What does salmonella enteritidis need to survive

Histological examination reveals fatty degeneration of the liver, occasionally accompanied by areas of necrosis, disintegration of muscle fibers, and congestion and perivascular infiltration of mononuclear cells in the kidneys [ 47 ]. Salmonella Pullorum and S. Gallinarum have been eradicated in developed regions including the US, Canada, and Western Europe but are still problems in other parts of the world. Control programs that incorporated good hygiene management, biosecurity enforcement, serological tests, and slaughter policies helped with the eradication of these pathogens.

In the s, poultry breeders and hatchers in US implemented tests blood analysis, tube agglutination, and rapid serum test for S. Gallinarum on a regular basis while uniform national management standards were adopted. Furthermore, in the s vaccination was implemented to control Pullorum disease and fowl typhoid.

Two decades later both diseases were eradicated and by there was no evidence of infection in commercial poultry [ 43 , 48 , 49 ]. It has been suggested that clearing poultry flocks of S. Gallinarum and S. Pullorum opened a favorable niche for S. Enteritidis [ 50 — 52 ]. The use of mathematical models with data from Europe and US suggests that S. Gallinarum excluded S. Enteritidis from poultry [ 53 ]. Coincidently, S. Enteritidis detection was on the rise after eradication of S.

Pullorum, and by the s it was the most frequently reported serovars in the US. Unlike avian Salmonella pathogens, serovar Enteritidis has rodents as reservoirs, making it more difficult to control on the farms. Enteritidis and S. Gallinarum are antigenic similar, both belonging to serogroup D1 possessing a similar lipopolysaccharide structure and O9 antigens. When commercial flocks were cleared from S. Gallinarum, serovar Enteritidis was able to colonize chickens without noticeable signs of disease.

It is believed that seropositive S. Pullorum had an enhanced immunity dominant O9 antigen that protected against S. Enteritidis infection [ 50 ]. Clinically, salmonellosis may be manifested as gastroenteritis, septicemia, or enteric fever.

Enteric fevers are caused by the human-specific pathogens S. Infection severity may vary by the resistance of each individual and the immune system as well as the virulence of the Salmonella isolate. Salmonella Typhi is a motile, nonlactose fermenting bacillus that causes most endemic and epidemic cases of typhoid fever globally [ 54 , 55 ]. Enteric fevers cause , deaths and 22 million illnesses per year, with the highest incidence happening in Southeast and Central Asia where it is endemic [ 56 ].

Like enteric fevers, nontyphoidal salmonellosis NTS is spread via the fecal-oral route, but estimated cases of NTS worldwide greatly surpass those for enteric fevers. Unlike Typhi and Paratyphi, nontyphoidal Salmonellae are not human-restricted. Many serovars closely related to foodborne outbreaks include S. Typhimurium, S. Enteritidis, S. Newport, and S. Heidelberg and have reservoirs in farm animals [ 9 , 58 ]. Among other foodborne pathogens, NTS is the leading cause of death and hospitalizations [ 59 ].

In NTS, cases are characterized by gastroenteritis or bacteraemia; symptoms may involve nausea, vomiting, and diarrhea and are typically self-limiting lasting approximately 7 days. Salmonella can also induce chronic conditions including aseptic reactive arthritis and Reiter's syndrome.

Different Salmonella serovars may demonstrate unique reservoirs and pathogeneses. It is still poorly understood why a few Salmonella serovars are responsible for a majority of human diseases, but nearly all of them belong to subspecies enterica. In a global survey, serotypes Enteritidis and Typhimurium were the most prevalent serovars of all isolates [ 60 ]. The biggest difference among severity and treatment methods is between enteric fever salmonellae and nontyphoid salmonellae Table 7.

It is suggested that a combination of factors specific to each serovar including the presence of plasmid virulence genes spv , surface cell structure, flagellin, and pathogenity islands SPIs is involved in severity of salmonellosis.

It has been demonstrated that S. Seftenberg and S. Litchfield have large deletions in invasion related genes, which might have been the result of a selective advantage in the intestinal environment [ 61 ]. Jones et al. From these data, most illnesses were related to serovars Typhimurium, Enteritidis, and Newport, while fatality rates reported were in most cases related to serovars Dublin, Muenster, and Choleraesuis.

Resistant Salmonella strains are commonly found in food animal sources [ 63 , 64 ]. Mismanagement of antimicrobial agents for treatment in humans and animals and the use of growth promoters in livestock have promoted antimicrobial resistance in Salmonellae [ 64 , 65 ]. The occurrence of Salmonella serovars resistant to quinolones, fluoroquinones, and third generation cephalosporins which are medically significant treatments has increased [ 66 — 68 ].

