Energy imbalance related predisposition to mastitis in group-fed high-producing postpartum dairy cows.

The energy imbalance related predisposition to mastitis was studied in group-fed postpartum dairy cows (n = 333) kept in 4 large-scale units and producing milk of low somatic cell count (SCC). Blood samples were taken on Days 1-3 after calving for assaying some metabolites and hormones related to the negative energy balance (NEB). If mastitis was diagnosed later, aseptic milk samples were taken to identify the pathogens. Considering pathogen types [contagious pathogens: Staphylococcus (S.) aureus, Gram-positive (GP) environmental pathogens, and Gram-negative (GN) environmental pathogens + mastitis with no detectable pathogens (NDP)] separately, stepwise logistic regression was used to analyse the relation between the potential prognostic value of hormones and metabolites and mastitis outbreak. Only the elevated (> or = 1.00 mmol/l) serum beta-hydroxybutyrate (BHB) levels predisposed the cows to mastitis in the subsequent 4 weeks. This prognostic value of BHB was significant only in GN + NDP mastitis and in cases caused by GP environmental pathogens, but not in S. aureus mastitis (odds ratio: 5.333, 3.600 and 1.333, respectively).

Putative peripheral neuropathy in suckling piglets.

Over a period of almost 2 years, a progressive motor disturbance was found to occur in 20-50% of the litters of both primiparous and multiparous sows in a large pig herd of 1000 sows. The motor disturbance sometimes affected the entire litter; however, in most cases only a few piglets per litter were affected. The clinical signs appeared at 3-5 days of age and consisted of difficult movement followed by anteflexion or retroflexion of the tarsal joints or 'rabbit-like posture'. Subsequently, primarily after weaning, inflammatory and necrotic lesions developed on the paralysed limbs as a result of secondary infections of injuries. The tibial nerve and the common fibular nerve of recently affected (5- to 6-day-old) piglets showed degeneration, demyelination and necrosis of some of the nerve fibres, accompanied by restorative changes in more chronic cases. The central nervous system, bones, skeletal muscles, tendons and joints showed no lesions that could have accounted for the symptoms of motor disturbance. Aetiological investigations excluded the possibility of lead, copper and cadmium toxicity. Vitamin B2 administered orally at 1 day old proved to be ineffective. The disease did not develop in piglets of sows kept at another farm under the same management and fed a diet prepared according to an identical formula from the same ingredients as those used on the affected farm, but with no milk whey added. This raised the suspicion of triaryl phosphate (TAP) poisoning, but this was found not to be the cause of the disease. New boars had not been brought to the farm in the year preceding the onset of disease, and the disease could not be linked to a specific boar or boar line. The aetiology of the disease has remained unclear.

Infectious stunting syndrome associated with disturbances of mineral metabolism and bone development in broiler chickens.

On a broiler farm with a rearing capacity of about 200,000 chickens, a disease characterised by growth retardation, variability in chick size, 'leg weakness', diarrhoea and increased mortality at 3 weeks of age occurred repeatedly, in several successive broiler flocks. Gross and histopathological findings were dominated by widening of the hypertrophic and ossification layers of the physes of long bones as well as by thickening, unevenness and defective calcification of the cartilage trabeculae. In the parathyroid gland, vacuolar degeneration of the cytoplasm of glandular epithelial cells, connective tissue proliferation and, here and there, cyst formation were seen. Additional findings included severe cerebellar oedema and neuronal degeneration. The pancreatic, myocardial and intestinal changes typical of infectious stunting syndrome (ISS) occurred only in a mild form. Four-week-old chickens exhibiting 'leg weakness' had significantly lower blood inorganic phosphate concentration and tibial ash content as compared to healthy chickens. The disease was successfully transmitted by oral administration of small intestinal homogenate from affected chickens. In a second experiment, however, the disease could not be transmitted with intestinal homogenate sterilized by irradiation. Large doses of vitamin D3 reduced the rate of growth retardation and defective calcification of bones. The digestive enzyme activities of the pancreas and small intestinal mucosa of 'infected' chickens were decreased as is typical of ISS.

Massive goitre (struma parenchymatosa) in geese.

