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Review Article
ARTICLE IN PRESS
doi:
10.25259/JNRP_72_2024

Parvimonas micra-related spondylodiscitis: A case report and systematic literature review

Department of Aging, Orthopaedic and Rheumatological Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy
Department of Orthopedic and Traumatology, IRCCS Casa Sollievo Della Sofferenza, San Giovanni Rotondo, Italy

*Corresponding author: Calogero Velluto, Department of Aging, Orthopaedic and Rheumatological Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy. calogerovelluto@gmail.com

Licence
This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Mazzella G, Velluto C, Caredda M, Messina F, Perna A, Meluzio M, et al. Parvimonas micra-related spondylodiscitis: A case report and systematic literature review. J Neurosci Rural Pract. doi: 10.25259/JNRP_72_2024

Abstract

The purpose of this study is to report a case of Parvimonas micra-related spondylodiscitis (PMSD) and conduct a systematic review of the literature to identify clinical, microbiologic, and radiographic assessment and treatment outcomes. This research was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. A systematic review of the Literature indexed in PubMed, MEDLINE, and Scopus databases was performed from 1970 to December 2023 using search terms “vertebral,” “spinal,” “infection,” “spondylodiscitis,” “discitis,” “osteomyelitis,” “Parvimonas,” and “micra.” The systematic review identified 34 cases of PMSD in addition to the reported case after the screening of 472 titles and abstracts. Patients reported several clinical presentations, with back pain being the most common symptom. Treatment strategies included antibiotic therapy alone or in combination with surgery, resulting in favorable outcomes for the majority of patients. However, challenges such as delayed diagnosis and lack of standardized treatment protocols were observed. The P. micra is an emerging pathogen in spinal infections, particularly in patients with predisposing factors. This study highlights the need for heightened awareness among healthcare providers regarding the potential role of anaerobic bacteria in spondylodiscitis. Standardized diagnostic and treatment protocols are warranted to improve outcomes for patients with PMSD.

Keywords

Spondylodiscitis
Vertebral osteomyelitis
Parvimonas micra
Anaerobic bacteria
Spinal infections

INTRODUCTION

Pyogenic Spondylodiscitis is uncommon; however, it is associated with several pathological conditions and has a mortality of up to 20%.[1] This condition requires long-term antibiotic therapy and, in some cases, surgical treatment.[2-4] The pathophysiology of spondylodiscitis is linked to the introduction of pyogenic bacteria, either directly during spinal surgery or through the bloodstream, resulting in the infectious deterioration of the vertebral body and intervertebral disc.[5] The incidence of spondylodiscitis, particularly among individuals aged 75 years and older, has considerably increased.[6] The clinical presentation of pyogenic spondylodiscitis typically manifests as back pain or radiating discomfort, followed by fever, neurological deficits, and systemic symptoms such as weight loss and night sweats.[7] Elevation of laboratory parameters, including inflammatory markers such as C-reactive protein, is commonly observed at presentation and tends to correlate with the response to treatment.[8] A microbiological diagnosis of the responsible pathogen is crucial for effective treatment and is linked to improved clinical outcomes.[9] Despite its rarity, anaerobic spondylodiscitis, accounting for <3% of cases of pyogenic vertebral osteomyelitis, should always be considered and pursued through microbiological investigation.[5] Spondylodiscitis is often caused by Gram-positive aerobic bacteria, such as Staphylococcus aureus, with a reported incidence of around 80%.[10] Other pathogens, such as Escherichia coli (a Gram-negative aerobic bacteria) and Mycobacterium tuberculosis, are also reported in the Literature.[11] Anaerobic bacteria are rarely responsible for spondylodiscitis, include Parvimonas micra, a Gram-positive anaerobic coccus (GPAC), typically found in the oral cavity, respiratory system, gastrointestinal tract, and the female genitourinary tract. Originally identified as Peptostreptococcus micros, the organism was reclassified as P. micra in 2006.[12] It is widely recognized as a principal oral pathogen[13,14] and has also been implicated in meningitis,[15] cervical and cerebral abscesses,[16,17] infectious endocarditis,[18] and rarely spondylodiscitis.[19] The aim of this study is to report a case of P. micra-related spondylodiscitis (PMSD) and to conduct a systematic review of the literature to identify clinical, microbiologic, and radiographic assessments, offering insights into treatment options and clinical outcomes.

