Changes of the regional vascular bed in toes septic diseases of cattle

Determination of the level of pathological changes in the vascular bed of fibrous formations of acropods in septic diseases of the fingers in cattle. An adaptive mechanism that prevents hemostasis. The process of compensatory hypertrophy of blood vessels.

Рубрика Сельское, лесное хозяйство и землепользование
Вид статья
Язык английский
Дата добавления 26.12.2023
Размер файла 1,0 M

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Changes of the regional vascular bed in toes septic diseases of cattle

Enciu V.Z., PhD, DVS, professor

Technical University of Moldova

Hudz N.V., PhD, Senior Researcher

Institute of Veterinary Medicine of the NAAS

In the present work, the results of the research on the study of the anatomical, histological and morphopathological aspects of the blood vessels of the support and movement apparatus are presented, a study stimulated by the requirements of theoretical and practical veterinary medicine, for the correct and effective intervention in the cattle toes region.

It has been established that in hidden laminitis the horn of the hoog becomes visibly softer, yellow spots appear caused by the leakage of blood from the vessels into the solar dermis, especially at the white line. Arterioles, under the action of pathological processes that develop in the adjacent tissues, lose their muscle tone and then an acute parietal paresis occurs. In severe forms, there are obvious changes in the vessels walls accompanied by changes in their trajectory architectonics. Due to necrosis and deformations of the horn wall of the hoof and the third phalanx, the arteries flatten dorso-palmar (plantar), which causes a major infiltration of the adjacent tissues, worsening of lameness, increased morbidity, decrease or complete cessation of animal productivity.

Keywords: cow's toes, horn wall, arterial vessels, regional hemorrhage, infiltration, necrosis.

Зміни регіонарного судинного русла при септичних захворюваннях пальців великої рогатої худоби

Єнчу В.З., Гудзь Н.В.

Вступ

Вивчення негативних наслідків акроподіальних хвороб особливо важливе, оскільки вони знижують ефективність ферм та інвестицій у галузі виробництва коров 'ячого молока. Знання джерел васкуляризації, розподілу та анастомозів у м 'яких утвореннях пальців стопи великої рогатої худоби відіграє надзвичайно важливу роль не тільки в умовах нормального функціонування опорно-рухового апарату, а й за різних його захворювань на рівні акроподій. Таким чином, детальне знання всіх морфофункціональних аспектів акроподіального судинного русла може значною мірою сприяти вибору та застосування відповідного та ефективного лікування.

Мета роботи. Встановити на макро- і мікроскопічних анатомічних розтинах, за фарбування реактивом Шиффа і рентгенограмах, рівень патологічних змін судинного русла фіброзних утворень акроподів при септичних захворюваннях цієї ділянки у великої рогатої худоби.

Матеріали і методи досліджень. Матеріалом для досліджень були грудні та тазові кінцівки великої рогатої худоби з захворюваннями на різних стадіях розвитку. Проводили дисекцію артерій, на макро-мікроскопічному рівні застосовували бінокулярну лупу після тотального забарвлення окістя та суглобових капсул реактивом Шиффа. Гістологічні зразки фарбували гематоксилін-еозином. У чотирьох аутоподіях з різним ступенем тяжкості в артеріальні судини вводили суміш фарб, що містять свинець і барій, і піддавали рентгенологічному дослідженню.

Результати досліджень та їх обговорення. На препаратах у легкій стадії захворювання встановлено, що артеріальна система поширюється у вигляді мереж та «очей» полігонального виду, що мають з обох боків периферично розташовані відгалуження.

Артеріоли 3-5 порядку на початковому етапі запалення реагують розширенням судинних стінок. У вогнищах захворювання спостерігається характерна картина гострого серозного запалення. Дерма та гіподерма стають набряковими, інфільтруються форменими елементами крові. Відзначаються зміни гістоструктури стінок артерій на рівні окістя і капсули, що проявляються набряком і появою чергування ширших і вужчих ділянок, що свідчить про вегетосудинну дистонію.

На середніх стадіях розвитку септичних захворювань реакція судин стає більш вираженою. Прихований ламініт розвивається у вигляді повільного безперервного процесу в залежності від кількості та тривалості інсультів. Ріг стає помітно м 'якшим, з 'являються жовті плями, викликані просочуванням крові з судин у дерму стопи. Геморагічні петехії також можна побачити на різних ділянках підошви, особливо білої лінії.

