UTA MICROBIOLOGY EXAM 4

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230 Terms

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disease
a condition where normal structure and/or function are damaged or impaired
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infection
invasion of pathogen or parasite that lead to disease
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signs
things that can be directly measured by clinician (ex: blood cell counts)
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symptoms
things felt by patient that cannot be clinically measured (ex: nausea)
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syndrome
groups of signs and symptoms that help indicate a particular disease
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asymptomatic/subclinical
only signs can be observed through correct testing (ex: patient with herpes and no symptoms)
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International Classification of Diseases (ICD)
World Health Organization codes that are used globally to classify and monitor diseases
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infectious
disease caused by direct effect of a pathogen
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communicable
capable of spreading person-to-person
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contagious
easily spread
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iatrogenic
acquired as result of medical procedure
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nosocomial
acquired from hospital setting
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zoonotic
acquired from animal
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non-communicable
obtained from non-living thing such as soil or contaminated object
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non-infectious
not caused by pathogen
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malaria
- communicable
- infectious
- zoonotic
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sickle cell anemia
- non-communicable
- non-infectious (genetic)
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5 stages of infectious disease
1. incubation
2. prodromal
3. illness
4. decline
5. convalescence
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incubation
initial entry of pathogen; replication begins
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prodromal
replication continues; host shows signs and symptoms
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illness
signs and symptoms are most severe in host
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decline
pathogen number starts to decrease; host's immune system is weak and vulnerable to secondary infection
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convalescence
host starts to recover
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acute disease
relatively short (hours, days, week)
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chronic disease
longer time (months, years, lifetime)
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latent disease
comes in episodes; pathogen replicates when disease is active
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Koch's postulates
set of standards that must be met to demonstrate that X pathogen causes X disease
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Koch's postulates
1) The suspected pathogen must be found in every case of disease and not be found in healthy individuals.

2) The suspected pathogen can be isolated and grown in pure culture.

3) A healthy test subject infected with the suspected pathogen must develop the same signs and symptoms of disease as seen in postulate 1.

4) The pathogen must be re-isolated from the new host and must be identical to the pathogen from postulate 2.
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Koch's assumptions (WRONG)
1) Pathogens are found only in diseased individuals.

2) All subjects are equally susceptible to infection.

3) All pathogens can be grown in culture.
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Molecular Koch's postulates
identifies gene instead of pathogen; improved postulates that overcame some of Koch's limitations
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Limitations of Molecular Koch's postulates
1. genetic manipulation of some organisms isn't possible with current techniques
2. some diseases do not have suitable animal models
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pathogenicity
ability of a pathogen to cause disease
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virulence
degree of pathogenicity
ex: highly virulent - Bacillus anthracis induces severe signs and symptoms
ex: low virulent - Rhinovirus induces low signs and symptoms
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virulence curve
how virulence can be modeled in controlled experiments
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median infectious dose (ID50)
number of pathogens required to infect 50% of those inoculated
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median lethal dose (LD50)
number of pathogens required to kill 50% of those infected
- LD50 is 10^4 pathogen cells or virions
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primary pathogen
can cause disease in a host regardless of the host's resident microbiota or immune system
ex: enterohemorrhagic E. coli (mainly due to Shiga toxin)
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opportunistic pathogen
can only cause disease in situations that compromise the host's defenses (protective barriers, immune system, or normal microbiota)
ex: Candida albicans with disrupted microbiota
ex: UTI caused by E. coli
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influencers of susceptibility
drugs, resident microbiota, genetics, & age
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5 stages of pathogenicity/infection
1. Exposure to host
2. Adhesion
3. Invasion
4. Infection
5. Transmission
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exposure (contact)
can occur in many ways: pathogens must be exposed to portals of entry to begin adhesion
- some portals are worse than others (ex: mucosa)
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TORCH infections
pathogens that can cross placental barrier as portal of entry
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Torch
toxoplasmosis --\> Toxoplasma gondii (protozoan)
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tOrch
syphilis --\> Treponema pallidum (bacterium)
chickenpox --\> Varicella-zoster virus (human herpesvirus 3)
hepatitis B --\> Hepatitis B virus (hepadnavirus)
HIV --\> Retrovirus
fifth disease (erythema infectiosum) --\> Parvovirus B19
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toRch
rubella (german measles) --\> Togavirus
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torCh
cytomegalovirus --\> Human herpesvirus 5
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torcH
herpes --\> herpes simplex virus (HSV) 1 & 2
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adhesion
pathogens' varying capability of colonization
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adhesins
molecules/structures that bind to certain host receptors
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biofilm
production of community glycocalyx
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invasion
occurs when colonization is established; pathogens generally produce toxins to allow further colonization into body/tissue and protection from immune system
- virulence plays a role in degree of invasion
ex: Helicobacter pylori urease production
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intracellular pathogens
invade via endocytosis and evasion of host immune defenses
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invasion mechanisms
1. Effector proteins are secreted to trigger entry - membrane ruffling
(ex: Salmonella and Shigella spp.)

