CASE NOTES


FACIAL ECZEMA IN CATTLE—FMD EXCLUDED

Kylie Greentree, District Veterinarian, Cumberland LHPA

Posted Flock & Herd December 2011

INTRODUCTION

This case study outlines a disease investigation that was in response to a farmer contacting the Emergency Disease hotline. The syndrome reported by the farmer could have been consistent with an exotic disease. The case study outlines the approach that the Cumberland LHPA took to reach a diagnosis and exclude important exotic disease.

Figure 1: Cattle with facial eczema constantly licking their noses

HISTORY

In early March 2011 the Cumberland LHPA was tasked to respond to a producer enquiry that had come through the Emergency Animal Disease Hotline. A local producer reported three Murray Grey cows with excessive head shaking, bleeding from the nose and frothing at the mouth. When further history was collected on the following day by the Cumberland LHPA, there were now five affected animals and some of the cattle were reported to have a dry cough. It was also reported that 1-2 weeks prior they had had very watery scours.

There were 10 cows in this affected mob. The cows were in a predominant rye grass paddock (also with phalaris and clover) that had been slashed 3 weeks prior. The paddock had been fertilised with chicken manure 12 months earlier. All cows were vaccinated with either 7-in-1 or a 5-in-1, there was a selenium lick block in the paddock and the water (in a concrete trough) looked clear. The cattle ranged in age from 4-7 years. Three cows had calves and did not appear to be affected. All cattle had been moved to an adjoining paddock with similar pasture content but had not been slashed. All cattle were in good condition body score. One cow had aborted a calf and several others that were supposed to be heavily in calf appeared empty.

WEATHER CONDITIONS LEADING UP TO THE EVENT

FEBRUARY

DATE MIN-MAX TEMP RAINFALL RELATIVE HUMIDITY
1 18.5-38.6 0 51
2 25.7-35.8 0 52
3 25.2-37.7 0 58
4 20.9-34.8 0 73
5 23.3-38.9 0 52
6 25.2-34.0 0 56
7 13.5-20.2 11.8 93
8 15.0-24.7 0 84
9 15.1-24.3 1.0 81
10 16.3-26.7 1.2 91
11 16.7-34.2 0 77
12 21.3-22.0 0.2 90
13 17.3-21.1 7.0 97
14 16.2-20.2 9.8 99
15 15.4-22.5 0.2 96
16 16.4-24.5 1.2 90
17 18.6-29.7 0 96
18 19.2-25.3 2.6 95
19 19.0-34.5 0 97
20 21.3-34.9 0.2 64
21 17.8-23.9 3.0 97
22 14.4-19.9 0.8 78
23 14.4-22.8 1.2 92
24 12.0-26.5 0 92
25 13.1-25.8 0.2 79
26 15.4-30.3 0 97
27 16.8-28.7 0 76
28 19.4-29.6 0.2 87

The mean statistics for February were:

Min-max temp= 18-28.3

Relative humidity= 81%

MARCH

DATE MIN-MAX TEMP °C RAINFALL mm RELATIVE HUMIDITY %
1 21-32.1 5.4 61
2 16.1-19.2 0.8 76
3 15.6-30.4 0.4 95
4 16.4-29.2 0.2 81
5 14.9-20.7 0.6 84
6 10.8-21 0.2 58
7 13.7-23 1.4 97

Over the entire month of March the mean statistics for the month were:

Min-max temp= 15.9-25.4

Relative Humidity= 86%

The weather leading up to the disease event was favourable for the production of fungal spores. Overnight temperatures were greater than 12°C most nights, there were consistent small amounts of rain to keep the grass moist and the relative humidity during February and March was quite high, sometimes reaching 99%.

CLINICAL EXAMINATION

The cattle were very agitated; they were shaking their heads like a dog with a grass seed in its external ear canal. Their noses appeared sunburnt, red and bleeding. The cattle were continuously licking their noses and hypersalivating.

Figure 2: Photosensitisation to the nose

On examination of the tongue, most of the cases had ulceration on the ventral and lateral margins. Several cows had crusty scabs over the skin on the neck and behind the ears. The margins of the eyelids and the vulva appeared crusty and burnt. Only the light coloured Murray Grey cattle were showing these clinical signs. All the cattle that were examined had an elevated temperature 39.4 - 40.5°C but they were also very agitated getting into the crush which would have elevated their temperature.

DIAGNOSTIC AIDS

Serum and EDTA blood was collected from five cattle. These samples were submitted to the State Diagnostic Laboratory to exclude Foot and Mouth Disease, Vesicular Stomatitis and undertake a liver profile.

Results of the liver profiles are summarised in Table One: Liver profiles of serum samples 1-5.

Sample 1 2 3 4 5
GGT ( 0-35U/L) 1055 599 734 1688 296
GLDH (0-30U/L) 1595 759 472 657 87
AST (0-120U/L) 478 129 340 155 294
BIL (0.0-24.0umol/L) 38.8 138.9 116.4 48.2 148.1
BIL-C umol/L 23.8 64.4 71.2 21.8 35.7
CK (0-300U/L) 752 156 385 183 977
PROTEIN (60-85g/L) 71.8 73.9 69.6 81.8 70.3
ALBUMIN (25-38g/L) 32.6 34.7 39.5 33.9 33.4
GLOB (30-45g/L)v 39.2 39.2 30.1 47.9 36.0
ALB/GLOB (0.7-1.1) 0.8 0.9 1.3 0.7 0.9

The liver profile results were interpreted by a pathologist from the EMAI State Diagnostic Laboratory as being indicative of hepatopathy with biliary disease. Elevated CK and AST are likely due to myopathy associated with recumbency.

