Brain abscess caused by multidrug-resistant Acinetobacter baumannii

2009 ◽  
Vol 111 (2) ◽  
pp. 306-310 ◽  
Author(s):  
Carlos H. Guinand Vives ◽  
Guillermo A. Monsalve Duarte ◽  
Sandra Valderrama Beltrán ◽  
Johanna Osorio Pinzón
Keyword(s):  
Acinetobacter Baumannii ◽  
Brain Abscess ◽  
Antibiotic Treatment ◽  
Clinical Course ◽  
Infectious Agent ◽  
Multidrug Resistant ◽  
Etiological Agent ◽  
History Of

This 24-year-old soldier had a history of polytrauma caused by firearm missiles of a fragmentation weapon. He was referred to the Hospital Militar Central, where multiple shrapnel wounds in the head, face, thorax, and extremities were found. A brain abscess was documented and drained, and a culture grew a multidrug-resistant Acinetobacter baumannii. An appropriate antibiotic treatment was started but did not lead to a good response, and the patient died. The clinical course of the illness is presented, as is its treatment and the role of A baumannii as an etiological agent of a brain abscess. To the authors' knowledge, there have been no reported cases in the worldwide literature of brain abscess by this infectious agent.

scholarly journals Colistin heteroresistance and the involvement of the PmrAB regulatory system in Acinetobacter baumannii

2018 ◽  
Author(s):  
Yannick Charretier ◽  
Seydina M. Diene ◽  
Damien Baud ◽  
Sonia Chatellier ◽  
Emmanuelle Santiago-Allexant ◽  
...  
Keyword(s):  
Acinetobacter Baumannii ◽  
Population Analysis ◽  
Regulatory System ◽  
Clinical Problem ◽  
Multidrug Resistant ◽  
Regulatory Pathway ◽  
Colistin Resistance ◽  
Bacterial Killing ◽  
One Step

AbstractMultidrug-resistant Acinetobacter baumannii infection has recently emerged as a worldwide clinical problem and colistin is increasingly being used as last resort therapy. Despite its favorable bacterial killing, resistance and heteroresistance to colistin have been described. Mutations in the PmrAB regulatory pathway have been already associated with colistin resistance whereas the mechanisms for heteroresistance remain largely unknown. The purpose of the present study is to investigate the role of PmrAB in laboratory-selected mutants representative of global epidemic strains. During brief colistin exposure, colistin resistant and colistin heteroresistant mutants were selected in a one-step strategy. Population Analysis Profiling (PAP) was performed to confirm the suspected phenotype. Upon withdrawal of selective pressure, compensatory mutations were evaluated in another one-step strategy. A trans-complementation assay was designed to delineate the involvement of the PmrAB regulatory system using qPCR and PAP. Mutations in the PmrAB regulatory pathway were associated with colistin resistance and colistin heteroresistance as well. The transcomplementation assay provides a proof for the role played by changes in the PmrAB regulatory pathway. The level of colistin resistance is correlated to the level of expression of pmrC. The resistance phenotype was partially restored since the complemented strain became heteroresistant. This report shows the role of different mutations in the PmrAB regulatory pathway and warns on the development of colistin heteroresistance that could be present but not easily detected with routine testing.

scholarly journals Wolf’s Panniculitis

2017 ◽  
Vol 5 (3) ◽  
pp. 397-398
Author(s):  
Anastasiya Atanasova Chokoeva ◽  
Georgi Tchernev
Keyword(s):  
Bacterial Infection ◽  
Treatment Regimen ◽  
Antibiotic Treatment ◽  
Male Patient ◽  
Topical Application ◽  
Clinical Resolution ◽  
History Of ◽  
History Of Pain ◽  
Systemic Antibiotic Treatment

