In this study, eight hyper-virulent strains of K. pneumoniae were reported positive for carbapenems resistant genes (OXA-48 and NDM). The presence of these strains in the clinical setting will complicate clinical practice and will cause fatal nosocomial infections . Although antimicrobial-resistant hvKP strains are rarely reported worldwide [18–20], but here in Sudan they appear to be more prevalent.
Eight neonatal blood isolates were multidrug-resistant, and three of them were extensively resistant to all antibiotics that were used. Consequently the emergence of MDR pathogens would increase the mortality and morbidity and prolong hospitalization and cost of treatment .
All neonatal blood isolates (15) were resistant to ceftazidime. Ceftazidime-resistant Klebsiella pneumoniae (CRKP) in the pediatric oncology units of some Sudanese hospitals may be the cause of recent reports of high mortality rate associated with K. pneumoniae infections among this group in different Sudanese hospitals . According to Schiappa , high resistance rates to ceftazidime could be due to the presence of a predominant enzyme (TEM-10) responsible for ceftazidime resistance in bloodstream isolates.
The isolates showed varying degrees of resistance to the other antibiotics; ciprofloxacin 30%, gentamicin 40%, and ceftazidime (70%). Resistance to these antibiotics may also be due to the presence of Extended-Spectrum Beta-lactamases (ESBLs) and other mechanisms like efflux pumps and porin mutations , which were not covered in this study.
Although chloramphenicol is used as a treatment of choice for MDR gram-negative bacilli bacteria , 38% of our isolates were resistant to it, which may be caused by transferable enzymatic resistance to aminoglycosides, thatis common in some hospitals .
In the current study, 94% (51/54) of the isolates harboring carbapenem-resistant genes were phenotypically susceptible to imipenem. This confirms what Walsh  said that this gene is not stable and relies upon other synergistic mechanisms to mediate resistance against carbapenems. In addition to imipenem, other antibiotics were analyzed in this study.
Of 48 K. pneumoniae isolates detected of having carbapenem-resistant genes, 10 had multiple genes co-occurring. This finding agrees with Ali & Omer  and Satir , which showed a multiplicity of genes in their isolates.
A total of 80% (4/5) of KPC and 100% (2/2) of IMP genes were positive among infant blood samples, and this may be due to organisms harboring these genes have a high ability to cause systemic infections, particularly in immunocompromised patients .
In this study, we found the essential gene for K. pneumoniae siderophores system entB gene is positive in 93.3% of all K. pneumoniae isolates, the rest (6.7%) of isolates that do not possess entB may contain other enterobactin (entA, C, D, E or F), or other siderophores systems like yersiniabactin or aerobactin as reported by Lawlor . Furthermore, mrkD gene is presented in 78.3% of the isolate. This gene has been found to be important in adhesion as reported by Chen et al. (2012). The rmpA gene was detected in 5% of isolates, in contrast with Aljanaby and Alhasani  who found the rmpA gene present in 62.5% of K. pneumoniae isolates. This difference may be attributed to its mode of inheritance as plasmid-mediated as mentioned by  indicating the limited spread of this gene in our local strains in Sudan.
The capsular serotype gene K2 was present in 51.7% of isolates; the rest of isolates may contain other capsular serotypes, as mentioned by Ho . This study showed that K2 is present in 80% of hypermucoviscous strains, indicating that there is a relationship between the presence of K2 gene and hypermucoviscous strains of K. pneumoniae, which is in agreement with the study by Guo  which found that K2 is the most common capsular serotype in hypermucoviscous strain. In contrast to other studies [21, 33] [34, 35], which found K1 was the most prevalent capsular serotype among hypermucoviscous K. pneumoniae.
The kfu gene (which codes for an iron uptake system) was present in 60% of isolates. The study showed no association between the presence of kfu gene and hypermucoviscosity. This finding disagrees with previous studies [21, 36, 37], which showed that kfu gene is associated with hypermucoviscosity phenotype; which may be attributed to diversity in geographical locations of studies.
The magA gene was found in 13.3% of isolates. The study showed no association between the presence of magA gene and hypermucoviscous strains. Although this gene is highly essential for K. pneumoniae, which confirms bacterial mucoviscosity, its prevalence among local isolates is not high, suggesting that other genes play a role in the formation of mucoviscosity .