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PubMed1997

Expression of memory immunity in the lung following re-exposure to Mycobacterium tuberculosis.

OBJECTIVE: To examine the memory immunity expressed in the lung in response to a low-dose aerosol challenge. DESIGN: Memory-immune C57BL/6 mice were generated by infection followed by drug treatment with isoniazid and rifabutin. Both memory-immune and naive mice were then rechallenged via both the aerosol and intravenous routes. The growth of bacteria in target organs, the expression of cytokines within these organs and the ability of T cells to recognize selected mycobacterial protein antigens were determined over time. RESULTS: There was a finite delay before immunity was expressed in the lungs of the memory-immune mice. This was in contrast to the immediate control of bacterial growth seen in the liver of intravenously challenged mice. In both cases, the expression of interferon-gamma (IFN-gamma) mRNA in the target organ correlated with the control of bacterial growth. Memory immunity in the spleen and lung differed: whereas splenic T cells strongly recognized the major Ag85 protein, the 45 kDa protein, and a synthetic peptide representing the ESAT molecule, only the Ag85 molecule was recognized by T cells harvested from thoracic lymph nodes after pulmonary rechallenge. CONCLUSIONS: Immunity, as mediated by IFN-gamma, is expressed more slowly following an aerosol rechallenge and appears to be restricted in terms of antigen specificity. Moreover, very strong levels of memory immunity can prevent progressive disease in the lungs, but cannot prevent the establishment of secondary infection.

Animals↗
PubMed1998

Host response to mycobacterial infection in the alcoholic rat: male and female dimorphism.

Increased susceptibility to tuberculosis occurs in the alcoholic. One explanation for the altered susceptibility is a change in T-lymphocyte modulation. To evaluate this, 24 male and 24 female Sprague-Dawley rats were treated with either a Lieber-type liquid ethanol diet (LED) or an isocaloric control (LCD). After 2 weeks, half the subjects were infected with BCG (10(8) colony-forming units) and sacrificed after 42 days. Splenic helper (CD4) and suppressor/cytoxic (CD8) cells were quantitated by flow cytometry. By three-way analysis of variance, splenic cellularity was significantly increased by infection (p < 0.0001) but suppressed by LED (p = 0.0002). There was a marginal sexual difference (p = 0.065) with females exhibiting a 35% lower response while on alcohol. Examining lymphocyte subsets, the most significant changes were observed after infection (BCG) and alcohol treatment (LED). CD4 levels were diminished by LED (p = 0.0002) but markedly increased by infection (p < 0.0001), producing a highly significant interaction that affected both absolute number (p < 0.0001) and relative percent present (p = 0.0078). CD8 was influenced only by infection (p < 0.0001). This resulted in a infection-related increase in the CD4/CD8 ratio which was lower with LED (p = 0.0032). Splenic T-lymphocytes, predominately CD4, are involved in the host response to BCG hepatitis and are adversely influenced by LED, which may contribute to increased susceptibility.

Alcoholism↗
PubMed1993

Myelin-liposome protection against experimental autoimmune encephalomyelitis is associated with reduced neuroantigen-specific T-cell-mediated responses.

Lewis rats undergo a relapsing paralytic disease upon challenge with spinal cord emulsified in complete Freund's adjuvant (CFA). Treatment with two intracardiac injections of liposomes composed of whole myelin significantly reduced the severity of disease. Protection was disease-specific since treatment with myelin liposomes did not protect Lewis rats against adjuvant arthritis (AA), a CNS-unrelated T-cell-mediated autoimmune disease. Myelin-liposome-treated, spinal cord/CFA-immunized rats displayed borderline reduction of delayed-type hypersensitivity (DTH) (ear swelling) reactions to myelin and myelin basic protein (MBP), but significantly reduced in vitro lymphnode cell proliferation in response to these antigens. Responses to purified protein derivative of Mycobacterium tuberculosis (PPD) were not reduced, emphasizing the antigen-specific nature of the myelin-liposome-mediated suppression. Spleen cell proliferative responses were inconsistent and often poor. However, when cultured in the presence of NG-monomethyl-L-arginine (MMA), antigen-specific proliferation of spleen cells from both treated and control rats was greatly enhanced, indicating that reactive nitrogen intermediates contributed to the decrease in spleen cell proliferation. Purified splenic T cells from treated rats displayed a pattern of proliferation similar to that of unseparated lymphnode cells. Treatment of rats with a single injection of myelin liposomes after recovery from the first clinical episode significantly reduced the severity of the relapses.

