Host-Microbe Relationships Flashcards
Close association and interaction of two dissimilar organisms living together.
Symbiosis
Microorganisms which are normally and consistently found in or on the body in the absence of disease.
Normal flora
association between organisms in which one is benefitted and the other is neither benefitted nor harmed.
Commensalism
both the microbe and host derive benefits from the relationship
Mutualism
disease traits of the resident flora are demonstrated only when normal host-microbe relationship is altered
opportunism
Alterations to the host-microbe relationship are common results from these circumstances:
Prolonged antibiotic therapy alters flora
Traumatic injury, surgery
Immunological compromise
Hormonal or chemical changes
Resident microbe
always present
transient microbe
can be normal, if present, but not always present (environmental, aging/birthing circumstances)
Nature/variety of microbes are often distinctive for different regions of the ____
body
Normal flora of one area may cause ____ of another
infection
symbiotic relationship in which a microorganism lives in or on a host at the expense of the host
parasitism
a carrier of microbes from one host to another
Vector (usually refers to a living entity, but could be non-living)
Vector could be insects/animals or an inanimate object, called a ____
fomite
the growth and spread of a pathogen in or on a host resulting in injury to the host tissue
Infectious dz
a microbe capable of causing disease by invading tissues, producing toxins, or both
pathogen
the degree of pathogenicity
virulence
how easily the microbe survives the normal host defenses and establishes infection
infectivity
Two virulence components
Infectivity
Severity
Modes of transmission
Direct contact
Inhalation
Ingestion
Parenteral
direct contamination of blood, body fluids, or tissues by arthropod and other animal vectors and by nonsterile syringes and needles
Parenteral
Virulence factors
Attachment/Establishment Factors
Antiphagocyctic Factors
“Invasive” Enzymes
Exotoxins
Endotoxins
Genetic Alterations
Special Antimicrobic Resistance Situations
Global & US Antimicrobial Health Threat
enable the establishment of infection
Attachment & Establishment Factors
The organism must enter the correct portion of the body (e.g. ingestion vs. inhalation vs wound), which requires:
(Attachment & Establishment Factors)
overcoming local defenses
Finding the best environment for growth/survival
(portal of entry)
The attachment of the microbe to tissue is required in order to establish a site of infection.
Attachment mechanisms:
(Attachment & Establishment Factors)
fimbrae
surface chemicals
Adhesive Matrix Molecules
attach to specific receptor sites on specific tissue
Attachment & Establishment Factors
fimbrae
Dissolve covering of cells and aid chemical attachment
Attachment & Establishment Factors
surface chemicals
produce biofilm thus providing “protection” for bacteria within harsh human environment
(Attachment & Establishment Factors)
adhesive matrix molecules
a certain minimum number of organisms are required to establish infection – presumably needed to overcome host defenses
(Attachment & Establishment Factors)
Quantity (also a component of a pathogen’s virulence)
various chemicals that (1) restrain the disease-causing actions of the microbe until sufficient quantity of microbes are present, then (2) switch on the disease-causing actions all at once.
