Alzheimer type II astrocytes in the brains of pigs with salt poisoning (water deprivation/intoxication)

The finding of Alzheimer type II astrocytes, in addition to the pathognomonic combination of laminar cerebrocortical necrosis and eosinophil infiltration, in the brains of pigs is reported for the first time in cases of indirect salt poisoning following water deprivation.     

Unusual type of reactive astrocytes in the feline central nervous system

An unusual type of hypertrophic astrocytes termed plump polygonal astrocytes (PPA) has been observed in the feline central nervous system which was characterized in a first preliminary study of 17 cats.These cells presented an oval to polygonal shape, measured about 20 microm in diameter, and displayed short, barely detectable processes.The condensed, hyperchromatic, eccentric nucleus was surrounded by an abundant, homogenous, eosinophilic cytoplasm.These GFAP-and S-100-positive and vimentin-negative cells were predominantly found in brains showing status spongiosus and less frequently in association with inflammation and in brains lacking histological lesions.They were mainly detected in white matter areas of the hindbrain. In addition, these cells were also observed in the dentate hilar region adjacent to degenerated neurons and a small amount of PPA were positive for caspase-3. It remains to be determined if PPA represent a specific type of reactive astrocytes and whether they are characteristic for a specific cause or response in the feline brain.     

Intervertebral disc disease of the cervical and cranial thoracic vertebrae in equidae: eight cases

Intervertebral disc disease in the cervical and cranial thoracic vertebrae is unusual in horses and the majority of documented cases have been associated with infection and resulted in ataxia. The current retrospective study documents the clinical and imaging features, and outcome in eight Equidae with neck stiffness ± forelimb lameness (n = 3) or ataxia (n = 2) assessed during a 10-year period at two clinics. The Equidae (one donkey and seven horses) ranged in age from 1.5 to 12 years (median 5.5 years). The duration of clinical signs ranged from 1 to 6 months (median 1.5 months). The donkey had a depressed demeanour. All Equidae had reduced range of neck movement. The donkey and one horse showed mild and severe ataxia respectively. Two horses showed a propensity to stumble on each forelimb, one of which exhibited forelimb lameness on the lunge or ridden. Two additional horses showed lameness in hand. One horse experienced ‘neck locking’ during grazing. Radiological abnormalities were identified involving the intervertebral symphysis between the sixth cervical vertebra (C6) and C7 in four Equidae; in two horses the articulation between C7 and the first thoracic vertebra (T1) was involved. One horse had abnormalities of the intervertebral symphyses of both C7 and T1, and T1 and T2. In one horse the articulation between C2 and 3 was affected. The donkey was treated with a prolonged course of doxycycline and improved. An advanced dressage horse returned to full-function after surgical fusion of the affected intervertebral symphysis. Intervertebral disc disease is a rare cause of neck stiffness ± lameness or ataxia.     

Sequential histopathologic changes of type I, pre-type II and type II ostertagiasis in cattle

Yearling cattle in Louisiana were examined at monthly intervals for abomasal nematode burdens and histological lesions over a year. Tracer calves were grazed for 3 to 4 weeks and removed from pasture for 2 to 3 weeks, then slaughtered; a few animals were killed in extremis shortly after removal from pasture. Histological changes were correlated with worm burdens and characterized according to the type of Ostertagia ostertagi infection present. In cattle with acute Type I ostertagiasis, changes varied from eosinophil infiltration to glandular dilation and slight mucous cell hyperplasia with submucosal edema. During the summer months the cattle had worm burdens that were primarily early 4th stage larvae (EL4), with changes characterized by minimal glandular dilation and mucous cell metaplasia and moderate lymphoid cell proliferation and with intramucosal migration of EL4. In the autumn, the maturation of EL4 produced the Type II syndrome with severe glandular changes, prominent mucosal hyperplasia and marked lymphoid cell accumulation. With increased duration of the pre-Type II interval, there was greater development of the subepithelial lymphoid tissue and increased frequency of epithelial globule leukocytes. The lymphoproliferation which occurred during the prolonged pre-Type II interval appeared to be related to the increased severity and mortality seen with the Type II ostertagiasis syndrome.     

