Materiały źródłowe

• #1 Dysentery – Wikipedia

  https://en.wikipedia.org/wiki/Dysentery

  Dysentery results from bacterial or parasitic infections. Viruses do not generally cause the disease. These pathogens typically reach the large intestine after entering orally, through ingestion of contaminated food or water, oral contact with contaminated objects or hands, and so on. Each specific pathogen has its own mechanism or pathogenesis, but in general, the result is damage to the intestinal linings, leading to the inflammatory immune responses. This can cause elevated physical temperature, painful spasms of the intestinal muscles (cramping), swelling due to fluid leaking from capillaries of the intestine (edema) and further tissue damage by the body’s immune cells and the chemicals, called cytokines, which are released to fight the infection. The result can be impaired nutrient absorption, excessive water and mineral loss through the stools due to breakdown of the control mechanisms in the intestinal tissue that normally remove water from the stools, and in severe cases, the entry of pathogenic organisms into the bloodstream. Anemia may also arise due to the blood loss through diarrhea. […] The underlying mechanism involves inflammation of the intestine, especially of the colon.

• #2 Bacillary dysentery – Wikipedia

  https://en.wikipedia.org/wiki/Bacillary_dysentery

  Bacillary dysentery is a type of dysentery, and is a severe form of shigellosis. It is associated with species of bacteria from the family Enterobacteriaceae. The term is usually restricted to Shigella infections. […] Shigellosis is caused by one of several types of Shigella bacteria. Three species are associated with bacillary dysentery: Shigella sonnei, Shigella flexneri and Shigella dysenteriae. […] One characteristic of bacillary dysentery is blood in stool, which is the result of invasion of the mucosa by the pathogen. […] Transmission is fecal-oral and is remarkable for the small number of organisms that may cause disease (10 ingested organisms cause illness in 10% of volunteers, and 500 organisms cause disease in 50% of volunteers). Shigella bacteria invade the intestinal mucosal cells but do not usually go beyond the lamina propria. Dysentery is caused when the bacteria escape the epithelial cell phagolysosome, multiply within the cytoplasm, and destroy host cells. Shiga toxin causes hemorrhagic colitis and hemolytic-uremic syndrome by damaging endothelial cells in the microvasculature of the colon and the glomeruli, respectively. […] In addition, chronic arthritis secondary to S. flexneri infection, called reactive arthritis, may be caused by a bacterial antigen; the occurrence of this syndrome is strongly linked to HLA-B27 genotype, but the immunologic basis of this reaction is not understood.

• #3 Shigella Infection: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/968773-overview

  Shigella infection is a major public health problem in developing countries where sanitation is poor. […] Shigellosis is spread by means of fecal-oral transmission. Other modes of transmission include ingestion of contaminated food or water (untreated wading pools, interactive water fountain), contact with a contaminated inanimate object, and certain mode of sexual contact. Vectors like the housefly can spread the disease by physically transporting infected feces. […] The infectivity dose (ID) is extremely low. As few as 10 S dysenteriae bacilli can cause clinical disease, whereas 100-200 bacilli are needed for S sonnei or S flexneri infection. The reasons for this low-dose response are not completely clear. One possible explanation is that virulent Shigellae can withstand the low pH of gastric juice. Most isolates of Shigella survive acidic treatment at pH 2.5 for at least 2 hours.

• #4 Bacillary Dysentery: Causes, Symptoms & Treatment

  https://my.clevelandclinic.org/health/diseases/22617-bacillary-dysentery

  Bacillary dysentery is a gastrointestinal disease. Bacillary means related to bacteria, and dysentery is severe diarrhea containing blood or mucus. […] With bacillary dysentery, a bacterial infection becomes more invasive and severe, causing inflammation in the intestines. Symptoms can range from mild to life-threatening. […] Bacillary dysentery occurs when foreign bacteria enter a persons body and the infection becomes severe. […] Some of the most common bacteria that lead to bacillary dysentery are: Shigella, which leads to shigellosis. […] The symptoms of bacillary dysentery range from mild to severe, including: Diarrhea containing blood or mucus. […] Complications of severe disease include extreme inflammation, dilation (widening) of the large intestine and acute kidney disease.

• #5 Molecular Mechanisms of Shigella Pathogenesis; Recent Advances

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9917014/

  Shigella strains have commonly been isolated from contaminated ground beef, oysters, potato salads, bean dip, raw vegetables and fish. […] Shigella foodborne outbreaks are usually common when consuming foods subjected to processing by hand, exposed to a limited thermal treatment or raw foods. […] Shigellosis, a global health problem in developed and developing countries, is a contagious infectious disease caused by different species of Shigella via the consumption of contaminated food and water. […] Investigation of the pathogenicity mechanisms of Shigella species helps us to determine more successful, preventive, specific and effective strategies against shigellosis. […] The virulence and pathogenesis of Shigella strains require T3SS, the most important pathogenicity mechanism of Shigella species.

• #6 Shigella Infection: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/968773-overview

  Shigella infection is a major public health problem in developing countries where sanitation is poor. […] Shigellosis is spread by means of fecal-oral transmission. Other modes of transmission include ingestion of contaminated food or water (untreated wading pools, interactive water fountain), contact with a contaminated inanimate object, and certain mode of sexual contact. Vectors like the housefly can spread the disease by physically transporting infected feces. […] The infectivity dose (ID) is extremely low. As few as 10 S dysenteriae bacilli can cause clinical disease, whereas 100-200 bacilli are needed for S sonnei or S flexneri infection. The reasons for this low-dose response are not completely clear. One possible explanation is that virulent Shigellae can withstand the low pH of gastric juice. Most isolates of Shigella survive acidic treatment at pH 2.5 for at least 2 hours.

• #7 Shigella Infection: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/968773-overview

  Shigella infection is a major public health problem in developing countries where sanitation is poor. […] Shigellosis is spread by means of fecal-oral transmission. Other modes of transmission include ingestion of contaminated food or water (untreated wading pools, interactive water fountain), contact with a contaminated inanimate object, and certain mode of sexual contact. Vectors like the housefly can spread the disease by physically transporting infected feces. […] The infectivity dose (ID) is extremely low. As few as 10 S dysenteriae bacilli can cause clinical disease, whereas 100-200 bacilli are needed for S sonnei or S flexneri infection. The reasons for this low-dose response are not completely clear. One possible explanation is that virulent Shigellae can withstand the low pH of gastric juice. Most isolates of Shigella survive acidic treatment at pH 2.5 for at least 2 hours.

• #8 Approach to the adult with acute diarrhea in resource-limited settings – UpToDate

  https://www.uptodate.com/contents/approach-to-the-adult-with-acute-diarrhea-in-resource-limited-settings

  Dysentery is commonly associated with fever and abdominal pain. […] Important features accounting for the association between Shigella spp and large, regional epidemics of dysentery include the low infective dose (10 to 100 organisms), which facilitates person-to-person spread of infection, and increasing resistance to commonly used antimicrobials. […] Serious complications may occur with Shigella infection, including sepsis, seizures, rectal prolapse, toxic megacolon, and the hemolytic-uremic syndrome. […] Antibiotic therapy is warranted in some circumstances, as outlined below. […] Dysentery — Adults with bloody diarrhea (especially older adults and individuals with AIDS) should be treated promptly with an antimicrobial that is effective against Shigella. […] In several trials of patients with dysentery, antibiotics reduced the duration of diarrhea and fever in infections caused by Shigella, which is the most common cause of dysentery in resource-limited settings and can otherwise be associated with severe complications.

• #9 Shigella – Medical Microbiology – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK8038/

  Infection is initiated by ingestion of shigellae (usually via fecal-oral contamination). An early symptom, diarrhea (possibly elicited by enterotoxins and/or cytotoxin), may occur as the organisms pass through the small intestine. The hallmarks of shigellosis are bacterial invasion of the colonic epithelium and inflammatory colitis. These are interdependent processes amplified by local release of cytokines and by the infiltration of inflammatory elements. Colitis in the rectosigmoid mucosa, with concomitant malabsorption, results in the characteristic sign of bacillary dysentery: scanty, unformed stools tinged with blood and mucus. […] The pathogenic mechanism of shigellosis is complex, involving a possible enterotoxic and/or cytotoxic diarrheal prodrome, cytokine-mediated inflammation of the colon, and necrosis of the colonic epithelium. The underlying physiological insult that initiates this inflammatory cascade is the invasion of Shigella into the colonic epithelium and the lamina propria. The resulting colitis and ulceration of the mucosa result in bloody, mucoid stools, and/or febrile diarrhea.

