Lecture 19 and 20 Respiratory Infections Flashcards
(209 cards)
1
Q
What are streptococci classifications based off of?
A
cell wall carbohydrates (known as Lancefield grouping)
2
Q
What were streptococci previously classified by?
A
Type of blood agar hemolysis
3
Q
Streptococci have _______________ on their surface that correlate with disease-causing potential
A
antigens
4
Q
Most strains of beta hemolytic strep from human infections have same…
A
cell wall carbohydrate
5
Q
What protein is on streptococcus pyogenes?
A
M protein
6
Q
Illnesses range from…
A
trivial to fatal
7
Q
What are the two divisions of respiratory system infections?
A
Divided into infections of upper respiratory tract (head and neck) and lower respiratory tract (chest)
8
Q
Which type of respiratory infection is more fatal?
A
lower respiratory infections
9
Q
Examples of upper respiratory infections
A
colds
10
Q
Examples of lower respiratory infections
A
pneumonia, tuberculosis
11
Q
The respiratory system replenishes ________ and releases __________
A
O2, CO2
12
Q
What are the structures of the upper respiratory tract?
A
nose and nasal cavity, pharynx, and epiglottis
13
Q
What is the upper respiratory tract lined by?
A
mucous membranes
14
Q
Goblet cells produce….
A
mucus, a slimy glycoprotein
15
Q
Function of mucus
A
Traps air-borne dust and particles including microbes
16
Q
Function of mucociliary escalator
A
propels mucus, trapped particles away from lungs
17
Q
What is the mucociliary escalator impaired by?
A
Impaired by smoking, alcohol/drug abuse, viral infections; increases chance
of infection
18
Q
What are tonsils and what do they come into contact with?
A
lymphoid organs, come into contact with microbes entering
upper respiratory tract
19
Q
What type of air do the nose and nasal cavity carry?
A
warm, humidified air
20
Q
Approx. 30% of healthy people carry…
A
staphylococcus aureus
21
Q
Infection of the nose is usually by….and results in…
A
viruses….rhinitis
22
Q
Sinuses in the skull cause…
A
sinus headache or post-nasal drip
23
Q
Inflammation of the throat is called…
A
pharyngitis
24
Q
Epiglottis covers ________ during swallowing
A
lower respiratory tract
25
Characteristics of Corynebacterium
Pleomorphic, often club-shaped Gram-
positive rods; non-motile
26
Describe cornyebacterium
Aerobic or facultatively anaerobic.
Those that look similar to C.
diphtheriae, the cause of diphtheria, are included in a
group called diphtheroids.
27
Characteristics of Haemophilus
Small, Gram-negative rods
28
Describe Haemophilus
Facultative anaerobes.
Commonly include the potential pathogen H. influenza
29
Characteristics of Staphylococcus
Gram-positive cocci in clusters
30
Describe staphylococcus
Facultative anaerobes. Potential pathogen
Staphylococcus aureus commonly inhabits the nostrils.
31
Characteristics of streptococcus
Gram-positive cocci in chains
32
Describe streptococcus
Aerotolerant (obligate fermenters)
33
Viridans streptococci are....
alpha hemolytic
34
Eyes and linings of eyelids are covered by...
conjunctiva
35
What are tears rich in?
lysozyme and secretory IgA
36
Tear ducts connect to....
nasal cavity
37
External ear protected by.....
cerumen
38
Middle ear is sterile and connected by.......to pharynx
Eustachain tubes
39
Purpose of eustachian tubes
Allow drainage, equalize pressure
40
Infection of middle ear
otitis media
41
Inner ear is typically....
microbe free
42
How can infectious agents get to the inner ear?
may enter from upper respiratory tract infection; may
spread to mastoid air cells
43
Sign and symptoms of streptococcal pharyngitis
Strep throat
Sore throat, difficulty swallowing, fever
* Throat is red with patches of pus, tiny hemorrhages
* Most patients recover after about a week; some have mild or no symptoms
44
Causative agent of strep throat
streptococcus pyogenes
45
Streptococcus pyogenes is gram...
positive
46
Streptococcus pyogenes grows in...
chains
47
Streptococcus pyogenes causes ..... of blood agar
beta hemolysis
48
............. from Lancefield grouping
Group A streptococcus
49
Different strains within GAS distinguished by....
