Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Groups of Swiss white mice weighing 25-28 grams were infected orally with 500, 2,000, 5,000 or 20,000 oocysts of Eimeria falciformis var pragensis. Depression, anorexia, weight loss, diarrhea or dysentery, and dehydration were most pronounced at eight to ten days postinfection. The highest mortality, 31%, occurred in mice infected with 20,000 oocysts. None of the mice infected with 500 oocysts died. The pathological findings were equally severe in mice infected with 5,000 and 20,000 oocysts. The enteric lesions, most pronounced at eight to ten days postinfection, were restricted mainly to the large intestine and consisted initially of both cryptal and absorptive epithelial cell destruction and submucosal edema. These changes were followed in 12 to 24 hours by a transient influx of neutrophils into the lamina propria followed by mononuclear cell infiltration which lasted for five to ten days. As the infective dose decreased, the inflammatory response occurred later and was less extensive. When seen, hemorrhage occurred seven to 11 days postinfection. In 50% of the mice infected with 5,000 and 20,000 oocysts, varying degrees of a nonselective mucosal necrosis were seen at eight to 12 days postinfection. In mice infected with 500 oocysts, mucosal destruction was restricted to the epithelium. Neutrophils predominated when necrosis was extensive, otherwise, mononuclear cells were the main inflammatory cells. Two to three days following necrosis, crypt hyperplasia was marked and mucosal integrity was restored. Ulcers, some of which extended into the submucosa, healed by days 14 to 20. Localized granulomatous colitis, induced by trapped oocysts within the lamina propria, was seen until the experiment was terminated at 25 days postinfection. Infection was followed by lymphoid hyperplasia in the lymph nodes and the spleen.
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PMID:The pathological changes caused by Eimeria falciformis var pragensis in mice. 74 2

A field trial was set up to test the prophylactic properties of the organophosphorous drug metrifonate (Bilarcil Bayer AG). Subjects were rural African children living in an area of Rhodesia where Schistosoma haematobium and S. mansoni are highly endemic. The trial was conducted in three stages, a preliminary period of therapy followed by two six-month periods of prophylaxis. Parasitological and haematological tests were carried out monthly and major assessments (including clinical examinations) were carried out prior to the start of the trial and at the end of each of the three stages. Drug was given to the appropriate groups at a dose rate of 7-5 mg/kg once per fortnight for three doses during the therapy stage and four-weekly during the prophylaxis stage. Results with S. haematobium were very good. A 60% cure-rate was observed six weeks aection was obtained in those children continuing to receive the drug as a prophylactic, even during the season of highest transmission; intensities of infection in those who became infected were very low. Infection rates in the treated but unprotected group rose steadily from 40% at week 11 to 95% at week 70. There was a sigificant effect upon the intensity of S. mansoni infections only when pre- and post-trial data were compared. Apart from the anticipated (and previously reported) depression of plasma cholinesterase values no side effects were recorded. Drug tolerance and acceptibility were very high. It is likely that the costs of a year's protection against S. Haematobium using metrifonate will be significantly lower than protection by molluscicidal techniques or single courses of treatment with established drugs.
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PMID:Field trial of metrifonate in the treatment and prevention of schistosomiasis infection in man. 84 20

In November 1976 an investigator at the Microbiological Research Establishment accidentally inoculated himself while processing material from patients in Africa who had been suffering from a haemorrhagic fever of unknown cause. He developed an illness closely resembling Marburg disease, and a virus was isolated from his blood that resembled Marburg virus but was distinct serologically. The course of the illness was mild and may have been modified by treatment with human interferon and convalescent serum. Convalescence was protracted; there was evidence of bone-marrow depression and virus was excreted in low titre for some weeks. Recovery was complete. Infection was contained by barrier-nursing techniques using a negative-pressure plastic isolator and infection did not spread to attendant staff or to the community.
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PMID:A case of Ebola virus infection. 89 Apr 13