• #10 Molecular Mechanisms of Shigella Pathogenesis; Recent Advances

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9917014/

  Shigella employs these seven steps, and releases different effector proteins to damage, invade and suppress the immune system of the host gastrointestinal epithelial cells, contributing, eventually, to mild diarrhoeal symptoms in the patient. […] S. dysenteriae type 1 is also considered one of the leading causes of bacillary dysentery or shigellosis and is transmitted to humans through the ingestion of contaminated water or food. […] S. dysenteriae type 1 adheres to the human colonic mucin and attaches to the epithelial cells by using the same mechanisms and virulence factor genes employed by other species. […] After attachment and adherence, Stxs are secreted by this organism. […] S. dysenteriae type 1 uses type 2 secretion system (T2SS) as an effector delivery system to inject protein effectors into the host cell. […] Shiga toxins contribute to HUS and bloody diarrhoea in humans, with a high rate of fatality.

• #11 Shigella-Epidemiology, Pathogenesis, and Treatment – Microbiology Notes

  https://microbiologynotes.org/shigella-epidemiology-pathogenesis-and-treatment/

  Shigella is an invasive pathogen, capable of invading and multiplying within a wide variety of epithelial cells, especially enterocytes. […] The event of the pathogenesis of Shigella includes invasion of the mucosa of the colon. […] Shigella strains are acid-resistant because of that it survives the stomach passage to extend in the intestines. […] Shigella cross the mucosal membrane by M cells located in the Peyers patches, which is related to the follicle of the intestines, which is devoid of a highly organized absorptive layer of enterocytes. […] The adherence is selective to the M cells and it is transcytosed through them, into the underlying phagocytic cells which cause apoptosis, in which IL-1 is, released which results in the draw the polymorphonuclear leukocytes towards the infected tissues.

• #12 shigella webpage

  https://www2.gvsu.edu/chm463/toxins/shigella.htm

  Shigella dysenteriae cause a Bacillary dysentery disease. The bacteria release the Shiga exotoxin that inhibits protein synthesis by lysing 28S rRNA. […] Shigella invade the villus cells of the large intestine by penetrating the colonic mucosa, but do not invade the blood, or perforate the intestine beyond the epithelium into the lamina propria. Shigella enter the intestinal mucosa by attaching to, and invading lymphoid cells in Peyer’s patches. These specialized lymphoid cells are called „M cells,” and normally transport foreign antigens from the intestine to underlying macrophages. The bacteria are internalized by the epithelial cells via a process similar to phagocytosis. This usually occurs with an endosome, but these bacteria have the ability to lyse the phagocytic vacuoles of macrophage cells and replicate in their cytoplasm. The bacteria are then spread into adjacent epithelial cells by propulsive movements of actin. This way, the bacteria avoid antibody-mediated humoral immunity. Shigella produce Ipa proteins in order to help escape from the endosome, but also produce them early on in order to initiate a cascade of cellular signalization that internalizes the bacteria with endosomes. While present in the mucosa, Shigella typically cause an inflammatory response that results in extensive tissue damage. They release a heat-stabile lipopolysaccharide endotoxin that can cause fever. The LPS of Gram-negative bacteria contains cell wall antigens (O antigens) that can elicit a variety of inflammatory responses in an animal. This endotoxin is part of the outer membrane of the Shigella cell, and has a low degree of specificity and a low degree of potency. It has an MW of 10kDa, and does not show enzymatic activity. Shigella also use apoptosis in order to intentionally activate the host’s inflammatory response. Subsequent infiltration and diapedisis by leukocytes disrupts the tight-junction of the bowel epithelium, thus allowing a massive invasion by bacteria still in the colon, resulting in a massive invasion and degradation of the intestinal mucosa.

• #13 shigella webpage

  https://www2.gvsu.edu/chm463/toxins/shigella.htm

  Shigella dysenteriae cause a Bacillary dysentery disease. The bacteria release the Shiga exotoxin that inhibits protein synthesis by lysing 28S rRNA. […] Shigella invade the villus cells of the large intestine by penetrating the colonic mucosa, but do not invade the blood, or perforate the intestine beyond the epithelium into the lamina propria. Shigella enter the intestinal mucosa by attaching to, and invading lymphoid cells in Peyer’s patches. These specialized lymphoid cells are called „M cells,” and normally transport foreign antigens from the intestine to underlying macrophages. The bacteria are internalized by the epithelial cells via a process similar to phagocytosis. This usually occurs with an endosome, but these bacteria have the ability to lyse the phagocytic vacuoles of macrophage cells and replicate in their cytoplasm. The bacteria are then spread into adjacent epithelial cells by propulsive movements of actin. This way, the bacteria avoid antibody-mediated humoral immunity. Shigella produce Ipa proteins in order to help escape from the endosome, but also produce them early on in order to initiate a cascade of cellular signalization that internalizes the bacteria with endosomes. While present in the mucosa, Shigella typically cause an inflammatory response that results in extensive tissue damage. They release a heat-stabile lipopolysaccharide endotoxin that can cause fever. The LPS of Gram-negative bacteria contains cell wall antigens (O antigens) that can elicit a variety of inflammatory responses in an animal. This endotoxin is part of the outer membrane of the Shigella cell, and has a low degree of specificity and a low degree of potency. It has an MW of 10kDa, and does not show enzymatic activity. Shigella also use apoptosis in order to intentionally activate the host’s inflammatory response. Subsequent infiltration and diapedisis by leukocytes disrupts the tight-junction of the bowel epithelium, thus allowing a massive invasion by bacteria still in the colon, resulting in a massive invasion and degradation of the intestinal mucosa.

• #14 Shigella dysentery: Applied microbiology & clinical cases at www.microrao.com

  https://www.microrao.com/bact9.htm

  Shigellosis is basically an enteric disease and the transmission involves feco-oral route. Shigella is transmitted via food, fingers, fomites or flies. Ingestion of small numbers of bacilli (approximately 102) can initiate infection in a susceptible person. As few as 10 S. dysenteriae bacilli can cause clinical disease, whereas 100-200 bacilli are needed for S. sonnei or S. flexneri infection. Once they survive the gastric juices, they reach large intestine and penetrate the cells of the epithelial lining. Pathogenesis requires invasion and toxin production. The characteristic virulence factor is encoded on a large (220 kb) plasmid that is responsible for synthesis of polypeptides that cause cytotoxicity. Shigella also produce siderophores that are coded on plasmid can chelate iron from host cells from its protein-bound state. Shiga toxin (Stx) is not essential for virulence of S dysenteriae type 1 but contributes to the severity of dysentery. The chromosomally encoded enterotoxin are are potent cytotoxins that are responsible for many pathogenic features of Shigella infection. Lipopolysaccaharide plays an important role in resistance to nonspecific host defense encountered during tissue invasion. The bacilli multiplies in the epithelia and spreads laterally to adjacent tissue and penetrate lamina propria. Inflammatory response ensues which ultimately leads to capillary thrombosis and sloughing off of epithelium due to necrosis leaving behind superficial ulcers. Some strains produce enterotoxin (Shiga toxin) that has neurotoxic, cytotoxic and enterotoxic action. The accumulation of inflammatory cells leads to the formation of microabscesses, which spread and coalesce to form larger abscesses. Bleeding occurs from superficial ulcerations. Bacterial shedding usually ceases within 4 weeks of the onset of illness. Chronic carriers are extremely rare.

• #15 Shigella Infection: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/968773-overview

  The incubation period varies from 12 hours to 7 days but is typically 2-4 days; the incubation period is inversely proportional to the load of ingested bacteria. The disease is communicable as long as an infected person excretes the organism in the stool, which can extend as long as 4 weeks from the onset of illness. Bacterial shedding usually ceases within 4 weeks of the onset of illness; rarely, it can persist for months. Appropriate antimicrobial treatment can reduce the duration of carriage to a few days. […] Virulence in Shigella species involves both chromosomal-coded and plasmid-coded genes. Virulent Shigella strains produce disease after invading the intestinal mucosa; the organism only rarely penetrates beyond the mucosa. […] The characteristic virulence trait is encoded on a large (220 kb) plasmid responsible for synthesis of polypeptides that cause cytotoxicity. Shigellae that lose the virulence plasmid are no longer pathogenic.

