Infectious illnesses trigger significant morbidity and mortality, particularly in people who are most vulnerable to illness: the really young, the elderly, the immunocompromised, and also the disenfranchised. The pathogenesis of infectious diseases is dependent on the relationship among the human host, the infectious agent, and also the external surroundings.
The infectious agent can be either exogenous (ie, not usually discovered on or within the body) or endogenous (ie, one that might be routinely cultured from a particular anatomic website but that does not normally trigger disease within the host). Virus results when an exogenous agent is introduced into a host from the environment or when an endogenous agent overcomes innate host immunity to cause illness. Host susceptibility plays an important role in either of these settings.
The environment includes vectors (insects and other carriers that transmit infectious agents) and zoonotic hosts or reservoirs (animals that harbor infectious agents and frequently act to amplify the infectious agent). For example, the white-footed mouse (Peromyscus leucopus) serves as an animal reservoir for Borrelia burgdorferi, the bacterium that brings about Lyme illness.
The Ixodes tick serves as an insect vector. Infection within the mouse is asymptomatic, and also the bacteria can multiply to higher levels in this animal. When the tick larva feeds on an infected mouse, it becomes secondarily infected with B burgdorferi, and this virus persists when the tick molts into a nymph.
Subsequently, when an infected nymph feeds on a human, the bacterium is transmitted into the host bloodstream, causing disease. The study of infectious diseases requires understanding of pathogenesis in the level from the population, the individual, the cell, and the gene. For example, in the population level, the spread of tuberculosis within the community is related to the social interactions of an infectious human host.
Outbreaks of tuberculosis have occurred in homeless shelters, prisons, bars, and nursing homes when an index case comes in close contact with susceptible persons. At the individual degree, tuberculosis outcomes from inhalation of respiratory droplets containing airborne tubercul bacilli. At the cellular degree, these bacilli activate T cells, which play a critical role in containing the infection.
Individuals with an impaired T-cell response (eg, those infected with HIV) are at particularly high chance for primary tuberculosis in the time from the initial infection or for reactivation of latent tuberculosis as their immunity wanes. Finally, at the genetic degree, individuals with specific polymorphisms in a macrophage protein gene may be at substantially higher chance for pulmonary tuberculosis.
Specific microorganisms have a tendency to trigger certain kinds of infections: Streptococcus pneumoniae commonly causes pneumonia, meningitis, and bacteremia but rarely about endocarditis (infection from the heart valves); Escherichia coli is a common cause of GI and urinary tract infections; Plasmodium species infect red blood cells and liver cells to trigger malaria; Entamoeba histolytica brings about amebic dysentery, liver abscesses, and so on.