Lectures 13&14: Pathogenicity of Microorganisms Flashcards
(77 cards)
1
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Parasites are organisms that
A
- Live on or within a host organism and are metabolically dependent on the host
- are any organism that cause disease
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The host is
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larger organism that supports the survival and growth of a smaller organism
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Infection
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- A parasite growing and multiplying within/on a host
- may or may not result in overt infectious disease
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Pathogen
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- Any parasite organism causing infectious disease
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Primary (frank) pathogen
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Causes disease by direct interaction with healthy host
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Opportunistic pathogen
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May be part of normal flora and causes disease when it has gained access to other tissue sites or host is immunocomprimised
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Pathogenicity
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ability to cause disease
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Chain of events for a successful infection
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- agent identitiy
- virulence of agent
- means of exposure to agent
- dose of agent
- susceptibility of host to agen
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infections passed from animal to human are termed
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zoonoses
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What does animate mean
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from other humans or animals
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what does inanimate mean
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from water, soil, and food
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Natural enviromental location in which the pathogen resides
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Reservoir (can be animate or inanimate)
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organisms that spread disease from one host to another
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vector
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infectious disease
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infection with viruses, bacteria, fungi, protozoa, and helminths
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Objective changes in body that can be directly observed
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Signs
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subjective changes experienced by patient
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symptoms
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Set of characteristic signs and symtpoms
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disease syndrome
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Incubation period
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period after pathogen entry, before signs and symptoms
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Prodromal stage
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- Onset of signs and symptoms
- not clear enough for diagnosis
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Period of illness
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- disease is most severe, signs and symptoms
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Convalescence
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Signs and symptoms begin to disappear
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Course of infectious disease
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- Incubation period
- Prodromal stage
- Period of illness
- Convalescence
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Q
A pathogen must contact a host and survive within it to cause a disease. To survive, it needs
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- A suitable environment
- A source of nutrients
- in competition with eukaryotic host cells
- Protection from harmful elements
- virulence factors allow a pathogen to oucompete host cells and resist their defenses
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Q
Some survival strategies for pathogens once in the host are
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- Adhesins
- Enzymes
- Toxins
- Invasins
- Autoinducers
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Virulence factors determine the
degree to which a pathogen causes damage, invasion, infectivity
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What is virulence
degree or intensity of pathogenicity
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Virulence is determined in part by pathogen's ability to
* survive outside of host
* more dependent on host (cannot survive outside of host)= less virulent
*
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What does pathogenicity islands mean
* Major virulence factors on large segments on chromosomal or plasmid DNA
* Increase bacterial virulence
* absent in nonpathogenic members
* common sequence characteristics
* insertion-like seqquences for mobility
* G + C content different from bacterial genome
* several open reading frames
* Can be spread through horizontal transfer of virulence genes to bacteria
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What is the first step in disease
* entrance and attachment
* Portal of entry
* Skin, respiratory, gastrointestinal, urogenital systems, or conjunctiva of eye, parental route (break in barrier defenses)
* Vector borne, sexual contact, blood transfusion, or organ transplant
* Adherence
* medated by special molecules called adhesins
* Colonization
* A site of microbial reproduction on or within host
* does not necessarily result in tissue invasion or damage
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What are the adherence structures of microbes
* Pili or fimbriae (adhesion molecules on bacterium's cell surface) bind complementary receptor sies on host cell surface
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what is microbial colonization site
* Site of microbial reporduction on/in host
* does not necessarily result in tissue damage
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* Adhesin/ligans bind to receptors on host cells
* examples on
* Streptococcus mutans
* Escherichia coli
* Streptococcus pyogenes
* Streptococcus mutans: Glycocalyx
* Escherichia coli: Fimbriae
* Streptococcus pyogenes: M protein
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Examples of microbial attachment mechanisms in Eschericia coli
* Type I fimbrae ( leads to diarrhea and UTI)
* P pili (leads to Hemolytic uremic syndrome)
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Adhesion mechanism of Streptococcus pyogenes
* Protein F (causes strep throat)
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Attachement mechanism of streptococcus mutans
sugar residue/glycocalyx (causes dental caries)
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Infectivity
ability to create a discrete point of infection
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invasiveness
ability to spread to adjacent tissues
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Penetration can be active or passive explain both
* active occurs through lytic substances which
* attack the extracellular matrix and basement membranes of integuments and intestinal linings
* degrade carbohydrate-protein complexes between cells
* disrupts host cell surface
* passive (e.g. Skin lesions, insect bites, wounds)
* spread to deeper tissues involves production of specific products and/or enzymes that promote spreading
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Virulence factor produced by Staphylococcus aureus for bacterial pathogen invasion and dissemination
Coagulase: Coagulates (clots) the fibrinogen in plasma/ The clot protects the pathogen from phagocytosis and isolates it from other host defenses.