• #16 Shigella Infection: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/968773-overview

  Siderophores, a group of plasmid-coded genes, control the acquisition of iron from host cells from its protein-bound state. […] Regulatory genes control expression of virulence genes. Shiga toxin (Stx) is not essential for virulence of S dysenteriae type 1 but contributes to the severity of dysentery. […] Regarding chromosomally encoded enterotoxin, many pathogenic features of Shigella infection are due to the production of potent cytotoxins known as Stx, a potent protein synthesis-inhibiting exotoxin. […] Shigella strains produce distinct enterotoxins. These are a family of cytotoxins that contain 2 major immunologically noncross-reactive groups called Stx1 and Stx2. […] Stx adheres to small-intestine receptors and blocks the absorption of electrolytes, glucose, and amino acids from intestinal lumen.

• #17 Molecular Mechanisms of Shigella Pathogenesis; Recent Advances

  https://www.mdpi.com/1422-0067/24/3/2448

  Shigella species are the main cause of bacillary diarrhoea or shigellosis in humans. […] In this study, we reviewed and summarised the previous studies and recent advances in molecular mechanisms of pathogenesis of Shigella Dysenteriae and non-Dysenteriae species. […] Shigella species uses attachment, invasion, intracellular motility, toxin secretion and host cell interruption mechanisms, causing mild diarrhoea, haemorrhagic colitis and haemolytic uremic syndrome diseases in humans through the expression of effector delivery systems, protein effectors, toxins, host cell immune system evasion and iron uptake genes. […] The virulence and pathogenesis of Shigella strains require T3SS, the most important pathogenicity mechanism of Shigella species. […] Shigella dysenteriae type 1 adheres to the human colonic mucin and attaches to the epithelial cells by using the same mechanisms and virulence factor genes employed by other species.

• #18 Molecular Mechanisms of Shigella Pathogenesis; Recent Advances

  https://www.mdpi.com/1422-0067/24/3/2448

  After attachment and adherence, Stxs are secreted by this organism. […] S. dysenteriae type 1 uses type 2 secretion system (T2SS) as an effector delivery system to inject protein effectors into the host cell. […] S. dysenteriae type 1 also uses a specific heme uptake system as a protective virulence factor encoded by Shu genes. […] Stxs are responsible for HUS, haemorrhagic colitis and bloody diarrhoea in the human host, since they target both intestinal and kidney epithelial cells.

• #19 shigella webpage

  https://www2.gvsu.edu/chm463/toxins/shigella.htm

  Additionally, a heat-labile exotoxin is released by Shigella dysenteriae that damages the mucosa and villi. This toxin, Shiga toxin, has enterotoxic, cytotoxic, and neurotoxic effects. The protein has a MW of 50-1000kDa, diffuses extracellularly, is highly potent and has a high degree of specificity. It causes local areas of erosion that give rise to bleeding and heavy mucous secretion. The toxin also leads to nerve cell damage. Shiga toxin is composed of A (enzymatic) and B (binding) subunits in a ratio of 1:5. One component binds to the host cell surface, while the other passes into the cell membrane or cytoplasm before acting. The B subunit binds host cell glycolipids, while the A1 domain causes inactivation of the 60S ribosomal subunit, leading to cell death from inhibition of protein synthesis. Part of an A subunit has N-glycosidase activity on a single adenosine residue, lysing the bond between the base and ribose. This two-domain (A-5B) structure is similar to the Shiga-like toxin of enterohemorrhagic E. Coli (EHEC), but coded by a lysogenic bacteria.

• #20 shigella webpage

  https://www2.gvsu.edu/chm463/toxins/shigella.htm

  Shiga toxin blocks absorption of electrolytes, glucose, and amino acids from the intestinal lumen by adhering to small intestine receptors. B subunit of Shiga toxin binds host cell glycolipid in large intestine, A1 domain internalized via receptor-mediated endocytosis (coated pits) and causes irreversible inactivation of the 60S ribosomal subunit, thereby inhibiting protein synthesis, causing cell death, microvasculature damage to the intestine, and hemorrhage (blood and fecal leukocytes in stool). Fever and abdominal cramping are considered signs of neurotoxicity.

• #21 Shigella Infection: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/968773-overview

  Siderophores, a group of plasmid-coded genes, control the acquisition of iron from host cells from its protein-bound state. […] Regulatory genes control expression of virulence genes. Shiga toxin (Stx) is not essential for virulence of S dysenteriae type 1 but contributes to the severity of dysentery. […] Regarding chromosomally encoded enterotoxin, many pathogenic features of Shigella infection are due to the production of potent cytotoxins known as Stx, a potent protein synthesis-inhibiting exotoxin. […] Shigella strains produce distinct enterotoxins. These are a family of cytotoxins that contain 2 major immunologically noncross-reactive groups called Stx1 and Stx2. […] Stx adheres to small-intestine receptors and blocks the absorption of electrolytes, glucose, and amino acids from intestinal lumen.

• #22 Shigellosis: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/182767-overview

  Shigella organisms cause bacillary dysentery, a disease that has been described since early recorded history. […] Shigella species (eg, S dysenteriae, S flexneri, S sonnei, S boydii) are aerobic, nonmotile, glucose-fermenting, gram-negative rods that are highly contagious, causing diarrhea after ingestion of as few as 180 organisms. […] These pathogens cause damage by two mechanisms, (1) invasion of the colonic epithelium, which is dependent on a plasmid-mediated virulence factor, and (2) production of an enterotoxin, which is not essential for colitis but enhances the virulence. […] Lapaquette et al indicate that S flexneri uses a calcium/calpain-dependent mechanism to cause sumoylation inhibition, thereby allowing pathogenic bacterial entry. […] The pathogenesis of HUS or TTP involves cytotoxic damage to the vascular endothelium. In most studies, Shiga toxin production by type 1 S dysenteriae is thought to be directly involved.

• #23 Dysentery pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Dysentery_pathophysiology

  Dysentery results from viral infections, bacterial infections, or parasitic infestations. Te pathogens typically reach the large intestine after entering orally, through ingestion of contaminated food or water, oral contact with contaminated objects or hands, and so on. […] Each specific pathogen has its own mechanism or pathogenesis, but in general the result is damage to the intestinal lining, leading to the inflammatory immune response. This can cause elevated temperature, painful spasms of the intestinal muscles (cramping), swelling due to water leaking from capillaries of the intestine (edema), and further tissue damage by the body’s immune cells and the chemicals, called cytokines, they release to fight the infection. The result can be impaired nutrient absorption, excessive water and mineral loss through the stools due to breakdown of the control mechanisms in the intestinal tissue that normally remove water from the stools, and in severe cases the entry of pathogenic organisms into the bloodstream. […] Some microorganisms for example, bacteria of the genus Shigella secrete substances known as cytotoxins, which kill and damage intestinal tissue on contact. Viruses directly attack the intestinal cells, taking over their metabolic machinery to make copies of themselves, which leads to cell death.

• #24 Shigella Infection: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/968773-overview

  Chromosomal genes control lipopolysaccharide (LPS) antigens in cell walls. LPS plays an important role in resistance to nonspecific host defense encountered during tissue invasion. […] 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. In addition to this series of pathogenic events, only S dysenteriae type 1 has the ability to elaborate the potent Shiga toxin that inhibits protein synthesis in eukaryotic cells and that may lead to extraintestinal complications, including hemolytic-uremic syndrome and death.

• #25 Shigella-Epidemiology, Pathogenesis, and Treatment – Microbiology Notes

  https://microbiologynotes.org/shigella-epidemiology-pathogenesis-and-treatment/

  In this case, diarrhea caused by the process is majorly inflammatory, consists of a small volume of stool consist of RBCs, WBCs, and bacteria. It is called classic dysentery. […] dysentery strains of Shigella produce exotoxins like Shiga toxin, which has one A subunit and five B subunits. […] The A subunit functions to cleave the 28S rRNA in the 60S ribosomal subunit, which prevents the binding of the aminoacyl in RNA transfer and disrupts the synthesis of the proteins. […] The combined action of toxin subunits damages the epithelial cells of the intestines, in the rare case of some patients, Shiga toxin can damage the glomerular endothelial cells, which causes renal failure.