M protein
50
M protein in Streptococcus pyogenes acts as...
adhesin
51
How many types of M protein are there in Streptococcus pyogenes?
80 different types
52
Antibodies that bind to M protein....
prevent infection
53
Do antibodies to one strain of infection stop others?
No
54
Protein F adheres to.....
fibrin of epithelial cells in throat
55
Protein G binds the Fc region of......
IgG antibodies
56
What degrades intracellular connections for Streptococcus pyogenes?
DNase, hyaluronidase, proteases
57
What does streptokinase do in Streptococcus pyogenes?
breaks blood clots
58
Some strains of Streptococcus pyogenes have a ____________________ capsule thought to disguise bacteria
from immune system
hyaluronic acid capsule (bc it is found in human tissue)
59
M protein prevents opsonization via...
C3B
60
Protein G is an _______ receptor
Fc
61
Protein G prevents....
IgG mediated phagocytosis
62
Streptococcus pyogenes produces C5a peptidase which....
destroys C5a responsible for attracting phagocytes to site of infection
63
Streptolysis O and S make.....
holes in membranes of erythrocytes and leukocytes
64
Streptolysins O and S yield....
Beta hemolysis
65
What are streptococcal pyrogenic
exotoxins (SPEs)?
Produced by a few strains of Streptococcus pyogenes, leads to high fever, May lead to scarlet fever, streptococcal toxic shock
syndrome, or “flesh-eating disease”
66
Effect of C5a peptidase
Inhibits recruitment of phagocytes by destroying
complement component C5a
Inhibits phagocytosis
67
Effect of Hyaluronic acid capsule
Interferes with phagocytosis by causing
inactivation of complement component C3b, an
opsonin; involved in attachment to host cells
68
Effect of M protein
Interferes with phagocytosis by causing
inactivation of complement component C3b, an
opsonin; involved in attachment to host cells
69
Effect of Protein F
Responsible for attachment to host cells
70
Effect of Protein G
Binds to Fc portion of antibodies, thereby
interfering with opsonization
71
Effect of Streptococcal pyrogenic exotoxins (SPEs)
Superantigens responsible for scarlet fever, toxic
shock, “flesh-eating” fasciitis
72
Effect of Streptolysins O and S
Lyse leukocytes and erythrocytes
73
Effect of tissue-degrading enzymes
Enhance spread of bacteria by breaking down
DNA, proteins, blood clots, tissue, hyaluronic acid
74
Streptococcus pyogenes naturally only infects...
humans
75
Streptococcus pyogenes spreads by...
respiratory droplets or contaminated food
76
____________ carriers more likely to spread than pharyngeal
nasal
77
In Streptococcus pyogenes, individuals can be _________ for weeks
asymptomatic
78
Streptococcus pyogenes usually becomes deficient in ______ in long-term carriers
M protein
79
Treatment and prevention of Streptococcus pyogenes
Confirmation via diagnostic tests and throat culture
Treatment with penicillin prevents some post-streptococcal sequelae
80
What is Post-streptococcal sequelae?
Complications that develop after streptococcal infections. Result from an
autoreactive immune respons
81
When does acute rheumatic fever begin?
can begin approximately 3 weeks after recovery
82
Symptoms of acute rheumatic fever
Fever, joint pains, chest pains, rash, nodules under ski
83
What are chorea?
Uncontrollable body movements that can occur during acute rheumatic fever
84
What disease can carditis develops in 30 to 50% of patients, can lead to chronic rheumatic heart disease
Acute rheumatic fever
85
Some ____________ involved in susceptibility in Acute Rheumatic Fever
MHC Class II alleles
86
Statistics for Acute Rheumatic Fever?
