Salmonellae are common infections in both humans and animals. They practically populate any animal, including livestock, poultry, birds, reptiles, rodents, domesticated animals, and people. One of three clinical syndromes, such as gastroenteritis, enteric fever, or localised disease, are frequently brought on by salmonella infections in humans. Salmonella infections in animals also result in significant losses of cattle.

What is Salmonella?

• Salmonella is a significant food-borne pathogen that causes both systemic and enteric infections, affecting millions of people worldwide each year.
• The discovery of Salmonella can be attributed to Dr. Daniel Salmon, who isolated the first organism, Salmonella choleraesuis, from a pig intestine.
• Belonging to the Enterobacteriaceae family, Salmonella consists of two pathogenic species that cause illness in humans: S. enterica and S. bongori.
• Salmonella bacteria are Gram-negative, flagellated, and facultative anaerobic bacilli. They possess O, H, and Vi antigens, which contribute to their classification and identification.
• The taxonomy of Salmonella is complex. The genus Salmonella is divided into two species based on DNA homology and host range: Salmonella Enterica and Salmonella Bongori. Subspecies of S. enterica, namely I, II, IIa, IIIb, IV, and VI, have also been identified.
• Most disease-causing salmonellae for humans are found in subgroup I of S. enterica subsp. enterica. This subgroup includes the bacilli responsible for typhoid and paratyphoid infections, as well as numerous other serotypes.
• Each Salmonella isolate is further classified into a serotype based on the presence of specific somatic O, flagellar H, and surface Vi antigens. Currently, there are over 2400 described serotypes.
• Salmonella serotypes are considered separate species, emphasizing their distinct characteristics. For example, Salmonella serotype Enteritidis, a subspecies of S. enterica subsp. enterica, is commonly referred to as S. Enteritidis or simply Enteritidis in clinical settings.
• To maintain clarity, serotypes are denoted using Roman rather than italic font.

What is Salmonellosis?

• Salmonellosis is a significant disease characterized by a range of clinical manifestations, including gastroenteritis and typhoid fever.
• Typhoid fever, primarily caused by Salmonella Typhi and Salmonella Paratyphi A, is prevalent in regions such as South and Southeast Asia.
• Non-typhoidal Salmonellae, specifically Salmonella Typhimurium and Salmonella Enteritidis, are responsible for invasive bacterial disease, with sub-Saharan Africa being the most affected region.
• The overall fatality rate of Salmonellosis is relatively low, typically less than 1%. However, certain populations are at a higher risk of severe complications and mortality, including malnourished children, immunocompromised individuals, and adults with HIV.

Salmonella Characteristics

• Gram-negative: Salmonella is classified as a Gram-negative bacterium based on its cell wall structure.
• Facultative anaerobes: These bacteria have the ability to survive and grow in both the presence and absence of oxygen.
• Motile, rod-shaped bacteria: Salmonella bacteria are characterized by their rod-shaped morphology and possess flagella that enable them to move in a motile manner.
• Non-spore former: Unlike some other bacteria, Salmonella does not produce spores as a means of survival and reproduction.
• Non-capsulated (except S. Typhi and S. Paratyphi): Most Salmonella strains do not possess a capsule, a protective layer outside the cell wall. However, Salmonella Typhi and Salmonella Paratyphi, which cause typhoid fever, are encapsulated.
• Growth temperature range: Salmonella can grow within a temperature range of 5 to 45°C, with the optimal temperature for growth being around 35 to 37°C, which is similar to the human body temperature.
• Broad pH range: Salmonella is capable of surviving and growing within a broad pH range of 3.8 to 9.5, displaying adaptability to various acidic and alkaline conditions.
• Resists bile salts: Salmonella has developed mechanisms to resist the harmful effects of bile salts found in the digestive system, allowing it to survive and establish infection.
• Produces H2S: Salmonella bacteria are known to produce hydrogen sulfide (H2S) gas as a byproduct of metabolism, which can be detected using specific biochemical tests.

Morphology of Salmonella

• Salmonellae are 1-3 m in diameter Gram-negative bacilli.
• They have peritrichous flagella and are motile (Salmonella Gallinarum and Salmonella Pullorum are exceptions, which are nonmotile).
• They don’t produce capsules and spores.
• Salmonellae strains can develop fimbriae, although the majority of Salmonella Paratyphi A strains and a small number of Salmonella Paratyphi B, Salmonella Typhi, and Salmonella Typhimurium strains do not.

Geographical distribution of Salmonella

• Enteric fever is endemic in many underdeveloped nations and is most frequently observed in those nations where sanitary standards are subpar.
• The Indian subcontinent, Southeast and Far East Asia, the Middle East, Africa, Central America, and South America are all regions where typhoid disease is endemic.
• Each year, there are roughly 12–13 million cases of typhoid fever worldwide, resulting in 600,000 fatalities. In all of India, enteric fever is widespread.
• Due to advancements in water supply and sanitation over the past several decades, typhoid disease has been almost completely eradicated in developed nations.
• Health issues related to typhoid fever still exist in both industrialised and developing nations. S. paratyphi A is common in South Asia, Eastern Europe, and South America; S. paratyphi B is common in North America, the United Kingdom, and Western Europe; and S. paratyphi C is common in Guyana and Eastern Europe.

Habitat of Salmonella

• Only human pathogens, S. Typhi and S. Paratyphi (A, B, and C).
• They are not present in any other hosts of animals.
• They settle infected human hosts’ small intestines, particularly the ileac mucosa.
• Long-term asymptomatic colonisation happens frequently in infected hosts.
• A variety of household animals, rodents, reptiles, and birds are parasitized by other salmonellae.
• S. Typhimurium affects a variety of hosts, including people, animals, and birds, in contrast to Salmonella Abortus-equi, Salmonella Abortus-oris, and S. Gallinarum, which are exclusively found in horses, sheep, and poultry, respectively.

