In the early months of 2020, there was abundant growth of paspalum on the North Coast of NSW. Autumn rain and high humidity followed and subsequently large numbers of cattle in the Casino and Lismore regions were affected by paspalum staggers.
Paspalum dilatatum (common paspalum) and Paspalum distichum (water couch) are species of exotic perennial grass. In NSW, it is commonly found in tropical, subtropical and temperate regions along the east coast.1,2 It grows quickly in summer under ideal conditions and produces large quantities of seeds between late January to April.3
Claviceps paspali is an ergot-producing fungus that grows on seed heads of paspalum grasses (Image 1).2 The fungus starts off sticky and yellow-grey in appearance and becomes hard and black when it matures.2 Ingestion of the mature ergot by cattle can lead to neurological signs, including muscle tremors, head shaking, and incoordination, with recumbency when cattle are stressed or overstimulated.4 This presentation is referred to as paspalum staggers or Claviceps paspali intoxication.2
This report describes cases of paspalum staggers in cattle on six properties from the north-eastern region of NSW.
Case Report/Series:
In April 2020, Local Land Services District Veterinarians from the districts of Casino and Lismore were called out to properties to investigate reports of cattle with neurological signs suspected to be from Claviceps paspali intoxication.
Case 1
On 1 April, a property was visited where 8/50 adult mixed-sex Charolais cattle in good condition (fat score 4) were displaying muscle fasciculation and mild head bobbing. One cow displayed signs of hind leg hypermetria, spasmodic tonic-clonic tightening of muscles and aggression to other cattle in the yard with signs becoming more severe when put under pressure. The pasture was predominantly made up of paspalum with high infestation of the seed heads with ergot at different stages of maturity. Humid conditions preceded the development of clinical signs in these cattle.
The differential diagnoses for this case included paspalum staggers and bovine ephemeral fever (BEF) or some unknown toxicity. Polymerase chain reaction (PCR) assay for bovine ephemeral fever virus (BEFV) came back negative.
The main findings from haematology and biochemistry were mild lymphocytopaenia most likely caused by stress, mild hyperproteinaemia most likely caused by dehydration and mild hypocalcaemia most likely caused by decreased feed intake.
As paspalum staggers was the most likely differential, the owner was advised to remove cattle from the ergot-infested pasture, slash the tops of the infested paspalum to remove the seed heads, provide cattle with hay and supplement with lick blocks for trace elements and calcium.
Case 2
On 2 April, another property was visited where 4/100, seven-year-old female Braford cattle were showing clinical signs of ataxia and incoordination. The pasture was predominantly composed of paspalum.
One of these cows was in lateral recumbency at the time of the property visit. On physical examination the cow was in good body condition (fat score 4), had injected and pink mucous membranes, muscle fasciculations, green rumen material coming out her nose and increased respiratory sounds.
Despite being placed in sternal recumbency and treated with antibiotics (oxytetracycline) intramuscularly as well as calcium and magnesium subcutaneously, she later died.
Haematology and biochemistry from this animal revealed mild hyperfibrinogenaemia, mild neutrophilia and mild lymphocytosis, indicating an inflammatory process and a mild hypocalcaemia (once again most likely due to decreased feed intake). PCR for BEFV was negative.
The cause of death was most likely aspiration and there was a high suspicion that the cow went down due to Claviceps paspali intoxication. A post-mortem was not performed for this case.
Case 3
On 16 April, a property was visited where 15 individuals from a mob of 100 mixed-sex adult beef cattle displayed signs of hindlimb ataxia, fine muscle tremors, head bobbing and aggression when mustered. A three-year-old Limousin bull went down in the yards and was unable to rise. He was in sternal recumbency on concrete, very aggressive and when disturbed displayed hyperesthesia of hind limbs, muscle fasciculations and had a wide-eyed look. The bull was still down two days later. The pasture on this property contained a large amount of paspalum with high levels of infestation of Claviceps paspali.
The cause was determined to be Claviceps paspali intoxication. No laboratory tests or post-mortems were performed for this case.
The owner was advised to remove cattle from the ergot-infested pasture.