Про адаптаційний механізм, що перешкоджає гемостазу, свідчать звужений просвіт судин, відносно товста стінка дрібних артерій і наявність оболонки з еластичних волокон. Виразно видно процес компенсаторної гіпертрофії судин, залучених до запального процесу.

Тяжкі форми акроподіальних порушень супроводжуються не тільки вираженими змінами стінок судин, але і зміною архітектури їх траєкторії. Через некроз і деформацію рогової стінки копитець і третьої фаланги, артерії сплющуються дорсо-пальмарним шляхом, що викликає виражену інфільтрацію прилеглих тканин, посилення кульгавості, підвищення хворобливості, зниження або повне скорочення продуктивності тварин.

Висновки та перспективи подальших досліджень. Артеріальна кровоносна система акроподію розподілена у вигляді полігональних мереж та «осередків» з периферично розташованими відгалуженнями з боків.

Патологічні зміни судинного русла проявляються гіперплазією, гіперемією, деструкцією та некрозом термінальних артеріальних судин. Важкі форми акроподіальних порушень супроводжуються як вираженими змінами стінок судин, а й зміною архітектури їх траєкторії.

Ключові слова: пальці корови, стінка рога, артеріальні судини, регіонарні крововиливи, інфільтрати, некрози.

Introduction

The study of the negative effects produced by acropodial diseases is particularly important, because they reduce th e efficacy of farms and investments in the field of cow milk production [1, 2].

Cattle with moderate limb injuries stay 14-16 hours a day in recumbency, compared to healthy ones that stay only 11 -12 hours. By this they reduce the time reserved for the food consumption and inevitably the amount of matter they would transform into milk [3] or meat. Prolongation of estrus, decrease in breeding performance and deterioration of maintenance state are noted [4]. The lameness costs for milk producers in Great Britain, according to research in Liverpool, reach the imposing figure of 30 million. pounds [5].

The authors Spinu M. [6] provide data on the fact that mild forms of foot diseases decrease milk productivity by 5-10%, and severe forms - up to 30%. In cows at the peak of lactation, milk losses can reach up to 50%, and the expenses on a dairy farm with a herd of 1,100 cows due to acropodial diseases were 19,868 rubles per year, i.e. 490.0 rubles, on average, per sick cow.

Knowing the vascularization sources, distribution and anastomoses in the cattle toes soft formations plays an extremely important role not only in the conditions of the normal functioning of the support and movement apparatus, but also in its various diseases at the level of the acropodias [2, 7]. Therefore, detailed knowledge of all the morphofunctional aspects of the acropodial vascular bed can greatly contribute to the choice and application of an appropriate and effective treatment [1, 7-10].

The goal of the work. To establish, by macro- and microscopic anatomical dissections, by staining with the Shiff reagent and radiographs, the level of pathological changes in the vascular bed of the fibrous formations of the acropods in septic diseases of this region in cattle.

Materials and methods

The thoracic and pelvic acropods of cattle with acropodial diseases in different stages of development served as research material. The classic dissection method of the arteries up to the visible ramifications was used, and at the macro-microscopic level - under the control of the binocular magnifier (MBS-9) after the total staining of the periosteum and joint capsules with Schiffs reagent. Histological samples were stained with hematoxylin -eosin. In four autopodia, with different degrees of severity, the arterial vessels were injected with a mixture of paints containing lead and barium and subjected to X-ray examination.

Results of research and discussion

On the samples stained with the Schiff reagent and radiological cliches, in the mild stage of the disease it was found that the arterial system is distributed in the form of networks and "eyes" with a polygonal appearance, having peripherally arranged branches on the sides. Arterioles and capillaries create a diffuse picture, similar to a shadow, due to the density of the branches. Intermagistral anastomoses stand out less (Fig. 1, 2).

Fig. 1. The tiered distribution of the vascular network in the superficial layer of the periosteum of the first phalanx diaphysis: 1 - nerves; 2 - arteries; 3 - veins. Cow, age 5 years. Schiff reagent staining, x32.

