Giant-cell osteosarcoma in a female ranch mink (Mustela vision).
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Animals↗
Biomedical subjects
B Martineau-Doizé
Publications and source records attributed to B Martineau-Doizé.
Virulence mechanisms of avian fimbriated Escherichia coli in experimentally inoculated chickens.
Virulence mechanisms of avian pathogenic Escherichia coli were investigated by inoculating commercial broiler chickens via the left caudal thoracic air sac with three highly pathogenic and three less pathogenic E. coli isolates. At 6 h postinoculation, all isolates had colonized the respiratory tract (trachea, lungs, and air sacs) and internal organs (liver, spleen, and kidney) of inoculated birds, but bacteria were recovered from pericardial fluid and blood only of birds inoculated with the more pathogenic isolates. F1 fimbriae were expressed on a high proportion of bacteria colonizing the trachea and to a lesser extent on bacteria in the lungs of birds inoculated with each of the isolates. F1 fimbriae were also expressed on bacteria in air sacs only for the less pathogenic isolates. P(F11) fimbriae were expressed on bacteria present in air sacs, lungs, kidney, blood, and pericardial fluid of birds inoculated with one of the more virulent isolates. On electron microscopy, bacteria of the more pathogenic isolates but not of the less pathogenic isolates were observed often associated with or within macrophages, which appeared to be viable, in the air sacs and lungs. In in vitro assays, the more pathogenic but not the less pathogenic isolates, were resistant to opsonization and phagocytosis in the absence of F1 fimbriae, whereas bacteria of all isolates were rapidly killed by avian macrophages when they expressed F1 fimbriae. These results suggest that resistance to phagocytosis may be an important mechanism in avian colisepticemia. They also suggest that F1 fimbrial phase variation to the nonfimbriated phase is favored in the avian lower respiratory tract, is more marked for the more pathogenic-isolates, and may be a virulence mechanism.
Air Sacs↗
Ultrastructural characterization of the nasal respiratory epithelium in the piglet.
BACKGROUND: Very little information is available on the ultrastructure of the nasal cavity epithelium of the piglet. However, the nasal respiratory epithelium plays an important role in the pathology of atrophic rhintis of the piglet. Indeed, ciliated cells and mucus play a co-ordinate role in the colonization of the nasal cavity by the etiological agents of the disease. METHODS: In the present study, samples of the ventral nasal turbinates of germ-free piglets were processed for observation in the transmission electron microcope to describe the ultrastructure of their covering respiratory epithelium. RESULTS: Five morphologically distinct cell types were observed. Ciliated cells and basal cells were similar to that described in the nasal cavity of other species. On the basis of their secretory granule morphology, five forms of goblet cells were observed. Nonciliated, nonsecretory columnar cells with short, thick, regularly and densely spaced apical microvilli were identified as brush cells. A distinct type of secretory cells was found. Their apical surface protruded above the adjacent cells and had a few microvilli covered with thin hairlike projections. They were rich in smooth endoplasmic reticulum and had an apocrinelike type of secretion. CONCLUSIONS: These findings indicate the complexity of cell types of the piglet nasal respiratory epithelium.
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In vitro phagocytosis and survival of Streptococcus suis capsular type 2 inside murine macrophages.
In this study, data on phagocytosis of Streptococcus suis and its survival inside macrophages are presented. Mouse peritoneal macrophages were incubated in the presence of one of five different strains of S. suis capsular type 2: a virulent wild-type strain (1591), a non-capsulated non-virulent mutant strain (M2), a poorly capsulated non-virulent mutant strain (M42), a non-virulent capsulated strain (1330), and the wild-type reference (virulent) strain S735. Opsonized or non-opsonized bacteria were incubated with macrophages in vitro and samples were obtained after 1 and 3 h incubation. Phagocytosis as well as live and dead intracellular organisms were determined by acridine orange and crystal violet staining. After 1 h incubation, non-opsonized virulent and non-virulent capsulated bacteria were poorly phagocytosed (by less than 7% of the macrophages), whereas the non-capsulated non-virulent mutant strain was highly phagocytosed (by more than 68% of the macrophages). The M42 mutant strain was more phagocytosed than the capsulated strains but less than the non-capsulated M2 mutant strain (35%). In contrast, a higher percentage of live bacteria was observed inside macrophages for the capsulated strains (1591 and S735) than for the non- or poorly capsulated mutant strains (M2 and M42). Opsonization of bacteria with rabbit serum or heat-inactivated rabbit serum significantly increased phagocytosis. For every opsonized strain, after 3 h incubation, the percentage of live bacteria within macrophages was considerably lower than the corresponding non-opsonized strains. In conclusion, the capsule of S. suis type 2 appears to act as an important anti-phagocytic factor. However, virulent capsulated non-opsonized strains can be phagocytosed by mouse peritoneal macrophages within which they appear to survive for at least 3 h. Serum factors other than complement increase not only phagocytosis but also intracellular killing of S. suis of both capsulated and non-capsulated strains.