Animals↗
PubMed1990

Adenocarcinoma of the cardia: treatment by thoracoabdominal R3 radical gastrectomy.

The complications and mortality rate of R3 radical gastrectomy using a left thoracoabdominal approach were studied in 38 patients with adenocarcinoma of the gastric cardia. There were two hospital deaths and two anastomotic leaks. There was a high rate of complications following surgery (subphrenic abscess, eight; severe chest infection, five; aspiration pneumonia, two; wound infection, two; and reactivation of tuberculosis, one). The hospital stay ranged from 11 to 39 days (median 21 days). Thirty-five patients had microscopic evidence of serosal involvement (S2). Thirty-three of the patients had lymph node metastases and 17 patients had involvement of N2 nodes. Four patients had histological evidence of residual suture line tumour, but only two of these returned with recurrence at the anastomosis. Follow-up (median 3 years) revealed that splenic artery nodal involvement (N2) did not worsen the prognosis after radical resection. Despite a high complication rate, thoracoabdominal radical gastrectomy is associated with an acceptable perioperative mortality rate, adequate symptom palliation and encouraging medium-term survival. The left thoracoabdominal approach gives excellent exposure for radical resection of cancer of the gastric cardia and should be the procedure of choice for curative resection of this tumour.

Adenocarcinoma↗
PubMed1988

Pleiotropic effects of the Bcg gene: III. Respiratory burst in Bcg-congenic macrophages.

Macrophage respiratory burst, as assessed by H2O2 and O2- production, and HMS and chemiluminescence activity was investigated in a variety of conditions in macrophages from Bcg-congenic mice. Measurement of HMS and chemiluminescence in splenic macrophages challenged in vitro with BCG showed that the Bcgr cells were more stimulated by the challenge than their Bcgs counterparts. H2O2 production was measured in Bcgr and Bcgs splenic macrophages. PMA-triggering and LK-triggering were shown to stimulate a similar degree of H2O2 production Bcgr and Bcgs macrophages. In contrast, in vitro phagocytosis of BCG was shown to trigger superior production of H2O2 and O2- in the Bcgr splenic macrophages as compared to their Bcgs congenics. Finally, following the in vivo infection with BCG Montreal, Bcgr splenic macrophages were superior producers of H2O2 (both spontaneous and PMA-triggered) in the early phase of infection.

Animals↗
PubMed1998

Infections in nonleukopenic compromised hosts (diabetes mellitus, SLE, steroids, and asplenia) in critical care.

Acutely ill patients who are immunocompromised but not neutropenic most commonly are: (1) diabetic; (2) on chronic high-dose steroid therapy; (3) have lupus; or (4) have impaired or absent splenic function. These patients often present in the CCU because of the severity of their infection. Differential diagnosis may be approached by first considering the patient's underlying disease, i.e., SLE. The next step in the diagnostic process is to appreciate the immune defect associated with these disorders. The nature of the immune defect determines which clinical pathogens are related to the immune defect. Pathogens are associated with a sterotyped pattern of organ involvement. The object of the diagnostic analysis is to determine the most likely organism affecting a particular organ system, given the defect in host defenses associated with the patient's underlying illness. In this way, a useful clinical diagnosis can be made rapidly, and appropriate clinical specimens obtained for diagnostic testing. Often empiric therapy must be started pending the results of diagnostic testing. In such situations, empiric therapy ordinarily is directed against the bacterial pathogens most likely to cause disease relevant to the patient's impaired defenses. Specific therapy for unusual or exotic pathogens should not be empiric and should be based on demonstration of a pathogenic role by the microorganism. In the case of miliary tuberculosis or invasive fungal disease, a case may be made for early empiric therapy to cover these organisms if there is sufficient clinical suspicion based on the presenting signs and symptoms as well as the pattern of organ involvement. As with all infections, but particularly in immunocompromised patients, the early initiation of appropriate antimicrobial therapy is essential and often life-saving.

Adrenal Cortex Hormones↗
PubMed1990

Characteristics of immunosuppressive macrophages induced in spleen cells by Mycobacterium avium complex infections in mice.

