Lactobacillus rhamnosus sepsis, endocarditis and septic emboli in a patient with ulcerative colitis taking probiotics
- Christian Karime ,
- Maria S Barrios ,
- Nathaniel E Wiest and
- Fernando Stancampiano
- Department of Internal Medicine, Mayo Clinic Florida, Jacksonville, Florida, USA
- Correspondence to Dr Christian Karime; chriskarime@hotmail.com
Abstract
A man in his 60s presented to the emergency room with fever and fatigue after a 2.5-month course of corticosteroids. His medical history was significant for bioprosthetic aortic valve replacement and moderately severe ulcerative colitis treated with balsalazide and daily lactobacillus-containing probiotics. Initial investigations revealed Lactobacillus rhamnosus bacteraemia without complication. Four days after hospital discharge, the patient experienced acute-onset right-sided paraesthesia and lower-limb paresis. On return to the emergency room, MRI of the brain demonstrated innumerable ring-enhancing lesions with haemorrhagic transformation. Transoesophageal echocardiogram revealed a small mobile density on the bioprosthetic aortic valve, raising the suspicion for L. rhamnosus infective endocarditis with secondary septic emboli to the brain. The patient was subsequently treated with intravenous gentamycin and ampicillin, with transition to indefinite oral amoxicillin suppressive therapy. The current case highlights the potential risk of lactobacilli translocation in an immunosuppressed patient with ulcerative colitis taking probiotics.
Background
Probiotics are live micro-organisms that, when consumed in sufficient quantity, are intended to confer a health benefit. According to the National Institute of Health, probiotics are the third most commonly used dietary supplement in the USA.1 While their exact mechanism of action remains poorly understood, probiotics have been associated with improved intestinal microbial balance, competitive inhibition of pathogenic micro-organisms, enhanced intestinal epithelial barrier function, and beneficial modulation of local and systemic immune responses.2–4 Available probiotic formulations contain a variety of micro-organisms designated as Generally Regarded As Safe by the US Food and Drug Administration, with the most common formulations containing bacteria of the Lactobacillus and Bifidobacterium genus.1 3
Despite limited clinical evidence supporting their use, probiotics are commonly used to promote or restore the intestinal microbial balance in both healthy and ill patients. Probiotic use in patients with inflammatory bowel disease (IBD) has gained increasing scientific interest. Studies have demonstrated that patients with IBD have a significant intestinal microbial imbalance, including reduced biodiversity of beneficial commensal flora and increased number of pathogenic micro-organisms.5–7 Although the pathophysiology of IBD is multifactorial, it is widely hypothesised that IBD ultimately results from a dysregulated and persistent immune response towards endogenous intestinal flora and luminal antigens, leading to significant inflammatory cell infiltration and eventual mucosal damage.8 9 While current therapeutic strategies in IBD focus primarily on targeting the immune system with pharmacological agents, there has been a growing interest in the prophylactic and therapeutic potential of probiotics.8 10 Nevertheless, several studies have highlighted the risk of bacterial translocation following probiotic administration, especially in individuals with inflammation-mediated enhanced mucosal permeability or taking immunosuppressive medications.4 11–16
To the best of our knowledge, we report the first case of L. rhamnosus sepsis complicated by bioprosthetic aortic valve endocarditis and septic emboli to the brain in a patient with moderately severe ulcerative colitis taking lactobacilli-containing probiotic supplementation.
Case presentation
A man in his late 60s presented to the emergency room with a 1-week history of fever, fatigue, generalised arthralgias and productive cough. His symptoms started shortly after completion of a 2.5-month course of oral prednisone (20–40 mg) and intermittent 5-day courses levofloxacin 500 mg for chronic unresolving cough. The patient’s medical history included moderately severe ulcerative colitis (Montreal classification S2 E2), treated for the past 6 months with two times a day 750 mg balsalazide and daily 550 mg probiotic supplementation containing a blend of six Lactobacilli species at a concentration of 26 billion colony-forming units (L. paracasein, L. acidophilus, L. plantarium, L. casei, L. salivarius, L. rhamnosus). Medical history also included a bioprosthetic aortic valve replacement 22 months earlier, complicated by acute respiratory distress syndrome requiring tracheostomy and extracorporeal membrane oxygenation.
