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PubMed1977

Protective effect of vaccines on Mycoplasma pulmonis-induced respiratory disease of mice.

Mice inoculated intranasally with either a virulent or an avirulent strain of live Mycoplasma pulmonis were resistant to respiratory disease induced by a subsequent intranasal challenge with virulent organisms. Similarly, mice inoculated intravenously with the virulent strain were resistant to intranasal challenge with the same strain. In contrast, mice inoculated intravenously with avirulent M. pulmonis were not resistant to intranasal challenge with the virulent mycoplasma strain. Studies on mice inoculated intravenously with the two strains of M. pulmonis indicated that persistance of mycoplasmas in the respiratory tract may be important in inducing resistance to intranasal challenge with M. pulmonis. These observations, together with the lack of correlation between the level of serum antibodies and resistance to M. pulmonis-induced respiratory disease, suggested that local immune mechanisms were important in resistance. It is proposed that an effective vaccination schedule to protect mice against M. pulmonis-induced respiratory disease may be one that stimulates both systemic and local immune defenses. This suggestion is supported by the observation that systemic followed by local administration of inactivated M. pulmonis was more effective in inducing resistance in mice to intranasal challenge with live organisms than was systemic administration alone. In addition, mice inoculated solely by the intranasal route with inactivated mycoplasmas were resistant to M. pulmonis-induced respiratory disease. These studies indicate the importance of local defense mechanisms in the induction of resistance to M. pulmonis-induced respiratory disease in mice.

Administration, Intranasal↗
PubMed2002

Isolation of mycoplasma species from the lower respiratory tract of healthy cattle and cattle with respiratory disease in Belgium.

Between 1997 and 2000, a total of 150 healthy cattle and 238 animals with respiratory disease were examined for six Mycoplasma species. Attempts were made to detect Mycoplasma canis, Mycoplasma dispar and Ureaplasma diversum in calves with recurrent disease, and all three of these species were identified in calves with recurrent disease and in healthy lungs. In healthy calves, 84 per cent of bronchoalveolar lavage fluids were mycoplasma free; when cultures were positive, Mycoplasma bovirhinis was the only species isolated. Mycoplasmas were isolated from 78 per cent of animals suffering recurrent respiratory disease and from 65 per cent of acute respiratory cases. Mycoplasma bovis was isolated from bronchoalveolar lavages from 35 per cent of calves suffering recurrent respiratory disease, and from 50 per cent of acute cases, and from 20 per cent of pneumonic cases examined postmortem. M bovis was associated with other Mycoplasma species in 44 per cent of cases. M dispar was also isolated from 45.5 per cent of calves suffering recurrent respiratory disease, often in association with M bovis. M canis was identified for the first time in diseased Belgian cattle. Other mycoplasmas, including Mycoplasma arginini, Mycoplasma alkalescens and U diversum, were isolated less frequently. Associations between mycoplasmas and other pathogens were often observed. Among lungs infected with Pasteurella and/or Mannheimia species, more than 50 per cent were mixed infections with M bovis.

Acute Disease↗
PubMed1998

Utility of antibody in identifying individuals who have or will develop anhydride-induced respiratory disease.

OBJECTIVE: To define the utility of serum antibody against trimellitic anhydride (TMA) in predicting which individuals employed, at Amoco Corporation, in the manufacture of TMA have or will develop immunologically mediated respiratory disease, such as asthma, due to exposure to TMA. METHODS: In 1990 we initiated a clinical and immunologic cross-sectional study of 181 subjects exposed to TMA for at least 1 year who had not been diagnosed with an immunologic respiratory disease. We then clinically and immunologically followed 119 of these subjects for the next 5 years to determine whether they would develop an immunologic respiratory disease due to TMA exposure. RESULTS: Of the 16 individuals with IgE against TMA conjugated to human serum albumin (TM-HSA) in 1990, 3 had immediate asthma and another 6 developed asthma during the 5-year follow-up. Of the 165 individuals without IgE against TM-HSA, none had immediate asthma in 1990 and only 1 of 102 individuals followed for 5 years developed asthma. Of the 44 subjects with IgG against TM-HSA, 6 had an immunologic respiratory disease in 1990 and 2 more developed it in the ensuing 5 years. Of the 137 subjects without IgG against TM-HSA, none had an immunologic respiratory disease in 1990 and none of the 80 subjects followed for 5 years developed it. CONCLUSIONS: Development of antibody against TM-HSA, both IgE and IgG, is predictive of subjects who have or will develop immunologically mediated respiratory disease due to TMA exposure. The absence of antibody is a potent negative predictor.

