
Bacteremia Susceptibility: Decoding the Genetic Blueprint to Combat a Silent Threat
A hypervirulent Klebsiella pneumoniae strain carrying MCR-1, NDM-1 and OXA-10 shows why resistance matters here, and how genetic markers flag higher-risk patients.

MD · MBA
Physician specializing in genetic analysis and personalized preventive medicine, and author of Outsmart Your Genes.
Brandon Colby is a physician-expert in the fields of genetic analysis and Personalized Preventive Medicine. He holds an MD from the Mount Sinai School of Medicine, an MBA from Stanford University's Graduate School of Business, and a degree in Genetics from the University of Michigan.
Dr. Colby is the author of the book Outsmart Your Genes and has developed numerous technologies that improve the analysis, interpretation, and actionability of genome sequencing data. He is an Affiliate Specialist of the American College of Medical Genetics and Genomics (ACMG), an Associate of the American College of Preventive Medicine (ACPM), and a member of the National Society of Genetic Counselors (NSGC).
Articles by Brandon Colby, MD are reviewed for accuracy by Sequencing's medical and scientific team. This page is for informational purposes and does not constitute medical advice.

A hypervirulent Klebsiella pneumoniae strain carrying MCR-1, NDM-1 and OXA-10 shows why resistance matters here, and how genetic markers flag higher-risk patients.

Uveal melanoma, mesothelioma, renal cell carcinoma and cutaneous melanoma cluster in families carrying a BAP1 mutation, which passes in an autosomal dominant pattern.

Changes in the ACTG1 gene disturb the actin cytoskeleton, causing intellectual disability, distinctive craniofacial features and, in some cases, ocular abnormalities.

SLC52A2 mutations disrupt riboflavin transport, causing the muscle weakness, hearing loss and cranial nerve problems of BVVLS2 that high-dose riboflavin may ease.

Features of both demyelinating and axonal neuropathy meet in CMT-DIE; studies of AARS-related neuropathy in UK and Irish families widened its known spectrum.

Inflamed lesions on fingers, toes, ears and nose mark chilblain lupus 2; its TLR7 gain-of-function variant points to TLR7 and MyD88 inhibitors under study.

Ataxia, developmental regression and dystonia that worsen after viral infections follow TPK deficiency; TPK1 testing confirms it and supports thiamine use.

Deletions at 2p16.3 are tied to intellectual disability and facial dysmorphisms, and contiguous gene deletions connect the region to Lynch syndrome.