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Role of capsular sialic acid in virulence and resistance to phagocytosis of Streptococcus suis capsular type 2.
Streptococcus suis capsular type 2 has a capsule rich in sialic acid (NANA). Sialic acid, known to be an antiphagocytic factor for many bacterial species, inhibits the activation of the alternative complement pathway. The role of capsular NANA in virulence, resistance to phagocytosis and intracellular survival of S. suis capsular type 2 was evaluated. In general, a low concentration of NANA was observed for all the S. suis strains tested. In addition, no difference could be found in NANA concentrations between strains of different virulence degrees. Sialic acid concentration increased in the virulent strain 89-1591 and the avirulent strain 90-1330 after in vivo growth with an increased capsular material thickness compared to growth in vitro. No significant difference could be found in the phagocytosis rate by porcine blood monocytes of either strain and strain 89-1591 treated with sialidase or the sialic acid-binding lectin from Sambucus nigra (SNA I). Intracellular survival of strain 89-1591 decreased after treatments with sialidase or lectin, becoming comparable to that of strain 90-1330. Finally, no difference could be seen in virulence using a murine model, even if strain 89-1591 was treated with the enzyme or the lectin. Thus, NANA does not seem to be a critical virulence factor for S. suis capsular type 2.
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Stimulation of osteoclast-like cell formation by Pasteurella multocida toxin from hemopoietic progenitor cells in mouse bone marrow cultures.
The effects of purified Pasteurella multocida toxin (PMT) on osteoclast formation from hemopoietic progenitor cells were studied using an in vitro system. Mononuclear adherent mouse bone marrow cells were cultured for 7 or 14 days in the presence of PMT, or 1,25-dihydroxy-vitamin D3, or both. Mononuclear osteoclast-like cells, which are postmitotic osteoclast precursor cells, were identified as tartrate-resistant acid phosphatase (TRAP)-positive mononuclear cells possessing calcitonin receptors. Multinucleated osteoclast-like cells were TRAP-positive multinuclear cells with calcitonin receptors. The results demonstrate that, as does 1,25(OH)2D3, Pasteurella multocida toxin stimulates proliferation of adherent bone marrow mononuclear cells (progenitor cells), and their differentiation into postmitotic mononuclear osteoclast precursor cells. It also causes fusion of the latter into multinuclear osteoclasts; however, the number of osteoclasts obtained with PMT is smaller than with 1,25-dihydroxy-vitamin D3.
Acid Phosphatase↗
Septicemia-inducing Escherichia coli O115:K"V165"F165(1) resists killing by porcine polymorphonuclear leukocytes in vitro: role of F165(1) fimbriae and K"V165" O-antigen capsule.
