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Botulismus bei einer Golden-Retriever-Hündin: Ein Fallbericht
Abstract
Zusammenfassung
Gegenstand und Ziel: Beschreibung einer Intoxikation mit Clostridium botulinum. Material und Methode: Fallbericht einer fünfjährigen Golden-Retriever-Hündin. Die Diagnose erfolgte durch den Toxinnachweis in verendeten Hähnchenkadavern, an denen das Tier geleckt hatte. Ergebnisse: Die Hündin entwickelte innerhalb von 24 Stunden eine schlaffe Tetraplegie, die nach drei Tagen unter symptomatischer Therapie eine beginnende Reversibilität zeigte. Schlussfolgerung: Botulismus sollte beim Hund differenzialdiagnostisch bei einer progressiven Nachhandschwäche, aszendierend bis zur Tetraplegie berücksichtigt werden. Klinische Relevanz: Neben der Fallbeschreibung wird eine Übersicht über Pathogenese und Klinik gegeben und die aktuellen diagnostischen und therapeutischen Möglichkeiten aufgezeigt.
... GİRİŞ otulismus, nöro toksin (A, B, Cα, Cβ, D, E, F ve G) üreten Clostridium botulinium tarafından oluşturulan (1,2) ve botulismus toksini içeren gıda, içme suyu ya da kadavraların tarafından kontamine edilen yemlerin alınması sonucunda, tüm memeliler, kuşlar ve balıkların etkilendiği bir intoksikasyondur (3)(4)(5). Sığırlarda genellikle Tip C ve D, ender olarak da Tip B toksinlerinin alınmasıyla toksikasyon oluşmaktadır (5)(6)(7)(8). İçerisinde toksin oluşmuş tavuk artıklarının yem olarak kullanılmasının da bir enfeksiyon kaynağı olabileceği bildirilmiştir (8). ...
... GİRİŞ otulismus, nöro toksin (A, B, Cα, Cβ, D, E, F ve G) üreten Clostridium botulinium tarafından oluşturulan (1,2) ve botulismus toksini içeren gıda, içme suyu ya da kadavraların tarafından kontamine edilen yemlerin alınması sonucunda, tüm memeliler, kuşlar ve balıkların etkilendiği bir intoksikasyondur (3)(4)(5). Sığırlarda genellikle Tip C ve D, ender olarak da Tip B toksinlerinin alınmasıyla toksikasyon oluşmaktadır (5)(6)(7)(8). İçerisinde toksin oluşmuş tavuk artıklarının yem olarak kullanılmasının da bir enfeksiyon kaynağı olabileceği bildirilmiştir (8). ...
... GİRİŞ otulismus, nöro toksin (A, B, Cα, Cβ, D, E, F ve G) üreten Clostridium botulinium tarafından oluşturulan (1,2) ve botulismus toksini içeren gıda, içme suyu ya da kadavraların tarafından kontamine edilen yemlerin alınması sonucunda, tüm memeliler, kuşlar ve balıkların etkilendiği bir intoksikasyondur (3)(4)(5). Sığırlarda genellikle Tip C ve D, ender olarak da Tip B toksinlerinin alınmasıyla toksikasyon oluşmaktadır (5)(6)(7)(8). İçerisinde toksin oluşmuş tavuk artıklarının yem olarak kullanılmasının da bir enfeksiyon kaynağı olabileceği bildirilmiştir (8). ...
... GİRİŞ otulismus, nöro toksin (A, B, Cα, Cβ, D, E, F ve G) üreten Clostridium botulinium tarafından oluşturulan (1,2) ve botulismus toksini içeren gıda, içme suyu ya da kadavraların tarafından kontamine edilen yemlerin alınması sonucunda, tüm memeliler, kuşlar ve balıkların etkilendiği bir intoksikasyondur (3)(4)(5). Sığırlarda genellikle Tip C ve D, ender olarak da Tip B toksinlerinin alınmasıyla toksikasyon oluşmaktadır (5)(6)(7)(8). İçerisinde toksin oluşmuş tavuk artıklarının yem olarak kullanılmasının da bir enfeksiyon kaynağı olabileceği bildirilmiştir (8). ...
