CHAPTER ONE

INTRODUCTION

1.0 Background of Study

Salmonella is a species in the genus with worldwide public health implications and is the major

cause of foodborne disease, accounting for deaths of thousands of people worldwide (Xiong et

al., 2018). Salmonella is anaerobic in nature and is a Gram-negative, rod-shaped bacterium

belonging to the Enterobacteriaceae family. Salmonella is divided into two species: Salmonella

enterica and Salmonella bongori. More than 2600 S. enterica serovars have been defined so far,

with most of these serotypes likely to cause diseases in both humans and animals, whereas a few

S. enterica variants, such as Salmonella gallinarum (SG) and Salmonella pullorum (SP), are non-

flagellated and non-motile, the large percentage of Salmonella members are motile by

peritrichous flagella. The SG and SP are linked to clinical disease in poultry and cause

significant economic losses to poultry farming, particularly in developing countries (Eguale,

2018). According to recent data from the United States, Europe, and Low and Middle Income

Countries (LMICs), Salmonella is frequently occurring international cause of foodborne disease.

Salmonella also enhances food contamination in many natural environments (Alzwghaibi et al.,

2018). Salmonella enteric found in the gut of food animals more persistently, is characterized by

chronic transmitters which remove the bacterium with their own fecal matter. As a result, these

carriers act as a reservoir for future bacterial contamination, allowing Salmonella to spread

through infected milk, meat, eggs, and other agricultural products fertilized and developed in

Salmonella-infested manure. Salmonella have been isolated from variety of animals and their

food products. These include poultry, ovine, porcine, bovine, lizards and snakes (Eriksson et al.,

2018).
1.1 Morphology, Physical and Biochemical Characteristics

Salmonella are anaerobic, chemo-organotrophic, rod-shaped with size 0.2–1.5 × 2–5 μm and are

Gram negative in nature (Stanaway et al., 2019). Except a few serovars viz S. choleraesuis, all

other members of this genus produce hydrogen sulphide and majority of them do not perform

lactose fermentation (Stanaway et al., 2019). This crucial trait has been used to produce a

number of selective and differential media for Salmonella culture, isolation, and presumptive

identification. Salmonella-Shigella agar (SS), brilliant green agar (BGA), xylose lysine

deoxycholate (XLD) agar, Hektoen enteric (HE) agar, MacConkey agar, lysine iron agar (LIA),

and triple sugar iron (TSI) agar are among the media frequently used (Hiyoshi et al., 2018).

Salmonella is non-fastidious, as outside the living hosts it can grow and multiply in a variety of

environments. Salmonella is heat-sensitive, and is frequently killed at temperatures of 70°C or

above. The majority of serotypes thrive and grow in temperatures ranging from 5 to 47°C with

an optimum of 32 to 35°C. Few serotypes, however, may thrive at temperatures as low as 2–4°C

and as high as 54°C (Nair et al., 2020). Salmonella grow at pH ranging from 4 to 9, with

optimum range of 6.5–7.5. Salmonella require high water activity of about 0.99–0.94 for

survival. At pH greater than 3.8, water activity greater than 0.94 and temperature higher than

70°C, it shows no growth. While almost all serotypes do not make indole, hydrolyze urea, or

deaminate phenylalanine or tryptophan, the majority of serotypes rapidly convert nitrate to

nitrite, ferment a range of carbohydrates with acid production (Nair et al., 2020).
Figure 1. Sources of Salmonella enterica infection

Source. (Nair et al., 2020).

1.2. Salmonella Nomenclature, Taxonomy and Serovars

The nomenclature system of Salmonella is a complex process. This genus is composed of two

main species, Salmonella enterica and Salmonella bongori. Salmonella enteric is further divided

into 06 subspecies on the basis of biochemical properties and genomic relatedness (Tanveer et

al., 2021). The subspecies are denoted by Roman numerals: I. S. enterica subsp. enterica; II. S.

enterica subsp. salamae; III. S. enterica subsp. arizonae; IIIa. S. enterica subsp. diarizonae; IV. S.

enterica subsp. houtenae; V. S. enterica subsp. indica. The S. enterica subsp. enterica (I) is most

common subspecies of Salmonella and is found to be predominantly associated with around 99%

of Salmonella infections in humans and warm blooded animals. The remaining 05 subspecies

and S. bongori are mainly attributed to Salmonella infections in cold blooded animals and are

rarely found in humans (Baldassarre et al., 2021). For serotypes in subspecies (I), CDC uses

names i.e. Enteritidis, Typhimurium, Choleraesuis and Typhi while as for the unnamed serotypes

described post 1966 antigenic formulae are used in subspecies II, IV, VI and S. bongori. The

name generally refers to the location (geographic) where the serovar/serotype was isolated first.

