Definite Respiratory Tract Pathogens

Corynebacterium diphtheriae (toxin-producing)

Mycobacterium tuberculosis

Mycoplasma pneumoniae

Chlamydia trachomatis

Chlamydophila pneumoniae

Bordetella pertussis

Legionella spp.

Pneumocystis jiroveci (Pneumocystis carinii) Nocardia spp. Histoplasma capsulatum Coccidioides immitis

Cryptococcus neoformans (may also be recovered from patients without disease) Blastomyces dermatitidis

Viruses (respiratory syncytial virus, human metapneumovirus, adenoviruses, enteroviruses, Hantavirus, herpes simplex virus, influenza and parainfluenza virus, rhinoviruses, severe acute respiratory syndrome) RARE RESPIRATORY TRACT PATHOGENS Francisella tularensis Bacillus anthracis Yersinia pestis Burkhoideria pseudomallei Coxiella bumetti Chlamydophila psittaei Brucella spp. Salmonella spp. Pasteurella multocida Klebsiella rhinoscleromatis Varicella-zoster virus (VZV) Parasites respiratory tract. Staphylococcus aureus and beta-hemo-lytic streptococci produce extracellular enzymes that ad to damage host cells or tissues. Extracellular products of staphylococci aid in production of tissue necrosis and destruction of phagocytic cells, contributing to the commonly seen phenomenon of abscess formation associated with infection caused by this organism. Although S. aureus can be recovered from throat specimens, it has not been proved to cause pharyngitis. Enzymes of streptococci, including hyaluronidase, allow rapid dissemination of the bacteria. Many other etiologic agents of respiratory tract infection also produce extracellular enzymes and toxins.

Microorganism Growth. In addition to adherence and toxin production, pathogens cause disease by merely growing in host tissue, interfering with normal tissue function, and attracting host immune effectors, such as neutrophils and macrophages. Once these cells begin to attack the invading pathogens and repair the damaged host tissue, an expanding reaction ensues with more nonspecific and immunologic factors being attracted to the area, increasing the amount of host tissue damage. Respiratory viral infections usually progress in this manner, as do many types of pneumonias, such as those caused by Streptococcus pneumoniae, S. pyogenes, Staphylococcus aureus, Haemophilus influenzae, Neisseria meningitidis, Moraxella catarrhalis, Mycoplasma pneumoniae, Mycobacterium tuberculosis, and most gram-negative bacilli.

Avoiding the Host Response. Another virulence mechanism that certain respiratory tract pathogens possess is the ability to evade host defense mechanisms, S. pneumoniae, N. meningitidis, H. influenzae, Klebsiella pneumoniae, mucoid P. aeruginosa, Oryptococcus neoformans, and others possess polysaccharide capsules that serve both to prevent engulfmentby phagocytic host cells and to protect somatic antigens from being exposed to host immunoglobulins, the capsular material is produced in such abundance by certain bacteria, such as pneumococcal that soluble polysaccharide antigen particles can bind host antibodies, blocking them from serving as opsonins. Proof that the capsular polysaccharide is a major virulence mechanism of H. influenzae, S. pneumoniae, and N. meningitidis was established when vaccines consisting of capsular antigens alone were shown to protect individuals from disease.

Some respiratory pathogens evade the host immune system by multiplying within host cells. Chlamydia trachomatis, Chlamydophila psittad (Chlamydia psittaci), and all viruses replicate within host cells. They have evolved methods for being taken in by the "nonprofessional" phagocytic cells of the host to achieve their required environment. Once within these cells, the organism is protected from host humoral immune factors and other phagocytic cells. This protection lasts until the host œil becomes suffidentiy damaged that the organism is then recognized as foreign by the host and is attacked. A second group of organisms that cause respiratory tract disease comprises those that are able to be taken up by phagocytic host cells {usually macrophages). Once within the phagocytic cell, these respiratory tract pathogens are able to multiply. Legionella, Pneumocystis jtroved (Pneumocystis carinii), and Histoplasma capsulatum are some of these more common intracellular pathogens.

Mycobacterium tuberculosis is the classic representative of an intracellular pathogen. In primary tuberculosis the organism is carried to an alveolus in a droplet nucleus, a tiny aerosol particle containing a few tubercle bacilli (the minimum infective dose is small). Once pha-gocytized by alveolar macrophages, organisms are carried to the nearest lymph node, usually in the hilar or other mediastinal chains. In the lymph node, the organisms slowly multiply within macrophages. Ultimately, Ai. tuberculosis destroys the macrophage and is subsequendy taken up by other phagocytic cells. Tubercle bacilli multiply to a critical mass within the protected environment of the macrophages, which are prevented from accomplishing lysosomal fusion by the bacteria. Having reached a critical mass, the organisms spill out of the destroyed macrophages, through the lymphatics, and into the bloodstream, producing myco-bacteremia and carrying tubercle bacilli to many parts of the body. In most cases, the host immune system reacts suffidendy at this point to kill the bacilli; however, a small reservoir of live bacteria may be left in areas of normally high oxygen concentration, such as the apical (top) portion of die lung. These bacilli are walled off, and years later, an insult to the host, either immunologic or physical, may cause breakdown of the focus of latent tuberde bacilli, allowing active multiplication and disease (secondary tuberculosis). In certain patients with primary immune defects, the initial bacteremia seeds bacteria throughout a host that is unable to control them, leading to disseminated or miliary tuberculosis. Growth of the bacteria within host macrophages and histiocytes in the lung causes an influx of more effector cells, inducting lymphocytes, neutrophils, and histiocytes, eventually resulting in granuloma formation, then tissue destruction and cavity formation. The lesion is characteristically a semisolid, amorphous tissue mass resembling semisoft cheese, from which it received the name caseating necrosis (death of cells or tissues). The infection can extend into bronchioles and bronchi from which bacteria are disseminated via respiratory secretions by coughing. Aerosol droplets produced by coughing and containing organisms are then inhaled by the next victim. Other portions of the patient's own lungs may become infected as well through aspiration (inhalation of a fluid or solid).

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  • miya
    Where does the tubercle bacilli taken up by phagocytes from the bronchioles?
    3 years ago

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