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PubMed2003

Graft protective effects of heme oxygenase 1 in mouse tracheal transplant-related obliterative bronchiolitis.

BACKGROUND: Heme oxygenase (HO)-1, long believed to be a cytoprotective protein, has recently been identified as a graft survival gene. This study evaluates the role of HO-1 in a murine heterotopic tracheal allograft model for obliterative bronchiolitis. METHODS: Mice with deficient or experimentally enhanced HO-1 expression underwent subcutaneous implantation of murine tracheal isografts and allografts. Grafts were excised after 9, 16, or 21 days and evaluated by histologic examination, immunohistochemistry for HO-1 and interleukin (IL)-10 proteins, and terminal deoxynucleotide transferase-mediated dUTP nick-end labeling. To evaluate the relationships between IL-10 and HO-1, the effects of modulation of HO-1 expression on IL-10 expression were evaluated and HO-1 expression was examined in tracheal transplants from IL-10 null mice. RESULTS: Isografts demonstrated normal histology with minimal HO-1 staining, whereas allografts showed features of human airway rejection (loss of respiratory epithelium, luminal granulation tissue, lymphocytic tracheitis) with increased HO-1 staining in macrophages and mesenchymal cells. HO-1-deficient mice demonstrated a more rapid progression of the tracheal allograft injury as compared with control allografts, and this was associated with a decrease in the anti-inflammatory cytokine, IL-10. Tracheal transplants using IL-10-deficient mice also resulted in a more severe injury, and this was accompanied by a decrease in HO-1 staining. CONCLUSIONS: HO-1 protein expression is increased in murine heterotopic airway rejection, and deficiency of HO-1 accelerates the development of the obliterative bronchiolitis-like lesion. IL-10 protein expression parallels expression of HO-1, suggesting that IL-10 may participate in the genesis of HO-1's effects on the inflammatory processes triggered by allotransplantation.

Animals↗
PubMed1990

Mast cells in normal and pathological specimens of the equine lung.

In lungs from 22 horses, the number and type of mast cells in histologically normal specimens were compared with those in specimens with various histological lesions. Tissues fixed in Carnoy's solution were superior to those fixed in formalin for the identification of mast cells. Fixation of lung specimens from eight horses in Carnoy's solution and formalin allowed the identification of two subpopulations of mast cells: formalin-sensitive, which predominated and formalin-resistant. Specimens with mild chronic tracheitis and mild and moderate chronic bronchitis generally had slight increases in mast cell numbers in comparison to histologically normal specimens. An increase in mast cell numbers was also observed around small and large bronchioles with mild, moderate and severe bronchiolitis and in fibrosed pulmonary pleurae in comparison to specimens with no histological lesions. The most striking increase in mast cell numbers was seen in fibrosed alveolar septa; there were approximately four times as many mast cells in these specimens as in specimens with normal histology.

Animals↗
PubMed1991

Intranasal infection of ferrets (Mustela putorius furo) with canine parainfluenza virus.

Immunocompetent and cyclophosphamide-immunosuppressed ferrets were intranasally infected with canine parainfluenza virus (CPIV) and observed for clinical signs, histopathologic lesions, the immunocytochemical demonstration of CPIV antigen in the respiratory tract and scanning electron microscopic alterations of the tracheal epithelium until 36 days post infection (p.i.). In both groups, clinical signs were minimal, restricted to the upper respiratory tract and consisted of cough elicited by tracheal compression between 3 and 7 days p.i. Microscopically, inflammatory and degenerative lesions were observed in the trachea and less frequently in the nasal cavity; bronchiolitis or interstitial pneumonia was not demonstrated. By immunocytochemistry, CPIV antigen was demonstrated in tracheal epithelial cells, whereas nasal cavity, bronchi, bronchioles and lung were devoid of viral antigen. Ferrets given CPIV alone developed a minimal lymphocytic tracheitis with minimal loss of cilia and CPIV antigen was observed only 4 days p.i. 17 days p.i., normal epithelial organization and ciliary reappearance was reestablished. Ferrets treated with cyclophosphamide and infected with CPIV exhibited mild to moderate histological lesions as above with similar scanning electron microscopic changes until 36 p.i. Tracheal lesions consisted of intraepithelial and submucosal infiltration of lymphocytes and macrophages, focal epithelial hyperplasia and multifocal loss of cilia. In addition, mild and transient neutrophilic infiltration was observed. In immunosuppressed ferrets, viral antigen expression was prominent and demonstrated 4 and 8 days p.i. These data suggest that ferrets are susceptible to aerosol CPIV infection.

