Nursing sickness in the mink — a metabolic mystery or a familiar foe?

Nursing sickness, the largest single cause of mortality in adult female mink (Mustela vison), is an example of a metabolic disorder, which develops when the demands for lactation require extensive mobilization of body energy reserves. The condition is characterized by progressive weight loss, emaciation, and dehydration with high concentrations of glucose and insulin in the blood. Morbidity due to nursing sickness can be as high as 15% with mortality around 8%, but the incidence is known to vary from year to year. Stress has been shown to trigger the onset of the disease and old females and females with large litters are most often affected. Increasing demand for gluconeogenesis from amino acids due to heavy milk production may be a predisposing factor. Glucose metabolism is inextricably linked to that of protein and fats. In obesity (or lipodystrophy), the ability of adipose tissue to buffer the daily influx of nutrients is overwhelmed (or absent), interfering with insulin-mediated glucose disposal and leading to insulin resistance. Polyunsaturated fatty acids of the n-3 family play an important role in modulating insulin signalling and glucose uptake by peripheral tissue. The increasing demand on these fatty acids for milk fat synthesis towards late lactation may result in deficiency in the lactating female, thus impairing glucose disposal. It is suggested that the underlying cause of mink nursing sickness is the development of acquired insulin resistance with 3 contributing key elements: obesity (or lipodystrophy), n-3 fatty acid deficiency, and high protein oxidation rate. It is recommended that mink breeder females be kept in moderate body condition during fall and winter to avoid fattening or emaciation. A dietary n-3 fatty acid supplement during the lactation period may be beneficial for improved glycemic control. Lowering of dietary protein reduces (oxidative) stress and improves water balance in the nursing females and may, therefore, prevent the development and help in the management of nursing sickness. It is also surmised that other, thus far unexplained, metabolic disorders seen in male and female mink may be related to acquired insulin resistance.     

Nursing sickness in lactating mink (Mustela vison). I. Epidemiological and pathological observations.

In a retrospective survey, the epidemiological characteristics of nursing sickness in Standard Black and Pastel mink (Mustela vison) were examined in a Danish fur research farm. Based on the clinical diagnosis of the disease, the overall morbidity in a total of 1774 lactating females amounted to 14.4% and the case fatality rate to 7.8%. Apparently healthy females weaned an average of 5.0 kits per litter, while dams suffering from nursing sickness raised and weaned an average of 5.4 kits per litter (p less than 0.01). Based on logistic regression analysis, the increasing age of the lactating dam, followed by littersize and female weight loss, appeared to be major determinants for the development of nursing sickness. The impact of additional covariates such as litter weight gain and female color type were remarkably low. At weaning (day 43) the mean individual live weight of the kits of either sex did not differ between healthy and sick dams. In Standard Black, the total biomass of the offspring raised by sick dams was significantly larger than that of the healthy controls (p less than 0.01). During the final two weeks of lactation, apparently healthy dams lost on average 14% of their body mass, whereas those affected by nursing sickness had a mean weight loss of about 31% (p less than 0.001). Postmortem examination of 25 dams with severe nursing sickness verified the clinical findings of progressive dehydration and emaciation. The gastrointestinal tract was empty and gastric ulcers and melaena were frequently present. Other common findings included small livers,enlarged adrenals and pitted kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)     

Incidence of nursing sickness and biochemical observations in lactating mink with and without dietary salt supplementation.

The impact of dietary sodium on the incidence of nursing sickness in mink dams and on the average litter biomass of 28 and 42 day old kits was studied. One group (n = 115 including 12 barren females) was given a standard feed mixture with a natural content of 0.53 g NaCl/MJ and another group (n = 115 including 8 barren females) was given the same feed mixture supplemented with NaCl to a final content of 1.00 g/MJ. The average dam weight at weaning was significantly lower (P < 0.001) and the incidence of nursing sickness during the last part of the lactation period 3 times higher in the nonsupplemented group. The average litter biomass at weaning did not differ between the 2 experimental groups. A number of biochemical markers of preclinical nursing sickness, e.g. plasma aldosterone and osmolality, Na+ and Cl concentrations in plasma and urine, were studied during the last part of the lactation period and at weaning in 20 dams of the nonsupplemented group, in 10 dams of the salt supplemented group and, for comparison, in 5 + 5 barren females on the day corresponding to day 34 after parturition in nursing mink. The nonsupplemented group had significantly lower concentrations of sodium and chloride in plasma and urine and a significantly higher concentration of plasma aldosterone as compared to the salt supplemented group. Distinct signs of relative salt deficiency and preclinical nursing sickness thus characterized the nonsupplemented group throughout this period, while more blurred hints of electrolyte imbalances were noticed in the sodium chloride supplemented group at weaning. A beneficial effect of salt supplementation on the incidence of nursing sickness was shown; however, it remains unclear whether salt deficiency can cause nursing sickness or whether salt acts as an appetite stimulant preventing inanition and the development of the disorder.     

