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Biomedical subjects

D H Walker

Publications and source records attributed to D H Walker.

At least 235 records · Page 13Linked to original sources
PubMed1980

Phycomycosis: a cause of bronchial obstruction.

A patient with diabetes mellitus presented with an obstructing mycetoma in the right bronchus intermedius due to Phycomycetes. Review of the literature revealed eight prior case reports of patients with prominent endobronchial disease attributable to phycomycosis. Indolent, obstructing lesions in large bronchi were noted in diabetics. The clinical illness differed from the fulminant fungal pneumonia noted in leukemics but was also lethal because of localized complications such as erosion into the pulmonary artery. The differential diagnosis included mucoid impaction, bronchocentric granulomatosis, and mycotic bronchitis. Surgical resection appears to be the appropriate therapy for well localized bronchial lesions.

Airway Obstruction↗
PubMed1979

Invasive pulmonary aspergillosis associated with influenza.

Fatal invasive pulmonary aspergillosis may follow viral influenza infections. Two cases with verified influenza A infection were followed by fatal necrotizing pneumonia due to Aspergillus fumigatus. Both patients demonstrated cutaneous anergy and lymphocytopenia. Influenza and perhaps other viruses that depress T-cell function may result in increased susceptibility to infections in which T cells are important in host defenses.

Antigens, Bacterial↗
PubMed1979

Permutation of the DNA in small-headed virions of coliphage P1.

Use of restriction endonucleases Bg/II, EcoRI, BamHI, and HindIII, has established that in small-headed (P1S) virions of coliphage P1, as a population, the entire genome found in big-headed (P1B) virions is represented. In addition, the origin and direction of DNA packaging are identical in P1S and P1B virions.

Coliphages↗
PubMed1979

Ultrastructural and virological aspects of Langat virus-induced SSPE in suckling hamsters.

The morphology of subacute sclerosing panencephalitis (SSPE) lesions in hamsters following i.p. inoculation of Langat virus was studied by light microscopy and electron microscopy. The lesions' temporal relationship to virus presence and antibody production was studied by immunofluorescence, virus isolation from brains and brain cell cultures, and by antibody assay of serum and spinal fluid. All 10-day-old hamsters infected with Langat virus developed SSPE lesions, most prominently in the cerebellum, without any overt signs. The lesions appeared 10 days after infection, progressed in severity until Day 21 and persisted unaltered at least 3 months. They consisted of neuronal degeneration, calcification, and intracellular lipid accumulation. Virus was isolated from Days 3 to 15 and disappeared on Day 21. Demonstration by cerebellar immunofluorescence of viral antigen was observed 10 days after inoculation. Antibody appeared in the serum on Day 6, rose to very high titres by Day 21, and thereafter declined. Cell-associated virus was not demonstrable in negative brain-cell cultures. These findings suggest that SSPE in hamsters, associated with Langat virus infection, is biologically different from measles SSPE. Purkinje-cell lipid accumulation and mineralization sparing mitochondria were manifestations of the response of neurons to cell injury at the threshold of irreversibility.

Animals↗
PubMed1979

Acute renal failure in Rocky Mountain spotted fever.

Review of clinical and pathologic data from ten fatal cases of Rocky Mountain spotted fever (RMSF) revealed the importance of acute renal failure in the clinical course and of multifocal perivascular interstitial nephritis as the principal pathologic lesion. In nine cases, Rickettsia rickettsii were demonstrated by immunofluorescence in the areas of vasculitis. Evidence was lacking for the role of disseminated intravascular coagulation, glomerulonephritis, or myoglobinuria in the pathogenesis of acute renal failure in these cases. Rickettsia-induced vascular injury led to acute renal failure by several mechanisms. Hypovolemia early in the course resulted in reversible, prerenal azotemia. Transient hypotension in midcourse produced acute tubular necrosis. In fulminant cases, preterminal circulatory collapse was associated with coma and oliguria. The interstitial nephritis could not be demonstrated conclusively to contribute to the acute renal failure.

Acute Kidney Injury↗
PubMed1978

Fatal viscerotropic Rocky Mountain spotted fever. Report of a case diagnosed by immunofluorescence.