2. Surface proteins allow for binding to host cell (trojan horse approach)
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Phagolysosome survivors
- Listeria monocytogenes
- Mycobacterium tuberculosis
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local infection
small area of body
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focal infection
pathogen or toxin spreads to secondary location
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systemic infection
occurs throughout body (ex: septicemia)
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primary infection
can lead to secondary infections of different pathogen
ex: HIV lowers immune system and opens door for yeast and others; rhinoviruses can lead to bacterial pneumonia
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transmission
persistence passes on pathogen onto a new host through a portal of exit
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virulence factors
pathogen product that assists in ability to cause infection and disease
- dictate how severe and extensive a disease is; some have more than one
ex: adhesion factors, exoenzymes, toxins, immune evasion
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adhesins
proteins that aid in attachment to host cell receptors
- found in ALL microbial types (viral, fungal, bacterial, etc.)
- commonly found on fimbriae or pili
- can initiate biofilm formation in some species
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-emia
presence of pathogen in blood
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bacteremia
bacteria in blood
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viremia
viruses in blood
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toxemia
toxins in blood
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septicemia
bacteria present and multiplying in blood
- patients with septicemia (septic) can lead to shock (life threatening disease in BP)
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exoenzymes
extracellular enzymes used to invade host tissues
- glycohydrolases, nucleases, phospholipases, proteases
ex: collagenase produced by C. perfringens causing necrosis and gas gangrene
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toxins
biological poisons that assist in ability to invade and cause tissue damage (toxigenicity)
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endotoxins
lipopolysaccharides that triggers host inflammatory responses; can cause severe fever and shock
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exotoxins
proteins mostly produced by Gram (+)
- targets receptors in specific cells
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detectors of endotoxins
1. Limulus amebocyte lysate (LAL) test
2. Enzyme-linked immunosorbent assay (ELISA)
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LAL test
blood cells of the horseshoe crab mixed with patient's serum; observed chromogenically or by coagulation
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ELISA
uses antibodies to detect endotoxins
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intracellular targeting
a division of exotoxins with A & B regions for activity and binding
ex: diptheria and botulinum toxin
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membrane disrupting
division of exotoxins aka phospholipases that degrade bilayer membrane
ex: Bacillus anthracis and Rickettsia spp.
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hemolysins and leukocidins
membrane disruptors that can target RBC, WBC, and other cells
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superantigen
division of exotoxins that trigger excessive production of cytokines by immune cells
ex: Staphylococcus aureus and Toxic Shock Syndrome
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host evasion
mechanisms to evade phagocytosis
ex: capsules that enlarge bacterial cell so phagocytes cannot engulf pathogens
ex: proteases digest host antibody molecules
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antigenic variation
alteration of cell surface proteins to hide from immune cell recognition (example of host evasion mechanism)
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antigenic drift
result of point mutations causing slight changes in spike proteins (H & N)
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antigenic shift
major change in spike proteins due to gen reassortment
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virulence in fungi
Many properties similar to bacteria; adhesins, proteases, and toxins
ex: Capsule (+) Cryptococcus spp. can cause pneumoniae and meningitis
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mycotoxins
fungal toxins produced by Claviceps purpurea and Aspergillus spp. that contaminate grains and other staple crops
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virulence in protozoans
have unique features for attachment
ex: Giargia lamblia uses adhesive disk of microtubules to attach to intestines
ex: Plasmodium falciparum quickly changes adhesive protein for RBCs to avoid immune recognition; causes chronicity in malaria patients
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virulence in helminths
tissue penetration commonly achieved with proteases (worms that burrow into skin)
ex: roundworms produce cuticle to last longer against host defense assaults
ex: Schistosoma mansoni degrades host antibodies to halt immune defense
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"Glycan gimmickry"
mimic host cells to evade immune system
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epidemiology
field that studies distribution and timing of diseases (infectious and non-infectious)
Determines:
1) Etiology
2) Transmission
3) Susceptible populations
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morbidity
number of individuals with disease
rate calculation: \#/population
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mortality
number of deaths from disease
rate calculation: \#/population
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prevalence
number of individuals at certain time
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incidence
number of new cases
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4 patterns of incidence
1. Sporadic
2. Endemic
3. Epidemic
4. Pandemic
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sporadic
occurs occasionally without regional concentration
ex: tetanus, rabies, plague
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endemic
constantly present in certain region
ex: malaria, ebola, chickenpox
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epidemic
larger than normal amount of cases
ex: influenza, west nile
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pandemic
epidemic that is cross continental
ex: virulent influenza, ebola, etc.
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etiology
determining the causative (etiological) agent of infectious disease; epidemiology helps provide clues and the standard procedure is Koch's postulates
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CDC (Center for Disease Control)
protects public from disease/injury by providing physicians and health-care workers with updates on public health issues & latest data on notifiable diseases
ex: publication of the MMWR (Morbidity and Mortality Weekly Report)
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NNDSS (National Notifiable Disease Surveillance System)
system where all cases must be reported by physicians; these studies track notifiable diseases to determine risks
ex: west nile, HIV, measles, etc.
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John Snow
British physician and father of epidemiology; his study led to the discovery of the contaminated water pump that was responsible for the 1854 cholera London epidemic