90 < Back to Research Top Published Date 18/12/2019 Detection of Borrelia crocidurae in a vaginal swab after miscarriage, rural Senegal, Western Africa Journal International Journal of Infectious Diseases Citation Int J Infect Dis . 2020 Feb;91:261-263 DOI 10.1016/j.ijid.2019.12.020 Authors Fall N.S, Diagne N, Mediannikov O, Fenollar F, Parola P, Sokhna C, Raoult D, Lagier J-C Abstract Tick-borne relapsing fever (TBRF) borreliae are one of the main causes of fever in rural Africa and can cause miscarriages. This article reports Borrelia crocidurae as a probable cause of spontaneous miscarriage, which was detected through vaginal self-sampling. This appears to be the first such report. URL Previous https://www.ijidonline.com/article/S1201-9712(19)30493-X/fulltext No Review Needed? Next

< Back New CME course on "Diagnostic Challenges in Lyme disease" LRC 29 Jan 2023 Previous Next

291 < Back to Research Top Published Date 08/04/2010 Bartonella vinsonii subsp. berkhoffii and Bartonella henselae bacteremia in a father and daughter with neurological disease Journal Parasites & Vectors Citation Parasit Vectors. 2010 Apr 8;3(1):29 DOI 10.1186/1756-3305-3-29 Authors Breitschwerdt EB, Maggi RG, Lantos PM, Woods CW, Hegarty BC, Bradley JM Abstract BACKGROUND: Bartonella vinsonii subsp. berkhoffii is an important, emerging, intravascular bacterial pathogen that has been recently isolated from immunocompetent patients with endocarditis, arthritis, neurological disease and vasoproliferative neoplasia. Vector transmission is suspected among dogs and wild canines, which are the primary reservoir hosts. This investigation was initiated to determine if pets and family members were infected with one or more Bartonella species. METHODS: PCR and enrichment blood culture in Bartonella alpha Proteobacteria growth medium (BAPGM) was used to determine infection status. Antibody titers to B. vinsonii subsp. berkhoffii genotypes I-III and B. henselae were determined using a previously described indirect fluorescent antibody test. Two patients were tested sequentially for over a year to assess the response to antibiotic treatment. RESULTS: Intravascular infection with B. vinsonii subsp. berkhoffii genotype II and Bartonella henselae (Houston 1 strain) were confirmed in a veterinarian and his daughter by enrichment blood culture, followed by PCR and DNA sequencing. Symptoms included progressive weight loss, muscle weakness, lack of coordination (the father) and headaches, muscle pain and insomnia (the daughter). B. vinsonii subsp. berkhoffii genotype II was also sequenced from a cerebrospinal fluid BAPGM enrichment culture and from a periodontal swab sample. After repeated courses of antibiotics, post-treatment blood cultures were negative, there was a decremental decrease in antibody titers to non-detectable levels and symptoms resolved in both patients. CONCLUSIONS: B. vinsonii subsp. berkhoffii and B. henselae are zoonotic pathogens that can be isolated from the blood of immunocompetent family members with arthralgias, fatigue and neurological symptoms. Therapeutic elimination of Bartonella spp. infections can be challenging, and follow-up testing is recommended. An increasing number of arthropod vectors, including biting flies, fleas, keds, lice, sandflies and ticks have been confirmed or are suspected as the primary mode of transmission of Bartonella species among animal populations and may also pose a risk to human beings. URL Previous https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2859367 No Review Needed? Next

184 < Back to Research Top Published Date 04/11/2015 Quantification of Borrelia burgdorferi Membrane Proteins in Human Serum: A New Concept for Detection of Bacterial Infection Journal Analytical Chemistry Citation Anal Chem. 2015 Nov 17;87(22):11383-8 DOI 10.1021/acs.analchem.5b02803 Authors Cheung CS, Anderson KW, Benitez KY, Soloski MJ, Aucott JN, Phinney KW, Turko IV Abstract The Borrelia burgdorferi spirochete is the causative agent of Lyme disease, the most common tick-borne disease in the United States. The low abundance of bacterial proteins in human serum during infection imposes a challenge for early proteomic detection of Lyme disease. To address this challenge, we propose to detect membrane proteins released from bacteria due to disruption of their plasma membrane triggered by the innate