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Mein Pferd ist an Hufrehe erkrankt und wie kann ich ihm jetzt helfen ???
 
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Kohlenhydratassoziierte Hufrehe (Gelesen: 4390 mal)
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Beiträge: 1902

Langelsheim, Niedersachsen, Germany
Zeige den Link zu diesem Beitrag Kohlenhydratassoziierte Hufrehe
29. Mai 2006 um 20:21
 
„Kohlenhydratassoziierte Hufrehe als 
extraintestinale Erkrankung caecaler Genese“

PD Dr. Annette Zeyner, Institut für Tierernährung, Ernährungsschäden und Diätetik, Veterinärmedizinische Fakultät, Universität Leipzig

Den experimentellen Beweis für den Zusammenhang zwischen Kohlenhydratüberfütterung, caecaler Acidose und akuter Hufrehe erbrachten Garner et al. (1975) bzw. Pollitt und van Eps (2002) nach Zwangsfütterung von 15 g Maisstärke bzw. 7,5 g Fructan (Raftilose) pro Kilogramm Lebendmasse (LM). French und Pollit (2004) zeigten, dass die einmalige orale Verabfolgung von 7,5, 10 und 12 g Oligofructose (OF) pro Kilogramm LM an Pferde innerhalb von 48 Stunden zur akuten Hufrehe führt. Die Untersuchung der Hufwand nach Euthanasie verwies auf einen OF-Dosis-abhängigen Verlust lamellärer Hemidesmosomen in den epidermalen Sekundärlamellen. Ohne die akkurate Anordnung der Hemidesmosomen kommt es zur Adhäsionstrennung zwischen Lamina densa der Basalmembran und den epidermalen Basalzellen. In dieser Studie nahmen die rehetypischen ultrastrukturellen Veränderungen im Schweregrad ebenfalls in Abhängigkeit von der OF-Dosis zu. Moore et al. (2004), Budras und König (2005) sowie Mülling und Budras (2005) äußerten sich zusammenfassend über Strukturen caecaler Genese, welche nach erleichterter Translokation durch eine inkompetente Darmschranke (Weiss et al. 1998) über vasokon-striktorische oder toxische Effekte, auch über die Aktivierung digitaler Metalloproteinasen, zur Auslösung einer akuten Hufehe führen können. So ist bezüglich der Mikroflora die fortgeschrittene Dickdarmacidose beim Pferd durch den weitgehenden Zelltod Gram-negativer Bakterien und die Zunahme Gram-positiver Keime charakterisiert, wobei Streptococcus bovis zu dominieren scheint. Pathognomotisch sind pyrogenes Exotoxin B von Streptococcus bovis, Endotoxine sowie vasoaktive Substanzen wie bestimmte biogene Amine caecaler Genese von Interesse. Im Dickdarm werden diese durch Dekarboxylierung von Aminosäuren durch Gram-positive Bakterien (Laktobacillen, Streptokokken) freigesetzt (Bailey et al. 2004), wobei bereits bei klinisch unauffälligen Pferden allein Gras- gegenüber Heufütterung die Konzentration bestimmter biogener Amine im Caecuminhalt erhöht (Bailey et al. 2003). Insgesamt stellt sich die sog. Fütterungsrehe als multifaktorielles, äußerst komplexes Geschehen dar, dessen Verständnis sich noch in weiten Teilen entzieht. 
 

Literatur

Baily SR, Marr CM, Elliott J (2003): Identification and quantification of amines in the equine caecum. Res vet Sci 74, 113-118.
Bailey SR, Menzies-Gow NJ, Marr MC, Elliott J (2004): The effects of vasoactive amines found in the equine hindgut on digital blood flow in the normal horse. Equine Vet J 36, 267-272.
Budras KD, König H (2005): Pathogenese und Ätiologie der Hufrehe. Pferdeheilkd 21, 344-345.
French KR, Pollit CC (2004): Equine laminitis: loss of hemidesmosomes in hoof secondary epidermal lamellae correlates to dose in an oligofructose induced model: an ultrastructural study. Equine Vet J 36, 230-235.
Garner HE, Coffman JR, Hahn AW, Hutcheson DP, Tumbleson ME (1975): Equine laminitis of alimentary origin: an experimental model. Am J Vet Sci 30, 441-444. 
Moore RM, Eades SC, Stokes AM (2004): Evidence for vascular and enzymatic events in the pathophysiology of acute laminitis: which pathway is responsible for initiation of this process in horses? Equine Vet J 36, 204-209.
Mülling C, Budras K-D (2005): Hufrehe – Prospektive auf der Basis des gegenwärtigen Forschungsstandes. Pferdeheilkd 21, 347-348.
Pollitt CC, van Eps AW (2002): Equine laminitis: A new induction model based on alimentary overload with fructan. Proc Australian Equine Vet Assoc. Bain-Fallon Memorial Lectures.
Weiss DJ, Evanson OA, MacLeay J, Brown DR (1998): Transient alteration in intestinal permeability to technitium Tc99m diethylenetriaminopentaacetate during the proximal stages of alimentary laminitis in ponies. Am J Vet Res 59, 1431-1434.


