Encephalitis > Volume 3(3); 2023 > Article
Mastroianni, Vangeli, Mauro, Urso, Manfredi, and Greco: Intrathecal tigecycline is a safe and effective treatment for central nervous system infections


Both the safety and effectiveness of intrathecal tigecycline (TGC) for treatment of infections of the central nervous system (CNS) are discussed using the clinical findings from a study of a recent patient who came to our attention, along with a literature review. Although penetration into the CNS is low (approximately 11%), intraventricular TGC could help treat patients with severe post-neurosurgical CNS infections. The use of multiple routes of TGC administration appears to be encouraging and should be considered in managing life-threatening intraventricular infections.


Tigecycline (TGC) is a glycylcycline antibiotic widely employed for systemic (intravenous) treatment of skin-skin structures and intraabdominal infections caused by susceptible gram-positive and gram-negative bacteria. Experiences with infections of the central nervous system (CNS) are limited [1], while those encompassing intrathecal administration are even rare. Combined intravenous and intrathecal treatment has been used in a few cases of CNS infections due to multi-resistant, gram-negative pathogens [219].
The report was approved by the Institutional Review Board of Azienda Ospedaliera di Cosenza, Cosenza, Italy and written informed consent was obtained from the patient for publication of this case report.

Case Report

After a subarachnoid hemorrhage, a 51-year-old male received external ventricular drainage (EVD) after a ventriculoperitoneal shunt became infected by Staphylococcus aureus, leading to a clinical picture of CNS infection (ventriculitis). A baseline computed tomography (CT) scan of his head revealed endovascular treatment of embolization at the apex of the basilar artery using a simple coiling technique, with evidence of metal coils at the level of the interpeduncular cistern, which generated artifacts. The scan also revealed the presence of a cerebral spinal fluid (CSF) shunt catheter with right transfrontal and extreme proximal access in the anterior recesses of the third ventricle, with thickening and inhomogeneity of the frontoparietal subgaleal soft tissues delimiting the shunt catheter, a ventricular system of dimensions within the limits, and midline structures on axis.
The S. aureus strain proved to be resistant to beta-lactams, macrolides, and clindamycin but fully susceptible to glycopeptides and TGC (minimum inhibitory concentration, <0.12 μg/mL).
Together with full-dose intravenous teicoplanin, TGC was administered by both intravenous (full dose) and intraventricular (IVT) routes, the latter at 1 mg twice daily, followed by 5 mg twice daily in a 0.9% saline solution (at a final concentration of 1 mg/mL), maintaining a closed IVT shunt for 2 hours.
Recommended antimicrobial therapy has included the use of 400 mg of teicoplanin in sodium chloride 0.9% intravenous solution 100 mL injection every 12 hours for 3 days, then 400 mg/day plus 100 mg of TGC in sodium chloride 0.9% intravenous solution of 250 mL as a loading dose, followed by 50 mg in sodium chloride 0.9% intravenous solution 100 mL every 12 hours. To enhance antimicrobial activity, use of the IVT route followed a recommended protocol. First, on the second day of therapy, the dose of intravenous TGC was reduced to 49 mg in sodium chloride 0.9% intravenous solution 100 mL every 12 hours, and 1 mg of TGC was administered intraventricularly every 12 hours (slow injection into the lateral ventricles via an EVD was recommended). On the 3rd day of therapy, assuming adequate tolerability, the dose of TGC was reduced to 45 mg in sodium chloride 0.9 intravenous solution 100 mL every 12 hours, administering 5 mg TGC intraventricularly every 12 hours. The overall duration of therapy was 14 days, with microbial sterilization of the CSF and negativity of blood cultures. The TGC used in each intrathecal injection was diluted in 10 mL of 0.9% NaCl, resulting in a concentration of 1 mg/mL. After each IVT injection, the CSF drain was temporarily closed for 2 hours to prevent premature lavage of the drug. Daily chemophysical and microbiological monitoring of the CSF was performed using EVD. Complete blood counts were obtained, and C-reactive protein, procalcitonin, creatinine, creatine phosphokinase, alanine transaminase, lipase, and electrolyte levels were monitored daily. A CT scan of the head on day 14 documented shunt catheter removal along the proximal path in which air was bubbling and hypodensity due to parenchymal pain was highlighted. The ventricular system was slightly reduced in size. Together with full normalization of CSF parameters, these assessments demonstrated both efficacy and safety of TGC administered by an intrathecal route (Table 1). The patient was discharged from the hospital after confirming no residual infection or ventricular enlargement.
The decision to use TGC both intravenously and intrathecally was based on three considerations. First, the intensive care and neurosurgery units of our hospital have a high risk of nosocomial infections due to gram-negative microorganisms, particularly Escherichia coli, Klebsiella pneumoniae, and Acinetobacter baumannii. Second, because the patient had been recently hospitalized for more than 4 weeks, we assumed he had been colonized by nosocomial organisms. Third, during the first days of treatment with teicoplanin, the patient continued to have a fever.


