Viral Pharyngitis Flashcards
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 Sneezing Runny nose Sore throat
Pharyngitis
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
Rhinovirus
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
Enterovirus
Naked viral particles
Plus sense RNA genome
Large group of viruses:
Febrile pharyngitis
Herpangina
Hand, foot and mouth disease
Herpangina
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
EBV
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
Herpesvirus
Important group of human pathogens Herpes simplex viruses (types 1 and 2) Varicella Zoster virus Cytomegalovirus 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
Dissemination:
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
Symptoms Fever Sore throat Lymphadenopathy (cervical) Malaise Headache Physical exam - splenomegaly May present with mild jaundice and rash
Primary EBV Infection
Pathology
Atypcial lymphocytosis – polyclonal B cell activation
Early
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
EBV Dx
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
Non-specific
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
Malignancies:
Burkitt’s lymphoma
Nasopharyngeal carcinoma
Mumps Virus Transmission and Symptoms
Transmission: respiratory droplets and saliva, direct contact, or fomites
Symptoms: 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
