(Diagnosis, Diagnostics, Immunodiagnosis, Immunodiagnostics, Pathogenesis,  Vaccines & Drugs)


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1306. Arora SK.  Kumar B.  Sehgal S. Development of a polymerase chain reaction dot-blotting system for detecting cutaneous tuberculosis. British Journal of Dermatology.  142(1):72-6, 2000 Jan.


For a definitive diagnosis of cutaneous tuberculosis the demonstration of  mycobacteria is essential, but this is generally not possible in skin  lesions. Routinely available techniques have poor sensitivity and are time  consuming, therefore, delaying the institution of timely therapy. The high  sensitivity and speed of polymerase chain reaction (PCR) for the detection  of infectious agents has prompted investigators to use this technique for  the detection of Mycobacterium tuberculosis in body fluids such as  cerebrospinal fluid or pleural fluid. In the present study, PCR was used  to examine punch biopsy specimens from the affected skin of 10 patients  with clinical diagnoses of tuberculosis verrucosa cutis, lupus vulgaris,  scrofuloderma, papulonecrotic tuberculide and erythema induratum. A  control group of 20 patients included individuals having skin  manifestations with definite clinical diagnoses other than cutaneous  tuberculosis, such as leprosy, fungal mycetoma, chronic bullous disease of  childhood and pemphigus vulgaris. The PCR amplified products were dot  hybridized with a probe which was random prime labelled with 32P. The  results were compared with routine microbiological and histological findings. Among the test group, six of 10 (60%) were positive for M. tuberculosis by PCR, although their histopathology showed non-specific chronic inflammation with no definite diagnosis. Microbiological investigations, including acid-fast bacillus smear and culture, were positive in a single case of scrofuloderma. All patients in the control group were negative by PCR for M. tuberculosis. The data indicate that the combination of dot hybridization with PCR markedly increased the  sensitivity and specificity of PCR. This may be a useful tool in the diagnosis of tuberculosis when conventional methods fail.



1307. Chen S.  Han C.  Li B.  Zheng R.  Zhang L. A survey on knowledge and skills in the early diagnosis of leprosy in general health services at different levels in Shandong Province, The People's Republic of China. Leprosy Review.  71(1):57-61, 2000 Mar.


In the late phase of a leprosy control programme, problems arise with regard to the early detection and treatment of a small number of new incident cases. We describe a study in the province of Shandong, People's Republic of China, on the knowledge and skills regarding leprosy of general health service staff, including rural doctors, paramedical doctors at township level, doctors from county general and provincial hospitals and dermatologists. The results showed that there is a continuing need for suitable training programmes for medical staff in the general health services. Most dermatologists had good levels of knowledge and skills and more than 80% of new cases have been diagnosed in skin clinics in this province since 1990. Their participation in early diagnosis and training of staff should be strengthened.


1308. No Abstract


1309. No Abstract



1310. Halliday G.  Robinson SR.  Shepherd C.  Kril J. Alzheimer's disease and inflammation: a review of cellular and therapeutic mechanisms. [Review] [75 refs] Clinical & Experimental Pharmacology & Physiology.  27(1-2):1-8, 2000  Jan-Feb.


1. Of the neurodegenerative diseases that cause dementia, Alzheimer's  disease (AD) is the most common. Three major pathologies characterize the  disease: senile plaques, neurofibrillary tangles and inflammation. We  review the literature on events contributing to the inflammation and the  treatments thought to target this pathology. 2. The senile plaques of AD  consist primarily of complexes of the beta-amyloid protein. This protein  is central to the pathogenesis of the disease. 3. Inflammatory microglia are consistently associated with senile plaques in AD, although the classic inflammatory response (immunoglobulin and leucocyte infiltration) is absent. beta-Amyloid fragments appear to mediate such inflammatory mechanisms by activating the complement pathway in a similar fashion to immunoglobulin. 4. Epidemiological studies have identified a reduced risk of AD in patients with arthritis and in leprosy patients treated with anti-inflammatory drugs. Longitudinal studies have shown that the  consumption of anti-inflammatory medications reduces the risk of AD only  in younger patients (< 75 years). 5. There is a considerable body of in  vitro evidence indicating that the inflammatory response of microglial  cells is reduced by non-steroidal anti-inflammatory drugs (NSAID).  However, no published data are available concerning the effects of these  medications on brain pathology in AD. 6. Cyclo-oxygenase 2 enzyme is  constitutively expressed in neurons and is up-regulated in degenerative  brain regions in AD. Non-steroidal anti-inflammatory drugs may reduce this  expression. 7. Platelets are a source of beta-amyloid and increased  platelet activation and increased circulating beta-amyloid have been  identified in AD. Anti-platelet medication (including NSAID) would prevent  such activation and its potentially harmful consequences. 8. Increased  levels of luminal beta-amyloid permeabilizes the blood-brain barrier (BBB)  and increases vasoconstriction of arterial vessels, paralleling the  alterations observed with infection and inflammation. Cerebral amyloidosis  is highly prevalent in AD, compromising the BBB and vasoactivity.  Anti-inflammatory medications may alleviate these problems. [References: 75]


1311. Hoffner RJ.  Esekogwu V.  Mallon WK. Leprosy in the emergency department.

Academic Emergency Medicine.  7(4):372-6, 2000 Apr.