Long-term outcome associated with intratumoral chemotherapy with cisplatin for cutaneous tumors in equidae: 573 cases (1995-2004)

OBJECTIVE: To determine outcome associated with cutaneous tumors treated via intratumoral chemotherapy with cisplatin and identify risk factors affecting local tumor control and complications in equidae. DESIGN: Retrospective case series. ANIMALS: 573 equidae with 630 cutaneous tumors. PROCEDURES: Medical records of horses, mules, donkeys, and ponies with cutaneous tumors treated via intratumoral chemotherapy with cisplatin were analyzed. RESULTS: 549 horses, 13 mules, 8 donkeys, and 3 ponies with 630 histologically confirmed cutaneous tumors were included. Tumors included sarcoids (n = 409), squamous cell carcinomas (151), soft tissue sarcomas (28), cutaneous lymphomas (26), and melanomas (16). Overall cure rate, defined as local control at 4 years, was 93.3%. For all tumor stages combined, cure rates after 1 course of treatment were 96.3% for sarcoids, 96% for lymphomas, 88% for squamous cell carcinomas, 85% for soft tissue sarcomas, and 81% for melanomas. Treatment protocol, tumor stage, and prior treatment were significant prognostic factors for tumor control. Treatment efficacy was lower for large tumors, those with gross postoperative residual disease, and those that had been treated previously with other modalities. Treatment was well tolerated. Local reactions were more likely to occur and to be more severe after the third and fourth treatment sessions. CONCLUSIONS AND CLINICAL RELEVANCE: Results confirmed the value of intratumoral chemotherapy with cisplatin for treatment of cutaneous tumors in equidae.The results cannot be extrapolated to other formulations of cisplatin or other protocols that might be used.     

The sequential development of type I and type II ostertagiasis in young cattle with special reference to biochemical and serological changes

The sequential development of Type I and Type II ostertagiasis over a 2-year period in the same naturally infected cattle is described for the first time. Particular reference is made to biochemical and serological changes. Positive relationships were demonstrated between the clinical signs of both Type I and Type II disease, and marked increases in the levels of plasma pepsinogen, plasma gastrin and antibody titres to adult Ostertagia antigen. At necropsy, there were significant relationships between the combined total of adult and developing 5th stage larvae of Ostertagia spp. and the levels of both plasma pepsinogen and gastrin. By the end of the second grazing season the cattle had acquired an immunity to infection with Ostertagia spp. and had very low burdens of this parasite at necropsy. However some of these cattle maintained elevated plasma pepsinogen levels when under natural challenge by Ostertagia spp. larvae and the aetiology of these changes and the problems of diagnosis using this parameter are discussed. Similar trends of infection were observed for Cooperia oncophora, although resistance to the parasite developed more rapidly.     

自发性急性犬瘟热的原发性脱髓性脑病

为了进一步观察犬瘟热病毒引起的原发性脑损伤和包涵体形成的特点，调查脑组织的损伤与神经症状的关系，对10只急性犬瘟热病犬的脑组织进行了详细的病理学研究。为了仔细地观察病变，本试验按照解剖学关系将脑组织分成3个大部分和11个切面，即大脑(4个切面)，脑干(5个切面)和小脑(2个切面)。组织切片经HE、LFB和免疫组织化学染色后进行检查，结果表明：在大脑，脱髓呈弥漫性发生，程度较轻；脑干的周围或靠近第三脑室的白质脱髓较重；小脑在轻度或中度脱髓的基础上常出现严重的多发性脱髓灶。脱髓部呈空泡或海绵状，有少量胶质细胞存在，但无炎性反应。脱髓性病损是非时称性发生，对神经束没有特殊的亲和力。在脑室的室管膜细胞内发现有较多的嗜酸性胞浆或核内包涵体。用抗犬瘟热病毒抗体染色，带有包涵体的室管膜细胞呈现强阳性反应。部分锥体细胞，神经核细胞和漓氏细胞变性、溶解或胞浆深染。胞核浓缩。这种变化以小锥体神经细胞表现得最为明显。根据此研究结果，作者认为由犬瘟热病毒引起的原发性脑组织损伤是一种脱髓性脑病，而不是脑炎变化；位于室管膜细胞内的包涵体对于脑组织犬瘟热的确诊具有重要的作用；由于犬瘟热病毒引起神经细胞的损伤是非特异性的，对脑组织的侵害是非对称性的。对神经束的作用无特殊的亲和力，所以患犬瘟热的犬在临床上可出现不同的神经症状。     

