Why is klebsiella pneumoniae good




















If a doctor notices that a bacterial infection persists after the initial treatment, they may order tests to identify the specific bacteria responsible. The results help them choose the most appropriate antibiotic treatment. Anyone who suspects that they have a urinary tract infection, pneumonia, meningitis, or cellulitis — all of which can result from K. Doctors treat K. When an infection is hospital-associated, doctors use a class of antibiotics called carbapenems until results of sensitivity testing are available.

If a doctor suspects that the bacteria have developed antibiotic resistance, they can order tests to determine how sensitive the bacteria are to specific antibiotics, before selecting the most effective option. It may be challenging for doctors to treat K.

Most recently, for example, some K. A doctor may prescribe a combination of antibiotics. One study observed lower mortality rates in people with bacteremia from K. When a person develops pneumonia from K. Doctors usually diagnose Klebsiella infections by examining either a sample of infected tissue or a sample of:. Once the doctor confirms the diagnosis, they may run sensitivity tests to determine which antibiotic will most effectively treat the infection.

Anyone who suspects that they have a K. If any infection persists after home care or an initial course of antibiotics, it is important to seek medical attention. The doctor may ask for additional testing to check the susceptibility of the bacteria to antibiotics. A person must come into contact with the bacteria, which do not spread through the air. In hospitals, K.

People may also come into contact with the bacteria through environmental exposure, though this occurs less often. Healthy family members of people with K. Some Klebsiella bacteria have become highly resistant to antibiotics. When bacteria such as Klebsiella pneumoniae produce an enzyme known as a carbapenemase referred to as KPC-producing organisms , then the class of antibiotics called carbapenems will not work to kill the bacteria and treat the infection.

Klebsiella species are examples of Enterobacterales, a normal part of the human gut bacteria, that can become carbapenem-resistant. CRE, which stands for carbapenem-resistant Enterobacterales, are an order of germs that are difficult to treat because they have high levels of resistance to antibiotics. Unfortunately, carbapenem antibiotics often are the last line of defense against Gram-negative infections that are resistant to other antibiotics.

Klebsiella infections that are not drug-resistant can be treated with antibiotics. Infections caused by KPC-producing bacteria can be difficult to treat because fewer antibiotics are effective against them. In such cases, a microbiology laboratory must run tests to determine which antibiotics will treat the infection.

They must follow the treatment regimen prescribed by the healthcare provider. If the healthcare provider prescribes an antibiotic, patients must take it exactly as the healthcare provider instructs. Patients must complete the prescribed course of medication, even if symptoms are gone.

If treatment stops too soon, some bacteria may survive and the patient may become re-infected. Colistin recorded the lowest resistance rate of 2. The individual studies as seen in Table 3 , details the number of isolates which were resistant to these antimicrobials. From Table 4 , it can be seen that K. In this review, the selected resistant-mediated genes were in the decreasing order of CTX-M-1 The genes, Mag, Armp, ArmpA2, allS hypermucoviscous phenotype and mucoviscosity-related genes ; wabG, uge, wcaG biosynthesis of lipopolysaccharide genes ; iutA, icuA, iroN, iroB, ybtA, irp2, kfu, entB iron uptake and transport genes and Cf29a, fimH, mrkD Adhesion genes are all some virulent factors that are used by K.

Trends of resistance and isolation rate of K. Klebsiella pneumoniae can be broadly classified into two subtypes; classical Klebsiella pneumoniae cKp and non-classical Klebsiella pneumoniae ncKp. The antimicrobial resistance profiles and the virulence profiles of these strains vary with the former tagged as notorious [ 3 , 5 ].

Notwithstanding, several clones of these ncKp have also been implicated in causing severe and difficult to threat infections due to their continuous mutation and the acquisition of plasmids and transposons which carries resistant and virulent genes.

This has led to the emergences of strains such as hypervirulent Klebsiella pneumoniae hvKp or hypermucoviscous Klebsiella pneumoniae HMKP.

This strain was first identified in Eastern part of Asia and has since spread worldwide [ 6 ]. This subtype is non-resistant to most of the commonly used antimicrobials such as colistin and carbapenems. But the recent reports of carbapenem-resistant hvKp strains which belong to the sequence types 11 ST11 [ 7 ], ST25 and ST65 [ 8 ] poses a major clinical concern. HvKp strains can cause serious infections in both immunocompetent, diseased and healthy young individuals [ 9 ].

This hvKp is known to habour i sidephore; predominant of which is aerobactin which is concomitant with hypermucoviscosity, ii virulent factors such as; K1, K2, K20 capsular types, rmpA and rmpA2 mucoid-regulator genes [ 10 ]. The horizontal transfer of these plasmids and transposons has led to the multidrug resistance MDR and the extremely drug resistance XDR nature of most of these subtypes.

