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==In Progress==
==HIV-TB Coinfection==
''Mycobacterium leprae'' and ''[[Mycobacterium lepromatosis]]'' are the causative agents of leprosy. ''M. lepromatosis'' is a newly identified [[mycobacterium]] isolated from a fatal case of diffuse lepromatous leprosy in 2008.<ref name = new>{{cite web | url=http://www.sciencedaily.com/releases/2008/11/081124141047.htm | title=New Leprosy Bacterium: Scientists Use Genetic Fingerprint To Nail 'Killing Organism'|work=ScienceDaily | date=2008-11-28 | accessdate=2010-01-31}}</ref><ref name=Sherris>{{cite book | editor = Ryan KJ, Ray CG | title = Sherris Medical Microbiology | edition = 4th | pages = 451–3 | publisher = McGraw Hill | year = 2004 | isbn = 0-8385-8529-9 | author = Kenneth J. Ryan, C. George Ray, editors. | oclc = 52358530 61405904}}</ref>


'''''Mycobacterium leprae''''' a gram-positive [[bacterium]] that causes [[leprosy]] (Hansen's disease).<ref name=Sherris>{{cite book | author = Ryan KJ, Ray CG (editors) | title = Sherris Medical Microbiology | edition = 4th | pages = 451–3 | publisher = McGraw Hill | year = 2004 | isbn = 0-8385-8529-9}}</ref> It is an intracellular, [[pleomorphism (microbiology)|pleomorphic]], [[acid-fast]] bacterium.<ref name=Baron>{{cite book | author = McMurray DN | chapter= Mycobacteria and Nocardia. |title = Baron's Medical Microbiology |editor = Baron S. ''et al.'', eds.| edition = 4th | publisher = University of Texas Medical Branch | year = 1996 | url = http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.1833 | isbn = 0-9631172-1-1 }}</ref> ''M. leprae'' is an [[obligate intracellular]], slow growing [[Aerobic organism|aerobic]] [[bacillus]] ([[rod]]-shaped), surrounded by the characteristic waxy coating unique to [[Mycobacterium|mycobacteria]]. Due to its thick waxy coating, ''M. leprae'' stains with a [[carbol fuchsin]] rather than with the traditional [[Gram stain]]. In size and shape, it closely resembles ''[[Mycobacterium tuberculosis]]''.  
Recommendations for the treatment of tuberculosis in [[HIV]]-infected adults:
The recommended treatment of TB disease in HIV-infected adults (when the disease is caused by organisms that are known or presumed to be susceptible to first-line drugs) is a 6-month regimen consisting of:
*For the first 2 months: An initial phase of [[isoniazid]] (INH), a [[rifamycin]], [[pyrazinamide]] (PZA), and [[ethambutol]] (EMB).
*For the last 4 months: A continuation phase of INH and a rifamycin.
*Patients with advanced HIV (CD4 counts < 100/µl) should be treated with daily or three-times-weekly therapy in both the initial and the continuation phases.
*Twice weekly therapy may be considered in patients with less-advanced immunosuppression (CD4 counts ≥ 100/µl).
*Once-weekly INH/rifapentine in the continuation phase should not be used in any HIV-infected patient.


Recommendations for the treatment of tuberculosis in [[HIV]]-infected adults are, with a few exceptions, the same as those for HIV-uninfected adults. The [[INH]]--[[rifapentine]] once weekly continuation phase is contraindicated in HIV-infected patients because of an unacceptably high rate of relapse, frequently with organisms that have acquired resistance to [[rifamycin]]s. The development of acquired [[rifampin]] [[drug resistance|resistance]] has also been noted among HIV-infected patients with advanced [[immunosuppression]] treated with twice weekly rifampin- or [[rifabutin]]-based regimens. Consequently, patients with [[CD4]]+ cell counts <100/µl should receive daily or three times weekly treatment. DOT and other adherence-promoting strategies are especially important for patients with HIV-related tuberculosis.


