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УДК 576.8.095.38:576.893.1 ББК 56
BURKHOLDERIA CEPACIA AND BIOFIELD TREATMENT
HAFFARESSAS Y. Lobachevsky State University of Nizhny Novgorod
Abstract
Burkholderia cepacia complex (BCC), or simply Burkholderia cepacia, is a group of catalase-producing, lactose-nonfermenting, Gram-negative bacteria composed of at least 20 different species. B. cepacia is an opportunistic human pathogen that most often causes pneumonia in immunocompromised individuals with underlying lung disease (such as cystic fibrosis or chronic granulomatous disease). MDR infection has been increased suddenly, which leads to ineffective treatment and risk of spreading infections.
Keywords: Burkholderia cepacia; Multi drug Resistant; Antimicrobial Susceptibility; Biofield Treatment.
Although B. cepacia complex strains are frequently isolated from the natural environment, common environmental species are infrequently associated with human infection. Historically regarded as an organism of low pathogenicity, B. cepacia complex can be transmitted person to person in both healthcare and non-healthcare settings, and both direct and indirect contact with infectious secretions and droplet spread have been implicated in transmission [1, 2] B. cepacia complex can survive for long periods in water or disinfectants, and healthcare-associated outbreaks of B. cepacia complex infection have been linked to contaminated nebulized and intravenous medications and solutions, including compounded and commercially distributed products, skin care products, disinfectants, and to inadequate disinfection of reusable medical devices [3].
B. cepacia complex emerged in the late 1970s as a cystic fibrosis respiratory pathogen, associated with accelerated decline in pulmonary functions and reduced survival, especially among those with more advanced lung disease or who had undergone lung transplantation [4]. According to the U.S. Cystic Fibrosis Foundation's 2012 National Patient Registry, 2.6 percent of all persons with cystic fibrosis were infected with B. cepacia complex compared to 3.1% in 2005. The prevalence increases with age and varies widely between cystic fibrosis centers. In the United States, B. multivorans and B. cenocepacia account for ~70% of patient isolates, and the incidence of new infection with B. multivorans relative to B. cenocepacia has increased in recent years. In comparison, in Canada and some European countries, B. cenocepacia is the predominant species. Molecular typing and
epidemiologic investigations support person-to-person transmission of B. cepacia complex during hospitalization, while attending ambulatory clinics, and during social gatherings. Transmission is facilitated by prolonged close contact between cystic fibrosis patients, sharing of equipment and personal care items, and by bacterial virulence factors. Transmission of B. cepacia complex among cystic fibrosis patients has been reduced in recent years by stringent infection prevention and control efforts, supported by the finding that the majority of new B. cepacia complex infections involve acquisition of unique strains likely from independent environmental sources [5].
Pathogenesis. B. cepacia complex form biofilms in vitro and in vivo in the lungs of cystic fibrosis patients, potentially contributing to reduced antimicrobial susceptibility, treatment failure and persistent infection [6]. Compared to MICs for planktonic B. cepacia complex isolates, biofilm inhibitory concentrations are substantially higher for most P-lactam agents. Other putative virulence factors, include regulated gene expression by quorum sensing, exopolysaccharide production associated with the mucoid phenotype that promotes evasion of the host response and persistence, and lipopolysaccharide that contributes to immunemediated tissue damage. There is an inverse correlation between the quantity of mucoid exopolysaccharide production by B. cepacia strains and rate of decline in cystic fibrosis lung function, likely related to increased surface expression of virulence factors in non-mucoid strains [7]. Epidemic transmission of B. cenocepacia strains among both cystic fibrosis and non-cystic fibrosis patients has been associated with two genetic
markers, cable pilin subunit (cblA) that promotes respiratory colonization by binding the abnormal cystic fibrosis respiratory mucin and the transcriptional regulator Burkholderia cepacia epidemic strain marker (BCESM). However, the low frequency of both markers suggests that other factors are involved in B. cepacia complex virulence and transmissibility.
The pathogenicity of B. cepacia complex in persons with chronic granulomatous disease appears due to the ability of the organism to resist neutrophil-mediated non-oxidative killing and to induce neutrophil necrosis [8]. Clinical isolates from the same B. cepacia complex species display different virulence phenotypes likely related to differential expression of virulence factors that promote intracellular survival. In contrast to chronic B. cepacia complex infection in persons with cystic fibrosis that typically is associated with persistence of a single strain type, recurrent B. cepacia complex infection in persons with chronic granulomatous disease is usually caused by a new strain [9].
Antimicrobial susceptibility. The biofield treatment on MDR strain of B. cepacia showed a significant change in sensitivity pattern of different antimicrobials such as ceftazidime, ciprofloxacin, imipenem and levofloxacin changed from I^R. Aztreonam sensitivity converted from R^I while meropenem and piperacillin/tazobactam changed from S^R (Table 1) [10].
