[Chronic bee paralysis virus - quo vadis? Incidence in Bavaria and consideration of therapeutic measures]. / Chronische-Bienenparalyse-Virus ­ quo vadis? Auftreten in Bayern und Betrachtung von Therapiemaßnahmen.

OBJECTIVE: Chronic bee paralysis virus (CBPV), a so far unclassified RNA virus that may cause neurological signs and hairless black syndrome in honey bees, has become increasingly prevalent in various European countries in recent years. The disease occasionally leads to immense losses of worker bees and a significant drop in performance, especially in strong colonies. The aim of this retrospective study was to analyse the spread of CBPV in Bavaria from 2018 to 2020 as well as to evaluate therapeutic measures. MATERIAL AND METHODS: In part 1 of the study, analysis results of the Tiergesundheitsdienst Bayern e. V. (Bavarian Animal Health Service) from 302 bee colonies were examined with regard to virus diagnostics and clinical signs with a focus on CBPV. In part 2, data collected with the help of a questionnaire regarding 105 CBPV-positive and symptomatic colonies were evaluated. RESULTS: In part 1, a significant (p = 0.004) increase in CBPV-positive samples from 2018 to 2020 was detected within Bavaria. In addition, the number of cases with clinical signs also increased during the last 2 years. Part 2 of the study showed a clustering of reports of initial onset of CBPV symptoms during springtime. The colonies mostly with a combination of symptoms recovered from the disease in 57 % of the cases. Therapeutic intervention was one decisive factor. A large number of different combinations of measures led to survival, and a lack of intervention mostly resulted in the death of the colony. In 62 % of the diseased and isolated colonies, isolation prevented further spread in the apiary. CONCLUSION UND CLINICAL RELEVANCE: Based on the results, CBPV occurred more frequently in connection with clinical signs in Bavaria in recent years. Due to the large number of applied combinations of measures, no evidence-based therapy recommendation may be derived based on the current evaluations. However, it has been shown that any therapeutic intervention is superior to withholding treatment. For precise therapy recommendations, trials with treatment under standard conditions are necessary.

Egg binding and hind limb paralysis in an African penguin--a case report.

This case report assesses the role acupuncture played in the rehabilitation therapy of an African penguin with bilateral hind limb paresis and paralysis following egg binding and a caesarean section. Egg binding is the failure of the oviduct to pass the egg down into the cloaca. In avian species the sciatic nerve runs through the middle of the kidney. Swelling of the kidney tissue due to the pressure exerted by the retained egg will cause pressure on the sciatic nerve which may lead to hind limb paresis/paralysis. Acupuncture was used to relieve any muscle, joint or nerve pain and to attempt to stimulate recovery of the sciatic nerve. Acupuncture was incorporated into a fairly intensive physical rehabilitation programme to help the penguin to walk again so that it could be re-introduced back into the sanctuary's captive colony.

A tale of two foxes--case reports: 1. Radial nerve paralysis treated with acupuncture in a wild fox. 2. Acupuncture in a fox with aggressive and obsessive behaviour.

Case 1. This is believed to be the first report of acupuncture treatment for traumatic radial nerve paralysis in a wild fox. From the first treatment, improvement in the range of mobility and sensation of the limb was evident. Additionally, the attitude of this wild animal changed from fear and aggression to complete cooperation: he lay peacefully during every treatment in a calm, drowsy state. Case 2. This reports the calming effects of acupuncture on a fox which had been showing aggressive behaviour and obsessive circling following toxoplasma infection.

Selenium elimination in pigs after an outbreak of selenium toxicosis.

In May 1996, 150 grower pigs in 5 California counties were exposed to selenium-contaminated feed distributed by a single feed company. Feed samples from 20 herds had a mean selenium concentration of 121.7 ppm dry weight (range, 22.1-531 ppm). In San Luis Obispo County, 52 pigs in 24 herds were exposed to the feed, and 8 pigs died with signs of paralysis. Bilateral symmetrical poliomyelomalacia involving the ventral horns of the cervical and lumbar intumescence was evident on histologic examination of spinal cord from affected pigs. Of 44 surviving exposed pigs, 33 (75%) exhibited signs of selenosis, including anorexia, alopecia, and hoof lesions. Thirty-nine of 44 pigs (88.6%) had elevated (>1 ppm) blood selenium concentrations. Surviving exposed pigs were changed to a standard commercial ration containing approximately 0.5 ppm (dry weight) selenium. Blood selenium concentrations were determined weekly for 46 days following removal of the contaminated feed and were compared with values of 20 control pigs fed a standard commercial ration. Mean (+/-SD) blood selenium concentrations of exposed pigs were 3.2 +/- 2.6 ppm at the initial sampling and 0.4 +/- 0.1 ppm after 46 days. Mean blood selenium concentrations of < or = 0.3 ppm for control pigs at all samplings were significantly lower (P < 0.001) than concentrations for exposed pigs. Muscle and liver samples of 22 of the 44 exposed pigs were collected at slaughter approximately 72 days after withdrawal of the selenium-contaminated feed. Muscle samples had a mean selenium concentration of 0.36 ppm (wet weight). Liver samples had a mean selenium concentration of 1.26 ppm (wet weight). One liver sample had a selenium value in the toxic range for pigs (3.3 ppm wet weight; reference range, 0.4-1.2 ppm). A 1-compartment pharmacokinetic model of selenium elimination in exposed pigs was generated, and the geometric mean blood selenium elimination half-life was estimated to be 12 days. The 60-day withdrawal time recommended by the Food Animal Residue Avoidance Database was considered sufficient to allow safe human consumption of tissues from exposed pigs.

