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Infection & Immunity Block > Viral Pharyngitis > Flashcards

Flashcards in Viral Pharyngitis Deck (25):

Infections of Oropharynx

Viruses most common invaders of nasopharynx
Rhinoviruses, coronaviruses: >50% of upper respiratory tract infections
Release of virus-rich fluid
Shedding of virus
Duration – 7 days

Following replication in epithelial cell layer, the release of the viruses are in extracellular fluid so when sneeze or cough there is shedding of virus


Upper Respiratory Tract Infections

Generally mild and self-limiting
Laboratory tests are generally not worthwhile
Treatment is symptomatic

Group of similar illnesses - different causes

Rhinitis with variable degrees of pharyngitis:
Nasal stuffiness
Runny nose
Sore throat



Primary complaint of sore throat

With nasal symptoms: predominantly viral
Without nasal symptoms: diverse etiologies

Salt water: shrinks the cells and unable to replicate viruses well so shortens the life cycle of the infection


Acute Pharyngitis and Tonsilitis

Acute pharyngitis = 70% viral causes

Common causes:
Viruses: Adenoviruses, EBV, HSV, Coxsackie virus
Bacteria: Strep. pyogenes, C. diptheriae, H. influenza

Less than 3 years of age = usually viral


Laryngitis and Tracheitis

Parainfluenza viruses
RSV and influenza viruses

Swelling of mucous membrane leads to croup: dry cough and inspiratory stridor

Croup: kids that have barking like cough because respiratory tracts have become swollen and have difficulty breathing
See in kids more because airways are smaller and more affected by swelling process



Very small particle
Carries well in small droplets
Naked – so survives in environment well
Plus sense RNA genome


Cycle of Rhinovirus

Transmission: through inhalation of respiratory droplets or fomites

Replication: in upper respiratory tract at 33C

Infection: confined to ciliated nasal mucosal epithelial cells

Symptoms mediated by inflammatory molecules

Incubation period : once infected, virus replicates and tissue damage occurs and development of symptoms within 2-3 days


Pathophysiology of Rhinovirus

Inflammation: decreased mucociliary transport

Secretory IgA: signs of pharyngeal inflammation are uncommon

IgA – eventually brings viral infection under control
Common cause of colds, nasal symptomology
Inflammation: nasal and sinus areas are where this occurs



Naked viral particles
Plus sense RNA genome

Large group of viruses:
Febrile pharyngitis
Hand, foot and mouth disease



Group A Coxsackie viruses
Children from 1-7 years of age; occasional in adults

Abrupt onset of fever
Associated sore throat
Dysphagia and malaise
Small vesicular lesions of the soft palate
¼ - vomiting and abdominal pain
Grayish white vesicles on the palate; discrete, surrounded by erythema
Other respiratory symptoms are usually lacking
Very painful pharyngitis

Tx: rest and symptomatic care; no specific treatments


Hand, Foot, and Mouth

Hand, foot and mouth disease
Fever, herpangina, skin rash
Usually under the age of 5
Coxsackie viruses, Enterovirus 71
Vesicle Lesions can be present, and rash can be present in other places of the body (auto-inoculation from break in the skin)

Can be swallowed and carried through the GI tract and this can spread virus to family members that is caring for infants (diaper changing)
Can present with herpangina in older kids because do not stick their feet and hands in their mouths



Capsid virus – does not survive in environment as well
Double stranded DNA genome

Member of the herpesviruses
Replicates in oropharyngeal epithelial cells
Latent infection in B cells; once infected you have it for the rest of your life
Clinical presentation: Infectious Mononucleosis



Important group of human pathogens
Herpes simplex viruses (types 1 and 2)
Varicella Zoster virus
Epstein Barr Virus
HHV 6 and 7
Kaposi sarcoma-associated virus


EBV Transmission, Infection, Dissemination

Transmission: propharyngeal secretions

Infection: oropharyneal epithelial cells and lymphoid cells in tonsillar epithelium

Infection of B cells in oropharynx
Dissemination via reticuloendothelial system


Infectious Mononucleosis

Incubation period from initial contact to large numbers of infected B cells is 30-50 days

Sore throat
Lymphadenopathy (cervical)
Physical exam - splenomegaly
May present with mild jaundice and rash


Primary EBV Infection

Atypcial lymphocytosis – polyclonal B cell activation

Large numbers of EBV-infected peripheral B cells
heterophile antibodies useful dx, but non-specific

Specific immune response
Activated T cells, NK cells
Mediators of clinical symptoms


Pathogenesis of EBV

Establishment of latent infection
1 in a million B cells - latently infected
Viral persistence
Restricted viral gene expression from altered cell growth and proliferation
Potential for reactivation - mostly if immunocompromised


Latency of EBV

Virus gains access to reticuloendothelial system and infect B cells and get recirculation of EBV infected B cells
Memory B cells so EBV will persist in these cells and have latency

EBV infects a naïve B cell causing activation and proliferation of B cells with EBV latency III, then the surviving memory B cells contain EBV latency II. This occurs in the germinal centers, then the cells go through lymph vessels where the EBV persistence continues without EBV gene expression and EBV latency I. These memory B cells then recirculate within the periphery where EBV replication (EBV lytic cycle) can occur via signaling to mature B plasma cells to secrete antibodies that enter the high endothelial venules and continue the process all over again.


EBV in Children

Frequently asymptomatic
EBV-specific serology is needed (serum EBV)

Young children below 12

Specific immune responses to EBV
Immune starts to respond via IgM EBV Ab
Then different types of IgG against specific viral proteins formed



Clinical presentation

Laboratory results:
Atypical lymphocytes
Heterophile antibodies (non specific)
Specific antibodies
Liver function tests

CBC and differential
See nucleus is enlarged and cytoplasm is ruffled in atypical lymphocytes
Hepatosplenomegaly can occur, so see elevated liver function tests


Heterophile Antibodies

IgM antibody produced by plasmacytoid cells
Agglutinate horse, sheep or cow RBCs
Often not seen in young children

B cells are pumping out Ab that are not designed to target specific Ag (non-specific) = IgM
Called heterophiles because react with RBCs from non human sources
Monospot test: patient serum + animal RBC = clumping/agglutinate of RBCs
Produced because of hyperplastic B cell response


EBV Complications

Splenic rupture
Airway obstruction

Burkitt’s lymphoma
Nasopharyngeal carcinoma


Mumps Virus Transmission and Symptoms

Transmission: respiratory droplets and saliva, direct contact, or fomites

Parotitis – swollen salivary glands
Fever and headache
Weakness and fatigue
Loss of appetite
Pain while chewing or swallowing


Mumps Epidemiology, Incubation Period, Prodromal Symptoms, and Clinical Presentation

Epidemiology: asymptomatic in 20-30%, and adults tend to be more severely affected

Incubation period -16-18 days

Prodromal symptoms - 3-5 days

Clinically – presentation depends organ affected
The most common –parotitis
CNS involvement
One third of post-pubertal male patients develop unilateral orchitis


Mumps Dx

Difficult to diagnose clinically
Mumps virus - no longer the most common cause of parotid swelling

Other causes:
cytomegalovirus, parainfluenza virus 1 and 3, influenza A, and HIV
Bacterial infections, drug reactions, and metabolic disorders