Serovars Newport, Heidelberg, Dublin, and I4, [ 5 ], i:- were also shown to be resistant to various antimicrobial groups Table 8.

In terms of multidrug resistance more than 5 antimicrobials the most prevalent serovars of epidemiological importance are Typhimurium, Heidelberg, Dublin, Paratyphi B, and I4, [ 5 ], i:- Table 9. Although S. Enteritidis is highly prevalent in human infections; it has lower antimicrobial resistance compared to other serovars. Antimicrobial resistance in Salmonella can be associated with horizontal transference of antibiotic resistant genes characteristically found on mobile genetic elements among Salmonella strains and other Enterobacteria or by clonal spread of antimicrobial drug resistant serovars that are particularly effective in worldwide dissemination [ 69 — 72 ].

Examples of nontyphoidal Salmonella isolates from US patients and resistance profile of specific antimicrobial agents [ 75 ]. Examples of nontyphoidal Salmonella isolates from US patients and their multidrug resistance profile [ 75 ]. Farm animals have been a common source of isolation for antimicrobial resistant Salmonella serovars [ 76 — 78 ].

A predominantly infectious S. Typhimurium DT emerged in the s and has managed to spread worldwide. This serovar commonly carries chromosomally based resistance to five antimicrobials ACSSuT and it is believed that it was disseminated worldwide by human travel and then spread locally by the absence of effective antimicrobials [ 76 , 79 , 80 ].

In human isolates from S. It is believed that horizontal transmission of virulence genes in multidrug resistant Salmonella strains can increase virulence and invasiveness and cause higher mortality rates compared to susceptible Salmonella [ 79 , 81 , 82 ]. Salmonellosis in cattle is caused by numerous serovars, with S. Typhimurium and S. Dublin being the most common [ 83 ]. Salmonella Dublin serovar is commonly detected in calves and adult cattle.

Most infections are introduced into Salmonella free herds by the purchase of infected animals that might have acquired infection on farm premises, in transit or on dealer's premises [ 84 ]. Another route of contamination can be waterborne infection. During the early stages of the acute enteric disease affected animals develop fever, dullness, loss of appetite, and depressed milk yield and adult pregnant animals may abort [ 83 , 85 ].

Infection of S. Dublin in humans is commonly developed after contact with carrier animals but can also be transmitted through contaminated food and may cause gastroenteritis [ 86 , 87 ]. Furthermore, when steers and heifers were submitted to the same testing S. Dublin, S. Montevideo, S. Typhimirium, S. Anatum, and S. Newport were more prevalent than other serovars Table Beef products are among the top five products related to Salmonella foodborne outbreaks Table 2.

When ground beef was tested, a constant increase in S. Montevideo and S. Dublin isolates was detected from to , followed by serovars Newport, Typhimurium, and Anatum Table A multistate sample collection from dairy cows reported that 7. Examples of Salmonella serovars profiles from cows and bulls in the US [ 36 ]. Examples of Salmonella serovars profiles from steers and heifers in the US [ 36 ].

Examples of Salmonella serovars profiles from ground beef collected in the US [ 36 ]. Pigs are an important reservoir of human nontyphoidal salmonellosis and the isolation of the organism from pork and pork products is very common. Porcine salmonellae consist of two groups separated by host range and clinical presentation.

The first group consists of the host-adapted serovar S. Choleraesuis and tends to elicit systemic disease in the form of septicaemia with a high mortality rate in young pigs. The second group consists of all the other serovars, which have a broader host range and tend to produce momentary enteritis.

Like other animal farms, the prevalence of Salmonella from swine varies depending on the region and type of farm surveyed. When fecal samples were taken from grower and finisher pigs, the prevalence among serovars was higher for S.

Derby and S. Typhimurium followed by Agona and Anatum, which are among the serovars with highest incidence in human foodborne outbreaks [ 91 ]. Moreover, Antimicrobial resistance has been more likely associated with S. Derby and pigs can become asymptomatic carriers [ 92 ].

In the US, from to the most prevalent serovars isolated from market hogs were Derby, Typhimurium, Johannesburg, Infantis, and Anatum, two of which were also in the top five serotypes isolated from humans in the same period [ 36 ].

Other serovars commonly isolated from pigs in recent years include Heidelberg, Saintpaul, and Agona Table Since the early s there has been a shift in the predominant serovar isolated from swine, where Choleraesuis has a higher incidence and replaced S. Examples of Salmonella serovars profiles from market hogs in the US [ 36 ]. Chicks may acquire Salmonella via vertical transmission from the parent, but horizontal transmission from environmental facilities, transportation, feed, and vectors including humans, rodents, and insects can be a significant problem [ 90 , 93 ].

