Listeria monocytogenes Brain Abscess: Controversial Issues for the Treatment--Two Cases and Literature Review.
Listeria monocytogenes (LM) is a facultative intracellular Gram-positive bacillus, widely distributed in nature and therefore found in multiple ecological sites, which can cause listeriosis, a serious foodborne bacterial infection . Invasive listeriosis is classified into three forms: bacteraemia, neurolisteriosis, and maternal-neonatal infection. The incidence of listeriosis in the western hemisphere is estimated to be approximately three to six cases per 1 million population per year . Epidemiological studies have identified host risk factors for bacteraemia and neurolisteriosis which include old age, innate and cellular immune deficiencies, cancer, HIV infection, cirrhosis, diabetes mellitus, alcoholism, and immunosuppressive therapies [3-6]. The most common central nervous system manifestation is meningitidis, while meningoencephalitis, rhombencephalitis, and cerebritis are less common . Brain abscesses are extremely rare as they account for approximately 1-10% of CNS listerial infections and are observed in 1% of all listerial infections . There are unresolved issues regarding surgical drainage of the abscess, selection of antibiotic regimen, and optimal treatment duration. We describe two cases (the first without evident immunodeficiency and the second affected by bullous pemphigoid) of brain abscess due to Listeria monocytogenes and discuss them by reviewing the literature on this topic.
2. Case Report
2.1. Case 1. A 62-year-old immunocompetent man with no significant previous medical history was hospitalized for high-grade fever, intractable hiccup, and interscapular pain. On admission, his white blood cell count was 11 x [10.sup.9]/L (normal range 4.50-10.80 [10.sup.3] mmc), his C-reactive protein (CRP) was elevated at 4.30 mg/dl (normal range 0.00-0.75 mg/dl), while his chest radiograph, abdomen ultrasound, and echocardiography were normal. A computed tomography (CT) scan of the brain revealed a diffuse abnormal pattern (presence of a specific inflammatory material) with hypodense lesions located in the trigonum of lateral ventricle in an underlying condition of demyelination and gliosis, suspicious for chronic ischemic vascular disease. A broad-spectrum antibiotic therapy with vancomycin and ceftriaxone was initiated. The patient became afebrile within a few days. A neurological examination found him to be alert and oriented, and he did not have a stiff neck. However, the patient had persistent hiccups and headache. Magnetic resonance imaging (MRI) showed enhancement of both trigeminal nerves and white spot lesions on the pons, cerebral peduncle, midbrain, and thalamus. He was then transferred to the Neurology Department where a lumbar puncture was carried out. His cerebrospinal fluid (CSF) was clear, WBC count was 50 cells/[micro]l, 100% lymphocytes, normal glucose level (normal range 40-70 mg/dl), 103 mg/dl protein (normal range 15-45 mg/dl), and the CSF culture was negative. As a viral etiology was suspected, antibiotic therapy with vancomycin + ceftriaxone was discontinued and treatment with acyclovir and steroid was initiated. After 72 hours, a progressive deterioration of his clinical-neurological condition occurred: he became hyperpyretic and aphasic and Glasgow Coma Score (GCS) was 9. CT brain imaging showed the involvement of the subcortical left temporoparietal lobe, and he was then transferred to the Infectious Disease Department. Blood cultures were performed, and another lumbar puncture was carried out. A cerebrospinal fluid (CSF) analysis showed cloudy CSF with increased spinal column pressure, granulocytic pleocytosis (180 cells/[micro]l, with PMN 90%), normoglychorrachia, and 145 mg/dl spinal fluid protein. A combination antimicrobial therapy with ampicillin 3 g/6 h + gentamicin 80 mg/8 h was initiated; 72 hours later, fever and other systemic signs and symptoms disappeared resulting in complete recovery (GCS15). Listeria monocytogenes were isolated from the patient's blood and recognized from CSF using the molecular technique (Multiplex Real-Time PCR Meningitis/ Encephalitis Filmarray bioMerieux). The patient was treated with intravenous ampicillin for 4 weeks, with combination intravenous gentamicin for the initial 2 weeks and switched to oral trimethoprim/sulfamethoxazole 160/800 mg/8 h for 1 month. An MRI was repeated after 8 weeks of antibiotic therapy due to the persistence of fluent aphasia. MR imaging showed a ring-enhancing lesion in the left frontotemporoparietal lobe, consistent with a brain abscess with significant perilesional edema (Figure 1). Surgical excision of the lesion was performed. Molecular identification of the pus using polymerase chain reaction (PCR) identified DNA of Listeria monocytogenes. The patient was represcribed intravenous ampicillin + gentamicin for 4 weeks, and therapy was then switched to oral trimethoprim/sulfamethoxazole 160/800 mg/12h for further 4 weeks. Patient's condition has improved progressively and with a complete recovery of linguistic abilities.
