Lyme disease is a multisystem tick-borne transmissive disease with heterogeneous manifestations, frequently making the diagnosis difficult in clinical practice. Herein, we report a case of a 43-year-old female patient who presented with generalized lymphadenopathy requiring a further diagnostic evaluation towards lymphoma. The patient also had clinical signs of Sjögren’s syndrome. Lymph node excision with subsequent histological and immunohistochemical studies were performed. While light microscopy findings were suspicious for lymphoma, immunohistochemistry results were consistent with cortical and paracortical lymph node hyperplasia with no evidence of lymphoproliferative disorder. Further laboratory testing confirmed the presence of Lyme borreliosis.Effectiveness of the administered antibiotic therapy confirmed Borrelia burgdorferi infection. Interrelationships between Sjögren’s syndrome, lymphadenopathy and Lyme disease are discussed.
Green spaces in the city are important for human wellbeing, but are also zones in which humans can become infected with zoonotic diseases. Therefore, there is a need to understand how infection risk is related to green space characteristics, wildlife communities and connectivity with rural areas hosting reservoir populations of hosts. Our hypothesis is that wildlife hosts in urban green spaces, and thereby the prevalence of questing ticks and their Lyme disease causing pathogens (Borrelia burgdorferi s.l.), can be partly predicted based on green space characteristics as well as measures of connectivity to known source areas. We sampled ticks in twenty-two green spaces during Spring (2014 and 2016) and Autumn 2016, located along an urbanization gradient in Antwerp (Belgium). More than 18,000 m2 was sampled, with tick densities ranging from 0 to 386 individuals/100 m2. We estimated connectivity using the least-cost algorithm as either the cost distance to the nearest green space, or to a known population of roe deer (Capreolus capreolus), known to be an important tick propagation host. Both connectivity measures turned out to be correlated, reflecting a gradient in green space isolation from the periphery to the urban center.
In 87% of plots where ticks were trapped, at least one Borrelia-infected tick was found.
The overall Borrelia-prevalence in nymphs was 17.8%, in adults 32.6%.
Density of infected ticks decreased with urbanization and increased with connectivity.
Nymphs in larger green spaces were more likely to be infected.
Density and infection prevalence for adults increased with the amount of neighboring agricultural land, the larval density and nymphal infection prevalence decreased.
Interestingly, the proportion of Borrelia genospecies associated with birds or mammals was comparable in rural and (sub)urban areas (bird/mammal: 0.38), suggesting that even in small green spaces Borrelia infections can persist in local host populations.
This is a colony in urine. (spirochetes in pleomorphic colony in Lyme patient’s urine stain with acridine orange)
We get to the ways that burgdorferi is transmitted. I laugh at all this stuff about looking for the Woodtick. That’s so ridiculous because most of the people who get Lyme disease have never heard or seen a tick. We know now it’s in tears and people wipe their eyes and then you shake hands with them. Or we don’t laugh so hard about the physician we had in the hospital who wouldn’t touch the doorknobs in the hospital without taking his white coat and handling the doorknob through a coat. Maybe he wasn’t so insane after all.
So we think this is spread by what is called fomites(an inanimateobject or substancethat is capable of transmittinginfectiousorganismsfromoneindividual to another) which is the pencil in the bag as you pick up a pen to write a check or anything you handle. So it’s in urine and in tears and it’s also spread by mosquitoes and who hasn’t had a mosquito bite? We’ve tested the mosquitoes in Michigan and sure enough they can carry the Lyme spirochete.
Oh, this is very interesting, I thought. This is a culture of that dreadful spirochete of Lou Gehrig’s and it’s stained with acridine orange and it’s staining red showing it’s still full of pep and multiplying and it’s a 10 day culture. We repeat this with the spirochete of Lyme or MS and at 10 days they are only green so if you have your choice you’re not going to take this one are you? Lou Gehrig’s is the last thing you’d want.
And this is something else where the ordinary lab that doesn’t have florescent antibody – this is a simple stain – Sudan black B. Sudan Black only stains a few things. It stains pseudomonas, you don’t run into pseudomonas in the average patient. Sudan black B. is something you can purchase and doesn’t cost very money like a florescent antibody does – that is very useful. (slide says “membrane *& outgrowth of L-body in blood culture of Lyme patient. Stained with Sudan Black B.) That’s probably my last slide. (Slide says: “To me they’re not just a bunch of microbes – they’re personalities!”)
