exanthema of swine virus (VESV)



No

119

Vesicular Stomatitis Virus (SVV)


(Acha and Szyfres, 2003b)

No

120 Yersinia enterocolitica

(Martins et al. 2018) (Fosse et al., 2008) Yes

121

Yersinia pseudotuberculosis


(Fosse et al., 2008) Yes

*Considered naturally present in pigs or ubiquitous

Appendix B. Input data retrieved from the literature to assess release, exposure and to characterize the hazards and risk. The ‘release’ is combined with ‘probability of amplification/reduction’ (see figure 2 and table 1) to assess the ‘exposure’. The ‘exposure’ is then combined with ‘pathogenicity’ (see table 2) to assess the occurrence and finally the occurrence is combined with adverse effects (see table 3) to characterize the risk.

Hazard Data available and retrieved from the literature

Aeromonas spp.

There is no data related to the occurrence of Aeromonas spp. in pig herds in Brazil. To date there is just one study investigating this pathogen in pig carcasses, and a high frequency (86.7%) in carcasses originated from 15 different farms was reported (Lucena, 2007). Thus, the release is assumed to be VERY HIGH with VERY HIGH uncertainty.

Aeromonas spp. habitat is primarily freshwater and soil but it is also found in the intestinal tract of human and animals (Bhunia, 2018). The type specie A. hydrophila is neither salt (<5%) nor acid (min. pH 6.0) tolerant and grows optimally around 28C. However, it is able to grow in temperatures as low as -0.1C (Adams and Moss, 2008). Aeromonas spp. include opportunistic pathogens causing disease in fish and reptiles with rare reports of infection in mammals (Markey et al., 2013). A. hydrophila has been reported as cause of septicemia in piglets in Portugal (Queiroga et al., 2012). Aeromonas spp. have been isolated from pig feces and carcass processing equipment (Fontes, M. C., Saavedra, M. J., Martins, C., Martínez-Murcia, 2011) It is a nonspore forming bacteria, and D-values of 1.5, 0.10 and 0.03 min, respectively, at 51, 57 and 60°C were reported (Shedon and Schuman, 1996). Thus, the exposure is HIGH with LOW uncertainty;

Foodborne disease can occasionally be caused by Aeromonas spp. Water, fish and inadequate sanitized raw vegetables are the most common vehicle of this pathogen (Laird, 2015). It is believed to be an opportunistic emergent foodborne pathogen especially to immunocompromised humans (Daskalov, 2006; Pal, 2018). Disease is most common in children under 5 years of age, the elderly, and the immunocompromised. Gastrointestinal disease associated with aeromonads is variable. Typical diarrheal disease is cholera-like with profuse, watery diarrhea and mild fever. Normally, the disease is self-limiting with low lethality (Dodd, 2017). Disease has been associated with a very high infective dose (1010 CFU) (Acha and Szyfres, 2003b). Thus, the pathogenicity is VERY LOW and the adverse effects is VERY LOW, both with LOW uncertainty;

Thus, the risk is VERY LOW with VERY HIGH uncertainty.

Arcobacter spp. There are few studies about the prevalence of Arcobacter spp. in Brazilian pig herds. A study investigating this genus in pig carcasses suggested that the hazard is present in almost all herds with a within herd prevalence of approximately 30% (Oliveira et al., 2009). Gobbi et al. (2018) reported Arcobacter spp. in 73% of pig carcasses and 4% of feces

sampled at two slaughterhouses. In the same study 10% of pork sampled at markets was positive for Arcobacter spp. This genus have been isolated from pig fetuses and sows with reproductive symptoms in Brazil (De Oliveira et al., 1997). Thus, the release is VERY HIGH with MODERATE uncertainty;

Arcobacter spp. have been reported worldwide in chickens, domestic mammals (cattle, pigs, sheep, horses, dogs), reptiles (lizards, snakes and chelonians), meat (poultry, pork, goat, lamb, beef, rabbit), vegetables and humans (Ramees et al., 2017). Most of the infections caused by Arcobacter remain asymptomatic and only few cases results in clinical disease. In pigs, cattle and horses, A. butzleri cause enteritis and/or diarrhea. A. cryaerophilus has been associated with porcine abortion and other reproductive symptoms (De Oliveira et al., 1997; Neill et al., 1985). A. butzleri and A. skirrowii have been less frequently reported in aborted animals (Collado et al., 2009; De Oliveira et al., 1997). A. butzleri can grow within a temperature range from 15C to 37C with optimal growth at 30C (Hilton et al., 2001). The genus Arcobacter is nonspore forming and thermal tolerance studies on three strains of A. butzleri determined that the D-values at pH 7.3 had a range of 0.07-0.12 min (at 60°C), 0.38-0.76 min (at 55°C) and 5.12-5.81 min (at 50°C) (D’Sa and Harrison, 2005). Arcobacter survival was further underlined by (Ho et al., 2008),who showed that A. butzleri, A. cryaerophilus and A. skirrowii may survive to the scalding process conditions (52 °C, 3 min) in poultry slaughterhouses. The genus Arcobacter is aerotolerant and able to grow aerobically. Thus, exposure is HIGH with VERY LOW uncertainty;

During the recent years, Arcobacter spp. have gained attention as an emerging food-borne enteropathogen. Arcobacters are mainly transmitted through contaminated food (vegetables, chicken and pork) and water, which may be contaminated through sewage. Several reports regarding the presence of Arcobacter in water have been documented and hence consumption of contaminated water acts as an efficient source of infection (Collado et al., 2009; Lee and Choi, 2013). Among all Arcobacters, A. butzleri is the most common specie and has been associated with human disease, such as enteritis, severe diarrhea, bacteremia and septicemia (Collado and Figueras, 2011; Van den Abeele et al., 2014). Arcobacter has been isolated from feces and blood samples of humans and symptoms may range from diarrhea to septicemia (Fisher et al., 2014). Gastrointestinal manifestations are the common signs in humans and may be exhibited as watery diarrhea in case of A. butzleri infection (Collado and Figueras, 2011). Cases of bacteremia due to A. butzleri and A. cryaerophilus have infrequently been documented (Ramees et al., 2017). An invasive form of Arcobacter infection in an 85-year-old immunocompromised

man was documented (Arguello et al., 2015). In general, health individuals recover spontaneously with no sequelae (Fernández et al., 2004). Thus, the pathogenicity is VERY LOW and the adverse effects LOW with VERY HIGH and HIGH uncertainty, respectively.

Thus, the risk is VERY LOW with a VERY HIGH uncertainty.

Brucella suis Few brucellosis surveys in swine have been carried out in Brazil. A national survey carried out during 1981 in 66,770 serum samples revealed a prevalence of 2.19% (Carrillo, 1987) The intensification of production changed this scenario and the last report indicated a prevalence of 0.34% (Brasil, 2009). More recently, Motta et al. (2010) subjected 27,300 serum samples originated from 13 Brazilian states, and none was confirmed as positive in agglutination tests. Similarly, Rosa et al. (2012) subjected 910 serum samples collected at slaughter and originated from 30 commercial pig farms to agglutination tests and none was confirmed as positive. The control of brucellosis in pig farms that sell breeding stock is very strict and carried out under official supervision (Poester et al., 2002). For this reason, the release is VERY LOW with VERY LOW uncertainty;

Brucella species are obligate parasites and each species has a preferred natural host, which serves as a reservoir of infection. B. suis can infect swine, including wild boar; its biovar 1 can also infect cattle and be excreted in milk (Markey et al., 2013). Bacteria shed by infected animals can remain viable in a moist environment for several months. Infected pigs may be asymptomatic or present abortion, orchitis, spondylitis and herd infertility (Megid et al., 2010); abscesses may occur in organs and tissues (Acha and Szyfres, 2003a). It grows optimally around 37C and is killed by heating at 63C for 7–10 min (Adams and Moss, 2008). Thus, the exposure is VERY LOW with MODERATE uncertainty;

B.suis can cause severe infection in humans. Infection most often occurs through occupational or recreational exposure to infected animals (Ketheesan et al., 2010; Meirelles-Bartoli et al., 2012). Although human brucellosis has sometimes been associated with the consumption of inadequately cooked meat from an infected animal, raw milk or cream are the principal food vehicles (Adams and Moss, 2008). Muscle tissue generally contains a small number of organisms and contaminated meat and meat products may represent a source of infection especially if they come from animals slaughtered during the acute phase of the disease and if they are consumed raw or undercooked (Casalinuovo et al., 2016). Teske et al. (2011) reported that 30 cfu (median) are need to start an infection in guinea pig’s skin. In milk it is believed that low doses (10–100 organisms) are sufficient to cause infection (Logue et al., 2017; Pappas et al., 2006). The consequences of infection with B. suis range from

asymptomatic infections to diverse syndromes that may appear insidiously or abruptly. Acute brucellosis is usually a febrile illness with nonspecific flu-like signs such as fever, chills, headache, malaise, back pain, myalgia and lymphadenopathy, which may be accompanied by splenomegaly and/ or hepatomegaly. Patients may experience drenching sweats, particularly at night. Nonspecific gastrointestinal signs including anorexia, vomiting, diarrhea and constipation may also be seen. Deaths are uncommon except in infants, and are usually caused by endocarditis or infections affecting the brain (Acha and Szyfres, 2003a). Thus, the pathogenicity is HIGH and the adverse effects is HIGH with MODERATE and LOW uncertainty, respectively;

Thus, the risk is VERY LOW with MODERATE uncertainty.

Clostridium botulinum There is no report about the prevalence of pigs carrying C. botulinum in Brazilian herds. Botulism cases are common in ruminants, birds and dogs, and have also been described in other species (Oliveira Júnior et al., 2016). Despite botulism being worldwide rare in swine, there is one report in Brazil. In this case, the animals were fed with food residues originating from restaurant and hotel kitchens that were stored at room temperaturein barrels and offered to the animals without a prior thermal treatment (Raymundo et al., 2012). Thus, the release is assumed to be VERY LOW with a VERY HIGH uncertainty;

Clostridium species are anaerobic endospore-producing rods. The endospores are widely, but unevenly, distributed in soils and aquatic environments. Germination of the endospores, with growth of vegetative cells and production of toxin, occurs in anaerobic environments such as contaminated can of meat, fish or vegetables, carcasses of invertebrate and vertebrate animals and rotting vegetation. C. botulinum is part of the gut microbiota of animals. In pigs, a study identified nine Operational Taxonomic Units (OTUs) in the gut microbiome, which belonged to the Clostridium botulinum group (Leser et al., 2002). In other study, which aimed to enumerate C. botulinum in pig feces, thirty-four (71%) of the positive samples had a spore load of less than 4 spores per gram (Dahlenborg et al., 2001). Botulism in animals is an intoxication usually caused by ingestion of preformed toxin. Pigs affected in a botulism outbreak presented flaccid paralysis, anorexia, weakness, lack of coordination, locomotion difficulties with the evolution of lateral decubitus, and involuntary urination and defecation (Raymundo et al., 2012). Physiological diversity within the species C. botulinum is recognized by its division into four groups. Groups I, III and IV present minimum growth temperature between 10C and 15C, while group II is considered psychrotrophic and is able to growth at 3-5C. Group I is more tolerant to salt, and can growth in a aw 0.94,

while the other groups are inhibited by salt concentrations of 3-5% (Adams and Moss, 2008) In any case, the optimal temperature lies between 30-37C. The optimum pH is neutral to slightly alkaline (pH 7.0-7.6). The consensus has long been that a pH around 4.7 represents an absolute minimum. The maximum pH for growth is 8.5–8.9 and the toxin is unstable at alkaline pH values (Adams and Moss, 2008; Markey et al., 2013). The most important common feature of the groups is the production of pharmacologically similar neurotoxins responsible for botulism. Eight serologically distinct toxins are recognized (A, B, C1, C2, D, E, F, and G), a single strain of C. botulinum will usually produce only one toxin type. Pigs are often a healthy carrier of C. botulinum that produces type B toxin (Serdev, 2018). Spores of group I are highly heat-resistant, and at 121C the D is 0.1 to 0.25; spores of group II in turn display a D values of 0.6-3.3 min at 80C. The botulin toxins are heat sensitive and may be destroyed by heating at 80C for 10 min, or boiling temperature for few minutes (Jay et al., 2005) .Thus, the exposure is VERY LOW with VERY LOW uncertainty;

Three types of botulism are recognized in human: foodborne botulism, infant or infectious botulism and wound botulism. Only in the first type is food invariably involved (Adams and Moss, 2008). Foodborne botulism results from the ingestion of the exotoxin produced by C. botulinum growing in the food. The botulinum toxins are the most toxic substances known, with a lethal dose for an adult human in the order of 10-8 g. Initial symptoms of botulism occur from 8 h to 8 days, most commonly 12–48 h, after consumption of the toxin-containing food. Symptoms include vomiting, constipation, urine retention, double vision, dysphagia, dry mouth and dysphonia. The patient remains conscious until, in fatal cases, shortly before the end, when the progressive weakness results in respiratory or heart failure. This usually occurs 1–7 days after the onset of symptoms. Surviving patients may take as long as 8 months to recover fully (Adams and Moss, 2008). Insufficient or inadequate sanitary measures in the preparation of pork and absence or insufficient heat treatment are the main risk factors. Human botulism is caused by the ingestion of toxins A, B, E and rarely F. Ready-to-eat foods in low oxygen-packaging are more frequently involved in cases of foodborne botulism (WHO, 2019a) Foodborne botulism is a rare illness. In 2017, only three outbreaks were reported in the USA, with 19 cases and three deaths (CDC, 2017). Between 1999 and 2014, 83 confirmed cases of foodborne botulism were registered in Brazil. The five most involved foods were mortadella, canned meat, sausage, chicken pie and pickled heart-of-palm (Vilmar et al., 2017). Thus, both the pathogenicity and the adverse effects were VERY HIGH with VERY LOW uncertainty;


Clostridium perfringens C. perfringens is believed to be isolated from feces of a low number of pigs (5%) in more than 70% of the commercial herds in Brazil (Barcellos and Sobestiansky, 2012). In a field-based case-control study in 16 pig farms, no difference was observed in the frequency of C. perfringens isolation from piglets with/without diarrhea (Ruiz et al., 2016). Moreno et al. (2003) reported four outbreaks of neonatal pig diarrhea in Brazil, which were caused by C. perfringens type A producer of 2+toxin. In a study conducted in three slaughterhouses, out of the 90 carcass swabs and fecal samples, 53 carcasses (58.8%) and 53 fecal samples (58.8%) were positive for C. perfringens. All strains were classified as C. perfringens biotype A, negative for enterotoxin production and negative to the 2 toxin gene (Ferreira et al., 2012) Thus, the release is HIGH with VERY LOW uncertainty;

C perfringens is an anaerobic, endospore-producing species, classified into five types designated A–E, based on the production of four major exotoxins and eight minor ones. C. perfringens type A, which is responsible for food poisoning and gas gangrene, produces only the major toxin, which has lecithinase activity. This toxin plays an important role in gas gangrene lesion, but does not have any role in the food poisoning syndrome (Adams and Moss, 2008) C. perfringens type A occurs in the intestinal tract of humans and animals as well as in soil (Markey et al., 2013). C. perfringens type A commonly affects piglets in the first week of life. Once it is part of the microbiota in swine, sows can transfer this bacterium to piglets. The disease is described as a non-hemorrhagic mucoid diarrhea and is characterized by mucosal necrosis and villus atrophy, without attachment and invasion by the microorganism (Songer and Uzal, 2005). C. perfringens has an optimum growth between 37C and 45C. The lowest temperature for growth is around 20C, and the highest is around 50C. Regarding pH, many strains grow over the range 5.5-8.0 but generally not below 5.0 or above 8.5. The lowest reported aw for growth and spore germination lie between 0.97 and 0.95 (Jay et al., 2005). On carcass and meat surface, Clostridium spores can occur but are not able to multiply. However, if carcass meat is exposed to temperatures above 20C clostridia can multiply within the tissues. In large pieces of meat and comminuted meat products, spores can survive cooking and may germinate into vegetative cells, which can growth during storage and produce enterotoxins. Enterotoxin is produced during sporulation and its biological activity destroyed within 5 minutes at 60C (ICMSF, 1996). The heat resistance of vegetative cells is comparable to that of non spore forming bacteria with D values at 60C in beef of a few minutes; D values of spores at 100C show a wide inter-strain variation with recorded values from 0.31min to more than 38min (Adams and Moss, 2008). Thus, the exposure is HIGH with VERY LOW uncertainty;

