Kimberly Kline 🏔

Congratulations Fellows!

The American Academy of Microbiology proudly announces the election of 63 fellows to the Class of 2026. Over the past 50 years, the Academy has elected +2,700 distinguished scientists. This year, the new fellows hail from 14 countries. Read press release: asm.social/2OC

New in JB: Weiss, Tamayo et al. describe a very cool microbial interaction wherein Enterococcus faecalis, an opportunist found in the inflamed gut, impacts phase-variation noted by chaining & rough colony morphology of C. diff.
journals.asm.org/doi/10.1128/...
@asm.org #JBacteriology

Abstract deadline Mon for 6th Clinical & Scientific Advances in UTI, the premier biennial gathering of our international community. Privileged to be co-organising this year. See you in Nashville! utiga.org/2026-6th-csa... #UTI #UTISky #IDSky #MicroSky @globaluti.bsky.social utiga.org/2026-6th-csa...

Scientist's way of saying 'I ❤️ you'

"I found this paper/preprint that made me think of your project."
"I checked the mice/cells/plates already."
"I just sent you the edits you requested."
"I have a slide/diagram that will work for that."
"I had that problem with [lab equipment], I have a fix."

🎉 New paper out!
Taking a closer look at Enterococcus thailandicus, a species long considered of low clinical relevance.

doi.org/10.1016/j.nm...

Great 3 continent team effort including Brenda Tien, Patrick Kao, Jianzhu Chen and BlueSkyers @harisantypas.bsky.social @cenkcelik.bsky.social @gthibault.bsky.social @scelse.bsky.social

Enterococcus faecalis-derived lactic acid suppresses macrophage activation to facilitate persistent and polymicrobial wound infections Macrophage activation is essential for innate immunity and antimicrobial defense. We show that Enterococcus faecalis suppresses macrophage activation …

Lactic acid lover? Check out @ronni.bsky.social 's new work in
@cp-cellhostmicrobe.bsky.social showing how Enterococcus faecalis-derived LA suppresses macrophage activation, in turn promoting bacterial persistence and polymicrobial wound infection in vivo.
www.sciencedirect.com/science/arti...

Strep/Enterococcal colleagues!

Streptococcal Biology GRC/GRS are open for applications. Acceptances are underway and the meeting is on track to fill up.

If you’re aiming for a short talk (lots of slots), registering early matters for full consideration.

Share widely!

www.grc.org/streptococca...

I remember well this very cool study by @kayla-king.bsky.social et al. Thanks for highlighting the possible link to our work here!

Enterococcus fans: Check out our latest on E. faecalis EET, advancing our understanding of both the fundamental physiology of this bug and new mechanisms of its virulence. This is the product of a thrilling collaboration with friends in Singapore @gthibault.bsky.social led by @aarontan.bsky.social.

YouTube video by KeystoneSymposia KSQA: Drs. Joseph P. Zackular & Mariana X. Byndloss (Beyond Antibiotics)

⏰ Deadline Jan 7 (11:59 pm MST) to submit a short talk abstract or apply for a scholarship for the Keystone Symposium Beyond Antibiotics. Hear from @joeyzacks.bsky.social, @maribyndloss.bsky.social: youtu.be/8Ppjx-MnvxA

keysym.us/KSBeyondAnti... @kimingeneva.bsky.social & @dariavantyne.bsky.social

Global burden, inequalities and projections of vancomycin-resistant Enterococcus faecium and Enterococcus faecalis, 1990–2050: a systematic global analysis Vancomycin-resistant Enterococcus faecium (VREfm) and Enterococcus faecalis (VREfs) are major antimicrobial resistance threats. Previous assessments r…

'In 2021, 11,021 deaths and 353,634 DALYs were attributable to VREfm worldwide, (...) 2,991 deaths and 82,025 DALYs attributable to VREfs. (...) VREfm burden is projected to continue rising across all indicators by 2050, while VREfs shows a sustained decline.'

www.sciencedirect.com/science/arti...

What’s next? Big questions we're excited about:
• How does Ef hijack intracellular trafficking machinery for its replication?
• What host pathways define “permissive” vs “restrictive” intracellular states?
• How does intracellular replication impact chronicity/relapse in vivo?
Stay tuned...🧐
6/6

Gelatinase regulates the egress of intracellular replicating populations during Enterococcus faecalis infection Enterococcus faecalis is a common opportunistic pathogen, frequently isolated from chronic wounds, yet the mechanisms underlying its virulence and persistence in this niche remain incompletely underst...

There's more! @frederickreinhart.bsky.social now shows Fsr quorum sensing turns on during intracellular replication, driving GelE-dependent host cell lysis/egress, a model for how intracellular “factories” become new extracellular inocula, primed for reinfection. 5/n www.biorxiv.org/content/10.6...

Enterococcus faecalis persists and replicates intracellularly within neutrophils | Infection and Immunity Chronic wound infection represents a major global public health concern, impacting both healthcare costs and patient quality of life (1, 2). Enterococcus faecalis is a Gram-positive opportunistic pathogen associated with infections in a range of contexts, including urinary tract infection, endocarditis, neonatal sepsis, and chronic wound infection (3–7). A facultative anaerobic bacterium and commensal of the human gastrointestinal tract, E. faecalis exhibits both intrinsic and acquired antibiotic resistance (8), making these infections inherently and increasingly difficult to treat. Long considered an extracellular pathogen, E. faecalis aggregates and forms biofilms, enhancing its persistence capacity in chronic infections (9). However, increasing evidence across a range of host cell types points to an intracellular niche and lifestyle of this multifaceted persistent bacterium (10–13).