The profile of generation and characteristics of splenic macrophages (M phi s) which suppress the concanavalin A (Con A) mitogenic response of splenic T cells (designated as 'immunosuppressive M phi s') in host CBA/JN mice during the course of Mycobacterium avium complex (MAC) infection were investigated. In MAC-infected mice, reductions in some cellular functions of host splenic T cells, such as the Con A mitogenic response and mixed leucocyte reaction, were seen around 2 weeks after challenge of organisms, and this was accompanied by appearance of immunosuppressive M phi s in spleen cells. In this case, increase in immunosuppressive M phi activity was seen in terms of both activity per spleen and activity per individual M phi. In this phase of the infection, MAC-induced splenic M phi s showed a markedly increased ability to produce reactive oxygen radicals in response to phorbol myristate acetate. Thus, the expression of suppressor activity of MAC-induced M phi s seems to be closely linked to their activated state. A large proportion of the immunosuppressive M phi s exhibited suppressor activity dependent on prostaglandins and membrane functions related to microfilaments. It was also found that the generation of IL-2-reactive T cell populations in response to Con A was markedly inhibited by MAC-induced splenic M phi s, whereas they caused no significant reduction in the IL-2-producing ability of normal spleen cells.

Animals↗
PubMedDate not supplied

Induction of colony-stimulating factors by a 30-kDa secretory protein of Mycobacterium tuberculosis H37Rv.

Colony-stimulating factors (CSFs)-induced increased hematopoietic activity is known to occur in various microbial diseases; however, not much is known during tuberculosis (TB). We investigated the CSF-inducing capability of a Mycobacterium tuberculosis H37Rv component. Swiss mice intravenously injected with purified 30-kDa secretory protein of M. tuberculosis H37Rv (Mtb30; 0.1-10 mg/kg) showed enhanced levels of serum CSFs; maximum response (142 +/- 16 colonies) occurred at 1 mg/kg. In vitro, Mtb30 (1-50 mug/mL) induced mouse peritoneal macrophages (PMs) to elaborate CSFs in the conditioned medium (CM); 25 mug/mL appeared optimal (97 +/- 11 colonies). Both in vivo and in vitro, peak CSF production occurred 24 h after stimulation which levelled-off to background levels by 72 h. Rabbit anti-Mtb30 antibody significantly (p<0.05) reduced CSF production by both Mtb30-stimulated and M. tuberculosis-infected PMs, in vitro. The induced CSFs, both in the serum and CM, appeared to be functionally similar, as they supported the formation of granulocyte (G), monocyte (M) and GM colonies, in similar proportions; the GM colonies were maximum (>79 %). Neutralizing (100%) rabbit anti-mouse interleukin-1 (IL-1) polyclonal antibody did not affect the Mtb30-induced CSF production, indicating it to be IL-1-independent; whereas, CSF production was partly dependent on tumour necrosis factor-alpha (TNF-alpha), as goat anti-mouse TNF-alpha immunoglobulin G only partly inhibited it. Mtb30-induced PM production of CSFs was de novo as it was completely blocked by cycloheximide (50 mug/mL). The CSF-inducing capability of Mtb30 appeared to be proteinaceous in nature as it was heat (70 degrees C; 1 h)-labile, was destroyed by proteases (pronase E and trypsin) and was unaffected by sodium periodate treatment. Further, compared to the controls, Mtb30 induced significantly (p<0.05) high levels of immunoreactive GM-CSF (9+/-1 and 7.5+/-0.8 ng/mL) and M-CSF (4.3+/-0.5 and 3.9+/-0.4 ng/mL) in serum and CM, respectively; G-CSF levels did not increase significantly (p>0.05). Mtb30-treated mice showed a maximum of 2.23- and 2.36-fold increase, in the splenic and femur colony forming unit-GM counts, respectively, as compared to the controls. This is the first report which demonstrates Mtb30-induced production of CSFs that is up-regulated both posttranscriptionally and functionally, and thus adds to our understanding of the molecular pathogenetic mechanisms of TB.

Animals↗
PubMed2005

Vaccine-induced cytokine responses in a guinea pig model of pulmonary tuberculosis.

