• DNA binding protein
• Salmonella typhi
• cell division activator protein
• inhibitors
• intrinsic apoptosis
• macrophages

• Salmonella typhi/drug effects
• Salmonella typhi/genetics
• Salmonella typhi/pathogenicity
• Humans
• Bacterial Proteins/metabolism
• Bacterial Proteins/genetics
• Apoptosis/drug effects
• Macrophages/microbiology
• Macrophages/drug effects
• THP-1 Cells
• DNA-Binding Proteins/metabolism
• DNA-Binding Proteins/genetics
• Autophagy/drug effects
• Typhoid Fever/microbiology
• Cell Division/drug effects

• bacteria
• biofilm formation
• chronic inflammation
• fungi
• gallbladder cancer
• metabolites
• virulence factors
• viruses

• Humans
• Gastrointestinal Microbiome
• Gallbladder Neoplasms/microbiology
• Bacteria/classification
• Bacteria/isolation & purification
• Animals
• Dysbiosis/microbiology
• Virulence Factors
• Fungi/pathogenicity
• Fungi/classification

• COVID
• SARS-CoV-2
• acalculous cholecystitis
• gallbladder

• Adult
• Humans
• COVID-19
• SARS-CoV-2/metabolism
• Acalculous Cholecystitis/diagnosis
• Peptidyl-Dipeptidase A/metabolism
• Cholecystitis, Acute
• Cholecystitis

• MDR
• QRDR
• XDR
• persistence
• quinolone-resistant

• Humans
• Salmonella typhi/genetics
• Typhoid Fever/drug therapy
• Typhoid Fever/microbiology
• Anti-Bacterial Agents/pharmacology
• Salmonella Infections/drug therapy
• DNA
• Microbial Sensitivity Tests

• ASTRA Chair Professorship and TATA Innovation fellowship funds
• CSIR-SRF fellowship
• DBT-IISc Partnership Program
• DAE0195 Department of Atomic Energy, Government of India
• Department of Biotechnology (DBT)
• IISc fellowship
• Ministry of Science and Technology; Department of Science and Technology (DST)

• Biliary perforation
• gall bladder
• peritonitis
• typhoid fever

• C. rodentium colitis
• colonic host defense peptides
• epithelial damage
• goblet cells
• high-fat/high cholesterol diets
• intestinal permeability
• mucus layer

The gallbladder (GB) microbiota plays critical roles in mammalian metabolism and immune homeostasis, and its relationship with human disease has been extensively studied over the past decade. However, very little is known about the interplay between GB microbiota and the immune functions of teleost fish, the earliest bony vertebrate with a GB. Therefore, this study sought to investigate the composition of the teleost GB microbiota and the potential mechanisms through which it affects mucosal immunity. In our results, we found that the GB mucosa (GM) and bile bacterial community shared a similar microbiological composition with that of the gut mucosa in naïve individuals. IHNV infection induced a profound GB inflammation and disrupted their microbial homeostasis followed by a strong anti-bacterial response. Interestingly, beneficial bacteria from the Lactobacillales order showed a significant increase in the abundance of the bile microbial community, whereas the structure of the Mycoplasmatales order in the gut microbial community was markedly changed. All in all, our study characterized the structure of the GB microbial ecosystem in teleost fish, and the fish GB microbiome shared a high similarity with the gut microbiota. More importantly, our findings offer solid evidence that the teleost GB evolved immune functions to preserve its mucosal microbial homeostasis, suggesting that both the microbiota and mucosal immunity of the GB might have co-evolved in early vertebrates.