immune system. These membrane proteins can be separated from the bulk of serum proteins by high-speed centrifugation causing substantial sample enrichment prior to targeted protein quantification using multiple reaction monitoring mass spectrometry. This new approach was first applied to detection of B. burgdorferi membrane proteins supplemented in human serum. Our results indicated that detection of B. burgdorferi membrane proteins, which are ?10(7) lower in abundance than major serum proteins, is feasible. Therefore, quantitative analysis was also carried out for serum samples from three patients with acute Lyme disease. We were able to demonstrate the detection of ospA, the major B. burgdorferi lipoprotein at the level of 4.0 fmol of ospA/mg of serum protein. The results confirm the concept and suggest that the proposed approach can be expanded to detect other bacterial infections in humans, particularly where existing diagnostics are unreliable. URL Previous https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4809138 No Review Needed? Next

In normal erythrocytes, small quantities of methaemoglobin are formed constantly and are continuously reduced, almost entirely by the reduced nicotine adenine dinucleotide (NADH) diaphorase system, rather than the reduced nicotine adenine dinucleotide phosphate (NADPH) diaphorase system. < Back Drug-Induced Methaemoglobinaemia LRC 19 Oct 2022 Source: Drug-Induced Methaemoglobinaemia | SpringerLink In normal erythrocytes, small quantities of methaemoglobin are formed constantly and are continuously reduced, almost entirely by the reduced nicotine adenine dinucleotide (NADH) diaphorase system, rather than the reduced nicotine adenine dinucleotide phosphate (NADPH) diaphorase system. Methaemoglobinaemias are usually the result of xenobiotics, either those that may directly oxidise haemoglobin or those that require metabolic activation to an oxidising species. The most clinically relevant direct methaemoglobin formers include local anaesthetics (such as benzocaine and, to a much lesser extent, prilocaine) as well as amyl nitrite and isobutyl nitrite, which have become drugs of abuse. Indirect, or metabolically activated, methaemoglobin formation by dapsone and primaquine may cause adverse reactions. The clinical consequences of methaemoglobinaemia are related to the blood level of methaemoglobin; dyspnoea, nausea and tachycardia occur at methaemoglobin levels of ≤30%, while lethargy, stupor and deteriorating consciousness occur as methaemoglobin levels approach 55%. Higher levels may cause cardiac arrhythmias, circulatory failure and neurological depression, while levels of 70% are usually fatal. Cyanosis accompanied by a lack of responsiveness to 100% oxygen indicates a diagnosis of methaemoglobinaemia, which should be confirmed using a CO-oximeter. Pulse oximeters do not detect methaemoglobin and may give a misleading impression of patient oxygenation. Methaemoglobinaemia is treated with intravenous methylene blue (methyl-thioninium chloride; 1 to 2 mg/kg of a 1% solution). If the patient does not respond, perhaps because of glucose-6-phosphate dehydrogenase (G6PD) deficiency or continued presence of toxin, admission to an intensive care unit and exchange transfusion may be required. Dapsone-mediated chronic methaemoglobin formation can be reduced by co-administration of cimetidine to aid patient tolerance. Increasing knowledge and awareness of drug-mediated acute methaemoglobinaemia among physicians should lead to prompt diagnosis and treatment of this potentially life-threatening condition. References Misra HP, Fridovitch I. The generation of Superoxide radical during the autoxidation of hemoglobin. J Biol Chem 1972; 247: 6960–2 PubMed CAS Google Scholar Mansouri A, Lurie AA. Methemoglobinaemia. Am J Hematol 1993; 42: 7–12 Article PubMed CAS Google Scholar Bunn HF, Forget BG. Hemoglobin: molecular, genetic and clinical aspects. Philadelphia: WB Saunders, 1986: 634–62 Google Scholar Rodriguez LF, Smolik LM, Zbehlik AJ. Benzocaine-induced methaemoglobinaemia: report of a severe reaction and review of the literature. Ann Pharmacother 1994; 28(5): 643–9 PubMed CAS Google Scholar Lindstrom TR, Ho C, Pisciotta AV. Nuclear magnetic resonance studies of haemoglobin. M Milwaukee Nat New Biol 1972; 237: 263–5 CAS Google Scholar Wilson G, Borthwick T, Lamb R. Toxic