OBJECTIVES: Los Angeles County-University of Southern California Medical  Center, like many large urban hospitals, has a large immigrant population  from regions of the world where leprosy is endemic. Emergency physicians  (EPs) in these settings can expect to encounter leprosy patients. This  study reviewed the emergency department (ED) course of patients with  confirmed leprosy in an attempt to describe the most common presenting  patterns so that future cases can be more easily recognized. METHODS: This  was a retrospective chart review of all patients followed in the Hansen's  disease clinic. Demographics, leprosy type, clinical presentations to the  ED, and medications were recorded. RESULTS: Of the total number of  patients (415), most were of Mexican (52%), Filipino (15%), Vietnamese  (14%), and Chinese (5%) origin. Leprosy was classified as lepromatous  (56%), borderline (40%), and tuberculoid (4%). There were a total of 118  ED visits by 74 patients. The mean age was 46 years, with 51% male and 49%  female. Dermatologic (68%), neurologic (23%), and ophthalmologic (9%)  complaints were the most common reasons for ED presentation related to  leprosy. The EP did not elicit a history of leprosy in 34% of those  patients followed in the leprosy clinic. The ED diagnosis of leprosy was  made in 3 of 15 (20%) undiagnosed cases. Of the 63 patients prescribed  medications in the leprosy clinic at the time of their ED visits, 22 (35%)  ED charts did not report leprosy drugs. CONCLUSION: Patients with leprosy  present to U.S. EDs, and new cases can be identified. Early recognition is  important given leprosy's devastating consequences, major drug side  effects of medications used for treatment, and improved prognosis with multidrug therapy. A history of leprosy and associated medications are often not documented in the ED chart, which may reflect a continued fear of stigmatization among these patients.


1312. Kajihara H.  Paturusi IA.  Saleh RM.  Rasyad C.  Ikuta Y. Light and electron microscopic study of peripheral nerve damage in patients with lepromatous leprosy (LL) and borderline lepromatous leprosy (BL). Hiroshima Journal of Medical Sciences.  49(1):83-92, 2000 Mar.


Cutaneous branches of radial nerves in patients with lepromatous leprosy (LL) and borderline lepromatous (BL) were studied by light and electron microscopy. Foamy macrophages were found more or less in the nerve fibers of all leprosy patients and distributed in the epineurial, perineurial and  endoneurial areas. In the endoneurium, the foamy macrophages were mainly  located in the subperineurial and perivascular spaces. Vacuolated Schwann  cells were also found in the nerve fasciculus. In electron microscopy,  these foamy macrophages and vacuolated Schwann cells contained numerous  small dense materials, irregular in size and shape, considered to be  degenerated and fragmented mycobacterium leprae. These dense materials  were found also in the cytoplasm of vascular endothelial cells. These  findings suggest that mycobacteria enter into the endoneurium via the  blood vessels. In our present study, on the other hand, it was very  difficult to find the intact mycobacteria in the cytoplasm of the foamy  macrophages, Schwann cells or endothelial cells, as well as in the  Ziehl-Neelsen staining of paraffin sections. The disappearance of intact  bacilli in our present study might have been caused by multi drug therapy.  The myelinated nerve fibers were degenerated and disappeared in variable  degrees. Degenerative changes of the myelin sheath developed from the  outer layer to the inner layer with disarrangement of the lamellar  structure. These findings were different from myelin destruction of  peripheral nerves in Wallerian degeneration. The degenerative changes of the myelin sheath are caused by degeneration and destruction of Schwann cells in leprosy patients. Fibrosis surrounding myelinated and unmyelinated nerve fibers, i.e., periaxonal fibrosis, was found to a greater or lesser extent in the endoneurium. In the present study, it is still unclear whether the periaxonal fibrosis was due to necrosis of the Schwann cells by infection of mycobacteria or to an autoimmune mechanism  such as antiperipheral nerve antibody. However, lamellated concentric  fibrosis surrounding regenerative myelinated and unmyelinated nerve fibers  with the disappearance of mycobacteria suggests that degenerations and  regenerations of nerve axons were repeated during clinical cause. These  findings indicated that autoimmune mechanisms play an important role in  the pathogenesis of periaxonal fibrosis.


1313. Mahaisavariya P.  Jiamton S.  Manonukul J.  Khemngern S.Mast cells in leprosy and leprosy reaction. International Journal of Dermatology.  39(4):274-7, 2000 Apr.


