PATHOPHYSIOLOGY OF INFECTION
DEFINITIONS
1. Infection : it is the penetration, development and proliferation in a living being of pathogenic microbes or pathogenic agents, which can remain localized (abscess, pneumonia, etc.), spread through the blood or spread their toxins in the body (toxic infection). It is the aggression of a living organism by pathogenic micro-organisms.
2. Virulence (quantitative concept): it is the ability of a germ to multiply in an organism. Virulence often implies multiplication and pathogenicity.
3. Pathogenic power : this is the ability to cause disorders in the parasitized organ.
4. Pathophysiology or pathological physiology : this is the study of disorders in the functioning of the organism or its parts, during an illness.
5. Community infection : this is an infection contracted outside of healthcare services.
6. Nosocomial infection : infection contracted during and/or in healthcare services.
I. PATHOGENIC AGENTS :
1. Bacteria
2. Virus
3. Unicellular fungi or micromycetes
4. Unicellular parasites or protozoa
II. BACTERIAL INFECTION : this is the aggression of the host by pathogenic bacteria.
1. PHYSIOPATHOLOGY OF A BACTERIAL INFECTION
1.1. The different types of host-bacteria relationships (interactions) : most bacteria lead a life independent of another living organism; they are called “ saprophytes ”; they live in nature on organic waste (environment); their presence in the organism is only transitory. Other bacteria will find the conditions necessary for their growth on the surface or inside another living organism, they are called “ parasites ”.
Parasitism is expressed in three ways:
* commensalism : obligatory parasitism but the host and the parasite do not benefit from it.
*Symbiosis : both host and parasite benefit from their association e.g. intestinal bacteria play a role in the ingestion and synthesis of vitamin K.
* True parasitism : the parasite benefits from the host, which does not benefit from it; the bacteria is harmful to the host. In this case we have:
° specific pathogenic bacteria : BK and Salmonella Typhi
° opportunistic pathogenic bacteria : these are commensal or saprophytic bacteria (germs of the oral flora).
1.2. The main mechanisms of bacteria-host interaction and pathogenicity factors : the pathogenic power of bacteria responds to successive stages:
* establish close contact with the host “membership”
*persist in host
* attack the host and possibly enter it “invasion”
PATHOPHYSIOLOGY OF INFECTION
2. FACTORS OF BACTERIAL VIRULENCE
2.1. Factors related to microbes (factors of bacterial aggression) : we can cite:
the surface or wall structure elements of the microorganism;
enzymes with deleterious effects on tissue components (outside the cell), secreted by the bacteria;
and protein toxins (endo and exotoxins) released by the bacteria which have a deleterious effect on cells.
2.2. Host-related factors : age, quality of nutrition, general condition (diabetes), current treatment, etc.
3. FACTORS ALLOWING BACTERIA TO ESCAPE HOST DEFENSES
3.1. Resistance to phagocytosis
3.2 . Resistance in the phagocyte: intracellular pathogen: exp BK
3.3 . Escape from the action of antibodies (encapsulated spores and bacteria)
4. THE DIFFERENT TYPES OF BACTERIAL INFECTIONS
4.1. Non-specific infection : It is caused by opportunistic bacteria (saprophytes), the latter do not usually cause diseases in healthy subjects. They can become pathogenic in subjects with altered natural defenses, these are commensal bacteria.
4.1.1. Pyogenic infection : The germs involved are called pyogenic, staphylococci produce a yellowish pus, streptococci a sero-lumpy pus and pneumococci a greenish pus.
Microbial dissemination occurs from a gateway or a first inflammatory focus.
* Extension by contiguity : the aggressor spreads from near to far, example of maxillary osteitis or sinusitis from a dental abscess.
* Lymphogenous extension : the causative agent penetrates the lymphatic pathways and reaches the neighboring lymph nodes; example, dental adenitis and syphilis.
*Hematogenous extension : the intravascular macrophage system generally allows minimal disseminations to be controlled by phagocytosis and digestion; this is then a simple bacteremia. Sometimes, the germs carried by the blood will graft onto an organ (heart, lungs, brain, etc.) or even cause septicemia.
* Extension by ductal route : this is extension by ascending route (infection of the salivary glands).
4.1.2. Non-suppurative infections : these are usually caused by Gram-negative germs. They most often have a digestive starting point. These are essentially acute local, toxic and septicemic reactions (toxic-infectious shock).