MATERIALS AND METHODS

This research was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines [Figure 1].[20]

Preferred Reporting Items for Systematic Reviews and Meta-Analyses flow-chart. n: Number of records, GGM: Giovan Giuseppe Mazzella, CV: Calogero Velluto, MC: Matteo Caredda.
Figure 1:
Preferred Reporting Items for Systematic Reviews and Meta-Analyses flow-chart. n: Number of records, GGM: Giovan Giuseppe Mazzella, CV: Calogero Velluto, MC: Matteo Caredda.

Search strategy

A systematic review of the Literature indexed in PubMed, MEDLINE, and Scopus databases, using search terms: “vertebral,” “spinal,” “infection,” “spondylodiscitis,” “discitis,” “osteomyelitis,” “parvimonas,” “micra,” and their medical subject headings (MeSH) terms in any possible combination, using the Boolean operator “AND” and “OR,” was performed from 1970 to December 2023. The search was reiterated until December 15, 2023. The reference lists of relevant studies were screened to identify other studies of interest.

Inclusion and exclusion criteria

Included in this review are studies reporting demographic features, symptoms, diagnostic settings, treatment, possible complications, and outcomes in patients with PMSD. Only articles written in English with available abstracts were included in the study. Excluded from this review were reports of surgical technique, expert opinions, animal studies, unpublished reports, cadaver or in vitro investigations, book chapters, and abstracts from scientific meetings.

Data collection

Two authors (G.G.M and C.V.) independently conducted the research by title and abstract. If the articles met the inclusion criteria, the full text was obtained and subsequently reviewed. Any discordance was resolved through consensus with a third author (M.C.). The reported items/data from the included articles encompassed: the age and gender of the patients, location of the PMSD, type of surgical treatment performed, underlying conditions, presence and location of any abscesses, presence of any immunosuppressive therapy, antibiotic therapy used, duration of antibiotic therapy, outcome, and complications.

Statistical analysis

Numbers software (Apple Inc., Cupertino, CA) was used to tabulate the obtained data. Categorical variables are presented as frequencies and percentages. Continuous variables are expressed as means and standard deviations.

CASE REPORT

In March 2021, a 64-year-old man with a history of Parkinson’s disease and diabetes, treated with L-Dopa, dopamine agonists, and oral hypoglycemic agents, was admitted to our emergency unit due to worsening back pain, associated with urinary incontinence and a walking deficit. He had undergone total hip arthroplasty and total knee arthroplasty in 2001 following multiple fractures from a car accident. A history of chronic low back pain led to an L3-L4 discectomy at another hospital in June 2019, which initially significantly alleviated his symptoms. However, 18 months post-surgery, his low back pain gradually returned and worsened. A magnetic resonance imaging (MRI) conducted 20 days before his current presentation revealed L2-L3-L4 spondylodiscitis with hyperintensity in T2 and STIR sequences [Figure 2].

(a) Sagittal T2 and (b) short T1 inversion recovery (STIR)-weighted images showing hyperintensity of L2, L3, and L4 with alteration of vertebral bodies. (c and d) Axial T2-weighted images showing hyperintensity of the right iliopsoas and of the vertebral body of L4. (e) Coronal T2-weighted view showing L3 collapse with complete disruption of L2-L3 and L3-L4 discs.
Figure 2:
(a) Sagittal T2 and (b) short T1 inversion recovery (STIR)-weighted images showing hyperintensity of L2, L3, and L4 with alteration of vertebral bodies. (c and d) Axial T2-weighted images showing hyperintensity of the right iliopsoas and of the vertebral body of L4. (e) Coronal T2-weighted view showing L3 collapse with complete disruption of L2-L3 and L3-L4 discs.

On arrival at the emergency room, a neurological examination and complete blood tests were performed. He showed no motor deficits in the upper limbs, but hypoesthesia and motor deficits were observed in the right lower limb (3/5 MRC in hip flexion, leg extension, ankle flexion, and extension). Patellar and Achilles reflexes were absent in the right limb. The visual analog scale for back pain was rated 8, and sensory disturbances in the saddle area and loss of visceral functions were noted. The latest MRI scans suggested cauda equina syndrome. Complete blood counts and blood chemistry tests were within normal limits for his age, except for elevated white blood cells at 22.96 × 109/L, neutrophils at 7.75 × 109/L, and mild thrombocythemia (578 × 109/L). Two sets of blood cultures were taken, indicating high inflammation rates with procalcitonin at 0.5 mg/dL and C-reactive protein at 98 mg/dL.

