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Respiratory 2 > Viral Respiratory Infections > Flashcards

Viral Respiratory Infections Flashcards

1
Q

Rhinovirus is a what type of virus? Classification? Immunity?

A

• RNA Viruses • Classification: Picornavirus • Serotypes: >100 • Immunity: –Variable, type-specific immunity with little crossprotection. Brief duration. –Mediated by secretory IgA (not humoral Ab)

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2
Q

Influenza is what type of virus? Classification? General types?

A

• Enveloped RNA Viruses • Classification: Orthomyxoviruses • Genera: A, B, C

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3
Q

Influenza has what kind of genome? Nucleocapsid? Explain the outer lipoprotein envelope?

A

–Segmented single-stranded RNA genome –Helical nucleocapsid –Outer lipoprotein envelope • Envelope covered with hemagglutinin (HA) and neuraminidase (NA). • HA- binds to cell surface receptor to initiate infection. Target of neutralizing Ab. • NA- cleaves neuraminic acid to release virus from infected cell. In addition, helps to degrade protective respiratory mucus .

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4
Q

What are the matrix proteins of influenza? The antigens? Nonstructural proteins/Virulence?

A

• Matrix Proteins –M1- structural. –M2- forms ion channel between internal and external environment. Role in virion uncoating. • Antigens –Internal ribonucleoprotein-group-specific. –HA and NA- type-specific. • Nonstructural protein- NS1-determines virulence by inhibiting production of interferon mRNA.

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5
Q

What is the genome, classification, and types of parainfluenza virus?

A

• Enveloped RNA Viruses • Classification: Paramyxoviruses • Types: 1,2,3,4 (with 2 subtypes, 4A and 4B).

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6
Q

Respiratory Syncticial Virus genome? Classification? Attachments? Groups?

A

• Enveloped, nonsegmented RNA virus • Classification: Paramyxovirus • Attachment (G) and fusion proteins (F) . • Two strains-groups A and B, with many genotypes. • Strains of both groups often circulate concurrently. • Immunity is incomplete.

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7
Q

Adenovirus genome? Serotypes? Some associated with what system disease?

A

• Double-stranded, nonenveloped DNA viruses. • Serotypes: minimum of 51 divided into six species (A-F) • Some types associated more with respiratory disease and others with GI disease.

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8
Q

Structure of adenovirus?

A

• Structure: • Icosahedral nucleocapsid • Fiber protrudes from each of the vertices of the capsid. • The fiber is used for attachment and is a hemaglutinin. • Fiber protein is type-specific antigen. • Group-specific antigen located on hexon.

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9
Q

Explain the infection of Adenovirus?

A

• Capability to reside in host for a period of several years or longer with prolonged, intermittent shedding of virus after initial infection • Latency • Immunity is based on neutralizing antibody, is type-specific, and is lifelong.

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10
Q

Human metapneumonia virus genome? Classification? How many genotypes?

A

• Enveloped, single-stranded RNA virus. • Classification: Paramyxovirus • Four genotypes. • Two major antigenic subgroups-A and B.

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11
Q

What is the Cornovirus

A

• Enveloped RNA viruses. • 80-160 nm in diameter. • Three antigenic groups- I, II, III • 3 or 4 proteins –surface glycoprotein (S protein) –hemagglutinin-esterase –membrane glycoprotein –nucleocapsid

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12
Q

Hantavirus genome? Classification? What is the major cause of hantavirus?

A

• RNA viruses, 3 RNA segments, lipid envelope • Classification: Bunyaviridae • Sin Nombre Virus is the major cause of Hantavirus Pulmonary Syndrome in the 4corners region of the United States.

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13
Q

Spectrum, Pathogenicity, and the clinical disease and diagnosis of Respiratory Viral infections?

A

• Spectrum of viral agents - overwhelming majority of acute respiratory disease • Pathogenicity - problem is secondary bacterial infection, (bronchopneumonia, otitis, sinusitis) • Clinical disease and diagnosis –Specific agents or groups of agents differ in frequency with which infection results in a particular syndrome, i.e. coryza and rhinovirus, croup and parainfluenza virus, bronchiolitis and respiratory syncytial virus. –Almost any syndrome can be caused by almost any viral respiratory pathogen

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14
Q

Risk factors influencing the incidence and severity of Viral respiratory tract infection in infants and children?