• Animals
• Bacteria
• Fishes
• Gallbladder
• Homeostasis
• Humans
• Mammals
• Microbiota
• Mucous Membrane

• Abdominal Pain/etiology
• Acalculous Cholecystitis/diagnosis
• Acalculous Cholecystitis/diagnostic imaging
• Adolescent
• Female
• Hepatitis A/complications
• Hepatitis A/diagnosis
• Humans
• Jaundice
• Ultrasonography

• Salmonella
• bile salts
• pathogen
• translational fidelity

• Bile Acids and Salts
• Mutation
• Ribosomes
• Salmonella enterica

• R35 GM136213 NIGMS NIH HHS

Enteric fever is one of the major public health problems mainly in developing countries. Gallbladder perforation is very unusual. Enteric fever rarely causes gallbladder perforation. We report a case of gallbladder perforation due to enteric fever in an adult patient.

A 50-year-old female without any medical illness presented with a history of intermittent fever for two weeks and three days duration of severe abdominal pain. Upper abdominal tenderness and guarding were found in the abdominal examination. Ultrasonography showed thickening of the gallbladder wall and pericholecystic fluid collection. Magnetic resonance cholangiopancreatography revealed a distended gallbladder with sludge, diffuse wall thickening, and contained perforation with a mild amount of free fluid seen in the abdomen. With the diagnosis of type II gallbladder perforation, percutaneous ultrasonography-guided drainage was done. The culture of bile revealed positivity for Salmonella Typhi. Intra-venous antibiotic (ceftriaxone and gentamicin) was administered for 14 days. Four weeks later, cholecystectomy with peritoneal lavage was done. She was discharged on the 8th postoperative day.

Preoperative diagnosing of gallbladder perforation is challenging. The accurate treatment and precise timing of the surgery remain important. In most cases, cholecystectomy and abdominal lavage are adequate to treat gallbladder perforation.

Gallbladder perforation is a life-threatening surgical problem. The clinician should have a high index of awareness about this unusual surgical entity due to enteric fever and early diagnosis with prompt surgical intervention is necessary to improve patient outcomes.

•

Enteric fever is one of the major public health problems mainly in developing countries.

• Adult patient
• Case report
• Enteric fever
• Gallbladder perforation

• Salmonella
• gall bladder
• host–pathogen interaction
• invasion
• poultry

• Dublin
• Gallinarum
• Pullorum
• Salmonella
• Typhi
• carrier state
• immunity
• typhoid

Acute acalculous cholecystitis (AAC) is an inflammation of the gallbladder not associated with the presence of gallstones. It usually occurs in critically ill patients but it has also been implicated as a cause of cholecystitis in previously healthy individuals. In this subgroup of patients, infectious causes comprise the primary etiology. We, herein, discuss the pathophysiological mechanisms involved in AAC, focusing on the infectious causes. AAC associated with critical medical conditions is caused by bile stasis and gallbladder ischemia. Several mechanisms are reported to be involved in AAC in patients without underlying critical illness including direct invasion of the gallbladder epithelial cells, gallbladder vasculitis, obstruction of the biliary tree, and sequestration. We emphasize that multiple pathogenic mechanisms may concurrently contribute to the development of AAC in varying degrees. Awareness of the implicated pathogens is essential since it will allow a more focused examination of the histopathological specimens. In conclusion, additional research and a high degree of clinical suspicion are needed to clarify the complex spectrum of mechanisms that are involved in the pathogenesis of AAC.

• Cholecystitis
• Infectious causes
• Vasculitis
• Sequestration
• Epstein-Barr virus

Conrad Waddington’s epigenetic landscape, a visual metaphor for the development of multicellular organisms, is appropriate to depict the formation of phenotypic variants of bacterial cells. Examples of bacterial differentiation that result in morphological change have been known for decades. In addition, bacterial populations contain phenotypic cell variants that lack morphological change, and the advent of fluorescent protein technology and single-cell analysis has unveiled scores of examples. Cell-specific gene expression patterns can have a random origin or arise as a programmed event. When phenotypic cell-to-cell differences are heritable, bacterial lineages are formed. The mechanisms that transmit epigenetic states to daughter cells can have strikingly different levels of complexity, from the propagation of simple feedback loops to the formation of complex DNA methylation patterns. Game theory predicts that phenotypic heterogeneity can facilitate bacterial adaptation to hostile or unpredictable environments, serving either as a division of labor or as a bet hedging that anticipates future challenges. Experimental observation confirms the existence of both types of strategies in the bacterial world.