While combined intravenous and intrathecal antibiotics have been used successfully to treat multidrug-resistant (MDR) CNS infections, most of these were nosocomial in origin, and intrathecal TGC has been used in only a few cases of spinal arachnoiditis or intracranial infections caused by MDR A. baumannii strains [219]. The present report is the first to apply TGC to patients with gram-positive CNS infections. TGC is a new, intravenous, broad-spectrum antibiotic that is a derivative of minocycline and a member of the glycylcyclines. It is part of a new class of semisynthetic antibacterial agents developed to treat polymicrobial infections caused by MDR to gram-positive and gram-negative pathogens, overcoming the main tetracycline-resistance genetic mechanisms associated with efflux pumps and ribosomal protection proteins that decrease the activity of other tetracyclines.
TGC is structurally similar to tetracyclines but is a chemically modified monocycline with addition of a t-butylglycylamido side chain to the C9 carbon of the “D” tetracycline ring, resulting in expansion of the TGC spectrum of antibacterial activity against a wide spectrum of gram-positive and gram-negative pathogens.
As a bacteriostatic inhibitor of bacterial protein translation via reversible binding to a helical region on the 30S subunit of bacterial ribosomes, TGC prevents the incorporation of amino acid residues into elongated peptide chains, inhibiting peptide formation and bacterial growth.
TGC is the first glycylcycline antibacterial drug that inhibits protein translation in bacteria by binding to the 30S ribosomal subunit and blocking the entry of aminoacyl transfer RNA molecules into the A site of the ribosome.
Both the dose and administration schedules of intrathecal TGC remain to be defined, but when a CNS infection is of concern, intravenous administration must be ruled out because of poor drug penetration of the blood-brain barrier. IVT administration of TGC is emerging as an effective therapeutic option for the treatment of CNS infections, particularly those caused by MDR organisms for which there are few other therapeutic opportunities.
Although the descriptions are limited, a narrative review of a letter summarized in Table 2 [2-19] highlights many relevant articles published, attesting to the strength of interest in this topic. Considering the potential neutral but irreversible effects correlated with high concentrations of TGC, further studies are needed to verify the safest and most effective dosages. IVT therapy remains an off-label therapeutic possibility and, pending further precision therapy studies, should be reserved as an individualized therapy resource for the treatment of severe infections, possibly under therapeutic drug monitoring guidance. The dose of TGC used by Soto-Hernández et al. [12] produced levels 15 to 20 times the minimum inhibitory concentration of the bacteria for up to six hours with adequate tolerance. Doses smaller than 5 mg and those administered more than twice daily have been recommended as the safest and most effective regimen [16]. Moreover, further research is necessary to determine the role of TGC in the treatment of CNS infection. The safety of IVT injections of this drug, as well as the pharmacokinetics and pharmacodynamics in this patient setting, should be analyzed in larger studies involving patients with postsurgical and serious infections by gram-positive organisms.
We recently published a brief report, the first of its kind, documenting the safety and efficacy of high-dose TGC as a salvage therapy in five Italian patients with serious CNS rickettsiosis [1]. Despite the low concentrations of TGC in the CSF compared with the minimum inhibitory concentration, some reports describe a positive evolution of the therapy for CNS infections by MDR organisms with TGC [1]. A drug may accumulate in polymorphonuclear cells and then be delivered to the site of infection in higher-than-anticipated concentrations or lead to minor subinhibitory effects. Although penetration into the CNS is minimal (approximately 11%), TGC delivered by IVT may be able to treat patients with severe post-neurosurgical CNS infections [1]. The decision to use TGC both intravenously and intrathecally in our patient was based on three considerations. First, the intensive care unit and neurosurgery units of our hospital both have a high risk of nosocomial infections due to gram-negative microorganisms, particularly E. coli, K. pneumoniae, and A. baumannii. Second, the patient had been recently hospitalized for more than 4 weeks and was assumed to be colonized by nosocomial organisms. Third. during the first days of treatment with teicoplanin, the patient continued to run a fever.
The use of multi-route TGC appears to be effective and should be considered for managing life-threatening IVT infections.


