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Biomedical subjects

I Uhnoo

Publications and source records attributed to I Uhnoo.

6 recordsLinked to original sources
PubMed1992

First documented case of human babesiosis in Sweden.

A 34-year-old splenectomized man presented with fever, myalgia and dysuria. His condition rapidly deteriorated, he became anuric and developed severe haemolytic anaemia, thrombocytopenia and fibrinolysis. Peripheral blood smears revealed intra-erythrocytic parasites consistent with Babesia divergens in 40% of the erythrocytes. The diagnosis was confirmed by gerbil inoculation and by a significant rise in antibody titer. Blood exchange transfusion reduced the number of babesia infected erythrocytes to 1%. Parenteral therapy with a combination of quinine and clindamycin eradicated parasitaemia after 10 days of treatment and the patient rapidly improved. Renal failure necessitated haemodialysis for one month, whereafter the patient made a full recovery. Human babesiosis is a rare disease, but with a potential fatal outcome and should be considered as a diagnostic alternative in splenectomized and otherwise immunocompromised individuals with severe febrile illnesses.

Adult↗
PubMed1990

Enteric adenoviruses.

Human adenoviruses are classified into 47 serotypes and six subgenera (A-F) with different tropisms. In recent years adenovirus type 40 (Ad40) and 41 (Ad41) of subgenus F have been shown to be causative agents in enteric infections, which is second in importance only to rotaviruses as a cause of infantile gastroenteritis. Infection with EAds occurs worldwide and has been associated with 4-17% of cases of diarrhoea in children. AD40 and Ad41 primarily affect young children less than 2 years of age and occur throughout the year. The clinical characteristics include watery diarrhoea accompanied by vomiting, low grade fever and mild dehydration. A distinct feature of EAds infection is the protracted diarrhoea (mean 8.6 and 12.2 days for Ad40 and Ad41, respectively). Respiratory symptoms are infrequent. Serotypes Ad40 and Ad41 differ from all other (established) adenoviruses by being unable to replicate in conventional cell cultures. These fastidious viruses only grow in selected cell lines, 293 cells being the most commonly used. In spite of the difficulty of isolating Ad40 and Ad41, they can be directly identified and typed by ELISA and solid-phase immune electron microscopy. The amount of viral DNA in stool specimens is sufficient for identification by DNA restriction and dot-blot assays. The recent development of highly sensitive and specific monoclonal antibody-based ELISAs enable accurate diagnosis of adenovirus gastroenteritis in routine work and make possible the evaluation of the role of the enteric adenoviruses in diarrhoeal disease in the developing countries.

Adenoviridae↗
PubMed1990

Extramucosal spread and development of hepatitis in immunodeficient and normal mice infected with rhesus rotavirus.

The pathogenic profiles of two heterologous animal rotaviruses, rhesus rotavirus strain MMU 18006 and bovine rotavirus strain WC3, were evaluated in mice with severe combined immunodeficiency (SCID mice) and normal BALB/c mice. Control animals were inoculated with homologous murine strain EDIM 5099 or a tissue culture-adapted murine rotavirus. Heterologous infection with rhesus rotavirus resulted in hepatitis in 84% of SCID and 21% of BALB/c mice, with mortality rates of 27 and 0%, respectively. Surviving SCID animals developed chronic liver disease, while symptoms in BALB/c mice resolved in 2 to 4 weeks after onset. Histopathologic examination revealed a diffuse hepatitis with focal areas of parenchymal necrosis. Rotavirus was detected in liver tissue from 100% of 29 SCID and 85% (11 of 13) BALB/c animals tested by cell culture infectivity, immunofluorescence, or electron microscopy. No extramucosal spread of virus or hepatitis was observed after infection with heterologous bovine strain WC3 or homologous murine rotaviruses. This finding of a novel rotavirus-induced disease manifestation suggests altered tissue tropism in a heterologous host for a group of viruses previously shown to replicate exclusively in the gut mucosa. The implications of our observations suggest that in human vaccine trials utilizing heterologous rotavirus strains, special attention should be paid to children with immunodeficiency disorders, and screening for hepatic function should be included in vaccine protocols.

Animals↗
PubMedDate not supplied

Effect of nutritional deprivation on mucosal viral infections.

Suckling BALB-c mice, subjected to nutritional deprivation in artificially expanded litters (18 to 20 pups), were compared to normally nourished pups (7-9 per litter) in a series of experiments designed to provide data on morphologic and functional alterations of the small intestine during malnutrition and infection. The effects of protein calorie malnutrition (PCM) on the viral replication pattern and severity of clinical disease were examined in suckling mice infected with murine rotavirus (MRV). The infection in nutritionally deprived animals was characterized by a significant decrease in the minimal infectious dose and in the incubation period for the onset of diarrhea as well as increased severity of disease when compared to well nourished controls. Rotavirus-specific antibody, administered orally prior to virus inoculation, significantly reduced MRV replication in both groups but most strikingly in malnourished animals. Additional studies of the uptake of a macromolecule [ovalbumin (OVA)] following oral administration to experimental and control groups showed more rapid and complete absorption in the malnourished animals. Infection further enhanced the uptake of OVA, suggesting that both PCM and rotavirus infection alter the permeability of the small intestine. An unexpected observation of rotavirus-associated hepatitis in CB-17scid mice was also made in nearly 40% of malnourished mice inoculated with 10(6) PFU of Rhesus rotavirus (RRV). Mice with PCM exhibited a susceptibility to hepatitis between SCID mice (80%) and immunologically normal mice (18%). While these data are not sufficient to confirm a nutritionally-mediated immunoincompetence, they do suggest that either loss of immune competence and/or increased gut permeability in malnourished animals may allow a more severe homologous rotavirus infection as well as extraintestinal spread of heterologous rotavirus.

Animals↗