Camel trypanosomoses is considered a devastating disease with severe health consequences that can be caused by different hemoprotozoan parasites. Camel samples (388) from the five regions in Northern Oman were assessed using a thin blood film. In addition, 95 seropositive samples were analyzed using various primers of mechanically transmitted trypanosomes. Out of the 388 blood smears examined, 0.8% (CI 95%, 2/388) were found to be positive for Trypanosoma sp. using a microscope. The parasitologically positive cases were detected in samples from females. The overall molecular prevalences were as follows: TBR was 78/95, 77% (CI 73.1–89.2%); ITS was 30/95, 31.6% (CI 73.1–89.2%); and T. evansi type A (RoTat 1.2) was 8/95, 8.4% (CI 4.0–16.0%). There were two species of trypanosomes that were observed in the camels.

Objectives: Identification of the high risk alleles, genotypes and haplotypes of the human leukocyte antigens (HLA) in different populations is beneficial for understanding their roles in type 1 diabetes (T1D) pathogenesis and intervention practices. This study aimed to identify T1D-associated HLA gene alleles in the Omani population. Methods: The present case-control study included 73 diabetic seropositive children (mean age 9.08 ± 3.27 years) attending the paediatric clinic at Sultan Qaboos University Hospital in Muscat, Oman, and 110 healthy controls. HLA–A, -B, -C, -DRB1 and -DQB1 genes were genotyped using a sequence-specific primer polymerase chain reaction (SSP-PCR). Results: Two HLA class I alleles (B*08, B*58) and three class II alleles (DQB1*02, DRB1*03 and DRB1*04) were associated with T1D susceptibility, while one class I (B*51) and three class II (DQB1*05, DQB1*06 and DRB1*16) alleles were associated with T1D protection. HLA-DRB1*03 and DQB1*02 alleles showed the strongest risk association among all alleles. Six DRB1 residues (E9, S11, S13, Y30, V70 and K71) were significantly associated with T1D susceptibility. Heterozygous genotypes, HLA-DRB1*03/*04 and DQB1*02/*03 were significantly associated with T1D susceptibility (P <0.0001, odds ratio [OR] = 63.21 and P = 0.02, OR = 3.63, respectively). Furthermore, a significant combined action of DRB1*03-DQB1*02 haplotype in T1D risk (P = 0.000176, OR = 15) and DRB1*16-DQB1*05 haplotype in protection (P = 0.0312, OR = 0.48) was detected. Conclusion: Known HLA class II gene alleles are associated with T1D in Omani children.

The Sultanate of Oman hosts large annual nesting aggregations of up to 23,000 Loggerhead Sea Turtles (Caretta caretta) and 10,000 Green Sea Turtles (Chelonia mydas). Both populations have until now been poorly sampled (eight samples for C. caretta and fifteen for C. mydas). Genetic diversity information is needed for both species because these populations are increasingly threatened as the coastlines of Oman become more developed. It is currently unclear how diverse these rookeries are relative to other rookeries in the Atlantic, Mediterranean, Indian, or Pacific oceans. We explored mitochondrial DNA (mtDNA) diversity in 100 C. caretta from Masirah Island and 42 C. mydas from Ras al Hadd, Oman. We also analyzed C. caretta with four nuclear DNA (nDNA) microsatellites to investigate nuclear diversity. Loggerhead populations in Oman showed extremely low mtDNA diversity, but high nDNA diversity, suggesting isolation of genetically impoverished matrilineal lines, but relatively high male-mediated gene flow. In contrast, C. mydas populations in Oman consist of two clusters of distinct haplotypes that yield extremely high estimates of haplotype and nucleotide diversity relative to other global rookeries. These results describe the diversity of C. caretta and C. mydas rookeries in Oman with implications for global conservation.

Objectives: Pompe disease (glycogen storage disease type II) is a rare autosomal recessive lysosomal storage disease that is caused by acid alpha-glucosidase deficiency. Early enzyme replacement therapy can benefit infants with the disease but the diagnosis is complicated by the rarity of the disease and the heterogeneity of the clinical manifestations. In this study, DNA extracted from archival postmortem formalin-fixed paraffin-embedded tissues was used to identify Pompe disease mutations in Oman and develop a rapid molecular-based test. Methods: Intronic primers were designed to amplify short fragments (193–454 base pairs [bp]) from coding exons (2–20) and screen for mutations using direct sequencing (DS). Results: Two mutations known to cause severe disease were identified in two infants. One was a coding mutation, c.2560C>T (p.Arg854X), and the second was found at a splice acceptor site, c.1327-2A>G. Polymerase chain reaction- and restriction fragment length polymorphism-based tests were designed for the rapid genotyping of the identified mutations. Conclusion: These tests can facilitate prenatal diagnosis and help in identifying carriers in families with the identified mutations.