{"id":9596,"date":"2026-05-21T11:19:00","date_gmt":"2026-05-21T09:19:00","guid":{"rendered":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/?p=9596"},"modified":"2026-08-04T11:29:05","modified_gmt":"2026-08-04T09:29:05","slug":"the-golden-staph-paradox","status":"publish","type":"post","link":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/the-golden-staph-paradox\/","title":{"rendered":"The golden staph paradox: Does a \u201csticky\u201d bacterium reduce the risk of death?"},"content":{"rendered":"\n

Staphylococcus aureus<\/em>, or golden staph, is one of the leading causes of severe bloodstream infections. Although the bacterium \u2013\u00a0well known to clinicians\u00a0\u2013\u00a0is associated with high virulence and antibiotic resistance, the course of infection can vary widely between patients. In some cases, the infection is quickly brought under control; in others, it leads to sepsis, organ failure, and even death. What explains these differences?<\/p>\n\n\n\n

A new study suggests that it is the balance between the bacterial factors of an invading isolate and patient\u2019s response.  Key bacterial factors involved may be those that bind to human fibrinogen (an important blood-clotting protein) and the \u03b1-toxin that weakens the immune system.<\/p>\n\n\n\n

\u201cStaphylococcus aureus<\/em> is highly adapted to living in the human body. People are likely to already have antibodies against this bacterium, but it can also produce toxins that suppress immune function,\u201d says Prof. Marta Zapotoczna, the project leader.<\/p>\n\n\n\n

Looking beyond resistance genes<\/strong><\/h3>\n\n\n\n

The team led by Prof. Marta Zapotoczna from the Infection Biology Laboratory at the University of Warsaw Biological and Chemical Research Centre, analyzed a cohort of S. aureus<\/em> isolates obtained from patients with bloodstream infections.<\/p>\n\n\n\n

A novel aspect of the study was integration of bacterial DNA analysis \u2013 including genome-wide association studies (GWAS), used to identify genetic variants \u2013 with measurements of bacterial traits and data on patients\u2019 complications and clinical outcomes.<\/p>\n\n\n\n

Previous research on Staphylococcus aureus<\/em> has focused mainly on comparing the genomes of different strains. Much less attention has been paid to how traits such as adhesion \u2013 the ability to attach to human tissues \u2013 or the production of immune-weakening toxins influence disease progression and the genetic variability of isolates.<\/p>\n\n\n\n

This time, the scientists linked bacterial genetic data with biological characteristics and patient outcomes. This approach allowed them to identify which specific bacterial traits are associated with a higher risk of severe disease.<\/p>\n\n\n\n

The study was based on data from patients treated in three Polish hospitals \u2013 in Warsaw, Krak\u00f3w, and Katowice. Participants had to provide consent for both the use of their clinical data and the bacterial isolates cultured from their blood. These samples were later used for laboratory experiments and genome sequencing.<\/p>\n\n\n\n

The project was conducted during the COVID-19 pandemic, which further complicated patient recruitment and coordination between clinical and laboratory teams.<\/p>\n\n\n\n

\u201cThis is the first in a series of studies combining clinical patient data, bacterial traits, and genotypes. We can already see that this approach reveals relationships that classical laboratory models fail to capture,\u201d says Prof. Marta Zapotoczna.<\/p>\n\n\n\n

Staphylococcus aureus<\/em> can bind to important proteins in the human body \u2013 fibrinogen and fibronectin. This helps it persist in tissues and more effectively establish infection.<\/p>\n\n\n\n

The scientists tested how strongly different bacterial strains bind to these proteins and then compared the results with bacterial DNA sequences and clinical data on disease progression in patients.<\/p>\n\n\n\n

The \u201cstickiness\u201d paradox: When bacterial adhesion works in the patient\u2019s favor<\/strong><\/h3>\n\n\n\n

The results came as a surprise. Staphylococcus aureus<\/em> strains that bound more strongly to fibrinogen were more likely to trigger a rapid immune response. This was reflected, among other things, in levels of C-reactive protein (CRP), which increases during inflammation.<\/p>\n\n\n\n

At the same time, these bacteria \u2013 especially when they did not produce the active immune-suppressing \u03b1-toxin \u2013 were associated with a lower risk of patient death.<\/p>\n\n\n\n

This suggests that under certain conditions, more \u201cadhesive\u201d bacteria may be more easily recognized by the immune system, which helps the body contain the infection more quickly.<\/p>\n\n\n\n

Previous studies, mainly conducted in animals or under laboratory conditions, suggested that the \u201cstickiness\u201d of Staphylococcus aureus<\/em> \u2013 its ability to adhere to tissues \u2013 primarily benefits the pathogen. However, the latest findings indicate that in humans this mechanism may be far more complex.<\/p>\n\n\n\n

One hypothesis currently under investigation is that some individuals may have antibodies targeting the proteins responsible for this \u201cstickiness.\u201d This would mean that, at the population level, we may have partially developed immune protection against this bacterial trait.<\/p>\n\n\n\n

An evolutionary game<\/strong><\/h3>\n\n\n\n

Staphylococcus aureus<\/em> strains that strongly adhere to human tissues but produce fewer toxins were more likely to trigger a robust immune response. While inflammation itself is not beneficial, in this case it may help the body detect the infection more quickly and keep it under better control.<\/p>\n\n\n\n

In contrast, bacteria that adhere less strongly to tissues but produce \u03b1-toxin may be more effective at \u201chiding\u201d from the immune system and are more often associated with severe disease outcomes.<\/p>\n\n\n\n