Due to worsening neurological symptoms, decompressive surgery was necessary. Under general anesthesia and in a prone position, a debulking of pseudomembranous tissue with a right L3 laminoarthrectomy was performed, although no purulent material was found. Large biopsy samples were taken for histological and microbiological evaluation. The intraoperative findings suggested a low likelihood of infection; hence, no empirical antibiotic therapy was initiated. The patient was discharged two days later in good clinical and neurological condition, free from back pain.

A post-operative computed tomography (CT) scan was conducted [Figure 3], and a lumbar custom-made brace was prescribed for early mobilization. Close outpatient follow-up was initiated to monitor clinical outcomes. Histological analysis confirmed chronic inflammation, and the intraoperative samples tested positive for P. micra. Consequently, targeted antibiotic therapy with amoxicillin/clavulanate (Augmentin 875/125 mg every 6 h) was initiated. One month post-procedure, neurological examinations showed no signs suggestive of cauda equina syndrome. The patient ceased antibiotic therapy two months later and began weaning from the brace. Conservative treatment continued for three months until a decrease in all inflammatory markers, including C-reactive protein, was observed. At the 12-month follow-up, he was in good health, without neurological signs or limitations in walking. A CT scan confirmed vertebral fusion between L2, L3, and L4 [Figure 4]. The patient’s postoperative follow-up was managed by a multidisciplinary team including a spine surgeon and an infectious disease specialist. Two years post-event, the patient reported no low back pain and an Oswestry Disability Index score of 22%. All procedures performed adhered to the 1964 Helsinki Declaration. Due to the retrospective nature of the research and the use of de-identified patient data, the Institutional Review Board waived the need for ethical review and approval. Written informed consent for scientific purposes and clinical data collection was obtained in accordance with institutional protocols.

(a) Sagittal, (b) coronal, and (c) axial post-operative computed tomography scans of the patient affected by Parvimonas micra-related spondylodiscitis, showing complete structural alteration of L2, L3, and L4 and the presence of laminectomy, as shown in the (c) axial view.
Figure 3:
(a) Sagittal, (b) coronal, and (c) axial post-operative computed tomography scans of the patient affected by Parvimonas micra-related spondylodiscitis, showing complete structural alteration of L2, L3, and L4 and the presence of laminectomy, as shown in the (c) axial view.
(a) Sagittal, (b) coronal, and (c) axial computed tomography scan images at 12 months follow-up, showing vertebral fusion of L2-L3-L4.
Figure 4:
(a) Sagittal, (b) coronal, and (c) axial computed tomography scan images at 12 months follow-up, showing vertebral fusion of L2-L3-L4.

LITERATURE REVIEW

After screening 472 titles and abstracts, we identified 46 papers deemed eligible for full-text analysis. Among these, 24 studies meeting inclusion criteria were ultimately included in the review. In total, including our report, 35 patients affected by PMSD were analyzed in this systematic review.[19,21-43]

Demographical data

The mean age of the included patients was 65.3 (8–86) years. Two (5.7%) were pediatric (<18 years old), and 22 (62.8%) were elderly (>65 years old). Among the included patients, 19 (54.3%) were male, and 16 (45.7%) were female. Demographic and clinical data are presented in Table 1.