Among commercial layers, contaminated eggs will typically result from flock infections acquired via persistent environmental Salmonella and are associated with the serovar Enteritidis [ 94 — 96 ]. It appears that Salmonella Enteritidis filled an ecological niche that was available after eradication of serovars Pullorum and Gallinarum.

Enteritidis was the most prevalent serovar isolated from chickens during the s but that has changed in the following decade. Salmonella outbreaks linked to consumption of nonmeat foods have rapidly increased during the last decades. Salmonella Saintpaul, S. Rubislaw, and S. Javiana spread by paprika and paprika-powdered potato chips caused outbreaks with more than infected people [ ].

An increase of S. Oranienburg infections was registered in the early s where multistate control studies revealed the consumption of chocolate as the apparent cause of infection [ ]. Epidemiological and environmental investigations indicate that cross contamination in the manufacturing plants may be the cause of outbreaks associated with low moisture foods [ ].

Salmonella Typhimurium, S. Ofda, S. Tennessee, and S. Poona were isolated from sesame paste and sesame seed which were sold for raw consumption in cereals [ ]. It is known that bacteria on plant surfaces may form large biofilms with other bacteria [ ].

The persistence of these biofilms makes it difficult to clean and sanitize the crops. These factors are thought to contribute to outbreaks related to plant products including fruits, nuts, and vine stalk vegetables as common sources Table 3.

Outbreaks of salmonellosis associated with seafood that occurred in the US were from cross contamination during farming, processing, preparation, and transportation. From to , serovars Newport, Typhimurium, Dublin, Montevideo, and Java were reported to have caused outbreaks associated with consumption of milk and cheese products in the US [ ].

The reason some Salmonella serovars are more prevalent in specific food products is not completely understood. It is suggested that Salmonellae react in a serovar dependent manner to environmental stresses including differences in temperature, chemicals, and low-nutrient available conditions that can vary by food [ — ].

Sigma factors are proteins that compose fundamental subunits of prokaryotic RNA polymerase and provide a mechanism for cellular responses by redirecting transcription initiation [ ]. Alternate sigma factors control the gene expression of bacteria by sensing the changes in the environment. The sigma factors can sense perturbation in the outer membrane and activate genes in response to heat stress in order to adapt to high temperatures.

The mechanism used is by specific activation and transcription of rpo H genes under high temperature [ ]. Transcription of rpo H genes in S. Additionally all virulence genes were upregulated in response to high temperature [ , ]. Water activity a w in foods is defined as the ratio of the vapor pressure of water in a food matrix compared to that of pure water at the same temperature.

The surrounding moisture and the conformation of the food matrix can influence the thermotolerance of Salmonella by increasing the temperature required to inactivate the organism. Under low a w conditions in high carbohydrate or high fat products, the heat resistance of S. Seftenberg strain W was greater than S. Typhimurium [ — ]. It is widely known that S. Seftenberg strain W has high resistance to heat, with a thermotolerance approximately 30 times more than S. The thermotolerance of Salmonella in poultry products including liquid egg yolks and chicken meat highlights the distinctiveness of S.

Seftenberg to survive high cooking temperatures. Other strains of S. Bedford have shown similar inactivation temperatures to strain W. Salmonella Senftenberg and S. Typhimurium exhibited higher resistance to heat in chicken litter among other Salmonella serovars [ — ]. Heat stress encountered during feed processing increased the thermotolerance of S. Enteritidis strains and may induce expression of virulence gene hil A in S.

Typhimurium, and S. Seftenberg [ , ]. It is believed that heat resistance confers a preadaptation to temperatures and it is influenced by the strain tested and culture conditions [ , ]. Salmonella uses cold shock proteins CSP as a response for quick adaptation to temperature downshifts in the environment.

During the downshift CSPs are synthesized for the cell to later resume growth [ — ]. There are a wide variety of potential chemical stresses, including pH, oxidation, membrane disruption, and denaturation of critical macromolecules or metabolic poisons that can affect pathogenic bacteria [ , ].

Chlorine, commonly used to disinfect water, can be antimicrobial to Salmonella. Salmonellae are capable of producing biofilms providing the organism with an exopolysaccharide matrix that inhibits chemical attack against chlorine [ — ]. However, chlorination by itself is not enough to reduce Salmonella incidence and infection in birds [ ]. Decontamination of broiler carcasses occurs during immersion in the chilling tank and the bacterial load in each carcass is expected to be lower than an initial count.

Chlorine is also used as a sanitizing method in poultry processing plants along with organic acids, inorganic phosphates, and other organic preservatives. Treatments for decontamination of carcasses were performed on different strains of Salmonella in the presence of acidified sodium chlorite varied widely with serotype; the highest resistance levels were shown by serotypes Typhimurium, Newport, and Derby [ ]. Among organic acids the use of acetic and propionic acid has shown inhibitory effects against Salmonella [ , ].