• DNA methylation
• bistability
• lineage formation
• noise
• phenotypic heterogeneity

• C57BL/6
• In silico
• Intracellular replication
• Salmonella
• Toxin–antitoxin system
• Virulence

Within the species of Salmonella enterica, there is significant diversity represented among the numerous subspecies and serovars. Collectively, these account for microbes with variable host ranges, from common plant and animal colonizers to extremely pathogenic and human-specific serovars. Despite these differences, many Salmonella species find commonality in the ability to form biofilms and the ability to cause acute, latent, or chronic disease. The exact outcome of infection depends on many factors such as the growth state of Salmonella, the environmental conditions encountered at the time of infection, as well as the infected host and immune response elicited. Here, we review the numerous biofilm lifestyles of Salmonella (on biotic and abiotic surfaces) and how the production of extracellular polymeric substances not only enhances long-term persistence outside the host but also is an essential function in chronic human infections. Furthermore, careful consideration is made for the events during initial infection that allow for gut transcytosis which, in conjunction with host immune functions, often determine the progression of disease. Both typhoidal and non-typhoidal salmonellae can cause chronic and/or secondary infections, thus the adaptive immune responses to both types of bacteria are discussed with particular attention to the differences between Salmonella Typhi, Salmonella Typhimurium, and invasive non-typhoidal Salmonella that can result in differential immune responses. Finally, while strides have been made in our understanding of immunity to Salmonella in the lymphoid organs, fewer definitive studies exist for intestinal and hepatobiliary immunity. By examining our current knowledge and what remains to be determined, we provide insight into new directions in the field of Salmonella immunity, particularly as it relates to chronic infection.

• Salmonella
• biofilm
• chronic infection
• hepatobiliary
• immunity

• gangrenous cholecystitis
• paediatric surgery
• subtotal cholecystectomy
• typhoid fever

• Inflammasome activation
• Salmonella Typhi
• Salmonella pathogenicity island-1
• Type III secretion System

Worldwide, neoplasms of the gastrointestinal tract have a very high incidence and mortality. Among these, colorectal cancer, which includes colon and rectum malignancies, representing both highest incidence and mortality. While gallbladder cancer, another neoplasm associated to gastrointestinal tract occurs less frequently. Genetic factors, inflammation and nutrition are important risk factors associated with colorectal cancer development. Likewise, pathogenic microorganisms inducing intestinal dysbiosis have become an important scope to determine the role of bacterial infection on tumorigenesis. Interestingly, in human biopsies of different types of gastrointestinal tract cancer, the presence of different bacterial strains, such as Fusobacterium nucleatum, Escherichia coli, Bacteroides fragilis and Salmonella enterica have been detected, and it has been considered as a high-risk factor to cancer development. Therefore, pathogens infection could contribute to neoplastic development through different mechanisms; including intestinal dysbiosis, inflammation, evasion of tumoral immune response and activation of pro-tumoral signaling pathways, such as β catenin. Here, we have reviewed the suggested bacterial molecular mechanisms and their possible role on development and progression of gastrointestinal neoplasms, focusing mainly on colon neoplasms, where the bacteria Fusobacterium nucleatum, Escherichia coli, Bacteroides fragilis and Salmonella enterica infect.

Neutrophil mobilization is a crucial response to protect the host against invading microorganisms. Neutrophil recruitment and removal have to be tightly regulated to prevent uncontrolled inflammation and excessive release of their toxic content causing tissue damage and subsequent organ dysfunctions. We show here the presence of live and apoptotic neutrophils in the cytoplasm of inflamed mammary, urinary and gall bladder epithelial cells following infection with E. coli and Salmonella bacteria. The entry process commenced with adherence of transmigrated neutrophils to the apical membrane of inflamed epithelial cells. Next, nuclear rearrangement and elongation associated with extensive actin polymerization enabled neutrophils to crawl and invaginate the apical membrane into cytoplasmic double membrane compartments. Scission of the invaginated cell membrane from the entry point and loss of these surrounding membranes released intracellular neutrophils into the cytoplasm where they undergone apoptotic death. The co-occurrence of this observation with bacterial invasion and formation of intracellular bacterial communities (IBCs) might link entry of infected neutrophils to the formation of IBCs and chronic carriage in E. coli mastitis and cystitis and Salmonella cholecystitis.