Conflicts of Interest

No potential conflict of interest relevant to this article was reported.

Author Contributions

Conceptualization, Investigation: Mastroianni A; Data curation: Greco S, Mauro MV; Formal analysis: all authors; Writing–original draft: all authors; Writing–review and editing: all authors

Table 1
Laboratory and cerebrospinal fluid characteristics
Characteristic Baseline Day 14
Laboratory characteristic
 White blood cell (×106/mL) 18.9 10
 Neutrophils (×106/mL) 14.8 5.7
  Percentage 78.4 57.9
 Lymphocytes 2.1 2.7
  Percentage 11.2 27.1
 Monocytes (×106/mL) 1.8 1.2
  Percentage 9.7 12.1
 C-reactive protein (mg/L) 301.7 62.9
 Fibrinogen (mg/dL) 763 337
Cerebrospinal fluid test
 Appearance Colorless, hazy Colorless, clear
 Karyocyte cell 33 9
 Red blood cell 0 0
 Mononuclear cell (%) 25 40
 Multinucleated cell (%) 75 60
 Immunoglobulin G (mg/dL) 16.8 4.99
 Albumin (mg/dL) 84.9 37.4
 Glucose (mg/dL) 64 54.9
 Gram stain Occasional gram-positive cocci No organisms seen
 Culture Staphylococcus aureus No growth
Table 2
Characteristics of adults previously reported with CNS infection treated with intraventricular TGS (2020–2022)
Patient No. Study Year Age (yr)/sex Country Underlying disease (s) Primary infection Organism(s) TGC MIC (mg/L) TGC concentrations (mg/L) Side effects TGC, IV/CVI/IVT LOT (days) Co-administered antibiotics Outcome Time to CSF sterilization (day)
1 Lauretti et al. [2] 2017 22/M Italy A giant pituitary adenoma, post-resection CSF leak Post-neurosurgical meningitis XDRAB 2 μg/mL NR Chemical ventriculitis, myelitis (CST) IV, 100 mg/q12 hr; IVT, 2 mg/(q24–12 hr) IVT, 45; 1 month from the restart of the IVT IV, 14; IVT, 14 CST IVT, 120,000/q12 hr; MEP IV, 2 g/q8 hr; VAN IV, 1 g/q12 hr Improved 75
2 Fang et al. [3] 2017 50/M China Craniocerebral injury Post-neurosurgical meningitis XDRAB 2 μg/mL NR None IV, 100 mg/q12 hr; IVT, 3–4 mg/q12 hr IV, 14; ITV, 14 CES IV, 3 g/q12 hr Improved 14
3 Wang et al. [4] 2017 45/M China Post-lumbar puncture meningitis MDRAB NR (Kirby-Bauer antibiotic test, 17 mm) 1 mg/mL None IV, 50 mg q12 hr; IVT, 10 mg q12 hr IV, 7 (discontinued before starting IVT TGC); IVT, 6 None Improved 6
4 Long et al. [5] 2018 55/M India Intracerebellar hemorrhage, CSF leak, hydrocephalus, EVD Post-neurosurgical ventriculitis MDRAB 16 μg/mL NR None IV, 100 mg q12; IVT, 4 mg/day IV, 14; CVI, 14; IVT, 3 CES IV, 2 g/q8 hr Improved 12
5 Tsolaki et al. [6] 2018 55/F Greece Aneurysmal subarachnoid hemorrhage Post-neurosurgical VM MDRAB 2 μg/mL NR None IV, 100 mg q12 yr; IVT, 4 mg/day IV TGC, 14; IVT TGC, 15; IVT CST, 22 IVT CST, 250 ×103 IU qd Improved 4