methaemoglobinaemia. J Tenn Med Assoc 1989; 82: 581–3 PubMed CAS Google Scholar Jaffe ER. Methaemoglobinaemia in the differential diagnosis of cyanosis. Hosp Pract 1985; 20: 92–110 CAS Google Scholar Winterhalter KH, Di Iorio EE, Beetlestone JG, et al. The electronic structure of haem in haemoglobin Zurich β63-His-Arg. J Mol Biol 1972; 70: 665–74 Article PubMed CAS Google Scholar Coleman MD, Ogg MS, Holmes JL, et al. Studies on the differential sensitivity between diabetic and non-diabetic human erythrocytes to monoacetyl dapsone hydroxylamine-mediated methaemoglobin formation in vitro. Env Toxicol Pharmacol 1996; 1: 97–102 Article CAS Google Scholar Park CM, Nagel RL. Sulfhemoglobinemia: clinical and molecular aspects. N Engl J Med 1984; 310: 1579–84 Article PubMed CAS Google Scholar Smith RP. Toxic responses of the blood. In: Klaasen CD, Amdur MO, Doull J, editors. Casarett and Doull’s toxicology. New York: MacMillan, 1986: 223–45 Google Scholar Jaffe ER, Hultquist DE. Cytochrome b5 reductase deficiency and enzymopenic hereditary methemoglobinaemia. In: Scriver CR, Beaudel AL, Sly WS, et al., editors. The metabolic basis for hereditary disease. New York: McGraw-Hill, 1989: 2267–80 Google Scholar Posthumus MD, van Berkel W. Cytochrome b 5 reductase deficiency and uncommon cause of cyanosis. Neth J Med 1994; 44: 136–40 PubMed CAS Google Scholar Yubisui T, Miyata T, Iwanaga S, et al. 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Clin Physiol Biochem 1990; 8: 204–10 PubMed CAS Google Scholar DeGowin RL, Bennet Eppes R, Powell RD. The haemolytic effects of diphenylsulphone (DDS) in normal subjects and in those with glucose-6-phosphate dehydrogenase deficiency. Bull World Health Organ 1966; 35: 165–79 PubMed CAS Google Scholar Beutler E, Baluda MC. Methemoglobin reduction-studies of the interaction between red cell populations and of the role of methylene blue. Blood 1963; 22: 323–33 PubMed CAS Google Scholar Bhutani A, Bhutani MS, Patel R. Methaemoglobinaemia in a patient undergoing gastrointestinal endoscopy. Ann Pharmacother 1992; 26(10): 1239–40 PubMed CAS Google Scholar Frayling IM, Addison GM, Chattergee K. Methaemoglobinaemia in children treated with prilocaine-lignocaine cream. BMJ 1990; 301: 153–4 Article PubMed CAS Google Scholar Tarburton JP, Metcalf WK. The kinetic differences between sodium nitrite, amyl nitrite and nitroglycerin oxidation of hemoglobin. Histol Histopathol 1986; 1: 213–7 PubMed CAS Google Scholar Bradberry SM, Whittington RM, Parry DA, et al. Fatal methemoglobinemia due to inhalation of isobutyl nitrite. J Toxicol Clin Toxicol 1994; 32(2): 179–84 Article PubMed CAS Google Scholar Machabert R, Testud F, Descotes J. Methaemoglobinaemia due to nitrite inhalation: a case report. Hum Exp Toxicol 1994; 13(5): 313–4 Article PubMed CAS Google Scholar Johnson WS, Hall AH, Rumack BH. Cyanide poisoning successfully treated without ‘therapeutic methaemoglobin levels’. Am J Emerg Med 1989; 7(4): 437–40 Article PubMed CAS Google Scholar Bruning-Fann CS, Kaneene JB. The effects of nitrate, nitrite and N-nitroso compounds on human health. Vet Hum Toxicol 1993; 35(6): 521–38 PubMed CAS Google Scholar Dusdieker LB, Getchell JP, Liarakos TM, et al. Nitrate in baby foods-adding to the nitrate mosaic. Arch Pediatr Adolesc Med 1994; 148(5): 490–4 Article PubMed CAS Google Scholar Kaplan A, Smith C, Promnitz, et al. Methaemoglobinaemia due to accidental sodium nitrite poisoning. S Afr Med J 1990; 77: 300–1 PubMed CAS Google Scholar Ellis Y, Hiss Y, Shenkman L. Fatal methemoglobinemia caused by inadvertent contamination of a laxative solution with sodium nitrite. Isr J Med Sci 1992; 28(5): 289–91 PubMed CAS Google Scholar Ternberg JL, Luce E. Methaemoglobinaemia: a complication of the silver nitrate treatment of burns. Paediatric Surg 1968; 63: 328–30 Google Scholar Adatia I, Lillehei C, Arnold JH. Inhaled nitric oxide in the treatment of post-operative graft dysfunction after lung transplantation. Ann Thorac Surg 1994; 57(5): 1311–8 Article PubMed CAS Google Scholar Shah N, Jacob T, Exler R. Inhaled nitric oxide in congenital diaphragmatic hernia. J Pediatr Surg 1994; 29(8): 1010–5 Article PubMed CAS Google Scholar Rossaint R, Gerlach H, Schmidt-Ruhnke H. Efficacy of inhaled nitric oxide in patients with severe ARDS. Chest 1995; 107(4): 1107–15 Article PubMed CAS Google Scholar Williams