Ruminal Acidosis/Rumen overload for Vet. Students /Ali sadiek

Diseases of Digestive SystemDiseases of Digestive System

ByByDr. Ali H. Dr. Ali H. SadiekSadiek

Prof. of Internal Veterinary Medicine and Clinical Prof. of Internal Veterinary Medicine and Clinical Laboratory DiagnosisLaboratory Diagnosis

Dept. of Animal MedicineDept. of Animal MedicineFaculty of Veterinary Medicine Faculty of Veterinary Medicine

AssiutAssiut UniversityUniversity-- AssiutAssiut, EGYPT, EGYPT

EE--mail: [email protected]: [email protected]

Prof. Dr. Ali SadiekProf. Dr. Ali Sadiek 22

Diseases of the Ruminant stomachDiseases of the Ruminant stomachIt composed of:1-Forestomach: Reticulo-rumen & Omasum2- True stomach: “Abomasum”


ReticulorumenReticulorumen• Occupies entire left half of abdominal

cavity• 90 kg capacity• Nerve supply is Vagus nerve =

parasympathetic• Four specialized contraction patterns

– Primary or mixing cycle– Eructation (secondary) cycle– Rumination/cud chewing– Esophageal groove closure


numerous papillae numerous papillae numerous papillae

polygonal cells

numerous papilae

broad longitudinal fold


full of folded tissue water

absorption

Microorganism, catches hardware

pepsinHCl

•Digest roughages to VFA,•make protein, make Vit. K and B CPX


ReticuloReticulo--RumenRumen• Motility controlled by gastric center in

Med. oblongata• Frequency of 1ry contractions = rough

indication of overall health of the ruminant– Primary cycle contractions = 60/hour–▼ to 50/hour during rumination–▲105/hour during feeding


Diseases of the RumenDiseases of the Rumen1. Ruminal Acidosis 2. Simple indigestion3. Tympany/ Bloat4. Traumatic reticuloperitonitis TRP5. Vagus Indigestion.


11--Ruminal acidosisRuminal acidosisSynonym1. Ruminal impaction2. Ruminant Carbohydrate

Engorgement3. Grain overload /Grain engorgement4. Lactic acidosis5. Carbohydrate intoxication6. Founder


Ruminal acidosisRuminal acidosis• Access to highly fermentable

feedstuffs–by unaccustomed animals, or– in larger than normal amounts

• Rapid clinical course of acute ruminal acidosis because of excessive prod. Of lactic acid in the rumen.

• It is ch. By: Toxemia, Dehydration, Ruminal atony, Recumbency and Deaths


Daily diet for High producing cowsDaily diet for High producing cows


What feeds can cause carbohydrate What feeds can cause carbohydrate engorgement?engorgement?

• Cereal grains• Indust. byproduct (brewers grains, sugars)• Fruits, Tubers (potatoes, sugar beets)• Finely ground feeds with large surface area

promote rapid fermentation

• Hay and grass are not highly fermentable due to cellulose and large particle size

• Corn silage usually not a problem because much of CHO already reduced to VFAs in ensiling process and also due to large particle size


PathogenesisPathogenesis


PathogenesisPathogenesis• Histamine levels increase• Ethanol, methanol, tyramine,

tryptamine production contribute to CNS depression

• Thiaminase production may result in development of polioencephalomalecia

• Death of Gram – bacteria can cause endotoxin release


Clinical signsClinical signs1. Abdominal pain2. Dehydration (6-12 %)3. Diarrhea – fluid, fetid4. Splashy rumen, bloat5. Depression6. Lameness7. Scleral injection


Clinical signsClinical signs8. TemperatureL: Elevated initially, may

be subnormal when presented9. HR = 80-140 bpm10.RR elevated (blow off CO2)11.Rumen fluid analysis

– pH < 5– sour odor– protozoa dead, predominance of gram +


P.M: Consequences of P.M: Consequences of RuminitisRuminitis

1- Ruminal ulcer and perforation2- Mycotic infection3- Hepatic abscess.4- Laminitis


Consequence of Consequence of RuminitisRuminitis

Rumen ulcers & perforation Mycotic infection

damages mucosal surfaces


Dry impacted R. contentDry impacted R. contentNormal R. mucosaNormal R. mucosa

RuminitisRuminitisMycoticMycotic ruminitisruminitis


Laboratory findingsLaboratory findingsI-Blood: Metabolic acidosis

Increased PCV, Glucose, Phosphate, BUN, creatinine , anion gapDecreased pH <7.0 and calcium

II-Ruminal fluid:Decreased pH< 5.0Decreased activity of microflra & fauna.

III-Urine:Decreased pHproteinuria


DiagnosisDiagnosisCase history: Sudden access to excess CHOClinical signs: Impaction, depression, toxemia.Laboratory findings: •Blood: CBC, BUN, blood gas.

•Rumen fluid analysis.•Urine pH and sp. Gr.

Differental Diagnosis:•Milk fever (incidence, decreased ca)•Liver disease (jaundice & liver function).•Lead and arsenic toxicity (Acuteness & nervous signs)


TherapyTherapyI- Evacuation of

rumen• Kingman tube

–Rumenotomy–Ice water administration


TherapyTherapyII- Medicinal therapy:1-Anti-inflammatory agents –flunixin

meglumine (Banamine)2-Antibiotics:Procaine pen G (10 million IU,

P.O.)3-Antimycotic therapy (Fungicid)III- Supportive therapy1-Fluid and electrolyte replacement IV2-Rumen transfaunation3-Thiamine and B-complex vitamins


ControlControl• Make dietary changes very gradually

– Addition of antibiotics– ionophore antibiotics e.g Monensin (Na+)

and Ionomycin (Ca++) ) to the feed have been beneficial but do not replace

– HCO3- (Antacid)– Good management.

• Rumen adaptation may take 6 weeks

Ruminal Acidosis/Rumen overload for Vet. Students /Ali sadiek

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