eMedicine Specialties > Infectious Diseases > Viral Infections

Rhinoviruses

Michael Rajnik, MD, Assistant Professor, Department of Pediatrics, Acting Program Director, Pediatric Infectious Disease Fellowship Program, Uniformed Services University of the Health Sciences
Clinton Murray, MD, Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium; Duane R Hospenthal, MD, PhD, Chief, Infectious Disease Service, San Antonio Military Medical Center, Brooke Army Medical Center; Professor of Medicine, Uniformed Services University of the Health Sciences

Updated: Jun 30, 2008

Introduction

Background

The common cold is an acute respiratory tract infection (ARTI) characterized by mild coryzal symptoms, rhinorrhea, nasal obstruction, and sneezing. Although the incidence of ARTI cannot be clearly defined because of seasonal and locational variability, it is estimated to vary from 3-6 cases per person per year in the United States. Children younger than 1 year have experienced an average of 6-8 episodes of ARTI. This figure decreases to 3-4 episodes per year by adulthood. Although the list of agents that cause the common cold is large, 66-75% of cases are due to 200 antigenically distinct viruses from 8 different genera. The most common of these are the rhinoviruses (25-80% of cases), followed by coronaviruses (10-20%), influenza viruses (10-15%), and adenoviruses (5%).

Rhinoviruses are members of the Picornaviridae family, which includes the human pathogens enteroviruses and hepadnaviruses (notably, hepatitis A). Rhinoviruses are small, nonenveloped, positive (sense) stranded RNA viruses. Their structure is an icosahedral capsid of 12 pentamers containing the 4 viral proteins. A deep cleft is involved in viral attachment. Attachment to cellular receptors can be blocked by a specific antibody. More than 100 different subtypes exist in 3 major groups and are categorized based on receptor specificity: intercellular adhesion molecule-1 (ICAM-1), low-density lipoprotein (LDL) receptors, and sialoprotein cell receptors.

Rhinoviral infections are chiefly limited to the upper respiratory tract but may cause otitis media and sinusitis. Rhinoviral infections may exacerbate asthma, cystic fibrosis, chronic bronchitis, and serious lower respiratory tract illness in infants, elderly persons, and immunocompromised persons. Although infections occur year-round, the greatest incidence occurs in the fall and spring. Of persons exposed to the virus, 70-80% have symptomatic disease.

Pathophysiology

Rhinoviruses are transmitted to susceptible individuals by direct contact or by 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. Symptoms 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.

Detectable histopathology that causes 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.

Deficient interferon-beta production by asthmatic bronchial epithelial cells has been proposed as a mechanism for increased susceptibility to rhinoviral infections in individuals with asthma.

Viral 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).

The virus grows in a limited temperature range (33-35°C) 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 increased temperature in both the lower respiratory and gastrointestinal tracts.

Frequency

United States

The frequency of rhinoviral infection averages 1 episode every 1-2 years per person. Rhinoviruses cause up to 80% of colds during the autumn months in temperate climates.

International

Rhinoviruses have been found in all countries, even in remote areas such as the Kaluhi Islands and the Amazon. In Brazil, rhinoviruses reportedly cause 46% of ARTIs.

Mortality/Morbidity

Although not associated with fatal disease, rhinoviruses are associated with significant morbidity. ARTIs, predominantly rhinoviral infections, are estimated to cause 30-50% of time lost from work by adults and 60-80% of time lost from school by children. Complications of rhinoviral infections include otitis media, sinusitis, chronic bronchitis, and exacerbations of reactive airway disease in children and adults. These viruses are possibly involved in lower respiratory tract infections in elderly persons, infants, persons with cystic fibrosis, and immunosuppressed patients. The true impact of lower respiratory tract infection is not clear. Recovery of rhinovirus in these patients may be a marker of an underlying disease process or a precursor to a bacterial infection.

Race

No difference in susceptibility to infection or disease course has been described among different races.

Sex

Some reports indicate a male predominance of infection in children younger than 3 years, which switches to a female predominance in children older than 3 years. No difference in rates of infection in adults is apparent.

Age

Rhinoviral infection is most common in children, with decreasing incidence as they approach adulthood. Children are instrumental in transmission of infection, commonly passing infection to family members after contracting the virus in nurseries, daycare facilities, and schools.

