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Biomedical subjects

D H Walker

Publications and source records attributed to D H Walker.

At least 199 records · Page 11Linked to original sources
PubMed1983

The histology of "taches noires" of boutonneuse fever and demonstration of Rickettsia conorii in them by immunofluorescence.

The recent increase in the incidence of boutonneuse fever in Italy provided the opportunity to study the pathology of six "taches noires," the lesions at the site of tick bite. The center of the lesion has either an ulcer or an area of necrosis of the epidermis and superficial dermis; in some cases the epidermis is intact. The alterations are mainly in the dermis and subcutaneous tissues where the small vessels show endothelial swelling and intramural and perivascular oedema and inflammation with macrophages, lymphocytes and smaller numbers of plasma cells, PMNs and eosinophils. In a few small arteries and fewer veins there are either nonocclusive mural or occlusive thrombi; there is no spatial or quantitative correlation between thrombosis and necrosis. We propose that cutaneous necrosis results from severe injury to many small vessels. Rickettsiae which had not been previously observed in "taches noires" were demonstrated in blood vessels by immunofluorescence, a finding that may be used as a means for early aetiological diagnosis of the disease. The "tache noire" is an excellent human model for localized rickettsial injury.

Adult↗
PubMed1983

Disseminated infection by Aspergillus terreus.

A patient with acute nonlymphocytic leukemia who received chemotherapy developed lung nodules and later central nervous system symptoms consistent with disseminated aspergillosis. The diagnosis was made at open lung biopsy by culturing the organism and observing in tissue sections conidia borne laterally along the hyphae, a characteristic of the Aspergillus terreus-flavipes group. This is the first reported case of disseminated A. terreus infection in an immunocompromised host.

Acute Disease↗
PubMed1983

A fatal eosinophilic process in a Laotian refugee.

A 17-year-old Laotian refugee developed an ultimately fatal disease process characterized by formation of an abdominal eosinophilic mass, peripheral eosinophilia, and elevated serum IgE. No parasitic pathogens that could explain her disease were isolated during life or identified at autopsy. Furthermore, the disease was not consistent with previously described neoplastic, inflammatory, or idiopathic diseases. We believe this process represents a unique, aggressive variation of the hypereosinophilic syndrome, and that immunosuppressive therapy may be warranted.

Adolescent↗
PubMed1983

Role of phospholipase-associated penetration mechanism in cell injury by Rickettsia rickettsii.

The cholesterol receptor-binding drugs amphotericin B and digitonin reduced rickettsial plaque formation, presumably by blocking rickettsial attachment, even when added to the plaque model on day 4 post-inoculation when infected foci were well established. The phospholipase inhibitor phentermine reduced plaque formation, presumably by inhibiting the phospholipase-associated entry step of penetration.

Amphotericin B↗
PubMed1983

Rocky Mountain spotted fever vaccine in an animal model.

Formalin-killed, purified Rickettsia rickettsii vaccine was evaluated in a guinea pig model of R. rickettsii infection. Vaccinated guinea pigs were partially protected by the vaccine when challenged with virulent, viable rickettsiae. Greater protection was observed when higher doses of vaccine were given and when frequent booster injections were administered. Stimulation of cell-mediated immunity to the vaccine antigens was variable and also appeared to be achieved more reproducibly with booster vaccinations. Serum antibody was elicited by high doses of vaccine and by booster vaccinations. The presence of serum antibody was useful in predicting immunity to challenge with R. rickettsii.

Animals↗
PubMed1983

Coliphage P1 morphogenesis: analysis of mutants by electron microscopy.

We used electron microscopy and serum blocking power tests to determine the phenotypes of 47 phage P1 amber mutants that have defects in particle morphogenesis. Eleven mutants showed head defects, 30 showed tail defects, and 6 had a defect in particle maturation (which could be either in the head or in the tail). Consideration of previous complementation test results, genetic and physical positions of the mutations, and phenotypes of the mutants allowed assignment of most of the 47 mutations to genes. Thus, a minimum of 12 tail genes, 4 head genes, and 1 particle maturation gene are now known for P1. Of the 12 tail genes, 1 (gene 19, located within the invertible C loop) codes for tail fibers, 6 (genes 3, 5, 16, 20, 21, and 26) code for baseplate components (although one of these genes could code for the tail tube), 1 (gene 22) codes for the sheath, 1 (gene 6) affects tail length, 2 (genes 7 and 25) are involved in tail stability, and 1 (gene 24) either codes for a baseplate component or is involved in tail stability. Of the four head genes, gene 9 codes for a protein required for DNA packaging. The function of head gene 4 is unclear. Head gene 8 probably codes for a minor head protein, whereas head gene 23 could code for either a minor head protein or the major head protein. Excluding the particle maturation gene (gene 1), the 12 tail genes are clustered in three regions of the P1 physical genome. The four head genes are at four separate locations. However, some P1 head genes have not yet been detected and could be located in two regions (for which there are no known genes) adjacent to genes 4 and 8. The P1 morphogenetic gene clusters are interrupted by many genes that are expressed in the prophage.

