BIOL 251 - Ch. 15 Study Points

Disease

Any condition in which the normal structure or functions of the body are damaged or impaired

Infection

Microbe is established, growing and dividing in a host and has signs or symptoms

Infectious disease

When normal structure or functions of the body are damaged or impaired

Caused by direct effect of a pathogen

Colonization

Microbe is established growing and dividing in host and has no signs or symptoms

Person isn’t sick

Microbes can still be passed from person to person

Iatrogenic disease

Contracted as the result of a medical procedure

Nosocomial disease

Acquired in hospital settings

Zoonotic disease

Infectious disease not transmitted between humans directly but transmitted from animals to humans

Communicable disease

Capable of being spread from person to person thru direct or indirect mechanisms

Noncommunicable disease

Not spread from person to person

Non-infectious disease

Disease caused by genetics, the environment, or inappropriate immune response

Pathogen

Colonized microbe capable of causing harm to host

Cellular - bacteria, parasites, fungi

Acellular - viruses, viroids, prions

Pathogenicity

Ability to cause disease

Virulence

Degree of pathogenicity

Virulence as it relates to a microorganism, virus, or toxin

Degree or amount of disease

Some pathogens cause more disease or damage (more virulent)

Related to collection of harmful genes

Virulence factors

How microbes evade host defenses

Determine extent and severity of disease

Adhesions, exoenzymes, exotoxins, endotoxins, anti-phagocytic factors, biofilm formation, phase variation/antigenic shift

Primary pathogen

Causes initial primary infection

Might predispose individual to a secondary infection

Opportunistic pathogen

Causes infection when host’s immune defenses are compromised

Examples of opportunistic pathogens

Staphylococcus epidermidis - nosocomial infections

E. coli - normal microbiota, can cause UTI

Candida albicans - overgrowth in patients on antibiotics

Difference between signs and symptoms

Signs - can be observed and measured; ex) fever

Symptoms - very subjective, experienced by patient, can’t be objectively measured; ex) muscle cramps, malaise, pain

Course of disease

Incubation → prodromal → illness → decline → convalescence

Incubation

Pathogen has entered host and begun multiplying

Variable - number of microbes, condition of host, etc.

Prodromal

Pathogen continues to multiply

Host experiences symptoms

Immune system is activated

Illness

Host experiences most obvious/severe symptoms

Decline

Number of pathogen particles decreases, signs/symptoms decline

Immune system has been weakened by pathogen - secondary infection risk

Convalescence

Recovery, recuperation, etc.

Acute disease

Illness is short term because pathogen is eliminated by host defenses

Person is usually immune to reinfection

Incubation → illness (short) → convalescence

Ex) influenza, Strep throat

Chronic disease

Illness persists over a long time period

Incubation → illness (long)

Helicobacter pylori, TB

Latent disease

Illness may recur if immunity weakens

Incubation → illness → convalescence → latency → recurrence

Varicella-zoster virus (shingles)

Limitations of Koch’s postulates

Not all individuals are equally susceptible

Not all individuals show the same signs and symptoms

Not all pathogens can be grown alone in a pure culture

Not all diseases can be replicated in animals

Molecular postulates

Described by Stanley Falkow

Some pathogens can cause different diseases depending on virulence factors produced

Virulence factor gene or its product should be found in pathogenic strains of the organism

Mutating the virulence gene to disrupt its function should reduce the virulence of the pathogen

Reversion of the mutated virulence gene or replacement with a wild-type version should restore virulence to the strain

Host factors that can affect the establishment of an infectious disease

Actual effective dose for an individual can vary widely

Depend on factors such as route of entry, age, health, and immune status of the host

Steps of pathogenesis

Exposure/contact → attachment (adhesion) → invasion/colonization → infection and damage to the host

Exposure/contact

First encounter with pathogen

Not all contact with pathogens results in infection and disease

Pathogen gains access to host via portal of entry

Attachment (adhesion)

Pathogen attaches to host cell receptors using adhesion factors

Slime layers and capsules can also make some bacteria adherent

Invasion/colonization

Pathogen disseminates thru the body

Virulence factors are produced - toxins, exoenzymes

How do pathogens or toxins invade and affect the host?

Enzymes produced by the bacteria breakdown cell structures which allow bacteria and toxins to invade and cause damage to host

Importance of adhesion molecules in the establishment of infectious diseases

Adhesion to the host cell is needed for pathogen since it’s needed for the activation of toxins and virulence factors

Provides stable surface for pathogen

Example of adhesion

Streptococcus pyogenes - adheres to respiratory epithelial cells thru Protein F

Botulinum toxin

Inhibits acetylcholine release from presynpatic nerve terminal

Causes paralysis due to not being able to contract muscles - death by respiratory failure

Tetanus toxin

Binds to inhibitory interneurons

Causes violent muscle spasms - death by respiratory failure

Cholera toxin

Causes increased secretion of fluids and electrolytes out of cell (makes cell leaky) - results in diarrhea

Shiga toxin

Cytotoxin

Potent inhibitor of protein synthesis - incites intense inflammatory response leading to hemolytic uremic syndrome

Damage lining of blood vessel walls, destruction of RBCs, kidney failure

Hyaluronidase

Degrades hyaluronic acid which connects adjacent cells of the epidermis together

Opening allows pathogen to spread thru tissue

Ex) Streptococcus pyogenes, Clostridium perfringens

Collagenase

Degrades the collagen between endothelial cells

Opening allows pathogen to enter the bloodstream

Ex) Clostridium perfringens

Streptococcus pyogenes and necrotizing fasciitis

Cystein protease - exoenzyme that hydrolyzes peptide bonds that have cysteine

This allows bacteria to reach deeper layers of skin and CT

Virulence factors destroy host tissues

Endotoxins

Source - Gram -

Composition - Lipid A component of lipopolysaccharide

Effect on host - general systemic symptoms of inflammation and fever

Heat stability - heat stable

Higher dose needed - toxin not potent

Exotoxins

Source - Gram -/+

Composition - Protein

Effect on host - specific damage to cells dependent upon receptor-mediated targeting of cells and specific mechanisms of action

Heat stability - most are heat labile but some are heat stable

Lower dose needed - toxin is potent

Cytotoxins

Exotoxin

Kill host cells or inhibit functions

Enterotoxins

Exotoxin

Cause intestinal disturbance

Neurotoxins

Exotoxin

Damage nervous system

Intracellular targeting toxin (AB toxin)

Exotoxin

B component binds to host cell thru its interaction with specific cell surface receptors

Toxin is brought in thru endocytosis

Once inside, A component separates from B component, and A component gains access to cytoplasm

Ex) diptheria, cholera, botulinum, tetanus toxin

Membrane disrupting toxin

Phospholipases that disrupt eukaryotic cytoplasmic membranes - hydrolyze phospholipids of membrane, lyses cells

Ex) alpha-toxin of C. perfringens; hemolysins of S. pyogenes

Superantigens

Stimulate high number of T-cells - overstimulate the nervous system

Create cytokine storm

How does vaccination of tetanus work?

Antibodies bind to the cells before tetanus toxin can

How do capsules help bacteria evade host defenses?

Antibodies normally function by binding to antigen → phagocyte binds to antibody and performs phagocytosis

Capsule inhibits the attachment of antibody or produces proteases to break down host antibodies