From an evolutionary perspective, the goal of bacteria is not to kill the host, but to survive and continue replicating within it. The problem is that both the progression of the infection itself \u2013 the bacterial growth \u2013 and the immune response can cause serious damage to the body, and sometimes even lead to patient death.<\/p>\n\n\n\n

The findings suggest that no single \u201cdangerous gene\u201d or isolated factor determines the course of infection. Instead, what matters is the complex interplay between multiple bacterial mechanisms and the human immune system.<\/p>\n\n\n\n

\u201cOur study shows a clear link between bacterial traits and mortality in infected patients. If we learn to quickly identify how a given strain behaves, in the future we may be able to tailor targeted therapies to the mechanism of infection,\u201d says Prof. Marta Zapotoczna.<\/p>\n\n\n\n

Genetic signatures of infection<\/strong><\/h3>\n\n\n\n

It is estimated that around 20% of people are persistently colonized by Staphylococcus aureus<\/em>, while in the rest of the population the bacterium may appear only temporarily or not at all.<\/p>\n\n\n\n

Staphylococci are part of our microbial environment. However, individual strains differ significantly at the genetic level. Some carry genes that promote toxin production, while others are more strongly equipped with mechanisms that enable adhesion to host cells.<\/p>\n\n\n\n

\u201cThis means that people may be colonized by distinct variants of Staphylococcus aureus<\/em>,<\/strong> with varying disease-causing potential and different strategies of interacting with the human body,\u201d says the scientist. <\/strong><\/p>\n\n\n\n

Genomic analyses conducted in the study allowed the researchers to identify genetic traits responsible for bacterial \u201cstickiness\u201d \u2013 genes that may, in the future, serve as biomarkers.<\/p>\n\n\n\n

\"\"
Staphylococcus aureus<\/em>, the bacterium known as golden staph.<\/figcaption><\/figure>\n\n\n\n

A step toward patient-specific diagnosis of infection<\/strong><\/h3>\n\n\n\n

The findings may be important not only for a better understanding of the bacterium\u2019s biology, but also for the future diagnosis and treatment of infections.<\/p>\n\n\n\n

The scientists suggest that analyzing how strongly Staphylococcus aureus<\/em> adheres to tissues and which toxins it produces could help improve assessments of a patient\u2019s risk of severe disease.<\/p>\n\n\n\n

The University of Warsaw team now plans to expand the study to around 500 patients and to investigate the antibodies present in individuals infected with Staphylococcus aureus<\/em>.<\/p>\n\n\n\n

At the same time, the scientists suspect that strains producing \u03b1-toxin may be particularly dangerous, as this toxin helps the bacterium weaken the immune response and evade detection. This may explain why some infections take a severe course even when the bacterium is not especially resistant to antibiotics.<\/p>\n\n\n\n

\u201cOur work shows that to understand the pathogenic potential of bacteria, we need to study not only antibiotic resistance, but also the mechanisms through which pathogens interact with the host. Focusing on these mechanisms can bring us closer to better predicting and controlling the risk of infection and its most severe outcomes, and complement classical approaches based on resistance genes,\u201d adds Prof. Marta Zapotoczna.<\/p>\n\n\n\n

\u201cThe better we understand how bacteria manipulate the host immune response and which mechanisms determine the course of infection, the more effectively we will be able to combat disease. It is not always antibiotic resistance that drives the most severe cases,\u201d the researcher emphasizes.<\/p>\n\n\n\n

Read more in Nature Communications<\/a>.<\/p>\n\n\n\n

The text was originally published in Polish on the Serwis Naukowy UW website on May 21, 2026.<\/em><\/p>\n\n\n\n

<\/p>\n","protected":false},"excerpt":{"rendered":"

Why do some patients recover relatively easily from staph infections, while others die despite treatment? Scientists at the University of Warsaw suggest that the answer may lie in the bacterium\u2019s reservoir of virulence factors incl. the ability to \u201cstick\u201d to human tissues and manipulate the immune system.<\/p>\n","protected":false},"author":10,"featured_media":9597,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[199],"tags":[1821,1824,1826,1822,1823,1827,1825,1621],"class_list":["post-9596","post","type-post","status-publish","format-standard","has-post-thumbnail","category-biology","tag-adhesion","tag-antibiotic-resistance","tag-course-of-infection","tag-genome-wide-association-studies","tag-gwas","tag-infection-biology-laboratory","tag-staphylococcus-aureus-golden-staph","tag-university-of-warsaw-biological-and-chemical-research-centre"],"acf":[],"_links":{"self":[{"href":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/wp-json\/wp\/v2\/posts\/9596","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/wp-json\/wp\/v2\/users\/10"}],"replies":[{"embeddable":true,"href":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/wp-json\/wp\/v2\/comments?post=9596"}],"version-history":[{"count":1,"href":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/wp-json\/wp\/v2\/posts\/9596\/revisions"}],"predecessor-version":[{"id":9600,"href":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/wp-json\/wp\/v2\/posts\/9596\/revisions\/9600"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/wp-json\/wp\/v2\/media\/9597"}],"wp:attachment":[{"href":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/wp-json\/wp\/v2\/media?parent=9596"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/wp-json\/wp\/v2\/categories?post=9596"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/serwisnaukowy.uw.edu.pl\/en\/wp-json\/wp\/v2\/tags?post=9596"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}