2.2. Case 2. A 72-year-old man with a history of bullous pemphigoid treated with a monoclonal antibody was admitted to another hospital due to a balance disorder. A neurological examination identified a left hemiplegia with no sensory deficits. An immediate CT brain scan showed a ring-enhancing cortical-subcortical lesion on the right frontal-parietal hemisphere. In view of the CTscan findings, gadolinium MRI of the brain was performed. MRI showed a caudal extension of the lesion with irregular enhancement and a necrotic region (Figure 2). Blood cultures were collected before initiating antimicrobial therapy. A few days later, his blood cultures grew Listeria monocytogenes. Based on organism sensitivity, intravenous therapy with ampicillin 3 g/6 h +gentamicin 80 mg/8 h +vancomycin 1 g/12h was initiated. Steroid therapy was also administered due to the associated moderate mass effect. The patient was then transferred to our Infectious Diseases Department for further workup and management. Forty-eight hours after the initiation of target therapy, the patient was afebrile. Twenty days later, he showed progressive clinical and neurologic deterioration characterized by visual hallucinations, frontal symptoms with disinhibition, and persistent hemiplegia. An MRI brain scan showed a substantial increase in lesion size, and new lesions appeared on splenium of corpus callosum and right temporal lobe with a significant mass effect on the right lateral ventricle. Trimethoprim/sulfamethoxazole 160/800 mg/8 h was added. The patient underwent a surgical biopsy of the lesion. Molecular identification of the brain tissue using PCR identified Listeria monocytogenes DNA. At the follow-up appointment five weeks later, additional imaging studies were performed which showed a considerable reduction in the size and enhancement of the lesions. Ampicillin, gentamicin, and vancomycin therapy was stopped while trimethoprim/sulfamethoxazole therapy was continued. The patient's neurological condition improved. An MRI brain scan performed after 8 weeks of antibiotic therapy, showed significant improvement, with noticeable decrease in the amount of vasogenic edema. Trimethoprim/sulfamethoxazole therapy was discontinued, and the patient was discharged. A year after the listeria brain abscess diagnosis, the patient does not show any significant neurologic deficits and is able to carry out all activities of daily living.
Listeria monocytogenes can invade tissues that are normally resistant to infection, such as the CNS, a gravid uterus, or a fetus. This bacterium reaches the CNS due to hematogenous spread from the gastrointestinal tract . The epithelium of the choroid plexus enables LM to gain access to CNS and causes a meningitides infection. On the other hand, LM may reach the brain parenchyma via the cerebral capillary endothelium, a single layer of brain microvascular endothelial cells characterized by tight junctions. It has been reported that LM-infected macrophages may pass through endothelial cells via the middle cerebral artery resulting in cerebritis which leads to brain abscess formation [10-13].
Furthermore, LM can use a peripheral intraneural route to invade the CNS. A recent animal study suggests that once the bacteria have gained access to the CNS via the peripheral nervous system, the infection can spread along the axons, producing additional lesions by traveling within the axons of the trigeminal nerve [14-16]. According to Bojanowski et al., once inside the CNS, the bacterium may travel along the white fiber tracts of the brain, resulting in a distinct anatomical imaging thus enabling early diagnosis . The spreading of multiple listeria brain abscess within the cerebral nervous system through the intrassonal pathway justified their specific pattern and why they have more detrimental effects than bacterial brain abscess. In our case 1, MRI shows that the spreading follows the arcuate fasciculus. In case 2, the caudal extension of the lesions may also suggest that the lesion follows the projection fiber tracts.
