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Query: UMLS:C0004623 (bacterial infection)
 15,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor necrosis factor (TNF), a pleiotropic cytokine, is produced by macrophages and other cells in a variety of infectious and noninfectious diseases. Ultimately, the net biological effects of TNF may be either beneficial or injurious to the host. For instance, during overwhelming bacterial infection, the acute overproduction of TNF causes septic shock syndrome characterized by hypotension, organ failure, and death. Antibodies against TNF prevent and reverse these sequelae in animal models of septic shock, and their use in humans is currently under investigation in clinical trials. In another instance, TNF has been implicated as an injurious mediator in the state of malnutrition that complicates the course of chronic infection and cancer. Termed cachexia, this chronic syndrome inevitably causes the afflicted host to succumb from weight loss, anorexia, and catabolism of protein and lipid. Experimental studies of animals exposed to TNF for protracted periods indicate that this cytokine is capable of causing cachexia, and the biochemical basis for these catabolic changes has been identified. More recent data indicate that the detrimental metabolic effects of TNF are not dependent upon its circulating levels in the bloodstream, but rather are dependent upon its actions locally in vital organs (e.g., brain). Thus, the metabolic basis for cachexia in infection may be largely dependent upon the amount of cytokine produced in metabolically important tissues. As a result, circulating TNF levels in cachectic patients may not accurately reflect the metabolic state of the host, and do not correlate to weight loss.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tumor necrosis factor and regulation of metabolism in infection: role of systemic versus tissue levels. 157 88

For further characterization of the mechanism involved in the anorexia during bacterial infection, we investigated whether muramyl dipeptide (MDP), the minimal immunologically active structure of gram-positive bacterial cell walls, affects rats' food intake in the same way as lipopolysaccharide (LPS) from E. coli. MDP (1.6 mg/kg body weight = b.wt.) injected intraperitoneally (IP) reduced food intake by decreasing meal frequency without affecting meal size. Indomethacin (2.5 mg/kg b.wt., IP) but not verapamil (5 mg/kg b.wt., IP) attenuated the hypophagic effect of MDP. In further experiments, MDP and LPS (100 micrograms/kg b.wt., IP) both inhibited gastric emptying and indomethacin failed to block this effect of LPS. Hepatic vagotomy did not attenuate the hypophagic effects of MDP or LPS. LPS reduced water intake only when food was available, but reduced food intake also during water deprivation. MDP did not affect water intake. MDP and LPS both had an aversive effect, but LiCl, which was also aversive, failed to reduce feeding under the conditions tested. This questions the role of a conditioned taste aversion in the hypophagia induced by MDP or LPS. The results suggest that a stimulation of eicosanoid synthesis contributes to MDP-induced hypophagia and may therefore also contribute to the anorexia during infection. In contrast, an inhibition of gastric emptying, an activation of hepatic satiety signals or a reduction of water intake, does not seem to be crucial for the hypophagic effects of MDP or LPS.
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PMID:Comparison of the effects of bacterial lipopolysaccharide and muramyl dipeptide on food intake. 238 34

Proventricular dilatation was diagnosed in 16 psittacine birds. Signs included anorexia, lethargy, weight loss, and intermittent vomiting. The proventriculus in all birds was thin-walled and impacted with ingesta and occupied most of the body cavity. Microscopic changes in the proventriculus varied from none to an infiltration of lymphocytes, macrophages, and heterophils. There was no evidence of viral or bacterial infection or lead toxicity.
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PMID:Proventricular dilatation syndrome in large psittacine birds. 638 50

The cascade of physiologic mechanisms in response to infection, the acute-phase response, is recognized as playing a major role in host defence. One such response is the hypoferremia that is consistently reported to occur during bacterial infection. This study aimed to determine whether the alterations in plasma iron were conditionable using the conditioned taste aversion (CTA) paradigm. The regime involved the pairing of a novel-tasting saccharin solution with bacterial endotoxin. Seven days after the initial pairing of these stimuli (the test day), the saccharin solution was represented. Animals exposed to this condition displayed a significant reduction in the level of plasma iron. Animals treated with an intraperitoneal dose of 400 micrograms/Kg lipopolysaccharide (LPS) displayed lower conditioned iron levels than rats infused with 100 micrograms/Kg LPS; however, this difference was not significant. These results showed that in addition to other acute-phase responses (fever and anorexia), plasma iron alterations are able to be manipulated through behavioral manipulations.
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PMID:Behavioral conditioning of endotoxin-induced plasma iron alterations. 761 18

