Chronic Salmonella Infection
Chronic Salmonella Infection - Related Videos
09:01
Chronic Salmonella Infected Mouse Model
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Cited by 12 •
2010
Establish a chronic bacterial infected mouse model with persistent Salmonella typhimurium colonization in intestine for 27 weeks.
08:40
Chronic Salmonella Infection Induced Intestinal Fibrosis
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Cited by 4 •
2019
This protocol describes a mouse model of Salmonella driven intestinal fibrosis that resembles key pathological hallmarks of Crohn’s disease including transmural inflammation and fibrosis. This method can be used to evaluate host factors that alter fibrotic outcomes using mutant mice maintained on a C57Bl/6 genetic background.
06:50
A Protocol to Infect Caenorhabditis elegans with Salmonella typhimurium
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Cited by 1 •
2014
C. elegans has emerged as a new genetic model to study host-pathogen interactions. Here we describe a protocol to infect C. elegans with Salmonella typhimurium coupled with the double-strand RNAi interference technique to examine the role of host genes in defense against Salmonella infection.
06:27
An Assay to Quantify Cytosolic and Vacuolar Salmonella in Infected Primary Macrophages
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2025
This video demonstrates an assay to quantify cytosolic and vacuolar Salmonella typhimurium inside bone marrow-derived macrophages using differential permeabilization. The macrophages are infected with a fluorescent protein-expressing Salmonella, which is internalized inside a specialized vacuolar structure called Salmonella-containing vacuole or SCV. A subset of bacteria escape the SCV and enter the cytosol. The cholesterol-rich plasma membrane of macrophages is permeabilized using digitonin,...
15:43
Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice
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Cited by 78 •
2014
We describe the agar-beads method to establish persistent long-term chronic Pseudomonas aeruginosa airway infection in the mouse model.
FAQs
Persistence within macrophages can help Salmonella remain protected in host tissues after the initial illness. This intracellular location is important because it links cellular survival with prolonged infection and may help explain why some infections relapse. In biology research, examining host-pathogen interactions at this cellular level clarifies how bacterial persistence differs from a short-lived infection.
For Salmonella Typhi, the gallbladder can provide a site for long-term colonization, while biofilms forming on gallstones may support bacterial persistence. A biofilm is a structured bacterial community attached to a surface. This arrangement matters because it can contribute to intermittent shedding in feces, connecting gallbladder colonization with continued transmission and chronic carriage.
A person may have few or no symptoms while Salmonella remains present and is shed intermittently in feces. This creates an important difference between clinical illness and transmission risk: the absence of obvious disease does not necessarily indicate that persistence has ended. Studying this pattern helps explain prolonged spread, relapse, and the difficulty of recognizing chronic carriers.
Investigators may use culture-based or molecular detection approaches to look for persistent Salmonella after the initial illness. These strategies support assessment of whether bacteria remain present even when symptoms are limited or absent. Their use is relevant to studying chronic carriage, evaluating possible relapse, and informing decisions about treatment and transmission control.
This condition provides a model for studying bacterial persistence, intracellular survival, colonization of host sites, and host-pathogen interactions. Researchers can also examine how prolonged carriage relates to intermittent fecal shedding and transmission. These questions connect cellular mechanisms with broader biological outcomes, including relapse and the maintenance of infection over an extended period.
Persistent infection can require attention beyond the resolution of initial symptoms because bacteria may remain capable of transmission. Understanding where Salmonella survives and how it is detected can guide treatment strategies and support antimicrobial stewardship. The same knowledge helps inform outbreak prevention by identifying mechanisms that contribute to continued shedding and spread.