• #26 Shigella dysentery: Applied microbiology & clinical cases at www.microrao.com

  https://www.microrao.com/bact9.htm

  Shigellosis is basically an enteric disease and the transmission involves feco-oral route. Shigella is transmitted via food, fingers, fomites or flies. Ingestion of small numbers of bacilli (approximately 102) can initiate infection in a susceptible person. As few as 10 S. dysenteriae bacilli can cause clinical disease, whereas 100-200 bacilli are needed for S. sonnei or S. flexneri infection. Once they survive the gastric juices, they reach large intestine and penetrate the cells of the epithelial lining. Pathogenesis requires invasion and toxin production. The characteristic virulence factor is encoded on a large (220 kb) plasmid that is responsible for synthesis of polypeptides that cause cytotoxicity. Shigella also produce siderophores that are coded on plasmid can chelate iron from host cells from its protein-bound state. Shiga toxin (Stx) is not essential for virulence of S dysenteriae type 1 but contributes to the severity of dysentery. The chromosomally encoded enterotoxin are are potent cytotoxins that are responsible for many pathogenic features of Shigella infection. Lipopolysaccaharide plays an important role in resistance to nonspecific host defense encountered during tissue invasion. The bacilli multiplies in the epithelia and spreads laterally to adjacent tissue and penetrate lamina propria. Inflammatory response ensues which ultimately leads to capillary thrombosis and sloughing off of epithelium due to necrosis leaving behind superficial ulcers. Some strains produce enterotoxin (Shiga toxin) that has neurotoxic, cytotoxic and enterotoxic action. The accumulation of inflammatory cells leads to the formation of microabscesses, which spread and coalesce to form larger abscesses. Bleeding occurs from superficial ulcerations. Bacterial shedding usually ceases within 4 weeks of the onset of illness. Chronic carriers are extremely rare.

• #27 Bacillary dysentery – Wikipedia

  https://en.wikipedia.org/wiki/Bacillary_dysentery

  Bacillary dysentery is a type of dysentery, and is a severe form of shigellosis. It is associated with species of bacteria from the family Enterobacteriaceae. The term is usually restricted to Shigella infections. […] Shigellosis is caused by one of several types of Shigella bacteria. Three species are associated with bacillary dysentery: Shigella sonnei, Shigella flexneri and Shigella dysenteriae. […] One characteristic of bacillary dysentery is blood in stool, which is the result of invasion of the mucosa by the pathogen. […] Transmission is fecal-oral and is remarkable for the small number of organisms that may cause disease (10 ingested organisms cause illness in 10% of volunteers, and 500 organisms cause disease in 50% of volunteers). Shigella bacteria invade the intestinal mucosal cells but do not usually go beyond the lamina propria. Dysentery is caused when the bacteria escape the epithelial cell phagolysosome, multiply within the cytoplasm, and destroy host cells. Shiga toxin causes hemorrhagic colitis and hemolytic-uremic syndrome by damaging endothelial cells in the microvasculature of the colon and the glomeruli, respectively. […] In addition, chronic arthritis secondary to S. flexneri infection, called reactive arthritis, may be caused by a bacterial antigen; the occurrence of this syndrome is strongly linked to HLA-B27 genotype, but the immunologic basis of this reaction is not understood.

• #28 Shigella-Epidemiology, Pathogenesis, and Treatment – Microbiology Notes

  https://microbiologynotes.org/shigella-epidemiology-pathogenesis-and-treatment/

  This process destabilized the intestinal wall integrity, which allows bacteria to reach the deeper epithelial cells. […] Bacteria are released from the M cells and make contact with the basolateral side of the enterocytes and again multistep invasion process is mediated by the set of the invasion plasmid antigens which includes IpaA, IpaB, and IpaC. […] Shigella is highly adaptive to intracellular conditions and uniquely uses it to continue the course of the infection. […] The radial stretching or expansion of the cell during the pathogenesis of the bacteria forms focal mucosal ulcers of the colon. […] Because of the ulcers, the hemorrhagic component is added and an intense acute inflammatory response is evoked when bacteria reach the lamina propria (thin layers of the connective tissue), usually, infection is not extended beyond the lamina.

• #29 Bacillary dysentery (shigellosis | PPT

  https://www.slideshare.net/slideshow/bacillary-dysentery-shigellosis-70342392/70342392

  Bacillary dysentery, also known as shigellosis, is an acute infectious disease of the intestine caused by dysentery bacilli. The bacilli attach and penetrate the intestinal mucosa, multiplying and releasing endotoxins that cause inflammation, necrosis, and ulceration of the sigmoid colon and rectum. Symptoms include fever, abdominal pain, bloody diarrhea, and tenesmus. There are both acute and chronic forms. Treatment involves antibiotics, rehydration, and controlling symptoms. Prevention focuses on controlling infectious sources, interrupting fecal-oral transmission routes, and vaccinating susceptible populations. […] Pathogenicity: – virulence endotoxin – exotoxin – invasiveness (attach-penetrate-multiply) Resistance: Strong, 1-2 week in fruits, vegetable and dirty soil, heat for 60 30 min

• #30 Bacillary dysentery (shigellosis | PPT

  https://www.slideshare.net/slideshow/bacillary-dysentery-shigellosis-70342392/70342392

  Pathogenesis number of bacteria toxicity invasiveness attachment penetration multiplication immunity […] common Bacteria intestine normal intestinal flora sIg A prevent attaching penetrate mucus multiply in epithelia cell proper lamina endotoxin endogenous pyrogen fever inflammation vessel contraction superficial mucosal necrosis and ulcer diarrhea mixed with blood pus, abdominal pain […] Pathogenesis-toxic strong – allergy to endotoxin demethyl-adrenaline DIC micro-circulatory failure shock, cerebral edema cerebral hernia […] Pathology site of lesion: entire large bowel- sigmoid colon rectum feature: acute: diffuse fibrinous exudative inflammation

• #31 Shigella – Medical Microbiology – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK8038/

  Infection is initiated by ingestion of shigellae (usually via fecal-oral contamination). An early symptom, diarrhea (possibly elicited by enterotoxins and/or cytotoxin), may occur as the organisms pass through the small intestine. The hallmarks of shigellosis are bacterial invasion of the colonic epithelium and inflammatory colitis. These are interdependent processes amplified by local release of cytokines and by the infiltration of inflammatory elements. Colitis in the rectosigmoid mucosa, with concomitant malabsorption, results in the characteristic sign of bacillary dysentery: scanty, unformed stools tinged with blood and mucus. […] The pathogenic mechanism of shigellosis is complex, involving a possible enterotoxic and/or cytotoxic diarrheal prodrome, cytokine-mediated inflammation of the colon, and necrosis of the colonic epithelium. The underlying physiological insult that initiates this inflammatory cascade is the invasion of Shigella into the colonic epithelium and the lamina propria. The resulting colitis and ulceration of the mucosa result in bloody, mucoid stools, and/or febrile diarrhea.

• #32 Mechanisms of infectious diarrhea | Nature Reviews Gastroenterology & Hepatology

  https://www.nature.com/articles/ncpgasthep1264

  The cytotoxin-producing organisms adhere to the mucosa, activate cytokines and stimulate the intestinal mucosa to release inflammatory mediators. Invasive organisms, which can also produce cytotoxins, invade the intestinal mucosa to induce an acute inflammatory reaction, involving the activation of cytokines and inflammatory mediators. […] Regardless of the underlying mechanism they use, these various types of pathogen have all successfully evolved to evade and modulate the host defense systems. The mechanisms by which the different pathogens invade the host and cause infectious diarrhea are the topic of this Review. […] Inflammatory diarrhea is caused by two groups of organisms: cytotoxin-producing, noninvasive bacteria (enteroaggregative E. coli, enterohemorrhagic E. coli, and Clostridium difficile); and invasive organisms (e.g. Salmonella spp., Shigella spp., Campylobacter jejuni).

• #33 Mechanisms of infectious diarrhea | Nature Reviews Gastroenterology & Hepatology

  https://www.nature.com/articles/ncpgasthep1264

  Cytotoxin-producing organisms adhere to the mucosa, activate cytokines and stimulate the intestinal mucosa to release inflammatory mediators; invasive organisms, which can also secrete cytotoxins, invade the intestinal mucosa to induce an acute inflammatory reaction and activate cytokines and inflammatory mediators.

• #34 Shigella-Epidemiology, Pathogenesis, and Treatment – Microbiology Notes

  https://microbiologynotes.org/shigella-epidemiology-pathogenesis-and-treatment/

  Shigella is an invasive pathogen, capable of invading and multiplying within a wide variety of epithelial cells, especially enterocytes. […] The event of the pathogenesis of Shigella includes invasion of the mucosa of the colon. […] Shigella strains are acid-resistant because of that it survives the stomach passage to extend in the intestines. […] Shigella cross the mucosal membrane by M cells located in the Peyers patches, which is related to the follicle of the intestines, which is devoid of a highly organized absorptive layer of enterocytes. […] The adherence is selective to the M cells and it is transcytosed through them, into the underlying phagocytic cells which cause apoptosis, in which IL-1 is, released which results in the draw the polymorphonuclear leukocytes towards the infected tissues.

