RhinovirusRhinovirus infections are chiefly limited to the upper respiratory tract but may include otitis media and sinusitis. Rhinovirus plays a role in exacerbations of asthma, cystic fibrosis, chronic bronchitis, and serious lower respiratory tract illness in infants, elderly persons, and patients who are immunocompromised. Although infections occur year-round, the greatest incidence is in the fall and spring. Of persons exposed to the virus, 70-80% have symptomatic disease.

RhinovirusBelong to the picornavirus family the smallest (pico) RNA viruses (24-30 nm)ssRNA virusAcid-labileRhinovirus Capsid consists of 4 proteins VP1, VP2, VP3& VP4At least 100 serotypes are knownIntercellular Adhesion Protein-1 (ICAM-1) Receptor for most human rhinovirus serotypes

Rhinovirus bonded to a CAM 1 receptorAntibodies bonded to a rhinovirus

Functions of Viral RNARNA genome is mRNA Positive strand. A viral-coded peptide (VPg) is attached to the 5 end.When introduced into cells, viral RNA can produce infectious virus. Viral RNA serves as a template for its replication Optimum growth occurs between 33 and 34 oC Viruses replicate rapidly in the cytoplasmdo not require DNA for reproduction

Functions of Viral ProteinsDerived from one polyprotein precursor Processed by post-translational cleavingStructural proteinsResponsible for host tropismsProtection of genomeAntigenicityNon-structural proteins ProteasesRNA polymeraseInhibitors of normal host cell functions

Virus Replication CycleInternal ribosome entry segment (IRES)

CoronavirusssRNA VirusEnveloped, pleomorphic morphology2 serogroups: OC43 and 229E

Transmission Routes Cold viruses may be transmitted by three routes:Large-particle droplets, which can travel a short distance to directly inoculate another personSmall-particle aerosols, which can travel longer distances and depositSecretion, which are transmitted by direct physical contactdirectly in alveoli of other individuals

How does it spread?Very contagiousSpread from person to personUsually from nasal secretions and from fingers of the affected personMost contagious in the first 3 days after symptoms beginViruses can last up to 5 hours on the skin and hard surfaces

Rhinovirus Higher rates occur in humid, crowded conditions, as found in nurseries, day care centers, and schools, especially during cooler months in temperate regions and rainy season in tropical regions.

Pathogenesis The offending virus invades the epithelial cells of URT.Inflammatory mediators are released.They alter the vascular permeability and cause tissue edema and stuffiness.Stimulation of cholinergic nerves in the nose and URT leads to increased mucus production (rhinorrhea) and occasionally to bronchocontriction Injury to cilia in the nasal epithelial cells may decrease ciliary function and impair clearance of nasal secretions.

Pathophysiology Rhinoviruses are transmitted to susceptible individuals by :Direct contact Aerosol particles infecting both ciliated areas of the nose and nonciliated areas of the nasopharynx through receptors, most frequently ICAM-1 (found in high quantities in the posterior nasopharynx). Few cells are actually infected by the virus, and the infection involves only a small portion of the epithelium.

PathophysiologySymptoms develop 1-2 days after viral infection, peaking 2-4 days after inoculation, although reports have described symptoms as early as 2 hours after inoculation with primary symptoms 8-16 hours later.

PathophysiologyDetectable histopathology causing the associated nasal obstruction, rhinorrhea, and sneezing is lacking: which leads to the hypothesis that the host immune response plays a major role in rhinovirus pathogenesis.

Infected cells release interleukin-8 (IL-8), which is a potent polymorphonuclear (PMN) chemoattractant. Concentrations of IL-8 in secretions correlate proportionally with the severity of common cold symptoms. Inflammatory mediators, such as kinins and prostaglandins, may cause vasodilatation, increased vascular permeability, and exocrine gland secretion.These, together with local parasympathetic nerve-ending stimulation, lead to cold symptoms

PathophysiologyViral clearance is associated with the host response and is due, in part, to the local production of nitric oxide. Serotype-specific neutralizing antibodies are found 7-21 days after infection in 80% of patients. Although these antibodies persist for years, providing long-lasting immunity, recovery from illness is more likely related to cell-mediated immunity. Persistent protection from repeat infection by that serotype appears to be partially attributable to immunoglobulin A (IgA) antibodies in nasal secretions, serum immunoglobulin G (IgG), and, possibly, serum immunoglobulin M (IgM).