Figure 3: Predominant Ryegrass pastures

The PCR results for Foot and Mouth and Vesicular Stomatitis were negative

Pasture samples were taken from two paddocks and also submitted to the State Diagnostic Laboratory:

1. The initial Ryegrass paddock that had been slashed and the Ryegrass was lying in wind rows.

2. The second paddock that they went into that was not slashed but was still predominant Ryegrass.

The report from the laboratory indicated that there was an average of Pithomyces at 175, 000 spores per gram of pasture and that this level is dangerous. Interpretation also included the comment that counts of 100, 000 will cause facial eczema and photosensitisation. Higher counts such as seen here will almost certainly cause liver damage in grazing sheep and cattle. This is also indicated by high serum levels in the liver of the affected animals. Parkinson, Malmo and Vermunt (2010) also report that counts of 40,000 spores per gram of pasture over many days can also be toxic especially when animals are grazing towards the base of the sward.

Both paddocks had a similar spore count so it was recommended that the few cows and calves in the second paddock were removed from this paddock also.

On the 28th March 2011 the producer took further pasture samples from the two paddocks in question. Over the 3 weeks there had been some considerable rain (71.4mm). The results on these paddocks were:

Sample 1: (Upper Paddock): 85,000 spores/gm pasture

Sample 2: 100,000 spores/gm pasture

In May 2011 the property was revisited by the Cumberland LHPA as another cow had lost a lot of condition over the last two weeks. On clinical examination of the cow you could see that she had skin damage to the nose that had recovered and that there was a decrease in the pigmentation. Bloods were taken and a liver profile requested. The results are summarised in Table Two:

Table Two: Laboratory results for bloods collected in May 2011.

Lab parameter Result
GGT 0-35 U/L 1123 H
GLDH 0-30 U/L 62 H
AST 0-120 U/L 142 H
BIL 0.0-24.0 umol/L 17.3
BIL 0.0-24.0 umol/L 17.3
CK 0-300 U/L 496 H
PROTEIN 60.0-85.0 g/L 72.3
ALBUMIN 25.0-38.0 g/L 32.7
GLOB 30.0-45.0 g/L 39.6
ALB/GLOB 0.7-1.1 0.8

The liver profile indicating a severe cholangiohepatopathy.

Parkinson, Vermunt and Malmo (2010) indicate that serum GGT gives the best indication as to the severity of bile duct damage. A serum concentration of GGT between 70-300IU/L may be seen with mild liver damage, 300-700IU/L with moderate damage and higher than 800IU/L with severe liver damage. GGT levels between 30-70IU/L are not clinically significant.

Figure 4: Ulceration of the tip of the tongue - Foot and Mouth exclusion was done

POST MORTEM

No post mortems were undertaken. One cow died but was buried immediately. As the owner knew the cause of death she did not ring for a post mortem to be done.

If a Post Mortem was done on these cattle you would expect:

Macroscopic evidence of oedema and fibrosis of the biliary tracts

Histologically: duct hyperplasia and fibrosis may be seen

Chronic cholangitis will eventually lead to left lobe atrophy in the liver of ruminants. Cattle with an enlarged right lobe and a thin, tough and small left lobe should always consider the possibility of sporidesmin toxicity.

DIAGNOSIS

A diagnosis of Facial Eczema was made on the basis of the history, clinical signs, liver profile and fungal spore results.

FOLLOW UP

Over the few months since the initial incident of Facial Eczema there have been two deaths. One died 3-4 days after the first visit on the 7th March 2011 and the other cow died mid June 2011. The first one that died only had moderately high GGT levels but was very agitated on examination, and the other cow (Z6) was not blood tested. 'Z6' lost weight over several months and was found dead. The producer said she definitely had the same clinical signs as the other Facial Eczema cases.

Three months after the initial visit the remaining cows have put back on some condition and seem to be doing well. The last cow we blood tested appears bright and eating well but is still very thin so it will be interesting to see how she progresses.

DISCUSSION

Facial Eczema is caused by the ingestion of fungal spores of Pithomyces chartarum. These spores contain the hepatotoxic compound, sporidesmin. The liver damage from sporidesmin causes the photosensitisation lesions that are a characteristic symptom of facial eczema. Facial Eczema normally occurs in hot humid conditions, in late summer to early autumn. The greatest risk occurs when humidity is close to 100% and when the grass temperatures have reached a minimum of 12°C for 4 consecutive nights. These conditions are normally found when more than 4mm of rain falls within 48hrs or when soil is kept moist by irrigation. Two or more repetitions in these weather conditions can lead to the fungus increasing to dangerous levels.

The fungus grows on dead litter of pasture, but can be found along the entire sward. The disease tends to be associated mainly with Perennial Ryegrass (Lolium perenne) because of its ability to produce dead litter.

When the spores are eaten by the ruminant, the spores release the sporidesmin toxin in the digestive tract. From here it is absorbed into the bloodstream, removed by the liver and excreted into the biliary system. The sporidesmin concentrates in the biliary system causing severe necrosis of the mucosal surface of the biliary ducts. The resulting peri-cholangitis leads to obstructive jaundice and accumulation of phytoporphyrin in the skin. The reaction between sunlight and circulating phytoporphyrin leads to tissue damage especially at muco-cutaneous junctions in lightly coloured or non-pigmented skin. Dark pigmented cattle may not show clinical signs.

Facial eczema can affect all ruminants to varying degrees. Alpacas and sheep are highly susceptible, cattle are moderately susceptible and goats have low susceptibility. Interestingly some family lines have greater susceptibilities, which illustrate the importance of selecting for resistance.

When the investigating veterinarian collected the initial history and heard that the cattle were head shaking they developed a list of differentials focused on neurological head shaking:


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