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Biomedical subjects

M K Njenga

Publications and source records attributed to M K Njenga.

26 records · Page 2Linked to original sources

Intimal lipid accretion and elevated serum cholesterol in Marek's disease virus-inoculated chickens.

In our previous studies of the early pathogenesis of the Marek's disease virus (MDV)-associated model of atherosclerosis, the brachiocephalic arteries and ascending aortas of MDV-inoculated chickens failed to develop lipid accretion and intimal/medial proliferation consistent with atherosclerotic lesions, as described in the original reports of this model. The role of cholesterol supplementation in the formation of MDV-associated atherosclerotic lesions was reexamined. At 3 days of age, 40 chicks were inoculated with the CU-2 strain of MDV. Another 40 chicks were sham inoculated. At 15 weeks postinfection, half of the sham- and MDV-inoculated birds received 2% cholesterol supplementation in the diet for the rest of the experimental period. At 30 weeks postinfection, the aortas and brachiocephalic arteries were evaluated. Several observations were different from the original description of the model. None of the chickens among the four experimental groups developed atherosclerotic lesions, regardless of MDV inoculation or cholesterol supplementation. However, intimal thickening and marked oil red O-positive foam cell accumulation were observed in all 11 MDV-inoculated, cholesterol-supplemented chickens. None of the nine MDV-inoculated, unsupplemented chickens manifested arterial lipid accumulation, despite the presence of an intimal cellular infiltrate. Also in contrast to the original model description, both cholesterol-supplemented and unsupplemented MDV-inoculated chickens manifested significant increases in serum cholesterol in comparison with the respective sham-inoculated groups.

Animals↗

Multi-organ reactivity of a monoclonal natural autoantibody that promotes remyelination in a mouse model of multiple sclerosis.

A contemporary view of autoimmunity suggests that self-reactivity is a normal phenomenon, in contrast to the classical association between autoimmunity and immunopathology. We have previously demonstrated that monoclonal antibody SCH94.03, a natural autoantibody with polyreactivity towards several purified protein and hapten antigens, promotes central nervous system remyelination when passively transferred to SJL/J mice chronically infected with Theiler's murine encephalomyelitis virus, an established experimental model of multiple sclerosis. In this study we characterized the autoreactivity of SCH94.03 with endogenous mouse tissue using immunoperoxide and multiple-color immunofluorescence staining techniques on frozen tissue sections. Within the nervous system, SCH94.03 labeled fibrous astrocytes, ependymal cells, ganglion satellite cells, and a sub-population of microglia, oligodendrocytes, and peripheral nervous system neurons. Outside the nervous system, SCH94.03 labeled gastrointestinal tract smooth muscle and luminal epithelium, erythrocytes, and interdigitating dendritic cells in peripheral lymphoid organs. These data indicate that SCH94.03 is a multi-organ reactive autoantibody and support the hypothesis that autoantibodies can have a beneficial rather than a pathogenic function in central nervous system demyelinating diseases.

Animals↗

Spontaneous CNS remyelination in beta 2 microglobulin-deficient mice following virus-induced demyelination.

Animal models with selective genetic immunodeficiencies are useful tools to identify pathogenic mechanisms of disease. Resistant (C57BL/6F 129/J) (H-2b) mice are rendered susceptible to Theiler's murine encephalomyelitis virus-induced demyelination by genetic disruption of the beta 2 microglobulin gene [beta 2 m(-l-)]. The absence of beta 2 m prevents the expression of major histocompatibility complex class I molecules and normal levels of functional CD8+ T cells. We tested whether genetic depletion of beta 2 m would permit CNS remyelination after chronic demyelination induced by the Daniel's strain of Theiler's virus. In contrast to the minimal spontaneous remyelination observed in SJL/J mice after infection with the Daniel's strain of Theiler's virus, chronically infected beta 2 m(-I-) mice showed extensive and progressive spontaneous CNS remyelination at 6, 12, and 18 months after infection. Spontaneous remyelination by both oligodendrocytes and Schwann cells occurred despite the presence of persistent virus antigen and RNA, but was associated with diminished virus-specific humoral and delayed-type hypersensitivity responses. These experiments support the hypothesis that the immune response inhibits myelin regeneration after virus-induced CNS demyelination.