A 28-year-old male patient, presented with a one-week history of pain and itching on the skin of the left upper leg. Erythematous indurated, warm and painful on palpation, subcutaneous plaques and nodules were clinically observed, affecting the skin of the left upper leg, within a recent black-wolf tattoo. The diagnosis of traumatic panniculitis with superposed bacterial infection, provoked by a wolf tattoo was made.  The patient underwent 7-days systemic antibiotic treatment regimen and topical application of iodine povidone unguent under occlusion for 7 days. Significant alleviation of the subjective complaints was achieved within the first week, with a total clinical resolution of the symptoms. The role of the procedure as a source of trauma for subcutaneous inflammation (traumatic panniculitis) and the contamination of the equipment or the staff (infective panniculitis) in simultaneously triggering of the pathogenetic chain of the reported Wolf’s panniculitis could be present.

scholarly journals Characterization of RelA in Acinetobacter baumannii

2020 ◽  
Vol 202 (12) ◽  
Author(s):  
María Pérez-Varela ◽  
Aimee R. P. Tierney ◽  
Ju-Sim Kim ◽  
Andrés Vázquez-Torres ◽  
Philip Rather
Keyword(s):  
Acinetobacter Baumannii ◽  
Galleria Mellonella ◽  
Multidrug Resistant ◽  
Cell Physiology ◽  
Content Type ◽  
Content Model ◽  
Transposon Insertion ◽  
Downstream Effectors

ABSTRACT In response to nutrient depletion, the RelA and SpoT proteins generate the signaling molecule (p)ppGpp, which then controls a number of downstream effectors to modulate cell physiology. In Acinetobacter baumannii strain AB5075, a relA ortholog (ABUW_3302) was identified by a transposon insertion that conferred an unusual colony phenotype. An in-frame deletion in relA (ΔrelA) failed to produce detectable levels of ppGpp when amino acid starvation was induced with serine hydroxamate. The ΔrelA mutant was blocked from switching from the virulent opaque colony variant (VIR-O) to the avirulent translucent colony variant (AV-T), but the rate of AV-T to VIR-O switching was unchanged. In addition, the ΔrelA mutation resulted in a pronounced hypermotile phenotype on 0.35% agar plates. This hypermotility was dependent on the activation of a LysR regulator ABUW_1132, which was required for expression of AbaR, a LuxR family quorum-sensing regulator. In the ΔrelA mutant, ABUW_1132 was also required for the increased expression of an operon composed of the ABUW_3766-ABUW_3773 genes required for production of the surfactant-like lipopeptide acinetin 505. Additional phenotypes identified in the ΔrelA mutant included (i) cell elongation at high density, (ii) reduced formation of persister cells tolerant to colistin and rifampin, and (iii) decreased virulence in a Galleria mellonella model. IMPORTANCE Acinetobacter baumannii is a pathogen of worldwide importance. Due to the increasing prevalence of antibiotic resistance, these infections are becoming increasingly difficult to treat. New therapies are required to combat multidrug-resistant isolates. The role of RelA in A. baumannii is largely unknown. This study demonstrates that like in other bacteria, RelA controls a variety of functions, including virulence. Strategies to inhibit the activity of RelA and the resulting production of ppGpp could inhibit virulence and may represent a new therapeutic approach.

scholarly journals Rett Syndrome in Males: The Different Clinical Course in Two Brothers with the Same Microduplication MECP2 Xq28

2019 ◽  
Vol 16 (17) ◽  
pp. 3075
Author(s):  
Maria Bernarda Pitzianti ◽  
Angelo Santamaria Palombo ◽  
Susanna Esposito ◽  
Augusto Pasini
Keyword(s):  
Rett Syndrome ◽  
Genetic Basis ◽  
Normal Development ◽  
Clinical Course ◽  
Neurodevelopmental Disorder ◽  
Dominant Inheritance ◽  
Clinical Form ◽  
Inactivation Pattern ◽  
History Of

Rett syndrome (RTT) is a neurodevelopmental disorder with a genetic basis that is associated with the mutation of the X-linked methyl-CpG binding protein 2 (MECP2) gene in approximately 90% of patients. RTT is characterized by a brief period of normal development followed by loss of acquired skills and evolution towards impairment of brain and motor functions and multi-organ dysfunction. Originally, RTT was considered lethal in males as it has an X-linked dominant inheritance. However, although this syndrome has a higher incidence in females, rare cases are also documented in males. Here, we describe the case of an 11-year-old male patient with a microduplication MECP2 Xq28. Our patient is currently living, while his older brother with the same mutation died at the age of 9 years. We showed that the role of MECP2 as an epigenetic modulator and the X-chromosome inactivation pattern can explain the lethal clinical form of the older brother with the same microduplication MECP2 Xq28 presented by our patient who is still alive. Given the limited case history of RTT in males, further studies are needed to better characterize this syndrome in males and consequently improve the currently available therapeutic strategies.