Enteric fever is a common infectious disease, especially in countries with poor sanitation and in the tropics. It is caused mainly by Salmonella typhi and accounts for nearly 27 million cases worldwide and 200,000 deaths annually. Enteric fever involves the reticuloendothelial system such as bone marrow, spleen, and liver. As it mostly involves the Peyer’s patches of the terminal ileum, enteric perforation occurs commonly. However, gallbladder perforation can also occur, though not very often. Ultrasound as well as computerized tomography (CT) abdomen and pelvis lack specificity for detecting gallbladder perforations in enteric fever. Diagnosis is usually confirmed intraoperatively when the gallbladder is visualized and perforation is seen. Gallbladder perforation is usually seen in acute cholecystitis when the gallbladder becomes necrotic and gangrenous. In acalculous cholecystitis, perforation is rare. Enteric fever is one of the rarest causes of acalculous cholecystitis, leading to perforation. Here, we present the case of a 20-year-old man who presented with fever for 10 days along with loose stools, vomiting, and acute abdomen. Labs showed leukopenia, positive Typhidot test but X-ray erect abdomen and ultrasound abdomen and pelvis were nonspecific. Only after resuscitation and exploration of the abdomen was it found that the gallbladder had multiple perforations. The patient was improved after eight days of postoperative intravenous antibiotics. This is a unique and rare presentation of such a common infectious disease.

• cholecystectomy
• cholecystitis
• enteric fever
• gallbladder
• perforation

• Cold shock protein
• RNA chaperone
• RNA–protein interaction
• Salmonella enterica
• YciF
• bile acid
• cell stress
• permeability
• porins
• stress response

During systemic infection of susceptible hosts, Salmonella enterica colonizes the gall bladder, which contains lethal concentrations of bile salts. Recovery of Salmonella cells from the gall bladder of infected mice yields two types of isolates: (i) bile-resistant mutants; (ii) isolates that survive lethal selection without mutation. Bile-resistant mutants are recovered at frequencies high enough to suggest that increased mutation rates may occur in the gall bladder, thus providing a tentative example of stress-induced mutation in a natural environment. However, most bile-resistant mutants characterized in this study show defects in traits that are relevant for Salmonella colonization of the animal host. Mutation may thus permit short-term adaptation to the gall bladder at the expense of losing fitness for transmission to new hosts. In contrast, non mutational adaptation may have evolved as a fitness-preserving strategy. Failure of RpoS⁻ mutants to colonize the gall bladder supports the involvement of the general stress response in non mutational adaptation.

• Salmonella enterica
• bacterial evolution
• enteric pathogens
• gene regulation
• host-pathogen interaction
• immunopathogenesis
• pathogenicity islands
• persistence
• virulence

• Carrier State
• Humans
• Risk Factors
• Salmonella Infections/diagnosis
• Salmonella Infections/drug therapy
• Salmonella Infections/microbiology
• Salmonella Infections/pathology
• Salmonella enterica/classification
• Salmonella enterica/pathogenicity
• Serogroup

• German-Israeli Foundation for Scientific Research and Development (GIF)
• Israel Science Foundation (ISF)

• Antibiotic susceptibility
• beta-glucuronidase
• biliary microbiome
• gallstone
• mucin
• phospholipase

Acute acalculous cholecystitis (AAC) is the inflammatory disease of the gallbladder in the absence of gallstones. AAC is estimated to represent at least 50% to 70% of all cases of acute cholecystitis during childhood. Although this pathology was originally described in critically ill or post-surgical patients, most pediatric cases have been observed during several infectious diseases. In addition to cases caused by bacterial and parasitic infections, most pediatric reports after 2000 described children developing AAC during viral illnesses (such as Epstein-Barr virus and hepatitis A virus infections). Moreover, some pediatric cases have been associated with several underlying chronic diseases and, in particular, with immune-mediated disorders. Here, we review the epidemiological aspects of pediatric AAC, and we discuss etiology, pathophysiology and clinical management, according to the cases reported in the medical literature.

