CH 21 - Respiratory Infections Flashcards
Antigenic drift
(definition)
Minor changes that occur naturally in influenza virus antigens as a result of mutation
Antigenic shift
(definition)
Major changes in the antigenic composition of influenza viruses that result from reassortment of viral RNA during infection of the same host cell by different viral strains
Granuloma
(definition)
Collections of lymphocytes & macrophages found in a chronic inflammatory response
An attempt by the body to wall off & contain persistent organisms & antigens
Mucociliary escalator
(definition)
Moving layers of mucus propelled by cilia lining the respiratory tract that traps bacteria & other particles & carries them toward the throat
Otitis media
(definition)
Inflammation of the middle ear
Pharyngitis
(definition)
Inflammation of the throat
Pneumonia
(definition)
Inflammation of the lungs accompanied by filling of the air sacs with fluids (ex: pus & blood)
Sputum
(definition)
Thick fluid containing mucus, pus, & other material coughed up from lungs
Normal flora:
Nose
Staphylococcus aureus
Normal flora:
Throat
Non-pathogens:
- S. viridans
- Neisseria species
- S. epidermidis
Throat flora INHIBITORY to (pathogens):
- Streptococcus pyogenes
- Neisseria meningitidis
- Staphylococcus aureus
Normal flora:
Mouth
Streptococcus viridans
- S. mutans in dental plaque (precursor to caries & perhaps endocarditis)
Anaerobic bacteria (gingival crevices):
1. Bacteroides
2. Fusobacterium
3. Clostridium
4. Peptostreptococcus
Actinomyces israelii
- Fungal organism (gingival crevices)
- Abscesses of jaw, lungs, or abdomen
Normal flora:
Lower respiratory tract & alveoli
Sterile
(little to no microbes)
Normal flora:
Conjunctiva
Commonly have no bacteria
- Invading organisms swept into tear ducts & nasal pharynx
Lower Respiratory Tract Infections
(listed)
- Influenza
- Pneumococcal pneumoniae
- Klebsiella pneumoniae
- Mycoplasmal pneumoniae
- Whooping cough
- Tuberculosis
- Legionnaires’ disease
- Respiratory syncytial virus infection
- Systemic mycoses
Influenza:
Causative agent
Influenza A virus
- Orthomyxovirus
- ssRNA genome (8 segments)
- Spiked envelope
H spike = hemagglutinin
- Aids in attachment
N spikes = neuraminidase
- Aids in viral spread (leaving cell)
Influenza:
Symptoms
Short incubation period (~2 days)
- Headache
- Fever
- Muscle pain
- Dry cough
Acute symptoms abate within 1 week
- Cough, fatigue, generalized weakness may linger
Influenza:
Pathogenesis
- Acquired through inhalation of respiratory secretions (aerosols)
- Attaches to host cell via hemagglutinin (H) spikes
- Envelope fuses with host membrane & replicates within cell - Mature virus buds from host cell
- Picks up viral envelope - Infected cells die/slough off
- Destroys mucociliary escalator - Host immunity quickly controls viral spread
Influenza:
Epidemiology
Outbreaks each year in US
- 10-40,000 deaths
Pandemics periodically
- 1918 = “Spanish flu”
- Higher than normal morbidity
Spread caused by major antigenic changes
Influenza:
Antigenic drift
Consists of minor mutations overtime
- Particularly hemagglutinin
Minimizes effectiveness of immunity to previous strains
- Enough susceptible people for continued viral spread)
Influenza:
Antigenic shift
More dramatic/sudden changes
Virus strains drastically antigenically different from previous
- Often more virulent
New virus comes from genetic reassortment
- 2 viruses infect cell at same time
- Genetic mixing results
Influenza:
Prevention
Vaccine 80-90% effective
New vaccine each year due to antigenic drift
Influenza:
Treatment
Antiviral medications: amantadine & rimantidine
- 70-80% effective
- MUST be taken early (not sub for vaccine)
- Inhibit uncoating of viral RNA in infected cells (prevents from leaving capsule)
Antineuraminidase: Tamiflu (Oseltamivir)
- Prevents virus from leaving cell to infect others
Pneumococcal pneumonia:
Causative agent
1 cause of bacterial pneumonia
Streptococcus pneumoniae
- G+
- Diplococci/short chains
- Thick polysaccharide capsule
- NO Lancefield grouping
- Known for producing hemolysin
- Primary virulent factor = capsule
- > 90 different types of S. pneumoniae based on capsular Ag
Nasopharyngeal colonizer
- Biofilm formation = immunoquiescent state (commensal)
- Growth requires convering sodium pyruvate into acetyl-phosphate (hydrogen peroxide byproduct inhibits growth of other colonizers - H. influenzae)
Pneumococcal pneumonia:
Symptoms
Cough
Fever
Chest pain
- Aggravated with cough/breathing
- Breathing becomes shallow/rapid
- Poor oxygenation (dusky skin, supplemental needed)
Sputum production
Runny nose & upper respiratory congestion
- Precedes above symptoms
Symptoms abate in individuals who survive 7-10 days without treatment
Pneumococcal pneumonia:
Epidemiology
30% carry encapsulated strain in throat (biofilm form)
Bacteria rarely reach lung due to mucociliary escalator
- Risk increases when escalator destroyed (ex: after flu)
Underlying disease & age increase risk of disease
Pneumococcal pneumonia:
Pathogenesis
Bacteria inhaled into alveoli
- Inflammatory response in lung
- Capsule interferes with phagocytosis
Pneumococci that enter bloodstream lead to 3 often fatal complications:
1. Septicemia (infection of bloodstream)
2. Endocarditis (infection of heart valves)
3. Meningitis (infection of membranes covering brain & spinal cord)
Recovery usually complete
- Most bacterial strains do NOT destroy lung tissue
Pneumococcal pneumonia:
Prevention
Polysaccharide vaccine
- Immunity to 23 strains (of pneumonia only)
- Does NOT work in children under 2yrs
Conjugate vaccine
- Against 13 types (in 2010; 7 types in 2000)
- Available for children
- Recently approved for adults
- Prevents colonization
Pneumococcal pneumonia:
Treatment
Antibiotics: penicillin & erythromycin
- Successful if given early
- More strains becoming antibiotic-resistant
Pneumococcal pneumonia:
Pore-forming toxins (PFTs)
Pneumolysin
- PFT of Streptococcus pneumonia
- High concentrations causes lysis (tissue damage)
- Lower concentrations causes ion dysregulation (pyroptosis or necroptosis)
Klebsiella pneumonia:
Causative agent
Several species of Klebsiella
Klebsiella pneumoniae = primary cause
- G- bacillus (LPS)
- Encapsulated (avoids phagocytosis, recognitions, & complement)
- ESKAPE pathogen
Klebsiella pneumonia:
Symptoms
Most symptoms indistinguishable from pneumococcal pneumonia
- Cough
- Fever
- Chest pain
Other symptoms:
- Repeated chills
- Red/gelatinous sputum (bloody/”currant-jelly”)
50-80% mortality in untreated pts
- Tend to die sooner than other pneumonia
Klebsiella pneumonia:
Epidemiology
Normal flora of intestine (GI) in small population
Colonization of mouth/throat more common in debilitated individuals
- Very young/old
- Alcoholics
- Institutional settings
Klebsiella pneumonia:
Pathogenesis
- Colonizes mouth & throat
- Carried to lung with inspired air/mucus
- Survival in lung aided by capsule
- Interferes with phagocytosis - Causes tissue death
- Necrosis & formation of lung abscesses = necrotizing pneumonia - Infection in bloodstream leads to abscesses in other tissues
- DIC
Klebsiella pneumonia:
Prevention & treatment
NO specific prevention measures
- Disinfect environment (medical equipment)
Use antimicrobials ONLY when necessary
- Help control resistance
Mycoplasmal pneumonia:
Causative agent
Mycoplasma pneumoniae
- Small (found in some cell lines)
- Deformed bacteria lacking cell wall
- Slow growing
- Aerobic
- Distinctive “fried egg” appearance
Mycoplasmal pneumonia:
Symptoms
Onset typically gradual
1st symptoms:
- Fever
- Headache
- Muscle pain
- Fatigue
Later symptoms:
- Dry cough (resembling “atypical pneumonia”
Usually no hospitalization required
- “Walking pneumonia”
Mycoplasmal pneumonia:
Epidemiology