BACKGROUND: Mast cells can be visualized in routine, acid-fast-staining,  paraffin tissue section as metachromatic staining cells, and can be  activated to release inflammatory mediators which play a role in the  cell-mediated immune response. METHODS: Skin biopsy tissues were taken  from the most active skin lesion of each leprosy patient at the time of  diagnosis (nonreactional group) and at the time of reaction (reactional  group) during the years 1994-1997 in the leprosy clinic at the Department  of Dermatology, Faculty of Medicine, Siriraj Hospital, Mahidol University,  Thailand. Mast cells were identified by metachromatic staining (purple) in  Fite's stain sections and reported as the average number of cells per high  power field in three compartments: at the center and periphery of the  granuloma and in the interstitium. The data were analyzed in three groups:  nonreactional group, type I, and type II leprosy reactions. The mast cell  count of each group and each compartment of the section, expressed as the  mean  standard error, was compared. RESULTS: A total of 95 persons were  included in the study, but 108 tissue sections were obtained due to nine  cases having more than one section. Of these patients, 63 cases (66.32%) had no reaction, 19 cases (20%) had type I reaction, and 13 cases had type II reaction. There was no difference in age and sex among these groups.  The mast cell count in the interstitium was higher than that within the  granuloma, both at the center and at the periphery, in every type, and the  count in this area reduced significantly in leprosy reactions, both type I  and type II, compared with the nonreactional group. CONCLUSIONS: The  change in the average mast cell number in nonreactional leprosy and  leprosy reactions may indicate the important role of mast cells in dynamic  changes in the cell-mediated immune response in leprosy and leprosy  reactions.


1314. Maslov AK. Phagocytic myeloperoxidase in leprosy pathogenesis [letter].  International Journal of Leprosy & Other Mycobacterial Diseases.   68(1):71-3, 2000 Mar.


1315. Patil SA.  Ramu G.  Prasad R. Detection of disease related immune complexes in the serum of leprosy patients. A novel single step method. Journal of Neuroimmunology.  105(1):64-8, 2000 Jun 1.


Mycobacterium leprae antigen and antibody complexes could be detected in the serum of leprosy patients using monoclonal antibody ML34 and anti-BCG antibodies by enzyme-linked immunosorbent assay. This simplified system  detects disease related complexes without the need for isolating and purifying them from the serum. Immune complexes captured using monoclonal  antibody ML34 revealed positivity in seven out of eight neuritic, two out  of nine tuberculoid (TT), five out of ten borderline tuberculoid (BT),  four out of ten borderline lepromatous (BL) and four out of ten  lepromatous (LL), leprosy cases. One of the controls also showed immune  complex of an IgM type. Anti-BCG based IgG immune complexes assay revealed positivity in six out of eight neuritic, one out of nine TT, four out of ten BT, two out of ten BL, four out of ten LL leprosy cases, and two out of 24 healthy controls. IgM type of mycobacterial immune complexes were almost negligible. Capture of complexes using monoclonal antibody ML34 which is against lipoarabinomannan of M. leprae seems to work better than  polyclonal anti-BCG antibody. The probable role of immune complexes in nerve damage needs to be evaluated, as very high levels of immune complexes are found in neuritic leprosy by both the assays. The above test would be useful in immunodiagnosis of neuritic leprosy and also in cases where antibody response is not detectable because of the formation of immune complexes.


1316.  Ramesh V.  Beena KR.  Mukherjee A. Sporotrichoid presentations in leprosy. Clinical & Experimental Dermatology.  25(3):227-30, 2000 May.


  Two adult patients of leprosy, one woman and one man, presented with a

  clinical picture simulating sporotrichosis. The skin and regional nerve

  trunk was affected in one, and in the other the disease was confined to

  the nerve. Both had features of an upgrading reaction following

  anti-leprosy therapy; this was seen as erosion and scarring of the plaque,

  and acute onset of abscesses along the easily palpable and thickened nerve

  that ruptured through the skin. The diagnosis was supported by

  histopathology. In the light of other infections that give rise to a

  sporotrichoid pattern of infection it is concluded that leprosy should

  also be included in this category so that early diagnosis and use of

  corticosteroids can be implemented quickly to prevent nerve destruction.



1317.   Young RJ 3rd.  Gilson RT.  Elston DM. Generalized annular borderline tuberculoid leprosy and update in  management of Hansen's disease. Cutis.  65(4):203-6, 2000 Apr.


We describe a patient with widespread borderline tuberculoid leprosy and  significant peripheral nerve involvement. Despite the presence of  widespread lesions, Fite stains and polymerase chain reaction studies were  initially negative. We discuss the diagnosis and treatment of leprosy  including recent changes in treatment regimens and duration.




1746. Authors

  Haimanot RT.  Melaku Z.


  Leprosy. [Review] [63 refs]


  Current Opinion in Neurology.  13(3):317-22, 2000 Jun.


  Leprosy is a unique infectious disease with a prolonged incubation period

  and a predilection for skin and nerves. The involvement of nerves by the

  primary infection as well as the immunologically mediated reversal

  reactions result in impairment of nerve function and severe disabilities.