• Acute acalculous cholecystitis
• Children
• Viral biliary disorders

• Acalculous Cholecystitis/diagnosis
• Acalculous Cholecystitis/epidemiology
• Acalculous Cholecystitis/etiology
• Acalculous Cholecystitis/therapy
• Anti-Bacterial Agents/therapeutic use
• Child
• Cholecystectomy
• Cholecystitis, Acute/epidemiology
• Cholecystitis, Acute/therapy
• Cholecystitis, Acute/virology
• Epstein-Barr Virus Infections/complications
• Epstein-Barr Virus Infections/immunology
• Epstein-Barr Virus Infections/virology
• Gallbladder/immunology
• Gallbladder/surgery
• Gallbladder/virology
• Hepatitis A/complications
• Hepatitis A/immunology
• Hepatitis A/virology
• Hepatitis A Virus, Human/isolation & purification
• Herpesvirus 4, Human/isolation & purification
• Humans
• Incidence
• Risk Factors
• Treatment Outcome

Salmonella enterica serovars Typhi and Typhimurium cause typhoid fever and gastroenteritis, respectively. A unique feature of typhoid infection is asymptomatic carriage within the gallbladder, which is linked with S. Typhi transmission. Despite this, S. Typhi responses to bile have been poorly studied. Transcriptome sequencing (RNA-Seq) of S. Typhi Ty2 and a clinical S. Typhi isolate belonging to the globally dominant H58 lineage (strain 129-0238), as well as S. Typhimurium 14028, revealed that 249, 389, and 453 genes, respectively, were differentially expressed in the presence of 3% bile compared to control cultures lacking bile. fad genes, the actP-acs operon, and putative sialic acid uptake and metabolism genes (t1787 to t1790) were upregulated in all strains following bile exposure, which may represent adaptation to the small intestine environment. Genes within the Salmonella pathogenicity island 1 (SPI-1), those encoding a type IIII secretion system (T3SS), and motility genes were significantly upregulated in both S. Typhi strains in bile but downregulated in S. Typhimurium. Western blots of the SPI-1 proteins SipC, SipD, SopB, and SopE validated the gene expression data. Consistent with this, bile significantly increased S. Typhi HeLa cell invasion, while S. Typhimurium invasion was significantly repressed. Protein stability assays demonstrated that in S. Typhi the half-life of HilD, the dominant regulator of SPI-1, is three times longer in the presence of bile; this increase in stability was independent of the acetyltransferase Pat. Overall, we found that S. Typhi exhibits a specific response to bile, especially with regard to virulence gene expression, which could impact pathogenesis and transmission.

• H58 clade
• RNA-Seq
• SPI-1 regulation
• bile responses
• cell invasion
• typhoid fever

• Salmonella
• bile salts
• chronic infection
• gall bladder
• gene regulation
• intestinal microbiome
• resistance to bile

• Salmonella-containing vacuole
• autophagy
• carrier state
• cytosolic bacteria
• extracellular
• intracellular lifestyle
• persistence
• transmission

• Animals
• Autophagy
• Host-Pathogen Interactions
• Humans
• Salmonella/genetics
• Salmonella/physiology
• Salmonella Infections/microbiology
• Salmonella Infections/physiopathology
• Salmonella Infections/transmission

• Citrobacter rodentium
• Salmonella enterica
• bile acids
• intestinal antimicrobial peptides
• mucins
• mucosal immunity

