logging in or signing up Acute Carbohydrates engorgement vetgreen Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 1079 Category: Education License: All Rights Reserved Like it (4) Dislike it (0) Added: December 04, 2009 This Presentation is Public Favorites: 0 Presentation Description It describe an important disease in ruminants which may results in many losses among cattle and other ruminants. Comments Posting comment... By: vetgreen (23 month(s) ago) Dear Naveen, Thank you for your letter concerning downloading my presentation of CHO engorgement in ruminants. I made it public for every one to download, if you find it difficult to have it please send me you email and I will send it to you as attachment, with my best wishes. I have more presentations in other website like DOCSTOCK and SCRIBD.COM. Dr. Ghalib. (Alaridi@yahoo.com) Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript Acute carbohydrates engorgement of ruminants : 4-Dec-09 Dr. Ghalib's Lectures. 1 Acute carbohydrates engorgement of ruminants Synonyms: Rumen overload Lactic acidosis Acute rumen impaction Acute grain overload Ruminal acidosis. It is an acute disease which characterized by indigestion, rumen stasis, dehydration, acidosis, toxemia, incoordination, collapse and frequently death. Slide 2: 4-Dec-09 Dr. Ghalib's Lectures. 2 Etiology: Any ruminant is susceptible to ruminal acidosis. It is most common in cattle that accidentally gain access to large amounts of highly soluble CHO such as finely ground grains e.g., wheat, barley and corn. Less common causes include apples, pears, potatoes & beets. The amount of feed which produce the disease depends on; Amount & type of grain and previous experience with the grain. The morbidity varies from 10-50%,& mortality rate is 90% in untreated cases and 30-40% in treated animals. Condition nutritional status of animal. The nature of microflora. Slide 3: 4-Dec-09 Dr. Ghalib's Lectures. 3 Pathogenesis: Within 2-6 hr of feeding on large amount of highly fermentable CHO particularly finely ground feeds, which increase the surface exposed to the fermentation bacteria, the microbial population in the rumen is changed with increase of gram-positive Streptococcus. bovis which utilizes the CHO to produce large quantities of lactic acid will decreases the pH to 5 or less, at this point the cellulolytic bacteria and protozoa are destroyed and replaced by lactobacilli and gram positive rods . VFA level is also increased & contributes to the fall of ruminal pH. The low pH allows the lactobacilli to utilize CHO to produce more excessive quantities of lactic acid . Slide 4: 4-Dec-09 Dr. Ghalib's Lectures. 4 Slide 5: 4-Dec-09 Dr. Ghalib's Lectures. 5 Excess D and L lactic acid causes rise in ruminal osmotic pressure which result in movements of excessive quantities of water and fluid from body tissues and blood into the rumen resulted in rumen distention, diarrhea, hemoconcentration and dehydration These conditions lead to hypovolemia, circulatory collapse, metabolic acidosis and death. The accumulation of VFAs produce rumen stasis. Finely ground CHO also decreases the amount of saliva secreted by the animal which lessens the amount of buffer flowing into the rumen. Slide 6: 4-Dec-09 Dr. Ghalib's Lectures. 6 Affected animals may develop chemical rumenitis due to the corrosive nature of lactic acid with high concentration in the rumen. Survived animals may develop peritonitis, mycotic rumenitis in several days, liver abscesses within weeks and ruminal scars. The released toxins may produce chronic laminitis as well. Rumen ulcer & perforation : 4-Dec-09 Dr. Ghalib's Lectures. 7 Rumen ulcer & perforation Mycotic rumenitis (image on left)Normal rumen mucosa (image on right) : 4-Dec-09 Dr. Ghalib's Lectures. 8 Mycotic rumenitis (image on left)Normal rumen mucosa (image on right) Slide 9: 4-Dec-09 Dr. Ghalib's Lectures. 