Spread by aerosolized droplets from respiratory secretions
- Survive long periods in secretions (aids in transmission)
- Small infecting dose
~1/5 of bacterial pneumonias
Peak incidence in young people
Mycoplasmal pneumonia:
Pathogenesis
- Attaches to receptors on epithelium
- Interferes with ciliated cell action
- Ciliated cells slough off - Inflammation initiates thickening of bronchial & alveolar walls
- Difficulty breathing
Produces toxin (thought to be possible cause of asthma)
Mycoplasmal pneumonia:
Prevention & treatment
NO practical prevention
- Avoid crowding in schools & military facilities (particularly dorms/barracks)
Cell wall synthesis inhibitors = INEFFECTUAL
- Ex: penicillin
Antibiotics of choice: tetracycline & erythromycin
- Must be given early
- Bacteriostatic (inhibit growth, don’t kill)
Whooping cough:
Causative agent
Bordetella pertussis
- G- bacillus
- ONLY infects humans (particularly young children)
Whooping cough:
Symptoms
Mild upper respiratory infection
Followed by paroxysmal coughing
- Series of hacking coughs
- Accompanied by copious mucus production
- End with inspiratory “whoop” (air rushes past narrow glottis)
Whooping cough:
Epidemiology
Spreads via infected respiratory droplets
- Most infectious during runny nose period
- Number of organisms decrease with onset of cough
Primarily occurs in infants & young children
- Milder forms seen in older children/adults
Whooping cough:
Pathogenesis
- Enters respiratory tract via inspired air
- Attaches to ciliated cells via filamentous hemagglutinin (Fha) - Mucus secretion increases
- Ciliary action decreases while ciliated cells sloughed off
- Cough relex = only way to clear secretions - Produces numerous toxic products
- Pertussis toxin
- Adenylate cyclase toxin
- Tracheal toxin
Whooping cough:
Pertussis toxin
A-B toxin
B portion attaches to cell surface
A portion enters cell & inactivates cAMP regulation (overproduction)
- Increased mucus formation
- Inhibits many leukocyte functions (chemotaxis, phagocytosis, respiratory burst)
- Impairs NK cell killing
- Contributes to bacterial binding to ciliated epithelial cells
Whooping cough:
Adenylate cyclase toxin
Increased production of cAMP
Increased mucus formation
Decreased phagocytic & NK cell killing
Whooping cough:
Tracheal cytotoxin
Causes release of NO from goblet cells
- Death of ciliated epithelial cells
Release of IL-1
- Fever causing cytokine
Whooping cough:
Prevention
Vaccination of infants
- Preventions disease in 70% of individuals
- Injections given at 6 weeks & 4, 6, 18 months
DPT = combined with diphtheria & tetanus toxoids
Whooping cough:
Treatment
Erythromycin
- Reduces symptoms if given early
Antibiotic eliminates bacteria from respiratory secretions
- Little bearing on course of disease due to toxin productive
Supportive therapy
- O2 therapy
- Suction of mucus (especially infants)
Tuberculosis:
Causative agent
1 respiratory bacterial infection in world (affects 1/3 of population)
Mycobacterium tuberculosis
- G+ rod
- Obligate anaerobe
- Mycolic acid in cell wall (acid fast staining)
Slow growing
- Generation time = 12 hrs or more
Resists most methods of control
Tuberculosis:
Symptoms
Chronic illness
- Slight fever with night sweats
- Progressive weight loss
- Chronic productive cough
- Sputum often blood-streaked
Tuberculosis:
Pathogenesis
- Inhalation of airborne organisms
- Taken up by pulmonary macrophages in lungs - Resists destruction within phagocyte
- Prevents fusion of phagosome with lysosome
- Allows multiplication in protected vacuole - Activated macrophages can kill bacteria
- Intense immune reaction occurs ~ 2 weeks post infection
- Macrophages fuse & form multinucleated giant cells
- Granuloma (tubercle) forms when macrophages & lymphocytes surround large cell to wall off infected tissue - Lysis of activated macrophages release contents into infected tissue