  The introduction of the World Health Organization Multi Drug Therapy over

  the last two decades has produced dramatic changes in the management and

  control programmes of leprosy. A recent important contribution to the

  understanding of leprosy pathogenesis has been the elucidation of the

  molecular basis for the entry of Mycobacterium leprae into the Schwann

  cell and the peripheral nerve. Leprosy still remains the commonest cause

  of peripheral neuropathy in developing countries. [References: 63]


1747. Authors

  Hermon-Taylor J. Bull TJ. Sheridan JM.  Cheng J.  Stellakis ML. Sumar N.


  Causation of Crohn's disease by Mycobacterium avium subspecies

  paratuberculosis [see comments] [comment]. [Review] [369 refs]


  Canadian Journal of Gastroenterology.  14(6):521-39, 2000 Jun.


  Mycobacterium avium subspecies paratuberculosis (MAP) is a member of the M

  avium complex (MAC). It differs genetically from other MAC in having 14 to

  18 copies of IS900 and a single cassette of DNA involved in the

  biosynthesis of surface carbohydrate. Unlike other MAC, MAP is a specific

  cause of chronic inflammation of the intestine in many animal species,

  including primates. The disease ranges from pluribacillary to

  paucimicrobial, with chronic granulomatous inflammation like leprosy in

  humans. MAP infection can persist for years without causing clinical

  disease. The herd prevalence of MAP infection in Western Europe and North

  America is reported in the range 21% to 54%. These subclinically infected

  animals shed MAP in their milk and onto pastures. MAP is more robust than

  tuberculosis, and the risk that is conveyed to human populations in retail

  milk and in domestic water supplies is high. MAP is harboured in the

  ileocolonic mucosa of a proportion of normal people and can be detected in

  a high proportion of full thickness samples of inflamed Crohn's disease

  gut by improved culture systems and IS900 polymerase chain reaction if the

  correct methods are used. MAP in Crohn's disease is present in a

  protease-resistant nonbacillary form, can evade immune recognition and

  probably causes an immune dysregulation. As with other MAC, MAP is

  resistant to most standard antituberculous drugs. Treatment of Crohn's

  disease with combinations of drugs more active against MAC such as

  rifabutin and clarithromycin can bring about a profound improvement and,

  in a few cases, apparent disease eradication. New drugs as well as

  effective MAP vaccines for animals and humans are needed. The problems

  caused by MAP constitute a public health issue of tragic proportions for

  which a range of remedial measures are urgently needed. [References: 369]


1748. Authors

  Jones PB.  Parrish NM.  Houston TA.  Stapon A.  Bansal NP.  Dick JD.

  Townsend CA.


  A new class of antituberculosis agents.


  Journal of Medicinal Chemistry.  43(17):3304-14, 2000 Aug 24.


  Long-chain lipid envelopes are characteristic of mycobacteria such as

  those that cause tuberculosis and leprosy. Inhibition of fatty acid

  synthesis or elongation is a strategy demonstrated to be clinically

  effective against M. tuberculosis. A new class of compounds designed to

  inhibit the beta-ketoacyl synthase reaction of fatty acid synthesis has

  been developed. Of >30 compounds described, the most active were

  acetamides containing alkylsulfonyl substituents. Inhibitory activities

  were acutely sensitive to net charge, chain length, and degree of

  unsaturation. The most active compound 5 (alkyl = C(10)) contained a

  single methylene spacer between the sulfone and carboxamide and exhibited

  an MIC of 0.75-1.5 &mgr;g/mL, comparable to first-line antituberculosis

  drugs. These compounds are species-specific, exhibiting no significant

  activity against bacterial species other than M. tuberculosis and closely

  related strains. The synthesis, biological activity, and specificity of

  these compounds are described.


1749. Authors

  Pennini SN.  Pedrosa L.  Rebello PF.


  Early diagnosis and treatment of leprosy in intradomiciliary contacts in a

  high prevalence area: Amazon region.


  Indian Journal of Leprosy.  70 Suppl:73S-77S, 1998.


  The importance of dermato-neurological examination of intradomiciliary

  contacts is well known as an important secondary preventive measure in

  leprosy control, due to the fact that it allows early diagnosis and

  treatment. This is an intervention trial in an area of high leprosy

  prevalence (Manaus/Brazil) where the proportion of contacts examined is

  low. The aim of the study is to assess whether a simple educational

  session conducted among patients increases contacts examination and leads

  to early case detection. The intervention group had examined more contacts

  (p < 0.05) but, paradoxically, presented fewer new cases than the control

  group. The authors discuss the probable causes for this unexpected

  outcome, the advantages of the intervention and other related issues.


1750. Authors

  Singh HB.  Katoch K.  Natrajan M.  Sharma RK.  Gupta UD.  Sharma VD.

  Singh D.  Chauhan DS.  Srivastava K.  Katoch VM.


  Effect of treatment on PCR positivity in multibacillary leprosy patients

  treated with conventional and newer drugs ofloxacin and minocycline.


