Biomedical subjects
Publications and source records attributed to F W Chandler.
In the histopathologic evaluation of inflammatory lesions, numerous structures suggestive but not representative of microbial agents are encountered and may lead to erroneous diagnoses. Examples of pseudomicrobes are illustrated and discussed to prevent potential incorrect histopathologic assessments.
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We have developed a new indirect immunofluorescence procedure for identifying Trypanosoma cruzi amastigotes in sections of Formalin-fixed, paraffin-embedded tissue pretreated with a 0.25% trypsin solution to enhance immunofluorescence. In sections of human and mouse myocardia infected with T. cruzi and stained by this procedure, both intact amastigotes and phagocytosed amorphous antigen were intensely fluorescent and easily detected; nonspecific background fluorescence was absent or minimal. No staining occurred in similarly treated sections of Formalin-fixed, paraffin-embedded tissue that contained Histoplasma capsulatum var. capsulatum, Toxoplasma gondii, or Leishmania donovani to control specificity. Because pathology laboratories usually receive Formalin-fixed tissues for evaluation, this rapid and reliable procedure can be used to extend the diagnostic capability of conventional histopathology.
Xylohypha emmonsii Padhye, McGinnis et Ajello is described as a new dematiaceous opportunistic pathogen of humans and lower animals. This hyphomycete differs from X. bantiana (Saccardo) McGinnis, Padhye, Borelli et Ajello by its inability to grow at 40 degrees C and by the development of short chains of asymmetrically bent to ellipsoid blastoconidia. In brain tissue of mice, experimentally infected with X. emmonsii, the host response to the invading fungus was similar to that observed in mice infected with X. bantiana. In tissues X. bantiana occurred predominantly as long, septate hyphae, in contrast to X. emmonsii, which was more polymorphic.
The first human phaeohyphomycotic infection caused by Xylohypha emmonsii is described. The patient, an 83-year-old woman, developed a purpuric lesion on her left arm. The pale brown fungal elements observed in biopsy tissue consisted of thin- to thick-walled, oval to spherical, yeastlike cells with single and, occasionally, multiple buds; chains of budding cells; cells with internal septations in one and, rarely, two planes; and septate hyphae. In culture, X. emmonsii grew moderately fast at 25 degrees C, showed minimal growth at 37 degrees C, and failed to grow at 40 degrees C. It produced acropetal chains of one-celled (rarely two-celled) conidia laterally and terminally directly from vegetative hyphal cells.
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Infection with Trichosporon spp was diagnosed in 2 cats. In one cat, infection consisted of a granulomatous dermatitis and was concurrent with disseminated lymphoblastic lymphosarcoma. In another cat, urinary cystitis caused by T beigelii was diagnosed.
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To further define the nature of Lyme carditis, electrophysiologic study and endomyocardial biopsy were performed in a patient with Lyme disease, whose principal cardiac manifestation was high-degree atrioventricular block. Intracardiac recording demonstrated supra-Hisian block and complete absence of an escape mechanism. Gallium 67 scanning demonstrated myocardial uptake, and right ventricular endomyocardial biopsy revealed active lymphocytic myocarditis. A structure compatible with a spirochetal organism was demonstrated in one biopsy specimen. It is concluded that Lyme disease can produce active myocarditis, as suggested by gallium 67 imaging and confirmed by endomyocardial biopsy. Furthermore, the presence of high-grade atrioventricular block in this disease requires aggressive management with temporary pacemaker and corticosteroid therapy.
Gomori's methenamine silver and the periodic acid--Schiff reaction stain cytoplasmic but not intranuclear cytomegalovirus inclusions. The biochemical basis of these staining qualities is discussed, and the staining characteristics are correlated with supporting ultrastructural observations. Failure to recognize this phenomenon may lead to erroneous diagnostic conclusions at the light microscopic level.
