Where is salmonella typhimurium found

Enterobacter sakazakii requires OmpA for invasion of brain endothelial cells via induction of microtubule condensation Singamsetty et al. The implications of Salmonella burden in various parts of the brain could be far reaching. Proliferation of the pathogen in various brain parts could be associated with an enormous variety of neurological symptoms.

Moreover, we found a very high proliferation capacity in neuronal cell lines bolstering our hypothesis that the neurological manifestations post-infection are effects of possible cell death or modulation in the brain. Further, cellular endotoxins are known to induce inflammation in substantia nigra dopaminergic neurons. Hippocampal slice cultures were found to undergo neurodegeneration in presence of Salmonella LPS Johansson et al.

Interestingly, sepsis has been found to make the blood-brain barrier leaky Brandtzaeg et al. Effects mediated by endotoxins could therefore lead to a battery of symptoms in context of the neurological manifestations. Glial cells could also serve as a niche for Salmonella in the brain. Conceivably, Salmonella would be less proliferative in glial cells, however, they may act as a niche harboring persister populations. With the average life-span of humans getting extended every decade and the complexities in modern lifestyles, we are also witnessing an increase in the incidences of neurological abnormalities ranging from depression, anxiety, bipolar disorders to diseases like Parkinson's disease and Alzheimer's disease.

In view of the enhanced incidences, the possible causes such as external pathogens are of outstanding importance. With genetic predisposition to such conditions on one hand, such external agents as bacterial infections could be viewed with heightened seriousness and in turn avoided. A recent report has drawn connections between Alzheimer's disease and Salmonella Kumar et al. Plaques were observed to be formed around the bacterial cells thereby entrapping them. Very conceivably, this phenomenon could easily steer toward an unpleasant outcome for the host in the absence of a very tight regulation.

This arena calls for a much greater understanding to actually unveil the cause and effect scenario of intracellular bacterial pathogens in the brain and allow active alleviation of the avoidable causes of neurological manifestations. Wild type WT S. Overnight cultures prepared from inoculation of a single colony from a fresh plate were used for infecting mice at the mentioned dosage. Either overnight culture or subcultured bacteria were used for cell-line experiments. Briefly, the kanamycin resistance gene cassette was PCR amplified from pKD4 plasmid using specific primers which also carried sequences homologous to the flanking region of the target gene.

The knockouts were confirmed using both primers against the gene of interest as well as Kan R cassette internal primers. Michael Hensel. The murine macrophage cell line RAW A monolayer of respective cells was infected with either overnight or 0.

Bacterial attachment to host cells was enhanced by centrifuging at —1, rpm for 5 min. Infected cells were lysed using 0. Fold Proliferation:. Percent invasion:. Percent invasion was calculated as: no. For immunofluorescence analysis, RAW At indicated time points post-infection, cells were washed with PBS and fixed with 3.

Post-washes, cells were then incubated with appropriate secondary antibody conjugated with fluorophores. Coverslips were mounted on a glass slide containing mounting medium. Images were analyzed using the Zen software provided by Zeiss.

Two strains of mice, 4—6 weeks old were used viz. For intraperitoneal infections, mice were injected with 10 4 bacterial cells into the peritoneal cavity and dissected 3rd day post-infection. Behavioral studies were carried out with the mice both pre and post-infection by water maze test. The dose was determined based on literature Brunner and Zeiler, and the length of treatment determined on the survival of the control group receiving placebo. The 5th day dissection was carried out to ensure proper infection of the cohort.

The main comparison of bacterial burden was done between the placebo treated group and the antibiotic treated group at the end of the entire experiment. Behavioral tests were carried out pre and post-infection as well as post-antibiotic treatment. In all the experiments, the mice were sacrificed and organs isolated under asceptic conditions. The samples were weighed, homogenized using a bead-beater and plated on Salmonella-Shigella agar to obtain the CFU burden in the organs.

