Studied by 61 PeopleCommensal
Tags & Description
Commensal
microbiota colonize a host in a typically non-harmful coexistence (benign)
Mutalistic
both benefit (i.e., vitamin production, immune system modulation, barrier against pathogens, nutrition, habitat)
Pathogenic
capable of causing disease
Positive effects of host-microbiome symbiosis
confers resistance to colonization by pathogens -regulates the cardiovascular system -supports host defense functions -has anti-inflammatory properties -provides additional metabolic potential -has antioxidant activity -maintains a healthy digestive tract
normal human microbiota (aka normal flora)
resident colonizing microbes (commensals) of our skin, respiratory, genitourinary, and digest system
-develops, expands, and evolves throughout life and plays a critical role in human health
-modified by many factors and has a close relationship with physiologic functions and development of diseases in different systems
The b acteria in our microbiomes are essential to human health and aid in biological processes such as:
extracting energy from food -providing essential vitamins -regulating our immune system -regulating our glucose levels and metabolism -protecting us against disease-causing microbes
Dysbiosis
disruption of normal microbiota balance that can compromise health
-increase risk for infections and disease
the immune system recognizes and responds to our normal microbiota
this defense system is critical to protect us from infection and disease
-our microbiota is critical for training our immune system
-childhood exposure to a variety of microorganisms is necessary for proper immune system development
Dysbiosis of the oral microbiome
can lead to periodontal disease
Pathogenicity
the ability of a microbe to infect a host and/or cause disease/damage
-host damage results from host-pathogen interactions
virulence
degree or extent of disease/damage that a pathogen causes (disease severity) or the ability of the pathogen to multiply within the host (pathogen's infectivity)
Host-Microbe Interactions
influence pathogenicity and virulence
-host properties (e.g., immune fitness, normal microbiota balance) combined with pathogenicity of the microorganism (virulence factors)
Virulence factors
mechanisms used by pathogens and/or components they produce to: infect, invade, damage host tissues, overcome defenses, or achieve transmission to a new host
-pathogens develop new virulence factors in response to the host and selective pressures
For a pathogen to persist in a population...
-it must endure over time -it must find a balance between breaking down defenses and living within an individual host -it must get readily transmitted to a new host
Pathogens that kill hosts quickly usually..
cause high-mortality outbreaks
are geographically isolated
are short-lived in duration or in a host/population
The goal of being a successful pathogen...
is to get transmitted to a new host to continue your life cycle
Making virulence factors requires
an energy investment
-pathogens only benefit/maintain a particular virulence factor when it bestows a benefit
The enviornment heavily influences?
production of virulence factors
Pathogens often become attenuated when grown in the lab
lose virulence factors needed to cause disease -still infectious but weakened -do not cause disease in an immunocompetent host -sometimes used in vaccines
Examples of bacterial virulence factors
avoidance and/or inhibition of the host's immune response -entry into and exit out of host cells and/or tissues -substances produced by or derived from microbes that have adverse host effects -attachment of host cells; includes colonization of host -obtained from the host for viability and multiplication
toxins
promote infection and disease by directly damaging host tissue or by disabling the immune system
toxigenic
microbes that make toxins
toxemia
toxins in the bloodstream
endotoxins
lipid A portion of LPS within the Gram-negative bacterial outer membrane; released upon cell lysis; inflammatory
Exotoxins
proteins (often enzymes) produced and actively secreted by growing cells; active in low concentrations
septic shock
characterized by fever, chills, fatigue, malaise, tachycardia, and hypotension -causes life-threatening drop in blood pressure and multiorgan failure -in the U.S., affects - 1 million people per year (fatal up to 1/2 of cases)
Endotoxins treatment issues
lipid-based endotoxins, not readily neutralized -no vaccines to prevent/protect available -appropriate antibiotic therapy is critical
type 1: membrane-acting extracellular toxins
the toxin binds at the host plasma membrane to generate a signal that changes host cell gene expression -Toxin does not enter cell
Type II membrane damaging toxins
toxins disrupt host cell membranes by forming pores or breaking down membrane lipids -results in cell lysis
Type III: Intracellular toxins
binding portion (B) of the toxin binds to the plasma membrane -toxin enters cell, often by endocytosis -active portion (A) enters the host cell and exerts an effect
For a pathogen to establish disease it must first
infect the host
Infectious dose-50 (ID50)
number of pathogens needed to establish an infection in 50% of exposed hosts -more infectious pathogens have a lower ID50 -HOWEVER: highly infectious does not equal especially dangerous
Lethal dose-50 (LD50)
amount of toxin needed to kill 50% of affected hosts that are not treated -lower LD50= higher virulence
ID50 and LD50 can change based on:
-species affected -host's immune fitness -route of exposure
Five steps to infection
enter the host
adhere to host tissues
invade tissues and obtain nutrients
replicate while warding off immune defenses
transmit to a new host
portal of entry
any site that a pathogen uses to enter the host
-determined by the mode of transmission -mucous membranes are the most common portal of entry -maybe site where disease develops (but not necessarily) -some pathogens have >1 portals of entry
Respiratory Mucosa (including ocular)
most common portal of entry -microbes transmitted by CONTACT with mucosa of mouth/eyes/nose or INHALATION of respiratory droplets, aerosols, or dust particles
Skin
largest body system -physical protective barrie -has to be penetrated for infection to occur
GI mucosa
infections frequently due to fecal-oral transmission via contaminated food, water, or fingers
disease may occur elsewhere
Urogenital systems
most STIs are acquired thru mucosa; some through the skin -urinary tract infections often normal flora
parental
introduced directly into bloodstream intravenously or by injection
Transplacental
some pathogens exhibit vertical transmission
spread from mother to developing child in utero
Attachment between pathogen and host dependent on:
Surface molecules on pathogens termed adhesions that bind to specific surface receptors on certain host cells -pili -species and tissue tropism
Pili (fimbriae)
bacterial adhesins that assemble into hair-like appendages and extend from the cell surface; other adhesins are directly associated with the microbial cell surface
Species and tropisms
due to specificity for attachment to a particular host cell surface marker
tropism
Preference of a pathogen for a specific host and/or a specific tissue within the host -Most microbes exhibit some level of tropism, but this factor can change over time -Pathogenic microbes require specific host/microbial features to interact with certain host tissues and establish an infection -Many host factors (i.e., age, gender, overall health, life habits) impact whether infection and/or disease develops
Adherence is Critical for Infection
if adhesins and/or receptors can be altered or masked to interfere with attachment, infection (and therefore disease) can be prevented or controlled
Bacteria alternate between two distinct life phases:
Planktonic (free-floating) -biofilm-associated (multicellular communities of attached sessile cells)
Planktonic bacterial attachment and colonization of surfaces is critical during
the development of a sustainable, persistent population within a mature biofilm