Clinical

History

Rhinoviral 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.
• Illness initially begins with a sore throat, which 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.
• Other associated complaints include headache, facial and ear pressure, and loss of smell and taste.
• Thirty percent of infected individuals develop a cough, and 20% develop hoarseness, both of which may persist up to a week, although they seldom become bothersome until nasal symptoms improve.
• Systemic signs and symptoms, such as fever and malaise, are unusual. If they are present, consider an alternative diagnosis.
• Symptoms generally last 7-11 days, although they persist up to 2 weeks in a quarter of patients. Rarely, patients complain of lingering symptoms that last more than 30 days.
• Infants and toddlers may display only nasal discharge. However, Calvo et al recently reported that, among infants younger than 2 years with viral respiratory tract infection requiring hospitalization in Spain, rhinoviral infections are second only to respiratory syncytial virus infections in terms of frequency.^{[46 ]} 
• School-aged children usually complain of nasal congestion, cough, and runny nose. These symptoms persist for an average of at least 10 days.^{[45 ]}
• 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 pulmonary disease.
• People who smoke do not appear to have more frequent rhinoviral infections; however, their infections are more severe and their symptoms of longer duration.

Physical

The physical examination findings are typically less severe than those reported by the patient.

• Red nose with dripping nasal discharge may be present.
• Nasal mucous membranes have a glistening glassy appearance without obvious erythema or 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.
• 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).
• Auscultation of the chest may reveal rhonchi.

Causes

• Rhinoviral transmission occurs with close exposure to infected respiratory secretions, including hand-to-hand, self-inoculation of eyes or nose, and, possibly, large- and small-particle aerosolization. The virus has been cultured from the skin after up to 2 hours and after up to 4 days on inanimate objects in ideal conditions. Donors are typically symptomatic with a cold at the time of transmission, and virus is detected on their hands and nasal mucosa.
• One recent study assessed the transfer of virus to surfaces in 15 adults with rhinoviral infection. Each stayed overnight in a hotel room. Afterward, 10 commonly-touched sites in each room were tested for viral contaminants. They found that virus could be recovered from 35% of these sites. Furthermore, they found that virus could be transferred back from inanimate objects to fingertips in many cases.^{[47 ]} 
• Higher rates occur in humid, crowded conditions, as found in nurseries, daycare centers, and schools, especially during cooler months in temperate regions and the rainy season in tropical regions.
• The likelihood of transmission does not appear to be related to exposure to cold temperatures, fatigue, or sleep deprivation.

Differential Diagnoses

Other Problems to Be Considered

Coronavirus
Sphenoid sinusitis
Nonallergic rhinitis
Respiratory syncytial virus infection

Workup

Laboratory Studies

• Because common-cold manifestations are so common, an aggressive workup is rarely necessary if findings from a thorough history and physical examination are consistent with a viral etiology and no complications are noted. Differentiation of one virus from another or one serotype of rhinovirus from another is difficult based on clinical presentation.
• Shedding of virus peaks at 48 hours but can persist for up to 3 weeks. Virus can be cultured on M-HeLa and human embryonic lung cells with typical cytopathic effect observed after culture, at 33-35°C on roller drums, for 2-6 days. Culture occasionally takes up to 14 days. Because of the prolonged time to obtain positive culture findings, it has rarely been found useful in clinical settings.
• Identity is confirmed by the acid sensitivity of the isolate. Specialized laboratories can identify serotypes by antibody neutralization, which requires a large battery of antisera.
• Polymerase chain reaction (PCR) is currently available. This testing is faster and more sensitive than culture. Real-time PCR has been shown to be a rapid and effective way to detect rhinoviruses and has been proposed as the clinical method of detection. PCR has been found most useful in clinical settings in testing patients who are severely immunocompromised, such as patients who have undergone bone marrow transplant. PCR must be used carefully. One study has reported persistent positive results for 5-6 weeks following admission of children for illnesses determined to be secondary to rhinoviral infection. Furthermore, the use of nested PCR techniques has resulted in up to 20% of illnesses being attributed to more than one organism.^{[19 ]}
• The large number of serotypes restricts the use of immunocytochemical methods and serology testing.
• Peripheral white blood cell counts may be elevated during the first 2-3 days of the infection, although use of common laboratory tests, such as complete blood count and erythrocyte sedimentation rate, are of virtually no benefit in managing rhinoviral infections.
• Consider bacterial throat culture or rapid strep test to identify the presence of GAS if oropharyngeal examination suggests streptococcal infection.

