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Practically each person is familiar with symptoms of acute infectious rhinitis. The individual susceptibility to a viral infection depends on many factors: age, physical development, sanitary and hygienic conditions, extent of adaptation to meteorological shifts, hardness of an organism to influence of low or contrast temperatures, existence of intercurrent diseases. Acute infectious rhinitis is especially widespread in children's age. It is considered that the children visiting preschool institutions transfer from 2 to 6 episodes of acute infectious rhinitis to a year. Because of a large number of activators which can cause this disease (see" The etiology and pathogeny"), its accurate seasonality does not exist. The outbreaks of an adenoviral infection often arise in the flying in children's recreation camps and among recruits in army. Epidemic of the diseases caused by a respiratory and syncytial virus is noted in the winter, peaks of a rinovirusny infection fall on spring and fall.
Data on prevalence of chronic infectious rhinitis are absent.
The international classification provides division of infectious rhinitis on acute and chronic. Allocate simple (catarral), hypertrophic and atrophic forms of chronic infectious rhinitis. A separate form of chronic infectious rhinitis is dry front rhinitis.
Etiology and pathogeny
Acute infectious rhinitis usually happens one of displays of a SARS, but can be also a consequence of injuries of a mucous membrane of a nose. The most often acute infectious rhinitis is caused by RV. Carry influenza viruses to more rare activators, a parainfluenza, adenoviruses, a respiratory and syncytial virus, coronaviruses. It is considered to be that RV cause from 1/3 to a half of all SARS in adults while coronaviruses — only 10%. In recent years RV role grows in developing of acute infectious rhinitis, they are responsible more than for 80% of cases during autumn epidemics.
The main bacterial causative agents of acute infectious rhinitis consider Streptococcus pneumoniae, by Streptococcus pyogenes and Haemophilus influenzae. Various serotypes of these microorganisms, consistently replacing each other, begin to colonize a nasopharynx right after the birth therefore even in healthy population they are present at a nasopharynx at 1/3 adults and 2/3 children.
The range of causative agents of chronic infectious rhinitis are significantly wider. It includes Staphylococcus epidermidis, Staphylococcus aureus, Pseudomonas spp., Klebsiella spp. and many others, including opportunistic pathogenic bacteriums. Patients with immunodeficiency causative agents of rhinitis can have fungi, bacterial and fungal associations and opportunistic microorganisms. Besides, the chronic form of inflammatory process can be caused also by the specific activator (Corinebacterium diphtheriae at diphtheria, Klebsiella rhinoscleromatis at a scleroma, Treponema pallidum at syphilis, etc.). However specific chronic infectious rhinitises are very rare.
Pathogeny. Getting on a mucous membrane, RV connects to molecules of intracellular adhesion which are constantly expressed on epithelial cells of a nasal cavity and a nasopharynx. About 90% of RV get into the owner's organism in the field of the pharyngeal almond rich with the mentioned receptors. After connection with adhesion molecules the virus gets through a cell membrane into its cytoplasm and brings the RNA (RNA) for replication there. After replication of RV extends on a mucous membrane of a nasal cavity, without striking it it is total, but forming the scattered islands of the infected epithelium. At infection of RV the main part of a ciliary epithelium of a nasal cavity remains rather intact in this connection rhinitis proceeds rather easily and less often is followed by complications. Unlike RV, influenza viruses and adenoviruses cause more extensive damage and desquamation of an epithelium.
Virus infection initiates the cascade of defense reactions and forming of an immune response. The inflammatory changes happening in a mucous membrane include expansion of blood vessels and increase of their permeability, a cellular infiltration, hyperproduction of glands, allocation of mediators and stimulation of sensitive nerve terminations. The allocation mediated by adhesion molecules cells of an epithelium of cytokines and mediators of an inflammation (SILT, interferon at, a factor of a necrosis of a tumor and a colony stimulating factor) leads to stimulation of two main protective mechanisms. The first of them is an activation of the cells killers possessing virutsidny activity, migration in a mucous membrane of neutrophils and activation of monocytes. The second mechanism — education from naive T lymphocytes of the T lymphocytes of the 2nd type capable, in particular, to produce specific antiviral antibodies which are defined in serum and in a nasal secret 2 — 3 weeks later after infection. Thus, the cascade of defense reactions adjusted by cytokines leads to elimination of a virus and forming of the protective immune mechanism. This mechanism is not resistant and does not prevent repeated virus infection.