On presentation to the emergency room, the patient was noted to have a respiratory rate of 30, blood pressure of 80/48 mm Hg, heart rate of 102 and oral temperature of 39.4°C. The initial physical examination was notable for scattered end-expiratory rales in the bilateral lower lung fields and a systolic murmur consistent with his bioprosthetic aortic valve. The abdomen was soft and non-tender to palpation with preserved bowel sounds.
Investigations and treatment
Initial laboratory studies in the emergency room were notable for mild neutrophilic leucocytosis, normocytic anaemia, thrombocytopenia, mild elevation of lactate and marked elevation of procalcitonin (table 1). Initial chest X-ray revealed non-specific bilateral interstitial infiltrates. With the patient meeting 3 of 4 SIRS criteria for shock and a presumed respiratory source of infection on chest X-ray and physical examination, sepsis protocol was initiated. Peripheral blood cultures, urine culture and sampling from the nasopharynx and sputum were collected. The patient was empirically treated with intravenous lactate ringer and intravenous antibiotics (vancomycin, cefepime and azithromycin) for suspected levofloxacin-resistant respiratory tract infection. Midodrine and hydrocortisone were added due to the mean arterial pressure remaining below 65 mm Hg despite adequate fluid resuscitation.
Initial laboratory tests on presentation to emergency department
| Initial laboratory results | |
| Haemoglobin (reference range: 132–166 g/L) |
110.0* |
| Haematocrit (reference range: 38.3%–48.6%) |
34.4* |
| Erythrocytes (reference range: 4.35–5.65×1012/L) |
3.98* |
| Mean corpuscular volume (reference range: 78.2–97.9 fL) |
86.4 |
| Mean corpuscular haemoglobin (reference range: 25.4–32.7 pg) |
27.6 |
| Mean corpuscular haemoglobin concentration (reference range: 321–356 g/L) |
320* |
| Red cell distribution width—SD (reference range: 35.1–43.9 fL) |
49.1* |
| Red cell distribution width—CV (reference range: 11.8%–14.5%) |
15.3* |
| Platelet count (reference range: 135–317×109/L) |
126* |
| White cell count (reference range: 3.4–9.6×109 cells/L) |
11.4* |
| Neutrophile % (reference range: 50%–75%) |
92.4* |
| Immature granulocytes % (reference range: 0%–3%) |
0.5 |
| Lymphocytes % (reference range: 12%–42%) |
4.0* |
| Monocytes % (reference range: 2%–11%) |
2.9 |
| Eosinophils % (reference range: 1%–3%) |
0.0* |
| Basophiles % (reference range: <2%) |
0.2 |
| Neutrophiles (reference range: 1.56–6.45×109/L) |
9.61* |
| Lymphocytes (reference range: 0.95–3.07×109/L) |
0.42* |
| Monocytes (reference range: 0.26–0.81×109/L) |
0.30 |
| Eosinophils (reference range: 0.03–0.48×109/L) |
0.00 |
| Basophiles (reference range: 0.01–0.08×109/L) |
0.02 |
| Lactate (reference range 0.5–2.2 mmol/L) |
2.3* |
| Procalcitonin (reference range <0.08 ng/mL) |
6.4* |
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Notable for mild neutrophilic leucocytosis, normocytic anaemia, thrombocytopenia, mild elevation of lactate and marked elevation of procalcitonin.
-
*Abnormal.