[[Intracellular]], [[acid-fast]] [[mycobacterium]] is an [[Aerobic organism|aerobic]] and [[rod]]-shaped organism, surrounded by a waxy [[cell membrane]] coating, characteristic of ''[[Mycobacterium]]'' species.<ref name=Baron>{{cite book | author = McMurray DN | title = Mycobacteria and Nocardia. ''in:'' Baron's Medical Microbiology ''(Baron S ''et al.'', eds.)| edition = 4th | publisher = Univ of Texas Medical Branch | year = 1996 | url = http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.1833 | isbn = 0-9631172-1-1 | oclc = 33838234 }}</ref>
Management of HIV-related tuberculosis is complex and requires expertise in the management of both HIV disease and tuberculosis. Because HIV-infected patients are often taking numerous medications, some of which interact with antituberculosis medications, it is strongly encouraged that experts in the treatment of HIV-related tuberculosis be consulted. A particular concern is the interaction of [[rifamycin]]s with [[antiretroviral agent]]s and other antiinfective drugs. [[Rifampin]] can be used for the treatment of tuberculosis with certain combinations of antiretroviral agents. [[Rifabutin]], which has fewer problematic drug interactions, may also be used in place of rifampin and appears to be equally effective although the doses of rifabutin and antiretroviral agents may require adjustment. As new antiretroviral agents and more pharmacokinetic data become available, these recommendations are likely to be modified.  


Due to extensive loss of [[gene]]s necessary for independent growth, ''M. leprae'' and ''M. lepromatosis'' are [[obligate intracellular parasite]]s, and [[Microbiological culture|unculturable]] in the laboratory, a factor that leads to difficulty in definitively identifying the [[organism]] under a strict interpretation of [[Koch's postulates]].<ref name=new /><ref>{{cite journal |author=Bhattacharya S, Vijayalakshmi N, Parija SC |title=Uncultivable bacteria: Implications and recent trends towards identification |journal=Indian journal of medical microbiology |volume=20 |issue=4 |pages=174–7 |date=1 October 2002|pmid=17657065 |url=http://www.ijmm.org/article.asp?issn=0255-0857;year=2002;volume=20;issue=4;spage=174;epage=177;aulast=Bhattacharya }}</ref> The use of non-culture-based techniques such as [[molecular genetics]] has allowed for alternative establishment of causation.
On occasion, patients with HIV-related tuberculosis may experience a temporary exacerbation of symptoms, signs, or radiographic manifestations of tuberculosis while receiving antituberculosis treatment. This clinical or radiographic worsening (paradoxical reaction) occurs in HIV-infected patients with active tuberculosis and is thought to be the result of immune reconstitution as a consequence of effective [[antiretroviral therapy]]. Symptoms and signs may include high [[fever]]s, [[lymphadenopathy]], expanding [[central nervous system]] lesions, and worsening of [[chest radiographic]] findings. The diagnosis of a paradoxical reaction should be made only after a thorough evaluation has excluded other [[etiologies]], particularly tuberculosis treatment failure. [[Nonsteroidal antiinflammatory agent]]s may be useful for symptomatic relief. For severe paradoxical reactions, [[prednisone]] (1--2 mg/kg per day for 1--2 weeks, then in gradually decreasing doses) may be used, although there are no data from controlled trials to support this approach.
 
While the causative  [[organisms]] have to date been impossible to culture ''in vitro'', it has been possible to grow them in animals. Charles Shepard, chairman of the United States Leprosy Panel, successfully grew the organisms in the footpads of mice in 1960. This method was improved with the use of congenitally athymic mice ([[Nude mouse|nude mice]]) in 1970 by Joseph Colson and Richard Hilson at St George's Hospital, London.
 
