Several potential proximate causes may be implicated in a recent (post-1984) decline in moose (Alces alces andersoni) numbers at their southern range periphery in northwest Minnesota, USA. These causes include deleterious effects of infectious pathogens, some of which are associated with white-tailed deer (Odocoileus virginianus), negative effects of climate change, increased food competition with deer or moose, legal or illegal hunting, and increased predation by gray wolves (Canis lupus) and black bears (Ursus americanus). Long-standing factors that may have contributed to the moose decline include those typically associated with marginal habitat such as nutritional deficiencies. We examined survival and productivity among radiocollared (n = 152) adult female and juvenile moose in northwest Minnesota during 1995–2000, and assessed cause of death and pathology through carcass necropsy of radiocollared and non-radiocollared animals.
Aerial moose surveys suggested that hunting was an unlikely source of the numerical decline because the level of harvest was relatively low (i.e., approx. 15% / 2 yr) and the population usually grew in years following a hunt. The majority of moose mortalities (up to 87% of radiocollared moose [n = 76] and up to 65% of non-radiocollared moose [n = 84]) were proximally related to pathology associated with parasites and infectious disease. Liver fluke (Fascioloides magna) infections apparently constituted the greatest single source of mortality and caused significant pathology in the liver, thoracic and peritoneal cavities, pericardial sac, and lungs. Mortality due to meningeal worm (Parelaphostrongylus tenuis) was less prevalent and was manifested through characteristic neurological disease. Several mortalities apparently were associated with unidentified infectious disease, probably acting in close association with malnutrition. Bone-marrow fat was lower for moose dying of natural causes than those dying of anthropogenic factors or accidents, implying that acute malnutrition contributed to moose mortality. Blood profiles from live-captured animals indicated that those dying in the subsequent 18 months were chronically malnourished.
Relative to other populations, average annual survival rates for adult females (0.79 [0.74–0.84; 95% CI]) and yearlings (0.64 [0.48–0.86]) were low, whereas those for calves (0.66 [0.53–081]) were high. Pregnancy (48%) and twinning (19%) rates were among the lowest reported for moose, with reproductive senescence among females being apparent as early as 8 years. Pregnancy status was related to indices of acute (i.e., bone-marrow fat) and chronic (i.e., blood condition indices) malnutrition. Opportunistic carcass recovery indicated that there likely were few prime-aged males (>5 yr old) in the population.
Analysis of protein content in moose browse and fecal samples indicated that food quality was probably adequate to support moose over winter, but the higher fecal protein among animals that died in the subsequent 18 months could be indicative of protein catabolism associated with malnutrition. Trace element analysis from moose livers revealed apparent deficiencies in copper and selenium, but there was limited evidence of direct association between trace element concentrations and moose disease, pathology, or mortality. Time-series analysis of regional moose counts (1961–2000) indicated that annual population growth rate was related negatively to mean summer temperature, with winter and summer temperatures increasing by an average of 6.8 and 2.1 C, respectively, during the 40-year period. This change may have increased moose thermoregulatory costs and disrupted th