In a goose flock consisting of 2300 birds of 6 months of age severe goitre was diagnosed. To the best of our knowledge this is the first report of naturally occurring goitre in geese, which is not related to the feeding of rapeseed meal. The major pathological findings included retarded growth and plumage development, significantly (300%) increased relative thyroid weight, fat accumulation in the mesenteric and abdominal region, and lipid infiltration of liver and kidney cells. Subsequent hormone analysis showed undetectable thyroxine (T4) levels and a dramatic drop in triiodothyronine (T3) plasma levels of the diseased geese. Thyroidal histology displayed the typical signs of struma parenchymatosa. In order to get more information about the possible causes of the goitre, 10 geese from the affected farm were transferred into the laboratories of the Central Veterinary Institute. The geese were allotted into two groups. Group I received iodine supplementation for 55 days, while the other group served as sick control (Group S). Iodine treatment caused a dramatic improvement in the birds' clinical condition except in plumage growth in Group I, while the clinical and main pathological signs of goitre remained unchanged or worsened in the untreated Group S. Contrary to this, the serum levels of thyroid hormones and responsiveness to thyrotropin releasing hormone (TRH) improved not only in Group I but also in Group S. Almost euthyroid biochemical parameters were found after 55 days of iodine treatment in Group I and, surprisingly, a considerable improvement (especially in serum T3 levels) occurred also in Group S. These findings confirm the diagnosis of goitre but also call attention to the fact that iodine deficiency was not the only factor eliciting the disorder. The underlying possible goitrogenic substance could not be traced down.

Testing the compatibility of a combination of tiamulin/chlortetracycline 1:3 premix (Tetramutin-Novartis) given in feed at different levels with salinomycin in chickens.

The compatibility of salinomycin (SA) (60 mg/kg feed) and Tetramutin (TM), a combination of tiamulin (TI) and chlortetracycline (CTC) in a 1:3 ratio, included in varying concentrations, was tested in broiler chickens. Assessment was based on clinical signs, body weight gain, feed conversion efficiency, gross pathological lesions and histological lesions in liver, heart and pectoral muscles, as well as analysis of blood for lactate dehydrogenase (LDH), aspartate dehydrogenase (AST) and creatine phosphokinase (CPK) activity. It was shown that chickens can be safely treated in feed for 7 days with TM containing TI concentrations of 33 or 55mg/kg feed together with SA at 60mg/kg. However, higher levels of TI (100 and 150 mg/kg feed) caused some adverse effects. There was no mortality but there was mild depression, 'leg weakness' accompanied by specific histological lesions in pectoral muscles (obliteration of cross-striation and swelling of muscle fibres, nuclei of muscle cells, hyalinization and destruction of sarcoplasm), a mild increase of AST activity, and a significant increase of CPK and LDH activity in blood. These latter two parameters can be used as an early indication of TI and SA incompatibility.

Nutritional metabolic diseases of poultry and disorders of the biological antioxidant defence system.

Deficiencies or disturbances of nutrition cause a variety of diseases and can arise in different ways. The amount of a particular nutrient in the diet may be insufficient to meet the requirements, the diet may contain substances that inactivate the nutrient or inhibit its absorption/utilisation, or metabolism may be upset by the interaction of dietary and environmental factors. Peroxidation of lipids or oxygen free radical generation in general is a physiological process important for cell metabolism, division and differentiation and also for the biosynthesis of hormones and prostaglandins. Free radicals generated through these processes are effectively scavenged by the antioxidant defence system. Uncontrolled lipid oxidation caused by disturbances of that system may play a crucial role in some important poultry diseases and toxicoses. The first route of lipid peroxide loading of the organism is via the feed, such as through oxidised lipids. Oxidised fatty acids are absorbed from the intestine mainly in the form of unsaturated keto compounds and initiate lipid peroxidation in the tissues. The second problem is the insufficient amount of antioxidants in the feed, e.g. vitamin E deficiency. Nutritional encephalomalacia is a problem in poultry production which depends both on the actual vitamin E supply and the dietary amount of polyunsaturated fatty acids. In young birds the primary target of vitamin E deficiency is the brain because it contains low amounts of vitamin E, and the vitamin E content of the liver acting as store decreases rapidly during the first week of life. Besides vitamin E, other components of the antioxidant system, e.g. the antioxidant enzymes (catalase and glutathione peroxidase) also have low activity in the brain as compared to other major tissues. The brain is highly susceptible to oxidative stress because of the accumulation of polyunsaturated fatty acids. The third source of free radical generation is the toxic level of different feed ingredients, e.g. toxicoses caused by vitamin A, selenium, and ionophore antibiotics. Other important aspects of antioxidants (e.g. vitamin E and selenium) in poultry are stimulation of the immune response (e.g. in the case of vaccination) and reduction of the risks of free radical formation as a result of macrophage function.

Pancreatitis caused by reovirus in guinea-fowl.