Brain abscesses are extremely rare, accounting for approximately 1-10% of CNS listerial infections. These abscesses are generally located in the subcortical grey matter, especially in the thalamus and basal ganglia [18, 19]. Protection against LM is predominantly cell-mediated. Individuals with impaired cell-mediated immunity are at risk of developing listerial infections .
To the best of our knowledge, only 73 cases of brain abscess caused by L. monocytogenes were reported in the literature between 1968 and 2017. We report further two cases (Table 1) [1, 13, 17, 21-23].
Forty-eight of these patients were male (64%). The mean age of the patients was 51.9, and median age was 55 years (range 0-87 years). Fifty-nine out of 73 had one or more risk factors described in the literature for the development of neurolisteriosis (81%), 15/75 had no risk factors (19%), and in 1 case, nothing was specified. The mortality rate was 27.3%.
Blood cultures were reported for 63 cases: 50/63 were positive (79.5%).
L. monocytogenes was isolated from the CSF or brain abscesses in 31/61 patients (50.8%).
The therapeutic regimen was reported for 67/75 cases, while it is unknown in 8/75.
Twenty-seven out of 67 patients received a monotherapy regimen (40%), while a combination therapy was prescribed for 40/67 (60%) cases: a two-drug therapy was prescribed in 31 cases (50.8%) and a three-drug therapy was administered in 9 cases (14.7%).
The mortality rate in the monotherapy regimen group was 18.5% (five patients out of 27) while the group that received combination therapy showed a 20% mortality rate (eight patients out of 40). Fifty-nine out of 67 patients received a beta-lactam regimen, while 8/59 received a free beta-lactam regimen.
Considering the substantial numerical difference of the two samples, these are not comparable.
Ampicillin was the most commonly prescribed antibiotic as it was administered to 49 patients: in 21 patients, it was prescribed as monotherapy; in 23 cases, it was administered in combination with gentamicin; in 3 cases, it was administered in combination with trimethoprim/sulfamethoxazole while in 2 cases, it was administered in combination with other drugs such as vancomycin or macrolides.
There are currently no guidelines for brain abscess management. Starting from the 2010 consensus on the management and treatment of brain abscesses, we reviewed our case series .
Thirty-nine out of 75 patients underwent neurosurgery (52%). Four out of 31 died (13%). Thirty-four patients out of 75 (45.3%) had only been treated with medical therapy. Of these, 15/34 died (38.2%). In 2 cases, no data have been reported.
Therefore, in our case series, taking into account all of the possible bias, mortality would appear to be significantly higher in the group of patients treated exclusively with medical therapy.
In our opinion, this is a very interesting finding which requires further investigation.
However, as yet, there is no evidence concerning the appropriate duration of therapy for those patients who underwent neurosurgery.
According to a recent consensus study, antimicrobial treatment for brain abscesses should generally last 6-8 weeks and treatment for those undergoing neurosurgery should last 4-6 weeks .
From our literature review, the duration of therapy was known in 36/75 patients. Sixteen out of 36 received less than or equal to 6 weeks while 20/36 patients were treated for 8 weeks or more. Of the group of patients who received [less than or equal to] 6 weeks of therapy, 4/16 (25%) underwent neurosurgery, while of those belonging to the group who received [greater than or equal to] 8 weeks, 16/20 (80%) underwent neurosurgery.
A 12.5% mortality rate was observed for the first group while 0% died in the second group, thus suggesting that a combination of surgery and prolonged medical therapy has a positive impact on mortality.
We believe that it is essential to carry out this review as brain abscesses are rare, and there are no definitive guidelines on the optimal management, type, and duration of therapy. LM infection should also be suspected in immunocompetent patients, and new molecular biology techniques play key roles in the early diagnosis of this rare pathology.
In our literature review, we found that listeria brain abscess is not related to advanced age and that it is related to high mortality (27.3%).
