ANS 123: Animal Growth & Development
Discussion #2: Tissues Matter
(Richards & Edwards 1986)
Researchers reported a neurologic condition in nine beef calves, ranging in age from 1 day to 2 years. One of the calves failed to stand at birth and was euthanized that day. The 8 remaining calves had difficulty coordinating their hindquarters, causing them to sway while standing, fall frequently, and struggle to stand back up again. When walking, these calves would do so with exaggerated hindlimb movements. Initially, with the exception of their uncoordinated hindquarters, these calves did not appear to suffer from any other deficit; the calves with milder symptoms and slower progression even grazed successfully. However, over time, the symptoms gradually worsened to the extent that the calves could no longer stand up, resulting in their euthanasia. Once a calf’s condition had progressed and it was euthanized, the researchers collected tissue samples from each calf’s brain, spinal cord, and some major organs for analysis.
For the most part, the analysis did not reveal gross defects in the tissue samples collected. At the microscopic level, the organs all appeared normal as did most of the brain tissue samples. For the spinal cord samples, however, the researchers found bilaterally symmetric microscopic lesions. These lesions appeared in the white matter, or the myelinated regions, of the spinal cord. Using staining techniques, the researchers observed that the lesions were characterized by less stainable myelin with excess myelin in areas immediately adjacent to the lesions. In most of the lesions, the axons were normal. Interestingly, when microscopic brain abnormalities were detected, they presented as lesions in the medulla oblongata and cerebellum (white matter) and were identical to the spinal cord tissue lesions.
(Dalir‐Naghadeh, et al. 2004)
A team of veterinarians reported 3 case studies (2 calves and 1 spontaneously aborted fetus) that presented with similar congenital skin defects.
The first calf was 6 days old. She was brought to the clinic because she was anorexic, feverish, lethargic, and had bloody discharge from her mouth. Upon examination, she had very obvious areas on her legs, muzzle, and nostrils that were completely devoid of fur and/or skin. The skin- and fur-less areas on her legs were covered in crusts, but no blisters. Despite antibiotic and fluid therapy, the calf did not survive. The necropsy on this calf also revealed that her tongue was devoid of skin and the fur-less areas of her body lacked hair follicles and sebaceous glands.
The second calf was 8.5 months old. This calf also exhibited obvious blister-less areas on his legs that lacked skin and/or fur, but the size of the areas was not as extensive as the first calf. Although his vital his signs were normal, he was brought to the clinic because he was sickly. After treatment with antibiotics, this calf survived. The veterinarians were able to keep track of this calf for 2 months post-treatment during which time, the calf survived, but was not thriving.
In the case of the fetus, the necropsy showed that the hindlimbs were almost completely absent of skin, tongue, and hard palate. As with the first calf, this calf also did not possess hair follicles or sebaceous glands.
(Buczinski, et al. 2010, Nart, et al. 2004)
Beginning in 1982, veterinary reports began describing cattle that presented with severe congestive heart failure, dilated hearts, congested livers, ventral subcutaneous edema, and abdominal cavity fluid (Nart et al., 2004). Heart failure from this condition typically presents as an elevated heart rate, abnormal heart sounds, jugular distension, and edema (Buczinski et al., 2010). Based on tissue samples from 9 individuals, the cardiac tissue exhibited evidence of scarring (e.g., fibrosis) throughout the heart and degeneration of cardiac tissue. The remaining intact cardiac tissue was marked by significantly thicker and longer cardiac fibers. The researchers estimated that these cattle had experienced a loss of approximately 50% of their total cardiac tissue due to degeneration (Nart et al. 2004). Short of heart failure, heart conditions in cattle such as this are difficult to detect; likely as cardiac tissue possesses an incredible plasticity that enables it to accommodate to both short- and long-term stressors. In the few cases where this type of heart condition was diagnosed prior to heart failure, only one survived long-term (Buczinski et al. 2010).
(Besser, et al. 1990, Potter & Besser 1994)
Seven calves (3 castrated males & 4 females) from a single sire exhibited abnormal standing posture: they could not extend their limbs fully and stood on their dew claws due to joint looseness. In addition, when compared to normal calves, these 7 calves had longer, thinner limbs, eye defects in the lens, systolic heart murmurs, and enlarged aortic roots (Besser et al., 1990).
The 3 males were brought to the veterinarians at 8 months of age (Potter & Besser, 1994). The researchers euthanized 2 of the male calves at 8 and 12 months, respectively. A third male calf died suddenly at 16 months due to an aortic rupture. The researchers conducted necropsies on all three calves and collected tissue samples from each calf’s aorta. Necropsies confirmed the gross skeletal and ocular abnormalities identified during the live exams. The tissue sections of the aortae revealed that the while the collagen fibers were normal, the elastin fibers were short, fragmented, and widely separated from each other (Besser et al., 1990).
Of the 4 females, one was euthanized at 27 months for an unrelated condition. The 2nd was euthanized on the verge of death at 28 months. Her necropsy revealed that she was experiencing a tear in her pulmonary artery that had triggered a massive clot to form. The 3rd female died at 33 months due to an aortic rupture. Meanwhile, the 4th female remained stable at 55 months, after having produced 3 calves. For the females that were euthanized or died, the researchers sampled tissue from each individual’s aorta. Identical to the males, the collagen fibers were normal, while the elastin fibers were not (Potter & Besser, 1994).
- Which tissue type did your breakout group cover?
- What are the symptoms?
- Degree of impairment (e.g., compatible vs incompatible with life; fatal vs survivable) – Be prepared to explain
- If this condition is compatible with life/survivable, does the condition interfere with the purpose for which the animal was bred? – Be prepared to explain
- What type of tissue cell appears to be defective? – Be prepared to explain why that type of cell appears to be the cause of the condition