Imaging Studies

• Chest radiography is seldom needed and should be obtained only if another lower respiratory tract infection (eg, pneumonia) is suspected.
• Sinus films or CT scanning of the sinuses may be used in cases of suspected sinusitis, although this imaging cannot differentiate viral processes from bacterial processes.

Procedures

• Although respiratory tract aspirations, brushings, and biopsies have been used in research protocols to identify etiologies of infections, these tests are of limited value in individual patients.

Treatment

Medical Care

Rhinoviral 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, and nasal decongestants.

Antibacterial agents are not effective unless bacterial superinfection occurs. Development 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, antivirals have only a narrow window to positively affect a rhinoviral infection. In addition, the cause of the common cold is not always rhinoviral infection. Therefore, rapid and accurate diagnostic tests would be needed if a specific antiviral therapy were developed.

• 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.
• Because infection is spread by hand-to-hand contact, autoinoculation, and, possibly, aerosol particles, emphasize appropriate hand washing, avoidance of finger-to-eyes or finger-to-nose contact, and use of nasal tissue.
• Heated humidified air has been used for decades for the alleviation of symptoms due to rhinoviral infections but has never been shown to improve objective outcome measures.^{[34 ]}
• Numerous agents are under investigation for the treatment of viral infections.
  • Pleconaril inhibits approximately 92% of rhinovirus serotypes. Susceptibility to pleconaril depends on the viral capsid surface protein VP1. A double-blind, randomized, placebo-controlled trial of pleconaril 400 mg PO tid for 5 days, initiated within 24 hours of symptom onset, resulted in a decrease in the duration of symptoms by 1 day.^{[14 ]}
  • Steroids have been examined as a therapeutic modality and have shown little effect with rhinoviruses. One recent article noted that children who experienced wheezing during a rhinoviral infection and were treated with prednisolone experienced fewer wheezing episodes than untreated individuals in the subsequent 2 months. However, no change in time to discharge was noted.^{[18 ]}
  • A blinded, placebo-controlled trial using intranasal interferon-alpha-2b and ipratropium with oral naproxen started within 24 hours of rhinovirus inoculation decreased viral shedding, geometric mean virus titers, and symptoms in the treatment group. Similar findings were reported with the use of intranasal interferon-alpha-2b, chlorpheniramine, and ibuprofen. Recombinant interferon-alpha-2b applied topically to the nose at 5 million U or more per day prevented experimental infections. Unfortunately, the effect of this agent on symptomatic illness was limited.^{[11 ]}
  • A recombinant soluble intercellular adhesion molecule-1 (ICAM-1) administered intranasally 6 times per day and beginning either 7 hours before or 12 hours after rhinovirus challenge was analyzed in a randomized, double-blinded study. Neither strategy affected the incidence of infection, but combining results from both treatment groups found a 23% decrease in clinical colds, a 45% decrease in total symptom score, and a 56% decrease in total nasal secretion weight.^{[50 ]}
  • 3C protease inhibitors are currently being evaluated in human trials, but no data are currently available. A phase II study found that ruprintrivir, a 3C protease inhibitor, delivered as a nasal spray was well tolerated and decreased positive viral culture results and improved symptom scores but did not decrease the frequency of colds.^{[15 ]}These drugs act by interfering with the cleaving of a single large polyprotein that produces individual structures and enzymatic proteins of the virus.
  • Rhinoviruses are sensitive to low pH. In one recent study, citrate/phosphate buffers were administered intranasally, decreasing viral shedding but failing to decrease symptomatology.^{[48 ]}

Diet

Dietary supplements have been touted as possible therapeutic or preventive measures.