Diagnosis should not be suspected only in immunocompromised patients as it was found in 20% of patients who had no risk factor.
Blood cultures were positive in more than 80% of cases. Most patients received a beta-lactam regimen, and mortality appears to be lower in patients treated with combination regimens.
This result looks certainly very interesting and should be explored with dedicated studies (i.e., sharp difference in mortality between the group undergoing neurosurgery and the group that only received medical therapy). Furthermore, the specific pattern of brain diffusion, reported and highlighted in our two clinical cases, should be considered when this diagnosis is hypothesized.
Conflicts of Interest
The authors declare that there are no conflicts of interest regarding the publication of this article.
 S. Limmahakhun and M. Chayakulkeeree, "Listeria monocytogenes brain abscess: two cases and review of the literature," Southeast Asian Journal of Tropical Medicine and Public Health, vol. 44, no. 3, pp. 468-478, 2013.
 P. Pagliano, T. Ascione, G. Boccia, F. De Caro, and S. Esposito, "Listeria monocytogenes meningitis in the elderly: epidemiological, clinical and therapeutic findings," Le Infezioni in Medicina, vol. 24, no. 2, pp. 105-111, 2016.
 C. M. De Noordhout, B. Devleesschauwer, F. J. Angulo et al., "The global burden of listeriosis: a systematic review and meta-analysis," The Lancet Infectious Diseases, vol. 14, no. 11, pp. 1073-1082, 2014.
 P. Pagliano, F. Arslan, and T. Ascione, "Epidemiology and treatment of the commonest form of listeriosis: meningitis and bacteraemia," Le Infezioni in Medicina, vol. 25, no. 3, pp. 210-216, 2017.
 C. Charlier, E. Perrodeau, A. Leclercq et al., "Clinical features and prognostic factors of listeriosis: the MONALISA national prospective cohort study," The Lancet Infectious Diseases, vol. 17, no. 5, pp. 510-519, 2017.
 J. A. Vazquez-Boland, M. Kuhn, P. Berche et al., "Listeria pathogenesis and molecular virulence determinants," Clinical Microbiology Reviews, vol. 14, no. 3, pp. 584-640, 2001.
 S. Morosi, D. Francisci, and F. Baldelli, "A case of rhombencephalitis caused by Listeria monocytogenes successfully treated with linezolid," Journal of Infection, vol. 52, no. 3, pp. e73-e75, 2006.
 B. Lorber, "Listeriosis," Clinical Infectious Diseases, vol. 24, no. 1, pp. 1-11, 1997.
 J. A. Vazquez-Boland, E. Krypotou, and M. Scortti, "Listeria placental infection," mBio, vol. 8, no. 3, article e00949-17, 2017.
 O. Disson and M. Lecuit, "Targeting of the central nervous system by Listeria monocytogenes," Virulence, vol. 3, no. 2, pp. 213-221, 2012.
 D. A. Drevets and M. S. Bronze, "Listeria monocytogenes: epidemiology, human disease, and mechanisms of brain invasion," FEMS Immunology & Medical Microbiology, vol. 53, no. 2, pp. 151-165, 2008.
 D. Schluter, S. Chahoud, H. Lassmann, A. Schumann, H. Hof, and M. Deckert-Schluter, "Intracerebral targets and immunomodulation of murine Listeria monocytogenes meningoencephalitis," Journal of Neuropathology and Experimental Neurology, vol. 55, no. 1, pp. 14-24, 1996.
 L. A. Cone, M. M. Leung, R. G. Byrd, G. M. Annunziata, R. Y. Lam, and B. K. Herman, "Multiple cerebral abscesses because of Listeria monocytogenes: three case reports and a literature review of supratentorial listerial brain abscess(es)," Surgical Neurology, vol. 59, no. 4, pp. 320-328, 2003.
 L. Dons, K. Weclewicz, Y. Jin, E. Bindseil, J. E. Olsen, and K. Kristensson, "Rat dorsal root ganglia neurons as a model for Listeria monocytogenes infections in culture," Medical Microbiology and Immunology, vol. 188, no. 1, pp. 15-21,1999.