Pancreatitis caused by a reovirus was observed among 8- to 22-day-old guinea-fowls held under extensive conditions in groups of 10,000 birds. With the virus isolated from the affected birds the disease entity could be reproduced experimentally. Both the naturally affected and the experimentally infected birds showed depression, lack of appetite and weakness, followed by recumbency, opisthotonus and, occasionally, convulsions. A proportion of the survivors were retarded in growth and stunted. At the acute stage, the pancreas showed 2- to 5-fold enlargement and bright yellowish discoloration, was tense to the touch, and had haemorrhages and necroses both on its surface and within its substance. The main findings revealed by histopathological and electron microscopic examination included the degeneration and necrosis of secretory cells of the exocrine glands responsible for the secretion of digestive enzymes, and the intensive replication of viral particles in the cytoplasm of these cells. The subacute stage of the disease was characterized by an irreversible depletion of the glandular substance and reparative phenomena. The activity of amylase, trypsin, total protease and lipase significantly decreased in the infected birds' intestinal content; at the same time, in the injured pancreatic tissue the activity of these enzymes showed an increase. Hepatic deiodinase activity of the experimentally infected guinea-fowls underwent a significant decrease; parallel to that, serum T4 level increased and serum T3 concentration decreased.

Effect of acute selenium toxicosis on the lipid peroxide status and the glutathione system of broiler chickens.

The effect of acute oral selenium toxicosis on the rate of lipid peroxidation, on the amount of reduced glutathione as well as on glutathione-peroxidase activity of the blood (plasma and red blood cells) and liver was studied in broiler chicken. Cockerels (28-day-old) were treated with selenium (4.85 mg/kg b.w.) administered intraoesophageally in the form of sodium selenite. Samples were at the onset of clinical signs (3 h after treatment) and 2 and 4 h thereafter. The malondialdehyde content of the blood plasma rose significantly (P < 0.05) at the onset of clinical symptoms but decreased later. Malondialdehyde content of the liver was higher than the control value at the first sampling (P < 0.01) and steadily increased later. Reduced glutathione content did not change significantly in the blood plasma and liver. Glutathione peroxidase activity of the RBC was significantly elevated (P < 0.01) only at the first sampling (3 h after treatment) and decreased to the control level thereafter. Acute oral selenium toxicosis increases the rate of lipid peroxidation in a short period of time (7 h) without exerting a significant effect on the glutathione system.

Effect of acute salinomycin-tiamulin toxicity on the lipid peroxide and antioxidant status of broiler chicken.

The combined effect, if any, of salinomycin poisoning and salinomycin-tiamulin interaction on lipid-peroxidative processes and the antioxidative defence system of the liver was studied in domestic fowl. Male broilers (28-day-old), reared on a diet containing 60 mg/kg salinomycin, were treated intraoesophageally with salinomycin (140 mg/kg body mass) or tiamulin (50 mg/kg body mass). Malondialdehyde, reduced glutathione and cytochrome P-450 concentrations as well as glutathione peroxidase and catalase activities of the liver were determined. Liver malondialdehyde concentration rose in the salinomycin-treated group while the amount of cytochrome P-450 increased in both groups treated. Glutathione concentration and glutathione peroxidase activity of the liver decreased rapidly but hepatic catalase activity increased in both groups after the treatment. Manifestation of the effect exerted by salinomycin and salinomycin-tiamulin on lipid-peroxidative processes nearly coincided with the onset of clinical signs and preceded the increase of hepatic cytochrome P-450 concentration. According to the results, the background of the previously reported incompatibility between salinomycin and tiamulin is the synergistic effect exerted on the antioxidant (glutathione) system.

Changes in the lipid peroxide status of broiler chickens in acute monensin poisoning.

The effect exerted by overdosage of monensin, an ionophore antibiotic, on the lipid peroxide status of broiler chickens was studied. Three-week-old broiler cockerels were given 150 mg monensin/kg body mass through a tube, and the malondialdehyde (MDA) concentration, glutathione peroxidase (GSH-Px) and catalase activity of the liver and breast muscle, and MDA concentration and GSH-Px activity of the blood plasma were determined. Liver MDA and catalase values rose rapidly and significantly during the experimental period. GSH-Px activity initially decreased, then tended to rise. Blood plasma and breast muscle variables did not change during the experiment. Acute monensin poisoning induced substantial enhancement of lipid peroxidation processes in the liver, while it did not appreciably affect the lipid peroxide status of the blood plasma and breast muscle. The role of the observed phenomenon in the rather complex pathogenesis of monensin poisoning is not known sufficiently. Further studies are needed to elucidate the problem.