• Although large doses of vitamin C have been used for prevention and treatment of colds, controlled trials reveal minimal therapeutic benefit and no preventive qualities.^{[33 ]}
• Zinc has been found to inhibit rhinovirus replication in vitro, but no proven benefit has been shown in vivo on virus activity or immune modulation.
• The genus Echinacea consists of 3 species of plants used medicinally for their reported nonspecific stimulation of the immune system.
  • Echinacea purpurea has recently been studied and did not show any differences in rates of infection or severity of illness when compared with placebo. Although reports of improved symptoms have been described, validation and standardization of products is necessary.^{[36 ]}
  • Echinacea angustifolia has also been examined in the prophylaxis and treatment of experimental rhinoviral infection. Neither the rate of infection nor the severity of symptoms were found to be statistically significantly affected when E angustifolia was used either prophylactically or at the time of challenge.^{[39 ]}
  • In contrast, a recent meta-analysis of echinacea indicated that, in properly designed studies, patients receiving placebo were 55% more likely to experience cold symptoms than patients taking echinacea. The most striking part of this meta-analysis was that 231 of 234 articles identified were excluded because they did not control for the type of viruses causing the colds. Echinacea extracts will continue to be evaluated.^{[32 ]}

Activity

Patients may limit their activity during the course of the infection, with clinical improvement occurring 48-72 hours after the prodrome of symptoms.

Medication

Drugs used in the symptomatic treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), antihistamines, and anticholinergic nasal solutions. These agents have no preventive activity and appear to have no impact on complications. The combined effect of NSAIDs and antihistamines often relieves nasal obstruction; therefore, decongestion therapy is rarely needed. Oral (pseudoephedrine) and topical (oxymetazoline and phenylephrine) decongestants are commonly used for symptomatic relief.

First-generation antihistamines reduce rhinorrhea by 25-35%, as do topical anticholinergics and ipratropium bromide. Second-generation or nonsedating antihistamines appear to have no effect on common cold symptoms. Corticosteroids may actually increase viral replication and have no impact on cold symptoms.

Antihistamines

These agents act by competitive inhibition of histamine at the H1 receptor.

Diphenhydramine (Benylin, Benadryl)

Occasional drowsiness and is suitable for use on a day-to-day basis. Oral H1-blocker used in the treatment of allergic conjunctivitis and rhinitis, angioedema, pruritus, and urticaria.

Dosing

Adult

25-50 mg PO q6-8h prn; not to exceed 400 mg/d
10-50 mg IV/IM q6-8h prn; not to exceed 400 mg/d

Pediatric

12.5-25 mg PO tid/qid, or 5 mg/kg/d, or 150 mg/m²/d divided tid/qid; not to exceed 300 mg/d
5 mg/kg/d IV/IM or 150 mg/m²/d, divided qid; not to exceed 300 mg/d

Interactions

Potentiates effect of CNS depressants; because of alcohol content, do not administer syrup dosage form to patients taking medications that can cause disulfiram-like reactions

Contraindications

Documented hypersensitivity; MAOIs

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, or urinary tract obstruction; xerostomia may occur

Chlorpheniramine (Telachlor, Chlo-Amine, Chlor-Trimeton, Aller-Chlor)

Competes with histamine or H1-receptor sites on effector cells in blood vessels and respiratory tract.

Dosing

Adult

10-20 mg IV/IM/SC once; not to exceed 40 mg/d
4 mg PO q4-6h; not to exceed 24 mg/d or 8-12 mg SR q8-12h; not to exceed 24 mg/d

Pediatric

<2 years: Not established
2-6 years: 1 mg PO divided q4-6h; not to exceed 6 mg/d
6-12 years: 2 mg PO q4-6h; not to exceed 12 mg/d or 8 mg SR PO hs
>12 years: Administer as in adults

Interactions

CNS toxicity increases with coadministration of other CNS depressants, tricyclic antidepressants, MAOIs, and phenothiazines

Contraindications

Documented hypersensitivity; asthma attacks; narrow-angle glaucoma; symptomatic prostate hypertrophy; bladder-neck obstruction; stenosing peptic ulcer

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause significant confusional symptoms; not for administration to premature or full-term neonates

Brompheniramine maleate (Bromphen, Nasahist B, Dimetane Extentabs)

Does not tend to cause drowsiness and is suitable for use on a day-to-day basis. Oral H1-blocker used in the treatment of allergic conjunctivitis and rhinitis, angioedema, pruritus, and urticaria.

