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Current Literature INTERNATIONAL JOURNAL OF LEPROSY Volume 71, Number 4 Printed in the U.S.A. (ISSN 0148-916X) CURRENT LITERATURE This department carries selected abstracts of articles published in current medical journals dealing with leprosy and other mycobacterial diseases. General & Historical 383 Chemotherapy 384 Clinical Sciences 388 Immuno-Pathology 391 Leprosy 395 Tuberculosis 396 Microbiology 403 Leprosy 405 Tuberculosis 406 Experimental Infections 410 Epidemiology and Prevention 413 Rehabilitation and Social Concerns 414 Other Mycobacterial Diseases 415 Molecular & Genetic Studies 420 General and Historical Araujo, M. G. [Leprosy in Brazil]. Rev. use of specific therapy, suppression of lepra Soc. Bras. Med. Trop. 36(3) (2003) reactions, prevention of physical incapac- 373–382. [Article in Portuguese] ity, and physical and psychosocial rehabili- tation. Chemotherapy with rifampin, dap- Leprosy or Hansen’s disease is a chronic sone, and clofazimine have produced very infectious disease caused by the Mycobac- good results and the control of the disease terium leprae. The skin and nervous mani- in Brazil in the foreseeable future is festations of the disease present a singular likely.—Author’s Abstract clinical picture that is easily recognized. After India, Brazil still is the second coun- try with the greatest number of cases in the Dionne, M. S., Ghori, N., and Schneider, world. Around 94% of the known cases D. S. Drosophila melanogaster is a ge- and 94% of the new cases reported in netically tractable model host for Myco- America, come from Brazil. The disease bacterium marinum. Infect. Immun. presents itself in two well-defined stable 71(6) (2003) 3540–3550. and opposite poles (lepromatous and tuber- culoid) and two unstable groups (indeter- Mycobacterium marinum is a pathogenic minate and dimorphic). The spectrum of mycobacterial species that is closely re- presentation of the disease may also be lated to Mycobacterium tuberculosis and classified as: tuberculoid tuberculoid (TT), causes tuberculosis-like disease in fish and borderline tuberculoid (BT), borderline frogs. We infected the fruit fly Drosophila borderline (BB), borderline lepromatous melanogaster with M. marinum. This bac- (BL) and lepromatous lepromatous (LL). terium caused a lethal infection in the fly, The finding of acid fast bacillus in tissue is with a 50% lethal dose (LD(50)) of 5 CFU. the most useful method of diagnosis. The Death was accompanied by widespread tis- effective treatment of leprosy includes the sue damage. M. marinum initially prolifer- 383 384 International Journal of Leprosy 2003 ated inside the phagocytes of the fly; later identified by Ziehl-Neelsen staining, identi- in infection, bacteria were found both in- fication of MAP in human beings requires side and outside host cells. Intracellular M. culture or detection of MAP DNA or RNA. marinum blocked vacuolar acidification If infectious in origin, Crohn’s disease and failed to colocalize with dead Escheri- should be curable with appropriate antibi- chia coli, similar to infections of mouse otics. Many studies that argue against a macrophages. M. marinum lacking the causative role for MAP in Crohn’s disease mag24 gene were less virulent, as deter- have used antibiotics that are inactive mined both by LD(50) and by death kinet- against MAP. However, trials that include ics. Finally, in contrast to all other bacteria macrolide antibiotics indicate that a cure for examined, mycobacteria failed to elicit the Crohn’s disease is possible. The necessary production of antimicrobial peptides in length of therapy remains to be determined. DROSOPHILA: We believe that this sys- Mycobacterial diseases have protean clini- tem should be a useful genetically tractable cal manifestations, as does Crohn’s disease. model for mycobacterial infection.—Au- The necessity of stratifying Crohn’s disease thors’Abstract into two clinical manifestations (perforating and non-perforating) when interpreting the results of antibiotic therapy is discussed. Greenstein, R. J. Is Crohn’s disease caused Rational studies to evaluate appropriate by a mycobacterium? Comparisons with therapies to cure Crohn’s disease are pro- leprosy, tuberculosis, and Johne’s disease. posed.—Author’s Abstract Lancet Infect. Dis. 3(8) (2003) 507–514. Although Crohn’s disease is considered Hernandez, A., Martro, E., Matas, L., to be autoimmune in origin, there is in- and Ausina, V. In-vitro evaluation of creasing evidence that it may have an infec- Perasafe compared with 2% alkaline glu- tious cause. The most plausible candidate is taraldehyde against Mycobacterium spp. Mycobacterium avium subspecies paratu- J. Hosp. Infect. 