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Query: UMLS:C0021311 (Infection)
 38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rhizobia are soil microorganisms that can interact with leguminous plants to form root nodules within which conditions are favourable for bacterial nitrogen fixation. Legumes allow the development of very large rhizobial populations in the vicinity of their roots. Infections and nodule formation require the specific recognition of host and Rhizobium, probably mediated by plant lectins. Penetration of the host by a compatible Rhizobium species usually provokes host root cell division to form the nodule, and a process of differentiation by both partners then ensues. In most cases the rhizobia alter morphologically to form bacteroids, which are usually larger than the free-living bacteria and have altered cell walls. At all stages during infection, the bacteria are bounded by host cell plasmalemma. The enzyme nitrogenase is synthesized by the bacteria and, if leghaemoglobin is present, nitrogen fixation will occur. Leghaemoglobin is a product of the symbiotic interaction, since the globin is produced by the plant while the haem is synthesized by the bacteria. In the intracellular habitat the bacteria are dependent upon the plant for supplies of energy and the bacteroids, in particular, appear to differentiate so that they are no longer able to utilize the nitrogen that they fix. Regulation of the supply of carbohydrate and the use of the fixed nitrogen thus appear to be largely governed by the host.
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PMID:The Rhizobium--legume symbiosis. 3 24

Anaplasma marginale was experimentally transmitted from cattle to elk to cattle. Six intact adult elk (Cervus canadensis canadensis) inoculated with freshly collected heparinized blood from cattle chronically infected with A. marginale became asymptomatic carriers. Although the elk did not develop clinical or hematologic evidence of infection, they became seropositive by the serum(SRCA) and plasma rapid card agglutination (PRCA) tests. Blood from the experimentally-infected elk produced disease in splenectomized bovine calves and the carrier state persisted for at least one year. Infection did not occur when two elk were inoculated with 0.5 ml of frozen blood from known bovine carriers. The blood had been frozen for four weeks in liquid nitrogen with 6% dimethyl-sulfoxide. The bovine SRCA and PRCA tests were adapted for use with elk serum. To obtain accurate test results, serum collected from clotted elk blood had to be held for at least 72 h at 21-27 C before performance of the SRCA test. Comparative serologic and infectivity studies indicated that the carrier (reactor) status of elk was accurately identified with the serologic tests in 61 of 68 samples evaluated. Incorrect serologic results with the SRCA and PRCA tests were false-negative readings. In no case were uninfected elk identified as seropositive.
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PMID:Evaluation of the anaplasmosis rapid card agglutination test for detecting experimentally-infected elk. 50 40

Anaplasmosis was experimentally transmitted from cattle to elk to cattle. Six non-splenectomized adult elk (Cervus canadensis canadensis) that were inoculated with freshly collected heparinized blood from cattle chronically infected with Anaplasma marginale became asymptomatic carriers. Although the exposed elk did not develop clinical or hematologic evidence of infection they become seropositive by the serum and plasma rapid card agglutination (RCA) tests. Blood from the experimentally infected elk produced disease in splenectomized bovine calves and the carrier state persisted for at least one year. Infection did not occur when two elk were inoculated with 0.5 ml of frozen blood from known bovine carriers. The blood had been frozen for four weeks in liquid nitrogen with six percent dimethyl-sulfoxide.
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PMID:Evaluation of the anaplasmosis rapid card agglutination test for detecting experimentally infected elk. 52 45

Infection of glucose, sulphur or nitrogen starved cells with MS2 virus results in the production of progeny virus but the absence of cell lysis and the failure of progeny virus release. Addition of glucose of sulphur to the correspondingly starved cells results in the normal release of virus within 40 to 60 min. Return of nitrogen to nitrogen-starved cells, however, does not result in the release of virus, even after 1 1/2 h. In experiments with uninfected, starved cells it was found that glucose or sulphur starved cells begin dividing within 45 min after the limiting compound is returned. In contrast, nitrogen-starved cultures have not begun to divide 1 1/2 after the return of nitrogen. The correlation between the time it takes for starved, infected cultures to resume lysis after the return of the limiting compound and the time similarly starved, but infected, cells normally begin division after addition of the limiting compound supports the hypothesis that lysis by RNA phage is related to cell division and may result at the time of cell division from failure of the cells to divide properly.
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PMID:The effect of host-cell starvation on virus-induced lysis by MS2 bacteriophage. 77 38

