Unit 3 Flashcards
Endemic vs Epidemic vs Pandemic
Endemic: constant, always in the community, localized (STI’s)
Epidemic: outbreak within a country
Pandemic: cross-continental outbreak (COVID)
Acute vs Chronic vs Latent
Acute: Short (Incubation, prodromal, illness, decline, convalescence, recovery)
Chronic: Long lasting (Incubation, prodromal, illness)
Latent: Dormant until its not (Incubation, prodromal, illness, decline, convalescence, latent period, illness…etc)
Signs vs Symptoms
Sign: measured/seen (cough, vomiting, rash, etc.)
Symptom: how one feels (headaches, body aches, fatigue)
Primary vs Secondary infections
Primary: weakens the immune systems (AIDS)
Secondary: opportunistic, usually cause death (Tuberculosis)
Bacteremia vs Sepsis
Bacteremia: bacteria in the blood
Septicemia: bacteria growing in the blood
Reservoir
Where the microbe is naturally found
- Living: humans, animals (zoonosis), arthropods (mosquitos, ticks, fleas)
- Nonliving: soil, water, air
Portal of Entry
Microbe getting inside the host
- Mucus membranes: respiratory, gastrointestinal, genitourinary, conjunctiva
- Parenteral: punctures, any break in the skin
- Skin: microbe burrows through the skin (helminths)
Pathogen Transmission
Reservoir to the host
- Direct contact: person-to-person, droplets (coughing, sneezing), vector (biological-> bites, mechanical-> touching) (arthropods)
- Indirect contact: Fomites (inanimate objects), vehicles (food, water, air, soil)
“fecal-oral route” not a category, but can be added to further describe transmission.
Normal Flora
Long time, no harm, “good” bacteria
Transient flora
short term, pathogenic, “bad” bacteria
Microbial antagonism of normal flora
Normal flora compete with transient flora for space and nutrients
Bacterial Adhesins
Attach to host glycoproteins
Fimbriae, pili, biofilms
Bacterial Invasion
Membrane Ruffling: bacteria induces endocytosis and enters host cell
Bacterial Evasion
- Antiphagocytic structures: capsules, waxes (mycolic acid TB)
- Antigenic variation: changes how it looks
- mimicking host cells
- Hiding inside phagocytes
Enzymes that help bacteria
- Hyaluronidase: breaks down hyaluronic acid (holds together connective tissue)
- Kinase: breaks down blood clots
- Coagulase: forms blood clots
- IgA protease: breaks down antibodies (specifically IgA)
Host cell damage
- Siderophores: steals host nutrients (usually iron)
- Endotoxin
- Exotoxin
Endotoxin
- Shed LPS
- Only and ALL gram negative
- unintentional
- fever (IL-1), inflammation, septic shock
- systemic
- toxic at high amounts (low toxicity)
Exotoxin
- secreted proteins
- both can make (usually gram +)
- Intentional
- cell specific (usually target the plasma membrane)
- localized
- toxic at low amounts (high toxicity)
Lysogenic conversion
process through which a bacterium gains the ability to produce an exotoxin through bacteriophage
1. cholera 2. botulism 3. diphtheria
Viral attachment
spikes that attach to specific receptors
Viral entry
- Invasion: enveloped fusion, endocytosis
- Evasion: envelope-> camouflage
Viral Evasion
- envelope: camouflage
- antigenic variation
- Genetic shift: genetic re-assortment, segmented (major changes)
- Genetic Drift: mutations over time (small, longer changes)
- Latent
Viral cytopathic effects
- syncytia: host cell membrane fusion (evasion tactic)
- Transformation: virus induces rapid uncontrolled cell growth (cancer) (oncogenesis)
- Inclusion bodies: masses of proteins
DNA
- slower replication
- slower transmission
- bigger genome (ds)
- usually chronic or latent
- less mutations
RNA
- quick replication
- quick transmission
- smaller genome (ss)
- usually acute
- more mutations
- more likely to be zoonosis
Prions
- infectious proteins
- brain shrinkage and deterioration
- occurs rapidly
- same symptoms as Alzheimer’s
- can spread in the body
Lyme disease
- Gram stain: negative
- morphology: spirochete
- motile?: yes
- unique structures: slowing growing, LPS endotoxin, systemic and chronic, antigenic variations
- Reservoir: rodents, white footed mouse, deer (zoonotic)
- Transmission: vector, black legged tick (parenteral)
- signs: fever, swollen lymph nodes, bullseye rash
symps: chills, numbness, fatigue - Px: avoid tick bites
- Tx: tetracyclines
- “Endemic”
Necrotizing Fascitis: Streptococcus pyogene
- Gram stain: positive
- morphology: cocci
- Motile?: no
- Unique structures: exotoxin (streptolysin), capsules, enymes (hyaluronidase, streptokinase
- Reservoir: Humans and cattle
- Transmission: open wound, droplet, direct contact, indirect contact (parenteral-> cuts)
- Signs: Acute, blicsters, black spots, pus
- Symps: pain, dizziness, nausea
- Complications: sepsis, shock, organ failure, TSS
- Px: good wound care, hand hygiene, avoid swimming w/ wound
- Tx: surgical debridement, antibiotics (penicillin, ampicillin, clindamycin), Oxygen therapy
- “Endemic”
HPV carcinoma: Human papilloma Virus
-morphology: non-enveloped
-viral genome: ds DNA
-reservoir: humans, local in the body
-transmission: 40 strains transmitted sexual contact. Genital/skin contact, can be passed during child birth
-signs/symps: genital warts and lesions, can cause cancer (LATENT)
-entry: parenteral
-Tx: no treatment. most infections self-resolve in 1-2 yrs. warts burned out, cancer removed
-Px: abstinence/monogamy.
Vaccine: gardasil-> subunit proteins
-Endemic
Measles virus
- morphology: enveloped
- viral genome: negative sense ss RNA (antigenic drift)
- reservoir: humans
- transmission: droplet transmission, vehicle (air)
- Entry: respiratory, systemic
- signs: high fever, cough, kolpik spots (white), syncytia (rash)
- symps: sensitivity to light, loss of appetite, aches (ACUTE)
- complications: hearing loss, pneumonia, encephalitis(deaf),
- Px: vaccine-> attenuated, 2 doses
- Tx: supportive care, vitamin A, anti-measles antibodies
- Epidemic
Case Study 1: Bacteria Neisseria meningitidis
- causes meningitis
- IgA protease: enzyme that destroys antibodies (IgA)
- produces endotoxins -> released when cell dies
Case Study 2: Streptococcus pneumoniae
- IgA protease
- produces exotoxin pneumolysin: causes cell disruption and inflammation
- produces protein called PdgA: protects bacteria against host lysozyme modifies the NAG sugars of peptidoglycan
Case study: E. Coli
- reservoir: GI tract of animals
- transmission: indirect contact by vehicles
- Shiga toxin: disrupts cells protein synthesis. Exotoxin
- E. coli is gram (-) therefore producing endotoxins
- Tx: treat with rehydration. antibiotics and antidiarrheics not recommended. Antibiotics increase shiga toxins
Case Study: Influenza
- segmented negative strand RNA genome
- Antigenic shift: human flu crosses with flu virus that affects animals. Virus mutates and creates a new strain
- Antigenic drift: small mutations that change the surface proteins of virus. makes us have to create a new vaccine every year.