6 Tsolaki et al. [6] 2018 50/M Greece Intraventricular mass resection, cerebral edema, EVD Post-neurosurgical VM MDRAB 1 μg/mL NR None IV, NR; IVT IV TGC, 15; IVT TGC, 15; IVT CST, 30 CST, 250 ×103 IU qd Improved 5
7 Tsolaki et al. [6] 2018 48/M Greece Cerebellum spontaneous hemorrhage, EVD Post-neurosurgical VM MDRKP NR NR None IV, NR; IVT IV TGC, 9; IVT TGC, 9; IVT CST, 11 CST, 125 ×103 IU qd Improved 3
8 Liu et al. [7] 2018 70/F China Sub-arachnoid hemorrhage Post-neurosurgical ventriculitis XDRAB ≤1 μg/mL NR None IV, 50 mg q12 hr; IVT, 2 mg q12 yr IV TGC, 16; IVT TGC, 10 CES IV, 3 g/q8 hr Improved 10
9 Wu et al. [8] 2018 67/M China Cerebral hemorrhage, EVD Post-neurosurgical meningitis MDRKP NR The trough concentrations of TGC in CSF for the three different dosages of TGC IV-ICV combined administration were 0.313, 1.290, and 2.886 mg/L for 40 mg IV/10 mg ICV, 45 mg IV/5 mg ICV, and 50 mg IV/1 mg ICV TGC, respectively None IV, 45 mg q12 hr, 40 mg q12 hr; IVT, 1 mg q12 hr, 5 mg q12 hr, 10 mg q12 hr NR TMP/SMX 480 mg q12 hr per os Improved 42
10 Curebal et al. [9] 2018 28 days/M Turkey Congenital hydrocephalus, VPS placement VPS infection MDRAB 1 μg/mL NR None IV, 1.2 mg/kg/day; IVT, 4 mg/day IV TGC, 24; IVT TGC, 14 MEP IV, 120 mg/kg/day for 34 days Died after the 1st month of discharge, because of pneumonia and sepsis. Blood culture was positive for XDRAB sensitive for colistin. TGC MIC value was 16 μg/mL 7
After three negative CSF the patient was discharged IVT AMK, 30 mg/ day for 10 days discontinued before starting IVT TGC
11 Pratheep et al. [10] 2019 Baby born at 27 wk gestation India Baby was born to a mother with prelabor premature rupture of membranes. At birth, baby had respiratory distress Ventriculitis XDRAB NR NR None IVT, 3 mg/day IVT TGC, 2 wk IVT CST, 5 mg/day for 4 wk Improved 14
12 Deng et al. [11] 2019 17/M China Tuberculous meningitis Post-neurosurgery intracranial infection XDRAB 1 μg/mL NR None IV,47.5 mg q12 hr; IVT, 4 mg q12 hr (after 4 days the clinical pharmacist advised changing from IVT to TGC ITC infusions; 4 mg daily) IV TGC, 39; IVT TGC, 39 IV FOS, 4 g q8 hr; IV CES, 3 g q8 hr; after 4 days changed to IV MEP 2 g every q8 hr Improved 39
13 Soto-Hernández et al. [12] 2019 38/M México Recent review of VPS. Hydrocephalus after cryptococcal meningitis in HIV+ Post-neurosurgical ventriculitis MDRKO <2 μg/mL Peak concentrations achieved at 2 hr after the dose of between 178 and 310 μg/mL None IVT, 5 mg q24 hr IVT TGC, 11 MEP, 6 g qd; AMK 15 mg/kg/day Improved 3