Animals↗
PubMed1997

Deep Candida infection in children with leukaemia: clinical presentations, diagnosis and outcome.

OBJECTIVES: To analyse the clinical features associated with deep Candida infection (DCI) and the outcome in children with leukaemia, and to evaluate various diagnostic methods. MATERIALS AND METHODS: Serum samples were analysed to determine Candida IgA, IgM and IgG antibodies and defect free C. albicans glucoprotein antigen and C. enolase antigen in eight children who had nine episodes of DCI and six with suspected DCI. RESULTS: DCI occurred shortly after the leukaemia diagnosis (median 40 days) or after the leukaemia relapse (median 30 days). Children with DCI had fever (100%), skin lesions/exanthema (45%), oral thrush (45%), oesophagitis (22%) and laryngo-tracheitis (22%). Candida endocarditis, arthritis and hepatic candidosis were diagnosed in one patient each. Two children with disseminated candidosis died in leukaemia relapse. In patients with C. albicans infections serology had a sensitivity of 83%. However, in patients with C. parapsilosis infection antibody detection was negative. As the patients were cured of their Candida infection, the IgG antibodies disappeared and the IgM and IgA antibodies fell within the normal range for age. CONCLUSION: DCI in children occurs shortly after the leukaemia diagnosis or shortly after relapse of leukaemia. The clinical features are many. Candida serology may help to diagnose or confirm DCI. The dynamics of antibody titres may help to establish the efficacy of antifungal treatment.

Adolescent↗
PubMed2005

Enzootic pneumonia of pigs--a diagnostic dilemma.

In an enzootic pneumonia-free Australian pig herd, an outbreak of a severe respiratory disease in the grow-out herd was initially diagnosed as acute tracheitis and pneumonia precipitated by the dusty environment, with a superimposed mixed infection of Pasteurella multocida and Arcanobacterium pyogenes. Culture for Mycoplasma hyopneumoniae, Salmonella sp and fungi was negative. The outbreak persisted. Subsequently, gross lesions consistent with enzootic pneumonia occurred, but histological lesions were equivocal and definitive tests for M hyopneumoniae remained negative. Eighteen months after the initial outbreak, gross and histological lesions were consistent with enzootic pneumonia but serological tests were still negative. Almost 2 years later, one of four nasal swabs was positive by the polymerase chain reaction test for M hyopneumoniae, and then lung samples were sporadically positive. The pneumonic disease became endemic in the herd. Gross lesions consistent with enzootic pneumonia occurred in another herd belonging to the same company nearly 2 years after the initial outbreak. Again, results of laboratory tests were inconsistent. Despite sporadic positive polymerase chain reaction tests for M hyopneumoniae, the respiratory disease resolved within 4 months and there has been no clinical evidence of enzootic pneumonia during the subsequent 4 years. These cases raise important questions about the role of the diagnostic tests and their interpretation, and the ecology of M hyopneumoniae and its role in enzootic pneumonia.

Actinomycetaceae↗
PubMed1990

Biological evaluation of Mycoplasma pulmonis temperature-sensitive mutants for use as possible rodent vaccines.

Temperature-sensitive mutants (TSMs) of Mycoplasma pulmonis were produced by treating the wild-type strain with N-methyl-N'-nitro-N-nitrosoguanidine. Three TSMs were selected at 38 degrees C, as a restrictive temperature, and at 34 degrees C, as a permissive temperature. Two TSMs, UTCMI and UTCMII, were proven to be nonpathogenic but immunogenic. In addition, they did not induce pneumonia, tracheitis, or tympanitis but did induce mild rhinitis. They were stable after 10 passages in vitro and in vivo. They elicited excellent antibody production and cell-mediated immunity in vaccinated rats. They also were not mitogenic to rat lymphocytes. Rats immunized intranasally with these TSMs were significantly protected against challenge with wild-type organisms. These mutants were morphologically and serologically indistinguishable from the wild-type organisms. The growth characteristics and antibiotic sensitivities were similar to those of wild-type organisms, except that they grew only at 34 degrees C. In contrast to wild-type organisms, they did not bind to or lyse sheep erythrocytes. Thus, these TSMs may qualify as a vaccine to prevent M. pulmonis infection in rats.

