Necrotising fasciitis is a life-threatening condition characterised by inflammation, affecting the soft tissues, which spreads within a fascial plane. Skin changes can be delayed and can often go unnoticed. The condition arises from a bacterial infection, commonly being of polymicrobial aetiology. We describe an uncommon case of necrotising fasciitis caused by Finegoldia magna, an anaerobic coccus, in a 40-year-old patient with diabetes. F. magna is a Gram-positive anaerobic coccus, which was previously known as Peptostreptococcus magnus. The bacteria is found in the normal flora of the urogenital tract. The bacteria is associated with severe infections such as native valve endocarditis, paravalvular abscess around a bioprosthetic valve, purulent pericarditis complicated by mediastanitis, meningitis after pneumonia and necrotising pneumonia complicated by pyopneumothorax. There have been no cases in the literature describing necrotising fasciitis of the abdominal wall caused by F. magna.
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Necrotising fasciitis is a life-threatening condition characterised by inflammation, affecting the soft tissues, which spreads within a fascial plane. The inflammation causes thrombosis of blood vessels, which can in turn lead to ischaemia and necrosis of the subcutaneous tissue.1 Skin changes can be delayed and can often go unnoticed.
The condition arises from a bacterial infection, commonly being of polymicrobial aetiology. The most commonly grown organisms are Gram-positive cocci: group A streptococci and Staphylococcus aureus; and Gram-negative bacteria such as Escherichia coli and Pseudomonas aeruginosa.2 Necrotising fasciitis carries with it high morbidity and mortality, and it is considered a surgical emergency.
We describe a rare case of abdominal wall necrotising fasciitis caused by a single bacteria, Finegoldia magna.
A 40-year-old man was referred to the medical team by his general practitioner (GP) with an 11-day history of lower abdominal wall cellulitis which was not resolving after being treated with antibiotics. He had visited his GP who initially prescribed flucloxacillin 500 mg four times a day. As the patient did not get better after the 7-day course of antibiotics, he was started on co-amoxiclav 625 mg three times a day. On the third presentation, on day 11, to his GP with fever, worsening glycaemic control and increased lethargy, he was referred to the hospital.
The patient had type 2 diabetes, and was taking metformin and gliclazide. His other past medical history of note was hypertension for which he was taking ramipril. He reported an 11-day history of feeling unwell, a burning sensation on the skin overlying his abdominal panniculus which started from a lump that the he could feel underneath his skin. He also reported that this lump advanced into the suprapubic area after 7 days of oral antibiotics.
On admission the patient looked unwell. He had a heart rate of 118 bpm, a systolic blood pressure of 90/70 mm Hg and a respiratory rate of 24 breaths per minute. He had no fever. On examination he had a high body mass index of 37 with significant overhanging panniculus extending beyond his genitalia. There was a 15×15 cm area of a faint erythematous rash, which blanched on palpation and was not associated with crepitus, on the lower abdomen which was tender to touch. On deeper palpation a mobile 4×3 cm lump could be felt in the subcutaneous tissue, which was non-fluctant and not adherent to the underlying fascia. There was no skin excoriation, cutaneous lesion or entry marks to account for the source of the cellulitis. His abdomen was otherwise soft and non-tender with normal bowel sounds.
His initial blood results showed a lactate of 1.8 mmol/L, glucose 32.6 mmol/L, C reactive protein 281 mg/L, sodium 128 mmol/L, creatinine 84 umol/L, urea 6.2 mmol/L, unremarkable liver function tests, Haemoglobin 147 g/L, White Cell Count 19.6×109/L, with neutrophils 15.7×109/L.
The wound swab culture intraoperatively grew a provisional report of anaerobes and a final culture of F. magna, sensitive to metronidazole. No other antibiotic sensitivity was investigated by the microbiologists.
A CT scan of his abdomen and pelvis (figures 1 and 2) showed extensive fat stranding extending from the umbilicus to the pubic bone, with associated subcutaneous gas. Prominent groin lymphadenopathy was noted.
