Upper respiratory tract infections

cold inflammation of the respiratory tract

We will briefly look at infections of the upper respiratory tract, including infections of the nasal passages, paranasal sinuses, and pharynx. These diseases are the common cold, rhinosinusitis, pharyngitis and diphtheria. With the exception of diphtheria, viruses are the most common causes of all these diseases.


The common cold is caused by many organisms, and about 90% of cases are caused by viruses.

Etiology of the common cold

Most cases are caused by rhinoviruses; there are at least 100 immunologically distinct rhinoviruses.


Initially, the symptoms are a stuffy nose, sneezing and headache. Then rhinorrhea occurs which gradually worsens. Fatigue, lacrimation, sore throat, mild fever and anorexia are common in middle to severe colds. If organisms enter the trachea and bronchi, tracheobronchitis develops and coughing and a feeling of substernal discomfort may occur.


  • The common cold occurs everywhere in the world.
  • Children under the age of 5 will develop five to seven colds a year, and adults one or two.
  • The common cold is seen mainly in the winter months (probably because most person contacts occur more easily in the winter).
  • Viruses spread from person to person, usually during handling.

Pathogenesis of the common cold

Rhinovirus infects the nasal passages after direct contact with contaminated surfaces or by inhalation of infectious droplets. It then infects the cells lining the nasal passages and pharynx after capturing the intracellular adhesion molecule on the host cells. Inflammatory changes that occur are hyperemia, edema, and leukocyte inflammation. Cilia cells are destroyed and peeled off.

The peak of pathological changes occurs after the second to fifth day. Cell regeneration begins rapidly, and new cells form around 14. days. The acute phase of the disease begins with a runny nose, with the production of clear discharge. After one to two days, infection with the normal bacterial flora causes the secretion of mucopullorent discharge. If blockage of the sinus openings or eustachian tube occurs, paranasal sinusitis or otitis media occurs. Complications are usually associated with the spread of the infection to the lower respiratory tract, resulting in bronchitis.


The diagnosis of a cold depends on the symptoms, the localization and course of the disease, the season and the afebrile course. Laboratory virus cultures and serological testing are rarely performed.

Therapy and prevention

Treatment of the common cold includes supportive therapy to relieve symptoms, for example, a nasal gel containing zinc gluconate. Big doses of vitamin C. they can shorten the duration of the disease and reduce the severity of symptoms. Washing your hands and disinfecting contaminated items can prevent you from catching a cold as well as avoiding contact with others during the cold season.

Acute rhinosinusitis

Acute rhinosinusitis

Acute rhinosinusitis is defined as inflammation or infection of the lining of the nasal passages and at least one paranasal sinus that does not last longer than four weeks. Rhinitis and sinusitis usually occur together, so medical terminology has now changed from the term sinusitis to rhinosinusitis.


Most cases of acute rhinosinusitis occur due to respiratory viruses, which include rhinoviruses, parainfluenza virus, respiratory syncytial virus, and adenovirus. However, acute rhinosinusitis can occasionally be complicated by a bacterial infection and is then diagnosed as acute bacterial rhinosinusitis.

The two most common causes of community-acquired (CA) acute bacterial rhinosinusitis are Streptococcus pneumoniae and Haemophilus influenzae. The table lists the bacteria that cause over 70% of paranasal sinus infections. Immunosuppressed patients are also prone to sinus fungal infections due to Aspergillus and Mucor species.


Acute rhinosinusitis is characterized by inflammation of the mucous membranes of the nose and paranasal sinuses. Symptoms include sneezing, rhinorrhea, nasal congestion and runny nose, sinus pressure, feeling of pressure in the face and headache, sore throat, cough and fever, and myalgia. Viral infection of the upper respiratory tract usually occurs before bacterial rhinosinusitis, and the differentiation between bacterial infection and viral infection is difficult.


  • Respiratory viruses cause most acute rhinosinusitis. Symptoms usually subside after 5-7 days, and most people recover without the need for medical treatment.
  • Sinus infection can occur after a cold, tooth extraction, rhinitis due to allergies, and water entering the sinuses after bathing (or, for example, diving).
  • Sinus infections develop most often during the winter months when the common cold occurs more often.
  • In approximately 2% of adults and 10% of children, acute bacterial rhinosinusitis may follow viral rhinosinusitis, allergic rhinitis, or other upper respiratory tract infections.
  • Predisposing factors for acute bacterial rhinosinusitis are listed on the side.
  • Patients with nosocomial infections are more likely to be infected with gram-negative organisms when they develop acute bacterial rhinosinusitis.
  • Acute bacterial rhinosinusitis due to anaerobic bacteria is usually associated with dental infections or procedures.


