Science topic
Sepsis - Science topic
Systemic inflammatory response syndrome with a proven or suspected infectious etiology. When sepsis is associated with organ dysfunction distant from the site of infection, it is called severe sepsis. When sepsis is accompanied by HYPOTENSION despite adequate fluid infusion, it is called SEPTIC SHOCK.
Questions related to Sepsis
A new concept of regular product has been developed but needs further study. This is a new area for study that is just being discovered.
I am doing a metagenomic data analysis.
Where from cell free DNA of AML patients who have sepsis.
It is a illumina NOVA Seq paired end data.
When I used various algorithms like minimap2, bowtie2 etc I got mapped reads of each TAXA.
What's the best way to predict Species abundance from its number of mapped reads ?
I have ref seq length of species also.
Some do say abundance = mapped reads/ ref seq length.
I wanted to know if there is any literature of how abundance could be predicted which is a more dynamic and robust quantitative value ?
happy to engage !
Does an ip E.coli injection (10^8 ) cause death in 4 hours in C57BL/6? Do I need to hydrate the mouse? Is this a good concentration to mimic a septic situation?
Sepsis is a pervasive problem in hospital and other care facilities that causes an alarming amount of preventable deaths. Please review the attached document for more information on this problem to generate awareness and develop more scientific interest in eliminating the problem.
I have read different protocolos both fast and slow instillation methods and using various volumes of bacterial suspension. I would need to know a standard protocol for intranasal instillation with good recovery of bacteria in lung.
Hi,
I have been struggling to categorise two studies, which needs appraising. Both are 'before-and-after study', which implemented an intervention to the 'after' group and compared the results with 'before' group. Does this make it a cohort study? Which tool should I use?
The studies are:
UTI and maybe sepsis are occasionally encountered after URS and PCNL. From your daily practice What are the possible strategies to prevent infection after RIRS or PCNL?
i tried performing a CLP procedure to induce sepsis in mice and i followed all the instructions in advertised protocols and videos.
after performing the procedure, even a successfull and clean one, with minimal injury the mice did not wake up and even died right after.
any one has an idea what could go wrong?
i tried performing a CLP procedure to induce sepsis in mice and i followed all the instructions in advertised protocols and videos.
after performing the procedure, even a successfull and clean one, with minimal injury the mice did not wake up and even died right after.
any one has an idea what could go wrong?
What is the most common type of surgical site infection?
How do surgical site infections occur?
Can you get an infection 2 months after surgery?
What kind of infection can you get after surgery?
How common are surgical site infections?
What are the signs of sepsis after surgery?
I work on UTI and sepsis. We find occasionally community-acquired UTI due to ESBL-producing E. coli which does not fulfill the MDR criteria (Magiorakos et al. 2013), because they are sensible to all other antibiotics. I have been searching for literature about this, but I have not been able to find studies that describe this fact.
Have you read studies that describes non-MDR ESBL-producing Enterobacteriaceae? Have you also found this?
PCT (Procalcitonin) is a biomarker of sepsis. There has been a link established between SARS-COV-2 and sepsis, but the understanding for how they interact in the body is not well understood. Would monitoring a patient's PCT levels be important in controlling COVID's impact in the body? Could a person's PCT levels be a biomarker for SARS-COV-2 severity?
any research relating to pre-hospital treatment for sepsis in the UK.
will early treatment of sepsis from the ambulance reduce the mortality rate?
Dear RG researchers, may I know how many of you found low lactate level associate with high sepsis mortality? I do encounter many of these cases in Malaysia. Theoretical, the low lactate is due to low pyruvate reserved in patients who had poor oral intake lead to starving.
I am going to study about cell population data generated by automated hematology analyzers related to Neutrophils in sepsis.Study will compare medians of several parameters between normal control group and sepsis patent group.So what would be the sample size determination formula? study is case unmached type and conventional formula needs "Percent of controls exposed"
what food and nutrient will recommend to sepsis patients after recovery? This is related with covid-19 to suggest to patients after discharging.
Hi. I am looking for manual method for sepsis DNA extraction. No kit based method required. Can you please suggest some good protocols? I want DNA extraction of both, cfDNA and bacterial cell DNA.
- late sepsis is a very important cause of mortality and morbidity in NICU , I wanted to know is there any body have experience about covid 19 in neonates who hospitalized due to late sepsis but the final diagnosis is covid 19.