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Virulence factor produced by Groups A,B,C, and G streptococci, staphylococci, clostridia for bacterial pathogen invasion and dissemination
Hyaluronidase: hydrolyzes hyaluronic acid, a constituent of the extacellular matrix that cements cells together and render the intercellular spaces amenable to passage by the pathogen
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Virulence factor produced by Staphylococci, pneumonocci, and other streptococci for bacterial pathogen invasion and dissemination
Leukocidins: pore-forming exotoxins that kill leukocytes; cause degranulation of lysosomes within leukocytes, which decrease host resistance
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presence of viable bacteria in the blood
bacteremia
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Pathogens or their toxins in the blood
septicemia
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Invasiveness varies among pathogens. Examples
* Clostridium tetani (tetanus) produces a number of virulence factors but is non-invasive
* Bacillus anthracis (anthrax) and Yersinia pestis (plague) also produce many virulence factors and are highly invasive
* Streptococcus spp. span the spectrum of virulence factors and invasiveness
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what is toxigenicity
ability to produce toxins
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What is a toxin
a specific substance that damages host
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Diseases that result from entry of a specific preformed toxin into host (Ex. Tetanus toxin)
Intoxications
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Toxemia
condition caused by toxins in the blood of host
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Exotoxins
* Soluble, heat-labile, proteins
* secreted into surroundings as pathogen grows
* most exotoxin producers are gram-positive
* often travel form site of infection to other tissues or cells where they exert their effects
* Usually synthesized by specific bacteria that have toxin genes in their plasmids or prophage DNA
* Among the most lethal substances known
* Are highly immunogenic
* Stimulate production of neutralizing Ab (antitoxins)
* Chemically inactivated to form immunogenic toxoids
* e.g. Tetanus toxoid
* do not produce a fever (but they are heat labile)
* LD50 is small
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Types of Exotoxins
* AB exotoxins
* Composed of two subunits
* A subunit- responsible for toxic effect
* B subunit- binds to specific target cell
* Specific host site exotoxins
* Membrane-disrupting exotoxins
* Superantigens
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Botulinum toxin
* Organism:
* Clostridium botulinum
* Gene location:
* Prophage
* Toxin type:
* AB
* Mechanism of Action:
* Blocks neurotransmitter release, leading to paralysis (flaccid paralysis)
* specificially it attacks SNAP25 and Syntaxin and does not allow the Ach to be moved to the synaptic terminal and released into the synaptic cleft
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Tetanospasmin
* Organism:
* Clostridium tetani
* Gene location:
* Plasmid
* Toxin type:
* AB
* Mechanism of Action
* Blocks neurotransmitter, leadin to spastic paralysis
* proteolysis of Synaptobrevin
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Superantigens
* Stimulate about 30% of T cells of the immune system
* Causes the T cells to overexpress and release cytokines
* results in failure of multiple host organs allowing time for the microbe to disseminate
* Example
* Staphylococcal enterotoxin B
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Endotoxins
* Lipopolysaccharide (LPS) in Gram-negative cell wall can be toxic to specific hosts
* called endotoxin because it is an endogenous (part) of the bacterium and released when organism lyses
* some is also released during multiplication
* Toxic component is the lipid portion, lipid A
* Heat Stable (but do produce fever)
* Toxic (nanogram amounts)
* Weakly immunogenic
* Generally similar, despite source
* Cause general system effects
* Fever, weakness, diarrhea, inflammation, intestinal hemorrhage, and fibrinolysis, the enzymatic breakdown of fibrin, the major protein component of blood clots
* Bring about these effects indirectly:
* endotoxin interacts with host molecules and cells, activating host systems
* coagulation, complement, fibrinolytic, and kininogen system
* e.g. interaction with macrophages---\> release of endogenous pyrogen (induces fever)
* e.g. binding to LPS-binding protein ---\> release of cytokines
* tumor necrosis and others lead to septic shock
* LD50 is relatively large
* chemistry:
* lipid
* Source:
* Gram-negative
* Not neutralized by antitoxin
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Mycotoxins
* Secondary metabolites of fungi
* common contaminants of food crops
