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Medical Forum / Diseases and Disorders / Sinusitis / April 2008New Theory of Chronic Sinusitis: It's Mycobacteria
Dr. Tichenor of New York is advancing a new theory of chronic sinusitis: It may be caused by previously unsuspected infestation of mycobacteria. Abstract presented at the 2008 AAAAI meeting: Non-Tuberculous Mycobacteria (NTM)) as a cause of Chronic Rhinosinusitis W. S. Tichenor, M. D. New York, New York Non-tuberculous mycobacteria (ntm)) as a cause of chronic rhinosinusitis JC Walsh, WS Tichenor The Center for Allergy, Asthma and Sinusitis, New York, New York Rationale: Patients with chronic rhinosinusitis have persistent symptoms despite medical and surgical treatment. Current theories regarding causation include immunological reactions to fungi and bacteria, but there is no consensus regarding the cause. Since mycological causes have been investigated previously, NTM could also be a cause. Methods: Endoscopically directed cultures of all patients with chronic resistant rhinosinusitis were reviewed. Most patients have cultures done for mycobacteria. Those with positive cultures for NTM were selected. Treatment records were then reviewed. Results: Twenty-one patients grew out NTM from either the ostiomeatal unit or paranasal sinuses. Nineteen grew out Mycobacterium chelonae and 1 each of M. majoritense and M. immunogenum. Eighteen of 21 patients had previous sinus surgery and 19/21 used nasal irrigation. Based on sensitivities, patients were typically treated with a combination of 3 antibiotics: amikacin irrigation, an oral quinolone, and clarithromycin. Treatment time ranged from 6 weeks to 13 months. Eleven patients responded to treatment, 2 were not treated, 1 received inadequate treatment, 2 remained culture positive, 2 did not respond, 2 were lost to follow-up, and 1 responded but was treated at the same time for MRSA. There were negative follow up cultures on 14/19 patients. Conclusion: Patients with chronic rhinosinusitis resistant to treatment should have endoscopically directed cultures performed for NTM. Treatment is often successful with an extended course of multiple antibiotics. http://www.sinuses.com/NTMabstract.htm  SignatureSteven L. Email: sdlitvin@earthlinkNOSPAM.net Remove the NOSPAM before replying to me. >Treatment time ranged from 6 weeks to 13 months. Eek. Based on what I've heard of the results from the widespread treatment of postal workers with quinolones during the 2001 anthrax scare, chances of adverse side-effects from a 13-month course of any quinolone are very high. If courses that long are required for many patients, the cure may be worse than the disease. > >Treatment time ranged from 6 weeks to 13 months. > [quoted text clipped - 3 lines] > quinolone are very high. If courses that long are required for many > patients, the cure may be worse than the disease. No, one recovers spontaneously from quinolones. (which ARE my Least favorite antibiotic, they cause nausa, dizziness, and the symptoms of arthritis.) but over a few months one returns to normal. Unless one lucks out big time with the pahges, untreated sinusitis is forever. > > >Treatment time ranged from 6 weeks to 13 months. > [quoted text clipped - 8 lines] > and the symptoms of arthritis.) > but over a few months one returns to normal. Oh BTW the quinolones are almost a specific for impedeing the ability of piliated bacteria like e-coli to penetrate cells. They don't really kill them, but without the ability to access the inside of the next layer of cells down, they fall off when their old host cell layer does. > Unless one lucks out big time with the pahges, untreated sinusitis is > forever. >> Treatment time ranged from 6 weeks to 13 months. > [quoted text clipped - 3 lines] > quinolone are very high. If courses that long are required for many > patients, the cure may be worse than the disease. Mycobacteria are among the toughest bugs to treat. Their cell walls are able to resist many common antibiotics, and even common antiseptics. Several different antibiotics may need to be given simultaneously. What Dr. Tichenor has NOT yet done is prove that the introduction of mycobacteria into a patient (lab animal) can induce sinusitis in a previously healthy specimen. And until he is, who the heck knows if the mycobacteria are the real cause of sinusitis. They could be a coincidental accompaniment of the real cause. SignatureSteven L. Email: sdlitvin@earthlinkNOSPAM.net Remove the NOSPAM before replying to me. Quinolones are actually the one type of anti-biotic that I refuse to take. The reason being that I tend to acquire a sort of over-awareness of my own heartbeat that hasn't completely subsided over a year later. One of the listed side effects is heart fibrillations which I assume is somewhat connected to what I experienced, but a less than severe case. I understand that this wouldn't be the situation with everyone, but let it be known that there are large online communities, much like this one, for the suffers of quinolone side-effects that can take several years to subside. Just a word of warning... > Quinolones are actually the one type of anti-biotic that I refuse to > take. The reason being that I tend to acquire a sort of over-awareness [quoted text clipped - 7 lines] > > Just a word of warning... Not to mention longstanding tendon damage. Susan > x-no-archive: yes > [quoted text clipped - 11 lines] > > Not to mention longstanding tendon damage. Not to mention running off to a doctor to dose yourself with meds on the strength of the latest hot theory of sinusitis--a theory which usually has a half-life of a few years. Five years ago, Dr. Tichenor was utterly convinced that the Mayo Clinic theory of Allergic Fungal Sinusitis was correct, and prescribed amphotericin irrigation as a matter of course. But Accentia's commercial amphotericin wash just failed clinical trials. So now Dr. Tichenor has glommed onto this other theory. And so it goes. Maybe we should wait another 5 years before running off to treat this hypothetical mycobacteria infection that Dr. Tichenor claims we've all got up our noses. SignatureSteven L. Email: sdlitvin@earthlinkNOSPAM.net Remove the NOSPAM before replying to me. > > x-no-archive: yes > [quoted text clipped - 34 lines] > Email: sdlit...@earthlinkNOSPAM.net > Remove the NOSPAM before replying to me. Yeah some people prefer to run off and have the delicate internal airflow modulating structures of their nasal cavity carved out. Than have it redone every three years. Lab animals like chinchillas? Palmer at UPenn proved that bacterial biofilms cause ostia media using chinchillas 5 years ago. > x-no-archive: yes > [quoted text clipped - 14 lines] > > Susan " ...the introduction of mycobacteria into a patient (lab animal) can induce sinusitis in a previously healthy specimen. ..." The abstract below says infection occurred after the inadvertent introduction of Mycobacterium chelonae -- does any one have easy access to a full text to see if the infection is described and if it was like, or became, sinusitis? -- interesting that the source was a biofilm. Hospital outbreak of atypical mycobacterial infection of port sites after laparoscopic surgery. Vijayaraghavan R, Chandrashekhar R, Sujatha Y, Belagavi CS. Department of Laparoscopic Surgery, Rajmahal Vilas Hospital, Sanjaynagar, Bangalore, India. wetware@sify.com J Hosp Infect. 2006 Dec;64(4):344-7. A series of 145 laparoscopy port site infections due to Mycobacterium chelonae were found in 35 patients following laparoscopy at a single hospital over a six-week period. The contaminating source was ultimately identified as the rinsing water used for washing chemically disinfected instruments. The organism survived and grew within the biofilm at the bottom of disinfectant trays and within the outer sleeves of re-usable laparoscopic instruments. Remedial control measures included changing to ethylene oxide gas sterilization of laparoscopic equipment instead of chemical sterilization, thorough dismantling and manual precleaning of instruments, drying prior to gas sterilization, and random checks of environmental samples within the operating room complex for acid-fast bacilli. No further atypical mycobacterial infective episodes have occurred in the three years since the study. Awareness of this ubiquitous opportunistic organism that is not easily eradicated from the hospital environment, careful surveillance, detailed attention to disinfection methods of medical devices, and appropriate control measures are essential to prevent potential outbreaks. PMID: 17046106 The following suggests that prior to 1999 mycobacteria chelonae infections were unknown to the literature, other than in the immunocompramised:- Initial report of primary sinusitis caused by an atypical pathogen (Mycobacterium chelonae) in an immunocompetent adult. Spring PM, Miller RH. Department of