Splenic abscess caused by Cutibacterium acnes in a patient with multiple tooth extractions

  1. Madalyn Walsh 1,
  2. Nicholas Wasko 2,
  3. Andrew Joseph Simms 3 and
  4. Jacob Hodges 3
  1. 1 Internal Medicine, The University of Iowa Hospitals and Clinics, Iowa City, Iowa, USA
  2. 2 Internal Medicine—Neurology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa, USA
  3. 3 Internal Medicine—Infectious Diseases, The University of Iowa Hospitals and Clinics, Iowa City, Iowa, USA
  1. Correspondence to Dr Madalyn Walsh; madalyn-walsh@uiowa.edu

Publication history

Accepted:30 Nov 2022
First published:25 Jan 2023
Online issue publication:25 Jan 2023

Case reports

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Abstract

A woman in her 40s with a history of dental abscess presenting with a 3-month history of nightly fevers, malaise, fatigue and acutely worsening left flank pain was found to have a splenic abscess replacing almost the entire splenic parenchyma on abdominal CT. Abscess aspirate showed Gram-positive rods, and both aerobic and anaerobic cultures grew Cutibacterium acnes (previously Propionibacterium acnes), a common member of the skin microbiome. Prior case reports of C. acnes splenic abscess all involved parental inoculation via needle use. However, in the context of no percutaneous needle exposure and multiple tooth extractions immediately preceding her symptoms, the most likely source of her infection is oral flora with haematogenous or lymphatic spread to the spleen.

Background

Splenic abscesses are a relatively uncommon pathology but can be associated with mortality as high as 27.6%.1 The most common aetiology of splenic abscess is haematogenous spread from a distal infection, or seeding of the spleen in the context of transient or persistent bacteraemia, such as in infective endocarditis or septicemia.1 Risk of developing a splenic abscess increases in the context of immunosuppression, including diabetes mellitus or traumatic injury to the spleen.1–3 Subcutaneous or intravenous needle use provides an opportunity for commensal skin microbes to access circulation and form abscesses in vulnerable patients. Additionally, dental procedures can cause transient exposure of oral flora to the bloodstream, necessitating peri-procedural antibiotics in patients with high-risk comorbidities.4 Here, we describe the first splenic abscess caused by the oral and skin commensal microbe C. acnes that is attributable to a dental procedure, rather than percutaneous inoculation.

Case presentation

A woman in her 40s with a history of hypertension and type 2 diabetes mellitus (not using insulin) presented with a 3-month history of persistent nightly fevers, malaise, fatigue and acutely worsening left flank pain. She underwent extractions of tooth number 13 and number 14 due to dental abscesses 3 months prior to presentation. She received one peri-operative dose of intravenous ampicillin/sulbactam and a 7-day course of amoxicillin/clavulanic acid prescribed for treatment of her dental abscess. Shortly after the extraction, she began having recurrent nightly fevers, malaise and left flank pain. She presented to her local emergency department with severe left flank pain, and abdominal CT revealed a splenic abscess replacing almost the entire splenic parenchyma (figure 1A) as well as extensive non-occlusive thromboses throughout portal venous system. She denied intravenous drug use, insulin use or any other needle exposure outside of her dental procedures in the past 6 months. The patient was started on broad-spectrum antibiotic therapy with intravenous piperacillin-tazobactam, vancomycin and metronidazole and was transferred to our academic centre.

Figure 1

(A) Coronal CT abdomen with contrast showing splenic abscess. Notable for gas throughout splenic parenchyma. (B) Coronal CT abdomen after percutaneous drain placement. Drain resulted in 1.1 L of purulent fluid aspiration. (C) Pathology slide of necrotic spleen. Notable for loss of splenic architecture, few Gram-positive rods.

Investigations

Physical examination revealed left abdominal and flank tenderness as well as a newly recognised systolic murmur. Laboratory studies were significant for: elevated while cell count, 20 900/µL; platelet count,1.048/L; INR, 1.1; haemoglobin, 7.5 g/dL; glucose, 255 mg/dL; haemoglobin A1c, 12.9%. She underwent drain placement with interventional radiology. Given her concurrent dental infection at the time when constitutional symptoms began, antibiotics were narrowed to ampicillin–sulbactam to focus coverage on odontogenic sources. Abscess aspirate grew many Gram-positive rods, and anaerobic culture grew C. acnes within 48 hours of sample collection. Aerobic culture later also grew C. acnes; no other organisms grew in culture. Blood cultures were obtained but did not grow any organisms. Transoesophageal echocardiogram was obtained to evaluate for endocarditis given new murmur but showed no evidence of valvular disease. Patient remained febrile every night and showed little clinical improvement, so drain size was increased with 1.1 L of purulent drainage. She continued to have high abscess burden on abdominal CT.

Treatment

The patient underwent splenectomy for definitive treatment for her infection, though significant necrosis made formal splenic resection impossible; she required debridement of the capsule, copious washouts and drain placement in the splenic cavity. Surgical pathology revealed necrotic non-viable tissue with numerous bacterial aggregates consistent with necrotic splenic tissue. Postoperative care was complicated by segmental and subsegmental pulmonary embolisms, which were treated with apixaban. Due to concern for recurrent splenic abscess, a drain was placed in the splenic space.

Outcome and follow-up

The patient was discharged with her drain and a peripherally inserted central catheter in place and was prescribed 2 g ceftriaxone intravenous and 500 mg metronidazole for 4 weeks.