• Salmonella
• antibodies
• epidemiology
• immunity
• immunosuppression
• invasive disease
• modeling
• phagocytes
• vaccines

• DNABII
• Haemophilus influenzae
• Pseudomonas aeruginosa
• Salmonella
• animal models
• bacterial pathogenesis
• biofilm
• eDNA
• extracellular matrix
• matrix
• neutrophil
• phagocyte
• pilin
• polysaccharide

• Chronic inflammation
• Gallbladder cancer
• Gallstones
• Metaplasia
• Salmonella Typhi
• TP53

• Autoimmune Diseases/complications
• Bacterial Infections/complications
• Gallbladder Neoplasms/etiology
• Gallstones/complications
• Humans
• Inflammation/complications

• ZIA CP010218-01 Intramural NIH HHS

• Salmonella
• enteric fever
• flagella
• invasion
• motility
• paratyphoid
• pathogenicity
• pyrexia

• Cell Line
• Endocytosis/radiation effects
• Epithelial Cells/microbiology
• Epithelial Cells/radiation effects
• Fever
• Gene Expression Regulation, Bacterial/radiation effects
• Humans
• Locomotion/radiation effects
• Macrophages/microbiology
• Macrophages/radiation effects
• Salmonella enterica/genetics
• Salmonella enterica/physiology
• Salmonella enterica/radiation effects
• Temperature
• Virulence/radiation effects
• Virulence Factors/metabolism

• R01 AI073971 NIAID NIH HHS
• HHSN272200900040C NIAID NIH HHS
• HHSN272200900040C PHS HHS
• AI039557 NIAID NIH HHS
• AI073971 NIAID NIH HHS
• R01 AI083646 NIAID NIH HHS
• AI083646 NIAID NIH HHS
• R01 AI052237 NIAID NIH HHS
• R01 AI075093 NIAID NIH HHS
• AI052237 NIAID NIH HHS
• AI075093 NIAID NIH HHS
• AI077645 NIAID NIH HHS

The biliary system is in continuous contact with the complex microbiota of the intestine. Microbial products have recently been proposed as potential triggers for biliary diseases.

The aim of this review is to provide a summary of the current knowledge regarding the role of the biliary and intestinal microbiome in biliary inflammatory diseases.

Previously, it was suggested that the healthy biliary system is a sterile organ, while acute cholangitis and cholecystitis may occur from ascending infections. Although non-inflammatory biliary colonization by certain bacteria such as Salmonella spp. has been already recognized since several decades, human and animal studies indicated only very recently that the gallbladder harbors a complex microbiota also under non-pathologic conditions. Novel findings suggested that – similar to the situation in the intestine – the biliary mucosa features a chemical, mechanical, and immunological barrier, ensuring immunological tolerance against commensals. However, microbial triggers might influence acute and chronic inflammatory disease of the biliary system and the whole liver.

Although yet undefined, dysbiosis of the biliary or intestinal microbiota rather than a single microorganism may influence disease progression.

• Bile acids
• Cholecystolithiasis
• Gallstones
• Microbiome
• Microbiota
• PBC
• PSC
• Primary biliary cirrhosis
• Primary sclerosing cholangitis

The availability of ontologies and systematic documentations of phenotypes and their genetic associations has enabled large-scale network-based global analyses of the association between the complete collection of phenotypes (phenome) and genes. To provide a fundamental understanding of how the network information is relevant to phenotype-gene associations, we analyze the circular bigraphs (CBGs) in OMIM human disease phenotype-gene association network and MGI mouse phentoype-gene association network, and introduce a bi-random walk (BiRW) algorithm to capture the CBG patterns in the networks for unveiling human and mouse phenome-genome association. BiRW performs separate random walk simultaneously on gene interaction network and phenotype similarity network to explore gene paths and phenotype paths in CBGs of different sizes to summarize their associations as predictions.