Dosing

Adult

Capsule/elixir: 4-8 mg PO q6-8h prn
Extended-release form: 8 mg PO q8-12h or 12 mg PO q12h prn; not to exceed 24 mg/d

Pediatric

<2 years: Not established
2-5 years: 1 mg PO q4-6h prn; not to exceed 6 mg/d
6-11 years: 2-4 mg PO q6-8h prn; not to exceed 12 mg/d
>12 years: Administer as in adults

Interactions

MAOIs and beta-blockers increase the effects of sympathomimetics; may reduce antihypertensive effects of methyldopa, mecamylamine, reserpine, veratrum alkaloids; alcohol and other CNS depressants may have an addictive effect

Contraindications

Documented hypersensitivity; severe hypertension; severe coronary artery disease; current or within 14 days of MAOI use; narrow-angle glaucoma; urinary retention; peptic ulcer disease; during an asthma attack

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with hypertension, heart disease, diabetes, or thyroid disease; antihistamines may cause drowsiness

Anticholinergics

These agents have antisecretory properties and, when applied locally, inhibit secretions from serous and seromucous glands lining the nasal mucosa.

Ipratropium intranasal (Atrovent)

Two strengths of nasal spray: 0.03% for treatment of rhinorrhea associated with allergic and nonallergic perennial rhinitis and 0.06% for treatment of rhinorrhea associated with common cold. Chemically related to atropine.

Dosing

Adult

Rhinorrhea common cold 0.06% nasal solution: 2 sprays (42 mcg/spray) per nostril tid/qid
Rhinorrhea allergic/nonallergic perennial rhinitis 0.03% nasal solution: 2 sprays (21 mcg/spray) per nostril bid/tid

Pediatric

Administer as in adults

Interactions

Drugs with anticholinergic properties, such as dronabinol, may increase toxicity; albuterol may increase effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients with narrow-angle glaucoma, prostatic hypertrophy, or bladder-neck obstruction

Nonsteroidal anti-inflammatory drugs (NSAIDs)

These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms also may exist (eg, inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, various cell membrane functions).

Naproxen (Anaprox)

For relief of mild to moderate pain and antipyretic action; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Dosing

Adult

550 mg PO q12h or 275 mg PO q6-8h prn

Pediatric

<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

Ibuprofen (Ibuprin, Motrin)

For relief of mild to moderate pain and antipyretic action; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Dosing

Adult

200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d

Pediatric

<6 months: Not established
6 months to 12 years: 4-10 mg/kg/dose PO tid/qid
>12 years: Administer as in adults

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy

Follow-up

Further Inpatient Care

• Inpatient care is rarely required.

Further Outpatient Care

• Persons with rhinoviral infections are almost universally treated as outpatients.

Deterrence/Prevention

• Hand-washing and avoidance of finger-to-eye and finger-to-nose contact are crucial to decreasing spread of infection. One study suggests that hand cleansers with salicylic acid and pyroglutamic acid prevent the transmission of rhinovirus as well as the number of patients who become clinically infected.^{[38 ]}
• The use of nasal tissues is encouraged because of possible aerosol spread of the virus.

Complications

• Sinusitis: Viral infection of the sinus mucosa leads to alterations of sinus cavities, resulting in obstruction and entrapment of bacteria, such as Streptococcus pneumoniae and unencapsulated strains of Haemophilus influenzae, leading to bacterial sinusitis. The maxillary sinuses are involved most frequently.
• Otitis media: Rhinoviruses have been suggested as both rare pathogens and as copathogens with bacteria in the etiology of otitis media. They have been recovered in middle ear fluid of people with otitis media and potentially allow secondary bacterial infection from obstruction secondary to mucosal changes in the eustachian tubes.
• Precipitation of asthma: People with asthma develop more viral respiratory tract infections than people without asthma. Rhinoviral infection is also detected at the onset of symptoms; however, in a rhinovirus challenge model, exacerbations 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).^{[12 ]}Additionally, recent data suggest that, in children at high risk for developing allergies and asthma, rhinoviral infection during infancy is the most significant risk factor for episodes of symptomatic wheezing.^{[22 ]}One recent study in Nashville noted that the hospitalization rate in all children younger than 5 years was 5 per 1000, but a history of asthma in this population increased the rate to 25.3 per 1000.^{[49 ]}
• 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 rhinoviral infections.
• 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 a marker of disease severity or an inciting event for other infectious processes.
• Adults with chronic obstructive pulmonary disease may experience exacerbations attributed to rhinoviruses. One recent study noted that 20% of all exacerbations could be traced to concomitant rhinoviral infection. Bacterial colony counts and levels of proinflammatory cytokines were also more elevated when rhinoviruses were present.^{[41 ]}

Prognosis

• The prognosis is excellent.