Genotyping glycogen storage disease type II and type V in cattle reared in the Czech Republic

Genotyping was carried out for glycogen storage disease type II and type V in seven cattle breeds. The analysis was carried out using the polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP) method. In the breeds analysed [Charolais, Czech Spotted (Czech Simmental), Belgian Blue, Limousine, Blonde d'Aquitaine, Aberdeen Angus, and Beef Simmental sires reared in the Czech Republic], the recessive allele was not found in the PYGM (phosphorylase glycogen, muscle) responsible for the glycogen storage disease type V. In the same panel, the recessive allele in exon 7, exon 9 and exon 13 of the GAA (glucosidase alpha, acid), causing the glycogen storage disease type II was not found. Therefore, we have not revealed the recessives outside previous reported breeds. The knowledge of the breed-specific occurrence of inherited disorders facilitates focusing and reduces the costs of detecting the heterozygous carriers of recessive inherited disorders.     

Comparison of type I and type II bovine viral diarrhea virus infection in swine.

Some isolates of type II bovine viral diarrhea virus (BVDV) are capable of causing severe clinical disease in cattle. Bovine viral diarrhea virus infection has been reported in pigs, but the ability of these more virulent isolates of type II BVDV to induce severe clinical disease in pigs is unknown. It was our objective to compare clinical, virologic, and pathologic findings between type I and type II BVDV infection in pigs. Noninfected control and BVDV-infected 2-month-old pigs were used. A noncytopathic type I and a noncytopathic type II BVDV isolate were chosen for evaluation in feeder age swine based upon preliminary in vitro and in vivo experiments. A dose titration study was performed using 4 groups of 4 pigs for each viral isolate. The groups were inoculated intranasally with either sham (control), 10(3), 10(5), or 10(7) TCID50 of virus. The pigs were examined daily and clinical findings were recorded. Antemortem and postmortem samples were collected for virus isolation. Neither the type I nor type II BVDV isolates resulted in clinical signs of disease in pigs. Bovine viral diarrhea virus was isolated from antemortem and postmortem samples from groups of pigs receiving the 10(5) and the 10(7) TCID50 dose of the type I BVDV isolate. In contrast, BVDV was only isolated from postmortem samples in the group of pigs receiving the 10(7) TCID50 dose of the type II BVDV isolate. Type I BVDV was able to establish infection in pigs at lower doses by intranasal instillation than type II BVDV. Infection of pigs with a type II isolate of BVDV known to cause severe disease in calves did not result in clinically apparent disease in pigs.     