Effect of malabsorption syndrome on pancreatic function in broilers.

The effect of "malabsorption syndrome" on pancreatic function was studied in newly hatched broiler chicks orally inoculated during the first few hours of life with intestinal homogenates from birds with naturally occurring malabsorption syndrome. The control groups were treated with saline. Tissue samples were collected at 0, 2, 4, 6, 9, 13, 17, and 29 days of age from both groups. The BW of inoculated birds decreased significantly relative to that of controls as early as 9 days of age. Pancreatic amylase activity was significantly greater than that in controls by 2 days. Protease activity of inoculated birds increased significantly over that in controls on the 2nd day and decreased significantly on the 6th and 9th days. Reoviruses were detected in the fecal samples of inoculated birds on the 2nd and 3rd days and did not appear in control samples. Reoviruses were also isolated from the pancreatic tissue of two inoculated birds on the 3rd day. Symptoms characteristic of malabsorption syndrome may be elicited by maldigestion; in the present study, this probably resulted from reduced digestive enzyme production of the pancreas. Similarities of changes in plasma triiodothyronine and pancreatic protease levels suggested a possible relationship between thyroid and pancreatic dysfunction in the condition of the malabsorption syndrome.

Rapid decrease of the peripheral deiodination of thyroxine in malabsorption syndrome in artificially inoculated broilers.

Thyroid function of broilers inoculated with the intestinal homogenate from birds from a field case of malabsorption syndrome was investigated during the first 2 days postinoculation. In one experiment, different amounts of the inoculum were applied to see if there exists a dose-response relationship. As early as 3 hours after inoculation, there was a significant drop in the serum level of triiodothyronine and in the activity of the liver 5'-deiodinase (type I). Type II deiodinase activity was less impaired. A minimum of 0.3 ml of inoculum was effective, whereas 0.05 ml of the same homogenate elicited a significant (P less than 0.01) drop in liver deiodinase activity. These findings underline the importance of thyroid impairment in the pathogenesis of malabsorption syndrome.

Interaction of T-2 fusariotoxin and monensin in broiler chickens infected with Coccidia.

Field observations suggest that coccidiosis is a common cause of death in broiler chicken flocks fed diets containing sufficient amounts of ionophore antibiotics (monensin, narasin, etc.) and contaminated with mycotoxins, particularly with T-2 fusariotoxin. To study this phenomenon, broiler chickens fed diets containing different amounts of T-2 toxin and free from monensin, or containing a preventive dose (100 mg/kg of feed) of monensin, were infected experimentally with coccidian oocysts. In all groups fed a diet containing monensin plus T-2 toxin severe clinical symptoms of coccidiosis (blood-stained faeces etc). occurred. Deaths and retarded growth depended on the toxin dose and were considerable. The body mass gain of chicks fed a diet containing monensin and T-2 toxin but not infected with coccidia was inferior to that of groups fed diets which contained either monensin or T-2 toxin (experiment 2). On the basis of these findings a negative interaction of the two compounds is assumed. This seems to be supported by the results of experiment 3, i. e. the finding that the lethal dose of narasin, a compound closely related to monensin both in chemical structure and mechanism of action, proved to be much lower (LD50 = 102 mg/kg body mass) for chickens fed a diet supplemented with T-2 toxin than for the control chickens (LD50 = 176 mg/kg body mass). The present results suggest that the feeding of diets severely contaminated with T-2 toxin may alter the anticoccidial efficacy of monensin.

Decreased thyroxine, triiodothyronine, and 5'-deiodination levels in malabsorption syndrome (runting or stunting syndrome) in artificially inoculated broilers.

The effect of malabsorption syndrome (stunting or runting syndrome) on the thyroid function of broilers was investigated in control and inoculated broilers from 1 to 29 days of age. The broilers were infected at 1 day of age with intestinal homogenates from chickens naturally suffering from this syndrome. The body weight of inoculated broilers was significantly (P less than 0.05) lower 1 week after inoculation than that of controls. The level of thyroxine in the serum of inoculated birds was lower (P less than 0.05) from day 6 through the remainder of the trial. The level of triiodothyronine of inoculated birds was depressed (P less than 0.05) on day 4, but 1 week later it returned to normal. The earliest phenomenon indicative of disturbance of thyroid function was the significant depression of 5'-deiodination in liver homogenates of inoculated broilers as early as day 2. It is concluded that thyroid function is one of the earliest targets of this syndrome.