Acute Rhinosinusitis: Viral, Postviral, and Bacterial

Viral rhinosinusitis, or the common cold, is, by definition, an ARS induced by respiratory viruses. It is often associated with pharyngitis, laryngitis, tracheitis, bronchitis, and conjunctivitis, and usually lasts 5 to 7 days in most patients. The common symptoms include itchy nose, sneezing, nasal stuffiness, watery or mucoid rhinorrhea, pain in the throat, and headache. Rhinitis and sinusitis usually coexist, and the common cold is often associated with mucosal inflammation in not only the nasal cavity but also the paranasal sinuses.2 Hence, viral rhinosinusitis is probably a more correct term ( Figs. 15.1 and 15.2 ).

ARS comprises of viral ARS (common cold) and postviral ARS. In the EPOS 2007 the term nonviral ARS was chosen to indicate that most cases of ARS are not bacterial. However, this term apparently led to confusion and, for that reason, in the EPOS 20121 it was decided to choose the term postviral ARS to express the same phenomenon. A small percentage of the patients with postviral ARS will have bacterial ARS. Common cold/acute viral rhinosinusitis is defined as the duration of symptoms for less than 10 days. Acute postviral rhinosinusitis is defined as the increase of symptoms after 5 days or persistent symptoms after 10 days with less than 12 weeks duration. Acute bacterial rhinosinusitis (ABRS) is suggested by the presence of at least three symptoms/signs of:

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  Discolored discharge (with unilateral predominance) and purulent secretion in cavum nasi

  
  
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  Severe local pain (with unilateral predominance)

  
  
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  Fever (> 38° C)

  
  
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  Elevated erythrocyte sedimentation rate/C-reactive protein levels

  
  
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  “Double sickening“ (i.e., a deterioration after an initial milder phase of illness)

Rhinosinusitis

Vestibulitis

Vestibulitis is a bacterial infection of the nasal vestibular tissue (e.g., hair follicles and skin) around the entrance to the nose. Symptoms include redness, swelling, and pain. Sometimes the infected tissue becomes raw and may bleed and crust around the nostrils.

Epidemiology

Acute viral rhinitis (or rhinosinusitis) is one of the most common health complaints, affecting millions of people annually. Infection of the respiratory tract by viruses can result in a variety of specific syndromes, such as the common cold, pharyngitis, tracheobronchitis, croup, bronchiolitis, and pneumonia. It has been demonstrated by a sinus computed tomography (CT) scan study that the common cold is often associated with mucosal inflammation in not only the nasal cavity but also the paranasal sinuses.2 Therefore, viral rhinosinusitis is also a correct term.

The common cold (viral rhinitis) can be caused by any of the more than 200 different strains of families of viruses, such as rhinovirus, coronavirus, respiratory syncytial virus (RSV), influenza, parainfluenza, and adenoviruses. Rhinoviruses are most common in adults and are considered to be the causative organisms in ~50% of cases. This is followed by coronaviruses (~15%). Occasionally, other types of organisms, such as Mycoplasma pneumoniae, are responsible. In ~30% of patients, no virus or any other microorganism can be identified.5 In children, there is a wider variety of responsible viruses; besides rhinoviruses and coronaviruses, one can also expect to find RSV, parainfluenza, and adenoviruses.5 Viruses are clearly involved in the pathogenesis, especially in patients with comorbidities. Illness results from obstruction of sinus ostia by edematous mucosa, impairment of mucociliary clearance, and destruction of the epithelial integrity. For example, rhinovirus, influenza A virus, and parainfluenza virus have been recovered from aspirates in patients with acute purulent maxillary sinusitis. Saito et al6 documented high titers of neutralizing antibodies to parainfluenza virus (3 in 18 of 31 patients) following an acute exacerbation of rhinosinusitis.

The illness that results from the virus infection is influenced by host factors, including age, previous infection or immunization, preexisting respiratory or systemic disease, and immunosuppressed states. People living in crowded places and debilitated persons are more prone to viral infections. This is especially so for a rhinovirus, as there is evidence for its spread via direct contact and not by air. Self-inoculation with the virus via the eye or nose results in infection of nasal epithelial cells, including the ciliated cells. Rhinovirus infection of an epithelial cell may trigger an inflammatory cascade, which is thought to be responsible for the cold symptoms, but also forms the basis for immunologic defense.