Sepsis is a life-threatening condition that arises when the body's defense reactions against infection damage its own tissues and organs. It is one of the most serious complications of infectious diseases caused by bacteria, viruses, fungi or parasites. There is no scientific literature that shows a connection between surviving sepsis and developing the new coronavirus. There are sayings tell that there are many of cases have developed sepsis. Do any one has Information
Sepsis is a poorly understood condition with surge in cytokines. However there is functional immunosuppression. What's your view and experience?
In my hospital practice, I have a lot of patients with various acute infections of different severity, and most of them with severe infections and sepsis have hypoalbuminemia of various degrees, as we all know, as a part of the acute-phase response. My question: Should we treat this hypoalbuminemia with albumin substitution or not, and if yes, what would be the albumin serum levels when we should start treatment, and what would be dose and percentage of albumin solution for substitution? I would like some references also.
Dear researchers,
are any of u aware of any studies that have looked at obesity sepsis and metabolomics ? I am looking for studies that will look at obesity sepsis and metabolomics ?
I have a 13 amino acids peptide and I want to inject it in mice to induce immunization. The injection will be in the tail vein. After 12 days I expect to have a peak in the production of antibodies, so in the 12th day after injection I will challenge these mice and matched controls with bacteria and perform a mortality curve. I believe this kind of immunization will be protective and prolong mice survival. How much peptide should I use to induce the immune response? One dose is enough? Do I need to inject it several times? When and how much?
If everything works well, I want to produce a monoclonal antibody against this peptide and inject it after the bacteria injections in non-immunized mice to see if this monoclonal antibody works as a new treatment for infections. How much antibody should I inject to try to treat wild-type mice with a monoclonal antibody? One dose is enough? Do I need to inject it several times? When and how much?
Currently working on a paper trying to capture Failure to Rescue by utilizing a clinical decision tool embedded into the EHR. I want to base this tool on SOFA scores and have the RNs utilize a qSOFA for patient's they have concerns about.
While more than half of the ICU patients have either sepsis/infection or are on antimicrobial - How we practice infectious diseases differ significantly between an ICU and other even in the same country (sometimes even different ICUs in the same hospital).
Understanding such practice is fundamental to improve patients' outcome, antibiotic resistance, length of stay, morbidity as well as antimicrobial resistance.
Can you help by answering this survey:
I am currently working with sepsis patients and I want to extend my research to cultures of monocytes from human blood. Does anyone have a reliable method to purify monocytes for culture?
I want to run a meta-analysis on "corticosteroids in the treatment of severe sepsis and septic shock". Unfortunately it is already done. What do we do in such case? Can it be done again? Any suggestion would be appreciated. Thank you in advance.
If you have devised any new parameters for sepsis
Dear friends,
Recently, we use LPS to induce 24h-mouse spesis model to explore the effect of some drugs to splenic Treg expansion. However, sometimes we failed to induce sepsis and splenic Treg expansion after LPS i. p. injection. I asked some friends and they told me that the mice in USA and mice in China have different lethal dose of LPS injection. In addition, they encourage me to use LPS produced in China, which may be a misture instead of ultrapure LPS from sigma. I wonder why sometimes LPS failed to expand Tregs in mice? In addition, may I know the different between LPS from Sigma and beyotimes? May I know some details about LPS subtype and application in experiments.
Yours
Shuoyang Liu
LPS from sigma is:
L9764 Sigma-Aldrich Lipopolysaccharides (rough strains) from Salmonella enterica serotype minnesota Re 595 (Re mutant).
LPS from beyotime(China) is : lipopolysaccharide purified from E. coli O111:B4, which is specific for TLR4 activation or TLR2.
The mice are bought from other labs. The body weight is from 17g-19g. The mice from other labs and from our breeding sometimes are different in response to LPS induction.
How is it possible these threads are now appearing? Can there be a correlation?
I want general information about sepsis and related mechanisms. If you provide me general informatin and details I will thankfull.
Dear researchers,
Have any of you come across specifically publications looking at Right ventricular diastolic dysfunction and sepsis ? I dont there are any studies out there ? if there are any could you forward me the citation please
cheers,
Rakesh
kindly inform what dose is suitable to get sick. I hope not to lose them so quickly. I don't need a sepsis and septic shock model.
I want to conduct a parallel trial study in which 3 care bundles will be implemented aimed to decrease neonatal sepsis.How is sample size calculated?
