Virulence genes of salmonella

Food Microbiology

Foodborne Pathogens: Hygiene and Safety View all 49 Articles

University of Teramo, Italy

Faculty of Veterinary Medicine, University of Belgrade, Serbia

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Original Research ARTICLE

1 Department of Food Science, Faculty of Food Science and Technology, Universiti Putra Malaysia, Serdang, Malaysia
2 Laboratory of Food Safety and Food Integrity, Institute of Tropical Agriculture and Food Security (ITAFoS), Universiti Putra Malaysia, Serdang, Malaysia
3 Department of Veterinary Pathology and Microbiology, Faculty of Veterinary Medicine, Universiti Putra Malaysia, Serdang, Malaysia
4 Department of Diagnostic and Allied Science, Faculty of Health and Life Science, Management and Science University, Shah Alam, Malaysia
5 Division of Applied Biomedical Sciences and Biotechnology, School of Health Sciences, International Medical University, Kuala Lumpur, Malaysia
6 Department of Agricultural and Food Science, Faculty of Science, Universiti Tunku Abdul Rahman, Kampar, Malaysia
7 Novel Antibiotic Laboratory, School of Diagnostic and Applied Health Sciences, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia
8 Department of Science and Technology Studies, Faculty of Science, University of Malaya, Kuala Lumpur, Malaysia

The aim of the present study was to investigate the prevalence of Salmonella spp., Salmonella Enteritidis and Salmonella Typhimurium in retail beef from different retail markets of Selangor area, as well as, to assess their pathogenic potential and antimicrobial resistance. A total of 240 retail beef meat samples (chuck = 60; rib = 60; round = 60; sirloin = 60) were randomly collected. The multiplex polymerase chain reaction (mPCR) in combination with the most probable number (MPN) method was employed to detect Salmonella spp., S. Enteritidis and S. Typhimurium in the meat samples. The prevalence of Salmonella spp., S. Enteritidis and S. Typhimurium in 240 beef meat samples were 7.50, 1.25, and 0.83%, respectively. The microbial loads of total Salmonella was found in the range of 5 cfu/mL (data not shown). The optimized mPCR reaction mixture (25 μL) contained 2 μL of DNA template, 5 μL of 5 × PCR buffer, 2.5 μL of 25 mM MgCl₂, 0.5 μL of 10 mM deoxynucleotide triphosphate (dNTP), 0.5 μL of 1.2 μM primer mix and 14.2 μL of deionized water. The mixture was then treated with 0.3 μL (1.5 U) Taq DNA polymerase. PCR amplification was performed in triplicate with the following conditions: initial denaturation at 94°C for 2 min, 30 cycles of denaturation at 94°C for 45 s, annealing at 53°C for 1 min, extension at 72°C for 1 min and final extension at 72°C for 7 min. The positive controls used were S. Typhimurium ATCC 14028 and S. Enteritidis ATCC 13076. Escherichia coli ATCC 25922 was used as a negative control.

The turbid MPN tubes were confirmed to be Salmonella by plating on selective CHROMagar Salmonella (CHROMagar Microbiology, Paris, France) and Xylose Lysine Deoxycholate (XLD) (Merck, Darmstadt, Germany) agar plates, and incubated at 37°C for 24 h. All the Salmonella isolates were then serotyped by slide agglutination using polyvalent “O” and “H” antisera (BD, Franklin Lakes, USA) at Veterinary Research Institute (VRI), Ipoh, Malaysia in accordance with the Kauffmann-White scheme.

The antimicrobial susceptibility was evaluated according to Clinical and Laboratory Standarts Institude (2012) by using disc diffusion method. Briefly, isolates were cultured aerobically in 10 mL Mueller-Hinton (MH) broth (Merck, Darmstadt, Germany) at 37°C for 24 h. Overnight cultures, grown on MH broth (OD adjusted to 0.5 MacFarland unit), were swabbed evenly with sterile non-toxic cotton swab on MH agar plates and left to dry for 2 to 4 min. Then, antimicrobial sensitivity discs were placed on the culture by using a disk dispenser and incubated at 37°C for 24 h. The tested antimicrobials were amoxicillin/clavulanic acid (AMC, 30 μg), amoxycillin (AML, 30 μg), ceftazidime (CAZ, 30 μg), cephazolin (KZ, 30 μg), ciprofloxacin (CIP, 5 μg), erythromycin (E, 15 μg), chloramphenicol (C, 30 μg), ampicillin (AMP, 10 μg), penicillin (P, 10 μg), streptomycin (S, 10 μg), tetracycline (TE, 30 μg), kanamycin (K, 30 μg), gentamicin (CN, 10 μg), vancomycin (VA, 30 μg), nalidixic acid (NA, 30 μg), and suphamethoxazole/trimethoprim (SXT, 25 μg) (Oxoid, Hamphire, United Kingdom). The multiple antibiotic resistance (MAR) index was calculated as “a/b,” where “a” the number of antibiotics for a particular isolate was resistant and “b” the total number of antibiotics tested (Krumperman, 1983).