Reservoir, source, and transmission of infection

• Enteric fever infection reservoirs include the diseased person and, more usually, carriers.
• Patients who continue to discharge typhoid bacilli in faeces for 3 weeks to 3 months after a clinical cure are considered convalescent carriers.
• Those who shed the bacilli for 3 months but not for a year are considered temporary carriers.
• Chronic carriers are people who have excreted the bacilli for a year.
• Two to four percent of patients develop chronic carriers. The bacilli can remain in the kidney and release urine, or they can remain in the gallbladder and be expelled in faeces (faecal carrier) (urinary carrier).
• Less frequently seen than faecal carriers, urine carriers typically exhibit some urinary lesion, such as calculus or schistosomiasis.
• Women than men and those over 40 are more likely to be in the carrier condition than are those under 40.
• Cooks or food handlers who become carriers could be dangerous to the neighbourhood.
• A typical example of such a carrier was Mary Mallon (also known as Typhoid Mary), a New York chef who, over the course of 15 years, produced at least seven outbreaks affecting more than 200 people.
• S. Paratyphi infections also result in the carrier stage. S. paratyphi B infections affect animals like dogs and cows, whereas S. paratyphi A infections only affect humans.
• The most frequent sources of infection are human faeces contaminated with S. Typhi in food, vegetables, and water.
• Ingesting food or water contaminated by infected food handlers or as a result of inadequate personal hygiene might result in S. Typhi infections.
• Person-to-person transmission of S. Typhi infections is frequent since the infectious dosage is minimal.
• For those at high risk of illness due to age, immunosuppression, underlying disease (leukaemia, lymphoma, sickle cell disease), or decreased stomach acidity, the infectious dose is still smaller.
• Salmonellae of typhoidal ancestry have no known animal reservoirs. Only nontyphoidal salmonellae frequently transmit zoonotic pathogens from animals to humans.
• The main reservoirs for nontyphoidal Salmonella organisms include poultry, livestock, reptiles, and companion animals.
• The route of transmission involves consumption of inadequately prepared fruits, vegetables, items of animal origin, such as poultry, red meats, unpasteurized milk, and eggs that have been contaminated by diseased humans or infected animals.
• Ingestion of polluted water and contact with sick reptiles such iguanas, pet turtles, and tortoises are other means of transmission.

Classification and typing of Salmonella

1. Kauffmann–White scheme

• Salmonella strains are categorised using the Kauffmann-White scheme, which is based on the structural formulae of the strains’ O and H antigens, which are recognised through agglutination with particular antisera.
• Based on the presence of specific O antigen components, Salmonellae are divided into various O serogroups.
• There are several serotypes in each serogroup that share an O factor with no counterparts in other serogroups.
• These O factors were once known by the capital letters A-Z and later by the numerals 51–67; they are now known as 1, 2, 3, and so forth.
• Subserogroups were created from some serogroups (e.g., C1–C4; E1–E4). Instead of using letters, it makes sense to identify each serogroup by its distinctive O antigen factor numbers.
• As a result, it is now suggested that group A be designated as 2, B as 4, C1 as 7, C2 as 8, D as 9, and so on.
• The existence of phase 1 and phase 2 of the flagellar antigens allows for the differentiation of the many serotypes within each O serogroup.
• An antigenic formula, which has three parts and describes the O antigens, phase 1 H antigens, and phase 2 H antigens in that sequence, is used to identify the antigenic structure of a Salmonella serotype.
• The component antigens in each of the three components are separated by commas, with a colon separating each.
• According to the Kauffmann-White scheme, each serotype corresponds to a species. Currently, the Kauffmann-White system has described more than 2400 serotypes.

2. Bacteriophage typing

• The intraspecies classification of S. Typhi is called bacteriophage typing and was initially developed by Craigie and Yen (1937).
• They discovered that the bacteriophage (Vi phage II) attacking the S. Typhi Vi antigen is very adaptive. Phage A is the name of the parent phage.
• Serial propagation within a strain of S. Typhi could make it unique to that strain only.
• A phenotypic or genotypic variation led to this adaption. The sensitivity of the cultures to various Vi phase variations is used to carry out the phage typing.
• The majority of other types, however, are only susceptible to one or two related adaptations. Since the presence of Vi antigens is required for S. Typhi phage typing, some strains (Vi negative) will not be typable.
• Currently, 97 different Vi II phage varieties of S. Typhi are known. The most prevalent S. Typhi phage types in India are E1, O, and A.
• Additional markers have been utilised for the division of strains belonging to a phage type in order to increase the utility and discrimination of phage typing.
• These include (a) Kristensen’s biotyping, (b) Nicolle’s complementary phage typing, (c) tetrathionate reductase production, (d) bacteriocin production, and (e) antibiogram.
• In order to I identify the origin of epidemics and (ii) learn more about the trends and patterns of typhoid epidemiology at the local, national, and worldwide levels, phage typing is useful.
• S. Typhimurium, S. Enteritidis, S. Dublin, and other serotypes have also been subjected to phage typing methods.
• The National Phage Typing Centers at the Lady Hardinge Medical College in New Delhi are where phage typing is done in India.

3. Biotyping

• The classification of various Salmonella strains belonging to a single serotype into various biotypes based on their biochemical traits is known as biotyping.
• In 1975, Duguid et al. classified S. Typhimurium into 144 distinct biotypes based on 15 different biochemical traits.
• Salmonella Montevideo, S. Agona, and S. Paratyphi B have all been assigned biotypes using the same biochemical traits.
• Based on the fermentation of arabinose, dulcitol, and xylose, S. Typhi has been divided into various biotypes.
• Because it further classifies a huge number of untypable strains or members of common phage types, biotyping is a useful addition to phage typing.
• On the other hand, strains belonging to the same biotype may be rearranged into other phage types.
• As a result, phage typing and biotyping combined offer a stronger ability to distinguish between Salmonella strains than either technique used alone.

4. Molecular methods

• In modern facilities, more discriminating genotyping techniques such as plasmid fingerprinting, multilocus enzyme electrophoresis, IS-200 profiling, and random amplified polymorphic DNA analysis have been used to characterise Salmonella’s epidemiology.
• The Central Research Institute, Kasauli, is home to India’s National Salmonella Reference Center (Himachal Pradesh).
• At the Indian Veterinary Research Institute in Izatnagar, there is a reference centre for salmonellae of animal origin (UP).
• These reference centres offer services for the confirmation of other salmonellae serotypes and the identification of uncommon serotypes.

Culture of Salmonella

They thrive at an ideal temperature of 37°C in a pH range of 6–8, on a variety of nonselective (Mueller-Hinton agar) and selective (Wilson and Blair’s bismuth sulfite medium) media. They are aerobic and facultatively anaerobic.

Nonselective solid media

• After 18 to 24 hours of incubation, Salmonella spp. develop grey, moist colonies on nutritional agar and blood agar that have a smooth, convex surface.
• Rough strains result in grainy, opaque, and unevenly surfaced colonies.
• Large mucoid colonies are produced by some S. paratyphi B strains as a result of the generation of loose polysaccharide slime.
• Because they don’t digest lactose, they grow pale, colourless colonies on MacConkey agar. S. Typhi cannot flourish on this substrate.
• Deoxycholate citrate agar produces colonies that resemble those formed on MacConkey agar.
• Sometimes they develop colonies with a dark centre after 48 or more hours of incubation.

