Infection - CH. 9 Flashcards
Commensalism
Colonizing bacteria obtain what they need without host body being affected.
Portals of entry
Parenteral
Direct Contact
Ingestion
Inhalation
Communicability
Ability to spread from one individual to others and cause disease
Infectivity
Ability of pathogen to invade and multiply in host.
Virulence
Degree to which a microorganism is capable of causing infectious disease
Adhesion
Prevents pathogens from being swept from the body
Mechanisms of adhesion
Slime layer
Proteins (COVID-19 spike protein)
Pili or fimbriae
Biofilm
Community of bacteria that colonize together within a sticky web of extracellular material biofilms
Protects from antibiotics and host elimination
First stage of infection
Colonization
Mechanism of action
How microorganism damages tissue
Toxigenicity
Ability to produce soluble toxins or endotoxins, factors that greatly influence the pathogen’s degree of virulence
Endotoxins
LPS contained in the cell walls of gram-negative organisms released during cell destruction that activate the inflammatory response, immune, response, and produce fever (pyrogenic)
Exotoxin
Enzymes released during growth of the bacteria, can damage the plasma membranes of host cells or can inactivate enzymes critical to protein synthesis.
Stages of Infection
Exposure
Incubation
Prodromal
Acute stage (invasion)
Convalescent
Resolution
Exposure period
Host exposed and infected by infective agent
Incubation period
Begins active replication - asymptomatic
Prodromal stage
Generic symptoms appear and pathogens continue to multiply
Acute Stage (Invasion)
Maximum impact of infectious process
Convalescent Stage
Containment, repair of tissue
Immune system successfully removes pathogen and symptoms decline
Resolution stage
Total elimination of pathogen from body
What happens during acute stage?
Proliferation and dissemination of pathogen - invading further w/larger impact
Production of toxic byproducts
Inflammatory and immune responses triggered
SPECIFIC symptoms
Staphylococcus, Streptococcus, TB
Toxins alter function for immune system to fight off or resist immune defenses
Bacterial growth phases
Initial lag phase
Log phase
Stationary phase
Death/spore formation
Spores
Dehydrated structures that represent a formant or nonvegetative state of a bacteria
Formed during nutrient deprivation/harsh condition
Highly resilient, can survive for centuries
Germinate to VEGETATIVE state when water and nutrients are available
Escherichia Coli
Causes UTIs
Salmonella
Self-limiting gastroenteritis
Enteric typhoid fever
Pyogenic cocci
Bacteria that can cause fever and suppurative infections
Spirilla
Helicobacter pylori causes most peptic and duodenal ulcers
Pseudamonas
Frequent cause of hospital based post-surgical pneumonia and UTIs
Staphylococcus aureus
Produce systemic infections such as pneumonia, septic arthritis
Can cause: impetigo, furuncles, carbuncles
Impetigo
Usually appears as red sores on the face. Burst and develop honey-colored crusts
In children, commonly seen on child’s nose and mouth, hands and feet.
Furuncles
Skin abscesses that involve a hair follicle and surrounding tissue (boils)
Carbuncles
Red, swollen, and painful cluster of boils that are connected to each other under the skin
Streptococcus pyogenes
Can cause acute pharyngitis (strep throat)
Streptococcus pneumoniae
Most common cause of pneumonia and otitis media
Gut barrier failure
Decreased perfusion of gut -> Flora bacteria escape into outside fluid -> Inflammatory response -> vasodilation -> shock
Septicemia
Proliferation of bacteria in the blood
Gram - release endotoxin and gram + release exotoxins that cause excess of cytokines (TNF-a, IL-1, IL-6, ROS)
Septic shock
Most common vasodilatory shock
Symptoms of gram - septic shock produced by endotoxins
Symptoms of septic shock
Vasodilation, edema, third spacing, fever, increased WBCs, flushed skin, personality changes
Multiple organ dysfunction
Progressive dysfunction of two or more organ systems from uncontrolled inflammatory response to severe illness or injury
Characteristics of a virus
Protein coat (capsid) surrounding nucleic acid core
No metabolic enzymes of their own
Insert their genome into a host cell’s DNA
Use that cell’s metabolic machinery to make new viruses
Viral Replication – Early phase
Viral recognition of host target cell
Attachment to host cell
Penetration of host cell membrane
Release and uncoating of viral genome into a host cell’s cytoplasm
Viral replication - Late phase
Viral genome transcription
Synthesis of viral structural components
Assembly of new viral particles - capsid
Release of new viruses from the host cell
Eclipse period
Period of time from viral uncoating to release of new viruses, during which the virus loses its infectivity
Latent Period
Time during which extracellular viruses cannot be detected; includes eclipse period and ends with release of new virus from infected cells
Antigenic drift/shift
Viral mutation
Mutations constantly occur due to rapid rate of division.
Latent viral state
Virus is never eliminated - is harbored in the body in an inactive state but can be reactivated by stressors
Measles
Enters through oropharynx
Enters blood after 5-7 days and spreads to body surfaces
Virus replicates in tissues causing URI symptoms
End of overt symptoms, person sheds virus and is highly contagious
ABs are produced but absorbed quickly by viral particles
Common Cold
Most common RI
Rhinovirus: portal is nasal mucosa and conjunctiva
Spread person/person
Incubation: 5 days
Rhinorrhea, sinusitis, pharyngitis, laryngitis, headache
Flu/Influenza
Orthomyxoviridae family: A, B, and C
Inhalation of droplet nuclei or direct contact
More contagious than bacterial RI
Damages epithelial cells of respiratory tract by undergoing necrosis and ECF leaks out.
Influenza symptoms
Abrupt onset of symptoms
Severe body aches, fever, anorexia, headache, malaise, and a dry cough
If in lower RT = viral pneumonia
Fungi
Large microorganisms with rigid chitin- or cellulose-based cells walls
Diseases caused by fungi
Mycoses (yeasts or molds)
Where are most fungal infections located
Surface of the body
Dermatophytes
Fungi, cause athlete’s foot and ringworm
Pathogenicity of fungi
Adapt to host environment
Parasitic microorganism range
Unicellular protozoa to large worms
Method of infection - parasites
Vectors or through contaminated water/food
Protozoa
Malaria, amoebic dysentery, giardiasis, plasmodium
Helminths
Roundworms, tapeworms, flukes
Arthropods
Ticks, mosquitoes, mites, lice, fleas
Fever
Hallmark of infectious diseases
Reset hypothalamus = body temperature increases
Can be caused by exogenous and endogenous pyrogenes
Specific
Reflects site of infection
Nonspecific
Can be shared by a number of diverse infectious diseases
Obvious
Predictable patterns
Covert
May require lab testing to detect
Serology
Detection of characteristic antigens/antibody
Bacteriostatic
Inhibit growth until the microorganisms are destroyed by the individual’s own protective systems
Antibiotic methods
Inhibit synthesis of cell wall
Damage cytoplasmic membrane
Alter metabolism of nucleic acid
Inhibit protein synthesis
Modify energy metabolism
How do bacteria fight against antibiotics
Inactivating antibiotics
Changing antibiotic binding sites
Using different metabolic pathways
Changing their walls to keep antibiotics out
Antiviral agents kill viruses by blocking
Viral RNA or DNA synthesis
Viral binding to cells
Production of the protein coats (capsids) of new viruses
