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Biomedical subjects

H C Walvoort

Publications and source records attributed to H C Walvoort.

52 records · Page 3Linked to original sources
PubMed1986

Otitis media in guinea pigs: pathology and bacteriology.

In the course of post-mortem examination of conventional random-bred and inbred (immunosuppressed) strain 2/N guineapigs kept in separate quarters, otitis media was diagnosed in 62 of 462 animals (13.4%) and 18 of 66 animals (27.3%) respectively. Clinical signs of otitis media were seen in only two random-bred animals but in nearly 50% of affected inbred animals. In random-bred guineapigs, purulent, often bilateral, otitis media was associated mainly with the isolation of Streptococcus zooepidemicus, Bordetella bronchiseptica, Pasteurella and Actinobacillus spp. and micrococci. In strain 2/N guineapigs serous or purulent often bilateral otitis media was associated mainly with the isolation of B. bronchiseptica and Pseudomonas aeruginosa serotypes 10 and 11. The simultaneous occurrence of similar pathogenic bacteria in both ears of bilaterally affected animals and in pneumonic lung tissue (in random-bred animals) suggested ascending and descending infection originating from the upper respiratory tract. It is concluded that otitis media, associated with the isolation of a variety of respiratory bacterial species, must be considered a major disease problem in guineapigs.

Animals↗
PubMed1986

Opportunistic infections in hysterectomy-derived, barrier-maintained guinea pigs.

Guineapigs were rederived by hysterectomy and associated with a colonization-resistant enteric microflora (CRF) of mouse origin to establish a strict barrier-maintained breeding colony. Infections were suspected in 55 of 209 animals autopsied. From 65 of 67 tissue samples selected for bacteriological examination 167 isolates, belonging to 16 usually non-pathogenic bacterial species or groups, were isolated mostly from cases of mastitis, typhlitis, enteritis, otitis media and pneumonia. Faecal streptococci, Pseudomonas aeruginosa, Clostridium perfringens, Citrobacter spp., C. freundii, Escherichia coli, Klebsiella oxytoca and Enterobacter cloacae accounted for 86.8% of all isolates. Variations in the recovery rate of these 8 species during the study and a gradual decline in the incidence of infections were observed. Elimination by rederivation of the autochthonous bacterial flora seemed to have predisposed to opportunistic infections by aerobic and facultatively anaerobic bacteria. Enteric colonization resistance to the growth of these bacteria was presumably insufficiently provided by the CRF of mouse origin and might be remedied by using a flora of guineapig origin.

Animals↗
PubMed1986

An outbreak of a herpesvirus infection in harbor seals (Phoca vitulina).

During an outbreak of a herpesvirus infection in juvenile harbor seals, 11 out of 23 seals died. The duration of the disease in these 11 animals varied from 1-6 days. Nasal discharge, inflammation of the oral mucosa, vomiting, diarrhea and fever up to 40 degrees C were observed in the first days of the disease. In later stages coughing, anorexia and lethargy occurred. Severe necrosis of the liver and interstitial pneumonia were the most striking histopathological findings.

Animals↗
PubMed1985

Comparative pathology of the canine model of glycogen storage disease type II (Pompe's disease).

The pathology of canine glycogen storage disease type II (acid alpha-glucosidase deficiency, GSD II) was studied in three genetically related Lapland dogs and compared to the pathology of human GSD II (McKusick 23230). Canine GSD II closely parallels the infantile form of the human disease, except for the presence of oesophageal dilatation. Generalized glycogen storage particularly affected muscular tissues (skeletal, oesophageal, cardiac and smooth muscle). The altered cells showed glycogen accumulation in the cytosol and in autophagic membrane-bound vacuoles (glycogenosomes). They also showed increased acid phosphatase activity consistent with the lysosomal nature of this storage disorder. The cytopathology in canine and human GSD II appears to evolve from segregation of glycogen during regular cellular autophagy, phagolysosomal accumulation of the undigested glycogen, and eventually rupture of distended glycogenosomes. This study indicates that the usefulness of canine GSD II as an animal model of human disease, extends to the area of pathogenesis.

Acid Phosphatase↗
PubMed1985

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.

Animals↗
PubMed1985

Heterozygote detection in a family of Lapland dogs with a recessively inherited metabolic disease: canine glycogen storage disease type II.

The control of recessively inherited inborn errors of metabolism may benefit from quantitative biochemical screening assays enabling the identification of heterozygous individuals. Based on the principle of partial enzyme deficiency in heterozygotes, an attempt was made to identify heterozygous animals in a Lapland dog family with canine glycogen storage disease type II (acid alpha-glucosidase deficiency). Acid alpha-glucosidase activity was determined in peripheral blood leucocyte extracts of 12 related Lapland dogs, two of which were obligate heterozygotes. The use of an antiserum against acid alpha-glucosidase was necessary to increase the specificity of the assay. Twice the obligate heterozygous enzyme level was assumed to indicate the homozygous normal level. Five dogs were designated as presumptive heterozygotes, and five as presumptive normal homozygotes. The results in two dogs were inconclusive. The information obtained in this preliminary investigation may be helpful in the control of the disease in the Lapland dog breed.

Animals↗
PubMed1984

Biochemical genetics of the Lapland dog model of glycogen storage disease type II (acid alpha-glucosidase deficiency).