A

• Age, immunologic experience • Prematurity, low birth weight • Chronic cardiopulmonary diseases • Immunodeficiency syndromes • Malnutrition • Exposure –Other children in family –Crowding –Care setting, family versus day care • Environmental pollution, parental smoking • Lack of breast-feeding

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15
Q

What are the methods and specimens needed to detect respiratory viruses?

A

• Methods –Tissue culture –Serology –Rapid antigen detection –Molecular methods • Specimens –Nasal wash –Oropharyngeal swab –Bronchoalveolar lavage

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16
Q

Immunity of respiratory viruses?

A

–Largely IgA, short-lived –Reinfection frequently results in milder disease, immunological memory –Cell mediated immunity –Interferon

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17
Q

Integrated system for defense of the respiratory system?

A

• Mechanical defenses • Phagocytic defenses • Humoral Immunity • Cell-Mediated Immunity

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18
Q

in general how are respiratory infections spread?

A

• Spread via respiratory tract by airborne droplets, contact

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19
Q

Age, sex, incidence timing that can lead to an increase in Respiratory viral infections?

A

• Age: Increased frequency and seriousness in young children and old age • Sex: Increased in women after childhood • Incidence: Decreased summer, increased winter • Underlying disease can lead to more severe clinical manifestations.

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20
Q

How do viruses change?

A

• Viruses change their pathogenic qualities and epidemic potentialities yielding new strains each year • Host’s susceptibility changes as agents keep changing • Vaccination: lead time necessary for production of vaccine

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21
Q

What are the agents of the common cold, pharyngitis, and laryngitis?

A

–Bacteria not the primary pathogens in URI –Principally caused by viruses with rhinovirus being the most common agent.

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22
Q

Clinical course of common cold, pharyngitis, laryngitis?

A

–An infection of the superficial mucus membranes, an intense rhinitis in the absence of marked constitutional disturbance with or without cervical lymphadenitis and fever –Incubation period 24 hours, symptoms subside in 24-48 hours, gone 3-7 days –Cold, pharyngitis, laryngitis

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23
Q

Lab Diagnosis of common cold, pharyngitis, laryngitis?

A

–Culture to rule out bacterial pathogens in the pharynx and ideally only treat if positive –No diagnostic tests for rhinovirus.

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24
Q

Treatment and control of common cold, pharyngitis, laryngitis?

A

• Treatment: Supportive for viral causes. • Control –Hand Hygiene –Respiratory Hygiene –Vaccination for specific agents (none for rhinovirus, the most common cause of colds)

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25
Q

Agents of influenza?

A

Agents: Influenza viruses types A, B, and C, each with variants –RNA viruses (orthomyxoviruses), affinity for mucoprotein on cell surfaces, enzyme neuraminidase destroys these mucoprotein receptor sites –Influenza A and and B cause epidemics; antigens for both of these types are found in yearly influenza vaccine. –Influenza A has two subtypes based on surface antigens hemagglutinin (HA) and neuraminidase (NA). –Influenza C: broadly distributed in population, cause only mild upper respiratory infection, rare changes in antigenic composition; not found in vaccine.

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26
Q

What is a shift change in influenza?

A

• Major change, new subtype • Exchange of gene segments • Occurs in A subtypes only • May cause pandemic • Occurs infrequently

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27
Q

What is a drift change in influenza?

A

• Minor change, within subtype • Point mutations • Occurs in A and B subtypes • May cause epidemic • Occurs frequently

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28
Q

What is influenza transmission? highest attack rates in? Temp/climate? Incubation?

A

• Transmission via respiratory droplet. • Highest attack-rates among school-aged kids. • Temperate climates: peak activity in US November-May but highest January/February. • Circulation of more than one strain common. • Incubation-1-4 days, mean of 2 days.