Development of cladribine treatment in multiple sclerosis

1996 ◽  
Vol 1 (6) ◽  
pp. 343-347 ◽  
Author(s):  
JC Sipe ◽  
JS Romine ◽  
JA Koziol ◽  
R McMillan ◽  
J Zyroff ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Clinical Course ◽  
Progressive Multiple Sclerosis ◽  
Efficacy And Safety ◽  
Double Blind ◽  
Relapsing Remitting ◽  
History Of ◽  
New Type ◽  
Cns Demyelination

Cladribine is a new type of drug with properties of selective lymphocyte suppression that appear to favorably alter the clinical course of progressive multiple sclerosis (MS). The history of the development of cladribine treatment in chronic progressive MS is discussed, and the application of cladribine treatment to progressive multiple sclerosis in a double-blind, placebo crossover study is reviewed. Cladribine selectively targets both resting and dividing lymphocytes and may be able to destroy the activated lymphocytes that induce CNS demyelination, thus producing stabilization or improvement in chronic MS. Although the role of cladribine has not yet been fully defined, additional studies are underway to evaluate the efficacy and safety of cladribine in both progressive MS and relapsing-remitting MS.

scholarly journals Multidrug resistant Acinetobacter baumannii--the role of AdeABC (RND family) efflux pump in resistance to antibiotics.

2008 ◽  
Vol 46 (3) ◽  
Author(s):  
Piotr Wieczorek ◽  
Paweł Sacha ◽  
Tomasz Hauschild ◽  
Marcin Zórawski ◽  
Małgorzata Krawczyk ◽  
...  
Keyword(s):  
Acinetobacter Baumannii ◽  
Efflux Pump ◽  
Multidrug Resistant ◽  
Resistance To Antibiotics

scholarly journals In-Depth Analysis of the Role of the Acinetobactin Cluster in the Virulence of Acinetobacter baumannii

2021 ◽  
Vol 12 ◽  
Author(s):  
Kelly Conde-Pérez ◽  
Juan C. Vázquez-Ucha ◽  
Laura Álvarez-Fraga ◽  
Lucía Ageitos ◽  
Soraya Rumbo-Feal ◽  
...  
Keyword(s):  
Acinetobacter Baumannii ◽  
Multidrug Resistant ◽  
Significant Loss ◽  
Genetic Redundancy ◽  
Double Mutant Strain ◽  
Wide Range ◽  
Depth Analysis ◽  
High Level ◽  
Antivirulence Agents

Acinetobacter baumannii is a multidrug-resistant pathogen that represents a serious threat to global health. A. baumannii possesses a wide range of virulence factors that contribute to the bacterial pathogenicity. Among them, the siderophore acinetobactin is one of the most important, being essential for the development of the infection. In this study we performed an in-depth analysis of the acinetobactin cluster in the strain A. baumannii ATCC 17978. For this purpose, nineteen individual isogenic mutant strains were generated, and further phenotypical analysis were performed. Individual mutants lacking the biosynthetic genes entA, basG, basC, basD, and basB showed a significant loss in virulence, due to the disruption in the acinetobactin production. Similarly, the gene bauA, coding for the acinetobactin receptor, was also found to be crucial for the bacterial pathogenesis. In addition, the analysis of the ΔbasJ/ΔfbsB double mutant strain demonstrated the high level of genetic redundancy between siderophores where the role of specific genes of the acinetobactin cluster can be fulfilled by their fimsbactin redundant genes. Overall, this study highlights the essential role of entA, basG, basC, basD, basB and bauA in the pathogenicity of A. baumannii and provides potential therapeutic targets for the design of new antivirulence agents against this microorganism.

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