Shigella dysenteriae is a species of gram-negative, facultatively anaerobic, rod-shaped bacteria that is extremely pathogenic and causes severe dysentery.
Infection with this organism often leads to ulceration of the intestinal epithelium.
It is known to produce an exotoxin (Shiga toxin) which disrupts protein synthesis and produces endothelial damage.
Shigella spread via fecal-oral and person-to-person transmission.
Table of Contents
Pathogenicity of Shigella dysenteriae
- By entering and multiplying in the cells lining the colon, Shigella spread illness.
- The invasion, intracellular replication, and cell-to-cell dissemination of the organisms are all mediated by structural gene proteins.
- These genes are controlled by chromosomal genes while being carried on a large virulence plasmid. Therefore, the plasmid's existence does not guarantee that genes are functioning.
- They first bind to and infiltrate the M cells present in Peyer patches rather than differentiating mucosal cells.
- IpaA, IpaB, IpaC, and IpaD are four proteins that are secreted into macrophages and epithelial cells via the type III secretion system.
- These proteins cause the target cell's membrane to ripple, allowing the bacteria to be engulfed.
- Shigella, in contrast to Salmonella, lyse the phagocytic vacuole and multiply in the cytoplasm of the host cell.
- The bacteria are driven through the cytoplasm to neighbouring cells, where cell-to-cell transit takes place, thanks to the reorganisation of actin filaments in the host cells. Shigella germs are shielded from immune-mediated removal in this way.
- Shigella cause apoptosis (programmed cell death) to evade phagocytosis. Additionally, IL-1 is released during this process, which attracts polymorphonuclear leukocytes to the diseased tissues.
- As a result, the integrity of the intestinal wall is compromised, enabling bacteria to enter deeper epithelial cells.
- Shiga toxin is an exotoxin produced by S. dysenteriae strains.
- This toxin, which is made by STEC, has one A subunit and five B subunits.
- The B subunits help the A subunit enter the cell by binding to a glycolipid (Gb3) in the host cell.
- The 60S ribosomal subunit's 28S rRNA is cut by the A subunit, preventing aminoacyl-transfer RNA from binding and interfering with protein synthesis.
- However, in a rare proportion of individuals, the Shiga toxin can mediate damage to the glomerular endothelium cells, resulting in renal failure (HUS). Damage to the intestinal epithelium is the major sign of toxin activity.
Clinical Manifestation of Shigella dysenteriae
A. Shigellosis
Shigellosis is characterized by:
- Abdominal cramps
- Diarrhea
- Fever
- Bloody stools
- One to three days after ingesting the bacteria, the disease's clinical signs and symptoms start to manifest.
- Within the first 12 hours, Shigella colonise the small intestine and start to reproduce.
- An enterotoxin is the mediator of the initial symptom of infection, which is copious watery diarrhoea without histologic evidence of mucosal penetration.
- However, lower abdominal pains and tenesmus (straining to urinate), together with copious amounts of pus and blood in the stool, are the key symptoms of shigellosis. It happens as a result of germs getting within the intestinal mucosa.
- The faeces contains a lot of erythrocytes, mucous, and neutrophils.
- Although antibiotic therapy is advised to lower the risk of subsequent transmission to family members and other contacts, infections are often self-limited.
- Few people acquire asymptomatic colonisation of the organism in the colon, which serves as an ongoing infection reservoir.
B. Hemolytic Uremic Syndrome (HUS)
- A collection of blood illnesses known as hemolytic-uremic syndrome (HUS) are characterised by low red blood cell counts, acute renal failure, and low platelet counts.
- After infection with S. dysenteriae type 1, HUS may develop.
- Children may experience convulsions; the cause may be a fast rate of temperature rise or metabolic changes linked to the development of the Shiga toxin.
- It has a greater risk of morbidity and death than HUS associated with E. coli and is typically exacerbated by severe diarrhoea, intravascular volume depletion, and circulatory collapse.
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