Prevention of iron-deficiency anaemia in suckling piglets.
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During a five-year period the incidence of neonatal sepsis was 20 times higher in Polynesian newborns compared with European newborns (11 per 1,000 vs. 0.6 per 1,000 total births). This high incidence in Polynesians was confined to a period when the infants were being given intramuscular iron dextran. When the iron administration was stopped the incidence of disease in Polynesians decreased from 17 per 1,000 to 2.7 per 1,000 total births. An analysis of the Polynesian iron-treated and non-iron-treated groups showed a statistically significant difference in the incidence of sepsis, the type of causative organism, and mortality. The data suggest that the iron dextran injections have impaired the immunity of the treated infants, making them more susceptible to Escherichia coli sepsis.
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Iron-dextran (Imferon) significantly increases the concentration of 67Ga in abscess relative to muscle, when given intravenously to abscess bearing rabbits 24 hr after intravenous, carrier-free 67Ga-citrate. This increase is achieved by accelerating the clearance of 67Ga from the blood.
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Eight intramuscular injections of 200 mg/kg of iron (DFe), given as iron dextran twice weekly in the week before and the three weeks after intravenous infection with about 10(7.5) colony-forming units of Mycobacterium avium, significantly prolonged (by about 11 days) the mean 'time-to-death' of immature male fowl (Gallus domesticus) compared with corresponding regimes using dextran (Dx) only or saline, When a proportion of the birds were examined 21 days after infection many of the abnormalities associated with the disease, including a marked hypochromic anaemia, were less severe in DFe-treated than in the Dx- or saline-treated chicks and there were about 10- to 85-fold fewer viable tubercle bacilli in the liver and spleen of the DFe-treated birds.
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Chicks aged 15 days were infected orally with 10(6-4) living Salmonella gallinarum. Iron from iron dextran or ferric ammonium citrate (DFe and CFe respectively), in doses of 2-0 or 0-4 mg/kg given intramuscularly at the time of infection, had no effect on subsequent mortality compared with infected controls. Increasing the amount of CFe to the maximum (20 mg/kg) that was non-toxic intramuscularly was also ineffective but when the dose of DFe was increased to 20 or 50 mg/kg the survival rate rose sharply. If given at other times in relation to the time of infection, or more frequently, 50 mg/kg or more of DFe was less active. The increased survival rate among infected chicks given 50 mg/kg of DFe at the time of infection was accompanied by decreases in the severity of the morbid changes in the disease, and by reductions of between c 10- to 100-fold in the numbers of viable S gallinarum in the liver, spleen or blood at the height of the acute infection. DFe (50 mg/kg) given at the time of infection also eliminated the difference in the survival rate noted previously between infected chicks fed respectively with diets containing fish or meat meal as the sole source of supplementary protein.
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