RS, Mickell JJ, Young ES. Methaemoglobin levels during prolonged combined nitroglycerin and sodium nitroprusside infusions in infants after cardiac surgery. J Cardiothorac Anesth 1994; 8(6): 658–62 Article CAS Google Scholar Norambuena E, Videla LA, Lissi EA. Interaction of nitrobenzoates with haemoglobin in red blood cells and a haemolysate. Hum Exp Toxicol 1994; 13: 345–51 Article PubMed CAS Google Scholar Hornfeldt CS, Rabe WH. Nitroethane poisoning from an artificial fingernail remover. J Toxicol Clin Toxicol 1994; 32(3): 321–4 Article PubMed CAS Google Scholar Schimelman MA, Soler JM, Muller HA. Methemoglobinemia: nitrobenzene ingestion. J Amer Coll Emerg Phys 1994; 7(11): 406–8 Article Google Scholar Dinneen SF, Mohr DN, Fairbanks VF. Methemoglobinemia from topically applied anesthetic spray. Mayo Clin Proc 1994; 69(9): 886–8 PubMed CAS Google Scholar Guertler AT, Lagutchik MS, Martin DG. Topical anesthetic-induced methemoglobinemia in sheep: a comparison of benzocaine and lidocaine. Fundam Appl Toxicol 1992; 18: 294–8 Article PubMed CAS Google Scholar Jensen CB, Jollow DJ. The role of N-hydroxyphenetidine in phenacetin-induced hemolytic anemia. Toxicol App Pharmacol 1991; 111(1): 1–12 Article CAS Google Scholar Morais M da S, Augusto O. Peroxidation of the antimalarial drug primaquine: characterisation of a benzidine-like metabolite with methaemoglobin forming capacity. Xenobiotica 1993; 23(2): 133–9 Article CAS Google Scholar Zone JJ. Dermatitis Herpetiformis. Curr Probl Dermatol 1991; 3: 4–42 Article Google Scholar Coleman MD. Dapsone: modes of action, toxicity and possible strategies for increasing patient tolerance. Br J Dermatol 1993; 129: 507–13 Article PubMed CAS Google Scholar Kiese M, Reinwein D, Waller HD. Kinetik der Hamiglobinbildung. IV Mitteilung. Die Hamiglobinbildung durch Phenylhydroxylamin und Nitrosobenzol in roten Zellen in vitro. Naun Schmied Arch Exp Pathol Pharmakol 1950; 210: 393–8 CAS Google Scholar Coleman MD, Rhodes LA, Scott AK, et al. The use of cimetidine to reduce dapsone-dependent methaemoglobinaemia in dermatitis herpetiformis patients. Brit J Clin Pharmacol 1992; 34: 244–9 Article CAS Google Scholar Cribb AE, Spielberg SP. Sulfamethoxazole is metabolised to the hydroxylamine in humans. Clin Pharmacol Ther 1992; 51: 522–6 Article PubMed CAS Google Scholar Pirmohamed M, Coleman MD, Galvani D, et al. Lack of interaction between sulphasalazine and cimetidine in patients with rheumatoid arthritis. Br J Rheumatol 1993; 32: 222–6 Article PubMed CAS Google Scholar Brown TD, O’Rourke TJ, Kuhn JG, et al. Phase I trial of sulofenur (LY186641) given orally on a daily × 21 schedule. Anticancer Drugs 1994; 5(2): 151–9 Article PubMed CAS Google Scholar Ehlhardt WJ, Woodland JM, Worzalla JF. Comparison of metabolism and toxicity to the structure of the anticancer agent sulofenur and related sulphonyl ureas. Chem Res Toxicol 1992; 5(5): 667–73 Article PubMed CAS Google Scholar Heilmair R, Karreth S, Lenk W. The metabolism of 4-aminobiphenyl in the rat II. Reaction of 4-hydroxy-4-aminobiphenyl with rat blood in vitro. Xenobiotica 1991; 21: 805–15 Article PubMed CAS Google Scholar Schott AM, Vial T, Gozzo I. Flutamide-induced methaemoglobinaemia. DICP 1991 June; 25(6): 600–1 PubMed CAS Google Scholar Conroy JM, Baker JD, Martin WJ. Acquired methaemoglobinaemia from multiple oxidants. South Med J 1993; 86: 1156–9 Article PubMed CAS Google Scholar Kearns GL, Fiser DH. Metoclopramide-induced methaemoglobinaemia. Pediatrics 1988 Sep; 82(3): 364–6 PubMed CAS Google Scholar Blisard KS, Mieyal JJ. Characterisation of the aniline hydroxylase activity of red cells. J Biol Chem 1979; 254: 5104–10 PubMed CAS Google Scholar Van Veldhuizen PJ, Wyatt A. Metoclopramide-induced sulfhemoglobinemia. Am J Gastroenterol 1995; 90(6): 1010–11 PubMed Google Scholar Halvorsen SM, Dull WL. Phenazopyridine-induced sulfhemoglobinemia: inadvertent rechallenge. Am J Med 1991; 91(3): 315–7 Article PubMed CAS Google Scholar Savic M, Siriski-Sasic J, Djulizibaric D. Discomforts and laboratory findings in workers exposed to sulfur dioxide. Int Arch Occup Environ Health 1987; 59(5): 513–8 Article PubMed CAS Google Scholar Darling RC, Roughton FJW. The effect of methemoglobin on the equilibrium between oxygen and hemoglobin. Am J Physiol 1942; 137: 56–68 CAS Google Scholar Medina I, Mills J, Leoung G, et al. Oral therapy for Pneumocystis carinii pneumonia in the acquired immunodeficiency syndrome — a controlled trial of trimethoprim-sulfamethoxazole versus trimethoprim-dapsone. N Engl J Med 1990; 323: 776–82 Article PubMed CAS Google Scholar Banzato CEM, Magna LA. In vitro effect of dapsone on NADH-methaemoglobin reductase. Int J Lepr 1991; 59: 486–7 CAS Google Scholar Smith RP, Olson MV. Drug-induced methaemoglobinemia. Semin Hematol 1973; 10: 253–68 PubMed CAS Google Scholar Winthrobe MM, Lee GR, Boggs DR, et al., editors. Clinical hematology. 