Selective solid media

• The preferred culture medium for Salmonella spp., particularly S. Typhi, is Wilson and Blair’s bismuth sulfite agar.
• On this medium, the growth of Proteus species, coliforms, and Shigella species is suppressed.
• Salmonellae grow metallic-looking colonies that are jet black on this medium thanks to the generation of hydrogen sulphide.
• Green colonies are formed by S. Paratyphi A and other species that do not produce H2 S. Salmonella spp. are isolated using the selective medium XLD (xylose, lysine deoxycholate agar).
• Salmonella spp. develop pink colonies on this medium with black cores as a result of producing H2 S.
• Salmonella serotypes H2 S-negative create red colonies without black cores.

Liquid media

• Enrichment media that are frequently employed include selenite F and tetrathionate broth.
• For the enrichment of Salmonella spp. from clinical specimens, selenite F broth is widely utilised.
• The growth of several salmonellae, including Salmonella Choleraesuis and S. Paratyphi B, is occasionally inhibited by this medium.
• Although tetrathionate broth is used to treat salmonellae, it occasionally also promotes the growth of Shigella spp. and Proteus spp.
• Although tetrathionate broth is sometimes antagonistic to Salmonella spp., it does not promote the growth of Proteus species.

Biochemical reactions of Salmonella

• Salmonellae convert glucose, mannitol, and maltose into acid and gas by fermentation. In contrast, S. Typhi does not ferment the sugars.
• Salicin, sucrose, and lactose are not fermented by them.
• Indole is not produced by them.
• Except for S. Paratyphi A, S. choleraesuis, and a few other species, the majority of salmonellae don’t create H2 S.
• Urea is not hydrolyzed by them. They test positive for MR, but negative for VP and positive for citrate. However, S. Typhi and S. Paratyphi do not develop in Simmon’s citrate media because they require tryptophan as a growth factor.
• Lysine, ornithine, and arginine are all decarboxylated by salmonellae, while glutamic acids are not. However, neither S. Typhi nor S. Paratyphi A decarboxylate ornithine or lysine.
• Salmonellae are oxidase- and catalase-negative.

Susceptibility to physical and chemical agents

• At 55°C, the bacilli are destroyed in an hour, while at 60°C, they are destroyed in fifteen minutes.
• They are likewise destroyed in 5 minutes by 5% phenol or 0.2% mercuric chloride.
• The germs are eliminated by boiling, chlorinating water, and pasteurising milk.
• They can endure contaminated soil and water for weeks, and ice for months.
• If dried, cultures may remain viable for years.

Cell Wall Components and Antigenic Structure of Salmonella

Lipopolysaccharide (LPS) 

Like all other Gram-negative bacilli, salmonellae have a complex lipopolysaccharide (LPS) structure in their cell walls. During cell lysis and to some extent during culture, the LPS is released. The LPS moiety is a crucial part of the bacteria’s pathogenicity and serves as an endotoxin. The LPS complex is made up of three parts: an inner lipid A coat, a middle piece (the R core), and an outer O polysaccharide coat. The following justifications support the significance of salmonellae’s LPS:

• O-antigen specificity is caused by the outer O polysaccharide chain’s repeating sugar units. This aids in determining the bacteria’s pathogenicity. Rough strains of Salmonella are those that lack the entire sequence of O sugar repeat units. They received this name due of the colonies’ untidy look. The smooth strains, which have a full complement of the “O” sugar repeat unit, are more virulent or avirulent than the rough strains.
• The cell wall’s endotoxin component plays a significant role in the pathogenesis of Salmonella infections. Fever, activation of the coagulation and serum complement kinin systems, and myocardial function depression are all effects of endotoxins. A systemic infection’s potential for developing septic shock is also partly caused by the circulatory endotoxin.
• Because many different Gram-negative bacteria share a common core structure, antibodies made against the common enterobacterial antigen R core are protective against infection brought on by these bacteria. In some cases, the harmful effects of Gram-negative bacteria are mediated by antibodies to R core.

Antigenic properties

Three main antigens are present in salmonella: 1. Flagellar antigen or H 2. Somatic antigen, or O 3. Antigens on the skin (Vi antigen, M and N antigen, and F antigens).

H or flagellar antigen

• This antigen, which is heat- and alcohol-labile, is found on the flagella.
• Although boiling or treatment with alcohols and acids renders the antigens inert, 0.2-0.4% formaldehyde preserves them.
• Other enterobacteria do not share the Salmonella H antigens, which are genus-specific.
• The antigens are maintained in 0.2-0.4% formaldehyde but are eliminated by boiling or treatment with alcohols and acids.
• Strongly immunogenic, the H antigen is linked to the production of antibodies after infection or vaccination.
• Phase I and phase II versions of the H antigen may both coexist.
• The organisms frequently transition between phases.
• The detection of serological structure throughout both phases is necessary for comprehensive serotype identification.

O or somatic antigen

• O antigens are found on the outer membranes’ surface and are identified by certain sugar sequences there.
• The O antigen is an essential component of the cell wall and is an LPS complex.
• It is heat stable and can withstand boiling for two hours and thirty minutes.
• Additionally, it is stable to alcohol, resistant to a 4-hour treatment with 96% ethanol at 37°C, and resistant to 0.2% formaldehyde.
• Trichloroacetic acid treatment can be used to remove this antigen from cell walls.
• Phenol treatment eliminates the bacteria’s antigenicity but leaves them poisonous.
• Compared to H antigen, antigen is less immunogenic.
• O antibody titers are often lower than H antibody titers after infection or immunisation.
• The O antigen is a mosaic of two or more antigenic components rather than a single factor.
• Based on the presence of the distinctive O antigen on the bacterial surface, salmonella are categorised.
• There have been 67 “O” antigens identified to date. 46 “O” serogroups of Salmonella have been identified based on the somatic antigens.

Surface antigens

These include (a) Vi antigen, (b) M and N antigens, and (c) F antigens, and are discussed below. 

Viantigen

• Overlying the “O” antigen is the surface antigen known as “Vi.”
• The first people to describe this antigen were Felix and Pitt, who called it the “Vi antigen” because they thought it was connected to virulence.
• It is comparable to the coliform K antigens.
• Only a few serotypes of which S. Typhi is the most significant contain the antigen.
• Some strains of Citrobacter freundii, Salmonella Dublin, and Salmonella Paratyphi C also include this antigen.
• These bacteria are rendered inagglutinable by their unique O antiserum but agglutinable by Vi antisera due to the antigen present on their surface.
• Boiling the Vi antigen in water for one hour destroys it because it is heat labile.
• Treatment with phenol hydrochloric acid and 0.5 sodium hydroxide also results in the destruction of vi antigen, while 0.25% formaldehyde or alcohol had no effect on the antigen.
• Serial subculture is lost on the Vi antigen.
• less immunogenic and linked to low levels of antibodies produced following infection.
• Early in the healing process, the antibody vanishes. Its continued existence suggests the emergence of the carrier state.
• Poor prognosis is indicated by complete absence of Vi antibodies in a confirmed case of typhoid fever.
• Alcoholized vaccinations cause a low titer of Vi antibodies, whereas phenolized vaccines do not cause the production of Vi antibodies in serum.
• The Vi antigen is not examined in the Widal test because the Vi antibody cannot be used to diagnose typhoid patients.