A subsequent non-contrasted CT of the chest did not reveal evidence of pneumonia. Nasopharyngeal and sputum samples were negative for bacterial, viral and fungal pathogens (table 2). Urinary culture was negative for bacteria as well as streptococcus pneumonia and legionella antigen. Initial peripheral blood cultures were found to be positive for gram positive bacteria at 31 and 41 hours, both identified by matrix-assisted laser desorption/ionisation-time of flight mass spectrometry as L. rhamnosus with resistance to meropenem and susceptibility to penicillin. No other micro-organisms were identified despite 7 days of incubation with 24-hour monitoring. Given susceptibilities, the patient’s antibiotic therapy was changed to intravenous ampicillin 2 g every 6 hours for 14 days.
Microbiological testing on initial presentation to the emergency department
Nasopharyngeal sampling
|
Results
|
Sputum collection
|
Results
|
Peripheral blood - Immunofluorescent assay
|
Results
|
Peripheral blood—bacterial culture
|
Result
|
Urine—bacterial culture
|
Result
|
-
Notable for gram positive bacilli in two-of-two blood cultures, with speciation identifying both cultures as Lactobacillus rhamnosus.
-
*Abnormal.
-
Ab, antibody; Ag, antigen.
Given a presumed gastrointestinal source of bacterial translocation secondary to ulcerative colitis and probiotic supplement use, a contrasted CT of the abdomen and pelvis was performed. Results of the abdominal CT revealed a small fluid collection adjacent to the sigmoid mesocolon (figure 1). The patient also underwent a transoesophageal echocardiogram (TEE) given the presence of gram positive bacteraemia in the setting of prior aortic valve replacement, which did not reveal evidence of endocarditis or valvular abnormality. Repeat peripheral blood cultures collected on day 3 of hospitalisation re-demonstrating persistent L. rhamnosus bacteraemia, with identification at 48 and 70 hours, respectively. A third set of peripheral blood cultures were collected on day 5 of hospitalisation, which no longer yielded growth of micro-organisms. On clinical stabilisation and 48 hours negative blood cultures, the patient was discharged with instructions to discontinue probiotic supplementation indefinitely. All blood cultures continued to be monitored for 7 days, with no further growth of micro-organisms.
Contrast enhanced CT of the abdomen/pelvis. Image demonstrates small amount of fluid at the root of the sigmoid mesocolon (red arrow). No focal well-defined or peripherally enhancing fluid collection within the abdomen or pelvis to suggest abscess formation.
Outcome and follow-up
On post-hospitalisation day 4, the patient developed acute-onset transient right-sided paraesthesia involving portions of his right arm, right lateral trunk and anterior right thigh. The following morning symptoms reoccurred, with new onset right leg paresis and inability to ambulate. On presentation to the emergency room, a contrasted CT of the head and neck with angiogram and 3D post-processing demonstrated new juxtacortical foci of haemorrhage and oedema involving the left middle frontal gyrus and left paracentral lobule (figure 2). Minimal subarachnoid haemorrhage within the left central sulcus was also noted. No evidence of vascular stenosis, dissection, aneurism or malformation was found (figure 2). Brain MRI with and without contrast revealed innumerable ring-enhancing lesions with evidence of haemorrhagic transformation and minimal vasogenic oedema, greatest at the left middle frontal gyrus (figure 3).
Non-contrast enhanced CT of the head. (A) Subcortical oedema (green arrow) within the left paracentral lobule with minimal subarachnoid haemorrhage (red arrow) along the adjacent left central sulcus. (B) A small focus of haemorrhage (red arrow) and oedema (green arrow) involving the left middle frontal gyrus and left paracentral lobule.
Contrast enhanced MRI of the brain. (A–C) Numerous supratentorial ring-enhancing lesions involving the left parietal and left occipital regions (green arrows). (D) Susceptibility weighted-imaging shows evidence of haemorrhage (red arrow) within lesions, with greatest haemorrhage involving the left middle frontal gyrus.