8th ed. Philadelphia: Lea and Febiger, 1981: 97–100 Google Scholar Cline MS. Curing the ‘nitrate blues’. Postgrad Med 1994; 96(3): 124–6 PubMed CAS Google Scholar Henretig FM, Gribetz B, Kearney T, et al. Interpretation of color change in blood with varying degree of methemoglobinemia. J Toxicol Clin Toxicol 1988; 26: 293–301 PubMed CAS Google Scholar Severinghaus JW. Nomenclature of oxygen saturation. Adv Exp Med Biol 1994; 345: 921–3 Article PubMed CAS Google Scholar Barker SJ, Temper KK, Hyatt J. Effects of methemoglobinemia on pulse oximetry and mixed venous oximetry. Anaesthesiol 1989 70: 112–7 Article CAS Google Scholar Reynolds K, Palayiwa E, Moyle JT. The effect of dyshaemoglobins on pulse oximetry: Part 1, theoretical approach, and Part 2, experimental results using an in vitro system. J Clin Monit 1993; 9(2): 81–90 Article PubMed CAS Google Scholar Olsen ML, McEvoy GK. Methemoglobinemia induced by topical anesthetics. Am J Hosp Pharm 1981; 38: 89–93 Google Scholar Goluboff N, Wheaton R. Methylene blue induced cyanosis and acute hemolytic anemia complicating the treatment of methemoglobinemia. J Pediatr 1961; 58: 86–9 Article PubMed CAS Google Scholar Foxworth JW, Roberts JA, Mahmoud SF. Acquired methemoglobinemia: a case report. Mo Med 1987; 84: 187–9 PubMed CAS Google Scholar Moon RE, Camparesi EM. Respiratory Monitoring. In Anesthesia, 3rd ed. Ronald D. Miller, ed. New York: Churchill Livingston, 1990: 1140 Vol 1 Google Scholar Hall AH, Kulig KW, Rumack BH. Drug- and chemical-induced methemoglobinemia: clinical features and management. Med Toxicol 1986; 1: 253–60 PubMed CAS Google Scholar Prussick R, Ali MAM, Rosenthal D, et al. The protective effect of vitamin E on the hemolysis associated with dapsone treatment in patients with dermatitis herpetiformis. Arch Dermatol 1992; 128: 210–3 Article PubMed CAS Google Scholar Kelly JW, Scott J, Sandland M, et al. Vitamin E and dapsone-induced hemolysis. Arch Dermatol 1984; 120: 1582–4 Article PubMed CAS Google Scholar Rhodes LE, Tingle MD, Park BK, et al. Cimetidine improves the therapeutic/toxic ratio of dapsone in patients on chronic dapsone therapy. Br J Derm 1995; 132: 257–62 Article CAS Google Scholar Szeremeta W, Dohar JE. Dapsone-induced methemoglobinemia: an anesthetic risk. Int J Pediatr Otorhinolaryngol 1995; 33: 75–80 Article PubMed CAS Google Scholar Download references Author information Authors and Affiliations Department of Pharmaceutical and Biological Sciences, Aston University, Birmingham, B4 7ET, England Michael D. Coleman Department of Intensive Care, Royal Liverpool University Teaching Hospital, Liverpool, England Nicholas A. Coleman Corresponding author Correspondence to Michael D. Coleman . Rights and permissions Reprints and Permissions About this article Cite this article Coleman, M.D., Coleman, N.A. Drug-Induced Methaemoglobinaemia. Drug-Safety 14, 394–405 (1996). https://doi.org/10.2165/00002018-199614060-00005 Download citation Published26 October 2012 Issue DateJune 1996 DOI https://doi.org/10.2165/00002018-199614060-00005 Previous Next

29 < Back to Research Top Published Date 22/10/2020 Efficacy of Double-Dose Dapsone Combination Therapy in the Treatment of Chronic Lyme Disease/Post-Treatment Lyme Disease Syndrome (PTLDS) and Associated Co-infections: A Report of Three Cases and Retrospective Chart Review Journal Antibiotics (Basel) Citation 9(11):725 DOI 10.3390/antibiotics9110725 Authors Horowitz RI, Freeman PR Abstract Three patients with multi-year histories of relapsing and remitting Lyme disease and associated co-infections despite extended antibiotic therapy were each given double-dose dapsone combination therapy (DDD CT) for a total of 7-8 weeks. At the completion of therapy, all three patients' major Lyme symptoms remained in remission for a period of 25-30 months. A retrospective