Gnotobiotic and conventional dogs of different ages were examined for intradermal skin test responses and in virtro peripheral blood lymphocyte responses to the phytomitogens, phytohemagglutinin-P (PHA-P) and pokeweed mitogen (PWM). All adult dogs skin tested with these mitogens demonstrated a positive skin reaction consisting of erythema and induration within 24 hours. In contrast, a positive reaction was obtained only with PHA-P when both mitogens were tested in conventional and gnotobiotic neonatal dogs. Lymphocytes from both adult and neonatal dogs underwent blastogenesis if cultured with PHA-P and PWM. Infection of gnotobiotic dogs with canine distemper virus (CDV) resulted in depression of PHA-P skin test response along with in vitro depression of lymphocyte blastogenesis. Persistent loss of skin test response correlated with eventual death due to CDV-associated encephalitis, whereas dogs which responded to PHA-P 14 to 21 days after viral inoculation survived CDV infection. The results of this study indicated that intradermal mitogen tests can be used as a rapid method for in vivo assessment of cell-mediated immunity in this species.
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PMID:Intradermal mitogen response in dogs: correlation with outcome of infection by canine distemper virus. 93 Nov 36

Three experiments determined if the methionine requirement of broiler chicks was affected by coccidial infection. Chicks were fed a corn-soy or a corn-soy-pea basal diet containing 0.73% and 0.62% total sulfur amino acids (TSAA), respectively. Levels of 0 to 0.45% DL-methionine were added, with and without 0.01% monensin sodium. In two experiments, the chicks were inoculated at two weeks of age with a mixture of oocysts of E. acervulina, E. maxima, E. tenella, E. necatrix and E. brunetti. Lesion scores on the intestines and ceca, and blood carotenoid levels were determined at three weeks. The experiments were terminated at four weeks. A level of methionine greater than 0.47% and of TSAA greater than 0.83% was necessary to obtain maximum growth rate in uninoculated chicks. No evidence of dermatitis was observed. Growth rate and feed efficiency of chicks infected with coccidiosis were more severly depressed when the diet was not supplemented with methionine. Infections of coccidia and low levels of methionine, which in themselves did not produce any significant change in weight gain, did give a significant weight depression in combination. Adding monensin to the diet prevented a reduction in growth rate and feed efficiency of inoculated chicks fed adequate methionine. Monensin did not completely prevent the adverse effects of a coccidial infection, based on feed efficiency, when chicks were fed diets inadequate in methionine. Blood carotenoid levels were not affected by methionine level, but were significantly lowered by coccidial infection in the absence of monensin. Intestinal and cecal lesions in inoculated chicks were significantly reduced by including monesin in the diet. Although the coccidial infection more severly affected the performance of chicks fed diets deficient in methionine, satistical analysis of pooled data indicated no difference in the quantitative requirement of chicks for methionine. Therefore, a level of methionine and cystine adequate for optimum growth under the coccidial-free conditions should be adequate for chicks when infected with coccidia.
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PMID:Effect of dietary methionine status on response of chicks to coccidial infection. 93 21

Pathogenicity trials in poultry are reported with an isolate of mycoplasma, designated 'W8', which is serologically unrelated to Mycoplasma gallisepticum, M synoviae or M meleagridis. W8 killed fowl and turkey embryos when injected into the yold sacs of embryonating eggs. Infection of one-day-old fowls, turkeys and pheasants by the air sac route caused marked growth depression and a high incidence of osteomyelitis of the vertebral column in all species. A large proportion of infected turkeys and a smaller proportion of infected pheasants also developed chondrodystrophic changes of the long bones similar to those of turkey syndrome '65. Infection did not cause mortality or macroscopic air sacculitis. No obvious pathological changes occurred in fowls following W8 infection by the air sac route at two weeks of age and only minimal changes when infection was given at one week. Infection did not appear to spread to in-contact controls. W8 was recovered most frequently and in greatest profusion from the air sacs, tracheas, kidneys and vertebral columns of fowls and turkeys following air sac infection at one day of age.
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PMID:Pathogenicity studies in poultry with an undefined serotype of Mycoplasma. 93 70

The effect of Mycoplasma pneumoniae infection on cell-mediated immunity was examined by two methods: the first method was the tuberculin skin test and the other was the measurement of the in vitro lymphocyte stimulation response to purified protein derivative (PPD) of tuberculin. Twenty-nine patients out of a total of 47 patients with a lower respiratory tract illness caused by M. pneumoniae had a negative tuberculin skin test when first tested. Twenty-three out of 26 patients with a negative tuberculin reaction in the early phase of the illness had a positive skin test when they were retested several weeks or months after the illness. The lymphocyte stimulation response to PPD was examined in 13 patients. In eight of these cases the lymphocyte response to PPD was significantly lower during illness than after recovery. Six control subjects showed no significant difference in their lymphocyte responsiveness to PPD when examined on two different occasions. These studies show that M.pneumoniae infection causes transient depression of cell-mediated immunity.
Infection 1976
PMID:Effect of Mycoplasma pheumoniae infection on cell-mediated immunity. 95 96