Patient Education

• Emphasize environmental measures to control infections, including hand-washing, avoiding finger-to-eye and finger-to-nose contact, and covering coughs and sneezes with disposable nasal tissues.
• For excellent patient education resources, visit eMedicine's Cold and Flu Center. Also, see eMedicine's patient education article Colds.

References

1. Arola M, Ruuskanen O, Ziegler T, et al. Clinical role of respiratory virus infection in acute otitis media. Pediatrics. Dec 1990;86(6):848-55. [Medline].

2. Arruda E, Pitkaranta A, Witek TJ Jr, et al. Frequency and natural history of rhinovirus infections in adults during autumn. J Clin Microbiol. Nov 1997;35(11):2864-8. [Medline].

3. Dagher H, Donninger H, Hutchinson P, et al. Rhinovirus detection: comparison of real-time and conventional PCR. J Virol Methods. May 2004;117(2):113-21. [Medline].

4. Dick EC, Jennings LC, Mink KA, et al. Aerosol transmission of rhinovirus colds. J Infect Dis. Sep 1987;156(3):442-8. [Medline].

5. Douglas RG, Lindgren KM, Couch RB. Exposure to cold environment and rhinovirus common cold. Failure to demonstrate effect. N Eng J Med. 1968;279:742-7.

6. Ghosh S, Champlin R, Couch R, et al. Rhinovirus infections in myelosuppressed adult blood and marrow transplant recipients. Clin Infect Dis. Sep 1999;29(3):528-32. [Medline].

7. Goldmann DA. Transmission of viral respiratory infections in the home. Pediatr Infect Dis J. Oct 2000;19(10 Suppl):S97-102. [Medline].

8. Gwaltney JM Jr, Phillips CD, Miller RD, et al. Computed tomographic study of the common cold. N Engl J Med. Jan 6 1994;330(1):25-30. [Medline].

9. Gwaltney JM Jr, Hendley JO, Simon G, et al. Rhinovirus infections in an industrial population. I. The occurrence of illness. N Engl J Med. Dec 8 1966;275(23):1261-8. [Medline].

10. Gwaltney JM Jr, Hendley JO, Simon G, et al. Rhinovirus infections in an industrial population. II. Characteristics of illness and antibody response. JAMA. Nov 6 1967;202(6):494-500. [Medline].

11. Gwaltney JM Jr, Winther B, Patrie JT, et al. Combined antiviral-antimediator treatment for the common cold. J Infect Dis. Jul 15 2002;186(2):147-54. [Medline].

12. Halperin SA, Eggleston PA, Beasley P, et al. Exacerbations of asthma in adults during experimental rhinovirus infection. Am Rev Respir Dis. Nov 1985;132(5):976-80. [Medline].

13. Harris JM 2nd, Gwaltney JM Jr. Incubation periods of experimental rhinovirus infection and illness. Clin Infect Dis. Dec 1996;23(6):1287-90. [Medline].

14. Hayden FG, Herrington DT, Coats TL, et al. Efficacy and safety of oral pleconaril for treatment of colds due to picornaviruses in adults: results of 2 double-blind, randomized, placebo-controlled trials. Clin Infect Dis. Jun 15 2003;36(12):1523-32. [Medline].

15. Hayden FG, Turner RB, Gwaltney JM, et al. Phase II, randomized, double-blind, placebo-controlled studies of ruprintrivir nasal spray 2-percent suspension for prevention and treatment of experimentally induced rhinovirus colds in healthy volunteers. Antimicrob Agents Chemother. Dec 2003;47(12):3907-16. [Medline].

16. Hendley JO, Gwaltney JM Jr. Mechanisms of transmission of rhinovirus infections. Epidemiol Rev. 1988;10:243-58. [Medline].

17. Jartti T, Lehtinen P, Vuorinen T, et al. Persistence of rhinovirus and enterovirus RNA after acute respiratory illness in children. J Med Virol. Apr 2004;72(4):695-9. [Medline].

18. Jartti T, Lehtinen P, Vanto T, et al. Evaluation of the efficacy of prednisolone in early wheezing induced by rhinovirus or respiratory syncytial virus. Pediatr Infect Dis J. Jun 2006;25(6):482-8. [Medline].