Selenium toxicosis with focal symmetrical poliomyelomalacia in postweaning pigs in South Africa.

An outbreak of paralysis in finisher pigs in South Africa after ingestion of feed containing 54,581 mg/kg of selenium is described. The main and entirely consistent lesion was bilaterally symmetrical focal poliomalacia of the ventral horns of the spinal cord, which was most severe and consistent in the lumbar intumescence. Acute and subacute lesions were characterized by malacia with large numbers of gitter cells. The main features of chronic lesions were loss of neurons and gliosis. Focal degeneration and necrosis of the myocardium and skeletal muscles were also consistent, but there were fewer specific changes. Endothelial swelling, mild fibrinoid degeneration and perivascular leukocytic infiltration were present in the acute stage. Dermatitis, coronitis and hoof sloughing, usually present in more chronic cases of intoxication, were not a feature of the present outbreak, although alopecia and crusting were evident on the backs of a few pigs several weeks after the episode of intoxication. Serum-and tissue-selenium levels were elevated in the early stages after intoxication. Serum levels were nearly normal in chronic cases two months after the episode, while liver and kidney levels were still higher than normal. Higher levels were found in liver, kidney and serum than in muscle, with the highest levels in the kidney. Less than 20% of affected pigs recovered sufficiently to be marketed.

Selenium toxicosis in feeder pigs.

Selenium toxicosis was diagnosed in feeder pigs on a central Michigan farm. Use of a commercial supplement, found to contain approximately 20 times the intended Se concentration, resulted in a Se concentration of 8.1 mg/kg of the complete feed. This was fed for 34 days during which daily feed consumption decreased approximately 35%, several pigs developed weakness and forelimb paresis, and 1 pig died. The highest serum Se concentration measured was 1,550 ng/ml (normal range, 140 to 190 ng/ml). Normal feed consumption returned when an alternative feed was provided. Mean serum Se concentrations of representative pigs, monitored over the subsequent 26 days, decreased from 905 to 258 ng/ml. Histologic examination of a recovering pig revealed skeletal and cardiac myopathy and bilaterally symmetric malacia of the gray matter of the ventral horns of the spinal cord. During the developing toxicosis, the pigs consumed an estimated 11.4 mg of Se/pig/d.

Riboflavin requirement of turkey poults fed a corn-soybean meal diet from 1 to 21 days of age.

Two battery experiments involving a total of 816 Nicholas Large White turkey poults were conducted to determine the riboflavin requirement from 1 to 21 days of age. In Experiment 1, 480 poults were assigned to six dietary treatments: 0, .6, 1.1, 1.7, 3.1, and 4.4 mg supplemental riboflavin/kg basal diet. The corn-soybean meal basal diet was formulated to contain 28.5% crude protein. The vitamin premix was formulated to be devoid of riboflavin. The analyzed riboflavin content of the basal diet was 2.7 mg/kg feed. Ten replicates of eight birds per pen (four female and four male poults) were used per diet. In Experiment 2, 336 poults were assigned the same dietary treatments but with only seven replications. Using the broken line technique, it was determined that .79 +/- .03 mg supplemental riboflavin/kg diet or 3.5 mg riboflavin/kg diet was needed to maximize growth. However, in order to prevent leg paralysis, slightly more riboflavin appeared to be needed.

[A case of selenium poisoning in piglets]. / Een geval van seleniumvergiftiging bij biggen.

Acute paralysis was observed in suckling piglets and weaner piglets on a pig breeding farm. Pathomorphological investigations revealed characteristic lesions in the central nervous system. These lesions were indicative of selenium poisoning. This was verified by chemical-toxicological analysis of organs and tissues of the affected pigs. Poisoning was shown to have been caused by the feed: one feed preparation contained an extremely large amount of selenium, which was due to human failure.

Equine degenerative myeloencephalopathy: a vitamin E deficiency that may be familial.