Failure of loop diuretics to induce nursing sickness in mink at weaning.

Nursing sickness in mink is thought to be precipitated by inadequate salt intake, whether this is due to inadequate salt levels in the diet or inadequate total dietary intake. To test this hypothesis, lactating females raising large litters were given 2 daily intramuscular injections of the loop diuretic furosemide (Lasix, 4 + 4 mg/kg/day) for 2.5 d during the normal weaning period 6 wk after parturition or served as untreated controls. Following the same protocol, barren mink (i.e. unsuccessfully mated females) were treated similarly. Dams were carefully inspected for clinical signs of nursing sickness during and after the treatment. Urinary osmolality and concentrations of sodium, potassium, chloride, creatinine and carbamide (urea) were measured prior to treatment (day 1) and on day 3, immediately before and 4 h after the final diuretic treatment. Plasma concentrations of aldosterone and cortisol were determined by radioimmunassay 4 h after the last injection with furosemide on day 3. Biochemical changes in urine (a low osmolality, low concentrations of carbamide and creatinine, and extremely low sodium concentrations) and in plasma (aldosteronism) similar to those found in nursing sickness were elicited in the nursing dams. Nevertheless, none of the dams developed overt clinical signs of nursing sickness. It is concluded that the biochemical signs of volume and salt depletion associated with nursing sickness are sequelae rather than etiological factors of this disorder.     

Comparison of two oral electrolyte solutions for the treatment of dehydrated calves with experimentally-induced diarrhoea

We compared the ability of two oral electrolyte solutions to resuscitate calves with experimentally induced diarrhoea and dehydration. Sucrose solution, furosemide, spironolactone, and hydrochlorothiazide were administered to 18 male Holstein-Friesian calves to induce diarrhoea and dehydration. Clinical changes after 24 h included severe diarrhoea, moderate dehydration (8-10% body weight), azotemia, and clinical depression. Calves were then randomly assigned to one of three treatment groups (milk replacer, 2 L every 12 h; hyperosmotic oral electrolyte solution, 2 L every 12 h; iso-osmotic oral electrolyte solution, 1.5 L every 6 to 12 h) and followed for an additional 48 h.Compared to feeding milk replacer, the hyperosmotic solution significantly (P< 0.05) improved hydration status, increased body weight, maintained urine production, decreased the degree of clinical depression and prevented development of metabolic acidosis, although serum glucose concentration was decreased at 24 h and 48 h. The hyperosmotic solution produced a similar resuscitative response to the iso-osmotic solution, but maintained higher serum glucose concentrations and lower serum beta-OH butyrate and non-esterified fatty-acid concentrations, indicating that the hyperosmotic solution provided greater nutritional support. The hyperosmotic solution rehydrated calves faster and more effectively than feeding equivalent volumes of milk replacer and can, therefore, be recommended as part of the initial treatment of dehydrated calves with diarrhoea.     