All Salmonella isolates collected in this study were screened for the presence of virulence genes using PCR. The primers, the size in base pairs of the respective amplification products and the references used for detection of six virulence genes are presented in Table 1. The virulence genes under study were invA, pefA, hilA, sopB, stn, and spvC. Positive (S. Typhimurium ATCC 14028 and S. Enteritidis ATCC 13076) and negative control (E. coli ATCC 25922) were conducted in the detection procedure. To evaluate the reproducibility of the experiments, PCR amplification and electrophoresis experiments were carried out in triplicate.

Table 1. PCR primers used for amplification of virulence genes in Salmonella isolates.

All measurements were carried out in triplicate. Minitab (v. 14) statistical package (Minitab Inc., State College, PA) was used to determine if there was any significant difference between the prevalence of Salmonella in beef meat from wet market and hypermarket. For all analysis, P Keywords: beef meat, Salmonella, multiplex PCR, prevalence, antimicrobial resistance, virulence gene

Citation: Thung TY, Radu S, Mahyudin NA, Rukayadi Y, Zakaria Z, Mazlan N, Tan BH, Lee E, Yeoh SL, Chin YZ, Tan CW, Kuan CH, Basri DF and Wan Mohamed Radzi CWJ (2018) Prevalence, Virulence Genes and Antimicrobial Resistance Profiles of Salmonella Serovars from Retail Beef in Selangor, Malaysia. Front. Microbiol. 8:2697. doi: 10.3389/fmicb.2017.02697

Giovanna Suzzi, Università di Teramo, Italy

Milan Zivko Baltić, Faculty of Veterinary Medicine, University of Belgrade, Serbia
Giorgia Perpetuini, Università di Teramo, Italy

Salmonella enterica, one of the main causes of gastrointestinal infections, modulates its virulence gene expression, adapting it to each stage of the infection process, depending on the free iron concentration found in the intestinal epithelium of its host. Researchers at Universitat Autònoma de Barcelona (UAB) have demonstrated for the first time that the pathogen activates these genes through the Fur protein, which acts as a sensor of iron levels in its surroundings.

The research, published online in the journal PLoS ONE and entitled "Fur activates the expression of Salmonella enterica pathogenicity island 1 by directly interacting with the hilD operator in vivo and in vitro", was carried out by the Molecular Microbiology Group of the UAB Department of Genetics and Microbiology and coordinated by Dr Jordi Barbé. Dr Juan Carlos Alonso from the National Biotechnology Centre also collaborated in the research group.

Iron is an essential part of the development of almost all living organisms. This is why all organisms have developed an iron uptake system which guarantees that they can acquire it from their external environment. However, too much iron in the cell interior can have harmful effects and organisms have systems to control this as well.

In vertebrates, this control produces a first defence barrier known as nutritional immunity which limits the amount of free iron found in biological fluids and prevents the development of pathogens. Only the upper intestinal track, given its anaerobic condition, presents appreciable levels of free iron. In the majority of gram-negative bacteria, such as Salmonella enterica, the control of iron levels is carried out by the Fur protein (Ferric Uptake Regulator), which interacts with the DNA and adjusts the production of uptake and storage systems of this element to the cell's cytoplasm.

Salmonella enterica is one of the most common bacterial pathogens associated with foodborne illnesses and is responsible for a number of diseases, from gastroenteritis to systemic infections affecting a wide variety of animals, including humans. During the first stages of infection, the bacterium enters the host through the intestinal epithelium thanks to the presence of a complex system of proteins called T3SS. The activation of T3SS however requires a large amount of energy and therefore depends on many systems to control and make sure its expression is produced just at the right moment.

