Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diarrhea or respiratory infection constitutes the terminal illness in most starved children and adults. A major component of starvation diarrhea appears to be an organ-specific malnutrition of the inestinal epithelium, not bacterial overgrowth. Faced with an overburden of nutrients on refeeding, the intestine cannot salvage ions because its epithelium has insufficient energy to control absorption effectively. In many cases, patients have a worsening of diarrhea and die within the 1st few days of oral refeeding. Antibiotics are particularly detrimental in starvation because they prevent effective bacterial fermentation and thus production of substrates for mucosal growth and sodium absorption. Oral rehydration thereapy uses glucose to drive sodium absorption in the small intestine mucosa, but it provides little energy to the mucosa. Nutrition of the small bowel mucosa is promoted by increasing the vascular supply of amino acids. Once nutrition of the intestinal mucosa has been restored, absorption of orally supplied nutrients becomes efficient. Refeeding diets in starvation should have a relatively high content of ferementable complex polysaccharides and dietary fiber and smaller amounts of milk fats and glucose than are normally provided to severely malnourished children. The starved intestinal epithelium returns to functional capacity after 5-7 days. As a result of the therapeutic implications in severely malnourished children, it is essential that cases of infective diarrhea and starvational diarrhea be differentiated from each other.
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PMID:Metabolic basis of starvation diarrhoea: implications for treatment. 287 46

Mortalities and abortions associated with starvation occurred at Cape Cross, Namibia, in Cape fur seals (Arctocephalus pusillus pusillus). Affected seals showed lethargy and emaciation, and the most common pathological signs were those of a respiratory infection, both in adults and offspring. Streptococcus phocae was isolated from adult seals, a cub and aborted foetuses.
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PMID:Streptococcus phocae infections associated with starvation in Cape fur seals. 1085 31

Pseudomonas aeruginosa is a common cause of chronic respiratory infection in cystic fibrosis (CF) patients. Infection is established within the lung epithelial mucus layer through adhesion to mucins. Terminal residues on mucin oligosaccharide chains are highly sulfated and sialylated, which increases their resistance to degradation by bacterial enzymes. However, a number of microbes, including P. aeruginosa, display mucin sulfatase activity. Using ion chromatography, the levels of sulfation on different respiratory mucins and the availability of inorganic sulfate to pathogens in sputum from CF patients were quantified. The ability of clinical isolates of P. aeruginosa to desulfate mucin was tested by providing mucin as a sole sulfur source for growth. All tested P. aeruginosa strains isolated from the lungs of CF patients were able to use human respiratory mucin as a source of sulfur for growth, whereas other non-clinical species of the genus Pseudomonas were not. However, measured levels of inorganic sulfate in sputum from CF patients suggested that bacteria resident in the lung have sufficient inorganic sulfate for growth and are unlikely to require access to mucin sulfur as a sulfur source during chronic infection. This was confirmed when expression of sulfate-repressed P. aeruginosa genes atsK and msuE was found to be repressed in the sputum of CF patients, which was detected by using quantitative RT-PCR. These results indicate that sulfate starvation is unlikely to occur in pathogens residing in the sputum of CF patients and, therefore, mucin desulfation may have an alternative purpose in the association between P. aeruginosa and the airways of CF patients.
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PMID:Desulfurization of mucin by Pseudomonas aeruginosa: influence of sulfate in the lungs of cystic fibrosis patients. 2291 66

Bordetella bronchiseptica can use catecholamines to obtain iron from transferrin and lactoferrin via uptake pathways involving the BfrA, BfrD, and BfrE outer membrane receptor proteins, and although Bordetella pertussis has the bfrD and bfrE genes, the role of these genes in iron uptake has not been demonstrated. In this study, the bfrD and bfrE genes of B. pertussis were shown to be functional in B. bronchiseptica, but neither B. bronchiseptica bfrD nor bfrE imparted catecholamine utilization to B. pertussis. Gene fusion analyses found that expression of B. bronchiseptica bfrA was increased during iron starvation, as is common for iron receptor genes, but that expression of the bfrD and bfrE genes of both species was decreased during iron limitation. As shown previously for B. pertussis, bfrD expression in B. bronchiseptica was also dependent on the BvgAS virulence regulatory system; however, in contrast to the case in B. pertussis, the known modulators nicotinic acid and sulfate, which silence Bvg-activated genes, did not silence expression of bfrD in B. bronchiseptica. Further studies using a B. bronchiseptica bvgAS mutant expressing the B. pertussis bvgAS genes revealed that the interspecies differences in bfrD modulation are partly due to BvgAS differences. Mouse respiratory infection experiments determined that catecholamine utilization contributes to the in vivo fitness of B. bronchiseptica and B. pertussis. Additional evidence of the in vivo importance of the B. pertussis receptors was obtained from serologic studies demonstrating pertussis patient serum reactivity with the B. pertussis BfrD and BfrE proteins.
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PMID:Interspecies variations in Bordetella catecholamine receptor gene regulation and function. 2637 Nov 28