Causes of Encephalitis and Encephalopathy in Brazilian Equids

The etiology of diseases that affect the central nervous system (CNS) of equids was investigated. Samples (n = 218) collected from equids showing clinical signs of nervous or behavioral changes were analyzed, of which 37 (17.0%) were positive for rabies, 13 (6.0%) for the presence of protozoans (one Sarcocystis neurona, 12 Toxoplasma gondii), three (1.4%) for equine herpesvirus type 1 myeloencephalopathy, and 24 (11%) for bacterial encephalitis. Histopathology of the CNS revealed one (0.4%) case of cryptococcal myelomeningoencephalitis and 20 (9.2%) cases of equine leukoencephalomalacia. Central nervous system samples were positive for Sarcocystis neurona and Toxoplasma gondii by nested PCR-ITS1 followed by nucleotide sequencing. Diagnosis of equine herpesvirus 1 was confirmed by cell isolation and polymerase chain reaction followed by sequencing of the GD and polymerase (ORF 30) genes in three samples. No case of equine encephalomyelitis was diagnosed in samples analyzed by isolation in mice, VERO cell cultures, and RT-PCR for the nsP1 gene. Bacterial agents (Staphylococcus spp., Streptococcus spp., Bacillus spp., Enterobacteriaceae spp., Corynebacterium spp., and nonfermenting gram-negative bacillus) were detected in pure or preponderant cultures. Diagnosis was conclusive in 45% of samples, indicating that other infectious and noninfectious etiologies of encephalitis and encephalopathy should be considered for investigation.     

Mucolipidosis type II in a domestic shorthair cat

A seven-month-old, female domestic shorthair cat was presented to the Veterinary Teaching Hospital, University of Zurich, with abnormal facial features, retarded growth and progressive hindlimb paresis. On physical examination the cat had a flat, broad face with hypertelorism, frontal bossing, small ears and thickened upper and lower eyelids. The corneas of both eyes were clear and the pupils were dilated. The skin was generally thickened, most prominently on the dorsal aspect of the neck. Radiography of the entire skeleton revealed a severely deformed spinal column, bilateral hip luxation with hip dysplasia, an abnormally shaped skull and generalised decreased bone opacity. The clinical features and radiographic changes were suggestive of mucopolysaccharidosis. The toluidine blue spot test on a urine sample, however, was negative for glycosaminoglycans. Further biochemical investigations revealed a deficiency of the enzyme N-acetylglucosamine-1-phosphotransfer-ase (GlcNAc-phosphotransferase, EC 2.7.8.17) in peripheral leukocytes and an elevation of many lysosomal enzymes in the serum of the cat which is diagnostic for mucolipidosis type II. Histology and electron microscopy of different tissues are briefly summarised. The findings of this cat, the first reported case of mucolipidosis type II are compared with other similar storage diseases described in the cat.     

Vitamin D-dependent rickets type II in a cat

A cat with clinical signs Indicating rickets was diagnosed as having a defect of vitamin D receptors. Clinical signs had been seen from four months of age. Treatment with calcium supplementation and various forms of vitamin D did not alter plasma calcium levels or reverse skeletal lesions of lateral antebrachial bowing, lumbar spinal lordosis and costochondral beading. Analgesics were effective for relieving skeletal pain during the bone growth phase and were withdrawn when the animal reached skeletal maturity. Therapy for hip osteoarthritis was given from five years of age until the cat was euthanased at nine years of age as a result of refractory hip pain.     

Prevalence of equine herpesvirus-1 and equine herpesvirus-4 infections in equidae species in Turkey as determined by ELISA and multiplex nested PCR

In this report we examined the presence of specific antibodies against equine herpesvirus type 1 (EHV-1), and equine herpesvirus type 4 (EHV-4) in several equidae, including mules, donkeys, horses. The presence of EHV-1 and EHV-4 in respiratory diseases of equids, and ability of multiplex nested polymerase chain reaction (PCR) screening in simultaneous diagnosis of horses acutely infected by EHV-1 and EHV-4 were also investigated. Sera from 504 horses, mules and donkeys sampled were tested for the presence of EHV-1 and EHV-4 specific antibodies. Blood samples taken from 21 symptomatic horses and nasal swabs taken from 40 symptomatic horses were tested for the presence of EHV-1 and EHV-4 by a multiplex nested PCR. A total of 14.3% (3/21) of buffy coat samples and 32.5% (13/40) nasal swab samples were found to contain EHV-1 DNA, while 19% (4/21) buffy coat samples and 22.5% (9/40) nasal swab samples were found to be positive for EHV-4 DNA. By species, 14.5% of horses, 37.2% of mules and 24.2% of donkeys tested were EHV-1 seropositive. EHV-4 specific antibodies were detected in 237 (81.7%) of 290 horse sera tested. Results from this investigation demonstrate that EHV-1 and EHV-4 are prevalent throughout the equid population, and that donkeys and mules might also represent an important source of infection for other equids. We also showed that the multiplex nested PCR assay might be useful for diagnosis of mixed respiratory infections in horses due to EHV-1 and EHV-4.     

