Major role of levofloxacin in the treatment of a case of Listeria monocytogenes meningitis

Viale, Pierluigi; Furlanut, Mario; Cristini, Francesco; Cadeo, Barbara; Pavan, Federica; Pea, Federico

doi:10.1016/j.diagmicrobio.2006.11.010

Cited by 23 publications

(9 citation statements)

References 12 publications

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“…However, this dosing schedule of levofloxacin has not been evaluated thus far in the management of meningitis. 500 mg levofloxacin every 12 h has been successfully used in meningitis due to other organisms 128–130…”

Section: Treatmentmentioning

confidence: 99%

Management of meningitis due to antibiotic-resistant Acinetobacter species

Kim

Peleg

Lodise

et al. 2009

The Lancet Infectious Diseases

195

149

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Acinetobacter meningitis is becoming an increasingly common clinical entity, especially in the postneurosurgical setting, with mortality from this infection exceeding 15%. Infectious Diseases Society of America guidelines for therapy of postneurosurgical meningitis recommend either ceftazidime or cefepime as empirical coverage against Gram-negative pathogens. However, assessment of the pharmacodynamics of these cephalosporins in cerebrospinal fluid suggests that recommended doses will achieve pharmacodynamic targets against fewer than 10% of contemporary acinetobacter isolates. Thus, these antibiotics are poor options for suspected acinetobacter meningitis. From in vitro and pharmacodynamic perspectives, intravenous meropenem plus intraventricular administration of an aminoglycoside may represent a superior, albeit imperfect, regimen for suspected acinetobacter meningitis. For cases of meningitis due to carbapenem-resistant acinetobacter, use of tigecycline is not recommended on pharmacodynamic grounds. The greatest clinical experience rests with use of polymyxins, although an intravenous polymyxin alone is inadvisable. Combination with an intraventricularly administered antibiotic plus removal of infected neurosurgical hardware appears the therapeutic strategy most likely to succeed in this situation. Unfortunately, limited development of new antibiotics plus the growing threat of multidrug-resistant acinetobacter is likely to increase the problems posed by acinetobacter meningitis in the future.

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Section: Treatmentmentioning

confidence: 99%

Management of meningitis due to antibiotic-resistant Acinetobacter species

Kim

Peleg

Lodise

et al. 2009

The Lancet Infectious Diseases

195

149

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“…Some newer quinolones and linezolid show good in vitro activity, but clinical experience is mixed and too limited to support recommending these antimicrobials to treat CNS listeriosis [47][48][49].…”

Section: Treatmentmentioning

confidence: 99%

Central nervous system infection with Listeria monocytogenes

Clauss¹,

Lorber

2008

Curr Infect Dis Rep

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The foodborne pathogen Listeria monocytogenes has a particular tropism for the central nervous system and can produce infection in the meninges and brain substance. Well-recognized clinical syndromes include meningitis, brain abscess, rhombencephalitis, and spinal cord abscess; simultaneous infection of the meninges and brain is common. Although it is an uncommon cause of infection in the population at large, L. monocytogenes is an important cause of central nervous system infection in those with impaired cell-mediated immunity, whether due to underlying disease or treatment with immunosuppressive therapeutic agents; it is the etiology in 20% of bacterial meningitis cases in neonates and in 20% of cases in those older than 50 years. Ampicillin is considered the treatment of choice, and trimethoprim-sulfamethoxazole is recommended for those allergic to penicillin. At-risk patients should be advised to avoid unpasteurized milk and soft cheeses along with deli-style, ready-to-eat prepared meats, particularly poultry products.

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“…However, FQs are not recommended in the treatment of listeriosis even if newer compounds (i.e. levofloxacin, moxifloxacin) might represent an efficient alternative in the treatment of CNS listeriosis, as previously reported in one human case report [5] and several animal models [6], [7]. Due to the extensive use of FQs for the treatment of multiple infections, there is also an important selective pressure for recovery of in vivo FQ-resistant mutants in gram-positive bacteria including L. monocytogenes .…”

Section: Introductionmentioning

confidence: 99%

Overexpression of the Novel MATE Fluoroquinolone Efflux Pump FepA in Listeria monocytogenes Is Driven by Inactivation of Its Local Repressor FepR

et al. 2014

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Whereas fluoroquinolone resistance mainly results from target modifications in gram-positive bacteria, it is primarily due to active efflux in Listeria monocytogenes. The aim of this study was to dissect a novel molecular mechanism of fluoroquinolone resistance in this important human pathogen. Isogenic L. monocytogenes clinical isolates BM4715 and BM4716, respectively susceptible and resistant to fluoroquinolones, were studied. MICs of norfloxacin and ciprofloxacin were determined in the presence or in the absence of reserpine (10 mg/L). Strain BM4715 was susceptible to norfloxacin (MIC, 4 mg/L) and ciprofloxacin (MIC, 0.5 mg/L) whereas BM4716 was highly resistant to both drugs (MICs 128 and 32 mg/L, respectively). Reserpine was responsible for a 16-fold decrease in both norfloxacin and ciprofloxacin MICs against BM4716 suggesting efflux associated resistance. Whole-genome sequencing of the strains followed by comparative genomic analysis revealed a single point mutation in the gene for a transcriptional regulator, designated fepR (for fluoroquinolone efflux protein regulator) belonging to the TetR family. The frame-shift mutation was responsible for the introduction of a premature stop codon resulting in an inactive truncated protein. Just downstream from fepR, the structural gene for an efflux pump of the MATE family (named FepA) was identified. Gene expression was quantified by qRT-PCR and demonstrated that fepA expression was more than 64-fold higher in BM4716 than in BM4715. The clean deletion of the fepR gene from BM4715 was responsible for an overexpression of fepA with resistance to norfloxacin and ciprofloxacin, confirming the role of FepR as a local repressor of fepA. In conclusion, we demonstrated that overexpression of the new MATE efflux pump FepA is responsible for fluoroquinolone resistance in L. monocytogenes and secondary to inactivation of the FepR repressor.

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Major role of levofloxacin in the treatment of a case of Listeria monocytogenes meningitis

Cited by 23 publications

References 12 publications

Management of meningitis due to antibiotic-resistant Acinetobacter species

Management of meningitis due to antibiotic-resistant Acinetobacter species

Central nervous system infection with Listeria monocytogenes

Overexpression of the Novel MATE Fluoroquinolone Efflux Pump FepA in Listeria monocytogenes Is Driven by Inactivation of Its Local Repressor FepR

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