Toxic shock syndrome toxin 1 (TSST-1) was purified to apparent homogeneity by chromatofocusing and affinity chromatography. The amino acid composition of the toxin was very similar to that reported for TSST-1 by other investigators. The amino-terminal amino acid was serine. A partial specific volume of 0.73 ml/g was calculated for the toxin from the amino acid data, and a molecular weight of 19,200 +/- 1,300 was determined by hydrodynamic methods. New Zealand white rabbits of both sexes were equally susceptible to the lethal effects of the toxin; however, older rabbits (greater than 12 months) were far more susceptible than young adults or weanlings. The 50% lethal dose of TSST-1 in older rabbits was 50 to 60 micrograms/kg when injected subcutaneously and 20 to 30 micrograms/kg when injected intravenously. Enhancement of lethal endotoxin shock by TSST-1 could not be demonstrated when both toxins were injected subcutaneously; however, lethal shock did occur when endotoxin (10 micrograms/kg) was injected intravenously after TSST-1 had been injected by either the subcutaneous (50 to 60 micrograms/kg) or the intravenous (20 to 30 micrograms/kg) route. Endotoxin alone was not lethal at a dose of 500 micrograms/kg of body weight when injected subcutaneously. When injected intravenously, endotoxin at a dose of 500 micrograms/kg was not lethal in weanling males or in females in any age group; however, young (6 to 7 months) and adult (greater than 12 months) males were killed by endotoxin doses as low as 45 to 50 micrograms/kg. Histopathologic studies of rabbits by both sexes which died as a result of TSST-1 alone or in combination with endotoxin showed extensive damage to organs rich in lymphoid and mononuclear phagocytic cells such as the thymus, mesenteric lymph nodes, liver, and spleen. Severe congestion of these organs as well as erythrophagocytosis and lymphoid depletion in the spleen and mesenteric lymph nodes were noted. Congestion and hemorrhage were also found in the heart, lungs, trachea, and thymus. The systemic pathology produced by TSST-1 was strikingly similar to that seen in humans who had died of toxic shock syndrome and in rabbits with subcutaneous chamber inoculated with toxic shock case strains of Staphylococcus aureus. Rabbits that were not killed by the toxin suffered a very rapid and severe leukopenia followed by leukocytosis with a left shift. Lymphopenia was also noted as was a mild but persistent anemia. With the exception of the early leukopenia, very similar hematologic findings have been noted in humans with toxic shock syndrome.
Phialemonium obovatum was found to be the cause of osteomyelitis in a German shepherd dog. Histologic examination of the biopsied material from the left tibia revealed septate, irregularly branched hyphae, swollen cells, and ovate-to-spherical cells divided by a transverse septum. The majority of the fungal elements were hyaline, but a few had lightly pigmented cell walls that had a greenish yellow tint. The presence of melanin in the cell walls of the hyphae and especially in their septa was verified by the use of the Fontana-Masson silver stain. P. obovatum formed moist, off-white-to-ochraceous, spreading colonies with a characteristic green pigment on their reverse side. The pigment was more prominent in cultures grown at 37 degrees C than in those grown at 25 degrees C. The isolate also grew at 40 degrees C. The dog isolate produced characteristic adelophialides without conspicuous collarettes and also basal septa from the creeping vegetative hyphae growing on the surface of the medium. The numerous obovate phialoconidia were smooth and one-celled.
A case of systemic zygomycosis caused by Apophysomyces elegans in a 56-year-old man is described. The left kidney and the bladder showed presence of broad, nonseptate-to-infrequently septate hyphae in both the bladder lesion and in the septic kidney. Surgical debridement and treatment with amphotericin B cured the infection. No underlying immune defect was ever demonstrated, and the patient was not hyperglycemic or acidotic at any time. This zygomycetous fungus closely resembles Absidia corymbifera, but is distinguished by its distinctive morphological features.
A natural infection of Acanthamoeba castellani, a free-living ameba, was determined to be the cause of acute, hemorrhagic, necrotizing amebic meningoencephalitis in a dog. This case is unique because previous reports of infection by the Acanthamoeba spp in dogs have not indicated its presence in the brain. Naturally developing meningoencephalitis by Acanthamoeba spp in the dog may have a pathogenesis similar to that of human beings. The ameba in this case also was observed in the lungs and kidneys, which are believed to be the primary sites of lesions in human beings that develop amebic meningoencephalitis from Acanthamoeba spp.
Although toxic shock syndrome toxin-1 (TSST-1) has been proposed as the toxin responsible for toxic shock syndrome, its role in this disease has not been proved. To study this question, we examined Staphylococcus aureus strains isolated from normally sterile sites in patients with nonmenstrual toxic shock syndrome for the presence of TSST-1 production. Only 20 (62.5%) of 32 produced TSST-1, compared with 41 (93%) of 44 vaginal isolates from patients with menstrual toxic shock syndrome. Of strains of S aureus from patients with nonmenstrual toxic shock syndrome, TSST-1-negative isolates were more likely to be associated with a fatal outcome and to not be phage group 1 than TSST-1-positive isolates. Seven of the TSST-1-negative strains were evaluated in a rabbit subcutaneous chamber model of toxic shock syndrome. Fifteen (60%) of 25 rabbits developed a toxic shock syndrome-like illness and nine died. Clinical signs and histopathologic findings in the rabbits were similar to those seen in rabbits inoculated with TSST-1-positive S aureus isolates. These results suggest that other, as yet unrecognized, toxins play a role in toxic shock syndrome, and that TSST-1 production may not be essential to the pathogenesis of toxic shock syndrome.
A dog with exposure keratopathy developed secondary bilateral keratitis from which Aspergillus sp and Curvularia sp were identified. Mycotic keratitis, while rare in the dog, should be considered in the differential diagnosis of keratitis.
Systemic protothecosis was diagnosed in a 7-year-old dog that had only ocular manifestations. During the 3-month course of disease, a variety of drugs was administered, including amphotericin B, gentamicin, and ketoconazole. The ocular signs initially abated, but subsequently worsened during this period. The dog was found dead 3 months after initial examination, and systemic protothecosis was confirmed at necropsy.