Mycobacterium leprae causes leprosy. M leprae strains collected worldwide have been genetically clonal, which poorly explains the varying severity and clinical features of the disease. We discovered a new Mycobacterium species from 2 patients who died of diffuse lepromatous leprosy (DLL). The Mycobacterium was purified from heavily infected, freshly frozen autopsy liver tissue followed by DNA extraction in 1 case. Paraffin-embedded skin tissue was used for DNA extraction in another case. Six genes of the organism were amplified by polymerase chain reaction, sequenced on cloning or from amplicons, and analyzed. Significant genetic differences with M leprae were found, including a 2.1% divergence of the 16S ribosomal RNA (rRNA) gene, a highly conserved marker of bacterial evolution, and 6% to 14% mismatches among 5 less conserved genes. Phylogenetic analyses of the genes of 16S rRNA, rpoB, and hsp65 indicated that the 2 most related organisms evolved from a common ancestor that had branched from other mycobacteria. These results and the unique clinicopathologic features of DLL led us to propose Mycobacterium lepromatosis sp nov. This species may account for some of the clinical and geographic variability of leprosy. This finding may have implications for the research and diagnosis of leprosy.

Background  Mycobacterium leprae was the only known cause of leprosy until 2008, when a new species, named Mycobacterium lepromatosis, was found to cause diffuse lepromatous leprosy (DLL), a unique form of leprosy endemic in Mexico. Methods  We sought to differentiate the leprosy agents among 120 Mexican patients with various clinical forms of leprosy and to compare their relative prevalences and disease features. Archived skin biopsy specimens from these patients were tested for both M. leprae and M. lepromatosis using polymerase chain reaction‐based species‐specific assays. Results  Etiologic species were confirmed in 87 (72.5%) patients, of whom 55 were infected with M. lepromatosis, 18 with M. leprae, and 14 with both organisms. The endemic regions of each agent differed but overlapped. Patients with M. lepromatosis were younger and were distributed across more states; their clinical diagnoses included DLL (n = 13), lepromatous leprosy (LL) (n = 34), and eight other forms of leprosy. By contrast, the diagnoses of patients with M. leprae did not include DLL but did include LL (n = 15) and three other forms of leprosy. Thus, M. lepromatosis caused DLL specifically (P = 0.023). Patients with M. lepromatosis also showed more variable skin lesions; the extremities were the most common sites of biopsy in these patients. Finally, patients with dual infections manifested all clinical forms and accounted for 16.1% of all species‐confirmed cases. Conclusions  Mycobacterium lepromatosis is another cause of leprosy and is probably more prevalent than M. leprae in Mexico. It mainly causes LL and also specifically DLL. Dual infections caused by both species may occur in endemic areas.

B. diminuta is intrinsically resistant to fluoroquinolones and can be selected out to cause infections.

Clinical and microbiologic studies of 50 cases of viridans streptococcal bacteremia in cancer patients were performed. The bacteria were identified to species level by sequencing analysis of the 16S rRNA gene. At least nine Streptococcus spp. were found, including S. mitis (25 strains, 50.0% of 50); currently unnamed Streptococcus spp. (11 strains); S. parasanguis (five strains); S. anginosus (three strains); S. salivarius (two strains); and one strain each of S. gordonii, S. sanguis, S. sobrinus, and S. vestibularis. There were no S. oralis strains. Among 11 antibiotics of nine classes tested, no resistance to vancomycin, linezolid, or quinupristin-dalfopristin was seen. Resistance to penicillin (MIC, 4 to 12 g/ml) was noted only among S. mitis strains (28.0%, 7/25) and not non-S. mitis strains (0/25) (P ‫؍‬ 0.004). Significantly more S. mitis strains than non-S. mitis strains were resistant to fluoroquinolones and to >3 classes of antibiotics. Isolation of quinolone-resistant organisms was associated with the prior usage of quinolones (P ‫؍‬ 0.002). Quantitative blood cultures showed that the strains resistant to levofloxacin or gatifloxacin were associated with higher colony counts than were their corresponding nonresistant strains. The young and elderly patients also had higher levels of bacteremia caused predominantly by S. mitis. Septic shock was present in 17 (34.0% of 50) patients, and 13 of those cases were caused by S. mitis (P ‫؍‬ 0.007). These results suggest that S. mitis is the most common cause of viridans streptococcal bacteremia in cancer patients and is more resistant to antibiotics than other species.Viridans streptococci represent a group of 24 currently described Streptococcus species that are nutritionally fastidious and mainly alpha-hemolytic on sheep blood agar (30). These gram-positive cocci are commensals of the oral cavity, upper airway, and gastrointestinal and genitourinary tracts. Despite the overall low virulence, they may cause infective endocarditis, contribute to polymicrobic abscess, and invade the bloodstream during the state of neutropenia.The bloodstream infection usually occurs in cancer patients with mucositis and neutropenia due to antineoplastic chemotherapy-related toxicity. In these patients, studies have found that viridans streptococci are among the most common organisms isolated from the cultures of bacteremia samples (17). As cancer care has improved and intensified over recent decades and the patients survive longer, these and other infectious complications become more pronounced. A study from our institution showed that the rate of viridans streptococcal bacteremia increased from 1 per 10,000 admissions to 47 per 10,000 during the 13-year period from 1977 to 1989 (11). These bacteremias cause substantial morbidity, and mortality in these patients is at 6 to 12% (17, 29).The most common viridans streptococci that cause neutropenic bacteremia have been S. oralis, S. mitis, and S. salivarius (4,11,15,17). Identification of these species, however, was reached through...

BackgroundHemorrhagic cystitis is a common cause of morbidity after allogeneic stem cell transplantation, frequently associated with BK virus infection. We hypothesized that patients with positive BK viruria before unrelated or mismatched related donor allogeneic hematopoietic stem cell transplantation have a higher incidence of hemorrhagic cystitis. Design and MethodsTo test this hypothesis, we prospectively studied 209 patients (median age 49 years, range 19-71) with hematologic malignancies who received bone marrow (n=78), peripheral blood (n=108) or umbilical cord blood (n=23) allogeneic hematopoietic stem cell transplantation after myeloablative (n=110) or reduced intensity conditioning (n=99). Donors were unrelated (n=201) or haploidentical related (n=8). ResultsTwenty-five patients developed hemorrhagic cystitis. Pre-transplant BK viruria detected by quantitative PCR was positive in 96 patients. The one-year cumulative incidence of hemorrhagic cystitis was 16% in the PCR-positive group versus 9% in the PCR-negative group (P=0.1). The use of umbilical cord blood or a haploidentical donor was the only significant predictor of the incidence of hemorrhagic cystitis on univariate analysis. There was also a trend for a higher incidence after myeloablative conditioning. Multivariate analysis showed that patients who had a positive PCR pre-transplant and received haploidentical or cord blood grafts with myeloablative conditioning had a significantly higher risk of developing hemorrhagic cystitis (58%) than all other recipients (7%, P<0.001). ConclusionsHemorrhagic cystitis is the result of a complex interaction of donor type, preparative regimen intensity, and BK viruria.