Given the high suspicion for subacute bioprosthetic aortic valve endocarditis and secondary septic emboli to the brain, intravenous gentamycin 1 mg/kg every 12 hours was added to intravenous ampicillin for synergistic activity. Blood cultures were repeated, which were negative. A repeat contrasted CT of the chest, abdomen and pelvis did not demonstrate infectious or malignant origin of cranial emboli. Subsequently, a repeat TEE demonstrated a small mobile density on the posterior cusp of the bioprosthetic aortic valve, consistent with bacterial vegetation (figure 4).
Transoesophageal echocardiography. The image demonstrating a small mobile density on the aortic aspect of the posterior cusp of the bioprosthetic aortic valve.
Following clinical stabilisation and complete symptom resolution, the patient was discharged home and antibiotic therapy was transitioned to 6 weeks of intravenous ampicillin 2 g every 6 hours. Indefinite suppressive antibiotic therapy with oral amoxicillin 500 mg every 12 hours was also prescribed given subacute bacterial endocarditis complicated by septic emboli to the brain (figure 5 summarises illness episode). Outpatient TTE 7 days after hospital discharge demonstrated interval resolution of previously noted bioprosthetic aortic valve vegetation. An MRI 10-days after hospital discharge demonstrated persistent innumerable foci of enhancement with reduced oedema in the left frontal and occipital regions. No new enhancing regions were noted. Three months after first presenting with fever, the patient remains asymptomatic without reoccurrence of neurological symptoms. He continues to avoid probiotic supplements and has transitioned to chronic suppressive amoxicillin therapy.
Diagrammatic timeline of initial and subsequent hospitalisation. BID, two times a day; BP, blood pressure; CBC, complete blood count; CMP, comprehensive metabolic panel; HR, heart rate; IV, intravenous; PLT, platelets (×109/L); PO, per oral; QID, four times a day; RBC, red blood cells (×1012/L); RR, respiratory rate; TEE, transoesophagial echocardiography; Temp, temperature; WBC, white blood cells (×109 cells/L).
Discussion
Our case report highlights an exceedingly rare case of L. rhamnosus sepsis complicated by bioprosthetic aortic valve endocarditis and septic emboli to the brain in an immunosuppressed patient with ulcerative colitis taking daily L. rhamnosus-containing probiotic supplementation. Research has shown that although the human gastrointestinal microbial ecosystem is relatively stable and resistant to change, intestinal lactobacilli populations show considerable temporal fluctuations dependent on oral consumptive practices.17 18 While both persistent and transient gastrointestinal lactobacilli have been identified, research has shown that strains of L. rhamnosus do not form stable populations in the human gastrointestinal tract and are likely transient microbial inhabitants whose presence and numerical predominance depends on ingestion of food or probiotic supplementation.19 20
Although lactobacilli are usually considered non-pathogenic flora of the gastrointestinal and female urogenital tract, studies have identified intestinal translocation as a major portal of entry. Intestinal translocation and lactobacillus bacteraemia is more common in patients who are immunosuppressed, recently undergone microbiome-disrupting antibiotic therapy, or who suffer from disorders disrupting or enhancing the permeability of the intestinal epithelial barrier.4 21–23 Consistent with previous reports of lactobacillus bacteraemia, our current patient had received a prolonged 2.5-month course of systemic immunosuppressive therapy as well as microbiome-disrupting antibiotic therapy with no activity against lactobacilli.22 This environment may have created a favourable selection pressure for probiotic-derived lactobacilli intestinal overgrowth while hampering the immune system’s ability to combat potential bacterial translocation. Furthermore, given that research has shown L. rhamnosus exacerbates intestinal inflammation and translocates in conditions of extensive mucosal damage, our patient’s history of moderately severe ulcerative colitis and the associated inflammation-mediated enhanced intestinal permeability may have further facilitated bacterial translocation.24 A summary of reported risk factors for intestinal translocation of lactobacillus relevant to the current case can be found in figure 6. While previous case reports have demonstrated the association between L. rhamnosus bacteraemia and endocarditis, we believe our work represents the first case of L. rhamnosus endocarditis with secondary innumerable septic emboli to the brain.
