Most intestinal parasites enter the body by being ingested as cysts, eggs, or meat-borne larvae, but a few enter by penetrating the skin and finding their way to the intestine. Once in the intestine, these pathogens cause damage in several ways: • G. lamblia attaches to the epithelial brush border, but does not invade into cells or tissue. Attachment of the organisms leads to blunting of villi, loss of brush border, malabsorption, and chronic inflammation through mechanisms that are poorly understood.
Cryptosporidia are taken up by enterocytes, in which they replicate, leading to extensive mucosal damage, villous atrophy, and inflammation.
E. histolytica kills host cells by contact-mediated cytolysis through a channel-forming pore protein, with consequent ulceration and invasion of the colonic mucosa.
Intestinal helminths cause disease when they are present in large numbers or travel to ectopic sites. Large numbers of A. lumbricoides can obstruct the gut, and this organism can invade and damage the bile ducts as well.
Helminths also cause disease by depriving the host of nutrients. Hookworms cause iron-deficiency anemia by sucking blood from intestinal villi; Diphyllobothrium, the fish tapeworm, causes anemia by depriving the host of vitamin B12.
A large number of microorganisms, including viruses, bacteria, and fungi, are inhaled daily by every individual. In many cases, the microbes are inhaled in dust or aerosol particles. The distance these particles travel into the respiratory system is inversely proportional to their size. Large particles are trapped in the mucociliary blanket that lines the nose and the upper respiratory tract. Microorganisms trapped in the mucus secreted by goblet cells are transported by ciliary action to the back of the throat, where they are swallowed or coughed out. Particles smaller than 5 µm travel directly to the alveoli, where they are phagocytosed by alveolar macrophages or by neutrophils recruited to the lung by cytokines.
Microorganisms that invade the normal healthy respiratory tract have developed specific mechanisms to overcome mucociliary defenses or to avoid destruction by alveolar macrophages. Some successful respiratory viruses evade these defenses by attaching to and entering epithelial cells in the lower respiratory tract and pharynx. For example, influenza viruses possess hemagglutinin proteins that project from the surface of the virus and bind to sialic acid on the surface of epithelial cells. This attachment induces the host cell to engulf the virus, leading to viral entry and replication within the host cell.
Certain bacterial respiratory pathogens release toxins that paralyze cilia. Examples include Haemophilus influenzae, Mycoplasma pneumoniae, and Bordetella pertussis. Some bacteria lack the ability to overcome the defenses of the healthy lung and can cause respiratory infections only in compromised hosts. Streptococcus pneumoniae and S. aureus can cause pneumonia subsequent to influenza because the viral infection leads to the loss of the protective ciliated epithelium. Chronic damage to mucociliary defense mechanisms occurs in smokers and individuals with cystic fibrosis, while acute injury occurs in intubated patients and in those who aspirate gastric acid.
Some respiratory pathogens avoid phagocytosis or destruction after phagocytosis. M. tuberculosis, for example, gains a foothold in alveoli because it escapes killing within the phagolysosomes of macrophages. Opportunistic fungi infect the lungs when cellular immunity is depressed or when leukocytes are reduced in number (e.g., P. jiroveci in patients with AIDS, Aspergillus spp. after chemotherapy).
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