Occurs in up to 3% of severe untreated cases, results in about 10 to 20
million cases per year globally
87
Symptoms of Acute post-streptococcal glomerulonephritis
Fever, fluid retention, high blood pressure;
blood and protein in urine
88
When is S.pyogenes eliminated during Acute post-streptococcal glomerulonephritis?
Usually before symptoms appear
89
Damage to......from inflammatory reaction to streptococcal antigens in kidney glomeruli
kidnesy
90
Causative agent of diphtheria
Corynebacterium diphtheriae
91
Describe Corynebacterium diphtheriae
Pleomorphic, non-motile, non-spore forming Gram-positive rod that often stains irregularly due to metachromatic granules
Club-shaped, often occur side by side in “palisades”
92
What is the gene that releases diphtheria toxin carried by?
specific lysogenic bacteriophage
93
Where is Corynebacterium diphtheriae isolated?
Isolated on selective medium containing potassium-tellurite (inhibits normal microbiota; C. diphtheriae forms dark colonies)
Also grown on Loeffler’s
94
Signs and symptoms of Diphtheria
Mild sore throat, slight fever, extreme fatigue, malaise
Swelling of neck, formation of pseudomembrane on tonsils and throat or in nasal cavity
Heart and kidney failure and paralysis may occur later
95
What is diphtheria?
a deadly toxin-mediated disease
96
_______________ made of cells killed by the exotoxin along with blood clots, fibrin, and leukocytes in diphtheria
Pseudomembrane
97
What is the A-B exotoxin in diphtheria?
“B” subunit attaches to cell receptors; entire molecule
taken up by endocytosis
Cells lacking receptor are uneffected
“A” subunit is an ADP-ribosyl-transferase, catalyzes reaction covalent modification of cellular factor 2 (EF-2) required for movement of ribosome on mRNA (i.e. protein synthesis).
98
How does diphtheria spread?
Spread by air; acquired via inhalation or from fomites
Cutaneous diphtheria; caused from touching or handling infected materials from carrier or patient, results in ulcers on skin may become systemic, fatal. Patients suffer from extreme fatigue and malais
99
Treatment and prevention of diptheria
Injection of antiserum to toxin; delaying treatment to wait for culture results can be fatal
Antibiotics can clear C. diphtheriae, but toxins already absorbed are unaffected
Even with treatment, approximately 10% mortality
Immunization with toxoid very effective; inactivated toxoid included with childhood DTaP vaccination (diphtheria and tetanus toxoids with components of Bordetella pertussis)
100
Location of lower respiratory tract infections is usually....
sterile
101
What is a symptom of laryngitis?
hoarseness
102
Trachea branches into two....infection is....
bronchi; bronchities
103
Bronchitis if often from...
coral infection, coughing due to smoking
104
Bronchi branch repeatedly to become ------; viral infection is ------
bronchioles; bronchiolitis
105
Bronchioles end in.....
alveoli
106
Inflammation of lungs in ------- called pneumonia when-----
pneumonitis; alveoli fill with pus and fluid
107
Lung tissue contains many ----- to prevent infection
macrophages
108
Inflammation of lung membranes is?
pleurisy
109
Pneumonia is disease of....
lower respiratory tract
inflammatory response due to microbial infection
110
Alveoli fills with......during pneumonia
fluids like pus and blood
111
What is the leading cause of death due to infectious disease in the U.S.?
Pneaumoniae
112
Signs and symptoms of pneumonia
Cough, chills, shortness of breath, fever, chest pain, sometimes cyanosis (lips turning blue) due to poor oxygenation
Cough is often productive, sputum containing pus and blood comes up from lungs
May be examined microscopically to identify cause
Cracking or bubbling sound with stethoscope
White shadows on chest X ray
113
Pneumonia is often caused by opportunists when...
mucociliary escalator is
compromised
114
Damaging affects of pneumonia largely due to...