Head and Neck Surgery, M.D. Anderson Cancer Center, University of Texas, Houston 77030-4009, USA. pspring@mdanderson.org Ear Nose Throat J. 1999 May;78(5):358-9, 362-4.Links Primary sinonasal infections caused by atypical mycobacteria are rare. In fact, only four examples of a primary nontuberculous mycobacterial etiology of paranasal sinusitis have been cited in the literature. The patients in all these cases were infected with the human immunodeficiency virus and, by definition, they all had acquired immunodeficiency syndrome. We present a report of an immunocompetent adult with a history of chronic sinusitis who consistently and repeatedly manifested a fast-growing, nonpigmented, atypical mycobacterium of the Runyon group IV category: Mycobacterium chelonae. The patient was successfully treated over a 3-year period with a combination of antimicrobial agents, multiple limited endoscopic sinus surgeries, and eventually a total globe-sparing maxillectomy. At this time, the patient is disease-free and has received no further treatment. This case represents the first report of an immunocompetent adult host with a primary atypical mycobacterial infection of the paranasal sinuses. It also demonstrates the multimodal nature of the treatment of atypical mycobacterial infections. We also discuss the Byzantine classification scheme relative to atypical mycobacteria, the disease process in the immunocompromised host, and the various treatment options. PMID: 10355197 > > x-no-archive: yes > [quoted text clipped - 83 lines] > treatment options. > PMID: 10355197 Mycobacterium chelona was probably unknown in the literature because it is finiky, requires a special culture medium and/or a PCR to find it, which only became available in like 2003? but it is ubiquitous. > > > x-no-archive: yes > [quoted text clipped - 87 lines] > it is finiky, requires a special culture medium and/or a PCR to find > it, which only became available in like 2003? but it is ubiquitous. Oh and did I mention that it likes a lower temp than other bugs? 30C for it, thank you, so it just does not show up in the standard set. > > > > x-no-archive: yes > [quoted text clipped - 91 lines] > 30C for it, thank you, so it just does not show up in the standard > set. A while back, there was a theory going around that mycobacteria causes Crohn's disease. It was worked on for some time, and then just disappeared. Judy > > > > > x-no-archive: yes > [quoted text clipped - 97 lines] > > Judy I remember this. Summary Transmissible spongioform enchephalopathies (TSE's), include bovine spongiform encephalopathy (also called BSE or "mad cow disease"), Creutzfeldt-Jakob disease (CJD) in humans, and scrapie in sheep. They remain a mystery, their cause hotly debated. But between 1994 and 1996, 12 people in England came down with CJD, the human form of mad cow, and all had eaten beef from suspect cows. Current mad cow diagnosis lies solely in the detection of late appearing "prions", an acronym for hypothesized, gene-less, misfolded proteins, somehow claimed to cause the disease. Yet laboratory preparations of prions contain other things, which could include unidentified bacteria or viruses. Furthermore, the rigors of prion purification alone, might, in and of themselves, have killed the causative virus or bacteria. Therefore, even if samples appear to infect animals, it is impossible to prove that prions are causative. Manuelidis found viral-like particles, which even when separated from prions, were responsible for spongiform STE's. Subsequently, Lasmezas's study showed that 55% of mice injected with cattle BSE, and who came down with disease, had no detectable prions. Still, incredibly, prions, are held as existing TSE dogma and Heino Dringer, who did pioneer work on their nature, candidly predicts "it will turn out that the prion concept is wrong." Many animals that die of spongiform TSE's never show evidence of misfolded proteins, and Dr. Frank Bastian, of Tulane, an authority, thinks the disorder is caused by the bacterial DNA he found in this group of diseases. Recently, Roels and Walravens isolated Mycobacterium bovis it from the brain of a cow with the clinical and histopathological signs of mad cow. Moreover, epidemiologic maps of the origins and peak incidence of BSE in the UK, suggestively match those of England's areas of highest bovine tuberculosis, the Southwest, where Britain's mad cow epidemic began. The neurotaxic potential for cow tuberculosis