Pathogenesis and Putative Mechanisms

The nature and severity of disease observed is dependent on both the direct harmful effects of the virus itself and the damage caused to host tissues as a consequence of the host immune response to the virus. Some immunopathology may be unavoidable if the host is to eradicate the virus. An ideal immune response (via either cell or humoral immunity) would result in early elimination of the virus with minimal harm to the host.7 However, the pathogenic mechanisms of virus-induced inflammation and the pathogenesis of common cold symptoms are still not fully understood.

The antiviral immune response involves innate (nonspecific) and specific components and requires the coordinated actions of many different cell types, including neutrophils, macrophages, eosinophils, dendritic cells, epithelial cells, mast cells, natural killer cells, and B and T lymphocytes. Coordination of this response involves numerous cytokines and chemokines. T lymphocytes expressing type 1 cytokines, including interferon-γ, play a key role.7 It was reported that common cold symptoms may be produced as a result of the release of inflammatory mediators, such as bradykinin and [3H]-N-α-tosyl-L-arginine methyl ester (TAME)–esterase activity (but not histamine), into the nasal mucosa and secretions.8 There is a luminal entry of plasma, including large binding proteins such as fibrinogen and 2-macroglobulin, which may bind and transport a variety of cytokines in both the common cold and allergic rhinitis.9 In contrast, most of the nasal fluid volume during a common cold could also be due to a glandular product from goblet cells and glands rather than plasma exudates.

The role and involvement of different cells during viral infection are controversial. It has been shown during experimental rhinovirus infection that no change occurred in the overall degree of lymphocytic infiltration or in the numbers of T and B lymphocytes compared with control specimens.10 Another study showed that there was no evidence of an inflammatory cellular infiltrate at either submucosal or epithelial levels during experimental infection with human rhinoviruses.11 When looking at the cytokine profile, increased nasal lavage fluid levels of interferon-γ, but not granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin 4 (IL-4), and IL-6 were found in patients with a coronavirus-induced common cold.9

Winther reported that rhinovirus infection does not cause detectable damage of the mucosa, but results in a 100-fold increase in the number of polymorphonuclear leukocytes in the nasal secretion, which turns purulent in half of the patients with uncomplicated colds.12 In another study, a significant increase in soluble intercellular adhesion molecule-1 (ICAM-1), IL-1β, IL-6, IL-8, myeloperoxidase, interferon-γ, and IL-10 was found in nasal secretions of patients with the common cold. ICAM-1 seems to be playing a greater role in viral infections, because it serves as a receptor for ~90% of all human rhinoviruses.13 A recent study reported the pattern of cytokines in the nasal fluid of patients with naturally acquired acute viral rhinitis.14 In this study, activation of both T helper cell types was found; however, Th1 dominance was noted with an increase of IL-6, IL-10, granulocyte colony-stimulating factor (G-CSF), GM-CSF, macrophage inflammatory protein (MIP)–1β, interferon-γ, and tumor necrosis factor (TNF)–α in the nasal secretions of patients with viral rhinitis (as compared with patients with ongoing allergic rhinitis and healthy controls). In the same study, however, elevated concentrations of IL-4 and IL-13 have also been found. The authors explained that IL-4 may play a role in limiting inflammatory processes by inhibiting the production of inflammatory cytokines.14 In addition, other mechanisms dominated by the epithelium itself and neurogenic inflammation may have an important role in the host′s response to viral infection.

In some instances, both viruses and bacteria could be cultured from the same specimen. An infection can start from a small viral inoculum. Following exposure, the viral particle binds to the specific surface antigens of their target cells. In 90% of rhinovirus infections, binding occurs with the ICAM-1 molecules on the surface of the cell.15 In contrast to bacteria, binding is very target- and host-specific. For example, rhinoviruses are difficult to study experimentally because they only infect humans and higher primates. Following cellular invasion and replication, viremia may occur, or the infection may remain localized to the target cells and perhaps to the regional lymphoid tissue. Target specificity and regionalization can be documented by viral culture studies. When selective samples are cultured, rhinovirus can be isolated from nasal secretions in 90% of patients, 70% of throat cultures, saliva from Stensen duct in 50%, and 0% of sputum cultures.16 In an experimental design in which healthy volunteers were inoculated with rhinoviruses, a titer of specific neutralizing antibodies of 1 in 16 volunteers was found to be protective against infection with the same viral species. However, immunity is not long lasting, because 9 to 12 months after the infection, the antibodies had disappeared from the serum, and reinfection with the same species became possible once again.