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Zeige den Link zu diesem Beitrag Re: Kohlenhydratassoziierte Hufrehe
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Zeige den Link zu diesem Beitrag Re: Kohlenhydratassoziierte Hufrehe
Antwort #2 - 24. März 2008 um 21:04
 
Equine Vet J. 2007 Jul ;39 (4):360-4 17722730 (P,S,E,B)
Equine laminitis: ultrastructural lesions detected 24-30 hours after induction with oligofructose.

A R Nourian, G I Baldwin, A W van Eps, C C Pollitt

REASONS FOR PERFORMING STUDY: The pathology of equine laminitis has been well-documented 48 h after dosing with oligofructose when clinical lameness and lamellar disintegration is well advanced. Further analysis of the earliest lesions, by collecting lamellar samples at the first sign of foot lameness after oligofructose dosing is required in order to increase understanding of the disease.
OBJECTIVES: To investigate lamellar epidermal hemidesmosome damage and basement membrane dysadhesion by transmission electron microscopy (TEM).
METHODS: Eight clinically normal, mature Standardbred horses were divided randomly into 2 groups of 4. The treatment group were dosed with
oligofructose (10 g/kg bwt)
and subjected to euthanasia when shifting weight from one foot to other commenced and at the first sign of lameness during walking and turning. This occurred at 24 h in 3 horses and 30 h in one. The sham treatment control group were dosed with water and subjected to euthanasia after 48 h. Lamellar tissues of the front feet were harvested and processed for ultrastructural study using TEM. RESULTS: Examination by TEM showed excessive waviness of the basement membrane zone and pointed tips of some secondary epidermal lamellae, an ultrastructural lesion typical of laminitis. The average number of hemidesmosomes/microm of basement membrane was decreased and their distance from the centre of the lamina densa of the basement membrane was increased.
CONCLUSIONS: Laminitis lesions are detectable 24 h after oligofructose administration.
POTENTIAL RELEVANCE: Hindgut events occurring in the first 24 h after dosing have begun the destruction of the hoof lamellar interface. Prevention and treatment strategies should precede lameness if they are to be efficacious.
http://lib.bioinfo.pl/pmid:17722730


Equine Vet J. 2006 May ;38 (3):203-8 16706272 (P,S,E,B)
Equine laminitis induced with oligofructose.

A W van Eps, C C Pollitt
Australian Equine Laminitis Research Unit, School of Veterinary Science, Faculty of Natural Resources, Agriculture and Veterinary Science, The University of Queensland, Brisbane, Queensland 4072, Australia.
REASONS FOR PERFORMING STUDY: Experimental induction of equine laminitis with a reliable and clinically relevant model should facilitate understanding of the disease. Successful induction with oligofructose (OF) could link pasture consumption to laminitis. OBJECTIVES: To determine whether alimentary administration of OF induces laminitis.
METHODS: Twelve horses were dosed with OF and 6 received a sham (placebo) treatment. Clinical observations were made and blood collected at 4 h intervals over a 48 h study period. Stained sections of the hoof wall lamellae, examined by light microscopy, were graded for laminitis severity.
RESULTS: All horses administered OF, but no sham-treated controls, developed clinical and histological laminitis.
CONCLUSIONS AND POTENTIAL RELEVANCE: Alimentary overload with OF is a valid induction model for studying the pathogenesis of laminitis. A link is therefore established between field cases of laminitis and pasture fructan content.


Environ Microbiol. 2006 May ;8 (5):885-98 16623745 (P,S,E,B,D)
Changes in equine hindgut bacterial populations during oligofructose-induced laminitis.

G J Milinovich, D J Trott, P C Burrell, A W van Eps, M B Thoefner, L L Blackall, R A M Al Jassim, J M Morton, C C Pollitt

Australian Equine Laminitis Research Unit, School of Veterinary Science, The University of Queensland, Queensland, Australia.