Escherichia coli O115:K"V165":F165(1) wild-type strain 5131 survives in the bloodstream of experimentally inoculated gnotobiotic pigs and induces septicemia, whereas its afimbriate (F165(1)-negative) TnphoA mutant M48 and its acapsular (K"V165"-negative) spontaneous mutant 5131a are both nonpathogenic. We evaluated the role of the mannose-resistant F165(1) fimbrial system and of the O-antigen K"V165" capsule in resistance to phagocytosis by porcine polymorphonuclear leucocytes (PMNLs) in vitro. F165(1)-positive strains (5131 and 5131a) attached to and were ingested by PMNLs at a significantly higher level than afimbrial mutant M48 (P < 0.001) after 1 h of incubation. During incubation of these strains with PMNLs for up to 6 h, parental strain 5131 resisted killing whereas afimbriate mutant M48 and acapsular mutant 5131a were gradually killed and were found at significantly lower numbers than the parental strain 5131 at 2 (P < 0.05) and 6 (P < 0.001) h. When bacteria were opsonized with normal pig serum, the afimbriate and acapsular mutants survived less well than when the bacteria were nonopsonized. Upon examination by electron microscopy of PMNLs after 2 h of incubation with bacteria, structurally normal bacteria were observed more often within phagosomes of PMNLs incubated with the parental strain than within phagosomes of PMNLs incubated with the afimbriate or the acapsular mutant. The extracellular oxidative response (as tested by release of hydrogen peroxide) of PMNLs stimulated by phorbol myristate acetate was completely inhibited by F165(1)-positive strains but only partially inhibited by the afimbriate mutant. These results suggest that the F165(1) fimbrial system may mediate adherence of E. coli O115 to PMNLs. Survival of the parental strain in the presence of PMNLs, which may be intracellular, is at least partially due to the presence of the F165(1) fimbrial system and of the O-antigen capsule K"V165". Furthermore, the presence of the F165(1) fimbrial system may contribute to the bacterial inhibition of the oxidative response of porcine PMNLs.
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Evaluation of biocompatible osteoconductive polymer shelf arthroplasty for the surgical correction of hip dysplasia in normal dogs.
Biocompatible osteoconductive polymer (BOP) shelf arthroplasty was performed on ten nondysplastic dogs, divided into five groups. Each group was evaluated at 6, 13, 17, 26 or 39 weeks postsurgery. Evaluation consisted of clinical, radiological and histological studies. The dogs were injected with three fluorochrome markers, 28 days, 14 days and 6 hours before euthanasia. Transverse sections of undecalcified arthroplasty site were examined by microradiography and fluorescence microscopy; surface-stained sections were evaluated by light microscopy. The BOP shelf arthroplasty was not technically difficult. Minimal mineralization of the shelf was noted by radiography, 26 and 39 weeks postop. A moderate to large amount of fibrous mature connective tissue was observed around the BOP fibers throughout the study. Bone ingrowth occurred around the BOP fibers, but was minimal within them. This osseous proliferation of the arthroplasty was very slow to take place; it was first noted microscopically 17 weeks postsurgery and was still minimal 39 weeks after surgery. These findings suggest that there may be interference to the osteoconductive properties of BOP by fibrous tissue. Ossification of the shelf arthroplasty was too unsatisfactory to recommend its use for the treatment of canine hip dysplasia.
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Effects of Pasteurella multocida toxin on the osteoclast population of the rat.
Pasteurella multocida type D toxin is a peptide shown to induce severe atrophic rhinitis in the pig as the result of an increased osteoclastic resorption of the ventral nasal turbinates. In the present study, the effects of the toxin on the histological, cytochemical and ultrastructural features of the osteoclast population of the rat were examined. Pasteurella multocida toxin induced atrophy of the ventral and dorsal nasal turbinates and thinning of the nasal bones. The number and size of the long bone metaphyseal osteoclasts were significantly increased, but not the number of nuclei per cell. Osteoclasts of toxin-treated rats had more developed clear zones and ruffled borders than those of the controls and their cytoplasmic vacuoles were more abundant and larger. We concluded that P. multocida toxin stimulates bone resorption by osteoclasts in the rat by increasing resorption activity and by increasing their number. Its action is not limited to the nasal turbinates but occurs also in the other bones, such as the long bones.
Acid Phosphatase↗
Nasal epithelial changes induced in piglets by acetic acid and by Bordetella bronchiseptica.
Research on atrophic rhinitis of pigs has shown that both Bordetella bronchiseptica infection and experimental treatment with acetic acid predispose the nasal mucosa to colonization with Pasteurella multocida. Gnotobiotic piglets aged 3 days were dosed intranasally with either B. bronchiseptica (n = 6) or acetic acid 1 per cent (n = 10) and killed at intervals up to the 4th day after treatment. Samples of the ventral turbinates were examined by light microscopy and scanning and transmission electron microscopy. Within 12 h acetic acid induced loss of cilia, oedema, focal cell exfoliations, mitochondrial swelling and inflammatory cell infiltration. Bordetella bronchiseptica induced only a limited oedema and loss of cilia. Colonization of cilia by the bacteria was observed 96 h after infection. We conclude that, although acetic acid and B. bronchiseptica do not induce the same modifications of the nasal respiratory epithelium, their action causes stagnation of nasal mucus, which results in a nasal environment favourable to colonization by Pasteurella multocida.