Data to be collected from patients will be clinical signs of sepsis and blood samples for culture to determine the presence of infection. The outcome variable will be incidence of neonatal sepsis among participants.The study aims to evaluate the impact of the intervention on incidence of sepsis. What will be the best method to analyze this data
i think the methods used to detect the septicemia and bacteriemia is critical and need a professional Technic . isn't it?
Hi,
I am looking for the some common essential criteria for the pathological scoring system in mouse Lung sepsis model. I found some in this article.
I would be thankful if someone can help me.
thanks
Jitendra
Imagine you have sepsis whole human blood (heparin), if you centrifuge, where the bacteria/fungi will be at? Are the bugs in plasma or with human cell?
Dear Researchers, I am trying to induce Motile Aeromonas Septicemia in Loach (15 gram)fish by injecting fish pathogenic strain of Aeromonas, injecting intra- muscular,at different doses 10^6 ,10^7. But there are no sign of disease (7 days)
The water temperature is 26c .Fish were kept without any feed, 3 days prior to experiment to induce the stress.
Please provide your kind suggestions.
Dear researchers, I share with you this important and interesting article, I hope it is of your interest and that you recommend it and share it because it is of interest
Vitamin C is an important anti-oxidant and an enzyme cofactor for many important biological reactions . Sepsis is associated with an acute deficiency of vitamin C , recently vitamin C-containing regimens as adjunctive therapy in sepsis have received much attention.
What do you think, some experience?
Mouse models of endotoxemia (such as an LPS injection) are associated with increased cell death. Such as increases in cell death seen in the spleen.
In human patients with endotoxemia I think cell death is also observed. However, I am unsure where it occurs, to what degree, what cells? What similarities are there to the mouse model?
I would assume there is. However, I don't know any critical-care clinical pathologists to whom I can pose this puzzler.
I can mention that this 12 year old article by L. Moldawer makes reference to cell death in humans; http://www.fasebj.org/content/15/6/879.long Back then it was of course referred to as apoptosis. Which, IMO is a just a general term used by many people for cell death.
What new information is out there regarding cell death observed in humans? Are there any existing treatments which attempt to address/prevent cell death in human clinical endotoxemia (assuming it is looked for)?
I am interested both in positive outcomes and the implications of policy including: impact on practice, the amount of antibiotic use (maternal and neonatal) both where sepsis is proven and not proven, length of hospital stay, psychological effects on the mother. How many mothers and neonates are we treating to reduce the risk of negative sepsis outcomes? Does the use of broad spectrum antibiotics in the initial response provide us with a false re-assurance and delay recognition of the underlying infection that requires a different response?
We are addressing sepsis and how the family can be part of the alert process. We are partnering with our Patient and Family Engagement department and were just wondering if this will be part of your research ? thanks
Working in a medical college in India as the head of department of obstetrics I get to see a lot of cases of sepsis in obstetrics . My interest is both in enhancing my own knowledge and contributing our experiences to studies or analysis dealing with this issue
My email ID amitarays@gmail.com
I was wondering if any of you are aware of any sepsis pertinent severity score, not APCHE or SOFA?
Inflammatory mediators promote insulin resistance, suggesting perhaps that critical care patients may exhibit hyperinsulinemia. However, I have great difficulty finding an article referring to serum insulin levels (there is an overabundance of publications on hyperglycaemia and insulin resistance but not insulin).
I would very much appreciate it if anyone can refer me to a manuscript making reference on insulin levels in any severe inflammatory setting (burns, sepsis, trauma, and surgery… any context where a strong inflammatory response is solicited).
Note: hyperglycaemia is often treated with intensive insulin therapy –it would be super if the study refer to untreated patients.
I am currently writing an assignment on use of IVC Point Of Care Ultrasound to assess Dehydration in Elderly Patient, more talking about sepsis induced dehydration in Emergency Department. If you have personal experience or aware of a relevant publication please let me know
For example Patient came with Post trauma sepsis and doctor ordered Inj. Meropenem . Now If in this case doctors need emergency Craniotomy. now how would you suggest surgical prophylaxis in terms of Drug, dose and duration??
For exemple in sepsis model some researchers use intravenous inoculation and others intraperitoneal.
Any strong evidence for c-reactive protein and albumin ratio in sepsis as predictor of mortality ?