Klebsiella is a major source of carbapenem resistance worldwide by the dissemination of its plasmids which is facilitated by high genetic transfer HGT to other species. Once the bla KPC-2 gene is introduces into a certain location, especially in a hospital setup, under antibiotic selection pressure, further dissemination of this gene may occur which may lead to MDR and XDR strains.

Hypermucoviscous K. Liu et al. It is believed that several factors can cause the colonization of K. The cases of K. In a study by Ling et al. This is an indication that infections caused by K. Some epidemiological risk factors associated with K. In Asia, it has been reported that exposure to health care facility and history of previous overseas hospitalization OR: The higher rates of colonization are primarily related to the increasing use of antibiotics [ 3 , 17 , 18 ].

The increase in colonization rate of K. In a study in Taiwan, antibiotic use e. In a study by Saleem et al. The above listed factors can in combination or singly predispose individuals to K.

Klebsiella pneumoniae is rapidly becoming known for its resistance properties to most of the last-line antibiotics that are usually used. It is especially problematic in hospitals, where it causes a range of acute infections. The increasing trends in the isolation rate of K.

Economically developed areas such as China have a more advanced medical system which may increase the chance of exposure to antibiotics and this will increase the possibility of bacterial resistance.

In China, the higher population density may also have increased the isolation rate among the population. In this review, although there is an increasing trend in the isolation rate, their resistance rates were not in tandem as this was evident in the decreasing trends over the years. Although, imipenem and meropenem have shown good activity against Enterobacteriaceae [ 22 ], the situation observed in this review reiterates the public health implications of K.

In Fig. Generally, the decreasing resistant rate of K. The global emergence and spread of genes of antimicrobial resistance such as ESBL and carbapenemase genes in K. This is because carbapenems have long been deemed as the last therapeutic resort or option of antibiotics used to treat diseases and infections caused by multidrug-resistant gram-negative bacteria. The rapid global emergence of K.

The extensive use and misuse of carbapenems is one of the attributable reasons that has led to the evolution of plasmid-mediated carbapenemases, i. Different resistance-mediated genes mediate antimicrobial drug resistance in K. The high rate of resistance to carbapenems imipenem and meropenem observed in this study can be partly be attributed to the presence of some carbapenemase resistant-mediated genes such as bla OXA.

The detection of carbapenemases is important from an epidemiological perspective as they are plasmid-mediated and may be transferred horizontally between different bacterial species [ 24 ].

Dissemination of resistant determinants have been recognized as a major challenge in the treatment of bacterial infections worldwide [ 25 ]. Also, resistance of K.

This can therefore be used to identify KPC-mediated genes that are resistant to these cephalosporins e. Klebsiella pneumoniae resistance to Aminoglycosides amikacin and gentamicin as seen in this review may be as a result of modifications in cell permeability due to alterations in AcrAB-TolC and KpnEF efflux pump systems and due to loss of putative porin, KpnO. The 16S rRNA methylases which are encoded on the plasmids [ 27 ] confers resistance to all aminoglycosides.

Mutations which confer resistance via target modification can also be a possible attributable reason for the increasing resistance of K. The low prevalence of Polymyxin Colistin resistance in this review makes a lot of sense because of their restricted use in human medicine dating back between the s and s, due to their recognized toxicity.

Undoubtedly, the presence of resistance determinants will allow K. According to a report by Dong et al. Hypermucoviscous phenotype and mucoviscosity-related genes, genes for biosynthesis of lipopolysaccharide, iron uptake and transport genes and Adhesive genes are all virulent factors that are employed by K.

Iron is a key component for K. As free iron is scarce in host plasma, K. Pneumoniae acquires iron predominantly through the secretion of siderophores; molecules with a greater iron affinity than the host transport proteins [ 30 ]. Among the siderophores secreted by K. The rmpA and rmpA2 are Plasmid-carried genes, which contribute to the enhancement of capsular production. Also, the MagA gene is an important gene used by K. This gene can be used as a molecular marker for quick diagnosis and can also be useful in tracing the roots of emerging infectious diseases caused by K.

The linear map of plasmid p in comparison with the most similar plasmids from GenBank is shown in Figure 3. A total of open reading frames were predicted. Multiple toxin-antitoxin TA -based addiction systems i. A complete tra region which encodes for the transfer component was also identified in p Figure 3. Comparison of the p K.

Both E. In total, of the isolates Of the five non-biofilm producers, three were from broilers and two were from turkeys. The average OD for all isolates was OD 0. The average OD value for broiler and turkey isolates were OD of 0. Figure 4. The biofilm forming abilities of K. This is the first study characterizing K.

A low occurrence of antimicrobial resistance was detected, but interestingly, a hypervirulent clone with a novel ST was detected from turkeys, suggesting a clonal expansion of this lineage in the turkey production in Norway. The samples investigated in this study originated from NORM-VET, and the sampling in the monitoring program is performed to ensure representativeness of the national animal populations.