Table 1
Effect of biofield treatment on Burkholderia cepacia to antimicrobial susceptibility. _
Antimicrobial Control Treated
Amikacin R R
Aztreonam R I
Cefepime R R
Cefotaxime R R
Ceftazidime I R
Ceftriaxone R R
Chloramphenicol S -
Ciprofloxacin I R
Gentamicin R R
Imipenem I R
Levofloxacin I R
Meropenem S R
Piperacillin R R
Piperacillin/Tazobactam S R
Tetracycline R -
Ticarcillin/K-Clavulanate R R
Tobramycin R R
Trimethoprim/Sulfamethoxazole R -
R: Resistant; I: Intermediate; S: Susceptible; '-' Not Reported
Decrease in MIC value was reported in case of aztreonam (16p,g/mL) and tetracycline (8 p,g/mL)
after biofield treatment as compared to control. MIC (minimum inhibitory concentration) value was increased after biofield treatment in case of ceftazidime, chloramphenicol, ciprofloxacin, imipenem, levofloxacin, meropenem, and piperacillin/tazobactam (Table 2) [10].
Rest of the tested antimicrobials did not show any change in sensitivity pattern and MIC value. A change of 38.9% in susceptibility pattern and 30% in MIC values of tested antimicrobials after biofield treatment.
Table 2
Minimum inhibitory concentration (MIC) of Burkholderia cepacia for tested antimicrobials.
Antimicrobial Control Treated
Amikacin >32 >32
Amoxicillin/ Clavulanic acid >16/8 >16/8
Ampicillin/Sulbactam >16/8 >16/8
Ampicillin >16 >16
Aztreonam >16 >16
Cafazolin >16 >16
Cefepime >16 >16
Cefotaxime >32 >32
Cefotetan >32 >32
Cefoxitin >16 >16
Ceftazidime >16 >16
Ceftriaxone >32 >32
Cefuroxime >16 >16
Cephalothin >16 >16
Chloramphenicol <8 >16
Ciprofloxacin 2 2 >
Gatifloxacin 4 -
Gentamicin >8 >8
Imipenem >8 >8
Levofloxacin 4 >4
Meropenem <4 >8
Moxifloxacin 4 -
Nitrofurantoin >64 >64
Norfloxacin >8 >8
Piperacillin >64 >64
Piperacillin/Tazobactam <16 >64
Tetracycline >8 8
Ticarcillin/K-Clavulanate >64 >64
Tobramycin >8 >8
Trimethoprim/Sulfamethoxazole >2/38 >2/38
MIC values are presented in ^g/mL; '-': Not Reported
B. cepacia is a member of a group known as B. cepacia complex causing "cepacia syndrome", form of progressive necrotizing pneumonia. It was associated with acute systemic infections and may be fatal in some case [10, 11]. The emergence of MDR of B. cepacia harbored a global health problem and an emerging drug resistant microorganism commonly associated with immunocompromised patients or patients with underlying lung disease, such as cystic fibrosis. Due to continuous new drug discovery in antimicrobials,
rate of MDR microorganism increased causing serious health problems.
Cell membrane alterations in MDR microorganism results in decreased uptake of antimicrobials [10, 12], overexpression of drug target enzymes results in mutation [10, 13], and drug efflux pumps remains the predominant mechanism in multi-drug resistant organisms [10, 14]. Nowadays, B. cepacia acquires resistance against broad range of antibiotics, so it was very difficult to start drug therapy in chronically infected patients [10, 15]. Due to this, use of combination therapy is suggested rather than monotherapy against B. cepacia infection. United States in 2002, demonstrated most prevalent infection among B.
cepacia complex was B. cepacia followed by B. multivorans as the next most dominant [10, 16]. Contaminated disinfectants, ventilators, antiseptics, and different types of medical equipment were also responsible for B. cepacia infection. Even, person-to-person spread has also been documented. Best drug of choice in B. cepacia infection is co-trimoxazole, followed by ceftazidime and meropenem, alone or in combination with other antibiotics [10, 17]. Experimental results showed a significant alteration in sensitivity pattern after biofield treatment in azetronan, ceftazidime, ciprofloxacin, imipenam, levofloxacin, meropenam, and piperacillin/tazobactam.
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BURKHOLDERIA CEPACIA И ВОССТАНОВЛЕНИЕ БИОПОЛЯ
ХАФФАРЕССАС Я. Нижегородский государственный университет им. Н.И. Лобачевского
Аннотация
Комплекс Burkholderia cepacia (BCC), или просто Burkholderia cepacia, представляет собой группу каталаз-продуцирующих лактозо-неферментирующих грамотрицательных бактерий, состоящих по меньшей мере из 20 разных видов. B. cepacia оппортунистический патоген человека, который чаще всего вызывает пневмонию у лиц с ослабленным иммунитетом с основными заболеваниями легких (такими как кистозный фиброз или хроническое гранулематозное заболевание). Увеличилось количество мультирезистентных штаммов возбудителя, что привело к неэффективному лечению и риску распространения инфекции.
Ключевые слова: Burkholderia cepacia; Мультирезистентность; Противомикробная восприимчивость; восстановление биополя.