Seventy-five patients with congenital nephrotic syndrome of Finnish type were identified in Finland in the period 1965-1973, giving an incidence of 12-2/10(5). A large placenta and proteinuria from birth are the hallmarks of the disease. About one-quarter of the patients had oedema and/or abdominal distension at birth and in all cases the full nephrotic syndrome was documented before 2 months. More than half of the patients died before 6 months and none lived longer than 2 years 3 months. A slight rise in blood urea nitrogen or serum creatinine levels occurred in 14 cases, but in none of these did a frank uraemia develop before death. Infection appeared to be the immediate cause of death in 31% of the cases; in 43% no cause of death other than congenital nephrotic syndrome could be shown. Thrombi in large vessels were found in 11 out of 58 necropsies.
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PMID:Congenital nephrotic syndrome of Finnish type. Study of 75 patients. 93 78

1. Effects of Ascaridia galli infection on the energy and nitrogen (N) metabolism were studied on groups of 5 cross-bred cockerels aged about 5 weeks and given a diet deficient or adequate in vitamin A at two levels of feeding in respiration chambers. 2. Metabolisability of dietary energy was 67% and N retention 33% in infected chickens compared with 71 and 41% respectively, in uninfected chickens. 3. Maintenance energy requirement of vitamin A-deficient birds was 882 kJ/kgW d compared with 998 kJ/kgW d for normal birds. N balance of the deficient chickens was also less when compared at the same energy balance. Infection did not affect maintenance energy requirement nor N balance. 4. Starvation heat production of infected chickens (619 kJ/kgW d) was higher than that of uninfected controls (586 kJ/kgW d). When infection treatments were combined, vitamin A-adequate chickens had a higher heat production (615 kJ/kg d) than the vitamin A-deficient (580 kJ/kgW d). Endogenous N excretion (mg/gW) was less in vitamin A-deficient than in adequate, starved birds. 5. Deficient chickens had undetectable liver reserves of vitamin A and only very low plasma concentrations. There was a difference in the length of larvae (17 d after infection) associated with vitamin A status, and with level of feeding.
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PMID:Energy and nitrogen metabolism of diseased chickens: interaction of Ascaridia galli infestation and vitamin A status. 124 1

Fall weaned Angus calves grazed stockpiled 1) tall fescue (Festuca arundinacea Schreb.), 2) tall fescue-red clover (Trifolium pratense L.), or 3) tall fescue-alfalfa (Medicago sativa L.) or were barn-fed, 4) tall fescue hay, 5) orchardgrass (Dactylis glomerata L.)-alfalfa hay, or 6) tall fescue silage from late October to early April during each of 5 yr. Infection of the fescue with Acremonium coenophialum ranged from 0 to 55%. There were two replications each of steers and heifers for each forage system in a completely random design. Each replicate was grazed by three Angus stockers, except for System 1, which was grazed by six stockers, for a total of 420 stockers. Each pasture replicate contained .8 ha (except System 1, which was 1.6 ha), and the stocking rate was one stocker per .27 ha. Fescue hay and silage were harvested each spring for barn-fed systems from the area stockpiled for grazing by cattle in System 1. Nitrogen fertilizer (90 kg/ha) was applied in early spring and again in early August, before stockpiling; no N was applied to stockpiled fescue grown with legumes. Daily gains by calves grazing stockpiled fescue-alfalfa were greater (P less than .01) than by calves grazing stockpiled fescue-red clover or N-fertilized stockpiled fescue (.50, .33, and .34 kg/d, respectively), but fescue-alfalfa calves required more days (P less than .01) of supplemental hay feeding (105, 60, and 36, respectively). Calves fed fescue hay in the barn gained more (P less than .01) than those fed fescue silage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Forage systems for beef production from conception to slaughter: II. Stocker systems. 131 26