Case 4
On a property was visited on 17 April where 1/50 from a mob of eight-year-old female Charolais cattle was found dead that morning in a drain with her head slightly downhill and positioned in dorsal recumbency. There were faeces behind her and evidence of paddling in the dirt from her hind legs. The pasture contained a significant amount of Paspalum dilatatum with most of the seed heads infested with ergot at different stages of maturity.
On post-mortem examination, the cow was in good condition and five months pregnant. There were petechial haemorrhages and congestion in the carcass, which were more prevalent in the front half of the cow, with swelling and congestion of associated prescapular and submandibular lymph nodes. A distinct bloat line was visible on the ribs with congestion cranial from ribs.4-5 The lungs were congested and compressed with distinct 'tiger stripe' haemorrhages and ecchymosis of the tracheal mucosa. A low number of scattered petechia were visualised in the epicardium. The rumen contained gas (likely due to post-mortem changes) with moderately dry contents and the omasum was full but not impacted. A large quantity of paspalum seed was found in the abomasum. There was also a low level paramphistome burden. The rest of the gastrointestinal tract was deemed to be normal. Multiple hydatid cysts were found in the lungs and liver.
Death was determined to be due to compression of lungs and posterior vena cava from being cast. There was a high suspicion that the cow was down due to Claviceps paspali intoxication. No laboratory tests were performed in this case.
Case 5
Visit 1
Another property was visited on 20 April. Here, 5/20 head in a 2-year-old female Wagyu cattle mob displayed signs of muscle fasciculations and hypersensitivity to stimuli, with one individual down and unable to rise. The pasture was predominantly made up of paspalum with a high proportion the seed heads infected with ergot.
The down cow was two-and-a-half years old and heavily in calf. The owner reported that she was staggering around three days prior and went down yesterday. The cow was still eating and drinking at this time.
On physical examination, she was bright, alert, responsive, tachypnoeic (respiratory rate 70), hyperthermic (rectal temperature 41°C) with tacky pink/injected mucous membranes and a distended abdomen. She was very sensitive to touch, displayed mild muscle tremors and had flaccid paralysis, although she would attempt standing up.
Haematology of this cow revealed a hyperfibrinogenaemia indicating an inflammatory response and a PCR for BEFV was negative.
Biochemistry showed a marked elevation in both aspartate aminotransferase (AST) and creatinine kinase (CK). Beta-hydroxybutyrate (BHB) was markedly elevated and the haptoglobin was high.
These results indicated significant muscle damage most likely due to recumbency, severe ketosis and an inflammatory process.
As paspalum staggers was the most likely differential, the owner was advised to remove all cattle from the ergot-infested pasture and top the ergot infected paspalum using a slasher.
Visit 2
The district veterinarian revisited the property on 30 April. Despite the down cow having been lifted with a tractor daily, administered intramuscular injections of anti-inflammatories (Tolfedine) and antibiotics (oxytetracycline) daily for five days she showed no signs of improvement 10 days later and was humanely euthanased and a post-mortem performed.
During this time another cow was found down, however this second animal was able to self-ambulate after being lifted with the tractor. The other cow's clinical signs had resolved by the time of this visit.
On post-mortem exam of the first cow the liver appeared pale and there was mild inflammation of the abomasal lining. No paspalum seeds were visualised in the rumen, reticulum or omasum. The brain and spinal cord were removed.
Laboratory results returned a neutrophilia and hyperfibrinogenaemia indicating an inflammatory process. Elevated BHB, glutamate dehydrogenase (GLDH) and bilirubin in addition to decreased urea and creatine were likely due to starvation. There was also a suspicion of liver disease with elevated GLDH. Elevated CK and AST were most likely due to recumbency. There was a mild hypocalcaemia, hypoalbuminaemia and hypophosphataemia. There was a delay in separating the serum sample, therefore it cannot be determined whether there was a true hypoglycaemia and hyperkalaemia or whether this finding was an artefact of sample handling.
Histology of the liver indicated moderate diffuse centrilobular hepatic lipidosis, which is supported by the elevation in ketones and GLDH on haematology. Samples from the abomasum indicated moderate multifocal lymphoplasmacytic abomasitis. Histological samples from the heart, kidney, lung and spleen were examined with no abnormalities identified. Marked haemorrhage was visualised in the brain and cervical spinal cord and was due to captive bolt euthanasia. Histology of the spinal cord appeared vacuolated however few damaged axons were visualised. Digestion chambers were present but sparse.