Guinea pigs exposed to very small numbers of virulent tubercle bacilli by the respiratory route develop a disease which mimics many of the important features of the pathogenesis of human tuberculosis (TB), including the expression of strong protective immunity following vaccination with BCG. In order to elucidate the precise immunological mechanisms of vaccine-induced resistance in this model, both mRNA and protein assays for several guinea pig cytokines and chemokines have been developed. The coordinated expression of cytokine and chemokine mRNA and protein was examined in various leukocyte populations and in inflammatory cells and fluid collected following the induction of tuberculous pleurisy in BCG-vaccinated guinea pigs. Real-time RT-PCR assays revealed that the mRNA levels for IFNgamma, TNFalpha, and IL-8 rose over the first few days of TB pleuritis and then declined over the 9 days of the study. Injection of anti-TGFbeta on day 8 following pleurisy induction resulted in significant changes in cytokine mRNA levels and PPD-induced proliferation in pleural effusion lymphocytes taken 24h later. BCG vaccination induced significantly higher levels of bioactive TNFalpha protein in the supernatants of alveolar, peritoneal and splenic cells from BCG-vaccinated guinea pigs cultured in the presence of attenuated or virulent mycobacteria. In sharp contrast, following virulent challenge, all three cell types from BCG-vaccinated guinea pigs produced significantly less TNFalpha. Thus, BCG vaccination appears to modulate the potentially harmful effects of TNFalpha in this model of pulmonary TB. Levels of mRNA for IL-12p40 were upregulated by exposure of infected and uninfected macrophages to recombinant guinea pig (rgp)TNFalpha. The intracellular survival of mycobacteria was enhanced when endogeous TNFalpha activity was neutralized with anti-rgpTNFalpha antiserum. rgp RANTES (CCL5) upregulated mRNA levels for TNFalpha, IL-1beta, MCP-1 (CCL2), and IL-8 (CXCL8) in alveolar and peritoneal macrophages. These results illustrate the profound effects of prior vaccination with BCG on the cytokine and chemokine responses of distinct cell populations in the guinea pig following exposure to attenuated and virulent strains of M. tuberculosis.

Animals↗
PubMed2001

Effects of Z-100, a Mycobacterium-tuberculosis-derived arabinomannan, on the LP-BM5 murine leukemia virus infection in mice.

OBJECTIVE: To investigate the effects of Z-100, an arabinomannan extracted from Mycobacterium tuberculosis, on the LP-BM5 murine leukemia virus (LP-BM5 MuLV) infection in mice. METHODS: C57BL/6 mice infected intraperitoneally with 4.5 x 10(2) PFU/mouse of LP-BM5 MuLV (MAIDS mice) were treated intraperitoneally with a 10-mg/kg dose of Z-100 every other day beginning 1 day after the viral infection. MAIDS mice treated with Z-100 were compared with control mice (MAIDS mice treated with saline) for their survival and splenomegaly after LP-BM5 infection. Cytokine-producing profiles of splenic T cells from these two groups of mice were also compared. RESULTS: When MAIDS mice treated with Z-100 were compared with those of control mice, a decrease in splenomegaly and lymphadenopathy was observed. Splenomegaly was markedly enhanced in MAIDS mice treated intraperitoneally with IL-4 or IL-10. When MAIDS mice were treated with Z-100, their survival rates were significantly increased compared to those of controls. Splenic T cells from control mice produced type-2 cytokines (IL-4 and IL-10). However, a decreased production of type-2 cytokines by splenic T cells from MAIDS mice treated with Z-100 was demonstrated. CONCLUSION: Z-100 could decrease the severity of the LP-BM5 MuLV infection through the regulation of MAIDS-associated type-2 T-cell responses.

Animals↗
PubMed1990

Genetic influences on the immune repertoire following tuberculous infection in mice.

Differences in the antibody repertoire between B10 and BALB background strains have been found following intraperitoneal infection of mice with Mycobacterium tuberculosis. Western blot analysis showed that B10 sera reacted with only a few antigenic bands, whereas BALB sera reacted with multiple bands, irrespective of the H-2 (b or k) haplotype. The oligo-banded pattern was a feature of live infection, since immunization with the mycobacterial extract in incomplete Freunds' adjuvant (IFA) produced a multi-banded response in both intact and in previously infected B10 mice. The multibanded BALB phenotype was dominantly expressed in (BALB x B10) F1 hybrids. The extent to which antibody levels to individual antigens varied was influenced by the combined effects of background (non-H-2) and H-2 genes: anti-65,000 molecular weight (MW) and anti-71,000 MW IgG levels were high in BALB but absent or low in B10 mice, irrespective of H-2 haplotypes, anti-19,000 MW levels in B10 mice were strongly H-2 controlled, whilst anti-38,000 MW levels were high in all tested strains. Immunoglobulin G1 (IgG1) subclass antibody and splenic interleukin-4 (IL-4) mRNA levels were distinctly lower in B10 than in BALB mice, but in vitro T-cell proliferative responses to mycobacterial antigens did not differ between the tested strains. It is proposed that the limited extracellular release of mycobacterial antigens required to stimulate B cells and/or differential activation of T-cell subsets may explain the narrow antibody repertoire in B10 strains of mice. This may have relevance to the outcome of infection, as bacterial counts were higher in the BALB strains at 10 weeks post-infection.