The causative factor of C. perfringens food poisoning is the enterotoxin. The enterotoxin is produced and released upon C. perfringens infection, which often occurs when foods are prepared in large quantities and kept warm for a long time before consumed. This storage abuse allows the germination of spores in the food and multiplication of C. perfringens vegetative cells. In the gut, vegetative cells sporulate and release the enterotoxin (Bennett et al., 2013). Its production occurs in the late stages of sporulation, and the peak of its production occurs just before the lysis of cell’s sporangium (Jay et al., 2005). C. perfringens food poisoning is generally a self-limiting, non-febrile illness characterized by nausea, abdominal pain, diarrhea and, less commonly, vomiting. Onset is usually 8 to 24 h after consumption of food containing large numbers of the vegetative organism; estimated at 106–108 cfu. In otherwise healthy individuals, medical treatment is not usually required and recovery is complete within 1–2 days (Adams and Moss, 2008). Thus, the pathogenicity is LOW and adverse effects associated VERY LOW with VERY LOW uncertainty;

The risk is VERY LOW with VERY LOW uncertainty.Cysticercus cellulosae/ Taenia solium

According to the official data obtained from the Brazilian Federal Inspection System, only 0.00092% of the 94,000,00 pig carcasses inspected from 2012 to 2014 presented cysticercosis lesions. These findings were restricted to 25 slaughterhouses from a total of 114 establishments under federal inspection (Coldebella et al., 2017). Thus, the release is VERY LOW with VERY LOW uncertainty;

The definitive host of the Taenia solium is man; the natural intermediate hosts of the T. solium cysticercus (C. cellulosae) are the domestic pig and the wild boar, and also humans. The adult stage of T. solium lives in the small intestine of man and regularly eliminates gravid proglottids, which are generally expelled to the external environment with the feces; there they dry out and release the eggs. The eggs remain near the droppings or are disseminated by the wind, rain, or other climatic phenomena, contaminating water or food which may be consumed by pigs. Pigs carrying the C. cellulosae often do not have symptoms but naturally infested carcasses can be detected by inspection (R. M. da Silva et al., 2012). The cysts are restricted to muscle and organs and no multiplication happens in food (Acha and Szyfres, 2003c; Djurković-Djaković et al., 2013). The inactivation is easily reached by cooking pork at 60ºC (Pawlowski and Murrell, 2001; Rhoads and Murrell, 1988). Thus, the exposure is VERY LOW with HIGH uncertainty;

Infection with the T. solium tapeworm occurs when humans eat raw or undercooked, infected pork. Tapeworm eggs pass with the feces and are infective for pigs. Infection in humans with the T. solium tapeworm causes few clinical symptoms. The infective dose of Cysticercus is not determined. As well as being infective for pigs, T. solium eggs may also infect

humans if they are ingested, causing infection with the larval parasite in the tissues (human cysticercosis). In this case humans are the origin of transmission. This infection can result in devastating effects on human health. When cysts develop in the brain, the condition is referred to as neurocysticercosis. Symptoms include severe headache, blindness, convulsions, and epileptic seizures, and can be fatal (Acha and Szyfres, 2003c). Taenia solium is considered endemic in Brazil (WHO, 2015b). In a survey conducted in 110,144 people from Health of Family Program, 185 (0.2%) presented taeniasis; from 97 patients eliminating proglottides, in only 4 T. solium was identified (Esteves et al., 2005) Thus, the pathogenicity is VERY HIGH and the adverse effects is LOW with VERY HIGH uncertainty;


Escherichia coli [ETEC, EPEC]

Enterotoxigenic E. coli (ETEC) and enteropathogenic E.coli (EPEC) figure among the most important causes of diarrhea in pigs in Brazil. In growers and finishers an overall prevalence of 10.87% was estimated, occurring in 5.49% of the sampled herds (Viott et al., 2013). In piglets the reported ETEC frequency was similar (10%), but the pathogen was distributed in a wider range of herds sampled (26.7%) (Cruz Junior et al., 2013). Thus, the release is MODERATE with a MODERATE uncertainty;

E.coli is a natural inhabitant of the large intestine and lower small intestine of all mammals. It is excreted in feces and can survive in fecal particles, dust and water for weeks to months. E. coli is not commonly associated to lesions to pigs at slaughter age but it can be carried in intestine. Growth requirements of ETEC and EPEC are not different from other coliforms. They have been reported to grow at temperatures from -2C to 50C, although in foods the growth is poor or very slow at 5C. They can grow over a pH range of 4.4-9.0 (Jay et al., 2005). They can be expected to grow in large number of foods under the proper conditions. It is not spore forming and is considering a heat sensitive organism, with a D value lower than 1 minute at 60C, although some strains can be more heat resistant (Li and Gänzle, 2016). Thus, the exposure is MODERATE with VERY LOW uncertainty;

ETEC and EPEC have been frequently detected in children with diarrhea in Brazil (Trabulsi et al., 2002). ETEC strains causing diarrhea in human are transmitted by food or water contaminated with feces of humans, which is its only reservoir (Roussel et al., 2017). Typical EPEC serotypes causing diarrhea in humans have not been found in animals; in contrast, several common atypical EPEC serotypes were found in human and animal species (Trabulsi et al., 2002). An outbreak caused by EPEC was reported in South Korea associated with consumption of tuna (Park et al., 2014). The infectious dose is high, between 108 and 1010 cfu (Yang et al., 2017). EPEC and ETEC cause usually a self-limiting disease

whit watery diarrhea, abdominal pain and vomiting (Meng et al., 2013; WHO, 2015a). Thus, the pathogenicity is VERY LOW and the adverse effects are LOW, with MODERATE and VERY LOW uncertainty, respectively.

Thus, the risk is LOW with MODERATE uncertainty.Escherichia coli [STEC] Escherichia coli is the main bacterium involved in food

contamination in Brazil (Brasil, 2018c). Among the pathogenic groups, Shiga-toxin producing (STEC) is of particular importance to public health. STEC strains may produce two immunologically distinct toxins: Shiga-toxin type 1 and 2. In addition, STEC strains may have a pathogenicity island, LEE (Locus of Enterocyte Effacement), which encodes the proteins that include those responsible for induction of attaching-and-effacing lesions (Croxen and Finlay, 2010). In pigs, Stx2e-producer STEC may be involved in post weaning diarrhea and oedema disease (Casanova et al., 2018). The oedema disease occurs in Brazil, especially in the intensive pig production systems that do not adopt preventative measures after the weaning of piglets (Barcellos and Sobestiansky, 2012). In Brazil, most of the reports of STEC isolation were related to cattle with or without diarrhea (Castro et al., 2019). In pigs, STEC was reported in 2.2% samples of ileum from healthy pigs at slaughter in the state of Mato Grosso (Martins et al., 2013). In other study, STEC was not detected in pig carcasses (Machado et al., 2014). Thus, the release is VERY LOW with MODERATE uncertainty;

E.coli is a natural inhabitant of the large intestine and lower small intestine of all mammals. It is excreted in feces and can survive in fecal particles, dust and water for weeks or months. STEC strains able to cause oedema disease can be present in the large intestine of pigs (Markey et al., 2013), but it is not commonly associated with lesions in pigs at slaughter age (Martins et al., 2013). Growth requirements of STEC are not different from other coliforms. They have been reported to grow at temperatures from -2C to 50C, although in foods the growth is poor or very slow at 5C. They can grow over a pH range of 4.4-9.0. They can be expected to grow in large number of foods under the proper conditions. E.coli does not form spore, and at 60C the D value for STEC was determined in 0.37 to 0.55 in pork sausage (Jay et al., 2005). At 63 ºC a D value of 0.42 minutes were determined (Osaili et al., 2006; Smith et al., 2010). Thus, the exposure is VERY LOW with VERY LOW uncertainty;

Pathogenicity of STEC is complex but in general, infection entails three features: ingestion of a contaminated food or other vehicles; colonization of intestinal epithelial cells by STEC; and production of Shiga toxins (Stx) which disrupts normal cellular functions and causes the cell damage (FAO/WHO, 2018). The infectious doses associated to STEC is low and some studies reported 10 cfu (Meng et al., 2013; Teunis et al., 2004) as the infectious dose. Overall, beef,

vegetables and fruits, and dairy, were estimated to be the most frequently identified sources of foodborne STEC illness. In the region of Americas, 1.18 (CI 95%: 1.11-1.25) of STEC cases have been attributed to pork (FAO/WHO, 2018). The incubation period ranges from three to eight days. The typical presentation of infections with STEC is acute gastroenteritis, often accompanied with mild fever and sometimes vomiting. The typically bloody diarrhea is in most cases mild and self-limiting and most people recover within five to seven days. Around 15% of children diagnosed with STEC O157 infection develop the severe complication of HUS; this proportion is much lower among adults, and this proportion in outbreaks of non-O157 outbreaks is not well documented. The severity of STEC diarrhea is determined by several factors, including the E. coli serotype, the type of Shiga toxin produced and other virulence characteristics of the bacteria. The patient’s age and the infecting dose also play an important role. Children under the age of 5 years are at higher risk of developing clinical disease when infected, and infants are at increased risk of death from dehydration and septicemia (ECDP, 2017). Thus, pathogenicity and adverse effects are HIGH, both with a VERY LOW uncertainty.


Hepatitis E virus (HEV) There are studies evaluating the frequency of Hepatitis E virus (HEV) in swine in Brazil. Vilanova et al.(2018) tested 449 pigs, and 304 showed anti-HEV positive reactions (67.7%, 95% CI = 63.2% - 71.9%). The seroprevalence among farms ranged from 0% to 85.7%. A high prevalence of anti-HEV antibodies in pigs was also detected by Guimarães et al. (2005), in Mato Grosso state, and Vitral et al. (2005), in Rio de Janeiro state. Guimarães et al. (2005) tested 260 animals from 13 different counties and found a prevalence of anti-HEV IgG of 81.2%. Vitral et al. (2005) analyzed 357 swine sera and found a prevalence of 63.6%. Amorim et al. (2018) detected HEV in 51 of 335 bile samples (15.2%) from healthy slaughter pigs in Minas Gerais. Phylogenetic analysis assigned isolates to subtypes 3c and 3i. Thus, the release is HIGH with VERY LOW uncertainty;

Pigs are considered the main reservoir of genotypes 3 and 4 of the hepatitis E virus. These viruses are prevalent at a high level in swine herds globally, meaning that consumers may be exposed to HEV if the virus is present in pigs at slaughter

(Krog et al., 2019) The prevalence of contaminated pork products varied from less than 1% to more than 50% depending on the country and the product. The highest prevalence has been observed in products prepared with raw pork liver (Salines et al., 2017). Geng et al. (2019) detected HEV RNA in liver, kidney, and blood samples with positivity of 6.1% (7/114), 3.1% (4/129), and 1.2% (2/170), respectively. In pork the virus was not detected. The viral

loads ranged 102.4-104.4 genome equivalents per gram. Feurer et al. (2018) evaluated the prevalence of HEV RNA in pork ham muscles and pork livers at slaughterhouses. None of the 1,134 ham muscles tested was positive for the presence of HEV. In liver samples the frequency of positives was 2.8% with a level of contamination up to 1.46 108copies/g. In pork products sold in Brazil from 47 pâté samples tested, 17 (36.17%) were found positive for HEV RNA (Heldt et al., 2016). The thermal stability of HEV has been assessed. A study inoculated pigs with pork liver homogenates containing infectious genotype HEV3 heated to 56 °C for 1 h, fried for 5 min (71 °C internal temperature) or boiled for 5 min and showed that HEV was more likely to resist when heated to up to 56 °C and was inactivated at temperatures higher than 71°C (Feagins et al., 2008). Another study was conducted on more complex foodstuffs prepared according to industrial recipes (liver pâté) and showed that it was necessary to heat the food to an internal temperature of 71°C for 20 min to fully inactivate HEV (Barnaud et al., 2012). Thus, the exposure is LOW with LOW uncertainty.

HEV genotypes 3 and 4 are considered zoonotic and have

been linked to human cases (Amorim et al., 2018). A number of studies have shown that consumers may be exposed to HEV since porcine livers, bought in supermarkets, have been found to contain HEV-specific RNA (Krog et al., 2019). Outbreaks of hepatitis E have been reported. In one outbreak in Italy, a pig liver sausage, which is traditionally eaten raw, was found to be the cause of hepatitis in a significant number of people who consumed it (Colson et al., 2010). HEV causes an acute self-limiting hepatitis. The majority (>70%) of infections is asymptomatic and people only seroconvert (Guillois et al., 2016). Symptomatic cases show an acute self-limiting hepatitis initially with fatigue, asthenia, nausea and

fever. Clearance of infection is usually observed within 1–5 weeks, and the incubation period is estimated to be between 2 and 6 weeks (Lhomme et al., 2016). Most humans with an acute infection recover completely within a couple of weeks. However, HEV infection in patients with pre-existing chronic liver disease can also lead to a fatal outcome due to liver failure (Acha and Szyfres, 2003b). Thus, the pathogenicity is MODERATE with HIGH uncertainty and the adverse effects are MODERATE with MODERATE uncertainty;

Thus, the risk is LOW with HIGH uncertainty.

Listeria monocytogenes Data about L. monocytogenes occurrence in pig herds in Brazil are scarce. In a study conducted in four farms, Listeria spp. was found in 14.6% fecal samples, but none was identified as L. monocytogenes (Paixão et al., 2005). In another study, Listeria spp. was isolated from 66.7% of pen feces samples at slaughterhouses, but only one from a total of 12 isolates was confirmed as L. monocytogenes (Pissetti et al., 2012). Listeria monocytogenes has been investigated in

pig carcasses, slaughterhouse environment and pork in Brazil. While L. monocytogenes was not found in raw pork, it was isolated from the slaughter environment and manufactured sausages (von Laer et al., 2009). In other studies the pathogen was detected in up to 19.8% of carcasses sampled (Ferronatto et al., 2012; Martins, 2013; Pissetti et al., 2012; Santos et al., 2006). Thus, the release is MODERATE with MODERATE uncertainty;

Listeria species are widely distributed in the environment. They can be isolated from sewage, water, animal feed, poultry, various meats, slaughterhouse waste, raw milk and cheese. Asymptomatic fecal carriers of L. monocytogenes occur in man and animals (Markey et al., 2013). Pigs rarely have lesions or clinical disease caused by L. monocytogenes, but may be an asymptomatic carrier of this pathogen (Funk and Wagstrom, 2019). In swine, isolation of L. monocytogenes is more frequently reported from tonsils and tongue than from feces. Autio et al. (2000) reported its detection in 14% of tongues and 12% of tonsil samples from pigs sampled at slaughter. In the intestinal content, 9% of the samples were positive. At slaughter, up to 32% of porcine tonsils were found colonized by L. monocytogenes (Frederiksson-Ahomaa et al., 2009). The genus Listeria has the ability to grow over a very wide range of temperature (-1.5 to 45°C), but the optimum growth occurs between 30-37 C (Le Marc et al., 2002; Giffel and Zwietering, 1999). L. monocytogenes can survive a low pH of 5.5 through a phenomenon known as the acid tolerance response (Tabit, 2018). The optimal water activity for their development occurs in the range of 0.92 to 0.99 (Tabit, 2018). Listeria spp. is non spore forming, and the D values of L. monocytogenes at 55C varies from 38.94 to 81.37 min; while at 70C D values range from 0.04 to 0.31 min (Murphy et al., 2004, 2002; Osaili et al., 2006). The exposure is MODERATE with VERY LOW uncertainty;

Listeriosis is important foodborne diseases caused by L. monocytogenes. High risk foods include deli meat and ready-to-eat meat products (such as cooked, cured and/or fermented meats and sausages), soft cheeses and cold smoked fishery products (WHO, 2018). Foods stored at low temperatures for an extended time and consumed without further treatment, such as cooking, are the most associated with foodborne outbreaks. Pork has also been implicated in foodborne outbreaks (Thévenot et al., 2006). In Spain, an outbreak caused by L. monocytogenes was associated with the consumption of chilled roasted pork meat product, and involved 222 confirmed cases causing three deaths (WHO, 2019b). The infection is highly dependent on the immune status of the exposed. Invasive listeriosis is characterized by septicemia and meningitis. In pregnant women L. monocytogenes is cause of premature labor, stillbirth, abortion and neonatal infection. In individuals not included in

the risk group, the infection is usually not invasive and prominent symptoms will include fever, diarrhea, myalgia and headache (Cruz et al., 2008). In this group, a very low rate of hospitalization occurs and the illness tends to last between 1 and 3 days. In healthy individuals a moderate to high dose is needed to start a foodborne disease. For the general population the ingested dose was estimated to be 1.5x109 in a low-exposure scenario (Pouillot et al., 2015). In the elderly, neonate and pregnant women the infective dose may be lower (EC, 1999). In an outbreak involving immunocompromised patients in Finland the median estimated dose was 8.2x103 L. monocytogenes (FAO/WHO, 2004) Thus, the pathogenicity is LOW and the adverse effects is HIGH, both with VERY LOW uncertainty;

Thus, the risk is LOW with MODERATE uncertainty.

