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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human diseases caused by atypical mycobacteria are reviewed. Pulmonary illness and childrens' lymphadenitis are the commonest, but cutaneous, disseminated, bony, articular, renal and meningeal diseases are also produced by atypical mycobacteria. Disseminated infections are often manifested by fever, hepato-splenomegaly and hematologic changes. Most diagnosis are made by sputum and gastric-juice cultures, bonemarrow and liver biopsies. Disseminated diseases are often fatal but may be cured with medical treatment. In general, atypical mycobacterial diseases are quite similar to tuberculous diseases in different organs. A unique isolation of atypical mycobacteria is not diagnostic "by it self", and other conditions are required. Diagnostic criteria and treatment are discussed.
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PMID:[Pathogenicity of atypical mycobacteria]. 16 50

Marek's disease virus (MDV) and the turkey herpesvirus (HVT) may be assayed on the chorioallantoic membrane (CAM) of the chicken embryo after intravenous inoculation of chicken embryo fibroblasts (CEF) or chicken blood leukocytes infected with these viruses. Free HVT, MDV associated with Marek's tumor cells, and lymphoblastoid cell lines derived from Marek's tumors, may be assayed in the same way. The intravenous assay is quicker than the yolk sac assay and somewhat more sensitive than in vitro or conventional CAM assay after direct inoculation of the CAM. The optimal time for inoculation was day 10 of embryo incubation; therafter the log-10 CAM lesions decreased as a negative linear function of embryo age at the time of inoculation. The log-10 CAM lesions increased as a positive linear function of the time since inoculation. The optimal time for counts was day 5 after inoculation. The log-10 CAM lesions was a linear function of the log-10 cells in the inoculum; the slope was 1.0. Venous in ovo inoculation caused as increase in the weight of the spleen proportional to the number of CAM lesions. Repression of the splenomegaly, by prior X irradiation of the embryo, did not reduce the number of CAM lesions. Embryols from lines inbred for susceptibility to Marek's disease produced more CAM lesions than embryos from resistant lines. This difference did not depend on prior exposure of the mothers to MDV or HVT.
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PMID:In ovo assay for Marek's disease virus and turkey herpesvirus. 16 13

The single i.p. injection of 2.5 times 10-8 killed B. pertussis cells protected 23 out of a group of 24 NMRI mice (95.8%) against the subsequent intracerebral infection, whilst 13 out of 24 mice (54.2%) survived the intracerebral challenge with virulent B. pertussis cells after prior oral administration of 2.5 times 10-11 killed B. pertussis cells, as demonstrated by the mouse protection test. Similar treatment with non-specific substances, such as egg white and saline, did not result in any increase of resistance. Systemic anaphylactic hypersensitivity to bovine serum albumin could also be achieved, when either both the protein antigen and the B. pertussis vaccine were given by the oral route or when the B. pertussis vaccine was injected intraperitoneally into mice which had received the soluble protein antigen by the oral route. Such effects were not produced at all in the reverse situation, when the B. pertussis vaccine was orally administered in mice, which were given the soluble protein antigen by the intraperitoneal route. After oral inoculation of 6 times 10-11 killed B. pertussis cells neither splenomegaly nor blood lymphocytosis became detectable. It is still unknown, in which manner the orally administered B. pertussis vaccine effects protection against the intracerebral infection with virulent bacteria as well as susceptibility for systemic anaphylaxis. The data presented do not favor the view that those effects are due to the phenomenon of persorption.
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PMID:Studies on the immunizing capacity of orally administered particulate antigens. I. The efficiency of killed Bordetella pertussis cells. 16 35