• #35 Shigella – Medical Microbiology – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK8038/

  In summary, shigellosis can be characterized as an acute inflammatory bowel disease initiated by the uptake of only a few organisms into lymphoid follicles. Intracellular replication and intercellular spread leads to an amplified inflammatory cascade at the initial site of entry, and as this inflammation persists and expands, the infiltration of PMN facilitates the entry of additional bacteria into the epithelium. The inflammatory infiltrate can also cause detachment of sheets of epithelial cells in areas devoid of lymphoid structures or bacterial cells.

• #36 Diarrhea – Gastrointestinal Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/gastrointestinal-disorders/symptoms-of-gastrointestinal-disorders/diarrhea

  Diarrhea occurs when unabsorbable, water-soluble solutes remain in the bowel and retain water. Such solutes include polyethylene glycol, magnesium salts (hydroxide and sulfate), and sodium phosphate, which are used as laxatives. Osmotic diarrhea occurs with sugar intolerance (eg, lactose intolerance caused by lactase deficiency). Ingesting large amounts of hexitols (eg, sorbitol, mannitol, xylitol) or high fructose corn syrups, which are used as sugar substitutes in candy, gum, and fruit juices, causes osmotic diarrhea because hexitols are poorly absorbed. Lactulose, which is used as a laxative, causes diarrhea by a similar mechanism. Overingesting certain foodstuffs can cause osmotic diarrhea. […] Diarrhea occurs when the bowels secrete more electrolytes and water than they absorb. Causes of increased secretions include infections, unabsorbed fats, certain medications, and various intrinsic and extrinsic secretagogues.

• #37 Diarrhea – Gastrointestinal Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/gastrointestinal-disorders/symptoms-of-gastrointestinal-disorders/diarrhea

  Infections (eg, gastroenteritis) are the most common causes of secretory diarrhea. Infections combined with food poisoning are the most common causes of acute diarrhea (4 days in duration). Most enterotoxins block sodium-potassium exchange, which is an important driving force for fluid absorption in the small bowel and colon. […] Impaired absorption of bile salts, which can occur with several disorders, can cause diarrhea by stimulating water and electrolyte secretion. The stools have a green or orange color. […] Rapid intestinal transit and diminished surface area impair fluid absorption and cause diarrhea. Common causes include small-bowel or large-bowel resection or bypass, gastric resection, and inflammatory bowel disease. Other causes include microscopic colitis (collagenous or lymphocytic colitis) and celiac disease. Hyperthyroidism may cause diarrhea due to rapid transit.

• #38 Pathophysiology of Diarrhea

  https://vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/diarrhea.html

  Diarrhea is one of the most common clinical signs of gastrointestinal disease, but also can reflect primary disorders outside of the digestive system. […] There are numerous causes of diarrhea, but in almost all cases, this disorder is a manifestation of one of the four basic mechanisms described below. It is also common for more than one of the four mechanisms to be involved in the pathogenesis of a given case. […] Diarrhea occurs when secretion of water into the intestinal lumen exceeds absorption. […] Many millions of people have died of the secretory diarrhea associated with cholera. […] Destruction of the epithelium results not only in exudation of serum and blood into the lumen but often is associated with widespread destruction of absorptive epithelium. […] The immune response to inflammatory conditions in the bowel contributes substantively to development of diarrhea. […] In this way, components of an osmotic (malabsorption) diarrhea are added to the problem. […] Disorders in motility than accelerate transit time could decrease absorption, resulting in diarrhea even if the absorptive process per se was proceeding properly.

• #39 Shigella-Epidemiology, Pathogenesis, and Treatment – Microbiology Notes

  https://microbiologynotes.org/shigella-epidemiology-pathogenesis-and-treatment/

  In this case, diarrhea caused by the process is majorly inflammatory, consists of a small volume of stool consist of RBCs, WBCs, and bacteria. It is called classic dysentery. […] dysentery strains of Shigella produce exotoxins like Shiga toxin, which has one A subunit and five B subunits. […] The A subunit functions to cleave the 28S rRNA in the 60S ribosomal subunit, which prevents the binding of the aminoacyl in RNA transfer and disrupts the synthesis of the proteins. […] The combined action of toxin subunits damages the epithelial cells of the intestines, in the rare case of some patients, Shiga toxin can damage the glomerular endothelial cells, which causes renal failure.

• #40 Dysentery: Shigella, bacteria with adaptation to respiration – News from the Institut Pasteur

  https://www.pasteur.fr/en/press-area/press-documents/dysentery-shigella-bacteria-adaptation-respiration

  Bacillary dysentery caused by the intestinal bacteria Shigella is a major health problem in tropical regions and developing countries. […] Researchers from Inserm and the Institut Pasteur have studied the mechanisms of Shigella virulence. They found that these bacteria are not only able to consume the oxygen in colonic tissue in order to grow and create foci of infection, but can also adapt their mode of respiration so that they can continue to grow once the oxygen in these foci has been used up. […] The research group also found that foci of Shigella infection had abnormally low levels of oxygen (hypoxia). The denser the population of bacteria, the greater the consumption of O2. […] Shigella bacteria are „facultative anaerobes,” which means that while they favor aerobic respiration (which uses O2 as fuel), if oxygen is lacking they can also switch to „anaerobic” respiration, which does not require O2. This characteristic enables them to continue to grow in hypoxic, or even anoxic (O2-depleted) foci after they have consumed all the oxygen in the tissues.

• #41 Dysentery: Shigella, bacteria with adaptation to respiration – News from the Institut Pasteur

  https://www.pasteur.fr/en/press-area/press-documents/dysentery-shigella-bacteria-adaptation-respiration

  The researchers have thus shown that aerobic respiration of Shigella and their capacity to modulate the oxygenation of infected tissues enables the formation of hypoxic foci of infection within the intestinal mucosa, which constitutes the first stage in their colonization strategy, with over 99% of the bacterial population growing in these areas. […] When these foci are depleted of oxygen, the adaptability of the bacteria to O2-poor environments gives them a crucial advantage that explains their virulence and that of other facultative anaerobic enterobacteria.

• #42 Molecular switch plays central role in bacterial dysentery

  https://www.mpg.de/21406868/molecular-switch-plays-central-role-in-bacterial-dysentery

  The regulation of virulence genes in Shigella bacteria is mediated by a CTP-dependent transcription factor. […] The researchers studied the infection process of the bacterial cause of dysentery, Shigella flexneri. […] The researchers discovered that the regulation of virulence genes in Shigella is mediated by a CTP-dependent switch that is central to the infection process. […] Our studies then showed that it indeed uses a CTP-dependent switch mechanism to control the expression of virulence genes. […] This CTP-dependent loading and sliding mechanism enables VirB to act as a molecular switch to remotely control gene expression during bacterial pathogenesis. […] Mutations that prevent the binding of CTP inhibit the loading of VirB onto DNA in vitro and suppress the formation of VirB-DNA complexes as well as the expression of virulence genes in Shigella cells. […] Our work provides the first evidence for a CTP-dependent switch involved in gene regulation.

• #43 Dysentery: Shigella, bacteria with adaptation to respiration – News from the Institut Pasteur

  https://www.pasteur.fr/en/press-area/press-documents/dysentery-shigella-bacteria-adaptation-respiration

  The researchers have thus shown that aerobic respiration of Shigella and their capacity to modulate the oxygenation of infected tissues enables the formation of hypoxic foci of infection within the intestinal mucosa, which constitutes the first stage in their colonization strategy, with over 99% of the bacterial population growing in these areas. […] When these foci are depleted of oxygen, the adaptability of the bacteria to O2-poor environments gives them a crucial advantage that explains their virulence and that of other facultative anaerobic enterobacteria.

• #44

  https://link.springer.com/article/10.1007/BF00784965

  Dynamics of the concentration of ascorbic acid in the organs upon introduction of Flexner dysentery culture, and the total bovine antigen recovered from dysentery bacilli was used as an indicator of the change of reactivity of the organism. […] Injection of the toxin causes more pronounced reaction with involvement of the blood system and intestines. […] Thus, the condition of nutrition plays an important part in the pathogenesis of dysentery.

