Bacteriology III: Normal Flora and Pathogens

Normal Flora: endogenous microorganisms that live on another living organism without causing disease
Pathogen: an organism that can cause disease
Opportunistic pathogen: non-pathogenic organisms that cause serious disease in immuno-compromised individuals or when in other locations
Virulence Factors: bacterial features that contribute to infection
Pathogenesis: the mechanism by which infections lead to symptoms

Consists of all microorganisms present in the body
Microbiome refers to the microorganisms and their genes
Microbiota refers to the microbes themselves
Example: An adult human body has approximately 2 m2 of skin, and it contains about 10^12 numbers of bacteria
Normal flora prevents the colonization of pathogens by competing with them for essential nutrients and attachment sites

Initial colonization of bacteria occurs primarily in the first year of life
A healthy microbiome is highly diverse with beneficial bacteria
Microbiota vary in anatomic location and composition
Example: Ubiquitous on the skin (e.g., Staphylococcus), very high numbers in the intestine (e.g., Escherichia coli), and absent in sterile sites (e.g., blood, organs)
Loss of diversity leads to altered microbiota (dysbiosis) and is associated with many health conditions

Example of dysbiosis: Clostridiodes difficile infection
Dysbiosis may lead to infections, and fecal transplantation can be used to treat dysbiosis

Primary infection: Initial infection with an organism in the host
Reinfection: Subsequent infection by the same organism in the host (after recovery)
Secondary infection: An infection that follows on from, or is the indirect result of another infection
Superinfection: Secondary infection that occurs during treatment of a primary infection
Opportunistic infection (primary or secondary): caused by normally harmless bacteria that become pathogenic upon favorable changes in the environment

Adhesion: attachment to host tissue or abiotic surfaces
Invasion: penetration of host tissue
Resistance to environment and host immunity: ability to survive and evade host defense mechanisms
Secretion: release of exotoxins, enzymes, and effector proteins
Virulence factors are molecules that enhance the ability of a microorganism to cause disease beyond that intrinsic to the species

Glycocalyx: a gelatinous sugar material including proteoglycans, glycoproteins, and glycolipids
Functions to help the organism resist environmental insults and is anti-phagocytic
Asplenic individuals are vulnerable to sepsis, as the majority of antibodies against the capsule are produced in the spleen

Non-encapsulated organisms are resistant to unenhanced phagocytosis
Encapsulated organisms are resistant to phagocytosis and require antibodies and complement to be dealt with

Formed during harsh environmental growth conditions
Highly resistant to desiccation, chemicals, hot/cold temperatures, and radiation
Found in the environment
Germinate into vegetative (replicating) bacterial cells on contact with moisture and suitable temperature and pH

Bacteria are sheltered from harmful factors in the environment, such as desiccation, antibiotics, and a host body's immune system
Slimy extracellular matrix produced by the bacteria
Biofilm composed of extracellular polymeric substances (EPSs)

Secretion Systems: Found in several Gram-negative bacteria
Important in the release of exotoxins, enzymes, and effector proteins
Type 3 Secretion System (T3SS) acts as a "needle" to inject effector proteins into the host and modify host cellular characteristics

Exotoxins: produced by bacteria and secreted into the environment
Types: A/B-toxins (Type III toxin), Membrane disrupting toxins (Type II toxin), Superantigens (Type I toxin)
Examples: Cholera, Tetanus, Botulism

2 Components: A "active" subunit and B "binding" subunit
B-subunit binds to specific host cell receptor, leading to internalization
A-subunit disassociates from B-subunit in host cell and targets cellular function

Non-specific activation of T cells leads to massive cytokine release, causing Toxic Shock
Example: Staph aureus Toxic Shock Syndrome Toxin

Produced only on cell lysis (cell death)
Lipopolysaccharide (LPS) components of the outer membrane of Gram-negative bacteria
Endotoxins produce their effect in a host by activating the complement system by the alternative pathway
Pyrogenic in action (i.e., they produce fever in their host)### Bacterial Toxins: Endotoxins
Bacterial endotoxins can cause bacterial sepsis (shock) and intravascular coagulation, leading to conditions like meningococcemia and sepsis.

The disease process involves multiple steps, resulting in different outcomes, including acute, transient carrier, chronic latent, chronic persistent, and chronic recurrent.

Acute: finite duration of time of infection and symptoms, resulting in resolution.
Transient carrier: finite duration and absence of symptoms with low infections.
Chronic latent: long duration of time and no display of symptoms of disease.
Chronic persistent: long duration of time and continuous symptoms.
Chronic recurrent: long duration of time and symptoms that exacerbate and abate, often due to changes in a person's immune status.

The bacterial load affects the outcome of the disease process, with higher loads leading to more severe outcomes.
The relationship between bacterial load and disease outcome is complex, with multiple factors influencing the progression of the disease.