Mycobacterium tuberculosis/Mycobacterium bovis

Tuberculosis caused by M. tuberculosis or M. bovis is worldwide rare in intensive swine production. Almost no data is available about the prevalence of M. tuberculosis/bovis in commercial pig herds in Brazil. But related to identification in lymph nodes there is strong evidence that the prevalence is low. According to Coldebella et al. (2017) 0.000046% of all pig carcasses inspected from 2012 to 2014 by the Brazilian Federal Inspection System (SIF) presented tuberculosis lesions. This finding was restricted to 12 slaughterhouses. In a study conducted in southern Brazil, in a non-commercial wild boars population, 80 samples were evaluated for the presence of M. tuberculosis complex, of which 27.9% and 31.3% showed histopathological changes and M. bovis genome presence, respectively. Moreover, 23.8% of the animals had at least one organ with isolates classified as M. tuberculosis complex, demonstrating that this specie may be a reservoir of this pathogen (Maciel et al., 2018). On the other hand, granulomatous lymphadenitis caused by M. avium complex detected at slaughter are reported in pigs, and it is an important cause of carcass condemnation since the macroscopic lesions may be similar (Barcellos and Sobestiansky, 2012; Oliveira et al., 2006). Thus, the release is VERY LOW with VERY LOW uncertainty;

Mycobacteria are Gram-positive, non xspore forming, acid fast bacilli. They are highly resistant to most environmental factors, many disinfectants and a large and increasing number of antibiotics. Mycobacterium avium has survived for more than four years in poultry lot soil, in cages, and in sawdust used as litter. The three Mycobacterium species that cause tuberculosis in swine are M. avium, M. bovis and M. tuberculosis. These three species infect poultry, cattle and human, respectively. However, each of these three occasionally infects other animal species. Mycobacterium avium usually is the organism that infects swine. In swine, mycobacteria appear to infect the tonsils and intestinal

mucosa initially and then spread to the regional lymph nodes, especially those of the cervical area, and to mesenteric nodes. Lesions in the nodes tend to develop slowly and, in most cases, the bacilli are successfully walled off. Only occasionally does the infection generalize, usually in older breeding stock infected with M. bovis. In swine with localized infections, there usually are no signs. Condemnation of carcasses at slaughter is the usual presentation. In older breeding stock infected by M. bovis and M. tuberculosis, generalization does occur occasionally. Affected animals tend to waste away despite adequate feed. They eventually become emaciated and may die from tuberculosis (Morés et al., 2007). Mycobacterium tuberculosis and M. bovis have optimal growth at 37C, and growth is very slow (up to 60 days in solid media). Mycobacteria possess the same degree of susceptibility to heat as other non spore forming bacteria, and the cooking is enough to eliminate the contamination (Doig et al., 2002; Smith, 1899; Sung and Collins, 1998). Thus, the exposure was VERY LOW with MODERATE uncertainty.

In humans, tuberculosis is a disease caused by species of the Mycobacterium tuberculosis complex, predominantly M. tuberculosis, but an unknown proportion of zoonotic tuberculosis cases are due to M. bovis. This zoonotic pathogen can be transmitted from vertebrates, especially cattle, to humans directly by aerogenous routes or indirectly by the consumption of raw milk or its derivatives .Untreated meat products are less frequently a transmission source of zoonotic tuberculosis (WHO, 2019c). M. bovis seems to be less virulent than M. tuberculosis to human beings (Pasquali, 2004) Whatever the route, the infectious dose for humans is unknown, but estimated to be in the region of tens to hundreds of organisms by the respiratory route and millions by the gastrointestinal route (O’Reilly and Daborn, 1995). The incidence rates of this zoonotic disease are generally low on a worldwide level, but available data are a cause for increasing concern about the consequences of this disease in some population groups and settings, and HIV-positive individuals are more susceptible to M. bovis infections (Thoen et al., 2009). In Brazil, the proportion of zoonotic tuberculosis was 3.5% of 200 cases analyzed in 1974 (Corrêa and Corrêa, 1974), although more recent studies have shown that it may be lower (Rocha et al., 2011). Occupation and consumption of raw milk and derivative products that place individuals in direct and indirect contact with animals and their excretions/secretions increase the risk for zoonotic tuberculosis in Brazil (Silva et al., 2018). The human form of M. bovis infection has similar clinical forms as that caused by M. tuberculosis. The access to the tissues is followed by an initial macrophage response that is not, however, sufficient to prevent proliferation of the microorganism. Most commonly, clinical manifestation of M. bovis infection in human is

associated with the extra-pulmonary form of the disease, but about half the cases of post-primary (reactivation) disease involve the lung (Anaelom et al., 2010). In 2016 there were 147,000 new cases of zoonotic tuberculosis worldwide (mostly in Africa), and 12,500 deaths (WHO, 2019c). Thus, the pathogenicity is assumed to be MODERATE and the adverse effects is MODERATE both with VERY HIGH uncertainty;

Thus, the risk is VERY LOW and the uncertainty VERY HIGH.

Salmonella [non typhoidal] Salmonella is a widespread in commercial swine herds in Brazil with within herd seroprevalences approaching 100% in some herds (Corbellini et al., 2016; Costa, 2014; Kich et al., 2011; Viott et al., 2013). In most cases, the infection occurs without clinical signs, and pigs are asymptomatic carriers at slaughter. Many studies demonstrated frequencies around 30% of pigs carrying Salmonella in the intestinal content at slaughter (Kich et al., 2011; Paim et al., 2019; Silva et al., 2012). The reported frequency in carcasses range from 8.7 to 27.6% (Corbellini et al., 2016; Kich et al., 2011; Silva et al., 2011; Pissetti et al., 2012). An exploratory study conducted in slaughterhouses under federal inspection estimated a prevalence of 10% (CI 95% 7.5-13.22) of positive pre chill carcasses (Brasil, 2018c). Salmonella Typhimurium has been reported as cause of diarrhea in pigs (Viott et al., 2013); septicemia caused by S. Choleraesuis also occurs (Meneguzzi et al., 2017). Thus, the release is VERY HIGH with a VERY LOW uncertainty;

The reservoir of salmonellae is the intestinal tract of warm-blooded and cold-blooded animals, the majority of which are subclinical shedders. These bacteria can survive for many months in the environment (Markey et al., 2013). Most serovars of non-typhoidal Salmonella do not cause any clinical signs or lesion in pigs, which are asymptomatic carriers, shedding the bacteria in the feces (Fàbrega and Vila, 2013; Knetter et al., 2015). Most of the Salmonella serovars grow at a temperature range of 5–47°C with the optimum at 35–37°C. The pH for optimum growth is around the neutrality, with values above 9.0 and below 4.0 being bactericidal. They require high water activity (Aw) between 0.99 and 0.94. It is non spore forming, and is sensitive to heat and usually killed at temperatures ≥70°C (Graziani et al., 2017). D values for destruction of the most heat resistant serovar, S. Senftenberg, at 72C in milk is 0.09 min; at the same temperature S. Typhimurium has a D value of 0.003 min (Adams and Moss, 2008). Thus, the exposure is HIGH with a VERY LOW uncertainty.

Salmonella is one of the most important foodborne pathogens worldwide. In Brazil, it is reported as the second most isolated pathogen from foods involved in food poisoning outbreaks (Brasil, 2018b). The bacteria are generally transmitted to humans through consumption of contaminated

food of animal origin, mainly meat, poultry, eggs and milk (Chlebicz and Śliżewska, 2018).The symptoms of Salmonella infection usually appear 12–72 hours after infection, and include fever, abdominal pain, diarrhea, nausea and sometimes vomiting. The illness usually lasts 4–7 days, and most people recover without treatment. However, in some cases, particularly in children and elderly patients, the associated dehydration can become severe and life-threatening (Acha and Szyfres, 2003a). The infective dose ranges between 106 and 108 cells, but in some people, even the dose of 10 cells may lead to the development of salmonellosis (Chlebicz and Śliżewska, 2018). Thus, the pathogenicity and adverse effects are MODERATE both with VERY LOW uncertainty.

Thus, the risk is HIGH with VERY LOW uncertaintySarcocystis suishominis No data is available about the prevalence of S. suishominis in

commercial pig herds in Brazil. But concerning to cysts in carcasses, there is strong evidence that the prevalence is low. According to the official data of the Brazilian Federal Inspection System, only 0.00193% of the 94,000,00 pig carcasses inspected from 2012 to 2014 presented sarcoporidiosis lesions (Coldebella et al., 2017), only related to culling sows (Mores et al., 2019). Thus, the release is VERY LOW with VERY LOW uncertainty;

The animal host acquires infection by ingesting feed and water contaminated with Sarcocystis sporocysts. After sporocysts are ingested, sporozoites are liberated, and initiate a complex asexual cycle. The sporozoite migrates from the intestine to extra-intestinal tissues and form cysts. A sarcocyst may take a month or more to mature and become infectious for the carnivore host. Human can serve as the definite host and excretes sporocysts in feces eight or more days after ingesting raw pork (Dubey, 2015). S. suishominis is located in the muscles of infected pigs (Avapal et al., 2004; Lindsay et al., 2012) but rarely causes severe disease in pigs (Acha and Szyfres, 2003c). It does not multiply in muscle. Although almost no evidences about the thermal resistance of S. suishominis exists, models with Sarcocystis meischeriana suggests that cocking meat at 60ºC for 20 min makes the parasite noninfectious for dogs (Fayer et al., 2015). Thus, the exposure is VERY LOW with a MODERATE uncertainty;

There is few information about the infective dose of S. suishominis to humans. As definitive hosts, humans can experience nausea, vomiting, acute and severe enteritis, but many infections appear to be mild or asymptomatic (Fayer et al., 2015). In the case of ingestion of sporocystes, human is an accidental intermediary host. In such case the consequences may be larger than the intestinal form, but most of the humans are diagnosed accidentally during the autopsies (Chhabra and Samantaray, 2013; Fayer, 2004). Thus, the pathogenicity is VERY HIGH and the adverse effects is VERY LOW, both with MODERATE uncertainty;


Staphylococcus aureus Staphylococcus aureus colonize the mucous membranes of mammals, including pigs, and can also cause many infections. Isolation of S. aureus from pig and pork is reported in Brazil. Takeuti et al. (2018) investigated the nasal carrier state in finishing pigs, and found 18% of S. aureus positive animals distributed in four different farms. Moreira et al. (2018) collected 280 samples at slaughter and obtained 20% of the samples positive for S. aureus; lymph nodes and pre chill carcasses were the samples presenting the highest positive frequency. Lima et al. (2004) reported the presence of S. aureus in pig carcasses in counts varying from 1.2 to 1.5 log UFC.cm-2. Thus, release is HIGH and the uncertainty is VERY LOW;

S. aureus is widespread in nature and occurs worldwide in mammals and birds; moreover, this specie can be transient in the intestinal tract and survive for long periods in the environment (Markey et al., 2013). In pigs, S. aureus can cause mastitis, botryomycosis, endometritis and udder impetigo (Markey et al., 2013; Masson, 2011). Although these bacteria may be found in feces, the main location on carcasses is the skin (De Lima et al., 2004). The presence of small numbers of S. aureus in foods is not uncommon. It will occur naturally in poultry and other raw meats as a frequent component of the skin microbiota. As a poor competitor, it normally poses no problem in these situations since it is eliminated by cooking or pasteurization (Adams and Moss, 2008). The optimum growth temperature of S. aureus is 35 – 37 ºC (Baeza et al., 2009), but it can multiply between 7C and 48C (Adams and Moss, 2008). Similarly, the optimum pH ranges from 6.0 to 7.0, but growth occurs from pH 4.0 to 9.8. A characteristic of S. aureus which is particularly important in some foods is its tolerance of salt and reduced aw. It grows readily in media containing 5–7% NaCl and some strains are capable of growth in up to 20% NaCl. It will grow down to an aw of 0.83, where it has a generation time of 300 min (Adams and Moss, 2008). Environmental factors influence the enterotoxin production, and they may vary according to the enterotoxin type (Jay et al., 2005). The pH range over which enterotoxin production occurs is narrower than S. aureus growth pH, with little toxin production below pH 6.0. Similarly, the range over which enterotoxin production occurs is more limited with a minimum aw recorded of 0.86 (Adams and Moss, 2008). The organism has low heat resistance with a D62 of 20–65 seconds and a D72 of 4.1 seconds when measured in milk (Adams and Moss, 2008). However, the staphylococcal enterotoxin (SEB) is quite heat resistant and varies with the type. For instance, the biological activity of SEB may be retained after heating for 16 h at 60C (Jay et al., 2005). Thus, the exposure is HIGH with VERY LOW uncertainty;

Staphylococcus aureus foodborne disease is an intoxication caused by ingestion of food that contains enteroxins, which are produced by specific strains. The great majority of food poisoning cases are associated with the contamination of food during preparation with S. aureus strains colonizing carrier food handlers. Afterwards, temperature abuse during storage may allow the Staphylococcus multiplication and toxin production (Baer et al., 2013; Kadariya et al., 2014). Enterotoxins are neurotoxins, which are able to produce symptoms in doses lower than 1 g. This level of toxin production is usually reached when S. aureus population is higher than 106 CFU/g of food (Grace and Fetsch, 2018) . Once produced, the toxin is heat resistant and hardly destroyed during food preparation. Food poisoning by S. aureus is characterized by a short incubation period, typically 2–4 h. Nausea, vomiting, stomach cramps, retching and prostration are the predominant symptoms, although diarrhea is also reported. Recovery is normally complete within 1–2 days. In severe cases dehydration, marked pallor and collapse may require treatment by intravenous infusion. Rarely patients have sequelae (Grace and Fetsch, 2018; Peresi et al., 2004). Thus, the pathogenicity is LOW and the adverse effects is VERY LOW both with VERY LOW uncertainty;

Thus, the risk is VERY LOW with VERY LOW uncertainty.

