Alternative therapies in Staphylococcus aureus diseases.

Kurlenda, Julianna; Grinholc, Mariusz

doi:10.18388/abp.2012_2136

Cited by 51 publications

(37 citation statements)

References 187 publications

(280 reference statements)

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“…S. aureus causes a range of illnesses from minor skin infections to life-threatening diseases such as pneumonia, meningitis, and sepsis 5–7 . Many S. aureus strains, particularly those found in hospitals, carry antibiotic resistance genes 8 , 9 . Annual medical expenses caused by S. aureus in the United States and European Union have been estimated to exceed $2.5 billion 10–12 .…”

Section: Introductionmentioning

confidence: 99%

Structure and genome ejection mechanism of Podoviridae phage P68 infecting Staphylococcus aureus

Hrebik

Štveráková

Škubník

et al. 2018

Preprint

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17Phages infecting S. aureus have the potential to be used as therapeutics against antibiotic-18 resistant bacterial infections. However, there is limited information about the mechanism of 19 genome delivery of phages that infect Gram-positive bacteria. Here we present the structures of 20 S. aureus phage P68 in its native form, genome ejection intermediate, and empty particle. The 21P68 head contains seventy-two subunits of inner core protein, fifteen of which bind to and alter 22 the structure of adjacent major capsid proteins and thus specify attachment sites for head 23 fibers. Unlike in the previously studied phages, the head fibers of P68 enable its virion to 24 position itself at the cell surface for genome delivery. P68 genome ejection is triggered by 25 disruption of the interaction of one of the portal protein subunits with phage DNA. The inner 26 core proteins are released together with the DNA and enable the translocation of phage 27 genome across the bacterial membrane into the cytoplasm. 29Introduction 32 Phages from the family Podoviridae have complex virions composed of genome-containing 33 heads and short non-contractile tails. The tail is attached to a special fivefold vertex of the head 34 in which a pentamer of capsid proteins is replaced by a portal complex. The tails of podoviruses 35 are formed of lower collar proteins, knobs, spikes, and fibers 1 . Podoviruses that infect S. aureus 36 often use cell wall teichoic acid as a receptor 2,3 . After binding to a cell, podoviruses disrupt the 37 bacterial cell wall and eject their genomes into the cell cytoplasm 1 . 38Phages infecting S. aureus are of interest because of their potential use in phage therapy 39 against antibiotic-resistant infections 4 . S. aureus causes a range of illnesses from minor skin 40 infections to life-threatening diseases such as pneumonia, meningitis, and sepsis 5-7 . Many 41 S. aureus strains, particularly those found in hospitals, carry antibiotic resistance genes 8,9 . 42 Annual medical expenses caused by S. aureus in the United States and European Union have 43 been estimated to exceed $2.5 billion 10-12 . 44Bacteriophage P68 belongs to the subfamily Picovirinae, and the genus P68virus of 45 phages infecting S. aureus 13 . P68 has a 18,227-bp-long double-stranded DNA genome that 46 encodes 22 open reading frames 13 . Here we used a combination of cryo-electron microscopy 47 (cryo-EM) and X-ray crystallography to structurally characterize the virion of phage P68 and the 48 mechanism of its genome ejection. 49 50 4 Results and Discussion 51 Virion structure of phage P68 52The virion of P68 has an icosahedral head with a diameter of 480 Å and 395 Å-long tail, 53 which is decorated with tail fibers (Fig. 1ab, Table S1, S2). Electron micrographs of a purified P68 54 sample contained not only native virions but also particles that were in the process of genome 55 release and empty particles (SFig. 1). The complete structure of the native virion of P68 was 56 determined to a resolution of 4.7 Å (SFig. 2, 3, Table S1)....

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Section: Introductionmentioning

confidence: 99%

Structure and genome ejection mechanism of Podoviridae phage P68 infecting Staphylococcus aureus

Hrebik

Štveráková

Škubník

et al. 2018

Preprint

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“…Two decades ago, Community-acquired MRSA (CA-MRSA) started to emerge among MRSA isolates from individuals with no or minimal exposure to health care facilities [8,9]. Currently, this strain tends to be more common among S. aureus infections as it is increasingly reported, particularly among children and young adults [8-11]. CA-MRSA strains are roughly classified into two main groups.…”