14 Zhong et al. [13] 2020 33/M China Severe craniocerebral trauma Post-neurosurgical intracranial infection XDRAB 2 μg/mL NR Hepatic toxicity, no neurotoxic side effects IV, 100 mg/q12 hr; IVT, 5 mg/q12 hr IV TGC, 100 mg q12 hr for 7; IVT TGC, 5 mg q12 hr for 7 Sequential use of POLB IV, 100 mg q12 hr IV, POLB IVT, 10 mg qd, changed to qod × 2 wk IVT 4 days later Improved 7 (after starting IV/IVT POLB)
During the 7 days of the use IV/IVT TGC, CSF cellular and biochemical CSF markers improved; however, XDRAB was still present.
15 Abdallah et al. [14] 2020 53/M Saudi Arabia Cerebral hemorrhage in DM and uncontrolled hypertension Post-neurosurgical meningitis and ventriculitis MDRAB 4 μg/mL (intermediate susceptibility) NR After 8 hr of administering the first dose of IVT TGC, the patient developed myoclonic seizures for 4 min IVT, TGC 2 mg q12 hr IV TGC, 22; IVT TGC, 14; IV MEP, 24; IV TMP-SMX, 19 High-dose tigecycline (200-mg IV stat dose followed by 100-mg IV q12 hr), TMP/SMX (1,920-mg IV q6 hr) Improved 14 (after starting IVT TGC)
16 Li et al. [15] 2021 68/M China Decompressive craniectomy and evacuation of traumatic cerebellar hematoma Post-neurosurgical ventriculitis MDRAB NR NR None IV, 50 mg q12 hr +; CVI, 4 mg q24 hr (in 50 mL of NS, at a rate of 12.5 mL/hr at a frequency of q6 hr) IV TGC + CVI, 3; IV TGC + IVT, 7 Improved 10 (after starting IV + CVI),
After 3 days: IV, 50 mg q12 day + IVT, 2 mg in 4 mL of NS in 2 min at a frequency of q8 hr 7 (after starting IV + IVT)
17 Huang et al. [16] 2022 16/F China Craniotomy for resection of vestibular schwannomas Post-neurosurgery meningitis XDRAB 2 μg/mL NR None IV, 50 mg q12 hr; IVT, 5 mg q24 days IV TGC + IVT TGC, 4 wk IV CES, 3 g q8 days for 4 wk Improved 4 wk
18 Huang et al. [16] 2022 80/M China Craniotomy for removal of frontal meningiomas Post-neurosurgical ventriculitis XDRAB 2 μg/mL NR None IV, 50 mg q12 hr; IVT, 5 mg q24 days IV TGC + IVT TGC, 10 IV CES, 3 g q8 days for 10 days Improved 10
19 Li et al. [17] 2022 57/M China Hematoma removal after craniocerebral injury Post-neurosurgical ventriculitis CRKP 2 μg/mL NR None IV, 100 mg qd; IVT, 3 mg q12 hr 14 IVT AMK, 0.8 g IV + 30 mg IVT qd Improved 14
20 Wang et al. [18] 2022 53/M China Suboccipital decompression for an acute cerebellar infarction Post-neurosurgical ventriculitis CRKP 0.5 μg/mL NR None IVT, 5 mg q12 days IVT TGC, 6 (after intracerebroventricular injection of POLIB) IV CAZ/AVI, 2.5 g + MAP, 2 g q 8 dahs Improved 6 (22nd day of hospitalization)
21 Li et al. [19] 2022 31/M China Ventricular drainage performed subarachnoid hemorrhage Post-neurosurgical ventriculitis XDRAB ≤2 μg/mL NR None IV, 100 mg q12 hr combined with IVT 5 mg qd IVT TGC + IVT TGC, 33 IV MEP, 2 g IV q8 hr; VAN, 1 g q12 hr; IVT POLB, 50,000 IU qd Improved 33 (after IV + IVT TGC),
29 (after IVT POLB)