Together with her collegue JoAnne Whittacker, Mattman did groundbreaking work on Lyme testing. Her Gold Standard Culture Method has disappeared thanks to the concerted suppression on microscopy. In 2004 she already claimed that she could not find any uninfected blood in the USA anymore.
Dr. Lida Mattman studied borrelia for decades and was nominated for the Nobel Prize. She is recognized for her work with diseases such as rheumatoid arthritis, Lou Gehrig’s disease, scleroderma and Parkinson’s. She described the etiology of interstitial cystitis and worked to discern the causes of rheumatoid arthritis and anterior uveitis, the most common cause of blindness.She also taught and used a new method to diagnose tuberculosis in 48 hours.
Having earned her bachelor’s and master’s degrees in microbiology and virology respectively from the University of Kansas and a doctorate in immunology from Yale University in 1940, she was professor of microbiology at Wayne State University since 1949 and is credited with ushering thousands of would-be doctors and nurses into the medical profession. She was awarded the university’s President’s Award for Outstanding Teaching and Research in 1977, retired in 1982, and was inducted into the Michigan Women’s Hall of Fame in 2005. Her book, “Cell Wall Deficient Forms,” written in 1974, is regarded as an invaluable education tool among researchers, students and physicians in the field of microbiology.
In addition to doing research at the universities of Iowa and Pennsylvania, she served as director of clinical laboratories for the United Nations Relief and Rehabilitation Commission and was an instructor at the Harvard School of Public Health.Dr. Mattman died in 2008 at 96 due to liver failure. https://www.findagrave.com/memorial/29190964/lida-mattman
Mattman isolated living Borrelia spirochetes in mosquitoes, fleas, mites, semen, urine, blood, plasma and Cerebral Spinal Fluid. She discovered that this bacteria is dangerous because it can survive and spread without cell wall (L shape). Because L-forms do not possess cell wall, they are resistant to antibiotics that act upon the cell wall.
Others have found various ways Bb is transmitted as well:
Burgess could infect cats with Bb orally, ocularly, and via IV
“The presence of live spirochetes in a genital lesion strongly suggests that sexual transmission of Lyme disease occurs,” said Middelveen. “We need to do more research to determine the risk of sexual transmission of this syphilis-like organism.”
The CDC/IDSA/NIH are on vacation and still haven’t received the memo
But like so many other pioneers who expose inconvenient truths about Lyme, the Michigan State Attorney’s Office told Dr. Mattman to stop testing for Lyme using her gold standard direct culture technique. She also successfully duplicated the results of the Bowen Q-RiBb test, which provided a preliminary report of the findings within 24 hours of receiving the specimen. The final report included digital photographs of the finding, which was useful in evaluating treatment by comparing pre and post serial dilution results.
Mattman was subsequently threatened with time in jail or a fine of 5,000 dollars a day. State police arrived at her lab with handcuffs and tried to find evidence that she was still testing but they didn’t find what they were looking for. She was forced to stop her valuable work and leave her lab.
The continued adherence to worthless 2-tier CDC testing is on purpose. They don’t want an accurate test – they had two and buried them!
Outer surface protein C (OspC) is one of the most abundant surface lipoproteins produced during early infection by the Borrelia spirochete, the causative agent of Lyme disease. The high sequence variability of the ospC gene results in the production of several and strongly divergent OspC types. One of the known roles of OspC is the recruitment of blood components, including complement regulators, to facilitate the bloodstream survival of Borrelia at an essential stage of host infection. Here, we identify and describe a new interaction between OspC and human fibrinogen. To test the ability of OspC to bind fibrinogen, we developed a microscale thermophoresis assay using four fluorescently labeled types of OspC. We show that OspC binds fibrinogen tightly, with nanomolar Kd, and that the binding depends on the OspC type. The binding assays combined with SAXS studies allowed us to map the OspC-binding site on the fibrinogen molecule. Spectrometric measurements of fibrinogen clotting in the presence of OspC indicate that OspC negatively influences the clot formation process. Taken together, our findings are consistent with the hypothesis that OspC interacts with blood protein partners to facilitate Borrelia spreading by the hematogenous route.
