Lesions in Brangus cattle with Chediak-Higashi syndrome

Hair, peripheral blood leukocytes, and other tissues from two related Brangus calves with phenotypic characteristics of Chediak-Higashi syndrome were examined by light and electron microscopy. Enlarged, pleomorphic, cytoplasmic granules, morphologically compatible with lysosomes, were seen in several neutrophils, many eosinophils, renal tubular epithelial cells, and Kupffer cells. Hair shafts of the calves showed irregular distribution and clumping of melanin granules. Severe infection and a possible hemorrhagic tendency were recognized. These Brangus calves represent the third breed of cattle affected with this genetic disease.     

Platelet aggregation, storage pool deficiency, and protein phosphorylation in mice with Chediak-Higashi syndrome.

The beige (bgJ/bgJ) mouse is a well-described murine model of Chediak-Higashi syndrome. Platelet function was examined in normal and beige mice to better characterize the defective aggregation response in platelets from mice with Chediak-Higashi syndrome. Platelet aggregation after collagen, thrombin, and phorbol-12-myristate 13-acetate stimulation was significantly (P less than 0.025) decreased in platelets from beige mice, relative to platelets from normal mice. Compared with beige and normal mice, those heterozygous for the bg trait had intermediate responses to collagen and thrombin, but not phorbol-12-myristate 13-acetate. The defect(s) in aggregation of platelets from beige mice was associated with a dense granule storage pool deficiency and decreased stores of serotonin and adenine nucleotides in platelets. Mice heterozygous for the bg trait had normal platelet serotonin and adenine nucleotide concentrations. Platelets from beige mice were approximately 10 times more sensitive to prostacyclin inhibition of collagen-induced aggregation than were platelets from control mice. However, a significant difference in platelet cyclic AMP concentration was not apparent between beige and normal mice after prostacyclin stimulation. Platelet endoperoxide synthesis measured by quantification of thromboxane B2, was normal in beige mice. Protein phosphorylation patterns in mouse platelets were similar to those seen in human platelets. Thrombin and collagen-induced [32P] phosphorylation of 40- and 20-kD proteins in platelets from normal and beige mice was similar. Results indicate that the biochemical defect(s) in platelet function in beige mice is partially attributable to storage pool deficiency and does not result in an absolute defect in phosphorylation of 40- and 20-kD proteins.     

Radiographic evidence of pulmonary dysfunction in anaesthetised cattle

The effects of fasting, sedation, recumbency and general anaesthesia on the radiographic appearance of the thoracic cavity of adult cattle were investigated. Fasting and sedation had little effect on the visible lung field but recumbency and general anaesthesia were followed by a reduction in lung field area. The reduction in area appeared to be greatest in the more dependent parts of the lung and was associated with the development of a persistent radiographic opacity. The changes were similar to those previously observed in horses.     

Neutropenia in cats with the Chediak-Higashi syndrome.

Thirteen cats with Chediak-Higashi syndrome and 22 control cats from the same colony, were evaluated for neutropenia. The absolute neutrophil counts of the Chediak-Higashi syndrome cats were significantly less (P less than 0.05) than those of the control cats. It is concluded that Chediak-Higashi syndrome cats, like Chediak-Higashi syndrome humans, have a neutropenia associated with the other manifestations of the syndrome. Lysozyme activity which was undetectable in the serum of both Chediak-Higashi syndrome and control cats was not of use for determining if the neutropenia was the result of neutrophil destruction.     

Secondary amyloidosis in a bull with Chediak-Higashi syndrome.

A ten year old Hereford bull with Chediak-Higashi syndrome was examined at necropsy after a lifelong history of recurrent bacterial infections. Amyloidosis, which has not been previously reported in Chediak-Higashi, was identified in liver, spleen and kidney.     

Alteration of release and role of adenosine diphosphate and thromboxane A2 during collagen-induced aggregation of platelets from cattle with Chediak-Higashi syndrome

OBJECTIVE: To compare the interaction of endogenous ADP with collagen and thromboxane A(2) (TXA(2)) during collagen-induced platelet aggregation between platelets from healthy cattle and those with Chediak-Higashi syndrome (CHS). POPULATION SAMPLE: Platelets harvested from blood samples from healthy Japanese Black cattle and those with CHS. PROCEDURES: Aggregation of gel-filtered platelets; release of ATP-ADP; and generation of thromboxane B(2) (TXB(2)), a metabolite of TXA(2), were measured. RESULTS: The potency of collagen to induce aggregation in platelets of cattle with CHS (ie, CHS platelets) was less than a tenth of that in platelets of healthy cattle (ie, control platelets). Platelet aggregation induced by collagen at an intermediate concentration depended on the coexistence of ADP and TXA(2), suggesting that released ADP cannot cause platelet aggregation by itself. Collagen-induced ADP release was markedly decreased, whereas TXB(2) production was slightly low in CHS platelets, compared with that in control platelets. A combination of subthreshold amounts of ADP and 9,11-dideoxy-9alpha, 11alpha-methano-epoxy-prostaglandin F(2) (U46619), a TXA(2) analogue, caused platelet aggregation. Similarly, a combination of subthreshold amounts of collagen and ADP caused platelet aggregation, whereas collagen and U46619 were not synergistic. CONCLUSIONS AND CLINICAL RELEVANCE: Deficient ADP release ensuing from the delta-storage pool deficiency in platelets from cattle with CHS resulted in reduction of collagen-induced platelet aggregation, through attenuation of synergism between TXA(2) and ADP and between ADP and collagen. Furthermore, results of the study reported here indicated that TXA(2) was important for aggregation of bovine platelets.     

