A Trivia On Viral Respiratory Infection! Quiz

CROUP (ACUTE LARYNGOTRACHEOBRONCHITIS)
Etiology
Acute laryngotracheobronchitis, or croup, is mostly caused by human parainfluenza viruses (3 cases out of 4). HPIV-1, HPIV-2 and HPIV-3 are the most common culprits (mostly HPIV-1 & HPIV-3; children between 1 & 5 yoa), but other viruses are associated with acute croup: These include influenza A and B viruses (mostly influenza A; children >5 yoa), RSV (in children 5 yoa).
Incidence
10 to 20% of lower respiratory tract diseases of children
Epidemiology
• Croup is almost exclusively an illness of young children ( • Transmission through droplets, direct contact, fomites
• Seasonality: Early fall (every other year) (HPIV-1 & HPIV-2) and late winter-early spring (HPIV-3), winter to early spring (influenza), and winter RSV

Incubation period
10 hours to a few days (adenoviruses)
Duration
3 to 4 days
Symptoms
• Rhinorrhea
• Sore throat
• Mild cough
• Brassy, barking cough, “seal’s bark” (2 - 3 d after symptoms onset)

•Inspiratory stridor
• Fever (except if due to RSV)
• Elevated respiratory rate
• Chest wall retractions (supraclavicular & suprasternal areas)
Fluctuating course (i. e. the child may appear to improve or worsen within an hour)
Diagnosis
Clinical syndrome and seasonality are sufficient for diagnosis, although viral isolation and identification can be obtained from nasopharyngeal samples. Differential diagnosis should include bacterial epiglottitis, supraglottitis, bacterial tracheitis and non-infectious causes of obstruction.

Pathogenesis
Most of the symptoms are the result of inflammation and seem proportional to viral replication (in the case of HPIVs at least) in both the upper and lower respiratory tract (respiratory epithelium). Viral infection is initiated in the upper respiratory tract, with inflammation of the nasal passages and nasopharynx, and then moves to the lower respiratory tract. Stridor, hoarseness and cough result from the inflammation of the larynx and trachea, especially at the subglottic level.
Immunity
• Very limited specific immunity, as re-infections with HPIVs, influenzaviruses and RSV are frequent
• Cellular immunity is thought to be important in viral clearance and avoidance of lethal outcome

Progression-complications (rare)
• Otitis-media
• Sinusitis
• Pneumonia

Prevention and Treatment
• Good hygiene practices
• Vaccination (influenza A and B)
• Alleviation of symptoms

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BRONCHIOLITIS
Etiology
RESPIRATORY SYNCYTIAL VIRUS (RSV) is the main virus responsible for bronchiolitis.
Other viruses associated with bronchiolitis are human metapneumoviruses, HPIVs (especially HPIV-3), influenzaviruses A and B, mumps virus, adenoviruses (types 3, 7 & 21), and rhinoviruses.
Incidence
11% ( Epidemiology
• Typically an infection of infants and early childhood (usually children under 2 yoa)
• More common in boys (1.5♂:1♀)
• Transmission through droplets, direct contact (respiratory secretions), fomites
• Seasonality: Late fall to early spring (rainy season in the tropics)

Incubation period
4 to 5 days
Duration
1 to 2 weeks
Symptoms
• Rhinorrhea
• Cough
• Expiratory wheezing
• *******Air trapping ******

• ********Nasal flairing*********
•******* Subcostal retractions*******
• ******8Hypoxia********
• Cyanosis
• Fever (occasional)

Risk Factors
• Children with underlying cardiopulmonary disease conditions
• Immunocompromised children
• Children born prematurely

