Chapter 15 flashcards

pathogenicity

ability to produce disease

virulence

the severity or degree to which a microorganism can cause disease

Portal of entry

Ways of disease to enter the body and multiply:

• Mucous membrane: tongue, cheeks, lips

• respiratory entry: travels down the trachea

• gastrointestinal: stomach and intestines

• genitourinary: genital and urinary

• hair follicles/sweat ducts

• inoculation: parental route; the process of introducing microbes into a culture media so that it reproduces there

mucous membrane

tongue, cheeks, lips

respiratory entry

The respiratory tract is a common entry point because it is constantly exposed to the air. Microbes can enter when a person inhales, and contact the mucosal surfaces of the nose, throat, or lungs.

gastrointestinal

stomach and intestines

genitourinary

genital and urinary

hair follicles/ sweat ducts

the skin's protective barrier by entering through the opening of the hair follicle to establish an infection. 

inoculation

the process of introducing microbes into a culture media so that it reproduces there

virulence

LD50—→ Lethal dose of 50 (potency of a toxin)

Less LD50 means more potency

More LD50 is less potency 

and

ID50———> Infectious dose (# of pathogens required to cause an infection in 50% of a tested population

Less ID50 means the pathogen is more virulent (more toxic because it needs less of them to cause disease)

Attachment: Adherence

Adherence for the pathogen’s side with help of ligands ( glycoproteins, lipoproteins, fimbriae)

Surface receptors

For host’s side with help of sugar receptors and mannose receptors ( most common)

Biofilms

provide attachment + resistance to antimicrobes

How do pathogens get past host defense?

Using a capsule in form of ECM (extracellular matrix proteins) it’s a protective layer secreted by some bacteria

Encapsulation

Increase virulence while still in a protective shell

Cell wall components

Protein in cell wall can facilitate adherence and prevent phagocytosis for bacteria:

• Mycolic Acid

• M protein

• Opa + fimbriae

Mycolic acid

(mycobacterium) Prevents digestion by phagocytes (resist digestion by phagocytes)

M- protein

( s.pyogenes + fimbriae) allows the bacteria to resist phagocytosis (being engulfed by immune cells), adhere to host cells, and interfere with complement activation and antibody deposition.

Opa + fimbriae

entry into cells as a mean of evading the host immune system by attaching to surface(fimbriae)  and host cell adhesion and invasion (opa)

Fibrin clot- coagulase

allows bacteria to form a protective fibrin clot: coat formed around bacteria to help them hide from the immune system,

3 important enzymes

• Hyaluronidase

• Collagenase

• kinases 

Kinases

"molecular switches" that control nearly all cellular activities, allowing bacteria to sense and rapidly adapt to their environment, survive stress, and cause disease.

Hyaluronidase

"spreading factor," helping the bacteria invade and move through host tissues by breaking down hyaluronic acid, a natural barrier. This allows the bacteria to spread more easily, increasing the severity of an infection, and some bacteria can even use the broken-down hyaluronic acid as a food source. 

Collagenase

it allows them to break down collagen,

Destroying immune molecules:

• IgA antibodies

• IgA protease

IgA antibodies

act as the primary security system at the body's mucosal surfaces (like the gut, lungs, nose, and reproductive tract), where most bacteria try to enters and attaches to bacteria, which stops them from binding to and infecting your body's cells.

IgA protease

a bacterial enzyme that helps certain pathogenic (disease-causing) bacteria survive and infect the body by destroying the function of human IgA antibodies

Antigenic variation

allows them to change their surface appearance to the host's immune system. This effectively lets the bacteria hide from, or confuse, the immune response, enabling them to persist

Penetration

alter actin (cytoskeleton) of a host cell to entry into a cell, a pathogen enters a host cell to initiate infection (allows them to to survive, get food, cause disease, and resist treatment)

How do they actually damage the host cell?