(Attachment & Establishment Factors)
Quorum-sensing Regulators
an OPERON
In this attachment/establishment feature, symptoms maybe unnoticed or mild until the bacteria reach a certain number
Quorum-sensing Regulators
an OPERON
prevent microbe from being engulfed and/or destroyed by white blood cell (physical protection or chemical poison)
Antiphagocytic factors
Antiphagocytic factors examples:
Capsule
Coagulase
Leukocidin
Survival of phagocytosis
slippery & slimy nature assists bacteria from being engulfed by phagocyte
(Antiphagocytic factors)
capsule
causes destruction of white blood cells
Antiphagocytic factors
Leukocidin (staphylococci, streptococci, & certain bacilli)
causes fibrin clot to form around the microbes
Antiphagocytic factors
Coagulase (Staphylococcus aureus)
resistance to killing within a phagocyte (e.g. mycobacteria, gonococcus, Listeria)
(Antiphagocytic factors)
survival of phagocytosis
factors that promote the invasion and spread of a pathogen in/on the tissue
enable the pathogen to invade the tissue or the site of infection to spread
“Invasive” Enzymes
“Invasive” Enzymes examples
Collagenase Fibrinolysin/Streptokinase Hyaluronidase Hemolysins Lecithinase Lipase Proteases Super Antigens
breaks down collagen fibers thus destroying tissue integrity
“Invasive” Enzymes
Collagenase
destructive to cell membranes of red blood cells and other tissue cells
(“Invasive” Enzymes)
Lecithinase
breaks down hyaluronic acid in cell membranes
“Invasive” Enzymes
Hyaluronidase
Staphylococcus, Streptococcus, Clostridium perfringens
lyses fibrin in blood clots thus preventing isolation of the infection
(“Invasive” Enzymes)
Fibrinolysin & Streptokinase
dissolve red blood cell membranes
“Invasive” Enzymes
Hemolysins
Staphylococcus, Streptococcus, C. perfringens
digest lipids allowing bacteria to enter
“Invasive” Enzymes
Lipase
digest proteins (e.g. IgA, certain other protective chemicals) thus permitting bacteria to evade entrapment, digestion, etc.
(“Invasive” Enzymes)
proteases
cause exacerbated immune or inflammatory response
“Invasive” Enzymes
Super Antigens
Proteins excreted from the cell that can cause specific and widespread biological effects on the body
Exotoxin
(1) Cytolytic and Receptor-binding proteins (usually)
(2) Many are dimeric: A & B subunits; facilitates entry into tissue cells
(3) Tissues affected are very defined and limited
(4) Superantigens are special group of toxins
(5) Often coded on plasmid or lysogenic phage
exotoxin
Examples of exotoxins
Tetanus neurotoxin (attacks motor nerves)
Staphylococcal enterotoxin (diarrhea, vomiting)
Cholera toxin (diarrhea)
Diptheria toxin (causes overprodcution of mucous blockage of respiratory tract and causes protein production issues in the heart)
Streptococcal erythrogenic toxin (Scarlet fever)
Elicit good, protective antibodies
Exotoxins (due to its protein nature)
the lipopolysaccharide (LPS) component of gram-negative cell walls which is released upon disintegration of the cell
(endotoxin)
Lipid A
Binds to CD14 and TLR4 (Toll-Like Receptor 4) on macrophages, B-cells, other cells.
“Lipid A”
Stimulates production and release of Acute-phase Cytokines, e.g. IL-1, TNF, IL-6 (i.e. it triggers white blood cells to discharge chemicals which induce fever, pain, hemorrhage, blood pressure drop, etc.
“Lipid A”
Not very potent per unit weight; however, very high levels in bloodstream can trigger very large effects including shock and death
“Lipid A”
Because it’s an LPS, lipid “A” doesn’t elict a good…
immune response
Genetic Alterations include:
plasmid
lysogeny
gene recombination
(1) Code for some exotoxins, antibiotic resistance, invasive enzymes, etc.
(2) Transmitted to daughter cells during cell division
(3) Passed to another bacterium during conjugation
plasmid
genetic alteration
Viral DNA incorporated into bacterial DNA
(1) Code for some exotoxins and invasive enzymes
(2) Introduced by viral infection of the bacteria and transmitted to daughter bacterial cells during cell division
lysogeny
Gene recombination – pieces of genetic material from one organism are incorporated into the genetic material of another organism. Results in:
(1) Different (new types) antigens are produced – current immunity not effective (e.g. Influenza virus)
(2) Causes increased resistance to antibiotics
Many bacteria gain antibiotic resistance by:
(a) Mutated genes (“successful” about 1 in 10 billion cell reproductions ?)
(b) Plasmid encoded genes
(c) Lysogenic virus
Presence of an antibiotic-resistant bacterium in the community / hospital leads to:
(a) Survival of the mutant
(b) Increasing numbers of the mutant in the population
(c) Disease problems increase and spread to new geographic locations
Abx-resistant examples
Beta lactamase
MRSA
Carbapenem-resistant enterobacteriaceae-Carbapenemase-producing Enterobacteriaceae (CPE)
Bacterial enzyme which inactivates many beta-lactam antimicrobics (e.g. penicillin, cephalosporin, carbapenem, monobactam classes).