  Acta Leprologica.  11(4):179-82, 1999.


  In order to develop objective criteria to monitor trends of therapeutic

  responses positivity of PCR signals and ATP assay methods has been

  compared in multibacillary (MB) leprosy patients. Biopsies from lesions of

  95 BL/LL patients before and after one year of treatment with a new drug

  regimen comprising of conventional and newer drugs ofloxacin and

  minocycline have been studied. These biopsies were processed for bacillary

  ATP assay and PCR positivity for a 36 kDa gene target by earlier published

  methods. In the untreated patients bacillary ATP levels were detectable in

  all specimens and ranged from 0.02 to more than 36 pg/millions organisms.

  After one year of treatment ATP levels were not detectable in any of the

  57 biopsies specimens available for analysis. However, PCR signals were

  detectable in 3 out of 57 biopsies. In two specimens signals were very

  weak detectable only by hybridization. It may be concluded that DNA based

  PCR assay may be useful in monitoring the trends of therapeutic responses

  in MB patients under treatment.


1751. Authors

  Spierings E.  De Boer T.  Zulianello L.  Ottenhoff TH.


  Novel mechanisms in the immunopathogenesis of leprosy nerve damage: the

  role of Schwann cells, T cells and Mycobacterium leprae. [Review] [64



  Immunology & Cell Biology.  78(4):349-55, 2000 Aug.


  The major complication of reversal (or type 1) reactions in leprosy is

  peripheral nerve damage. The pathogenesis of nerve damage remains largely

  unresolved. In situ analyses suggest an important role for type 1 T cells.

  Mycobacterium leprae is known to have a remarkable tropism for Schwann

  cells that surround peripheral axons. Reversal reactions in leprosy are

  often accompanied by severe and irreversible nerve destruction and are

  associated with increased cellular immune reactivity against M. leprae.

  Thus, a likely immunopathogenic mechanism of Schwann cell and nerve damage

  in leprosy is that infected Schwann cells process and present antigens of

  M. Leprae to antigen-specific, inflammatory type 1 T cells and that these

  T cells subsequently damage and lyse infected Schwann cells. Previous

  studies using rodent CD8+ T cells and Schwann cells have revealed evidence

  for the existence of such a mechanism. Recently, a similar role has been

  suggested for human CD4+ T cells. These cells may be more important in

  causing leprosy nerve damage in vivo, given the predilection of M. leprae

  for Schwann cells and the dominant role of CD4+ serine esterase+ Th1 cells

  in leprosy lesions. Antagonism of molecular interactions between M.

  leprae, Schwann cells and inflammatory T cells may therefore provide a

  rational strategy to prevent Schwann cell and nerve damage in leprosy.

  [References: 64]


1752. Authors

  Suarez RE.  Lombardi C.


  Leprosy elimination at sub-national level.


  Leprosy Review.  71(2):206-11, 2000 Jun.


  New strategies for the countries that have already achieved the

  elimination goal, which includes the great majority of the endemic

  countries, are needed. There is current concern in these countries about

  the reduction in the political-technical commitment when the goal is

  achieved and the possibility of the re-emergence of the disease. A review

  of the literature on the leprosy post-elimination strategy is done. The

  proposal to estimate the true prevalence using hidden prevalence based on

  late diagnosis of the new cases is made. Suggestions are explored for

  strategies of the work after elimination at national level is attained

  such as the stratification at the first sub-national level, using

  estimated true prevalence. It is considered necessary to define strategies

  for the post-elimination phase with the aim of continuing to the long-term

  objective of the interruption of transmission and the consequent leprosy




2221. Cho SN.  Cellona RV.  Villahermosa LG.  Fajardo TT Jr.  Balagon MV. Abalos RM.  Tan EV.  Walsh GP.  Kim JD.  Brennan PJ. Detection of phenolic glycolipid I of Mycobacterium leprae in sera from leprosy patients before and after start of multidrug therapy. Clinical & Diagnostic Laboratory Immunology.  8(1):138-42, 2001 Jan.


  A total of 100 untreated new leprosy patients were recruited prospectively and examined for the presence of phenolic glycolipid I (PGL-I) antigen in their serum specimens by dot enzyme-linked immunosorbent assay (ELISA) using rabbit anti-PGL-I antiserum. The presence of circulating PGL-I antigen was closely related to the bacterial indices (BI) of the patients. The PGL-I antigen was detectable in 27 (93.1%) of 29 patients with a BI of 4.0 or above and in 15 (68.2%) of 22 patients with a BI of 3.0 to 3.9. However, none of the 37 patients with a BI of less than 1.9 had detectable PGL-I antigen by the methods used in this study. The level of PGL-I in serum declined rapidly by about 90% 1 month after the start of multidrug therapy. This study showed clearly that anti-PGL-I IgM antibodies and circulating PGL-I antigen levels reflect the bacterial loads in untreated leprosy patients. The serological parameters based on the PGL-I antigen may therefore be useful in the assessment of leprosy patients at the time of diagnosis and possibly in monitoring patients following chemotherapy.


