Test 3 Flashcards
Vectors
“zoonosis”
- disease of animals transmissible to humans
- can be direct or indirect transmission
Reservoirs
Hold pathogen between infections
- vectors, vehicles, and fomites can be reservoirs if pathogen survives in/on them and infects many individuals over time
- carriers
- always indirect because individuals are not sick
Direct transmission
Diseased and those they infect are in the same place at the same time
Must stay warm, if cook and dry no longer direct transmission
-touching
-respiratory droplets (if they remain suspended and moist)
-sexual contact
-bites (only if thing that bites you has the same disease that you get - pass same disease via bite)
-kissing
-fecal contact
Indirect transmission
Diseased not in the same place and time with those they infect
-vehicles, fomites, vectors
Vehicles
Anything taken into body voluntarily that pathogens can hitch a ride on
- contaminated food, water, air (dust)
- pathogens in dust use air to transport
Fomites
Inanimate objects
-fork, knife, spoon, table
Vectors
Living organisms (not diseased) -mosquitos carrying Zika, flies, mites, ticks
Carriers
Ex. of reservoir
Asymptomatic infected individuals who infect many overtime
-transmit directly or indirectly
-“all carriers are reservoirs but not all reservoirs are carriers”
5 stages of disease
- Incubation
- Prodromal
- Acute
- Decline
- Convalescence
Incubation phase
No symptoms, pathogen is in body and growing, immune system hasn’t recognized pathogen yet
-can be used to determine when someone should come out of quarantine
Prodromal phase
First vague symptoms appear: fever, malaise, lack of appetite)
Acute phase
Recognizable, severe symptoms
-usually when diagnosis occurs
Decline phase
Pathogen and symptoms are “declining” recognizable symptoms are still there but become less severe or less frequent
Convalescence
Symptoms gone, strength/stamina diminished
-dont have specific symptoms, but have overall weakness
Acute disease
- rapid onset (incubation and prodromal are short)
- Severe symptoms - peak of cut period has characteristic “crisis point”
- rapid recovery
Crisis point
- point during acute disease where symptoms are the worst
- if an individual is going to die they are most likely to die during this phase
Chronic disease
- delayed onset
- less severe symptoms - no crisis point, gradual transition between acute and decline
- prolonged recovery (ex. with tuberculosis, lungs will always be somewhat immunocompromised)
- never leave convalescence stage
Primary disease
- occurs in previously healthy individuals
- can make someone sick even if you are not immunocompromised
- ex. flu, strep
Secondary disease
- “piggy back” another disease, due to immunocompromised host
ex. flu (primary), pneumonia (secondary) - almost never occur on their own
- could be same pathogen gaining strength or spreading to another location (sequelae)
Sequelae
Type of secondary disease
Same pathogen gaining strength or spreading to another location
ex. scarlet fever (strep with rash) - if strep is left untreated, makes toxin that causes rash, if still gone untreated can get in blood and infect heart and kidneys
Nosocomial infection
- acquired in health care setting
- 40% of hospital deaths are from nosocomial infections
- ex. MRSA, VRE, C. Dif
Local infection
Pathogen remains at portal of entry
ex. strep, skin anthrax
Systemic infection
Spread throughout system or entire body
Septicemia
Specific type of systemic blood infection (systemic infection involving the blood)
Bacteriocemia
Specific type of septicemia
Bacteria in blood
Viremia
Specific type of septicemia
Virus in the blood
Fungemia
Specific type of septicemia
Fungus in the blood ex. yeasts
Focal infections
- internal site of further spread
- re-localization of widespread pathogen
Endemic
Disease that exists at stable, predictable levels
ex. common cold, chicken pox
- can be high or low incidence as long as numbers are steady
Epidemic
“outbreak”
- high number of cases in one place at one time
ex. TSS in women using super absorbent tampons
Pandemic
Global epidemic on 2 continents or more at the same time
Examples of specific secondary disease
Sequelae, nosocomial
Level 1 defense
Skin
- non specific (helps protect against any pathogen)
- non solicited (surfaces have these defenses in place 24/7, 365)
Level 2 defense
Within the wall defenses
-non specific, semi-solicited (defenses that are always present but change activity in response to pathogen ex. phagocytic WBS…there are always some in the blood but numbers increase when pathogen detected)
Level 3 defense
Final defenses (throughout)
- specific (geared toward 1 protein in/on the pathogen)
- solicited (only made when the pathogen is present)
Correct entry - pathogen attack
- Portal and dose
- Most have to come in the correct portal or else won’t cause disease
- have to usually have multiple organisms to get sick
Pathogen physical weapons
- adhesion
- fimbrae
- capsules
Adhesion
viruses and bacteria
-ligands (adhesins)
Fimbrae
Fimbrae help with adhesion to linings
Capsules
adhesion, neutralize drugs, avoid phagocytosis, delay immune response to pathogen by masking bacteria surface
Chemical weapons bacteria use to attack your body
enzymes of pathogens that alter substrate in host tissue
toxins
How are flagella used to penetrate tissues
Flagella in combination with invasion to allow penetration into tissues
Allow bacteria to go right through the middle of the cell
ex. syphilis, borrelia
bacteria can go from local to septicemia to focal