The analysis of both OMIM and MGI associations revealed that majority of the phenotype-gene associations are covered by CBG patterns of small path lengths, and there is a clear correlation between the CBG coverage and the predictability of the phenotype-gene associations. In the experiments on recovering known associations in cross-validations on human disease phenotypes and mouse phenotypes, BiRW effectively improved prediction performance over the compared methods. The constructed global human disease phenome-genome association map also revealed interesting new predictions and phenotype-gene modules by disease classes.

• Algorithms
• Animals
• Area Under Curve
• Gastrointestinal Diseases/genetics
• Gene Regulatory Networks
• Genetic Association Studies
• Genome
• Humans
• Mice
• Phenotype
• Protein Interaction Maps

• bacterial pathogens
• cellular slime moulds
• glycoside hydrolase family 18
• virulence factors

• Animals
• Cell Line
• Chitinases/genetics
• Chitinases/metabolism
• Dictyostelium/microbiology
• Gene Expression Regulation, Bacterial
• HeLa Cells
• Humans
• Listeria monocytogenes/enzymology
• Listeria monocytogenes/pathogenicity
• Listeria monocytogenes/physiology
• Mice
• Microbial Viability
• Salmonella Infections, Animal/microbiology
• Salmonella typhimurium/enzymology
• Salmonella typhimurium/pathogenicity
• Salmonella typhimurium/physiology
• Sequence Deletion
• Virulence Factors/genetics
• Virulence Factors/metabolism

• Autism
• Parkinson's disease
• cholestasis
• glyphosate
• manganese

• Aged
• Aged, 80 and over
• Cholecystectomy
• Cholecystitis, Acute/diagnostic imaging
• Cholecystitis, Acute/surgery
• Female
• Humans
• Male
• Middle Aged
• Retrospective Studies
• Severity of Illness Index
• Ultrasonography

• Salmonella
• antimicrobials
• gallbladder
• pig

• Salmonella
• chronic carrier
• diagnostics
• epidemiology
• typhoid fever

• Carrier State/microbiology
• Gallbladder/microbiology
• Host-Pathogen Interactions
• Humans
• Paratyphoid Fever/microbiology
• Salmonella paratyphi A/growth & development
• Salmonella typhi/growth & development
• Typhoid Fever/microbiology

• AI058935 NIAID NIH HHS
• R01 AI066208 NIAID NIH HHS
• AI100023 NIAID NIH HHS
• R33 AI100023 NIAID NIH HHS
• R01 AI106878 NIAID NIH HHS
• U01 AI058935 NIAID NIH HHS
• AI066208 NIAID NIH HHS
• R21 AI100023 NIAID NIH HHS
• 100087 Wellcome Trust
• AI106878 NIAID NIH HHS
• K08 AI089721 NIAID NIH HHS
• Wellcome Trust
• R56 AI109002 NIAID NIH HHS
• R56 AI106878 NIAID NIH HHS
• R37 AI106878 NIAID NIH HHS
• 100087/Z/12/Z Wellcome Trust

Human infections by the bacterial pathogen Salmonella enterica represent major disease burdens worldwide. This highly ubiquitous species consists of more than 2600 different serovars that can be divided into typhoidal and non-typhoidal Salmonella (NTS) serovars. Despite their genetic similarity, these two groups elicit very different diseases and distinct immune responses in humans. Comparative analyses of the genomes of multiple Salmonella serovars have begun to explain the basis of the variation in disease manifestations. Recent advances in modeling both enteric fever and intestinal gastroenteritis in mice will facilitate investigation into both the bacterial- and host-mediated mechanisms involved in salmonelloses. Understanding the genetic and molecular mechanisms responsible for differences in disease outcome will augment our understanding of Salmonella pathogenesis, host immunity, and the molecular basis of host specificity. This review outlines the differences in epidemiology, clinical manifestations, and the human immune response to typhoidal and NTS infections and summarizes the current thinking on why these differences might exist.

• NTS
• Salmonella enterica
• enteric fever
• gastroenteritis
• salmonellosis
• typhoid

• promoters
• ramR
• surface plasmon resonance
• transcriptional regulation