inflammatory response
* Fluids collect in alveoli, along with leukocytes and mucus
* May cause consolidation, clogged alveoli
* May affect nerve endings in pleura, causing pain
115
Causative agent often has ---- that delays phagocytosis by lung----
capsule, macrophages
116
Causative agent of Pneumococcal pneumonia
Streptococcus pneumoniae
117
Describe Streptococcus pneumoniae
Gram-positive diplococcus known as pneumococcus; lancet-shaped
Thick polysaccharide capsule responsible for virulence
90 different serotypes each with different capsular antigens
* Certain serotypes more commonly invasive
* Strains lacking capsule do not cause invasive disease
118
Strains lacking ---- do not cause invasive disease in Streptococcus pneumoniae
capsule
119
Signs and symptoms of Streptococcus pneumoniae
cough, fever, chest pain, sputum production
(incubation period 1 to 3 days)
* Usually preceded by 1 to 2 days of runny nose, congestion that ends with
sudden fever and shaking chills
* Sputum becomes pinkish or rust-colored from blood
* Severe chest pain aggravated by each breath or cough
* Causes shallow rapid breathing
* Patient develops cyanosis from poor oxygenation
120
Due to S. pneumoniae, survivors ----- without treatment
sweat heavily and return to normal temperature after 7 to 10 days
121
Pneumolysin damages....
ciliated epithelium
122
Pneumococci may enter blood-stream, lead to.....
sepsis of blood,endocarditis (heart valve infection), meningitis (infection of brain, spinal cord membranes)
123
Capsule, pneumococcal surface protein (PspA) interfere with....
C3b of complement system, block phagocytosi
124
Epidemiology of pneumococcal pneumonia
up to 30% of healthy people carry encapsulated
pneumococci in throat; mucociliary escalator effectively keeps from reaching lungs
* Risk of infection increases when this defense mechanism is impaired
* Increased risk in those over 50, or with heart or lung disease, diabetes or
cancer, or severe alcoholism
* Increased risk during or following Influenza A infectio
125
Treatment and Prevention of pneumococcal pneumonia
penicillin cures if given early; resistant
strains increasingly more common
* Conjugate vaccine (PCV13) against 13 strains available for children under
2, adults over 65 and those with certain health conditions
* Vaccine (PPSV23) available for 23 most common pneumococcal strai
126
Causative agent of pertussis
Bordetella pertussis
127
Describe Bordetella pertussis
Tiny encapsulated aerobic Gram-negative rod
Sensitive to sunlight, drying: quickly die outside of host
128
Pathogenesis of Bordetella pertussis
bacteria are inhaled, attach to ciliated cells of epithelium
129
What is the effect of bacteria attaching to ciliated cells of epithelium during Pertussis?
Increased mucus production, decreased ciliary action results in severe
cough
Some bronchioles completely obstructed, lead to small areas of collapsed
lung
Spasms occur when partial mucus plug in airway allows air in let but not
out... patient gasps for air when finally able to expel breath.
130
What is the chief cause of death of pertussis?
Chief cause of death is pneumonia due to B. pertussis or (more
commonly) secondary bacterial infections
131
How many toxins are released in pertussis?
three
132
What are the three stages of pertussis?
Catarrhal Stage
Paroxysmal Stage
Convalescent Stage
133
What Is the catarrhal stage?
(inflammation of mucous membranes)
1 to 2 weeks of signs resembling upper respiratory infection (runny nose,
sneezing, low fever, mild cough)
134
What is the paroxysmal stage?
(repeated sudden attacks)
* Frequent bursts of violent uncontrollable coughing lasting 2 to 4 weeks or
longer
* Dry but severe; small blood vessels in eyes rupture, tongue protrudes, neck
veins stand out
* Forceful inhalation of air: “whoop” sound
* Vomiting, seizures, cyanosis may occur
135
What is the convalescent stage?
(recovery)
* Not contagious; coughing decreases over several weeks
136
Epidemiology of Pertussis
Vaccination-preventable disease, but still endemic in many countries
including U.S.
* Causes up to half a million deaths annually globally
137
What are the three main toxins deployed by B.pertussis?