9 Clinical findings: The severity of signs varies from simple indigestion to fatal acidosis. The speed of onset of illness depend on the nature of feed as the ground is more dangerous than whole grain and severity increases with larger amount of feed eaten. Clinical signs appear few hrs after feed consumption with enlarged rumen and kicking at the belly. A- In severe grain overload, 1-2 hr later after the onset of overload some animals will be recumbent others shows staggery drunken gait with blind appearance that bump into objects and others standing quietly. All are anorexic and depressed. Slide 10: 4-Dec-09 Dr. Ghalib's Lectures. 10 Affected animals show temperature below normal with heart rate is usually increased with the severity of acidosis (120-140 beats/ minutes is poor prognosis). The respiration is shallow and increased up to 70-90/ minutes. In sheep and goats, the temperature is slightly higher than normal and the heart rate may be higher than 100/minute. Tooth grinding may occur in 25% of affected sheep and goats. Profuse diarrhea is common ; the feces are soft to liquid with sweet-sour odor, may contain undigested grains. Dehydration rate is equal to 10-12% in severe overload. Absence of feces is grave prognostic sign. Anuria is common in acute cases & diuresis following therapy is a good prognostic sign. Slide 11: 4-Dec-09 Dr. Ghalib's Lectures. 11 Ruminal stasis is evident with gurgling sounds are usually audible on auscultation, and fluid splashing sound may be heard in the rumen after ballottement of left flank. In animals fed roughage before engorgement on excess grain, the rumen content may feel firm and doughy. Those become ill with smaller amount of grain, the content feel resilient because of fluid-filled rumen. In severely affected, acute laminitis may occur and chronic laminitis may be evident within weeks to months. Pregnant cattle survived severe form may abort 10-14 days. A herd with a high prevalence of lameness. The cows are standing with arched back and lowered heads especially to take the weight off their hind limbs. : 4-Dec-09 Dr. Ghalib's Lectures. 12 A herd with a high prevalence of lameness. The cows are standing with arched back and lowered heads especially to take the weight off their hind limbs. Left photo: Paint brush sole hemorrhages & white line disease.Right photo: Laminitic rings. The result of an outbreak of acute laminitis. : 4-Dec-09 Dr. Ghalib's Lectures. 13 Left photo: Paint brush sole hemorrhages & white line disease.Right photo: Laminitic rings. The result of an outbreak of acute laminitis. Abnormal horn formation : 4-Dec-09 Dr. Ghalib's Lectures. 14 Abnormal horn formation Bubbly scours- a clinical sign of ruminal acidosis : 4-Dec-09 Dr. Ghalib's Lectures. 15 Bubbly scours- a clinical sign of ruminal acidosis Slide 16: 4-Dec-09 Dr. Ghalib's Lectures. 16 Sternal recumbency may follow within 2 days with head turned into the flank & less response to stimuli resembling cases of milk fever. (early recumbency suggest unfavorable prognosis). Death may occur 1-3 days when acute signs develop quickly. Temporary improvements may be followed by relapse within 3-4 days later probably because of mycotic rumenitis and death may occur within 2-3 days due to acute diffuse peritonitis. Acidotic cows showing poor rumen fill, arched backs associated with lameness and loose feces : 4-Dec-09 Dr. Ghalib's Lectures. 17 Acidotic cows showing poor rumen fill, arched backs associated with lameness and loose feces Slide 18: 4-Dec-09 Dr. Ghalib's Lectures. 18 Favorable prognostic signs may include the following; Passage of large amount of soft feces. Rise in temperature Return of ruminal movements to normal Reduction of heart rate. B- In the mild form: affected cattle are anorectic bright, alert and diarrhea is common. Dehydration equal to 4-6%. Ruminal movements are reduced but not absent. Animal will start eating within 3 days without any treatment. Slide 19: 4-Dec-09 Dr. Ghalib's Lectures. 