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Biomedical subjects

J L Meier

Publications and source records attributed to J L Meier.

At least 37 records · Page 2Linked to original sources
PubMed1987

Pathogenesis of Sarcocystis falcatula in the budgerigar. I. Early pulmonary schizogony.

Sarcocystis falcatula is a protozoan parasite which obligatorily alternates its definitive host, the opossum (Didelphis virginiana), and a uniquely wide range of avian intermediate hosts. The disease produced by this coccidian parasite in intermediate hosts was studied in the budgerigar bird (Melopsittacus undulatus). The ultrastructure of pulmonary sporozoites, meronts and merozoites of this Sarcocystis species is described. Early schizogony occurs progressively in pulmonary capillary and in venular and venous endothelial cells.

Animals↗
PubMed1987

Pathogenesis of Sarcocystis falcatula in the budgerigar. II. Pulmonary pathology.

Sarcocystis falcatula is a protozoan parasite which obligatorily alternates its definitive host, the opossum (Didelphis virginiana), and a uniquely wide range of avian intermediate hosts. The disease produced by this coccidian parasite in intermediate hosts was studied in the budgerigar bird (Melopsittacus undulatus). Early schizogony occurs in pulmonary endothelial cells, resulting in endothelial cell hypertrophy, capillary obstruction preceding endothelial lysis, acute endophlebitis, and chronic periphlebitis. These impede outflow of the pulmonary vascular system resulting in interstitial, subpneumocytic, and then air-space edema. The edema is associated with retraction and degeneration of squamous pneumocytic processes, loss of the myelinoid "surfactant" covering over the pneumocytes, and atelectasis of the respiratory labyrinth. Epithelial repair is effected by migration of granular pneumocytes (normally confined to the parabronchi and their atria) down the infundibula and into the respiratory labyrinth. This pattern of injury and repair is comparable to diffuse alveolar damage (acute interstitital pneumonitis) of mammals despite the markedly different structure of the avian lung. The implications of this peculiar tissue tropism are discussed.

Animals↗
PubMed1986

Microscopic and submicroscopic anatomy of the parabronchi, air sacs, and respiratory space of the budgerigar (Melopsittacus undulatus).

The normal microscopic and submicroscopic structure of the lower respiratory tract of the budgerigar (Melopsittacus undulatus) is described and compared with other birds and mammals. Granular (type II) pneumocytes are confined to linings of air sacs, parabronchi, and their atria; however, their secretions (surfactant) cover the surfaces of the infundibula and respiratory space. Infundibula extend from the atria and give rise to the air capillaries, which branch and anastomose freely with those of adjacent infundibula and other parabronchi (interparabronchial septa are not found). Infundibula and the respiratory labyrinth are lined by a continuous epithelium of squamous pneumocytes, whose perikarya are concentrated in the infundibula and whose peripheral cytoplasm is markedly attenuated. The squamous pneumocytes of the respiratory labyrinth share a basal lamina with the blood capillaries that they envelop.

Animals↗
PubMed1986

Calcitonin and reflex sympathetic dystrophy syndrome.

Reflex sympathetic dystrophy syndrome is a difficult condition to treat. Many modalities have been proposed, all of them being clinically effective but whose efficacy is often difficult to assess, and has not been properly compared. A regimen of physical therapy (pressure therapy, antalgic electrotherapy and exercise therapy) with or without calcitonin was investigated in 24 patients randomly assigned to 2 groups, one given physical therapy alone (Group I) and the other physical therapy plus salmon calcitonin 100 MRC units daily for 3 weeks (Group II). Efficacy assessment was based on clinical (pain, oedema and movement in the affected parts), biochemical (blood and urinary phosphorus and calcium levels, plasma 25-OH-D, plasma parathyroid hormone (PTH), creatinin, alkaline phosphatases and urinary hydroxyproline) and scintigraphic parameters, as well as on the patient's ability to resume working. There was significant improvement in pain in the Group II patients after one week of treatment. As a result the authors advocate the use of calcitonin in addition to physical therapy in reflex sympathetic dystrophy syndrome - and even of calcitonin alone where physical therapy is not possible.

Adult↗
PubMed1986

Attachment of Pneumocystis carinii to rat pneumocytes.