Two horse farms, on which there was a high incidence of proven and suspected equine degenerative myeloencephalopathy (EDM), were studied. Symmetric ataxia and paresis, along with laryngeal adductor, cervicofacial, local cervical, and cutaneous trunci hyporeflexia, characterized the syndrome. Serum vitamin E concentration reflected a deficient state in affected and unaffected horses on both farms when compared with selected reference groups and with published values. A high incidence of the disease was evident in offspring of two particular sires on one farm. Vitamin E supplementation resulted in correction of the deficient state in most horses and was associated with a drastic reduction in the incidence of EDM on one farm from 40% to less than 10% the year following vitamin E supplementation. In addition, during the last year, the severity of signs in the few cases was dramatically reduced. This information substantiates the hypothesis that EDM is a vitamin E-responsive disorder of Equidae with a possible familial predisposition.

Incompatibility between lasalocid and chloramphenicol in broiler chicks after a long-term simultaneous administration.

Two growth experiments were conducted to evaluate in broiler chicks the compatibility between lasalocid medication in the feed (at 90 or 125 ppm) and a long-term administration of chloramphenicol either via the feed (500 ppm) or via the drinking water (500 mg/liter). The simultaneous administration of lasalocid and chloramphenicol generally caused severe growth depression, decreased feed intake and impaired feed conversion. Several chicks showed evident symptoms of intoxication, such as ataxia, leg weakness and paralysis. The development and frequency of these symptoms were dependent on the dosage of lasalocid and on the duration of the simultaneous administration. Biochemical examinations (Experiment 2) revealed in the affected chicks significant changes in several parameters, in particular a markedly increased activity of creatine kinase and GOT in the plasma. It confirmed that the observed leg weakness and paralysis were caused by myodegeneration.

Selenium toxicosis in swine.

Selenium toxicosis was diagnosed as the cause of fatal paralytic disease in a group of feeder pigs. Lumbar poliomyelomalacia and coronary band necrosis were the principal lesions. High selenium concentrations were detected in liver and kidney. Excessive selenium was traced to the premix added to the complete ration.

Paralysis in swine due to focal symmetrical poliomalacia: possible selenium toxicosis.

A paralytic disease in swine was observed on three farms located in the same geographical area of Georgia. Postmortem examinations revealed the paralysis to be related to spinal poliomalacia. Feed collected from two of the affected farms was used in a feeding study, and the paralytic condition was reproduced. In pigs from both the feeding trial and field cases, the poliomyelomalacia was characterized by focal, symmetrical lesions located in the cervical and lumbar intumescences. Selenium was detected in the feed at levels ranging from 19 to 24 ppm.

Suspected vitamin E-selenium deficiency in two ostriches.

Paresis of the limbs of two 4-month-old ostriches fed a diet predominantly of crushed maize was investigated. Raised levels of serum aspartate transaminase and creatine kinase were demonstrated in both birds. The less severely affected ostrich recovered after a single intramuscular injection of a vitamin E-selenium preparation but the other died despite therapy. An autopsy of the latter revealed focal pale areas in the thigh muscle. Microscopically affected muscle fibres showed degeneration, necrosis and regenerative changes. Fibrinoid degeneration and necrosis of some arterioles was observed as well as varying degrees of interstitial fibrosis. The above findings suggest a diagnosis of vitamin E-selenium deficiency.

Efficacy of different phosphorus supplements for sows during gestation and lactation.

PIP: This study was undertaken to compare dicalcium, Curacao, and soft ph sophates as supplemental feeding during gestation and lactation. In Exp eriment 1, 37 crossbred sows at 11 months of age were mated and each of 4 groups given an experimental diet. The basal diet was a 16% crude pro tein-fortified corn-soybean meal containing .34% of phosphorus and .72% of calcium. The test diets were fortified with either dicalcium, Curaca o, or soft phosphate to provide .52% of phosphorus. Limestone was given to maintain .72% of calcium. Animals were confined in a concrete feedin g area and fed 1.8 kg of diet per head per day until Day 94 of gestation . At that time the diet was increased to 2.3 kg/day. On Day 109 of gestation animals were moved to farrowing crates until 10 days postpartu m and then to wooden units until weening at 8 weeks. Sows were sacrific ed after 8 weeks lactation, or if they developed posterior paralysis. In this experiment, the different phosphate sources were without observed influence on the livability or performance of pigs up to 8 weeks of age (p less than .05). Gilts receiving no supplemental phosphorus had significantly lower bone ash and phosphorus than did those receiving either of the supplements. Posterior paralysis was observed in 5 of 9 sows fed the unsupplemented diet, in 3 of 9 fed the soft supplemented diet, and in 2 of 10 fed the Curacao phosphate supplement. None fed dicalcium phosphate developed paralysis. The paralysis usually occurred after 6 weeks of lactation and was often accompanied by a fractured femur. In Experiment 2, 70 sows were bred at 10 months of age and fed 1.8 kg of the experimental diets. During 36 days of lactation, phosphorus digestibility, retention, and balance were shown to be lower for those fed only the basal diet. Bone ash, bone phosphorus, and bone strength were lower in those fed the unsupplemented diet. Results of these studies indicate the need for supplemental phosphorus in sow feeding. When feeding dicalcium phosphate or Curacao phosphate the use of over .5% phosphorus in the sow's diet is unnecessary during gestation and lactation.^ieng