We performed a 17-year retrospective analysis of 10 cases of hepatocellular carcinoma presenting as pyogenic liver abscess. Spontaneous tumor necrosis and biliary obstruction caused by tumor thrombi, superimposed with bacterial infection, were the two major pathogeneses. Exact diagnosis of the underlying hepatocellular carcinoma was made for five of the 10 patients before management was attempted. Main clinical manifestations included fever, chills, right-upper-quadrant pain, malaise, anorexia, jaundice, and hepatomegaly. Characteristics such as middle age and male sex, seropositivity for hepatitis B and/or hepatitis C, chronic liver disease, unexplained anemia, marked weight loss, and a severely inversed albumin/globulin ratio raise suspicions about the underlying hepatocellular carcinoma. Management strategies included percutaneous drainage (n = 3), surgical drainage (n = 4), and hepatectomy (n = 3) in addition to administration of parenteral antibiotics in all cases. The prognosis was dismal, with a mean survival of 3.5 months (range, 8 days to 6 months).
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PMID:Hepatocellular carcinoma presenting as pyogenic liver abscess: characteristics, diagnosis, and management. 959 57

The pattern of acute illness was determined in 102 adolescents and adults with sickle cell anaemia who presented to the emergency unit of a Lagos hospital. The patients had a mean age of 20.5 years (SD 13.1) and a male-female ratio of 1.5. The symptoms included fever (72%), fatigue and weakness (59%), anorexia (59%) and pain (57.5%) while major clinical signs were pallor (100%), jaundice (71%) and hepatomegaly (68%). Sixty-eight per cent of patients had sickle cell crises, including one with hemiplegic stroke, 10% with combined anaemia and pain crises, 33% with anaemia crises only and 23.5% with pain crises only. Sixty-three per cent had infection which was malaria in 24.5%, bacterial in 17% and viral in 6%. Of 16 patients with pyrexia of unknown origin, seven responded to treatment with chloroquine and eight to antibiotics. Infection was detected in 50% of the patients with sickle cell crises. The association between anaemia crises and malaria was significant (P < 0.05). Of the eight deaths, seven (88%) had anaemia crises. In contrast to studies conducted two decades ago in the same hospital, the prevalence of anaemia crises now exceeds that of pain crises and malaria now exceeds that of bacterial infection. Severe symptomatic anaemia (anaemia crisis) was more frequently associated with infection (mostly malaria) than was bone pain crisis. The Girdle pain crisis more frequently resulted in a fatal outcome than the uncomplicated bone pain crisis.
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PMID:Acute sickle cell syndromes in Nigerian adults. 1093 Nov 63

Cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) are assumed to mediate anorexia during bacterial infections. To improve our understanding of the role that these two cytokines serve in mediating infection during anorexia, we investigated the ability of pentoxifylline (PTX), a potent inhibitor of TNF-alpha production, to block the anorectic effects of the bacterial products lipopolysaccharide (LPS) and muramyl dipeptide (MDP) in rats. Intraperitoneally injected PTX (100 mg/kg body wt) completely eliminated the anorectic effect of intraperitoneally injected LPS (100 microg/kg body wt) and attenuated the anorectic effect of a higher dose of intraperitoneally injected LPS (250 microg/kg body wt). Concurrently, PTX pretreatment suppressed low-dose LPS-induced TNF-alpha production by more than 95% and IL-1beta production 39%, as measured by ELISA. Similarly, high-dose LPS-induced TNF-alpha production was reduced by approximately 90%. PTX administration also attenuated the tolerance that is normally observed with a second injection of LPS. In addition, PTX pretreatment attenuated the hypophagic effect of intraperitoneally injected MDP (2 mg/kg body wt) but had no effect on the anorectic response to intraperitoneally injected recombinant human TNF-alpha (150 ug/kg body wt). The results suggest that suppression of TNF-alpha production is sufficient to attenuate LPS- and MDP-induced anorexia. This is consistent with the hypothesis that TNF-alpha plays a major role in the anorexia associated with bacterial infection.
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PMID:Inhibition of TNF-alpha production contributes to the attenuation of LPS-induced hypophagia by pentoxifylline. 1108 76