Diagrammatic representation of reported risk factors for intestinal translocation of lactobacillus in relation to current patient. Figure summarises the most important applicable risk factors in the current patient for lactobacillus translocation and development of subacute bioprosthetic valve endocarditis. Diagram does not represent an exhaustive list of plausible risk factors. CFU, colony forming units.
Prior research has identified lactobacilli as one of the most common bacteria to translocate the intestinal epithelium.23 25 While lactobacilli bacteraemia is rare in healthy individuals owing to an intact intestinal barrier and immune clearance of translocated bacteria, several cases of opportunistic infections have been reported in patients with a history of immunosuppression, solid organ transplant, abdominal surgery, cancer and IBD.15 22 26 These opportunistic infections include infective endocarditis, peritonitis, intrabdominal abscess and meningitis, with L. rhamnosus and casei being the most commonly isolated organisms.22 26 Although the incidence of lactobacillus endocarditis is very low, endocarditis is one of the most commonly associated sequelae of L. rhamnosus bacteraemia. In these cases, isolated strains were reported to possess the ability to bind fibronectin, fibrinogen and collagen as well as induce platelet aggregation.27–29 Only three cases of L. rhamnosus bacteraemia in patients with ulcerative colitis taking probiotic supplementation have been reported previously.12 15 16 However, evidence demonstrating elevated serum bacterial lipopolysaccharide (LPS), bacterial DNA, LPS-binding protein and LPS-directed antibodies in patients with IBD suggests microbial translocation is a common occurrence.30–33
While the aetiology of IBD remains incompletely understood, significant alterations to the gut microbiota function and biodiversity (collectively referred to as dysbiosis) has been observed.8 34 However, whether dysbiosis serves as the inciting event, functions to perpetuate the underlying inflammatory dysregulation, or is simply the result of altered gastrointestinal conditions remains unclear.10 While current therapeutic strategies in IBD focus primarily on targeting the immune system with pharmacological agents, there has been an increasing focus on the therapeutic potential of probiotic supplementation to induce or maintain disease remission.8 10 Although extensive research supports the physiological and immunological function of the microbiome through yet incompletely understood mechanisms, a 2020 comprehensive technical review of available human randomised control trials (RCTs) by the American Gastroenterological Association concluded that there was insufficient evidence to recommend probiotic use in patients with IBD, with significant knowledge gaps remaining.10 For a summary of RCTs included, see table 3. Furthermore, in a systemic review of probiotic, prebiotic and synbiotic therapy RCTs by Bafeta et al, severe inadequacy of therapeutic harm reporting was noted.35 Of 384 RCTs (of which 69% were probiotic RCTs), no harm-related data, safety results or number of serious adverse events were reported in 28%, 37% and 80% of RCTs, respectively. Importantly, 98% of trials did not provide a definition of adverse events, report number of participant withdrawal due to harm, or report number of adverse events per study group.35 As such, it is difficult to broadly conclude that these interventions are safe without the reporting of safety data.