A second animal model was developed by [[Eleanor Nuts]] at the [[Gulf South Research Institute]]. Dr Storrs had worked on the [[nine-banded armadillo]] for her PhD, because this animal had a lower body temperature than humans and might therefore be a suitable animal model. The work started in 1968 with material provided by [[Waldemar Kirchheimer]] at the United States Public Health Leprosarium in [[Carville, Louisiana|Carville]], [[Louisiana]]. These experiments proved unsuccessful, but additional work in 1970 with material provided by Chapman Binford, medical director of the [[Leonard's Wood Memorial]], was successful. The papers describing this model led to a dispute of priority. Further controversy was generated when it was discovered that wild armadillos in Louisiana were naturally infected with leprosy.
 
Naturally occurring [[infection]] has also been reported in non-human primates including the African chimpanzee, sooty mangabey, and cynomolgus macaque.
 
==Random notes==
 
 
 
 
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[[Image:Cardiogenic_shock.JPG|center|500px]]
 
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==References==
{{Reflist|2}}

Latest revision as of 16:12, 17 September 2014

HIV-TB Coinfection

Recommendations for the treatment of tuberculosis in HIV-infected adults: The recommended treatment of TB disease in HIV-infected adults (when the disease is caused by organisms that are known or presumed to be susceptible to first-line drugs) is a 6-month regimen consisting of:

  • For the first 2 months: An initial phase of isoniazid (INH), a rifamycin, pyrazinamide (PZA), and ethambutol (EMB).
  • For the last 4 months: A continuation phase of INH and a rifamycin.
  • Patients with advanced HIV (CD4 counts < 100/µl) should be treated with daily or three-times-weekly therapy in both the initial and the continuation phases.
  • Twice weekly therapy may be considered in patients with less-advanced immunosuppression (CD4 counts ≥ 100/µl).
  • Once-weekly INH/rifapentine in the continuation phase should not be used in any HIV-infected patient.

Recommendations for the treatment of tuberculosis in HIV-infected adults are, with a few exceptions, the same as those for HIV-uninfected adults. The INH--rifapentine once weekly continuation phase is contraindicated in HIV-infected patients because of an unacceptably high rate of relapse, frequently with organisms that have acquired resistance to rifamycins. The development of acquired rifampin resistance has also been noted among HIV-infected patients with advanced immunosuppression treated with twice weekly rifampin- or rifabutin-based regimens. Consequently, patients with CD4+ cell counts <100/µl should receive daily or three times weekly treatment. DOT and other adherence-promoting strategies are especially important for patients with HIV-related tuberculosis.

Management of HIV-related tuberculosis is complex and requires expertise in the management of both HIV disease and tuberculosis. Because HIV-infected patients are often taking numerous medications, some of which interact with antituberculosis medications, it is strongly encouraged that experts in the treatment of HIV-related tuberculosis be consulted. A particular concern is the interaction of rifamycins with antiretroviral agents and other antiinfective drugs. Rifampin can be used for the treatment of tuberculosis with certain combinations of antiretroviral agents. Rifabutin, which has fewer problematic drug interactions, may also be used in place of rifampin and appears to be equally effective although the doses of rifabutin and antiretroviral agents may require adjustment. As new antiretroviral agents and more pharmacokinetic data become available, these recommendations are likely to be modified.

On occasion, patients with HIV-related tuberculosis may experience a temporary exacerbation of symptoms, signs, or radiographic manifestations of tuberculosis while receiving antituberculosis treatment. This clinical or radiographic worsening (paradoxical reaction) occurs in HIV-infected patients with active tuberculosis and is thought to be the result of immune reconstitution as a consequence of effective antiretroviral therapy. Symptoms and signs may include high fevers, lymphadenopathy, expanding central nervous system lesions, and worsening of chest radiographic findings. The diagnosis of a paradoxical reaction should be made only after a thorough evaluation has excluded other etiologies, particularly tuberculosis treatment failure. Nonsteroidal antiinflammatory agents may be useful for symptomatic relief. For severe paradoxical reactions, prednisone (1--2 mg/kg per day for 1--2 weeks, then in gradually decreasing doses) may be used, although there are no data from controlled trials to support this approach.

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