Discussion

Abscesses can form in any organ, but splenic abscesses make up a minority of cases, with an estimated frequency between 0.1% and 0.7%.3 5 Splenic abscesses arise via inoculation from outside sources, including haematogenous spread of remote infection (eg, infective endocarditis), contiguous infection, trauma and embolic events with subsequent infection.1 3 Case series indicate Gram-positive cocci (Streptococcus viridans, Staphylococcus aureus, Enterococcus species), Gram-negative rods (Escherichia coli, Klebsiella pneumoniae, Pseudomonas species, Salmonella species) and Mycobacterium tuberculosis are among the most frequent culprit organisms.2 5 Including the present report, only six cases of splenic abscess caused by C. acnes have ever been described in the literature as described in table 1.5–9

Table 1

A summary of case reports concerning Propionibacterium acnes splenic abscesses

Case number Year Age, years Sex Risk factors Antibiotic therapy and duration Surgical intervention Outcome
*This was a retrospective study encompassing 67 individual patients that did not include details about specific cases.
1 1981 27 Male Sickle cell trait, intravenous drug use6 Intravenous penicillin Splenectomy Survived
2 1982 59 Male Diabetes with subcutaneous insulin therapy7 Intravenous penicillin Splenectomy Survived
3* 2006 NA NA NA5 NA NA Survived
4 2013 64 Male Chronic lymphocytic leukaemia8 Levofloxacin Splenectomy Survived
5 2017 64 Female Diabetes with subcutaneous insulin therapy, intravenous and subcutaneous drug use9 Clindamycin Splenectomy Survived
Presenting case 2022 40s Female Metronidazole, Ceftriaxone Metronidazole, Ceftriaxone Splenectomy Survived

Ethics statements

Patient consent for publication

Footnotes

  • Contributors MW was the general medicine resident caring for patient, drafted and revised portions of the manuscript, submitted the manuscript for publishing. NW was the infectious disease resident caring for patient, drafted and revised portions of the manuscript. AJS was the infectious disease fellow caring for patient, obtained and formatted figures, revised manuscript. JH was the staff physician caring for patient, revised manuscript, gave insight into publishing and journal selection.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

References

    1. Lee MC
    . Splenic abscess: an uncommon entity with potentially life-threatening evolution. Can J Infect Dis Med Microbiol 2018;2018. doi:10.1155/2018/8610657
    1. Llenas-García J ,
    2. Fernández-Ruiz M ,
    3. Caurcel L , et al
    . Splenic abscess: a review of 22 cases in a single institution. Eur J Intern Med 2009;20:537–9. doi:10.1016/j.ejim.2009.04.009
    1. Nelken N ,
    2. Ignatius J ,
    3. Skinner M , et al
    . Changing clinical spectrum of splenic abscess. A multicenter study and review of the literature. Am J Surg 1987;154:27–34. doi:10.1016/0002-9610(87)90285-6
    1. Suda KJ ,
    2. Calip GS ,
    3. Zhou J , et al
    . Assessment of the appropriateness of antibiotic prescriptions for infection prophylaxis before dental procedures, 2011 to 2015. JAMA Netw Open 2019;2:e193909. doi:10.1001/jamanetworkopen.2019.3909
    1. Chang K-C ,
    2. Chuah S-K ,
    3. Changchien C-S , et al
    . Clinical characteristics and prognostic factors of splenic abscess: a review of 67 cases in a single medical center of Taiwan. World J Gastroenterol 2006;12:460–4. doi:10.3748/wjg.v12.i3.460
    1. Gangahar DM ,
    2. Delany HM
    . Intrasplenic abscess: two case reports and review of the literature. Am Surg 1981;47:488–91.
    1. Gekowski KM ,
    2. Lopes R ,
    3. LiCalzi L , et al
    . Splenic abscess caused by Propionibacterium acnes. Yale J Biol Med 1982;55:65–9.
    1. Kiritani S ,
    2. Kaneko J ,
    3. Aoki T , et al
    . Multiple splenic nodules with fever: a case of splenic abscess due to Propionibacterium acnes. Clin J Gastroenterol 2013;6:434–7. doi:10.1007/s12328-013-0427-5
    1. Mohammed S ,
    2. Kollu VS
    . Rare case of Propionibacterium acnes-related splenic abscess. BMJ Case Rep 2018;2018:bcr2018225858. doi:10.1136/bcr-2018-225858
    1. Mayslich C ,
    2. Grange PA ,
    3. Dupin N
    . Cutibacterium acnes as an opportunistic pathogen: an update of its virulence-associated factors. Microorganisms 2021;9:303. doi:10.3390/microorganisms9020303
    1. Perry A ,
    2. Lambert P
    . Propionibacterium acnes: infection beyond the skin. Expert Rev Anti Infect Ther 2011;9:1149–56. doi:10.1586/eri.11.137
    1. Niazi SA ,
    2. Clarke D ,
    3. Do T , et al
    . Propionibacterium acnes and Staphylococcus epidermidis isolated from refractory endodontic lesions are opportunistic pathogens. J Clin Microbiol 2010;48:3859–69. doi:10.1128/JCM.01326-10
    1. Niazi SA ,
    2. Al Kharusi HS ,
    3. Patel S , et al
    . Isolation of Propionibacterium acnes among the microbiota of primary endodontic infections with and without intraoral communication. Clin Oral Investig 2016;20:2149–60. doi:10.1007/s00784-016-1739-x
    1. McDowell A ,
    2. Valanne S ,
    3. Ramage G , et al
    . Propionibacterium acnes types I and II represent phylogenetically distinct groups. J Clin Microbiol 2005;43:326–34. doi:10.1128/JCM.43.1.326-334.2005

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