Distal limb necrosis is occasionally encountered secondary to septicaemia, most notably from Salmonella, and from the ingestion of fungal toxins. Known fungal toxins associated with distal limb necrosis include the sclerotium of Claviceps purpurea (ergotism) and moulds on tall fescue, Festuca arundinacea (fescue foot). In addition, wire can occlude distal limbs leading to necrosis and extreme heat or cold can damage tissues with a similar outcome. This case describes distal limb necrosis in a single, otherwise well grown, robust, nursing Hereford calf grazing on a native pasture on the central tablelands of NSW. An investigation did not identify the cause of this condition but septicaemia is suspected.
The owner of a herd of 35 Hereford cows with 1-2 month old calves at foot called because one calf had what he described as an infection of all feet that was unresponsive to antibiotics. The calf, examined on 8 October 2010 was a well-grown, bright and alert 7-week-old Hereford heifer. The skin covering all feet was dry and black although this was less extensive on the left front foot. This necrotic skin extended proximally to about the fetlock. The right hind fetlock joint was palpably unstable. No other extremities appeared to be affected and the calf was not febrile.
The mob of cattle grazed a pasture dominated by perennial native grasses and naturalised exotic species on a light granite soil. The pastures also contained an abundant residue of summer grasses. In view of the prognosis, the calf was euthanased and was subsequently autopsied.
A distal foreleg was submitted to the laboratory for examination. This limb had necrosis (dry gangrene) with a sharp demarcation between normal and necrotic tissue overlying the distal metacarpus (Image 3). The lesion had an unpleasant smell. The affected skin was black and hard. The underlying subcutis contained areas of haemorrhage and yellow discolouration. The digital flexor tendon contained some localised, fibrinous exudate within the tendon sheath. The metacarpo-phalangeal joint contained scant, tacky material within the joint, which was not present within interphalangeal joints. Longitudinal sectioning of phalangeal and distal metacarpal bones did not reveal any obvious lesions.
A section of skin and subcutis was examined at the junction of normal and necrotic skin. Inflammatory crusts were overlying the surface of the necrotic skin. There was full-thickness coagulative necrosis of affected skin and subcutis. Necrotic tissue was surrounded by a proximal zone of haemorrhage with moderate infiltrates of macrophages, neutrophils, proliferating fibroblasts and collagen. The flexor tendon contained localised fibrinosuppurative exudate within the tendon sheath.
Hepatocytes had a swollen, pale cytoplasm indicating non-specific hydropic degeneration. The heart section contained a single, small focal area of necrosis and mineralisation of myofibres. This was presumed to be incidental.
The calf tested negative on the Pestivirus antigen ELISA (PACE). Salmonella culture was negative on a pooled sample comprised of three swabs taken from the subcutis, metacarpo-phalangeal joint and tendon sheath
Gangrene, the necrosis and sloughing of tissues, can be either moist or dry. Moist gangrene occurs when lymphatic and venous vessels are obstructed and is usually accompanied by infection. When arterioles become damaged by trauma, pressure or toxins or obstructed by microemboli or spasms; while the lymphatic and venous return vessels remain patent; dry gangrene occurs (Radostits et al. 2007, Diver and Peek, 2008).
Fungal toxins are the best known agents that damage arterioles or cause them to spasm. These include the parasitic fungus Claviceps purpurea, which produces ‘ergots’ on the seed heads of a range of grasses, especially ryegrass. Fungal endophytes within tall fescue (Festuca arundinacea) also damage or impair the function of arterioles leading to local vascular obstruction but Aspergillus terreus and mushrooms are also described as causing this disorder (Radostits et al., 2007).
Calves can suffer from dry gangrene of the extremities subsequent to Salmonella infection. In this condition, there is a clear line of demarcation of the skin from normal to necrotic at the fetlock joint. The tips of the ears and tail may also be affected (Radostits et al., 2007). In this case, there is no evidence for the presence of any of the known agents that cause distal limb necrosis in calves. Histopathology was not definitive for any cause, though the fibrinosuppurative tendonitis could have been due to bacterial infection. A previous episode of salmonellosis is possible but seems unlikely in an otherwise apparently healthy calf grazing at a low stocking rate on pasture.
Tall fescue is an introduced grass grown in NSW in lawns and pastures (PlantNET). There is no evidence that it is present on this property. The dry residues may have contained fungal toxins but a nursing calf would not normally consume much of this material. This calf was also not febrile, as might be expected with ergotism, although any febrile episode may have passed.
We presume that this calf suffered a recent septicaemia leading to either endothelial damage or micro emboli, obstructing the arterioles supplying blood to the feet.
Distal limb necrosis secondary to Salmonella was particularly common during the ’70s. One herd of dairy cross calves in particular had significant problems. The calves, reared in a woolshed died in droves from Salmonella dublin. At least a dozen lost the distal 6-12 inches (pre-metric) of one or more limbs. There were a few other incidents but mostly ones or twos. The problem stopped when it stopped raining.
Dan Salmon, Riverina LHPA