# Unusual Cutibacterium acnes splenic abscess with bacteremia in an immunocompetent man: phylotyping and clonal complex analysis

Angèle Roudeau, Stéphane Corvec, Beate Heym, Louise Ruffier D'epenoux,
Olivier Lidove, Valérie Zeller

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► To cite this version:

Angèle Roudeau, Stéphane Corvec, Beate Heym, Louise Ruffier D'epenoux, Olivier Lidove, et al.. Unusual Cutibacterium acnes splenic abscess with bacteremia in an immunocompetent man: phylotyping and clonal complex analysis. BMC Infectious Diseases, 2024, 24 (1), pp.601. 10.1186/s12879-024-09467-x. inserm-04618976

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# Unusual *Cutibacterium acnes* splenic abscess with bacteremia in an immunocompetent man: phylotyping and clonal complex analysis

Angèle Roudeau<fnref n="1" />, Stéphane Corvec<fnref n="2" />, Beate Heym<fnref n="3" />, Louise Ruffier d'Epenoux<fnref n="2" />, Olivier Lidove<fnref n="1" /> and Valérie Zeller<fnref n="1" />*

**Abstract**

**Background** *Cutibacterium acnes* is an anaerobic bacterium mostly implicated in cutaneous and body-implant infections. Splenic abscess is a rare entity and *C. acnes* abscesses have only exceptionally been reported. We describe a spontaneous splenic *C. acnes* abscess in an immunocompetent man with no predisposing factors or identified portal of entry. His isolates were subjected to single-locus sequence typing (SLST) to explore their genetic relatedness and better understand this rare infection.

**Case presentation** A splenic abscess was diagnosed on a computed-tomography scan in a 74-year-old man with chronic abdominal pain. No risk factor was identified. Abscess-drained pus and post-drainage blood cultures grew *C. acnes*. SLST of abscess and blood isolates showed that they belonged to the same *C. acnes* SLST type C1 found in normal skin and rarely in inflammatory skin disease. Specific virulence factors could not be identified.

**Conclusion** *C. acnes* abscesses are extremely rare and can develop in immunocompetent patients without an identifiable portal of entry. Molecular typing of clinical isolates can help confirm infection (versus contamination) and enables genetic background comparisons. Further research is needed to understand *C. acnes* tropism and virulence.

**Keywords** Abscess, Spleen, *Cutibacterium acnes*, Single-locus sequence typing, Phylotypes, Case report

**Background**

Splenic abscess develops extremely rarely (<0.7% according to autopsy studies) [1] and *Cutibacterium acnes* abscesses have exceptionally been reported. Splenic abscesses are usually discovered in patients with endocarditis and considered to be of hematogenous origin

[1]. Gram-positive cocci (*Staphylococcus aureus*, *Streptococcus viridans*) or Enterobacterales (*Klebsiella pneumoniae*) are classically responsible for these abscesses. Treatment requires splenectomy or percutaneous drainage and antibiotics. Reported mortality is 15–30% [1, 2].

*C. acnes* is a slow-growing, facultative, anaerobic, Gram-positive bacillus, mostly recovered as a saprophytic bacterium from human skin, the oral cavity, and gastrointestinal and genitourinary tracts. Its involvement in acne pathophysiology is well-known. Historically, *C. acnes* was considered a low-virulence microorganism. However, its pathogenic role, facilitated by its ability to produce biofilm, is now clearly established [3, 4].

We describe a spontaneous splenic *C. acnes* abscess, with bacteremia after abscess drainage, in an

<footnote>*Correspondence:
Valérie Zeller
vzeller@hopital-dcss.org</footnote>

<footnote n="1">¹Department of Internal Medicine and Infectious Diseases, Groupe Hospitalier Diaconesses– Croix Saint-Simon, 125, rue d’Avron, Paris 75020, France</footnote>

<footnote n="2">²Service de Bactériologie et des Contrôles Microbiologiques, CHU Nantes, Université de Nantes, INSERM, INCIT U1302, Nantes, France</footnote>

<footnote n="3">³Laboratoire des Centres de Santé et Hôpitaux d’Île-de-France, Groupe Hospitalier Diaconesses– Croix Saint-Simon, 125, rue d’Avron, Paris, France</footnote>
<figure><img src="image_3.png" /></figure>

# Unusual *Cutibacterium acnes* splenic abscess with bacteremia in an immunocompetent man: phylotyping and clonal complex analysis

Angèle Roudeau<fnref n="1" />, Stéphane Corvec<fnref n="2" />, Beate Heym<fnref n="3" />, Louise Ruffier d'Epenoux<fnref n="2" />, Olivier Lidove<fnref n="1" /> and Valérie Zeller<fnref n="1" />*

**Abstract**

**Background** *Cutibacterium acnes* is an anaerobic bacterium mostly implicated in cutaneous and body-implant infections. Splenic abscess is a rare entity and *C. acnes* abscesses have only exceptionally been reported. We describe a spontaneous splenic *C. acnes* abscess in an immunocompetent man with no predisposing factors or identified portal of entry. His isolates were subjected to single-locus sequence typing (SLST) to explore their genetic relatedness and better understand this rare infection.

**Case presentation** A splenic abscess was diagnosed on a computed-tomography scan in a 74-year-old man with chronic abdominal pain. No risk factor was identified. Abscess-drained pus and post-drainage blood cultures grew *C. acnes*. SLST of abscess and blood isolates showed that they belonged to the same *C. acnes* SLST type C1 found in normal skin and rarely in inflammatory skin disease. Specific virulence factors could not be identified.

**Conclusion** *C. acnes* abscesses are extremely rare and can develop in immunocompetent patients without an identifiable portal of entry. Molecular typing of clinical isolates can help confirm infection (versus contamination) and enables genetic background comparisons. Further research is needed to understand *C. acnes* tropism and virulence.