was shown in pre-1960 England, where one quarter of all tuberculous meningitis victims suffered from Mycobacterium bovis infection. And Harley's study showed pathology identical to "mad cow" from systemic M. bovis in cattle, causing a tuberculous spongiform encephalitis. In addition to M. bovis, Mycobacterium avium subspecies paratuberculosis (fowl tuberculosis) causes Johne's disease, a problem known and neglected in cattle and sheep for almost a century, and rapidly emerging as the disease of the new millennium. Not only has M. paratuberculosis been found in human Crohn's disease, but both Crohn's and Johne's both cross-react with the antigens of cattle paratuberculosis. Furthermore, central neurologic manifestations of Crohn's disease are not unknown. There is no known disease which better fits into what is occurring in Mad Cow and the spongiform enchephalopathies than bovine tuberculosis and its blood-brain barrier penetrating, virus-like, cell- wall-deficient forms. It is for these reasons that future research needs to be aimed in this direction. http://drbroxmeyer.netfirms.com/MadCow.pdf > > > > > > x-no-archive: yes > [quoted text clipped - 152 lines] > wall-deficient forms. It is for these reasons that > future research needs to be aimed in this direction.http://drbroxmeyer.netfirms.com/MadCow.pdf I found this bit preticularly interesting. Amyloid: the common denominator in all spongioform encephalopathies "It is an astounding finding, because we never would have dreamed that amyloid and prions are the same", proclaimed Stanley Prusiner [1]. In the past amyloid was usually the deposition that took place due in the course of chronic inflammatory disease, mainly tuberculosis, the usual precipitating cause. The very term "amyloidosis", coined by Virchow, was a misnomer, assuming that the infiltrative material had chemical similarities to the starch (or amylum) of plants, which it did not. Nevertheless, by force of use and habit, the word stuck. Hass's study proved a direct correlation between amyloid deposition and the mycobacteria by injecting M. bovis into rabbits and following M. tuberculosis in humans. He concluded that the only infectious disease which served as an apparent cause of amyloidosis was tuberculosis [59]. All 21 human subjects with amyloid in Hass's investigation had chronic pulmonary tuberculosis. In a 50-year study based upon autopsy, Schwartz saw amyloidosis, primary and secondary, in the brain and elsewhere as a by-product of underlying infectious tuberculosis, either reactivating itself or being reactivated by a host of traumatic, chemical, biologic or physical insults [60]. Microscopically, in the brain, Schwartz found plaques and amyloid degeneration of nerve fibrils. When Schwartz injected 22 guinea pigs with M. tuberculosis, all but four came down with amyloidosis. His uninfected controls, with the exception of one showed no amyloid. He thereby confirmed Hass, who's large series of rabbits showed that three out of four inoculated with bovine tuberculosis had amyloid disease within 15 months [59]. Hass's amyloid uniformly showed a principal protein fraction as well as a minor fraction whose physical behavior also implied another protein. The amyloid issue had surfaced previously when in 1978, Researcher Pat Merz, in breakthrough work, identified tiny fibrils in the brains of scrapie infected mice not present in well controls. Prion purists refused to admit that their prion rods were related to Merz's find, citing her entities as longer fibrils and claiming that Merz stated plainly that her scrapie associated fibrils (or SAF) were not amyloid and therefore could not be prion rods, the term Prusiner used for amyloid fibrils. Actually Merz said that her Scrapie associated filaments were amyloid-like on more than one occasion and workers in the field suggested that the two entities in Merz and Prusiner's papers were identical [1]. Delgado saw such fibrils in either case as typical features of amyloid [62]. Meanwhile, by 1994, de Beer, studying the relationship between a major rise of serum amyloid and having tuberculosis, saw a rapid descent in amyloid in patients treated with anti-tubercular drugs [63]. As an offshoot of de Beer's work, Tomiyama dissolved b-amyloid plaque with rifampin, a first line drug in the treatment of TB, and one of the few agents, to this day, that is able to dissolve amyloid plaque [64]. |
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