ThermophilicCampylobacter

There are some studies reporting the isolation of thermophilic Campylobacter from swine in Brazil. Modolo et al. (1999) reported their isolation from pigs with (43%) and without (34%) diarrhea. C. coli was the most prevalent specie. In a case-control study, C. coli was isolated in 38.59% of pigs from 15 farms; no difference between groups with or without diarrhea was found (Ruiz et al., 2016). From 37 carcasses sampled, Campylobacter spp. was isolated from five after dehairing and one after chilling (Biasi et al., 2011). There is one report comparing the prevalence of both Campylobacter species in pigs in Brazil, and C. coli was present in 42% of samples and C. jejuni in 16% (Modolo et al., 1999). Thus, release is HIGH for C. coli and it is LOW for C. jejuni, both with MODERATE uncertainty;

The principal reservoir of thermophilic Campylobacter is the alimentary tract of wild and domestic mammalians and birds. C. jejuni and to a lesser extent C. coli are the species most often encountered in medical laboratories as causes of acute enterocolitis in man. They are distinguished from most other species by their high optimum growth temperature (42°C) and are, thus, referred as thermophilic Campylobacter (Møller Nielsen et al., 1997). C. jejuni is predominantly associated with poultry (Tauxe, 1997), but has also been isolated from cattle, sheep, goats, dogs, cats and pigs (Møller Nielsen et al., 1997). In a study conducted in Canada, C. coli was the dominant Campylobacter species, and because it is isolated from over 99% of pigs it was regarded as a normal

inhabitant of a pig’s gastrointestinal system (Varela et al., 2007). In swine, Campylobacter primarily affects piglets. The key clinical signs include mild diarrhea, sometimes with blood or mucus, dehydration and loss of condition. Thermophilic Campylobacter presents optimum growth at 42-43C, and is not able to growth below 30C (Stanley and Jones, 2003). C. jejuni and C. coli are considered to be microaerophilic, thus they are unable to grow in the presence of air and grow optimally in atmospheres containing 5% oxygen. In addition, campylobacters have a restricted temperature growth range and whilst they grow optimally at 42 °C, the organisms do not grow at temperatures below 30 °C. These two growth characteristics place severe restrictions on the ability of campylobacters to multiply outside of an animal host and, consequently, unlike most other bacterial foodborne pathogens, these bacteria are not normally capable of multiplication in food during either processing or storage (Park, 2002). Campylobacter is particularly sensitive to drying and reduced pH, and it is inhibited at pH values below 5.1. In addition, Campylobacter is sensitive to salt concentrations above 1.5% (ICMSF, 1996). C. jejuni and C. coli are rather sensitive to heat and do not survive cooking or pasteurization temperatures (D-values are 0.21-2.25 minutes at 55-60°C) (ICMSF, 1996). Thus, the exposure is MODERATE for C. coli and it is LOW for C. jejuni both with VERY LOW uncertainty.

Campylobacter spp. is one of the most frequently occurring bacterial agents of gastroenteritis in humans. The true incidence of gastroenteritis due to Campylobacter spp. is poorly known, particularly in low- and middle-income countries; studies in high-income countries have estimated the annual incidence at between 4.4 and 9.3 per 1,000 population (WHO, 2012). The majority of foodborne‐related campylobacteriosis is caused by C. jejuni, which is most commonly associated with poultry; however; low levels have been attributed to pork (Schuppers et al., 2005). Enteropathogenic Campylobacter can cause an acute enterocolitis, which is not easily distinguished from illness caused by other enteric pathogens. The incubation period may vary from one to 11 days, typically 1-3 days. The main symptoms are malaise, fever, severe abdominal pain and diarrhea. Vomiting is not common. The diarrhea may produce stools that can vary from profuse and watery to bloody and dysenteric. In most cases the diarrhea is self-limiting and may persist for up to a week, although mild relapses often occur. In 20% of the cases symptoms may last from one to three weeks. The late complications associated with Campylobacter infections are reactive arthritis and the Guillain-Barré syndrome. These complications show different pictures of symptoms or disorders. The infective dose of C. jejuni has been investigated in a few experiments involving volunteers. In one experiment a dose of 500

organisms ingested with milk caused illness in one volunteer (Robinson, 1981). In another experiment involving 111 healthy young adults, doses ranging from 800 to 20,000,000 organisms caused diarrheal illness (Black et al., 1988). Thus, the pathogenicity to humans is HIGH for C. jejuni and it was assumed to be LOW for C. coli with LOW and VERY HIGH uncertainty, respectively. The adverse effects is MODERATE for both hazards with MODERATE uncertainty.

Thus, the risk is LOW for both hazards, with MODERATE uncertainty, for C. jejuni and VERY HIGH uncertainty for C. coli.

Toxoplasma gondii There are several studies reporting the frequency of seropositive pigs in Brazil. The reported within-herd seroprevalence in commercial swine herds range from 3% to 90.4% and more than 50% of the tested farms presented at least one positive animal (Garcia et al., 1999; Gumarães et al., 1992; Marques-Santos et al., 2017; Suarez-Aranda et al., 2000). Viable cysts were found in brain, heart and tongue of pigs (Dos Santos et al., 2005; Farzão-Teixeira et al., 2006). Dias et al. (2005) isolated T. gondii from 13 of 149 pork sausages sampled on market. The sausages were made with an unknown contact time with salt, and samples were digested in pepsin and bio assayed in mice. Viable T. gondii was isolated from one sample; for the 12 other samples mice inoculated with sausage digests developed T. gondii antibodies, but viable parasites were not found. Thus, the release is HIGH with LOW uncertainty.

Toxoplasma gondii is an intestinal coccidia that parasitizes members of the cat family as definitive hosts and has a wide range of intermediate hosts. Infection is common in many warm-blooded animals, including humans. In most cases infection is asymptomatic (Acha and Szyfres, 2003c). Pigs are infected mostly by consumption of feed or water contaminated with oocists. In pregnant sows, T. gondii can cross the placenta and infect the fetus, which can result in abortion and stillbirth (Barcellos and Sobestiansky, 2012). Severe clinical toxoplasmosis in pigs is considered rare, but reports of clinical toxoplasmosis in neonatal and weaned pigs, and associated with abortion are available (Dubey, 2009). Clinical signs in piglets are fever, anorexia, dyspnea, cough and nervous signs (Barcellos and Sobestiansky, 2012). Viable T. gondii was identified in 7 pork pools from a total of 2,094 pork samples collected at retail level in the USA, demonstrating a low level of contaminated pork (Dubey et al., 2005). T. gondii cannot multiply outside the host. Tissue cysts remained viable at 52 C for 9.5 min; they are generally rendered nonviable by heating to 61 C or higher temperature for 3.6 min (Dubey et al., 1990). Salting, curing, and pickling procedures used to make sausages and other preparations do often kill tissue cysts, but these procedures have not been standardized universally (Dubey et al., 2012). Thus, the

exposure is LOW with HIGH uncertainty. Toxoplasma gondii infection is usually non-pathogenic in

immunocompetent adults. The major pathogenic factor is proliferation of tachyzoites, destroying host cells faster than they can regenerate. In acute infection, mild symptoms can arise, including fever, rash, headache, lymphadenopathy, organomegaly (liver and/or spleen), weight loss, weakness, pneumonia, and myalgia. More severe symptoms are rare and mostly affect immunocompromised patients, although they can also develop in immunocompetent individuals. These include retinochoroiditis, and severe encephalitis. Congenital infection can result in abortion or stillbirth, and live births may demonstrate the congenital toxoplasmosis syndrome - mental retardation, malformation, retinochoroiditis, strabismus, nystagmus, microphthalmia, and cataracts. Severity of transplacental infection is inversely proportional to gestational age, but the rate of vertical transmission is more frequent as the pregnancy progresses. Ocular toxoplasmosis is responsible for 30% – 60% of retinochoroiditis cases. The most common sequelae related to T. gondii is the ocular form in which there is an inflammation of retina and blindness (Almeida et al., 2006; Derouin, 1992; Jones and Dubey, 2012; Saadatnia and Golkar, 2012). Humans can become infected from food or water contaminated with oocysts. Eating of unwashed raw vegetables or fruits or ingestion of water contaminated with oocysts, have been identified as important risk factors. Moreover, toxoplasmosis can be acquired via consumption of undercooked contaminated meat (Dubey and Jones, 2008). Among the food animals, infected pigs are the most likely meat source of T. gondii infection for people in many countries, including Brazil (Dubey and Jones, 2008; Silva et al., 2010). In a reported outbreak, a whole family had clinical toxoplasmosis epidemiologically linked to consumption of raw pork sausage at a party in Santa Vitória do Palmar, RS (Almeida et al., 2006). In a serological survey conducted in military recruits (18-21 years old) in Brazil, 56% were seropositive, and 27% presented antibodies titers 1:256 in the dye-test (Niederman et al., 1967). Up to 32% of 0–5-year-old, 19·5–59% of 6–10-year-old, and 28·4–84·5% of 11–15-year-old children in Brazil were seropositive. Limited data indicate that in certain areas approximately 50% of pre-teenage children have been exposed to the parasite (Jones and Dubey, 2012). Very high (36–92%) seroprevalences were found in pregnant women. These data indicate that seroprevalence of T. gondii in children and in pregnant women in Brazil is one of the highest worldwide (Dubey et al., 2012). A population-based study on ocular toxoplasmosis prevalence was reported by Portela et al. (2004). A door-to-door survey was conducted in rural area of Governador Valadares, MG. A total of 414 persons were enrolled in the study. Half (49%) of them had T. gondii antibodies with a very high (47% of 49)

seroprevalence in children less than 9 years old. A total of 29 of 414 (7%) persons had ocular lesions. Overall, 28 (12·9%) of 216 seropositives had ocular lesions, while only 1 (0·5%) of 198 seronegatives had ocular lesions. Currently, most of the eye disease is thought to be post-natal acquired (Jones and Dubey, 2012). A follow-up study performed a decade later evaluated risk factors associated with ocular toxoplasmosis in the same locality (Jones et al., 2006). Important risk factors associated with toxoplasmosis were: eating rare meat, eating home-made cured, dried or smoked meat, having a garden, having soil-related activity, being male, and past and present pregnancy. Thus, the pathogenicity is LOW with a HIGH uncertainty; the adverse effect is HIGH with a LOW uncertainty.

Thus, the risk is LOW with HIGH uncertaintyYersinia enterocolitica Data regarding the presence of Yersinia enterocolitica in

Brazilian pig farms is limited. Two pig farms were investigated for the presence of Y. enterocolitica on the barn floor. From twenty samples, none was positive. In the same study, Y. enterocolitica was detected in palatine tonsils, mesenteric lymph nodes and carcasses (1%) of pigs (Martins et al., 2018). Similarly, Y. enterocolitica was isolated from 8% of samples of tongue, tonsils and lymph nodes of slaughtered pigs (Saba et al., 2013). In other study, Y. enterocolitica was isolated from the pig farm environment and in several steps of the slaughter line (Moreira et al., 2019). Among 400 pigs originated from 15 farms sampled at slaughter, 25.5% were positive for Y. enterocolitica (Wildemann et al., 2018). Fattening pigs proved to be an important reservoir of Y. enterocolitica biotype 4/O:3 carrying virulence genes in Brazil (Paixão et al., 2013). Thus, the release is MODERATE and the uncertainty as MODERATE;

The habitat of Y. enterocolitica is the intestinal tract of wild and domestic animals and the environment (Markey et al., 2013). Y. enterocolitica is a highly heterogeneous species, consisting of six biotypes of different virulence. Pigs are the most important reservoir for human pathogenic strains. Y. enterocolitica is often found colonizing the lymphoid tissues and intestine of asymptomatic pigs (Drummond et al., 2012). Since the oral cavity is frequently contaminated, handling the head during slaughter (removal of the tongue, splitting of the carcass and post mortem inspection) may lead to the spreading of the contamination present in this part of the carcass. Muscles situated near the tonsils can be frequently contaminated (De Zutter and Van Hoof, 1987). As a consequence, edible offal such as tongues, hearts and livers are more frequently and to a greater extent contaminated than pig carcasses (EFSA, 2007). Y. enterocolitica can growth over the temperature range -2 to 45 C, with an optimum between 22 and 29 C. Y. enterocolitica is not able to grow at pH <4.2 or >9.0 or at salt concentrations greater than 7%

(aw <0.945) (Barton, 2011). Species of genus Yersinia are non spore forming, and can be destroyed in 1-3 min at 60C (Jay et al., 2005). Thus, the exposure is MODERATE with a VERY LOW uncertainty;

Infection with Y. enterocolitica has been linked most clearly to the handling and consumption of raw and undercooked pork. The same serotypes (principally O:3, O:9, and O:5,27) and genotypes isolated from pigs have been reported in affected humans (Barton, 2011). Yersinia enterocolitica is an enteric pathogen, which in susceptible people can cause extra-intestinal disease. Enterocolitis is the most common manifestation and is seen principally in young children. Older children and adolescents may develop mesenteric lymphadenitis. Some cases are subclinical and in the clinical cases onset of clinical signs usually occurs within 24–48 h of ingestion of the organism. The illness usually lasts 1–3 days, with diarrhea seen in most cases plus fever; headache and vomiting occur in many cases. Involvement of mesenteric lymph nodes leads to severe abdominal pain. The minimum infective dose for humans is not known; however it is believed that a minimum concentration of 108 CFU/g of food is needed to start an infection (Brachman, 2001). The clinical illness caused by this pathogen ranges from self-limited enterocolitis, in healthy individuals, to potentially fatal systemic infection (Bottone, 1997; Cover and Aber, 1989). Thus, the pathogenicity is MODERATE and the adverse effects is LOW, both with HIGH uncertainty.

Thus, the risk is LOW with HIGH uncertaintyYersinia pseudotuberculosis

There is almost no information available about the prevalence of Y. pseudotuberculosis in Brazilian pig herds (Falcão et al., 2008). This specie has been responsible for more than 100 reported episodes of hemorrhagic gastroenteritis in Bos taurus indicus and Bubalus bubalis and only one suspected case in Sus scrofa domesticus. The isolation of this pathogen from humans has never been reported in Brazil (Falcão et al., 2008; Warth et al., 2012). Thus, the release is assumed as VERY LOW, and the uncertainty as VERY HIGH;

Y. pseudotuberculosis is widely spread in the environment, where it can survive for a long time. Soil and water may be contaminated by feces of infected animals, mainly rodents and birds (Fredriksson-Ahomaa, 2007). This specie is pathogenic for many animal species and occasionally humans, causing mesenteric adenitis, chronic diarrhea and severe septicemia. Usually Y. pseudotuberculosis does not cause disease in pigs, in rare cases it may cause small abscesses in the intestine of weaned pigs (Markey et al., 2013). In Luria-Bertani broth strains of Y. pseudotubercusosis were able to growth between 0 and 43.7C, in pH between 4.5 and 9.3, and most strains were able to growth in the presence of 5% NaCl (Keto-Timonen et al., 2018). In milk, its population increased significantly at 4C and 24C after one and two weeks of storage (Yehualaeshet et al., 2013). Species

of genus Yersinia are no spore forming, and can be destroyed in 1-3 min at 60C. Thus, the exposure is VERY LOW with VERY HIGH uncertainty;

Human Y. pseudotuberculosis infections can be acquired from contaminated food or water; however, the foodborne transmission has been less well documented (EFSA, 2018; Nuorti et al., 2004). In reported outbreaks, vegetable juice, untreated surface water, homogenized milk, ice lettuce and fresh carrots have been suggested as the vehicle (Nuorti et al., 2004; Williamson et al., 2017). Clinically, infections typically present as abscess-forming mesenteric lymphadenitis and diarrhea but can also lead to secondary complications, such as perforation, subacute obstruction syndrome, intussusceptions, and acute renal failure in rare cases. Infection is usually self-limiting, but rare cases of sepsis can lead to a very high mortality (Galindo et al., 2011). Thus, the pathogenicity is assumed to be VERY LOW and the adverse effects is MODERATE, with VERY HIGH and HIGH uncertainty, respectively;

Thus, the risk is LOW with VERY HIGH uncertainty

References

Abilleira, F., Musskopf, G., Fauth, E., Silva, V.B., Scartezzini, M., Vogt, F.I., Oliveira, S.J., 2010. Análise bacterioógica de casos de aderência pulmonar em suínos de diferentes lotes abatidos em um frigorifico no Rio Grande do Sul. Rev. Bras. Hig. e Sanidade Anim. 4, 16–22. https://doi.org/10.5935/1981-2965.20100002

Acha, P.N., Szyfres, B., 2003a. Zoonoses and communicable diseases common to man and animals: Volume I. Bacterioses and mycoses, PAHO Scientific and Technical Publication No. 580. https://doi.org/10.1590/S1135-57272005000300012

Acha, P.N., Szyfres, B., 2003b. Zoonoses and communicable diseases common to man and animals: Volume II: Chlamydioses, rickettsioses, and viroses, PAHO Scientific and Technical Publication No. 580. https://doi.org/10.1016/0167-5877(89)90014-7

Acha, P.N., Szyfres, B., 2003c. Zoonoses and communicable diseases common to man and animals: Volume III. Parasitoses, PAHO Scientific and Technical Publication No. 580. https://doi.org/10.1590/S1135-57272005000300012

Almeida, F.S., Rigobelo, E.C., Marin, J.M., Maluta, R.P., Ávila, F.A., 2007. Diarréia suína: estudo da etiologia, virulência e resistência a antimicrobianos de agentes isolados em leitões na região de Ribeirão Preto-SP, Brasil. ARS Vet. 23, 151–157.

