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Salmonella Enterica

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Angela Su

on 18 November 2014

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Transcript of Salmonella Enterica

Salmonella Enterica
Background
Spread of Bacteria
Enterica is a effective pathogen because it produces an endotoxin similar to gram negative bacteria called invasin which allows non pathogenic cells to take up the bacteria, where it is able to live intracellular, it is also able to inhibit the oxidative burst of leukocytes making innate immuno response enefective.

The most common source of infection is drinking water tainted by urine and feces of infected individuals.

The bacteria enters the human body by ingestion and incubates in the intestine for about 3 - 5 days, and then infiltrates the body and infects the organ system. The human body cannot fight the bacteria because of the inhibition of oxidative lysis.

Systematic inflammatory response triggered by pathogenic gram-negative bacteria largely depends on the release of lipoposacharides LPS from the bacterial cell wall.
Research Focus
Study of BapA - 2005
BapA is a cell-surface protein required for biofilm formation by Salmonella Enterica S. Enteritidis.
biofilm is usually composed of curli fimbriae and cellulose.
With out BapA a biofilm matrix is not formed
orally inoculated animals with a bapA-deficient strain survived longer than those inoculated with the wild-type strain.
why salmonella enterica can survive in harsh environments(GI track)
they have to withstand nutrient differences, temperature, pH, and osmotic pressure
Cell Metabolism
prevention
Thoroughly cook all meats and eggs.
Use proper cooking temperatures for certain meats.
Wash hands, counters, utensils, with hot soapy water.
Separation of meats to other food items inside the refrigerator.
Red meat, poultry and sea food are more susceptible in carrying the bacteria.
it is possible to control transmission by proper hygiene, waste management, water purification and treatment of the sick.
Treatment
There is no treatment for humans as of today, the only thing to do is to let the body expel the bacteria through the feces.
The bacteria causes gastrointestinal inflammation which ends up causing diarrhea and dehydrates the body. Diarrhea is the bacterias way to infect other individuals, a way of transmission.
For more extreme cases like babies or the elderly, they are given a combination of antibiotics in order to kill the bacteria, but so,stiles this method is hard since there are several strans of the bacteria which are strong or immune to antibiotics.
Mixed-acid fermentation of glucose to produce ATP, CO2 and H2 with various acid end-products.

S. enterica can also feed on maltose through a type I, ATP-binding cassette(ABC) transporter.

From a gene sequence salmonella was predicted to have 3 membrane associated enzyme, this enzyme allow the bacteria to use obtain energy by splitting the hydrogen.
The development of disease from Salmonella Enterica depends on the Type III secretion system (T3SS) encoded by Salmonella Pathogencity island-2 (SPI-2). T3SS allows Salmonella to secrete effector proteins into the host cell causing symptoms and enables bacterial replication.

The main feature of the T3SS is the needle complex (NC), bacterial proteins that need to secreted into the host cytoplasm are passed through the NC. It provides a smooth passage though the highly selective and almost impermeable membranes, it is also used as a sensory probe to detect the presence of eukaryotic organisms.

Salmonella replicate and invade better in the ileum than the cecum of animal intestine due to the different ion presented in these regions, the ileum contains formate and acetate which triggers the secretion mechanism, molecules such as propionate and butyrate in the cecum serves as an inhibitor to the T3SS.

Secretion proteins are involved in host cell invasion and intercellular proliferation, once internalized by the host cell Salmonella subverts the endolysosome trafficking path way to create Salmonella containing vacuole (SCV)

A large number of fimbrial and non-fimbrial adhesins are present in Salmonella, which mediate biofilm formation which can form contact with the host cells.
Type 3 Sceretion system
(T3SS)
T3SS continued...
Salmonella Enterica (Background: Structure and Lifecycle)
- Discovered by Dr. Daniel Salmon
- 95-99% genetically identical
- Enteric : infect the intestine
3 Main Serovars
1) Typhimurium
2) Enteritidis
3) Tyhi
- Serovars: used to identify bacteria based on external (surface) antigen.
S. Typhimurium
- Gram Negative
- LPS (endotoxin) = O-antigen is the outermost on LPS
- Damages epithelial cells lining intestine
- Responsible for induction of immune response
- Typhimurium has the ability to acetylate O-antigen, which lead to a change in conformation, making it difficult to be recognized by antibodies
- Causes Gastroenteritis (aka infectious diarrhea)
- Secretes Auto inducers (LuxS): communicate with nearby cells (quorum sensing)
- Infects through direct contact with other cells
- contact is followed by the formation of appendages on the bacterial surface (shorter but thicker than flagella)
S. Typhi
- Gram Negative
- Causes Typhoid fever
- Rod-shaped + flagellated
- Only infects humans
- Spreads through contaminated water and undercooked food
- Has evolved resistance to antibiotics
- 2 membranes (inner + outer)
- Lipopolysaccharide chains (endotoxin)
- V(i) antigen: increases resistance to human macrophages and oxidative killing (not required for infection )
- Produces Invasin (protein): allows for non-phagocytotic cells to engulf the bacteria (survive internally)

Enteritidis
- Rod-shaped, Gram Negative
- Non-Motile
- Adapted to infect animal hosts (humans not most prominent victims)
- AHL (Quorum sensing)

Life Cycle
VBNC State
- Enhanced external survival: increases transmission to new host
- Viable but non-culturable state (stressful/ external conditions)
- Constantly released into environment from infected host
- phoN gene: periplasmic nonspecific acid phosphatase
-Detoxification of heavy metals that accumulate in metal-contaminated soil.
Study on the effects of cinnamon, mustard essential oils and Zein coatings on cherry tomatoes - Salmonella Enterica Enterica serovar Typhimurium -2014
zein is class of prolamine protein found in corn and is used in many industrial and food uses.
cinnamon and mustard oils are used because they have a natural antimicrobial mechanism that is still not well understood.
the cell hydrophobicity of essential oils are associated with cell membrane damage by disrupting cell structures and function.
leakage of ions and other cell contents.
loss of original shape and a development of a bumpy surface.
control had greater loss in water, firmness, color and vitamin C in 21 days of storage.
Enterica strains overproduce a cell- destroying toxin. Salmonella Enterica disables the microphages by switching their gene expression pattern from a less virulent state to a more virulent state during infection. This results in the overproduction of its toxin, an actin- destroying protein which severely weakens the outer structure of cells, particularly targeting the immune system.
Quorum Sensing: Modification of gene expression patterns in response to extracellular concentration of species-specific signal molecules
LuxS-mediated quorum sensing system in S. enterica
Autoinducer-2 (AI-2) is signaling molecule
invF gene expression (transcription) directly related to AI-2 activity
AI-2 activity significantly increases during early log phase, peaking at late log phase, then decreasing to approximately 25% of maximum
Serotype Typhimurium: LuxS gene required for AI-2 “burst” since it encodes AI-2 synthase
invF transcription necessitates LuxS protein
SPI-1 pathogenicity island encodes proteins allowing for invasion of epithelial cells/virulence (Type III Secretion System)
LuxS deletion mutant results in attenuation of virulence
mRNA levels in particular components of SPI-1 (virulent) decreased significantly with LuxS mutant
Quorum Sensing
Full transcript