Equipment sanitization is also important, and previous studies have shown the importance of combining sanitizing agents, including detergents and acids. Treatments with sanitizers and detergent successfully inactivated S. In general, chlorate preparations act as selective toxic agents to enteric pathogens by disrupting cell membrane causing the leakage of intracellular components in bacterium. In the case of organic acids their bactericidal activity is related to pH, affecting creation of undissociated acids that will acidify the cytoplasm and disrupt key biochemical processes.

In chickens, Salmonella first reaches the crop with a pH range of 4 to 5, as a result of bacterial lactic acid fermentation. If adaptation to that pH occurs, Salmonella can survive and adapt to a more acidic pH and therefore oppose antibacterial effects of the stomach [ ].

PhoP genes act on the bacterial cell envelope by increasing the resistance to low pH and enhancing survival within the macrophage [ ]. Salmonella responds to acidic environmental challenges of pH 5. It has been shown that RpoS and PhoPQ provide protection against inorganic acids, while regulators RpoS, iron regulatory protein Fur, and adaptive response protein Ada provide a major tolerance to stress of organic acids [ , , ].

The PhoP locus is a crucial virulence determinant and Salmonella pho P strains are very sensitive to microbial peptides. Several genes, including rpo S, and some acid shock proteins and heat shock proteins are implicated in Salmonella virulence. Commonly isolated from chicken carcasses S. Kentucky shows more acid sensitivity pH 5. When virulence gene presence was surveyed, acid adaptive stress genes including rpo S, fur , and pho PQ were detected in S.

Kentucky [ ]. Begin typing your search term above and press enter to search. Press ESC to cancel. Skip to content Home Essay What does Salmonella enteritidis need to thrive? Ben Davis April 4, What does Salmonella enteritidis need to thrive? What does Salmonella enteritidis eat? How does Salmonella survive in the stomach? People who have had salmonella are at higher risk of developing reactive arthritis. Also known as Reiter's syndrome, reactive arthritis typically causes:.

The Department of Agriculture has created a Salmonella Action Plan, which involves updating the poultry slaughter inspection system and enhancing sampling and testing programs for poultry and meat.

The plan's purpose is to cut the number of salmonella infections in the United States. You can also take care to avoid spreading bacteria to others. Preventive methods are especially important when preparing food or providing care for infants, older adults and people with weakened immune systems. Be sure to cook food thoroughly and refrigerate or freeze food promptly. Washing your hands thoroughly can help prevent the transfer of salmonella bacteria to your mouth or to any food you're preparing.

Wash your hands after you:. Cookie dough, homemade ice cream and eggnog all contain raw eggs. If you must consume raw eggs, make sure they've been pasteurized.

Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission. This content does not have an English version. This content does not have an Arabic version. Overview Salmonella infection salmonellosis is a common bacterial disease that affects the intestinal tract.

Pet food can sometimes be the source of Salmonella infection. If people handle contaminated pet food or a contaminated utensil and then touch their mouth, they can accidentally ingest the bacteria. Pet food that contains raw or uncooked meat is more likely than processed pet food to test positive for Salmonella. Many animals, especially cattle, chickens, rodents, reptiles, and amphibians, can naturally carry Salmonella in their intestines and show no signs of illness.

People can get salmonellosis from handling these animals. Salmonella can also get on the inside and outside of cages, aquariums and terrariums. Feeder rodents fed to some pet reptiles and amphibians can be a source of the bacteria. Direct contact with feeder rodents or contaminated items in animal habitats can spread Salmonella to people. Salmonella infection most often causes gastroenteritis, which can range from mild to severe.

Symptoms in people start within 6 hours to 6 days after ingesting the bacteria and include:. Most people recover from salmonellosis in 4 to 7 days without treatment. In some cases, the diarrhea may be so severe that the person needs to be hospitalized. In a person with severe diarrhea, the bacteria may spread from the intestines to the bloodstream and then to other places in the body.

If this happens, the disease can be fatal unless the person is treated promptly with antibiotics. Children under 5, pregnant women, the elderly, and people with weakened immune systems such as those with cancer or other diseases have a higher risk of getting salmonellosis and are more likely to have severe symptoms.

Salmonellosis is uncommon in dogs and cats, but they can be carriers of the bacteria. For example, cats can spread Salmonella through shared litter boxes or when roaming throughout the house, such as on kitchen countertops. Some ways dogs can spread the bacteria is when they give people kisses or have stool accidents inside the home.

Pet waste from both sick and healthy pets can be a source of infection for people. When the disease is seen in an adult dog or cat, the animal typically has another infection or health problem at the same time.