**Keywords** Abscess, Spleen, *Cutibacterium acnes*, Single-locus sequence typing, Phylotypes, Case report

**Background**

Splenic abscess develops extremely rarely (<0.7% according to autopsy studies) [1] and *Cutibacterium acnes* abscesses have exceptionally been reported. Splenic abscesses are usually discovered in patients with endocarditis and considered to be of hematogenous origin

[1]. Gram-positive cocci (*Staphylococcus aureus*, *Streptococcus viridans*) or Enterobacterales (*Klebsiella pneumoniae*) are classically responsible for these abscesses. Treatment requires splenectomy or percutaneous drainage and antibiotics. Reported mortality is 15–30% [1, 2].

*C. acnes* is a slow-growing, facultative, anaerobic, Gram-positive bacillus, mostly recovered as a saprophytic bacterium from human skin, the oral cavity, and gastrointestinal and genitourinary tracts. Its involvement in acne pathophysiology is well-known. Historically, *C. acnes* was considered a low-virulence microorganism. However, its pathogenic role, facilitated by its ability to produce biofilm, is now clearly established [3, 4].

We describe a spontaneous splenic *C. acnes* abscess, with bacteremia after abscess drainage, in an

<footnote>*Correspondence:
Valérie Zeller
vzeller@hopital-dcss.org</footnote>

<footnote n="1">¹Department of Internal Medicine and Infectious Diseases, Groupe Hospitalier Diaconesses– Croix Saint-Simon, 125, rue d’Avron, Paris 75020, France</footnote>

<footnote n="2">²Service de Bactériologie et des Contrôles Microbiologiques, CHU Nantes, Université de Nantes, INSERM, INCIT U1302, Nantes, France</footnote>

<footnote n="3">³Laboratoire des Centres de Santé et Hôpitaux d’Île-de-France, Groupe Hospitalier Diaconesses– Croix Saint-Simon, 125, rue d’Avron, Paris, France</footnote>
immunocompetent man with no predisposing factors or identified portal of entry, unlike the four cases reported in the literature [5-8]. The *C. acnes* isolates were subjected to single-locus sequence typing (SLST) to better understand this rare infection.

Case presentation

A 74-year-old male was admitted to our Internal Medi-
cine and Infectious Diseases Department in June 2022 for
a second episode of abdominal pain, diarrhea, vomiting
and fever, with 5-kg weight loss within 2 months. The first
episode, 1 month earlier, had lasted 2 weeks. Abdominal
computed-tomography (CT) scan showed a 7-cm splenic
abscess (Fig. 1a). The gallbladder was normal. No blood
cultures or other microbiological testing were performed.
Admission findings were: weight 61 kg; afebrile with-
out chills; complained of left hypochondrium and dor-
sal pains; stable hemodynamics and respiratory status;
diminished breath sounds at the left lung base; no heart

murmur, skin lesion or lymphadenopathy; soft but tender
abdomen. Blood analyses showed: elevated C-reactive
protein (CRP) 80 mg/L; normal neutrophil and eosino-
phil counts, creatinemia and liver enzymes.

Other remarkable history included: 2013, normal colo-
noscopy; 2009, normal coronarography; 2000, ischemic
stroke; 1998, acute pulmonary edema. He reported no
history of drug abuse.

Infective endocarditis was excluded in the absence of
major and minor diagnostic criteria: transthoracic and
transesophageal echographies showed no valvular lesion
or suspicious image, but did reveal chronic heart fail-
ure. Three aerobic and anaerobic blood bottle cultures
(FN plus bottle, bioMérieux, Inc Durham, NC27712,
USA) of day-2, -6 and -8 postadmission samples incu-
bated for 120 h (5 days) were negative. He had no fever,
cardiac murmur, predisposing heart condition enhanc-
ing the risk of infective endocarditis (no history of valvu-
lopathy, previous endocarditis, prosthetic valve or other

<figure><img src="image_2.png" /><figcaption>**Fig. 1** Thoracic-abdominal computed-tomography scan (a) before and (b) after abscess drainage. Splenic abscess (circle), pleural effusion (star) and drain (arrow)</figcaption></figure>
immunocompetent man with no predisposing factors or identified portal of entry, unlike the four cases reported in the literature [5-8]. The *C. acnes* isolates were subjected to single-locus sequence typing (SLST) to better understand this rare infection.

Case presentation

A 74-year-old male was admitted to our Internal Medi-
cine and Infectious Diseases Department in June 2022 for
a second episode of abdominal pain, diarrhea, vomiting
and fever, with 5-kg weight loss within 2 months. The first
episode, 1 month earlier, had lasted 2 weeks. Abdominal
computed-tomography (CT) scan showed a 7-cm splenic
abscess (Fig. 1a). The gallbladder was normal. No blood
cultures or other microbiological testing were performed.
Admission findings were: weight 61 kg; afebrile with-
out chills; complained of left hypochondrium and dor-
sal pains; stable hemodynamics and respiratory status;
diminished breath sounds at the left lung base; no heart

murmur, skin lesion or lymphadenopathy; soft but tender
abdomen. Blood analyses showed: elevated C-reactive
protein (CRP) 80 mg/L; normal neutrophil and eosino-
phil counts, creatinemia and liver enzymes.

Other remarkable history included: 2013, normal colo-
noscopy; 2009, normal coronarography; 2000, ischemic
stroke; 1998, acute pulmonary edema. He reported no
history of drug abuse.

Infective endocarditis was excluded in the absence of
major and minor diagnostic criteria: transthoracic and
transesophageal echographies showed no valvular lesion
or suspicious image, but did reveal chronic heart fail-
ure. Three aerobic and anaerobic blood bottle cultures
(FN plus bottle, bioMérieux, Inc Durham, NC27712,
USA) of day-2, -6 and -8 postadmission samples incu-
bated for 120 h (5 days) were negative. He had no fever,
cardiac murmur, predisposing heart condition enhanc-
ing the risk of infective endocarditis (no history of valvu-
lopathy, previous endocarditis, prosthetic valve or other

<figure><img src="image_4.png" /><figcaption>**Fig. 1** Thoracic-abdominal computed-tomography scan (a) before and (b) after abscess drainage. Splenic abscess (circle), pleural effusion (star) and drain (arrow)</figcaption></figure>
cardiac implants), other infectious sites in favor of septic embolism or immunological phenomena. Because of his African childhood, brucellosis, rickettsiosis, bartonellosis, echinococcosis and amoebiasis serologies were performed and were negative.