Eighteen volunteers in tow study groups were inoculated with influenza A (H3N2) and their peripheral blood T, B and null cells enumerated at subsequent intervals. Infection with wild-type virus or with a live, attenuated virus vaccine markedly reduced the proportion and absolute number of T-cell rosettes 24 hours after inoculation. T-Cell depression preceded the onset of clinical illness in symptomatic subjects, continued during illness, and returned to normal with recovery. T-cell lymphopenia was most pronounced in volunteers infected with wild-type virus and was accompanied by an increase in null cells. Lymphocytes from six wild-virus recipients with T-cell leukopenia were incubated in vitro with a calfthymus extract (thymosin), significantly increasing the percentage of T rosettes in all six subjects (P less than 0.0001). These data indicate that influenza is accompanied by pronounced quantitative and functional changes in T cells.
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PMID:Influenza: response of T-cell lymphopenia to thymosin. 108 84

In the present study, the immunodepressive effects of canine distemper virus (CDV) infection of dogs on two parameters of lymphocyte function, namely phytomitogen-induced cellular proliferation and skin allograft rejection, were investigated. Infection of susceptible gnotobiotic dogs with virulent R252-CDV resulted in a depression of peripheral blood lymphocyte mitogen response as measured by (3H)thymidine incorporation for up to 10 weeks after inoculation. This effect coincided with the appearance of viral antigen by immunofluorescence in leukocytes but persisted after the virus was no longer detectable. Loss of mitogen reactivity was seen in all infected dogs. However, when these same CDV-infected dogs were challenged with foreign skin allografts, no significant retention of grafts over controls was observed despite the depressed lymphocyte activity. Considering the in vitro and in vivo data it was concluded that, although immunodepressive effects of CDV were demonstrated in vitro, paralled in vivo experiments indicated that less than complete suppression of immune functions occurs during the course of CDV infection.
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PMID:Effects of canine distemper virus infection on lymphoid function in vitro and in vivo. 109 60

To determine the functional impact of alterations in lymphocyte concentrations and ratios following infection with chicken anemia agent (CAA) alone or in combination with infectious bursal disease virus (IBDV) on the immune system of young chickens, in vitro lymphoproliferation assays and in vivo responses to vaccination with several common viral agents were assessed at various time intervals post-inoculation (PI). Concanavalin A (Con A), phytohemagglutinin (PHA) and pokeweed mitogen (PWM) stimulation of splenic lymphocytes (SPL) collected from control birds could not be detected until 10-14 days PI. Infection with CAA was characterized by significantly higher PWM stimulation of SPL at 17 days PI and significantly lower PWM stimulation of peripheral blood lymphocytes (PBL) at 14 days PI, compared with uninfected controls. Concanavalin A and PWM stimulation of SPL was significantly increased in birds inoculated with IBDV alone. Lymphocytes harvested from birds inoculated simultaneously with CAA and IBDV had significantly lower responses. Effects on humoral and cell-mediated immunity following CAA and/or IBDV were determined by evaluating vaccination responses to Newcastle disease virus (NDV), fowl pox virus (FPV) and infectious laryngotracheitis virus (ILTV) during the acute phase of CAA infection (2 weeks PI). Vaccination of birds 2 weeks following CAA infection at 1 day of age resulted in decreased protection against NDV (85.7%) and ILTV (7.1%) challenge compared with protection rates in control birds (100% and 53.3% respectively). Infectious bursal disease virus infection was associated with decreased protection against NDV (60%) only. Concomitant infection at 1 day of age resulted in a greater reduction in NDV challenge protection (33.3%), slightly decreased FPV protection (87.5%), increased numbers of persistent FPV vaccination lesions and increased protection against ILTV challenge (71.4%). Vaccination of birds 2 weeks following CAA infection at 2 weeks of age resulted in slightly decreased NDV humoral antibody, development of persistent FPV vaccination lesions (17%) and increased immunity to ILTV challenge compared with control birds (83.3% vs. 66.7%). Chickens inoculated with IBDV alone displayed a more severe depression in NDV antibody titers and only a slight decrease in ILTV protection. Vaccination following concomitant infection at 2 weeks of age resulted in a higher percentage of FPV persistent vaccination lesions (39%) and greatly enhanced immunity to ILTV challenge (100%).
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PMID:Immune dysfunction following infection with chicken anemia agent and infectious bursal disease virus. II. Alterations of in vitro lymphoproliferation and in vivo immune responses. 133 77


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