rifampin and Immunologic-Deficiency-Syndromes

Topics: Animals; Binding Sites, Antibody; Dose-Response Relationship, Drug; Guinea Pigs; Humans; Immunity; Immunity, Cellular; Immunologic Deficiency Syndromes; Immunosuppressive Agents; Lymphocytes; Macrophages; Rabbits; Rifampin; Rifamycins; Skin Transplantation; Time Factors; Transplantation, Homologous

Anti-interferon-gamma (IFN-γ) autoantibodies has been recognised as an adult-onset immunodeficiency in the past decade in people who originate from Southeast Asia. These patients are susceptible to particular opportunistic infections, especially non-tuberculous mycobacteria (NTM). We present the case of a woman whom originally came from Thailand with disseminated

Topics: Adult; Anti-Bacterial Agents; Asian People; Autoantibodies; Azithromycin; Bacteremia; Disease Progression; Ethambutol; Female; Humans; Immunologic Deficiency Syndromes; Immunologic Factors; Interferon-gamma; Mycobacterium avium Complex; Mycobacterium avium-intracellulare Infection; Pericarditis; Pleurisy; Pneumonia, Bacterial; Recurrence; Rifampin; Rituximab; Thailand

It is well known that disseminated Mycobacterium bovis BCG infection is developed after BCG vaccination in infants with congenital cellular immune deficiencies such as mutations in genes along the interleukin (IL)-12/interferon (IFN)-γ pathway and mutations in nuclear factor-kB essential modulator (NEMO). In this report, a rifampicin-resistant M.bovis BCG strain isolated from an infant with NEMO defect was presented. An 8-month-old male infant with NEMO defect admitted to the pediatric outpatient clinic of our hospital with fever, generalized lymphadenopathy and hepatosplenomegaly. Microscopic examination of the smears prepared from lymph node and liver biopsy specimens revealed abundant amount (3+) of acid-fast bacilli (AFB). Rifampicin-susceptible Mycobacterium tuberculosis complex (MTC) was detected by real-time PCR (GeneXpert MTB/RIF; Cepheid, USA) in the samples. The growth of mycobacteria was determined on the 20th day of culture performed in MGIT960 system (Becton Dickinson, USA). The isolate was identified as M.bovis BCG by GenoType MTBC kit (Hain Lifescience, Germany) and defined as M.bovis BCG [SIT 482 (BOV_1)] by spoligotyping. In the primary anti-tuberculosis drug susceptibility test performed by MGIT960 system, the isolate was found susceptible to rifampicin (RIF), isoniazid (INH), streptomycin (STM) and ethambutol (EMB). Then anti-tuberculosis treatment was started to the patient. However, the patient at the age of 2 years, re-admitted to the hospital with the complaint of hepatosplenomegaly. Smear of spontaneously draining abscess material obtained from subcutaneous nodules revealed intensive AFB positivity (3+) once again. In the present instance RIF-resistant MTC was detected with GeneXpert system in the specimen. The growth of mycobacteria was determined on the 13th day of culture and isolate was identified as M.bovis BCG. The present isolate was found susceptible to INH, STM and EMB but resistant to RIF. A mutation in the rpoB gene (codon 531, S531L) associated with RIF resistance was detected by using the partial sequencing of the rpoB gene. Patient died due to disseminated bovis BCG infection and multiple organ failure. To our knowledge, there are only six RIF-resistant M.bovis BCG strains isolated from patients in the literature. However, this is the first RIF-resistant M.bovis BCG strain isolated from a NEMO-deficient patient.