Male Sprague-Dawley rats were immunosuppressed by subcutaneous injections of cortisone acetate for 8 weeks to induce Pneumocystis carinii pneumonia. Rats were killed with ether, their lungs were filled in situ with cold glutaraldehyde, and sections were examined by transmission electron microscopy. P. carinii trophozoites were observed in lungs for as long as 6 weeks after cessation of corticosteroid injections. Trophozoites were attached most frequently to type I pneumocytes but were seen on several occasions to be attached to type II pneumocytes. In attachment, trophozoites in contact with alveolar epithelial cells produced cytoplasmic modifications of three basic forms: one was an invagination of parasite surface to pinch cytoplasmic extensions on the surface of the epithelial cells. A second was an extension that was inserted into a crevice of the host surface and enlarged at the tip to form an anchor. The third was an extension that remained pointed at the tip and was recurved to form a hook. None of these modifications was seen on the surface of the trophozoites. Filopodia did not appear to be involved in attachment but were seen on both attached and lumenal surfaces of the trophozoites. Trophozoites and cysts were also observed to be partially or completely enveloped by extensions of the host cell's cytoplasm. In these instances, parasites had rounded surfaces but appeared viable. No fusion of cell membranes between parasite and host cells was ever seen. These observations may help explain why P. carinii can attach tenaciously to lung epithelium without cell-membrane fusion, production of a glycocalyx, or invasion of host cells.

Animals↗
PubMed1985

Perturbation of lymphatic endothelial cells in experimental Brugia malayi infections.

Infection with filarial nematodes induces lymphatic dysfunction in many individuals in endemic areas. The present morphometric study describes changes in lymphatic endothelial cells of Brugia-infected cats. Transmission electron microscopy revealed a decrease in the number of cytoplasmic vesicles in endothelial cells from lymphatic vessels harboring filarial nematodes (4.9 vesicles per micron 2 cytoplasm) when compared with similar cells from the contralateral uninfected control vessels (9.0 vesicles per micron 2). The size of the vesicles and their location within the cytoplasm was not changed. Irregular large vacuoles, often containing degenerating organelles, were common in endothelial cells lining Brugia-infected lymphatic vessels. These studies suggest that damage of cells by living or dead worms or worm products may have a direct effect on the endothelial lining of lymphatic vessels. This may compromise the efficiency of vessels that collect and transport edematous fluid in affected limbs.

Animals↗
PubMed1984

Description of Sarcocystis falcatula stiles, 1893, a parasite of birds and opossums.

Sarcocystis falcatula Stiles, 1893 is re-described. Intermediate hosts of the parasite which was earlier described as Sarcocystis debonei Vogelsang, 1929 are species of passeriform, psittaciform, and columbiform birds. In these birds, muscle zoites are 6.88 X 2.19 (4.8-8.4 X 1.2-3.6) micron and are enclosed in a cyst wall with regular protrusions, 1-5 micron long. The convoluted primary wall has multiple thin areas in the osmiophilic layer. Microtubules originate in the ground substance and extend to the tips of the protrusions. The only known definitive host is the opossum, Didelphis virginiana; rats, cats, a dog, and a ferret could not be infected from muscle cysts. Sporocysts from opossums infected from five different infected avian sources measure 11.2 X 7.4 (9.6-12.0 X 6.0-8.4) micron.

Animals↗
PubMed1983

Leprosy in wild armadillos (Dasypus novemcinctus) on the Texas Gulf Coast. Ultrastructure of the liver and spleen.

Recent studies have established that the "naturally-occurring leprosy-like disease of wild armadillos" is, indeed, caused by Mycobacterium leprae indistinguishable from M. leprae from human lepromatous leprosy. The present study reports the ultrastructure of the mycobacteria and host response in deep viscera, liver and spleen, in Texas armadillos with sylvatic leprosy. Evidence for acid-fast bacillary proliferation in these organs and penetration of hepatocytes is given. Acid-fast bacilli concentrated in activated macrophages in Billroth cords and sheaths of Schweigger-Seidel of the spleen and in Kupffer cells of the liver. Both mycobacteria and host response seen in lepromata of sylvatic leprosy, lepromatous lesions produced by injection of inocula from human lepromata and human lepromata, are compared.

Animal Diseases↗
PubMed1983

Bursitis and tenosynovitis caused by group G streptococci.

Two cases of extraarticular Group G streptococcal infection are reported: one patient suffered from tenosynovitis of the extensor digitorum communis tendons of a wrist and the other from a prepatellar bursitis. In both cases penicillin therapy rapidly cleared all signs of infection.

Adult↗