- Death of tissue & formation of “cheesy” material - Granulomas can contain live organisms & lead to reactivation TB
Tuberculosis:
Epidemiology
Tuberculin test (Mantoux)
- Type IV hypersensitivity response
- Small amounts of TB Ag injected under skin
- Does NOT detect very recent infection (< 4 weeks)
+ test = red/firm
- Exposed to TB
- Doesn’t indicate active disease
Tuberculosis:
Prevention
Vaccination used in many parts of world
- NOT given in US (eliminates TB test as diagnostic tool)
Bacillus of Calmette & Guérin (BCG)
- Derived from Mycobacterium bovis
- Gives partial immunity against TB
Tuberculosis:
Treatment
Antibiotic treatment for active TB
- 2 or more meds given together (to reduce resistance)
Rifampin & isoniazid (INH)
- Target actively growing organisms & metabolically inactive intracellular organisms
Prolonged therapy
- At least 6 months (tubercle)
- 2 years for active infection
Legionnaires’ disease:
Causative agent
Legionella pneumophila
- G- bacillus
Legionnaires’ disease:
Symptoms
Early:
- Headache
- Muscle ache
- Rapid rise in temp
- Confusion
- Shaking chills
Later:
- Dry cough
- Sputum production
- Pleurisy
Alimentary tract symptoms (1/4 of cases):
- Diarrhea
- Abdominal pain
- Vomiting
Legionnaires’ disease:
Epidemiology
Widespread in natural warm waters (within amoebae)
Relatively resistant to chlorine
Survives well in water system of buildings
- Lives in A/C
Person-to-person transmission does NOT occur
Legionnaires’ disease:
Pathogenesis
- Breathe aerosolized contaminated water
- Healthy people = resistant - Lodge in/near alveoli
- Stimulate phagocytosis - Bacteria release macrophage invasion potentiator (MIP)
- Aids in entry of macrophage - Necrosis of alveolar cells & inflammatory response
- Small abscesses, pneumonia, pleurisy
- Fatal arrest in 15% of hospitalized cases
Legionnaires’ disease:
Prevention
Prevention focused on equipment to minimize risk of infectious aerosols
Adequate disinfection
Legionnaires’ disease:
Treatment
Antibiotics = successful
Erythromycin
- High doses
Rifampin
- Administered concurrently in some cases
Bacteria produce beta-lactamase enzymes
- Resistant to penicillins & cephalosporins
Respiratory syncytial virus infection:
Causative agent
Respiratory syncytial virus (RSV)
- Paramyxovirus family
- ssRNA
- Enveloped (lacks hemagglutinin & neuraminidase)
Respiratory syncytial virus infection:
Symptoms
Incubation period 1-4 days
- Runny nose
- Cough & wheezing
- Difficulty breathing
- Fever (may/may not be present)
- Dusky skin (poor oxygenation)
1 of causes of croup in older infants
Respiratory syncytial virus infection:
Pathogenesis
- Enters through inhalation
- Infects respiratory epithelium
- Death & sloughing off of infected cells - Bronchiolitis
- Common feature
- Bronchioles obstructed by sloughing cells (wheezing)
Respiratory syncytial virus infection:
Epidemiology
Outbreaks = common
- Late fall to late spring
- Peak = mid-winter
Recovery produces short-lived immunity
Healthy adults/children = mild disease
- Rapidly spread infection
~60,000 hospitalization & ~6,000 deaths (65+ yrs)
Respiratory syncytial virus infection:
Prevention & treatment
Vaccine (May 23)
- Recommended for 60+ yrs & pregnant mothers (week 32-36)
Isolation of sick = best prevention
NO effective antiviral meds
Systemic mycoses
(listed)
- Coccidiodomycosis (Valley Fever)
- Histoplasmosis (Spelunker’s Disease)
- Blastomycosis
Coccidiodomycosis:
Causative Agent
Coccidiodes immitis
Dimorphic fungus
- Mold in soil (barrel-shaped arthrospores on ends of hyphae)
- Spherule in tissue (containing endospores)
Coccidiodomycosis:
Transmission
Inhalation of arthrospores (mold form)
Endemic in arid regions of SW USA & Latin America
Coccidiodomycosis:
Symptoms
Often asymptomatic
- Mild pneumonia/flu-like symptoms
May spread from lungs to bones & CNS
Overall rate of dissemination = ~1%