Topics: Antibiotics, Antitubercular; Bacterial Proteins; DNA-Directed RNA Polymerases; Drug Resistance, Bacterial; Ectodermal Dysplasia; Fatal Outcome; Genetic Diseases, X-Linked; Humans; Immunologic Deficiency Syndromes; Infant; Liver; Lymph Nodes; Male; Multiple Organ Failure; Mutation; Mycobacterium bovis; Primary Immunodeficiency Diseases; Rifampin; Tuberculosis

Topics: Adult; Dapsone; Diagnosis, Differential; Drug Therapy, Combination; Humans; Immunologic Deficiency Syndromes; Infections; Leishmaniasis; Leprostatic Agents; Leprosy, Multibacillary; Male; Minocycline; Mycobacterium leprae; Ofloxacin; Palate; Prednisone; Rifampin; Strongyloidiasis; Treatment Outcome

The authors investigated spontaneous and induced secretion of cytokins at different stages of generalized tuberculosis. In the development of infection there were inhibited IL-2 synthesis in response to ConA, emerging activity of PNO-alpha in response to the inductors in blood serum and culture of peritoneal macrophages, enhanced secretion of IL-6. Complete immunodeficiency was associated with cessation of IL-2 synthesis by splenocytes, elevated production of IL-6 by peritoneal macrophages, low concentrations of PNO-alpha in the serum and peritoneal macrophage cultures. In the treatment of M. bovis-infected mice with antibacterial drugs alone IL-6 secretion by peritoneal macrophages and PNO-alpha activity in the serum were increased. Immunocorrection resulted in marked activation of IL-2 production by splenocytes in response to ConA as well as enhanced synthesis of IL-6 in unstimulated cultures of peritoneal macrophages.

Topics: Adjuvants, Immunologic; Animals; Antitubercular Agents; Concanavalin A; Drug Evaluation, Preclinical; Drug Therapy, Combination; Immunity, Cellular; Immunologic Deficiency Syndromes; Interleukin-2; Interleukin-6; Isoniazid; Mice; Mycobacterium bovis; Rifampin; Thymus Hormones; Tuberculosis; Tumor Necrosis Factor-alpha

Soon after more than 10(6) Mycobacterium leprae, freshly harvested from armadillo liver or harvested and 60CO irradiated, were inoculated into the hind footpads of either normal or thymectomized and irradiated (T900R) mice, the organisms were found to reside within phagosomes of polymorphonuclear and mononuclear cells. On the other hand, 7 and 8 months after 10(4) freshly harvested M. leprae were inoculated into the footpads of normal or T900R mice and the organisms had multiplied to their maximum in the normal mice, many organisms, largely intact by electron-microscopic criteria, were found to reside free in the cytoplasm of the footpad macrophages, whereas damaged organisms were contained within phagosomes. After 11 months, many intact organisms were found to lie free in the cytoplasm of the macrophages of T900R mice, whereas only damaged intraphagosomal M. leprae cells were observed in the macrophages of normal mice. Finally, a remarkably large proportion of damaged extraphagosomal M. leprae was found in T900R mice administered rifampin for 2 days in a bactericidal dosage. It appears that M. leprae multiplies free in the cytoplasm of the footpad macrophages of infected mice, whereas the M. leprae cells resident within the phagosomes of the macrophages are dead. As the result of treatment with rifampin, the organisms appeared to have been killed in their extraphagosomal location, only afterwards being incorporated into phagosomes. However, the intracellular site in which M. leprae is killed in the course of an effective immune response remains unclear.

Topics: Animals; Female; Immunologic Deficiency Syndromes; Leprosy; Macrophages; Mice; Mice, Inbred Strains; Microscopy, Electron; Mycobacterium leprae; Phagocytosis; Rifampin; Thymectomy

Topics: Adolescent; Adrenal Cortex Hormones; Anemia; Antibodies; BCG Vaccine; Biopsy; Bone Marrow Diseases; Ethambutol; Female; Fever; Hepatomegaly; Humans; Immunity, Cellular; Immunoglobulins; Immunologic Deficiency Syndromes; Iron; Isoniazid; Leukocyte Count; Lymph Nodes; Lymphocytes; Lymphopenia; Mycobacterium bovis; Mycobacterium Infections; Rifampin; Splenic Diseases; Splenomegaly; Tuberculin Test

Topics: Adolescent; Adult; Antibodies, Bacterial; Child; Child, Preschool; Female; Humans; Immunoglobulin M; Immunologic Deficiency Syndromes; Infant; Male; Meningitis; Meningococcal Infections; Rifampin; Sulfadiazine