Animals↗
PubMed1987

Pathology of the spleen in the acquired immunodeficiency syndrome.

The pathologic findings of the spleen at autopsy in 101 patients with the acquired immunodeficiency syndrome are described. Grossly visible lesions were present in 52 patients. Microscopically, the histologic patterns of red and/or white pulp could be classified into five groups: group 1, in white pulp only, was characterized by lymphoid depletion; group 2, in red or white pulp, by a proliferation of histiocytes; group 3, in red or white pulp, by a plasma cell/immunoblastic reaction; group 4, in red or white pulp, by a mixture of cells in malpighian corpuscles or trabeculae without significant proliferation or depletion; and group 5, in red pulp only, by packed cords with empty sinuses. These patterns of reaction could be correlated with infectious agents. Disseminated opportunistic infections involved the spleen in 27 cases; of these, the red pulp had a histiocytic or mixed pattern in 89%, and the white pulp showed lymphoid depletion in 52%. Other lesions, including neoplasms in five patients, did not predominate in any group. Splenic opportunistic infections in acquired immunodeficiency syndrome may correlate with histologic patterns of reaction and give an indication of immune response.

Acquired Immunodeficiency Syndrome↗
PubMed2003

Enhanced murine antigen-specific gamma interferon and immunoglobulin G2a responses by using mycobacterial ESAT-6 sequences in DNA vaccines.

The Mycobacterium tuberculosis protein ESAT-6 has unusual immune stimulating activities, has been implicated in the recall of long-lived immunity, and induces protection against tuberculosis in mice. For many diseases caused by bacterial or viral pathogens, a strong cell-mediated immune (i.e., type 1) response is often required for recovery or protection. Therefore, it is important to design immunization regimens that induce agent-specific type 1 immunity. We have shown in previous studies that ESAT-6 could enhance antigen-specific type 1 immune responses in BALB/c mice against a second antigen when presented as a purified fusion protein. It was also of interest to determine if ESAT-6 could enhance the type 1 response against a second antigen beyond that afforded by DNA vaccination through CpG motifs. This was tested by using gene fusions of ESAT-6 and the Mycoplasma hyopneumoniae surface antigen P71. Modified P71 gene sequences were cloned with or without ESAT-6 sequences into a DNA vaccine vector and were used to immunize mice. Splenic lymphocytes from vaccinated mice were tested for gamma interferon (IFN-gamma) and interleukin-10 (IL-10) secretion. Serum antibodies were examined for P71 antigen-specific isotype responses. When stimulated in vitro with purified P71 antigen, splenocytes from the ESAT-6:P71 vaccinates secreted higher levels of IFN-gamma and lower levels of IL-10 compared to those of vaccinates receiving the P71 construct alone. Furthermore, the immunoglobulin G2a serum antibody levels were significantly higher in the ESAT-6:P71 vaccinates compared to those of the vaccinates receiving P71 alone. In conclusion, ESAT-6 was shown to enhance antigen-specific type 1 immune responses in BALB/c mice when used in DNA vaccines.

Animals↗
PubMed1996

Key epitopes on the ESAT-6 antigen recognized in mice during the recall of protective immunity to Mycobacterium tuberculosis.