His clinical and biological parameters remained unchanged during week 1. On day-9 postadmission, before receiving any antibiotic therapy, he underwent CT-guided percutaneous spleen-abscess drainage. Drain placement was easy but the thick abscess pus was difficult to drain. Twenty-four hours later, he developed fever, chills, hypoxemia. A new CT scan showed enlargement of the left pleural effusion (Fig. 1b). Two blood cultures were initiated. Intravenous piperacillin–tazobactam was started but, upon appearance of an urticarial rash, switched immediately to ceftriaxone, amikacin, linezolid and metronidazole. Supplemental oxygen therapy was started (3 L/min) when breathing difficulty began before he was transferred to another hospital’s Thoracic Surgery Unit for left pleural drainage.

Direct examination of the splenic abscess pus found abundant Gram-positive bacilli. Numerous *C. acnes* colonies grew in pus cultures after 72 h of incubation and one of two anaerobic blood cultures, initiated just before starting antibiotics, also yielded *C. acnes* after 120 h of incubation. Isolate antibiotic susceptibilities were tested according to EUCAST guidelines using *Brucella*-agar plates containing 5% sheep blood, vitamin K1 (1 mg/L) and hemin (5 mg/L). A 1 McFarland-standard inoculum suspension was deposited on plates and incubated anaerobically. Gradient concentration strips were read after 48 h. The *C. acnes* strain was susceptible to amoxicillin (minimum inhibitory concentration (MIC)=0.023 mg/L), ceftriaxone (MIC=0.047 mg/L), rifampicin (MIC=0.008 mg/L), vancomycin (MIC=1 mg/L), daptomycin (MIC=1.5 mg/L), clindamycin (MIC=0.094 mg/L), doxycycline (MIC=0.094 mg/L), moxifloxacin (MIC=0.094 mg/L), levofloxacin (MIC=0.25 mg/L) and linezolid (MIC=0.094 mg/L) but resistant to metronidazole (MIC>256 mg/L). Pleural effusion, collected 2 days after starting antibiotics, showed no growth. The differential cell count comprised 80% neutrophils; no absolute cell count was available.

Percutaneous spleen and pleural drainage lasted 10 days. The patient's general condition progressively improved; he remained afebrile and supplemental oxygen was stopped after 1 week. His white blood count decreased from 18,600/mm³ to 8,800/mm³ and C-reactive protein (CRP) from 254 to 15 mg/L within 2 weeks. Antibiotic administration lasted 3 weeks. Intravenous (IV) ceftriaxone (2 g/day), oral linezolid (600 mg q12h) and oral metronidazole (500 mg q8h) were maintained for 10 days to treat the acalculous cholecystitis detected by abdominal echography. Treatment was then switched

to oral clindamycin (600 mg, q8h) for 10 days to complete treatment of the *C. acnes* spleen abscess.

Immunosuppression searches remained negative: glycemia, protein electrophoresis, complete blood count, and immunoglobulin IgA, IgM and IgG rates were normal. Human immunodeficiency virus, hepatitis B and C virus serologies were negative.

The patient was discharged to home. One and a half years later, he was well, without any abdominal or infectious signs of relapse.

The *C. acnes* clinical isolates were sent to the *Cutibacterium* Species Reference Center (Nantes University Hospital) to investigate their genetic relatedness with molecular-typing methods including SLST [9, 10]. They belonged to SLST type C1, corresponding to phylotype IA₂ and the University of Aarhus multilocus sequence typing clonal complex CC28 [11].

## Discussion and conclusion

To our knowledge, six cases of *C. acnes* splenic abscess have been published [5–8, 12, 13]; four were monomicrobial [5–8], like ours, and fully described, as summarized in Table 1. Another case in a retrospective study on splenic abscesses provided no further details [12], and the last, published >40 years ago [13], reported a polymicrobial *S. aureus*, *Clostridium* sp.- and *C. acnes*-containing abscess for which cross-contamination could not be excluded.

Our case, the fifth monomicrobial one, provides the first phylotyping of *C. acnes* abscess and blood isolates. It confirmed their genetic relatedness, better characterized them and excluded contamination.

Three previous cases [5, 6, 8] had usual clinical pictures, similar to our patient's (Table 1). However, case 2 [7], was different; that heavily immunocompromised 64-year-old man was febrile without any gastrointestinal symptoms. His CT scan was normal. ¹⁸F-fluorodeoxyglucose-positron-emission tomography with high spleen uptake led to splenic abscess diagnosis.

Possible risk factors or portals of entry were sought for each of those rare infections. Because *C. acnes* is a human skin and buccal saprophytic bacterium, skin breaks were evoked for all of them: subcutaneous insulin [5], IV-drug abuse [6], IV chemotherapy [7] or tooth extractions [8]. However, those are common cutaneous breaks and splenic abscesses remain rare. The immunocompromised status of cases 1 and 2 (respectively, acute respiratory failure syndrome post-left myocardial infarction (8) or leukemia [7]) could explain their infections.

Major predisposing factors for *C. acnes* infection are previous surgeries and foreign-body implants, such as prosthetic heart valves, ventriculoperitoneal shunts, orthopedic implants and joint prostheses. *C. acnes* contamination most likely occurs during surgery. This
cardiac implants), other infectious sites in favor of septic embolism or immunological phenomena. Because of his African childhood, brucellosis, rickettsiosis, bartonellosis, echinococcosis and amoebiasis serologies were performed and were negative.