Animals↗

Intestinal helminths of public health importance in dogs in Nairobi.

In a survey of intestinal canine zoonotic helminths in Nairobi, 156 dogs were autopsied. Of these, 10% were infected with Echinococcus granulosus, 88% with Ancylostoma caninum, 45% with Dipylidium caninum and 3% with Toxocara canis. All the infected dogs with E. granulosus originated from around abottoirs in Dagoretti. The risk of infection in man with hydatid disease is considered to be high around Dagoretti and control measures are recommended.

Abattoirs↗

Pathogenic and immunosuppressive effects of avian pneumovirus in turkeys.

Avian pneumovirus (APV) causes a respiratory disease in turkeys. The virus has been associated with morbidity and mortality due to secondary infections. Our objective was to determine if APV caused immunosuppression in the T-cell or B-cell compartments and to study the pathogenesis of the disease in APV maternal antibody-lacking 2-wk-old commercial turkeys. APV was administered by the eyedrop/intranasal route. Observations were made for gross lesions, viral genome, and T-cell mitogenesis and cytokine secretion at 3, 5, 7, 14, and 21 days postinoculation (DPI). During the acute phase of the disease that lasted for about 1 wk, the turkeys exposed to APV showed clinical signs characterized by nasal discharge and sinus swelling. Virus genome was detected by in situ hybridization in cells of turbinates and trachea at 3 and 5 DPI. At 3 and 5 DPI, spleen cells of the birds infected with APV markedly decreased proliferative response to concanavalin A (Con A). Con A and lipopolysaccharide stimulation of spleen cells from virus-exposed turkeys resulted in accumulation of nitric oxide-inducing factors (NOIF) in the culture fluid. NOIF were not detected in culture fluids of Con A-stimulated spleen cells of virus-free turkeys. APV did not compromise the antibody-producing ability of turkeys against several extraneous antigens such as Brucella abortus and tetanus toxoid.

Administration, Intranasal↗

Neonatal avian pneumovirus infection in commercial turkeys.

Eleven market turkey flocks developed a respiratory disease characterized by coughing, swollen sinuses and nasal discharge. These symptoms first appeared between 3 and 16 days of age. Avian pneumovirus (APV) RNA was detected by reverse transcriptase (RT)-polymerase chain reaction (PCR) in six of six flocks tested. APV was detected by immunohistochemistry in turbinates of three of three affected flocks tested. Virus isolation attempts were negative. Ten of 11 flocks became seropositive on the APV enzyme-linked immunosorbent assay. Five weeks prior to hatch of these affected market turkeys, several breeder flocks in one geographic area had developed clinical signs and experienced decline in egg production typical of APV infection. In two breeder flocks, acute and convalescent sera indicated APV infection during the period of declining egg production. Attempts to detect APV RNA by RT-PCR from choanal cleft swabs of newly hatched poults were successful. Attempts to isolate the virus from these PCR-positive samples were negative.

Age Factors↗

Detection of avian pneumovirus in wild Canada (Branta canadensis) and blue-winged teal (Anas discors) geese.

Choanal cleft swab samples from 770 wild Canada geese (Branta canadensis) and 358 blue-winged teal (Anas discors), captured for relocation or banding, were examined for the presence of avian pneumovirus (APV) RNA by reverse transcription (RT)-polymerase chain reaction (PCR) and for virus isolation. The swab samples were pooled into groups of 5 or 10. Sixty eight of 102 (66.7%) pooled goose samples were RT-PCR positive for APV RNA. Thirteen of 52 (25.0%) pooled blue-winged teal samples were RT-PCR positive for APV RNA. APV RNA-positive samples were inoculated onto chick embryo fibroblasts (CEF) and QT-35 cells. Infectious APV was isolated from five Canada goose pooled samples in CEF and from one Canada goose pool in QT-35 cells but not from blue-winged teal.

Animals↗