chart review of 37 additional patients undergoing DDD CT therapy (40 patients in total) was also performed, which demonstrated tick-borne symptom improvements in 98% of patients, with 45% remaining in remission for 1 year or longer. In conclusion, double-dose dapsone therapy could represent a novel and effective anti-infective strategy in chronic Lyme disease/ post-treatment Lyme disease syndrome (PTLDS), especially in those individuals who have failed regular dose dapsone combination therapy (DDS CT) or standard antibiotic protocols. A randomized, blinded, placebo-controlled trial is warranted to evaluate the efficacy of DDD CT in those individuals with chronic Lyme disease/PTLDS. Keywords: Lyme disease; babesiosis; bartonellosis; dapsone combination therapy (DDS CT); double-dose dapsone combination therapy (DDD CT); florescent in situ hybridization (FISH); persistent infection; post-treatment Lyme disease syndrome (PTLDS). URL Previous https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7690415/ No Review Needed? Next

< Back The Tick/Lyme Prevention Issue LRC 17 Jul 2023 Previous Next

It is Lyme awareness month & in honor of that the LDF has placed its Lifetime TV Network award-winning documentary online for people to view. < Back Lyme TV documentary online and free for viewing LRC 9 May 2023 It is Lyme awareness month & in honor of that the LDF has placed its Lifetime TV Network award-winning documentary online for people to view. Go to https://lyme.org linked via youtube: Previous Next

By Stephanie Brown Published on June 07, 2023 Fact checked by Nick Blackmer < Back Low-Dose Naltrexone Could Treat Long COVID Symptoms LRC 8 Jun 2023 By Stephanie Brown Published on June 07, 2023 Fact checked by Nick Blackmer Wladimir Bulgar / Science Photo Library / Getty Images. Key Takeaways Long COVID is still not well understood, making it difficult for scientists to develop treatments. Low-dose naltrexone may be a promising treatment for long COVID, but more studies are needed. Naltrexone is FDA-approved to treat alcohol use disorder and opioid addiction, but it has also been used off-label in low doses to treat inflammatory diseases. Naltrexone is a drug approved by the Food and Drug Administration (FDA) to treat alcohol use disorder and opioid addiction. Low-dose naltrexone (LDN) , usually at a fraction of the regular dose, has been used to treat fibromyalgia and multiple sclerosis. Now, research shows that LDN might also be a promising treatment for long COVID. As many as 23 million Americans may have been affected by long COVID, but the lack of understanding about this condition makes it hard to develop treatments. “I want to encourage people that it is possible to improve and for their symptoms to get better, but I want to discourage people from the belief that there’s one medicine that will cure long COVID,” said Jessica A. Bender, MD, MPH , co-director of UW Medicine’s Post-COVID-19 Rehabilitation and Recovery Clinic. Related: Have Long COVID and Can't Work? Here's What to Do How Might Low-Dose Naltrexone Treat Long COVID? While LDN might not cure all long COVID symptoms, it could serve as part of a treatment plan. A small study published last year found that LDN improved some self-reported symptoms, such as pain and energy levels, for long COVID patients. “It looks like it worked for most people. So I think it’s part of the solution because it’s targeting two of the four issues that I see really critical with long COVID, which is brain inflammation and immune dysregulation,” said Jack Lambert, MD, PhD , a co-author of the study and a professor of infectious disease at the University College Dublin School of Medicine in Ireland. People with long COVID reportedly have an increased level of inflammatory cytokines , which are involved in the body’s immune response, according to Hector Bonilla, MD , co-director of the Stanford Post-Acute COVID-19 Syndrome Clinic. Related: What Should We Expect From Long COVID Treatment? LDN has demonstrated effects on reducing inflammatory cytokines, which might be why it shows promise as a potential treatment for long COVID patients, Bonilla said. LDN is sometimes used to treat chronic inflammatory diseases like inflammatory bowel disease (IBS). Lambert said he has used LDN for patients with chronic Lyme disease , a condition that can lead to inflammation of the