His clinical and biological parameters remained unchanged during week 1. On day-9 postadmission, before receiving any antibiotic therapy, he underwent CT-guided percutaneous spleen-abscess drainage. Drain placement was easy but the thick abscess pus was difficult to drain. Twenty-four hours later, he developed fever, chills, hypoxemia. A new CT scan showed enlargement of the left pleural effusion (Fig. 1b). Two blood cultures were initiated. Intravenous piperacillin–tazobactam was started but, upon appearance of an urticarial rash, switched immediately to ceftriaxone, amikacin, linezolid and metronidazole. Supplemental oxygen therapy was started (3 L/min) when breathing difficulty began before he was transferred to another hospital’s Thoracic Surgery Unit for left pleural drainage.

Direct examination of the splenic abscess pus found abundant Gram-positive bacilli. Numerous *C. acnes* colonies grew in pus cultures after 72 h of incubation and one of two anaerobic blood cultures, initiated just before starting antibiotics, also yielded *C. acnes* after 120 h of incubation. Isolate antibiotic susceptibilities were tested according to EUCAST guidelines using *Brucella*-agar plates containing 5% sheep blood, vitamin K1 (1 mg/L) and hemin (5 mg/L). A 1 McFarland-standard inoculum suspension was deposited on plates and incubated anaerobically. Gradient concentration strips were read after 48 h. The *C. acnes* strain was susceptible to amoxicillin (minimum inhibitory concentration (MIC)=0.023 mg/L), ceftriaxone (MIC=0.047 mg/L), rifampicin (MIC=0.008 mg/L), vancomycin (MIC=1 mg/L), daptomycin (MIC=1.5 mg/L), clindamycin (MIC=0.094 mg/L), doxycycline (MIC=0.094 mg/L), moxifloxacin (MIC=0.094 mg/L), levofloxacin (MIC=0.25 mg/L) and linezolid (MIC=0.094 mg/L) but resistant to metronidazole (MIC>256 mg/L). Pleural effusion, collected 2 days after starting antibiotics, showed no growth. The differential cell count comprised 80% neutrophils; no absolute cell count was available.

Percutaneous spleen and pleural drainage lasted 10 days. The patient's general condition progressively improved; he remained afebrile and supplemental oxygen was stopped after 1 week. His white blood count decreased from 18,600/mm³ to 8,800/mm³ and C-reactive protein (CRP) from 254 to 15 mg/L within 2 weeks. Antibiotic administration lasted 3 weeks. Intravenous (IV) ceftriaxone (2 g/day), oral linezolid (600 mg q12h) and oral metronidazole (500 mg q8h) were maintained for 10 days to treat the acalculous cholecystitis detected by abdominal echography. Treatment was then switched

to oral clindamycin (600 mg, q8h) for 10 days to complete treatment of the *C. acnes* spleen abscess.

Immunosuppression searches remained negative: glycemia, protein electrophoresis, complete blood count, and immunoglobulin IgA, IgM and IgG rates were normal. Human immunodeficiency virus, hepatitis B and C virus serologies were negative.

The patient was discharged to home. One and a half years later, he was well, without any abdominal or infectious signs of relapse.

The *C. acnes* clinical isolates were sent to the *Cutibacterium* Species Reference Center (Nantes University Hospital) to investigate their genetic relatedness with molecular-typing methods including SLST [9, 10]. They belonged to SLST type C1, corresponding to phylotype IA₂ and the University of Aarhus multilocus sequence typing clonal complex CC28 [11].

## Discussion and conclusion

To our knowledge, six cases of *C. acnes* splenic abscess have been published [5–8, 12, 13]; four were monomicrobial [5–8], like ours, and fully described, as summarized in Table 1. Another case in a retrospective study on splenic abscesses provided no further details [12], and the last, published >40 years ago [13], reported a polymicrobial *S. aureus*, *Clostridium* sp.- and *C. acnes*-containing abscess for which cross-contamination could not be excluded.

Our case, the fifth monomicrobial one, provides the first phylotyping of *C. acnes* abscess and blood isolates. It confirmed their genetic relatedness, better characterized them and excluded contamination.

Three previous cases [5, 6, 8] had usual clinical pictures, similar to our patient's (Table 1). However, case 2 [7], was different; that heavily immunocompromised 64-year-old man was febrile without any gastrointestinal symptoms. His CT scan was normal. ¹⁸F-fluorodeoxyglucose-positron-emission tomography with high spleen uptake led to splenic abscess diagnosis.

Possible risk factors or portals of entry were sought for each of those rare infections. Because *C. acnes* is a human skin and buccal saprophytic bacterium, skin breaks were evoked for all of them: subcutaneous insulin [5], IV-drug abuse [6], IV chemotherapy [7] or tooth extractions [8]. However, those are common cutaneous breaks and splenic abscesses remain rare. The immunocompromised status of cases 1 and 2 (respectively, acute respiratory failure syndrome post-left myocardial infarction (8) or leukemia [7]) could explain their infections.

