Lower Respiratory Tract Infections
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General Goal: To know the major mechanisms of defense in the LRT, the major mechanisms invaders use to avoid the defenses of the LRT, and the common modes of transmission.

Specific Educational Objectives: The student should be able to:

1. describe most common modes of transmission of pneumonia.

3. describe defense mechanisms the body uses to protect itself from infections.

4. the mechanisms microbes use to infect the LRT.

Reading: Mosby's Color Atlas and Text of Infectious Diseases by Christopher P. Conlon and David R. Snydman. pp. 67-76.

Lecture: Dr. Neal R. Chamberlain

References: 


A. Epidemiology of lower respiratory tract (LRT) or parenchymal respiratory infections. B. General Anatomy
  1. As mentioned previously the respiratory tract is usually divided into three segments.
  2. The alveoli are lined with two types of cells, the Type 1 and Type 2 pneumocyte. The Type 1 pneumocyte is a very large thin cell stretched over a very large area. This cell can not replicate and is susceptible to a large number of toxic insults. Type 1 pneumocytes are responsible for gas exchanges occurring in the alveoli. The Type 2 granular pneumocyte is smaller, roughly cuboidal cell that is usually found at the alveolar septal junctions. This cell is responsible for the production and secretion of surfactant. The Type 2 pneumocyte can replicate in the alveoli and will replicate to replace damaged Type 1 pneumocytes.
C. Mechanisms of defense.
  1. Particles from 2 um to 0.2 um can go all the way down inside the alveoli avoiding the defenses of the upper respiratory tract and the mucociliary elevator. (Note: Most bacteria and all viruses are 2 mm and smaller.)
  2. The following defense mechanisms in the alveoli protect the parenchymal cells from invasion by microorganisms.
  3. Once a microorganism arrives in the alveoli it can be opsonized by IgG in the fluid lining the alveoli. These organisms will then be ingested by the macrophage. If no specific antibody to the organism is present then the macrophage may still be able to phagocytize the invader however, at a slower rate. Once the microorganism is phagocytized the macrophage will destroy the organism, if it can, and present microbial antigens on the surface to awaiting B and T cells. Once activated the B and T cells can produce more antibody and/or activate the macrophage. Meanwhile the macrophage is also releasing factors that help bring in polymorphoneutrophils (PMN) from the blood stream and initiate an inflammatory response. Along with the PMNs come more antibodies and complement components useful in destroying the invader. The invaders can also at this time leave the lung and get into the general circulation. This is probably why systemic signs of infection (fever, malaise, myalgia, etc.) occur in pneumonia.
D. Mechanisms invaders use to avoid the normal defense mechanisms of the lung.
    1. To kill the microorganism in the alveoli it must be phagocytized by the alveolar macrophage. If these microbes can avoid phagocytosis or survive once phagocytized they can survive in the lung. Microorganisms have developed a number of ways to avoid phagocytosis. Once phagocytized certain organisms can survive in the phagocyte.
    2. Mechanisms used to avoid phagocytosis.
    3. Mechanisms used to survive in the phagocyte.
E. Modes of transmission
  1. Inhalation of small airborne infectious particles (airborne transmission). Most microorganisms that cause pneumonia are able to survive on airborne droplets. These droplets can float in the air for quite a long time and if still infectious can sometimes cause pneumonia.
  2. Aspiration of resident naso-oropharyngeal flora or large airborne particles after deposition in the naso-oropharynx (aspiration pneumonia). Usually aspiration of material into the lungs occurs during sleep. Certain people aspirate more than others during sleep and as a result have more problems with LRT infections. Other groups of people bothered by aspiration related LRT infections are alcohol abusers, drug abusers, and comatose patients.
  3. Hematogenous spread to the lung from another site of infection. People with endocarditis, septic pelvic or jugular thrombophlebitis may also experience LRT infections. Pneumonia acquired by hematogenous spread to the lungs often times is bilateral and uniform. Pneumonia transmitted by bronchogenic infection (inhalation, aspiration) are usually unilateral and tend to localize in the lung.
  4. Direct extension from a contiguous site of infection. Entamoeba histolytica can cause pneumonia by direct extension from an amebic abscess in the liver. Influenza and Respiratory Syncytial Viruses can spread from the upper respiratory tract to the LRT via infection of the respiratory epithelium.
  5. Exogenous penetration and contamination of the lung can occur due to accidental trauma (car accident) or surgery.
Inhalation and aspiration are the two most common means of acquiring an infectious pneumonia.