Adult↗
PubMed2004

The combination of PRRS virus and bacterial endotoxin as a model for multifactorial respiratory disease in pigs.

This paper reviews in vivo studies on the interaction between porcine reproductive and respiratory syndrome virus (PRRSV) and LPS performed in the authors' laboratory. The main aim was to develop a reproducible model to study the pathogenesis of PRRSV-induced multifactorial respiratory disease. The central hypothesis was that respiratory disease results from an overproduction of proinflammatory cytokines in the lungs. In a first series of studies, PRRSV was shown to be a poor inducer of TNF-alpha and IFN-alpha in the lungs, whereas IL-1 and the anti-inflammatory cytokine IL-10 were produced consistently during infection. We then set up a dual inoculation model in which pigs were inoculated intratracheally with PRRSV and 3-14 days later with LPS. PRRSV-infected pigs developed acute respiratory signs for 12-24h upon intratracheal LPS inoculation, in contrast to pigs inoculated with PRRSV or LPS only. Moreover, peak TNF-alpha, IL-1 and IL-6 titers were 10-100 times higher in PRRSV-LPS inoculated pigs than in the singly inoculated pigs and the cytokine overproduction was associated with disease. To further prove the role of proinflammatory cytokines, we studied the effect of pentoxifylline, a known inhibitor of TNF-alpha and IL-1, on PRRSV-LPS induced cytokine production and disease. The clinical effects of two non-steroidal anti-inflammatory drugs (NSAIDs), meloxicam and flunixin meglumine, were also examined. Pentoxifylline, but not the NSAIDs, significantly reduced fever and respiratory signs from 2 to 6h after LPS. The levels of TNF-alpha and IL-1 in the lungs of pentoxifylline-treated pigs were moderately reduced, but were still 26 and 3.5-fold higher than in pigs inoculated with PRRSV or LPS only. This indicates that pathways other than inhibition of cytokine production contributed to the clinical improvement. Finally, we studied a mechanism by which PRRSV may sensitize the lungs for LPS. We hypothesized that PRRSV would increase the amount of LPS receptor complex in the lungs leading to LPS sensitisation. Both CD14 and LPS-binding protein, two components of this complex, increased significantly during infection and the amount of CD14 in particular was correlated with LPS sensitisation. The increase of CD14 was mainly due to infiltration of strongly CD14-positive monocytes in the lungs. The PRRSV-LPS combination proved to be a simple and reproducible experimental model for multifactorial respiratory disease in pigs. To what extent the interaction between PRRSV and LPS contributes to the development of complex respiratory disease is still a matter of debate.

Animals↗
PubMed1983

Respiratory disease among workers exposed to man-made mineral fibers.

Fibrous glass and mineral wool workers exposed to airborne man-made mineral fibers prior to 1964 were identified and followed for deaths caused by respiratory disease. Fiber exposure levels were estimated for each worker. Average fiber concentrations were very low in relation to a National Institute of Occupational Safety and Health recommendation that exposure to man-made mineral fibers less than 3.5 microns in diameter be limited to 3 fibers per cubic centimeter of air. Fibrous glass workers were exposed to about one hundredth and mineral wool workers to about one tenth of that amount. Respiratory cancer death rates were not excessive for the fibrous glass workers, but they were significantly elevated for the mineral wool workers. When respiratory cancer deaths were compared with fiber exposure levels, however, there was in no instance a strong positive correlation. There was a significant excess in nonmalignant respiratory disease deaths (excluding influenza and pneumonia) for fibrous glass workers and for the total cohort. When these nonmalignant respiratory disease deaths were compared with fiber exposure levels, however, there was in no instance a strong positive association. A special study was made of workers exposed to small diameter fibers. Respiratory cancer deaths were not in excess; however, there was an excess in nonmalignant respiratory disease deaths. This study provided no consistent evidence of a respiratory disease hazard related to exposure to man-made mineral fibers among the workers who produce these fibers. Results must be interpreted in relation to the relatively low exposure levels for these workers.

