Acinetobacter baumannii is a Gram-negative bacterium known for its intrinsic pan-antibiotic resistance and ability to cause healthcare-associated infections. A potential treatment option rapidly gaining interest is “phage therapy”. We have recently isolated three novel myoviruses vB_AbaM-DLP1, vB_AbaM-DLP2, and vB_AbaM-DLP3 from sewage samples using the A. baumannii strain AB5075. Host range analysis of these phages against 107 A. baumannii clinical strains shows a limited host range, with 15, 21, and 19 isolates sensitive to DLP1, DLP2 and DLP3, respectively.  All phages exhibit large burst sizes of approximately 250 PFU/cell, with short latency periods of 15-20 min. A restriction fragment length polymorphism analysis using a panel of 16 enzymes shows that all genomes are highly resistant to digestion. Only NdeI can cut the DNA when incubated for the maximum allowable time, suggesting significant steric hindrance of the enzyme. More significantly, mass spectrometry of the nucleosides revealed a hypermodified deoxycytidine with a molecular weight of 640 kDa, nearly 2.6 times the size of a normal cytidine. NMR analysis confirmed significant modifications to the deoxycytidine with three arabinose moieties, producing the structure β-D-Araf-5-β-D-Araf-3-α-D-Araf-5-deoxycytidine. Further investigation into the genomes of these A. baumannii T4-like phages reveals a conserved region with eight genes encoding enzymes potentially involved in the DNA modification pathway. CRISPR interference experiments are underway to target these genes during host infection to elucidate the enzymes responsible for this significant DNA modification. The identification of this unique, previously unreported DNA modification provides insight into the types of DNA modifications bacteriophages employ to protect their genomes from degradation caused by resident restriction systems of the host.