Amorim, A.R., Mendes, G.S., Pena, G.P.A., Santos, N., 2018. Hepatitis E virus infection of slaughtered healthy pigs in Brazil. Zoonoses Public Health 65, 501–504. https://doi.org/10.1111/zph.12455

Anaelom, N.J., Ikechukwu, O.J., Sunday, E.W., Nnaemeka, U.C., 2010. Zoonotic tuberculosis: A review of epidemiology, clinical presentation, prevention and control. J. Public Heal. Epidemiol. 2, 118–124.

Arguello, E., Otto, C.C., Mead, P., Babady, N.E., 2015. Bacteremia caused by arcobacter butzleri in an immunocompromised host. J. Clin. Microbiol. https://doi.org/10.1128/JCM.03450-14

Autio, T., Sateri, T., Fredriksson-ahomaa, M., Rahkio, M., Lunden, J., Korkeala, H., 2000. Listeria monocytogenes Contamination Pattern in Pig Slaughterhouses. J. Food Prot. 63, 1438–1442. https://doi.org/10.4315/0362-028X-63.10.1438

Avapal, R.S., Sharma, J.K., Juyal, P.D., 2004. Pathological changes in Sarcocystis infection in domestic pigs (Sus scrofa). Vet. J. 168, 358–361. https://doi.org/10.1016/j.tvjl.2003.11.006

Barnaud, E., Rogee, S., Garry, P., Rose, N., Pavio, N., 2012. Thermal inactivation of infectious hepatitis E virus in experimentally contaminated food. Appl. Environ. Microbiol. 78, 5153–5159. https://doi.org/10.1128/AEM.00436-12

Barcellos, D.E.S.N., de Uzeda, M., Mathiesen, M.R., Duhamel, G.E., Kader, I.I.T.A., 2000. Prevalence of Brachyspira species isolated from diarrhoeic pigs in Brazil. Vet. Rec. 146, 398–403. https://doi.org/10.1136/vr.146.14.398

Baeza, R., Rossler, C., Mielnicki, D., Zamora, C., Chirife, J., 2009. Theoretical

modelling of Staphylococcus aureus growth in a cooked meat product kept at ambient temperature using temperature profiles of selected Mexican cities. Ciênc. Tecnol. Aliment 29, 81–84.

Baer, A.A., Miller, M.J., Dilger, A.C., 2013. Pathogens of Interest to the Pork Industry: A Review of Research on Interventions to Assure Food Safety. Compr. Rev. Food Sci. Food Saf. 12, 183–217. https://doi.org/10.1111/1541-4337.12001

Barcellos, D.E.S.N., Sobestiansky, J., 2012. Doença dos Suínos, 2nd ed. Cânone Editorial, Goiânia.

Bhunia, A.K., 2018. Opportunistic and Emerging Foodborne Pathogens: Aeromonas hydrophila, Plesiomonas shigelloides, Cronobacter sakazakii, and Brucella abortus. https://doi.org/10.1007/978-1-4939-7349-1_20

Bodnar, L., Alcântara, B., Milinari, B., Moraes, D., Cascales, R., Gardinali, N., Leme, R. de A., Alfieri, A., 2010. Detecção do vírus da Hepatite E em fígado de suínos de abatedouro, in: XiX Encontro Anual de Iniciação Científica. Unicentro, Guarapuava, p. 4.

Bottone, E.J., 1997. Yersinia enterocolitica: The charisma continues. Clin. Microbiol. Rev. 10, 257–276. https://doi.org/file://Z:\References\Text Files\00000004540.txt

Brasil, 2009. Programas nacionais de saúde no Brasil, 1st ed. Ministério da Agricultura, Pecuária e Abastecimento, Brasilia.

Brentano, L.; Zanella, J.R.C.; Mores, N.; Piffer, I.A., 2002. Levantamento soroepidemiológico para coronavírus respiratório e da gastroenterite transmissível e dos vírus de influenza H3N2 e H1N1 em rebanhos suínos no Brasil. Comun. Técnico Embrapa Suínos e Aves 1–6.

Carrillo, C.G., 1987. Animal brucellosis in America and its relationship with the human infection. OIE, Paris.

Casalinuovo, F., Ciambrone, L., Cacia, A., Rippa, P., 2016. Contamination of bovine, sheep and goat meat with Brucella spp. Ital. J. Food Saf. https://doi.org/10.4081/ijfs.2016.5913

Casanova, N.A., Redondo, L.M., Dailoff, G.C., Arenas, D., Fernández Miyakawa, M.E., 2018. Overview of the role of Shiga toxins in porcine edema disease pathogenesis. Toxicon 148, 149–154. https://doi.org/10.1016/j.toxicon.2018.04.019

Castro, V.S., Figueiredo, E.E. de S., Stanford, K., McAllister, T., Conte-Junior, C.A., 2019. Shiga-Toxin Producing Escherichia Coli in Brazil: A Systematic Review. Microorganisms 7. https://doi.org/10.3390/microorganisms7050137

CDC, 2017. National botulism surveillance summary 2017 [WWW Document]. URL https://www.cdc.gov/botulism/surv/2017/index.html

Chhabra, M.B., Samantaray, S., 2013. Sarcocystis and sarcocystosis in India: Status and emerging perspectives. J. Parasit. Dis. 37, 1–10. https://doi.org/10.1007/s12639-012-0135-y

Chlebicz, A., Śliżewska, K., 2018. Campylobacteriosis, Salmonellosis, Yersiniosis, and

Listeriosis as Zoonotic Foodborne Diseases: A Review. Int. J. Environ. Res. Public Health 15, 863. https://doi.org/10.3390/ijerph15050863

Collado, L., Figueras, M.J., 2011. Taxonomy, Epidemiology, and Clinical Relevance of the Genus Arcobacter. Clin. Microbiol. Rev. 24, 174–192. https://doi.org/10.1128/CMR.00034-10

Collado, L., Guarro, J., Figueras, M.J., 2009. Prevalence of Arcobacter in meat and shellfish. J. Food Prot. 72, 1102–1106.

Corbellini, L.G.L.G., Júnior, A.B., de Freitas Costa, E., Duarte, A.S.R., Albuquerque, E.R., Kich, J.D., Cardoso, M., Nauta, M., Junior, A.B., de Freitas Costa, E., Duarte, A.S.R., Albuquerque, E.R., Kich, J.D., Cardoso, M., Nauta, M., 2016. Effect of slaughterhouse and day of sample on the probability of a pig carcass being Salmonella-positive according to the Enterobacteriaceae count in the largest Brazilian pork production region. Int. J. Food Microbiol. 228, 58–66. https://doi.org/10.1016/j.ijfoodmicro.2016.03.030

Corrêa, C.N., Corrêa, W.M., 1974. Human tuberculosis by bovine bacilli in São Paulo, Brasil. Arq. Inst. Biol. (Sao. Paulo). 41, 131–4.

Costa, E. de F., 2014. Validação de estratégias a campo para o controle de Salmonella sp. na cadeia de produção de suínos. Master Thesis. Universidade Federal do Rio Grande do Sul.

Coutinho, T.A., Bernardi, M.L., Cardoso, M.R. de I., Borowski, S.M., Moreno, A.M., Barcellos, D.E.S.N. de, 2009. Performance of transport and selective media for swine Bordetella bronchiseptica recovery and it comparison to polymerase chain reaction detection. Brazilian J. Microbiol. 40, 470–479. https://doi.org/10.1590/S1517-83822009000300009

Coutinho, T.A., Imada, Y., de Barcellos, D.E.S.N., de Oliveira, S.J., Moreno, A.M., 2011. Genotyping of Brazilian Erysipelothrix spp. strains by amplified fragment length polymorphism. J. Microbiol. Methods 84, 27–32. https://doi.org/10.1016/j.mimet.2010.10.003

Cover, T.L., Aber, R.C., 1989. Yersinia Enterocolitica. N. Engl. J. Med. 321, 16–24. https://doi.org/10.1056/NEJM198907063210104

Croxen, M. a, Finlay, B.B., 2010. Molecular mechanisms of Escherichia coli pathogenicity. Nat. Rev. Microbiol. 8, 26–38. https://doi.org/10.1038/nrmicro2265

Cruz, C.D., Martinez, M.B., Destro, M.T., 2008. Listeria monocytogenes : UM AGENTE INFECCIOSO AINDA POUCO CONHECIDO NO BRASIL. Alim Nutr 19, 195–206.

Cruz Junior, E.C., Salvarani, F.M., Silva, R.O.S., Silva, M.X., Lobato, F.C.F., Guedes, R.M.C., 2013. A surveillance of enteropathogens in piglets from birth to seven days of age in Brazil. Pesqui. Veterinária Bras. 33, 963–969. https://doi.org/10.1590/S0100-736X2013000800002

Cunha, J.B., de Mendonça, M.C.L., Miagostovich, M.P., Leite, J.P.G., 2010. Genetic diversity of porcine enteric caliciviruses in pigs raised in Rio de Janeiro State, Brazil. Arch. Virol. 155, 1301–1305. https://doi.org/10.1007/s00705-010-0695-z

D’Alencar, A.S., Farias, M.P.D.O., Rosas, E.D.O., Lima, M.M. De, Menezes, M.M., Santos, F.L. Dos, Alves, L.C., Faustino, M.A.D.G., 2011. Influência do manejo higiênico sanitário na infecção por helmintos gasreintestinais em suínos de granjas tecnificadas e de subsistência abatidos na região metropolitana de recife e zona da mata do estado de pernambuco, Brasil. Arq. do Inst. Biológico; Arq. do Inst. Biológico 78, 207–2015. https://doi.org/10.5433/1679-0359.2011v32n3p1111

D’Sa, E.M., Harrison, M.A., 2005. Effect of pH, NaCl content, and temperature on growth and survival of Arcobacter spp. J. Food Prot. 68, 18–25.

Dahlenborg, M., Borch, E., Radstrom, P., 2001. Development of a Combined Selection and Enrichment PCR Procedure for Clostridium botulinum Types B, E, and F and Its Use To Determine Prevalence in Fecal Samples from Slaughtered Pigs. Appl. Environ. Microbiol. 67, 4781–4788. https://doi.org/10.1128/AEM.67.10.4781-4788.2001

Daskalov, H., 2006. The importance of Aeromonas hydrophila in food safety. Food Control 17, 474–483. https://doi.org/10.1016/j.foodcont.2005.02.009

De Lima, E.D.S.C., Pinto, P.S.D.A., Dos Santos, J.L., Vanetti, M.C.D., Bevilacqua, P.D., De Almeida, L.P., Pinto, M.S., Dias, F.S., 2004. Isolamento de Salmonella sp e Staphylococcus aureus no processo do abate suíno como subsídio ao sistema de Análise de Perigos e Pontos Críticos de Controle - APPCC. Pesqui. Vet. Bras. 24, 185–190. https://doi.org/10.1590/S0100-736X2004000400003

De Oliveira, S.J., Baetz, A.L., Wesley, I. V., Harmon, K.M., 1997. Classification of Arcobacter species isolated from aborted pig fetuses and sows with reproductive problems in Brazil. Vet. Microbiol. 57, 347–354. https://doi.org/10.1016/S0378-1135(97)00106-5

De Zutter, L., Van Hoof, J., 1987. Isolation of Yersinia enterocolitica from pork meat, in: 33th ICoMST. Helsinki.

Derouin, F., 1992. Pathogeny and immunological control of toxoplasmosis. Brazilian J. Med. Biol. Res. 25, 1163–1169.

Dias, R.A.F., Navarro, I.T., Ruffolo, B.B., Bugni, F.M., De Castro, M.V., Freire, R.L., 2005. Toxoplasma gondii in fresh pork sausage and seroprevalence in butchers from factories in Londrina, Paraná State, Brazil. Rev. Inst. Med. Trop. Sao Paulo. https://doi.org/10.1590/S0036-46652005000400002

Dixon, B.R., 2015. Foodborne Parasites in the Food Supply Web, Foodborne Parasites in the Food Supply Web. Elsevier. https://doi.org/10.1016/B978-1-78242-332-4.00013-8

Djurković-Djaković, O., Bobić, B., Nikolić, A., Klun, I., Dupouy-Camet, J., 2013. Pork as a source of human parasitic infection. Clin. Microbiol. Infect. 19, 586–594. https://doi.org/10.1111/1469-0691.12162

Dodd, C.E.R., 2017. Infrequent Microbial Infections, in: Foodborne Diseases. Elsevier, pp. 277–288. https://doi.org/10.1016/B978-0-12-385007-2.00013-9

Doig, C., Seagar, A.L., Watt, B., Forbes, K.J., 2002. The efficacy of the heat killing of Mycobacterium tuberculosis. J. Clin. Pathol. 55, 778–779.

Dubey, J.P., 2015. Foodborne and waterborne zoonotic sarcocystosis. Food Waterborne Parasitol. 1, 2–11. https://doi.org/10.1016/j.fawpar.2015.09.001

Dubey, J.P., 2009. Toxoplasmosis in pigs-The last 20 years. Vet. Parasitol. https://doi.org/10.1016/j.vetpar.2009.05.018

Dubey, J.P., Hill, D.E., Jones, J.L., Hightower, A.W., Kirkland, E., Roberts, J.M., Marcet, P.L., Lehmann, T., Vianna, M.C.B., Miska, K., Sreekumar, C., Kwok, O.C.H., Shen, S.K., Gamble, H.R., 2005. Prevalence of viable Toxoplasma gondii in beef, chicken, and pork from retail meat stores in the United States: risk assessment to consumers. J. Parasitol. 91, 1082–1093. https://doi.org/10.1645/GE-683.1

Dubey, J.P., Jones, J.L., 2008. Toxoplasma gondii infection in humans and animals in the United States. Int. J. Parasitol. https://doi.org/10.1016/j.ijpara.2008.03.007

Dubey, J.P., Kotula, A.W., Sharar, A., Andrews, C.D., Lindsay, D.S., 1990. Effect of High Temperature on Infectivity of Toxoplasma gondii Tissue Cysts in Pork. J. Parasitol. 76, 201. https://doi.org/10.2307/3283016

Dutra, M.C., Moreno, L.Z., Amigo, C.R., Felizardo, M.R., Ferreira, T.S.P., Coutinho, T.A., Sanches, A.A., Galvis, J.A., Moreno, M., Moreno, A.M., 2016. Molecular survey of Cytomegalovirus shedding profile in commercial pig herds in Brazil. J. Infect. Dev. Ctries. https://doi.org/10.3855/jidc.7367

EC, 1999. Opinion of the scientific committee on veterinary measures relating to public health on Listeria monocytogenes.

ECDP, 2017. Facts about Escherichia coli [WWW Document]. URL https://www.ecdc.europa.eu/en/escherichia-coli-ecoli/facts (accessed 12.7.19).

