An outbreak of bovine respiratory disease in selenium deficient cattle in NSW

Erin Davis, veterinary undergraduate CSU, and Dave Gardiner, District Veterinarian, Central North LHPA, Mudgee

Posted Flock & Herd March 2011

Case report

A herd investigation was undertaken of cattle on a property in the Central North area of the Livestock Health and Pest Authority region of New South Wales. The property runs a stud Wagyu and Angus female breeding operation, with an artificial breeding program using semen imported from the U.S., and backup bulls to achieve an overall conception rate of 96% across the herd.

At weaning time May 2009, while mustering a mob of 49 cows and 24 calves, the owner discovered one dead cow and calf with advanced decomposition. Many cattle in the mob were coughing, dropping to the back of the mob, and obviously sick. There was no history of vitamin or mineral treatments in the herd, though it was a known selenium deficient area with previous problems in the herd. Another mob of 26 cows and 26 calves were showing similar signs.

Condition score of the cows and calves was generally poor and ranged from 1-3 in the cows and 1-2 in the calves. There was evidence of bottle jaw and green scour in some of the cows and calves. Moist non-productive coughs were regularly heard in the mob and they appeared depressed. Two weaners were noticed with nasal discharges and these were swabbed. Four cows and calves were sampled for bacteriology, parasitology and serum for selenium levels. Temperatures for these cattle ranged from 37.1°C to 40°C.

Initial testing was based upon suspicion of Bovine Respiratory Disease (BRD), Bovine Virus Diarrhoea Virus (BVDV- pestivirus), as well as exclusion of Theileria and anthrax. Results from initial testing showed no significant bacterial culture, negative Fluke ELISA, negative Infectious Bovine Rhinotracheitis (IBR) on PCR and low worm egg counts (WEC). Glutathione peroxidise levels came back as low, indicating that the herd was selenium deficient. The owner treated the affected cattle with a selenium supplementation (Selpor), vitamin A, D & E, and a booster 7 in 1.

Sample ID Temp Age Samples
1 2781 38.1 4T R & G
2 B370 37.7 2T R & G
3 B325 38.8 2T R, G, P
4 B385 39 2T R, G, P
5 D111 38.5 5 milk R & G & F
6 D119 39.2 6 milk R, G, P & S
7 D130 39.7 7 milk R, G, P & S
8 D183 40 8 milk R, G, P & F
Table 1: Specimen advice ID of cattle examined and samples collected

Number & Type of Specimens Tests Requested
8 x plain bloods Serology - Fluke ELISA 1 to 4
8 x Li Hep GSHPx
5 x EDTA FBC & path profile if indicated
2 x dry and buffered swabs Bacto - virology
2 x faeces calves WEC
3 x blood smears Atypical Theleria in pure bred Wagyu
Ear piece from dead cow Anthrax exclusion please
Table 2: Tests Requested

Test Number of samples Result
IBR real time PCR 2 Negative
Bacteriology Bacillus anthracis 3 Negative
Bacteriology culture 2 No significant findings or growth
Fluke ELISA 4 Negative
WEC 2 200, 160 epg strongyle
Table 3: Laboratory test results farm visit

Sample number GSHPx U/gHb (range 40-300)
1 17- low
2 14- low
3 12- low
4 12- low
5 4- low
6 5- low
7 4- low
8 4- low
Table 4: Glutathione peroxidise test results farm visit #1

A second farm visit for examination and sampling of cattle took place a week later. By this stage, three mobs were affected, with an estimated 100% morbidity for coughing and 10% with severe clinical signs of malaise and ill thrift. Further investigation revealed that all mobs were running in adjoining paddocks along a creek with kikuyu and couch pastures with heavy grazing of this area noted. BRD, Acute Bovine Pulmonary Emphysema and Oedema (Fog Fever) and coronavirus were on the list of suspected diseases. Many animals were scouring. One animal that appeared very weak and dehydrated was sacrificed for post-mortem. Post-mortem revealed greyish lungs with a consolidated appearance, especially cardiac and to lesser extent apical and diaphragmatic lobes. There was excess pericardial fluid, and the heart was flabby and pale. The liver was also pale, and the pancreas and small intestine appeared congested.

Results from lab testing revealed hypoproteinaemia, negative or no significant bacterial growth, negative for Pestivirus antibody and Coronavirus, and WEC negative. Histopathology of the lung was suggestive of a nonspecific immune response not consistent with Acute Bovine Pulmonary Emphysema and Oedema (Fog Fever) or pneumonia. One sample showed positive for Rotavirus. Based on these results, a protein losing enteropathy was associated with scouring induced by rotavirus, which in this case was likely to be a secondary infection in immunocompromised animals. The laboratory recommended further testing in 3 weeks for antibody to Pestivirus, as well as repeat testing of animals for seroconversion to bovine respiratory viruses, including Parainfluenza-3 virus (PI3), Bovine Respiratory Syncytial Virus (BRSV) and IBR.

