How does Shigella invade cells?

During intracellular replication, Shigella moves by polymerizing actin at one bacterial pole, forming actin comet tails, allowing the formation of bacteria-containing protrusions at the cell plasma membrane that invade adjacent cells.

What is the mode of transmission for Shigella?

Shigella can pass from stool or soiled fingers of one person to the mouth of another person, including during sexual activity. Many Shigella outbreaks among this population have been reported in the United States, Canada, Japan, and Europe since 1999.

What is the molecular mechanism by which Shigella enters host cells?

Effector proteins Invasion of plasmid antigen B (IpaB) initiates binding to the host cell while also initiating pathways that kill macrophages upon infection, IpaC activates proteins to form the actin-polymerizing complex that allows Shigella to move and spread within host cells [3].

What are the virulence factors of Shigella?

Invasion plasmid antigens (Ipas) include IpaA, IpaB, IpaC and IpaD proteins. Ipa proteins are the important virulence factors in Shigella. IpaA structure has three vinculin binding sites (VBSs) that can activate vinculin by the binding to the vinculin head domain (Park et al., 2011).

How do virulence factors work?

Virulence factors help bacteria to (1) invade the host, (2) cause disease, and (3) evade host defenses. The following are types of virulence factors: Adherence Factors: Many pathogenic bacteria colonize mucosal sites by using pili (fimbriae) to adhere to cells.

Who is shigellosis?

Shigella bacteria cause an infection called shigellosis. Most people with Shigella infection have diarrhea (sometimes bloody), fever, and stomach cramps. Symptoms usually begin 1–2 days after infection and last 7 days. Most people recover without needing antibiotics.

What is the difference between salmonella and Shigella?

Salmonella will not ferment lactose, but produce hydrogen sulfide (H2S) gas. The resulting bacterial colonies will appear colorless with black centers. Shigella do not ferment lactose or produce hydrogen sulfide gas, so the resulting colonies will be colorless.

What is the pathophysiology of Shigella?

Shigella bacteria invade the intestinal epithelium through M cells and proceed to spread from cell to cell, causing death and sloughing of contiguously invaded epithelial cells and inducing a potent inflammatory response resulting in the characteristic dysentery syndrome.

How does Shigella enter the body?

Shigella spp. are transmitted by the fecal-oral route and enter the human body via the ingestion of contaminated food or water. The bacteria are highly infectious, since as few as 10 to 100 microorganisms are sufficient to cause disease (61).

What is the pathogenesis of Shigella?

Pathogenesis. Shigella infection is typically by ingestion. Depending on the health of the host, fewer than 100 bacterial cells can be enough to cause an infection. Shigella species generally invade the epithelial lining of the colon, causing severe inflammation and death of the cells lining the colon.

What is the morphology of Shigella?

Shigella species are small Gram negative rods, 0.3 – 1µm in diameter and 1 – 6µm in length, appearing singly, in pairs and in chains. Shigella species are facultative anaerobes and are non-spore formers.

What kind of secretion system does Shigella have?

Shigella possesses a Type III secretion system (T3SS), which is a needle-like structure that penetrates the host cell membrane, and is an important virulence factor for cell entry. The T3SS injects a protein called IpaC into host cells, which causes the host cells to produce actin-rich filaments (a component of the cell’s skeleton).

How does Shigella initiate the process of adhesion?

In Shigella, the bacterial proteins responsible for adhesion are the same as those that initiate the process of invasion. Following adherence, Shigella initiate activation of T3SS and secretion of effector proteins into the host cell (Fig. 2a).

What happens to the macrophage when exposed to Shigella?

When the macrophage is exposed to shigella, it undergoes apoptosis (programmed cell death) and releases proinflammatory cytokine interleukin 1 (IL-1). Cytokines are small, soluble proteins that mediate inflammatory reactions and immunity.

How does Shigella dysenteriae enter the host cell?

The process begins when the B subunits bind to the host cell at a surface receptor, globotriaosylceramide (Gb3) (see figure 2). This initiates an uptake mechanism by the host cell, and eventually the toxin will gain access to the cytoplasm, which is the interior part of the host cell.