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Pathogenicity of an Escherichia coli O115:K"V165" mutant negative for F165(1) fimbriae in septicemia of gnotobiotic pigs.
To evaluate the role of the F165(1) fimbrial system in the pathogenesis of septicemia, 2-day-old germfree pigs were inoculated intragastrically with Escherichia coli O115:K"V165":F165 wild-type strain 5131, its F165(1)-negative TnphoA mutant M48, or E. coli O115:K(-):F165(-) wild-type strain 862B. Pigs were sacrificed at different times (3, 6, 12, 24, 48, and 96 h) postinfection (p.i.). Pigs inoculated with strain 5131 developed clinical signs (anorexia, lameness, reluctance to move, or lack of motor coordination) and were moribund within 48 h p.i., and, at necropsy, infecting bacteria were isolated in various extraintestinal organs. Strain 5131 was isolated as early as 6 h p.i. from the blood of inoculated pigs. Pigs inoculated with mutant M48 developed only mild clinical signs at 96 h p.i. Mutant M48 colonized extraintestinal organs of pigs but to a lesser extent than the parent strain did. In contrast to the parent strain, this mutant was not isolated in the blood of inoculated pigs. Pigs inoculated with strain 862B remained normal during the experiment. All of the strains colonized the mucus layer of the intestine, but no histological changes of intestinal mucosa were observed by either light or electron microscopy. The parent strain, but not the mutant M48, expressed F165(1) in vivo. In a competitive study in which the parent strain and its afimbrial mutant were inoculated simultaneously, clinical signs of septicemia developed 24 h after inoculation, and only the parent strain 5131 was isolated from the blood of inoculated pigs. Our results suggest that the F165(1) fimbrial system of E. coli O115:K"V165" strains may play an important role in the ability of the bacteria to survive in the blood and spread systemically through the porcine host.
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Osteogenesis and growth of the nasal ventral conchae of the piglet.
The present study investigated the osteogenesis and growth of the nasal ventral conchae of piglets aged from 1 to 28 days. Serial transverse sections of paraffin wax-embedded noses were stained and examined by light microscopy. Bone formation occurred in a rostrocaudal direction in the ventral scroll, dorsal scroll, connecting zone, transverse lamina and articular lamina, successively, and occurred by two ossification processes: endochondral ossification and intramembranous bone apposition. Endochondral ossification was responsible for the longitudinally, rostrally directed growth. Rapid transverse bone growth and modelling were centrifugally directed and occurred by intramembranous bone apposition at the eccentric side of the scrolls and resorption at the concentric scroll side. Elongation of the distal scroll extremities took place by intramembranous bone apposition.
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Distribution and histochemical characterization of goblet cells in the nasal cavity of piglets.
The present study was designed to compare the distribution of goblet cells and the histochemical composition of mucosubstances produced by these cells in the nasal cavity of piglets aged from 1 to 28 days. Serial transverse sections were stained to demonstrate neutral, acidic, and sulfated mucosubstances. Sections located at eight reference levels rostrocaudally in the nasal cavity and defined regions on these sections were used for goblet-cell counting. There was a nonhomogeneous distribution of goblet cells in the nasal cavity of piglets. A rostrocaudal increase in goblet-cell density was observed with the highest densities found in the ventral meatus and on the septum. There was no difference in this pattern of distribution according to age of the piglets. However, age-related differences were observed in the prevalence of goblet cells containing sialomucins, sulfomucins, or both. While sialomucins were prevalent at 1 and 14 days, sulfomucins predominated in the rostral half of the cavity at 28 days. Our results indicate a maturation of the products of secretion with aging in piglets. The affinity of infectious agents for sialylated glycoconjugates and the predominance of sialomucins in the nasal cavity of newborn piglets could account for their greater susceptibility to bacterial infection.
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Localization of epidermal growth factor receptors in cells of the enamel organ of the rat incisor.