Platelet aggregation responses and virus isolation from platelets in calves experimentally infected with type I or type II bovine viral diarrhea virus.

Altered platelet function has been reported in calves experimentally infected with type II bovine viral diarrhea virus (BVDV). The purpose of the present study was to further evaluate the ability of BVDV isolates to alter platelet function and to examine for the presence of a virus-platelet interaction during BVDV infection. Colostrum-deprived Holstein calves were obtained immediately after birth, housed in isolation, and assigned to 1 of 4 groups (1 control and 3 treatment groups). Control calves (n = 4) were sham inoculated, while calves in the infected groups (n = 4 for each group) were inoculated by intranasal instillation with 10(7) TCID50 of either BVDV 890 (type II), BVDV 7937 (type II), or BVDV TGAN (type I). Whole blood was collected prior to inoculation (day 0) and on days 4, 6, 8, 10, and 12 after inoculation for platelet function testing by optical aggregometry by using adenosine diphosphate and platelet activating factor. The maximum percentage aggregation and the slope of the aggregation curve decreased over time in BVDV-infected calves; however, statistically significant differences (Freidman repeated measures ANOVA on ranks, P < 0.05) were only observed in calves infected with the type II BVDV isolates. Bovine viral diarrhea virus was not isolated from control calves, but was isolated from all calves infected with both type II BVDV isolates from days 4 through 12 after inoculation. In calves infected with type I BVDV, virus was isolated from 1 of 4 calves on days 4 and 12 after inoculation and from all calves on days 6 and 8 after inoculation. Altered platelet function was observed in calves infected with both type II BVDV isolates, but was not observed in calves infected with type I BVDV. Altered platelet function may be important as a difference in virulence between type I and type II BVDV infection.     

Glycogen storage disease type II in the Lapland dog

Summary

A newly recognized inherited metabolic disease in the Lapland dog is described. The metabolic defect is a deficiency of acid‐α‐glucosidase, a lysosomal hydrolase. The clinical picture is dominated by vomiting related to megaoesophagus, and progressive muscle weakness leading to exhaustion and death before two years of age. Cardiac abnormalities are observed. The main histopathologic lesion consists of glycogen accumulation, notably in membrane‐bound vacuoles (glycogenosomes), involving all kinds of muscular tissue in particular. Recessive inheritance of the disease was demonstrated by complementation analysis. The enzyme protein is present in affected tissues, although in an inactive form. Based on the gene dosage phenomenon, an attempt was made to identify carrier dogs by means of a biochemical assay. Glycogen storage disease type II in the Lapland dog appears to be a homologous model for the infantile manifestation of glycogen storage disease type II (Pompe's disease) in man.     

Glycogen storage disease type II in the Lapland dog

A newly recognized inherited metabolic disease in the Lapland dog is described. The metabolic defect is a deficiency of acid-alpha-glucosidase, a lysosomal hydrolase. The clinical picture is dominated by vomiting related to megaoesophagus, and progressive muscle weakness leading to exhaustion and death before two years of age. Cardiac abnormalities are observed. The main histopathologic lesion consists of glycogen accumulation, notably in membrane-bound vacuoles (glycogenosomes), involving all kinds of muscular tissue in particular. Recessive inheritance of the disease was demonstrated by complementation analysis. The enzyme protein is present in affected tissues, although in an inactive form. Based on the gene dosage phenomenon, an attempt was made to identify carrier dogs by means of a biochemical assay. Glycogen storage disease type II in the Lapland dog appears to be a homologous model for the infantile manifestation of glycogen storage disease type II (Pompe's disease) in man.