Major predisposing factors for *C. acnes* infection are previous surgeries and foreign-body implants, such as prosthetic heart valves, ventriculoperitoneal shunts, orthopedic implants and joint prostheses. *C. acnes* contamination most likely occurs during surgery. This
<table><caption>**Table 1** Summary of case reports on monobacterial *C. acnes* splenic abscesses</caption><thead><tr><th>Case [Ref] year</th><th>Age, yr, Sex</th><th>Risk factor(s)</th><th>Findings Clinical</th><th>Imaging</th><th>Microbiology result(s), sample</th><th>Treatment</th><th>Outcome</th></tr></thead><tbody><tr><td>1 [5] 1982</td><td>59, male</td><td>Diabetes, subcutaneous insulin, myocardial infarction</td><td>Left abdominal pain, nausea, vomiting, fever</td><td>11-cm splenic cystic deformity (ultrasonography & CT scan)</td><td>Positive blood-bottle cultures & spleen-pus culture</td><td>Splenectomy & IV penicillin</td><td>Survived</td></tr><tr><td>2 [6] 2013</td><td>64, male</td><td>Lymphocytic leukemia on IV chemotherapy</td><td>Fever of unknown origin</td><td>No anomaly on CT scan, high splenic uptake (FDG-PET)</td><td>Positive spleen specimen culture<br>Sterile blood-bottle cultures</td><td>Splenectomy & levofloxacin</td><td>Survived</td></tr><tr><td>3 [7] 2017</td><td>64, female</td><td>Diabetes, IV-drug abuse</td><td>Nausea, vomiting, left abdominal pain</td><td>9-cm splenic hydropodensity (CT scan)</td><td>Positive radio-guided spleen aspirate & spleen specimen cultures<br>Sterile blood-bottle cultures</td><td>Metronidazole, ciprofloxacin & vancomycin, then splenectomy & clindamycin</td><td>Survived</td></tr><tr><td>4 [8] 2023</td><td>40, female</td><td>Tooth extraction</td><td>3-month history of fever, fatigue & left flank pain</td><td>Splenial abscess replacing almost the entire spleen parenchyma (CT scan)</td><td>Positive radio-guided spleen aspirate culture<br>Sterile blood-bottle cultures</td><td>Metronidazole, ceftriaxone & splenectomy</td><td>Survived</td></tr><tr><td>5, This report 2023</td><td>72, male</td><td>None</td><td>2 episodes of nausea, vomiting, fever & left abdominal pain</td><td>7-cm splenic abscess (CT scan)</td><td>Positive radio-guided spleen aspirate & blood-bottle cultures</td><td>Percutaneous drainage; ceftriaxone, metronidazole & linezolid, then clindamycin</td><td>Survived</td></tr></tbody></table>

Abbreviations: CT, computed tomography; FDG-PET, ¹⁸F-fluorodeoxyglucose-positron emission tomography; IV, intravenous.

bacterium has the capacity to adhere to the implant surface and persist through biofilm formation, with the latter being one of its major virulence factors [4]. Spontaneous *C. acnes* infections with bacteremia are very unusual. It is worth noting that, even though prosthesis *C. acnes* infections are now more common because of the higher number of prosthesis arthroplasties, none of the splenic abscess patients had a prosthetic device. Their infections are most probably attributable to contiguous cutaneous or mucosal contamination sources.

Our patient, unlike all previously reported cases, had no risk factor or determined source of *C. acnes* infection: no skin break (no IV or subcutaneous treatment, no recent surgery, no drug abuse, no dental work) and no prosthesis. He had not been hospitalized for more than 9 years. It is unlikely that contamination occurred at that time via IV infusion, for example, even if *C. acnes* is a slow-growing bacteria and the clone isolated from our patient is found in normal or chronically inflamed skin (see below). He was not immunosuppressed or immunocompromised and had neither endocarditis nor known splenic infarct. It seems improbable that acalculous cholecystitis caused the splenic abscess via the bloodstream, because *C. acnes* mainly inhabits deep skin layers. The patient had no right hypochondrial pain and his gallbladder was normal on the initial CT scan. It also seems unlikely that the CT-guided percutaneous abscess drainage infected the spleen: the puncture extracted large amounts of pus that, upon direct examination, contained

numerous Gram-positive bacilli and cultures grew abundant *C. acnes* colonies.

Because we were unable to identify any risk factors for our patient, we investigated the idea that the risk was rather linked to the bacterium itself. Indeed, *C. acnes* expresses different antigens that could be involved in its pathogenicity [3]. The broad heterogenicity of *C. acnes* pathogenicity led to the development of several different accurate *C. acnes* phylogenetic determination methods [5]. *C. acnes* strains can be divided into at least six main phylotypes (IA₁, IA₂, IB, IC, II and III). SLST determined different lineages and divided them into at least 194 phenotypes [10], which are increasingly linked to different pathogenic capabilities [14]. Our patient's three isolates (one from blood bottle cultures and two from splenic pus) were subjected to molecular typing including SLST, phylotyping and multilocus sequence typing. All three belonged to the same clone: SLST type C1, phylotype IA₂ and clonal complex CC28. Notably, this cluster has been found in normal skin and rarely in chronic inflammatory skin diseases, e.g., acne [3, 15]. It seems to have high biofilm-formation capacity and strong adhesive properties [14]. Despite genomic investigations, it has proven difficult to identify specific virulence factors [9, 15] for this *C. acnes* subtype. These results suggest that the skin was the most likely source of infection. The bacteria might have spread either via the blood or locally from a nearby source. The clinical picture and the absence of an identified portal of entry could not confirm that hypothesis, despite our investigations.
<table><caption>**Table 1** Summary of case reports on monobacterial *C. acnes* splenic abscesses</caption><thead><tr><th>Case [Ref] year</th><th>Age, yr, Sex</th><th>Risk factor(s)</th><th>Findings Clinical</th><th>Imaging</th><th>Microbiology result(s), sample</th><th>Treatment</th><th>Outcome</th></tr></thead><tbody><tr><td>1 [5] 1982</td><td>59, male</td><td>Diabetes, subcutaneous insulin, myocardial infarction</td><td>Left abdominal pain, nausea, vomiting, fever</td><td>11-cm splenic cystic deformity (ultrasonography & CT scan)</td><td>Positive blood-bottle cultures & spleen-pus culture</td><td>Splenectomy & IV penicillin</td><td>Survived</td></tr><tr><td>2 [6] 2013</td><td>64, male</td><td>Lymphocytic leukemia on IV chemotherapy</td><td>Fever of unknown origin</td><td>No anomaly on CT scan, high splenic uptake (FDG-PET)</td><td>Positive spleen specimen culture<br>Sterile blood-bottle cultures</td><td>Splenectomy & levofloxacin</td><td>Survived</td></tr><tr><td>3 [7] 2017</td><td>64, female</td><td>Diabetes, IV-drug abuse</td><td>Nausea, vomiting, left abdominal pain</td><td>9-cm splenic hypodensity (CT scan)</td><td>Positive radio-guided spleen aspirate & spleen specimen cultures<br>Sterile blood-bottle cultures</td><td>Metronidazole, ciprofloxacin & vancomycin, then splenectomy & clindamycin</td><td>Survived</td></tr><tr><td>4 [8] 2023</td><td>40, female</td><td>Tooth extraction</td><td>3-month history of fever, fatigue & left flank pain</td><td>Splenial abscess replacing almost the entire spleen parenchyma (CT scan)</td><td>Positive radio-guided spleen aspirate culture<br>Sterile blood-bottle cultures</td><td>Metronidazole, ceftriaxone & splenectomy</td><td>Survived</td></tr><tr><td>5, This report 2023</td><td>72, male</td><td>None</td><td>2 episodes of nausea, vomiting, fever & left abdominal pain</td><td>7-cm splenic abscess (CT scan)</td><td>Positive radio-guided spleen aspirate & blood-bottle cultures</td><td>Percutaneous drainage; ceftriaxone, metronidazole & linezolid, then clindamycin</td><td>Survived</td></tr></tbody></table>