Pilot project for eradicating maedi-visna in Walliser blacknose sheep

Maedi-Visna is a lentiviral disease of sheep with a worldwide distribution. The transmission of the virus occurs primarily via colostrum and milk from the infected ewe to its newborn lamb but also horizontally between sheep. The most obvious clinical symptoms are progressive dyspnea and emaciation. In this prospective study an eradication based on serological testing and removing of seropositive animals was performed in 24 flocks of sheep of the breed "Walliser Schwarznasenschafe" leading to a reduction of the seroprevalence from 36% to 1% within two years. The control group consisted of 21 flocks of sheep. Lambs of seropositive ewes had a 7.6 times higher risk to seroconvert within their first two years of life compared to those of seronegative ewes. The dynamics of the spread of the infection were studied in birth cohort groups. Cohort animals of seropositive ewes showed an obvious trend to seroconvert slowly. Seropositive ewes had a significantly lower reproduction rate and their lambs suffered from significantly higher death and lower growth rates, probably due to a reduced milk production, resulting in economic losses.     

Johne's disease in Canada Part I: clinical symptoms, pathophysiology, diagnosis, and prevalence in dairy herds

Recent international developments in the area of infectious disease control and nontariff trade barriers, along with possible zoonotic concerns, have provoked a revival of interest in Johne's disease in Canada and elsewhere. The bacterium causing Johne's disease, Mycobacterium avium subspecies paratuberculosis, is distributed worldwide and causes chronic granulomatous enteritis, also known as paratuberculosis, in domestic and exotic ruminants, including cattle. The subclinical form of this disease results in progressive weight loss, reduced milk production, lower slaughter value, and premature culling, with possible impacts on fertility and udder health. Eventually, infection can lead to the clinical form that manifests as chronic diarrhea, emaciation, debilitation, and eventual death. Currently, available tests to detect infected animals produce many false-negative results and some false-positives, particularly in subclinically infected animals, thus making their interpretation and utilization challenging in control programs. The objective of this 2-part review is to critically review the literature about Johne's disease in dairy cattle for bovine practitioners in Canada. Part I covers the clinical stages, pathophysiology, diagnosis, and prevalence of infection in Canada, while Part II discusses impacts, risk factors, and control programs relevant to Canadian dairy farms. By reviewing the scientific literature about Johne's disease, control of the disease could be pursued through informed implementation of rational biosecurity efforts and the strategic use of testing and culling.     

Senecio jacobaea: deceiving beauty. Senecio jacobaea poisoning

In a cattle herd problems were noticed during 1.5 years, characterised by emaciation and loss of milk production with lower fat- and protein%, tenesmus, central nervous symptoms (aggression, circling and blindness), diarrhoea, eczema solare and death. Clinical, laboratory and post mortem examinations did not reveal a specific cause at first. An intoxication was suspected based on the clinical symptoms, the course of the disease in sick animals and severe liver cirrhosis found in a sudden death cow: The animals were fed grassilage derived from an air force base on which an overwhelming amount of tansy ragwort (Senecio jacobaea) was present. On subsequent microscopic examination of the livers of 11 slaughtered clinically healthy animals all of these showed fibrosis in varying extension. Cirrhosis and fibrosis of the liver and the clinical symptoms are all features of chronic pyrrolyzidine alkaloidosis. Tansy ragwort poisoning has not been diagnosed in the Netherlands for years. The rise in cases is due to more extensive use of land.     

A review of exertional rhabdomyolysis in wild and domestic animals and man.

Exertional rhabdomyolysis is a condition arising in several species of newly captured wild animals after some form of physical exertion and stress. It is characterized by muscle necrosis and myoglobinuria. Death may result from secondary renal failure, acute or chronic heart failure and progressive emaciation.     

Chronic metabolic acidosis in dairy cows]

Complex clinical and clinico-biochemical examination of the blood, urine and rumen liquor in a herd of dairy cows revealed chronical metabolic acidosis accompanied by rumen dysfunction and by a reduced butterfat content of milk. During the first examination of the acid-base state of the blood was almost at a standard level. An increased level of urea in blood plasma and a higher GOT transaminase activity testified to an excessive load on the liver. Urine pH was considerably deviated towards the acidic side and inorganic phosphorus was present in urine in a greater concentration. The pH of rumen liquor was slightly shifted towards alkalinity owing to the release of NH3 from urea in the food ration. The diagnosis--suspect chronical metabolic acidosis--was determined on the basis of the first examination. Chronical metabolic acidosis was definitely proved by the second examination when urea had been excluded from the feed ration. Repeated examinations revealed chronical metabolic acidosis which had originally been accompanied by a higher rumen liquor pH. On the basis of case histories and mechanisms of chronical acidosis, measures were proposed, resulting in an increase of the butterfat content of milk. Chronical metabolic disorders often follow a long-lasting latent pattern, manifesting themselves as a reduced milk yield and lower resistance; the clinical form of disease appears only at a later stage. The system of preventive diagnostics provides information on the changes in the composition of internal medium and of the faeces before a drop occurs in milk and fat production. These measures prevent metabolic disorders and high losses of produce which otherwise remain hidden for a long time.     