Diagnosis
The clinical syndrome and seasonality are the main diagnostic features, although differential diagnosis must include all other causes of lower respiratory illnesses (e.g. asthma, retropharyngeal abscess, enlarged adenoids, foreign body, vascular rings) and infections and, for infants younger than 6 months, must include Chlamydia trachomatis, and Pneumocystis jirovecii for infants less than 4 months. Diagnosis is through isolation and culture of etiological agent from nasopharyngeal secretions. Rapid diagnosis is also achieved by detection of viral proteins (immunofluorescence & ELISA) or viral RNA (RT-PCR) in nasopharyngeal secretions when antiviral therapy is possible (influenza, RSV).
Pathogenesis
Viral replication first starts in the nasopharynx. Spread of the virus to the lower respiratory tract is rapid and likely due to secretion aspiration (but also from cell to cell). Viral replication is mainly restricted to the respiratory epithelium, but RSV also infects mononuclear phagocytes thus interfering with their functions. Severity of disease correlates with viral load and epithelial cell destruction and sloughing (bronchiolar epithelium). Inflammation, inflammatory cell infiltration and increased mucous production by mucous secreting cells also contribute to the pathogenesis of the disease (necrosis, peribronchiolar infiltration, oedema, and mucous/fibrin/alveolar debris plugs), especially in young infants as they possess bronchioles of smaller diameters.
Immunity
Infection provides only short-term humoral immunity, as RSV (& other bronchiolitis agents) re-infections are common. Effective vaccines against RSV are unavailable at the present moment.
Protection against RSV relies on non-specific host defense mechanisms such as surfactants and interferons, as well as cell-mediated immunity (CTL) and adaptive immunity (IgM, IgG, & IgA).
Progression-complications (rare)
• Otitis-media
• Sinusitis
• Asthma
• Pneumonia

Prevention and Treatment
• Good hygiene practices
• Alleviation of symptoms
• Ribavirin (RSV in some cases)

CROUP (ACUTE LARYNGOTRACHEOBRONCHITIS)
Etiology
Acute laryngotracheobronchitis, or CROUP, IS MOSTLY CAUSED BY HUMAN PARAINFLUENZA VIRUSES (3 CASES OUT OF 4).
HPIV-1, HPIV-2 and HPIV-3 are the most common culprits (mostly HPIV-1 & HPIV-3; children between 1 & 5 yoa), but other viruses are associated with acute croup: These include influenza A and B viruses (mostly influenza A; children >5 yoa), RSV (in children 5 yoa).
Incidence
10 to 20% of lower respiratory tract diseases of children
Epidemiology
• Croup is almost exclusively an illness of young children ( • Transmission through droplets, direct contact, fomites
• Seasonality: Early fall (every other year) (HPIV-1 & HPIV-2) and late winter-early spring (HPIV-3), winter to early spring (influenza), and winter RSV

Incubation period
10 hours to a few days (adenoviruses)
Duration
3 to 4 days
Symptoms
• Rhinorrhea
• Sore throat
• Mild cough
• Brassy, barking cough, “seal’s bark” (2 - 3 d after symptoms onset)

•Inspiratory stridor
• Fever (except if due to RSV)
• Elevated respiratory rate
• Chest wall retractions (supraclavicular & suprasternal areas)
Fluctuating course (i. e. the child may appear to improve or worsen within an hour)
Diagnosis
Clinical syndrome and seasonality are sufficient for diagnosis, although viral isolation and identification can be obtained from nasopharyngeal samples. Differential diagnosis should include bacterial epiglottitis, supraglottitis, bacterial tracheitis and non-infectious causes of obstruction.

Pathogenesis
Most of the symptoms are the result of inflammation and seem proportional to viral replication (in the case of HPIVs at least) in both the upper and lower respiratory tract (respiratory epithelium). Viral infection is initiated in the upper respiratory tract, with inflammation of the nasal passages and nasopharynx, and then moves to the lower respiratory tract. Stridor, hoarseness and cough result from the inflammation of the larynx and trachea, especially at the subglottic level.
Immunity
• Very limited specific immunity, as re-infections with HPIVs, influenzaviruses and RSV are frequent
• Cellular immunity is thought to be important in viral clearance and avoidance of lethal outcome

Progression-complications (rare)
• Otitis-media
• Sinusitis
• Pneumonia

Prevention and Treatment
• Good hygiene practices
• Vaccination (influenza A and B)
• Alleviation of symptoms