Table 1: Demographic data of patients and systematic review.
Author Year Age, years Sex Initial presentation Comorbidities Surgical treatment Antibiotic treatment Primary focus of infection Outcome
Mazzella et al.
(current study)
2024 64 M Lower back pain associated with urinary incontinence and walking deficit Parkinson disease, diabetes, THA, TKA, L3-L4 discectomy Debridement and L3 laminoarthrectomy and decompression Amoxicillin/clavulanate 875/125 mg cpr OS every 6 h for 2 months Unknown No relapse
Kalmoukos et al.[21] 2023 68 F Lower back pain and lower extremities pain Rheumatoid arthritis, Osteoporotic vertebral fractures T12-L1 None Penicillin, clindamycin, 8 weeks Hematogenous No relapse
Paul et al.[22] 2023 70 F Lower back pain Chronic lymphocytic leukemia in remission, autoimmune hemolytic anemia, DM, hypertension, hypothyroidism, right THA T9-L3 stabilization with T12 laminectomy Vancomycin and cefepime 1 week; on 7th day meropenem 1 g 3 times daily, based on the positive Parvimonas micra report Dental caries in the left maxillary molar No relapse
Shimizu et al.[23] 2022 54 M Persistent fever and pulsated headaches Hypertension and stroke None NO (transient bacteremia that resolved spontaneously) History of dental treatment, oral contamination, a painful mouth No relapse
Durovic et al.[24] 2022 82 M Acute immobilizing pain of the lower back and in both shoulder joints Renal failure
Gout
Decompressive spinal surgery due to spinal stenosis in L1-L5
Acute paraplegia resulting from the abscesses, emergency decompression T12–L5 with laminectomy of L2-4 Empiric antibiotic therapy with amoxicillin/clavulanic acid Several tooth root granulomas Death unrelated to spondylodiscitis
69 M Lower back pain for 3 weeks and new hyposensitivity of the left thigh Coronary heart disease
Renal failure
DM II
Previous spinal surgery: decompression and left discectomy L2/3
CT-guided biopsy 14 days of IV amoxicillin/clavulanic acid; oral amoxicillin for an additional 4 weeks A single episode of fever following a tooth extraction 10 days before the back pain began No relapse
72 M Back pain for 2 weeks Parkinson’s disease CT-guided biopsy; followed by an open discectomy with drainage of the abscess Empiric antibiotic therapy with amoxicillin/clavulanic acid; after identification penicillin IV for 2 weeks, and later amoxicillin orally for an additional 4 weeks Dental procedure Not reported
72 F Persistent lower back pain for 6 weeks Metastatic breast cancer with vertebral metastases Fenestration and evacuation of the abscess 5 weeks of IV treatment with amoxicillin/clavulanic acid; oral moxifloxacin for an additional 6 weeks No primary focus of infection Not reported
72 M Lumbago for 3 months Operated for spinal stenosis in L2–5 Two CT-guided biopsies followed by transpedicular biopsy of L5 and the L4-5 disc Penicillin and ertapenem IV for 2 weeks. Clindamycin for a further 12 weeks for treatment of chronic osteomyelitis No primary focus of infection No relapse
63 F Lower back pain for 6 weeks None Transpedicular and disc open biopsy Amoxicillin/clavulanic acid intravenously for 14 days, followed by oral amoxicillin for 6 weeks Persistent inflammation of a molar following a dental procedure Persistent pain
Miyazaki et al.[25] 2019 83 F Lower back pain; tenderness and stabbing pain in his left thigh, accompanied by an erythematous rash Prostatic cancer, DM, hypertension and hyperuricemia None 2 g of meropenem and 1200 mg of clindamycin daily Not identified Died of multiple organ failure on the 3rd day of his hospitalization
Yoo et al.[26] 2019 77 F Acute on chronic lower back pain, aggravated by heavy lifting Cerebrovascular accident, hypertension, hyperlipidemia and osteoporosis Not required surgical intervention IV ceftriaxone 2g once daily and IV metronidazole, dual cover with IV ceftriaxone and oral metronidazole (8-week course of ceftriaxone and 5-week course of metronidazole) Not identified Relapse-free 4 months after discharge
Van Duijvenbode et al.[27] 2018 78 M Severe pain in right leg and in the lumbar spine Bilateral THA, revision of the left THA, left TKA, hypertension, ulcerative colitis Decompression of L2 and L3 and a posterior spondylodesis T12-L5 Vancomycin and ciprofloxacin, after cultures results 12 g daily penicillin IV for 2 weeks, oral clindamycin 600 mg 3 times daily for 4 weeks Laminectomy of L3-L5 performed 1.5 years before, collapse of the vertebral bodies of L2 and L3, compression of right nerve root and spinal stenosis at L3 Occasional back pain at 1 year after surgery
Mizuta et al. 2018 86 F Lower back pain Not reported None Metronidazole 7 weeks Unknown Not reported
Cleaver et al.[28] 2017 45 F 8 week history of lumbar back Klippel–Trenaunay syndrome, copper intrauterine device in situ since 2009 CT-guided vertebral biopsy; 6 days post-biopsy, percutaneous posterior spinal stabilization T10-L3 Empirically postoperatively intravenous teicoplanin, piperacillin-tazobactam and amikacin; IV ertapenem, 1 g once daily, and oral clindamycin, 450mg 4 times daily, for a total of 6 weeks Some years previously, dental cavity filling and some subsequent dental hygienist procedures, but good oral health At 6 week follow-up, no spinal pain, with a tender but non-erythematous operative site