Summary of published randomised control trials for induction and maintenance of remission in patients with inflammatory bowel disease
| Study groups | Main finding | Probiotic species | Reference |
| Induction of remission (Crohn’s disease) | |||
| Probiotic vs placebo after 1 week of antibiotics (both receiving concomitant tapering steroids) | No difference in induction or maintenance of remission at 6 months | Lactobacillus rhamnosus | Schultz et al 36 |
| Maintenance of remission (Crohn’s disease) | |||
| Probiotic vs placebo (no other treatment allowed) after surgical induction | No difference in relapse prevention at (a) 3 months or (b) 6 months | Lactobacillus johnsonii | (a) Van Gossum et al 37 (b)Marteau et al. (2006)38 |
| Probiotic vs placebo after surgical induction | No difference in relapse prevention at 3 and 12 months. Reduced mucosal inflammatory cytokine levels compared with placebo at 3 months. Crohn’s disease activity index and inflammatory bowel disease quality of life scores were similar |
Lactobacilli (paracasei, plantarum, acidophilus, delbrueckii) and Bifidobacterium (longum, breve, infantis), and Streptococcus salivarius thermophilus. | Fedorak et al 39 |
| Probiotic vs placebo after medical induction (steroids or salicylates) | No difference in relapse prevention at 1 year. No significant difference between groups in mean Crohn’s disease activity index scores or erythrocyte sedimentation rates or in median levels of C reactive protein |
Saccharomyces boulardii | Bourreille et al 40 |
| Induction of remission (ulcerative colitis) | |||
| Probiotic vs placebo (both groups continued treatment with steroid induction and mesalamine maintenance) | Higher rate of remission induction in probiotic vs placebo treated children at 1 year. At 6 months, 12 months or at time of relapse, endoscopic and histological scores were significantly lower in the probiotic group than in the placebo group |
Lactobacilli (paracasei, plantarum, acidophilus, delbrueckii) and Bifidobacterium (longum, breve, infantis), and Streptococcus salivarius thermophilus | Miele et al 41 |
| Probiotic with low-dose balsalazide vs medium-dose balsalazide alone or mesalazine alone | Higher rate of remission induction in probiotic with low-dose balsalazide group at 8 weeks | Lactobacilli (paracasei, plantarum, acidophilus, delbrueckii) and Bifidobacterium (longum, breve, infantis), and Streptococcus salivarius thermophilus | Tursi et al 42 |
| Probiotic vs placebo (both groups continued treatment with mesalamine, azathioprine or 6-mercaptopurine) | Higher rate of remission induction at 12 weeks. Significantly greater decreases in ulcerative colitis disease activity index scores and individual symptoms at weeks 6 and 12 in probiotic group |
Lactobacilli (paracasei, plantarum, acidophilus, delbrueckii) and Bifidobacterium (longum, breve, infantis), and Streptococcus salivarius thermophilus | Sood et al 43 |
| Probiotic vs placebo (both groups continued treatment with sulfasalazine, or mesalazine) | No difference in rate of remission at 12 weeks. Significantly reduced endoscopic activity index and histological score in probiotic group |
Bifidobacterium breve, Bifidobacterium bifidum, Lactobacillus acidophillus | Kato et al 44 |
| Probiotic vs placebo enema (both receiving mesalazine) | Increased rate of remission at 8 weeks. Decrease endoscopic and histological mucosal damage in probiotic group |
Lactobacillus reuteri | Oliva et al 45 |
| Probiotic vs placebo (both groups continued treatment with mesalamine, prednisolone, azathioprine and/or 6-mercaptopurine) | No difference in rate of remission at 8 weeks. Significant decrease of ulcerative colitis disease activity index scores, and endoscopic index scores |
Bifidobacterium longum | Tamaki et al 46 |
| Probiotic vs placebo after treatment with ciprofloxacin (add on therapy allowed except immunotherapy or systemic steroids) | Significantly fewer patients treated with probiotic reached remission. Patients treated with probiotics without an initial antibiotic cure did worse |
Non-pathogenic Escherichia coli | Petersen et al 47 |
| Maintenance of remission (ulcerative colitis) | |||
| Probiotics vs mesalamine after induction of remission with oral steroids and 1 week of gentamicin | No difference in rate of remission maintenance at 1 year | Non-pathogenic Escherichia coli | Rembacken et al 48 |
| Probiotic vs mesalamine | Equivalence, with no difference in relapse rates at 12 weeks. No difference in clinical activity index difference between the two groups |
Non-pathogenic Escherichia coli | Kruis et al 49 |
| Probiotics vs mesalamine | Equivalence, with no difference in relapse rates at 12 months. Clinical activity index showed a slightly larger increase in the probiotic group. No significant differences between groups on endoscopic index of histological examination |