In all experiments, each group contained 4—6 mice and 2—6 independent experiments were performed unless otherwise mentioned. Mouse organs were isolated aseptically and fixed with paraformaldehyde. Following dehydration, sections embedded in paraffin were obtained using a microtome. Haematoxylin-eosin staining was performed for some sections while others were processed for staining with antibody against Salmonella O antigen. DC designed and carried out all experiments.

BB helped in the cell line experiments. AR carried out animal experiments with DC. DC and DiC wrote the manuscript. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Shyamala Mani is acknowledged for Neuro2a cell line. Central animal facility, IISc is acknowledged. Vani Ravikumar is acknowledged for helping with histological analysis. Ali, G. Spectrum of neuropsychiatric complications in cases of typhoid fever. Health 2, — Bauler, T. Salmonella meningitis associated with monocyte infiltration in mice.

Bollen, W. Presence of wild-type and attenuated Salmonella enterica strains in brain tissues following inoculation of mice by different routes. Brandtzaeg, P. Plasma endotoxin as a predictor of multiple organ failure and death in systemic meningococcal disease.

Brunner, H. Oral ciprofloxacin treatment for Salmonella typhimurium infection of normal and immunocompromised mice. Agents Chemother. Datsenko, K. Dewan, P. Isolated cerebellar ataxia: an early neurological complication of enteric fever. Drevets, D. Invasion of the central nervous system by intracellular bacteria.

Herrera, A. The single intranigral injection of LPS as a new model for studying the selective effects of inflammatory reactions on dopaminergic system. Huang, S. Cellular mechanisms of microbial proteins contributing to invasion of the blood-brain barrier. Inoue, H. Rinsho Shinkeigaku 35, — PubMed Abstract Google Scholar. Jeannin, P.

Outer membrane protein A OmpA : a new pathogen-associated molecular pattern that interacts with antigen presenting cells-impact on vaccine strategies. Vaccine 20 Suppl. Jin, Y. Neural route of cerebral Listeria monocytogenes murine infection: role of immune response mechanisms in controlling bacterial neuroinvasion. Johansson, S. Salmonella lipopolysaccharide LPS mediated neurodegeneration in hippocampal slice cultures. Joshi, N.

Cranial nerve palsies in typhoid fever: report of three cases. Read the full Outbreak Investigation. Sign up for RSS Feed. Section Navigation. Facebook Twitter LinkedIn Syndicate. Minus Related Pages. What are the signs and symptoms of Salmonella infection? Most people infected with Salmonella develop the following signs and symptoms hours after being exposed to the bacteria: Diarrhea Fever Abdominal cramps How long does the illness last?

Others develop diarrhea, fever and abdominal cramps within eight to 72 hours. Most healthy people recover within a few days without specific treatment. In some cases, the diarrhea associated with salmonella infection can be so dehydrating as to require prompt medical attention.

Life-threatening complications also may develop if the infection spreads beyond your intestines. Your risk of acquiring salmonella infection is higher if you travel to countries with poor sanitation.

Salmonella infection is usually caused by eating raw or undercooked meat, poultry, eggs or egg products. The incubation period ranges from several hours to two days. Most salmonella infections can be classified as stomach flu gastroenteritis. Possible signs and symptoms include:. Signs and symptoms of salmonella infection generally last two to seven days.

Diarrhea may last up to 10 days, although it may take several months before bowels return to normal. A few varieties of salmonella bacteria result in typhoid fever, a sometimes deadly disease that is more common in developing countries.

Salmonella bacteria live in the intestines of people, animals and birds. Most people are infected with salmonella by eating foods that have been contaminated by feces. Commonly infected foods include:. The Food and Drug Administration also indicates that some salmonella outbreaks have been traced to contaminants in spices. The agency is seeking ways to increase the safety of spices. Many foods become contaminated when prepared by people who don't wash their hands thoroughly after using the toilet or changing a diaper.

Infection also can occur if you touch something that is contaminated, including pets, especially birds and reptiles, and then put your fingers in your mouth. Factors that may increase your risk of salmonella infection include activities that may bring you into closer contact with salmonella bacteria and health problems that may weaken your resistance to infection in general. Your body has many natural defenses against salmonella infection.