M and N antigens

• These polysaccharide-based antigens are found on the surface of bacteria.
• These antigens stop O antiserum from agglutinating.
• These antigens are destroyed after two and a half hours of boiling.
• The mucoid form of Salmonella colonies is caused by the M antigen’s presence.

F antigen

• The fimbriae include these antigens.
• There are two phases to them: one with F antigen and the other without.

Antigenic variation

Salmonellae antigens undergo phenotypic and genotypic variations as follows: 1. OH–O variation 2. V–W variation 3. S–R variation 4. Phase variation 5. Variations in O antigens

OH–O variation

• Sometimes strains of nonflagellated salmonellae (O) develop from flagellated salmonellae (OH).
• The loss of flagella is connected to this variant, also known as the OH-O variation.
• Flagella do not form when salmonellae are cultivated on agar with phenol (1:800).
• Because flagella reappear when the strain is subcultured on conditions devoid of phenol, this alteration is transient and phenotypic.
• Typically, just a partial loss of flagella, as well as a reduction in the amount of the H antigen, occurs.
• Small quantities of flagellated bacteria are also present in these cultures. A population of flagellated bacteria is obtained from such cultures by subculture in Craigie’s tube.
• A broad tube filled with semisolid agar (0.2%) is employed in Craigie’s tube method.
• The upper end of a small, narrow tube that is open at both ends is inserted into the tube’s agar so that it protrudes significantly above the agar.
• A population of motile cells is produced in subcultures made from the top of the agar outside the central tube after the bacterial strain is introduced into the inner tube and incubated for 8–16 hours.
• Instead of using a Craigie’s tube, you may use a U-tube constructed of soft agar, which would allow you to inoculate one limb while harvesting cultures from the other.
• Rarely, salmonellae may mutate and lose their flagella. One stable nonmotile mutant is the S. Typhi 901-O strain, which is utilised to make O-agglutinable bacterial antigen solutions for the Widal test and other serological testing.

V–W variation

• Almost all S. Typhi strains that have recently been discovered have a coating of Vi antigen on their surface that totally obscures the O antigen.
• Such bacilli can be agglutinated by Vi antiserum but not by O antiserum when fully expressed. The V shape is what we have here.
• The Vi antigen entirely disappears after several subcultures.
• With the Vi antiserum, these cultures are inagglutinable, while the O antiserum readily agglutinates them.
• The W form is what we have here. The bacillus is agglutinable with both Vi and O antisera in partial loss of the Vi antigen; these forms are referred to as “VW forms.”
• However, in S. Paratyphi C and S. Dublin, the O antigen is not entirely covered by Vi antigens.

S–R variation

• The smooth-to-rough (S-R) variation is caused by mutation and is connected to I a change from smooth to rough colony morphology, (ii) the loss of the O antigen, and (iii) a reduction in virulence.
• The irregular, big, and rough colonies are autoagglutinable in saline. These colonies exhibit a deficient ability to produce O antigen.
• Though it happens infrequently in nature, laboratory strains kept by serial cultures on common media frequently convert into rough forms.
• Maintaining cultures on Dorset’s egg media or lyophilizing them can help to some extent prevent the smooth S-R fluctuation.

Phase variation

• Most salmonellae exhibit phase 1 and phase 2 alternate phases of their flagellar or H antigens.
• Phase 1 antigens are classified as “specific” or “species” because they are either unique to a serotype or shared by a small number of species.
• More than 80 flagellar antigens have been discovered during this phase. These are classified as little letters of the alphabets a to z, with the exception of j, and then z1 to z68.
• Based on the discovery of the antigen in phase 1, the serotype is presumed to be identified. The second phase, sometimes referred to as the “nonspecific” or “group” phase, uses a lot of common antigens.
• Phase 2 antigens are significantly fewer and are numbered from 1 to 12 in Arabic (1, 2, and 3 . . . up to 12).
• Salmonella strains that appear in both phases are referred to as biphasic, while those that appear in only one phase are referred to as monophasic (e.g., S. Typhi, S. Paratyphi A, etc.).
• A culture comprises cells bearing both phases’ flagellar or H antigens, but often one phase predominates over the other, causing only one of the phases’ antisera to agglutinate the culture.
• Finding the H antigens of both phases is crucial for the accurate serotyping identification of Salmonella isolates.
• Using Craigie’s tube approach, isolates can be changed from one phase to another.
• In this approach, a phase 1 culture is changed to a phase 2 culture by passing it through a Craigie’s tube containing a specific phase 1 antiserum, and a phase 2 antiserum is used to effect the reverse conversion.

Variations in O antigen

• By lysogenizing with some converting phages, the structural formulas of the O antigen may change, changing the bacterial serotypes as a result.
• Thus, phage 15 changes Salmonella Anatum (serotype 3,10:e,h:1,6) into Salmonella Newington (serotype 3,15:e,h:1,6), while phage 34 changes the latter into Salmonella Minneapolis (serotype 3,15,34:e,h:1,6).
• The anatum var. 15 and anatum var. 15, 34 serotypes are the Newington and Minneapolis, respectively.

Virulence factors of Salmonella

Complex factors contribute to salmonellae’s virulence. These are encoded on the chromosome of the organism as well as on big (34-120 kDa) plasmids.

Type III secretion systems

• Salmonella virulence factors can be secreted into host cells more easily thanks to Type III secretion systems (TTSS), which are made up of around 20 proteins.
• A number of Salmonella pathogenicity islands, including phoP/phoQ and Salmonella pathogenicity-island 1 (SPI-1) and 2 (SPI-2), encode these.
• The bacterium becomes non-virulent when these pathogenicity islands are absent.
• Bacteria are taken in by epithelial cells by TTSS.
• Invasion by nonphagocytic cells is mediated by SPI-1, and Salmonella is helped to survive and reproduce inside of macrophages by SPI-2.

Endotoxin

• Many of the systemic symptoms of the sickness induced by Salmonella spp. are produced by endotoxin.

Fimbriae

• Salmonella binds to M (microfold) cells found in Peyer patches of the terminal section of the small intestine via species-specific fimbriae. Normally, these M cells deliver foreign antigens, such germs, to the subordinate macrophages for clearance.

Acid tolerance response gene

• The acid tolerance response (ATR) gene helps bacteria survive in phagosomes by shielding Salmonella spp. from stomach acids and the acidic pH of the phagosome.

Enzymes

• The enzymes catalase and superoxide dismutase guard the bacteria against intracellular death by macrophages.

Pathogenesis of enteric fever

The virulence traits of the infecting strain and the human host both affect how sick people who have salmonellae infection will get.

