The type of capsular polysaccharide (CPS) on the cell surface of Acinetobacter baumannii can determine the specificity of lytic bacteriophage under consideration for therapeutic use. We have previously shown that the CPS biosynthesis gene clusters, KL3, KL22 and KL159, that produce the K3 type capsule are over-represented in available sequenced genomes. However, further studies have shown that deletion of the gtr6 gene results in the production of a variant CPS form, K3-v1, that lacks the b-d-GlсpNAc side chain, which leads to hypervirulence. Our studies have also shown that frameshifts in the gtr6 gene also influence the ability of some phage to digest the capsule. Hence, knowledge of the frequency and distribution of gtr6 mutations, and whether these occur in the most resistant isolates, is important. We manually examined the gtr6 sequence in 1776 genomes from NCBI that carry either KL3, KL22, or KL159 loci. A total of 1228 genomes (69%) were found to carry a complete gtr6 coding sequence (387 aa), whereas 330 (18.6%) had detectable frameshifts in gtr6 caused by indels or single nucleotide polymorphisms (SNPs), and 39 (3.18%) included an insertion sequence (IS) interrupting gtr6. Mutations in gtr6 that predict the K3-v1 hypervirulent phenotype were found in genomes from all geographical regions, except those from sub-Saharan Africa, with the earliest observed isolate carrying gtr6 with a frameshift recovered in 1931. A recombination-free core SNP phylogeny was also constructed using a subset of 50 KL3 sequence type (ST) 2 isolates originating from Asia and Australia, which demonstrated that gtr6 frameshifts are random and are not associated with recombination. Hence, gtr6 mutations appear to occur spontaneously in globally disseminated extensively antibiotic resistant isolates, indicating a need for improved detection of small changes in the gtr6 gene that may predict hypervirulence and altered phage susceptibility.