CASE NOTES

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Acute bovine pulmonary oedema and emphysema in a single heifer on dry pastures in central west New South Wales

Nik Cronin, District Veterinarian Central West Local Land Services, Forbes, and Anthony Chamings, Veterinary Pathologist Elizabeth Macarthur Agricultural Institute, Menangle

Posted Flock and Herd June 2025

INTRODUCTION

Acute bovine pulmonary oedema and emphysema (ABPE) is the name given to a syndrome also known as 'fog fever'. In England the disease is often associated with rapidly growing pasture that is lush, known as 'foggage', hence the common term². This report describes a case of ABPE, 'fog fever', in a single animal in central west NSW.

HISTORY

A producer in the Parkes district requested a post-mortem on an 18-month-old Angus heifer that died suddenly in early January 2025. She was part of a mob of 120 head, 70 of which were homebred, and 50 of which were bought in several months earlier. They had been grazing mixed paddocks, pasture and stubble, since harvest. They were on regrowth forage sorghum for about a month until late December 2024, then moved onto barley stubble with drying summer grasses also present. There was a dry creek bed with light timber shelter running through the paddock, and fresh dam water supply.

A wet period had occurred late November into early December associated with particularly warm and humid conditions. Temperatures through the rest of December were slightly above average, and particularly warm toward the end of the month.

The producer was working in the paddock around the middle of the day and from a distance noticed the heifer sitting on her own. She stood and attempted to move to the mob but after a short distance lay down and died. While all other animals looked well the producer was concerned because another animal in the same mob which was noticed unwell around mid-December had died. No investigation was carried out at the time.

INVESTIGATION

It was a very hot day and late in the afternoon. Feed in the paddock was dry, apart from a small number of green shooting plants.

The well-grown heifer, in excellent body condition, was in right lateral recumbency in the middle of the paddock. It was 4-5 hours since death, and she was in rigor mortis. Her oral mucous membranes were dark purple and there was a small amount of watery blood-stained fluid pooled in her nostrils, and no other discharges apart from clear mucous around the vulva. An anthrax ICT was negative.

Figure 1. Dead heifer in situ in dry stubble paddock

After the ICT the heifer was moved to a different location for post-mortem and ease of disposal.

During post-mortem the most significant findings were in the chest cavity. The pleural surface of the chest wall was severely inflamed, with roughening and marked ecchymotic haemorrhages. The lung surfaces were shiny and mottled in colour. Lung tissue was wet, firm and heavy. The tracheal lumen contained blood-stained fluid, and the mucosal surface was roughened with sub-mucosal haemorrhages. The extent of pulmonary congestion and the presence of moderate interlobular oedema and emphysema was more apparent on cut section. A thick, stable foam was present in the small airways.

Figure 2. Left chest wall, with inflammation and ecchymotic haemorrhages

Figure 3. Left lung, shiny surfaces with firm lung tissue mottled in colour

Figure 4. Tracheal lumen, with blood-stained fluid

Figure 5. Lung, severe pulmonary congestion, interlobular oedema, emphysema, and foam exuding from small airways

The liver was slightly enlarged. The rumen was normal size and full, containing mostly dry ingesta, and there were a large number of small summer grass seeds in the abomasum.

LABORATORY

Samples were submitted to NSW Animal and Plant Health Laboratories at the Elizabeth Macarthur Agricultural Institute (EMAI). Fresh lung tissue yielded no growth on routine culture, and a lung swab reported a sparse pure growth that was determined not to be significant.

Histopathology of two sections of the lung revealed that the alveolar spaces were filled with oedema fluid and inflammatory cells (neutrophils and macrophages) as well as small amounts of haemorrhage. The respiratory epithelium of the alveoli was replaced by dead or dying cells (necrosis) and eosinophilic cellular debris (hyaline membranes) and the alveolar septae were expanded by oedema fluid and small numbers of inflammatory cells. Inflammation, necrosis and oedema were also seen affecting smaller bronchioles. The changes were consistent with an acute interstitial pneumonia.

Figure 6. Lung, alveolar lining replaced by fibrillar eosinophilic material (hyaline membranes) ( ✯ ), alveolar space filled with neutrophils, macrophages and cellular debris ( ✚ ) and expanded alveolar septae containing neutrophils, lymphocytes and congested capillaries ( < ).

