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Abstract: The main purpose of this article is to review the previously published data on so-called “moose sickness” in the light of two case studies presented here. Molybdenosis and Mo-induced disturbances of Cu metabolism in moose are characterized by numerous severe lesions caused by reduced activity of Cu-containing enzymes such as ceruloplasmin, superoxide dismutase in blood, and myocardial cytochrome c oxidase. Consequences of such metabolic disturbances (e.g. glucose intolerance, insulin resistance, and noninsulin-dependent diabetes mellitus) were first reported in moose in 2000. This was corroborated by the detection of furosine, pentosidine, and Ne-(carboxymethyl)-lysine in blood plasma and the kidney, indicating long-term hyperglycemia. Increased concentrations of insulin, glucose, and urea and reduced levels of phosphate, T4, and Mg in blood were also seen. Recently, a similar toxic endocrinopathy was reported in sheep treated therapeutically with thiomolybdates because of chronic Cu toxicosis. Two case reports illustrate the difficulty of diagnosing Mo-related disturbances of Cu metabolism in moose, as analyses of Cu and Mo have not proved entirely reliable because of interaction, accumulation, and the short biological half-life of Mo. The increased bioavailability of Mo is most probably the result of increased pH in the soil, caused, for example, by liming, making Mo accessible in forage plants consumed by moose. The etiology underlying the Swedish moose disease has been difficult to determine because of the complex clinical signs and unspecific pathological findings. However, a combination of clinical chemistry, trace element analysis, and biochemistry correlated with the pathological findings has corroborated molybdenosis and Mo-induced disturbances of Cu metabolism as the probable etiological factor. Alternative etiologies suggested for the moose disease, such as viral infection, starvation because of overpopulation, and/or shortage of forage as well as senescence and phytotoxic substances, are discussed.

A previously unreported urolith is presented. The concrement was found in the bladder of four Persian cats and one collie dog. It contained potassium, magnesium and phosphorus, all determined by chemical analysis. The infrared spectrum of the X-ray-dense urolith displayed absorption bands in the phosphate region. A single absorption maximum at 930 cm–1indicated the presence of inorganic pyrophosphate. A single crystal structure determination of the urolith has been performed. The results obtained are consistent with the formula [K1.0Mg1.5]4+[P2O7]4–.(H2O)5, which corresponds to 11.5% K, 10.7% Mg and 18.2% P. The structure contains negatively charged slabs of composition MgP2O7·(H2O)22– alternating with positively charged, hydrated Mg2+and K+ions. The observed P2O7is that of a distorted eclipsed synconformation, which is the most common geometry in the solid state according to a statistical analysis of known structural data. A simple numerical descriptor has been derived, classifying observed X2O7conformations. It is suggested that some genetic enzymatic dysfunction of pyrophosphate-hydrolysing alkaline phosphatase might cause the formation of this unusual urolith.

During the period 1973–1977, a number of mute swans (Cygnus olor) were submitted to the National Veterinary Institute in Stockholm and examined post mortem. Organ tissues from 58 swans were chemically analysed for concentrations of lead, cadmium, copper, zinc, iron and manganese. In 10 swans (17 %), elevated residues of lead were found indicating intoxication. Cadmium concentrations were significantly higher in adult than in juvenile swans; also in swans from the Swedish east coast compared with specimens from the west coast. Remarkably high copper concentrations were often found, with one exception yet without any signs of intoxication. High zinc and cadmium concentrations were often found in the same swans. The findings of iron and manganese were not remarkable.

In the determination of the total lead content of urine by the dithizone method a large part of the analysis time is spent in ashing. McCord and Zemp described a method using “wet ashing,” which shortened the ashing time to 30 min. The author, by using a modification of the above method, found that no loss of lead occurred as compared with a determination carried out with a longer ashing time. This method may be used for the analysis of urine from persons suffering from lead poisoning even after treatment with EDTA or penicillamine.