Now, @claudiajades.bsky.social shows that E. faecalis replicates robustly in primary mouse AND human neutrophils - cells we typically think of as executioners, not incubators. 4/n #IAI @asm.org journals.asm.org/doi/10.1128/...

The unforeseen intracellular lifestyle of Enterococcus faecalis in hepatocytes Enterococcus faecalis is a bacterial species present at a subdominant level in the human gut microbiota. This commensal turns into an opportunistic pathogen under specific conditions involving dysb...

In parallel, the team of Pascale Serror and Cristel Archambaud showed E. faecalis can also survive/divide in hepatocytes, forming intracellular clusters (and supporting the “intracellular niche” concept beyond classic phagocytes). 3/n www.tandfonline.com/doi/10.1080/...

Enterococcus faecalis alters endo-lysosomal trafficking to replicate and persist within mammalian cells Author summary Enterococcus faecalis is often isolated from chronic wounds. Prior to this study, E. faecalis has been observed within different cell types, suggesting that it can successfully colonize...

First, work from @ronni.bsky.social in our group showed E. faecalis can replicate inside macrophages + epithelial cells, and that the intracellularly “trained” population is primed for more efficient reinfection. 2/n #PLOSPathogens @plos.org dx.plos.org/10.1371/jour...

Enterococcus faecalis: an overlooked cell invader | Microbiology and Molecular Biology Reviews SUMMARYEnterococcus faecalis and Enterococcus faecium are human pathobionts that exhibit a dual lifestyle as commensal and pathogenic bacteria. The pathogenic lifestyle is associated with specific conditions involving host susceptibility and intestinal ...

🧵Enterococcus faecalis is not just an extracellular organism. 🧵 A growing body of work shows it can survive + REPLICATE inside host cells, and that intracellular life may seed persistence, dissemination, and reinfection. 1/n #MMBR @asm.org journals.asm.org/doi/10.1128/...

🤩 Long ago in 2021, Irina Afonina saw E. faecalis prophage tail fibers co-purify with membrane vesicles, but we didn't know their fxn: pmc.ncbi.nlm.nih.gov/articles/PMC.... In this new preprint, Mike Gilmore and colleagues show us what the tail fibers (aka efagins) actually do! Super cool work. 🤩

Proteoglycofili are glycosaminoglycan-containing fibrillar components released by neutrophils to neutralize bacteria Alternative to the formation of NETs, André et al. describe here that viable neutrophils may release a fibrillar component named proteoglycofili or PGF upon stimulation. PGF formation is associated wi...

Thrilled to share that neutrophils produce extra long fibrillar components named proteoglycofili or PGF. PGF are released by living neutrophils and do not contain DNA. They might look like NETs but are not NETs…

www.cell.com/cell-reports...

Diagram illustrating "feed the enemy's enemy": ampicillin inhibits Pseudomonas aeruginosa. Citrobacter freundii acidifies the environment, further inhibiting P. aeruginosa.

New preprint from our lab www.biorxiv.org/content/10.1...! Andrea Dos Santos and Clément Vulin combine experiments and models showing how adding glucose can strengthen negative interactions between microbial species. This can be used in tandem with antibiotic treatment to inhibit pathogens!

Excited to share our first look at Enterococcus faecium infection biology: diabetic wounds are complex, and E. faecium persists despite early immune responses. In diabetic mice, it shows impaired clearance + sustained neutrophil recruitment, worsening healing.

Metabolic cross-talk promotes persistence of Enterococcus in a model of polymicrobial catheter-associated urinary tract infection https://www.biorxiv.org/content/10.1101/2025.11.19.689321v1

Beyond Antibiotics: Emerging Strategies for Combating Bacterial Infection | Keystone Symposia Join us at the Keystone Symposia on Beyond Antibiotics: Emerging Strategies for Combating Bacterial Infection, May 2026, in Breckenridge, with field leaders!

Registration is now open for @keystonesymposia.bsky.social "Beyond #Antibiotics: Emerging Strategies Combating #BacterialInfection." Deadline for scholarships and abstract selected short talks is Jan 7! Join us this May for an amazing meeting! keysym.us/KSBeyondAntibiotics26 #KSBeyondAntibiotics26

Enterococcus being one step ahead when it comes to stress… once again! Loved figuring this one out🤓

bsky.app/profile/kimi...

The consequence: A rapid, phenotype-first membrane “hardening” unintentionally primes the cell for the mutations that lock in high-level resistance.

Sometimes evolution doesn’t wait. E. faeecalis rehearses the phenotypic resistance program before writing it into the genome. 😎

The driver? LTA synthase, which boosts glycolipids when the cell senses membrane damage.
The sensor network? LiaFSR + SapRS + BsrRS, working together to flip the switch on this lipid remodeling program.

New work from @colomer-winter.bsky.social shows that E. faecalis doesn’t wait for mutations at all - it immediately rewires its membrane lipids as a stress response to daptomycin. And surprisingly, the cell ends up looking a lot like a resistant strain before any genetic change happens.

Why does daptomycin resistance appear so fast in Enterococcus? We finally have a clue.

DAP resistance in enterococci pops up quickly. What’s been missing is why resistance-associated membrane changes look the way they do, and why the classic path of mutations is so predictable.

A conserved sRNA regulates mucin adhesion and gut colonization across the Enterococcaceae https://www.biorxiv.org/content/10.1101/2025.11.10.687296v1