Example: salmonellosis (typhoid and paratyphoid fever)
4.2. Specific infection : it is caused by pathogenic bacteria (tuberculosis, syphilis, cholera, etc.). It is an infection caused by the same bacteria, responsible for the same disease regardless of the means of defense (healthy or immunocompromised subject) with characteristic manifestations.
4.2.1. Tuberculosis : this is an infectious disease caused by the penetration and proliferation in the body of a mycobacterium: Koch’s bacillus ( BK ).
BK enters the body by crossing a mucous barrier. Sometimes, macrophages will be able to destroy all the BK and prevent the disease from developing, sometimes, the BK behaves like an intracellular parasite and multiplies in the histiocytes. These infected cells, by migrating, can contribute to the dissemination of the disease.
4.2.2. syphilis : this venereal disease is due to the penetration into the body and the proliferation of a spiral bacterium which is mobilized thanks to the undulations of an axial filament.
5. RESISTANCE OF BACTERIA TO ABTIBIOTICS :
5.1. Natural resistance
5.2 . Acquired resistance
PATHOPHYSIOLOGY OF INFECTION
6. USE OF ANTIBIOTICS
6.1. Antibiotic therapy : it is used to treat a proven infection. It is:
* probabilistic (most often)
* or after antibiogram
6.2 Antibiotic prophylaxis : It is used to prevent infection.
III . VIRAL INFECTION : Viruses are the smallest intracellular parasites, measuring between 10 and 300 nm. They are made up of a single type of nucleic acid (either DNA or RNA), surrounded by a protein capsid, the whole is called a nucleocapsid or viral unit. Sometimes the nucleocapsids are surrounded by a membrane envelope (peplos) of a lipoprotein nature.
Outside of cells, viruses survive for a long time, but they can only reproduce inside living cells. They hijack their metabolism and force them to synthesize the nucleic acids they are made of and the proteins that surround them. Viruses are on the borderline between inert and living matter; they have no metabolism.
1. THE VIRAL CYCLE : The virus can reproduce and become pathogenic only by penetrating a host cell to divert its metabolism to its advantage for the synthesis of its own constituents. From the harmless extracellular virus to the reproduction of new pathogenic viral units, there are several successive stages of viral activity which constitute the viral cycle.
1.1. Attachment or adhesion : This is the adhesion of the virus to specific sites on the cytoplasmic membrane of the host cell.
1.2. Penetration : this is the passage of the virus or its genetic material (nucleic acid) into the cell.
1.3. decapsidation : the viral structure is then degraded, with the exception of the genome which, freed from the capsid, is released into the cell and can interact with its machinery.
1.4. replication or synthesis of the constitutions of the new virus : the released viral genome takes the direction of syntheses in the host nucleus to produce copies (replicas) of the viral genome, viral proteins and the capsid as well as the peplos lipoproteins for enveloped viruses.
1.5. assembly or maturation : the new genome produced by the cell is surrounded by new viral proteins; it is the encapsidation of the genome which results in the formation of a new viral particle (several particles).
1.6. dispersion or release : after maturation, the cell bursts and the viruses leave it to seek other hosts.
2. CONSEQUENCES OF VIRAL MULTIPLICATION ON THE INFECTED CELL : Viral infection causes the following lesions:
2.1. degenerative lesions is the death of the cell by lytic infection.
2.2 . fusion or tolerance of the infectant
2.3 . malignant cellular transformation
3. MODES OF TRANSMISSION OF VIRUSES OR VIRUS-ORGANISM INTERACTION : There are several ways of transmitting viruses in the body:
3.1 . airborne transmission
3.2 . digestive or fecal-oral transmission
3.3 . sexual transmission
3.4 . Mother-to-child transmission
3.5 . iatrogenic or nosocomial transmission: blood transfusion , care, invasive explorations and tissue and organ transplants
3.6 . transmission by animals
4. FACTORS INFLUENCING PATHOGENESIS
4.1. Virus-related factors
* viral load or inoculum
* the route of inoculation
* cytopathogenicity
* the virus’s escape from the immune response
* resistance to antivirals
4.2. Host factors : generally represented by immune deficiency
5. FIGHT AGAINST VIRAL INFECTIONS
5.1. Passive immunotherapy : this is the preventive or curative administration of human immunoglobulins prepared from donor plasma.
5.2. active immunotherapy : it is provided by vaccination
5.3. antiviral chemotherapy : this is the introduction into the body of molecules to inhibit viral multiplication.
ACYCLOVIR is the first antiviral substance without cytotoxicity, it causes the inhibition of viral DNA polymerase, thus blocking the replication chain.
END
PATHOPHYSIOLOGY OF INFECTION
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