A recently described canine model (Lapland dog) of glycogen storage disease type II (GSD II, Pompe disease, acid alpha-glucosidase deficiency) was identified with several biochemical genetic methods. Complementation studies in which fibroblasts from a GSD II dog were fused with fibroblasts derived from control dogs and from human patients with different clinical forms of the disease did not lead to restoration of acid alpha-glucosidase activity in the heterokaryon cell populations. These results indicate that acid alpha-glucosidase deficiency is the primary defect in canine GSD II and that there is a close genetic parallelism with human GSD II. Immunotitration analysis of the residual acid alpha-glucosidase activity in the canine GSD II fibroblasts and liver demonstrated that this residual activity was not due to acid alpha-glucosidase enzyme, in which respect canine GSD II was similar to the infantile form of the human disease. Double immunodiffusion studies showed the presence of catalytically inactive acid alpha-glucosidase enzyme protein in canine GSD II. This is consistent with a structural gene mutation. It is concluded that canine GSD II in the Lapland dog is a homologous model of the infantile form of human GSD II, a conclusion in concordance with clinical and pathological studies.

Animals↗
PubMed1984

A biphasic serum glucose response in mice to inoculation with pertussis vaccine.

The effect of B. pertussis vaccine on the serum glucose level of mice was investigated. The results show that at least two components in the vaccine interfere with glucose metabolism. A heat-stable component which is assumed to be LPS induced hypoglycemia 3-5.5 h after inoculation, especially in LPS-sensitized mice. A heat-labile component which is possibly equivalent with the LPF/HSF/IAP complex, is responsible for persistence of the hypoglycaemia for at least 6 days. If hypoglycaemia contributes to the neurological side effects after pertussis vaccination both components have to be considered as being responsible for these effects.

Animals↗
PubMed1984

Vertical transmission of Bacillus piliformis infection (Tyzzer's disease) in a guinea pig: case report.

Tyzzer's disease (Bacillus piliformis infection) was diagnosed at necropsy in a hysterectomy-derived, gnotobiotically reared guinea pig. This is the first description of spontaneous vertical, presumably transplacental, transmission of B. piliformis infection. Subsequent horizontal transmission of the infection was concluded from the presence of specific anti-B. piliformis antibodies in the sera from guinea pigs originating from different litters but reared in the same isolator.

Animals↗
PubMed1983

Glycogen storage diseases in animals and their potential value as models of human disease.

Glycogen storage diseases (GSD) are inborn errors of glycogen metabolism. Of the eight human GSD types in which the enzymatic deficiency has been identified, spontaneous animal counterparts have been reported for GSD I (glucose-6-phosphatase deficiency) in the mouse, for GSD II (acid alpha-glucosidase deficiency) in the dog, in cattle and in the quail, for GSD III (debrancher enzyme deficiency) in the dog and for GSD VIII (phosphorylase kinase deficiency) in the rat and the mouse. Experimentally induced GSD-like conditions have been described in the rat (Acarbose-induced GSD II-like conditions, iodoacetate-induced symptoms of myophosphorylase (GSD V) and myophosphofructokinase (GSD VII) deficiency) and the chicken (ochratoxin A-induced symptoms of cyclic AMP-dependent protein kinase deficiency). Enzymatic defects that are typical of the human GSD types have not been clearly identified in the induced animal conditions. The homology of animal and human GSD types is discussed. It is concluded that clinical, pathogenic and therapeutic studies of GSD may benefit from the use of animal models. For genetic studies of human GSD these models may prove to be of limited value, as the picture of several human GSD types is already obscured by genetic heterogeneity.

Animals↗
PubMed1983

Granular cell myoblastoma in the tongue of a dog: a case report.

A granular cell myoblastoma was found in the dorsal side of the tongue of a 9-year-old female mongrel Pinscher. Macroscopically the tumour was white, well circumscribed, and 1 1/2 cm in diameter. Microscopically the tumour cells were arranged in small compact nests or cords with delicate, poorly vascularized collagen bundles in between. Acinar structures were found, also a few mitotic figures were present. Cytoplasmic granules showed a positive periodic acid Schiff reaction. Ultrastructural features included indented nuclei and small-sized vesicular cytoplasmic granules. The histogenesis of the neoplasm remains uncertain.

Animals↗
PubMed1983

Recovery of members of the Pasteurella-Actinobacillus-group from guinea pigs.

In the course of post-mortem bacteriological examination of conventional guinea pigs, 88 isolates belonging to the Pasteurella-Actinobacillus-group were recovered from 69 of 279 animals (25%). Most isolates were recovered from pneumonic lung, enteritic jejunum and inflamed mammary gland. No relationship was found between biotype and source of isolation. About 50% of isolates were recovered in pure culture or as the predominant micro-organism. It is concluded that members of the Pasteurella-Actinobacillus-group must be considered potentially pathogenic for guinea pigs.

Actinobacillus↗
PubMed1982

Canine glycogen storage disease type II. A biochemical study of an acid alpha-glucosidase-deficient Lapland dog.

A biochemical study was performed in a Lapland dog suspected of glycogen storage disease type II (acid alpha-glucosidase deficiency, Pompe's disease). Glycogen content was substantially elevated in heart and skeletal muscle but not in the liver. Severely reduced activities of acid alpha-glucosidase (EC 3.2.1.20) were found in heart, skeletal muscle, liver and cultured tongue fibroblasts. The deficiency was located in the glycoprotein fraction, which supported its lysosomal origin. The electrophorogram showed after acid incubation that the affected dog was missing the activity band, while after neutral incubation the pattern was similar to control. The obtained biochemical data are compared with the known data of the human pathology.

Animals↗
PubMed1978

[Abnormal respiration with dullness over the thorax in cattle. Due to an extensive lesion of the liver (author's transl)].

The case of a four-year-old cow is reported, in which a very extensive necropurulent lesion was localized in the left half of the liver. When the animal was studied clinically and by X-ray, a space-occupying lesion in the thorax was strongly suspected. The importance of including diseases of the liver in the differential diagnosis of thoracic disorders is stressed.

Animals↗