Test Number of Samples Result
Pestivirus antibody AGID 1 Antibody negative
Rotavirus real time PCR 1 Positive
Coronavirus real time PCR 1 Negative
PI3 virus antibody ELISA 1 Negative
Bacteriology culture 1 - lung No growth
Salmonella culture (faeces) 1 Negative
Yersinia culture (faeces) 1 Negative
WEC 1 0, negative
Blood Biochemistry 1 Hypoproteinaemia/albuminaemia, mild WBC degenerative changes.
Histopathology 4 Bronchiolitis, lympho-plasmacytic, multifocal, minimal
Table 5: Laboratory test results farm visit #2

A third visit took place in June, where further epidemiological information was gathered and paired convalescent blood samples collected. 168 cows and 62 calves had shown signs of illness in coughing across four mobs. Of these, 50 were Angus cows and the remainder purebred Wagyu cows and/or cross calves. Illness and ill thrift were worst in a portion of the original artificial insemination mob of 50 cows and 36 calves drafted off from a mob of 26 cows and 26 calves in early April. The 26 cows and calves were on similar pasture conditions but were not as badly affected. Two other mobs of 50 Angus cows with 50 crossbred calves and 42 Wagyu heifers were also affected. The suspected diseases at this stage included PI3, BRSV, BVDV and selenium deficiency. Following the initial discovery of a dead cow and calf and illness in May and subsequent treatment with Selpor, Vitamin A, D, and & and 7 in 1, all but a few animals improved in condition and recovered. Two calves were still coughing, and another two were ill thrifty and poor with scour, with one noted to have an ill thrifty mother. One weaner sampled at the original farm visit with a temperature of 40°C was missing from the muster and was presumed dead. One of the coughing calves had a mild serous discharge with flecks of white mucous in it, which was swabbed.

Test Number of Samples Result
Pestivirus antibody AGID 10 4 negative, 5 intermediate, 1 high
IRB real time PCR 1 Negative
IBR Antibody ELISA 10 Negative
PI3 Antibody ELISA 10 6 positive, 4 negative
BRSV Antibody ELISA 10 4 positive, 6 negative
Table 6: Laboratory test results farm visit #3

Sample number GSHPx U/gHb (range 40-300)
1 104
2 67
3 60
4 13- Low
Table 7: Glutathione peroxidise results farm visit #3

Testing of samples revealed IBR negative, but PI3 and BRSV antibody ELISA positive. Of four serum samples taken from animals for GSHPx, one was low, indicating selenium deficiency. Pestivirus antibody testing revealed 5 of 10 animals as transiently affected (2- intermediate) and one as transiently affected in the last 6-9 months (3- high). No further testing was undertaken after this farm visit. The conclusion was made that a primary nutritional deficiency in the form of low selenium led to cattle that were immunocompromised, which resulted in infection with rotavirus and enzootic pneumonia caused by PI3 virus.

Figure One: Affected cows and calves in the yards.


Selenium (Se) is an essential trace element in animal nutrition, and exerts multiple actions related to animal production, fertility and disease prevention (Hefnawy & Tortora-Perez, 2010). There is a high correlation between glutathione peroxidise (GSHPx) activity and Se in the blood, being the reason why this enzyme is used as an indicator of deficiencies (Ammerman & Miller, 1975). GSHPx enzyme was the first proven seloenzyme that can prevent oxidative damage of the cellular membrane by protecting against the peroxides generated in the intermediary metabolism of cells with the oxidation of fats and proteins of the membranes. A deficiency of Se prevents the synthesis and function of GSHPx, thus damage to cellular and mitochondrial membranes takes place (Combs & Combs, 1986). A relationship has also been established between Se and thyroid activity whereby thyroid peroxidise, a seloenzyme, plays a role in the process of iodization of globulin, avoiding thyroid epithelial cell membrane damage. Deiodinases of peripheral tissues are also seloenzymes, which are necessary for the activation of T3 from T4 (Beckett et al, 1987, 1993).