• #45 Dysentery: Causes, Symptoms, Diagnosis & Treatment

  https://my.clevelandclinic.org/health/diseases/23567-dysentery

  Dysentery is characterized by diarrhea, high fever, weight loss, an upset stomach and nausea and vomiting. If you have bacillary dysentery, your diarrhea may contain blood or mucus. […] The parasitic and bacterial infections that cause dysentery are very contagious. People usually transfer the parasite or bacteria to each other when poop (fecal matter) from an infected person gets into another person’s mouth. […] Bacillary dysentery occurs when foreign bacteria enter your body and the infection becomes severe. Some of the most common bacteria that cause bacillary dysentery include: Shigella, which leads to shigellosis. Salmonella, which causes salmonella. Campylobacter, which causes campylobacteriosis. Escherichia coli, which leads to E. coli infection. […] Without proper treatment, dysentery may be fatal. It’s especially deadly to: Young children. People 50 years of age and older. People who have dehydration or malnutrition.

• #46 Bacillary dysentery – Wikipedia

  https://en.wikipedia.org/wiki/Bacillary_dysentery

  Bacillary dysentery is a type of dysentery, and is a severe form of shigellosis. It is associated with species of bacteria from the family Enterobacteriaceae. The term is usually restricted to Shigella infections. […] Shigellosis is caused by one of several types of Shigella bacteria. Three species are associated with bacillary dysentery: Shigella sonnei, Shigella flexneri and Shigella dysenteriae. […] One characteristic of bacillary dysentery is blood in stool, which is the result of invasion of the mucosa by the pathogen. […] Transmission is fecal-oral and is remarkable for the small number of organisms that may cause disease (10 ingested organisms cause illness in 10% of volunteers, and 500 organisms cause disease in 50% of volunteers). Shigella bacteria invade the intestinal mucosal cells but do not usually go beyond the lamina propria. Dysentery is caused when the bacteria escape the epithelial cell phagolysosome, multiply within the cytoplasm, and destroy host cells. Shiga toxin causes hemorrhagic colitis and hemolytic-uremic syndrome by damaging endothelial cells in the microvasculature of the colon and the glomeruli, respectively. […] In addition, chronic arthritis secondary to S. flexneri infection, called reactive arthritis, may be caused by a bacterial antigen; the occurrence of this syndrome is strongly linked to HLA-B27 genotype, but the immunologic basis of this reaction is not understood.

• #47

  https://link.springer.com/article/10.1007/BF00830627

  In condition of dysenteric intoxication, changes of reflexes from the chemoreceptors of intestines are due to the toxic, not the antigenic group of the toxin. […] In animals immunized by dysenteric anatoxin the sensitivity of intestinal receptors to dysenteric toxin is decreased.

• #48 Approach to the adult with acute diarrhea in resource-limited settings – UpToDate

  https://www.uptodate.com/contents/approach-to-the-adult-with-acute-diarrhea-in-resource-limited-settings

  Dysentery is commonly associated with fever and abdominal pain. […] Important features accounting for the association between Shigella spp and large, regional epidemics of dysentery include the low infective dose (10 to 100 organisms), which facilitates person-to-person spread of infection, and increasing resistance to commonly used antimicrobials. […] Serious complications may occur with Shigella infection, including sepsis, seizures, rectal prolapse, toxic megacolon, and the hemolytic-uremic syndrome. […] Antibiotic therapy is warranted in some circumstances, as outlined below. […] Dysentery — Adults with bloody diarrhea (especially older adults and individuals with AIDS) should be treated promptly with an antimicrobial that is effective against Shigella. […] In several trials of patients with dysentery, antibiotics reduced the duration of diarrhea and fever in infections caused by Shigella, which is the most common cause of dysentery in resource-limited settings and can otherwise be associated with severe complications.

• #49 INFLAMMATORY DIARRHEA | Harrison’s Manual of Medicine

  https://harrisons.unboundmedicine.com/harrisons/view/Harrisons-Manual-of-Medicine/623642/all/INFLAMMATORY_DIARRHEA

  After an incubation period of 5-21 days, prolonged fever (75% of cases), headache (80%), chills (35-45%), anorexia (55%), and abdominal pain (30-40%) are common. […] Intestinal perforation and/or GI hemorrhage can occur in the third and fourth weeks of illness; neurologic manifestations (e.g., meningitis, Guillain-Barr syndrome) occur in 2-40% of pts. […] Most commonly caused by S. Typhimurium or S. Enteritidis, NTS typically presents within 6-48 h of exposure as gastroenteritis (nausea, vomiting, nonbloody diarrhea, abdominal cramping, and fever) that lasts 3-7 days. […] The main mode of transmission is via contaminated food products, such as eggs (S. Enteritidis), poultry, undercooked meat, dairy products, manufactured or processed foods, and fresh produce. […] Bacteremia, usually due to S. Choleraesuis and S. Dublin, develops in 8% of pts; of these pts, 5-10% develop localized infections (e.g., hepatosplenic abscesses, meningitis, pneumonia, osteomyelitis). […] Reactive arthritis can follow Salmonella gastroenteritis, particularly in persons with the HLA-B27 histocompatibility antigen.

• #50 Bacillary Dysentery: Causes, Symptoms & Treatment

  https://my.clevelandclinic.org/health/diseases/22617-bacillary-dysentery

  Bacillary dysentery is a gastrointestinal disease. Bacillary means related to bacteria, and dysentery is severe diarrhea containing blood or mucus. […] With bacillary dysentery, a bacterial infection becomes more invasive and severe, causing inflammation in the intestines. Symptoms can range from mild to life-threatening. […] Bacillary dysentery occurs when foreign bacteria enter a persons body and the infection becomes severe. […] Some of the most common bacteria that lead to bacillary dysentery are: Shigella, which leads to shigellosis. […] The symptoms of bacillary dysentery range from mild to severe, including: Diarrhea containing blood or mucus. […] Complications of severe disease include extreme inflammation, dilation (widening) of the large intestine and acute kidney disease.

• #51 Dysentery: Causes, Symptoms, Diagnosis & Treatment

  https://my.clevelandclinic.org/health/diseases/23567-dysentery

  Dysentery is characterized by diarrhea, high fever, weight loss, an upset stomach and nausea and vomiting. If you have bacillary dysentery, your diarrhea may contain blood or mucus. […] The parasitic and bacterial infections that cause dysentery are very contagious. People usually transfer the parasite or bacteria to each other when poop (fecal matter) from an infected person gets into another person’s mouth. […] Bacillary dysentery occurs when foreign bacteria enter your body and the infection becomes severe. Some of the most common bacteria that cause bacillary dysentery include: Shigella, which leads to shigellosis. Salmonella, which causes salmonella. Campylobacter, which causes campylobacteriosis. Escherichia coli, which leads to E. coli infection. […] Without proper treatment, dysentery may be fatal. It’s especially deadly to: Young children. People 50 years of age and older. People who have dehydration or malnutrition.

• #52 The role of type I interferon in Shigella flexneri pathogenesis

  https://repositories.lib.utexas.edu/items/37a358d8-2a7f-4788-8cc9-4c1bdef0a75e

  The type I interferon (IFN) response is part of the first line of defense against pathogens. […] This study delves into the effects of type I IFN signaling on the various stages of Shigella flexneri pathogenesis. Shigella spp. are the cause of bacterial dysentery. […] Following invasion, it replicates in the host cell cytosol and spreads to adjacent cells. This provokes an intense inflammatory response that is characteristic of shigellosis. […] Here, we show that type I IFN signaling inhibits invasion by S. flexneri; however, during later stages of S. flexneri pathogenesis, type I IFN signaling appears to promote cell-to-cell spread and host cell lysis. […] Type I IFN, IFN in particular, increased the size of plaques formed in cell culture monolayers by S. flexneri. […] Upon further investigation, we found that larger plaque sizes could be attributed to a combination of increasing the rate of cell-to-cell spread and the rate of host cell lysis by IFN signaling. […] We also found that IFN signaling produces larger plaque sizes in Listeria monocytogenes infections, suggesting that ISGs induced by IFN may have a generalizable effect on other invasive bacterial pathogens.