We investigated more than pooled samples and sampling was conducted throughout the whole year. The higher occurrence of K. This makes turkey an interesting candidate for further study regarding zoonotic transmission. There are many potential factors to why there is a distinct difference in detection rates between the two poultry species.

Diet, environment, genetics and the use of antimicrobial agents all influence gut microbiota and could therefore influence the presence of K. Broiler and turkey reared in large-scale food production have similar living conditions and diet.

A possible explanation for the difference in occurrence may be preventive treatment with the ionophores narasin and monensin. In Norway, broilers were previously given narasin and turkey flocks are given monensin as a preventive measure to reduce intestinal parasites Eimeria spp.

Currently, turkey flocks are still given monensin, while narasin has been phased out since in Norwegian broiler production. Ionophores may affect the gut microbiota, as both narasin and monensin have been found to have an antimicrobial effect on gram-positive bacteria Chan et al. A reduction of the gram-positive fraction of the gut microbiota may result in higher abundance of Gram-negative bacteria, such as K.

Since turkey flocks are still treated with monensin, such preventative treatment may be an explanatory factor for the observed occurrence of K. However, further studies are needed to deduce the effects of such treatment on the gut microbiota. Similarly, antimicrobial treatment may also affect the gut microbiota and change the competition dynamics in the gut for K. In Norway, the use of antibiotics in livestock is low, strictly controlled, and monitored European Medicines Agency, European Surveillance of Veterinary Antimicrobial Consumption, In other countries, however, it is used more liberally, not just to combat infections but also as a growth enhancer Ryan, ; European Medicines Agency, European Surveillance of Veterinary Antimicrobial Consumption, Animals have different microbiomes in their gastrointestinal-tract and excessive use of antibiotics could affect the prevalence of K.

The gut microbiome of broiler and turkey is dominated by Firmicutes and Bacteroidetes , followed by Proteobacteria, and Actinobacteria Oakley et al. Although these bacteria belong to the same phylum, a closer look at which species are present and their relative abundance, might give insight into whether they contribute to the variation of K.

The occurrence of antimicrobial resistance among obtained isolates in this study was low and this reflects the low antimicrobial usage pattern in Norwegian livestock production European Medicines Agency, European Surveillance of Veterinary Antimicrobial Consumption, The finding of low resistance rates is therefore not surprising.

The phylogenetic tree based on poultry genomes comprised several deep-branching lineages, which is typical for K. These isolates comprise a set of diverse K.

A recently published study from Norway screened 2, healthy persons for K. In the current study, ST35 represented a major ST identified in both poultry species. Compared to human carriage, the occurrence of ST35 in Norwegian poultry seem to be higher. Due to the detection of K. No virulence genes coincided with resistance genes in this dataset, which is typical for K. Virulence genes were detected in a relatively high fraction of the genomes, In the Norwegian study on healthy humans as carriers of K.

There could be several reasons for the lower rate in humans, but in the human study other phylogroups in addition to K. In contrast, the population in the present study comprised only K.

Our findings indicate that poultry may be a reservoir for hypervirulent K. The identified ST clone from turkeys is of particular concern, as all the ST genomes harbored genes that indicate a hypervirulent phenotype, located on a potentially conjugative IncF plasmid Huynh et al. These virulence operons, notably aerobactin and salmochelin, are highly important virulence determinants.

Plasmids with iuc5 and iro5 have previously been identified in E. However, this needs to be verified with conjugation experiments. The clonal spread of ST indicates a common source. Introduction via breeding animals is believed to be the reason for the occurrence of E. The latter results are only based on samples from broilers, therefore further studies are needed to look for the same pattern in the turkey production.

In the current study, almost all tested K. These findings correlate with the previous results from K. Additionally, a statistically significant difference in OD between broilers and turkeys was detected.

However, the difference in mean OD between the two animal species was small and therefore probably not of biological significance. The good biofilm formation displayed at this temperature indicates that K. While the isolates in the current study presented good biofilm forming abilities at room temperature, it is unknown if the same level of production efficiency will be observed at body temperature of poultry. Overall, a higher occurrence of K.

Our data indicate a low occurrence of antimicrobial resistance in K. However, the presence of a hypervirulent K. In addition, identification of STs found in both animals and in humans may indicate transmission between the reservoirs, but, further studies are required to evaluate the zoonotic potential of these STs. Taken together, the results from this study provides further understanding and knowledge about K. The p plasmid is available in GenBank under the accession number MW The data used in this study can be found in Supplementary Data Sheet 1.

MS conceptualized the study. LN oversaw the biofilm work. All authors contributed to writing and editing the manuscript. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

DNA extraction, purification, library preparation and sequencing was performed at Stavanger University Hospital. Eva Bernhoff is acknowledged for planning and organizing whole genome sequencing at Stavanger University Hospital.



0コメント

  • 1000 / 1000