Summary
In the horse, carbohydrate overload is thought to play an integral role in the onset of laminitis by drastically altering the profile of bacterial populations in the hindgut. The objectives of this study were to develop and validate microbial ecology methods to monitor changes in bacterial populations throughout the course of experimentally induced laminitis and to identify the predominant oligofructose-utilizing organisms. Laminitis was induced in five horses by administration of oligofructose. Faecal specimens were collected at 8 h intervals from 72 h before to 72 h after the administration of oligofructose. Hindgut microbiota able to utilize oligofructose were enumerated throughout the course of the experiment using habitat-simulating medium. Isolates were collected and representatives identified by 16S rRNA gene sequencing. The majority of these isolates collected belonged to the genus Streptococcus, 91% of which were identified as being most closely related to Streptococcus infantarius ssp. coli. Furthermore, S. infantarius ssp. coli was the predominant oligofructose-utilizing organism isolated before the onset of lameness. Fluorescence in situ hybridization probes developed to specifically target the isolated Streptococcus spp. demonstrated marked population increases between 8 and 16 h post oligofructose administration. This was followed by a rapid population decline which corresponded with a sharp decline in faecal pH and subsequently lameness at 24-32 h post oligofructose administration. This research suggests that streptococci within the Streptococcus bovis/equinus complex may be involved in the series of events which precede the onset of laminitis in the horse.


J Dairy Sci. 2005 Aug ;88 (8):2774-82 16027191 (P,S,E,B)
Histopathology of oligofructose-induced acute laminitis in heifers.

M B Thoefner, O Wattle, C C Pollitt, K R French, S S Nielsen

Department of Large Animal Sciences, The Royal Veterinary and Agricultural University of Copenhagen, DK-1870 Frederiksberg, Denmark. mbt@kvl.dk

Histopathology of the dermo-epidermal junction in the lamellar region of front claws was examined in 6 dairy heifers given an alimentary oligofructose overload and compared with sections from a control group of 6 heifers. Four of the 6 heifers administered oligofructose developed clinical signs of acute laminitis before they were euthanized. Postmortem samples from front claws were processed for histology. Eleven histopathologic characteristics were selected from the existing literature and used in a blinded evaluation of sections. In total, 104 front claw samples, including 8 samples from 2 cows having spontaneously occurring acute laminitis, were evaluated histologically using hematoxylin and eosin as well as periodic acid-Schiff staining. The major morphological features associated with oligofructose-induced acute clinical laminitis were stretching of lamellae, dermal edema, hemorrhage, changes in basal cell morphology, presence of white blood cells in dermis, and signs of basement membrane detachment. Changes at the lamellar junction of claw tissue affected by oligofructose-induced clinical laminitis resembled tissue from the 2 cows suffering from spontaneous acute clinical laminitis, and generally were consistent with existing descriptions of laminitis histopathology. Important exceptions to existing descriptions in the literature were stretching of lamellae and basement membrane changes. Not previously described, we considered these early signs of acute laminitis. In conclusion, this study documents that oligofructose-induced clinical laminitis is associated with histopathological changes at the lamellar interface. A weakened dermo-epidermal junction is a possible intermediate stage in the pathophysiology of bovine sole ulceration at the typical site.



Asia Pac J Clin Nutr. 2005 ;14 Suppl :S62 16326531 (P,S,E,B)
Glucose uptake in the equine hoof.

K E Asplin, B A Bevan, C M McGowan, C C Pollitt, M N Sillence

School of Veterinary Science, University of Queensland, St Lucia, QLD 4072.

Background - Laminitis is a crippling and potentially fatal condition of the equine hoof, associated with many causes, including carbohydrate overload, overfeeding, dietary oligofructans, metabolic syndrome, and Cushing's Syndrome. The mechanism of laminitis is unknown, but could be associated with impaired glucose uptake into the hoof.
Objectives - To characterise the physiological regulation of glucose transport in normal equine lamellae.
Design - Equine lamellar explants were incubated for up to 48 h in a cell culture medium. Glucose uptake was measured using 2-deoxy-D-[2,6-(3)H] glucose. Separation force was determined by tension testing. beta-Adrenoceptors were measured by radioligand binding using [(3)H]-CGP-12177.
Outcomes - Lamellar explants incubated in the presence of glucose remained intact at forces of up to 916 g, whereas without glucose, explants became separated from the hoof wall at 416 +/- 36 g. Insulin (300muU/mL) had no effect on glucose uptake, but Isoprenaline (40 nM) reduced glucose uptake to 60% of basal levels after 24 h and 48 h. Explants contained 90 +/- 2.6% beta(2)-adrenoceptors and 10 +/- 2.6% beta(1)-adrenoceptors.
Conclusion - Healthy lamellar tissue is dependent on glucose for structural integrity. Glucose uptake is impaired by catecholamines, which are associated with various stress conditions that can cause laminitis. Therefore, the data presented are consistent with the hypothesis that glucose uptake plays a role in certain types of laminitis.
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