A case of fatal viscerotropic Rocky Mountain spotted fever with virtual absence of cutaneous lesions was diagnosed at autopsy by specific immunofluorescent demonstration of Rickettsia rickettsii in spleen, kidney, epididymis and skin. The clinical presentation was that of insidious onset of fever, renal failure, hypotension, hyponatremia and obtundation over a 10 day period. The patient had respiratory insufficiency, hypocalcemia, increases in creatinine phosphokinase (CPK), serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), lactic dehydrogenase (LDH), alkaline phosphatase, billirubin and serum phosphate, grand mal seizure, myalgia and unremitting shock with death occurring on day 12 of illness. Postmortem examination revealed severe vasculitis with interstitial nephritis and multifocal tubular necrosis, pericholangitis with bile stasis, glial nodules in the brain, multifocal rhabdomyonecrosis, interstitial pneumonitis and mild interstitial myocarditis. Risk factors which this patient shared with other patients with fatal Rocky Mountain spotted fever were failure to recognize a rash, failure to obtain a tick bite history, male sex, black race and age greater than 30 years.

Autopsy↗
PubMed1978

Laboratory diagnosis of Rocky Mountain spotted fever by immunofluorescent demonstration of Rickettsia in Cutaneous lesions.

Direct immunofluorescent staining for Rickettsia rickettsii was performed on cryostat sections of skin biopsies from 27 patients suspected of having Rocky Mountain spotted fever. In nine of the 17 patients whose final diagnosis was Rocky Mountain spotted fever, coccobacillary forms of R. rickettsii were identified in endothelium and vascular walls within the dermis. Facotrs recognized as contributing to false-negative results were prior treatment with tetracycline or chloramphenicol for 24--48 hours or longer and failure to obtain a section through the focus of vasculitis. No false-positive result was obtained in the ten patients whose final diagnoses were not Rocky Mountain spotted fever. The laboratory test offers an immediate, positive laboratory diagnosis for this treatable, life-threatening disease.

Adolescent↗
PubMed1978

A method for specific diagnosis of Rocky Mountain spotted fever on fixed, paraffin-embedded tissue by immunofluorescence.

For specific demonstration of Rickettsia rickettsii in fixed, paraffin-embedded tissues, the technique of trypsin digestion of deparaffinized, rehydrated sections was investigated. It was determined that 3.5 hr of digestion was optimal for achieving discrete, bright, green immunofluorescence of rickettsiae. At autopsy kidneys from seven of 10 cases of probably Rocky Mountain spotted fever contained structures that were specifically stained and that had the size and shape of rickettsiae. These structures were strictly limited to the endothelium and vascular walls of renal capillaries, veins, and arteries. Results from controls indicated that specificity of the immunofluorescence. R. rickettsii may be demonstrated by this method with greater sensitivity and specificity than by current histological methods. The technique allows retrospective analysis of certain organs for pathogenesis of involvement in Rocky Moutain spotted fever and offers a specific diagnostic test.

Animals↗
PubMed1978

Effect of immunosuppression on Rickettsia rickettsii infection in guinea pigs.

The role of the immune response in the pathogenesis of Rickettsia rickettsii infection in guinea pigs was investigated by immunosuppression, using antilymphocyte serum. Twenty guinea pigs were inoculated with R. rickettsii, Sheila Smith strain, on day 0. Fifteen animals received antilymphocyte serum on days --1, 0, 2, 4, and 6. Five animals received normal rabbit serum on the same schedule. At necropsy, specimens were collected for histological examination, rickettsial immunofluorescence, rickettsial titration, and antirickettsial antibody titration. All normal rabbit serum recipients and 12 of 15 antilymphocyte serum recipients developed typical disease. Comparison of animals in terminal stages of disease revealed the same clinical course and gross lesions, but differing rickettsial burden and cellular response. Immunosuppressed animals had higher titers of splenic rickettsiae and greater numbers of immunofluorescent rickettsiae. Thus, although antibody was undetectable in both groups, there appeared to be an inhibition of antirickettsial immunity. Microscopic vasculitis was similar quantitatively, but differed qualitatively, with immunocompetent animals having the typical monouclear/lymphocytic inflammation and immunosuppressed animals having neutrophilic predominance. This study demonstrates that immunopathological mechanisms are not necessary for the pathogenesis of experimental Rocky Mountain spotted fever. The rickettsiae themselves seem capable of causing cellular and tissue damage.

Animals↗
PubMed1978

Disseminated petriellidosis (allescheriosis).

