Staphylococcus aureus
Firza Alexander Gronthoud in Practical Clinical Microbiology and Infectious Diseases, 2020
Staphylococcus aureus produces bound or free coagulase, which converts fibrinogen to fibrin, providing protection from phagocytes and enables S. aureus to form septic emboli and disseminate to other organs. It further prevents phagocytosis. Staphylococcus aureus can also produce several toxins which are associated with specific clinical syndromes. Examples are: Toxic shock syndrome toxin-1 (TSST-1) causing toxic shock syndrome characterized by fever, diarrhoea, shock, multiorgan failure and a scarlatiniform rash which desquamates. Blood cultures are almost always negative.Exfoliative toxin damages the epidermis, causing generalized skin desquamation, also known as scalded skin syndrome.Panton–Valentine leucocidin lyses white blood cells; is associated with recurrent skin boils and abscesses and necrotizing pneumonia.Enterotoxin causes food poisoning.
Gastrointestinal and liver infections
Michael JG Farthing, Anne B Ballinger in Drug Therapy for Gastrointestinal and Liver Diseases, 2019
Intestinal secretory processes in infective diarrhoea are generally activated by secretory entero toxins. Cholera toxin (CT) is the prototype enterotoxin and its mechanism of action has been studied in great detail.2, 3 Until recently, the main focus of the action of cholera toxin has been on the enterocyte and the enzymic activity of the A1 subunit of cholera toxin, which activates Gs—the catalytic unit of the enzyme adenlyate cyclase. This results in an increase in intracellular cyclic AMP, which, through a series of intermediate steps, results in phosphorylation of the transmembrane chloride channel protein, with opening of chloride channels in the apical membrane of the enterocyte.
Scientific Rationale for the Use of Single Herb Remedies in Ayurveda
D. Suresh Kumar in Ayurveda in the New Millennium, 2020
Daswani et al. (2011) studied the anti-diarrheal activity of the decoction of C. rotundus tubers using representative assays of diarrheal pathogenesis. Antibacterial, antigiardial and antirotaviral activities were also studied. Effects on adherence of enteropathogenic Escherichia coli and invasion of enteroinvasive E. coli and Shigella flexneri to HEp-2 cells were evaluated to measure the effect on colonization. Effect on enterotoxins such as enterotoxigenic E. coli, heat-labile toxin, heat-stable toxin and cholera toxin was also assessed. The decoction showed antigiardial activity, reduced bacterial adherence to and invasion of HEp-2 cells and affected production of cholera toxin and action of heat-labile toxin. The decoction of C. rotundus seems to exert the anti-diarrheal action by mechanisms other than direct killing of the pathogen.
Immunomodulatory regulation by heat-labile enterotoxins and potential therapeutic applications
Published in Expert Review of Vaccines, 2021
Mary-Peyton A. Knapp, Taylor A. Johnson, Madison K. Ritter, Robert O. Rainer, Steven E. Fiester, Jennifer T. Grier, Terry D. Connell, Sergio Arce
Mutant enterotoxins may also decrease toxicity by reducing excessive inflammatory responses. According to Scharton-Kersten et al., HLTs lacking ADP-ribosyltransferase, as evidenced by mutant LT-I and CT compared to their respective holotoxins, seemed to attenuate the immune response to diphtheria toxin, while still conferring some immunogenicity [67]. A study tested the immunogenicity of LT-IIa, LT-IIb, LT-IIb (T13I), and LT-IIc when co-administered with RiVax antigen. The mutant LT-IIb (T13I) demonstrated the least amount of inflammatory response when administered with RiVAx compared to the other HLTs tested [62]. In another study, intranasal administration of LT-IIb (T13I) with RiVax antigen caused a significant increase in RiVax-specific antibody levels compared to RiVax alone. There was also an increase in IgG and IgA antibodies in BAL fluid, saliva and fecal samples. These findings demonstrated that LT-IIb (T13I) was not less effective than LT-IIb as an adjuvant even though it was less toxic [13]. Taken together, this data reveals that it is possible to use mutant forms of HLTs as adjuvants to stimulate immunogenicity while decreasing the toxicity of the wildtype forms through loss of cAMP activation and reduced inflammation.
Phosphodiesterase 5 (PDE5) restricts intracellular cGMP accumulation during enterotoxigenic Escherichia coli infection
Published in Gut Microbes, 2020
Jennifer Foulke-Abel, Huimin Yu, Laxmi Sunuwar, Ruxian Lin, James M. Fleckenstein, James B. Kaper, Mark Donowitz
The Global Enteric Multi-Center Study (GEMS) identified enterotoxigenic Escherichia coli (ETEC) infection as one of the four leading causes of acute diarrhea and associated mortalities in developing countries.1 As the leading cause of traveler’s diarrhea, ETEC is also a recognized burden on deployed U.S. military personnel.2 The host diarrheal response is initiated by the secreted peptide heat-stable enterotoxin (ST) and/or the multi-subunit protein heat-labile enterotoxin (LT) via induction of second messenger cGMP and cAMP synthesis, respectively. ETEC strain H10407, originally isolated from a patient in Bangladesh with severe cholera-like diarrhea,3 employs additional factors to facilitate host interaction, including but not limited to the secreted mucinase EatA4 and surface adhesins EtpA5,6 and CfaE.7 Strains expressing ST, alone or in combination with LT, were more highly associated with diarrhea than LT-only expressing strains,8 confirming the importance of ST in disease pathogenesis. As such, recent renewed efforts to employ ST antigens for vaccine development are under way.9,10
Microbiota modulation-based therapy for luminal GI disorders: current applications of probiotics and fecal microbiota transplantation
Published in Expert Opinion on Biological Therapy, 2019
Abbinaya Elangovan, Jessica R. Allegretti, Monika Fischer
The pathophysiology of acute infectious diarrhea frequently involves one of the three mechanisms – ingestion of a preformed enterotoxin, production of an endotoxin following the ingestion of the culprit organism or inflammation of the intestinal epithelium by invasion of the organism [45].
Related Knowledge Centers
- Protein
- Exotoxin
- Gastrointestinal Tract
- Cytotoxicity
- Semipermeable Membrane
- Epithelium
- Pore-Forming Toxin
- Cell Membrane
- Travelers' Diarrhea
- Cyclic Adenosine Monophosphate