Beta lactamase
Plasmid encoded gene – Frequently carried by Enterobacteriaceae (family of gram-negative bacilli) Staphylococcus, Neisseria gonorrhoeae, Haemophilus influenzae) that frequently produce the enzyme
Beta lactamase
version that affects a larger group of antimicrobics that are typically not affected by typical beta-lactamase
Extended spectrum Beta lactamase
ESBL
Mutated mecA gene – encodes a low-affinity penicillin binding protein (PBP2a)
Methicillin-Resistant Staphylococcus aureus (MRSA)
Consider ____ to be resistant to all beta-lactam antibiotics (e.g. penicillins and cephalosporins regardless of the in vitro lab results.)
MRSA
Mutated genes for outer membrane porins (pore proteins) and PBP transpeptides
A form of beta-lactamase
Carried by plasmids
Carbapenem-Resistant Enterobacteriaceae (CRE) – Carbapenemase-producing Enterobacteriaceae (CPE)
CRE-CPE results in:
Loss of drug diffusion into periplasm
loss of cross-linking activity of PBP
Non-specific Factors
Host Resistance Factors
Innate species immunity/resistance
Physical/mechanical barriers
chemical barriers
phagocytosis
inflammation
(1) Intact skin prevents entry of organism
(2) Mucous membranes – sticky linings trap invading
organisms
(3) Cilia of respiratory tract – move particles to the
throat where they are swallowed
(4) Peristaltic action of gut – moves gut contents at a
slow, steady pace thus preventing overgrowth
(5) Normal flora – occupy attachment sites & compete
for nutrients
Physical/Mechanical Barriers
(1) Acid pH (stomach, skin, vagina, urine) – denatures
most organisms
Exceptions: typhoid & tubercule bacilli, protozoan
cysts, polio & hepatitis A viruses
(2) Bile salts (intestine) – inhibitory to many microbes
(3) Lysozyme (tears, saliva) – digests gram-positive
cell walls
(4) Antimicrobial chemicals from normal flora
(5) Interferon (a type of lymphokine) – human host cell protein(s) produced in response
to invasion by certain viruses. It acts as a local defense against certain viruses by
producing inhibiting substances that “interfere” with viral reproduction.
Chemical barriers
denatures
most organisms
(chemical barriers)
Acid pH (stomach, skin, vagina, urine)
Exceptions to acid pH efficacy
typhoid & tubercle bacilli, protozoan cysts, polio & hepatitis A viruses
Digests gram positive bacteria
chemical barriers
lysozyme
human host cell protein(s) produced in response
to invasion by certain viruses. It acts as a local defense against certain viruses by
producing inhibiting substances that “interfere” with viral reproduction.
(chemical barrier)
interferon (a type of lymphokine)
Paul Revere
moves gut contents at a
slow, steady pace thus preventing overgrowth
(physical/mechanical barrier)
peristaltic action of gut
occupy attachment sites & compete
for nutrients
(physical/mechanical barriers)
normal flora
inhibitory to many microbes
chemical barrier
bile salt
Antimicrobial chemicals from ____
chemical barrier
normal flora
(1) “Foreign” particles are ingested & digested by polymorphonuclear leukocytes, monocytes, and macrophages
(2) Numerous enzymes act to degrade and digest the ingested particles
(3) Local tissue damage may occur due to egestion of waste materials
phagocytosis
(1) Develops after mechanical injury or exposure to certain chemicals
(2) Inflammatory process limits the extent of injury
Inflammation
_____ is formed to enclose the pus (phagocytes, dead microbes, dead tissue cells, plasma)
(inflammation)
Fibrin clot/wall
Increased capillary ____ causes fluid accumulation and influx of phagocytic leukocytes
(inflammation)
permeability