Animals↗
PubMed2005

Systemic disease in Vaal rhebok (Pelea capreolus) caused by mycoplasmas in the mycoides cluster.

In the winter of 2002, an outbreak of mycoplasma infection in Vaal rhebok (Pelea capreolus) originating from South Africa occurred 15 weeks after their arrival in San Diego, Calif. Three rhebok developed inappetence, weight loss, lethargy, signs related to pulmonary or arthral dysfunction, and sepsis. All three rhebok died or were euthanized. Primary postmortem findings were erosive tracheitis, pleuropneumonia, regional cellulitis, and necrotizing lymphadenitis. Mycoplasmas were detected in numerous tissues by electron microscopy, immunohistochemistry, and PCR. The three deceased rhebok were coinfected with ovine herpesvirus-2, and two animals additionally had a novel gammaherpesvirus. However, no lesions indicative of herpesvirus were seen microscopically in any animal. The rheboks' mycoplasmas were characterized at the level of the 16S rRNA gene, the 16S-23S intergenic spacer region, and the fructose biphosphate aldolase gene. Denaturing gradient gel electrophoresis was carried out to address the possibility of infection with multiple strains. Two of the deceased rhebok were infected with a single strain of Mycoplasma capricolum subsp. capricolum, and the third animal had a single, unique strain most closely related to Mycoplasma mycoides subsp. mycoides large-colony. A PCR survey of DNA samples from 46 other ruminant species demonstrated the presence of several species of mycoplasmas in the mycoides cluster, including a strain of M. capricolum subsp. capricolum identical to that found in two of the rhebok. These findings demonstrate the pervasiveness of mycoplasmas in the mycoides cluster in small ruminants and the potential for interspecies transmission and disease when different animal taxa come in contact.

Animals↗
PubMed1982

Safety and efficacy of live and inactivated infectious bovine rhinotracheitis vaccines.

Two commercial live virus infectious bovine rhinotracheitis (IBR) vaccines for intranasal administration and an inactivated polyvalent calf pneumonia vaccine were compared for safety and efficacy in calves against experimental IBR infections. All three products were clinically safe for use in young calves; a mild, transient, febrile response was induced by one of the live vaccines. Vaccinal virus was recovered for up to 16 days after vaccination from nasal secretions of all calves given live vaccine. Both live vaccines stimulated a serum neutralising antibody response, but the inactivated vaccine failed to elicit any serological response. Following intranasal challenge four months after the first dose of vaccine, all live virus vaccinates remained systemically healthy. A slight nasal discharge and a few rapidly healing ulcers of the nasal mucosa were the only abnormalities observed. Both the group given the inactivated vaccine and the unvaccinated controls developed clinical IBR with pyrexia, ocular and nasal discharges, severe ulceration of the nasal mucosa and tracheitis and tachypnoea to varying degrees of severity. Parenteral administration of dexamethasone six months after challenge induced reactivation of virus shedding followed by a rise in humoral antibody titre irrespective of the original vaccination history.

Animals↗
PubMed1985

Inhaled beclomethasone dipropionate in acute infections of the respiratory tract.

100 patients with acute tracheitis, tracheobronchitis or bronchitis were randomly allocated to receive inhaled beclomethasone dipropionate (BDP) 100 micrograms qds or placebo as an adjunct to oral antihistamine and a tetracycline antibiotic. 2 patients were withdrawn from analysis, leaving 49 patients in each group. There was no evidence that inhaled BDP conferred any benefit or detriment on the progress of the condition as assessed by daily symptom scores and weekly clinic visits for up to 2 weeks. The same conclusion maintains when the patients were subdivided into two grades of severity as assessed by the physician when the patient first presented. Inhaled BDP would seem to have no role in the inflammatory process associated with those acute infections of presumed viral origins.

Acute Disease↗
PubMedDate not supplied

Osteomyelitis of the clavicle.

Osteomyelitis of the clavicle is rare; however, it may occur following head and neck surgery. Risk factors include radiation, long-standing tracheitis, disruption of the periosteum or the cortical bone with interruption of the blood supply to the clavicle. Proper management includes early diagnosis, surgical debridement of soft tissue and bone, appropriate antimicrobial therapy, and coverage of the defect with a myocutaneous flap to protect the great vessels of the upper mediastinum.

Clavicle↗
PubMedDate not supplied

Flexible minibronchoscopy in children.