2222. Donoghue HD.  Holton J.  Spigelman M. PCR primers that can detect low levels of Mycobacterium leprae DNA. Journal of Medical Microbiology.  50(2):177-82, 2001 Feb.


  There are several specific PCR-based methods to detect Mycobacterium leprae DNA, but the amplicons are quite large. For example, primers that target the 36-kDa antigen gene and are in common diagnostic use yield a 530-bp product. This may be a disadvantage when examining samples in which the DNA is likely to be damaged and fragmented. Therefore, two sets of M. leprae-specific nested primers were designed, based on existing primer pairs which have been shown to be specific for M. leprae. Primers that targeted the 18-kDa antigen gene gave an outer product of 136 bp and inner product of 110 bp. The primers based on the RLEP repetitive sequence yielded a 129-bp outer product and 99-bp nested product. With dilutions of a standard M. leprae killed whole-cell preparation as the source of DNA, both single-stage and nested PCR were performed after optimisation of the experimental conditions. Compared with the 36-kDa antigen gene primers, the 18-kDa antigen gene outer primers were 100-fold more sensitive and the RLEP outer primers were 1000-fold more sensitive. As an illustration of two possible applications of these new primers, positive results were obtained from three skin slit samples from treated lepromatous leprosy patients and three archaeological samples from human remains showing typical leprosy palaeopathology. It was concluded that these new primers are a useful means of detecting M. leprae DNA which is damaged or present at a very low level.


2223. John TJ.  Muliyil J. Care after cure in leprosy. Lancet.  357(9252):313, 2001 Jan 27.


2224.  Kalantri SP. Dr K. V. Desikan gets the Damien-Dutton Award. National Medical Journal of India.  14(1):61, 2001 Jan-Feb.


2225. Kim SK.  Dohlman CH. Causes of enlarged corneal nerves. [Review] [81 refs] International Ophthalmology Clinics.  41(1):13-23, 2001 Winter.


2226. Marques MA.  Ant nio VL.  Sarno EN.  Brennan PJ.  Pessolani MC. Binding of alpha2-laminins by pathogenic and non-pathogenic mycobacteria and adherence to Schwann cells. Journal of Medical Microbiology.  50(1):23-8, 2001 Jan.


  The ability of Mycobacterium leprae to specifically bind alpha2-laminins of Schwann cells has been described recently as being an important property of the leprosy bacillus, which could explain the neural tropism of M. leprae. Therefore, the extent of the expression of alpha2-laminin-binding properties among mycobacteria was investigated. In an ELISA-based assay, all three species of Mycobacterium tested (M. tuberculosis, M. chelonae and M. smegmatis) expressed laminin-binding capacity, suggesting that the ability to bind alpha2-laminins is conserved within the genus Mycobacterium. This report also demonstrated that not only M. leprae but all the mycobacterial species tested readily interacted with the ST88-14 cells, a human schwannoma cell line, and that the addition of soluble alpha2-laminins significantly increased their adherence to these cells. These results failed to demonstrate the presence in M. leprae of a unique system based on alpha2-laminins for adherence to Schwann cells.



2227. Moraes MO.  Sampaio EP.  Nery JA.  Saraiva BC.  Alvarenga FB.  Sarno EN. Sequential erythema nodosum leprosum and reversal reaction with similar lesional cytokine mRNA patterns in a borderline leprosy patient. British Journal of Dermatology.  144(1):175-81, 2001 Jan.


  We compare the clinical and histological data with the immunological status of a borderline leprosy patient who experienced an erythema nodosum leprosum (ENL) reaction followed by a reversal reaction (RR) after 12 weeks of anti-inflammatory treatment (pentoxifylline, PTX, 1200 mg daily). Skin biopsies, serum and blood samples were collected sequentially during the reactional episodes. At the outset of RR, the patient's lymphocytes secreted interferon (IFN) -gamma and there was a positive lymphoproliferative test in response to Mycobacterium leprae, which had been absent during ENL. The lepromin reaction reversed from negative (0 mm) at diagnosis, to positive (3 mm) 3 months after the development of RR. Tumour necrosis factor (TNF) -alpha levels in the serum decreased after 1 week of treatment and increased slightly thereafter. The immunohistochemical data for ENL showed a diffuse dermal and hypodermal infiltrate composed of mononuclear cells and neutrophils, while RR was characterized by an epithelioid granulomatous infiltrate with a marked presence of gammadelta T cells. Reverse transcription-polymerase chain reaction showed a mixed cytokine profile characterized by the expression of TNF-alpha, IFN-gamma, interleukin (IL) -6, IL-10 and IL-12 mRNA in the skin, which persisted throughout the development of ENL and RR lesions. IL-4 mRNA, first detected after 7 days of PTX treatment, was still present during RR. The results suggest the emergence of an initial Th0-like cytokine profile in ENL, typical of a state of immunoactivation, before conditions optimal for the appearance of an antigen-specific cell-mediated immune response and gammadelta T-cell migration are created.