Adult↗
PubMed1993

[State of pulmonary surfactant and hemodynamics of lesser blood circulation in Donets Basin coal miners during development of dust-induced respiratory tract diseases].

Respiratory diseases caused by dust in coal miners and high-risk group are manifested by accumulation of low surface-active surfactant masses, which thicken alveolar-capillary membrane, thus the smallest bronchi and alveoli collapse and diffusion of oxygen across blood-gas barrier becomes inadequate. Respiratory hypoxemia leads to reflectory construction of pulmonary arterioles, hence pulmonary hypertension occurs and cuts down blood supply to middle and lower portions of lungs, where dust is the most likely to invade. The blood supply is therefore shunted to the upper portions of lungs, which is compensatory. The stated changes appear at early stages of occupational respiratory diseases in miners.

Adult↗
PubMed2002

Depletion of CD8+ T cells exacerbates CD4+ Th cell-associated inflammatory lesions during murine mycoplasma respiratory disease.

Mycoplasma infection is a leading cause of pneumonia worldwide and can lead to other respiratory complications. A component of mycoplasma respiratory diseases is immunopathologic, suggesting that lymphocyte activation is a key event in the progression of these chronic inflammatory diseases. The present study delineates the changes in T cell populations and their activation after mycoplasma infection and determines their association with the pathogenesis of murine Mycoplasma respiratory disease, due to Mycoplasma pulmonis infection. Increases in T cell population numbers in lungs and lower respiratory lymph nodes were associated with the development of mycoplasma respiratory disease. Although both pulmonary Th and CD8(+) T cells increased after mycoplasma infection, there was a preferential expansion of Th cells. Mycoplasma-specific Th2 responses were dominant in lower respiratory lymph nodes, while Th1 responses predominated in spleen. However, both mycoplasma-specific Th1 and Th2 cytokine (IL-4 and IFN-gamma) responses were present in the lungs, with Th1 cell activation as a major component of the pulmonary Th cell response. Although a smaller component of the T cell response, mycoplasma-specific CD8(+) T cells were also a significant component of pulmonary lymphoid responses. In vivo depletion of CD8(+) T cells resulted in dramatically more severe pulmonary disease, while depletion of CD4(+) T cells reduced its severity, but there was no change in mycoplasma numbers in lungs after cell depletion. Thus, mycoplasma-specific Th1 and CD8(+) T cell activation in the lung plays a critical regulatory role in development of immunopathologic reactions in Mycoplasma respiratory disease.

Animals↗
PubMed2004

Immunization against viral respiratory disease: a review.

BACKGROUND: Healthy and at risk children are susceptible to the morbidity and mortality associated with viral-induced respiratory diseases, including respiratory syncytial virus (RSV) and influenza. The World Health Organization is attempting to develop and distribute effective vaccines to prevent/reduce key viral respiratory diseases. METHODS: The goals of a vaccination program for viral respiratory infections include the prevention of lower respiratory tract infections and prevention of infection-associated morbidities, hospitalization and mortality. This article explores influenza and RSV vaccine developments. RESULTS: There are 2 influenza vaccines, trivalent inactivated and live, cold-adapted, attenuated. Trivalent inactivated vaccine is indicated for persons older than 6 months of age. Currently <10%, <30% and <30% of healthy children, healthy adults and high risk children, respectively, are vaccinated. Efficacy is from 70 to 90% in healthy adults younger than 65 years of age and 30-90% in children, with lower efficacy in younger children. Live, cold-adapted, attenuated vaccine is indicated for healthy persons 5-49 years of age and usually is 70-90% effective. Various RSV vaccine formulations are being investigated. The Advisory Committee on Immunization Practices (ACIP) recommends influenza vaccination for children 6-23 months old. Studies support immunization of all children, not only those at high risk. Current ACIP recommendations focus on high risk persons and do not include school age children. A universal immunization program for all children could benefit the entire community. CONCLUSION: Effective vaccines are available for some viral respiratory pathogens (eg, influenza virus), but not for most mucosally restricted respiratory viral pathogens. Research should continue into safe and effective vaccines for all childhood viral illnesses.