Flexible endoscopy is assuming a role of increasing importance in the evaluation and diagnosis of upper aerodigestive tract disorders. With improved fiberoptic capabilities and miniaturization, these techniques are gaining in applicability to the pediatric population. At Children's Hospital, Boston, a newly designed Machida 1.9-mm bronchoscope has been employed in the evaluation of the upper airway. The use of this small caliber instrument has been investigated in 1) evaluation of endotracheal or tracheotomy tube position, thus decreasing the need for repeated chest radiographs to confirm location; 2) bedside evaluation of possible tracheal disease (eg, mucous plug, granuloma, tracheitis) in the intensive care unit patient to determine treatment plans and/or need for further rigid bronchoscopy, and 3) evaluation of airway dynamics in the awake patient. Our experience with the flexible fiberoptic minibronchoscope is reviewed, with a discussion of indications for its use, as well as possible limitations. Case studies are presented to demonstrate the usefulness of the instrument.

Airway Obstruction↗
PubMedDate not supplied

Tracheotomies: a 10-year experience in 319 children.

A retrospective analysis was made of 319 patients having tracheotomies at the Hospital for Sick Children in Toronto between 1976 and 1985. In comparison to a similar study at the same institution completed 15 years earlier, the average number of tracheotomies per year has declined by half, because almost no tracheotomies are now done in patients with epiglottitis and tracheitis. Tracheotomies for children with CNS disorders and craniofacial anomalies are relatively more frequent. The average duration of tracheotomy is almost 1 year (339 days). Complications occurred in 30% of patients, but tracheotomy-related mortality was less than 1%.

Adolescent↗
PubMed1985

Pathology of spontaneous colibacillosis in a broiler flock.

Forty-eight of 134 chickens collected from a flock on a broiler farm were diagnosed pathologically and microbiologically to have colibacillosis. Both acute septicemia (seven birds, 1 to 36 days old) and subacute serositis (41 birds, 5 to 57 days old) were found. The former consisted of necrosis with fibrinous exudates in the ellipsoids and lymphoid follicles of the spleen, and fibrinous thrombi in sinusoids of the liver with occasional necrosis of hepatic cells. The latter had fibrinopurulent inflammation with granulomatous changes in the serosal tissues--including the epicardium, pericardium, and hepatic peritoneal sac--accompanied by septicemic lesions in the spleen and liver. Respiratory lesions (airsacculitis, pneumonia, and tracheitis) were noted in most chickens affected with acute septicemia and subacute serositis. Degenerative changes also were observed in the bursa of Fabricius.

Acute Disease↗
PubMed1986

Sialodacryoadenitis virus-associated lesions in the lower respiratory tract of rats.

Eight- to 10-week-old outbred Wistar rats were inoculated intranasally with 10(2.9) medium mouse lethal infective doses of sialodacryoadenitis (SDA) virus. Sham inoculated control rats and challenged rats were killed at 1 day intervals for the first 8 days, then on days 10, 12, 14, and 20. Typical lesions associated with SDA were seen microscopically in the salivary and lacrimal glands of inoculated rats. In addition, laryngitis, tracheitis, bronchitis, bronchiolitis, and multifocal alveolitis were present during the acute stages of the disease. Viral antigen was demonstrated in epithelial cells lining airways by immunofluorescence microscopy. SDA virus was recovered from the lower respiratory tract from days 2 to 6 post-inoculation (PI). Serum antibodies to SDA virus, but not to Sendai virus or Mycoplasma pulmonis were present in rats tested at day 20 PI. These findings demonstrate that during the acute stages of the disease, significant lesions do occur in the lower respiratory tract of SDA virus-infected rats.

Animals↗
PubMed1990

Experimental primary postnatal bovine viral diarrhea viral infections in six-month-old calves.

Eight clinically healthy calves were inoculated intranasally, four with either noncytopathic or four with cytopathic bovine viral diarrhea virus, and were necropsied 5 or 12 days post-inoculation. The most frequent gross lesion associated with noncytopathic or cytopathic viral infection was proximal colonic mural edema. Consistent microscopic findings were acute to subacute tracheitis, mild enterocolitis with edema, petechial hemorrhages of mesenteric lymph nodes with mild follicular lymphocytic depletion, and paracortical lymphocytic hyperplasia. At necropsy, cytopathic virus was recovered from 4/4 calves and noncytopathic virus was isolated from 2/4 calves. Neutralizing antibodies to noncytopathic bovine viral diarrhea virus were detected in the two calves from which noncytopathic virus was not recovered. Immunohistochemical analysis of lymphoid tissues demonstrated a small, randomly distributed population of mononuclear cells that contained bovine viral diarrhea viral antigen in 7/8 calves.