Diagnosis for this cow was ketosis and hepatic lipidosis secondary to prolonged recumbency due to Claviceps paspali intoxication.
Case 6
On 28 April, a property was visited where 1/32 from a mob of one-year-old female Angus and Brangus cattle was found dead. The cow had been observed grazing on water couch prior to death. She showed signs of incoordination and ataxia, with increased severity of signs after being mustered. She went down, she had a 20-second-long seizure before rising again and walking a few metres before collapsing again. She had fine muscle tremors, aggressive behaviour, a head bob and a wide-eyed look. She died that afternoon and a post-mortem was done within two hours of death.
Differential diagnoses for this case included paspalum staggers and BEF. PCR for BEFV came back negative.
Post-mortem examination of the dead cow revealed multiple subcutaneous petechial haemorrhages and a large amount of paspalum seed in the abomasum. Histology showed no brain or spinal cord pathology.
There was a high suspicion of Claviceps paspali intoxication due to grazing of ergot-infested water couch seed heads.
Infections of Claviceps paspali generally occur in autumn and tend to be highest after wet humid summers.2,5-8 Lismore and Casino received higher-than-average monthly rainfall for the months of January and February (Figures 1 and 3) which resulted in prolific growth of Paspalum spp.2,9,10 In April, these regions also experienced close to the highest mean maximum monthly temperature ever recorded (Figures 2 and 4).11,12 High rainfall, humidity and day temperatures negatively impact pollination, which results in the paspalum floret remaining open for a longer period of time, making them more susceptible to infection from Claviceps paspali as the fungus most effectively infects florets that have not been pollinated or have been pollinated just prior to infection.13
The mycotoxins in Claviceps paspali believed to cause the staggers are tremorgenic indole-diterpenes.18 The types isolated so far including paspalitrem A, B and C as well as paspalinine.18 The specific pathophysiology of Claviceps paspali intoxication is not yet completely understood.18 It is thought to be due to inhibition of gamma aminobutyric acid receptors and release of neurotransmitters from synaptosomes at the neuromuscular junction in the central and peripheral nervous systems.13,18
In one study of sheep and cattle, 1g/kg/day of infected seed heads over a period of four or more days produced severe staggers,19 another study reported toxic dose amounts of 100g of infected seed heads per day for two days,2 and another reported 1-5kg over 2-6 days being the toxic amount.20 It is important to note that different stages of the ergot produce differing amounts of toxin, with the stage just before the fungus matures to become hard and black being the most toxic stage.2
Deaths directly from ingestion of the ergot are uncommon, however cattle can go down, sustain injuries and can die secondary to clinical intoxication.2 Younger animals appear to be more commonly affected as they appear to preferentially graze on these plants.2 The immature yellow stage of the ergot produces a nectar-like secretion called honeydew, which aids in the ergot's dispersal by insects and has been suggested to be palatable to cattle.13,19
Diagnosis is made via a combination of observing typical clinical signs, finding a history of exposure to ergot-infected paspalum pasture, obtaining a response to removal from infected pasture, and ruling out other differential diagnoses.2,13 Affected animals may appear normal prior to being moved or stressed.18
No effective treatment is available.2 Cattle should be removed gently from the infected pasture and placed in a safe paddock with no ponds, drains or steep slopes.2,20 Exercise and stress will exacerbate the clinical signs.19,20 Once moved, these animals should be monitored closely as a precaution since delay in onset of clinical signs has been described in paspalum staggers in horses.18 Clinical signs are expected to disappear within 10 days of removal from infected pasture.20
Effective pasture management is key in prevention of Claviceps paspali intoxication and involves frequent/heavy grazing during the major growth period of paspalum in the summer, which reduces the number of seed heads available for infection by the fungus.20 Mowing or slashing the paspalum pasture is also effective.20
I would like to thank Nathan Jenning for sharing his knowledge. I would also like to thank Prof. Jenny-Ann Toribio for organising this opportunity.