In order to avoid any confusion between species and serotype, the first letter of the named

serotype is written in capital and is not italicized. At the first citation of a serotype, the genus

name is given first, followed by the word “serotype” or abbreviated form “ser” and finally the

serotype name is written. One of the examples is Salmonella serotype or ser. Typhimurium.

Afterwards the genus name can be directly written followed by serotype name (e.g. Salmonella

Typhimurium or S. Typhimurium (Baldassarre et al., 2021).

1.2 Signs and Symptoms of Salmonella

Patients can have influenza like symptoms, a dull frontal headache, malaise, anorexia, a dry

cough, sore throat, and occasionally epistaxis. Constipation is a recurrent early symptom

although many patients will experience diarrhea at some point. Enteric fever can present as a

diarrheal illness and occasionally with bloody diarrhea. Most patients have abdominal pain that
is diffuse and poorly localized. Nausea is common, and vomiting occurs in more severe cases

(Daley et al., 2017). Other frequent symptoms include chills, hepatosplenomegaly, rash (rose

spots). Serotype analysis is the most common method that used for identification and

classification of Salmonella. The genus Salmonella includes 2000 serotypes of clinical standing

which are reported to be associated with human infection. Depending on the common clinical

symptoms, they have been divided into two groups (Enteric fever and food poisoning) (Dahora

et al., 2019).

1.3 Sources and Modes of Transmission of Salmonella Infection

Typhoidal Salmonella is transmitted predominantly through water or food contaminated with

human feces. The risk for infection is high in low- and middle-income countries where typhoidal

Salmonella is endemic and that have poor sanitation and lack of access to safe food and water

(7). Enteric fever in high-income countries is usually acquired abroad and is associated with

travel to areas of endemicity, although clusters may be associated with food preparers who are

chronic carriers of Salmonella serovar typhi (Carden et al., 2017).

 Table I. Clinically Important Salmonella Groups

Enteric fever group Food Poisoning group

Species Key features Species Key features

Salmonella typhi Typhoid S. typhimurium Gastroenteritis, Septicemia

Salmonella paratyphi Paratyphoid S. enetriditis Gastroenteritis, Septicemia

A, B, C

S. heidlberg Gastroenteritis

S. agona Gastroenteritis

S. indiana Gastroenteritis

S. newport Gastroenteritis

S. anatum Gastroenteritis, Septicemia

Source. (Carden et al., 2017).

1.3.1 Transmission of Salmonella Infection

The ingestion of contaminated food, these bacteria will colonize the intestines by invading

dendritic cells and enterocytes of the intestinal epithelium barrier. Salmonella species, which are

successful in passing this barrier, are confronted by proximal macrophages and may be

phagocytosed, or actively, invade the macrophages, using T3SS-1 and fimbriae, among other

bacterial surface adhesions (Betz et al., 2018). After being internalized by macrophages,

Salmonella then reside within a membrane bound compartment distinct from the phagosome and

lysosome known as the SCV. In this cellular compartment, Salmonella can survive and replicate

in the absence of host antimicrobial defense mechanisms, thereby evading endosomal fusion

with the NADPH oxidase complex (Blohmke et al., 2016). From within the SCVs, SPI-2 genes

are expressed encoding T3SS-2, which enables Salmonella to translocate a range of effector

proteins into the cytoplasm of the host cell including SigD/SopB, SipA, SipC, SodC-1, SopE2,

and Spt Pleading to their arrangement of the actin cytoskeleton. T3SS-2 has been described as

necessary for systemic virulence in murine models and survival within macrophages (Blohmke

et al., 2017).
 CHAPTER TWO

LITERATURE REVIEW

2.0 Pathogenicity of Salmonella

2.0.1 Anatomical Barriers to Infection

Upon ingestion of contaminated food or water by a human host, S. Typhi faces hostile conditions

in the stomach and small intestinal lumen before invading the terminal ileum (Bronner et al.,