19 Diagnosis: A history of overeating of toxic doses of highly fermentable CHO particularly grain is diagnostic and may be confirmed by; 1- Characteristic clinical signs of rumen stasis, gurgling sound of fluid in the distended rumen, staggering gait, normal temperature and diarrhea. 2- Examination of pH of ruminal fluid (e.g. pH test strips). Normal pH in cattle on roughage is 6-7 and in cattle fed on grain diet is 5.5-6. pH <5 indicates severe acidosis. 3- Examination of rumen protozoa: On microscopic exam of ruminal fluid, 5-7 protozoa are normal findings. In lactic acidosis the protozoa are absent. pH test strips : 4-Dec-09 Dr. Ghalib's Lectures. 20 pH test strips Slide 21: 4-Dec-09 Dr. Ghalib's Lectures. 21 A Gram’s stain will reveal a change from normal predominant gram-negative bacteria to gram-positive bacteria in acidosis. Differential diagnosis: the disease should be differentiated from the following septic and toxic cases such as, Parturient paresis Acute diffuse peritonitis Septic mastitis or metritis Slide 22: 4-Dec-09 Dr. Ghalib's Lectures. 22 Treatment: Water intake should be restricted to all animals engorged on large quantities of concentrate for 24 hr. Severely affected animals removal of rumen contents and replacement with ingesta taken from healthy animals is necessary. Rumen lavage may be considered in animals that are still standing using large-bore stomach tube (2.5 cm diameter) to add water enough to distend the left paralumber fossa then empty out through gravity flow and repeat this for 15-20 times to empty the rumen. Slide 23: 4-Dec-09 Dr. Ghalib's Lectures. 23 This should be followed by; 1- Rumen inoculation of fresh ruminal fluid (the best ruminotoric) because it contains viable bacteria & protozoa. 2- Administration of antifoaming agents (PO) to reduce foam stability and to promote release of free gas to be eructated. Examples of these agents are; a- Poloxalene b- polymerized methyl silicone c- Vegetable oil (peanut, soyabean & sunflower oil). 3- Ruminal alkalinizing agents (antacids) such as magnesium hydroxide & magnesium carbonate. Slide 24: 4-Dec-09 Dr. Ghalib's Lectures. 24 Administration of activated charcoal (PO) is to protect ruminal mucosa from injury by toxins. To correct lactic acidemia and dehydration and to restore renal function, rigorous fluid therapy should be given. Initially as 5% sod bicarb solution given IV followed in the next 6-12 hr by solution of 1.3% sod bicarb in saline. In this case it is unnecessary to administer antacids orally. In less severe cases (pH >5 and the animal in standing position and alert) emptying the rumen is unnecessary and administration of mag hydroxide added to warm water into the rumen is sufficient therapy. Slide 25: 4-Dec-09 Dr. Ghalib's Lectures. 25 If appetite returns within 3 days, the prognosis is good. Supportive treatment may include the following: A- Antibiotics should be given to reduce the risk of liver abscessation. B- Antihistaminic may be used to control histamine production. C- Calcium/magnesium solution (IV or SC) to counteract 2ndary hypocalcemia and hypomagnesemia. D- Thiamine (10mg/kg) every 1-2 days for up to 3 doses may also by helpful to prevent PEM. Slide 26: 4-Dec-09 Dr. Ghalib's Lectures. 26 Treatment of mild cases of acidosis includes a- withholding concentrates and b- feeding hay to stimulate saliva flow. Additional therapy includes; Oral antacids (magnesium hydroxide, magnesium oxide or sodium bicarbonate to alkalinize the rumen. Oral electrolytes solutions to treat metabolic acidosis. Slide 27: 4-Dec-09 Dr. Ghalib's Lectures. 27 Prevention Avoid giving concentrates to animal in large quantity. Feedlot cattle should be introduced to concentrate rations gradually and mixed with roughage. The ionophore antibiotics salinomycin, monensin, and lasalocid may have a protective effects to prevent lactic acidosis and salinomycin was found to be more effective than others. You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