Abbreviations: CT, computed tomography; FDG-PET, ¹⁸F-fluorodeoxyglucose-positron emission tomography; IV, intravenous.

bacterium has the capacity to adhere to the implant surface and persist through biofilm formation, with the latter being one of its major virulence factors [4]. Spontaneous *C. acnes* infections with bacteremia are very unusual. It is worth noting that, even though prosthesis *C. acnes* infections are now more common because of the higher number of prosthesis arthroplasties, none of the splenic abscess patients had a prosthetic device. Their infections are most probably attributable to contiguous cutaneous or mucosal contamination sources.

Our patient, unlike all previously reported cases, had no risk factor or determined source of *C. acnes* infection: no skin break (no IV or subcutaneous treatment, no recent surgery, no drug abuse, no dental work) and no prosthesis. He had not been hospitalized for more than 9 years. It is unlikely that contamination occurred at that time via IV infusion, for example, even if *C. acnes* is a slow-growing bacteria and the clone isolated from our patient is found in normal or chronically inflamed skin (see below). He was not immunosuppressed or immunocompromised and had neither endocarditis nor known splenic infarct. It seems improbable that acalculous cholecystitis caused the splenic abscess via the bloodstream, because *C. acnes* mainly inhabits deep skin layers. The patient had no right hypochondrial pain and his gallbladder was normal on the initial CT scan. It also seems unlikely that the CT-guided percutaneous abscess drainage infected the spleen: the puncture extracted large amounts of pus that, upon direct examination, contained

numerous Gram-positive bacilli and cultures grew abundant *C. acnes* colonies.

Because we were unable to identify any risk factors for our patient, we investigated the idea that the risk was rather linked to the bacterium itself. Indeed, *C. acnes* expresses different antigens that could be involved in its pathogenicity [3]. The broad heterogenicity of *C. acnes* pathogenicity led to the development of several different accurate *C. acnes* phylogenetic determination methods [5]. *C. acnes* strains can be divided into at least six main phylotypes (IA₁, IA₂, IB, IC, II and III). SLST determined different lineages and divided them into at least 194 phenotypes [10], which are increasingly linked to different pathogenic capabilities [14]. Our patient's three isolates (one from blood bottle cultures and two from splenic pus) were subjected to molecular typing including SLST, phylotyping and multilocus sequence typing. All three belonged to the same clone: SLST type C1, phylotype IA₂ and clonal complex CC28. Notably, this cluster has been found in normal skin and rarely in chronic inflammatory skin diseases, e.g., acne [3, 15]. It seems to have high biofilm-formation capacity and strong adhesive properties [14]. Despite genomic investigations, it has proven difficult to identify specific virulence factors [9, 15] for this *C. acnes* subtype. These results suggest that the skin was the most likely source of infection. The bacteria might have spread either via the blood or locally from a nearby source. The clinical picture and the absence of an identified portal of entry could not confirm that hypothesis, despite our investigations.
Our patient underwent CT-controlled percutaneous drainage, which was developed for splenic abscesses in the 1990's [16]. The other *C. acnes* splenic abscesses were treated with splenectomy [5–8] (Table 1). Percutaneous drainage was chosen because the patient was pauci-symptomatic and his chronic heart failure put him at high risk for surgery. The initial drainage was difficult because of pus thickness and led to sepsis 24 h later, and worsening of the pleural effusion requiring prolonged drainage. Finally, 10 days of percutaneous drainage and 3 weeks of antibiotics eradicated his infection.

C. acnes is naturally metronidazole- and fosfomycin-
resistant, and susceptible to a wide range of antibiotics
(β-lactam, clindamycin, rifampicin, vancomycin, dap-
tomycin and fluoroquinolones). No consensus exists for
first-choice and alternative antibiotic regimens, which
remain controversial [3]: amoxicillin, clindamycin or flu-
oroquinolones. Available data derive from implant-asso-
ciated infection [4]. Large-scale studies on homogeneous
populations are rare, the antibiotic regimens used to treat
these infections are heterogeneous and no recommenda-
tions based on a high level of evidence can be devised.
The antibiotic regimens prescribed for all reported C.
acnes splenic abscesses differed (Table 1). Our patient
initially received a broad-spectrum antibiotic combina-
tion to cover other gastrointestinal bacteria and acalcu-
lous cholecystitis, before being narrowed to clindamycin
to treat the C. acnes spleen abscess. Clindamycin was
chosen because of its good activity, bioavailability and tis-
sue diffusion. Amoxicillin is another highly active agent.

Conclusion

This *C. acnes* splenic abscess developed in a patient without any potentially responsible comorbidity. It illustrates that immunocompetent patients—without an evident skin break or other portal of entry—can develop this extremely rare infection. Molecular typing of clinical isolates can help confirm infection (versus contamination) and enable genetic background comparisons. Further research, especially on virulence factors, is still needed to understand this unusual tropism.

