Noriyuki Horiuchi

Experimental induction of amyloidosis by bovine amyloid fibrils in Sore Hock rabbits.

We report the experimental amyloidosis associated with administration of bovine amyloid fibrils in rabbits afflicted by Sore Hock (SH), which is ulcerative pododermatitis. Two groups of SH-afflicted rabbits were subjected to five inflammatory stimulations at intervals of 4 days by intraepithelial injection of a mixture consisting of Freunds complete adjuvant and lipopolysaccharide. One group of rabbits was administered amyloid in conjunction with the last inflammatory stimulation and the other group was not. For additional control, two groups were designed. A third group consisted of rabbits without SH, which were subjected to five stimulations and were administered amyloid. A fourth group consisted of SH-afflicted rabbits, subjected to 0–4 stimulations and administered amyloid. Amyloid depositions were observed in SH-afflicted rabbits, which had been stimulated five times and given amyloid (18/18). In the 4th group, only one rabbit, which had been subjected to four stimulations, showed amyloid depositions. No amyloid depositions were observed in the other rabbits. These results suggest that bovine AA amyloid fibrils have an amyloid-enhancing factor-like effect on SH-afflicted rabbits.

Histological features of the vomeronasal organ in the giraffe, Giraffa camelopardalis

The vomeronasal organ (VNO) that preferentially detects species‐specific substances is diverse among animal species, and its morphological properties seem to reflect the ecological features of animals. This histological study of two female reticulated giraffes (Giraffa camelopardalis reticulata) found that the VNO is developed in giraffes. The lateral and medial regions of the vomeronasal lumen were covered with sensory and nonsensory epithelia, respectively. The vomeronasal glands were positive for periodic acid‐Schiff and alcian blue (pH 2.5) stains. The VNO comprises several large veins like others in the order Cetartiodactyla, suggesting that these veins function in a pumping mechanism in this order. In addition, numerous thin‐walled vessels located immediately beneath the epithelia covering the lumen entirely surrounded the vomeronasal lumen. This sponge‐like structure might function as a specific secondary pump in giraffes.

Lambda-carrageenan treatment exacerbates the severity of cerebral malaria caused by Plasmodium berghei ANKA in BALB/c mice

BackgroundThere is an urgent need to develop and test novel compounds against malaria infection. Carrageenans, sulphated polysaccharides derived from seaweeds, have been previously shown to inhibit Plasmodium falciparum in vitro. However, they are inflammatory and alter the permeability of the blood–brain barrier, raising concerns that their use as a treatment for malaria could lead to cerebral malaria (CM), a severe complication of the disease. In this work, the authors look into the effects of the administration of λ-carrageenan to the development and severity of CM in BALB/c mice, a relatively non-susceptible model, during infection with the ANKA strain of Plasmodium berghei.MethodsFive-week-old female BALB/c mice were infected with P. berghei intraperitoneally. One group was treated with λ-carrageenan (PbCGN) following the 4-day suppressive test protocol, whereas the other group was not treated (PbN). Another group of healthy BALB/c mice was similarly given λ-carrageenan (CGN) for comparison. The following parameters were assessed: parasitaemia, clinical signs of CM, and mortality. Brain and other vital organs were collected and examined for gross and histopathological lesions. Evans blue dye assays were employed to assess blood–brain barrier integrity.ResultsPlasmodium berghei ANKA-infected BALB/c mice treated with λ-carrageenan died earlier than those that received no treatment. Histopathological examination revealed that intracerebral haemorrhages related to CM were present in both groups of infected BALB/c mice, but were more numerous in those treated with λ-carrageenan than in mock-treated animals. Inflammatory lesions were also observed only in the λ-carrageenan-treated mice. These observations are consistent with the clinical signs associated with CM, such as head tilt, convulsions, and coma, which were observed only in this group, and may account for the earlier death of the mice.ConclusionThe results of this study indicate that the administration of λ-carrageenan exacerbates the severe brain lesions and clinical signs associated with CM in BALB/c mice infected with P. berghei ANKA.

Proventriculitis Associated with Cryptosporidium baileyi in a Snowy Owl (Bubo scandiacus) and Its Epidemiological Investigation

Abstract We describe an unusual case of proventriculitis associated with Cryptosporidium baileyi in a 7-wk-old snowy owl (Bubo scandiacus) chick kept at a zoo. Necropsy of this animal revealed diffuse mucosal thickening of the proventriculus. Subsequent histopathological examinations of the proventriculus showed marked ductal epithelial hyperplasia with intestinal metaplasia and severe inflammatory cell infiltration in the lamina propria and submucosa. These lesions were associated with numerous periodic-acid-Schiff–positive cryptosporidia-like protozoan parasites. Moreover, oocysts found within the lamina propria had a noticeably thicker wall and displayed Ziehl-Neelsen–positive test results. PCR sequencing analyses of the 18S rDNA, actin, and 70 kDa heat shock protein gene loci identified the protozoan to be C. baileyi, of which two novel sets of primers were designed for use with formalin-fixed paraffin-embedded tissue. An epidemiological survey was carried out at the zoo to investigate the source of infection, but all owl species surveyed proved negative for cryptosporidiosis. It is most likely that small animal vectors such as wild birds or rodents were responsible for this particular lethal case. This is the first report of C. baileyi associated with proventriculitis and also the first report of cryptosporidiosis in a raptor species in Asia.

