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This article was published in 1993
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Heat Stress Losses in Feedlot Cattle at Texas, February 1991
John Cronin, Veterinary Officer, QDPI, TOOWOOMBA
On 9 February 1991, the QDPI Regional Manager in Toowoomba, T.S., was contacted by the manager of W. Feedlot advising of the death of approximately 450 head of cattle that afternoon. I was contacted that night by T.S. to investigate on behalf of the Department. On 10 February 1991, when I arrived at the feedlot there were over 1000 dead animals, Dr J.B., a private veterinary consultant from Texas had been there on 9 February 1991 and 10 February 1991. After several autopsies and the receipt of the laboratory results for specimens collected by J.B. and his associates on 9 February 1991, both J.B. and I were of the opinion that heat stress was the cause of the mortalities. This was based on the clinical symptoms, environmental conditions and initial blood results.
The ambient temperature was 37°C at midday on 10 February 1991 and higher in the afternoon. It was quite humid and the previous day had been more humid. On 11 February 1991 J.G., a QDPI Veterinary Pathologist and Manager of the Regional Veterinary Laboratory in Toowoomba and T.S. visited the feedlot. There were further losses that day and by 12 February 1991, 2284 head had been buried. By 2.00 pm on 13 February 1991, 2681 head had been buried. One additional contributing factor was the higher than normal temperatures experienced at night. Deaths occurred mostly during the afternoon. T.S. and J.G. made a number of visits that week and conducted more autopsies and investigations.
The Pathologists report submitted by J.G. came to the conclusion that all of the findings were 'consistent with a diagnosis of heat stroke'. During that same week an epidemiological investigation was done by I.D., a QDPI Veterinarian and Manager of the Animal Health Program for Veterinary Services Branch, Brisbane, I.D. came to the conclusion that 'the diagnosis of heat stress made on clinical, pathological and clinico-pathological grounds is supported by the epidemiological pattern of the outbreak'. He went on to say that 'accepting heat stress as a cause of death, it is likely that a complex of factors interplayed to produce the effect seen'. A copy of his summary report is attached. In his investigations, I.D. pursued all possible leads to try to find any precipitating causes. One hypothesis was based on a period of water deprivation due to a pump failure. However this hypothesis was not able to be sustained. Furthermore the feedlot management has stated that water was always available to every pen.
The executive summary of the report by I.D., J.G. and T.S. came to the following conclusion: 'No unequivocal solution to the question of what predisposed this feedlot to these deaths may be available.... A number of potential risk factors have been identified and the limitations to interpreting the significance of each factor discussed in the epidemiological report'. Briefly these factors were:
environmental factors
animal factors
dietary factors.
These factors are expanded on in the attached summary of the epidemiologists report. A further comment made in the detailed epidemiologists report is of interest. To quote: 'Although the shade trial conducted as the incident was abating suggests that shade can lower rectal temperatures, the connection between this trial and the incident is tenuous'. Another comment in the Field Coordinator's Report by T.S. is of interest: 'The presence of dead cattle around water troughs in a number of pens markedly restricted access to water by other cattle. This contributed to higher mortalities'. Some earlier comments in T.S.'s report clarifies this: 'Staff were only able to bury cattle at night when it was cooler. The extra vehicle activity in cleaning pens of dead cattle during the day only excited the cattle and exacerbated the problem.
Having been present on the second day of the incident, it was obvious that the staff of the feedlot were doing a very good job of handling the problem. The removal of dead cattle did not have any obvious solution, as T.S. outlined.
One final comment of engineering interest was the site chosen for the mass burial of approximately 2700 carcases. The site chosen was a gravel quarry ranging from about four to ten metres deep. It was a large area of approximately 5000 m2. An officer from Water Resources visited the feedlot and made recommendations regarding the burial site. Water Resources had recommended that bentonite be added to the pit and backfilled for subsequent burials. As there was seepage from the initial 1200 carcases buried in the quarry, some banks of earth and bentonite as well as trenches were put in to alleviate this problem. The top of the quarry area where the carcases were buried was compacted and sealed with clay soil. Considering the size of the operation and the site selected, the disposal was successful and no problems have since occurred at the site. The disposal operation was supervised by Mr R.S., Senior Inspector of Stock with the QDPI in Toowoomba. Ray had extensive experience with the disposal of 3000 head at Binowee Feedlot in the Botulism outbreak in January 1990.