Infective dose

• Salmonellae-contaminated food or drink must be consumed to become infected. In trials involving human volunteers, the infective dosage (ID50) was discovered to be between 103 and 106 bacilli.
• A significant inoculum is required to overcome stomach acidity and to compete with normal intestinal flora, even though the infectious dosage differs between strains.
• Additionally, shorter incubation times and higher sickness rates are linked to large inocula.
• However, smaller infectious dosages might still be sufficient to spread infection if
  • These organisms are consumed along with foods that swiftly pass through the stomach (such liquids) or that raise the pH of the stomach (e.g., cheese, milk).
  • Antacids are taken simultaneously.
  • Those with compromised immune systems consume these microorganisms.
• When the salmonellae enter the intestine, they connect to the cells lining the ileal mucosa using fimbriae or pili.
• The bacteria only adhere to the Peyer patches’ specialised epithelial cells (M cells).
• The first invasion of S. Typhi into the intestinal mucosa is mediated by Salmonella TTSS. SPI-1 causes membrane ruffling by introducing Salmonella Secreted invasion proteins (Sips or Ssps) into the M cells.
• Salmonellae are encircled and swallowed by the ruffled membranes, which causes intracellular multiplication in the phagosome, host cell death, and dissemination to nearby epithelial cells and lymphoid tissue.
• Salmonella spp. are likewise shielded by an ATR gene against phagosome acidity and stomach acids.
• There are additional components that shield the bacteria from intracellular death, including catalase and superoxide dismutase.
• The phagosomes carry the bacteria to the lamina propria, where they are discharged.
• Salmonellae typhoidal strains cause the generation of macrophages in the lamina propria while nontyphoidal strains induce the production of neutrophils (nontyphoidal strains).
• Later, S. Typhi and other virulent Salmonella strains enter deeper tissues through capillaries and lymphatics, triggering a strong immunological reaction.
• The germs go from the submucosa to the mesenteric lymph nodes, where they proliferate before moving into the bloodstream (transient primary bacteremia) and dispersing to other tissues.
• The bacteria can infiltrate any organ during this bacteremic phase, but they are most frequently detected in the reticuloendothelial tissues of the liver, spleen, bone marrow, gallbladder, and Peyer patches in the terminal ileum.
• The liver infects the gallbladder, and the resulting cholecystitis is typically asymptomatic. Because of the contaminated bile, stool cultures are positive.
• Gallbladder disease that already exists makes a person more susceptible to a chronic biliary infection and long-term faecal carriage.
• During either the main intestinal infection or subsequent bacteremia, Peyer patches become infected, and the bacteria continue to spread through infected bile.
• The infiltration of chronically inflammatory cells causes the Peyer patches to become hyperplastic, which may result in the necrosis of the superficial layer and the creation of ulcers, as well as a risk of haemorrhage from blood vessel erosion or peritonitis from transmural perforation.
• There is a lack of knowledge on the aetiology of enteric fever toxaemia and protracted fever.
• It has been proposed that the causes of the protracted fever may be pyrogens and mediators released at the sites of inflammation.

Host immunity

• Since humoral antibodies do not play a significant role in disease prevention and Salmonella spp. are primarily intracellular pathogens, cell-mediated immunity (CMI) is a more effective defence against the infection.
• During the course of the illness, CMI appears to be prevalent among populations in typhoid fever-endemic regions.
• It seems that people with depressed CMI are more prone to contracting S. Typhi infections.
• O antibody first emerges in an acute infection, growing gradually, then dropping and frequently disappearing within a few months; H antibody comes a little later but lasts a little longer.
• While heightened levels of H antibody help to determine the type of enteric fever, rising or high O antibody titers typically suggest acute illness.

Clinical Syndromes 

Typhoid fever is brought on by S. Typhi, while paratyphoid fever is brought on by S. Paratyphi A, Salmonella Schottmuelleri (formerly S. Paratyphi B), and Salmonella Hirschfeldii (previously S. Paratyphi C). Typhoid and paratyphoid fever induced by these Salmonella spp. are both referred to as enteric fever.

Enteric fever

• The symptoms of enteric fever typically include a fever, headache, and gastrointestinal discomfort.
• The incubation period can last anywhere from 3 to 56 days, but it typically lasts between 7 and 14 days.
• A coated tongue, headache, lethargy, anorexia, and abdominal discomfort with either constipation or diarrhoea are typical symptoms of the disease’s insidious onset.
• The usual feature is a step-ladder pyrexia with relative bradycardia and toxaemia. An enlarged liver and a soft, palpable spleen are symptoms of the illness.
• A week or more of these symptoms are followed by gastrointestinal issues.
• This stage relates to the beginning of a bacterial infection, which is then followed by gallbladder colonisation and a subsequent re-infection of the intestines.
• The most significant problems are intestinal perforation, serious bleeding, and circulatory collapse.
• Other problems include toxic encephalopathy, cerebral thrombosis, hepatitis, pancreatitis, arthritis, and myocarditis.
• It takes time to recover. After early improvement, relapse occurs in 10–20% of patients using antibiotics.
• A relapse normally happens about a week after therapy is stopped, however it has been documented to happen even two months afterwards.
• Relapses typically last less time and are milder than the first illness. Rarely, a second or third relapse could happen.
• In cases of relapse, the blood culture and serum H, O, and Vi antibodies are once more positive.
• While often milder than typhoid fever, paratyphoid fever is caused by S. Paratyphi A and B. However, S. Paratyphi C more frequently results in a frank septicemia with suppurative consequences rather than paratyphoid fever.

Laboratory Diagnosis of Salmonella

Enteric fever is diagnosed in a laboratory using the following techniques:

• Salmonella spp. isolation by culture.
• Salmonella serodiagnosis by the presentation of antibodies and antigens.
• Molecular diagnosis using PCR and DNA probes.

Specimens 

• For the purpose of isolating typhoidal bacilli for culture, frequent material include blood, blood clots, bone marrow, and faeces.
• The cerebral fluid, peritoneal fluid, mesenteric lymph nodes, resected intestine, pharynx, tonsils, abscess, bone, and urine are among the additional specimens.

Culture 

Blood culture

• An extremely helpful method for identifying enteric fever is blood culture. In roughly 90% of instances during the first week of fever, 75% of cases during the second week, 60% of cases during the third week, and 25% of cases thereafter until the pyrexia subsides.
• The use of antibiotics, however, quickly results in negative blood cultures.
• An aseptic venepuncture is used to collect 5–10 mL of blood for inoculation into a culture bottle containing 50–100 mL of 0.5% bile broth.
• This 10-fold dilution of blood is accomplished by mixing 5–10 mL of blood with 50–100 mL of bile broth. This procedure is used to counteract the bactericidal effects of several chemicals found in blood.
• The bactericidal effects of blood are further countered by the addition of liquid (sodium polyanethol sulfonate). For up to 7 days, a blood culture bottle is incubated at 37°C.
• The bile broth is subcultured on Mac Conkey agar after being incubated at 37°C for an entire night. A blood culture is positive in about 90% of cases during the first week of fever, 75% of cases during the second week, 60% of cases during the third week, and 25% of cases throughout the remaining weeks until the pyrexia subsides.
• The use of antibiotics, however, quickly results in negative blood cultures.