Sialodacryoadenitis (SDA) is a highly contagious common viral infection in rats, akin to mumps in humans. Anorexia occurs during such viral infection. But the pattern of the decrease in food intake (a decrease in either meal size and meal number or both) during spontaneous viral infection has not been previously characterized. We observed the onset of anorexia and an abnormal feeding pattern during an opportunistic SDA viral infection in our rat colony. We thus studied seven male rats. Before the viral infection there was a positive association between food intake and meal number (P<.05). After infection food intake decreased by 68%. This occurred via a significant decrease in meal size (by 69%) (P<.05); and a nonsignificant decrease in meal number (P=.71). This pattern of decreased food intake is similar to that occurring during indomethacin-induced ulcerative ileitis, where we previously measured an increase in plasma tumor-necrosis factor (TNF)-alpha. Anorexia in response to bacterial lipopolysaccharide administration, which is also linked to plasma TNF-alpha, is however, caused only via a decrease in meal number. The differences in the decrease in the feeding pattern between the SDA viral and a bacterial infection suggest that factors other than TNF-alpha alone play a significant role in the mechanism of anorexia during a viral infection.
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PMID:Feeding behavior during sialodacryoadenitis viral infection in rats. 1133 4

Knowledge of the acute and late ionizing radiation exposure damage to the gastrointestinal tract, particularly injury of the small intestine, is of great significance in radiotherapy, as is management of accidental radiation exposure. Irradiation (X-ray, neutron, cobalt gamma) induces a series of events in this rapidly renewing tissue resulting in the well-known symptoms of the gastrointestinal (GI) radiation syndrome, such as GI haemorrhage, endotoxemia, bacterial infection, anorexia, nausea, vomiting, diarrhoea, and loss of electrolytes and fluid. In spite of the significant advances that have occurred in research on underlying mechanisms over the last two decades, the overall etiology and pathogenesis of the GI-syndrome still remains unclear. Currently, to our knowledge, these symptoms are probably due to a rapid modification of the intestinal motility and to the structural alteration of the intestinal mucosa (cell loss and altered crypt integrity). Several evidences suggest that radiation-induced dysfunctions and structural changes of this organ (either changes in subcellular, cellular, and histological structure) are mediated by concerted and interrelated changes of a plethora of various extracellular mediators and their intracellular messengers. The aim of this review is to summarize our current knowledge about the pathomorphology and cell biology of the ionizing radiation response of the GI tract with a focus on the small intestine.
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PMID:Morphological aspects of ionizing radiation response of small intestine. 1156 86

Bacterial infection alters whole-body protein homeostasis. Although immune cells are of prime importance for host defense, the effect of sepsis on their protein synthesis rates is poorly documented. We analyzed protein synthesis rates in rat primary lymphoid tissues and circulating lymphocytes after infection. Male Sprague-Dawley rats were studied 1, 2, 6 or 10 d after an intravenous injection of live Escherichia coli. Control healthy rats consumed food ad libitum (d 0) or were pair-fed to infected rats. Protein synthesis was quantified using a flooding dose of L-(4,4,4-(2)H(3))valine. Sepsis induced a delayed increase in total blood leukocytes and a rapid and persistent inversion of the counts. Basal fractional rates of protein synthesis (ks) were 117, 73 and 29%/d in bone marrow, thymus and circulating lymphocytes, respectively. Pair-feeding strongly depressed the absolute protein synthesis rates (ASR) of bone marrow (d 2 and 10) and thymus (d 2-10). The infection per se increased bone marrow, thymus and circulating lymphocyte ks but at various postinfection times. It decreased bone marrow (d 1) and thymus (d 1 and 2) ASR but increased lymphocyte (d 2 and 10) and bone marrow (d 10) ASR. Our results reflect the deleterious effect of anorexia on primary lymphoid tissues. The host defense against bacterial infection exhibited time- and tissue-dependent modifications of protein synthesis, indicating that blood lymphocyte protein data are not representative of the immune system as a whole. Optimization of nutritional supports would be facilitated by including protein synthesis measurements of the immune system.
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PMID:Bacterial infection affects protein synthesis in primary lymphoid tissues and circulating lymphocytes of rats. 1209 87


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