Initial concerns were of severe cellulitis with potential underlying abscess, potentially secondary to diverticular perforation and fistula. Surgical opinion was sought, and fistulation was thought unlikely. Necrotising fasciitis was not initially considered as a likely differential at this point.
The patient was reviewed by the on-call medical team and started on intravenous tazocin 4.5 g three times a day. The patient was admitted and managed as abdominal wall cellulitis according to the Sepsis Six protocol with aggressive fluid resuscitation.3 His observations failed to respond to initial resuscitation and antibiotic treatment. Due to concerns raised by the on-call medical consultant, he had a CT scan of his abdomen and pelvis, which showed locules of gas within the fat of his panniculus with significant fat stranding (figures 1 and 2). There were no hernias. His bowel and peritoneal cavity were intact. The infection was contained within the subcutaneous tissue and did not seem to breach the rectus sheath. This CT was compatible with the clinical findings, and confirmed the diagnosis of necrotising fasciitis.
His antibiotics were changed to the hospital’s empirical antibiotic protocol for necrotising fasciitis, intravenous tazocin 4.5 g three times a day and teicoplanin 900 mg two times per day for the first three doses then once a day. The patient was promptly escalated to the on-call surgical team who took the patient to theatre for debridement of the infection.
The patient was taken to the theatre for debridement of the infection at 10 hours from his admission to hospital. A stab incision was made just above the suprapubic region in the midline where the lump could be felt. Liquified necrotic fat and ‘dishwasher like’ fluid, pathognomic for necrotising fasciitis, was released from the wound along with an offensive smell. The incision was extended after a finger sweep test which showed separation of the facial plane. The area debrided extended further than the erythematous area on the skin and went as deep as just above the rectus sheath. After comprehensive debridement, the patient had a 25×15 cm defect in the lower abdominal panniculus (figure 3). The rectus sheath was not breached.
The wound was dressed with Collatamp G (Schering-Plough, Stockholm, Sweden), a gentamicin-impregnated collagen matrix containing 2.0 mg/cm2 of gentamicin sulphate which is released by a combination of diffusion and enzymatic breakdown of the collagen matrix, giving a high local concentration for at least 72 hours.
Tissue and wound swab cultures were taken intraoperatively and showed a growth of anaerobes, with F. magna the final isolated single organism.
The patient needed ionotropic support for 24 hours postoperation and remained intubated. After being extubated he returned to the ward while receiving intravenous antibiotics (tazocin and teicoplanin) and fluids. He reported feeling much better and his observations improved. The patient proceeded to return to theatre on two further occasions for a surgical relook and debridement. Despite this, the wound was not suitable for primary closure. Tissue viability nurses were involved and his wound was managed with a vacuum dressing system to good effect. He was discharged 7 days following admission, on sensitive oral antibiotics after discussion with microbiology, and follow-up was arranged for consideration of primary closure.
Outcome and follow-up
The patient was readmitted a fortnight after his discharge to the diabetic inpatient ward with difficulty in managing his glycaemic control. He was managed as sepsis of unknown origin—the wound at this time was granulating well and unlikely to be the source. He recovered quickly after 3 days of treatment.
His postoperative wound at 6 weeks had significantly reduced in size and had granulated well (figure 4).