Great article on homocysteine and fibrinogen, two biomarkers of inflammation: http://blog.wellnessfx.com/2013/09/16/take-deeper-look-two-biomarkers-inflammation/ There’s even a link between the two biomarkers. High homocysteine levels block the natural breakdown of fibrinogen, leading to a buildup of fibrinogen in the blood which can cause hyper coagulation.
If you struggle with hyper coagulation(thick blood) work with your practitioner as this can hamper the effectiveness of treatment as well as compromise nutrient and oxygen delivery to the body. Also, thicker blood requires the heart to work harder to circulate blood. Some also feel it can deprive the gut of nourishment and may be a factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. https://www.diagnose-me.com/symptoms-of/hypercoagulation-thickened-blood.php. This link also explains testing as well as potential treatments to discuss with your doctor.
Many Lyme/MSIDS struggle with hyper coagulation. My husband does and took heparin for years during treatment. He felt better immediately. He has since weaned from that onto increased fish oil, Berberine, and Systemic Enzymes. Nattokinase is also recommended.
The take home from this study is that Bb uses components of our blood to propagate itself.
Antibiotics can disturb gastrointestinal microbiota which may lead to reduced resistance to pathogens such as Clostridium difficile (C. difficile). Probiotics are live microbial preparations that, when administered in adequate amounts, may confer a health benefit to the host, and are a potential C. difficile prevention strategy. Recent clinical practice guidelines do not recommend probiotic prophylaxis, even though probiotics have the highest quality evidence among cited prophylactic therapies.
Objectives
To assess the efficacy and safety of probiotics for preventing C.difficile‐associated diarrhea (CDAD) in adults and children.
Search methods
We searched PubMed, EMBASE, CENTRAL, and the Cochrane IBD Group Specialized Register from inception to 21 March 2017. Additionally, we conducted an extensive grey literature search.
Selection criteria
Randomized controlled (placebo, alternative prophylaxis, or no treatment control) trials investigating probiotics (any strain, any dose) for prevention of CDAD, or C. difficile infection were considered for inclusion.
Data collection and analysis
Two authors (independently and in duplicate) extracted data and assessed risk of bias. The primary outcome was the incidence of CDAD. Secondary outcomes included detection of C. difficile infection in stool, adverse events, antibiotic‐associated diarrhea (AAD) and length of hospital stay. Dichotomous outcomes (e.g. incidence of CDAD) were pooled using a random‐effects model to calculate the risk ratio (RR) and corresponding 95% confidence interval (95% CI). We calculated the number needed to treat for an additional beneficial outcome (NNTB) where appropriate. Continuous outcomes (e.g. length of hospital stay) were pooled using a random‐effects model to calculate the mean difference and corresponding 95% CI. Sensitivity analyses were conducted to explore the impact of missing data on efficacy and safety outcomes. For the sensitivity analyses, we assumed that the event rate for those participants in the control group who had missing data was the same as the event rate for those participants in the control group who were successfully followed. For the probiotic group, we calculated effects using the following assumed ratios of event rates in those with missing data in comparison to those successfully followed: 1.5:1, 2:1, 3:1, and 5:1. To explore possible explanations for heterogeneity, a priori subgroup analyses were conducted on probiotic species, dose, adult versus pediatric population, and risk of bias as well as a post hoc subgroup analysis on baseline risk of CDAD (low 0% to 2%; moderate 3% to 5%; high > 5%). The overall quality of the evidence supporting each outcome was independently assessed using the GRADE criteria.
