Acinetobacter baumannii with plasmids resisting antibiotic attacks

Decoding Antibiotic Resistance: How Acinetobacter Baumannii Plasmids Are Evolving

Rhea Morgan in Health & Wellness December 2025 • 4 min read.

"A Deep Dive into the Genetic Structures Enabling This Superbug to Defy Treatment"

In the relentless battle against infectious diseases, Acinetobacter baumannii stands out as a particularly formidable adversary. This Gram-negative bacterium, an opportunistic pathogen, is a key member of the ESKAPE group—a collection of microbes notorious for their ability to evade antibiotic treatments. The rise of A. baumannii is a global concern, driven primarily by its increasing resistance to multiple drugs.

Globally, most A. baumannii strains resistant to multiple antibiotics are categorized under two main groups: global clone 1 (GC1) and global clone 2 (GC2). These classifications help scientists track and understand the spread of resistance. Research has shown that GC1 strains evolved around 1960 and diversified into two distinct lineages by 1967. In contrast to other Gram-negative bacteria, A. baumannii often houses resistance genes within genomic resistance islands located on its chromosome.

Acinetobacter baumannii isolate D36, belonging to lineage 2 of global clone 1, exhibits extensive antibiotic resistance. A recent study examined four plasmids within D36, revealing how these genetic structures contribute to the bacterium's ability to withstand antibiotic treatments. The study sheds light on the genetic mechanisms that facilitate resistance, providing insights crucial for developing new strategies to combat this resilient pathogen.

What Makes D36 So Resistant?

Acinetobacter baumannii with plasmids resisting antibiotic attacks

The D36 genome comprises a chromosome and four plasmids, named pD36-1 through pD36-4, ranging in size from 4.7 to 47.2 kb. Among these, PRAY (pD36-2, 6 kb) and pD36-4 (47.4 kb) carry antibiotic resistance genes, while pD36-1 (4.7 kb) and pD36-3 (7.2 kb) are cryptic plasmids without known resistance functions. The copy numbers vary, with pD36-1, PRAY, and pD36-3 present in 11–13 copies per cell, while pD36-4 exists in only 2–3 copies.

The smallest plasmid, pD36-1, contains mobilization genes mobA and mobC, which are related to those in pRAY. PRAY carries the aadB gene cassette, providing resistance to gentamicin, kanamycin, and tobramycin. These plasmids lack identifiable replication initiation proteins, suggesting alternative replication mechanisms. Notably, PRAY can be mobilized by the large conjugative plasmid pA297-3, further aiding its spread.

pD36-1: Contains mobA and mobC, facilitating mobilization.
PRAY: Carries aadB, conferring resistance to gentamicin, kanamycin, and tobramycin. Mobilized by pA297-3.
pD36-3: A RepAcil plasmid with unique dif modules.
pD36-4: Includes sul2 (sulfonamide resistance) and aphA1a (kanamycin/neomycin resistance), plus a mer module for mercury resistance.

The largest plasmid, pD36-4, includes the sul2 gene for sulfonamide resistance and aphA1a within Tn4352::ISAba1, which confers resistance to kanamycin and neomycin. It also harbors a hybrid Tn501/Tn1696 transposon that confers resistance to mercuric ions, demonstrating a broad spectrum of resistance mechanisms. Further diversifying its defense arsenal, pD36-4 contains two novel Rep_3 family proteins, suggesting a co-integrate structure.

The Implications and Future Directions

Understanding the genetic structures within A. baumannii, such as plasmids like pD36-4 and pRAY, is crucial for devising effective countermeasures. As these plasmids can transfer resistance genes, limiting their spread is essential. Future research should focus on developing novel antimicrobial agents and strategies that circumvent these resistance mechanisms, ensuring effective treatment options remain available. Continuous monitoring and genetic analysis of A. baumannii strains will also aid in tracking the evolution of resistance and informing public health policies.