The recall of long-lived immunity in a mouse model of tuberculosis (TB) is defined as an accelerated accumulation of reactive T cells in the target organs. We have recently identified Ag 85B and a 6-kilodalton early secretory antigenic target, designated ESAT-6, as key antigenic targets recognized by these cells. In the present study, preferential recognition of the ESAT-6 Ag during the recall of immunity was found to be shared by five of six genetically different strains of mice. Overlapping peptides spanning the sequence of ESAT-6 were used to map two T cell epitopes on this molecule. One epitope recognized in the context of H-2b,d was located in the N-terminal part of the molecule, whereas an epitope recognized in the context of H-2a,k covered amino acids 51 to 60. Shorter versions of the N-terminal epitope allowed the precise definition of a 13-amino acid core sequence recognized in the context of H-2b. The peptide covering the N-terminal epitope was immunogenic, and a T cell response with the same fine specificity as that induced during TB infection was generated by immunization with the peptide in IFA. In the C57BL/6j strain, this single epitope was recognized by an exceedingly high frequency of splenic T cells (approximately 1:1000), representing 25 to 35% of the total culture filtrate-reactive T cells recruited to the site of infection during the first phase of the recall response. These findings emphasize the relevance of this Ag in the immune response to TB and suggest that immunologic recognition in the first phase of infection is a highly restricted event dominated by a limited number of T cell clones.

Amino Acid Sequence↗
PubMed2001

Environmental modulation of autoimmune arthritis involves the spontaneous microbial induction of T cell responses to regulatory determinants within heat shock protein 65.

Both genetic and environmental factors are believed to be involved in the induction of autoimmune diseases. Adjuvant arthritis (AA) is inducible in susceptible rat strains by injection of Mycobacterium tuberculosis, and arthritic rats raise T cell responses to the 65-kDa mycobacterial heat-shock protein (Bhsp65). We observed that Fischer 344 (F344) rats raised in a barrier facility (BF-F344) are susceptible to AA, whereas F344 rats maintained in a conventional facility (CV-F344) show significantly reduced incidence and severity of AA, despite responding well to the arthritogenic determinant within Bhsp65. The acquisition of protection from AA can be circumvented if rats are maintained on neomycin/acidified water. Strikingly, naive unimmunized CV-F344 rats but not BF-F344 rats raised T cell responses to Bhsp65 C-terminal determinants (BCTD) (we have previously shown that BCTD are involved in regulation of acute AA in the Lewis rat); however, T cells of naive CV-F344 and BF-F344 gave a comparable level of proliferative response to a mitogen, but no response at all to an irrelevant Ag. Furthermore, adoptive transfer into naive BF-F344 rats of splenic cells of naive CV-F344 rats (restimulated with BCTD in vitro) before induction of AA resulted in a considerably reduced severity of AA. These results suggest that spontaneous (inadvertent) priming of BCTD-reactive T cells, owing to determinant mimicry between Bhsp65 and its homologues in microbial agents in the conventional environment, is involved in modulating the severity of AA in CV-F344 rats. These results have important implications in broadening understanding of the host-microbe interaction in human autoimmune diseases.

Adoptive Transfer↗
PubMed1995

The immunogenicity of recombinant Mycobacterium smegmatis bearing BCG genes.

Specific pathogen-free C57BL/6 mice infected with recombinant Mycobacterium smegmatis (rM. smegmatis) bearing BCG genes showed increased splenic survival compared to those receiving the vector control (plasmid DNA only). The mouse-passaged rM. smegmatis (J3R) survived in peritoneal macrophages better than the vector control, regardless of whether the macrophages were infected in vivo or in vitro. When rM. smegmatis J3R was cultured in synthetic Proskauer-Beck-Tween medium, protein bands characteristic of BCG culture filtrates and not present in the vector control preparation were observed. Mice immunized with two doses of heat-killed J3R suspended in Freund's adjuvant were able to limit the growth of virulent Mycobacterium tuberculosis within the lung and spleen compared to that observed in control mice receiving adjuvanted vector control or Freund's adjuvant alone.

Animals↗
PubMed1996

Roxithromycin alone and in combination with either ethambutol or levofloxacin for disseminated Mycobacterium avium infections in beige mice.

Roxithromycin alone reduced the level of bacteremia caused by Mycobacterium avium complex liver and splenic infection (in CFU per gram) of beige mice and mortality compared with untreated controls (P < 0.05). Roxithromycin plus ethambutol resulted in a significant reduction in the number of bacteria in splenic tissue compared with those in control splenic tissues of mice and mice treated with roxithromycin alone and ethambutol alone. Roxithromycin plus levofloxacin was not better than roxithromycin alone. Roxithromycin has in vivo activity against M. avium complex strains, and pilot studies with humans may be considered.

Animals↗