Infections trachea

Physiological Effects. The sulfur and nitrogen mustards act first as cell irritants and finally as a cell poison on all tissue surfaces contacted. The first symptoms usually appear in 4—6 h (4). The higher the concentration, the shorter the interval of time between the exposure to the agent and the first symptoms. Local action of the mustards results in conjunctivitis (inflammation of the eyes) erythema (redness of the skin), which may be followed by blistering or ulceration and an inflammatory reaction of the nose, throat, trachea, bronchi, and lung tissue. Injuries produced by mustard heal much more slowly and are much more Fable to infection than bums of similar intensity produced by physical means or by other chemicals. 

Infections of the respiratory tract are among the commonest of infections, and account for much consultation in general practice and a high percentage of acute hospital admissions. They are divided into infections of the upper respiratory tract, involving the ears, throat, nasal sinuses and the trachea, and the lower respiratory tract (LRT), where they affect the airways, lungs and pleura. 

Sendai virus infection potentiates neurogenic inflammation in the rat trachea. J. Appl. Physiol. 68, 754-760. 

Local host defenses of both the upper and lower respiratory tract, along with the anatomy of the airways, are important in preventing infection. Upper respiratory defenses include the mucodliary apparatus of the nasopharynx, nasal hair, normal bacterial flora, IgA antibodies, and complement. Local host defenses of the lower respiratory tract include cough, mucodliary apparatus of the trachea and bronchi, antibodies (IgA, IgM, and IgG), complement, and alveolar macrophages. Mucus lines the cells of the respiratory tract, forming a protective barrier for the cells. This minimizes the ability of organisms to attach to the cells and initiate the infectious process. The squamous epithelial cells of the upper respiratory tract are not ciliated, but those of the columnar epithelium of the lower tract are. The cilia beat in a uniform fashion upward, moving particles up and out of the lower respiratory tract. 

Infection of the trachea and bronchi causes hyperemic and edematous mucous membranes and an increase in bronchial secretions. Destruction of respiratory epithelium can range from mild to extensive and may affect bronchial mucociliary function. In addition, the increase in bronchial secretions, which can become thick and tenacious, further impairs mucociliary activity. Recurrent acute respiratory infections may be associated with increased airway hyperreactivity and possibly the pathogenesis of chronic obstructive lung disease. 

Dawley) 6hr/d Cardio 260 infection mucopurulent exudate in the nasal cavities lymphoid hyperplasia in the trachea and pneumonitis) ... 

Exposure to hexachloroethane vapors can cause irritation to the respiratory system. Acute exposure to 260 ppm hexachloroethane had no apparent effect on the lungs and air passages in rats, but acute exposure to a concentration where particulate hexachloroethane was present in the atmosphere caused lung irritation (Weeks et al. 1979). On the other hand, intermediate-duration exposure to 260 ppm hexachloroethane appeared to cause some irritation of the respiratory epithelium, which may have increased susceptibility to respiratory infection. When exposure ceased, the animals recovered, so there were no histopathological indications of tissue damage after a 12-week recovery period. Lesions of the nasal passages, trachea, and bronchi increased mycoplasma infections mucus in the nasal cavities and decreased oxygen consumption were indicators of respiratory tract irritation from repeated episodes of hexachloroethane exposure. 

Hexachloroethane vapors and ingested hexachloroethane act as irritants on the lining of the lung, nasal cavity, trachea, and other tissues of the respiratory tract. Pulmonary irritation was associated with an increased incidence of mycoplasma infection in rats. Hexachloroethane exposure can also irritate the eyes. The irritation of the eye and respiratory tract are reversible once exposure has ceased. 

Excess mucus in the nasal turbinates, irritation of the epithelium, and increased incidence of a mycoplasma respiratory infection were seen in rats with inhalation exposure to 260 ppm for 6 weeks and in pregnant rats with inhalation exposure to 48 ppm for 11 days. Pulmonary irritation was also present in pregnant rats treated with an oral dose of 500 mg/kg/day for 11 days (Weeks et al. 1979). Effects on the respiratory epithelium were not apparent in the tissue of the lungs, nasal cavity, nasal turbinates, larynx, trachea, or bronchi based on histopathological examination (NTP 1977, 1989 Weeks et al. 1979). Exposure to... 