Pertussis Toxin (PT)
Adenylate cyclase toxin (ACT)
Tracheal cytotoxin (TCT)
138
What is pertussis toxin (PT) and what does it do?
is A-B exotoxin: B attaches to cellular
receptors, “A” component moves through cytoplasmic
membrane
* Increases cAMP: yields increased mucus, decreased
killing ability of phagocytes, release of lymphocytes
into bloodstream, ineffectiveness of natural killer
cells, low blood sugar
139
What does adenylate cyclase toxin (ACT) do?
lyses leukocytes; catalyzes ATP
conversion to cAMP
140
What does tracheal cytotoxin (TCT) do?
causes release of fever-inducing interleukin-1; toxic to ciliated
epithelial cells
141
Epidemiology of Pertussis
highly contagious
Classically disease of infants; most fatalities in those under 1 year of age
* Milder in older children, adults; may be mistaken for another disease
such as a common cold, which fosters transmission
* Incidence increasing
* Better surveillance, suboptimal vaccination, decreasing immunity in vaccinated,
development of resistance
142
How does pertussis spread?
via respiratory secretions suspended in air
143
When are pertussis patients most infectious?
catarrhal stage
144
Treatment and prevention of pertussis
Macrolides during catarrhal stage; ineffective in paroxysmal stage
* Intensive supportive therapy sometimes needed in infants
* Prevented with acellular pertussis vaccine (aP) given in combination with
diphtheria and tetanus toxoids (DTaP)
* Additional booster for adolescents (Tdap)
* Also given to pregnant women to provide passive immunity to newborn
145
What is given in the catarrhal stage of pertussis, but not the paroxysmal stage?
macrolides (ineffective during paroxysmal stage)
146
Why did tuberculosis incidence begin to rise?
due to expanding AIDS epidemic, increasing prevalence of drug-resistant strain
147
Initial infection by Mycobacterium tuberculosis is usually...
asymptomatic (immune response controls, but unable to eliminate)
148
Signs and symptoms of tuberculosis
Yields latent tuberculosis infection (LTBI); later may develop
tuberculosis disease (TB disease), or active tuberculosis
* Slight fever, weight loss, night sweating, persistent cough, often
blood-streaked sputum, night sweating
* Primarily infects lungs, but bacterial cells can travel through
bloodstream to other tissues including kidneys, bones, joints, central
nervous system
– Called miliary TB because lesions caused by the bacteria resemble millet seeds
149
Causative agent of tuberculosis
Mycobacterium tuberculosis
150
Describe Mycobacterium tuberculosis
Slender, acid-fast, rod-shaped bacterium
Strict aerobe with generation time over 16 hours
Unusual cell wall contains mycolic acids: cells resist drying,
disinfectants, strong acids and alkali; responsible for acid-fast staining
Easily killed by pasteurization
151
What other strains can cause tuberculosis in humans and other animals (that are all a part of the Mycobacterium tuberculosis complex (MTBC))
M. bovis, M. africanum and
others,
152
Pathogeneis of tuberculosis: alveolar macrophages
airborne cells inhaled into lungs
Alveolar macrophages quickly engulf; unable to destroy
Ingested bacteria manipulate macrophage to create
environment in which they can multiply.
The bacteria then recruit more macrophages to the site,
increasing the number of host cells to multiply in
Lymphocytes wall off infected area, granuloma forms
– Called tubercles
In granuloma, effector helper T cells release cytokines
– Activate macrophages to destroy mycobacteria but some hosts have been induced to become foamy macrophages; thought to help bacteria survive in these cells
153
Pathogenesis of tuberculosis: why does it remain as latent TB infection?