Abbreviations

<table>
   <tr>
    <td>
     CRP
    </td>
    <td>
     C-reactive protein
    </td>
   </tr>
   <tr>
    <td>
     CT scan
    </td>
    <td>
     Computed tomography
    </td>
   </tr>
   <tr>
    <td>
     IV
    </td>
    <td>
     Intravenous
    </td>
   </tr>
   <tr>
    <td>
     MIC
    </td>
    <td>
     Minimum inhibitory concentration
    </td>
   </tr>
   <tr>
    <td>
     SLST
    </td>
    <td>
     Single-locus sequence typing
    </td>
   </tr>
  </table>

Acknowledgements

We would like to thank Janet Jacobson for editing and reviewing this
manuscript for English language.

Author contributions

A.R. contributed to the clinical management of the patient, was involved in acquisition and analysis of the data, and drafting of the manuscript. S.C. and B.H. contributed to the acquisition and analysis of the microbiological data, were involved in the supervision of the drafting and critical revision

of the manuscript. L.R.E. contributed to the acquisition and analysis of the
microbiological data. O.L. contributed to the critical revision of the manuscript.
V.Z. contributed to the clinical management of the patient and was involved
supervision of the drafting and critical revision of the manuscript. All authors
read and approved the final manuscript.

Funding

This research did not receive any specific grants from funding agencies in the public, commercial, or not-for-profit sectors.

Data availability

All data analyzed during this study are included in this article.

Declarations

Ethics approval and consent to participate

According to French law, Ethics Committee approval was not required for this
retrospective case report.

Consent for publication

Written informed consent was obtained from the patient for publication of
this case report and the accompanying images. A copy of the written consent
is available for review by the Editor-in-Chief of this journal on request.

Competing interests

The authors declare no competing interests.

Received: 4 January 2024 / Accepted: 3 June 2024

Published online: 19 June 2024

References

1. Lee MC, Lee CM. Splenic abscess: an uncommon entity with potentially life-threatening evolution. Can J Infect Dis Med Microbiol. 2018;2018:8610657.

2. Radcliffe C, Tang Z, Gisriel SD, Grant M. Splenic abscess in the new mil-
lennium: a descriptive, retrospective case series. Open Forum Infect Dis.
2022;9(4):ofac085.

3. Achermann Y, Goldstein EJC, Coenye T, Shirliff ME. *Propionibacterium acnes*: from commensal to opportunistic biofilm-associated implant pathogen. Clin Microbiol Rev. 2014;27(3):419–40.

4. Coenye T, Spittaels KJ, Achermann Y. The role of biofilm formation in the pathogenesis and antimicrobial susceptibility of Cutibacterium acnes. Biofilm. 2022;4:100063.

5. Gekowski KM, Licalzi L. Splenic abscess caused by *Propionibacterium acnes*. Yale J Biol Med. 1982;55(1):65–9.

6. Mohammed S, Kollu VS. Rare case of *Propionibacterium acnes*-related splenic abscess. BMJ Case Rep. 2018;2018:bcr2018225858.

7. Kiritani S, Kaneko J, Aoki T, Sakamoto Y, Hasegawa K, Sugawara Y, Kokudo N. Multiple splenic nodules with fever: a case of splenic abscess due to *Propionibacterium acnes*. Clin J Gastroenterol. 2013;6(6):434–7.

8. Walsh M, Wasko N, Simms AJ, Hodges J. Splenic abscess caused by *Cutibacterium acnes* in a patient with multiple tooth extractions. BMJ Case Rep. 2023;16(1):e250486.

9. Dagnelie MA, Khammari A, Dréno B, Corvec S. *Cutibacterium acnes* molecular typing: time to standardize the method. Clin Microbiol Infect. 2018;24(11):1149–55.

10. Scholz CFP, Jensen A, Lomholt HB, Brüggemann H, Kilian M. A novel high-resolution single locus sequence typing scheme for mixed populations of *Propionibacterium acnes* in vivo. PLoS ONE. 2014;9(8):e104199.

11. Kilian M, Scholz CFP, Lomholt HB. Multilocus sequence typing and phylogenetic analysis of *Propionibacterium acnes*. J Clin Microbiol. 2012;50(4):1158–65.

12. Chang KC, Chuah SK, Changchien CS, Tsai TL, Lu SN, Chiu YC, Chen YS, Wang CC, Lin JW, Lee CM, Hu TH. 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(3):460–4.

13. Gangahar D, Delany H. Intrasplenic abscess: two case reports and review of the literature. Am Surg. 1981;47(11):488–91.

14. Kuehnast T, Cakar F, Weinhäupl T, Pilz A, Selak S, Schmidt MA, Rüter C. Schild. Comparative analyses of biofilm formation among different *Cutibacterium acnes* isolates. Int J Med Microbiol. 2018;308(8):1027–35.
Our patient underwent CT-controlled percutaneous drainage, which was developed for splenic abscesses in the 1990's [16]. The other *C. acnes* splenic abscesses were treated with splenectomy [5–8] (Table 1). Percutaneous drainage was chosen because the patient was pauci-symptomatic and his chronic heart failure put him at high risk for surgery. The initial drainage was difficult because of pus thickness and led to sepsis 24 h later, and worsening of the pleural effusion requiring prolonged drainage. Finally, 10 days of percutaneous drainage and 3 weeks of antibiotics eradicated his infection.

C. acnes is naturally metronidazole- and fosfomycin-
resistant, and susceptible to a wide range of antibiotics
(β-lactam, clindamycin, rifampicin, vancomycin, dap-
tomycin and fluoroquinolones). No consensus exists for
first-choice and alternative antibiotic regimens, which
remain controversial [3]: amoxicillin, clindamycin or flu-
oroquinolones. Available data derive from implant-asso-
ciated infection [4]. Large-scale studies on homogeneous
populations are rare, the antibiotic regimens used to treat
these infections are heterogeneous and no recommenda-
tions based on a high level of evidence can be devised.
The antibiotic regimens prescribed for all reported C.
acnes splenic abscesses differed (Table 1). Our patient
initially received a broad-spectrum antibiotic combina-
tion to cover other gastrointestinal bacteria and acalcu-
lous cholecystitis, before being narrowed to clindamycin
to treat the C. acnes spleen abscess. Clindamycin was
chosen because of its good activity, bioavailability and tis-
sue diffusion. Amoxicillin is another highly active agent.