Acute Carbohydrates engorgement vetgreen Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 1079 Category: Education License: All Rights Reserved Like it (4) Dislike it (0) Added: December 04, 2009 This Presentation is Public Favorites: 0 Presentation Description It describe an important disease in ruminants which may results in many losses among cattle and other ruminants. Comments Posting comment... By: vetgreen (23 month(s) ago) Dear Naveen, Thank you for your letter concerning downloading my presentation of CHO engorgement in ruminants. I made it public for every one to download, if you find it difficult to have it please send me you email and I will send it to you as attachment, with my best wishes. I have more presentations in other website like DOCSTOCK and SCRIBD.COM. Dr. Ghalib. (Alaridi@yahoo.com) Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript Acute carbohydrates engorgement of ruminants : 4-Dec-09 Dr. Ghalib's Lectures. 1 Acute carbohydrates engorgement of ruminants Synonyms: Rumen overload Lactic acidosis Acute rumen impaction Acute grain overload Ruminal acidosis. It is an acute disease which characterized by indigestion, rumen stasis, dehydration, acidosis, toxemia, incoordination, collapse and frequently death. Slide 2: 4-Dec-09 Dr. Ghalib's Lectures. 2 Etiology: Any ruminant is susceptible to ruminal acidosis. It is most common in cattle that accidentally gain access to large amounts of highly soluble CHO such as finely ground grains e.g., wheat, barley and corn. Less common causes include apples, pears, potatoes & beets. The amount of feed which produce the disease depends on; Amount & type of grain and previous experience with the grain. The morbidity varies from 10-50%,& mortality rate is 90% in untreated cases and 30-40% in treated animals. Condition nutritional status of animal. The nature of microflora. Slide 3: 4-Dec-09 Dr. Ghalib's Lectures. 3 Pathogenesis: Within 2-6 hr of feeding on large amount of highly fermentable CHO particularly finely ground feeds, which increase the surface exposed to the fermentation bacteria, the microbial population in the rumen is changed with increase of gram-positive Streptococcus. bovis which utilizes the CHO to produce large quantities of lactic acid will decreases the pH to 5 or less, at this point the cellulolytic bacteria and protozoa are destroyed and replaced by lactobacilli and gram positive rods . VFA level is also increased & contributes to the fall of ruminal pH. The low pH allows the lactobacilli to utilize CHO to produce more excessive quantities of lactic acid . Slide 4: 4-Dec-09 Dr. Ghalib's Lectures. 4 Slide 5: 4-Dec-09 Dr. Ghalib's Lectures. 5 Excess D and L lactic acid causes rise in ruminal osmotic pressure which result in movements of excessive quantities of water and fluid from body tissues and blood into the rumen resulted in rumen distention, diarrhea, hemoconcentration and dehydration These conditions lead to hypovolemia, circulatory collapse, metabolic acidosis and death. The accumulation of VFAs produce rumen stasis. Finely ground CHO also decreases the amount of saliva secreted by the animal which lessens the amount of buffer flowing into the rumen. Slide 6: 4-Dec-09 Dr. Ghalib's Lectures. 6 Affected animals may develop chemical rumenitis due to the corrosive nature of lactic acid with high concentration in the rumen. Survived animals may develop peritonitis, mycotic rumenitis in several days, liver abscesses within weeks and ruminal scars. The released toxins may produce chronic laminitis as well. Rumen ulcer & perforation : 4-Dec-09 Dr. Ghalib's Lectures. 7 Rumen ulcer & perforation Mycotic rumenitis (image on left)Normal rumen mucosa (image on right) : 4-Dec-09 Dr. Ghalib's Lectures. 8 Mycotic rumenitis (image on left)Normal rumen mucosa (image on right) Slide 9: 4-Dec-09 Dr. Ghalib's Lectures. 