Fibrous layer forms around macrophages, keeps lymphocytes
outside of tubercle
– Layer calcifies and can be seen on X-rays as Ghon foci
– Called Ghon complex if adjacent lymph nodes involved
* Some mycobacteria survive; prevented from multiplying by low pH and low O2
154
When results in active TB?
if inflammatory response cannot contain or destroy
mycobacteria if immunity becomes impaired by stress, age, or disease
155
What is released when macrophages in tubercle die? What does this form?
bacteria, enzymes, cytokines released
Forms area of necrosis
156
What is caseous necrosis?
foamy macrophages (with lipids) thought to play
important role
157
What is a tuberculous cavity and what is it caused by?
large lung defect
tubercle ruptures, releases bacteria and dead material, causes....
158
What is the result of a tuberculous cavity?
Spreads bacteria in lungs
Lung cavity persists, enlarges for months or years, spreads bacteria; can be transmitted by coughing
159
Epidemiology of TB
Approximately 13 million Americans have LTBI
* Only approximately 5 to 10% will reactivate, progress to active TB
* Transmission almost entirely via respiratory route
– 10 or fewer inhaled mycobacterium can cause infection
160
What is important to notice in TB?
Frequency of coughing, ventilation,
crowding, immunodeficiency
(especially AIDS) important
161
How do you identify TB?
– Tuberculin skin test (TST; Mantoux test)
– Blood tests (IGRAs)
– Xpert MTB/RIF (detect Mycobacterium
DNA)
162
Treatment and prevention of TB
multiple drugs over long time
* Combination therapy needed; mycobacteria grow slowly, resist body
defenses; mutants likely present given high numbers of cells involved
in infection
* Rifampin (RIF), isoniazid (INH), pyrazinamide (PZA), and ethambutol
(EMB) given for 2 months; then INH, RIF for another 4 to 7 months
* Resistant strains often evolve as symptoms disappear, and patient
becomes careless in taking medications
163
What are DOTS and what disease are they used for?
DOTS (directly observed therapy short-course) used for TB
164
What does Multi-drug-resistant TB (MDR-TB) resist?
RIF, INH
165
What does Extensively drug-resistant TB (XDR-TB) resist?
both first and many
second-line drugs; threaten global control
166
What is the new regimen of medications for XDR-TB?
pretomanid, along
with bedaquiline and linezolid
167
What is used in the US to identify TB?
skin or blood tests, lung X-rays used to identify cases;
both TB disease and are LTBI treated
168
What is the BGG vaccine? What is it used against?
BCG vaccine used in many countries (live attenuated from M.
bovis); prevents childhood TB, but ineffective against LTBI
reactivation
169
Why is the BGG vaccine discouraged in US?
as it causes positive tuberculin
test
– Interferes with disease prevention
– Not safe in severely immunocompromised patient
170
What is the causative agent of Legionellosis?
Legionella pneumophila
171
Describe Legionella pneumophila
Gram-negative rod; fastidious
* Stains poorly in tissue; immunofluorescence
* Facultative intracellular parasite; survives well in freshwater amebas,
which can form cysts during adverse conditions, allowing bacteria within
to survive
* Persist in biofilms; if disturbed, huge numbers released
172
Signs and symptoms of Legionellosis
headache, muscle aches, high fever, confusion,
shaking chills (incubation 2 to 10 days)
* Dry cough develops, produces sputum, sometimes blood
* Shortness of breath or pleurisy can occur
* About 25% of cases have digestive tract symptoms (for example, diarrhea,
abdominal pain, vomiting)
* Recovery is slow; weakness, fatigue last for weeks
173
Pathogenesis of Legionellosis
Acquired by inhaling aerosolized water with organism
* Promote uptake by alveolar macrophages
* Mip (macrophage invasion potentiator) aids entry into macrophages
* Bind C3b, an opsonin
* Bacteria survive by preventing phagosome-lysosome fusion; multiply
within macrophages
* Necrosis of host cells and inflammatory response lead to abscesses,
pneumonia, pleurisy, and often bacteremia
* Fatal in about 15% of hospitalized cases
174
Epidemiology of Legionellosis
Widespread in warm natural waters containing protozoa, which house
the bacteria
* Also found in water systems
* L. pneumophila protected from chlorine inside protozoa
* Cases have originated from aerosols from central air-conditioning
systems, nebulizers, sprays to freshen produce, showers, and water
faucets,
* No direct person-to-person spread
175
Treatment and prevention of Legionellosis
Appropriate antibiotic (for example, macrolides)
* Produces a
* Antibiotic must reach high level within phagocytic cell to kill bacterium
* Some patients require O2 therapy
* Prevention directed at air conditioning equipment
design to minimize aerosols, disinfection procedures
for cooling water holding tank
176
Causative agent of influenza
Influenza A, a member of the Orthomyxoviridae
177
Describe Influenza A
Enveloped virus with 8 segments of single-stranded, negative sense RNAs
178
What are the glycoproteins in influenza A?
