Rhinovirus (RV) Infection (Common Cold) Clinical Presentation

Updated: Sep 11, 2017
  • Author: Joseph Adrian L Buensalido, MD; Chief Editor: Mark R Wallace, MD, FACP, FIDSA  more...
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Presentation

History

Rhinoviruses (RVs) cause or predispose to various upper respiratory tract infections (URTIs) and lower respiratory tract infections (LRTIs), which are less common. The most common manifestation of rhinovirus infection is the common cold. Rhinovirus infections are typically indistinguishable from colds of other viral etiologies. Individual patients exhibit a wide variety of signs and symptoms.

The incubation period is 12-72 hours, averaging 8-16 hours after viral inoculation of the nose. Symptomatic complaints 2 hours after viral inoculation have been described. Symptoms generally last 7-11 days, though they may persist for up to 2 weeks in roughly 25% of patients. Rarely, patients complain of lingering symptoms that last more than 30 days.

Nasal dryness or irritation may be the first symptom of rhinovirus infection. A sore throat or throat irritation is also a common initial symptom and is frequently the most bothersome of the early symptoms. This is followed by nasal discharge, nasal congestion, and sneezing, which intensify over the next 2-3 days. Nasal secretions typically become thicker and colored after the first few days of illness. Nasal obstruction can interfere with sleep and feeding.

Other associated complaints include headache, facial and ear pressure, and loss of smell and taste. About 30% of infected individuals develop a cough, and 20% develop hoarseness, both of which may persist for up to 1 week, though they seldom become bothersome until nasal symptoms improve. Posttussive vomiting can occur. Irritability or restlessness is common.

Systemic signs and symptoms, such as fever and malaise, are unusual. If they are present, consider an alternative diagnosis. When fever is present, it is typically low-grade. Infants and preschoolers are more likely to experience fevers, which are often 38-39°C.

Infants and toddlers may display only nasal discharge. However, Calvo et al reported that among infants younger than 2 years with viral respiratory tract infection requiring hospitalization in Spain, rhinovirus infections are second only to respiratory syncytial virus (RSV) infections in terms of frequency. [29]

School-aged children usually complain of nasal congestion, cough, and runny nose. These symptoms persist for an average of at least 10 days. [30]

Most patients have obstruction and mucosal abnormalities of sinuses, eustachian tubes, and middle ear, which causes a predisposition to secondary bacterial infection in up to 2% of patients. Infection may exacerbate underlying asthma and chronic obstructive pulmonary disease (COPD; see Complications).

People who smoke do not appear to have more frequent rhinovirus infections; however, their infections are more severe, and their symptoms last longer.

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Physical Examination

The physical examination findings in patients with rhinovirus infections are typically less severe than the symptoms reported by the patients themselves.

Fever is not common, though temperatures of 38-39°C are possible in younger children.

A red nose with a profuse, dripping nasal discharge may be present. The discharge can be clear and watery or mucopurulent (yellow or green). Purulent secretions are common after the first few days of illness because a large number of white blood cells (WBCs) migrate to the site of viral infection. Such secretions should not be taken as implying bacterial infection unless they persist for more than 10-14 days.

The nasal mucous membranes have a glistening, glassy appearance, usually (though not always) without obvious erythema or edema. Despite the sore throat, the pharynx typically appears normal, without any erythema, exudate, or ulceration. If marked erythema, edema, exudates, or small vesicles are observed in the oropharynx or if conjunctivitis or polyps in the nasal mucosa occur, consider other etiologies, including infection with adenovirus, herpes simplex virus, mononucleosis, diphtheria, coxsackievirus A, or group A streptococci (GAS).

Mildly enlarged, nontender cervical lymph nodes are present. Auscultation of the chest may reveal rhonchi.

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Complications

Complications of rhinovirus infection include otitis media, sinusitis, chronic bronchitis, and exacerbations of reactive airway disease in children and adults.

Otitis media

Rhinoviruses have been suggested both as rare primary pathogens and as co-pathogens with bacteria in the etiology of otitis media. It is believed that by causing respiratory mucosal inflammation that leads to eustachian tube obstruction, they potentially allow secondary bacterial infection.

Respiratory viruses are found in either the middle ear fluid or the nasopharynx in approximately 40% of patients with otitis media. In particular, as many as 24% of these patients have rhinovirus in nasopharyngeal secretions; rhinovirus has also been obtained from middle ear fluid. Patients whose symptoms are refractory to treatment with antibiotics are more likely to have positive viral cultures from the middle ear.

Sinusitis

Infection of the sinus mucosa with rhinovirus leads to alterations of sinus cavities, resulting in obstruction and entrapment of bacteria (eg, Streptococcus pneumoniae and unencapsulated strains of Haemophilus influenzae) and giving rise to bacterial sinusitis. The maxillary sinuses are involved most frequently.

