Cerebrocortical Necrosis (CCN) is a sporadic neurological disorder of the central nervous system affecting young bovines, especially calves and store cattle. Although often seen as an isolated event on farms, CCN can recur in herds exposed to dietary and management conditions, particularly those predisposing to ruminal acidosis and thiamine (Vitamin B₁) deficiency.
This guide explores the underlying causes of CCN, the clinical signs to watch for and the key nutritional and management strategies that can help reduce the risk of the disease. It also highlights the importance of supporting rumen health to minimise the conditions that predispose cattle to CCN and outlines practical measures that can be implemented on farm to help protect herd health and performance.
Pathogenesis and underlying mechanism:
CCN is a functional deficiency of thiamine (Vitamin B₁). Thiamine is a cofactor in several metabolic pathways including carbohydrate metabolism. In ruminants, thiamine is normally synthesised by rumen micro‑organisms and absorbed via the small intestine. Under normal conditions this endogenous production is sufficient to meet the animal’s requirements, and it is not normal to supplement Vitamin B1 in ruminant diets. Due to the sporadic nature of the disease the underlying causes are not fully understood.
CCN arises when there is an imbalance between thiamine synthesis and destruction within the rumen. It is thought bacteria, such as Clostridium sporogenes and Bacillus thiaminolyticus, can proliferate under specific dietary conditions and produce thiaminase enzymes. These enzymes break down thiamine before it can be absorbed, leading to the deficiency.
Recent work suggests that a drop in rumen pH seen in subacute or clinical acidosis may be a factor. This drop in pH causes thiaminase bound up in the cell wall of certain bacteria (in Clostridium sporogenes and Bacillus thiaminolyticus) to be released into the ruminal fluid. This provides an explanation for the frequent association of CCN with high‑concentrate diets, sudden introduction of grain, or very lush low‑fibre forages. As thiamine levels fall, energy metabolism in the brain is impaired, leading to symptoms commonly seen with the disease.
Sulphur toxicity can also cause symptoms like CCN. High sulphur levels in water sources, forages and feedstuffs can lead to the production of hydrogen sulphide (H₂S) gas within the rumen. Hydrogen sulphide is directly neurotoxic and interferes with cellular energy metabolism, producing lesions in the brain similar to that caused by thiamine deficiency.(Refer to Inform Nutrition Technical article on Sulphur).
Plants such as bracken fern (Pteridium aquilinum) and horsetail (Equisetum spp.) also contain thiaminase and may contribute when grazed in significant quantities.
Clinical signs and diagnosis:
Affected animals may first appear dull, then show signs of blindness, head‑pressing against walls or posts, uncontrolled eye movements, un-coordinated movements. Muscle tremors, and separation from the herd are also common. In severe cases the animal may become recumbent and progress to coma and death within hours to a few days.
Risk factors and predisposing conditions:
CCN is sporadic overall, but certain management and dietary factors markedly increase risk.
The most important include:
- High‑concentrate or low‑fibre diets: Sudden introduction or excessive levels of concentrates reduce rumen pH, slows rumen motility, and favour the growth of thiaminase‑producing bacteria. If feeding over 1 kilo (2.2 lbs) of a concentrate to calves, then, split it into 2 feeds.
- Lush low‑fibre grass: Calves grazing any combination of very green, leafy, wet, rapidly growing swards, especially after topping or tight grazing, consume high levels of fermentable carbohydrate with low fibre. This increases the risk of acidosis and thiaminase release. High covers of stemmy grass can also be an issue as calves will selectively consume the leaf first.
- Dietary transitions: Abrupt changes from pasture to high‑grain rations, or from a low‑fibre to a high‑energy diet, increase the risk a CCN breakout.
On some farms, repeated outbreaks suggest that local conditions, such as specific pasture types, feeding systems, rumen development or timing of turnout consistently create high‑risk environments.