Castañeda’s biphasic method of blood culture

• The risk of contamination during repeated subcultures is lower with this type of culture.
• The approach also offers the advantages of being more affordable and safe. In this technique, the agar slant in the culture bottle’s one side is filled with bile broth.
• Following blood inoculation, the bottle is incubated upright to ensure that the agar’s surface is left free of any broth covering the slant.
• Only the lowest slope of the agar retains any remaining broth. To re-incubate the broth for subculture, the bottle is simply tilted such that it flows over the agar slant’s surface.
• Colonies form on the agar slant if salmonellae are present.

Clot culture

• Because certain inhibitory chemicals that are present in the serum are missing in the clot proper, clot culture is a more sensitive approach than blood culture.
• Another benefit of this approach is the ability to demonstrate Salmonella antigens or antibodies using serum that is eluted from blood during the clotting process.
• In this procedure, 5 mL of the patient’s blood are drawn under strictly controlled aseptic conditions, placed in a sterile test tube, and allowed to clot.
• Serological tests are performed using the serum that was pipetted off. A bottle of bile broth containing streptokinase (100 units/mL) is filled with the broken-up clot after being broken up with a sterile glass rod.
• The release of microorganisms that have been trapped inside the clot is facilitated by streptokinase.
• In the same manner as was previously described for blood culture, the bile broth is incubated and subcultured on media.

Bone marrow culture

• One of the most sensitive methods is bone marrow culture.
• Even though blood cultures are negative, it is usually positive.
• It is also encouraging, independent of how long patients have had enteric fever or how long they have been taking antibiotics.
• Patients whose initial blood culture results are negative, potentially as a result of earlier antibiotic therapy, are advised to have this test.

Feces culture

• Salmonellae are excreted in faeces with varied frequency throughout the illness and even during the recovery period, making faeces culture helpful as well.
• The patient’s faeces are collected in a sterile container, and they are then transported right away to the lab.
• The stool samples may be collected in a buffered glycerol saline transport medium if a delay is expected.
• Direct inoculations of the faecal samples are performed on MacConkey, DCA, and Wilson-Blair medium.
• The Wilson-Blair medium receives a somewhat heavy inoculation of stool due to its great selectivity.
• Before subculture onto selective media, one tube of each selenite and tetrathionate broth is inoculated for enrichment and incubated for 12 to 18 hours.
• Overnight, the plates are incubated at 37 °C. Large, black colonies with a metallic sheen are produced by S. Typhi on the Wilson-Blair medium.
• Due to the lack of H2 S production on this medium, S. Paratyphi A colonies grow in a green colour.
• On MacConkey and DCA media, Salmonellae produce pale nonlactose fermenting colonies.
• As noted before, tests are used to identify the colonies. After 7 days, the culture is deemed negative if no growth is seen.

Other specimens for culture

• Salmonellae can be isolated by culture from a variety of specimens, although they are rarely used.
• These samples consist of bile, sputum, rose spots, pus from suppurative lesions, urine, and CSF.
• At autopsy, cultures can be taken from the mesenteric lymph nodes, liver, spleen, and gallbladder.
• To diagnose enteric fever, the organism must be isolated from bone marrow, blood, or blood clots.
• Fecal cultures are helpful, however they might be positive in both patients and carriers. Bile culture can be used to identify carriers.

Identification of Salmonella bacteria

Motility tests, biochemical analyses, and slide agglutination with particular Salmonella antisera are used to identify colonies.

Slide agglutination test

• On a clean slide, the test is conducted using a loopful of growth from a nutrient agar plate or slope that has been emulsified in two drops of saline.
• One drop of bacterial emulsion on the slide is added to a loopful of typhoid O antiserum (factor 9/group D) if S. Typhi is detected, which is the case when no gas is generated from glucose. The slide is gently rocked.
• Salmonella strain tested likely belongs to Salmonella group D, according to the development of quick agglutination.
• The flagellar antiserum is used to agglutinate S. Typhi to determine its identity (anti-d serum).
• Fresh S. Typhi isolates can occasionally be found in the V form, which does not agglutinate with the O antiserum.
• Tests for agglutination against anti-Vi serum can be performed on these strains. As an alternative, after boiling for 20 minutes, the growth that was scraped off is tested for agglutination with the O antiserum.
• It is tested for agglutination with O and H antisera for groups A, B, C, etc. if the isolate is a nontyphoidal Salmonella that produces gas from carbohydrates.

Identifying features of Salmonella Typhi

• produces on MacConkey agar pale, non-lactose-fermenting colonies.
• produces colonies on Wilson and Blair’s bismuth sulfite agar that are jet black and have a metallic shine around them.
• Anaerogenic; produces only acid, not gas, during the fermentation of glucose, mannitol, and maltose.
• Decarboxylate ornithine not.
• Oxidase is negative and catalase is positive.
• Motile.
• H2 S is present, catalase is active, indole is not, and oxidase is not.
• Typhoid O antiserum (factor 9/group D) agglutination is positive.

Serodiagnosis

Enteric fever is diagnosed using a variety of serological tests that look for specific Salmonella antigens or antibodies in the serum and urine.