Fig. 2. Vasculo-nervous plexus in the periosteum of the distal phalanx - the adventitial layer. Bull, 2 years old. Fully prepared. Schiff reagent staining, x32.

vascular bed septic cattle

Arterioles of order 3-5, at the initial stage of inflammation, react by dilating the vascular walls. In the foci of the disease, a characteristic picture of acute serous inflammation is observed. The dermis and hypodermis become edematous, infiltrated with the formed elements of blood. There are changes in the histostructure of the arterial walls at the level of the periosteum and the capsules, manifested by edema and the appearance of an alternation between wider and narrower portions, which informs us of a vascular dystonia. Congestion can be seen in the coronary arteries (Fig. 3).

F Fig. 3. The acute phase of laminitis with hemorrhagic areas on the solar face. Vascular congestion occurs at this level: 1 - vascular congestion; 2 - coronary edema; 3 -discoloration of the horn wall; 4 - sole hemorrhage; 5 - capillary bed; 6 - venules; 7 - arterioles; 8 - arterio-venous anastomosis.

Fig. 4. Various signs of vascular insult. The distal phalanx moves vertically, causing the spread of vascular congestion. 1 - vascular congestion; 2 - the beginning of the distal phalanx separation; 3 - white line of hoof; 4 - sole ulcer; 5 - discoloration of the horn wall; 6 - sole hemorrhage; 7 - double sole; 8 - capillary bed; 9 - venules; 10 - arterioles; 11 - arterio-venous anastomosis.

In the middle stages of the septic diseases development, in cattle acropodia, the reaction of the vessels becomes more obvious. Hidden laminitis develops in a slow, continuous process, depending on the number and duration of insults. The horn becomes visibly softer, yellow spots appear caused by blood leaking from the vessels into the solar dermis. Hemorrhagic petechiae can also be seen in various sole areas, especially at the white line. Arterioles, under the action of pathological processes that develop in the adjacent tissues, lose their muscle tone and then an acute parietal paresis occurs. As a result, it is observed that the inflammatory hyperemia of the vessels recorded in the initial period of the disease is replaced by the reaction of the muscular wall of the arteries and arterioles (Fig. 4).

It should be mentioned that the adaptation mechanism preventing hemostasis is well developed. This is demonstrated by the narrowed lumen, the relatively thick wall of the small arteries and the presence of an elastic fiber casing. A process of compensatory hypertrophy of the blood vessels involved in the inflammatory process is clearly visible on the histological samples. A narrowing of the vascular lumen is highlighted, until its closure. This happens due to hypertrophy of the muscular elements of the vascular walls. In parallel with these changes, the architecture of arterioles and their histostructure change. In vessels 80-120 mk in diameter, parietal thrombi are detected. When vessel obliteration occurs, thrombosis becomes organised. At the level of tissues, injured by the inflammatory process, the presence of haema pigment and dense phagocytic infiltration are detected, which implies an active local defence process during the animal's life. (Fig. 5, 6).

Fig. 5. Interdigital dermatitis - podophilic tissue with oedema, conjunctival proliferation, polymorphonuclear infiltration. Cow, 4 years old. HE stain, x250.

Fig. 6. Blood stasis, necrosis, local neutrophilic infiltration, podophil-keratophil congestion. Pelvic limb, cow, 4 years old. HE stain, x250.

Small arterioles become flexuous, with uneven narrowing of the lumen. The 5-7th order arteries, located at the level of the claw and heel, undergo a process of reduction, and as a result, deregulation of the terminal arterial arch of the hoof occurs. The muscular tunic of these vessels is hypertrophied and thickened. Perivascular sclerosis, hyperelastosis and thickening of the intima is detected. These changes are conditioned by the regional inflammatory process, its intensity and severity. Progression of the pathological process in cattle toes causes irreversible changes in the axial and soleus magistral arteries. In these vessels, on histological samples, sclerotic processes are highlighted, which cause arteries'obturation with a diameter of 150-250 pk and even larger. A large proportion of these vessels acquire a flexuous appearance, with a spindle-like trajectory. The anastomoses appear to be „amputated”, indicating that the microcirculatory process is severely disrupted (Fig. 7).

The transition from the healthy portion of the vessel to the stenotic and sclerotic portion is abrupt, obvious, with unregulated contours. Demonstrative in this regard are the branches in the axial digital arteries altered due to interdigital ficus, in which, at a distance of 1.5-2.0 cm after branching, the process of sclerosis is attested, the wall thickens and the terminations reduce. In two other cases strangulations of the magistral arteries with obvious flexures were observed. Terminal arterioles derived from the magistral arteries acquire a granular appearance and histologically appear as necrotic remnants of the arterioles.

