Molecular frequency of bovine leukemia virus in Creole cattle of Eastern Colombia.

Enzootic Bovine Leukosis (EBL), caused by the bovine leukosis virus (BLV), is a global infectious disease affecting livestock. This study focuses on studying the frequency and genetic traits of BLV in three Creole breeds including Chino Santandereano (Chino), Casanareño (CAS), and Sanmartinero (SM) in Eastern Colombia. We implemented a cross-sectional survey between 2019 and 2020 across four departments (Arauca, Casanare, Santander and Meta) in Eastern Colombia to assess the molecular characteristics of BLV infection in these breeds. A total of 253 cattle were analyzed, of which 42.6 %, 28.8 %, and 28.4 % belonged to the Chino, CAS, and SM breeds, respectively. BLV provirus was detected using nested polymerase chain reaction (n-PCR) targeting the conserved region of the env viral gene. Subsequently, the obtained amplicons were sequenced and subjected to phylogenetic analyses. The overall BLV infection frequency was 26.48 % (95 % CI: 21.01 - 31.98 %), with Chino exhibiting the highest frequency (35.1 %) following by SAM and CAS, respectively (P < 0.05). Other epidemiological variables associated with the infection included age, department, and season (P < 0.05). BLV-positive animals exhibited elevated levels of total serum proteins (P < 0.05), while molecular characterization revealed the exclusive circulation of BLV genotype 1 within these breeds. This study provides an updated assessment of BLV infection in Creole breeds from the eastern of Colombia, underscoring their lower infection frequency compared to introduced breeds and their reduced susceptibility to developing clinical signs. The epidemiological and molecular characteristics observed should be considered in developing control programs aimed at improving genetic resistance to BLV in Colombian cattle.

Molecular detection and characterization of Giardia spp., Cryptosporidium spp., and Blastocystis in captive wild animals rescued from central Colombia.

Cryptosporidium, Giardia, and Blastocystis are significant causes of diarrhea worldwide. However, studies on their prevalence in wild animals are limited, compared to humans and domestic animals. In this study, we collected 23 stool samples from captive wild rescued animals in Boyacá, Colombia. Using conventional PCR, we detected Cryptosporidium spp., Giardia spp., and Blastocystis in over half of the samples (69.6%). Cryptosporidium spp. (43.5%) were the most commonly found, followed by Giardia spp. (39.1%) and Blastocystis (13.0%). Co-infections involving these parasites were also observed. Subsequent genotyping revealed Cryptosporidium canis and Cryptosporidium ryanae as the predominant species. These findings contribute valuable information about the ecoepidemiology of intestinal parasites in Colombian wild animals.

Neonatal upper airway obstruction in osteogenesis imperfecta: series of three cases and review of the literature.

OBJECTIVES: Osteogenesis imperfecta (OI) is a genetic disorder characterized by variable degrees of dysfunction in type I collagen formation. We sought to explore an association between OI and upper airway obstruction (UAO) in light of our recent experience. METHODS: We performed a retrospective chart audit and a review of the literature. RESULTS: Three consecutive cases of OI at our institution required otolaryngological evaluation for UAO. The first patient had the mildest mutation type and did well until he developed severe reflux-triggered laryngospasm that improved with Nissen fundoplication and gastrostomy tube placement. He had mild hypotonia on endoscopy. The second patient had severe OI and the greatest acute fracture burden at birth. He required tracheotomy after early respiratory failure, and some mild bronchomalacia was noted. The third patient had severe OI and underwent cesarean section delivery. She developed respiratory failure after 1 month, requiring tracheotomy; mild tracheomalacia and glottic narrowing were noted on endoscopy. CONCLUSIONS: The UAO consisted of mild hypotonia or malacia in 3 consecutive cases of OI, and may have contributed to pulmonary and mechanical causes of tracheotomy requirement. The greatest predictors of tracheotomy requirement appear to be the severity of the OI mutation and the fracture burden. Elective cesarean section should be considered in severe cases of OI.

A family of anti-sigma70 proteins in T4-type phages and bacteria that are similar to AsiA, a Transcription inhibitor and co-activator of bacteriophage T4.

Anti-sigma70 factors interact with sigma70 proteins, the specificity subunits of prokaryotic RNA polymerase. The bacteriophage T4 anti-sigma70 protein, AsiA, binds tightly to regions 4.1 and 4.2 of the sigma70 subunit of Escherichia coli RNA polymerase and inhibits transcription from sigma70 promoters that require recognition of the canonical sigma70 -35 DNA sequence. In the presence of the T4 transcription activator MotA, AsiA also functions as a co-activator of transcription from T4 middle promoters, which retain the canonical sigma70 -10 consensus sequence but have a MotA box sequence centered at -30 rather than the sigma70 -35 sequence. The E.coli anti-sigma70 protein Rsd also interacts with region 4.2 of sigma70 and inhibits transcription from sigma70 promoters. Our sequence comparisons of T4 AsiA with Rsd, with the predicted AsiA orthologs of the T4-type phages RB69, 44RR, KVP40, and Aeh1, and with AlgQ, a regulator of alginate production in Pseudomonas aeruginosa indicate that these proteins share conserved amino acid residues at positions known to be important for the binding of T4 AsiA to sigma70 region 4. We show that, like T4 AsiA, Rsd binds to sigma70 in a native protein gel and, as with T4 AsiA, a L18S substitution in Rsd disrupts this complex. Previous work has assigned sigma70 amino acid F563, within region 4.1, as a critical determinant for AsiA binding. This residue is also involved in the binding of sigma70 to the beta-flap of core, suggesting that AsiA inhibits transcription by disrupting the interaction between sigma70 region 4.1 and the beta-flap. We find that as with T4 AsiA, the interaction of KVP40 AsiA, Rsd, or AlgQ with sigma70 region 4 is diminished by the substitution F563Y. We also demonstrate that like T4 AsiA and Rsd, KVP40 AsiA inhibits transcription from sigma70-dependent promoters. We speculate that the phage AsiA orthologs, Rsd, and AlgQ are members of a related family in T4-type phage and bacteria, which interact similarly with primary sigma factors. In addition, we show that even though a clear MotA ortholog has not been identified in the KVP40 genome and the phage genome appears to lack typical middle promoter sequences, KVP40 AsiA activates transcription from T4 middle promoters in the presence of T4 MotA. We speculate that KVP40 encodes a protein that is dissimilar in sequence, but functionally equivalent, to T4 MotA.