 C. Guldimann, B. Lejeune, S. Hofer et al., "Ruminant organotypic brain-slice cultures as a model for the investigation of CNS listeriosis," International Journal of Experimental Pathology, vol. 93, no. 4, pp. 259-268, 2012.
 A. Oevermann, S. Di Palma, M. G. Doherr, C. Abril, A. Zurbriggen, and M. Vandevelde, "Neuropathogenesis of naturally occurring encephalitis caused by Listeria monocytogenes in ruminants," Brain Pathology, vol. 20, no. 2, pp. 378-390, 2010.
 M. W. Bojanowski, R. Seizeur, K. Effendi, P. Bourgouin, E. Magro, and L. Letourneau-Guillon, "Spreading of multiple Listeria monocytogenes abscesses via central nervous system fiber tracts: case report," Journal of Neurosurgery, vol. 123, no. 6, pp. 1593-1599, 2015.
 R. Bartt, "Listeria and atypical presentations of Listeria in the central nervous system," Seminars in Neurology, vol. 20, no. 3, pp. 361-373, 2000.
 S. Matano, S. Satoh, Y. Harada, H. Nagata, and T. Sugimoto, "Antibiotic treatment for bacterial meningitis caused by Listeria monocytogenes in a patient with multiple myeloma," Journal of Infection and Chemotherapy, vol. 16, no. 2, pp. 123-125, 2010.
 O. Leiti, J. W. Gross, and C. U. Tuazon, "Treatment of brain abscess caused by Listeria monocytogenes in a patient with allergy to penicillin and trimethoprim-sulfamethoxazole," Clinical Infectious Diseases, vol. 40, no. 6, pp. 907-908, 2005.
 Y. Maezawa, A. Hirasawa, T. Abe et al., "Successful treatment of listerial brain abscess: a case report and literature review," Internal Medicine, vol. 41, no. 11, pp. 1073-1078, 2002.
 P. B. Eckburg, J. G. Montoya, and K. L. Vosti, "Brain abscess due to Listeria monocytogenes: five cases and a review of the literature," Medicine, vol. 80, no. 4, pp. 223-235, 2001.
 Y. Samra, M. Hertz, and G. Altmann, "Adult listeriosis-a review of 18 cases," Postgraduate Medical Journal, vol. 60, no. 702, pp. 267-269, 1984.
 M. Arlotti, P. Grossi, F. Pea et al., "Consensus document on controversial issues for the treatment of infections of the central nervous system: bacterial brain abscesses," International Journal of Infectious Diseases, vol. 14, no. 4, pp. S79-S92, 2010.
Beatrice Tiri (iD), (1) Giulia Priante, (1) Lavinia Maria Saraca, (1) Lucia Assunta Martella, (2) Stefano Cappanera, (2) and Daniela Francisci (1)
(1) Infectious Diseases Clinic, Department of Medicine, University of Perugia, Perugia, Italy
(2) Infectious Diseases Clinic, Department of Medicine, "S. Maria" Hospital, Terni, Italy
Correspondence should be addressed to Beatrice Tiri; firstname.lastname@example.org
Received 12 March 2018; Revised 11 June 2018; Accepted 8 July 2018; Published 24 July 2018
Academic Editor: Tomoyuki Shibata
Caption: Figure 1: MR image showing the evolution of the ring-enhancing lesion in the left fronto-temporoparietal lobe in a brain abscess with significant perilesional edema.
Caption: Figure 2: MR image showing a caudal extension of the lesion with irregular enhancement with irregular enhancement and a necrotic region (FLAIR/long TR).
