Detection of mrkD and fimH Biofilm Genes and Antibiotic Susceptibility of Uropathogenic Biofilm-Producing Klebsiella pneumoniae in Sana'a City, Yemen

In the human body, the urinary tract is a busy highway for bacteria, but for some, it becomes a fortress. One of the most common invaders is a bacterium called Klebsiella pneumoniae. While this germ can cause pneumonia and other serious infections, it is particularly notorious for causing urinary tract infections, especially in people who have catheters or weakened immune systems. The danger lies not just in the bacteria itself, but in how it survives. Instead of floating freely, these bacteria can stick together and to surfaces, wrapping themselves in a slimy, protective shield known as a biofilm. Think of this biofilm as a microscopic city wall that keeps antibiotics out and protects the bacteria from the body's immune defenses. Once this shield is built, infections become difficult to treat and often return repeatedly. Compounding this problem is the fact that many of these bacteria have evolved to resist the very drugs doctors use to kill them, creating a growing public health crisis where standard treatments no longer work.

Researchers in Sana'a City, Yemen, set out to understand this specific threat within their local hospitals. They collected urine samples from patients suffering from urinary tract infections and focused their attention on the Klebsiella pneumoniae bacteria found there. Their goal was threefold: to see how many of these bacteria could build the protective biofilm shield, to test how well current antibiotics could stop them, and to look for specific genetic instructions inside the bacteria that might explain why some build stronger shields than others. They were particularly interested in two known genetic markers, fimH and mrkD, which act like molecular tools helping the bacteria stick to surfaces and form these communities. By connecting the presence of these genes to the strength of the biofilm and the bacteria's resistance to drugs, the team hoped to map the landscape of this infection in their region.

The study began with 241 urine samples taken from patients showing clear signs of infection. After careful laboratory processing, the researchers confirmed that Klebsiella pneumoniae was the cause in 79 of those cases. When they tested these 79 bacterial strains to see if they could form biofilms, the results were striking. More than half, specifically 40 isolates, were capable of building these protective shields. Among the biofilm builders, the researchers found that none were weak; they were either moderate or strong builders. Nearly half of the biofilm producers created particularly robust shields, while the rest formed moderate ones. This confirmed that in this specific population, the ability to form a biofilm is a common and potent trait.

The situation became more concerning when the researchers tested these biofilm-forming bacteria against a wide range of antibiotics. The results showed a high level of resistance, meaning the drugs were often ineffective. Among the bacteria that built biofilms, almost half were classified as extensively drug-resistant, meaning they were immune to nearly all available treatments. Another third were multidrug-resistant, and a small number were even pan-drug-resistant, showing no susceptibility to any of the tested antibiotics. Only a tiny fraction, about 15 percent, remained fully susceptible to the drugs. This pattern suggests that the bacteria forming these biofilms are not only harder to wash away but are also the ones most likely to survive modern medical treatments.

To understand why some bacteria built such strong shields, the team looked inside the genetic code of the 40 biofilm-producing strains. They searched for the mrkD and fimH genes, which are known to help bacteria stick together. They found that every single one of the 40 biofilm-forming bacteria carried the mrkD gene. This gene appears to be a fundamental requirement for these bacteria to form biofilms in this region, as it was present in every case without exception. However, the story was different for the fimH gene. While this gene was also very common, appearing in 87.5 percent of the strains, its presence told a more specific story. The researchers found a clear statistical link between the fimH gene and the strength of the biofilm. Every single one of the strongest biofilm builders carried this gene, whereas a few of the moderate builders did not. This suggests that while mrkD is essential for the bacteria to start building a biofilm, the presence of fimH may be what pushes the structure to become a particularly strong and difficult-to-treat fortress.

The study concludes that in Sana'a City, the bacteria causing urinary tract infections are frequently building strong biofilms and are highly resistant to antibiotics. The research highlights that the mrkD gene is a universal feature of these biofilm formers, while the fimH gene is a strong indicator of the most aggressive, hard-to-treat strains. These findings do not prove that the genes cause the resistance directly, but they show a clear association that helps identify the most dangerous bacteria. The high frequency of drug-resistant strains underscores an urgent need for better infection control and more careful use of antibiotics in local hospitals. Furthermore, the strong link between the fimH gene and powerful biofilms suggests that looking for this specific gene could help doctors identify which infections are likely to be the most severe, potentially guiding better treatment choices in the future.