There are a number of consequences of Se deficiency. Reduced reproductive efficiency and animal health, along with high mortality in offspring as a result of degenerative lesions in the myocardium (Ramirez-Bribiesca et al, 2001), lower weight gains, lower milk and wool production, and low seminal quality (Beckett & Arthur, 2005) have been described. Dairy cattle research has demonstrated that Se deficiency in dairy cattle reduces the ability of blood and milk neutrophils to kill bacteria, leading to higher incidence and duration of mastitis in Se deficient animals (Spears & Weiss, 2008: Smith et al, 1984). Pre-partum Se supplementation is thought to reduce the incidence of retained placenta (Allison & Laven, 2000). Se deficiency was found to affect blood levels of IgG and T cell function (Arthur et al, 2003), but another study found the response of IgG variable, responding to Se supplementation in cows and calves, and adult sheep, but not lambs. Positive correlations have been found between blood Se levels and increased concentrations of IgG in serum and increased concentrations of IgG in their calves (Hefnawy & Tortora-Perez, 2010). The activity and lifespan of neutrophils, macrophages and lymphocytes diminishes in the Se deficient animal, thought to be a result of a decrease in the activity of GSHPx. This condition would limit further antigen processing and antigen presentation, thus limiting the humoral response (Hefnawy & Tortora-Perez, 2010). The use of Se as an immune stimulant has a positive effect on the immune response and quality of colostrum (Jendrycsko, 1994). Neutrophils from Se supplemented cows shows a greater phagocytic and bactericide activities against Staphylococcus aureus and Candida albicans, and increased production of leukotrines (Grasso et al, 1990: Jukola et al, 1996). In cows with poor body condition a deficient immune response was associated with smaller amounts of T-lymphocytes, whereas Se supplementation induced 'immunostimulant' effects (Pollock et al, 2004), and increased the humoral immune response, especially when used in conjunction with vitamin E (Spears, 2000). A study with beef cows and calves fed on feeds marginally deficient in Se indicated that bimonthly Se-vitamin E injections reduced calf death losses (4.2% versus 15.3%) from birth to weaning. Most of the deaths in the study were attributed to diarrhoea and subsequent lack of thrift (Spears, 2000). Separate studies have demonstrated an enhanced antibody response associated with Se supplementation in beef cattle (Droke & Loerch, 1989: Swecker et al, 1989: Cao et al, 1992).

In this case study, the combination of poor body condition and Se deficiency is thought to have led to an immune compromised state in the animals. A reduction in the function of the immune system including a decreased number and function of T-lymphocytes could have contributed to the inability of the cattle to overcome PI3 and BRSV when exposed to these viruses. The improvement seen in the herd after treatment with Se and vitamins A, D and E supports the theory that Se deficiency was a factor contributing to disease outbreak in the herd. As PI3 virus normally causes a mild clinical to subclinical infection (Merck & Co, 2008), morbidity close to 100% in this herd could indicate that these were immune compromised animals with a reduced ability to fight disease. In one study however, the clinical signs and duration of infection were not affected by Se deficiency in calves inoculated with IBR virus (Reffett et al, 1988a), although in a similar study into lambs (Reffett et al 1988b), there was found to be an enhanced immune response in lambs when challenged with PI3 virus. Se deficiency, also, did not affect susceptibility of stressed steers to Pasteurella haemolytica challenge (Stabel et al, 1989).

Bovine Respiratory Disease Complex (BRDC) is caused by a variety of pathogens, both viral and bacterial, that may interact with each other to cause disease. Pestivirus is known to cause immune suppression and may lead to BRDC. As there was one animal that had a high antibody titre to Pestivirus (transiently affected in the last 6-9 months) in this case, Pestivirus may have also been a factor in the development of clinical respiratory disease in the herd. It is interesting to note, however, this animal (a weaner calf) tested negative to PI3, IBR and BRSV, and it had a temperature of 39.7 on clinical exam. Further testing was not undertaken. If further testing had taken place, re-testing of those animals that tested negative to BRDC viruses to see if they seroconverted would have provided good evidence that these viruses were involved in the clinical picture. A Pestivirus antigen capture ELISA (PACE) could have also been undertaken on negative animals for Pestivirus antibodies to look for a persistently affected animal.


This case report associated the primary nutritional stress of selenium deficiency in cows and calves with secondary respiratory disease infection. It has been normal practice to routinely supplement with selenium in this herd since a severe deficiency was recognised in February 2005 associated with ill thrift [6]. The routine treatment was not applied in 2009 due to a severely depressed Wagyu market and drought. The observed response to selenium treatment, being the disappearance of clinical signs of respiratory disease and a general improvement in the condition of the cattle during the winter feed pinch months, suggests Selenium deficiency was the primary cause of the observed respiratory disease and ill thrift. The excellent reproductive rates achieved in the stud herd, suggests the deficiency occurred rapidly during the autumn months preceding the observed outbreak of coughing in May 2009.

Further evidence of Selenium deficiency during 2009 was observed during October on a neighbouring property. A mob of Wagyu Angus cross heifers was inspected for movement to Tasmania on the 6th October. They showed signs of ill thrift and a rough red tinged coat colour. The owners agreed they looked Selenium deficient and said they did not treat this mob with a supplement due to drought cost cuts. They only did the steers that year and these were sold fat and shiny.


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