Epidermal growth factor (EGF) is a peptide shown to effect precocious incisor tooth eruption in rat pups. Binding sites for EGF were visualized in the continuously erupting adult rat incisor by light and electron microscope radioautography after in vivo injection of 125I-EGF. These binding sites represented EGF receptors because of (i) competition between 125I-EGF binding at 2 min after injection and a coinjected excess of unlabeled EGF; (ii) the receptor-mediated endocytosis of 125I-EGF at 15 and 30 min after injection; and (iii) the demonstration of EGF receptor kinase activation in vivo. The stem and the mitotic cells in the epithelial odontogenic organ at the growing end of the tooth develop into two nondividing layers of the enamel organ: (i) ameloblasts which secrete enamel and are subsequently involved in the enamel maturation process, and (ii) papillary layer cells situated between the blood supply and the ameloblasts. Although few EGF receptors were present at the mitotic end, receptor density was highest at the mature end of the enamel organ. High levels of 125I-EGF binding were found on papillary layer cells and ruffle-ended, but not smooth-ended, ameloblasts. This implies a cyclical exteriorization and internalization of receptors during modulations between the two cell types. These data suggest that the EGF receptor mediates a major function of the enamel organ in the formation of enamel.
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Effects of purified Pasteurella multocida dermonecrotoxin on the nasal ventral turbinates of fattening pigs: histological observations.
Fattening specific pathogen-free derived pigs were injected intramuscularly with dermonecrotoxin of Pasteurella multocida, capsular type D. Ten days later, the nasal ventral turbinates and liver were examined histologically. A moderate turbinate atrophy was observed due to an increased number of osteoclasts and the absence of intramembranous bone apposition. Liver lesions were limited to some hepatocyte necrosis, sinusoid neutrophil infiltration and Kupffer cell hypertrophy. This study demonstrated that adult pigs are sensitive to P. multocida dermonecrotoxin.
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Histological changes in the nasal ventral conchae of piglets infected with Bordetella bronchiseptica.
Piglets infected intranasally with Bordetella bronchiseptica were injected with two fluorochrome markers. Transverse sections of undecalcified nasal conchae (cut between the third incisor and the third premolar teeth) were examined by microradiography and fluorescence microscopy; surface-stained sections were evaluated by light microscopy. The fluorescent surface of the nasal ventral conchae from the infected piglets was increased as compared with the controls. This was due to an increased amount of fluorescent mineralization fronts as well as to the presence of abnormal fluorescent areas within trabeculae. Trabecular mineral content of the microradiographs was irregular and varied from hypo- to hypermineralized. When compared with the corresponding surface-stained sections, no correlation could be made between the mineral content and the type of tissue. These findings suggest that an increased number of osteoblasts which secrete prebone matrix but are modified so that mineralization does not occur normally.
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Atrophic rhinitis caused by Pasteurella multocida type D: morphometric analysis.
In order to study the distribution and the extent of atrophy caused by Pasteurella multocida in the nasal conchae, experimental piglets were injected intramuscularly at seven days of age with either two or four 50% mouse lethal doses per kg body weight of P. multocida type D dermonecrotoxin. Experimental and control piglets were killed four, six and ten days postinjection. Serial transverse paraffin embedded sections of the noses were cut throughout the entire length of the nasal conchae. The area of the nasal ventral conchae was measured and the morphometric index of the nasal cavity was calculated. It was observed that P. multocida type D dermonecrotoxin induced severe atrophy of the nasal ventral conchae. This atrophy was present along the entire conchae. However, it was most severe at the level of the first and second premolar teeth.
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Distribution of atrophy in the nasal ventral conchae of piglets infected experimentally with Bordetella bronchiseptica.
The distribution and extent of atrophy caused by Bordetella bronchiseptica in the nasal ventral conchae were investigated by intranasally infecting piglets at day 4 of life. Experimental and control piglets were killed at one, two, three, four, five and six weeks of age. Serial transverse 80 microns thick nondecalcified sections were cut throughout the entire length of the nasal ventral conchae, and microradiographed. It was observed that the distribution and extent of atrophy was not uniform along the ventral conchae. The articular and transverse laminae as well as the connecting zone were not atrophied, except at their rostral extremity. The entire dorsal scroll was atrophied. This atrophy was moderate, except at the rostral and caudal extremities of the dorsal scroll, where its size was less than half that of the controls. The ventral scroll was less atrophied than the dorsal scroll, although a marked atrophy was present at its rostral extremity. From these observations, it is suggested that two transverse sections should be made through the nose of pigs in order to establish a diagnosis of atrophic rhinitis at slaughter: one section at the level of the first-second premolar tooth and one more rostral section, at the level of the canine tooth.
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