Extract from Field Coordinators Report
Clinical Symptoms and PM Findings:
These are listed as per:
J.B. (PP) 09/02 and 10/02/91
J.C. 10/02/91
T.S. & J.G. 11/02/91 and beyond.
(a) 09/02 and am 10/02/91 - J.B.
Salivation, bellowing, anoxia, recumbency and death, in less than one hour. A lot of animals were panting, grunting and showing signs of distress. Some pens had up to 90% of cattle affected. Some cattle had acute gastroenteritis, often passing pure blood. Scleral vessels were injected. Animals in lateral recumbency were destroyed. On autopsy there were ecchymotic haemorrhages of the heart, pleura and watery bloody small intestinal contents.
(b) pm 10/02/91 - J.C.
Similar symptoms were observed. Temperatures of affected cattle ranged from 42°C to 44°C. A full range of samples were collected and despatched to Toowoomba Vet. Lab. and Veterinary Pathology Services, Brisbane for analysis.
Other Observations: (i) Pens containing Aberdeen Angus had higher mortality rates. (ii) The ambient temperature on 10/02/91 was 37°C at midday and felt humid. Management reported a temperature of 41°C. The humidity was considered higher on Saturday. (iii) By late afternoon 10/02/91 both J.C. and J.B. were of the opinion that heat stress was the cause of mortalities based on clinical symptoms, environmental conditions and initial blood results (CPK and AST) from the laboratory. Management were advised but options were limited as no suitable shaded paddocks [were] available. Cattle were in no condition to move.
(c) 11/02/91 - J.G. and T.S.
Ambient temperature was 37°C and relatively humid.
Up to 60-70% of cattle in some pens were affected showing symptoms described previously, but with fewer mortalities. Severely affected animals found difficulty in drinking. Many cattle had reddened pasterns with some knuckling of the fetlocks occurring. One animal displayed a goose stepping gait. Rectal temperatures ranged from 42.5°C to 44°C in recumbent animals.
On post-mortem, no significant abnormalities were observed.
12/02/91
Ambient temperature 36°C with relative humidity of 45-50%.
Fewer cattle showed clinical symptoms with more animals chewing their cuds than previously observed. A number of animals showed tenderness of hind feet with some knuckling. Animals were generally more distressed from 4.00 pm (Daylight saving) onwards with a number of mortalities occurring during this period. This was considered the hottest part of the day.
13/02/91 - 15/02/91
Ambient temperatures 35-36°C with relative humidity of 40%.
Most of the animals that died during this period were destroyed because of knuckling at the fetlocks and therefore unable to reach food or water.
It was thought that knuckling resulted from muscle damage due to increased body temperatures and pressure necrosis from recumbency. This had affected contraction of the extensor tendons thus resulting in knuckling.
A ground temperature of 47°C was recorded during the outbreak. The reddening of the pasterns and feet tenderness were also observed in late November-December when high ambient temperatures were recorded. A number of pens had been scraped since then which would contribute to the ground radiation.
Quarantine: Formal quarantine was imposed on the 11/2/91, although the feedlot was under voluntary quarantine as from the 9/2/91. The quarantine was formally revoked on the 15/2/91.
The only movements off the property since the 28/1/91 were 2324 bullocks to Oakey abattoir.
Mortalities:
Approximate mortality figures are as follows:
| 09/02/91 | 569 |
| 10/02/91 | 1000 |
| 11/02/91 | 3-400 |
| 12/02/91 | 2284 buried by 6.00 am |
| 100 | |
| 13/02/91 | 2681 buried by 2.00 pm |
| 14/02/91 | sporadic losses |
| 15/02/91 | sporadic losses |
Comment:
It is highly probable that the mortality figures over the first two and a half days were higher than estimated. This is based on daily observations and the presence of cattle, which had been dead for some time, remaining in a number of pens late on 12/02/91.
Staff were only able to bury cattle at night when it was cooler. The extra vehicle activity in cleaning pens of dead cattle during the day only excited the cattle and exacerbated the problem.
Another contributing factor to the high and continued losses was the higher than normal temperatures experienced at night.
The presence of dead cattle around water troughs in a number of pens markedly restricted access to water by other cattle. This contributed to higher mortalities.
The use of water trucks was only effective when used inside the pens and water sprayed for some time on affected cattle. In some instances this stirred cattle up so again care was needed.