2018). The very first barrier to infection is gastric acid. While a high proportion of bacteria are

likely killed in the stomach, for those that do survive, the exposure to acid may signal arrival in a

new host, acting as a stimulus for S. Typhi replication (Salerno-Goncalves et al., 2018). The

human gut microbiota, consisting of commensal bacteria colonising the gut lumen and mucosa,

is thought to play a key role in defence against pathogen invasion. Unlike S. Typhimurium,

which is able to metabolise butyrate produced by the microbiota and colonise the intestinal

lumen, S. Typhi and S. Paratyphi A lack the required operon (Bronner et al., 2018). Despite this,

stools rich in transcripts from methane-producing archaea have been associated with a

marginally lower risk of developing typhoid after human challenge, suggesting that the

microbiome may play a role in enteric fever susceptibility (Zhang et al., 2018). Salmonella

Typhi must traverse the bactericidal layer of mucus coating the intestinal wall. Mucus

predominantly consists of highly glycosylated proteins called mucins (Johansson and Hansson

2016). This layer changes dynamically in response to infection to strengthen the barrier; S. Typhi

infection induces upregulation of secreted gel-forming mucins MUC2 and MUC5B in an

intestinal co-culture model and ex vivo intestinal biopsies, respectively (Nickerson et al., 2018).
In addition to acting as a barrier, the mucus is enriched with antimicrobial peptides, including α-

defensins HD5 and HD6, and human β-defensins 1 and 2. In intestinal biopsies from human

volunteers administered S. Typhi vaccine strain Ty21a, HD5 messenger RNA (mRNA) was

downregulated, potentially representing a means of immune evasion (Jaslow et al., 2018).

However, β-defensins, shown to be bactericidal against S. Typhi in vitro, and protective in mice

infected intraperitoneally with S. Typhi, were unchanged. The bactericidal activity of β-defensins

against S. Typhi suggests that antimicrobial peptides could have potential as a therapy for

antibiotic-resistant enteric fever. In a Phase 3 trial, antimicrobial peptide surotomycin has been

demonstrated as non-inferior to vancomycin for Clostridium difficile treatment, indicating that

such an approach could be effective against gastrointestinal infections. Such a treatment could

hypothetically be used as a prophylactic in outbreak settings or reduce transmission through stool

shedding (Daley et al., 2017).

In addition to antimicrobial peptides, secretory immunoglobulin A (IgA) is thought to protect the

intestinal epithelium by blocking bacterial uptake and inhibiting flagellar motility (Betz et al.,

2018). The role of secretory IgA in protection against enteric fever is not yet well characterised.

In human challenge participants, a drop in peripheral B cells and a rise in B cell α4β7 expression

are observed during acute disease, suggestive of gut homing, while oral vaccination with

attenuated S. Typhi strain Ty21a significantly increases S. Typhi-specific stool IgA (Dahora et

al., 2019). Serum IgA is associated with protection in Vi-polysaccharide-vaccinated human

challenge participants, but no relationship has been elucidated between gut IgA and protection

against enteric fever. Interestingly, mice lacking the polymeric immunoglobulin receptor

required for IgA transport to the intestinal lumen are significantly more resistant to S.

Typhimurium infection, although the potential reasons for this are numerous—possibly due to

changes in the microbiome, compensation by serum antibodies or IgG, or reduced M-cell-

mediated uptake—and may act in combination. Underneath the mucus layer, the glycocalyx,
composed of glycolipids and glycoproteins extending from the plasma membrane of intestinal

epithelial cells, serves as an additional protective barrier (Betz et al., 2018). Salmonella

Typhimurium uses two glycosyl hydrolases, nanH and malS, to degrade the glycocalyx, without

which it is cannot efficiently invade. While the typhoidal serovars do not possess nanH, malS is

present in S. Typhi, S. Paratyphi A and S. Paratyphi B with over 97% sequence identity (UniProt

2019).

2.0.2 Invasion of the Intestinal Epithelium

The favorable outcome of a pathogen is based on its capability to enter a host, evade host defense

barrier and initiate infection. Salmonella has developed contrasting schedule to destabilize

normal host cellular functions that allow it to get involved in and multiple inside the host cell.

