There are many genetic and acquired risk factors that are known to cause venous thromboembolic disorders (VTE). One of these is the Prothrombin G20210A mutation, which has been identified in 1996. Prothrombin G20210A mutation causes higher levels of the clotting factor prothrombin in the blood of carriers, which creates a higher tendency towards blood clotting (hypercoagulability), and therefore the carriers become at higher risk of developing VTE. High prevalence of Prothrombin G20210A mutation was reported in Caucasian populations, but the prevalence was almost absent in non-Caucasians. That was most obvious in countries of South Europe and the Mediterranean region. This review article discusses Prothrombin G20210A mutation, how it causes VTE, the origin of the mutation, and its distribution worldwide with special concentration on the Mediterranean area.
Blood isolates of Salmonella enterica serovar Typhi from two recently returned Bangladeshi patients in Kuwait were ciprofloxacin resistant, with ciprofloxacin MICs of 12 mg/liter for both isolates. Both isolates had three novel gyrA mutations (55-Leu3Trp, 87-Asp3Ala, and 106-Gln3Arg) and three novel parC mutations (84-Glu3Lys, 106-Trp3Gly, and 128-Tyr3Asp).
Venous thromboembolic disorders (VTE) are serious disorders with high morbidity and mortality rates. Many genetic and acquired risk factors were identified to cause VTE. The most common genetic risk factor is Factor V Leiden mutation (FVL). FVL was found in high percentage of populations of Caucasian origin but was almost absent in non-Caucasians. It was also reported in populations living in North Africa and the Middle East. This review article briefly explains FVL and how it causes VTE, the distribution of FVL worldwide, and then it elaborates on the epidemiology of FVL in the Mediterranean Region and how this brought speculations that FVL might have originated in the Eastern Mediterranean area.
The spread of antibiotic-resistant bacteria has become a large problem in most countries including Kuwait. This antibiotic resistance is usually due to the production of extended-spectrum b-lactamase (ESBL) enzymes such as SHV, TEM and CTX-M. This study reports the emergence and spread of an ESBL-producing Klebsiella pneumoniae clone in a neonatal intensive care unit (NICU) in a Kuwaiti hospital. Eight ESBL-producing K. pneumoniae isolates were from blood cultures of seven neonates, and two were from the fingers of two healthcare workers in a NICU in Al Jahra Hospital, Kuwait. All isolates were obtained in February-March 2006, except for one, which was obtained in August 2005. Identification of the bacteria was based on traditional bacteriological and biochemical tests using the Vitek system. Antibiotic susceptibility was tested by the disc diffusion method using 16 different antibiotics. ESBLs were detected using disc approximation and double-disc synergy methods and confirmed as ESBLs using Etest. PCR and DNA sequencing were performed to determine the genotypes and mutations in the b-lactamase genes (bla TEM , bla SHV and bla CTX-M). Genetic relatedness was determined by PFGE. All isolates were confirmed to have ESBLs by the Vitek system, disc approximation test, double-disc diffusion test and Etest, being resistant to cefotaxime, ceftazidime, cefepime, gentamicin, tobramycin and ciprofloxacin but susceptible to tetracycline and trimethoprim-sulfamethoxazole. Molecular studies showed the isolates to have TEM-1 b-lactamase, a CTX-M-15-like ESBL and the newly discovered SHV-112 ESBL. PFGE showed that all isolates had identical banding patterns. The results indicate that a single clone of ESBL-producing K. pneumoniae caused bloodstream infections among babies in a NICU of a Kuwaiti hospital, and may have emerged at least 5 years ago. This clone was also present on the hands of healthcare workers, suggesting that they may have been involved in its transmission. Further studies are recommended to determine whether this clone is also spreading in other Kuwaiti hospitals.
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