Coagulase
- Forms clots
- Localizing enzyme - helps pathogen form local infection
- can protect pathogen while it reproduces
(strepto) kinase
- dissolves clots
- allows septicemia (spread into blood stream)
Hyaluronidase
- digests hyaluronic acid “cell cement”
- allows bacteria to spread between cells
Collagenase
-breaks down collagen
-works with hyaluronidase to spread into tissues
Benefit: avoids, WBC’s and dangerous chemicals even though is slower spread through adjacent tissues
Leucocidin
- kills white blood cells, causes them to take on water and die
- contributes to pus formation
M-protein
- structural protein embedded in cell membrane
- prevents WBC’s from being able to grab and eat bacteria
Hemolysins
Enzymes that selectively cause lysis of red blood cells
- reduce O2 and increase CO2 for microaerophiles
- release protein, iron for nutrients
Digestive enzymes
- pathogens use you for food
- proteases, lipases, amylases
Toxins
Affect functionality of host tissue
-2 general categories: endo and exo
Exotoxins
- all proteins excreted from living cell (bacterial cell is still alive)
- both Gr- and Gr+produce exotoxins
- effects: specific cells/tissues
- effects seen in acute phase
Immune response to exotoxins
Antitoxins - antibodies produced by the body
Toxoid
Production possible by denaturation, to be used as a vaccine
ex. tetanus shot is a toxoid
Types of exotoxins
- cytotoxins
- enterotoxins
- neurotoxin
Cytotoxins
- directly kill cells
- bind to any nearby cell membrane causing it to take on water and lyse
- cause lesions
- benefit to bacterium: nutrients from host cell
Enterotoxins
- affect digestive tract (usually intestines)
- effect: fluid loss from cells and/or increased peristalsis
- results: diarrhea, cramping, nausea
- staph, cholera, e. coli, salmonella
- benefit to bacterium: allows quick spreading of pathogen
Neurotoxin
Affect nervous system
- botulism
- tetanus
Botulism causes what type of paralysis
Flaccid
Tetanus causes what type of paralysis
Rigid
Mechanism of action of botulism toxin
- prevents vesicles of NT from fusing with membrane and releasing NT
- no muscle contraction occurs = flaccid paralysis
- outbreak caused by: preformed toxin, in anaerobic conditions with a lot of protein: canned foods (beans)
- symptoms: slurred speech, relaxed facial muscles, blurred vision
Infant botulism
Caused by botulism spores, can colonize anaerobic pockets of intestines. Adult bodies have gut flora which can kill the spores whereas baby intestines are not fully colonized yet
Botox
potent botulism toxin, injected into face to cause paralysis
Mechanism of tetanus toxin
- binds to nerve ending
- prevents inhibitory neuron neurotransmitter release
- muscles fail to relax = rigid paralysis
What phase would the effects of exotoxins be seen?
Acute phase
What phase would the effects of endotoxins be seen?
End of decline/maybe into convalescence
Endotoxins
- lipids - do not trigger specific immune response
- –cannot be made into vaccines bc can’t be denatured! (no toxoid possible)
- located in LPS layer of cell wall (only gr- have LPS layer)
- produced by Gr- cells only
- released only when the cell dies
- systemic effect (widespread)
- fever, inflammation, BP drop, shock, blood coagulation
Viral cytopathic effects
Viral infected cell abnormalities visible through microscope biopsies/cultures
-may often be enough to be diagnostic
Syncytium formation
- CPE
- Adjacent cells merge into a continuous mass
- big blob of cytoplasm with multiple nuclei
Multi-nucleated cells
- CPE
- cells contain more than 1 nucleus
- when mitosis occurs without cytokinesis
ex. herpes
Inclusion bodies
- CPE
- Clumps of host cell organelles, or viral products seen inside cells
Nucleomegaly
- CPE
- bigger nuclei inside cells
Enlargement
- CPE
- cells get significantly larger
Rounding
- CPE
- cells go from flat to spherical, and turn lose from neighbors (disrupts protective layer)
- effect that leaves you vulnerable to secondary infections
Level 1 defense
- found on the surface
- non specific - help protect against any pathogen (bacteria, fungi, viruses)
- non-solicited - surfaces have these defenses in place 24/7, 365 and don’t need to be triggered
Level 2 defenses
- beneath the surfaces
- non specific
- semi solicited - defenses that are always present but change activity in response to pathogen ex. phagocytic WBC’s (they are always in the blood but if a pathogen is detected more will be made)
Level 1: skin defenses
- close fitting cells - prevent bacteria from getting through
- skin is dry - bacteria can’t grow well in dry conditions
- keratin - prevents skin from tearing
- salt and sebum - gets rid of bacteria via osmotic pressure and antibacterial oil respectively
- lysozyme and defensins - antibacterial
- epidermis and dermis - multilayered, a lot of layers for bacteria to get through
- sloughing - old layers of skin falling off
- normal flora - good bacteria that outcompete bad for food
- hair - help protect surfaces like eyes
Level 1: respiratory defenses
- hair turbines
- cough, sneeze reflexes
- ciliary escalator
Level 1: eyes
- blinking reflex
- eyelashes
- tears
- lysozyme in tears
- saltiness of tears
Level 1: mouth
- lysozyme in saliva
- digestive enzymes
- normal flora
Level 1 urinary tract: Male and F
-flushing of urine
Level 1 reproductive tract F
- low pH
- ciliary escalator
- vaginal normal flora
Level 1: digestive tract
- peristalsis
- mucous (lysozyme)
- normal lora
Phagocytosis what level of defense?