CNS, central nervous system; TGC, tygecicline; MIC, minimum inhibitory concentration; IV, intravenous; CVI, continuous ventricular irrigation; IVT, intraventricular therapy; LOT, length of treatment; CSF, cerebrospinal fluid; M, male; F, female; XDRAB, extensive drug resistant Acinetobacter baumannii; NR, not reported; CST, chemical sterilization therapy; MEP, meropenem; VAN, vancomycin; CES, cefoperazone-sulbactam; MDRAB, multidrug-resistant Acinetobacter baumannii; EVD, external ventricular device; MDRKP, multidrug resistant Klebsiella pneumoniae; TMP/SMX, trimethoprim-sulfamethoxazole; VPS, ventriculo-peritoneal shunt; AMK, amikacyn; ITC, intrathecal; FOS, fosfomycin; POLB, polimixyn B; DM, diabetes mellitus; POLIB, polimyxin B; CAZ/AVI, ceftazidime/avibactam.


1. Mastroianni A, Greco S, Urso F, Mauro MV, Vangeli V. Does tigecycline have a place in therapy for rickettsial infection of the central nervous system? Infect Chemother 2022;54:165–172.
crossref pmid pmc pdf
2. Lauretti L, D’Alessandris QG, Fantoni M, et al. First reported case of intraventricular tigecycline for meningitis from extremely drug-resistant Acinetobacter baumannii. J Neurosurg 2017;127:370–373.
crossref pmid
3. Fang YQ, Zhan RC, Jia W, Zhang BQ, Wang JJ. A case report of intraventricular tigecycline therapy for intracranial infection with extremely drug resistant Acinetobacter baumannii. Medicine (Baltimore) 2017;96:e7703.
crossref pmid pmc
4. Wang L, Zhang J, Yu X, et al. Intrathecal injection of tigecycline in treatment of multidrug-resistant Acinetobacter baumannii meningitis: a case report. Eur J Hosp Pharm 2017;24:182–184.
crossref pmid pmc
5. Long W, Yuan J, Liu J, et al. Multidrug resistant brain abscess due to Acinetobacter baumannii ventriculitis cleared by intraventricular and intravenous tigecycline therapy: a case report and review of literature. Front Neurol 2018;9:518.
crossref pmid pmc
6. Tsolaki V, Karvouniaris M, Manoulakas E, et al. Intraventricular CNS treatment with Colistin-Tigecycline combination: a case series. J Crit Care 2018;47:338–341.
crossref pmid
7. Liu Y, Pu Z, Zhao M. Case report of successful treatment of extensively drug-resistant Acinetobacter baumannii ventriculitis with intravenous plus intraventricular tigecycline. Antimicrob Agents Chemother 2018;62:e01625–18.
crossref pmid pmc pdf
8. Wu Y, Chen K, Zhao J, Wang Q, Zhou J. Intraventricular administration of tigecycline for the treatment of multidrug-resistant bacterial meningitis after craniotomy: a case report. J Chemother 2018;30:49–52.
crossref pmid
9. Curebal B, Dalgic N, Bayraktar B. Intraventricular tigecycline for the treatment of shunt infection: a case in pediatrics. J Neurosurg Pediatr 2018;23:247–250.
crossref pmid
10. Pratheep R, Ray S, Mukhopadhyay K, et al. First case report of intraventricular tigecycline in a neonate with extensively drug-resistant Acinetobacter baumannii ventriculitis. Pediatr Infect Dis J 2019;38:e172–e174.
crossref pmid
11. Deng ZW, Wang J, Qiu CF, Yang Y, Shi ZH, Zhou JL. A case report of intraventricular and intrathecal tigecycline infusions for an extensively drug-resistant intracranial Acinetobacter baumannii infection. Medicine (Baltimore) 2019;98:e15139.
crossref pmid pmc
12. Soto-Hernández JL, Soto-Ramírez A, Pérez-Neri I, Angeles-Morales V, Cárdenas G, Barradas VA. Multidrug-resistant Klebsiella oxytoca ventriculitis, successfully treated with intraventricular tigecycline: a case report. Clin Neurol Neurosurg 2020;188:105592.
crossref pmid
13. Zhong L, Shi XZ, Su L, Liu ZF. Sequential intraventricular injection of tigecycline and polymyxin B in the treatment of intracranial Acinetobacter baumannii infection after trauma: a case report and review of the literature. Mil Med Res 2020;7:23.
crossref pmid pmc pdf
14. Abdallah M, Alsaleh H, Baradwan A, et al. Intraventricular tigecycline as a last resort therapy in a patient with difficult-to-treat healthcare-associated Acinetobacter baumannii ventriculitis: a case report. SN Compr Clin Med 2020;2:1683–1687.
crossref pmid pmc pdf
15. Li W, Li DD, Yin B, Lin DD, Sheng HS, Zhang N. Successful treatment of pyogenic ventriculitis caused by extensively drug-resistant Acinetobacter baumannii with multi-route tigecycline: a case report. World J Clin Cases 2021;9:651–658.
crossref pmid pmc
16. Huang G, Lai W, Wu D, Huang Q, Zhong Q, Ye X. Two cases report of intrathecal tigecycline therapy for intracranial infection with Acinetobacter baumannii and review of literatures. Infect Drug Resist 2022;15:2211–2217.
crossref pmid pmc pdf
17. Li J, Liu Y, Wu G, Wang H, Xu X. Intravenous plus intraventricular tigecycline-amikacin therapy for the treatment of carbapenem-resistant Klebsiella pneumoniae ventriculitis: a case report. Medicine (Baltimore) 2022;101:e29635.
crossref pmid pmc
18. Wang H, Zhou Q, Huang K, Yang X, Wen L. Intraventricular plus systemic antibiotic therapy for treating polymyxin-resistant Klebsiella pneumoniae ventriculitis: a case report. Open Forum Infect Dis 20225;9:ofac084.
crossref pmid pmc pdf
19. Li Z, An Y, Li L, Yi H. Intrathecal injection of tigecycline and polymyxin B in the treatment of extensively drug-resistant intracranial Acinetobacter baumannii infection: a case report and review of the literature. Infect Drug Resist 2022;15:1411–1423.
crossref pmid pmc pdf
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Antonio Mastroianni

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