- 10x higher in Filipinos & African Americans
- Occurs most often in immunocompromised
Resolution of disease results in long-term immunity against reinfection
Histoplasmosis:
Causative Agent
Histoplasma capsulatum
Dimorphic fungus
- Mold in soil (contaminated with bat/bird droppings; caves)
- Yeast in tissue (tuberculate macromicroconidia multiply within macrophages)
Histoplasmosis:
Transmission
Inhalation of conidia
Endemic in central & eastern states (especially Ohio & MS River Valleys)
Histoplasmosis:
Symptoms
Often asymptomatic
- Mild respiratory symptoms
Spreads throughout body within macrophages
- Small granulomatous foci of infection heals by calcification
Dissemination occurs most often in immunocompromised
Blastomycosis:
Causative Agent
Blastomyces dermatitidis
Dimorphic fungus
- Mold in soil
- Yeast in tissue (broad-based bud)
Blastomycosis:
Transmission
Inhalation of conidia
Blastomycosis:
Symptoms
Chronic granulomatous disease
Primary pulmonary stage frequently followed by spread to other sites (ex: skin & bones)
Dissemination may result in ulcerated granulomas of skin, bone, & other sites
Upper respiratory tract infections
(listed)
- Streptococcal pharyngitis
- Diphtheria
- Pinkeye, earache, & sinus infections
- Common cold
- Adenoviral pharyngitis
- SARS & COVID-19
Streptococcal Pharyngitis:
Causative Agent
Streptococcus pyogenes
- G+ coccus in chains
- B-hemolytic
- Group A
(Lancefield grouping - carbohydrate in cell wall)
Streptococcal Pharyngitis:
Symptoms
- Difficulty swallowing
- Fever
- Red throat with pus patches
- Enlarged tender lymph nodes (localized to neck)
Streptococcal Pharyngitis:
Epidemiology
Spread readily by respiratory droplets
Streptococcal Pharyngitis:
Pathogenesis
Causes wide variety of illnesses
Numerous virulence factors
Streptococcal Pharyngitis:
Viruelence factors
- C5a peptidase
- Hyaluronic acid capsule
- M protein
- Protein F
- Protein G
- SPEs
- Streptolysins O & S
- Tissue degrading enzymes
Streptococcal Pharyngitis:
C5a peptidase
Inhibits attraction of phagocytes by destroying C5as
Streptococcal Pharyngitis:
Hyaluronic capsule
Inhibits phagocytosis
Aids penetration of epithelium
Streptococcal Pharyngitis:
M protein
Interferes with phagocytosis by causing breakdown of C3b opsonin
Streptococcal Pharyngitis:
Protein F
Responsible for attachment to host cells
Streptococcal Pharyngitis:
Protein G
Interferes with phagocytosis by binding Fc segment of IgG
Streptococcal Pharyngitis:
SPEs
Superantigens responsible for scarlet fever, toxic shock, & “flesh-eating” fascilitisT
Streptococcal Pharyngitis:
Tissue degrading enzymes
Enhance spread of bacteria by breaking down:
- DNA
- Proteins
- Blood clots
- Tissue hyaluronic acid
Streptococcal Pharyngitis:
Treatment
Most pts recover uneventfully in ~1 week
Confirmed strep throat treated with 10 days of antibiotics
- Penicillin or erythromycin
Streptococcal Pharyngitis:
Complications during acute illness
- Scarlet fever
- Erythrogenic toxin enter bloodstream & circulates throughout body
- Causes redness of skin & whitish coating of tongue - Quinsy
- Painful abscess develops around 1 of tonsils
Streptococcal Pharyngitis:
Secondary sequelae
Occurs week after infection (organism NOT present)
Acute glomerulonephritis
- Skin infections & pharyngitis
- Immune complexes deposited in glomeruli (provoking inflammatory reaction)
Acute rheumatic fever
- Pharyngitis
- Due to cross-reactions between streptococcal Ags & Ags of joint/heart tissue (M protein)
- Prevented by treatment of pharyngitis within 8 days of onset
Diphtheria:
Causative Agent
Corynebacterium diphtheria
- Variably shaped
- G+
- Non-spore forming
Certain strains produce diphtheria toxin
Diphtheria:
Symptoms
Begins with mild sore throat/fever
- Fatigue & malaise
- Dramatic neck swelling
- Whitish-gray “pseudomembrane”
(forms on tonsils or in nasal cavity & can detach into larynx/trachea - airway obstruction)