The study published by UAB researchers indicates that one of the external signals controlling T3SS activation is the level of free iron of the host and that this control is carried out by the Fur protein. Thus, thanks to the Fur protein, when the bacterium detects that levels are high it interacts with its DNA and activates T3SS expression which allows it to invade the epithelium. Once it penetrates the epithelial barrier, however, the levels of free iron reduce drastically due to all of the iron secretion systems the host has at its disposal. In this case T3SS remains silent and thus avoids an unnecessary expenditure of energy.

The study demonstrates for the first time that Fur not only acts as an iron level sensor and regulator of this element in the cell's interior, but also helps the pathogen detect its location during the infection process, acting as a direct activator for the invasion. The research reinforces the idea that Fur is capable of modulating gene expression, adapting it to the needs of each stage of the infection.

The results obtained demonstrate that delving deeper into the study at molecular level of the interactions between host - pathogen in relation to iron must lead in the future to the development of new strategies in the design of vaccines, as well as discover new targets for antibacterial action to fight against infectious diseases. In fact, the Molecular Microbiology Group of the UAB Department of Genetics and Microbiology has studied for years bacterial mechanisms of divalent cation uptake and its control systems. This line of research has given way to the publication of several scientific articles in prestigious journals, and has led to the patenting and licensing of a vaccine for the bacterial pathogen Pasteurella multocida based on its iron uptake methods.

Researchers have discovered a novel mechanism in Salmonella that affects its virulence and its susceptibility to antibiotics by changing its production of proteins in a previously unheard of manner. This allows Salmonella to selectively change its levels of certain proteins to respond to inhospitable conditions.

Although the mechanism had not been recognized before, the scientists were intrigued to find evidence of a similar mechanism in all five kingdoms of life - animals, plants, fungi, protista, and monera.

The findings were published today, July 29, in Molecular Cell. The senior author of the study is Dr. Ferric C. Fang, professor of microbiology, laboratory medicine, and medicine at the University of Washington (UW). Fang also directs the Clinical Microbiology Laboratory at Harborview Medical Center in Seattle. The lead author is William Wiley Navarre, who began the study as a postdoctoral fellow in the Fang lab and is now an assistant professor at the University of Toronto.

Salmonella enters the gut when people eat contaminated food, and can sometimes spread to other parts of the body. Illness outbreaks and grocery recalls related to Salmonella are often in the news. Babies, young children, the elderly, and people with cancer or HIV are especially prone to severe illness from Salmonella.

Salmonella is adaptable and can withstand many of the body's attempts to fight it. The bacteria live and multiply in a special compartment inside the cells of an infected person or animal. Salmonella can alter its physiology as it moves from a free-swimming life to its residence in a host cell. Salmonella's metabolism also changes over time to make use of the nutrients available in the host cell, and to survive damage from the build-up of oxidants and nitric oxide in the infected cell.

While screening mutant Salmonella that were resistant to a form of nitric oxide that normally stops the bacteria from dividing, Navarre, Fang and their research collaborators found mutations in two little-known genes. These are the closely linked poxA and yjeK genes. In a number of bacteria, these two genes are associated with a third gene that encodes the Bacterial Elongation Factor P, which is involved in protein production.

The researchers discovered that these three genes operate in a common pathway that is critical for the ability of the Salmonella bacteria to cause disease and resist several classes of antibiotics. Salmonella with mutations in either the poxA gene or the yjeK genes, the study noted, appear to be nearly identical and show similar changes in proteins involved in metabolism. Strains with mutations in both genes resemble the single mutant strains, an observation that suggests the two genes work in the same pathway.

The mutant strains exhibited many abnormalities under stressful conditions.

"The wide spectrum of compounds that dramatically inhibited the growth of these mutant strains suggest that the defect lies in a general stress response," the researchers noted. The mutant bacteria measurably differed from the wild-type Salmonella under 300 different conditions. In addition, their aberrant production of virulence factors reduces their ability to survive in the host.

The researchers' analysis also suggests that the way poxA and yjeK modify the bacterial protein elongation factor is essential in the production of proteins that allow the bacteria to use alternative energy sources when they are deprived of nutrients, as occurs after they enter host cells.

Unexpectedly the researchers found that the Salmonella with mutations in poxA and yjeK continued to respire inappropriately under nutrient-poor conditions in which wild-type Salmonella cease respiration.