Table 1: Seventy-three cases of brain abscess caused by Listeria monocytogenes reported in the literature between 1968 and 2017 (we described two other cases). CSF/ Age/ Underlying brain N. sex diseases Blood abscess 1 70/M Myasthenia + - gravis in immunosuppressive TP 2 57/F Cirrhosis; DM + + 3 60/M DM; rheumatoid - + arthritis methotrexate 4 52/M OLT in HCC + + secondary to hepatitis C and alcoholic cirrhosis; cyclosporine 5 56/F Primary biliary + + cirrhosis; OLT; tacrolimus, azathioprine, prednisone 6 42/M None + + 7 47/F SLE; - + mycophenolate 8 16/F SLE; + - mycophenolate 9 81/M Myelodys plastic + + syndrome; basal cell skin carcinoma, prostate cancer treated 10 52/F DM, + - hypothyroidism, prednisolone, azathioprine 11 81/F DM NR + 12 74/F DM + NR 13 32/F LAC + NR 14 72/M None - + 15 52/M Inflammatory + - myositis treated with prednisolone and azathioprine 16 70/M Alcoholism + + 17 56/M AIDS + - 18 49/M Rheumatic fever, + - alcoholism, DM 19 64/M DM, aortic valve + - replacement 20 71/M DM, rheumatic + - heart disease 21 56/M AIDS + - 22 70/F Cirrhosis, DM, + ND heart failure 23 25/F Ulcerative NR NR colitis 24 87/M None + + 25 63/M None + - 26 24/M None + - 27 53/F None + - 28 63/F None - - 29 43/F None - - 30 39/M None NR - 31 54/F None NR NR 32 1 + None NR NR 1/4/M 33 70/M NONE - + 34 53/M Cirrhosis, + - seizure 35 85/M DM + - 36 43/M OSAS, + - alcoholism 37 0/M Pronatis + - 38 63/M MM + - 39 61/M DM NR NR 40 60/M HIV NR + 41 68/M Leukemia NR NR 42 NR/M None NR NR 43 2/M NR NR + 44 49/M Renal + + transplant 45 16/M ALL + + 46 20/M ALL + + 47 6/F ALL + + 48 46/F Ulcerative + + colitis 49 58/F SLE + - 50 58/F Immunoblastic + - lymphadenopathy 51 65/M DM + NR 52 19/M Juvenile NR + rheumatoid arthritis, tetralogy of Fallot 53 55/M Renal transplant + - 54 45/M Renal transplant + - 55 60/F Rheumatoid + - arthritis 56 66/F AML, Crohn's + + disease 57 47/M AIDS + - 58 54/F Sarcoidosis + - 59 23/F ITP + - 60 58/M MM + - 61 55/M Glioblastoma - + multiforme 62 51/M Cardiac + + transplant 63 37/M Cardiac + + transplant 64 56/F Primary biliary + + cirrhosis 65 50/M Sarcoidosis - + 66 51/F Crohn's - + disease 67 50/M Cardiac - + transplant, DM 68 75/M None ND 69 77/M CLL - NR 70 58/M CLL - + 71 Child ALL NR NR 72 68/F Breast cancer + ND 73 47/F Evans syndrome, + - SLE, DM Case 62/M None + + 1 Case 72/M Bullous + + 2 pemphigoid Surgery/ Duration N. type Antibiotic of therapy 1 ND Ampicillin + 6 weeks gentamicin; ampicillin + trimethoprim/ gentamicin for sulfamethoxazole 10 days trimethoprim/ sulfamethoxazole 2 Biopsy Ampicillin + NR gentamicin (a) Amoxicillin + (a) 17 days trimethoprim/ sulfamethoxazole 3 ND (b) Trimethoprim/ (b) 20 days sulfamethoxazole (c) Linezolid (c) 33 days (d) Amoxicillin (d) NR 4 Craniotomy Ampicillin + 3 weeks with resection gentamicin + (gentamicin of the lesion penicillin G only for 2 weeks) 5 Biopsy Ampicillin + 8 weeks gentamicin (gentamicin only for 2 weeks) 6 Biopsy and Ampicillin + NR drainage gentamicin + meropenem 7 ND Ampicillin 6 weeks 8 External Trimethoprim/ 13 weeks ventricles sulfamethoxazole trimethoprim/ device + ampicillin sulfamethoxazole; + meropenem ampicillin for 4 weeks; meropenem for 5 weeks (total of 22 weeks) 9 Craniotomy with Ampicillin NR resection of the lesion 10 Biopsy Ampicillin + 6 weeks gentamicin 11 Biopsy Ampicillin 8 weeks 12 NR Vancomycin + NR ampicillin + ceftriaxone 13 NR Ampicillin + 8 weeks; trimethoprim/ linezolid sulfamethoxazole for 10 days + linezolid 14 ND Ampicillin NR 15 ND Ampicillin 6 weeks 16 ND Ampicillin + 3-6 weeks gentamicin + vancomycin 17 ND Ampicillin + Article not gentamicin available 18 ND Penicillin G + NR streptomycin + tetracycline 19 ND Ampicillin + 4 weeks + gentamicin ampicillin for 2 weeks 20 ND Ampicillin + NR gentamicin 21 ND Ampicillin + Article not gentamicin available 22 ND Ampicillin + Article not trimethoprim/ available sulfamethoxazole 23 ND NR NR 24 ND Penicillin G + NR chloramphenicol 25 ND Ampicillin NR 26 ND Ampicillin + 6 weeks, gentamicin gentamicin only for 10 days 27 ND Minocycline, 2 weeks gentamicin 28 ND NR NR 29 ND Ampicillin NR 30 ND NR NR 31 ND NR NR 32 ND Amoxicillin Article not available 33 Craniectomy Ampicillin NR and open biopsy 34 + Penicillin G + Article not erythromycin available 35 + Ampicillin Article not available 36 + NR Article not available 37 + Ampicillin + Article not gentamicin available 38 Biopsy (a) Ampicillin (a) 5 weeks (b) Linezolid + (b) 15 weeks rifampin 39 Biopsy Trimethoprim/ 3 weeks, sulfamethoxazole + trimethoprim/ chloramphenicol sulfamethoxazole alone for 20 weeks 40 Craniotomy and Penicillin G + NR intraoperative chloramphenicol cultures 41 ND Chloramphenicol NR 42 ND NR NR 43 Craniotomy with NR NR resection of the lesion 44 ND Chloramphenicol NR 45 ND Penicillin G + NR chloramphenicol 46 ND Ampicillin + 8 weeks chloramphenicol + erythromycin, gentamicin 47 ND Ampicillin, NR vancomycin, netilmicin 48 ND Ampicillin, 8 weeks, gentamicin 4 weeks 49 ND Penicillin G + ARTICLE NOT tobramycin AVAILABLE 50 ND Ampicillin 8 weeks 51 ND Ampicillin + 4 weeks gentamicin 52 ND Vancomycin + Article not ampicillin available 53 + Ampicillin Article not available 54 Craniotomy Ampicillin 10 weeks and drainage 55 Biopsy Ampicillin, 8 weeks, amoxicillin 24 months 56 Biopsy Ampicillin 4 weeks 57 Craniotomy Ampicillin, NR gentamicin, vancomycin 58 Biopsy Ampicillin + NR gentamicin 59 Drainage of Trimethoprim/ 12 months the abscess sulfamethoxazole 60 Craniotomy (a) Trimethoprim/ (a) 12 weeks and drainage sulfamethoxazole + (gentamicin gentamicin only 2 weeks) (b) Trimethoprim/ (b) 5 months sulfamethoxazole 61 Biopsy Amoxicillin + 12 weeks gentamicin 62 Stereotactic Ampicillin + 6 weeks, brain aspiration gentamicin gentamicin only 2 weeks 63 Craniotomy with penicillin G 8 weeks resection of the lesion 64 Biopsy Ampicillin + 6 weeks gentamicin gentamicin only 2 weeks 65 Craniotomy Trimethoprim/ Article not sulfamethoxazole available 66 Biopsy Ampicillin + 12 weeks gentamicin (gentamicin not reported) 67 Biopsy and Ampicillin + 18 weeks of aspiration gentamicin ampicillin; 14 weeks gentamicin 68 + Ampicillin + Article not gentamicin available 69 + Chloramphenicol Article not available 70 Biopsy Ampicillin + 6 weeks gentamicin 71 + NR Article not available 72 Biopsy Ampicillin, 10 weeks, amoxicillin 24 weeks 73 ND Ampicillin, 6 weeks, NR amoxicillin