Extract from Pathologist's Report
Biochemistry:
Biochemical profiles covering up to 26 biochemical parameters were performed on two groups of clinically affected animals.
Group A (n = 15) were animals suffering heat exhaustion, they were unable to rise and had rectal temperatures > 43°C.
Group B (n = 6) were animals used in a shade experiment, some exhibited heat stress (that is, tonguing, panting) but all were ambulant and rectal temperatures ranged from 39.7 to 41°C.
Biochemistry Results - Summary
| XA | XB | Normal Range | |
|---|---|---|---|
| Calcium mmol/L | 1.7* | 2.35 | 2.1 - 2.8 |
| Magnesium mmol/L | 0.77 | 0.95 | 0.65 - 1.3 |
| Total Protein g/L | 74 | 75 | 60 - 85 |
| Bilirubin uM/L | 25.7* | 10.8 | 1 - 10 |
| Creatinine umol/L | 315* | 199 | 40 - 220 |
| BUN mmol/L | 12.8* | 5.2 | 2.0 - 8.5 |
| Gamma-GT IU/L | 14.0 | 22.5 | 10 - 35 |
| CPK IU/L | 46,250** | 333 | 10 - 200 |
| AST(GOT) IU/L | 1490* | 103 | 30 - 170 |
| GLDH IU/L | 17.2 | 26.5 | 0 - 20 |
| Phosphorus mmol/L | 1.8 | 2.1 | 1.13 - 2.25 |
| 3-OH butyrate mmol/L | 1.4* | 0.6 | 0 - 0.9 |
Consistent biochemical findings included renal insufficiency (as evidenced by elevated creatinine and BUN levels), hypocalcaemia, severe skeletal muscle necrosis (that is, elevated CPK and AST), mild ketosis and bilirubinaemia.
Epidemiologist's Report
by I.C. Douglas B.V.Sc., M.Sc., Manager, Animal Health, Veterinary Services Branch, Brisbane
Summary
The diagnosis of heat stress made on clinical, pathological and clinico-pathological grounds is supported by the epidemiological pattern of the outbreak.
The deaths occurred suddenly and in too great a number to be caused by an infectious disease. Recovery of affected animals was too rapid and too irregular to suggest a toxic cause. There was no consistent link between any feed ingredient or contaminant of the water supply. Heat-tolerant breeds seemed unaffected.
Accepting heat stress as a cause of death it is likely that a complex of factors interplayed to produce the effect seen.
Environmental Factors
Information on climatic conditions suggests that the combination of high maximum and minimum temperatures, high relative humidity and a lack of wind was unusual for the area. The maxima recorded in surrounding areas were not exceptional however the variations between maxima and minima were small, maintaining hot conditions at all times, and the relative humidity rose abruptly and maintained a high level for several days.
The layout of the feedlot seemed important with deaths concentrated in the higher rows.
Several local environmental parameters deserve consideration.
a. Amount of reflected radiation
Losses towards the boundary of the feedlot adjoining heavily grassed areas were low.
b. The slope of the feedlot
This probably increased the intensity of absorbed radiation. Some variation in slope was present with the higher rows more highly sloped.
c. Cleanliness of the pens
The higher pens had been recently cleaned of manure. This may have created different micro-climates down the feedlot increasing the humidity and lowering the shade temperatures at the lower levels and increasing reflected radiation from the cleaner pens.
The shade trial conducted indicated that shade was capable of assisting animals to maintain lower core body temperatures. The trial was conducted after the main effect had subsided, involved small stock numbers (20 head) and did not relate to the prevention of death or clinical signs of stress. It is not unreasonable to assume however, that the absence of shade in the feedlot played some part in the syndrome.
Animal Factors
Breed type was correlated with death rates with Angus-type cattle at significantly greater risk than the bulk of the cattle which were of Hereford-type. Brahman-cross or Simmental-cross animals were seemingly unaffected.
The size, weight, and fat cover of the animals did not appear to influence death rate. This is contrary to what would normally be expected.
The time since arrival at the feedlot did influence the death rate with introductions within the previous one to two months being significantly less at risk.
There is no evidence to suggest that the geographic origin of the animals influenced this syndrome.
Dietary Factors
The presence of a consistent dietary element did not explain the losses however there is a suggestion that the high energy content of the ration may have predisposed. This assumption is not strongly supported by the data and the effect was not absolute.
Management Factors
There was nothing apparent in the management of this feedlot which would have predisposed to loss.