2228. Mvogo CE.  Bella-Hiag AL.  Ellong A.  Achu JH.  Nkeng PF. Ocular complications of leprosy in Cameroon. Acta Ophthalmologica Scandinavica.  79(1):31-3, 2001 Feb.


  PURPOSE: This study aimed to identify the main ocular complications of leprosy in Cameroon. PATIENTS AND METHODS: It is a prospective cross-sectional study which took place from July 1998 to January 1999 in five leprosaria in Cameroon. The ophthalmological examination of all patients was performed by the same team. RESULTS: Of the 218 patients examined, 60.1% were males and 39.9% females. 72.5% had a paucibacillary leprosy and 27.5% a multibacillary form. 77.5% of patients had at least one ocular lesion and 38.3% of eyes had visual acuity < or = 1/10. Madarosis and anterior uveitis were more frequent in multibacillary forms while lagophthalmos and cataract were so in paucibacillary forms. CONCLUSION: Ocular complications are frequent in leprosy in Cameroonians. It is a true public health problem and it is important to prevent these lesions by early diagnosis and adequate treatment.


2229. Nunez-Gussman J.  Hwang L.  Hsu S. Guess what! Targetoid erythematous plaques: an unusual morphological presentation of multibacillary Hansen's disease. European Journal of Dermatology.  11(1):65-7, 2001 Jan-Feb.


2230. Ochoa MT.  Stenger S.  Sieling PA.  Thoma-Uszynski S.  Sabet S.  Cho S. Krensky AM.  Rollinghoff M.  Nunes Sarno E.  Burdick AE.  Rea TH.  Modlin RL. T-cell release of granulysin contributes to host defense in leprosy. Nature Medicine.  7(2):174-9, 2001 Feb.


  A novel mechanism by which T cells contribute to host defense against microbial pathogens is release of the antimicrobial protein granulysin. We investigated the role of granulysin in human infectious disease using leprosy as a model. Granulysin-expressing T cells were detected in cutaneous leprosy lesions at a six-fold greater frequency in patients with the localized tuberculoid as compared with the disseminated lepromatous form of the disease. In contrast, perforin, a cytolytic molecule that colocalizes with granulysin in cytotoxic granules, was expressed at similar levels across the spectrum of disease. Within leprosy lesions, granulysin colocalized in CD4+ T cells and was expressed in CD4+ T-cell lines derived from skin lesions. These CD4+ T-cell lines lysed targets by  the granule exocytosis pathway and reduced the viability of mycobacteria in infected targets. Given the broad antimicrobial spectrum of granulysin, these data provide evidence that T-cell release of granulysin contributes to host defense in human infectious disease.

2231. Rambukkana A. How does Mycobacterium leprae target the peripheral nervous system? [see comments]. [Review] [44 refs] Trends in Microbiology.  8(1):23-8, 2000 Jan.


  Mycobacterium leprae has the capacity to invade the peripheral nervous system and cause neuropathy. The molecular mechanisms responsible have remained unknown until recently. Identification of the endoneurial laminin-2 isoform and its receptor alpha-dystroglycan as neural targets of M. leprae has not only opened up a new area of scientific inquiry into the pathogenesis of neurological damage in leprosy, but has also revealed unexpected biological properties of these important host molecules. [References: 44]


2232. Salvadori M. Index of suspicion. Case 2. Diagnosis: Leprosy. Pediatrics in Review.  22(1):22-31, 2001 Jan.


2233. Santos DO.  Santos SL.  Esquenazi D.  Nery JA.  Defruyt M.  Lorre K.  Van Heuverswyn H. Evaluation of B7-1 (CD80) and B7-2 (CD86) costimulatory molecules and dendritic cells on the immune response in leprosy. Nihon Hansenbyo Gakkai Zasshi. Japanese Journal of Leprosy.  70(1):15-24, 2001 Feb.


  The cell activation depends on T cell antigen receptor binding to antigen plus MHC and costimulation. The binding of CD28, expressed on the T cell surface to B7 (B7-1 or CD80/B7-2 or CD86) present on the antigen--presenting cells (APCs), determines, in several T cell function models, if activation or anergy follows antigenic stimulation. In leprosy, the role of CD80 and CD86 as costimulatory signal in M. leprae-specific cellular immunity has not yet been defined. We investigated the role of B7-CD28 pathway of T cell activation in the in vitro response to M. leprae, following stimulation in the presence of monocytes or dendritic cells (DCs) as APCs. Monocytes were purified, by cold aggregation, from peripheral blood mononuclear leukocytes (PBMC), isolated from leprosy  patients. In order to obtain DCs, the monocytes were cultured in the presence of IL-4 and GM-CSF. T cells were purified from PBMC by negative selection with mABs and C'. The phenotype of the cell populations was monitored by FACS. Lymphoproliferative assays were performed with T cells, in the presence of monocytes or DCs. The cells were stimulated by M. leprae in the presence of anti-CD80 antibody (Ab) and/or anti-CD86 antibody (Ab) (Innogenetics). In some experiments Il-10, Il-12 and anti-Il-12 Ab were also added to the culture. We observed a significantly more efficient APC function for DCs when compared to monocytes in T cell in vitro responses to M. leprae. Regardless of the clinical form of Leprosy, the M. leprae-specific immune response was markedly reduced in the presence of anti-CD86 Ab. Il-12 increase the immune response to M. leprae while IL-10 or anti-IL-12 Ab reduce this response when monocytes or DCs were used as APCs.