DISCUSSION

'Fog fever' is an acute atypical interstitial pneumonia seen in cattle. More recent names now tend to be more descriptive of its pathophysiology, such as ABPE.

"ABPE is one of the more common causes of acute respiratory distress in adult cattle on pasture, usually in the 'fall', 5-10 days after a change to a better, often lush pasture".¹

The disease is rare in Australia⁵.

Classic 'fog fever' is seen when cattle are introduced to protein-rich, lush pasture where previous grazing was dry feed. The new diet has high levels of tryptophan, which is converted into 3-methylindole (3-MI) in the rumen. This metabolite enters circulation where it is further broken down in the lungs by mixed function oxidases to a pneumotoxin. This compound causes extensive localized damage leading to oedema, interstitial pneumonia, and alveolar and interstitial emphysema³. It most commonly presents as an outbreak with multiple animals affected, although there may be mild, as well as severely affected animals⁵. Spontaneous recovery is possible in mild cases¹.

Histopathology of the lung determined that this animal had died of ABPE as above - but the pasture available was clearly not 'foggage'. Agents other than foggage/tryptophan can cause ABPE. One is a pneumotoxin found in mouldy sweet potatoes. Purple mint (Perilla fruitescens), stinkwood (Ziera arborescens) and rapeseed and kale (brassica spp.) have also been implicated⁴. Viral infections, septicaemia, inhaled toxins and hypersensitivity reactions (e.g. to lung worm/Dictyocaulus sp.) can also cause similar histopathological changes⁴. In this case no lung worm sections were observed, and the epidemiology was less supportive of a virus (as deaths were sporadic and no clinical disease was seen in other animals). Interestingly, the disease is reported to occur commonly in western Canada when cattle have been placed in a stubble field following the harvest of any of the cereal crops⁵, as were the cattle in this case. The reference does not define whether cases in this scenario are isolated/sporadic or occur as part of an outbreak.

Searching available disease investigation records for the district, we reviewed a previous case of 'fog fever' diagnosed by a private practitioner. It occurred in March 2019, which was during an extended drought period. A single steer was affected. Case history notes were minimal, however it was reported that the animal had escaped a paddock to access a 'lush' pasture for one day and then was returned to the original paddock with sparse feed and sorghum hay on offer.

A search was also performed in Sample Manager at EMAI looking for cases in which the terms 'Fog Fever' or 'Acute Bovine Pulmonary Oedema and Emphysema' were mentioned between 1 January 2020 and 1 April 2025. In this period five cases were identified with histological changes consistent with acute interstitial pneumonia and where the pathologist suggested toxic pneumonia as a possible differential. These cases occurred sporadically and were from Keerrong (near Lismore; March 2020), Narrabri (August 2020), Young (May 2021), Tamworth (June 2023) and Brewongle (near Bathurst; May 2024). Cattle were found dead, or observed with respiratory signs such as stridor or coughing. Consolidated or heavy, wet lungs were a common post-mortem finding described in the submissions. Two cases were on lush pasture and one on oat stubble (still green). The other two case reports did not describe the feed available. One animal was persistently infected by pestivirus, and therefore an underlying viral cause was considered a potential contributing factor. In another case there was an accompanying bronchitis, and a secondary bacterial infection, in addition to the interstitial pneumonia, was likely. In a third case another animal in the herd had died recently from bacterial septicaemia, and therefore septicaemia was also considered as a potential cause of the post-mortem findings in the animal with acute interstitial pneumonia. In the same period, EMAI received over 33,300 submissions from cattle herds, and therefore toxic pneumonia is a relatively rare diagnosis in NSW.

REFERENCES

1. Campbell J (2022) Pulmonary Emphysema, Edema, and Interstitial Pneumonia in Cattle www.msdvetmanual.com Accessed April 2025
2. Maas J (2001) Fog fever, UC Davis Veterinary Medicine Extension my.ucanr.edu Accessed April 2025
3. McGavin MD & Zachary JF. Pathologic Basis of Veterinary Disease 4^th edn. Mosby Elsevier, pages 527-8
4. McGavin MD & Zachary JF. Pathologic Basis of Veterinary Disease 7^th edn. Mosby Elsevier, pages 839
5. Radostits OM, Blood DC, & Gay CC (2000) Veterinary Medicine; A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses. 9^th edn. WB Saunders Company Ltd, page 1782