Perhaps the mutant strains don't know when to quit. Wild-type Salmonella might enter a state of suspended animation to weather harsh conditions, whereas the mutants fail to respond properly to environmental stress. The fact that the mutants continue to respire when they are in dire straits might lead to the production of toxic oxygen-containing compounds.

"This might explain," the authors suggested, "why the mutants are broadly sensitive to a large number of unrelated compounds and cellular stresses."

The researchers also noticed a resemblance between the astounding manner in which the poxA gene modifies the bacterial elongation factor to regulate stress resistance, and the way a similarly acting factor is regulated in plant and animal cells.

During the manufacture of a protein, transfer RNA, also called tRNA, normally places an amino acid at the end of a growing chain of protein building blocks. A certain type of enzyme normally hands the tRNA the amino acid for it to place. However, in this study, researchers have shown for the first time that the poxA enzyme steps in and directly attaches an amino acid to the Elongation Factor P protein, rather than to the tRNA.

Fang said, "Sometimes it seems as if the most basic discoveries in biology have already been made. It was fun and unexpected to learn something new about a process as fundamental as protein synthesis."

"This is an interesting illustration of molecular evolution," Fang continued. "This essential, but previously unrecognized mechanism, for regulating the production of proteins appears to have been conserved over evolutionary time and continues to take place in cells belonging to all five kingdoms of life."

Future studies in his lab will address the specific reasons behind the defective stress response in poxA- and yjeK-deficient bacteria and the explanation for its different effects on the amounts of individual proteins. The lab will also look further into the roles of the normal poxA and yjeK proteins, the intriguing way in which the bacterial elongation protein is modified, the apparent universality of this protein-modifying mechanism in living cells and its conservation throughout the course of evolution.

Salmonella enterica, one of the main causes of gastrointestinal infections, modulates its virulence gene expression, adapting it to each stage of the infection process, depending on the free iron concentration found in the intestinal epithelium of its host. Researchers at Universitat Autònoma de Barcelona (UAB) have demonstrated for the first time that the pathogen activates these genes through the Fur protein, which acts as a sensor of iron levels in its surroundings.

The research, published online in the journal PLoS ONE, was carried out by the Molecular Microbiology Group of the UAB Department of Genetics and Microbiology and coordinated by Dr Jordi Barbé. Dr Juan Carlos Alonso from the National Biotechnology Centre also collaborated in the research group.

In vertebrates, this control produces a first defence barrier known as nutritional immunity which limits the amount of free iron found in biological fluids and prevents the development of pathogens. Only the upper intestinal track, given its anaerobic condition, presents appreciable levels of free iron. In the majority of gram-negative bacteria, such as Salmonella enterica, the control of iron levels is carried out by the Fur protein (Ferric Uptake Regulator), which interacts with the DNA and adjusts the production of uptake and storage systems of this element to the cell's cytoplasm.

Salmonella enterica is one of the most common bacterial pathogens associated with food-borne illnesses and is responsible for a number of diseases, from gastroenteritis to systemic infections affecting a wide variety of animals, including humans. During the first stages of infection, the bacterium enters the host through the intestinal epithelium thanks to the presence of a complex system of proteins called T3SS. The activation of T3SS however requires a large amount of energy and therefore depends on many systems to control and make sure its expression is produced just at the right moment.

The results obtained demonstrate that delving deeper into the study at molecular level of the interactions between host -- pathogen in relation to iron must lead in the future to the development of new strategies in the design of vaccines, as well as discover new targets for antibacterial action to fight against infectious diseases. In fact, the Molecular Microbiology Group of the UAB Department of Genetics and Microbiology has studied for years bacterial mechanisms of divalent cation uptake and its control systems. This line of research has given way to the publication of several scientific articles in various journals, and has led to the patenting and licensing of a vaccine for the bacterial pathogen Pasteurella multocida based on its iron uptake methods.

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Сальмонеллы - лактозонегативные грамотрицательные палочки удлиненной формы, с закругленными концами длиной 1. 4 и шириной 0,3. 0,8 мкм. Подавляющее большинство представителей рода Salmonella подвижны (за исключением S. gallinarum-рullorum), органами их движения являются 4-5 жгутиков, расположенных равномерно по всей поверхности микробной клетки [1, 3, 12]. Геном сальмонелл состоит из одной кольцевой хромосомы размером 4,8 млн пар нуклеотидов и ряда плазмид от 3 до 100 тысяч пар нуклеотидов (т.п.н.), при этом обнаружено значительное сходство между плазмидами вирулентности различных серотипов [8, 43, 46].