Case Craniotomy with (a) Ampicillin + (a) 8 weeks 1 resection of gentamicin (gentamicin the lesion (b) Trimethoprim/ only 4 weeks) sulfamethoxazole (b) 8 weeks Case Biopsy (a) Ampicillin + (a) 5 weeks 2 gentamicin + (b) 3 weeks trimethoprim/ sulfamethoxazole (b) Trimethoprim/ sulfamethoxazole N. Outcome References 1 Survived Chalouhi et al., 2013 2 Died Matera et al., 2012 3 Survived Coste et al., 2012 4 Survived Choudhury et al., 2013 5 Survived Tseng et al., 2013 6 Survived Beynon et al., 2013 7 Survived Horta-Baas et al., 2013 8 Survived Perini et al., 2014 9 Survived West et al., 2015 10 Survived Al-Harabi et al., 2015 11 Survived Dejesus-Alvelo et al., 2015 12 Survived Bojanowski et al.  13 Survived Fervienza et al., 2016 14 Survived Mano et al., 2017 15 Survived Onder et al., 2016 16 Died Cone et al.  17 Survived Patey et al., 1989 18 Died Buchner and Schneierson, 1968 19 Survived Soto and Sliman, 1992 20 Died Eckburg et al.  21 Survived Patey et al., 1989 22 Died Sivalinga et al., 1992 23 Died Larsson and Linell, 1979 24 Died Spilkin et al., 1968 25 Died Kennard et al., 1979 26 Survived Smiatacz et al., 2006 27 Survived Mrowka et al., 2002 28 Died Brun-Buisson et al., 1985 29 Died Brun-Buisson et al., 1985 30 Died Kwantes and Isaac, 1971 31 Died Larsson and Linell, 1979 32 Survived Mancini et al., 1990 33 Survived Salgado et al., 1996 34 Survived Halkin et al., 1971 35 Died Brown et al., 1991 36 Survived Douen and Bourque, 1997 37 Survived Banerji and Noya, 1999 38 Survived Leiti et al.  39 Survived Sjostrom et al., 1995 40 Died Harris et al., 1989 41 Died Larsson et al., 1978 42 Died Pollock et al., 1984 43 Survived Umenai et al., 1978 44 Died Crocker and Leicester, 1976 45 Survived Dykes et al., 1979 46 Survived Hutchinson and Heyn, 1983 47 Survived Viscoli et al., 1991 48 Survived Soares-Fernandes et al., 2008 49 Survived Takano et al., 1999 50 Survived Maezawa et al.  51 Died Wu et al., 2010 52 Survived Turner et al., 1995 53 Survived Lechtenberg et al., 1979 54 Survived Stam et al., 1982 55 Survived Updike et al., 1990 56 Survived Eckburg et al.  57 Died Cone et al.  58 Died Ackermann et al., 2001 59 Survived Treebupachatsaul et al., 2006 60 Survived Al-Khatti and Al-Tawfiq, 2010 61 Survived Ganiere et al., 2006 62 Survived Eckburg et al.  63 NR Eckburg et al.  64 Survived Cone et al.  65 Survived Poropatich and Phillips, 1992 66 Survived Stefanovich et al., 2010 67 Survived Eckburg et al.  68 Survived Mylonakis et al., 1998 69 NR Cleveland and Gelfand, 1993 70 Survived Dee and Lorber, 1986 71 Survived An tunes et al., 1998 72 Survived Limmahakhun and Chayakulkeeree  73 Survived Limmahakhun and Chayakulkeeree  Case Survived 1 Case Survived 2
|Printer friendly Cite/link Email Feedback|
|Title Annotation:||Case Report|
|Author:||Tiri, Beatrice; Priante, Giulia; Saraca, Lavinia Maria; Martella, Lucia Assunta; Cappanera, Stefano;|
|Publication:||Case Reports in Infectious Diseases|
|Date:||Jan 1, 2018|
|Previous Article:||Corrigendum to "Community-Acquired Cavitary Pseudomonas Pneumonia Linked to Use of a Home Humidifier".|
|Next Article:||Actinomyces europaeus Isolated from a Breast Abscess in a Penicillin-Allergic Patient.|