Level 2
Neutrophils
Carry out phagocytosis
-work in bloodstream and tissues
Monocytes
Only called this when they are in the blood stream
-phagocytosis
Macrophage
A monocyte that has moved into a tissue and differentiated.
-phagocytosis
Kuppfer cells
Monocyte that has moved into a tissue and differentiated into a macrophage that has then differentiated into a liver macrophage
-phagocytosis
Microglial cells
monocyte that has moved into a tissue and differentiated into a macrophage that has then differentiated into a brain tissue macrophage
- only ones that have pseudopods
- phagocytosis
Dendritic cells
- phagocytosis
- specialize in epithelial and endothelial
- have long thin pseudopods
- type of macrophage
- protect coverings and linings
What chemical weapon would allow the pathogen to enter the bloodstream and spread rapidly throughout the body?
(strepto) kinase
What chemical weapon might allow a microaerophilic pathogen to adjust the body’s tissues to favor its reproduction?
Hemolysin – ruptures red blood cells to prevent the arrival of O2 and removal of CO2 in the tissues
If Aubrey inhales bacteria, what hair-like structure might allow the pathogens to cling to her
respiratory mucosa?
Fimbrae
Exotoxins are _____ molecules while endotoxins are _____
proteins; lipids
What specific toxin type causes cell death and necrosis?
Cytotoxins
All ____ are ____, but not all ____ are _____.
a. Septicemia, systemic diseases ; systemic diseases, septicemia
b. reservoirs, carriers ; carriers, reservoirs
c. secondary diseases, sequalae ; sequelae, secondary diseases
d. bacteremia, septicemia ; septicemia, bacteremia
a or d
Scrub typhus is a disease normally seen in bats, but humans entering caves can become infected if they breathe in bacteria from the bats breath “misting” down as they fly overhead. The disease is said to be a(n)________, and the infection route would be: ________
Zoonosis, direct
Antitoxins are _______, while toxoids are _____, but BOTH are ________.
a. Protein ; lipid ; toxins
b. Made in the body ; made in a laboratory ; able to prevent disease symptoms from occurring
c. Lipid ; protein ; endotoxins
d. Secreted ; a part of the bacterial cell wall ; found in response to endotoxins
B
Adult botulism and infant botulism differ in that:
Adult botulism is a food intoxication, infant botulism is a food infection
If the organism may exist harmlessly in the throat, but can become pathogenic when your immune system is lowered, what term describes the organism?
Opportunistic
What virulence factor would be most likely to allow the bacteria to spread into the bloodstream?
Kinase
What term SPECIFIC TIMING word describes the meningitis, following the earlier URI?
Sequelae
What are the GENERAL and SPECIFIC terms for this virulence factor that is responsible for the life-threatening diarrhea seen in the disease?
enterotoxins and exotoxins
If this human pathogen also causes disease in mammals in nature, what term describes this disease?
Zoonosis
Severity and progression refer to
Acute v. chronic
Timing refers to..
primary v secondary
specific secondary = sequelae, nosocomial
Location refers to
Local v systemic v focal
- spec. type of systemic = septicemia
- –spec types of septicemia = bacteriemia, viremia, fungemia
patterns in population refers to
endemic, pandemic, epidemic
Steps in phagocytosis
- WBC find target by taxis
- Pseudopods surround particle and secrete alert signal
How do WBC’s find their target
Taxis
All WBC’s must have
lysozyme, acids, superoxide, digestive enzymes
Phagolysosome
Fusion of phagosome and lysosome
-digest material, or eject it