Геном серовара S.typhimurium полностью расшифрован в 2001 г.[4, 31, 42]. Ранее было установлено, что большинство штаммов S.typhimurium состоят из вирулентных плазмид размером около 90 т.п.н. [18, 19, 25].

Плазмида S. dublin размером 76 т.п.н., включает 3 района вирулентности [43]. По данным азиатских ученых плазмида S. choleraesuis варьирует от 50 до 110 т.п.н., а у S. enteritidis - 60 т.п.н. [11]. Известно, что некоторые штаммы сальмонелл не имеют плазмид вирулентности, при этом они не теряют своей инвазивной способности [9, 24]. Хромосома S. enterica очень сходна с таковой E.coli и состоит из единственной циркулярной молекулы ДНК размером около 4 млн пар оснований. Среднее суммарное содержание в ней цитозина и гуанина составляет 52% [4].

Информацию о ферментах, ответственных за синтез и сборку полисахаридных частей О-антигена, кодирует кластер генов в локусе rfb хромосомы. Изменения О-антигена происходят в результате лизогенной конверсии хромосомных генов бактериофагами или мутаций [4, 39].

Образование жгутиков зависит от 3 классов генов, функции которых контролируются рядом регуляторов, в т.ч. сигма-фактором FliA и его антагонистом антисигма-фактором FlgM. У многих сероваров сальмонелл 2 набора генов флагеллина, из которых в экспрессии белка задействована только 1 аллель. Опероны, контролирующие синтез каждой фазы жгутикового антигена, также кодируют репрессор синтеза другой фазы флагеллина.

У S. enterica имеется 4 пильных оперона: fim (типа 1), lpf (длинных полярных пилей), pef (плазмидокодируемых пилей) и agf (тонких агрегативных пилей) [4].

Хромосомный локус inv включает 14 генов, наиболее известными из них являются invA, invE. Продукты данных генов необходимы для инвазии бактерий через эпителиальные клетки кишечника Часть этих генов гомологична генам E.coli, регулирующим сборку жгутиков [16, 28].

В тесной связи с локусом inv функционирует рядом лежащий локус Spa. Между его 12 генами и генами плазмиды вирулентности шигелл выявлена высокая степень идентичности и сходная последовательность локализации. Сходство ряда генов этих локусов с генами LcrD, LcrE и YscA йерсиний позволяет предположить, что транспортировка инвазивных протеинов сальмонелл осуществляется по тем же механизмам, что и экспорт жгутиковых белков.