Bu raporda Bolu yoresindeki bir sigir surusunde tespit edilen Botulismus vakalarinda klinik, hematolojik ve biyokimyasal degisikliklerin belirlenmesi amaclanmistir. Bu amacla calismanin materyalini salgin sonucunda sag kalan 10 sigir olusturdu ve bu sigirlarin klinik, hematolojik ve biyokimyasal muayeneleri yapildi. Anamnezde yetersiz mera kosullari nedeni ile tavuk gubresi ve tavuk lesleri ile kontamine olmus arazide otlayan sigirlarda 3 gun sonra ilk semptomlarin ortaya ciktigi belirlendi. Klinik semptom olarak; sallantili yuruyus, kas tremoru, dilin disari cikmasi, kuyrukta paraliz, costo-sternal yatma, on ve arka bacaklarda paraliz belirlendi. Hematolojik muayenede butun parametrelerin referans degerler arasinda oldugu tespit edildi. Biyokimyasal incelemelerde serum kolesterol ve aspartat aminotransferaz (AST) degerleri yuksek bulunurken bakir (Cu), demir (Fe), fosfor (P), mangan (Mn) ve selenyum (Se) degerlerinin referans degerlerden dusuk oldugu saptandi. Klinik olarak Botulismus tanisi konulan sigirlarda hematolojik parametrelerde degisiklik olmadigi belirlendi. Botulismustan korunmak ve kontrol etmek icin; toksin kaynaginin engellenmesi ve yok edilmesi, mera islahi, mineral takviyesi ve kadavralarin uygun sekilde yok edilmesi ile asilama gibi tedbirlerin uygulanmasi gerektigi kanisina varildi.
Obwohl Frettchen (Mustela putorius furo) ursprünglich Europäer sind, bringen sie mit ihrer quirligen und lustigen Art etwas Exotik in die heimischen Wohnzimmer. Bei aller Ähnlichkeit zu Hund und Katze sollte man dennoch nicht vergessen, dass Frettchen Tiere mit spezifischen Ansprüchen sind, die Tierbesitzer und Tierärzte vor Herausforderungen stellen. Aufklärung, Beratung und Prävention sind demnach insbesondere in Bezug auf vermeidbare Erkrankungen durch Fütterungs- oder Haltungsfehler enorm wichtig.
Botulismus is an intoxication caused by the neurotoxin of Clostridium botulinum. Clinical signs are characterized by progressive, symmetric, generalized LMN (lower motor neuron) dysfunction. The severity of the illness depends on the amount of neurotoxin in the circulation and on the susceptibility of the animal. The incubation period may vary from a few hours to 6 days, and the course may last about 14-24 days. In case of recovery, muscle weakness dissolves in a descending way, starting from the muscle of the head, through the front legs, and the trunk to the hind legs. The diagnosis of botulismus can be based on the detection of the toxin in serum, faeces, vomitus or contaminated feed. The most widespread method is the toxin isolation and neutralization test performed in mice. In their 3 patients, ataxia beginning with the weakness of the hind legs occurred one day before hospitalization. The three foxterriers came from the same household, thus all the circumstances: nutrition, environment were the same. Flaccid tetraplegia developed within five hours after admission, following an ascending route, including the paralysis of the neck and head muscles, as well as the eyelids (Figure 1). Anamnesis and the results of the clinical examination arose the suspect of botulism, whilst no characteristic alterations of the blood count, blood chemistry and acid-base analysis were found (Table 1). Toxin isolation from the serum using mice inoculation toxin-neutralization test confirmed the diagnosis, and revealed Type C toxin. List of differentials included polyradiculoneuritis, tick paralysis, monensin toxicosis, and traumatic spinal cord lesions (Table 2). No antitoxin preparation was available to provide adequate serum therapy. Supportive treatment consisted of parenteral nutrition (Figure 2) and parenteral amoxicilline-clavulanic acid therapy to reduce any potential intestinal population of C botulinum. Besides placing a permanent urinary catheter to ensure urination, soft bedding was provided, and the animals were turned regularly to prevent haemostasis in the lungs. One dog died on the 4(th) and an other on the 8(th) hospitalization day, but the third one left the hospital in improving status due to intensive therapy on day 18(th).