Demonstration of serum antibodies

Widal test

• Traditional serologic test for diagnosing typhoid fever is the Widal test. The test analyses agglutinating antibodies against flagellar (H) and somatic (O) antigens of S. Typhi in the patient’s serum for typhoid and paratyphoid bacilli.
• In this tube agglutination test, Dreyer’s narrow agglutination tube with a conical bottom is used for H agglutination, whereas Felix’s short round-bottomed tube is used for O agglutination.
• The test utilises the H and O antigens of S. Typhi and the H antigens of S. Paratyphi A and B.
• Due to the fact that antigenic factor 12 is shared by the paratyphi O antigen and the typhoid O antigen, the paratyphi O antigens are not utilised.
• The H antigens of S. Typhi and S. Paratyphi A and B are employed separately because the H antigens of these bacteria lack cross-reactivity.
• The ‘O’ and ‘H’ strains of S. Typhi 901 are used to produce antigen. The O antigen is produced by growing S. Typhi on phenol agar (1:800) and collecting the resulting growth in a small volume of saline. The saline bacterial solution is then mixed with 20 times its volume of 100% alcohol, heated at 40–50oC for 30 minutes, centrifuged, and the deposit is resuspended in saline to the desired concentration. It is utilised as a preservative.
• Antigen preparation must always utilise standard smooth strains supplied from reference sites.
• After antigen preparation, every batch of antigen is compared to a standard.
• Adding 0.1% formalin to a 24-hour broth culture or saline solution of an agar culture produces H antigens.
• Taking equal amounts (0.4 mL) of serial dilutions of the serum (from 1/20 to 1/640) and H antigen of S. Typhi (TH), S. Paratyphi A (AH), S. Paratyphi B (BH), and O antigens of S. Typhi (TO) and mixing in Dreyer’s tubes and Felix’s tubes, respectively, is how the test is conducted.
• The tubes are then incubated overnight at 37oC in a water bath. Some suggest a 4-hour incubation at 37oC, followed by an overnight incubation at 4oC.
• To test for autoagglutination, antigen- and normal saline-filled control tubes are utilised.
• Serum agglutination titers are measured. H agglutination is characterised by the production of loose, cotton-like clusters, whereas O agglutination is marked by a disc-like pattern at the tube’s bottom.
• In both forms of agglutination, the supernatant fluid stays clear. The highest serum dilution exhibiting agglutination with H or O antigens indicates the patient’s serum antibody titer.
• Interpretation of the Widal test findings should take the following into account:
  1. Antibodies against H and O antigens often emerge between the seventh and tenth day of illness, grow steadily until the third or fourth week, and then drop gradually. Therefore, blood obtained prior to 7–10 days will be antibody-free.
  2. The display of antibodies in matched samples, one sample taken in the first week and the second sample collected in the third week, is more beneficial than the showing of antibodies in a single serum.
  3. A titer of 1/100 or greater for O antibodies and 1/200 or greater for H antibodies is indicative of enteric fever in most cases. However, a single test result should be regarded with caution. In addition, before determining a diagnostic cutoff titer for H and O antibodies, it is required to collect baseline antibody titer levels in “normal sera” from various regions.
  4. An high amount of antibodies may be detected in the sera of patients who have previously suffered from enteric fever, as well as in the sera of individuals with an asymptomatic infection or immunisation against enteric fever. Therefore, the simple presence of antibodies in the Widal test should not be interpreted as evidence of enteric fever.
  5. Antibodies against S. Typhi and S. Paratyphi A and B may be detectable at high titers in the serum of vaccinated individuals. In the event of infection, however, elevated antibody titers will only be observed against the infecting species. After vaccination, H antibodies linger for many months, whereas O antibodies vanish after six months. In the event of infection, however, high titres of antibodies will only be detected against the infecting species.
  6. Those who have suffered from enteric diseases in the past or who have been inoculated may develop an anamnestic response during a fever that is unrelated, such as malaria, influenza, etc. The anamnestic reaction exhibits just a temporary increase in antibodies, whereas enteric fever exhibits a prolonged increase in antibodies.
  7. Patients who are treated early with antibiotics, such as chloramphenicol, may exhibit a diminished antibody response.
• It has been demonstrated that the sensitivity, specificity, and predictive values of the Widal test differ significantly between laboratories.
• Various antigens, procedures, and patient populations are responsible for this vast variance.
• At the time of admission, the Widal test is positive in only 40–60% of patients with enteric fever.

Other serological tests

• Variations on the indirect hemagglutination assay, the countercurrent immunoelectrophoresis assay, the indirect fluorescent Vi antibody assay, and the indirect enzyme-linked immunosorbent assay (ELISA) for immunoglobulin M (IgM) and IgG antibodies to S. Typhi polysaccharide are all available for the diagnosis of typhoid fever.
• The specificity of the antibody ELISA has been improved by testing monoclonal antibodies against S. Typhi flagellin.

Demonstration of serum antigens

• Serum and urine from an infected person with typhoid fever both contain circulating S. Typhi antigen, whereas serum from a cured patient does not.
• Since typhoid fever is usually present or recent when serum antigen is present, this is the case.
• Different tests, including ELISA, co-agglutination, and counter-current immunoelectrophoresis, are used to identify circulating antigen in serum and urine for typhoid fever diagnosis.

Molecular Diagnosis 

• Testing methods for identifying typhoid illness include DNA probes and polymerase chain reaction (PCR).
• Although DNA probes for recognising S. Typhi from bacterial culture isolates and directly from blood have been developed, they are not yet commercially accessible. The use of PCR is still in the testing phase.

Treatment of Salmonella

• Since its release in 1948, chloramphenicol has been the antibiotic of choice for treating enteric fever.
• It blocks protein synthesis in bacteria by attaching to their 50S ribosomal subunits.
• Chloramphenicol is still used to treat typhoid fever due to its low cost and effectiveness against sensitive strains of S. Typhi.
• Antibiotics such as fluoroquinolones (such as ciprofloxacin, pefloxacin, norfloxacin) and third-generation cephalosporins (such as ceftazidime, ceftriaxone, cefotaxime) are now the best options for treating multidrug-resistant S. Typhi.
• For typhoid, they are increasingly employed due to their efficiency, low relapse rates, and low carrier rates.
• Cefotaxime suppresses the formation of bacterial cell walls, which stunts their development. With respect to typhoid fever, the antibiotic has moderate efficacy and displays excellent in vitro activity against S. Typhi and other salmonellae.
• It has been reported recently that ceftriaxone-resistant Salmonella infections are becoming more common in the United States.
• Third-generation cephalosporins have been criticised for their high price tag and the fact that they must be given intravenously.
• In cases of S. Typhi infection, it is recommended to treat the infection with a 14-day course of chloramphenicol, ampicillin, or trimethoprim and sulfamethoxazole.

Chloramphenicol-resistant S. Typhi 

• In 1972, a S. Typhi strain that was resistant to the antibiotic chloramphenicol caused a deadly outbreak in Mexico and quickly expanded to North America and Europe.
• The first multidrug-resistant S. Typhi epidemic in India was documented in 1972 in the city of Calicut (Kerala). By 1978, it had become endemic only in Kerala.
• These drug-resistant germs quickly spread to other regions of India. Additionally, these antibiotic-resistant isolates exhibited resistance to streptomycin, sulfadiazine, and tetracycline as a result of the presence of a transmissible plasmid encoding resistant determinants to these antibiotics.
• The antibiotics ampicillin, amoxicillin, cotrimoxazole, and furazolidone were initially effective against these resistant bacteria.
• S. Typhi strains resistant to multiple or even all of these medications first emerged in various parts of India in the late 1980s.

Prevention and Control of Salmonella

The most efficient methods of reducing the prevalence of typhoid fever in endemic nations are the provision of clean drinking water, the practise of good food hygiene, and the disposal of human waste in an environmentally friendly manner. Typhoid fever is one of the leading causes of illness and death in developing countries, but these methods have the added benefit of reducing the prevalence of other enteric illnesses as well.