Rhinoviruses:
• Picornaviridae
• (+) ssRNA
• NAKED icosahedral capsid
• 30 nm
• >100 serotypes in 3 groups based on receptor specificity
• Seasonality: Mostly early fall and late spring (but rhinoviruses still account for half of the colds during the SUMMER…)
• Narrow host range (primates)

Enteroviruses:
• Picornaviridae
• (+) ssRNA
• NAKED icosahedral capsid
• 27 nm to 30 nm
• Tens of numbered serotypes
• Seasonality: Mostly SUMMER and early fall
• Fairly wide host range depending on serotype (mice, primates)


Adenoviruses, often associated with pharyngitis, are naked dsDNA viruses of the Adenoviridae family;
Adenoviruses (types 1, 2, 3, 4, 5, 6, 7, 14 & 21):
• Adenoviridae
• Linear dsDNA
• NAKED icosahedral capsid
• 65 nm to 80 nm
• 49 serotypes
• NO SEASONALITY
• Wide host specificity

VIRAL PHARYNGITIS SYNDROME
Etiology
Pharyngitis is often associated with the common cold and flu (influenza) and, consequently, many of the viruses that cause common colds and the flu also can cause pharyngitis. These include rhinoviruses, adenoviruses (types 3, 4, 7, 14 & 21; types 3 & 7 are associated with bilateral conjunctivitis),
enteroviruses [COXSACKIEVIRUS A (types 2, 4, 5, 6, 8 & 10)
and echoviruses], influenzaviruses A and B, human parainfluenzaviruses (HPIV-1, HPIV-2 & HPIV-3), coronaviruses, and RSV. Other viruses associated with pharyngitis include Epstein-Barr virus (Human herpesvirus 4 or EBV), human cytomegalovirus (Human herpesvirus 5 or CMV), herpes simplex viruses (Human herpesvirus 1 & Human herpesvirus 2 or HSV-1 & HSV-2 respectively), and Human immunodeficiency virus 1 (HIV-1).

Symptoms associated with specific viral etiologies:
• Exudate (adenoviruses 3 & 7, HSV & EBV)
• Conjunctivitis (influenzaviruses A & B & adenoviruses 3 & 7)
• Influenza A and B pharyngitis is associated with the flu syndrome
• Vesicular lesions and ulcers [COXSACKIEVIRUSES (enteroviruses) cause HERPANGINA & HAND-&-FOOT-&-MOUTH DISEASE

& echoviruses (enteroviruses) also cause herpangina. HSV pharyngitis is also associated with vesicular lesions & ulcers]

The most likely time frame until the appearance of the H9N2 influenza A virus in the person's community is unknown, as stated in the answer. It is not possible to determine when or if the virus will reach their community based on the given information.

Parainfluenzaviruses:
• Paramyxoviridae
• (-) ssRNA
• Enveloped pleomorphic
• 150 nm to 200 nm
• Four types HPIV-1 to HPIV-4; no clinically relevant antigenic strains
• Seasonality: Early fall of even-numbered years until 1970 (HPIV-1), early fall of odd-numbered years since 1973 (HPIV-1 and HPIV-2), and late winter-early spring (HPIV-3)
• Narrow host range (humans), although human counterparts infect other mammals (rodents, cattle, sheep, dogs)

BRONCHIOLITIS
Etiology
RESPIRATORY SYNCYTIAL VIRUS (RSV) is the main virus responsible for bronchiolitis.
Other viruses associated with bronchiolitis are human metapneumoviruses, HPIVs (especially HPIV-3), influenzaviruses A and B, mumps virus, adenoviruses (types 3, 7 & 21), and rhinoviruses.
Incidence
11% ( Epidemiology
• Typically an infection of infants and early childhood (usually children under 2 yoa)
• More common in boys (1.5♂:1♀)
• Transmission through droplets, direct contact (respiratory secretions), fomites
• Seasonality: Late fall to early spring (rainy season in the tropics)

Incubation period
4 to 5 days
Duration
1 to 2 weeks
Symptoms
• Rhinorrhea
• Cough
• Expiratory wheezing
• *******Air trapping ******
• ******Nasal flairing*********
•*******Subcostal retractions*******
• ******Hypoxia********
• Cyanosis
• Fever (occasional)