Child Welfare↗
PubMed1987

Field trial of a quadrivalent vaccine against calf respiratory disease.

A quadrivalent vaccine containing the killed antigens of respiratory syncytial virus, parainfluenza virus type 3, Mycoplasma dispar and M bovis, emulsified with an oil adjuvant, was tested for efficacy against naturally occurring calf respiratory disease. Three batches of beef cattle aged 12, seven and three weeks at the time of first vaccination were used. Within each batch of approximately 100 animals, half were vaccinated subcutaneously on three occasions, three weeks apart and half served as unvaccinated controls. Over the trial period, from November 1981 to May 1982, 27 per cent of the control calves were treated for respiratory disease compared with 16.3 per cent of the vaccinated animals. This reduction of non-fatal disease in the vaccinated animals represented a protection rate of almost 40 per cent and was statistically significant (P less than 0.05). Mortality was also reduced from 3.4 per cent in the control calves to 1.9 per cent in the vaccinated animals but this difference was not statistically significant. During a major outbreak of disease associated with respiratory syncytial virus, the protection rate increased to 69 per cent (P less than 0.01). Furthermore, in the batch of cattle aged seven weeks at first vaccination there was significantly less pneumonic consolidation at death in the vaccinated animals than in the control animals (P less than 0.05).

Animals↗
PubMed1979

Studies of respiratory disease in random-source laboratory dogs: viral infections in unconditioned dogs.

A prospective study was conducted to identify the viruses causing respiratory diseases in unconditioned, random-source dogs. During the quarantine period, respiratory disease occurred in 86 of 167 (52%) dogs, and 34 (21%) died. Most affected dogs had a distemper-like illness which required extensive and prolonged care. Histopathologic studies confirmed the diagnosis of canine distemper in 10 of 12 (83%) fatal infections examined. Sixty-seven of 91 (74%) dogs which arrived without canine distemper antibody became ill, and 30 (32%) died. In contrast, only 16 of 67 (24%) dogs with canine distemper antibody had respiratory disease, and only 3 (4%) died. Parainfluenza SV5 and canine adenovirus--type II were recovered from 27 of 54 and 22 of 54 sick dogs, respectively. Canine herpesviruses, canine coronaviruses, and canine parvoviruses were less frequently isolated. Increased antibody titers to SV5 were found consistently, and rises in titer to the other viruses were demonstrated. Many of the sick dogs were infected with two or more viruses. Although several viral agents were detected during these epizootics, prevention of canine distemper appeared to be the key to controlling severe, prolonged, and often fatal respiratory disease.

Adenoviridae↗
PubMed1998

SWORD '97: surveillance of work-related and occupational respiratory disease in the UK.

SWORD is one of seven clinically based reporting schemes which together now provide almost comprehensive coverage of occupational diseases across the UK. Although SWORD is now in its tenth year, participation rates remain high. Of an estimated 3,903 new cases seen this year, 1,031 (26%) were of occupational asthma, 978 (25%) of mesothelioma, 794 (20%) of non-malignant pleural disease, 336 (9%) of pneumoconiosis and 233 (6%) of inhalation accidents. Incidence rates of occupational asthma were generally highest among workers in the manufacture of wood products, textiles and food (particularly grain products and crustaceans) and additionally, in the production of precious and non-ferrous metals, rubber goods, detergents and perfumes, and in mining. Health care workers were noted to have a surprisingly high incidence of inhalation accidents. Occupational asthma attributed to latex has increased dramatically; the highest rates are among laboratory technicians, shoe workers and health care workers.

Humans↗