Comparative severity of experimentally induced mycobacteriosis in striped bass Morone saxatilis and hybrid tilapia Oreochromis spp.
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Twenty striped bass Morone saxatilis and 20 hybrid tilapia Oreochromis niloticus x O. mossambicus x O. aureus each received a single intramuscular injection of 1.6 x 10(6) colony forming units per gram body weight of Mycobacterium marinum. Striped bass manifested significantly greater clinical and microscopic disease compared to tilapia. Whereas all the striped bass had died or were clinically ill by Day 8 post-infection, there was no apparent disruption of normal behaviour, physical appearance, or growth in any of the sacrificed or surviving tilapia. Histologically, granulomas in striped bass were generally larger and less discrete, with a higher proportion of heavily vacuolated macrophages, and large cores of necrotic cells. Visceral granulomas in tilapia were smaller, with a higher proportion of epithelioid macrophages, more pigment-containing cells, more peripheral lymphocytes, and virtually no central necrosis. Visceral granulomas were 18-fold more numerous in striped bass than in tilapia. Based upon histomorphometric data, mean proportions of acid-fast bacteria within pronephros granulomas were 4-fold greater in striped bass than tilapia, and striped bass granulomas averaged more than twice as large as tilapia granulomas. In the anterior kidney of striped bass, a positive correlation existed between mean mycobacterial proportions and mean necrosis scores. In tilapia, mean mycobacterial proportions correlated negatively with mean granuloma numbers, whereas there was no correlation between these parameters in striped bass. Results suggest that intrinsic functional differences in the immunologic systems of striped bass and hybrid tilapia may contribute to inter-species variation in mycobacteriosis susceptibility. (+info)
The pathology of untreated and antibiotic-treated experimental tularaemia in monkeys.
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Grivet monkeys were infected intranasally with the virulent Schu-S4 strain of F. tularensis. One group of animals remained untreated and two other groups received a 7-day course of kanamycin therapy starting on either the third or fourth day after infection. Untreated monkeys developed pyrexia and mucopurulent oculonasal discharge and died 5--7 days after infection. All had pyogranulomatous lesions in the liver, spleen, respiratory tract and lymph nodes. Electron microscopy of liver and spleen showed phagocytosis of F. tularensis organisms by macrophages and polymorphonuclear leucocytes, but many bacteria survived phagocytosis and were released on destruction of the cells. Kanamycin therapy enabled most monkeys to survive the disease, but it did not prevent the development of persistent lesions in all animals. Caseous nodules were larger and more widespread in the organs of monkeys in which treatment was delayed until the fourth day of infection. (+info)
Identification by 16S rRNA gene analyses of a potential novel mycobacterial species as an etiological agent of canine leproid granuloma syndrome.
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PCR amplifications of the 16S rRNA gene were performed on 46 specimens obtained from 43 dogs with canine leproid granuloma syndrome to help determine its etiology. Sequence capture PCR was applied to 37 paraffin-embedded specimens from 37 dogs, and nested PCR was attempted on DNA from 9 fresh tissue specimens derived from 3 of the 37 aforementioned dogs and from an additional 6 dogs. Molecular analyses of the paraffin-embedded tissues and fresh tissue specimen analyses were performed at separate institutions. PCR products with identical sequences over a 350-bp region encompassing variable regions 2 and 3 of the 16S rRNA gene were obtained from 4 of 37 paraffin-embedded specimens and from all 9 specimens of fresh tissue originating from 12 of the 43 dogs. Identical sequences were determined from amplicons obtained from paraffin-embedded and fresh specimens from one dog. The consensus DNA sequence, amplified from paraffin-embedded tissue and represented by GenBank accession no. AF144747, shared highest nucleotide identity (99.4% over 519 bp) with mycobacterial strain IWGMT 90413 but did not correspond exactly to any EMBL or GenBank database sequence. With a probe derived from the V2 region of the novel canine sequence, reverse cross blot hybridization identified an additional four paraffin-embedded specimens containing the same novel sequence. In total, molecular methodologies identified the proposed novel mycobacterial sequence in 16 of 43 dogs with canine leproid granuloma syndrome, indicating that the species represented by this sequence may be the principal etiological agent of canine leproid granuloma syndrome. (+info)
Trehalose 6,6'-dimycolate (Cord factor) enhances neovascularization through vascular endothelial growth factor production by neutrophils and macrophages.