Quantitative evaluation of cervical cord compression by computed tomographic myelography in Thoroughbred foals

ABSTRACT Five Thoroughbred foals (age, 8–33 weeks; median age, 31 weeks; weight, 122–270 kg; median weight, 249 kg) exhibiting ataxia with suspected cervical myelopathy (n=4) and limb malformation (n=1) were subjected to computed tomographic (CT) myelography. The areas of the subarachnoid space and cervical cord were measured on transverse CT images. The area of the cervical cord was divided by the area of subarachnoid space, and stenosis ratios were quantitatively evaluated and compared on the basis of histopathological examination. The sites with a ratio above 52.8% could have been primary lesion sites in the histopathological examination, although one site with a ratio of 54.1% was not a primary lesion site. Therefore, in this study, a ratio between 52.8–54.1% was suggested to be borderline for physical compression that damages the cervical cord. All the cervical vertebrae could not be scanned in three of the five cases. Therefore, CT myelography is not a suitable method for locating the site of compression, but it should be used for quantitative evaluation of cervical stenosis diagnosed by conventional myelography. In conclusion, the stenosis ratios determined using CT myelography could be applicable for detecting primary lesion sites in the cervical cord.

A cutaneous mixed tumor in a dog

The atypical cutaneous tumor of a 9-year-old mixed breed female dog was examined. The tumor was well-demarcated and histologically composed of a trichoblastic area, tricholemmal area and apocrine glandular area. Neoplastic cells in trichoblastic area and tricholemmal area had PAS-positive granules in the cytoplasm and were positive for pan-cytokeratin, cytokeratin 5/6, 14 and 19 and p63. Neoplastic cells in trichoblastic area were also positive for cytokeratin 15 and CD34. Neoplastic cells in apocrine glandular area were positive for pan-cytokeratin and cytokeratin 7, 18 and 19. Myoepithelial cell proliferation with osteocartilaginous metaplasia was observed in this area. Since neoplastic cells showed multiphenotypic differentiation for hair follicles and apocrine glands, the present case was diagnosed as a cutaneous mixed tumor.

A clinical case of neosporosis in a 4-week-old holstein friesian calf which developed hindlimb paresis postnatally

A 4-week-old female Holstein Friesian calf presented with hindlimb paresis. Neurologic examination of spinal reflexes revealed depressed or absent reflexes of the hindlimbs. Menace responses on both sides disappeared on examination of cranial nerves. The calf was finally diagnosed with Neospora caninum infection by pathological findings including nonsuppurative inflammation associated with cysts in the cerebrum and spinal cord. High levels of antibody against recombinant surface antigen 1 of N. caninum (NcSAG1) were detected by ELISA from both serum and cerebrospinal fluid (CSF) samples. This result suggests that detection of antibodies against N. caninum by NcSAG1-ELISA in serum and CSF could be useful for the clinical diagnosis of neosporosis in calves with acquired neurological signs.

Detection of monoclonal integration of bovine leukemia virus proviral DNA as a malignant marker in two enzootic bovine leukosis cases with difficult clinical diagnosis.

Monoclonal integration of bovine leukemia virus (BLV) proviral DNA into bovine genomes was detected in peripheral blood from two clinical cases of enzootic bovine leukosis (EBL) without enlargement of superficial lymph nodes. A BLV-specific probe hybridized with 1 to 3 EcoRI and HindIII fragments in these 2 atypical EBL cattle by Southern blotting and hybridization, as well as in 3 typical EBL cattle. The probe also hybridized to a large number of EcoRI and HindIII fragments in 5 cattle with persistent leukosis. These results suggest that the detection of monoclonal integration of BLV provirus into the host genome may serve as a marker of monoclonal proliferation and malignancy in difficult to diagnose EBL cattle.

Detection of the nonsense mutation of OPA3 gene in Holstein Friesian cattle with dilated cardiomyopathy in Japan.

Bovine dilated cardiomyopathy (DCM) is an autosomal recessive genetic disorder causing congestive heart failure and subsequent death. Recently, a nonsense mutation c.343C>T in the bovine optic atrophy 3 (OPA3) gene had been reported to cause the DCM in Holstein cattle in Switzerland. However, the mutation has not been confirmed in bovine DCM outside Switzerland. Nine Holstein Friesian cows that were macroscopically and histologically diagnosed with or suspected of DCM and 12 control cows kept in Japan were tested for the mutation. The mutation surrounding OPA3 DNA fragment was amplified by PCR and subjected to direct sequences. The homogeneous c.343C>T mutation was proved to occur in all the affected cows and not in the control cows. The present study is the first report of the mutation in the DCM affected cows outside Switzerland.

Glomus tumor of the liver in a cow.

An 11-year-old Holstein-Friesian cow exhibited anorexia and jaundice. A large mass was found in the liver during necropsy. Macroscopically, the mass was composed of dark red multilobular tissue and a centrally located abscess, which was connected to the hepatic duct. Histologically, the mass consisted of proliferation of small neoplastic cells and was demarcated from the hepatic parenchyma by a thick region of granulation tissue. The neoplastic cells were predominantly arranged in solid sheets, but they also formed blood-filled cancellous structures, and proliferating foci were seen around blood vessels. Periodic acid-Schiff reaction demonstrated that a fine basement membrane-like structure surrounded the neoplastic cells. Immunohistochemically, the neoplastic cells were positive for vimentin and alpha smooth muscle actin and negative for cytokeratin, factor VIII-related antigen, chromogranin and desmin. Based on its histopathological features, the hepatic neoplasm was diagnosed as a primary glomus tumor. This is the first report about a primary glomus tumor of the liver in a cow.