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29
Q

Influenza accounts for? secondary attack rates? Hospitalization rates? Morbidity greater in which high risk groups?

A

• Accounts for many visits to physician and ER among children. • High secondary attack-rates in families. • Hospitalization rates higher among those <2 yrs and >65 yrs. • Morbidity greater for certain high-risk groups: –Hemoglobinopathies –Chronic lung disease –Asthma –Cystic fibrosis –Malignancy –Diabetes –Chronic renal disease –Chronic heart disease –***Note: Although deaths are more common among kids with risk factors for influenza complications, most pediatric deaths occur among previously healthy children

30
Q

Pathogenesis of influenza?

A

–Spread via respiratory tract droplets –Selective action for the ciliated epithelium, and in humans invades those areas of the bronchial tree covered by ciliated epithelium –Inflammation, necrosis and desquamation of the respiratory tract epithelial cells

31
Q

Clinical disease of influenza?

A

–Abrupt onset of fever, shaking chills, severe headache, muscle aches, rhinitis, sore throat, cough, prostration –Less common: conjunctival injection, abdominal pain, nausea, emesis, diarrhea. –In neonates, can look like sepsis. –Major complication bacterial superinfection –Other complications of influenza : Reye’s syndrome, myositis, neurologic (ranging from febrile seizures to encephalitis).

32
Q

Lab diagnosis of influenza?

A

–Best if perform testing on upper respiratory tract specimens (nasophrayngeal or nasal swabs) within 4 days of symptom onset. –Isolation in egg or cell culture: 2-6 days –Rapid diagnostic tests for A and B Ags- sensitivity and specificity variable. DFA and IFA staining for detection of A and B Ags in nasopharyngeal or nasal specimens- rapid-3-4 hours. • Interpret rapid and immunofluorescent tests with caution. – False+ likely during low activity. – False- likely during high activity. –Serology: hemagglutination inhibition testing, CF, neutralization testing, or EIAnot useful for patient management-need 2 serum samples 10-14 days apart. –RT-PCR-high sensitivity and specificity.

33
Q

Vaccines for influenza?

A

• Ability of the virus to mutate periodically to entirely circumvent immunity to its ancestors • Inactivated virus; live attenuated virus

34
Q

Live attenuated vaccine versus inactivated vaccine?

A

Low effectiveness of LAIV during the 2010-2016 Influenza Seasons against Influenza a (H1N1).

» Therefore, during the 2016-2017 and 2017-2018 seasons, LAIV was not recommended for use.

» However, in the 2018-2019 season, LAIV is being recommended because it has been effective against flu B and H3N2. Some data also shows that new H1N1 vaccine virus in LAIV may have improved effectiveness.

35
Q

Who is at high risk for influenza complications?

A

–Children younger than 5, but especially children younger than 2 years old

–Adults 65 and older.

–Pregnant women.

–American Indians and Alaskan Natives

– People who have medical conditions including: • Asthma • Neurological and neurodevelopmental conditions • Chronic lung disease • Heart disease • Blood disorders • Endocrine disorders • Kidney disorders • Liver disorders • Metabolic disorders. • Weakened immune system due to disease or medication • People younger than 19 years of age who are receiving long-term aspirin therapy • People who are morbidly obese (BMI40 or greater)

36
Q

Treatments for influenza?

A
  • Two types of antiviral drugs:
  • Adamantanes- widespread resistance among influenza A strains and influenza B viruses not susceptible. No longer in use.
  • Neuraminidase Inhibitors- can be used for A and B –Oseltamivir (tamiflu)-oral –Zanamivir-inhaled –Peramivir- IV
37
Q

When to give antivirals? Administer when? Oseltamivir treatment is how long? main side effect?

A
  • Antivirals offered for any hospitalized child that has worsening/severe illness associated with influenza.
  • Offer to any outpatient who has risk of severe complications from influenza.
  • Offer to child suspected of having influenza who has high-risk person living in house.
  • Administer early- within 48 hours-for best outcome.
  • Oseltamivir treatment is 5 days and main side effect is GI.
38
Q

Agents of a parainfluenza virus infection?