F. magna is a Gram-positive anaerobic coccus, which was previously known by the name Peptostreptococcus magnus. The bacteria is found in the normal flora of the urogenital tract. It is also known to be part of the prepubertal vaginal flora and it is found in 50% of the vaginal flora of pregnant women.4 Other research has demonstrated evidence of the anaerobe in stool cultures.5 6 Murdoch et al noted its association with skin infections, which could indicate it’s presence as normal skin flora.7 The bacteria has been found to be a causative organism in cases of native valve endocarditis, paravalvular abscess around a bioprosthetic valve, purulent pericarditis complicated by mediastanitis, meningitis after pneumonia and necrotising pneumonia complicated by pyopneumothorax.4 8
F. magna has been found to signal neutrophils to release reactive oxygen species and several proinflammatory proteins such as the monosaccharide d-glycero-D-manno-heptose 1,7-bisphosphate (HBP), Interferon gamma (IFN-y) and interleukin 8. Furthermore, it produces a protein called FAF (F. magna adhesion factor) which is able to degrade the host’s immune response with antimicrobial properties similar to protein M, which is produced by Streptococcus pyogenes.9 10 It is also known to create a biofilm which contributes to its survival capabilities.9
There have been no cases in the literature describing necrotising fasciitis of the abdominal wall caused by F. magna. Scapaticci et al have published a case of F. magna causing lower limb necrotising fasciitis originating from a diabetic foot ulcer.11 The patient in this case had caused a small laceration of his toe while clipping his nails, which indicates a clear focus of entry of skin flora. Our patient in this case had no excoriation marks to indicate that the bacteria had penetrated into the subcutaneous tissue through the skin. However, the patient had previously seen his GP and was prescribed antibiotics for a presumed cellulitis which started as an internal lump in his lower abdomen. Our theory is that a minor skin infection or irritation, not excluding a folliculitis, may have led to the introduction of skin F. magna flora into the subcutaneous tissue. The courses of antibiotics given by the GP would have treated his initial skin infection, however given his relatively immunocompromised state caused by his diabetes, the antibiotics were not sufficient to penetrate into the subcutanous plane in a timely fashion, leading to the progression to necrotising fasciitis.
In retrospect, the diagnosis could have been made in a more timely matter; however the atypical appearance of the abdominal rash and examination findings made it difficult to consider necrotising fasciitis as a primary diagnosis. The Laboratory Risk Indicator for Necrotising Fasciitis (LRINEC) Score could have been used to escalate concerns of necrotising fasciitis.12 Calculation in retrospect, reveals a score of 8 at the time of admission, which indicates a high risk for necrotising fasciitis. It is important to be aware that although LRINEC is not validated as a diagnostic score for necrotising fasciitis, it can be used as an adjunct to aid clinical decision making in equivocal cases.12 13
Second, the value of cross-sectional imaging in the form of CT was highlighted, as this was the modality of choice to achieve a diagnosis in this case. A study on use of CT scan in the emergency department concluded that CT is the most appropriate scan in aiding the diagnosis of necrotising fasciitis due to the high spatial resolution. The hallmark of necrotising faciitis on CT is gas within subcutaneous tissues.14 Although gas is not observed in all cases of necrotising fasciitis, other CT findings have been shown to be diagnostic, such as thickening of the affected fascia, fluid collections along the deep fascial sheaths and extension of oedema into the intermuscular septa and the muscles.15
In equivocal cases such as ours with minimal skin compromise, it reiterates the value of cross-sectional imaging in the diagnositc pathway of necrotising fasciitis, however treatment should not be delayed in cases with strong clinical suspicion.
Necrotising fasciitis carries high morbidity and mortality and is a condition which needs prompt and effective treatment. This case report demonstrates that it is not always a clear diagnosis and is accompanied by a spectrum of clinical signs. A high index of clinical suspicion should be maintained in all cases of cellulitis especially in high-risk groups such as patients with diabetes, and immunocompromised, chronic disease and elderly patients. This is the first case in literature describing necrotising fasciitis of the abdominal wall by F. magna, an atypical bacterium in this condition.
This is a rare case of monomicrobial necrotising fasciitis of the abdominal wall.
It is important to have a low threshold of concern for necrotising fasciitis in patients with diabetes, particularly in atypical presentations such as the case described.
Early use of the Laboratory Risk Indicator for Necrotising Fasciitis Score may escalate concerns regarding necrotising fasciitis, enabling earlier definitive management.
Cross-sectional imaging is a valid and easily accessible method of diagnosing necrotising fasciitis when diagnostic uncertainty exists.
Contributors AB performed a literature search and wrote the first draft of the case report. RCM provided further edits, followed up the patient and guided the writing of introduction and discussion. PB followed up the patient and reviewed and edited the final draft.
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.
Competing interests None declared.
Patient consent for publication Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
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