EFSA, 2018. The European Union summary report on trends and sources of zoonoses, zoonotic agents and food‐borne outbreaks in 2017. EFSA J. 16. https://doi.org/10.2903/j.efsa.2018.5500

EFSA, 2007. Monitoring and identification of human enteropathogenic Yersinia spp. - Scientific Opinion of the Panel on Biological Hazards. EFSA J. https://doi.org/10.2903/j.efsa.2007.595

Esteves, F.M., Silva-Vergara, M.L., Carvalho, Â.C.F.B. de, 2005. Inquérito epidemiológico sobre teníase em população do programa saúde da família no município de Uberaba, MG. Rev. Soc. Bras. Med. Trop. 38, 530–531. https://doi.org/10.1590/S0037-86822005000600017

Fàbrega, A., Vila, J., 2013. Salmonella enterica serovar Typhimurium skills to succeed in the host: Virulence and regulation. Clin. Microbiol. Rev. https://doi.org/10.1128/CMR.00066-12

Falcão, J.P., Corrêa, E.F., Martins, C.H.G., Falcão, D.P., 2008. Panoramic view of the occurrence of Yersinia species other than Y. pestis in Brazil. Rev. Ciencias Farm. Basica e Apl. 29, 1–16.

FAO/WHO, 2018. Shiga toxin-producing Escherichia coli (STEC) and food: attribution, characterization, and monitoring. Rome.

FAO/WHO, 2004. Risk assessment of Listeria monocytogene s in ready-to-eat foods, Microbiological Risk Assessment Series. Rome.

Fayer, R., 2004. Sarcocystis spp. in human infections. Clin. Microbiol. Rev. https://doi.org/10.1128/CMR.17.4.894-902.2004

Farzão-Teixeira, E., Oliveira, F.C. de, Pelissari-Sant’Ana, V., Lopes, C.W., 2006. Toxoplasma gondii em encéfalos de suínos comercializados no município de Campos dos Goytacazes, Estado do Rio de Janeiro, Brasil. Rev. Bras. Parasitol. Veterinária 15, 33–36.

Fayer, R., Esposito, D.H., Dubey, J.P., 2015. Human infections with Sarcocystis species. Clin. Microbiol. Rev. 28, 295–311. https://doi.org/10.1128/CMR.00113-14

Feagins, A.R., Opriessnig, T., Guenette, D.K., Halbur, P.G., Meng, X.J., 2008. Inactivation of infectious hepatitis E virus present in commercial pig livers sold in local grocery stores in the United States. Int. J. Food Microbiol. https://doi.org/10.1016/j.ijfoodmicro.2007.11.068

Fernández, H., Krause, S., Villanueva, M.P., 2004. Arcobacter butzleri an emerging enteropathogen: Communication of two cases with chronic diarrhea. Brazilian J. Microbiol. 35, 216–218. https://doi.org/10.1590/S1517-83822004000200008

Ferreira, T.S.P., Moreno, A.M., Almeida, R.R. de, Gomes, C.R., Gobbi, D.D.S. de, Filsner, P.H.N. de L., Moreno, M., 2012. Molecular typing of Clostridium perfringens isolated from swine in slaughterhouses from São Paulo State, Brazil. Ciência Rural 42, 1450–1456. https://doi.org/10.1590/S0103-84782012000800020

Ferronatto, A.I., Pellegrini, D.D.C.P., Guerra, P., Cardoso, M.R. de I., 2012. Distribuição de grupos clonais de Lysteria monocytogenes em carcaças e no ambiente de matadouros frigoríficos de suínos. Arch. Vet. Sci. 17. https://doi.org/10.5380/avs.v17i3.24940

Filsner, P.H.N. de L., 2013. Isolamento e caracterização de Enterococcus faecallis resistentes a vancomicina ou a altas concentrações de aminoglicosídeos provenientes de suínos no Brasil. Universidade de São Paulo.

Fisher, J.C., Levican, A., Figueras, M.J., McLellan, S.L., 2014. Population dynamics and ecology of Arcobacter in sewage. Front. Microbiol. 5. https://doi.org/10.3389/fmicb.2014.00525

Fontes, M. C., Saavedra, M. J., Martins, C., Martínez-Murcia, A.J., 2011. Phylogenetic identification of Aeromonas from pigs slaughtered for consumption in slaughterhouses at the North of Portugal. Int. J. Food Microbiol. 118–122.

Fosse, J., Seegers, H., Magras, C., 2008. Foodborne zoonoses due to meat: A quantitative approach for a comparative risk assessment applied to pig slaughtering in Europe. Vet. Res. 39, 1–16. https://doi.org/10.1051/vetres:2007039

Fredriksson-Ahomaa, M., 2007. Yersinia enterocolitica and Yersinia pseudotuberculosis, in: Simjee, S. (Ed.), Foodborne Diseases. Humana Press, Totowa, NJ, pp. 79–113. https://doi.org/10.1007/978-1-59745-501-5_4

Funk, J., Wagstrom, E., 2019. Preharvest Food Safety, Zoonotic Diseases, and the Human Health Interface, in: Diseases of Swine. John Wiley & Sons, Inc., Hoboken, NJ, USA, pp. 197–210. https://doi.org/10.1002/9781119350927.ch12

Galindo, C.L., Rosenzweig, J.A., Kirtley, M.L., Chopra, A.K., 2011. Pathogenesis of Y. enterocolitica and Y. pseudotuberculosis in Human Yersiniosis. J. Pathog. 2011, 1–16. https://doi.org/10.4061/2011/182051

Garcia, J.L., Navarro, I.T., Ogawa, L., Oliveira, R.C. De, 1999. Soroprevalência do toxoplasma gondii, em suínos, bovinos, ovinos e eqüinos, e sua correlação com humanos, felinos e caninos, oriundos de propriedades rurais do norte do Paraná-Brasil. Ciência Rural 29, 91–97. https://doi.org/10.1590/S0103-84781999000100017

Garcia, L.A.T., 2011. Estudo da incidência de adenovírus humano e suíno, norovírus humano e circovírus suíno, em amostras de água de consumo e descedentação animal do município de Concórdia, Santa Catarina. UFSC.

Gava, D., Streck, A.F., Souza, C.K., Gonçalves, K.R., Bortolozzo, F.P., Canal, C.W., Wentz, I., 2009. Atualização sobre a parvovirose na suinocultura. Acta Sci. Vet. 37, 105–115.

Gobbi, D.D.S., Spindola, M.G., Moreno, L.Z., Matajira, C.E.C., Oliveira, M.G.X., Paixão, R., Ferreira, T.S.P., Moreno, A.M., 2018. Isolation and molecular characterization of Arcobacter butzleri and Arcobacter cryaerophilus from the pork production chain in Brazil. Pesqui. Vet. Bras. https://doi.org/10.1590/1678-5150-PVB-4709

Graziani, C., Losasso, C., Luzzi, I., Ricci, A., Scavia, G., Pasquali, P., 2017. Salmonella, in: Foodborne Diseases. Elsevier, pp. 133–169. https://doi.org/10.1016/B978-0-12-385007-2.00005-X

Guillois, Y., Abravanel, F., Miura, T., Pavio, N., Vaillant, V., Lhomme, S., Le Guyader, F.S., Rose, N., Le Saux, J.-C., King, L.A., Izopet, J., Couturier, E., 2016. High Proportion of Asymptomatic Infections in an Outbreak of Hepatitis E Associated With a Spit-Roasted Piglet, France, 2013. Clin. Infect. Dis. 62, 351–357. https://doi.org/10.1093/cid/civ862

Guimarães, F.R., Saddi, T.M., Vitral, C.L., Pinto, M.A., Gaspar, A.M.C., Souto, F.J.D., 2005. Hepatitis E virus antibodies in swine herds of Mato Grosso state, Central Brazil. Brazilian J. Microbiol. 36, 223–226. https://doi.org/10.1590/S1517-83822005000300004

Gumarães, A.M., Ribeiro, M.F.B., Lima, J.D., Almeida, T.M.B., 1992. Frequência de anticorpos anti-Toxoplasma gondii em suínos da raça Piau. Arq. Bras. Med. Veterinária e Zootec. 44, 69–71.

Heldt, F.H., Staggmeier, R., Gularte, J.S., Demoliner, M., Henzel, A., Spilki, F.R., 2016. Hepatitis E Virus in Surface Water, Sediments, and Pork Products Marketed in Southern Brazil. Food Environ. Virol. https://doi.org/10.1007/s12560-016-9243-7

Hilton, C.L., Mackey, B.M., Hargreaves, A.J., Forsythe, S.J., 2001. The recovery of

Arcobacter butzleri NCTC 12481 from various temperature treatments. J. Appl. Microbiol. 91, 929–932. https://doi.org/10.1046/j.1365-2672.2001.01457.x

Ho, H.T.K., Lipman, L.J.A., Gaastra, W., 2008. The introduction of Arcobacter spp. in poultry slaughterhouses. Int. J. Food Microbiol. 125, 223–229. https://doi.org/10.1016/j.ijfoodmicro.2008.02.012

ICMSF, 1996. Microorganisms in foods 5. Characteristics of microbial pathogens, 1st ed. BlackieAcademic & Professional, London.

Igbinosa, I.H., Igumbor, E.U., Aghdasi, F., Tom, M., Okoh, A.I., 2012. Emerging Aeromonas Species Infections and Their Significance in Public Health. Sci. World J. 2012, 1–13. https://doi.org/10.1100/2012/625023

Jay, J., Loessner, M., Golden, D., 2005. Modern food microbiology, 7th ed. Springer, New York.

Jones, J.L., Dubey, J.P., 2012. Foodborne toxoplasmosis. Clin. Infect. Dis. 55, 845–851. https://doi.org/10.1093/cid/cis508

Jones, J.L., Muccioli, C., Belfort, R., Holland, G.N., Roberts, J.M., Silveira, C., 2006. Recently acquired Toxoplasma gondii infection, Brazil. Emerg. Infect. Dis. https://doi.org/10.3201/eid1204.051081

Kadariya, J., Smith, T.C., Thapaliya, D., 2014. Staphylococcus aureus and Staphylococcal Food-Borne Disease: An Ongoing Challenge in Public Health. Biomed Res. Int. 2014, 1–9. https://doi.org/10.1155/2014/827965

Kanuganti, S.R., Wesley, I. V., Reddy, P.G., McKean, J., Hurd, H.S., 2002. Detection of Listeria monocytogenes in pigs and pork. J. Food Prot. https://doi.org/10.4315/0362-028X-65.9.1470

Ketheesan, N., Norton, R.E., Eales, K.M., 2010. Brucellosis in Northern Australia. Am. J. Trop. Med. Hyg. 83, 876–878. https://doi.org/10.4269/ajtmh.2010.10-0237

Keto-Timonen, R., Pöntinen, A., Aalto-Araneda, M., Korkeala, H., 2018. Growth of Yersinia pseudotuberculosis Strains at Different Temperatures, pH Values, and NaCl and Ethanol Concentrations. J. Food Prot. 81, 142–149. https://doi.org/10.4315/0362-028X.JFP-17-223

Knetter, S.M., Bearson, S.M.D., Huang, T.H., Kurkiewicz, D., Schroyen, M., Nettleton, D., Berman, D., Cohen, V., Lunney, J.K., Ramer-Tait, A.E., Wannemuehler, M.J., Tuggle, C.K., 2015. Salmonella enterica serovar Typhimurium-infected pigs with different shedding levels exhibit distinct clinical, peripheral cytokine and transcriptomic immune response phenotypes. Innate Immun. https://doi.org/10.1177/1753425914525812

Krog, J.S., Larsen, L.E., Breum, S.Ø., 2019. Tracing Hepatitis E Virus in Pigs From Birth to Slaughter. Front. Vet. Sci. 6. https://doi.org/10.3389/fvets.2019.00050

Kruger, C.D., Cavaglieri, L.R., Direito, G.M., Keller, K.M., Dalcero, A.M., da Rocha Rosa, C.A., da, R.R.C.A., Krüger, C.D., Cavaglieri, L.R., Direito, G.M., Keller, K.M., Dalcero, A.M., da Rosa, C.A.R., 2010. Ochratoxin a in serum of swine from different Brazilian states. J. Vet. Diagnostic Investig. 22, 753–756.

https://doi.org/10.1177/104063871002200516

Laird, K., 2015. New and Emerging Bacterial Food Pathogens, in: Food Safety. Elsevier, pp. 309–316. https://doi.org/10.1016/B978-0-12-800245-2.00014-9

Le Marc, Y., Huchet, V., Bourgeois, C.M., Guyonnet, J.P., Mafart, P., Thuault, D., 2002. Modelling the growth kinetics of Listeria as a function of temperature, pH and organic acid concentration. Int. J. Food Microbiol. https://doi.org/10.1016/S0168-1605(01)00640-7

Lee, M.H., Choi, C., 2013. Survival of Arcobacter butzleri in Apple and Pear Purees. J. Food Saf. 33, 333–339. https://doi.org/10.1111/jfs.12057

Leser, T.D., Amenuvor, J.Z., Jensen, T.K., Lindecrona, R.H., Boye, M., Moller, K., 2002. Culture-Independent Analysis of Gut Bacteria: the Pig Gastrointestinal Tract Microbiota Revisited. Appl. Environ. Microbiol. 68, 673–690. https://doi.org/10.1128/AEM.68.2.673-690.2002

Lhomme, S., Marion, O., Abravanel, F., Chapuy-Regaud, S., Kamar, N., Izopet, J., 2016. Hepatitis E Pathogenesis. Viruses 8. https://doi.org/10.3390/v8080212

Li, H., Gänzle, M., 2016. Some Like It Hot: Heat Resistance of Escherichia coli in Food. Front. Microbiol. 7. https://doi.org/10.3389/fmicb.2016.01763

Lima, E. do S.C. de, Pinto, P.S. de A., Santos, J.L. dos, Vanetti, M.C.D., Bevilacqua, P.D., Almeida, L.P. de, Pinto, M.S., Dias, F.S., 2004. Isolamento de Salmonella sp e Staphylococcus aureus no processo do abate suíno como subsídio ao sistema de Análise de Perigos e Pontos Críticos de Controle - APPCC. Pesqui. Veterinária Bras. 24, 185–190. https://doi.org/10.1590/S0100-736X2004000400003

Lindsay, D.S., Dubey, J.P., Santin-Duran, M., Fayer, R., 2012. Coccidia and Other Protozoa, in: Zimmerman, J. (Ed.), Disease of Swine. John Wiley & Sons.

Logue, C.M., Barbieri, N.L., Nielsen, D.W., 2017. Pathogens of Food Animals: Sources, Characteristics, Human Risk, and Methods of Detection, in: Told, F. (Ed.), Advances in Food and Nutrition Research. Elsevier, pp. 277–365. https://doi.org/10.1016/bs.afnr.2016.12.009

Lucena, R.F., 2007. Isolamento e caracterização de Aeromonas em carcaças suínas. Master Thesis. Universidade de Caxias.

Machado, L.A.P., Lucca, F., Alves, J., Pozzobon, A., Bustamante-Filho, I.C., 2014. Prevalence and genotyping of pathogenic Escherichia coli on carcasses of pigs slaughtered in commercial slaughterhouses in southern region of Brazil. Rev. Bras. Hig. e Sanidade Anim. 8. https://doi.org/10.5935/1981-2965.20140009

Maciel, A.L.G., Loiko, M.R., Bueno, T.S., Moreira, J.G., Coppola, M., Dalla Costa, E.R., Schmid, K.B., Rodrigues, R.O., Cibulski, S.P., Bertagnolli, A.C., Mayer, F.Q., 2018. Tuberculosis in Southern Brazilian wild boars ( Sus scrofa ): First epidemiological findings. Transbound. Emerg. Dis. 65, 518–526. https://doi.org/10.1111/tbed.12734

Markey, B., Leonard, F., Archambault, M., Cullinane, A., Maguire, D., 2013. Clinical Veterinary Microbiology, 2nd ed. Elsevier.