Immunization

• Typhoid vaccination at recommended intervals also significantly reduces the prevalence of typhoidal Salmonella infections.
• People who are I in close contact with S. Typhi cases or carriers (e.g., live in the same household), (ii) travelling to areas with a higher risk of exposure to S. Typhi, or (iii) working with S. Typhi in a microbiology laboratory should be vaccinated against typhoid.
• Typhoid vaccinations come in two forms, killed and oral, and they are as follows:

1. Killed vaccines 

TAB vaccine

• The TAB vaccine is a killed whole cell vaccination that includes S. Typhi (at 1000 million/mL) and S. Paratyphi A and B (at 750 million/mL) that have been heat killed and stored with 0.5% phenol.
• India and other nations where enteric fever is common have utilised the vaccine for quite some time.
• The vaccination is administered subcutaneously twice, with a 4- to 6-week interval between doses; a third dose is given every three years.
• Over the course of a 3-to-7-year field study, the cure rate for typhoid fever increased from 70 percent to 90 percent.
• The negative effects include a high temperature and discomfort at the injection site. The administration of excessive amounts of antigen through injection is another area of concern.
• Since S. Paratyphi B infection is uncommon in India, the divalent typhoid-paratyphoid A vaccine without S. Paratyphi B is used instead of the trivalent TAB vaccine.

Vi capsular polysaccharide antigen vaccine (ViCPS)

• Vaccines containing ViCPS antigen are made from purified Vi antigen, which is the capsular polysaccharide produced by S. Typhi and isolated from blood cultures.
• A single 0.5 mL parenteral dose of ViCPS is administered for the primary immunisation (25 g IM).
• To stay protected from S. Typhi, booster shots must be administered every 2 years.
• Overall protection rates in two field trials ranged from 50-64% in South Africa and 72% in Nepal, two countries where the illness is particularly prevalent.
• Some of the adverse reactions include heat rash, headache, redness, and induration. Underage children are not advised to get the immunisation.

Acetone-inactivated parenteral vaccine

• The United States military is the only group with access to this vaccination at the moment.
• The vaccine has a success rate of between 75% and 94%.
• If repeated exposure is anticipated, booster shots are administered every three years.

Ty21a oral vaccine

• This is an oral vaccine comprising live attenuated S. Typhi Ty21a strains in an enteric-coated capsule. The S. Typhi Ty21a strain lacks the enzyme UDPgalactose-4-epimerase and is a stable mutant.
• The strain can establish an infection when ingested, but will self-destruct after only four or five cell divisions.
• Vaccine appears to increase both serum and gut antibodies and cell-mediated immune responses; however, the mechanism by which this occurs is uncertain.
• One entericcoated capsule of Ty21a is administered on alternate days for the first vaccine, for a total of four capsules.
• If exposure is predicted to persist or resume, a booster shot every 5 years is necessary to maintain protection.
• If you want the capsules to have the most effect, you must keep them in the fridge at 4oC and take all four of them.
• Vaccine recipients sometimes experience mild to severe adverse reactions, including but not limited to abdominal pain, nausea, vomiting, fever, headache, and rash/urticaria.
• In a field study conducted in Chile, participants who received four doses of vaccine had a significantly lower risk of contracting typhoid fever compared to those who received two or three doses of vaccine (P 0.001), respectively.
• In Indonesia, however, the vaccine’s efficacy was just 42%, suggesting that it may not be useful in regions with heavy exposure to S. Typhi.
• Anyone with a damaged immune system should not get the vaccine. This includes people who are HIV positive and children under the age of 6.

Salmonella Gastroenteritis 

• The majority of cases of salmonellosis are due to salmonella gastroenteritis. Salmonella gastroenteritis, sometimes known as food poisoning, is mostly caused by nontyphoidal salmonellae, which are largely animal pathogens, and thus is considered a zoonotic disease.
• In many regions of the world, S. Typhimurium is the most frequent species responsible for the disease. S. Enteritidis, S. Hadar, S. Heidelberg, S. Agona, S. Virchow, S. Seftenberg, S. Indiana, S. Newport, and S. Anatum are also prevalent species of Salmonella.
• Infection in humans typically arises after eating tainted food. Salmonellae can be found in a variety of foods, although milk and dairy products, meat, poultry, and eggs are the most common vectors.
• The safety of eggs and other egg-based foods is a major concern. Salmonellae can grow inside an egg if it is put on contaminated chicken feed or manure.
• Food can also be tainted by the faeces of rodents, lizards, and other tiny animals. Produce, dairy products, and seafood can spread disease if they are not properly cleaned or handled to prevent contamination by manure or other germs.
• There is a 6-72 hour incubation period. Common symptoms include feeling sick, throwing up, and having diarrhoea that is loose and runny.
• Common symptoms include a high temperature, nausea, vomiting, diarrhoea, and muscle aches and headaches. About half of infected people experience fever, which typically does not go above 39 degrees Celsius.
• A normal recovery time for symptoms is between 2 and 7 days. Salmonellae in the faeces are cultured in a lab to confirm the diagnosis.
• Isolation of salmonellae from the meal provides definitive proof of the diagnosis in cases of mass food poisoning.
• The symptoms of mild salmonellosis are treated rather than the underlying cause. However, there is no evidence that antimicrobial treatment can reduce the course of an infection, so it is not recommended.
• Antibiotics are often prescribed only for the most severe, invasive illnesses. Antibiotic therapy is suggested for:
  • Infants younger than 3 months and younger than 12 months with high fever and undetermined blood culture results due to Salmonella gastroenteritis.
  • patients with anemia, an immune deficiency (from HIV or another cause), cancer, or a long-term gastrointestinal (GI) disorder. 
• Antibiotics such as ampicillin, amoxicillin, trimethoprim-sulfamethoxazole, cefotaxime, and ceftriaxone are useful in curing the illness.
• Salmonella gastroenteritis can be avoided by taking precautions against food contamination at multiple stages, beginning with the animal or bird itself.
• Salmonellae can be eliminated from food by boiling it thoroughly.

Salmonella Bacteremia 

• There is no Salmonella species that cannot produce septic shock by entering the bloodstream. However, Salmonella choleraesuis, Salmonella paratyphi, and Salmonella typhi are the most common causes of bacteremia.
• Patients of all ages, especially those with compromised immune systems like those suffering from AIDS or who are very young, are at increased risk for contracting Salmonella bacteremia.
• Salmonella bacteremia has symptoms similar to those of other Gram-negative bacteremias.
• However, as much as 10% of individuals can develop localised suppurative infections like osteomyelitis, deep abscesses, endocarditis, arthritis, and meningitis.
• Case mortality rates have been estimated at 25%.
• Salmonellae can be isolated from the patient’s blood or suppurative lesion pus (but not the faeces) to confirm the diagnosis.

FAQ