Treatment strategies:
Animals are often acutely ill when first seen by the farmer. Because several diseases (e.g., listeriosis, meningitis, lead poisoning, and other encephalopathies) can mimic CCN, prompt veterinary diagnosis and treatment is important.
Diagnosis is based on a combination of history, clinical findings, and response to treatment. A history of recent dietary change (e.g., sudden increase in concentrates, move to lush grass, or feeding of high‑grain rations) strongly supports the diagnosis of CCN.
The primary treatment is high‑dose thiamine administration, usually given intramuscularly or intravenously. Doses are typically higher than those used for general vitamin supplementation and may need to be repeated over several days, depending on clinical response.
Calves that respond to treatment often show improvement within hours to a day, although some may have residual symptoms. Supportive therapy may include intravenous fluids and electrolytes to correct dehydration and acid‑base imbalances, along with measures to ensure adequate energy intake such as drenching with glucose or using parenteral nutrition (ie. short term intravenous therapy) if the animal is not eating.
CCN Premix:
Our experience has shown that supplementing Inform Nutrition’s CCN Premix (a proven formulation including a large concentration of a specific thiamine (Vit B1) source) through feed for non-clinical cases has been effective in reducing the number of subsequent cases appearing in the herd. Generally, we have found that once you pass 10 days from the initial case, the risk of a subsequent case is reduced.
Prevention and management:
Because CCN is triggered primarily by diet and management, prevention focuses on minimising factors that promote thiaminase production and ruminal acidosis:
Rumen development in calves. We typically don’t see CCN in suckler calves so poor rumen development and factors associated with artificial rearing may be an issue in some outbreaks. Calves neutralise acids produced when digesting feed by absorption of these acids in the rumen and production of natural buffers in saliva.
- Good rumen development is essential prior to weaning to prevent problems later.
- Any acidosis experienced by the calf during the rearing or postweaning phase can damage the rumen and reduce the ability of the calf to absorb these acids.
- Low fibre grasses reduce chewing, essential for production of saliva buffers and mixing in the rumen.
A reduction in rumen motility can slow down absorption of acids and lead to Subacute Ruminal Acidosis SARA or acute acidosis. In practice, we have found the inclusion of Rumbuff + Yeast at 2% (ie. 20 kilos per tonne of finished calf feed) to be a highly effective and key element in the solution to managing feed-related issues in young growing calves. At a concentrate feeding level of 1.0-1.5 kilos per head per day at grass this delivers an intake of 20-30 grammes per calf. As previously advised, ideally calves getting over 1.0 kilo per head should be fed twice per day.
Later born calves are often weaned close to turn out. The stress of weaning coupled with adaptating to a new diet can cause significant digestive problems. There is a strong argument, on problem farms, to keep these calves housed for at least a month longer to allow for further rumen development after weaning before turnout to grass.
Gradual diet changes: Introduce concentrates slowly over several days to allow the rumen microflora to adapt.
Ensuring adequate fibre: Maintain sufficient effective fibre in the diet (e.g., hay or straw) to buffer rumen pH and stimulate rumination. For fibre to be of benefit the calves must eat it. Fibre needs to be fed fresh daily when feeding in the field.
Grazing management: Avoid turning calves onto very lush, wet, low‑fibre swards immediately after topping or tight grazing. Strip grazing high covers can help reduce selective grazing and improve fibre intakes.
Monitoring and supplementation: In high‑risk situations (e.g., sudden move to high‑grain rations or lush grass), consider the temporary use or inclusion of Inform Nutrition CCN Premix. If you are experiencing an outbreak feed concentrates and monitor calves at least twice per day.
Although CCN is often a sporadic condition, understanding the nutritional and management factors that contribute to its development can significantly reduce the risk of future cases. Maintaining good rumen health through gradual dietary transitions, adequate fibre intake and effective nutritional management plays a key role in prevention. By recognising the early warning signs and implementing appropriate feeding strategies, farmers can help protect animal health, minimise losses and support optimum performance in young cattle.
For further information and/or stockists in your area, please contact your local Inform Nutrition Sales representative.