A

Agents - Types 1 through 4 –Paramyxoviruses, receptor destroying enzyme neuraminidase, hemagglutinins (cause hemadsorption in tissue culture)

39
Q

Parainfluenza epidemiology?

A
  • Transmission: direct contact and droplets/fomites.
  • Sporadic and epidemic disease.
  • Cyclic and distinct pattern: –Type 1-usually causes croup every other autumn –Type 2-same as 1and often concurrent but less common and less severe –Type 3-spring and summer but often into autumn when 1 and 2 are less prominent. –Type 4- least common.
  • Primary infection with all usually by age 5y. –Type 3-often in infancy. –Type 1-most common among 1-5 yr olds.
  • Incubation-2-6 days.
40
Q

Explain how viral infections can lead to respiratory effort?

A
41
Q

Conditions that favor an increased rate of infection?

A

–Absent serum antibody –Low levels of serum antibody –Absent or decreased secretory antibody

42
Q

conditions that favor an increased level of disease severity?

A

–Large inoculum –Young age or prematurity –Low levels of maternal antibody –Immune deficiency –Abnormal pulmonary circulation –Abnormal airway

43
Q

lab diagnosis of parainfluenza virus?

A

–Viral isolation –RT-PCR –Rapid Ag identification: immunofluorescent techniques typically employed. –Serology - retrospective

44
Q

Explain the control of parainfluenza?

A

• Control –Contact precautions among hospitalized. –Hand hygiene.

45
Q

explain the management of viral croup?

A
46
Q

What is the Respiratory syncytial virus agent?

A

• The agent: respiratory syncytial virus (RSV), groups A and B –Paramyxovirus, quite unstable, ability to form syncytial masses in growing cell monolayers

47
Q

What is the transmission of RSV?

A
  • Transmission: direct exposure or contact with secretions/fomites. Note-can survive on surfaces for several hrs and hands for minmum of 30 minutes.
  • Winter and early spring in temperate areas.
  • Incubation: 2-8 days.
48
Q

Clinical disease in RSV?

A

Clinical disease –Major cause in children under 6 months of bronchiolitis (URI, fever, respiratory distress, wheezing and over-expansion of the lungs) or bronchopneumonia

49
Q

What are the clinical signs of lower respiratory infection in RSV? The xray findings?

A
  • Fever, usually present early with upper respiratory tract signs, but frequently disappears as disease progresses
  • Retractions • Tachypnea • Crackles • Wheezing • Hypoxemia • Cough may persist for weeks
  • X-ray findings do not always reflect severity of illness –Bilateral interstitial pneumonitis or mild changes (peribronchial thickening and hyperinflation) with hyperinflation of lung (most common) –Lobar, segmental, or subsegmental consolidation, mimicking bacterial pneumonia (20% of children)
50
Q

Risk factors for RSV in the lower respiratory area?

A

–Absence of breast-feeding –Crowding –Maternal smoking –Asthma in immediate family –Increased airway reactivity in infants –Anatomically small airways –Formation of RSV-specific IgE antibody

51
Q

When is hospitalization needed for RSV infection?

A

–Premature birth –Bronchopulmonary dysplasia –Congenital heart disease with pulmonary hypertension –Cystic fibrosis –Immune suppression –Organ or bone marrow transplantation

52
Q

Short term and long term effects of RSV?

A
  • Short-term –Apnea most common complication in young infants
  • Long-term –Recurrent wheezing –Pulmonary function abnormalities
53
Q

Lab diagnosis of RSV?

A

Laboratory diagnosis –isolation in known sensitive cell cultures –rapid antigen detection systems: immunofluorescent and enzyme immunoassay techniques. –RT-PCR- preferred –serology not generally reliable in infants

54
Q

RSV treatment?

A

• Primarily Supportive • Ribavirin for life-threatening disease only. • Note: corticosteroids, alpha and beta adrenergic agents, and antimicrobials not routinely recommended.

55
Q

RSV prevention?