Marques-Santos, F., Amendoeira, M.R.R., Carrijo, K.F., Santos, J.P.A.F., Arruda, I.F., Sudré, A.P., Brener, B., Millar, P.R., 2017. Occurrence of Toxoplasma gondii and risk factors for infection in pigs raised and slaughtered in the Triângulo Mineiro region, Minas Gerais, Brazil. Pesqui. Vet. Bras. 37, 570–576. https://doi.org/10.1590/S0100-736X2017000600006

Martins, R.P., da Silva, M.C., Dutra, V., Nakazato, L., Leite, D. da S., 2013. Preliminary virulence genotyping and phylogeny of Escherichia coli from the gut of pigs at slaughtering stage in Brazil. Meat Sci. 93, 437–440. https://doi.org/10.1016/j.meatsci.2012.10.007

Martins, R.P., Da Silva, M.C., Dutra, V., Nakazato, L., Leite, D.D.S., 2011. Prevalence of enterotoxigenic and Shiga toxin-producing Escherichia coli in pigs slaughtered in Mato Grosso, Brazil. J. Infect. Dev. Ctries. 5. https://doi.org/10.3855/jidc.1217

Martins, T.S., 2013. Pesquisa e quantificação de listeria sp.em carcaças suínas antes e após o processo de maturação em câmara fria. Master Thesis. UDESC.

Masson, G.C.I.H., 2011. Staphylococcus aureus na cadeia produtiva de suínos e perfil de resistência a antimicrobianos. Universidade Estadual Paulista.

Matajira, C.E.C., Moreno, L.Z., Amigo, C., Gomes, V.T. de M., Silva, A.P.S., Mesquita, R.E., Nakasone, D.H., Christ, A.P.G., Sato, M.I.Z., Moreno, A.M., 2015. Identificação de Aerococcus viridans como agente etiológico de infecção urinária em matrizes, in: Congresso Brasileiro de Veterinários Especialistas Em Suínos - ABRAVES. Embrapa Suínos e Aves.

Megid, J., Antonio Mathias, L., A. Robles, C., 2010. Clinical Manifestations of Brucellosis in Domestic Animals and Humans. Open Vet. Sci. J. 4, 119–126. https://doi.org/10.2174/1874318801004010119

Meirelles-Bartoli, R.B., Mathias, L.A., Samartino, L.E., 2012. Brucellosis due to Brucella suis in a swine herd associated with a human clinical case in the State of São Paulo, Brazil. Trop. Anim. Health Prod. 44, 1575–1579. https://doi.org/10.1007/s11250-012-0108-2

Meneguzzi, M., Kich, J.D., Rebelatto, R., Pissetti, C., Kuchiishi, S.S., Reis, A.T., Guedes, R.M.C., Leão, J.A., Reichen, C., 2017. Salmonella clinical isolates from Brazilian pig herds: genetic relationship and antibiotic resistance profiling, in: International Conference on the Epidemiology and Control of Biological, Chemical and Physical Hazards in Pigs and Pork. Iowa State University, Digital Press, Foz do Iguaçu, pp. 170–174. https://doi.org/10.31274/safepork-180809-378

Meng, J., LeJeune, J.T., Zhao, T., Doyle, M.P., 2013. Enterohemorrhagic Escherichia coli, in: Doyle, M.P., L.Buchanan, R. (Eds.), Food Microbiology: Fundamentals and Frontiers, Fourth Edition. American Society of Microbiology, pp. 287–309. https://doi.org/10.1128/9781555818463.ch12

Modolo, J.R., Margato, L.F.F., Gottschalk, A.F., Lopes, C.A. de M., 1999. Incidence of Campylobacter in pigs with and without diarrhea. Rev. Microbiol. 30, 19–21. https://doi.org/10.1590/S0001-37141999000100004

Møller Nielsen, E., Engberg, J., Madsen, M., 1997. Distribution of serotypes of

Campylobacter jejuni and C. coli from Danish patients, poultry, cattle and swine. FEMS Immunol. Med. Microbiol. 19, 47–56. https://doi.org/10.1111/j.1574-695X.1997.tb01071.x

Moreira, L.M., Tavares, A.B., Ebersol, C.N., Gonçalves, T.G., Lima, H.G. de, Cereser, N.D., Timm, C.D., 2018. Holding Pens as Sources of Contamination of Coagulase-Positive Staphylococcus to Pigs Waiting for Slaughter. Acta Sci. Vet. 46, 6. https://doi.org/10.22456/1679-9216.84208

Moreno, A., Baccaro, M., Ferreira, A., 2003. Detection of the Î22-toxin gene from Clostridium perfringens isolated in diarrheic piglets. Arq. Inst. … 70, 135–138.

Mores, M., Mores, N., Albuquerque, E., Kich, J.D., 2019. Pathologic diagnosis of zoonotic parasitosis in slaughter pigs in Brazil, in: Proceedings of the 13th SafePork. Berlin, p. 111.

Morés, N., Ventura, L., Dutra, V., Silva, V.S., Jr, B., Oliveira, S.R., Kramer, B., Neto, S.F., N, A.M., Ventura, L., Dutra, V., Silva, V.S., W, B.J., Oliveira, S.R., Kramer, B., Barioni Júnior, W., Oliveira, S.R., Kramer, B., Ferreira Neto, J.S., 2007. Linfadenite granulomatosa em suínos: linfonodos afetados e diagnóstico patológico da infecção causada por agentes do complexo Mycobacterium avium. Pesqui. vet. bras 27, 13–17.

Motta, P.M.C., Jr., A.A.F., Oliveira, A.M. de, Nascimento, K.F., Filho, P.M.S., Serra, C.V., Jesus, A.L., Jr., A.V.R., Ramalho, A.K., Mota, P.M.P.C., Assis, R.A., Camargos, M.F., 2010. Inquérito soroepidemiológico para brucelose em suídeos do Brasil. Vet. em Foco 7, 141–147.

Murphy, R.Y., Duncan, L.K., Johnson, E.R., Davis, M.D., Smith, J.N., 2002. Thermal inactivation D- and z-values of Salmonella serotypes and listeria innocua in chicken patties, chicken tenders, franks, beef patties, and blended beef and turkey patties. J. Food Prot. 65, 53–60.

Murphy, R.Y., Osaili, T., Duncan, L.K., Marcy, J.A., 2004. Thermal inactivation of Salmonella and Listeria monocytogenes in ground chicken thigh/leg meat and skin. Poult. Sci. 83, 1218–1225.

Neill, S.D., Campbell, J.N., O’Brien, J.J., 1985. Taxonomic position of Campylobacter cryaerophila sp. nov. Int. J. Syst. Bacteriol. https://doi.org/10.1099/00207713-35-3-342

Niederman, J.C., Henderson, J.R., Opton, E.M., Black, F.L., Skvrnova, K., 1967. A nationalwilde serum survey of Brazilian military recruits, 1964: II. Antibody patterns with Arbovirures, Poliovirus, Measles ans Mumps1. Am. J. Epidemiol. 86, 319–329. https://doi.org/10.1093/oxfordjournals.aje.a120742

Nishi, S.M., Gennari, S.M., Lisboa, M.N.T.S., Silvestrim, A., Caproni Junior, L., Umehara, O., 2000. Parasitas intestinais em suínos confinados nos Estados de São Paulo e Minas Gerais. Arq. Inst. Biol. (Sao. Paulo). 67, 199–203.

Nuorti, J.P., Niskanen, T., Hallanvuo, S., Mikkola, J., Kela, E., Hatakka, M., Fredriksson‐Ahomaa, M., Lyytikäinen, O., Siitonen, A., Korkeala, H., Ruutu, P., 2004. A Widespread Outbreak of Yersinia pseudotuberculosis O:3 Infection from

Iceberg Lettuce. J. Infect. Dis. 189, 766–774. https://doi.org/10.1086/381766

O’Reilly, L.M., Daborn, C.J., 1995. The epidemiology of Mycobacterium bovis infections in animals and man: A review. Tuber. Lung Dis. https://doi.org/10.1016/0962-8479(95)90591-X

OIE, 2010. Chapter 2.1.1, in: OIE (Ed.), Terrestrial Animal Health Code. Paris, p. 6.

OIE, 2008. Campylobacter Jejuni and Campylobacter coli, in: Manual of Diagnostic Tests and Vaccines for Terrestrial Animals 2015. OIE, Paris, pp. 1185–1191.

Oldoni, M.L., Teixeira, A.D.R.M.L., 2012. Análises micotoxicológicas em rações comercializadas no oeste de Santa Catarina. Rev. Bras. Prod. Agroindustriais 14, 373–379.

Oliveira, S. de, Bernardi, R., Mottin, V., Hepp, D., Thompsen, P., 2009. Observação de diferentes graus de lesões em estômagos e úlcera gástrica em leitões de creche. Isolamento de Arcobacter cryaerophilus. Acta Sci. Vet. 37, 119–123.

Oliveira, S.J. de, Bernardi, R.T., Vogt, F.I., Scartezzini, M., Hepp, D., Lunge, V.R., 2010. Úlceras gástricas em suínos de abate: cultivo de Arcobacter spp. a partir de estômagos com diferentes graus de lesões. Acta Sci. Vet. 38, 351–356.

Oliveira, E.M.D., Rodriguez, C.A.R., Leão, S.C., Maku, M., Neto, J.S.F., 2006. Estudo da dinâmica da infecção por Mycobacterium avium em uma população suína através de modelagem matemática. Arq. Inst. Biol. (Sao. Paulo). 73, 409–414.

Oliveira Filho, J.X. de, Morés, M.A.Z., Rebellato, R., Kich, J.D., Cantão, M.E., Klein, C.S., Guedes, R.M.C., Coldebella, A., Barcellos, D.E.S.N. de, Morés, N., 2018. Pathogenic variability among Pasteurella multocida type A isolates from Brazilian pig farms. BMC Vet. Res. 14, 244. https://doi.org/10.1186/s12917-018-1565-2

Oliveira Júnior, C.A. de, Silva, R.O.S., Olinda, R.G., Lobato, F.C.F., 2016. Botulism in non-ruminants in Brazil. Ciência Rural 46, 2158–2165. https://doi.org/10.1590/0103-8478cr20160394

Osaili, T., Griffis, C.L., Martin, E.M., Beard, B.L., Keener, A., Marcy, J.A., 2006. Thermal inactivation studies of Escherichia coli O157:H7, Salmonella, and Listeria monocytogenes in ready-to-eat chicken-fried beef patties. J. Food Prot. 69, 1080–1086.

Paim, D.S., Pisseti, C., Vieira, T.R., Werlang, G.O., Costa, E.D.F., Deon Kich, J., Cardoso, M., 2019. Enumeration, Antimicrobial Resistance and Typing of Salmonella enterica: Profile of Strains Carried in the Intestinal Contents of Pigs at Slaughter in Southern Brazil. Acta Sci. Vet. 47. https://doi.org/10.22456/1679-9216.89668

Paixão, R., Moreno, A.M., Cavalcante, D.A., Doto, D.S., Gobbi, D.D.S., Campos, D.F.S., Castilla, K.S., Ferreira, A.J.P., 2005. Occurrence of Listeria monocytogenes in Brazilian swine herds, in: International Conference on the Epidemiology and Control of Biological, Chemical and Physical Hazards in Pigs and Pork. Iowa State University, Digital Press, pp. 256–258. https://doi.org/10.31274/safepork-180809-773

Pal, M., 2018. Is Aeromonas hydrophila a potential pathogen of food safety concern? J. Food Microbiol. 2, 1–2.

Pappas, G., Panagopoulou, P., Christou, L., Akritidis, N., 2006. Biological weapons. Cell. Mol. Life Sci. 63, 2229–2236. https://doi.org/10.1007/s00018-006-6311-4

Park, J.-H., Oh, S.-S., Oh, K.-H., Shin, J., Jang, E.J., Jun, B.-Y., Youn, S.-K., Cho, S.-H., 2014. Diarrheal Outbreak Caused by Atypical Enteropathogenic Escherichia coli O157:H45 in South Korea. Foodborne Pathog. Dis. 11, 775–781. https://doi.org/10.1089/fpd.2014.1754

Park, S.F., 2002. The physiology of Campylobacter species and its relevance to their role as foodborne pathogens. Int. J. Food Microbiol. 74, 177–188. https://doi.org/10.1016/S0168-1605(01)00678-X

Pasquali, P., 2004. Tuberculosis due to Mycobacterium bovis, in: Pasquali, P. (Ed.), HIV Infections Ans Zoonoses. FAO, Rome.

Pawlowski, Z.S., Murrell, K.D., 2001. Taeniasis and cysticercosis, in: YH Hui, SA Sattar, KD Murrell, WK Nip, P.S. (Ed.), Foodborne Disease Handbook: Viruses, Parasites, Pathogens and HACCP. CRC Press, New York, pp. 217–227. https://doi.org/10.1201/9781351072106

Poester, F.P., Gonçalves, V.S.P., Lage, A.P., 2002. Brucellosis in Brazil. Vet. Microbiol. 90, 55–62. https://doi.org/10.1016/S0378-1135(02)00245-6

Portela, R.W.D., Bethony, J., Costa, M.I., Gazzinelli, A., Vitor, R.W.A., Hermeto, F.M., Correa‐Oliveira, R., Gazzinelli, R.T., 2004. A Multihousehold Study Reveals a Positive Correlation between Age, Severity of Ocular Toxoplasmosis, and Levels of Glycoinositolphospholipid‐Specific Immunoglobulin A. J. Infect. Dis. https://doi.org/10.1086/421505

Pouillot, R., Hoelzer, K., Chen, Y., Dennis, S.B., 2015. Listeria monocytogenes dose response revisited--incorporating adjustments for variability in strain virulence and host susceptibility. Risk Anal. 35, 90–108. https://doi.org/10.1111/risa.12235

Praveen, P.K., Debnath, C., Shekhar, S., Dalai, N., Ganguly, S., 2016. Incidence of Aeromonas spp. infection in fish and chicken meat and its related public health hazards: A review. Vet. World 9, 6–11. https://doi.org/10.14202/vetworld.2016.6-11

Queiroga, M.C., Amaral, A.S.P., Branco, S.M., 2012. Short communication. Isolation of Aeromonas hydrophila in piglets. Spanish J. Agric. Res. 10, 383–387. https://doi.org/10.5424/sjar/2012102-495-11

Ramees, T.P., Dhama, K., Karthik, K., Rathore, R.S., Kumar, A., Saminathan, M., Tiwari, R., Malik, Y.S., Singh, R.K., 2017. Arcobacter : an emerging food-borne zoonotic pathogen, its public health concerns and advances in diagnosis and control – a comprehensive review. Vet. Q. 37, 136–161. https://doi.org/10.1080/01652176.2017.1323355

Raymundo, D.L., Gomes, D.C., Boabaid, F.M., Colodel, E.M., Schmitz, M., Correa, A.M.R., Dutra, I.S., Driemeier, D., 2012. Type C botulism in swine fed on restaurant waste. Pesqui. Veterinária Bras. 32, 1145–1147.

https://doi.org/10.1590/S0100-736X2012001100012

Reddy, P.N., Srirama, K., Dirisala, V.R., 2017. An Update on Clinical Burden, Diagnostic Tools, and Therapeutic Options of Staphylococcus aureus. Infect. Dis. Res. Treat. 10, 117991611770399. https://doi.org/10.1177/1179916117703999

Rhoads, M.L., Murrell, K.D., 1988. Taeniasis and Cysticercosis, in: Balows, A., Hausler, W.J., Ohashi, M., Turano, A., Lennete, E.H. (Eds.), Laboratory Diagnosis of Infectious Diseases: Principles and Practice. Springer New York, New York, NY, pp. 987–992. https://doi.org/10.1007/978-1-4612-3898-0_103

Ribeiro, M.G., Risseti, R.M., Bolaños, C.A.D., Caffaro, K.A., de Morais, A.C.B., Lara, G.H.B., Zamprogna, T.O., Paes, A.C., Listoni, F.J.P., Franco, M.M.J., 2015. Trueperella pyogenes multispecies infections in domestic animals: a retrospective study of 144 cases (2002 to 2012). Vet. Q. 35, 82–87. https://doi.org/10.1080/01652176.2015.1022667

