Dietary fat is a valuable energy source for dairy cows to aid in meeting the high energy requirements for milk production (Bauman et al., 2003). The trade-off however exists, that when fat is included in the ration, reduced cellulose, crude fibre and nitrogen free extract digestibilities may occur (Maczulak et al., 1981). Unsaturated long chain fatty acids suppress the activity of fibrolytic bacteria in the rumen (Palmquist & Jenkins, 1980), while medium chain fatty acids demonstrate strong antiprotozoal properties, and thus have effects on the formation of fermentation end products and methane production in the rumen (Sutton et al., 1983; Hristov et al., 2004; Soliva et al., 2004).
This report details a novel case of fat toxicity in an 800 cow Holstein-Friesian dairy located near Finley, Southern N.S.W, causing widespread mortality over a period of approximately one week, associated with the inclusion of desiccated coconut into the fed ration.
The affected group consisted of approximately 330 Holstein-Friesian females of mixed age ranging from multi- and primiparous dry cows, to yearling heifers. The animals were held in a feedlot-style system with ad libitum access to pasture silage and poor quality pasture and oaten hay, and limited access to a concentrate consisting of almond hulls and millrun. On Saturday 23-6-12, the concentrate was altered to include approximately 10 percent desiccated coconut, although subsequent analysis revealed it’s concentration to be 35 percent. The mix was fed at a rate of roughly 7 kg per head. Cattle had no access to other feed or pasture.
This desiccated coconut had previously been fed to the milking cow herd in the preceding days, however due to apparent unpalatability and drop in milk production, this was quickly withdrawn after just two days.
The following day, Sunday 24-6-12, the local veterinarian was called to find over 50 recumbent, weak, dehydrated cows with tachypnoea and ruminal stasis. More than 50 individuals were treated with intravenous Calcigol 4 in 1 and intravenous isotonic fluids. Numerous cows responded well by standing and walking, yet some relapsed and were subsequently retreated.
On Monday 25-6-12, recumbent and moribund individuals were again treated with intravenous isotonic fluids, and up to 6 bags (3 L) of Calcigol 4 in 1. A number of cows had died. Hypothermia, rumen stasis, tachypnoea, tachycardia, recession of the eyes into the orbit, profuse regurgitation of ruminal fluid from the nose, ketosis, hypocalcaemia, and death of rumen microflora (none observable in rumen fluid under light microscope) was reported in moribund individuals.
On Tuesday 26-6-12, the district veterinarian was called to find approximately 26 individuals had died, with an apparent over-representation of younger stock. Post mortem examinations were conducted and the results are shown below. By Saturday 30-6-12, approximately 30 of 100 yearling females, 80 of 200 pregnant heifers and dry cows, and roughly 20 springers had died.
Post mortem examination was undertaken on a number of individuals; the following were consistent findings: multifocal pericardial petechial haemorrhages; the rumen was grossly distended with an abnormally large amount of wet hay/straw fibrous content; abomasum containing a large amount of undigested fibre, and diffuse petechial haemorrhage of the mucosal surface and minimal intestinal contents were found distal to the abomasum. There was also red discolouration of the medullary region of the kidneys, with engorged blood vessels.
Histopathology conducted at EMAI revealed: rumenitis, reticulitis; ulcerative, multifocal, severe with corneal and subcorneal pustules; abomasitis, nodular, hyperplastic, moderate with mucus neck cell hyperplasia; glomerulonephritis, with fibrin thrombi and moderate tubular proteinosis.
The severe changes in the rumen and reticulum were consistent with a chemical/acidic rumenitis/reticulitis with extensive mucosal damage, ulceration, and complete absence of normal ciliated flora. The glomerular changes in the kidney were consistent with disseminated intravascular coagulopathy with the presence of glomerular damage, fibrin thrombi and protein leakage. Fibrin clots noted in the hematology report are also confirmatory (Dr M. Gabor, EMAI).
The biochemistry results supported renal damage with elevated BUN/creatinine and phosphorus, with both a prerenal (dehydration) and likely a renal component. Elevated PCV and protein confirmed the clinical dehydration noted in the history. The presence of hypocalcemia despite an elevated protein level is significant. Liver disease is a not a feature of this case. No evidence of lactic acidosis (grain overload fermentation) was seen. Elevated CK and AST were indicative of muscle damage i.e. downers.
No cases of such toxicity in ruminants have been reported in literature, and so unfortunately little evidence is available to explain the pathogenesis of this disease. Desiccated coconut contains a minimum of 62 % fat in the form of coconut oil, which contains approximately 75 % medium chain saturated fatty acids, the majority of which being lauric acid (LA) at 45 % and myristic acid (MA) at 18%. Whilst fat is an important energy component in the diet of ruminants, and fat supplementation has become a common practice to increase the energy density of the diet (Bauman et al., 2003), high levels may adversely affect microbial fermentation.
Medium chain fatty acids (MCFAs), such as LA and MA exhibit potent antiprotozoal properties and thus have effects on rumen fermentation and methane production (Sutton et al., 1983; Hristov et al., 2004a,b; Soliva et al., 2004). Suppression of ruminal methane production by LA, MA, or coconut oil as a source of these MCFAs, is known to be mediated by a reduction in ruminal protozoal numbers and also by direct inhibition of rumen methanogens (Dohme et al., 1999, 2001). Among the most sensitive to inhibition by dietary fats are fibrolytic bacteria, which are likely to have been affected in this case given the abnormally large amount of unfermented fibre located in the rumen and abomasum. Such defaunating agents as MCFAs are not protozoa-specific, and so can significantly and adversely affect the bacterial population in the rumen. Disseminated Intravascular Coagulation is a likely sequela of massive gram negative microbial death and ensuing endotoxaemia. In macrophages and monocytes, bacterial endotoxins stimulate increased synthesis and the release of tissue factor and proinflammatory mediators which induce procoagulatory functions of endothelial cells (Schoeniger, 2005).
Hristov et al. (2009) found treatment with LA to result in a decrease in milk production in lactating cows, and a significant reduction in dry matter intake. Similarly, trials completed by Hollmann (2011) found that feeding a diet of 4.6 % or more of coconut markedly reduced the dry matter intake of the cattle. This is likely explained by the increased production of ruminal proprionate, and reduced ruminal microbial protein synthesis.
Analysis of the total mixed ration fed to the affected herd found the ration to contain 28.65 % crude fat. Components of the mixed ration included almond hulls (3.5%), mill run (4.3%) and desiccated coconut (18 to 20%). Current recommendations for fat content, which vary slightly between sources, range from 2 to 3 % of dietary dry matter intake (Estridge, 2005), a range which is radically exceeded in this case.
Water is a major component of fat breakdown within the rumen. Therefore ruminants fed on a high fat diet have increased requirements for water within the rumen. When water concentration within the rumen is inadequate, fluid is drawn from extra-ruminal sources, which can lead to severe dehydration (Parry, K, 2012, NSW DPI- Livestock Officer Beef Cattle, pers. comm.), explaining the marked dehydration, and profuse regurgitation of ruminal fluid from the nose of affected animals in this case. Similarly, the clinical hypocalcaemia evident in these cows both antemortem, and following post mortem measurements, is probably a function of gut stasis and reduced intestinal absorption, increased utilisation of cations with fat digestion, and reduced renal reabsorption due to the DIC and renal failure (Parkinson et al, 2010).
It is likely that little could have been done to prevent mortality in many of these cows in this case. Rumen transfaunation would probably be the best treatment, along with fluid and electrolyte therapy, however to have a profound effect this would probably be required to be carried out early in the disease process, and the issue of providing enough donors in a case such as this is most likely unviable.