9 Clinical findings: The severity of signs varies from simple indigestion to fatal acidosis. The speed of onset of illness depend on the nature of feed as the ground is more dangerous than whole grain and severity increases with larger amount of feed eaten. Clinical signs appear few hrs after feed consumption with enlarged rumen and kicking at the belly. A- In severe grain overload, 1-2 hr later after the onset of overload some animals will be recumbent others shows staggery drunken gait with blind appearance that bump into objects and others standing quietly. All are anorexic and depressed. Slide 10: 4-Dec-09 Dr. Ghalib's Lectures. 10 Affected animals show temperature below normal with heart rate is usually increased with the severity of acidosis (120-140 beats/ minutes is poor prognosis). The respiration is shallow and increased up to 70-90/ minutes. In sheep and goats, the temperature is slightly higher than normal and the heart rate may be higher than 100/minute. Tooth grinding may occur in 25% of affected sheep and goats. Profuse diarrhea is common ; the feces are soft to liquid with sweet-sour odor, may contain undigested grains. Dehydration rate is equal to 10-12% in severe overload. Absence of feces is grave prognostic sign. Anuria is common in acute cases & diuresis following therapy is a good prognostic sign. Slide 11: 4-Dec-09 Dr. Ghalib's Lectures. 11 Ruminal stasis is evident with gurgling sounds are usually audible on auscultation, and fluid splashing sound may be heard in the rumen after ballottement of left flank. In animals fed roughage before engorgement on excess grain, the rumen content may feel firm and doughy. Those become ill with smaller amount of grain, the content feel resilient because of fluid-filled rumen. In severely affected, acute laminitis may occur and chronic laminitis may be evident within weeks to months. Pregnant cattle survived severe form may abort 10-14 days. A herd with a high prevalence of lameness. The cows are standing with arched back and lowered heads especially to take the weight off their hind limbs. : 4-Dec-09 Dr. Ghalib's Lectures. 12 A herd with a high prevalence of lameness. The cows are standing with arched back and lowered heads especially to take the weight off their hind limbs. Left photo: Paint brush sole hemorrhages & white line disease.Right photo: Laminitic rings. The result of an outbreak of acute laminitis. : 4-Dec-09 Dr. Ghalib's Lectures. 13 Left photo: Paint brush sole hemorrhages & white line disease.Right photo: Laminitic rings. The result of an outbreak of acute laminitis. Abnormal horn formation : 4-Dec-09 Dr. Ghalib's Lectures. 14 Abnormal horn formation Bubbly scours- a clinical sign of ruminal acidosis : 4-Dec-09 Dr. Ghalib's Lectures. 15 Bubbly scours- a clinical sign of ruminal acidosis Slide 16: 4-Dec-09 Dr. Ghalib's Lectures. 16 Sternal recumbency may follow within 2 days with head turned into the flank & less response to stimuli resembling cases of milk fever. (early recumbency suggest unfavorable prognosis). Death may occur 1-3 days when acute signs develop quickly. Temporary improvements may be followed by relapse within 3-4 days later probably because of mycotic rumenitis and death may occur within 2-3 days due to acute diffuse peritonitis. Acidotic cows showing poor rumen fill, arched backs associated with lameness and loose feces : 4-Dec-09 Dr. Ghalib's Lectures. 17 Acidotic cows showing poor rumen fill, arched backs associated with lameness and loose feces Slide 18: 4-Dec-09 Dr. Ghalib's Lectures. 18 Favorable prognostic signs may include the following; Passage of large amount of soft feces. Rise in temperature Return of ruminal movements to normal Reduction of heart rate. B- In the mild form: affected cattle are anorectic bright, alert and diarrhea is common. Dehydration equal to 4-6%. Ruminal movements are reduced but not absent. Animal will start eating within 3 days without any treatment. Slide 19: 4-Dec-09 Dr. Ghalib's Lectures. 