19. Jennings LC, Anderson TP, Werno AM, et al. Viral etiology of acute respiratory tract infections in children presenting to hospital: role of polymerase chain reaction and demonstration of multiple infections. Pediatr Infect Dis J. Nov 2004;23(11):1003-7. [Medline].

20. Kirkpatrick GL. The common cold. Prim Care. Dec 1996;23(4):657-75. [Medline].

21. Ledford RM, Patel NR, Demenczuk TM, et al. VP1 sequencing of all human rhinovirus serotypes: insights into genus phylogeny and susceptibility to antiviral capsid-binding compounds. J Virol. Apr 2004;78(7):3663-74. [Medline].

22. Lemanske RF Jr, Jackson DJ, Gangnon RE, et al. Rhinovirus illnesses during infancy predict subsequent childhood wheezing. J Allergy Clin Immunol. Sep 2005;116(3):571-7.

23. Makela MJ, Puhakka T, Ruuskanen O, et al. Viruses and bacteria in the etiology of the common cold. J Clin Microbiol. Feb 1998;36(2):539-42. [Medline].

24. Malcolm E, Arruda E, Hayden FG, et al. Clinical features of patients with acute respiratory illness and rhinovirus in their bronchoalveolar lavages. J Clin Virol. Apr 2001;21(1):9-16. [Medline].

25. McBride TP, Doyle WJ, Hayden FG, et al. Alterations of the eustachian tube, middle ear, and nose in rhinovirus infection. Arch Otolaryngol Head Neck Surg. Sep 1989;115(9):1054-9. [Medline].

26. Monto AS, Bryan ER, Ohmit S. Rhinovirus infections in Tecumseh, Michigan: frequency of illness and number of serotypes. J Infect Dis. Jul 1987;156(1):43-9. [Medline].

27. Monto AS, Ullman BM. Acute respiratory illness in an American community. The Tecumseh study. JAMA. Jan 14 1974;227(2):164-9. [Medline].

28. Naclerio RM, Proud D, Lichtenstein LM, et al. Kinins are generated during experimental rhinovirus colds. J Infect Dis. Jan 1988;157(1):133-42. [Medline].

29. Nicholson KG, Kent J, Hammersley V, et al. Acute viral infections of upper respiratory tract in elderly people living in the community: comparative, prospective, population based study of disease burden. BMJ. Oct 25 1997;315(7115):1060-4. [Medline].

30. Rotbart HA, Hayden FG. Picornavirus infections: a primer for the practitioner. Arch Fam Med. Sep-Oct 2000;9(9):913-20. [Medline].

31. Sanders SP, Proud D, Permutt S, et al. Role of nasal nitric oxide in the resolution of experimental rhinovirus infection. J Allergy Clin Immunol. Apr 2004;113(4):697-702. [Medline].

32. Schoop R, Klein P, Suter A, et al. Echinacea in the prevention of induced rhinovirus colds: a meta-analysis. Clin Ther. Feb 2006;28(2):174-83. [Medline].

33. Schwartz AR, Togo Y, Hornick RB, et al. Evaluation of the efficacy of ascorbic acid in prophylaxis of induced rhinovirus 44 infection in man. J Infect Dis. Oct 1973;128(4):500-5. [Medline].

34. Singh M. Heated, humidified air for the common cold. Cochrane Database Syst Rev. 2004;CD001728. [Medline].

35. Smith CB, Kanner RE, Golden CA, et al. Effect of viral infections on pulmonary function in patients with chronic obstructive pulmonary diseases. J Infect Dis. Mar 1980;141(3):271-80. [Medline].

36. Sperber SJ, Shah LP, Gilbert RD, et al. Echinacea purpurea for prevention of experimental rhinovirus colds. Clin Infect Dis. May 15 2004;38(10):1367-71. [Medline].

37. Turner RB. The treatment of rhinovirus infections: progress and potential. Antiviral Res. Jan 2001;49(1):1-14. [Medline].

38. Turner RB, Biedermann KA, Morgan JM, et al. Efficacy of organic acids in hand cleansers for prevention of rhinovirus infections. Antimicrob Agents Chemother. Jul 2004;48(7):2595-8. [Medline].