brain or spinal cord, and the positive results led him to conduct the pilot study on LDN in long COVID patients. LDN isn’t FDA-approved to treat long COVID, so healthcare providers can only prescribe it off-label. “We’re three years into long COVID, and we’ve not advanced very far in terms of interventions. This is just one of the few promise interventions that I can vouch for based on my clinical experience, and I encourage others to consider using it as well,” Lambert said. Related: How Do You Know if You Have Long COVID? LDN May Not Work for Everyone LDN doesn’t seem to come with many side effects, but this medication might not work for everyone. “I’ve had some people who had one or two doses and just didn’t feel like themselves or had some hard-to-describe side effects and so decided to not take it,” Bender said. When LDN is prescribed, Bender explained, people often start with a very low dose and work their way up to a higher dose. While people might see improvements after a few weeks, she said it is difficult to track how well the drug works because it’s often prescribed along with multiple treatments. Clinical trials are still needed to help healthcare providers understand exactly how this LDN works. A placebo-controlled study in British Columbia looking at the effects of LDN on long COVID fatigue may be underway soon, which could help provide some answers. “What we as a scientific community need to do is be able to prove that this medication works for this indication with relatively few side effects and that’s how we can help improve the health of the public and everybody with long COVID,” Bender said. Read Next: Low-Dose Naltrexone May Be Opioid Replacement for Chronic Pain What This Means For You If you or a loved one are experiencing long COVID symptoms, consider talking to your healthcare provider about the treatment options available to you. They can help you create a treatment plan that works best for your symptoms. Originally posted: Low-Dose Naltrexone Could Treat Long COVID Symptoms ( verywellhealth.com ) Sources Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy. Toljan K, Vrooman B. Low-dose naltrexone (LDN)—review of therapeutic utilization . Med Sci (Basel) . 2018;6(4):82. doi:10.3390/medsci6040082 Government Accountability Office. Science & tech spotlight: long COVID . O’Kelly B, Vidal L, McHugh T, Woo J, Avramovic G, Lambert JS. Safety and efficacy of low dose naltrexone in a long covid cohort; an interventional pre-post study . Brain Behav Immun Health . 2022;24:100485. doi:10.1016/j.bbih.2022.100485 Buonsenso D, Piazza M, Boner AL, Bellanti JA. Long COVID: A proposed hypothesis-driven model of viral persistence for the pathophysiology of the syndrome . Allergy Asthma Proc . 2022;43(3):187-193. doi:10.2500/aap.2022.43.220018 Lie MRKL, van der Giessen J, Fuhler GM, et al. Low dose naltrexone for induction of remission in inflammatory bowel disease patients . J Transl Med . 2018;16(1):55. doi:10.1186/s12967-018-1427-5 Bonilla H, Peluso MJ, Rodgers K, et al. Therapeutic trials for long COVID-19: a call to action from the interventions taskforce of the RECOVER initiative . Front Immunol . 2023;14:1129459. doi:10.3389/fimmu.2023.1129459 Bolton MJ, Chapman BP, Marwijk HV. Low-dose naltrexone as a treatment for chronic fatigue syndrome . BMJ Case Reports . 2020;13(1):e232502. doi:10.1136/bcr-2019-232502 Previous Next

2 < Back to Research Top Published Date 18/08/2021 Recent Progress in Lyme Disease and Remaining Challenges Journal Frontiers in Medicine Citation Front. Med., 18 August 2021 DOI 10.3389/fmed.2021.666554 Authors Bobe JR, Jutras BL, Horn EJ, Embers ME, Bailey A, Moritz RL, Zhang Y, Soloski MJ, Ostfeld RS, Marconi RT, Aucott J, Ma'ayan A, Keesing F, Lewis K, Mamoun CB, Rebman AW, McClune ME, Breitschwerdt EB, Reddy PJ, Maggi R, Yang F, Nemser B, Ozcan A, Garner O, Di Carlo D, Ballard Z, Joung H-A, Garcia-Romeu A, Griffiths RR, Baumgarth N, Fallon BA Abstract Lyme disease (also known as Lyme borreliosis) is the most common vector-borne disease in the United States with an estimated 476,000 cases per year. While historically, the long-term impact of Lyme disease on patients has been controversial, mounting evidence supports the idea that a substantial number of patients experience persistent symptoms following treatment. The research community has largely lacked the