Bacteria are bigger and more complex than viruses, though they can still spread through the air. A bacterium is a single cell, and it can live and reproduce almost anywhere on its own: in soil, in water and in our bodies.
For the most part, we live peacefully with bacteria—the colonies in our guts are helpful to us and strengthen our immune system. But like viruses, bacteria can also harm us by replicating quickly in our bodies, killing cells. Some bacteria also produce toxins which can kill cells and cause an outsized, damaging immune reaction. Broad-spectrum antibiotics were developed to kill bacteria in our bodies and in the food supply by inhibiting their growth.
But bacteria are extremely adaptive and can quickly evolve to evade antibiotics. Bacteria share their antibiotic-resistant genes with each other, meaning more strains generate resistance to the drugs we use. Common forms: Fungi are responsible for causing conditions such as yeast infections , valley fever and meningitis. Fungi are more complicated organisms than viruses and bacteria—they are "eukaryotes," which means they have cells. Of the three pathogens, fungi are most similar to animals in their structure.
There are two main types of fungi: environmental, which are yeast and mold that often live in soil and don't generally cause infection in most healthy people; and commensals, which live on and in us and generally don't hurt us. Certain environmental fungi reproduce "spores," particles that can enter our body through the lungs or on the skin. These fungi can be especially damaging for people with weakened immune systems, as the fungi can spread quickly and damage many organs.
Fungi are slower to mutate, so they are easier to target with antifungal medications than bacteria are with antibiotics. Skip to content. How viruses make us sick. Viruses also are capable of infecting any living thing, including bacteria and fungi. J Allergy Clin Immunol ; — Science ; —2. Viral interleukin 10 is critical for the induction of B cell growth transformation by Epstein—Barr virus.
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J Parasitol ; 59 Impairment of primary expulsion of Trichuris muris in mice concurrently infected with Nematospiroides dubius. Parasitology ; 75 —8. Trichinella spiralis : delayed rejection in mice concurrently infected with Nematospiroides dubius.
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Int J Parasitol ; 43 —9. Trichuris suis therapy for active ulcerative colitis: a randomized controlled trial. Gastroenterology ; — In this part of the chapter we will briefly examine the stages of infection, and the various types of infectious agents.
The process of infection can be broken down into stages, each of which can be blocked by different defense mechanisms. In the first stage, a new host is exposed to infectious particles shed by an infected individual.
The number, route, mode of transmission, and stability of an infectious agent outside the host determines its infectivity. Some pathogens, such as anthrax, are spread by spores that are highly resistant to heat and drying, while others, such as the human immunodeficiency virus HIV , are spread only by the exchange of bodily fluids or tissues because they are unable to survive as infectious agents outside the body. The first contact with a new host occurs through an epithelial surface.
This may be the skin or the internal mucosal surfaces of the respiratory, gastro-intestinal, and urogenital tracts. After making contact, an infectious agent must establish a focus of infection. This involves adhering to the epithelial surface, and then colonizing it, or penetrating it to replicate in the tissues Fig. Many microorganisms are repelled at this stage by innate immunity.
We have discussed the innate immune defense mediated by epithelia and by phagocytes and complement in the underlying tissues in Chapter 2. Chapter 2 also discusses how NK cells are activated in response to intracellular infections, and how a local inflammatory response and induced cytokines and chemokines can bring more effector cells and molecules to the site of an infection while preventing pathogen spread into the blood.
These innate immune responses use a variety of germline-encoded receptors to discriminate between microbial and host cell surfaces, or infected and normal cells. They are not as effective as adaptive immune responses, which can afford to be more powerful on account of their antigen specificity. However, they can prevent an infection being established, or failing that, contain it while an adaptive immune response develops. Infections and the responses to them can be divided into a series of stages.
These are illustrated here for an infectious microorganism entering across an epithelium, the commonest route of entry. The infectious organism must first adhere to epithelial more Only when a microorganism has successfully established a site of infection in the host does disease occur, and little damage will be caused unless the agent is able to spread from the original site of infection or can secrete toxins that can spread to other parts of the body.
Extracellular pathogens spread by direct extension of the focus of infection through the lymphatics or the bloodstream. Usually, spread by the bloodstream occurs only after the lymphatic system has been overwhelmed by the burden of infectious agent.
Obligate intracellular pathogens must spread from cell to cell; they do so either by direct transmission from one cell to the next or by release into the extracellular fluid and reinfection of both adjacent and distant cells. Many common food poisoning organisms cause pathology without spreading into the tissues. They establish a site of infection on the epithelial surface in the lumen of the gut and cause no direct pathology themselves, but they secrete toxins that cause damage either in situ or after crossing the epithelial barrier and entering the circulation.
Most infectious agents show a significant degree of host specificity , causing disease only in one or a few related species. What determines host specificity for every agent is not known, but the requirement for attachment to a particular cell-surface molecule is one critical factor. As other interactions with host cells are also commonly needed to support replication, most pathogens have a limited host range. The molecular mechanisms of host specificity comprise an area of research known as molecular pathogenesis, which falls outside the scope of this book.
While most microorganisms are repelled by innate host defenses, an initial infection, once established, generally leads to perceptible disease followed by an effective host adaptive immune response.
This is initiated in the local lymphoid tissue, in response to antigens presented by dendritic cells activated during the course of the innate immune response Fig. Antigen-specific effector T cells and antibody -secreting B cells are generated by clonal expansion and differentiation over the course of several days, during which time the induced responses of innate immunity continue to function.
Eventually, antigen -specific T cells and then antibodies are released into the blood and recruited to the site of infection Fig. A cure involves the clearance of extracellular infectious particles by antibodies and the clearance of intracellular residues of infection through the actions of effector T cells. After many types of infection there is little or no residual pathology following an effective primary response. In some cases, however, the infection or the response to it causes significant tissue damage.
In other cases, such as infection with cytomegalovirus or Mycobacterium tuberculosis , the infection is contained but not eliminated and can persist in a latent form.
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