39. Turner RB, Bauer R, Woelkart K, et al. An evaluation of Echinacea angustifolia in experimental rhinovirus infections. N Engl J Med. Jul 28 2005;353(4):341-8. [Medline].

40. Wark PA, Johnston SL, Bucchieri F, et al. Asthmatic bronchial epithelial cells have a deficient innate immune response to infection with rhinovirus. J Exp Med. Mar 21 2005;201(6):937-47. [Medline].

41. Wilkinson TM, Hurst JR, Perera WR, et al. Effect of interactions between lower airway bacterial and rhinoviral infection in exacerbations of COPD. Chest. Feb 2006;129(2):317-24.

42. Winther B, Brofeldt S, Christensen B, et al. Light and scanning electron microscopy of nasal biopsy material from patients with naturally acquired common colds. Acta Otolaryngol. Mar-Apr 1984;97(3-4):309-18. [Medline].

43. de Arruda E, Hayden FG, McAuliffe JF, et al. Acute respiratory viral infections in ambulatory children of urban northeast Brazil. J Infect Dis. Aug 1991;164(2):252-8. [Medline].

44. van Kraaij MG, van Elden LJ, van Loon AM, et al. Frequent detection of respiratory viruses in adult recipients of stem cell transplants with the use of real-time polymerase chain reaction, compared with viral culture. Clin Infect Dis. Mar 1 2005;40(5):662-9. [Medline].

45. Pappas DE, Hendley JO, Hayden FG, et al. Symptom profile of common colds in school-aged children. Pediatr Infect Dis J. Jan 2008;27(1):8-11. [Medline].

46. Calvo C, Garcia-Garcia ML, Blanco C, et al. Role of rhinovirus in hospitalized infants with respiratory tract infections in Spain. Pediatr Infect Dis J. Oct 2007;26(10):904-8. [Medline].

47. Winther B, McCue K, Ashe K, et al. Environmental contamination with rhinovirus and transfer to fingers of healthy individuals by daily life activity. J Med Virol. Oct 2007;79(10):1606-10. [Medline].

48. Gern JE, Mosser AG, Swenson CA, et al. Inhibition of rhinovirus replication in vitro and in vivo by acid-buffered saline. J Infect Dis. Apr 15 2007;195(8):1137-43. [Medline].

49. Miller EK, Lu X, Erdman DD, et al. Rhinovirus-associated hospitalizations in young children. J Infect Dis. Mar 15 2007;195(6):773-81. [Medline].

50. Turner RB, Wecker MT, Pohl G, et al. Efficacy of tremacamra, a soluble intercellular adhesion molecule 1, for experimental rhinovirus infection: a randomized clinical trial. JAMA. May 19 1999;281(19):1797-804. [Medline].

Keywords

rhinoviruses, rhinovirus infection, cold, common cold, respiratory virus, RV, acute respiratory tract infection, ARTI, upper respiratory tract infection, URTI, otitis media, sinusitis, chronic bronchitis, lower respiratory tract illness, rhinoviral infection, rhinorrhea

Contributor Information and Disclosures

Author

Michael Rajnik, MD, Assistant Professor, Department of Pediatrics, Acting Program Director, Pediatric Infectious Disease Fellowship Program, Uniformed Services University of the Health Sciences
Michael Rajnik, MD is a member of the following medical societies: American Academy of Pediatrics, Armed Forces Infectious Diseases Society, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

Coauthor(s)

Clinton Murray, MD, Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium
Clinton Murray, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Association of Military Surgeons of the US, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Duane R Hospenthal, MD, PhD, Chief, Infectious Disease Service, San Antonio Military Medical Center, Brooke Army Medical Center; Professor of Medicine, Uniformed Services University of the Health Sciences
Duane R Hospenthal, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Armed Forces Infectious Diseases Society, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Society for Infectious Diseases, International Society of Travel Medicine, and Medical Mycology Society of the Americas
Disclosure: Nothing to disclose.

Medical Editor

Gregory William Rutecki, MD, Associate Professor, Program Director, Department of Internal Medicine, Feinberg School of Medicine, Northwestern University
Gregory William Rutecki, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Nephrology, National Kidney Foundation, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gordon L Woods, MD, Consulting Staff, Department of Internal Medicine, University Medical Center
Gordon L Woods, MD is a member of the following medical societies: Society of General Internal Medicine
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

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