Fig. 7. Sole curvature and transverse crevices appearance in chronic laminitis. Distal phalanx is bent towards the sole, separating from the sole wall. 1 - vascular congestion; 2 - separation of distal phalanx from keraphysis; 3 - transverse fissures; 4 - soleus ulcer; 5 - horn wall discoloration; 6 - double sole; 7 - capillary bed; 8 - venules; 9 - arterioles; 10 - arteriovenous anastomoses.

Severe forms of acropodial disorders are accompanied not only by obvious changes in the vessel walls, but also by changes in the architecture of their trajectory. Due to necrosis and deformities of the horn wall of the hoof and third phalanx, the arteries flatten dorso-palmar, which will cause major infiltration of adjacent tissues, worsening of lameness, increased morbidity, decreased or complete cessation of animal productivity.

Conclusions and prospect for further researches

Knowledge of the vascularization sources, vessel distribution and vascular bed architecture in fibrous formations of the acropodia in cattle is of great importance not only in the normal functioning of the support and movement apparatus but also in various diseases of the toes region. Thus, on the basis of the research carried out we can draw the following conclusions:

1. The arterial circulatory system of acropods is distributed in the form of polygonal networks and 'meshes' with peripherally arranged branches on the sides. They are massively involved in the pathological changes occurring in this region.

2. Pathological changes in the vascular bed are manifested by hyperplasia, hyperemia, destruction and necrosis of terminal arterial vessels. Severe forms of acropodial disorders are accompanied not only by obvious changes in the vessel walls, but also by changes in the architecture of their trajectory. Due to necrosis and deformations of the horn wall of the hoof and the third phalanx, the arteries flatten dorso-palmar (plantar), causing infiltration of adjacent tissues, worsening of lameness, increased morbidity, decreased or complete cessation of animal productivity.

3. We would like to draw the attention of practising veterinarians to the fact that in the treatment of acropodial diseases in cattle, the vascular factor should also be taken into consideration and given the relevant protection.

References

1. Enciu, V. (2013). Efectul economic in profilaxia afectiunilor acropodiale la taurine. In: Lucrari Stiintifice. UASM, Vol. 40 (Medicina Veterinara). Chisinau, p. 7-10.

2. Enciu, V., & Gangal, N. (2017). Managementulpododermatitelor. Cap. 12, p. 327-352. In: Ghidmedical veterinar. Patologie §i clinica bovina, sub red. prof. Holban D., Chisinau. 384p.

3. Dewes, H. (1978). Some aspects of lameness in dairy cattle. New Zealand Veterinary Journal. № 26. p. 147-148.

4. Gasca, D. (2009). Studiul anatomo-clinic al afectiunilor podale la bovine in diferite sisteme de crestere. 35 ani de invatamant superior medical veterinar din Republica Moldova: Simpozion stiintific international. (p. 216-221).Chisinau.

5. Trial shows routine foot trim increases lameness. (1999). Farmers Weekly. p.32.

6. Spinu et al. (2009). Dinamica vosstanovlenia neirotrofii koji posle obrabotki rany conecinostei jivotnim krioghennom [Dynamics of skin neurotrophy recovery after treatment of the extremities wound with animal cryogen]. §ШЩа agricola - Agricultural science, № 1. 53-57 [in Russian]

7. Enciu, V. (2014). Sistemul nervos §i microcirculajia sanguina a formajiunilor fibroase ale autopodiilor la bovine in norma §ipatologie. Chisinau: Centrul editorial al UASM. 219p.

8. Blowey, R., & Done, S. (1995). Failure to demonstrate histological changes of digital and interdigital dermatitis in biopsies of slurry heel. Veterinary Record. № 137. p. 379-380.

9. Enciu, V. (2008). Morphologhicescaia cartina nervnogo aparata palytev u corov pri porajeniah distalinogo otdela conecinostei. Vestnic. Naucino-teoreticeschii sbornic - Herald. Scientific-theoretical collection. №1 (21). Is. 1, p. 96-102.

10. Step, D., Smith, R. (2006). Nonrespiratory Diseases of Stocker Cattle. Vet. clinics of North America, Vol. 22, № 2. 425-429.

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