Salmonella infections pose a serious threat to human and animal health.
Salmonella are commonly found in the bowels of healthy birds and mammals. In food, they are most commonly detected in eggs and raw pork, turkey and chicken. Usually Salmonella infections in humans are food-borne. While most of these gram-negative bacteria are largely species-specific, some have the potential to be transmitted to other species and / or humans.
In particular, Salmonella Typhimurium (STM) has this so-called “zoonotic” potential, i.e. the ability to infect various animal species and humans. STM is one of the major causes of human gastrointestinal disease (91,662 confirmed salmonellosis cases in 2017 in the EU). If the bacterium enters the bloodstream, it can be life-threatening. This pathogen increasingly spread in pig herds and is now the most frequently detected serovar of Salmonella in pigs. The monophasic serovar 1,4,,12:i:- of STM is also gaining in importance. It was first characterized in Spain 1997 and has nowadays a worldwide presence (Europe, USA, Thailand, Korea, Brazil). It is progressively described in outbreak descriptions.
In the EU, S 1,4,,12:i:- is considered an emergent serotype that causes human infections, with a remarkable increase in the incidence in pig and pork, surpassing even STM in the last years, when the detection in pig carcasses and pig meat are reported together.
(Source: The European Union summary report on trends and sources of zoonoses, zoonotic agents and food-borne outbreaks in 2017. EFSA J. 2018, 16, 5500)
Source: J. Campos at all., Non-typhoidal Salmonella in the Pig Production Chain: A Comprehensive Analysis of Its Impact on Human Health, Pathogens
Preventive measures should therefore start at the beginning of the production chain – in the breeding herd.
The best possible protective measure is the vaccination of sows and piglets. The vaccination program must be completed by an optimized cleaning and disinfection program, stricter biosecurity measures and optimized in-house management.
Visit https://www.pig333.com/salmonella/salmonella-in-pig-meat-from-the-abattoir-to-the-consumer_5914/ for more information about Salmonella in pork.
The Salmonella enterica species includes more than 2,600 serovars due to the broad variety of the antigens.
Salmonella are bacteria of the genus Salmonella, which belong to the family of Enterobacteria(ceae). There are two main species within the genus Salmonella: S. enterica and S. bongori. Salmonella enterica is further divided into six subspecies of which “enterica” is the most important.
99.5 % of the Salmonella strains that have been isolated and are of public health relevance belong to the species S. enterica.
Each subspecies is subdivided into serogroups, according to the composition of their bacterial cell wall antigens. That means, the somatic “O” antigen type is determined based on oligosaccharide chains associated with lipopolysaccharides of the cell wall. Due to the great variability, approximately 50 different serogroups have been identified to date.
Each serogroup is further subdivided into serovars, according to the classification of the flagellar H antigen and one of the capsular antigens.
Due to the protein structure and the associated high antigen variation of these H antigens, differentiation includes more than 2,600 serovars within the S. enterica species and approximately 1,500 of which belong to the enterica subspecies.
Some serotypes (mainly Typhimurium and Enteritidis) can be distinguished even further by their phage type. This is a classification based on the susceptibility to a particular set of bacteriophages (viruses that attack bacteria).
Based on the combination of somatic antigens (O) and flagellar antigens (H), a specific antigenic formula is obtained for each serotype.
Under “a” all somatic antigens are summarized, expressed as numbers for the serogroup of Salmonella Typhimurium. Summarized under “b“ and “c” are all flagellar antigens.
In one and the same Salmonella serovar, two different H antigens may occur, which can be distinguished in phase 1 (H1) and phase 2 (H2). Which of the two phases (flagella) or whether both phases are formed simultaneously depends on which of the responsible genes is active. H1 is always expressed with letters, and H2 always with numbers. If there is only H1, the serovar is named “monophasic”. The non existent H2 is indicated with a “minus”.
Monophasic serovars are of increasing importance. They were first characterized in Spain 1997. As they have a worldwide presence (Europe, USA, Thailand, Korea, Brazil) the description in Salmonella pig outbreaks increases.
Some Salmonella serovars are „host-adapted“, many others, however, are not. For example, Salmonella Typhimurium is not „host-adapted“ and can infect several species, which increases the zoonotic risk.
Salmonella pig infection can be caused by the pig-adapted serovar Salmonella Choleraesuis, but also by many other serovars that are not specific to pigs, mainly Salmonella Typhimurium, but also S. Rissen, S. Derby, and S. Anatum, among others.
Nonetheless, it is worth mentioning that people can also become infected with S. Choleraesuis and get very seriously ill from it.
Therefore the resulting serovar Choleraesuis reservoir in pigs is a concern, not only because of its potential for causing Salmonella infection in young pigs but also because of its public health implications for humans.
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Learn more about the infection process and the pathogen.
Salmonella are widespread bacteria with high tenacity that can enter the barn in many ways. They can survive there for long periods, posing a risk of Salmonella infection to pigs.
Among all Salmonella serovars, S. Typhimurium (STM) is of particular importance. This non-species-specific pathogen has become increasingly widespread on pig farms with a prevalence of around 30% of breeding farms and is most commonly detected in bacteriological testing to identify these Salmonella infected pigs.
(Source: EFSA baseline survey, 2008)
STM is usually introduced to the herd by bought-in Salmonella infected pigs. It might also be brought into a herd in a variety of other ways, for example by rodents, birds, dogs, cats, wild animals, or inanimate vectors such as contaminated feed, boots, clothing, equipment or vehicles. Once the stock is infected, Salmonella are shed by the pigs and the Salmonella infection circulates in the farm as the epidemiological unit.
How pigs become infected
Replication to about 107 organisms per gram of intestinal content is required for lesion production in pigs infected with S. Typhimurium, a finding that probably also applies to other serotypes causing enterocolitis.
The ability to invade is a requirement for pathogenesis and is encoded by a serotype-specific plasmid. During the invasion process, there is induction of synthesis of new proteins that enhance intracellular survival. The predominant portal of entry into the submucosa may occur at Peyer´s patches. Attachment of the bacteria to epithelial receptors triggers microfilament-controlled uptake, vacuole formation, vacuole transport through the cell cytoplasm, and entry into the laminal propria via exocytosis through the basement membrane.
Colon, salmonella infection, Source: Ceva
Spread to mesenteric lymph nodes is rapid, occurring within 24 hours after oral challenge. Early intestinal inflammation is considered a key feature of pathogenesis for enteric forms of Salmonella pig infection. In clinical cases mucosal inflammation and necrosis, as well as septicemia occur in concert with the diarrhoea in Salmonella infected pigs.
Source: Carlson et al. (2012) Salmonellosis, pg. 821-833, in: Diseases of swine, 10th edition, John Wiley & Sons, Inc.
It is important to remember the high tenacity of Salmonella on surfaces and in the environment. In particular, the fact of long persistence in dust leads to an almost inexhaustible source of infection with Salmonella in pigs in many farms. But also damp corners, which are not easily accessible for cleaning and disinfection, lead again and again to a long retention of Salmonella in the farm with numerous possibilities of re-infection.
|Location||Time to survival|
|Smooth metal surfaces||14 days|
|Dried faeces||2.5 years|
|Liquid waste||2.7 years|