A USDA Early Response Team investigated deaths of several horses and a mule in northern Arizona at the request of local animal health officials. Thirteen animals (12 horses and 1 mule) housed at 5 facilities in a 7.4 square mile area died between August 1998 and January 1999. Clinical signs consisted of muscular weakness that rapidly progressed to lateral recumbency. Ten animals had paresis of the tongue, throat, or lips. Affected animals appeared alert and were interested in eating and drinking, even while recumbent. All 13 animals were euthanatized. Clostridium botulinum type C was isolated from feces or intestinal contents from 3 affected horses. Preformed toxin was detected in samples of soil and bird droppings collected from a nearby horse burial site. It was hypothesized that the outbreak was a result of birds, presumably ravens, feeding at the burial site and at horse facilities in the area that transferred toxin to the affected animals.
Diffuse lower motor neuron dysfunction developed in a group of American Foxhounds while they were hunting. Of 19 dogs, 10 became weak and 9 became quadriplegic. Three of the quadriplegic dogs died before treatment could be instituted. The remaining quadriplegic dogs recovered after being given supportive treatment, with (4 dogs) or without (2 dogs) trivalent (types A, B, E) botulinal antitoxin. The 10 dogs that were weak recovered without treatment. A markedly decreased amplitude of evoked potentials and increased chronaxy were found by electromyographic examination of 2 of the quadriplegic dogs. A toxic substance that was neutralized by type C botulinal antitoxin in mouse inoculation tests was in the serum and feces of the most severly affected dog presented alive and in a fecal extract of another affected dog. In the one dog necropsied, neither gross nor histologic lesions were found in the central or peripheral nervous systems or in the skeletal musculature. The history, clinical signs, electromyographic findings, toxin neutralization tests in mice, and absence of histologic abnormalities in the neuromuscular system provided evidence for the diagnosis of C botulism.
In six dogs with botulism type C electrophysiological examinations showed: fibrillation potentials and prolonged insertional activity; low amplitude of the evoked muscle action potential; decrease in amplitude of the compound muscle action potential with slow repetitive stimulation; slowing of motor and sensory velocities in the peripheral nerve; and restoration of velocity and amplitude corresponding to clinical improvement. These findings indicate peripheral nerve dysfunction which cannot be explained adequately by current knowledge of the action of botulinum toxin on cholinergic nerve endings. It is therefore suggested that botulinum toxin also interferes with peripheral nerve conduction.
A diffuse lower motor neurone paralysis developed in a 6-month-old male Australian cattle dog pup 4 days after it had eaten the carcase of a rotting duck in Centennial Park, Sydney. Two other dogs which ate smaller portions of the same carcase were less severely affected. Clostridium botulinum type C was isolated from and C. botulinum type C toxin was detected in faeces from the severely affected dog. The serum contained 25 LD50 of toxin/ml. The high C. botulinum count and toxin level in the faeces declined progressively during the ensuing weeks, but 114 days after ingesting the carcase C. botulinum type C was still present in faeces and a low toxin titre persisted. Soil, mud and water samples in the area of the duck ponds in the park contained C. botulinum type C spores. Spores and high toxin titres were also found in the intestine of the carcases of 2 birds in the area.
Botulinum toxin is a presynaptically-acting polypeptide neurotoxin. The toxin causes an almost complete inhibition of evoked transmitter release from cholinergic nerve endings. Characteristics inhibition by the toxin of the quantal and nonquantal components of resting ACh output have also been described. In this context botulinum toxin has been a valuable probe of the transmitter release process. Under certain circumstances an effect of the toxin on ACh synthesis has also been found. A postulate has been advanced which could account for these multiple actions of botulinum toxin, and several tests of this nodel have been outlined. Regardless of the validity of the proposal, the avenues of pursuit which it suggests could lead to a firmer understanding of the mechanism of action of botulinum toxin and of the functioning of cholinergic nerve terminals.
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