Always we use low dose (max 75mg/die) of diclofenac intravenous infusion during septic shock or sepsis when physically or with others therapies it's not possible to reduce temperature to avoid its emodinamic and metabolic effects. Many times, without renal adverse effects, it seems a good choice and often it changes the global clinical set of the patient.
Have you any study regarding this aspect?
Presently I am using the following steps:
1. I'm using freshly collected blood in EDTA- vacutainer tube.
2. Then, the blood was dilution at 1:3 ratio (blood: Media) in a cell culture plate at 37oC, 5%CO2 for 2h. Then cells were stimulated with or without LPS (1-10 µg/ml) for 6 to 24 h.
3. Surface staining with CD14, HLA-DR, CD80, and CD86 was performed for flow cytometry.
I am trying to quantify the expression of above mentioned surface markers in monocytes gating. So far I have obtained poor results.
The problem is that I am not getting proper results and non-reproducible results.
Any hints or tips would be well highly appreciated.
While using antibiotic Ceftriaxone in mice for CLP model of sepsis, it is always used with some other antibiotics like metronidazole or clindamycin and not alone. Can't we use ceftriaxone alone at higher dose.
Thank you
sepsis among diabetic elderly- impact on their survival - is this too narrow or too wide?
Dear All!
I am going to start thesis work on identifying better methods of preprocessing including normalization and imputation of missing values of microRNA in microarray data . It is request if anyone can share with me regarding microRNA data preprocessing methods of sepsis and normal patients.
best regards, Awais
Hello Folks,
I am searching for mathematical models for Trauma induced patients with Hypovolemic shock, Spesis etc based on Non-Linear Adaptive Closed Loop Control Systems.
I would appreciate any articles or journals or thesis written that could help me develop the model various models.
Also how would you bench test these types of systems?
Thanks
Tim
We need to get the bacteria from the blood of patients with sepsis for diagnosis, is there any commercial device or prototype capable of efficiently purifying bacteria from blood sample (5-7ml)?
We would like to know if there is anything known about the safety en efficacy of Omega-3 fatty acid administration in patients with sepsis or SIRS.
Which antibiotic is used in the latest protocol?
Sepsis, Nephrology, Internal Medicine.
My group is trying to validate a real time PCR detection method for contaminated Total Parenteral Nutritional samples, using 16s rRNA as a target. For this, we need a method of isolating bacterial DNA from this lipid, glucose and amino acids rich sample. Our objective is to create a faster way of diagnosing sepsis in intensive care patients, as the traditional method of culturing takes up to 4 days.
Any clinical experience in using ursodeoxycholic acid in sepsis induced cholestatic jaundice?
According to analyses the strain is also able to adapt very quick.
I read in an article written by Daniel Rittirsch published in 2008 (Harmful molecular mechanisms in sepsis) that a sepsis can trigger thrombosis and large-scale haemorrhage simultaneously. I just wondering why patients with a sepsis triggered stroke are treated with thrombolytic substances. These substances are already hazardous for patients without sepsis in concern of brain haemorrhage. The combination of the enhanced bleeding risk due to the sepsis and the thrombolytic substance most likely result in a considerable higher probability of the occurrence of a brain haemorrhage compared to the treatment of a “normal” stroke.
Does anyone have an explanation for this doubtful therapeutic approach?
Our NICU wants to send heel prick blood for sepsis for work up. Query any experience in this? Any helpful suggestions to reduce contamination rate?
metabolic demands of fever vs the natural response to infection.
While reading different books ,I found many confusing things about the indication of anticoagulants in sepsis. Is there any particular guidelines for the indication of anticoagulants in sepsis?
Pre-transplant splenectomy enhances allograft survival in adults, but that possibilty is unknown in children, whereas splenectomy in children is associated with overwhelming sepsis.
Found many articles that there is always a pre-treatment before injecting the LPS (in mouse), but how can this data be interpreted considering the real status of a patient, who can't have a pre-treatment like this.
Is SIRS really not needed anymore? How does this new definition help physicians in a earlier recognition of sepsis if it is focus on organ damage (SOFA score/qSOFA)? Opinion question of course
my drug doesn't last long (~1hr at best) in the blood stream, so need know how long the lps actually remains there to cause sepsis.
I found that treating my drug (20mg/kg bw; i.p.) after 1hr of LPS (E. coli: O55:B5, 15mg/kg bw; i.p.) made the survival rate 100% up to 33hr and then all the mice in the group died wihtin 60hrs. If LPS lasts long in blood stream then I have to inject my drug at least 3 times at every 1hr after LPS administration.