A
  • Proper hand and repsiratory hygiene.
  • Palivizumab (Synagiso) humanized murine monoclonal antibody. Maximum- 5 doses. Strict criteria for certain high risk infants.
56
Q

what is human metapneumovirus (hMPV)? Similar to?

A
  • Paramyxovirus
  • Acute respiratory disease in children, elderly,and immunocompromised
  • Similar to RSV in range of severity of illness –Clinically apparent infections more common in children <2 years –Asymptomatic and mild infections more common in older children and adults
57
Q

hMPV seasonality?

A
  • Winter seasonality –up to 10% of “viral illness” in children
  • Global distribution (based on seroprevalence)
  • Circulating >40 years
58
Q

hMPV lab diagnosis and treatment?

A
  • Laboratory Diagnosis: –RT-PCR
  • Treatment: supportive
59
Q

Explain coronoviruses?

A
  • One of the leading cause of the common cold behind Rhinoviruses
  • Longer incubation period (3d vs. 2d)
  • Shorter duration (7d vs. 10d)
  • Similar symptoms (nasal obstruction, sneezing, runny nose, and cough)
  • Examples: Severe Acute respiratory Syndrome (SARS-CoV) and Middle East respiratory syndrome (MERS
60
Q

Coronoviruses antibody? Re-infection? S protein antibodies are?

A

• Host defenses • S protein-specific antibodies are neutralizing • Antibody is short-lived (2-3 yrs) • Re-infection is common

61
Q

Where are coronoviruses found?

A

• Epidemiology –Found all over the world –Winter and spring in temperate climates –Periodic epidemics (every 2-3 yrs) in the U.S.

62
Q

Coronovirus lab detection?

A

Laboratory detection –RT-PCR of respiratory specimens, stool, blood now employed for SARS infection and some MERS infections. –Serology in reference labs.

63
Q

What are the clinical manifestations of the SARS Coronovirus?

A

• Fever • Myalgia • Headache • Malaise • Cough • Chills • Dyspnea/Hypoxemia • Diarrhea • Respiratory failure • Higher mortality in adults

64
Q

Clinical manifestations of the MERS coronovirus?

A

• Similar to SARS. • Most infections in male adults with underlying renal, cardiac, or metabolic disease

65
Q

Coronovirus treatment?

A

• Supportive Mainly • No antiviral yet approved.

66
Q

Explain the Hantavirus Pulmonary syndrome Clinical? Labs?

A
  • Clinical –Fever and unexplained ARDS with hypoxemia OR –Unexplained fatal respiratory illness with autopsy
  • Laboratory H 4-fold rise in IgG antibody titer OR –Positive IgM antibody OR –Positive immunohistochemistry –Polymerase chain reaction evidence of MCV
67
Q

Hantavirus Pulmonary syndrome clinical manifestations?

A

• Prodromal Symptoms for 3-7 days: –Fever –Chills –Headache –Myalgias –Nausea/Emesis/Diarrhea –Dizziness –Cough FOLLOWED BY SEVERE HYPOXEMIA AND PULMONARY EDEMA!!!Can also see myocardial dysfucntion leading to hyptoension.

68
Q

Epidemiology of HPS?

A

Epidemiology –Rodent reservoir –Geographic distribution: • In US in 4 corners region primarily. –Mortality: 30-40%

69
Q

Diagnosis of HPS? Treatment? Control?

A
  • Diagnosis-serology is method of choice for diagnosis.
  • Treatment –Supportive –ECMO –?Ribavarin but no effect in cardiopulmonary stage
  • Control –Rodent control
70
Q

Explain the syndromes of Adenovirus in different age populations?

A
71
Q

Lab diagnosis of Adenovirus?

A

Laboratory diagnosis –Isolation in culture –Antigen detection –PCR-generally preferred in respiratory disease.

72
Q

What is the epidmiology and treatment of adenovirus?

A
  • Epidemiology –Type 1, 2 and 5 endemic in most populations (usually low level present at all times) –Types 3, 4, 7, 14 and 21 epidemic –Spread by respiratory droplet or fecal oral route
  • Treatment –Supportive –Cidofovir

Respiratory 2 (10 decks)

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