Investigation of virulence genes and carbapenem resistance genes in hypervirulent and classical klebsiella pneumoniae isolates isolated from various clinical specimens

Investigation of Virulence Genes and Carbapenem Resistance Genes in Hypervirulent and Classical Klebsiella pneumoniae Isolates Isolated from Various Clinical Specimens Klebsiella pneumoniae is a global pathogen that can cause hospital-acquired and community-acquired infections and is known for its resistance to antibiotics. The pathotype, which is defined as hypervirulent K. pneumoniae (hvKp) and is more lethal than classical K. pneumoniae (cKp) strains, causes many community-acquired infections such as liver abscess, endophthalmitis, pneumonia in healthy young adults. There are no clear clinical or microbiological criteria to define HvKp. The string test, which shows hypermucoviscosity, is performed by pulling the colonies grown on culture plates upwards with the help of a loop and measuring the elongation amount, and is the most commonly used microbiological test to define hvKp. In our study, 100 K. pneumoniae strains isolated from different clinical specimens were grouped as hvKp and cKp according to string test. The presence of 6 virulence genes (fimH-1, rmpA, magA, aerobactin, K1, K2) in all strains and 5 carbapenemase genes (OXA-48, KPC, IMP, VIM, NDM-1) in carbapenem resistant strains were investigated. Of the 100 K. pneumoniae strains 45% were defined as hvKp and 55% as cKp. The fimH-1 gene was found to be positive in 94% of the strains, the aerobactin gene in 37%, the magA and K1 gene in 34%, the rmpA gene in 5%, and the K2 gene in 3% of the strains. Aerobactin gene was positive in 68.9% of hvKp strains and 10.9% of cKp strains, and the presence of aerobactin gene in hvKp strains was statistically significant compared to cKp strains (p<0.05). MagA gene and K1 serotype were found in 28.9% of hvKp strains and 38.2% of cKp strains. Although the magA gene ratio was high in CKp strains, this difference was not statistically significant. (p>0.05). FimH-1 gene was found positive in 93.3% of hvKp strains and 94.5% of cKp strains. The difference between the two groups could not be evaluated statistically because the numbers were high. The RmpA gene was positive in 8.9% of hvKp strains and 1.8% of cKp strains. The K2 gene was positive in 4.4% of hvKp strains and 1.8% of cKp strains. The difference in the hvKp and cKp groups for these genes could not be evaluated statistically because 15 the numbers were low. Although there was no statistical difference in antibiotic susceptibility between hvKp and cKp strains, ceftriaxone, cefuroxime, ceftazidime, amikacin, cefoxitin, ertapenem, cefuroxime axetil and imipenem were found to be more effective in hvKp strains. Ciprofloxacin and trimethoprim sulfamethoxazole were found to be more effective in hvKp strains than cKp strains, and the difference was statistically significant (p<0.05). Although gentamicin, amoxicillin and piperacillin-tazobactam were found to be more effective against cKp than hvKp, the dfifference was not statistically significant (p>0.05). Of the 35 carbapenem resistant strains 65,7% were found to be cKp and 34,3% hvKp. Although it was not statistically significant, hvKp strains were found to be more sensitive to carbapenems. The most common gene in carbapenem resistant strains was OXA-48. While the KPC gene was detected in five strains, IMP, VIM and NDM-1 were not detected on any of the tested strains. Of the 29 OXA-48 positive samples 69% were found to belong to cKp strains and 31% to hvKp strains. It was determined that all of the KPC positive strains were hvKp strains. It was concluded that the string test and virulence factors alone cannot be sufficient to show hypervirulence, and that more than one virulence factor combination should be evaluated in the presence of clinical features of hypervirulent infections to show hypervirulence.