Energy intake and milk production in mink (Mustela vison)--effect of litter size.

Energy intake and milk production were measured in 12 mink dams raising litters of 3, 6 and 9 kits one to four weeks post partum by means of balance experiments and measurements of milk intake of the kits by the water isotope dilution technique. The dams were fed ad libitum on a conventional wet mink diet (DM: 323 g/kg; CP: 173 g/kg; ME: 4.4 MJ/kg). Milk samples collected from dams with corresponding litter sizes and lactation weeks, and body composition of kits nursed by these dams, were analysed for content of DM, ash, N and fat. The ME and drinking water consumption were higher in dams nursing 9 kits than in dams nursing 3 kits. The N and water balances as well as the live weight of dams were not affected by litter size. Daily milk production was higher in dams nursing 9 kits than in dams nursing 3 kits. The DM, N and fat content of the milk increased during lactation, but were not affected by litter size. Individual kit live weight was higher in litters of 3 than in litters of 6 and 9 kits four weeks post partum. The DM and fat content of the kits were lowest in kits from litters of 9 kits, whereas these kits had the highest protein content. Daily ME for maintenance of kits and the efficiency of utilisation of ME in milk for body gain were estimated to 356 kJ/kg0.75, kp approximately 0.53 and kf approximately 0.71, respectively. In conclusion, daily milk production increased with increasing litter size, but not in proportion to the number of kits, indicating that milk production limits the growth rate of the young. In the fourth week of lactation, milk production was not different between dams nursing 6 or 9 kits, indicating a maximum capacity.     

Candida albicans urocystitis in a cat.

Candida albicans urocystitis secondary to urethral stricture and administration of antibiotics was diagnosed in a cat by fungal culturing of urine and examination of specimens. Surgical repair of the stricture and administration of 5-fluorocytosine resulted in resolution of the cystitis. Related problems included anorexia and severe weight loss, which necessitated enteral nutritional support, dehydration, renal disease, and nosocomial Pseudomonas aeruginosa urocystitis.     

DIARRHOEA IN PIGLETS INOCULATED WITH ROTAVIRUS

A rotavirus isolated from a field outbreak of diarrhoea in artificially reared piglets was purified, filtered and administered orally to gnotobiotic and conventional piglets. Four successive passages of the virus in gnotobiotic piglets produced severe diarrhoea within 20 to 24 hours of administration. The diarrhoea lasted several days causing dehydration, emaciation, loss of body weight and some deaths. Virus was demonstrated in the faeces of the infected piglets by electron microscopy. Conventionally reared piglets developed little or no diarrhoea when given virus, whereas artificially reared piglets developed moderate to severe diarrhoea which lasted from 3 to 8 days with some deaths. No clinical disease was obvious in surviving piglets following challenge with the virus 10 or 17 days after initial infections.     

Diagnostic features of ovine progressive pneumonia.

Ovine progressive pneumonia, a chronic, insidious disease of adult sheep, has a relentless course leading to dyspnea, emaciation, and death. Clinical observations and serologic tests are adequate for making a tentative diagnosis. The agar gel immunodiffusion test seems to be the best serologic procedure for indicating infection with the virus but cannot be used to predict morphologic changes or clinical disease, inasmuch as many clinically unaffected animals carry the virus. A definitive diagnosis is based on finding lesions and isolating virus. Affected lungs are large and heavy as a result of interstitial accumulation of lymphoid cells and fibromuscular tissue. Frequently, interstitial lesions are accompanied by bronchopneumonia from secondary bacterial infection. The causal virus can be isolated from infected lungs by cocultivation with primary ovine or bovine cells.     

