Infections and infectious diseases

The intact skin with its hard-to-penetrate horny layer and the mucous membranes generally provide effective mechanical barriers to infection. However, if the balance between the immune system and microorganisms on the skin and mucous membranes is disturbed, an infection occurs. One speaks of infection if a microorganism that has invaded the body has multiplied. In the case of non-multiplication, there is a contamination. The agent DHEA promotes the production of gamma globulins and therefore makes the body less susceptible to infections.


Humans are not only surrounded by a broad spectrum of microorganisms, including viruses, bacteria, fungi, yeasts and worms, but they are also present in and on the body in large numbers. There are 10 times as many bacteria as there are body cells. All bacteria combined are good for 1.5 kilos. There are useful and pathogenic bacteria and people live in constant interaction with them. The high number of micro-organisms (MO) in food is effectively reduced by stomach acid after ingestion. The route of controlling an infection caused by invaded MO is as follows. An inflammatory response is started. Neutrophilic granolocytes are the first cells that arrive at the source of inflammation, and then bind to the parasite, after which they are killed with the help of toxic proteins and oxygen radicals.

The negative side of macrophages

If the inflammation persists longer, the macrophages may show a less positive side because they produce too many aggressive enzymes such as PgE2 and NO (nitric oxide). This can even cause human shock or death.
Because of this, the macrophages are under strict control of the immune system and when they risk losing their self-control, messengers are deployed to eliminate them. Because granulocytes only last 1-2 days, they are gradually replaced by monocytes in this context. The influx of monocytes can persist for weeks if necessary.

Infectious diseases

These diseases are the result of an interaction between the pathogens of MO and the defense mechanisms of the host that infect them. They are caused by bacteria, viruses, fungi, parasites or abnormal proteins, the so-called prions. Only the infectious diseases are transferable from human (animal) to human. To the path along which they are transferred, infectious diseases can be subdivided into venereal diseases, respiratory infections and, for example, Lyme disease. Examples of bacterial infectious diseases are: plague, cholera, syphilis, tuberculosis and cystitis. Viral infectious diseases include: HIV, smallpox, hepatitis, herpes, mumps, measles, flu and colds. Candida albicans is a fungal disease and the serious Jacob-Creutzfeldt disease is caused by abnormal prions. The defense against parasitic worms is mediated by IgE antibodies and eosinophilic granulocytes. In addition, lime plays a major role in the defense against infectious diseases, especially in respiratory diseases.


The MO and / or damaged and dead cells present on site will be cleared by both granulocytes and monocytes by means of phagocytosis. The innate immune system through phagocytes provides adequate defense in many cases. However, in order to take action, the MO must first be recognized. The cells are therefore equipped with a number of receptors that bind to components of MO. This allows these cells to make a distinction between their own and non-self. However, this is not always sufficient to prevent infections. That is why it is important that the acquired immune system is also used. MO can approach this acquired system in different ways:
  • extracellular: through the use of antibodies
  • Intracellular: via CD4-TH lymphocytes and CD8 cytotoxic T lymphocytes

Extracellular defense

The production of antibodies by plasma cells does not start properly after 5-10 days after the first contact with a certain MO. Many extracellular bacteria have developed surface structures, such as a polysaccharide capsule, that prevent direct recognition and thereby uptake by phagocytic cells. Pneumococci are an example of encapsulated bacteria. They are transmitted from person to person through saliva and cough. When the spleen is removed or malfunctions, there is a (greatly) increased risk of acute pneumococcal infections with severe sepsis. This is caused by failure or reduction of the spleen filtration function, but also because a certain subpopulation of B lymphocytes is now unique to the spleen, the so-called marginal zone B lymphocytes. With a pneumococcal infection, a severe acute inflammatory reaction occurs. This is started by cytokines and leads to the formation of the protein C-reactive protein (CRP) and is produced by the liver. It binds to phosphorylcholine from the cell wall of the bacterium, after which complement is activated.
The pneumococci can be divided into 90 serotypes and groups based on differences in the composition of the capsule saccharide. The antibody response to pneumococcal disease is serotype-specific to one specific serotype, not to one of the 89 other pneumococcal serotypes. Relevant antibodies to capsular saccharide are primarily of the IgA and further of the IgM and IgG2 class.

Intracellular defense

This complex defense is primarily aimed at viruses, which sometimes have ingenious routes to escape destruction. Viruses are not independently living organisms, they need cells to be able to reproduce. Once in the cells, they take over the metabolism, so that the infected cells only produce new viruses.
They can also remain latent in the body after successful control, in order to react to weakened defenses and cause a chronic infection. An example is the Epstein-barr virus (EBV). Mycobacteria, such as salmonella and legionella, have also developed such mechanisms. They can survive within the macrophages, among other things. There they are shielded from important parts of the defense such as complement and antibodies. In order to grow, they obtain the essential nutrients and minerals directly from the host cell. They also prevent them from ending up in the lysosomes, a large arsenal of bacteria-killing enzymes, which considerably increases their chances of survival. For the development of immunity, natural killer cells (NK cells) and Th1 lymphocytes are necessary to enhance the bactericidal capacity of the macrophage.

NK cells

These, like the other lymphocytes, come from progenitor cells in the bone marrow and they can be viruses and kill bacteria in the cell. In addition, CD8 cytotoxic T lymphocytes play a role in this context. These lymphocytes kill MO via perforin and granzyme, or by direct induction of apoptosis (killing) by Fas-Fas ligand interaction. Perforin is a protein stored in secretory lysosomes of cytotoxic T lymphocytes and NK cells. This protein forms pores in the cell membrane of target cells, after which granzymes, also from the secretory lysosomes, can enter the target cell and subsequently induce it to apoptosis.

Stopping the immune response

Due to the interaction of Fas and Fasl, an excess of activated lymphocytes can be cleared. That is, the same mechanisms used for the elimination of virus-infected target cells are also used to stop the immune response once it has reached its goal. The mucosa is protected by mucins, prostaglandins and macrophages, among other things. Mucines, which are the attachment sites for all kinds of organisms, including intestinal bacteria, are rich in sialic acid. When the content of sialic acid diminishes, adhesion of the beneficial flora decreases while the binding of fungi and also of cancer cells increases. Administration of whey, a substance rich in salic acid, restores the structure of the mucins. As a defense mechanism, the cell membrane can convert arachidonic acid into the hormone prostaglandin E2 as a defense.

Video: Infectious Diseases - An Introduction (April 2020).

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