Fecal contamination in natural water sources is a common problem in low-income countries. Several health risks are associated with unprotected water sources, such as gastrointestinal infections caused by parasites, viruses, and bacteria. Moreover, antibiotic-resistant bacteria in water sources have become an increasing problem worldwide. This study aimed to evaluate the bacterial pathogens present in water within a rural context in Ecuador, along with the efficiency of black ceramic water filters (BCWFs) as a sustainable household water treatment. We monitored five natural water sources that were used for human consumption in the highlands of Ecuador and analyzed the total coliforms and E. coli before and after BCWF installation. The results indicated a variable bacterial contamination (29–300 colony-forming units/100mL) in all unfiltered samples, and they were considered as high risk for human consumption, but after filtration, no bacteria were present. Moreover, extended-spectrum beta-lactamase-producing E. coli with bla_TEM, bla_CTX-M9, and bla_CTX-M1 genes, and two E. coli classified in the clonal complex ST10 (ST98) were detected in two of the locations sampled; these strains can severely impact public health. The clonal complex ST10, found in the E. coli isolates, possesses the potential to spread bacteria-resistant genes to humans and animals. The results of the use of BCWFs, however, argue for the filters’ potential impact within those contexts, as the BCWFs completely removed even antibiotic-resistant contaminants from the water.

Tracking cell death in vivo can enable a better understanding of the biological mechanisms underlying tissue homeostasis and disease. Unfortunately, existing cell death labeling methods lack compatibility with in vivo applications or suffer from low sensitivity, poor tissue penetration, and limited temporal resolution. Here, we fluorescently labeled dead cells in vivo with Trypan Blue (TBlue) to detect single scattered dead cells or to generate whole-mount three-dimensional maps of large areas of necrotic tissue during organ regeneration. TBlue effectively marked different types of cell death, including necrosis induced by CCl₄ intoxication in the liver, necrosis caused by ischemia-reperfusion in the skin, and apoptosis triggered by BAX overexpression in hepatocytes. Moreover, due to its short circulating lifespan in blood, TBlue labeling allowed in vivo “pulse and chase” tracking of two temporally spaced populations of dying hepatocytes in regenerating mouse livers. Additionally, upon treatment with cisplatin, TBlue labeled dead cancer cells in livers with cholangiocarcinoma and dead thymocytes due to chemotherapy-induced toxicity, showcasing its utility in assessing anticancer therapies in preclinical models. Thus, TBlue is a sensitive and selective cell death marker for in vivo applications, facilitating the understanding of the fundamental role of cell death in normal biological processes and its implications in disease.