Non-pathogenic Escherichia coli | Kruis et al 50 |
| Probiotic vs placebo (no other medications allowed) | No difference in remission maintenance at 1 year | Lactobacillus acidophilus and Bifidobacterium animalis | Wildt et al 51 |
| Probiotic vs mesalamine vs probiotic and mesalamine | No difference in relapse rates at 6 months and 12 months. No statistically significant differences were noted at 6 and 12 months on clinical, endoscopic or histological scores |
Lactobacillus rhamnosus | Zocco et al 52 |
| Probiotic vs placebo (both groups continued chronic medical treatment) | No difference in relapse rates at 6, 9 or 12 months | Streptococcus faecalis, Clostridium butyricum and Bacillus mesentericus | Yoshimatsu et al 53 |
| Probiotic vs placebo (no other therapy) | No difference in incidence of relapse or relapse-free survival at 48 weeks | Bifidobacterium breve and Lactobacillus acidophilus | Matsuoka et al 54 |
-
Studies included as per the American Gastroenterological Association technical review of probiotics in gastrointestinal disorders.10
In conclusion, the literature suggests that patients with ulcerative colitis who have recently undergone immunosuppressive and microbiome-disrupting antibiotic therapy have an elevated risk of intestinal bacterial translocation. Our current case highlights the risk and potential severe complications of lactobacillus bacteraemia in an elderly immunosuppressed patient taking lactobacilli-containing probiotics for ulcerative colitis management. Given the inconclusive benefit of probiotic supplementation in patients with IBD and under-reporting of adverse events in RCTs, the current case serves to raise awareness of potential adverse results and urges caution when probiotics are to be used in patients with immunosuppression and IBD.
Learning points
-
Bacteria of the lactobacilli genus, including Lactobacillus rhamnosus, are commonly used in oral probiotic formulations.
-
Research has shown that while both persistent and transient lactobacilli populations are found in the human gastrointestinal tract, L. rhamnosus is likely a transient inhabitant whose presence and numerical predominance depends on oral consumptive practices and probiotic supplementation.
-
Several studies have highlighted the risk of bacterial translocation following probiotic administration, in particular for patients who are immunocompromised or those with inflammatory bowel disease (IBD) whose intestinal mucosa has enhanced permeability.
-
Although the incidence lactobacillus endocarditis is very low, endocarditis is one of the most commonly associated sequelae of L. rhamnosus bacteraemia.
-
The 2020 comprehensive technical review by the American Gastroenterological Association on the potential benefit of probiotic supplementation in IBD was inconclusive and highlighted significant knowledge gaps, with independent systemic review of randomised control trials highlighting concerns for non-reporting of therapy harm and adverse events.
Ethics statements
Patient consent for publication
Acknowledgments
The authors would like to thank Sina O’Sullivan, Seyed M Seyedsaadat and Sabrina D Phillips for their expertise in preparing and interpreting radiographic and echocardiographic images for the current study.
Footnotes
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Twitter @MedWiest
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Contributors CK made substantial contributions to the conception or design of the work, contacted patient, summarised case, drafted the work and revised it critically for important intellectual content; and agreed to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. MB made substantial contributions to the conception or design of the work, drafted the work and revised it critically for important intellectual content; and agreed to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. NW made substantial contributions to the conception or design of the work, revised the work critically for important intellectual content and gave final approval of the version to be published. FS made substantial contributions to the conception or design of the work, revised the work critically for important intellectual content and gave final approval of the version to be published.
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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.
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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.
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Competing interests None declared.
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Provenance and peer review Not commissioned; externally peer reviewed.
- © BMJ Publishing Group Limited 2022. No commercial re-use. See rights and permissions. Published by BMJ.
References
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