Animals↗
PubMed1994

Comparative pathology of a chicken-origin and two duck-origin influenza virus isolates in chickens: the effect of route of inoculation.

Forty-nine 5-week-old chickens were inoculated by the intravenous (i.v.), intratracheal (IT), or intranasal (IN) routes with either a chicken-origin or one of two duck-origin type A influenza virus isolates. Twelve control chickens were inoculated with sterile chorioallantoic fluid. For all viruses, i.v. inoculation produced predominate lesions of renal tubule necrosis (nephrosis) and nephritis, and influenza virus nucleoprotein was localized in nuclei and cytoplasm of necrotic renal tubule epithelium. Chickens inoculated by the IT route, and to a lesser extent the IN route, had mild to severe tracheitis, bronchitis, and ventromedial pneumonia associated with secondary bronchi but lacked renal tubule necrosis and nephritis. These data indicate low-virulence avian-origin influenza viruses were nephrotropic during simulated systemic infection (i.v. inoculation) and pneumotropic during simulated local infection (IT and IN inoculation). Gross and histologic kidney lesions produced by i.v. inoculation of the chicken-origin influenza virus were similar to changes reported in outbreaks of low-virulence influenza virus in laying chickens.

Acute Disease↗
PubMed1995

Comparative severity of respiratory lesions of sialodacryoadenitis virus and Sendai virus infections in LEW and F344 rats.

In several chronic diseases, lesions are more severe in LEW rats than in F344 rats. To determine whether or not acute viral diseases also are more severe in LEW rats than in F344 rats, we inoculated 6-7-week-old LEW and F344 rats with 10(7.2) cell culture infective units of sialodacryoadenitis virus or 10(4.7) infective units of Sendai virus. Twenty-four rats of each strain were given each virus. Lesions in nasal passages, tracheas, intrapulmonary airways, and pulmonary alveoli in 6 or 12 rats inoculated with each virus were assessed by scoring 5, 10, and 14 days after inoculation. Both viruses caused typical patchy necrotizing rhinitis, tracheitis, bronchitis, and bronchiolitis, with multifocal pneumonitis, in rats of both strains. Mean lesion indices for LEW rats given sialodacryoadenitis virus were significantly different from those for F344 rats for nasal passages on days 10 (0.999 vs. 0.680) and 14 (0.736 vs. 0.278), bronchi on day 5 (0.479 vs. 0.361), and alveoli on day 5 (0.677 vs. 0.275). Lesion indices for LEW rats given Sendai virus were significantly different from those for F344 rats for nasal passages on days 10 (1.000 vs. 0.611) and 14 (0.778 vs. 0.583); trachea on day 10 (0.625 vs. 0.028); bronchi on days 5 (0.476 vs. 0.331), 10 (0.123 vs. 0.013), and 14 (0.038 vs. 0); and alveoli on days 5 (0.413 vs. 0.114) and 10 (0.185 vs. 0.020). Thus, at the tested doses, both viruses caused more severe respiratory tract lesions in LEW rats than in F344 rats.

Analysis of Variance↗
PubMed1996

Lesions of acute inhaled lethal ricin intoxication in rhesus monkeys.

Five unimmunized adult rhesus monkeys weighing 5.9-6.3 kg were challenged with a precalculated, inhaled dose of 20.95-41.8 micrograms/kg of aerosolized ricin. Two males and three females either died or were killed at the onset of respiratory distress between 36 and 48 hours post-ricin inhalation and were necropsied. Consistent gross and microscopic lesions were confined to the thoracic cavity. All monkeys had multifocal to coalescing fibrinopurulent pneumonia, diffuse necrosis, and acute inflammation of airways, and nearly diffuse alveolar flooding, with peribronchovascular edema. All monkeys also had purulent tracheitis, fibrinopurulent pleuritis, and purulent mediastinal lymphadenitis. One male monkey and one female monkey had bilateral adrenocortical necrosis. We attributed the cause of death to asphyxiation following massive pulmonary alveolar flooding. The lesions of acute inhaled ricin intoxication in rhesus monkeys closely resembled those lesions reported in rats with acute inhaled ricin intoxication.

Administration, Inhalation↗