Risk Factors
• Children with underlying cardiopulmonary disease conditions
• Immunocompromised children
• Children born prematurely

Diagnosis
The clinical syndrome and seasonality are the main diagnostic features, although differential diagnosis must include all other causes of lower respiratory illnesses (e.g. asthma, retropharyngeal abscess, enlarged adenoids, foreign body, vascular rings) and infections and, for infants younger than 6 months, must include Chlamydia trachomatis, and Pneumocystis jirovecii for infants less than 4 months. Diagnosis is through isolation and culture of etiological agent from nasopharyngeal secretions. Rapid diagnosis is also achieved by detection of viral proteins (immunofluorescence & ELISA) or viral RNA (RT-PCR) in nasopharyngeal secretions when antiviral therapy is possible (influenza, RSV).
Pathogenesis
Viral replication first starts in the nasopharynx. Spread of the virus to the lower respiratory tract is rapid and likely due to secretion aspiration (but also from cell to cell). Viral replication is mainly restricted to the respiratory epithelium, but RSV also infects mononuclear phagocytes thus interfering with their functions. Severity of disease correlates with viral load and epithelial cell destruction and sloughing (bronchiolar epithelium). Inflammation, inflammatory cell infiltration and increased mucous production by mucous secreting cells also contribute to the pathogenesis of the disease (necrosis, peribronchiolar infiltration, oedema, and mucous/fibrin/alveolar debris plugs), especially in young infants as they possess bronchioles of smaller diameters.
Immunity
Infection provides only short-term humoral immunity, as RSV (& other bronchiolitis agents) re-infections are common. Effective vaccines against RSV are unavailable at the present moment.
Protection against RSV relies on non-specific host defense mechanisms such as surfactants and interferons, as well as cell-mediated immunity (CTL) and adaptive immunity (IgM, IgG, & IgA).
Progression-complications (rare)
• Otitis-media
• Sinusitis
• Asthma
• Pneumonia

Prevention and Treatment
• Good hygiene practices
• Alleviation of symptoms
• Ribavirin (RSV in some cases)

Influenza A virus, which is the main etiological agent responsible for the flu, is an enveloped segmented (-) ssRNA virus of the Orthomyxoviridae family; Influenzaviruses: • Orthomyxoviridae • Segmented (7-8) (-) ssRNA • Enveloped spherical • 120 nm • Many types characterized by their hemagglutinin (15 HA recognized subtypes) and neuraminidase (9 recognized NA subtypes) • Seasonality: Winter to early spring • Wide host range (birds, swine, humans)

Respiratory Syncytial Virus (RSV):
• Paramyxoviridae
• (-) ssRNA
• Enveloped pleomorphic
• 100 nm to 350 nm
• 2 subgroups (A and B) based on the G surface glycoprotein
• Seasonality: Mid-winter to early spring
• Wide host specificity (humans and non-primates)

VIRAL COLD SYNDROME Etiology The plurality of common colds is due to rhinoviruses (30-50%, sometimes more). Other etiological agents include coronaviruses (10-15%), influenzaviruses A (5-15%; especially in children) and B, RSV (5%), other human parainfluenzaviruses (5%; HPIV-1, HPIV-2, HPIV-3 & HPIV-4), enteroviruses (<5%), adenoviruses (<5%; types 1, 2, 5, & 6 are endemic, types 4, 7, 14 & 21 cause epidemics, whereas type 3 is both), and metapneumoviruses. Other systemic viral infections can present with similar upper respiratory tract symptoms, but these are usually followed by other, more characteristic, symptoms. These include measles, or rubeola, (Morbillivirus, Paramyxoviridae), rubella (Rubivirus, Togaviridae) and mumps (Rubulavirus, Paramyxoviridae).



