Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been detected in domestic and wild cats. However, little is known about natural viral infections of domestic cats, although their importance for modelling disease spread, informing strategies for managing positive human-animal relationships and disease prevention. Here, we describe the SARS-CoV-2 infection in a household of two human adults and sibling cats (one male and two females) using real-time RT–PCR, an ELISA test, viral sequencing, and virus isolation. On May 5th, 2020, the cat-owners tested positive for SARS-CoV-2. Two days later, the male cat showed mild respiratory symptoms and tested positive. Four days after the male cat, the two female cats became positive, asymptomatically. Also, one human and one cat showed antibodies against SARS-CoV-2. All cats excreted detectable SARS-CoV-2 RNA for a shorter duration than humans and viral sequences analysis confirmed human-to-cat transmission. We could not determine if cat-to-cat transmission also occurred.

Salmonella enterica subsp. enterica serotype Enteritidis is a major cause of human salmonellosis worldwide; however, little is known about the genetic relationships between S . Enteritidis clinical strains and S . Enteritidis strains from other sources in Chile. We compared the whole genomes of 30 S . Enteritidis strains isolated from gulls, domestic chicken eggs, and humans in Chile, to investigate their phylogenetic relationships and to establish their relatedness to international strains. Core genome multilocus sequence typing (cgMLST) analysis showed that only 246/4,065 shared loci differed among these Chilean strains, separating them into two clusters (I and II), with cluster II being further divided into five subclusters. One subcluster (subcluster 2) contained strains from all surveyed sources that differed at 1 to 18 loci (of 4,065 loci) with 1 to 18 single-nucleotide polymorphisms (SNPs), suggesting interspecies transmission of S . Enteritidis in Chile. Moreover, clusters were formed by strains that were distant geographically, which could imply that gulls might be spreading the pathogen throughout the country. Our cgMLST analysis, using other S . Enteritidis genomes available in the National Center for Biotechnology Information (NCBI) database, showed that S . Enteritidis strains from Chile and the United States belonged to different lineages, which suggests that S . Enteritidis regional markers might exist and could be used for trace-back investigations. IMPORTANCE This study highlights the importance of gulls in the spread of Salmonella Enteritidis in Chile. We revealed a close genetic relationship between some human and gull S . Enteritidis strains (with as few as 2 of 4,065 genes being different), and we also found that gull strains were present in clusters formed by strains isolated from other sources or distant locations. Together with previously published evidence, this suggests that gulls might be spreading this pathogen between different regions in Chile and that some of those strains have been transmitted to humans. Moreover, we discovered that Chilean S . Enteritidis strains clustered separately from most of S . Enteritidis strains isolated throughout the world (in the GenBank database) and thus it might be possible to distinguish the geographical origins of strains based on specific genomic features. This could be useful for trace-back investigations of foodborne illnesses throughout the world.

Pandemic (H1N1) 2009 virus was detected in breeding turkeys on 2 farms in Valparaiso, Chile. Infection was associated with measurable declines in egg production and shell quality. Although the source of infection is not yet known, the outbreak was controlled, and the virus was eliminated from the birds.

Staphylococcus aureus is the most commonly isolated pathogen from clinical bovine mastitis samples and a difficult pathogen to combat. Mesenchymal stem cells (MSC) are multipotent progenitor cells equipped with a variety of factors that inhibit bacterial growth. The aim of the present study was to evaluate the in vitro antibacterial potential against S. aureus of conditioned medium (CM) from MSC derived from fetal bovine bone marrow (BM-MSC) and adipose tissue (AT-MSC). BM-MSC, AT-MSC and fetal fibroblasts (FB) cultures were activated by infection with S. aureus. Bacterial growth was evaluated in presence of CM, concentrated CM (CCM), activated CM (ACM) and concentrated ACM (CACM) from BM-MSC, AT-MSC and FB. Gene expression of β-defensin 4A (bBD-4A), NK-lysine 1 (NK1), cathelicidin 2 (CATHL2), hepcidin (HEP) and indoleamine 2,3 dioxygenase (IDO) and protein expression of bBD-4A were determined in activated and non-activated cells. The majority of BM-MSC and AT-MSC expressed CD73, Oct4 and Nanog, and were negative for CD34. Growth of S. aureus decreased when it was exposed to CM from BM-MSC, AT-MSC and FB. Moreover, growth of S. aureus in CCM, ACM and CACM was lower compared to controls of CM from BM-MSC and AT-MSC. Activated AT-MSC increased mRNA levels of bBD4A and NK1, and protein levels of bBD4A in CM. Thus, CM from fetal bovine BM-MSC and AT-MSC has the capacity to reduce in average ~30% of S. aureus relative growth under in vitro conditions. The in vitro antibacterial effect of fetal bovine MSC may be mediated by bBD4A and NK1 activity.

The MgtC is a virulence factor in Salmonella Typhimurium that is required for growth at low-Mg²⁺ concentrations and intramacrophage survival. This gene is codified in a conserved region of the Salmonella pathogenicity island 3 (SPI-3), and is also present in the chromosome of other Salmonella serovars. In this study we characterized the MgtC factor in S. Typhi, a human specific pathogen, by using mgtC and SPI-3 mutant strains. We found that MgtC is the most important factor codified in the SPI-3 of S. Typhi for growth in low-Mg²⁺ media and survival within human cells. In addition, by using reporter genes we determined that the low-Mg²⁺ concentration, acidic media and PhoP regulator induce mgtC expression in S. Typhi. We suggest that MgtC is the most important virulence factor codified in the SPI-3 of S. Typhi.