Best mouse strain for sepsis model. Is there any background for selecting the appropriate strain?
Hello!
I believe most of you must have read the new definitions of sepsis and septic shock published in the "JAMA" latest issue. A new definition in which the SOFA score becomes a diagnostic tool and not just a prognosis-assesment one.
The score in itself is quite easy to use but when it comes to the GCS, what should one do? Most of ICU patients or those with septic shock are sedated. How can we evaluate the GCS then, should we always use the last GCS measured before sedation, or should we assign a random medium number in such cases??
Many thanks for your insight.
Need to know the concentration, dosage and preparation of LPS, I am going to test my drug whether it has any anti-sepsis action.
Assay: Cytokine profile and Survival rate determination
Animal Model: C57BL/6 mouse (6weeks)
LPS: E. coli: O111:B4, O55:85, O127:B8, Salmonella enterica ser. enteritidis/typhimurium
Dose: 15mg/kg bw in 0.9% NaCl
Which one should I use?
Are there any rules/criteria for selecting LPS?
LPS mediated sepsis in mice for cytokine profile to test a drug's anti-inflammatory activity.
I want to check infection in the blood for identification of SEPSIS patients.
My name is Jeremy, I am a senior staff nurse working in a general medical and surgical ICU in the UK.
With recently reading some work on Immunomodulatory Effect of Continuous Venovenous Hemofiltration during Sepsis: Preliminary Data.
As such I would like to ask for the readers help and advice.
With some of our septic patients experiencing acute renal failure needing CVVHDF, I have posed the question, that as yet I can find no answer to.
With 'normal' patients in ARF on CVVHDF, they would become hypothermic to a temperature of 35 Degrees or below. Hence needing active warming through a Bear Hugger and filter heater aids.
With septic patients on CVVHDF, I have seen temperatures of 36-37 Degrees with no heater elements to aid this.
If this is the case, should we not then be complementing them with heater elements to achieve an active temperature of 38-38.5 Degrees? As you may see in the normal immune response to increase an individuals temperature.
Patients are not actively given antipyretic's due to the researched based evidence of increased mortality.
If we are placing septic patients on CVVHDF, then we are actively cooling them! As such, are we not increasing the patients chances of mortality and morbidity?
A patient with paraneoplastic hypercalcemia from metastatic neuroendocrine pancreatic neoplasia shows very high levels of both procalcitonin and calcitonin, in the absence of clinical and lab findings of sepsis. Does anyone have an explanation for this situation?
I am very concerned with if researchers are using values of Troponin T as an indicator of severity of septic patients. Reflecting on my experiences in intensive care unit, patients with septic shock supposedly showed elevated Troponin T whether they had apparent cardiac damages or not (regardless of normal findings of UCG and EKG). I hinted the article published in 2013 by Vasile VC et al entitled "Elevated cardiac troponin T levels in critically ill patients with sepsis.(Am J Med)". Could you give me any suggestion about the correlation of values of Trponin T and severity of sepsis?
Does anybody know the mechanism of sepsis-induced insulin resistance in Equines?
I am looking to use eritoran for blocking TLR4 in my experimental model, but I could not find it available from any commercial company. Can you suggest where I can purchase or how easy it is to get from Eisai Inc.?
Current application of the 3 & 6 hour bundles will necessitate patients seek treatment early for sepsis. I want to quantify the subjective symptoms of older adults with sepsis.
In several clinical settings such as pancreatitis and trauma, a secondary infection can be frequent and often causes death. I wonder if the body in a hyperactivated status would amplify the detrimental effect of bacterial infection. Is there any literatures on this aspect?
As described in literature, CGD usually complicates with frequent gram pos. (but not gram neg.) infections. Does anyone know about the severity (i.e. severe sepsis, septic shock, need of ICU administration) of these infections? And about treatment? How well reacts these patient to antibiotic treatment?
There are many markers of endothelial activation and damage (sVCAM-1, von Wilebrand factor, D-dimer, etc. etc. etc.), and I need to decide for one (ideally) or two to measure in human blood that can tell me if the endothlium has been activated, damaged or dead. We want to look for indicators of activation of any vascularity that can have impact at a systemic level, to the point of possibly participating in septic shock or acute respiratory inflammatory syndrome, empyema, lung edema, deep vein thrombosis, etc (any poor outcome related with inflammation). The patiens will be mainly critical or hospital-bound, with respiratory symptoms, mainly related with infectious diseases. I will thank any ideas.