Higashi et al.[30] 2017 67 M Progressive lower back pain for 2 months DM II Blood culture and transcutaneous vertebral biopsy; L4–S1 decompression and instrumented spinal fusion IV ampicillin/sulbactam; on day 19 of admission, ampicillin (8 g/day) until day 72 of admission Periodontitis Recovered
Jones et al.[31] 2015 72 M 4 weeks of back pain None Core biopsy 6 weeks of IV piperacillin+tazobactam, then 2 weeks of oral amoxicillin+clavulanate Uncomplicated tooth extraction 2 months before Relapse-free after 12-month follow-up
72 F 3 months of back pain, without fever or constitutional symptoms Chronic osteoarthritis involving both hips and spine Core biopsy of the T5 vertebral lesion and aspirate of the right paravertebral abscess IV piperacillin+tazobactam for 4 weeks Cervical spinal corticosteroid injections many years prior Relapse-free after 5-month follow-up
George et al.[32] 2015 49 M 3 week history of progressive low back pain Spondylolisthesis with L3-L4 decompression and instrumented spinal fusion 6 months earlier Debridement of soft tissue due to epidural abscess at L2-L3 and removal of the spinal hardware IV ceftriaxone and oral metronidazole for 6 weeks Dental work with tooth extraction Normal inflammatory markers at 3 months follow-up
Gahier et al.[33] 2015 59 F Cervical pain spreading to her left shoulder and asthenia of 6-week duration None None (6 blood cultures) IV gentamicin, metronidazole and amoxicillin later replaced by amoxicillin alone for 14 weeks Dental caries with an apical granuloma Full recovery
82 F Lower back pain None None (blood culture) IV ceftriaxone and gentamicin replaced by amoxicillin for 6 weeks Dental apical granuloma Positive clinical outcome
60 F Persistent lower back pain (2 months) despite a treatment with NSAIDs and morphine None None (blood culture) IV ceftriaxone and gentamicin, later replaced by amoxicillin for 12 weeks Portal of entry not identified Positive clinical and biological outcome
Endo et al.[34] 2015 55 F Lower back pain None Laminoplasty and debridement of the epidural abscess High-dose IV sulbactam/ampicillin (6 g daily) for 6 weeks, followed by oral metronidazole (1500 mg daily) for
10 weeks in total
Dental treatment before the onset of low back pain Complete recovery
Medina et al.[35] 2015 23 F 3-week history of fever associated with headache and dorsal paravertebral myalgia None None Amoxicillin/clavulanic acid; rifampicin/clindamycin for
8 weeks
Hematogenous Successful
Pilmis et al.[36] 2015 83 M Chronic lower back pain without fever Left hip/right knee joint surgery and an ischaemic heart disease Laminectomy L4-L5, four samples removed from the L4 and L5 vertebral bodies IV amoxicillin and gentamicin for fifteen days followed by oral clindamycin and rifampicin for a total duration of
3 months
No tooth infection or any portal of entry including gastrointestinal No relapse was noted in a 6-months follow-up
Dahya et al.[37] 2015 62 M 3-day history of fever, chills and intractable lumbar back pain Hepatitis C, status after liver transplantation,
Spinal stenosis
Degenerative joints disease
None Vancomycin/Ceftriaxone Endocarditis/Hematogenous Successful
Gonzalez et al.[38] 2014 62 M Lumbar back pain and weakness in lower left limb of 6 months duration Hypertension
DM
Right hemiparesis
Aphasia
Percutaneous biopsy T7-T8 Clindamycin for 4 months Unknown Successful
Uemura et al.[19] 2014 83 M Lower back pain of 6-week duration, tenderness over L3 Benign prostatic hypertrophy Surgical biopsy of the vertebral bones 3 g ampicillin-sulbactam every 6 h for 8 weeks, 625 mg oral amoxicillin-clavulanate every 8h for 4 weeks Periodontitis No relapse after 10 months
85 F Worsening malaise, anorexia of 1-month duration Hypertension None, blood culture Empiric doripenem IV for 12 days, IV ampicillin 3 g for
4 weeks, oral amoxicillin 500 mg every 6h for 8 weeks
Periodontitis No relapse
Fraisse et al.[39] 2009 75 M Lower back pain DM, hypercholesterolemia None Amoxicillin/Clavulanic acid+gentamicin, amoxicillin/clindamycin for 12 weeks Hematogenous Successful
Brook[40] 2001 10 M 6 weeks of low back pain, fever, abdominal pain None None Oral amoxicillin Unknown Successful
8 M Low back pain, fever None None Clindamycin Unknown Successful
Leder and Barlam[41] 2000 70 M Lower back pain Ulcerative colitis, osteoarthritis, benign prostatic hypertrophy None Amoxicillin/Metronidazole Paraspinal abscess Successful
Rousseau and Harlé[42] 1998 82 F Not reported None None Amoxicillin Unknown Successful
Papasian et al.[43] 1986 70 M Not reported Cataract operations, TURP, right inguinal herniorrhaphy None Nafcillin-clindamycin, 6 weeks Unknown Successful