Chromosome Mapping↗
PubMed1983

Immunity and rickettsial infection: a review.

Immunity to rickettsiae is enhanced by both T-lymphocytes and humoral antibodies; however, the principal effector of rickettsial killing is the macrophage. Lymphokines may play an important role. There is undoubtedly a complex in vivo interaction between the immune, phagocytic, and inflammatory host defenses against these obligate intracellular bacteria.

Antibody Formation↗
PubMed1983

Correlation of rickettsial titers, circulating endotoxin, and clinical features in Rocky Mountain spotted fever.

Blood rickettsial titers, skin biopsy results, and circulating endotoxin measurements were correlated with the clinical course of disease in patients with Rocky Mountain spotted fever (RMSF). Nine of 11 patients with documented RMSF had Rickettsia rickettsii isolated from plasma samples. Of the eight patients in whom rickettsial titers were measured, seven had 10(0.7) to 10(1.2) median tissue culture infective doses (TCID50) per milliliter; all seven had mild to moderately severe disease. One patient with fulminant, fatal untreated RMSF had 10(3) TCID50/mL of postmortem plasma. Two patients from whom rickettsiae were not isolated had positive direct immunofluorescent stains of skin biopsy material for R rickettsii. Circulating endotoxin was present in two patients, one with documented rickettsemia and one with a positive skin biopsy alone. Only low levels of circulating rickettsiae are present in patients with moderately severe disease. Measurement of plasma endotoxin is not useful in the early diagnosis of RMSF.

Adolescent↗
PubMed1983

Fulminant Rocky Mountain spotted fever. Its pathologic characteristics associated with glucose-6-phosphate dehydrogenase deficiency.

Three patients with documented fulminant Rocky Mountain spotted fever (RMSF) (death on or before day 5 of illness) had severe multisystemic injury as shown by clinical signs and laboratory data, but on microscopic examination showed minimal evidence of the typical mononuclear leukocytic response to rickettsial vascular infection and injury. Thrombosis was more extensive than in classic RMSF, with fibrin thrombi located in foci of rickettsial infection. These patients had a rash either preterminally or not at all, particularly severe Rickettsia-associated pulmonary lesions, and other shock-related lesions, eg, centrilobular hepatic necrosis. All three patients were male blacks with glucose-6-phosphate dehydrogenase deficiency, a condition recently associated with severity of RMSF. Diagnosis of fulminant RMSF requires awareness of its pathologic and epidemiologic aspects, and use of rickettsial isolation or specific immunofluorescence.

Adolescent↗
PubMed1982

Experimental infection of rhesus monkeys with Lassa virus and a closely related arenavirus, Mozambique virus.

As a model for the pathogenesis of Lassa fever in humans, nine rhesus monkeys were inoculated with Lassa virus. Three monkeys had had a previous asymptomatic experimental infection with Mozambique virus, a closely related arenavirus; these monkeys were protected from illness and viremia and manifested only mild pathologic lesions. The other animals developed severe disease and viremia. At necropsy, hepatocellular necrosis, interstitial pneumonia, a unique pulmonary arteritis, adrenal gland necrosis, encephalitis, and uveitis were prominent pathologic lesions which correlated with the organ titers of virus. One animal infected with Lassa virus developed prolonged viremia, a typical immune response, and sudden onset of lower limb paralysis after recovery; at necropsy chronic proliferative arteritis of the spinal cord, brain, and heart was evident. Similarities and differences in the pathologic lesions in this model and Lassa fever in humans indicate that care must be taken in interpreting the results of experiments concerning immune prophylaxis, pathogenesis, and treatment in rhesus monkeys.

Animals↗
PubMed1982

Human endothelial cell culture plaques induced by Rickettsia rickettsii.

Primary cultures of human umbilical vein endothelial cells were inoculated with plaque-purified Rickettsia rickettsii. After adsorption of rickettsiae, monolayers were overlaid with medium containing 0.5% agarose. Small plaques appeared on day 4 postinoculation, and distinct 1- to 2-mm plaques were observed on day 5. Plaquing efficiency was less than that of primary chicken embryo cells in the same medium. Human endothelial cell monolayers were susceptible to infection by R. rickettsii and underwent necrosis as demonstrated by supravital staining. The topographic association of endothelial cell necrosis and rickettsial infection in the plaque model confirmed the direct cytopathic effect of R. rickettsii on human endothelium. Uninfected cells appeared normal by supravital staining and transmission electron microscopy. This model offers the possibility of investigating rickettsial pathogenesis and mechanisms of enhanced severity of Rocky Mountain spotted fever in specific genetically determined conditions.

Cells, Cultured↗
PubMed1982

Zygomycosis caused by Cunninghamella bertholletiae: clinical and pathologic aspects.

Two cases of disseminated systemic zygomycosis caused by Cunninghamella bertholletiae in compromised persons were studied. The underlying disease in one patient was hematopoietic dysplasia (preleukemic syndrome) and in the other, postnecrotic hepatic cirrhosis. A definitive diagnosis of zygomycosis caused by C bertholletiae is achieved only by isolation and identification of the fungus and by demonstration of tissue invasion.

Adolescent↗