SYSTEMIC EFFECTS Occurs primarily through inhalation and ingestion. The T vapor or aerosol is less toxic to the skin or eyes than the liquid form. When inhaled, the upper respiratory tract (nose, throat, tracheae) is inflamed after a few hours latency period, accompanied by sneezing, coughing and bronchitis, loss of appetite, diarrhea, fever, and apathy. Exposure to nearly lethal doses of T can produce injury to bone marrow, lymph nodes, and spleen as indicated by a drop in white blood cell (WBC) count and, therefore, results in increased susceptibility to local and systemic infections. Ingestion of T will produce severe stomach pains, vomiting, and bloody stools after a 15-20 minute latency period. 

Major determinants of the efficiency of mucociliary clearance are cilia density, periciliary fluid, and composition of mucus. Some drugs and excipients, such as preservatives in drug formulations, may diminish the ciliary movement in the nasal cavity and trachea. A suggested adverse effect of ciliostasis (permanently or momentarily arrest or impairment of ciliary activity) is lower respiratory tract infection as a result of impaired nasal microbiological defense. 

The following protocols can be used for the isolation and structural characterization of any natural bioactive peptides from the immune system of invertebrates. The different procedures that will be detailed below refer to the identification and primary structure determination of the Drosophila immune-induced peptides (19,20,23,27,30) and of bioactive peptides from the immune system of other Diptera (17,21,24,31). These approaches were also successfully used for the discovery of bioactive peptides from crustaceans, arachnids, and mollusks. These methods should be considered as a guideline and not as the exact procedure to follow (see Note 3). The suggested procedures will be reported following the normal order of execution, (1) induction of the immune response by an experimental infection, (2) collection of the immunocompetent cells (hemocytes), tissues (epithelia, trachea, salivary glands, etc.)... 

Huang, H.-T., Haskell, A. and McDonald, D.M. (1989). Changes in epithelial secretory cells and potentiation of neurogenic inflammation in the trachea of rats with respiratory tract infections. Anat. Embtyol. 180, 325-341. 

Because acute bronchitis is primarily a self-limiting illness and rarely a cause of death, few data are available to describe the pathology. In general, infection of the trachea and bronchi yields... 

These studies help support the concept that the environment of the cystic fibrosis airway (at least in the fetus) is different from that of normal airways. They also suggest that the airways of cystic fibrosis patients have an innate tendency toward the development of an inflammatory response. Since the production of IL-8 occurred in sterile xenografts of cystic fibrosis tracheas, the findings also support the view that a chemokine necessary for the initiation of an inflammatory response (i.e., IL-8) can be produced in the absence of infection. However, it cannot be excluded that the production of IL-8 was not due to trauma or injury to the epithelium during the creation of the xenografts. In the next section, we will review recent studies that address the events, cell types, and mechanisms responsible for in the initiation and amplification of airway inflammation in cystic fibrosis. 

Ascariasis is the infestation of humans with the round worm, Ascaris lumbricoides. The adult worms normally live in the lumen of the small bowel of an infected individual. The eggs of the worm are passed in the faeces of these individuals and can contaminate water or food. Humans become infected when they ingest contaminated water or food. Gastric juices cause the eggs to hatch in the small bowel. The larvae penetrate the intestinal wall to enter the blood stream and reach the lungs. They migrate, or are carried by the bronchioles to bronchi, ascend the trachea to the glottis and pass down the oesopha-... 

Madden and coworkers (2002) reported in their series of placement of an Ultraflex self-expanding stent out of a total of 25 patients one patient, who presented with an esophagotracheal flstula due to advanced esophageal cancer. A previously placed esophageal stent had migrated through the tracheal wall. A covered stent was placed in the trachea and sealed off the fistula immediately. The patient was alive 9 months after tracheal stent placement without signs of further respiratory infection. 

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