Section: Introductionmentioning

confidence: 99%

Sccmec type II gene is common among clinical isolates of methicillin-resistant Staphylococcus aureus in Jakarta, Indonesia

et al. 2013

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BackgroundCommunity Acquired Methicillin Resistant Staphylococcus aureus (CA-MRSA) is a strain of MRSA that can cause infections in patients in the community, in which these patients had no previous risk factors for MRSA infection and the patient received 72 hours prior to infection when admitted to hospital. This study aims to determine and compare the characteristics of epidemiological, clinical, and molecular biology of CA-MRSA with HA-MRSA.MethodsA total of 11 clinical strains of Methicillin-resistant Staphylococcus aureus (MRSA) and Methicillin-sensitive Stapylococcus aureus (MSSA) were collected from 2 hospitals in Jakarta, Indonesia in 2012. SCCmec typing was performed by multiplex polymerase chain reaction (PCR) and the presence of six genes (vraR, vraG, vraA, vraF,fruA, and fruB) associated with vancomycin resistance was examined by simple PCR analysis.ResultsWe found three strains of community-acquired MRSA with SCCmec type II and one strain of hospital-acquired MRSA with SCCmec type IV. The other seven strains did not contain mecA genes and SCCmec. Plasmid pUB110 was found in one strain of community-acquired MRSA and two strains of hospital-acquired MRSA. vraA genes were present in 9 of the 11 strains, vraF in 4, vraG in 5, and vraR in 4. Note worthily, three quarters of strains without pUB110 contained vraR and vraF, and 70% contained vraA, whereas 60% of strains with pUB110 contained vraG.ConclusionBased on these results, we should be concerned about the possibility of transition from MRSA strains sensitive to vancomycin in VISA strains of MRSA strains obtained in clinical trials. But first we need to look the existence of natural VISA or hVISA among these MRSA strains.

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“…Staphylococcus aureus can be carried asymptomatically and it is one of the main causes of hospital and community-acquired infections (1). The extensive use of antibiotics for the treatment of S. aureus skin and soft tissue infections has caused selective pressure and eventually has given rise to multiple drug-resistant strains (2).…”

Section: Introductionmentioning

confidence: 99%

Genetic Determinants of Resistance to Fusidic Acid Among Staphylococcus aureus Isolates in Jordan

Aldasouqi

Abu-Qatouseh

Badran

et al. 2019

Jundishapur J Microbiol

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Background: Fusidic acid-resistant Staphylococcus aureus (FRSA) has been reported in many countries to have a remarkable difference in resistance determinants. Fusidic acid resistance is very important because it might lead to the failure of topical treatment, especially when it is used as empiric therapy. In addition, its resistance might be linked to other antibiotic resistances. The overall rate of fusidic acid resistance is still relatively low. However, there is an increase in the prevalence of clinical isolates of FRSA worldwide. Objectives: We aimed to characterize FRSA isolated from Jordanian patients and evaluate the occurrence of the genetic resistance caused by fusB and fusC. Methods: We conducted a prospective cross-sectional study to determine the prevalence and the resistance pattern of S. aureus to fusidic acid among Jordanian patients and healthy people. Staphylococcus aureus clinical isolates (n = 113) obtained from patients admitted to Prince Hamzah Hospital between February and July 2015 were compared with isolates (n = 288) obtained from healthy subjects. Conventional methods were used for the identification of S. aureus and further confirmations were done by the existence of the thermonuclease gene using polymerase chain reaction (PCR). Screenings of antibiotic resistance were performed using the disc diffusion method. The minimum inhibitory concentrations were calculated using the E-test. PCR was used to detect the presence of resistant genes. Results: The FRSA frequency was significantly higher among clinical isolates (31.9%) than among isolates from healthy subjects (1%) and in methicillin-resistant Staphylococcus aureus (MRSA) (66.7%) than in methicillin-sensitive Staphylococcus aureus (MSSA) (33.3%). Of the FRSA isolates, 38.9% and 16.7% carried fusB and fusC, respectively, and they displayed low resistance compared to non-fusB, non-fusC FRSA isolates. The rate of FRSA was significantly (P < 0.05) higher among MRSA than among MSSA isolates (n = 24, 66.7% and n = 12, 33.3%, respectively). We found no association between fusidic acid determinants among MRSA and MSSA (P > 0.05). Conclusions: A high occurrence of FRSA was detected in Jordanian clinical isolates of S. aureus, particularly among MRSA. Moreover, fusB was the predominant resistance determinant, with low-level resistance. Based on our findings, fusidic acid susceptibility testing is strongly recommended in medical laboratories. The restricted use of fusidic acid is advised.

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Alternative therapies in Staphylococcus aureus diseases.

Cited by 51 publications

References 187 publications

Structure and genome ejection mechanism of Podoviridae phage P68 infecting Staphylococcus aureus

Structure and genome ejection mechanism of Podoviridae phage P68 infecting Staphylococcus aureus

Sccmec type II gene is common among clinical isolates of methicillin-resistant Staphylococcus aureus in Jakarta, Indonesia

Genetic Determinants of Resistance to Fusidic Acid Among Staphylococcus aureus Isolates in Jordan

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