THA: Total hip arthroplasty, TKA: Total knee arthroplasty, DM: Diabetes mellitus, TURP: Transurethral resection of the prostate, IV: Intravenous, NSAIDs: Non-steroidal anti-inflammatory drugs.

Localization, presentation symptoms, and underlying conditions

In this literature review of PMSPD, several clinical scenarios are detailed, shedding light on the multifaceted nature of lower back pain associated with PMSD.

The PMSD involved the thoracic spine in three patients (8.6%) and the thoracolumbar spine area in seven patients (20%). The lumbar spine was involved in 20 (79.2%) patients, whereas the cervical spine was involved in two patients (5.7%, Gahier et al. and Medina et al.).[33,35] In one patient, no abnormalities were noted in the CT scan (Shimizu et al.).[23] A single level of spondylodiscitis was reported in 29 cases. On the other side, multi-level involvement was described in four patients. In 25.7% (9 patients), the infection was related to the presence of a paraspinal abscess that affected the psoas muscle. Among these, only one patient showed an intraspinal abscess (Durovic et al.).[24] In one patient, there was extraspinal localization: Miyazaki et al. reported the clinical history of a patient, who exhibited a significant pleural effusion in his left thoracic cavity, necessitating drainage through a thoracotomy tube.[25] Two patients experienced bloodstream infection with severe compromise of organs functionality. The most frequent presentation symptom was low back pain. Notably, the cases by Paul et al. (2023) and Yoo et al. (2019) reported acute exacerbations of lower back pain in individuals with chronic health conditions.[22,26] The study by Shimizu et al. (2022) described a unique case of persistent fever and pulsated headaches in a patient with a history of dental treatment, emphasizing the potential oral origin of PMSD.[23] Medina et al. reported a case of an atypical presentation of Lemierre’s syndrome.[35] Van Duijvenbode’s et al. case (2018) reported a patient with severe leg and lumbar spine pain postoperatively: laminectomy of L3-L5 was performed 1.5 years before his visit, due to lumbar stenosis as a result of degenerative lumbar deformity.[27] Cleaver et al. (2017) reported a case of PMSD related to KlippelTrenaunay syndrome.[29] Twelve patients (34.3%) had no comorbidities at the moment of hospitalization. No patients were immunocompromised, even though Miyazaki et al. reported a history of a patient with a background of prostatic cancer and diabetes mellitus (DM).[25] These conditions might have compromised his immune system and disrupted host defenses, potentially facilitating the entry of P. micra into his bloodstream. The most commonly reported predisposing conditions for PMSPD were previous spine or dental surgeries, although a primary focus of infection was frequently undetermined. In this review, 17 patients (48.6%) had no recorded details regarding the portal of infection. Uemura et al. suggested that advanced age might constitute another significant risk factor for P. micra-induced spondylodiscitis.[19]

Diagnosis

The diagnosis of PMSD varied among the included studies, with six authors, namely, Paul et al., Cleaver et al., Higashi et al., Jones et al., Pilmis et al., George et al., and Medina et al. relying on matrix-assisted laser desorption ionization time-of-flight mass spectrometry for a total of 8 patients (22.8%).[22,29-32,35,36] Shimizu et al., Durovic et al., Gahier et al., and Yoo et al. employed blood cultures for diagnosis, representing 11 patients (31.4%).[23,24,26,33] Van Duijvenbode et al. opted for intraoperative cultures.[27] Miyazaki et al., Endo et al., and Uemura et al. utilized 16S rRNA gene sequencing for three patients (8.6%).[19,25,34] Notably, Uemura et al. additionally utilized isolation by culture (RapID-ANA) in triplicate for one patient (2.85%).[19] However, Mizuta et al., Dahya et al., Gonzalez et al., Fraisse et al., Brook et al., Leder et al., Rousseau et al., and Papasian et al. did not disclose their specific diagnostic approaches in their respective studies.[28,37-43] This diversity underscores the need for standardized diagnostic protocols in the field of PMSD.