As compared to specifically pathogen-free NMRI mice, in principle, the immunological reactivity of germfree mice of the same strain and age was not found to be reduced. This is documented by the cellular kinetics of the primary immune responses, evoked by the intraperitoneal (i.p.) injection of either a "saturated" dose of 4 times 10(8) sheep erythrocytes (SE) or the simultaneous injection of 4 times 10(8) SE and 3 times 10(9) killed Bordetella pertussis organisms (PO). Thereby, adjuvancy of PO was not found to be reduced in germfree mice. The only difference consisted in the demonstration of significantly reduced numbers of both direct and indirect plaque-forming spleen cells (PFC) on the 4th day after primary antigenic stimulation. This is suggested to be due to a lack of sufficient training of the immunological apparatus of germfree mice. Both in germfree and conventional mice significant splenomegaly, blood leukocytosis as well as increase in the numbers of pre-existing "background" PFC became detectable following a single i.p. injection of 3 times 10(9) PO without SE. Similarly, the injection of endotoxin from Serratia marcescens produced a moderate increase in the numbers of "background" PFC. From the data presented it is suggested that strict gnotobiotic conditions do not cause noteworthy deficiency in immunological competence.
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PMID:Influence of Bordetella pertussis and bacterial endotoxins on the immunological reactivity of germfree mice. 16 52

A Graffi murine leukemia was utilized as a model system to investigate the effect of chemoimmunostimulation therapy. Subcutaneous inoculation of approximately 1.0 times 10(6) tumor cells resulted in a rapidly growing tumor at the site of inoculation and subsequent development of splenomegaly and lymphoadenopathy. All animals succumbed to the leukemia within 24 to 30 days. Treatment of diseased animals with two courses of cytoxan over a 2-week period resulted in a remission period of approximately 16 to 18 days before relapse and eventual death of approximately 70% of the drug-treated animals. A significant number of long-term survivors (50 to 83%) was obtained in groups of animals that received combined drug plus BCG or C. parvum therapy. In contrast, the administration of MER (a methanol-extracted residue of BCG) to animals in a drug-induced remission period was no more effective than drug alone. The protective effect afforded by BCG and C. parvum was dependent on the time interval between drug therapy and the administration of the immunostimulators. Treatment of leukemic animals with BCG, C. parvum, or MER alone proved ineffective as all mice died at approximately the same time as untreated control animals. No leukemic cells were observed in any of the histologically examined tissues taken from long-term survivors. The implication of these results for cancer therapy is discussed.
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PMID:Histological and combined chemoimmunostimulation therapy studies against a murine leukemia. 17 Feb 12

The authors report a case of Hodgkin's disease at the subdiaphragmatic II B b stage with cell type III, revealed by thrombopenic purpura. Laparotomy and splenectomy confirmed the invasion of the spleen whereas there was no clinical splenomegaly and splenic radio-isotope scan was normal. The course is at present favourable, the purpura has been treated by corticotherapy then splenectomy, and the disease has been brought under control by classical treatment (cobalt radiotherapy and chemotherapy). The authors then discuss eight other cases in the world literature. Splenectomy is of dual interest for the assessment of Hodgkin's disease, on the one hand, and for the treatment of thrombopenic purpura on the other hand.
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PMID:[Thrombopenic purpura revealing Hodgkin's disease]. 17 87

A chromophobic pituitary adenoma induced on BD IX-rats has been grafted on animals of the same strain. The transplanted tumour takes in 90-100%; it grows at a slow rate (in 7 months after grafting a weight of 7-20 g is attained). Tumour-bearing animals display gigantism and hypertrophy of adrenals; moreover, in 33% of cases, diabetes is observed. With non-diabetic animals, splenomegaly and marked leukocytosis are observed; immature white and red cells are present in the peripheral blood. Spontaneous regression of the tumour never occurs. After surgical removal, tumour regrowth and the formation of metastases are observed. Diabetes is characterised by pronounced hyperglycaemia, glucosuria, polyphagia and polydipsia. Histochemically, insulin cannot be detected in pancreas. Splenomegaly is never observed in diabetic animals. Transplanted adenoma frequently tends to stop growing. No recurrence is observable after extirpation. Spontaneous regression of the tumour sometimes occurs. Gigantism, hypertrophy of adrenals and diabetes are considered as consequences of growth hormone- and ACTH-secretion of the transplanted adenoma. At present the tumour is running in the 8th passage. It did not change its characteristics over a period of 5 years.
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PMID:Transplantable, STH-producing and diabetogenic pituitary adenoma of the BD IX-strain of rats. 17 13