• #53 The role of type I interferon in Shigella flexneri pathogenesis

  https://repositories.lib.utexas.edu/items/37a358d8-2a7f-4788-8cc9-4c1bdef0a75e

  The type I interferon (IFN) response is part of the first line of defense against pathogens. […] This study delves into the effects of type I IFN signaling on the various stages of Shigella flexneri pathogenesis. Shigella spp. are the cause of bacterial dysentery. […] Following invasion, it replicates in the host cell cytosol and spreads to adjacent cells. This provokes an intense inflammatory response that is characteristic of shigellosis. […] Here, we show that type I IFN signaling inhibits invasion by S. flexneri; however, during later stages of S. flexneri pathogenesis, type I IFN signaling appears to promote cell-to-cell spread and host cell lysis. […] Type I IFN, IFN in particular, increased the size of plaques formed in cell culture monolayers by S. flexneri. […] Upon further investigation, we found that larger plaque sizes could be attributed to a combination of increasing the rate of cell-to-cell spread and the rate of host cell lysis by IFN signaling. […] We also found that IFN signaling produces larger plaque sizes in Listeria monocytogenes infections, suggesting that ISGs induced by IFN may have a generalizable effect on other invasive bacterial pathogens.

• #54 How Salmonella Bacteria Cause Diarrhea In Their Host | ScienceDaily

  https://www.sciencedaily.com/releases/2009/09/090911205127.htm

  Salmonella bacteria are cunning when it comes to triggering diarrhoea in their host. […] Researchers have succeeded in explaining a molecular mechanism that enables the bacteria to activate their host cells non-specific immune response, thus making the host ill. […] A single virulence factor is sufficient to allow the bacteria to trigger disease. […] The bacteria inject the protein molecule into an intestinal epithelium cell, where it triggers a cascade of signals inside the cell. […] SopE tampers with two specific GTPases called Cdc42 and Rac1. […] When SopE binds to these two factors, the cell changes its surface and Salmonellae can penetrate into the cell. […] However, Hardt and his research group have now shown that Cdc42 and Rac1 are also a part of the cells early warning system.

• #55 How Salmonella Bacteria Cause Diarrhea In Their Host | ScienceDaily

  https://www.sciencedaily.com/releases/2009/09/090911205127.htm

  What the two molecules do is to activate, via a route that is still unknown, the molecule Caspase-1, which is a cornerstone of inflammatory responses in the cell. […] Caspase-1 in turn activates chemical messengers that attract phagocytes such as macrophages. […] The perfidiousness of SopE is that the bacteria tamper with, of all things, a communication system which a cell cannot simply replace or switch off, because otherwise the non-specific immune response would fail to happen or the cells skeleton would be paralysed. […] Consequently diarrhoea is the lesser of the two evils. […] Ironically, not all strains of Salmonella possess SopE. […] However, SopE is only one of 12 candidate chemical messengers that Salmonellae use to crack their hosts cell.

• #56 How Salmonella Bacteria Cause Diarrhea In Their Host | ScienceDaily

  https://www.sciencedaily.com/releases/2009/09/090911205127.htm

  Salmonella bacteria are cunning when it comes to triggering diarrhoea in their host. […] Researchers have succeeded in explaining a molecular mechanism that enables the bacteria to activate their host cells non-specific immune response, thus making the host ill. […] A single virulence factor is sufficient to allow the bacteria to trigger disease. […] The bacteria inject the protein molecule into an intestinal epithelium cell, where it triggers a cascade of signals inside the cell. […] SopE tampers with two specific GTPases called Cdc42 and Rac1. […] When SopE binds to these two factors, the cell changes its surface and Salmonellae can penetrate into the cell. […] However, Hardt and his research group have now shown that Cdc42 and Rac1 are also a part of the cells early warning system.

• #57 Dysentery: Shigella, bacteria with adaptation to respiration – News from the Institut Pasteur

  https://www.pasteur.fr/en/press-area/press-documents/dysentery-shigella-bacteria-adaptation-respiration

  Bacillary dysentery caused by the intestinal bacteria Shigella is a major health problem in tropical regions and developing countries. […] Researchers from Inserm and the Institut Pasteur have studied the mechanisms of Shigella virulence. They found that these bacteria are not only able to consume the oxygen in colonic tissue in order to grow and create foci of infection, but can also adapt their mode of respiration so that they can continue to grow once the oxygen in these foci has been used up. […] The research group also found that foci of Shigella infection had abnormally low levels of oxygen (hypoxia). The denser the population of bacteria, the greater the consumption of O2. […] Shigella bacteria are „facultative anaerobes,” which means that while they favor aerobic respiration (which uses O2 as fuel), if oxygen is lacking they can also switch to „anaerobic” respiration, which does not require O2. This characteristic enables them to continue to grow in hypoxic, or even anoxic (O2-depleted) foci after they have consumed all the oxygen in the tissues.

• #58 Dysentery: Shigella, bacteria with adaptation to respiration – News from the Institut Pasteur

  https://www.pasteur.fr/en/press-area/press-documents/dysentery-shigella-bacteria-adaptation-respiration

  The researchers have thus shown that aerobic respiration of Shigella and their capacity to modulate the oxygenation of infected tissues enables the formation of hypoxic foci of infection within the intestinal mucosa, which constitutes the first stage in their colonization strategy, with over 99% of the bacterial population growing in these areas. […] When these foci are depleted of oxygen, the adaptability of the bacteria to O2-poor environments gives them a crucial advantage that explains their virulence and that of other facultative anaerobic enterobacteria.

• #59 Molecular switch plays central role in bacterial dysentery

  https://www.mpg.de/21406868/molecular-switch-plays-central-role-in-bacterial-dysentery

  The regulation of virulence genes in Shigella bacteria is mediated by a CTP-dependent transcription factor. […] The researchers studied the infection process of the bacterial cause of dysentery, Shigella flexneri. […] The researchers discovered that the regulation of virulence genes in Shigella is mediated by a CTP-dependent switch that is central to the infection process. […] Our studies then showed that it indeed uses a CTP-dependent switch mechanism to control the expression of virulence genes. […] This CTP-dependent loading and sliding mechanism enables VirB to act as a molecular switch to remotely control gene expression during bacterial pathogenesis. […] Mutations that prevent the binding of CTP inhibit the loading of VirB onto DNA in vitro and suppress the formation of VirB-DNA complexes as well as the expression of virulence genes in Shigella cells. […] Our work provides the first evidence for a CTP-dependent switch involved in gene regulation.

• #60 Molecular switch plays central role in bacterial dysentery

  https://www.mpg.de/21406868/molecular-switch-plays-central-role-in-bacterial-dysentery

  The regulation of virulence genes in Shigella bacteria is mediated by a CTP-dependent transcription factor. […] The researchers studied the infection process of the bacterial cause of dysentery, Shigella flexneri. […] The researchers discovered that the regulation of virulence genes in Shigella is mediated by a CTP-dependent switch that is central to the infection process. […] Our studies then showed that it indeed uses a CTP-dependent switch mechanism to control the expression of virulence genes. […] This CTP-dependent loading and sliding mechanism enables VirB to act as a molecular switch to remotely control gene expression during bacterial pathogenesis. […] Mutations that prevent the binding of CTP inhibit the loading of VirB onto DNA in vitro and suppress the formation of VirB-DNA complexes as well as the expression of virulence genes in Shigella cells. […] Our work provides the first evidence for a CTP-dependent switch involved in gene regulation.

• #61 shigella webpage

  https://www2.gvsu.edu/chm463/toxins/shigella.htm

  Shigella dysenteriae cause a Bacillary dysentery disease. The bacteria release the Shiga exotoxin that inhibits protein synthesis by lysing 28S rRNA. […] Shigella invade the villus cells of the large intestine by penetrating the colonic mucosa, but do not invade the blood, or perforate the intestine beyond the epithelium into the lamina propria. Shigella enter the intestinal mucosa by attaching to, and invading lymphoid cells in Peyer’s patches. These specialized lymphoid cells are called „M cells,” and normally transport foreign antigens from the intestine to underlying macrophages. The bacteria are internalized by the epithelial cells via a process similar to phagocytosis. This usually occurs with an endosome, but these bacteria have the ability to lyse the phagocytic vacuoles of macrophage cells and replicate in their cytoplasm. The bacteria are then spread into adjacent epithelial cells by propulsive movements of actin. This way, the bacteria avoid antibody-mediated humoral immunity. Shigella produce Ipa proteins in order to help escape from the endosome, but also produce them early on in order to initiate a cascade of cellular signalization that internalizes the bacteria with endosomes. While present in the mucosa, Shigella typically cause an inflammatory response that results in extensive tissue damage. They release a heat-stabile lipopolysaccharide endotoxin that can cause fever. The LPS of Gram-negative bacteria contains cell wall antigens (O antigens) that can elicit a variety of inflammatory responses in an animal. This endotoxin is part of the outer membrane of the Shigella cell, and has a low degree of specificity and a low degree of potency. It has an MW of 10kDa, and does not show enzymatic activity. Shigella also use apoptosis in order to intentionally activate the host’s inflammatory response. Subsequent infiltration and diapedisis by leukocytes disrupts the tight-junction of the bowel epithelium, thus allowing a massive invasion by bacteria still in the colon, resulting in a massive invasion and degradation of the intestinal mucosa.