Do you think procalcitonin is a useful tool for early discovering the post-traumatic septic complications? Has anyone ever tried to assess the increase in plasma current day / day before?
What is the proper statistical test for:
Several (dichotomous) dependent variables WITH single polytomous
independent variable.
I'm trying to select the suitable statistical test to study the association of bacterial
genotype (single polytomous (0,1,2,3,....) independent variable) with several
clinical outcomes for patients (dichotomous (0,1)) dependent variables.
extra explanation:
*Several (dichotomous) dependent variables
1. Pneumonia (0,1) ...... 2. Sepsis (0,1)........3. Abcess (0,1) ,,,etc
*Single (polytomous) independent variable
1. Bacterial genotype (0,1,2,3,4,5)
Thanks
We have a patient with severe sepsis following bronchopneumonia while on cyclophosphamide therapy .
Severe Sepsis is often caused by germs that release LPS or ß-glucans, that are toxic for blood monocytes. Monocyte fragments generate systemically circulating thrombin.
Hi all,
For my MSc, my project is to use an ANN to diagnose Sepsis in patients using various vital signs as inputs. The aim was then to then develop an Android app that allows a user to put in the inputs at the point of care and receive a risk score (% likelihood of sepsis, etc).
I'm constructing my ANN using Matlab (using their pattern recognition network wizard), and I'm using MIT App Inventor 2 to build the App itself.
Where I'm struggling, is understanding how one would actually put the ANN to work with the app.
I've recently been informed that App Inventor 2 isn't powerful enough to host an ANN, and that a possible solution may be to use an online source, such as Google Spreadsheet, however I'm not sure how this would work either.
Another small complication is the nature of the ANN - I'm using 8 inputs to determine one of 2 outputs. However, as these are vital signs, and more useful over a time period (to get a trend), I've actually got something like 24 inputs (8x3) for each patient. Now, if I train the ANN, will that mean that I can't query it unless I have 24 inputs again?
Lots of questions here, I know, but I would really appreciate any feedback, no matter what it might be.
Thank you again,
Conor.
Hi everyone,
I would like to know if there is a putative relationship between sleep deprivation and a faster development of sepsis. Thanks a lot. Lo
I have mice which produced anti-bovine serum albumin. To enhance the antibody production, I administrated bovine serum albumin to these mice by ip. But all administrated mice die after one day. Does anyone explain this phenomina or introduce related papers?
A 44 year old man, was operated on 3 years ago for PVR of the mitral valve (rheumatic stenosis). After 1.5 years he presented an atrial fibrillation, treated with Amiodarone, and after he developed a hyperthyroid state (resolved at present).
Also, in the moment of hyperthyroid state, this patient was treated for an infection of upper airways (= amoxicillin + clavulanic acid 625 mg x 3 times per day – 2 days; but fever was still present; than = cefuroxime axetil 500 mg 1 tab x 2 times per day – 5 days; than = Ceftriaxone 2 gr per day i/v -7 days).
After one month the fever is back. The recommended treatment was with Moxifloxacin 400 mg intravenous- 3 days + 4 days PO; fever disappeared again. The patient continued to take prednisolone ( for cordarone hyperthyreosis). After another month, fever appeared again, with a non-significant sore throat.
At this moment it was performed blood culture (suspect ion for endocarditis.
At echo of heart no signs of endocarditis. In blood: Streptococcus gallolyticus multi sensible. Body scan was performed to determine the origin of this bacteria: all clean.
To treat this bacteremia a treatment with antibiotic was started:
Cefuroxime axetil 500 mg x 2 times per day – 7 days
Ciprofloxacin 500 mg x 2 times per day – 10 days
Moxifloxacin 400 mg IV – 5 days + 12 days PO.
After each scheme of treatment with antibiotics in blood culture was find Streptococcus gallolyticus with the same sensitivity. Clinically patient presents only fever, which disappear during antibiotherapy and is back after stop of this therapy.
It was suspected colon carcinoma (origin of persistent Str. gallolyticus described in the literature), but it was excluded after colonoscopy.
Did you have same situation in your practice: persistent bacteremia with Streptococcus gallolyticus without response to antibiotic treatment?
What you think about the origin of persistent bacteremia?