Robinson, D.A., 1981. Infective dose of Campylobacter jejuni in milk. BMJ 282, 1584–1584. https://doi.org/10.1136/bmj.282.6276.1584

Rocha, V.C.M., Corrêa, S.H.R., Oliveira, E.M.D., Rodriguez, C.A.R., Fedullo, J.D., Matrone, M., Setzer, A., Ikuta, C.Y., Vejarano, M.P., Figueiredo, S.M., Ferreira Neto, J.S., 2011. Tuberculosis determined by Mycobacterium bovis in captive waterbucks (Kobus ellipsiprymnus) in São Paulo, Brazil. Brazilian J. Microbiol. 42, 726–728. https://doi.org/10.1590/S1517-83822011000200040

Rosa, D.C., Garcia, K.C.O.D., Megid, J., 2012. Soropositividade para brucelose em suínos em abatedouros. Pesqui. Veterinária Bras. 32, 623–626. https://doi.org/10.1590/S0100-736X2012000700006

Roussel, C., Cordonnier, C., Livrelli, V., Wiele, T. Van de, Blanquet‐Diot, S., 2017. Enterotoxigenic and Enterohemorrhagic Escherichia coli: Survival and Modulation of Virulence in the Human Gastrointestinal Tract, in: Escherichia Coli - Recent Advances on Physiology, Pathogenesis and Biotechnological Applications. InTech. https://doi.org/10.5772/intechopen.68309

Ruiz, V.L.A., Bersano, J.G., Carvalho, A.F., Catroxo, M.H.B., Chiebao, D.P., Gregori, F., Miyashiro, S., Nassar, A.F.C., Oliveira, T.M.F.S., Ogata, R.A., Scarcelli, E.P., Tonietti, P.O., 2016. Case – control study of pathogens involved in piglet diarrhea. BMC Res. Notes 9, 22. https://doi.org/10.1186/s13104-015-1751-2

Saadatnia, G., Golkar, M., 2012. A review on human toxoplasmosis. Scand. J. Infect. Dis. 44, 805–814. https://doi.org/10.3109/00365548.2012.693197

Saba, R.Z., Rossi Junio, O.D., Kamimura, B.A., Lavezzo, L.F., Bürger, K.P., Vidal-Martins, A.M.C., 2013. Isolation of Yersinia enterocolitica in slaughtered swine. Ars Vet. 29, 92. https://doi.org/10.15361/2175-0106.2013v29n4p92

Biasi, R.S., Freitas de Macedo, R.E., Scaranello Malaquias, M.A., Franchin, P.R., 2011. Prevalence, strain identification and antimicrobial resistance of Campylobacter spp. isolated from slaughtered pig carcasses in Brazil. Food Control 22, 702–707. https://doi.org/10.1016/j.foodcont.2010.10.005

Salines, M., Andraud, M., Rose, N., 2017. From the epidemiology of hepatitis e virus

(HEV) within the swine reservoir to public health risk mitigation strategies: A comprehensive review. Vet. Res. https://doi.org/10.1186/s13567-017-0436-3

Santarém, V.A., Farias, M.R., Tostes, R.A., 2005. Demodectic mange in fattening pigs in São Paulo, Brazil. Vet. Parasitol. 131, 169–171. https://doi.org/10.1016/j.vetpar.2005.03.029

Santos, L. de A.G. dos, Pinto, P.S.A., Moraes, M.P., Vanetti, M.C.D., Bevilaqua, P.D., Pinto, M.S., Dias, F.S., 2006. Pesquisa molecular e convencional de Listeria monocytogenes para o controle de qualidade da carne suína. Rev. Ceres 53, 481–489.

Schuppers, M.E., Stephan, R., Ledergerber, U., Danuser, J., Bissig-Choisat, B., Stärk, K.D.C., Regula, G., 2005. Clinical herd health, farm management and antimicrobial resistance in Campylobacter coli on finishing pig farms in Switzerland. Prev. Vet. Med. 69, 189–202. https://doi.org/10.1016/j.prevetmed.2005.02.004

Serdev, N., 2018. Botulinum Toxin. IntechOpen. https://doi.org/10.5772/intechopen.73809

Sheldon, B.W., Schuman, J.D., 1996. Thermal and Biological Treatments to Control Psychrotrophic Pathogens. Poult. Sci. 75, 1126–1132. https://doi.org/10.3382/ps.0751126

Silva, R.C. da, Souza, L.C. de, Langoni, H., Tanaka, E.M., Lima, V.Y. de, Silva, A.V. da, 2010. Risk factors and presence of antibodies to Toxoplasma gondii in dogs from the coast of São Paulo State, Brazil. Pesqui. Veterinária Bras. 30, 161–166. https://doi.org/10.1590/S0100-736X2010000200011

Silva, R.M. da, Uyhara, C.N.S., Silva, F.H., Espindola, N.M., Poleti, M.D., Vaz, A.J., Meirelles, F. V., Maia, A.A.M., 2012. Cysticercosis in experimentally and naturally infected pigs: parasitological and immunological diagnosis. Pesqui. Veterinária Bras. 32, 297–302. https://doi.org/10.1590/S0100-736X2012000400005

Black, R.E., Levine, M.M., Clements, M.L., Hughes, T.P., Blaser, M.J., 1988. Experimental Campylobacter jejuni Infection in Humans. J. Infect. Dis. 157, 472–479. https://doi.org/10.1093/infdis/157.3.472

Silva, M.R., Rocha, A. da S., Araújo, F.R., Fonseca-Júnior, A.A., de Alencar, A.P., Suffys, P.N., da Costa, R.R., Moreira, M.A.S., Guimarães, M.D.C., 2018. Risk factors for human mycobacterium bovis infections in an urban area of Brazil. Mem. Inst. Oswaldo Cruz. https://doi.org/10.1590/0074-02760170445

Smith, D.R., Novotnaj, K., Smith, G., 2010. Preharvest food safety: what do the past and the present tell us about the future? J. Agromedicine 15, 275–280. https://doi.org/10.1080/1059924X.2010.484671

Smith, T., 1899. The Thermal Death-Point Of Tubercle Bacilli In Milk And Some Other Fluids. J. Exp. Med. 4, 217–233.

Soares, P., 2011. Identificação do Circovírus tipo 2 e do Torque Teno Vírus em suínos de criações intensivas do Estado de Goiás. Master Thesis. Universidade Federal de

Goiás.

Songer, J.G., Uzal, F. a, 2005. Clostridial enteric infections in pigs. J. Vet. Diagn. Invest. 17, 528–536. https://doi.org/10.1177/104063870501700602

Stanley, K., Jones, K., 2003. Cattle and sheep farms as reservoirs of Campylobacter. J. Appl. Microbiol. 94, 104–113. https://doi.org/10.1046/j.1365-2672.94.s1.12.x

Suarez-Aranda, F., Galisteo, A.J., Hiramoto, R.M., Cardoso, R.P., Meireles, L.R., Miguel, O., Andrade, H.F.J., 2000. The prevalence and avidity of Toxoplasma gondii IgG antibodies in pigs from Brazil and Peru. Vet. Parasitol. 91, 23–32.

Sung, N., Collins, M.T., 1998. Thermal tolerance of Mycobacterium paratuberculosis. Appl. Environ. Microbiol. 64, 999–1005.

Tabit, F.T., 2018. Contamination, Prevention and Control of Listeria monocytogenes in Food Processing and Food Service Environments, in: Listeria Monocytogenes. InTech. https://doi.org/10.5772/intechopen.76132

Taira, K., Saeed, I., Permin, a., Kapel, C.M.O., 2004. Zoonotic risk of Toxocara canis infection through consumption of pig or poultry viscera. Vet. Parasitol. 121, 115–124. https://doi.org/10.1016/j.vetpar.2004.01.018

Takeuti, K.L., de Barcellos, D.E.S.N., de Andrade, C.P., de Almeida, L.L., Pieters, M., 2017. Infection dynamics and genetic variability of Mycoplasma hyopneumoniae in self-replacement gilts. Vet. Microbiol. 208, 18–24. https://doi.org/10.1016/j.vetmic.2017.07.007

Takeuti, K.L., Malgarin, C.M., Amaral, A.F., Barcellos, D.E.S.N. de, 2018. Frequency of Methicillin-Resistant Staphylococcus aureus (MRSA) in Fattening Pigs in the State of Rio Grande do Sul, Brazil. Acta Sci. Vet. 44, 4. https://doi.org/10.22456/1679-9216.80934

Tauxe, R. V., 1997. Emerging Foodborne Diseases: An Evolving Public Health Challenge. Emerg. Infect. Dis. 3, 425–434. https://doi.org/10.3201/eid0304.970403

te Giffel, M.C., Zwietering, M.H., 1999. Validation of predictive models describing the growth of Listeria monocytogenes. Int. J. Food Microbiol. 46, 135–149. https://doi.org/10.1016/S0168-1605(98)00189-5

Teske, S.S., Huang, Y., Tamrakar, S.B., Bartrand, T.A., Weir, M.H., Haas, C.N., 2011. Animal and Human Dose-Response Models for Brucella Species. Risk Anal. 31, 1576–1596. https://doi.org/10.1111/j.1539-6924.2011.01602.x

Teunis, P., Takumi, K., Shinagawa, K., 2004. Dose Response for Infection by Escherichia coli O157:H7 from Outbreak Data. Risk Anal. 24, 401–407. https://doi.org/10.1111/j.0272-4332.2004.00441.x

Thévenot, D., Dernburg, A., Vernozy-Rozand, C., 2006. An updated review of Listeria monocytogenes in the pork meat industry and its products. J. Appl. Microbiol. 101, 7–17. https://doi.org/10.1111/j.1365-2672.2006.02962.x

Thoen, C.O., Lobue, P.A., Enarson, D.A., Kaneene, J.B., de Kantor, I.N., 2009. Tuberculosis: a re-emerging disease in animals and humans. Vet. Ital. 45, 135–81.

Trabulsi, L.R., Keller, R., Gomes, T.A.T., 2002. Typical and Atypical Enteropathogenic Escherichia coli. Emerg. Infect. Dis. 8, 508–513. https://doi.org/10.3201/eid0805.010385

Uddin Khan, S., Atanasova, K.R., Krueger, W.S., Ramirez, A., Gray, G.C., 2013. Epidemiology, geographical distribution, and economic consequences of swine zoonoses: a narrative review. Emerg. Microbes Infect. 2, e92. https://doi.org/10.1038/emi.2013.87

Valença, R.M.B., Mota, R.A.., Anderlini, G.A.., de Faria, E.B.., Cavalcanti, É.F.S.T.F., Albuquerque, P.P.F., Neto, O.L.D.S., Guerra, M.M.P., 2011. Prevalência e fatores de risco associados à infecção por Toxoplasma gondii em granjas suinícolas tecnificadas no estado de alagoas. Pesqui. Vet. Bras. 31, 121–126. https://doi.org/10.1590/S0100-736X2011000200005

Van den Abeele, A.-M., Vogelaers, D., Van Hende, J., Houf, K., 2014. Prevalence of Arcobacter Species among Humans, Belgium, 2008–2013. Emerg. Infect. Dis. 20, 1746–1749. https://doi.org/10.3201/eid2010.140433

Varela, N.P., Friendship, R.M., Dewey, C.E., 2007. Prevalence of Campylobacter spp isolated from grower-finisher pigs in Ontario. Can. Vet. J. = La Rev. Vet. Can. 48, 515–7.

Vilanova, L.F.L.S., Rigueira, L.L., Perecmanis, S., 2018. Seroprevalence of hepatitis E virus infection in domestic pigs in the Federal District, Brazil. Arq. Bras. Med. Veterinária e Zootec. 70, 469–474. https://doi.org/10.1590/1678-4162-9455

Vilmar, G., Souto, K., Barbosa, V.C., Coelho, K.O., 2017. Botulismo no Brasil: Ocorrência e distribuição nos últimos dez anos.

Viott, A.M., Lage, A.P., Cruz, E.C.C., Guedes, R.M.C., 2013. The prevalence of swine enteropathogens in Brazilian grower and finish herds. Braz. J. Microbiol. 44, 145–51. https://doi.org/10.1590/S1517-83822013005000033

Vitral, C.L., Pinto, M.A., Lewis-Ximenez, L.L., Khudyakov, Y.E., Santos, D.R. dos, Gaspar, A.M.C., 2005. Serological evidence of hepatitis E virus infection in different animal species from the Southeast of Brazil. Mem. Inst. Oswaldo Cruz 100, 117–122. https://doi.org/10.1590/S0074-02762005000200003

von Laer, A.E., Lima, A.S. de, Trindade, P. dos S., Andriguetto, C., Destro, M.T., Silva, W.P. da, 2009. Characterization of Listeria monocytogenes isolated from a fresh mixed sausage processing line in Pelotas-RS by PFGE. Brazilian J. Microbiol. 40, 574–582. https://doi.org/10.1590/S1517-83822009000300021

Brachman, P.S., 2001. Control of Communicable Diseases Manual, 17th Edition, American Journal of Epidemiology. https://doi.org/10.1093/aje/154.8.783-a

Warth, J.F.G., Biesdorf, S.M., De Souza, C., 2012. Yersinia pseudotuberculosis O III causes diarrhea in Brazilian cattle, in: Advances in Experimental Medicine and Biology. https://doi.org/10.1007/978-1-4614-3561-7_13

WHO, 2019a. Emergencies preparedness, response. Botulism [WWW Document]. URL https://www.who.int/csr/delibepidemics/botulism/en/

WHO, 2019b. Emergencies preparedness, response [WWW Document]. List. - Spain. URL https://www.who.int/csr/don/16-september-2019-listeriosis-spain/en/

WHO, 2019c. Global tuberculosis report. Geneva.

WHO, 2018. Listeriosis [WWW Document]. Listeriosis. URL https://www.who.int/news-room/fact-sheets/detail/listeriosis (accessed 12.7.19).

WHO, 2015b. Endemicity of Taenia soluim, 2015 [WWW Document]. URL https://www.who.int/taeniasis/Endemicity_Taenia_Solium_2015.jpg

WHO, 2012. The global viwe of Campylobacteriosis. Utrecht.

Williamson, D.A., Baines, S.L., Carter, G., Gonçalves da Silva, A., Ren, X., Sherwood, J., Dufour, M., Schultz, M.B., French, N.P., Seemann, T., Stinear, T.P., Howden, B.P., 2017. Genomic insights into a sustained national outbreak of Yersinia pseudotuberculosis. Genome Biol. Evol. evw285. https://doi.org/10.1093/gbe/evw285

Yamaguti, M., Oliveira, R.C., Marques, L.M., Buzinhani, M., Buim, M.R., Neto, R.L., Guimarães, A.M.S., Timenetsky, J., 2015. Molecular characterisation of Mycoplasma hyorhinis isolated from pigs using pulsed-field gel electrophoresis and 16S rRNA sequencing. Vet. Rec. Open 2, e000093. https://doi.org/10.1136/vetreco-2014-000093

Yamasaki, L., Boselli-Grotti, C.C., Alfieri, A.A., Silva, E.O., Oliveira, R.L., Camargo, P.L., Bracarense, A.P.F.R.L., 2009. Alterações histológicas da pars esophagea de suínos e sua relação com Helicobacter spp. Arq. Bras. Med. Veterinária e Zootec. 61, 553–560. https://doi.org/10.1590/S0102-09352009000300005

Yang, S.-C., Lin, C.-H., Aljuffali, I.A., Fang, J.-Y., 2017. Current pathogenic Escherichia coli foodborne outbreak cases and therapy development. Arch. Microbiol. 199, 811–825. https://doi.org/10.1007/s00203-017-1393-y

Yehualaeshet, T., Graham, M., Montgomery, M., Habtemariam, T., Samuel, T., Abdela, W., 2013. Effects of temperature on the viability, growth and gene profile of Yersinia pseudotuberculosis and Yersinia enterocolitica inoculated in milk. Food Control 34, 589–595. https://doi.org/10.1016/j.foodcont.2013.05.025

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