Case 4

Case 4 A very large group of us

Case 4 • The dead cow in the picture below is from the feedlot in the second picture.

Case 4 • On postmortem examination, the cow was markedly dehydrated and the opened rumen is pictured below.

Question 1 • Q: Acute ruminal acidosis is the tentative diagnosis. Describe the sequence of events that has taken place in this cow’s rumen, leading to her developing ruminal acidosis and to her becoming so dehydrated. • A: The cow, Kevin, has likely had a recent, sudden change in diet. She eats lots of tasty grains, chock-ablock full of highly fermentable carbohydrates (CHOs)…

Question 1 •

•

…Approximately 2-4 h after the ingestion of excess carbohydrate, Gram-positive cocci (Streptococcus bovis) multiply rapidly, utilizing the carbohydrate to produce lactic acid and long-chain volatile fatty acids. The buffering mechanisms in the rumen are rapidly overwhelmed and as ruminal pH falls below 5 (the normal pH ranges from 6.0 to 7.5) protozoa, cellulolytic organisms and lactate-utilizing organisms are destroyed. At pH 4.0-4.5 the streptococci are rapidly overgrown by Gram-positive rods (lactobacilli), whose pH optimum is below 5. By 24 hours these are the most numerous organisms in the rumen and ceacum. Additional important microbiologic changes include increased proportions of coliforms and clostridia in the rumen and cecum. Ruminal motility ceases and the animal becomes anorectic at the time of the initial decrease in ruminal pH. The stasis of the rumen at this time is thought to be due to the increased ruminal absorption of the short chain volatile fatty acids rather than to the absorption of lactic acid per se. Lactic acid probably provides the acid conditions in the rumen that convert the volatile fatty acids to their more readily absorbable, nondissociated form. Later in the course of the disease, histamine and endotoxins also play an important role in the inhibition of ruminal motility. Both these substances are produced in the ruminal fluid. Endotoxins are elaborated by the coliforms and clostridia, while histamine is produced by lactobacillary decarboxylation of histidine. Although histamine is poorly absorbed by the normal rumen, significant amounts may cross the acid-damaged epithelium…

Question 1 •

•

…Ruminal acidosis is typically associated with a severe metabolic acidosis, dehydration, shock, toxemia and diarrhea. Equal amounts of D- and Llactate are produced and both forms are slowly absorbed from the rumen. The blood lactate concentration usually reaches a peak 7-24 hours after acute overeating. As the L-lactate is metabolized more rapidly than the Dlactate, the metabolic acidosis is due in large part to the accumulation of the latter. However, the majority of the lactic acid produced is not absorbed but accumulates in the rumen to cause the sequestration of large quantities of water. This induces rapid contraction of the extracellular fluid volume, dehydration, shock and eventual renal failure. Diarrhea is the result of a lactate-based osmotic overloading of the large intestine, the lactate coming from the rumen. There is also a contribution from the further fermentation of undigested carbohydrate. Diarrhea exacerbates the acidosis, dehydration and shock, and endotoxins also contribute to the production of shock. Animals with acute ruminal acidosis often die in 1-3 days, and, in those that survive, overcompensation may produce a hypochloremic metabolic alkalosis after 4-7 days.

Question 1

Question 2 • Q: What other factors may have contributed to the dehydration in this cow? • A: The excess lactic acid is the primary cause of osmotic dehydration via the rumen. Also contributing are the presence of the ingested grain. Rumenitis damages the epithelium, resulting in passive loss of plasma proteins and associated further loss of water. Large amounts of fluid overload the large intestine, and are lost as diarrhoea. Undigested CHOs are fermented in the large intestine, causing further water loss. With hypocalcaemia due to malabsorption, she might have muscle weakness. With lethargy and anorexia, she might not want to get to the water. Endotoxaemia may result in acute renal failure, causing further water loss in urine.

Case 4 • A rapid sedimentation of particulate matter was noted.

Question 3 • Q: A rapid sedimentation of particulate matter was noted. Explain why this occurs with this condition? • A: As the pH falls below 5, protozoa and normal gut flora die. The protozoa act to maintain the rumenal contents in suspension; as they die, the rumenal contents settle out, as seen in the photograph.

Question 4 • Q: What would be the likely pH of this cow’s ruminal fluid (<4; 4 to 6; >6)? • A: 4-6; L. acidophilus begins to dominate S. bovis at pH < 5. Would L. acidophilus continue to ferment the grains, producing further lactic acid and, uncontrollably, further lowering pH?

Question 5 • Q: What would be the expected finding on a Gram stain of this cow’s ruminal fluid? • A: S. bovis would stain G+; at the point of death, this cow’s rumen would likely have been dominated instead by L. acidophilus, a G+ bacillus. Clostridium sporogenes, Bacillus thiaminolyticus, Bacillus aneurinolyticus, also G+, will be present.

Question 6 • • • • • • •

Q: Give the expected blood gas status of this cow and explain how this comes about? A: Metabolic acidosis – kidneys and lungs attempt to compensate. pH < 5 due to metabolic acidosis pO2 – normal??? pCO2 – slight increase, followed by significant decrease after 24 hours, with respiratory compensation (increased expiration to eliminate CO2) HCO3- – decreased due to overwhelming acidosis B.E. – ??? CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3↑↑↑

Case 4 • The last picture is of a 9 month old steer that is one of 200 in a feedlot. • This steer is 1 of 3 that appeared blind and had a staggering gait about 24 hours ago. • This animal has gone into sternal recumbency and has a “star gazing” appearance.

Case 4

Question 7 •

Q: What is the likely diagnosis of this steer’s neurological problem? Explain how has this problem occurred? What would be the appropriate therapy? • A: The G+ organisms in the rumen (Clostridium sporogenes, Bacillus thiaminolyticus, Bacillus aneurinolyticus) have thiaminase II activity. Overgrowth of these bacteria results in thiamine destruction, leading to polioencephalomalacia. Thiamine is required to convert pyruvate to acetyl CoA. A thiamine deficiency therefore inhibits the TCA cycle, drastically reducing the cell’s ability to produce energy. Neurons are particularly susceptible, and cerebrocortical necrosis results. • Treatment by IV thiamine… as well as supportive therapy and removing the source of acidosis. In the event of treatment failure, euthanasia is the best option.

Question 8 • Q: What lesions might be seen in the livers of some of these feedlot animals when they go for slaughter? How have these lesions occurred? • A: The rumenal epithelium is damaged by the excess lactic acid. Various fungal and bacterial species cross the rumen wall and enter the portal circulation, eventually reaching the liver. Examples include Arcanobacterium pyogenes, which causes liver abscesses, and Fusobacterium necrophorum, which causes necrobacillosis. Necrobacillosis manifests as necrosis, cellulitis or phlegmon (diffuse inflammation of the soft or connective tissue); the pus has a characteristic rotting odour.

Question 4 • Q: What would be the likely pH of this cow’s ruminal fluid (<4; 4 to 6; >6)? • A: < 4; L. acidophilus begins to dominate S. bovis at pH < 5. Presumably, L. acidophilus continues to ferment the grains, producing further lactic acid and, uncontrollably, further lowering pH.