Treatment options

Antibiotic therapy alone was administered in 16 patients (45.7%). In 18 patients (51.4%), a combination of medical and surgical treatment was described, while one patient (2.8%) suffered a transient bacteremia resolved spontaneously. In two cases (5.7%), a CT-guided biopsy was performed, in one case a percutaneous biopsy (2.85%, Gonzalez et al.), in four cases (11.4%) a surgical biopsy was reported, in three cases (8.6%) abscess drainage, in four cases (11.4%) posterior decompression, and in five cases (14.3%) posterior decompression and fusion.[38] Combination antibiotic treatment was prescribed in all cases, except one. The most commonly used antibiotic was amoxicillin/clavulanic acid (40%), followed by clindamycin (31.4%) and gentamicin (14.3). In 31 (88.6%) cases, the duration of antibiotic therapy was reported. The mean duration was 61.2 days. Dahya et al., Brook and Rousseau et al. had not reported the duration of therapy.[37,40,42] At the time, the case report was published, antibiotic therapy was still ongoing in no case.

Outcomes

The clinical outcomes were reported in 33 cases (94.3%). Twenty-eight (80%) had a complete recovery: They were relapse free at the last follow-up visit. Three patients (8.6%) complained of persistent lumbar back pain but an improvement in the radiological picture was observed. Two patients (5.7%) died during follow-up from causes unrelated to spondylodiscitis. A complication was reported in one patient: A Clostridium difficile infection occurred three weeks after completion of antimicrobial therapy.[26]

DISCUSSION

The P. micra, a GPAC, typically inhabits the normal oropharyngeal flora. Formerly classified as Peptostreptococcus micros, this bacterium also resides as a commensal in the gastrointestinal and urogenital tracts, though it infrequently leads to serious infections.[12] Infections involving P. micra typically arise within polymicrobial infections, originating from established microbial colonies, and its dissemination through the bloodstream can result in metastatic infections. The literature most commonly documents cases of endodontic infections and oropharyngeal abscesses, with pleural empyema and intra-abdominal abscesses being less common.[13] Papasian et al. reported the first case of vertebral osteomyelitis secondary to P. micra in 1986.[43] Since then, only a few works on this topic can be found in the literature, indicating that PMSDs are a clinical entity still being defined.[27] Most cases of spondylodiscitis result from the blood-borne spread of bacteria originating from remote infection sites, predominantly involving S. aureus, and to a smaller degree, Enterobacteriaceae and Streptococci.[24] Recognizing the causative microorganism of spinal infection is essential for timely and effective management but can be challenging in some cases. Due to the poor sensitivity of blood cultures, specific growth needs and slow propagation of the bacterium, along with negative spinal biopsies, identifying the responsible pathogen often requires several attempts, which can delay treatment.[24] Typically, detecting anaerobic bacteria in spinal biopsies is uncommon, with Cutibacterium acnes and Bacteroides fragilis being the species most frequently found.[44] The elderly population is at the greatest risk of developing spinal infections, and the lumbar area is the most affected. Additional significant risk factors include DM, intravenous drug use, and previous spinal surgeries[11] and recent dental procedures. In a recent systematic review of the literature, Van Duijvenbode et al. suspected an odontogenic focus in 50% of cases;[27] moreover, Durovic et al., in a case series of six patients with PMSD, suspected a dental focus as the source of infection in four out of six patients, with a short rest between dental infection and symptoms of spondylodiscitis, indicating a clear correlation between recent dental procedures and the development of PMSD.[24] The clinical presentation of patients with PMSD is generally a history of worsening back pain, associated or not with mild systemic inflammatory signs. In cases where symptoms are more severe, it is common to administer empiric broad-spectrum antibiotics before pinpointing the infection’s source and identifying the responsible pathogen. According to the 2015 guidelines from the Infectious Diseases Society of America (IDSA), a 6-week course of parenteral antimicrobial treatment is advised for the majority of patients suffering from bacterial vertebral osteomyelitis.[45] In cases of acute neurological compromise or pyogenic abscesses requiring evacuation and drainage, surgical treatment must be associated in addition to targeted antibiotic therapy.[26] MRI of the spine is considered the decisive method for assessing patients exhibiting signs or symptoms that may indicate spondylodiscitis. If results are uncertain, CT-guided biopsies, or open biopsies when necessary, are regarded as the definitive diagnostic tools. The guidelines from the IDSA state that a positive blood culture for S. aureus is adequate to confirm the infection source when spondylodiscitis is identified through MRI.[45] We performed a systematic review of the literature to define a correct diagnostic approach to PMSD that allows for timely treatment, whether pharmacological or surgical, which would improve the prognosis of these patients. The systematic review revealed the increasing incidence of spondylodiscitis, particularly among individuals aged 75 years and older, and emphasizes the importance of timely diagnosis and effective treatment to improve clinical outcomes. The clinical presentation of pyogenic spondylodiscitis typically manifests as back pain or radiating discomfort, along with fever, neurological deficits, and systemic symptoms. Laboratory parameters such as inflammatory markers play a crucial role in diagnosis and treatment response monitoring. Furthermore, while Gram-positive aerobic bacteria, particularly S. aureus, are commonly implicated in spondylodiscitis, our study highlights the rare occurrence of anaerobic spondylodiscitis, with P. micra being identified as one such pathogen. Radiological outcomes in our case report play a pivotal role in the comprehensive evaluation of PMSD, providing crucial insights into disease progression and treatment response. As shown in Figure 2, there was a complete disruption of bone associated with degenerative changes, such as vertebral endplate erosion and disc space narrowing. These findings offer valuable diagnostic clues, while assessments of sagittal and coronal balance highlight mechanical instability and potential neurological compromise. In our case, the patient reported symptoms including radiculopathy and severe back pain, which prompted emergency decompression surgery. Furthermore, in accordance with infectious disease recommendations, antibiotic therapy was initiated along with immobilization using a brace. These radiological and clinical parameters contribute to a holistic approach to managing this challenging condition, guiding therapeutic decisions, and optimizing patient outcomes.

