Explore chapters and articles related to this topic
Clinical profile in adult typhoid fever in patients at hospital X, East Jakarta, Indonesia, January–March 2018
Published in Ade Gafar Abdullah, Isma Widiaty, Cep Ubad Abdullah, Medical Technology and Environmental Health, 2020
Salmonella typhi, one of the subspecies of the genus Salmonella that causes typhoid fever, causes prolonged fever, headaches, nausea, vomiting, loss of appetite (anorexia), and constipation or not infrequently diarrhea. Severe cases can result in serious complications or even death. The average dose that can cause symptoms of clinical or subclinical infection in humans is around 105–108Salmonella bacteria (Salmonella typhi is enough with the number of 103 bacteria that may already be causing clinical symptoms). Infection is transmitted through food or water contaminated by feces or urine from the patient or carrier. Raw fruits and vegetables are the main cause of the spread of S. typhi bacteria. This happens in some countries where human feces are used as fertilizer for plants (fruits and vegetables) and contaminated water is used to make fruits look more attractive in the market (Brooks et al. 2010; Setiati et al. 2014).
Nutritional Disorders/Alternative Medicine
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Food poisoning involves gastrointestinal symptoms after consumption of foods or drink, usually due to salmonella or an enterotoxin. Foods, water or milk can also be carriers for the enteric (intestinal) fevers—typhoid or paratyphoid—caused by Salmonella organisms. Bacillary dysentery (Shigella) and cholera (Vibrio cholerae) are other bacterial diseases spread through food or drinking water. Amebic dysentery, caused by the protozoan Entamoeba histolytica, is transmitted by water or uncooked foods contaminated with human feces. The term traveler's diarrhea refers to the gastrointestinal disorder that occurs from strains of enterobacteria to which immunities have not been developed.
An Overview of Helminthiasis
Published in Venkatesan Jayaprakash, Daniele Castagnolo, Yusuf Özkay, Medicinal Chemistry of Neglected and Tropical Diseases, 2019
Leyla Yurttaș, Betül Kaya Çavușoğlu, Derya Osmaniye, Ulviye Acar Çevik
T. solium can cause two separate diseases in the human population: taeniasis, when the human is a primary host; and cysticercosis (a cyst containing an invaginated scolex) when the human is the secondary host (Berman 2012). When the intermediate host ingests a T. solium egg, the oncosphere is liberated after its passage through the stomach. After that it penetrates the intestinal wall and is transported through the blood or lymphatics to the muscles where it develops into a cysticercus. Cysticercoids move from the muscle to the brain and they cause cysticercosis, which can be lethal after moving to the brain. The analysis of human faeces is used in the diagnosis of taeniasis. Sedimentation, flotation, and Kato–Katz tests are concentration methods, but they have low sensitivity for Taenia eggs and cannot differentiate between T. solium and T. saginata taeniasis. In addition to this, serologic tests for a T. solium tapeworm stage-specific antibody have been advanced as a research technique (Geerts 2015).
The barrier and beyond: Roles of intestinal mucus and mucin-type O-glycosylation in resistance and tolerance defense strategies guiding host-microbe symbiosis
Published in Gut Microbes, 2022
Critically, the phenomena of the fecal mucus barrier association is conserved in other species including rat (which also has the b1/b2 layers), baboon,47 and human,47,50 although the b1/b2 subtypes have not been confirmed in the latter. Still, there is thick and clear mucus on the periphery of well-formed human and baboon stool that is impenetrable to the microbiota.47 The similarities between the rodent and primate/human mucus suggest a similar proximal colon-mediated mechanism leads to association of fecal mucus in humans and raises important questions as to what leads to mucus defects in human diseases like UC. Further, these studies raise new questions on the relative contribution of mucus production from proximal and distal sites to the niche and barrier functions of mucus. For example, are the native mucus studies in the mouse explant model system using distal colon representing the type II sulfated mucus? Does the encapsulating mucus on human feces represent a different type compared to that present in distal colon goblet cells as observed in rodents?
Antioxidant properties of polyphenols from snow chrysanthemum (Coreopsis tinctoria) and the modulation on intestinal microflora in vitro
Published in Pharmaceutical Biology, 2022
Minghao Zhang, Naiyu Zhao, Minhao Xie, Deqiao Dong, Weilin Chen, Yuanpeng He, Dalin Yan, Haiyan Fu, Xinlin Liang, Li Zhou
In vitro fermentation method was slightly modified according to the procedure described by Bai et al. (2021). Briefly, fresh human faeces were taken from 8 healthy donors (4 males and 4 females, 20–26 years old). All donors were without any antibiotic exposure for at least 6 months. The volunteers were mentally and physically able to participate in the study and informed written consent was obtained from each volunteer. In addition, the experiments were performed in compliance with the relevant laws and institutional guidelines. Fresh faecal samples were collected in anaerobic tubes and then dissolved in the physiological saline solution (NaCl 9.0 g/L, cysteine-HCl 0.5 g/L) to yield 10% (w/v) faecal slurry suspension after centrifugation. Autoclaved basal nutrient growth medium was supplied with C. tinctoria phenolics or nothing. Medium (18 mL) and 2 mL faecal slurry were added into the anaerobic tubes, then placed in the 37 °C anaerobic chambers. At each time point of fermentation (0, 12 and 24 h), assigned anaerobic tubes were taken out and stored at −80 °C for further analysis.
Clostridioides difficile: innovations in target discovery and potential for therapeutic success
Published in Expert Opinion on Therapeutic Targets, 2021
Tanya M Monaghan, Anna M Seekatz, Benjamin H Mullish, Claudia C. E. R Moore-Gillon, Lisa F. Dawson, Ammar Ahmed, Dina Kao, Weng C Chan
More recently, there is interest in targeting mixed bacterial populations to prevent C. difficile biofilm formation and thus persistence in the gut. Bacteroides fragilis, a gut commensal microbe that has been negatively associated with C. difficile during infection, was demonstrated to inhibit C. difficile biofilm formation in vitro in co-culture [44]. The presence of LuxS was observed to contribute to C. difficile growth inhibition in this co-culture [44], suggesting different metabolic and signaling pathways for mono- vs mixed-populations. In a bioreactor model consisting of human feces, C. difficile has been observed to co-colonize with Fusobacterium nucleatum, another prevalent human gut commensal bacterium [47]. Aggregation between the two was diminished when C. difficile flagella or the RadD protein of F. nucleatum was removed. Targeting of non-C. difficile factors, such as proteins of other bacteria that interact with C. difficile directly, could be a unique therapeutic landscape.