Biomedical subjects

T Glaus

Publications and source records attributed to T Glaus.

22 records · Page 2Linked to original sources

PubMed1990

Ultrastructural and biochemical findings in brain cell cultures infected with canine distemper virus.

To study the pathomechanism of demyelination in canine distemper (CD), dog brain cell cultures were infected with virulent A75/17-CD virus (CDV) and examined ultrastructurally. Special attention was paid to the oligodendrocytes, which were specifically immunolabelled. In addition, cerebroside sulfotransferase (CST), an enzyme specific for oligodendrocyte activity was assayed during the course of the infection. Infection and maturation as well as CDV-induced changes were found in astrocytes and brain macrophages. Infection of oligodendrocytes was rarely seen, although CST activity of the culture markedly decreased and vacuolar degeneration of these cells occurred, resulting in their complete disappearance. We concluded that the degeneration of oligodendrocytes and demyelination is not due to direct virus-oligodendrocyte interaction, but due to CDV-induced events in other glial cells.

Animals↗

PubMed1989

[What is your diagnosis? Key-Gaskell syndrome].

The first case of Key-Gaskell syndrome in Switzerland has been described. The disease is mainly characterized by damaged autonomous ganglia. Lesions of the parasympathicus account for dry mucous membranes, mydriasis, paralysis of the bladder, megaesophagus and paralysis of the remaining gastrointestinal tract. Lesions of the sympathicus are explained by bradycardia and prolapse of the third eyelid. Until now the etiology of the disease is not known.

Animals↗

PubMedDate not supplied

Neurological manifestations of hypothyroidism: a retrospective study of 29 dogs.

Neuromuscular signs in association with hypothyroidism are described in 29 dogs. Eleven dogs had lower motor neuron signs, 9 had peripheral vestibular deficits, 4 had megaesophagus, and 5 had laryngeal paralysis. Primarily older (mean = 9.5 years), large-breed dogs were affected, and there was no sex or breed predisposition. Duration of clinical signs before presentation ranged from 2 to 8 weeks (mean = 5 weeks). The diagnosis was based on (1) results of neurological examination (29 dogs); (2) electromyographic abnormalities (18 dogs), including fibrillation potentials (n = 18), positive sharp waves (n = 15), and complex repetitive discharges (n = 4); (3) high serum cholesterol concentration (10 dogs; mean = 335 mg/dL); (4) low response to thyroid-stimulating hormone (29 dogs; mean T4 prestimulation concentration = 0.8 micrograms/dL; mean T4 poststimulation = 1.2 microgram/dL); and (5) good response to thyroxine supplementation (26 dogs). Dogs with vestibular deficits had abnormal brainstem auditory-evoked responses (BAER), including increased latencies of P1-P6 and decreased amplitude of P4,5-N5. Seven other dogs had similar BAER abnormalities without manifesting clinical signs of vestibular involvement. Three dogs with vestibular signs had fibrillation potentials and positive sharp waves without exhibiting lower motor neuron signs. All dogs were supplemented with levothyroxine (0.02 mg/kg PO bid). The follow-up period ranged between 6 and 30 months (mean, 14 months). Serum T4 concentrations were measured at least 3 times for each dog every 2 months (mean T4 concentration = 2.6 micrograms/dL). All but 1 dog with lower motor neuron signs and 1 dog with vestibular signs recovered after 2 months (mean, 57 days).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Clinical, serologic, and parasitologic follow-up after long-term allopurinol therapy of dogs naturally infected with Leishmania infantum.

Canine leishmaniasis usually is treated with antimony compounds, but frequent relapses, adverse effects, high costs, and development of resistance to long-term antimonial therapy emphasize the importance of searching for alternative antileishmanial drugs. Allopurinol was used at a dosage of 10 mg/kg/day PO to treat 10 dogs naturally infected with Leishmania infantum for a period of 2-24 months. Nine dogs recovered within 2-6 months of chemotherapy, and no relapses were observed during the treatment of up to 20 months. However, 3 of 4 dogs relapsed after treatment was discontinued. These dogs again recovered clinically when therapy was resumed. Parasite-specific immunoglobulin concentrations (IgG2) were high in all dogs before therapy and remained high even in clinically cured dogs during or after therapy. On the other hand, specific IgG1 reactions, which have been shown to be detectable in symptomatic animals, persisted in 7 dogs for long periods after clinical recovery. Three of these dogs relapsed within 2-4 weeks after interrupting therapy. However, 1 dog with no detectable specific IgG1 reaction at the end of therapy did not relapse in the following 4 months. Parasites could be detected in 8 of 9 dogs after clinical improvement by in vitro cultivation or polymerase chain reaction (PCR) testing of lymph node aspirates. In 4 of these dogs, parasites also were detected in blood samples by PCR. Hence, these clinically cured dogs must be regarded as reservoirs of Leishmania and allopurinol cannot be recommended in endemic areas.

Allopurinol↗