PathophysiologyThe virus has a limited temperature range in which it can grow (33-35C) and cannot tolerate an acidic environment.

Thus, finding the virus outside of the nasopharynx is unlikely because of the acidic environment of the stomach and the temperature elevation in both the lower respiratory and gastrointestinal tracts.

VIRAL INFECTION OF NAZAL CELLSSNEEZING SORE THROATChemical Mediators of InflammationVascular DilatationNASAL OBSTRACTIONIncreased Vascular PermeabilityTissue EdemaSerum TransductionIncreased Mucus Production Sensitization of Irritated of Airways ReceptorsCholinergic StimulationBronchoconstrictionRHINORRHEACOUGHThe Common Cold

Physical examinationRed nose with dripping nasal discharge may be present.Nasal mucous membranes have a glistening, glassy appearance without obvious erythema and edema. Yellow or green nasal discharge does not indicate bacterial infection because a large number of white blood cells migrate to the site of viral infection.

Physical ExaminationIf marked:1. erythema, edema, exudates, or small vesicles are observed in the oropharynx 2. conjunctivitis3. polyps in the nasal mucosa occur, consider other etiologies, including: adenovirus, herpes simplex virus, mononucleosis, diphtheria, Coxsackie A virus, or group A streptococcus (GAS).

Clinical characteristicsIncubation period 12-72 hoursNasal obstruction, drainage, sneezing, scratchy throatMedian duration 1 week but 25% can last 2 weeksPharyngeal erythema is commoner with adenovirus than with rhino or coronavirus

SymptomsBegins with a feeling of dryness and stuffiness in the nasopharynx (nose)Nasal secretions (usually clear and watery)Watery eyesRed and swollen nasal mucous membranesHeadacheGeneralized tirednessChills (in severe cases)Fever (in severe cases)Exhaustion (in severe cases)

If the pharynx and larynx (throat) becomes involved:Sore throatHoarseness

ICEBERG CONCEPT INFECTIONSever SymptomsMild SymptomsInfection but no SymptomsExposure but no Symptoms

RISK FACTOR FOR MORE SEVER COMMON COLDLOW NEUTRALIZING AbCHRONIC LUNG DISEASEEXTREMES AGEASTHMA ALLERGY Ig E CYTOKINE PRODUCTION I F N -gamma I L-5

ComplicationsAcute otitis media Paranasal sinusitisNeck lymphonoditis Retropharyngeal abscessLaryngitis Lower respiratory tract diseaseAcute glomerulonephritis and rheumatic fever

Laboratory TestWhite cell count The viral infections is normal to low.The bacterial infections or viral-bacterial infection is high. Laboratory diagnosis of viral infectionsAntigen or nucleic acid detection Serologic testingIsolation of viruses by culture of the throat or nasopharynxUse of monoclonal antibodiesPolymerase chain reaction (PCR)

TREATMENT

Treatment of common coldAntihistaminesDecongestantsPain RelieversCough suppressantsNasal StripsAntibiotics are ineffective!!!

MEDICATION Drugs used in the symptomatic treatment include:Nonsteroidal anti-inflammatory drugs (NSAIDs) Antihistamines Anticholinergic nasal solutions These agents have no preventive activity and appear to have no impact on complications.

TREATMENT Rhinovirus infections are predominately mild and self-limited: thus, treatment is generally focused on symptomatic relief and prevention of person-to-person spread and complications. The mainstays of therapy include: Rest, Hydration, Antihistamines, Nasal decongestantsAntibacterial agents are not effective unless bacterial superinfection occurs.

TREATMENTDevelopment of effective antiviral medications has been hampered by the short course of these infections. Because peak symptom severity occurs at 24-36 hours after inoculation, only a narrow window of time exists in which antivirals could positively impact upon this infection. In addition, the cause of the common cold is not always rhinovirus. Therefore, rapid and accurate diagnostic tests would be needed if a specific antiviral therapy were developed.

VACCINATION Because of the large number of rhinovirus immunotypes and the inaccessibility of the conserved region of the viral capsid (the most likely effective site for targeting a vaccine), no rhinovirus vaccine is on the horizon.

PREVENTIONBecause infection is spread by: hand-to-hand contact, autoinoculation, possibly, aerosol particles, emphasize appropriate hand washing, avoidance of finger-to-eyes or finger-to-nose contact, and use of nasal tissue. Cough and sneeze into arm or tissue, not into your hand

SUMMARY

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