F. Pathogenesis of Pneumonia

  1. A microorganism enters the alveoli and proceeds to grow in the rich environment provided by the lung. Oftentimes the organism contains a capsule or is intracellular and can avoid phagocytosis for a period of time. As a result of tissue injury an inflammatory response occurs. Tissue injury can occur due to exotoxins produced by a bacteria, cell lysis caused by a virus, or death of alveolar macrophages and dumping of their lysosomal contents in the alveoli due to growth of an organism in the phagocyte. Vascular permeability increases and PMNs arrive at the area attempting to contain and eliminate the organisms. Along with PMNs come many of the serum components. Meanwhile other alveolar macrophages are being recruited to the area of inflammation. This accumulation of microorganism, immune cells, and serum components causes the alveoli to fill up and can result in spread to other alveoli in close proximity. This inflammatory response is what is described as an opacity or consolidation when viewing a roentgenograph (a X-ray film). Not only are serum components coming into the alveoli but certain products made by the microorganism are able to leave the lung and exert systemic effects. Examples include endotoxin from gram negative bacteria eventually resulting in fever and septic shock, and cell wall components of gram positive bacteria that can eventually lead to fever production and septic shock. All of the microbial products producing or indirectly resulting in systemic changes have yet to be clearly determined.
  2. The deleterious effects on the host fall into two categories:
G. Enumeration of organisms capable of causing pneumonia
Bacteria  Viruses
Streptococcus pneumoniae Influenza
Streptococcus pyogenes (Grp A) Parainfluenza
 Streptococcus agalactiae (Grp B) Cytomegalovirus
Staphylococcus aureus Adenovirus
Bacillus anthracis Epstein-Barr Virus
Other Bacillus sp. Herpes Simplex Virus 
Nocardia sp.  Varicella-Zoster
Enterobacteriaceae Coxsackievirus
Pseudomonas aeruginosa Measles
Acinetobacter sp. Rhinovirus
Burkholderia pseudomallei Respiratory Syncytial Virus
Burkholderia mallei Fungi
Yersinia pestis Aspergillus sp.
Francisella tularensis Mucorales sp
Hemophilus influenzae  Candida sp.
Bordetella pertussis Histoplasma capsulatum
Neisseria meningitidis Blastomyces dermatitidis
Legionella pneumophila Cryptococcus neoformans
Legionella-like bacteria  Coccidioides immitis
Bacteroides melaninogenicus Paracoccidioides brasiliensis
Fusobacterium nucleatum Pneumocystis carinii
Peptostreptococcus sp.  Parasites-Protozoa
Peptococcus sp. Plasmodium falciparum 
Actinomyces sp. Entamoeba histolytica
Mycobacterium tuberculosis Toxoplasma gondii
Other Mycobacterium sp.  Leishmania donovani
Mycoplasma pneumoniae  Parasites-Nematodes
Branhamella catarrhalis Ascaris lumbricoides
Chlamydia trachomatis Toxocara sp.
Chlamydia psittaci Ancyclostoma duodenale
Chlamydia pneumoniae Parasites-Cestodes 
Coxiella burnetii (Q-fever)  Echinococcus granulosus

H. Complications of Pneumonia- Basically there are two types of complications


Send comments and email to Dr. Neal R. Chamberlain,  nchamberlain@atsu.edu
Revised 8/5/02
©2002 Neal R. Chamberlain, Ph.D., All rights reserved.