Упомянутые локусы включают в себя острова патогенности, обуславливающие генетическое разнообразие сальмонелл. Сальмонеллы содержат ряд генов вирулентности, известных как модули или острова патогенности. На сегодняшний день известен двадцать один модуль SPI [35, 42]. Остров патогенности-1 (SPI-1) представляет собой участок ДНК размером 40 тысяч пар оснований [16]. Данный модуль кодирует 33 протеина, в т.ч. компоненты секреционной системы типа III (T3SS), регуляторные и секреционные эффекторные протеины, а также опероны. T3SS используются бактериями для введения белков, называемых эффекторами, непосредственно внутрь клеток-хозяев, которые будут выступать в качестве медиаторов вторжения клеток и модификаций, способствующих внутриклеточному росту [35]. Изменение генов invA, invF, invG, hilA, sipC, sipD, spaR и orgB этой системы ведет к 16-100-кратному снижению вирулентности S. enterica. Остров патогенности 2 (SPI-2) имеет размер 40 тысяч пар оснований. Он кодирует второй вид секреционной системы типа III, который участвует во внутриклеточной выживаемости и системе сборки жгутиков. Приобретение SPI-2 позволило сальмонеллам перейти от выживания к репродукции в клетках хозяина и от местной инфекции пищеварительного тракта к системной диссеминации. Остров патогенности-3 (SPI-3) имеет размер 36 тысяч пар оснований, участвует в процессе внутриклеточного выживания и кодирует транспорт магния. Только один его ген (mgtC) ассоциирован с вирулентностью - кодируемый им продукт обеспечивает рост бактерии в макрофагах и проявление системной вирулентности за счет адаптации к условиям низкого содержания ионов магния и низкому рН фагосомы [7]. SPI - 4 представляет собой 24 т.п.н. и участвует в адгезии к эпителиальным клеткам [17, 33, 34, 44]. SPI - 5 является небольшим островом патогенности размером менее 8 т.п.н., он необходим для инвазирования эпителия кишечника [44].SPI - 6 кодирует работу T6SS, safABCD фимбриальный кластер генов и инвазивный pagN [15, 41]. SPI - 7 самый большой остров патогенности на сегодняшний день (отсутствует в S . Typhimurium, но присутствует в S .Typhi) [35]. В S . Typhi размер данного модуля составляет 134 т.п.н., что соответствует примерно 150 генов [22, 36]. Этот остров содержит гены биосинтеза капсульного антигена Vi, отвечающего за вирулентность бактерии [23, 47]. SPI - 8 представляет собой фрагмент ДНК и является частью SPI-13 [35]. SPI-9 представляет собой локус размером 16 т.п.н. и содержит три гена, кодирующих T1SS [33, 34]. SPI-10 наиболее полно изучен в S. typhi, состоит из 33 т.п.н. и включает несколько функционально несвязанных генов [6, 13, 35]. Опыты Haneda et al.(2009) показали, что удаление SPI-10 из S. typhimurium штамм 14028 приводит к ослаблению вирулентности сальмонелл [21]. SPI-11 был первоначально идентифицирован в геномной последовательности серовара S. choleraesuis, его размер соответствовал 14 т.п.н. Несколько короче данный остров патогенности в S. typhimurium (6,7 т.п.н.) и в S. typhi (10 т.п.н.). SPI-11 участвует в интрамакрофагальной выживаемости сальмонелл [10, 20, 32]. SPI - 12 состоит из 15,8 т.п.н. в S. typhimurium и 6,3 т.п.н. в S. typhi, кодирует специфические О-антигены [22, 31, 39]. SPI - 13 был первоначально идентифицирован в серотипе S. gallinarum. Состоит из 25 т.п.н., однако 8 т.п.н. несут различную функциональную нагрузку в разных серотипах сальмонелл. Отвечают за гены, кодирующие работу лиазы, гидролазы, оксидазы; вирулентность бактерии; репликацию внутри макрофагов [21, 37, 38]. SPI-14 соответствует 9 т.п.н., (отсутствует в S. Typhi) [33, 37]. Функция SPI-14 на сегодняшний день невыяснена, но известно, что данный остров патогенности кодирует цитоплазматические белки [14]. SPI-15 остров патогенности размером 6,5 т.п.н. (отсутствует в S. typhimurium). SPI - 16 находится в S. typhimurium и S. typhi, размер его составляет 4,5 т.п.н. SPI-17 кодирует остров в 5 т.п.н. (отсутствует в S. typhimurium) [42]. SPI-18 был идентифицирован в S. Typhi, размером 2,3 т.п.н., в опытах in vitro установлено, что модуль отвечает за инвазию сальмонелл в эпителиальные клетки кишечника человека. Другие острова патогенности не были идентифицированы как модули SPI, но они кодируют гены, ответственные за вирулентность бактерии. [5, 26, 27].

Регуляторная система PhoP/PhoQ регулирует изменения липополисахаридов самой бактерии, что повышает ее резистентность к меняющимся условиям внешней среды и антимикробным препаратам, а также ведет к затруднению распознавания липополисахарида иммунной системой.

Гены spv (spvR, spvA, spvB, spvC и spvD) у S.typhimurium и S.enteritidis локализуются в крупной (размером 50-100 тысяч пар оснований) плазмиде, а у остальных сероваров в хромосоме. Кодируемые ими факторы обеспечивают распространение сальмонелл по организму, репродукцию в моноцитах, а также индукцию апоптоза последних.

Ген shdA размером в 6105 пар оснований проявляет гомологию с участками ДНК шигелл и диареегенных штаммов E.coli. Он обеспечил S. enterica адаптацию к теплокровным животным и регулирование интенсивности выделения бактерии с фекалиями.

Уникальный ген sifA состоит из 300 пар оснований и имеет более низкое суммарное содержание гуанина и цитозина (41%), чем другие части ДНК. Отвечает за образование филаментов, связывающих агента с мембраной фагосомы клеток эукариотов [4].

Итак, патогенные свойства микроорганизмов детерминированы в геноме. Причем некоторые из них имеют одну группу детерминант, другие - четыре, чем и определяются различия в патогенности сальмонелл [2].

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