Platelet function and association of bovine viral diarrhea virus with platelets of persistently infected cattle

OBJECTIVE: To determine whether viral involvement with platelets obtained from cattle persistently infected (PI) with bovine viral diarrhea virus (BVDV) is associated with altered platelet function or decreased platelet counts. SAMPLE POPULATION: Platelets obtained from 8 cattle PI with BVDV and 6 age-, sex-, and breed-matched uninfected control cattle. PROCEDURE: Manual platelet counts were determined, and platelet function was assessed through optical aggregometry by use of the aggregation agonists ADP and platelet-activating factor. Identification of BVDV in serum and preparations of purified platelets was determined by use of virus isolation tests. RESULTS: No significant difference in platelet counts was detected between cattle PI with BVDV and control cattle. In response to the aggregation agonists, maximum aggregation percentage and slope of the aggregation curve were not significantly different between cattle PI with BVDV and control cattle. We isolated BVDV from serum of all PI cattle and from purified platelets of 6 of 8 PI cattle, but BVDV was not isolated from serum or platelets of control cattle. CONCLUSIONS AND CLINICAL RELEVANCE: Isolation of BVDV from platelets in the peripheral circulation of cattle immunotolerant to BVDV does not result in altered platelet function or decreases in platelet counts.     

Platelet Aggregation in Feline Cardiomyopathy

Platelet aggregation in response to adenosine diphosphate (ADP) was evaluated in 16 healthy cats and in 10 cats with cardiomyopathy. The minimum threshold concentration of ADP required to induce irreversible (2nd-phase) aggregation was determined in each cat. The minimum ADP concentration needed for 2nd-phase aggregation in platelets from healthy cats ranged from 1 microM to 100 microM ADP, with 56% (9/16) requiring 100 microM ADP. Of the remaining seven normal cats, three had platelets responding irreversibly to 10 microM ADP, and four had platelets responding to 1 microM ADP. In cats with cardiomyopathy, the threshold concentrations ranged from 0.01 microM ADP to 10 microM ADP. Two cats had platelets responding irreversibly to 0.01 microM ADP, whereas another cat had a threshold response at 0.1 microM ADP. Platelets from the remaining seven cats with cardiomyopathy exhibited 2nd-phase aggregation in response to 1 microM ADP (five cats) or 10 microM ADP (two cats). Platelet counts ranged from 210,000/mm3 to 630,000/mm3 in healthy cats and from 218,000/mm3 to 624,000/mm3 in cats with cardiomyopathy. There was no apparent correlation between the platelet count and the magnitude of the threshold aggregation response, as measured by lag phase and slope of the aggregation curves. The results indicate that some cats with cardiomyopathy have platelets that are hyperaggregable to ADP in vitro.     

Platelet transfusion in thrombocytopenic horses

Platelet transfusions might be indicated in horses with thrombocytopenia. The need for a transfusion cannot be determined by platelet numbers alone, as primary or co‐existing disease processes, platelet function and age of the recipient also need to be considered. In patients with no co‐morbidities, relevant bleeding is uncommonly observed with platelet counts >10 x 10⁹/l and a therapeutic approach with initiation of treatment when signs of bleeding are observed might be justified.     

种牛场牛腐蹄病的防治研究

于2002年对种牛场42头肉用种公牛进行了腐蹄病的预防研究,对不同品种、不同年龄阶段的牛进行了统计,结果表明:患有腐蹄病的牛有9头,发病率为21.4%,在发病期间严重影响了种公牛采精、冷冻精液的生产及其质量,影响了优秀种公牛生产性能的发挥。经研究发现发病率主要是随年龄增长而上升,并与品种、季节和牛舍卫生条件等因素十分相关。经3年的防治研究,种牛场每年牛腐蹄病发病率逐年减少,分别为21.4%,9.5%,0,取得了较好的防治效果。腐蹄病总治愈率为84.6%,其中,急性腐蹄病的总治愈率为100%,慢性腐蹄病的总治愈率为60%。     

Defective in vitro motility of polymorphonuclear leukocytes of homozygote and heterozygote Chediak-Higashi cats.

The in vitro migratory responses of neutrophils of homozygote and heterozygote Chediak-Higashi cats were defective in an under-agarose assay when compared to the behavior of phagocytes of control cats. The linear distances traversed by the leading front of migrating Chediak-Higashi neutrophils toward streptococcal culture supernatant, zymosan-activated serum or buffer were reduced and smaller numbers of Chediak-Higashi phagocytes populated the resulting migration areas than did cells of control animals. The relative migration parameters of the Chediak-Higashi phagocytes, however, did not differ from the corresponding parameters of control neutrophils in the presence of streptococcal culture supernatant. Therefore, phagocytes of homozygote and heterozygote Chediak-Higashi cats recognized and responded equally well to the bacterial stimuli as did cells of control animals but traveled shorter distances primarily because of a reduced inherent motility. Similar results were also obtained when the feline phagocytes were attracted by zymosan-activated serum. In addition the relative migration parameters of the neutrophils of homozygote Chediak-Higashi cats were reduced and the normalized spatial distributions of their migrating cells were significantly different in the presence of 100% and 20% zymosan-activated serum when compared to the corresponding migration parameters of carrier and control animals. Defective recognition or responses to the higher concentrations of these host-derived attractants complicated, therefore, the already reduced inherent motility of the phagocytes of homozygote Chediak-Higashi cats.