* Glycoprotein spikes embedded in envelope: hemagglutinin antigen (HA) and neuraminidase antigen (NA)
179
What is the difference between HA and NA in influenza?
* HA attaches to receptors on host epithelial cells
* NA critical in release:
destroys surface receptors
that bind budding virion
180
What are the subtypes of influenza based off of?
HA and NA
181
How many HA and NA subtypes are there?
18 HA and 11 NA
182
Which HA and NA subtypes only infect humans?
H1, H2, H3 and N1, N2
infect humans
183
What is the most serious type of influenza in humans?
Influenza A
184
What are the three types of influenza and what are they based off of?
Three major virus types (A, B, and C) based on protein coat
185
Signs and symptoms of influenza
Headache, muscle aches, fever, sore throat, fatigue; peaks in 6 to 12 hours; dry
cough develops and worsens over a few days (incubation period approximately
2 days)
* Acute symptoms last approximately 1 week; lingering cough, fatigue, weakness
last additional days or weeks
* Influenza viruses do not cause vomiting and diarrhea “stomach flu” is a
misnomer.
186
Pathogenesis of influenza
inhalation of aerosolized secretions or from
contaminated fomites
Virions attach by HA spikes to respiratory epithelial cells; enter by endocytosis
Virus uncoats in the endosome and viral proteins and RNA traffic into cell nucleus where all RNA synthesis takes place.
Rapid synthesis of viral RNA and proteins
Host membrane embedded with HA and NA; mature virions acquire these as they bud from host cell
Infected cells die, slough off, destroy mucociliary escalator
Person susceptible to secondary respiratory infections
Immune system quickly controls influenza virus infections in most cases; complete recovery of respiratory epithelium may take 2 months or more
187
Epidemiology of Influenza
Only small percentage of cases are fatal, (Case Fatality Rate is about 0.1%) but the numbers of cases are high (40-50M/year in US), so overall number
of deaths is high (40,000-60,000/year in US).
Most deaths due to viral pneumonia on top of underlying illnesses and secondary bacterial pneumonia.
Epidemics occur annually; pandemics periodically
188
What is antigenic drift in relation to influenza?
minor mutations in HA and NA genes; responsible for
seasonal influenza
* Immunity developed from previous year less effective
189
What is antigenic shift in relation to influenza?
one species has concurrent infection with multiple types
allows mixture of 8 RNA segments; causes pandemic influenza
(uncommon)
* Human strain can gain novel HA and/or NA antigens from animal-directed viral
species to which humans have no immunity
190
All known influenza A viruses are found in --- but....
birds; most of these cause no disease in humans
191
What is LPAI?
(low pathogenic avian influenza)
192
What is HPAI?
(high pathogenic avian influenza)
193
Which virus spread from chickens to humans?
H5N1 (influenza)
194
What virus appeared in China in 2013?
H7N9 avian virus
30 to 40% case-fatality rate
* Found in birds in U.S., but no human cases
* Fear is that virus will evolve to allow transmission
from person to person
195
Treatment and prevention of influenza
Antiviral medications such as neuraminidase inhibitors are partially
effective
* Children 5 to 15 with influenza should not be given aspirin due to risk of
Reye’s syndrome
* Potentially fatal liver disease
* Variety of trivalent or quadrivalent vaccines
* Against 3 or 4 strains in circulation (two A strains and 1 to 2 B strains)
* New vaccine required each year because of antigenic drift
196
What is the most common cause of serious lower respiratory tract infections in infants and young children?