Conclusion

This *C. acnes* splenic abscess developed in a patient without any potentially responsible comorbidity. It illustrates that immunocompetent patients—without an evident skin break or other portal of entry—can develop this extremely rare infection. Molecular typing of clinical isolates can help confirm infection (versus contamination) and enable genetic background comparisons. Further research, especially on virulence factors, is still needed to understand this unusual tropism.

Abbreviations

CRP C-reactive protein

CT scan Computed tomography

IV Intravenous

MIC Minimum inhibitory concentration

SLST Single-locus sequence typing

Acknowledgements

We would like to thank Janet Jacobson for editing and reviewing this
manuscript for English language.

Author contributions

A.R. contributed to the clinical management of the patient, was involved in acquisition and analysis of the data, and drafting of the manuscript. S.C. and B.H. contributed to the acquisition and analysis of the microbiological data, were involved in the supervision of the drafting and critical revision

of the manuscript. L.R.E. contributed to the acquisition and analysis of the
microbiological data. O.L. contributed to the critical revision of the manuscript.
V.Z. contributed to the clinical management of the patient and was involved
supervision of the drafting and critical revision of the manuscript. All authors
read and approved the final manuscript.

Funding

This research did not receive any specific grants from funding agencies in the public, commercial, or not-for-profit sectors.

Data availability

All data analyzed during this study are included in this article.

Declarations

Ethics approval and consent to participate

According to French law, Ethics Committee approval was not required for this
retrospective case report.

Consent for publication

Written informed consent was obtained from the patient for publication of
this case report and the accompanying images. A copy of the written consent
is available for review by the Editor-in-Chief of this journal on request.

Competing interests

The authors declare no competing interests.

Received: 4 January 2024 / Accepted: 3 June 2024

Published online: 19 June 2024

References

1. Lee MC, Lee CM. Splenic abscess: an uncommon entity with potentially life-threatening evolution. Can J Infect Dis Med Microbiol. 2018;2018:8610657.

2. Radcliffe C, Tang Z, Gisriel SD, Grant M. Splenic abscess in the new mil-
ennium: a descriptive, retrospective case series. Open Forum Infect Dis.
2022;9(4):ofac085.

3. Achermann Y, Goldstein EJC, Coenye T, Shirliff ME. Propionibacterium acnes: from commensal to opportunistic biofilm-associated implant pathogen. Clin Microbiol Rev. 2014;27(3):419–40.

4. Coenye T, Spittaels KJ, Achermann Y. The role of biofilm formation in the pathogenesis and antimicrobial susceptibility of Cutibacterium acnes. Biofilm. 2022;4:100063.

5. Gekowski KM, Licalzi L. Splenic abscess caused by Propionibacterium acnes. Yale J Biol Med. 1982;55(1):65–9.

6. Mohammed S, Kollu VS. Rare case of Propionibacterium acnes-related splenic abscess. BMJ Case Rep. 2018;2018:bcr2018225858.

7. Kiritani S, Kaneko J, Aoki T, Sakamoto Y, Hasegawa K, Sugawara Y, Kokudo N. Multiple splenic nodules with fever: a case of splenic abscess due to Propionibacterium acnes. Clin J Gastroenterol. 2013;6(6):434–7.

8. Walsh M, Wasko N, Simms AJ, Hodges J. Splenic abscess caused by Cutibacterium acnes in a patient with multiple tooth extractions. BMJ Case Rep. 2023;16(1):e250486.

9. Dagnelie MA, Khammari A, Dréno B, Corvec S. Cutibacterium acnes molecular typing: time to standardize the method. Clin Microbiol Infect. 2018;24(11):1149–55.

10. Scholz CFP, Jensen A, Lomholt HB, Brüggemann H, Kilian M. A novel high-resolution single locus sequence typing scheme for mixed populations of Propionibacterium acnes *in vivo*. PLoS ONE. 2014;9(8):e104199.

11. Kilian M, Scholz CFP, Lomholt HB. Multilocus sequence typing and phylogenetic analysis of Propionibacterium acnes. J Clin Microbiol. 2012;50(4):1158–65.

12. Chang KC, Chuah SK, Changchien CS, Tsai TL, Lu SN, Chiu YC, Chen YS, Wang CC, Lin JW, Lee CM, Hu TH. 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(3):460–4.

13. Gangahar D, Delany H. Intrasplenic abscess: two case reports and review of the literature. Am Surg. 1981;47(11):488–91.

14. Kuehnast T, Cakar F, Weinhäupl T, Pilz A, Selak S, Schmidt MA, Rüter C. Schild. Comparative analyses of biofilm formation among different Cutibacterium acnes isolates. Int J Med Microbiol. 2018;308(8):1027–35.
15. Brüggemann H, Salar-Vidal L, Gollnick HPM, Lood R. A Janus-faced bacterium: host-beneficial and -detrimental roles of *Cutibacterium acnes*. Front Microbiol. 2021;12:673845.

16. Thanos L, Dailiana T, Papaioannou G, Nikita A, Koutrouvelis H, Kelekis DA. Percutaneous CT-guided drainage of splenic abscess. Am J Roentgenol. 2002;179(3):629-32.

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15. Brüggemann H, Salar-Vidal L, Gollnick HPM, Lood R. A Janus-faced bacterium: host-beneficial and -detrimental roles of *Cutibacterium acnes*. Front Microbiol. 2021;12:673845.

16. Thanos L, Dailiana T, Papaioannou G, Nikita A, Koutrouvelis H, Kelekis DA. Percutaneous CT-guided drainage of splenic abscess. Am J Roentgenol. 2002;179(3):629-32.

**Publisher's Note**

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.