2234.   Stockel S.  Meurer M.  Wozel G. Dapsone-induced photodermatitis in a patient with linear IgA dermatosis. [Review] [17 refs] European Journal of Dermatology.  11(1):50-3, 2001 Jan-Feb.


  Dapsone (4, 4' diaminodiphenylsulfone) is an efficient antiinflammatory agent. Its therapeutic use may result in a variety of adverse effects. The most frequent unwanted reactions are hemolytic anemia and methemoglobinemia. By oral route dapsone is mainly metabolized to monoacetyldapsone (MADDS) and hydroxylamine dapsone (DDS-NOH). We report a 76-year-old female patient with linear IgA dermatosis who developed a dapsone-induced photosensitivity 8 weeks after initiation of sulfone therapy. She showed a widespread erythematous eruption in UV-exposed skin area. After clearing of skin lesions the photopatch test revealed positive reactions to dapsone, MADDS and DDS-NOH. Dapsone-induced photosensitivity to date has been described only in leprosy patients. We demonstrate for the first time that this adverse reaction is not restricted to leprosy and that dapsone metabolites may also contribute to the mechanism of  photosensitivity like the parent sulfone. Dapsone-induced photosensitivity is a rare, not dose-related adverse effect of the sulfone and can also occur in patients with inflammatory skin disorders. [References: 17]


2819.    Bhake AS.  Desikan KV.  Jajoo UN. Cytodiagnosis of histoid leprosy. Leprosy Review.  72(1):78-82, 2001 Mar.

2820.    Charlab R.  Sarno EN.  Chatterjee D.  Pessolani MC. Effect of unique Mycobacterium leprae phenolic glycolipid-I (PGL-I) on tumour necrosis factor production by human mononuclear cells. Leprosy Review.  72(1):63-9, 2001 Mar.

2821.    Coleman MD. Dapsone-mediated agranulocytosis: risks, possible mechanisms and prevention. [Review] [51 refs]  Toxicology.  162(1):53-60, 2001 Apr 12.

2822.    Curtiss R 3rd.  Blower S.  Cooper K.  Russell D.  Silverstein S.  Young L. Leprosy research in the post-genome era. [0 refs]  Leprosy Review.  72(1):8-22, 2001 Mar.

2823.    de la Barrera S.  Fink S.  Finiasz M.  Aleman M.  Helena Farina M.  Pizzariello G.  del Carmen Sasiain M. Lysis of autologous macrophages pulsed with hsp10 from Mycobacterium leprae is associated to the absence of bacilli in leprosy. Immunology Letters.  76(1):55-62, 2001 Feb 1.

2824.    Lockwood DN.  Reid AJ. The diagnosis of leprosy is delayed in the United Kingdom. QJM.  94(4):207-12, 2001 Apr.

2825.    Ooi WW.  Moschella SL. Update on leprosy in immigrants in the United States: status in the year 2000. [Review] [38 refs] Clinical Infectious Diseases.  32(6):930-7, 2001 Mar 15.

2826.    Ramadan W.  Mourad B.  Fadel W.  Ghoraba E. Clinical, electrophysiological, and immunopathological study of peripheral nerves in Hansen's disease. Leprosy Review.  72(1):35-49, 2001 Mar.

2827.    Tovar-Rivera T.  Sanchez-Colon S.  Padierna-Olivos L.  Masso-Rojas F.  Estrada-Parra S.  Mondragon-Gonzalez R.  Jimenez-Martinez MC.  Sanchez-Garcia FJ. Connectivity patterns in tuberculosis and leprosy patients are indistinguishable from that of healthy donors. Scandinavian Journal of Immunology.  53(5):520-7, 2001 May.

2828.    Walsh DS.  Prieto-Go D.  Abalos RM.  Tuur-Saunders SM.  Villahermosa LG.  Jabien Z.  Walsh GP.  Fajardo TT. Malignant T-cell lymphoma mimicking lepromatous leprosy. Clinical & Experimental Dermatology.  26(2):173-5, 2001 Mar.

2829.    Zijlstra EE.  el-Hassan AM. Leishmaniasis in Sudan. Post kala-azar dermal leishmaniasis. Transactions of the Royal Society of Tropical Medicine & Hygiene.  95 Suppl 1:S59-76, 2001 Apr.




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