By using the host nutrients: Iron, steal it from the host by sidesphores by binding more tightly, or by engulfing entire IBP, or kill cells and take released iron from host cells 

Direct damage

By using cell lysis; the process of breaking open a bacterial cell to release its contents, like proteins and DNA

Toxins

• Toxemia

• Toxigenicity

• Exotoxins

Toxemia

bacterial infection releases poisons, or toxins, that spread throughout the body via the bloodstream

Toxigenicity

ability of a bacterium to produce poisons (toxins) that harm host cells and cause disease. 

Exotoxins

potent, poisonous proteins secreted by living bacteria that cause disease by destroying host cells or interfering with their normal functions. 

INTOXICATION final stage

• A-B toxin

• Membrane- disrupting

• Endotoxins

A-B toxin

Active compound: Diptheria toxin composed of two subunits: B that binds to a host cell and A that has the enzyme activity to damage the cell from the inside. Bacteria use these toxins to hijack the host's cellular machinery and cause disease. 

Membrane-disrupting toxins

hemolysins, leukocidins, and streptolysins: damage host cell membranes, leading to cell lysis and death

hemolysins target red blood cells

leukocidins target white blood cells

streptolysins (a type of hemolysin) are produced by Streptococcus pyogenes and target both red and white blood cells. 

Endotoxins

gram negative, outer membrane w LPS (lipopolyssacharides)

Fever & Shock

Cytokine release

LAL assay

Used to detect endotoxin on drugs or medical devices (sterelization does not get rid of endotoxin)

Plasmids

Can carry genes for antibiotic resistance, genes for toxins, genes for capsules

Lysogenic Conversion

bacteriophage that transfer virulance(toxins) to harmless bacteria :o

ex: cholera

Patoghenicity of viruses ( list of the various ways viral infections affect cells, leading to visible changes known as cytopathic effects (CPE) and other less visible) 

• CPE, slow visible signs a classic example found in the brain cells of animals and humans with rabies.

• Syncytia (RSV): The fuSlow visible signs (CPE): General term for the structural changes in host cells caused by viral invasion.

• Stop mitosis: Viruses can halt the normal cell division process of the host cell.

• Host lysosome release enzymes, that will destroy intracellular components: Viruses can trigger the release of destructive enzymes from the host cell's lysosomes, leading to self-destruction of the cell (apoptosis or necrosis).

• Inclusion bodies: Granules or abnormal structures within the cell that contain viral components (e.g., viral proteins, nucleic acids, or assembled virions). Negri bodies arsion of multiple adjacent host cells into a single, multinucleated giant cell. This is characteristic of certain viruses, such as Respiratory Syncytial Virus (RSV).

• Antigenic changes: The presence of viral proteins on the host cell surface can alter the cell's identity, making it a target for the immune system.

• Chromosomal changes: Viruses can interact with host cell DNA, leading to damage, rearrangement, or integration of viral genetic material into the host's chromosomes.

• Transformation and loss of contact inhibition (cancer, tumor formation): Some oncogenic viruses can transform normal host cells into cancerous cells. This often involves the loss of contact inhibition, a normal cellular process that stops cell growth when cells touch each other, leading to uncontrolled proliferation and tumor formation.

• Change in function of host cell (not visible): Viruses can alter the host cell's metabolic activities, hormone production, or other normal functions without immediate

Pathogenicity of fungi

• Capsules: To mask the fungus from the immune system.

• Allergic response: To trigger an inflammatory response in susceptible individuals

• toxins: To directly damage cells and tissues, causing disease.

Pathogenicity of Protozoa + Helminths

• Damage to host tissue by metabolic waste products(Parasitic)

• Antigenic variation

Pathogenicity of Algae

• Produce neurotoxins

Portals of exit

• Respiratory tract( sneezing, coughing)

• Gastrointestinal tract (saliva)

• Genitourinary tract( vaginal sacrations0

• Arthropods and syringes (transferring them to a new host)