Bio 230 Lecture Notes

Chapter 14. Host-Microbe Relationships and Disease Processes

Types of Symbiosis: Mutualism (beneficial to both host and microbes, e.g. gut microflora); Parasitism (harmful to the host, e.g., pathogens); Commensalism (neither harmful or beneficial to the host, e.g., skin microflora)
Pathogenicity (disease-causing ability of microorganisms); Virulence (degree of pathogenicity)
Evolution of virulence: commensalism with the human host is NOT the inevitable outcome of evolution of microbial parasites. Ease of transmission selects for strains with higher virulence, e.g. high virulent form of cholera thrives over low virulent forms in places lack of water-treatment systems.
Normal Microflora:

Commensal microbial populations on or in the human body. They exist in skin, upper respiratory tract (e.g., nasal mucosa), digestive tract (mouth mucosa, pharynx, stomach, large intestine, colon, rectum), and uro-genital tract (urethra, vagina).
Resident microflora are well-established microbial populations adapted to human body. They offer protection from colonization by harmful microbes through competitive exclusion (microbial antagonism).
Human Microbiome Project aims to identify all microbial species in resistant microflora

Opportunistic Pathogens: normally harmless microbes becoming pathogens under special conditions

Immune-compromised host
Introduction into non-resident body sites, e.g., E.coli in urinary tract
Disturbances to the normal microflora, e.g, yeast infection due to heavy antibiotics use

Experiment procedures for identifying the causative/etiological agent of an infectious disease
Steps & Exceptions

Agent isolated from diseased host in pure culture (Exception: many microbial species cannot grow, or grow slowly, in pure culture)
Isolated agent is injected into an healthy host (Exception: human-specific infection, e.g., HIV-1, cannot be experimentally introduced into healthy hosts)
The same disease symptoms are reproduced
Pure cultures are obtained and shown to be the same as the original culture

By causing direct tissue damage: e.g. destruction of epithelial cells by enterics; viruses cause visible deformation of the host cells (cytopathic effects); malaria pathogen grows in and destroys live tissues and red blood cells
By producing toxins: the mechanism of most bacterial damage (see details below)
By inducing hypersensitivity (allergic) reactions: e.g. arthritis caused by Lyme bacteria

Adhesins: molecules on the surface of microorganisms that binds to host cells. Permit attachment to cells, usually a part of fimbriae, mostly glycoproteins or lipoproteins. Attachment sites on host cells are called receptors, on the parasite called ligands. Ligand-receptor binding is highly specific.
Capsules: capsule is a virulent factor of Streptococcus pneumoniae. It resists the host's defense by impairing phagocytosis (destruction by engulfing of microbes).
Exoenzymes: digestive enzymes for tissue invasion, e.g., hemolysins produced by Streptococci to release iron from hemoglobin
Toxins: Most damage by bacterial pathogen is done by toxins, which are poisonous substances produced by microorganisms. Toxemia refers to the presence of toxins in the blood. Two types of toxins: exotoxins and endotoxins (see below)

Exotoxins are produced mostly by G+ and some G- bacteria
Exotoxins are made of proteins (many are enzymes): therefore can be denatured by heat, and easier to make anti-toxin (toxoid) vaccines
Exotoxins are among the most lethal substances known.
Examples: diphtheria toxin, anthrax toxin (three parts, one shields from immune system, one destroys immune cells, the third kills host cells), tetanus toxin (a neurotoxin produced by Clostridium tetanus), Staphylococcal toxin (an enterotoxin produced by Staphylococcus aureus, causing toxic shock syndrome), botulinum toxin (a neurotoxin causing muscle paralysis, used as Botox for removing wrinkles)

Endotoxins are part of the outer membrane of the Gram-negative cell walls
Endotoxins are lipopolysacchrides (LPS), therefore do not promote effective antitoxin production and are not denatured by heat
Released when bacteria cells die, causing similar symptoms, e.g., fever.
Lower toxicity compared with exotoxins
Examples: Salmonella typhi (causing typhoid fever), Neisseria meningitidis.

Communicable/Contagious infectious diseases: easily transmission from host to host
Non-communicable infectious diseases: NOT transmitted from host to host, e.g., opportunistic infections, enterotoxin in food, infections acquired from environmental reservoirs (tetanus, legionellosis, Lyme)

Incubation phage (no sign or symptoms)
Prodromal phase (vague symptoms)
Invasive phase and Acme (severe symptoms, most tissue damage, strongest host responses)
Declining phase
Convalescence phase (tissue repair)

Lack of prevention and health care (e.g., immunization)
Evolution of drug-resistance
Discovery of infectious cause of known diseases (e.g., H. pylori for peptic ulcer)
New social, behavioral, and, climate, technological conditions, e.g., legionellosis in centralized air conditioning system, expansion of tick habitats due to global warming
Pathogens shift host from non-human animals to humans ("zoonosis"), e.g., SARS, bird flu, AIDS