* Aspergillus flavus and A. parasiticus produce carcinogenic aflatoxin
* Stachybotrys produce tissue-damaging satratoxins
* Claviceps purpurea (ergot) produce hallucinogen lysergic acid (LSD)
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effects of pathogen biofilm growth
* May cause a chronic infection
* increases virulence
* become less sensitive to antibiotics
* make cells in biofilm more resistant to host defense ("frustrates" phagocytes)
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Cell wall components of pathogens that are increase virulence
* M protein resists phagocytosis
* ex. Streptococcus pyogenes
* Opa protein inhibits T helper cells
* Ex. Neisseria gonorrhoeae
* Mycolic acid (Waxy lipid) resists digestion
* Ex. Mycobacterium tuberculosis
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Resisting host defenses
* Production of decoy proteins to bind available neutralizing antibodies
* Lengthened O-chains to prevent host detection or lysis
* some survive inside host cells
* eject themselves form cell to cell using host actin
* ex. Shigella sp. and Rickettsia sp.
* Infection of immune system cells, diminishing function
* Fuse with adjacent cells to prevent exposure to antimicrobial proteins in host
* Capsules prevent phagocytosis
* Mutations change antigenic sites or alter expression of antigens
* thourhg downregulation or phase variation (ex. Altered Pilin protein, N. gonorrhea)
* Produce substances that resemble host tissue
* Produce proteases that degrade host proteins
* Special proteins that interfere with host defenses
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Examples of Capsules and function
* Prevent phagocytosis
* Streptococcus pneumoniae
* Haemophilus influenzae
* Bacillus anthracis
* Staphylococcus aureus
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Pathogen Enzymes
* Coagulase
* Coagulates fibrinogen
* Kinases
* Digest fibrin clots
* Hyaluronidase
* Hydrolyzes hyaluronic acid (found in CT)
* Collagenase
* Hydrolyzes collagen
* IgA proteases
* Destroy IgA antibodies
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Evidence suggests correlation between mode of transmission and degree of virulence
* Direct contact
* less virulent
* Vector-borne
* highly virulent in human host; relatively benign in vector
* Greater ability to survive ouside host
* means more virulent
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What is Tropism
* Tropism
* Pathogen must make contact with appropriate host tissue
* determined by specific cell surface receptors
* (note that transmission alone is not enough for infection to occur)
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What are the five main modes of transmission
* Airborne (indirect)
* contact
* vehicle (indirect)
* vector borne
* vertical
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inanimate materials or objects involved in pathogen transmission
Vehicles
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Fomites
Common vehicle such as surgical instruments, bedding, and eating utensils
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What is the difference between harborage transmission and biological transmission
* Both are types of internal transmission for vector-borne transmission
* Harborage transmission
* pathogen does not undergo changes within vector
* Biologic transmission
* pathogen undergoes changes within vector
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Occurss when the unborn child aquires a pathogen form an infected mother
Vertical transmission
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Examples of congential infection (born with infection)
* gonorrhea (especially in the eyes)
* herpes
* german measles
* toxoplasmosis
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What is infectious dose 50
Dose that causes 50% of the host organisms to become infected
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Infectious dose 50 for Bacillus anthracis in each of the 3 portals of entry
* ID50 through skin:
* is 10-50 endospores
* ID50 through inhalation:
* is 10,000 to 20,000 endospores
* ID50 through GI is 250,000-1,000,000 endospores
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Cytopathology
* Can be used to observe cells in tissue culture for death rates rather than entire organisms
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What are the two main factors of host susceptibility
* Defense mechanisms of host (innate and adapted/acquired immunity)
* Pathogenicity of pathogen
* (note that nutrition, genetic predisposition, and stress also play a role in host susceptibility to infection)
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What are the portals of exit for a pathogen
* Respiratory tract
* coughing and sneezing
* Gastrointestinal tract
* Feces and saliva
* Genitourinary tract
* urine and vaginal secretions
* Skin
* Blood
* biting arthropods and needles or syringes
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