With passing or resistant defects of immunity or disturbance of mukotsiliarny transport virus infection becomes only the first phase of a disease which opens a way of bacterial superinfection. When cilia of the cells of a ciliary epithelium affected with a virus temporarily do not function, the bacteria which are in a nasal cavity have an opportunity for rather long contact with an epithelium surface. Further through the defects formed as a result of influence of a virus in an epithelial cover these bacteria can get into own layer of a mucous membrane. It in turn leads to the strengthened migration of neutrophils and macrophages and activation of mechanisms of antibacterial protection.
Various forms of chronic infectious rhinitis seldom meet in pure form. Chronic catarral infectious rhinitis can pass into subatrophic (atrophic) or hypertrophic forms. The hyperplasia of a submucosal layer is often combined with atrophic changes of an epithelium or with increase in amount of glands and hyperproduction of slime. Hypertrophic processes concern more often the lower nasal sinks which increase in sizes, gradually occupying all lower parts of a nasal cavity. The hypertrophy can be local and take mainly back ends of sinks which in this case take a polyp form.
The etiology and pathogeny of dry front rhinitis are up to the end not found out. It can arise at long influence of dust and other harmful production factors — hot dry air, chemicals (ammonia, formalin, hydrochloric, nitric and sulfuric acids, etc.).
Clinical signs and symptoms of infectious rhinitis
In a typical situation clinical displays of acute infectious rhinitis take place three consecutive stages in the development. In each case separate stages can be more or less expressed or be absent completely, for example, if there does not come bacterial infection.
The first stage (reflex or prodromal) develops quickly owing to overcooling of an organism and several hours last. At first there is a spasm, and then paralytic vasodilatation and hypostasis of nasal sinks. Dryness, burning in nasal cavities, difficulty of nasal breath, repeated sneezing disturb. The mucous membrane of a nose at a front rinoskopiya looks hyperemic and dry.
The second stage (catarral or serous) lasts two-three days and develops as a result of virus infection. The nose congestion, plentiful transparent watery allocations from a nose, decrease in sense of smell, sometimes dacryagogue, a congestion of ears and a nasal shade of a voice are characteristic of this stage. Plentiful allocations can cause irritation of skin of a vestibule of the nose and an upper lip, especially in children. The mucous membrane of a nose at this stage edematous, wet, has bright red color.
The beginning of the third stage is connected with accession of a bacterial inflammation. The general state improves, nasal breath and sense of smell are gradually recovered, but allocations gain mucopurulent character and more dense consistence. At a front rinoskopiya such discharge is visible in the general nasal course and at the bottom of a nasal cavity. Running off of a nasal secret on a back wall of a nasopharynx can lead to development of painful cough that is especially characteristic of children. The mucous membrane of a nose at this stage remains hyperemic and edematous, but its color gradually comes nearer to normal, and the gleam of the nasal courses gradually extends. All cycle of an illness comes to the end in 7 — 10 days, but can have shorter abortal current or in unfavorable conditions drags on and leads to development of complications — sinusitis, otitis, a tracheobronchitis, etc.
Main symptom of chronic
infectious rhinitis is difficulty of nasal breath. It can be non-constant, be followed by a periodic congestion one, other half of a nose, amplify at night, practically always gradually progresses, forces to use vasoconstrictive drops and finally brings the patient to the doctor. Nasal breath can be complicated for various reasons: as a result of hypostasis or a hypertrophy of nasal sinks or because of accumulation of allocations or crusts in the general nasal course. Allocations at this disease usually dense, yellowish, greenish or gray color. They can depart from a nose in the form of crusts, sometimes in allocations there is a blood impurity.
The diagnosis and the recommended clinical trials
In typical cases diagnosis of acute infectious rhinitis is simple. The acute beginning, the previous contact with the patient of a SARS and/or overcooling, typical sequence of emergence of symptoms are characteristic. At the persistent course of chronic infectious rhinitis research of a smear from a nasal cavity on microflora and sensitivity to antibiotics is shown.
The differential diagnosis of recurrent acute infectious rhinitis and allergic rhinitis at children of younger age can represent big difficulties. At children it is necessary to carry out differential diagnosis of chronic infectious rhinitis with a foreign body (rhinolith), chronic sinusitis, primary tsiliarny dyskinesia, a mucoviscidosis and Young's syndrome.