Depending upon the serotype of Salmonella involved and health status of human host, the

acuteness of Salmonella infection varies. Elderly people, immune-suppression patients and

children below 05 years of age are more prone to Salmonella infection. The ability of Salmonella

to invade, replicate and remain alive within the human host makes it more morbific that finally

results into harmful mortal disease (Brewer et al., 2019).

Salmonella produces different virulence factors that play an important role in its pathogenicity.

These involve: the potential to invade the cell; a perfect lipopolysaccharide coat; to replicate

intra-cellularly; and feasibly the secretion of toxins (Bronner et al., 2018). The organisms

establish a colony in ileum and colon after ingestion followed by occupying the intestinal

epithelium and grows rapidly within the epithelium and lymphoid follicles. Salmonella invasion

mechanism is partially understood. On epithelial cell surface there is the presence of specific

receptors. When the organism incursion occurs, enterocyte membrane goes through

disarrangement that results in pinocytosis of organism (Betz et al., 2018). Invasion depends on

rearrangement of cell cytoskeleton and may be entailed to increase in cellular inositol phosphate
and calcium (Zhang et al., 2018). After invasion, organism has ability to proliferate intra-

cellularly thereby escalating to mesenteric lymph nodes and all over the body by systematic

circulation; absorbed by reticulo-endothelial cells that limits and checks the expansion of an

organism. There is a perceptible genetic control involving multiple genes in both chromosomes

and plasmids for attachment and invasion. Some organisms has the ability to infect liver, spleen,

gall bladder, bone, meninges etc. depending upon the host defense. Human Salmonella

(gastroenteritis) resides in intestine. However, most serotypes get perished on time (Salerno-

Goncalves et al., 2018). After invading the intestine, most of Salmonellae brings on an acute

inflammatory response that may lead to ulceration, also they might elaborate cytotoxins that

forbid protein synthesis. It is not clear if these cytotoxins play a role in the inflammatory

response or ulceration. On the other hand, invasion of the mucosa induces epithelial cells to

produce and release pro-inflammatory cytokines such as IL-1, IL-6, IL-8, TNF-2, IFN-U, MCP-

1, and GM-CSF. These trigger an acute inflammatory response in the body and may also be

accountable to harm the intestine (Nickerson et al., 2018). Due to the inflammatory reaction,

symptoms such as fever, chills, stomach pain, leukocytosis, and diarrhea are frequent.

Polymorphonuclear leukocytes, blood, and mucus may be seen in the stool (Nickerson et al.,

2018).

One of the features of Salmonella is non-phagocytic nature on human host cells during invasion,

where it literally induces its own phagocytosis in order to gain access to its host cell (Betz et al.,

2018). Salmonella pathogenicity islands (SPIs), gene clusters positioned at the major

chromosomal DNA region and encoding for the structures required in the invasion activity,

provide the remarkable genetics that enable this brilliant technique (Dahora et al., 2019).

Bacteria tend to infiltrate the epithelial cells of the intestinal wall when they enter the digestive

tract via contaminated water or food. Type III secretion systems, or SPIs, are multi-channel

proteins that allow Salmonella to infuse its effectors into the cytoplasm via the intestinal
epithelial cell membrane. The bacterial effectors subsequently activate the signal transduction

pathway and lead the host cell’s actin cytoskeleton to be rebuilt, causing the epithelial cell

membrane to ruffle outward and engulf the bacteria. The membrane ruffle’s morphology is

similar to the process of phagocytosis (UniProt, 2019). The ability of the Salmonella strains to

remain in the host cell is important for pathogens as strains lacking this capability are non-

virulent (UniProt, 2019). After the host cell engulfs Salmonella, the bacterium is enclosed in a

membrane compartment called a vacuole, which is formed of the host cell membrane. The

presence of the bacterial foreign body activates the host cell immune response under normal

circumstances, which result in the fusion of the lysosomes and the secretion of the digestive

enzymes to break down the intracellular bacteria. Although, Salmonella uses the type III

secretion system to inject other effector proteins into the vacuole, it causes the modification of

the compartment structure. The re-assembled vacuole obstructs the fusion of the lysosomes and

this allows the intracellular survival and replication of the bacteria inside the host cells. The

ability of the bacteria to continue within macrophages allows them to be carried in the reticulo-

endothelial system (RES) (Yue et al., 2017).