Respiratory syncytial virus (RSV) infections
197
What is the leading cause of death in infants worldwide?
Respiratory syncytial virus (RSV) infections
198
Signs and symptoms of Respiratory syncytial virus (RSV) infections
Runny nose followed by cough, wheezing,
difficulty breathing; possibly fever (incubation period 1 to 4
days)
* Bluish color around lips indicates insufficient O2 due to bronchiolitis
* In healthy older children and adults, similar to bad cold
* RSV causes croup; high-pitched cough and noisy inhalation from airway
obstruction
* Sometimes fatal for elderly with underlying diseases
199
Causative agent of Respiratory Syncytial Virus
Enveloped, single-stranded RNA
200
What are the two subtypes of Respiratory Syncytial Viruses in Pneumoviridae
A and B
201
What does the enveloped, single stranded RNA cause cells to do?
Causes cells in cultures to fuse into syncytia, giving name respiratory
syncytial virus (RSV)
202
Pathogenesis of Respiratory Syncytial Virus
enters body by inhalation and replicates in nasopharynx; spreads
to epithelium in bronchioles
* Cells die and slough off; bronchiolitis is common
* Bronchioles partially plugged by sloughed cells, mucus
* Obstruction causes wheezing; may allow air into lungs but not out
* Pneumonia often results; secondary infections common
203
Epidemiology of Respiratory Syncytial Virus
Recovery yields only weak and short-lived immunity
Healthy children, adults usually have mild illness and readily spread virus
204
Treatment and prevention of Respiratory Syncytial Virus
no effective antivirals
* Preventing healthcare-associated RSV requires strict isolation techniques
* Passive immunity via monthly injections of immune globulin or RhuMab (palivizumab)
* No vaccine
205
Signs and Symptoms of Hantavirus Pulmonary Syndrome
Begins with fever, fatigue, and muscle aches after incubation
period of 7 days to 8 weeks
Often followed by nausea, vomiting, and diarrhea
Unproductive cough and increasingly severe shortness of
breath appear within a few days, often followed by shock and
death
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Causative Agents of Hantavirus Pulmonary Syndrome
Caused by a hantavirus called the Sin Nombre virus (SNV)
– Enveloped viruses of the family Bunyaviridae
– Genome consists of three segments of single-stranded RNA
* Sin Nombre virus infects deer mice, which transmitted the virus to humans during the initial outbreak in 1993
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Pathogenesis of Hantavirus Pulmonary Syndrome
Enters the body by inhalation of airborne dust contaminated with the urine, feces, or saliva of infected rodents
* Taken up by phagocytes in lungs and transported to lymph nodes
* Enters the circulation and carried throughout the body, infecting endothelial cells that line capillaries, particularly in the lung
* Massive amounts of the viral antigen appear in lung capillaries
* Inflammatory response to antigen cause capillaries to leak fluid into the lungs
* Patients suffocate and their blood pressure to falls, leading to shock and death in almost 40% of the cases
* Few infectious virions enter the air passages so person-to-person transmission is rare
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Epidemiology of Hantavirus Pulmonary Syndrome
zoonosis; considered emerging disease
– Cases have been identified from Canada to Argentina, in
addition to the United States.
– Main risk factor is poorly ventilated rodent-infested homes
and buildings
– Infections more prevalent in the fall when wild rodents seek
shelter from the cold weather
– Ecological factors that affect mouse population levels, such
as numbers of predators and El Niño weather patterns, can
also affect transmission
– Example of how environmental change can result in
infectious human disease
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Treatment and Prevention of Hantavirus Pulmonary Syndrome
No proven treatment
Prevention based on
minimizing exposure to
rodents and contaminated
dust
– Control rodent population
– Mouse-proofing buildings,
keeping food in containers
– Use of mops rather than brooms
or vacuums