• #62 shigella webpage

  https://www2.gvsu.edu/chm463/toxins/shigella.htm

  Shigella dysenteriae cause a Bacillary dysentery disease. The bacteria release the Shiga exotoxin that inhibits protein synthesis by lysing 28S rRNA. […] Shigella invade the villus cells of the large intestine by penetrating the colonic mucosa, but do not invade the blood, or perforate the intestine beyond the epithelium into the lamina propria. Shigella enter the intestinal mucosa by attaching to, and invading lymphoid cells in Peyer’s patches. These specialized lymphoid cells are called „M cells,” and normally transport foreign antigens from the intestine to underlying macrophages. The bacteria are internalized by the epithelial cells via a process similar to phagocytosis. This usually occurs with an endosome, but these bacteria have the ability to lyse the phagocytic vacuoles of macrophage cells and replicate in their cytoplasm. The bacteria are then spread into adjacent epithelial cells by propulsive movements of actin. This way, the bacteria avoid antibody-mediated humoral immunity. Shigella produce Ipa proteins in order to help escape from the endosome, but also produce them early on in order to initiate a cascade of cellular signalization that internalizes the bacteria with endosomes. While present in the mucosa, Shigella typically cause an inflammatory response that results in extensive tissue damage. They release a heat-stabile lipopolysaccharide endotoxin that can cause fever. The LPS of Gram-negative bacteria contains cell wall antigens (O antigens) that can elicit a variety of inflammatory responses in an animal. This endotoxin is part of the outer membrane of the Shigella cell, and has a low degree of specificity and a low degree of potency. It has an MW of 10kDa, and does not show enzymatic activity. Shigella also use apoptosis in order to intentionally activate the host’s inflammatory response. Subsequent infiltration and diapedisis by leukocytes disrupts the tight-junction of the bowel epithelium, thus allowing a massive invasion by bacteria still in the colon, resulting in a massive invasion and degradation of the intestinal mucosa.

• #63 Molecular Mechanisms of Shigella Pathogenesis; Recent Advances

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9917014/

  Shigella species are the main cause of bacillary diarrhoea or shigellosis in humans. […] In this study, we reviewed and summarised the previous studies and recent advances in molecular mechanisms of pathogenesis of Shigella Dysenteriae and non-Dysenteriae species. […] Shigella species uses attachment, invasion, intracellular motility, toxin secretion and host cell interruption mechanisms, causing mild diarrhoea, haemorrhagic colitis and haemolytic uremic syndrome diseases in humans through the expression of effector delivery systems, protein effectors, toxins, host cell immune system evasion and iron uptake genes. […] The investigation of these genes and molecular mechanisms can help us to develop and design new methods to detect and differentiate these organisms in food and clinical samples and determine appropriate strategies to prevent and treat the intestinal and extraintestinal infections caused by these enteric pathogens.

• #64 Molecular Mechanisms of Shigella Pathogenesis; Recent Advances

  https://www.mdpi.com/1422-0067/24/3/2448

  Shigella species are the main cause of bacillary diarrhoea or shigellosis in humans. […] In this study, we reviewed and summarised the previous studies and recent advances in molecular mechanisms of pathogenesis of Shigella Dysenteriae and non-Dysenteriae species. […] Shigella species uses attachment, invasion, intracellular motility, toxin secretion and host cell interruption mechanisms, causing mild diarrhoea, haemorrhagic colitis and haemolytic uremic syndrome diseases in humans through the expression of effector delivery systems, protein effectors, toxins, host cell immune system evasion and iron uptake genes. […] The virulence and pathogenesis of Shigella strains require T3SS, the most important pathogenicity mechanism of Shigella species. […] Shigella dysenteriae type 1 adheres to the human colonic mucin and attaches to the epithelial cells by using the same mechanisms and virulence factor genes employed by other species.

• #65 Molecular Mechanisms of Shigella Pathogenesis; Recent Advances

  https://www.mdpi.com/1422-0067/24/3/2448

  After attachment and adherence, Stxs are secreted by this organism. […] S. dysenteriae type 1 uses type 2 secretion system (T2SS) as an effector delivery system to inject protein effectors into the host cell. […] S. dysenteriae type 1 also uses a specific heme uptake system as a protective virulence factor encoded by Shu genes. […] Stxs are responsible for HUS, haemorrhagic colitis and bloody diarrhoea in the human host, since they target both intestinal and kidney epithelial cells.

• #66 Molecular Mechanisms of Shigella Pathogenesis; Recent Advances

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9917014/

  Shigella species are the main cause of bacillary diarrhoea or shigellosis in humans. […] In this study, we reviewed and summarised the previous studies and recent advances in molecular mechanisms of pathogenesis of Shigella Dysenteriae and non-Dysenteriae species. […] Shigella species uses attachment, invasion, intracellular motility, toxin secretion and host cell interruption mechanisms, causing mild diarrhoea, haemorrhagic colitis and haemolytic uremic syndrome diseases in humans through the expression of effector delivery systems, protein effectors, toxins, host cell immune system evasion and iron uptake genes. […] The investigation of these genes and molecular mechanisms can help us to develop and design new methods to detect and differentiate these organisms in food and clinical samples and determine appropriate strategies to prevent and treat the intestinal and extraintestinal infections caused by these enteric pathogens.

• #67 Molecular Mechanisms of Shigella Pathogenesis; Recent Advances

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9917014/

  Shigella strains have commonly been isolated from contaminated ground beef, oysters, potato salads, bean dip, raw vegetables and fish. […] Shigella foodborne outbreaks are usually common when consuming foods subjected to processing by hand, exposed to a limited thermal treatment or raw foods. […] Shigellosis, a global health problem in developed and developing countries, is a contagious infectious disease caused by different species of Shigella via the consumption of contaminated food and water. […] Investigation of the pathogenicity mechanisms of Shigella species helps us to determine more successful, preventive, specific and effective strategies against shigellosis. […] The virulence and pathogenesis of Shigella strains require T3SS, the most important pathogenicity mechanism of Shigella species.

• #68 Approach to the adult with acute diarrhea in resource-limited settings – UpToDate

  https://www.uptodate.com/contents/approach-to-the-adult-with-acute-diarrhea-in-resource-limited-settings

  Dysentery is commonly associated with fever and abdominal pain. […] Important features accounting for the association between Shigella spp and large, regional epidemics of dysentery include the low infective dose (10 to 100 organisms), which facilitates person-to-person spread of infection, and increasing resistance to commonly used antimicrobials. […] Serious complications may occur with Shigella infection, including sepsis, seizures, rectal prolapse, toxic megacolon, and the hemolytic-uremic syndrome. […] Antibiotic therapy is warranted in some circumstances, as outlined below. […] Dysentery — Adults with bloody diarrhea (especially older adults and individuals with AIDS) should be treated promptly with an antimicrobial that is effective against Shigella. […] In several trials of patients with dysentery, antibiotics reduced the duration of diarrhea and fever in infections caused by Shigella, which is the most common cause of dysentery in resource-limited settings and can otherwise be associated with severe complications.

• #69 Approach to the adult with acute diarrhea in resource-limited settings – UpToDate

  https://www.uptodate.com/contents/approach-to-the-adult-with-acute-diarrhea-in-resource-limited-settings

  Dysentery is commonly associated with fever and abdominal pain. […] Important features accounting for the association between Shigella spp and large, regional epidemics of dysentery include the low infective dose (10 to 100 organisms), which facilitates person-to-person spread of infection, and increasing resistance to commonly used antimicrobials. […] Serious complications may occur with Shigella infection, including sepsis, seizures, rectal prolapse, toxic megacolon, and the hemolytic-uremic syndrome. […] Antibiotic therapy is warranted in some circumstances, as outlined below. […] Dysentery — Adults with bloody diarrhea (especially older adults and individuals with AIDS) should be treated promptly with an antimicrobial that is effective against Shigella. […] In several trials of patients with dysentery, antibiotics reduced the duration of diarrhea and fever in infections caused by Shigella, which is the most common cause of dysentery in resource-limited settings and can otherwise be associated with severe complications.

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