2.1 Clinical Manifestations of Salmonella

2.1.1 Enteric Fever

Salmonella typhi is the etiological agent of typhoid fever. Since the clinical symptoms of

Paratyphoid fever are indistinguishable from typhoid fever, the term “enteric fever” is used

collectively for both fevers, and both S. typhi and S. paratyphi are referred as typhoid

Salmonella (Yin et al., 2020). Humans are the sole reservoir for the two strains of typhoid

Salmonella. Diarrhea is more commonly observed in children, whereas patients with

immunosuppression are more likely to develop constipation (Zhang et al., 2018)). During the

illness, enteric fever displays a specific fever pattern with an initial low-grade fever (> 37.5°C to
38.2°C) which slowly develops to high-grade fever (> 38.2°C to 41.5°C) in the second week.

Besides fever, infected patients may also develop myalgia, bradycardia, hepatomegaly (enlarged

liver), splenomegaly (enlarged spleen), and rose spots on their chest and abdomen (Salerno-

Goncalves et al., 2019)). In endemic regions, approximately 15% of the infected patients develop

gastrointestinal complications which include pancreatitis, hepatitis and cholecystitis.

Haemorrhage is one of the most severe gastrointestinal complications that occur as a result of

perforation of Payer’s patches, lymphatic nodules located at the terminal ileum, resulting in

bloody diarrhea. On top of that, the ability of typhoid Salmonella to survive and persist in the

RES results in relapse in approximately 10% of the infected patients (Yin et al., 2020).

2.1.2 Bacteremia and Other Extra Intestinal Complications

Salmonella bacteremia is a condition whereby the bacteria enter the blodstream after invading

the intestinal barrier. Almost all the serotypes of Salmonella can cause bacteremia, while S.

dublin and S. cholearaesuis are two invasive strains that are highly associated with the

manifestations of bacteremia (38). Similar to enteric fever, high fever is the characteristic

symptom of bacteremia, but without the formation of rose spots as observed in patients with

enteric fever. In severe conditions, the immune response triggered by bacteremia can lead to

septic shock, with a high mortality rate. Other extra intestinal complications include cellulites,

urinary tract infections, pneumonia, endocarditis and meningitis (Liew et al., 2019).

2.1.3 Miscarriage

A 34-year old multi gravid woman presented at 16 weeks of gestation with a Six-hour history of

abdominal pain, Similar to uterine contractions, and mild vaginal bleeding or 24 h prior to the

onset of abdominal pain she had felt generally unwell, with flu-Like symptoms, a headache, and

mild pyrexia (Samykannu et al., 2018). She had no gastrointestinal disturbance. The pregnancy

had otherwise been un-eventful that had undergone an ultrasound scan at seven weeks of
gestation for reassurance, as she had a history of a previous miscarriage at 11 weeks of gestation.

Her obstetric history also included a normal delivery at term and two early termination of

pregnancy. On examination she was distressed, requiring opiate analgesia (Salerno-Goncalves et

al., 2019). She was pyrexia, with a temperature of 37.6 °C. She had a tense, tender uterus on

palpation, and proceeded to deliver a 16- week male fetus, but failed to deliver the placenta, and

required an evacuation of retained products of conception. Postoperatively, her temperature set to

38.2 °C, and antibiotic therapy was started (Salerno-Goncalves et al., 2019). Twenty-four hours

later she was pyrexia with no abdominal pain and minimal vaginal blood loss and was

discharged home on oral antibiotics. A full count taken on admission had initially shown a raised

white cell count with neutrophilia and a high monocyte count, which returned to normal 24 h

post-miscarriage. A high vaginal swab was taken at the time of the evacuation of the placenta.

This grew Salmonella group C, which was Later further identified as being Salmonella virchow.

As part of the investigation into the cause of the mid-trimester miscarriage, the fetus and placenta

were histologically examined. Histology of the fetus confirmed a male fetus weighing 85 g,

equivalent to 16 weeks of gestation (Nickerson et al., 2018). There were no fetal malformations.