Glycogen storage disease type II in the Lapland dog

A newly recognized inherited metabolic disease in the Lapland dog is described. The metabolic defect is a deficiency of acid-alpha-glucosidase, a lysosomal hydrolase. The clinical picture is dominated by vomiting related to megaoesophagus, and progressive muscle weakness leading to exhaustion and death before two years of age. Cardiac abnormalities are observed. The main histopathologic lesion consists of glycogen accumulation, notably in membrane-bound vacuoles (glycogenosomes), involving all kinds of muscular tissue in particular. Recessive inheritance of the disease was demonstrated by complementation analysis. The enzyme protein is present in affected tissues, although in an inactive form. Based on the gene dosage phenomenon, an attempt was made to identify carrier dogs by means of a biochemical assay. Glycogen storage disease type II in the Lapland dog appears to be a homologous model for the infantile manifestation of glycogen storage disease type II (Pompe's disease) in man.     

Experimental Streptococcus bovis infections in pigeons.

Thirty pigeons were experimentally infected with Streptococcus bovis using an intravenous infection model. Ninety percent of the inoculated pigeons developed clinical disease. Disease signs included acute death, inability to fly, lameness, inappetence, emaciation, polyuria, and the production of slimy, green droppings. At necropsy, the septicemic character of the disease was evident. Typical lesions included extensive well-circumscribed areas of necrosis in the pectoral muscle, tenosynovitis of the tendon of the Musculus pectoralis profundus, and arthritis of the stifle, tibiotarsal, or shoulder joints. Focal myocardial necrosis also was seen. Meningitis and encephalitis occurred in the cerebrum and the cerebellum. Disease signs and lesions described here after experimental infection were similar to those in naturally occurring cases of S. bovis septicemia.     

河南省郑州市某宠物医院2例犬巴贝斯虫病的诊治

犬巴贝斯虫病是一种由硬蜱传播的犬血液寄生虫病,以春、夏季节多发,患病犬出现高热、黄疸、尿液发红、严重贫血、消瘦、精神萎靡等临床症状。选取河南省郑州市某宠物医院的2例犬巴贝斯虫病例进行分析,总结了犬巴贝斯虫病的诊治方法。     

Mannosidosis in a litter of Persian cats

Three kittens in a litter of Persian cats showed, from the age of eight weeks, tremor, ataxia, dysmetria, progressive weakness and emaciation. Cytoplasmic vacuolation was observed in neurons, mesenchymal and epithelial cells of tissues taken post mortem. The alpha-mannosidase activity of brain tissue of one cat tested was 4.8 per cent of control values and the urine of two cats contained large amounts of mannose-rich oligosaccharides.     

Clinical and pathological features of Aspergillus fumigatus infections in poultry in southern Nigeria

This study was undertaken to supply information on Aspergillus fumigatus infection of poultry in Nigeria. The disease in broiler chicks was characterized by gasping, droopiness, emaciation and heavy mortality while affected grower chickens showed emaciation, weakness, diarrhoea and 17 per cent mortality. The disease was sporadic in laying flocks. Granulomatous nodules were observed in birds that died in each outbreak. The nodules were numerous and affected mainly the lungs and thoracic air sacs in the broiler chicks while only few large nodules were observed mainly in the abdominal air sacs in the layers.     

Water deprivation test in the dog: maximal normal values.

Studies were undertaken to determine maximal urine osmolality and urine specific gravity following water deprivation for 20 dogs with normal renal function. In addition, the reliability of body weight, skin pliability, total plasma protein concentration, and packed cell volume as indices of negative water balance was assessed. Following water deprivation for periods sufficient to induce dehydration, the mean maximal urine osmolality was 2,289 mOsm/kg. The corresponding mean maximal urine specific gravity was 1.062 and ranged from 1.050 to 1.076. The ratio of mean maximal urine osmolality to mean serum osmolality at the time of peak urine concentration was 7.3. There was no detectable difference in urine concentration indices between males and females. Changes in skin pliability and packed cell volume proved unreliable as estimates of dehydration. Weight loss and increases in total plasma protein concentration proved to be more consistent indicators of hydration status. Abnormal increases in serum urea nitrogen and serum creatinine concentrations occurred rarely, even though some dogs had water withheld for periods of up to 96 hours.