Diphtheria:
Epidemiology
Humans = primary reservoir
Spread by air
- Acquired through inhalation
Diphtheria:
Pathogenesis
Little invasive ability
Most strains release diphtheria toxin
- Production of toxin requires lysogenic conversion by bacteriophage
- Toxin produced in low iron environments (repressor shuts down in high iron, repressor removed in low iron)
Exotoxin released into bloodstream
- Damages heart, nerves, kidneys
Diphtheria:
Diphtheria toxin
A/B toxin
- Released from bacteria in inactive form
- Cleaved into A & B chains
B chain
- Attaches to host cell membrane
- Enters via endocytosis
A chain
- Becomes active enzyme that inhibits protein synthesis
- Inactivates elongation factor 2 (EF-2)
Other examples of A/B toxins:
(listed)
- Botulinum toxin
- Pertussis toxin
- Tetanus toxin
- Cholera toxin
- Heat-labile enterotoxin
Diphtheria:
Prevention
Diseases primarily results from toxin absorption
- NOT microbial invasion
Immunization
- DPT (neutralizes toxin)
- Booster every 10 years (immunity wanes after childhood)
Diphtheria:
Treatment
Early antiserum treatment
- Delay may be fatal
Antibiotics given to eliminate bacteria
- Penicillin & erythromycin
- Stops transmission of disease (NO effect on toxin absorption)
1 in 10 pts die (even with treatment)
Pink eye, earache, sinus infections:
Most common causative agents
Haemophilus influenza
- G- bacillus
Streptococcus pneumoniae
- G+ diplococci
(aka: pneumococcus)
Pink eye, earache, sinus infections:
Other causative agents
Otitis media
- Mycoplasma pneumoniae
- Streptococcus pyogenes
- Staphylococcus aureus
Respiratory viruses (1/3 of cases)
Pinkeye:
Symptoms
- Increased tears/redness of conjunctiva
- Swelling eyelids
- Sensitivity to bright light
- Large amounts of pus
(unless viral - minimal pus & swelling)
Sinusitis:
Symptoms
- Pain & pressure (localized)
- Tenderness over sinus
- Headache
- Severe malaise
Otitis media:
Symptoms
- Extreme ear pain
- Mild fever (may be absent)
- Vomiting
- Ear drum ruptures (trapped fluids released & pain ends abruptly)
More common in young children
Pinkeye:
Pathogenesis
Few details known (bacterial conjunctivitis)
Most likely from airborne respiratory droplets
Resist destruction by lysozyme
Sinusitis:
Pathogenesis
Begins with infection of nasopharynx
Spreads upwards to sinuses
Pathogenesis mechanism much like otitis media
Otitis media:
Pathogenesis
Often developing at time of conjunctivitis diagnosis
Begins with infection of nasal chamber & nasopharynx
- Moves to middle ear & damages ciliated cells
Ear drum often bursts
- Immediate pain relief
Pinkeye:
Prevention
Removal of infected individuals from school/daycare
Hand washing
Avoid rubbing/touching eyes
Avoid sharing towels
Pinkeye:
Treatment
Eyedrops/ointments containing antibacterial meds
Otitis media:
Prevention
Administration of pneumococcal vaccine (reduces incidence)
Otitis media:
Treatment
Antibiotic therapy
- Amoxicillin
Sinusitis:
Prevention & treatment
NO proven preventative measures
Treatment = supportive care
- Decongestants & antihistamines DISCOURAGED (ineffective)
Common cold:
Causative Agent
Rhinovirus (30-50%)
- Over 100 serotypes
- Picornavirus family
- Small
- ssRNA
- Acid labile (killed by gastric acid)
Coronavirus (~20%)
- ssRNA
Common cold:
Symptoms
- Malaise
- Scratchy mild sore throat
- Cough/hoarseness
- Nasal secretion (initially watery, later thick)
- NO fever (unless 2ndary infection)
Symptoms disappear in ~1 week
Common cold:
Epidemiology
Humans = only source
Close contact with infected persons/secretion necessary for transmission
- High concentrations in nasal secretions during 1st 2-3 days
Young children transmit easily
- Lack good hygiene
NO relationship btwn cold temp & development of cold virus
Common cold:
Pathogenesis
Viruses attach to specific receptors on respiratory epithelial cells
- Multiply in cells