However, the histologic assessment of the placenta revealed the presence of intervillous thrombi

with focal perivillous and villous inflammatory changes. This was a true villitis associated with a

hematogenous infection. The placental tissue was then Gramstained, and this revealed numerous

colonies of Gram-negative bacilli within the fibrin between the villas. There was no significant

inflammation or colonization of the membranes and placental bed, as would be expected if this

had been an ascending infection. Two weeks prior to the miscarriage, the woman had been on

holiday in Turkey and had eaten an omelet, which she felt was undercooked (Nickerson et al.,

2018). Twenty-four hours after this she had symptoms of loose stools and atemperature for

oneday, but these symptoms were mild and no medical attention had been sought. There were no

other dietary or animal exposures to Salmonella. Based on this history, it was suggested that she
had contracted a Salmonella infection from eating undercooked eggs while on a holiday but had

remained well until the time of the miscarriage. Even the evidence of swabs taken from the

posterior fornix growing Salmonella, the placenta, histology showing hematogenous infection

with a Gram-negative bacillus, and the woman’s pyrexia and neutrophilia, it appears that the

miscarriage was caused by a Salmonella sepsis, with crossing of the infection to the placenta

itself and subsequent choric ammonites (Nuccio et al., 2018).

2.1.4 Salmonella typhi and Gallbladder Cancer

Global annual incidence of gallbladder cancer (GC) is 17 million cases with high incidence rates

in certain populations. The malignancy is usually associated with gallstone disease, late

diagnosis, unsatisfactory treatment, and poor prognosis. The five-year survival rate is

approximately 32 percent for lesions confined to the gallbladder mucosa and one-year survival

rate of 10 percent for more advanced stages Involving gallstones in 78% – 85% of cases (Ortega

et al., 2016). Over 90 percent of gallbladder carcinomas are adeno carcinoma (Parquet et al.,

2018). There are several risk factors for gallbladder cancer. The main associated risk factors

include cholelithiasis (especially untreated chronic symptomatic gallstones), obesity,

reproductive factors, and environmental exposure to certain chemicals, congenital developmental

abnormalities of the pancreatic bile-duct junction and chronic infections of the gallbladder

(Velasquez et al., 2016). The interplay of genetic susceptibility, lifestyle factors and infections in

gallbladder carcinogenesis is still poorly understood. However, a link has been specifically

proposed between chronic bacterial infections of the gallbladder and Salmonella typhi the

strongest epidemiological evidence of bacterial oncogenic potential, aside of Helicobacter pylori,

concerns S. typhi. Infection with this bacterium of typhoid, can lead to chronic bacterial carriage

in the gallbladder (Villa et al., 2020). Recent epidemiological studies have shown that those who

become carriers of S. typhi have several times the increased risk of developing carcinoma of the
gallbladder compared with people who have had acute typhoid and have cleared the infection.

These findings agreed with earlier investigations by (Villa et al., 2020).

CHAPTER THREE

3.0 CONCLUSION

Globally, Salmonellosis is the main cause of bacterial disease in all living creatures. All over the

world it is posing very serious public health concerns and compromising the yield and output of

animal husbandry production. The effort of isolating, identifying, and reporting Salmonella

serotypes must continue for diagnostic, therapeutic, and public health objectives, despite the fact

that the nomenclature for Salmonella is constantly evolving and the argument over the naming

for the type species is still ongoing. Salmonella outbreaks have been linked to a variety of foods,

and researchers are scrambling to figure out how this infection impacts humans and animals.

This infection is a leading source of morbidity and mortality worldwide, with the host immune

response differing depending on nature of infection. The genetic makeup of Salmonella made it

possible for its strains to adapt to different environmental conditions. The implications of this

infectious disease in humans vary depending on its serotype and the health level of the human

host.

3.1 RECOMMENDATION

Thus for better understanding the genetics of Salmonella and to investigate the mechanisms that

contribute to pathogenesis evolution, a lot of work has been done. Occurrence of two different,
potentially complementary evolutionary approaches to host range and virulence were evaluated

using genome sequencing of Salmonella serovars. It includes horizontal gene transfer, gene loss

which actually affects its ability to colonize. Gene acquisition by horizontal transfer (associated

with SPIs, transposable elements, phages, and plasmids) and gene loss or loss of function, which

affects host range. In spite of the presence a greater amount of research findings related to

Salmonella infection and pathogenesis mechanism in host animals, several key queries remain

intact viz the exact role of virulence genes and genomic islands of particular serovar in animal

model. Thus the need of hour is to have an in depth understanding of Salmonella pathogenesis

for developing intervention strategy to minimize the disease’s prevalence and spread, as well as

assisting in the production of novel drugs and treatments which might lead to improved treatment

of Salmonellosis in living creatures.

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