Main results
Thirty‐nine studies (9955 participants) met the eligibility requirements for our review. Overall, 27 studies were rated as either high or unclear risk of bias. A complete case analysis (i.e. participants who completed the study) among trials investigating CDAD (31 trials, 8672 participants) suggests that probiotics reduce the risk of CDAD by 60%. The incidence of CDAD was 1.5% (70/4525) in the probiotic group compared to 4.0% (164/4147) in the placebo or no treatment control group (RR 0.40, 95% CI 0.30 to 0.52; GRADE = moderate). Twenty‐two of 31 trials had missing CDAD data ranging from 2% to 45%. Our complete case CDAD results proved robust to sensitivity analyses of plausible and worst‐plausible assumptions regarding missing outcome data and results were similar whether considering subgroups of trials in adults versus children, inpatients versus outpatients, different probiotic species, lower versus higher doses of probiotics, or studies at high versus low risk of bias. However, in a post hoc analysis, we did observe a subgroup effect with respect to baseline risk of developing CDAD. Trials with a baseline CDAD risk of 0% to 2% and 3% to 5% did not show any difference in risk but trials enrolling participants with a baseline risk of > 5% for developing CDAD demonstrated a large 70% risk reduction (interaction P value = 0.01). Among studies with a baseline risk > 5%, the incidence of CDAD in the probiotic group was 3.1% (43/1370) compared to 11.6% (126/1084) in the control group (13 trials, 2454 participants; RR 0.30, 95% CI 0.21 to 0.42; GRADE = moderate). With respect to detection of C. difficile in the stool pooled complete case results from 15 trials (1214 participants) did not show a reduction in infection rates. C. difficile infection was 15.5% (98/633) in the probiotics group compared to 17.0% (99/581) in the placebo or no treatment control group (RR 0.86, 95% CI 0.67 to 1.10; GRADE = moderate). Adverse events were assessed in 32 studies (8305 participants) and our pooled complete case analysis indicates probiotics reduce the risk of adverse events by 17% (RR 0.83, 95% CI 0.71 to 0.97; GRADE = very low). In both treatment and control groups the most common adverse events included abdominal cramping, nausea, fever, soft stools, flatulence, and taste disturbance.
Authors’ conclusions
Based on this systematic review and meta‐analysis of 31 randomized controlled trials including 8672 patients, moderate certainty evidence suggests that probiotics are effective for preventing CDAD (NNTB = 42 patients, 95% CI 32 to 58). Our post hoc subgroup analyses to explore heterogeneity indicated that probiotics are effective among trials with a CDAD baseline risk >5% (NNTB = 12; moderate certainty evidence), but not among trials with a baseline risk ≤5% (low to moderate certainty evidence). Although adverse effects were reported among 32 included trials, there were more adverse events among patients in the control groups. The short‐term use of probiotics appears to be safe and effective when used along with antibiotics in patients who are not immunocompromised or severely debilitated. Despite the need for further research, hospitalized patients, particularly those at high risk of CDAD, should be informed of the potential benefits and harms of probiotics.
What is Clostridium difficile‐associated diarrhea?
Antibiotics are among the most prescribed medications worldwide. Antibiotic treatment may disturb the balance of organisms that normally populate the gut. This can result in a range of symptoms, most notably, diarrhea. Clostridium difficile (C. difficile) is a particularly dangerous organism that may colonize the gut if the normal healthy balance has been disturbed. Clostridium difficile‐related disease varies from asymptomatic infection, diarrhea, colitis, and pseudo‐membranous colitis to toxic megacolon and death. The cost of treatment is expensive and the financial burden on the medical system is substantial.
What are probiotics?
Probiotics are live organisms (bacteria or yeast) thought to improve the balance of organisms that populate the gut, counteracting potential disturbances to the gut microbial balance that are associated with antibiotic use, and reducing the risk of colonization by pathogenic bacteria. Probiotics can be found in dietary supplements or yogurts and are becoming increasingly available as capsules sold in health food stores and supermarkets. As ‘functional food’ or ‘good bacteria’, probiotics have been suggested as a means of both preventing and treating C. difficile‐associated diarrhea (CDAD).
What did the researchers investigate?
The researchers investigated whether probiotics prevent CDAD in adults and children receiving antibiotic therapy and whether probiotics causes any harms (side effects). The researchers searched the medical literature extensively up to 21 March 2017.
What did the researchers find?
This review includes 39 randomized trials with a total of 9955 participants. Thirty‐one studies (8672 participants) assessed the effectiveness of probiotics for preventing CDAD among participants taking antibiotics. Our results suggest that when probiotics are given with antibiotics the risk of developing CDAD is reduced by 60% on average.Among trials enrolling participants at high risk of developing CDAD (> 5%), the potential benefit of probiotics is more pronounced with a 70% risk reduction on average. Side effects were assessed in 32 studies (8305 participants) and our results suggest that taking probiotics does not increase the risk of developing side effects. The most common side effects reported in these studies include abdominal cramping, nausea, fever, soft stools, flatulence, and taste disturbance. The short‐term use of probiotics appears to be safe and effective when used along with antibiotics in patients who are not immunocompromised or severely debilitated. Despite the need for further research, hospitalized patients, particularly those at high risk of CDAD, should be informed of the potential benefits and harms of probiotics.
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