- Large number of viruses released from infected cells
Injured cells cause inflammation
- Profuse nasal secretion, sneezing, & tissue swelling
Infection halted by:
1. Inflammatory response
2. Interferon release
3. Immune response
Infection can extend to ears, sinuses, & lower respiratory tract
Common cold:
Prevention
NO vaccine
- Too many different types of rhinovirus (impractical)
- Hand washing
- Keeping hands away from face
- Avoiding crowds during cold season
Common cold:
Treatment
Antibiotic therapy = INEFFECTUAL
Certain antiviral meds show promise (must be taken at 1st onset of symptoms)
Treatment with OTC meds may prolong duration (inhibit inflammation)
Adenoviral Pharyngitis:
Causative agent
Adenovirus
- Nonenveloped
- dsDNA
45 types infect humans
Remains infectious in environment for extended periods (transmitted easily on medical instruments)
Easily inactivated with heat & disinfectants
Adenoviral Pharyngitis:
Symptoms
- Runny nose
- Fever
- Sore throat (often pus on pharynx & tonsils)
- Lymph nodes in neck enlarged & tender
- Hemorrhagic conjunctivitis (certain strains)
- Mild cough (common; worsens when disease complicates)
Infection usually resolves 1-3 weeks (with/without treatment)
Adenoviral Pharyngitis:
Epidemiology
Human = only source of infection
Spread by respiratory droplets
- Common among school children
Endemic spread promoted by high # of asymptomatic carriers
Adenoviral Pharyngitis:
Pathogenesis
Virus infects epithelial cells
1. Attaches specific surface receptors
2. Multiples in nucleus
3. Escape to epithelial surface
4. Cell destruction initiates inflammation
Different viruses affect different tissues
- Adenovirus type 4 = sore throat & lymph node enlargement
- Adenovirus type 8 = extensive eye infection
Adenoviral Pharyngitis:
Prevention & Treatment
Same prevention as common cold
NO treatment
- Attenuated vaccine no longer used by military
- Patients usually recover uneventfully
- Bacterial 2ndary infections may occur (require antibiotics)
SARS & COVID-19:
Causative Agents
Similar coronaviruses:
- SARS-CoV (2002 outbreak)
- SARS-CoV-2 (Dec 2019 pandemic)
Enveloped +ssRNA
SARS source traced back to palm civets
- Infected from original reservoir (bats)
MERS (outbreak in 2012)
- Camels = intermediate host
SARS & COVID-19:
Symptoms
- Fever/chills
- Cough
- Shortness of breath
- Fatigue, muscle & body aches
- Loss of taste/smell
- Sore throat
- Headache
- Congestion
- Nausea/vom
- Diarrhea
SARS & COVID-19:
Pathogenesis
Enters cell through ACE2 binding
- Fusion of viral envelope with host cell membrane
- Mediated by spike protein
SARS & COVID-19:
Epidemiology
Direct person-to-person respiratory transmission
- Close-range contact via respiratory particles
- Transmitted longer distances via airborne route
Infected individuals more likely to be contagious in earlier stages of illness
- Larger amount of virus in upper respiratory tract
SARS & COVID-19:
Treatment
Treatments authorized by FDA for emergency use
SARS & COVID-19:
Treatments NOT in hospital
Symptoms < 5 days:
- Paxlovid
- Laegevrio (molnupiravir)
Symptoms < 7 days:
- Bebtelovimab (mAB)
- Remdesivir (Veklury)
SARS & COVID-19:
Treatments in hospital
COVID-19 convalescent plasma
- Blood taken from people recovered from COVID-19
- Contains Abs to treat (improves immune response)
Barcitinib (Olumiant)
- mAb treatment
Tolxilizumab (Actemra)
- mAB treatment
- May decrease risk of death
Remdesivir (Veklury)
- Antiviral
- Must be given within 7 days after 1st symptoms appear
SARS & COVID-19:
Prevention
mRNA vaccines
- Pfizer & Moderna
- Uses genetically engineered mRNA to express spike protein in host cells
Vector vaccines
- Johnson & Johnson (AstraZeneca)
- Uses viral vector to deliver material to host cells to induce spike protein production
Traditional protein subunit vaccine
- Developed by Novavax
Before vaccines: lockdowns & face masks