Spearmint Rhino is a club in vegas with NAKED women.

the Rhino virus is NAKED



Coronaviruses:

• Coronaviridae = (+) ssRNA • Enveloped PLEOMORPHIC • 100 nm to 150 nm

• 2 antigenic groups (229E and OC43)

• Seasonality: Winter or spring

• Narrow host range (humans)



Rhinoviruses:

• Picornaviridae • (+) ssRNA • NAKED icosahedral capsid • 30 nm

• >100 serotypes in 3 groups based on receptor specificity

• Seasonality: Mostly early fall and late spring (but rhinoviruses still account for half of the colds during the SUMMER…)

• Narrow host range (primates)

VIRAL COLD SYNDROME Etiology The plurality of common colds is due to rhinoviruses (30-50%, sometimes more). Other etiological agents include coronaviruses (10-15%), influenzaviruses A (5-15%; especially in children) and B, RSV (5%), other human parainfluenzaviruses (5%; HPIV-1, HPIV-2, HPIV-3 & HPIV-4), enteroviruses (<5%), adenoviruses (<5%; types 1, 2, 5, & 6 are endemic, types 4, 7, 14 & 21 cause epidemics, whereas type 3 is both), and metapneumoviruses. Other systemic viral infections can present with similar upper respiratory tract symptoms, but these are usually followed by other, more characteristic, symptoms. These include measles, or rubeola, (Morbillivirus, Paramyxoviridae), rubella (Rubivirus, Togaviridae) and mumps (Rubulavirus, Paramyxoviridae). Rhinoviruses: • Picornaviridae • (+) ssRNA • NAKED icosahedral capsid • 30 nm • >100 serotypes in 3 groups based on receptor specificity • Seasonality: Mostly early fall and late spring (but rhinoviruses still account for half of the colds during the SUMMER…) • Narrow host range (primates) Enteroviruses: • Picornaviridae • (+) ssRNA • NAKED icosahedral capsid • 27 nm to 30 nm • Tens of numbered serotypes • Seasonality: Mostly SUMMER and early fall • Fairly wide host range depending on serotype (mice, primates)

Pathogenesis
Most of the symptoms are the result of inflammation and seem proportional to viral replication (in the case of HPIVs at least) in both the upper and lower respiratory tract (respiratory epithelium). Viral infection is initiated in the upper respiratory tract, with inflammation of the nasal passages and nasopharynx, and then moves to the lower respiratory tract. STRIDOR, HOARSENESS AND COUGH RESULT FROM THE INFLAMMATION OF THE LARYNX AND TRACHEA, ESPECIALLY AT THE SUBGLOTTIC LEVEL.

Rhinoviruses:
• Picornaviridae
• (+) ssRNA
• NAKED icosahedral capsid
• 30 nm
• >100 serotypes in 3 groups based on receptor specificity
• Seasonality: Mostly early fall and late spring (but rhinoviruses still account for half of the colds during the ******SUMMER ******)
• Narrow host range (primates)

Enteroviruses:
• Picornaviridae
• (+) ssRNA
• NAKED icosahedral capsid
• 27 nm to 30 nm
• Tens of numbered serotypes
• Seasonality: Mostly SUMMER and early fall • Fairly wide host range depending on serotype (mice, primates)


Adenoviruses, often associated with pharyngitis, are naked dsDNA viruses of the Adenoviridae family;
Adenoviruses (types 1, 2, 3, 4, 5, 6, 7, 14 & 21):
• Adenoviridae
• Linear dsDNA
• NAKED icosahedral capsid
• 65 nm to 80 nm
• 49 serotypes
• NO SEASONALITY • Wide host specificity

infection initiates in the respiratory tract mucosa. Viral replication progresses along the respiratory epithelium, leading to a loss and desquamation of respiratory epithelial cells, associated with inflammatory cell infiltration. Direct cytopathic effects are believed to be responsible for most of the pathological changes, but inflammation is also involved
Pathogenesis --CROUP (ACUTE LARYNGOTRACHEOBRONCHITIS)
Most of the symptoms are the result of inflammation and seem proportional to viral replication (in the case of HPIVs at least) in both the upper and lower respiratory tract (respiratory epithelium). Viral infection is initiated in the upper respiratory tract, with inflammation of the nasal passages and nasopharynx, and then moves to the lower respiratory tract. Stridor, hoarseness and cough result from the inflammation of the larynx and trachea, especially at the subglottic level.