To investigate how T. vivax affects metabolism in dwarf goats, nine wethers (infection group) given alfalfa pellets ad libitum were infected intravenously and food intake was recorded up to 49 days after infection in the infection group and in the control group (n = 9). Controls received the same diet, ad libitum before infection and in restricted amounts after infection in order to obtain similar intakes in the two groups. Digestible organic matter intake (DOMI) and nitrogen balance (NB) were determined during four balance trials. All animals were bled regularly to measure parasitaemia, packed cell volume (PCV) and a number of serum metabolites. All infected animals showed symptoms typical for T. vivax infection as judged by parasitaemia, PCV and rectal temperature. Infection had a non-uniform negative effect on food intake. Compared with controls at equal DOMI, NB was lower in infected animals, the difference being significant 4 weeks after infection. This was caused by a gradual increase in NB at equal DOMI of the control group. The NB of the ad libitum fed infected animals 2 and 4 weeks after infection was comparable to values normally found in healthy ad libitum fed dwarf goats with an equal DOMI. NEFA values in serum were significantly elevated after infection. Except for two infected animals with an extremely low food intake towards the end of the experiment, no rise in serum ketone bodies was evident. After infection, serum protein increased, differences with controls being significant 4 and 7 weeks after infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of T. vivax infection in west African dwarf goats on energy and nitrogen metabolism. 141 47

Infection is detrimental to growth, making it a serious problem for both humans and animals. To explore factors responsible for the restoration of tissue protein stores following infection, we developed a model of Escherichia coli infection suitable for studies of protein metabolism in growing animals. Weanling female Sprague-Dawley rats were given a single intraperitoneal injection of E coli (approximately 10(9) colony forming units [CFU]/kg body weight); control rats were injected with vehicle alone. Two days later, infected rats had lower (P less than .05) body weight (-11%), food intake (-49%), daily nitrogen balance (-64%), and lower protein mass of gastrocnemius muscle (-21%), tibialis anterior muscle (-23%), gastrointestinal tract (-15%), skin (-16%), and carcass (14%), compared with control rats. There was complete catch-up in terms of body weight, cumulative nitrogen balance, and carcass and tissue protein masses within 3 weeks of infection. Catch-up was achieved predominantly by increasing (P less than .05) the apparent nitrogen digestibility of the diet, thereby increasing the amount of nitrogen available to the body. Food intake did not increase and urinary nitrogen did not decrease during catch-up growth. E coli peritonitis in weanling rats provides a simple and useful model for the study of the effects of infection on growth and protein metabolism in growing animals.
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PMID:Catch-up growth following Escherichia coli infection in weanling rats. 173 44

The complex interactions between nutrition, infection and immunity are still poorly understood and the precise role of each factor is difficult to ascertain. Infection itself induces profound metabolic alterations resulting in negative nitrogen balance. Protein energy malnutrition, whatever its origin, results in an immune deficiency characterized by impaired delayed cutaneous hypersensitivity, low production of lymphokines, low T cell counts, decreased T cell responses to specific or non specific mitogenic stimuli. Serum immunoglobulin levels are normal or elevated and antibody responses to most vaccines are normal or slightly altered. Secretory IgA levels, number of IgA plasma cells in jejunal mucosa and specific IgA antibody levels are depressed. Neutrophil chemotaxis and serum opsonic activity are normal but bacterial killing capacity is markedly reduced. C3 levels are usually reduced as a consequence of low hepatic synthesis and increased consumption but most other complement proteins remain within the normal range. Such alterations of immunological parameters can be induced by malnutrition itself but they are commonly observed in populations also exposed to a heavy load of infectious agents from birth. Various types of immunodeficiencies can be achieved by selective deficiencies of minerals trace elements and several vitamins. Several experimental and clinical studies showed that overnutrition could alter T cell immune responses and accelerate the development of spontaneous auto-immune diseases in selected strains. Conversely low calorie or low fat diets as well as supplementation in fish oil markedly enhanced survival in these models. Despite much controversy as regards the mechanisms of immune alterations of nutritional origin, the clinical and experimental data already available provide a framework for the design of further investigations and for prophylactic action.
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PMID:Experimental models and mechanisms of immune deficiencies of nutritional origin. 212 53


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