Natural infection with Machupo and Latino viruses occurs only in the cricetine rodent Calomys callosus. Machupo virus induces fatal infection in suckling mice and hamsters, and in adult guinea-pigs, marmosets, and rhesus monkeys. Latino virus kills only suckling hamsters; it produces chronic but non-viraemic infection in Calomys rodents.Machupo virus, in contrast, induces a viraemic immunotolerant infection in suckling Calomys, and a split response in animals more than 9 days of age. Tolerant infection is associated with haemolytic anaemia and splenomegaly, lesions not observed in animals able to clear viraemia and produce circulating neutralizing antibodies. Experimental increase in the fraction of tolerant response was obtained by decreasing the virus dose or by phenotypic inbreeding of rodents. Long-term effects of tolerant infection included mild runting, decreased survival time, and almost total sterility among females, largely caused by fatal virus infection of embryos.
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PMID:Infection of wild and laboratory animals with Machupo and Latino viruses. 18 99

Bolivian haemorrhagic fever (BHF) caused by Machupo virus is acquired by contact with the excretions and secretions of Calomys callosus, an indigenous cricetine rodent which is preadapted to peridomestic habitats. It competes successfully with Mus musculus, but not with Rattus rattus. A successful disease control programme has functioned in Beni Department since 1964. It is based on trapping surveys and the detection of splenomegaly in Calomys rodents as an index of chronic virus infection. Mass trapping and poisoning are used initially, and regular trapping is employed to control Calomys populations in towns where disease has occurred. More than 1000 cases of BHF were recorded from 1960-1964, but less than 200 in the past 10 years. The cost of this programme is approximately $30 000 annually.
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PMID:Rodent control programmes in areas affected by Bolivian haemorrhagic fever. 18 5

Two hundred and seventy-five male CBA/Birmingham mice including 84 mice over 80 wk of age were autopsied at intervals over the whole range of their natural life span of about 2 1/2 yr. Body weight increased progressively up to 30 wk of age when a plateau value of 30-40 g was attained. Subsequent to 80 wk a slight, progressive decrease was observed. The thymus showed a profound increase in size from about 5 mg at birth to approximately 60 mg by the 3rd wk. Thereafter, the weight of the thymus decreased, rapidly at first, to reach 20-30 mg by 15 wk of age. The thymus weight then decreased more slowly to around 10 mg by the 80th wk. The spleen weight reached a plateau value of 50-60 mg by 4 wk and this was maintained until the 80th wk. In mice older than 80 wk varying degrees of splenomegaly were observed. Histologically, the areas of white pulp in these spleens were very prominent, suggestive of an on-going immune response. It was possible to associate this splenomegaly with the appearance of gross and microscopic evidence of hepatomas. No hepatomas were observed prior to 80 wk, but between 80 and 120 wk the incidence increased progressively; and all the mice whose age at autopsy exceeded 120 wk had hepatomas. Histologically the hepatomas showed marked nuclear plemorphism with occasional mitotic figures. Thrombi, areas of avascular necrosis and collections of inflammatory cells were observed. The tumour metastasised to the lung in 12% of cases. The doubling time of the hepatoma in situ was estimated as 1-6 wk (range 1-3-1-8 wk). These hepatomas were transplantable and grew with a doubling of 2-25 wk in syngeneic adult recipients. To test if the more rapid progressive growth of the tumour in situ in old CBA mice might have resulted from a breakdown in "immunological surveillance" the same tumour was transplanted simultaneously to a group of young and old recipients. The tumour grew more slowly (doubling time, 2-5 wk) in the old recipients. This result would not appear to support the hypothesis of a prolonged breakdown of immunological surveillance as the cause of the progressive increase in the incidence and growth of these tumours in situ in old mice.
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PMID:The incidence, pathology and transplantation of hepatomas in CBA mice. 18 43


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