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Trehalose 6,6'-dimycolate (TDM) plays important roles in the development of granulomatous inflammation during infection with Mycobacterium spp., Rhodococcus spp., etc. To reveal the augmenting effect of TDM on vascular endothelial growth factor (VEGF) production and neovascularization, we investigated murine granulomatous tissue air pouches induced by Rhodococcus sp. strain 4306 TDM dissolved in Freund's incomplete adjuvant (FIA), comparing them to pouches treated with FIA alone. Histologically, granulomatous tissue and new vessel formation, which reached a maximum at day 7, was greatly enhanced by treatment with TDM. At day 1, VEGF-positive neutrophils accumulated in the pouch wall with frequency of 95% of total infiltrating cells, adhering to TDM-containing micelles. By day 3, granulomatous tissue and new vessels started to develop, and VEGF-positive macrophages appeared in a small number and gradually increased in number thereafter. The pouch contents of VEGF, interleukin-1beta, tumor necrosis factor alpha, and transforming growth factor beta were significantly elevated in TDM-treated pouches, with peaks at days 1, 0.5, 1, and 3, respectively, compared to those of control pouches, while that of basic fibroblast growth factor showed no significant increase. Treatment with anti-VEGF antibody inhibited TDM-induced granulomatous tissue formation and neovascularization, and administration of recombinant VEGF into pouches treated with FIA alone induced neovascularization comparable to that in the TDM-treated pouches. Incubation of neutrophils and macrophages on TDM-coated plastic dishes increased the VEGF release. The present results indicate that TDM augments VEGF production by neutrophils and macrophages and induces neovascularization in the granulomatous tissue. (+info)
Localized pigmented villonodular synovitis of the knee joint: neoplasm or reactive granuloma? A review of 18 cases.
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OBJECTIVE: The localized form of pigmented villonodular synovitis of the knee joint is a rare disease with limited alteration of the synovial membrane, the pathogenesis of which is the subject of controversial discussion. METHODS: Eighteen cases have been documented in our hospital since 1976. All of the patients had additional cartilage or meniscus damage. Treatment consisted of excision of the lesion and the adjacent synovial membrane, as well as therapy of the additional damage. RESULTS: The patients who had received such therapy were followed for 3-9 yr, without any clinical, sonographic or magnetic resonance tomographic signs of recurrence. In addition to the lack of a tendency towards recurrence, none of the cases displayed any further characteristics of the diffuse form of villonodular synovitis, such as invasiveness or malignant transformation. CONCLUSIONS: We therefore suggest that pigmented villonodular synovitis of the knee joint should be classified more strictly than before into a potentially neoplastic (diffuse) form and a reactive granulomatous (local) form. From the cases observed, we conclude that degenerative joint lesions may be the cause of the reactive granulomatous form. (+info)
B cell-deficient mice are highly resistant to Leishmania donovani infection, but develop neutrophil-mediated tissue pathology.
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Resolution of Leishmania infection is T cell-dependent, and B lymphocytes have been considered to play a minimal role in host defense. In this study, the contribution of B lymphocytes to the response against Leishmania donovani was investigated using genetically modified IgM transmembrane domain (muMT) mutant mice, which lack mature B lymphocytes. When compared with wild-type mice, muMT mice cleared parasites more rapidly from the liver, and infection failed to establish in the spleen. The rapid clearance of parasites in muMT mice was associated with accelerated and more extensive hepatic granuloma formation compared with wild-type mice. However, the liver of infected muMT mice also showed signs of destructive pathology, associated with the presence of increased numbers of neutrophils. The role of neutrophils in controlling parasite growth in the viscera was determined by depletion with the mAb RB6-8C5. This treatment led to a dramatic enhancement of parasite growth in both the liver and spleen of muMT and wild-type mice. As assessed by transfer of both normal and chronic-infection serum, Ig protects microMT mice from destructive hepatic pathology, but minimally alters their resistance compared with wild-type mice. However, adoptive transfer of CD4+ and CD8+ T cells into recombinase activating gene 1 (RAG1-/-) recipients, suggested that T cell function was not altered by maturation in a B cell-deficient environment. Taken together, these data suggest an inhibitory role for B lymphocytes in resistance to L. donovani unrelated to the presence or absence of Ig. However, Ig protects muMT mice from the exaggerated pathology that occurs during infection. (+info)
Non-specific granulomatous inflammatory lesions of small bowel.
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The entity of nonspecific granulomatous inflammatory lesions(NSGIL) of the small bowel is a diagnostic and therapeutic dilemma. Data of 52 histopathologically proven cases of NSGIL seen by us between 1986 and 1991 were analysed. All these patients presented with either intestinal obstruction or perforation. They were thoroughly evaluated and investigated for tuberculosis. Of the 52 patients, 6 patients received antitubercular therapy (ATT) before and after surgery and 32 patients only after surgery. Fourteen patients did not receive ATT. Surgical procedures undertaken included stricturoplasty, resection/anastomosis and simple suturing of perforation. No complications were seen in patients who received ATT; however, six of 14 patients who did not receive ATT developed wound sepsis and 2 developed partial wound dehiscence. Many of these NSGIL lesions could be tuberculous in etiology though typical caseating granulomas were not seen. (+info)
Enlarging single CT lesions can also spontaneously resolve.
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Computed tomography in two patients, aged 9 and 14 years, with history of focal seizures, revealed single, small, enhancing CT lesions. These patients were treated with albendazole and anticonvulsants. Follow-up CT scans revealed an increase in the size of the solitary lesions. They were managed conservatively and further follow-up CT scans revealed complete resolution of the lesions. The report suggests that some enlarging CT lesions may also spontaneously resolve. The most likely cause of the enlarging lesions was albendazole therapy. (+info)