Ticks themselves harbor their own parasites including the bacterium Borrelia burgdorferi, stained here with a vital dye that labels living bacteria green and dead bacteria red. These spiral-shaped bacteria live in deer ticks and can be transmitted to humans during a tick’s blood meal. Borrelia burgdorferi causes Lyme disease, which is characterized by a bull’s-eye-shaped skin rash and fever; if the infection is left untreated, various complications can result, including arthritis and neurological abnormalities. The idea that parasites have their own parasites was noted by Jonathan Swift in 1733: “So, naturalists observe, a flea Has smaller fleas that on him prey; And these have smaller still to bite ‘em; And so proceed ad infinitum.” (A, from Acorn, White-Footed Mice and Tick Cycle Augment Risks of Lyme Disease in 2012. March 14, 2012. Reprinted with permission of Anita Sil; B, courtesy of
M.
Embers.) microorganism to cause disease depends on many factors, it requires that the pathogen possess specialized pathogenic characteristics that allow it to live in humans.
Primary pathogens can cause overt disease in most healthy people. Some primary pathogens cause acute, life-threatening epidemic infections and spread rapidly from one sick or dying host to another; historically important examples include the bacterium Vibrio cholerae, which causes cholera, and the variola and influenza viruses, which cause smallpox and flu, respectively. Others may persistently infect a single individual for years without causing overt disease; examples include the bacterium Mycobacterium tuberculosis (which can cause the life-threatening lung infection tuberculosis) and the intestinal worm Ascaris. Although these potential primary pathogens can make some people critically ill, billions of people carry these foreign organisms in an asymptomatic way, often unaware that they are infected. It is sometimes difficult to draw a line between the asymptomatic presence of such pathogens and the normal microbiota. Some microbes of the normal flora can act as opportunistic pathogens, in that they cause disease only if our immune systems are weakened or if they gain access to a normally sterile part of the body.
In order to survive and multiply, a successful pathogen must be able to: (1) enter the host (usually by breaking an epithelial barrier); (2) find a nutritionally compatible niche in the host’s body; (3) avoid, subvert, or circumvent the host’s innate and adaptive immune responses; (4) replicate, using host resources; and (5) exit one host and spread to another. Pathogens have evolved various mechanisms that maximally exploit the biology of their host organisms to help accomplish these tasks. For some pathogens, these mechanisms are adapted to a unique host species, whereas for others the mechanisms are sufficiently general to permit invasion, survival, and replication in a wide variety of hosts. Because pathogens have evolved the ability to interface directly with the molecular machinery of host cells, we have learned a great deal about cell biological principles by studying them.
Our constant exposure to pathogens has strongly influenced human evolution. In modern times, humans have learned how to limit the ability of pathogens to infect us through improvements in public health measures and childhood nutrition, vaccines, antimicrobial drugs, and routine testing of blood used for transfusions. As we learn more about the mechanisms by which pathogens cause disease (called pathogenesis), our creativity and resourcefullness will continue to serve as an important addition to our immune systems in fighting infectious diseases.
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