Disseminated infection by Petriellidium (Allescheria) boydii occurred in an immunosuppressed renal allograft recipient. A probable airborne pulmonary infection underwent hematogenous spread to the brain, thyroid, and heart. The organism develops septate, branching hyphae in tissue and may be misdiagnosed as Aspergillus. The basic pathologic lesions are necrosis with a predominantly polymorphonuclear leukocytic reaction and abscess formation, and a mild granulomatous response with macrophages and multinucleated giant cells. A particular tropism for blood vessels was observed. The vascular organs, brain, and thyroid have been involved in all three disseminated cases reported thus far.

Abscess↗
PubMed1977

Anticonvulsant prolongation of survival in adult murine lymphocytic choriomeningitis. I. Drug treatment and virologic studies.

Lymphocytic choriomeningitis virus-induced central nervous system disease is characterized by death during a seizure approximately seven days after intracerebral inoculation. This process is mediated by thymus dependent lymphocytes, sensitized against viral antigens. Various forms of immunosuppressive treatment prevent the seizure death and produce persistently infected survivors. In this study, anticonvulsant treatment (particularly diazepam treatment) of LCM virus infected mice prolonged survival without affecting viral replication, or suppressing immune responsiveness. This prolongation of life did not lead to a reversal of pathologic processes and there were no survivors. However, anticonvulsant treatment permitted study of more advanced stages of the choriomeningitis than has previously been possible.

Animals↗
PubMed1977

Anticonvulsant prolongation of survival in adult murine lymphocytic choriomeningitis. II. Ultrastructural observations of pathogenetic events.

Because previous ultrastructural studies of murine lymphocytic choriomeningitis (LCM) had revealed only mononuclear cell infiltration with no cytopathology of target cells in the choroid plexus, ependyma, and leptomeninges, diazepam treatment was used to prolong survival for characterization of late pathogenetic events. Mice which were treated with diazepam and sacrificed 8, 9, and 10 days after intracerebral inoculation with LCM virus showed an increasing amount of inflammatory infiltration into choroid plexuses, leptomeninges, Virchow-Robin spaces, and ependyma. Mononuclear cells, lymphocytes, and polymorphonuclear (PMN) leukocytes increased in number as compared with terminally infected mice sacrificed 7 days after inoculation. Ultrastructurally, choroidal epithelial cells showed cytopathological changes varying from dilated endoplasmic reticulum through necrosis. Greater numbers of PMN leukocytes, macrophages, and activated macrophages and fewer undifferentiated mononuclear cells were seen in choroid plexuses of the drug-treated survivors. Virions and larger, more numerous arenavirus inclusions were present in choroid plexus and ependyma. Ultrastructurally the leptomeningitis was characterized by large numbers of activated macrophages. Choroidal epithelial necrosis appears to be the in vivo correlate of T-cell-mediated cytotoxicity in vitro.

Animals↗
PubMed1977

Identification of Rickettsia rickettsii in a guinea pig model by immunofluorescent and electron microscopic techniques.

Moribund guinea pigs infected with Richettsia rickettsii were examined by necropsy, histology, immunofluorescence, electron microscopy, and serology. Untreated animals died at 9 and 10 days after inoculation. Animals given saline subcutaneously survived from 1 to 4 days longer. Prolonged survival was accompanied by more severe lesions: scrotal necrosis; infarction of ears; and swollen, hemorrhagic footpads, epididymis, and cremaster muscle. Histopathologic examination demonstrated that acute, necrotizing vasculitis, perivascular hemorrhage, and focal necrosis were more extensive. Direct immunofluorescence indicated many more rickettsiae in endothelium and vascular wall of saline recipients. Ultrastructurally, typical rickettsiae were present focally in the cytoplasm of endothelial and vascular smooth muscle cells. Cytopathology in infected and adjacent cells included swelling, mitochondrial enlargement with decrease in matrix density and loss of cristae, and increased pinocytosis. In addition, treated animals had more cytonecrosis, thrombosis, extravascular fibrin deposition, prominent inflammatory cells with polymorphonuclear phagocytosis of rickettsiae, and antibody production.

Animals↗
PubMed1976

Genetic studies of coliphage P1. II. Relatedness to P7.

Using semiquantitative spot tests, 107 independently isolated amber mutants of P1 were shown to be rescued by a nonpermissive strain of Escherichia coli lysogenic for P7 (previously called phiamp), indicating extensive genetic relatedness between P1 and P7. The amount of rescue observed varied with mutants from different genetic linkage clusters of P1. Although these rescue tests cannot distinguish between recombination, complementation, transactivation, or combinations thereof, a major role is indicated for recombination.

Ampicillin↗