54(1) (2003) 52–56. berculosis (MAP). Intriguingly, Koch’s postulates may have been fulfilled for MAP Quantitative suspension and carrier tests and Crohn’s disease, even though they still were used to compare the activity of Perasafe have not been met for Mycobacterium lep- and Cidex against Mycobacterium tubercu- rae and leprosy. In animals MAP causes losis, Mycobacterium avium-intracellulare, Johne’s disease, a chronic wasting intestinal Mycobacterium fortuitum, and Mycobacte- diarrhoeal disease evocative of Crohn’s dis- rium chelonae. The interference of an or- ease. Johne’s disease occurs in wild and do- ganic load, and of hard water was also con- mesticated animals, including dairy herds. sidered. Both agents achieved reductions Viable MAP is found in human and cow exceeding 10(5)-fold within 20 and 30 min milk, and is not reliably killed by standard for all the strains tested. Perasafe is thus pasteurisation. MAP is ubiquitous in the en- mycobactericidal and a viable alternative to vironment including in potable water. Since Cidex for intermediate or high-level disin- cell-wall-deficient MAP usually cannot be fection.—Authors’Abstract Chemotherapy Babaoglu, K., Page, M. A., Jones, V. C., The emergence of multi-drug resistant tu- McNeil, M. R., Dong, C., Naismith, J. berculosis, coupled with the increasing over- H., and Lee, R. E. Novel inhibitors of lap of the AIDS and tuberculosis pandemics an emerging target in Mycobacterium tu- has brought tuberculosis to the forefront as a berculosis; substituted thiazolidinones as major worldwide health concern. In an at- inhibitors of dTDP-rhamnose synthesis. tempt to find new inhibitors of the enzymes Bioorg Med. Chem. Lett. 13(19) (2003) in the essential rhamnose biosynthetic path- 3227–3230. way, a virtual library of 2,3,5 trisubstituted- 71, 4 Current Literature, Chemotherapy 385 4-thiazolidinones was created. These com- berculosis. Expression profiles of M. tuber- pounds were then docked into the active site culosis treated with compounds that inhibit cavity of 6′hydroxyl; dTDP-6-deoxy-D- key metabolic pathways are required as ref- xylo-4-hexulose 3,5-epimerase (RmlC) from erences for the assessment of novel antimy- Mycobacterium tuberculosis. The resulting cobacterial agents. We have studied the re- docked conformations were consensus sponse of M. tuberculosis to treatment with scored and the top 5% were slated for syn- the mycolic acid biosynthesis inhibitors iso- thesis. Thus far, 94 compounds have been niazid, thiolactomycin, and triclosan. Thio- successfully synthesized and initially tested. lactomycin targets the beta-ketoacyl-acyl Of those, 30 (32%) have ≥50% inhibitory ac- carrier protein (ACP) synthases KasA and tivity (at 20 microM) in the coupled rham- KasB, while triclosan inhibits the enoyl- nose synthetic assay with seven of the 30 ACP reductase InhA. However, controversy also having modest activity against whole- surrounds the precise mode of action of iso- cell M.tuberculosis.—Authors’Abstract niazid, with both InhA and KasA having been proposed as the primary target. We have shown that although the global re- Bermudez, L. E., Reynolds, R., Kolo- sponse profiles of isoniazid and thiolacto- noski, P., Aralar, P., Inderlied, C. B., mycin are more closely related to each other and Young, L. S. Thiosemicarbazole than to that of triclosan, there are differences (thiacetazone-like) compound with ac- that distinguish the mode of action of these tivity against Mycobacterium avium in two drugs. In addition, we have identified mice. Antimicrob. Agents Chemother. two groups of genes, possibly forming ef- 47(8) (2003) 2685–2687. flux and detoxification systems, through which M. tuberculosis may limit the effects In vitro screening of thiacetazone deriva- of triclosan. We have developed a mathe- tives indicated that two derivatives, SRI- matical model, based on the expression of 286 and SRI-224, inhibited a panel of 25 21 genes, which is able to perfectly discrim- Mycobacterium avium complex (MAC) iso- inate between isoniazid-, thiolactomycin-, lates at concentrations of 2 micro g/ml or or triclosan-treated M. tuberculosis. This lower. In mice, SRI-224 and thiacetazone model is likely to prove invaluable as a tool had no significant activity against the MAC to improve the efficiency of our drug devel- in livers and spleens, but treatment with opment programs by providing a means to SRI-286 resulted in significant reduction of rapidly confirm the mode of action of thio- bacterial loads in livers and spleens. A com- lactomycin analogues or novel InhA in- bination of SRI-286 and moxifloxacin was hibitors as well as helping to translate en- significantly more active than single drug zyme activity into whole-cell activity.— regimens in liver and spleen.—Authors’ Authors’Abstract Abstract Ciccone, R., Mariani, F., Cavone, A., Persi- Betts, J. C., McLaren, A., Lennon, M. G., chini, T., Venturini, G., Ongini, E., Col- Kelly, F. M., Lukey, P. T., Blakemore, S. izzi, V., and Colasanti, M. Inhibitory ef- J., and Duncan, K. Signature gene ex- fect of NO-releasing ciprofloxacin (NCX pression profiles discriminate between 976) on Mycobacterium tuberculosis sur- isoniazid-, thiolactomycin-, and triclosan- vival. Antimicrob. Agents Chemother. treated Mycobacterium tuberculosis. An- 47(7) (2003) 2299–2302. timicrob. Agents Chemother. 47(9) (2003) 2903–2913. Here, we report the antimycobacterial ac- tivity of NCX 976, a new molecule ob- Genomic technologies have the potential tained adding a NO moiety to the fluoro- to greatly increase the efficiency of the drug quinolone ciprofloxacin, on Mycobacterium development process.
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