Acute infectious episodes in patients with chronic bronchitis

Although rhinoviral invasion of the bronchial tree is unclear, alterations in ventilation and exacerbations of bronchitis have been described with rhinovirus infections.

Exacerbation of reactive airway disease

In general, people with asthma develop more viral respiratory tract infections than people without asthma. Viral URTI is a common trigger for asthma exacerbations in children of all ages. In children younger than 5 years, rhinovirus and respiratory syncytial virus (RSV) are the most commonly implicated pathogens. Rhinovirus is the most commonly implicated pathogen in older children.

Rhinovirus infection has been implicated in asthma exacerbations and refractory wheezing. [31] In a rhinovirus challenge model, exacerbation of wheezing was shown in a minority of adults, and only 20% had a 10% or greater decrease in forced expiratory volume in 1 second (FEV1). [32] In children at high risk for allergies and asthma, rhinovirus infection during infancy is the most significant risk factor for symptomatic wheezing. [33] More specifically, human rhinovirus 1B infection affects airway epithelial tight-junction expression, increasing epithelial permeability. [34]

Recently, evidence has shown that rhinovirus induces the release of the chemokine CCL5, which causes airway smooth-muscle chemotaxis, influencing airway remodeling in persons with asthma. [35] Rhinovirus also induces T-helper-2 and T-helper-17 responses, leading to both eosinophilia and mucus hypersecretion during asthma exacerbations. [36]

Rhinovirus C has been implicated in apparent life-threatening events in infants, [37, 38, 39] and certain species are associated with hospitalization for severe respiratory tract infection. [40, 41] The role of rhinovirus infection early in life as a precursor to asthma later in life has been proposed. [33, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59]

Adults with COPD may experience exacerbations attributable to rhinoviruses. One study noted that 20% of all exacerbations could be traced to concomitant rhinoviral infection and found that bacterial colony counts and levels of proinflammatory cytokines were also more elevated when rhinoviruses were present. [60]

Rhinovirus is the implicated virus in as many as 57% of respiratory exacerbations in patients with cystic fibrosis.

Lower respiratory tract infection

Deep respiratory tract infections have been described in immunosuppressed patients, elderly persons, and infants and children with cystic fibrosis; however, determining the true impact of rhinovirus is difficult because it may be either a marker of disease severity or an inciting event for other infectious processes. Rhinovirus may cause both pneumonia [61] and bronchiolitis in infants. [62]

Other complications

Data suggest that antecedent rhinovirus infection circulating in the community predisposes children younger than 5 years to subsequent invasive pneumococcal disease. [63]

Rhinovirus may cause laryngotracheobronchitis in infants.

Rhinovirus is an uncommon cause of acute nasopharyngitis; common colds, by definition, are not characterized by objective evidence of pharyngeal irritation. Acute nasopharyngitis is most commonly caused by adenovirus, enteroviruses, influenza, and parainfluenza.

Rhinovirus C (RV-C), which includes rhinovirus C15 (RV-C15), has been associated with severe infections that usually require hospitalization in young children, particularly those with asthma. Rhinovirus C can also lead to serious respiratory problems in adults. [64]

Colds and other minor infections may increase stroke risk in children

Findings from a study by Hills and colleagues suggest that the strong effect of minor infections on the risk of stroke in children is short-lived. The risk appears to be highest during the three days following a doctor’s visit for an infection, after which it rapidly diminishes. [65, 66]

The researchers used the Kaiser Pediatric Stroke Study, which represents about 2.5 million children enrolled between 1993 and 2007 in Kaiser Permanente Northern California (KPNC). In a retrospective study of medical records, they identified 102 children who had sustained an arterial ischemic stroke and 306 control children without stroke. The total number of doctor visits during the 2 years before a stroke during which a diagnosis of 1 or more minor infections was made were included in the analysis. [66]

A total of 74 cases (73%) and 187 controls (61%) had at least 1 visit for infection during the 2-year observation period. The most common infection reported was upper respiratory tract infection representing 49% of infections in the cases and 45.4% of infections in the controls over the 2-year period. [66]

The rate of infection before the stroke or index date was greater for cases than controls in each of three time periods: within 3 days, 4 to 7 days, and 8 to 30 days. After adjustment for these periods, sex, immunologic, hematologic, and cardiac disease, and head and neck trauma in the preceding month, a diagnosis of infection 3 days before a stroke conferred a 12-fold increased risk for arterial ischemic stroke (odds ratio, 12.1; 95% confidence interval, 2.5 - 56.7; P = .002). The risk rapidly diminished after those 3 days, with no increased risk for stroke beyond 1 week. [66]

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