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This article is based on research published under:

DOI-LINK: 10.1371/journal.pone.0204357, Alternate LINK

Title: Genetic Structure Of Four Plasmids Found In Acinetobacter Baumannii Isolate D36 Belonging To Lineage 2 Of Global Clone 1

Subject: Multidisciplinary

Journal: PLOS ONE

Publisher: Public Library of Science (PLoS)

Authors: Mohammad Hamidian, Ruth M. Hall

Published: 2018-09-27

Everything You Need To Know

What is Acinetobacter baumannii, and why is it a global concern?

Acinetobacter baumannii is a Gram-negative bacterium classified as an opportunistic pathogen and is a member of the ESKAPE group, known for its resistance to antibiotic treatments. Its increasing resistance to multiple drugs has made it a global concern, particularly the strains categorized under global clone 1 (GC1) and global clone 2 (GC2), which are frequently multi-drug resistant. The rise of multi-drug resistant strains like Acinetobacter baumannii poses a significant threat to healthcare globally because it limits treatment options and increases the risk of treatment failure for infections.

What are plasmids, and how do they contribute to the antibiotic resistance of Acinetobacter baumannii?

Plasmids are small, circular DNA molecules found in bacteria, separate from the main chromosome, and they often carry genes that provide bacteria with advantageous traits, such as antibiotic resistance. In Acinetobacter baumannii, plasmids like pD36-2 (PRAY*) and pD36-4 harbor antibiotic resistance genes. For example, PRAY* contains the aadB gene, which confers resistance to gentamicin, kanamycin, and tobramycin. The presence of these plasmids allows Acinetobacter baumannii to withstand the effects of antibiotics, thus making infections harder to treat.

Can you explain the difference between pD36-1, PRAY*, pD36-3, and pD36-4 plasmids found in Acinetobacter baumannii isolate D36?

The Acinetobacter baumannii isolate D36 contains four plasmids: pD36-1, PRAY* (pD36-2), pD36-3, and pD36-4. pD36-1 contains mobilization genes mobA and mobC, which facilitate its movement between bacterial cells. PRAY* carries the aadB gene, providing resistance to gentamicin, kanamycin, and tobramycin, and is mobilized by the plasmid pA297-3. pD36-3 is a RepAcil plasmid with unique dif modules, the function is still not fully explored. pD36-4 includes the sul2 gene for sulfonamide resistance and aphA1a gene, which provides resistance to kanamycin and neomycin. It also carries a mer module, providing resistance to mercuric ions. These plasmids, each with their unique set of genes, contribute to the overall antibiotic resistance profile of the bacterium.

How does the genetic makeup of pD36-4, specifically, contribute to the broad-spectrum resistance seen in Acinetobacter baumannii?

The pD36-4 plasmid is crucial in understanding the broad-spectrum resistance of Acinetobacter baumannii because it carries several resistance genes. Notably, it includes the sul2 gene, providing resistance to sulfonamides, and the aphA1a gene within Tn4352::ISAba1, conferring resistance to kanamycin and neomycin. Additionally, it contains a hybrid Tn501/Tn1696 transposon that confers resistance to mercuric ions. Furthermore, pD36-4 contains two novel Rep_3 family proteins, suggesting a co-integrate structure which might further diversify its defense mechanisms. The presence of these genes and structures allows Acinetobacter baumannii to resist a wide range of antibiotics and other toxic substances, making the bacterium very difficult to treat.

What are the implications of understanding the genetic structures, like plasmids, within Acinetobacter baumannii for the future of antibiotic treatment?

Understanding the genetic structures within Acinetobacter baumannii, particularly the plasmids such as pD36-4 and PRAY*, is critical for developing effective countermeasures against this superbug. Since these plasmids can transfer resistance genes, limiting their spread is essential. Future research must focus on novel antimicrobial agents and strategies that can circumvent these resistance mechanisms, ensuring effective treatment options remain available. Continuous monitoring and genetic analysis of Acinetobacter baumannii strains will help track the evolution of resistance. This information is vital for informing public health policies and developing targeted interventions. Essentially, detailed knowledge of the plasmids and their mechanisms enables scientists to stay ahead of the bacterium's evolving resistance capabilities.