necessary funding to properly advance the scientific and clinical understanding of the disease, or to develop and evaluate innovative approaches for prevention, diagnosis, and treatment. Given the many outstanding questions raised into the diagnosis, clinical presentation and treatment of Lyme disease, and the underlying molecular mechanisms that trigger persistent disease, there is an urgent need for more support. This review article summarizes progress over the past 5 years in our understanding of Lyme and tick-borne diseases in the United States and highlights remaining challenges. URL Previous https://www.frontiersin.org/articles/10.3389/fmed.2021.666554/full No Review Needed? Next

10 < Back to Research Top Published Date 13/05/2021 The peptidoglycan-associated protein NapA plays an important role in the envelope integrity and in the pathogenesis of the lyme disease spirochete Journal PLoS Pathogen Citation 17(5):e1009546 DOI 10.1371/journal.ppat.1009546 Authors Davis MM, Brock AM, DeHart TG, Boribong BP, Lee K, McClune ME, Chang Y, Cramer N, Liu J, Jones CN, Jutras BL Abstract The bacterial pathogen responsible for causing Lyme disease, Borrelia burgdorferi, is an atypical Gram-negative spirochete that is transmitted to humans via the bite of an infected Ixodes tick. In diderms, peptidoglycan (PG) is sandwiched between the inner and outer membrane of the cell envelope. In many other Gram-negative bacteria, PG is bound by protein(s), which provide both structural integrity and continuity between envelope layers. Here, we present evidence of a peptidoglycan-associated protein (PAP) in B. burgdorferi. Using an unbiased proteomics approach, we identified Neutrophil Attracting Protein A (NapA) as a PAP. Interestingly, NapA is a Dps homologue, which typically functions to bind and protect cellular DNA from damage during times of stress. While B. burgdorferi NapA is known to be involved in the oxidative stress response, it lacks the critical residues necessary for DNA binding. Biochemical and cellular studies demonstrate that NapA is localized to the B. burgdorferi periplasm and is indeed a PAP. Cryo-electron microscopy indicates that mutant bacteria, unable to produce NapA, have structural abnormalities. Defects in cell-wall integrity impact growth rate and cause the napA mutant to be more susceptible to osmotic and PG-specific stresses. NapA-linked PG is secreted in outer membrane vesicles and augments IL-17 production, relative to PG alone. Using microfluidics, we demonstrate that NapA acts as a molecular beacon-exacerbating the pathogenic properties of B. burgdorferi PG. These studies further our understanding of the B. burgdorferi cell envelope, provide critical information that underlies its pathogenesis, and highlight how a highly conserved bacterial protein can evolve mechanistically, while maintaining biological function. URL Previous https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1009546 No Review Needed? Next

217 < Back to Research Top Published Date 05/06/2014 Pregnancy and infection Journal The New England Journal of Medicine Citation N Engl J Med. 2014 Jun 5; 370(23): 2211?2218. DOI 10.1056/NEJMra1213566 Authors Kourtis AP, Read JS, Jamieson DJ Abstract Before the advent of antibiotic agents, pregnancy was a recognized risk factor for severe complications of pneumococcal pneumonia, including death.1 The influenza pandemic of 2009 provided a more recent reminder that certain infections may disproportionately affect pregnant women. Are pregnant women at increased risk for acquiring infections? Are pregnant women with infection at increased risk for severe disease? During pregnancy, several mechanical and pathophysiological changes occur (e.g., a decrease in respiratory volumes and urinary stasis due to an enlarging uterus), and immune adaptations are required to accommodate the fetus. In this article, we review and synthesize new knowledge about the severity of and susceptibility to infections in pregnant women. We focus on the infections for which there is evidence of increased severity or susceptibility during pregnancy that is not fully explained by mechanical or anatomical changes, and we discuss these infections in light of new findings on immunologic changes during pregnancy. URL Previous https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459512/ No Review Needed? Next