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Immunity mutation discovered in zoonotic bacteria
The study investigated the response of Staphylococcus aureus to macrophages.
The mutation helps the bacteria survive immune responses and antibiotics.

New research has discovered a genetic mutation, which is helping zoonotic bacteria to develop a resistance to immune system defences and antibiotics.

Researchers from the Roslin Institute studied the response of Staphylococcus aureus, a major pathogen affecting both humans and animals, to immune cells known as macrophages.

The study aimed to discover how the bacteria was avoiding being killed by macrophages, and how it was adapting to immune responses.

Macrophages represent a significant component in the immune system response to S.aureus, and play a major part in disease outcomes. The researchers passaged strains of S.aureus along a macrophage cell line, where it collected mutations.

Exposure to the macrophages saw the bacteria undergo changes to its characteristics over time. Mutations meant that the bacteria developed many of its survival traits, including an ability to grow within immune cells and resist antibiotics.

However these advantages proved to be conditional, with the bacteria losing these mutations when grown in nutrient-rich conditions away from macrophages.

Further research revealed that the phenotype which was contributing to bacterial survival was a new type of small colony variant (SCV). These variants frequently contribute to more persistent, but less virulent, form of the pathogen.

These SCVs are often linked to chronic infections such as osteomyelitis and lung infections in cystic fibrosis patients. The adaptation has also led to the bacteria becoming more resistant to antibiotics, such as vancomycin.

The new model suggests that repeatedly exposing bacteria to macrophages could reveal the conditional way that bacteria adapts to specific niches.

It may also lead to a better understanding of how bacteria can evade the immune system, meaning scientists can consider potential treatment strategies for both humans and animals.

Dr Joana Alves, a research fellow at the Roslin Institute, said: “Our study uncovers a novel adaptation strategy by S. aureus in response to immune challenges, highlighting the remarkable ingenuity of pathogens in evading host defences.

“Our findings demonstrate the power of experimental models to unravel the complex mechanisms underlying bacterial adaptation during infection”

The full study can be found in the journal mBio.

Image © Shutterstock

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Equine Disease Surveillance report released for Q4 2025

News Story 1
 The latest Equine Disease Surveillance report has been released, with details on equine disease from Q4 of 2025.

The report, produced by Equine Infectious Disease Surveillance, includes advice on rule changes for equine influenza vaccination.

Statistics and maps detail recent outbreaks of equine herpes virus, equine influenza, equine strangles and equine grass sickness. A series of laboratory reports provides data on virology, bacteriology, parasitology and toxicosis.

This issue also features a case study of orthoflavivus-associated neurological disease in a horse in the UK. 

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News Shorts
RCVS annual renewal fee for vets due

RCVS' annual renewal fee for veterinary surgeons is now due. Vets must pay their renewal fee before Wednesday, 1 April 2026.

This year's standard annual fee has increased to 431 from last year's 418. This is an approximately three per cent increase, as approved by RCVS Council and the Privy Council.

Tshidi Gardner, RCVS treasurer, said: "The small fee increase will be used to help deliver both our everyday activities and our new ambitious Strategic Plan, which includes aims such as achieving new legislation, reviewing the Codes of Professional Conduct and supporting guidance, and continuing to support the professions through activities such as the Mind Matters Initiative, RCVS Academy and career development."

A full breakdown of the new fees is on the RCVS website. Information about tax relief is available on the UK government website.