19 Diagnosis: A history of overeating of toxic doses of highly fermentable CHO particularly grain is diagnostic and may be confirmed by; 1- Characteristic clinical signs of rumen stasis, gurgling sound of fluid in the distended rumen, staggering gait, normal temperature and diarrhea. 2- Examination of pH of ruminal fluid (e.g. pH test strips). Normal pH in cattle on roughage is 6-7 and in cattle fed on grain diet is 5.5-6. pH <5 indicates severe acidosis. 3- Examination of rumen protozoa: On microscopic exam of ruminal fluid, 5-7 protozoa are normal findings. In lactic acidosis the protozoa are absent. pH test strips : 4-Dec-09 Dr. Ghalib's Lectures. 20 pH test strips Slide 21: 4-Dec-09 Dr. Ghalib's Lectures. 21 A Gram’s stain will reveal a change from normal predominant gram-negative bacteria to gram-positive bacteria in acidosis. Differential diagnosis: the disease should be differentiated from the following septic and toxic cases such as, Parturient paresis Acute diffuse peritonitis Septic mastitis or metritis Slide 22: 4-Dec-09 Dr. Ghalib's Lectures. 22 Treatment: Water intake should be restricted to all animals engorged on large quantities of concentrate for 24 hr. Severely affected animals removal of rumen contents and replacement with ingesta taken from healthy animals is necessary. Rumen lavage may be considered in animals that are still standing using large-bore stomach tube (2.5 cm diameter) to add water enough to distend the left paralumber fossa then empty out through gravity flow and repeat this for 15-20 times to empty the rumen. Slide 23: 4-Dec-09 Dr. Ghalib's Lectures. 23 This should be followed by; 1- Rumen inoculation of fresh ruminal fluid (the best ruminotoric) because it contains viable bacteria & protozoa. 2- Administration of antifoaming agents (PO) to reduce foam stability and to promote release of free gas to be eructated. Examples of these agents are; a- Poloxalene b- polymerized methyl silicone c- Vegetable oil (peanut, soyabean & sunflower oil). 3- Ruminal alkalinizing agents (antacids) such as magnesium hydroxide & magnesium carbonate. Slide 24: 4-Dec-09 Dr. Ghalib's Lectures. 24 Administration of activated charcoal (PO) is to protect ruminal mucosa from injury by toxins. To correct lactic acidemia and dehydration and to restore renal function, rigorous fluid therapy should be given. Initially as 5% sod bicarb solution given IV followed in the next 6-12 hr by solution of 1.3% sod bicarb in saline. In this case it is unnecessary to administer antacids orally. In less severe cases (pH >5 and the animal in standing position and alert) emptying the rumen is unnecessary and administration of mag hydroxide added to warm water into the rumen is sufficient therapy. Slide 25: 4-Dec-09 Dr. Ghalib's Lectures. 25 If appetite returns within 3 days, the prognosis is good. Supportive treatment may include the following: A- Antibiotics should be given to reduce the risk of liver abscessation. B- Antihistaminic may be used to control histamine production. C- Calcium/magnesium solution (IV or SC) to counteract 2ndary hypocalcemia and hypomagnesemia. D- Thiamine (10mg/kg) every 1-2 days for up to 3 doses may also by helpful to prevent PEM. Slide 26: 4-Dec-09 Dr. Ghalib's Lectures. 26 Treatment of mild cases of acidosis includes a- withholding concentrates and b- feeding hay to stimulate saliva flow. Additional therapy includes; Oral antacids (magnesium hydroxide, magnesium oxide or sodium bicarbonate to alkalinize the rumen. Oral electrolytes solutions to treat metabolic acidosis. Slide 27: 4-Dec-09 Dr. Ghalib's Lectures. 27 Prevention Avoid giving concentrates to animal in large quantity. Feedlot cattle should be introduced to concentrate rations gradually and mixed with roughage. The ionophore antibiotics salinomycin, monensin, and lasalocid may have a protective effects to prevent lactic acidosis and salinomycin was found to be more effective than others.