In addressing the distinctive characteristics and clinical considerations of PMSD, our analysis reveals several points of interest that warrant further elucidation in the results section of the manuscript. First, the impact of P. micra on spondylodiscitis appears to diverge from more common pathogens due to its anaerobic nature, potentially contributing to a delayed diagnosis and subsequent treatment initiation, as the organism requires specific conditions for growth and identification in cultures.[19,24,43] Radiologically, PMSD does not present with uniquely distinguishing features when compared to other causes of spondylodiscitis; however, the propensity for abscess formation, particularly paraspinal, may be more pronounced given the anaerobic and polymicrobial tendencies of the infection.[19,26,27] The treatment duration for PMSD, while not inherently longer, must be prudently tailored to each case, often employing a combination of surgical intervention and targeted antibiotic therapy, with the duration guided by the patient’s clinical response and the resolution of symptoms and laboratory markers of infection.[45] P. micra’s role in spondylodiscitis is further underscored by its association with dental procedures, a potential primary source for infection spread through hematogenous routes.[19,24] In addition, risk factors such as prior spinal surgery, immunocompromised states, and the presence of other comorbid conditions play a significant role in the susceptibility to PMSD, delineating the need for heightened vigilance and targeted diagnostic strategies in at-risk patient populations.[11,19,37] Collectively, these insights into the pathogenicity, diagnosis, and management of PMSD contribute to a better understanding of this unique clinical entity, emphasizing the need for prompt and appropriate diagnostic and therapeutic measures to mitigate its impact on patient outcomes.

Thus, a comprehensive evaluation encompassing both radiological outcomes and reported symptoms is essential in the management of PMSD, facilitating timely diagnosis, treatment planning, and monitoring of disease progression. Future research efforts should focus on elucidating the optimal diagnostic modalities, treatment strategies, and outcomes associated with PMSD. Collaborative endeavors are essential to accumulate larger datasets that can inform evidence-based guidelines for the management of this rare but potentially debilitating condition. Ultimately, our study contributes valuable insights to the existing literature and underscores the need for continued vigilance and research in the field of infectious spondylodiscitis, with specific attention to the role of P. micra as a causative pathogen.

CONCLUSION

P. micra is a potential causative agent in spinal infections, particularly in patients with underlying risk factors such as dental or gastrointestinal pathologies. The systematic literature review revealed a limited but growing body of evidence implicating P. micra in spondylodiscitis, emphasizing the need for heightened awareness among spine surgeons. Early detection is crucial for implementing timely and effective therapeutic interventions. In addition, the review sheds light on the diverse treatment approaches reported in the literature, emphasizing the absence of standardized guidelines for managing PMSD.

Acknowledgments

Giovan Giuseppe Mazzella and Calogero Velluto contributed equally.

Authors’ contributions

Conceptualization, GGM, CV, LP. Methodology, GGM, LP. Data curation, GGM, CV. Formal analysis, MCM, CV. Investigation, GGM, CV, FM, MC. Validation, CV, FM, MC, LP. Writing – original draft preparation, GGM, CV. Writing – review and editing GGM, CV. Visualization, FM, MC, LP. Supervision, LP. All authors have read and agreed to the published version of the manuscript.

Ethical approval

The Institutional Review Board has waived the ethical approval for this study.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent.

Conflicts of interest

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

Financial support and sponsorship

Nil.

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