The most common precursor to acute bacterial rhinosinusitis is a viral infection of the upper respiratory tract followed by sinus obstruction due to mucosal edema. Obstruction of the mouth of the paranasal sinuses makes it difficult to drain mucous secretions. Bacteria grow in these secretions, irritating the underlying mucosa and producing more secretions. Mucosal cell death and exfoliation occurs, but the cells will regenerate once the infection has passed.


The diagnosis of acute rhinosinusitis is based on the patient’s clinical signs and symptoms. Acute bacterial rhinosinusitis is correctly diagnosed in half of the cases only on clinical signs. Acute bacterial rhinosinusitis and viral rhinosinusitis are difficult to distinguish because no clinical sign can accurately distinguish between acute viral rhinosinusitis and acute bacterial rhinosinusitis. However, acute bacterial rhinosinusitis has a higher chance of developing into a chronic disease.

A diagnosis of acute bacterial rhinosinusitis is likely when the patient has symptoms of rhinosinusitis that include purulent nasal discharge that worsens after 5 days and persists for more than 10 days or is out of proportion to the symptoms seen with viral upper respiratory tract infection.

Signs and symptoms considered closer to the bacterial pathogen include high and persistent fever (> 39), periorbital swelling, severe facial or dental pain, altered mental status, diplopia, and infraorbital hypersthesia.

The four symptoms that appear to be most helpful in diagnosing a patient with acute bacterial rhinosinusitis are purulent nasal discharge, maxillary tooth pain, or facial pain (especially unilateral), unilateral maxillary sinus pain, and worsening symptoms after initial improvement. The criteria for diagnosis are in the table.

Therapy and prevention

Several different treatments can be used to aid in recovery. Symptomatic treatment is recommended for viral rhinosinusitis, but if the patient has bacterial rhinosinusitis, symptomatic and antibiotic treatment is required.

Symptomatic treatment

  • Increase oral hydration with the use of nasal solution and steam to encourage drainage;
  • antipyretics, analgesics, and decongestants may be required for fever, headache, and facial pain;
  • mucolytics are useful for “thinning” thick nasal secretions.

Antibiotic treatment

Recommendations for initial antibiotic therapy in patients with acute bacterial rhinosinusitis include amoxicillin or cefdinir. If patients are allergic to beta-lactam antibiotics, trimethoprim-sulfamethoxazole or azithromycin are the antibiotics of choice.

There is no vaccine for acute viral or bacterial rhinosinusitis, but patients can avoid future problems by avoiding jumping into the water without a stuffy nose, correcting septal deviations or removing polyps, and proper dental care.


Pharyngitis disease

Pharyngitis or sore throat is a common disease, and most cases are caused by viruses.


Pharyngitis can be caused by many different microorganisms, however, for 90% of cases in adults and 60-75% of cases in children, viruses are responsible. S.pyogenes (beta hemolytic group A streptococcus) is the most common bacterial cause of acute pharyngitis.

Manifestations of pharyngitis

Fever, inflammation, edema, and hyperemia of the tonsils and pharyngeal walls are commonly found in patients with viral and bacterial pharyngitis. Other findings indicating viral rather than bacterial pharyngitis include conjunctivitis, cough, nasal congestion, hoarseness, and diarrhea; anterior stomatitis and small ulcerative lesions; and viral exanthema.

Patients with S. pyogenes pharyngitis (streptococcal pharyngitis, streptococcal angina or purulent angina ) often present with fever and pain on swallowing (usually sudden onset). Headache, nausea and vomiting, and abdominal pain may be present, especially in children. On examination, patients have tosylopharyngeal erythema, with or without exudate, and palpable enlarged anterior cervical lymph nodes (lymphadenitis). They may also have red and swollen uvula; petechiae on the palate; and scarlet fever rash. However, none of these signs are specific for S. pyogenes pharyngitis.

If left untreated, patients with S. pyogenes pharyngitis may develop suppurative and nonsupurative complications. Suppurative complications include peritonsillar abscesses, cervical lymphadenitis, and mastoiditis. A major non-suppurative complication is rheumatic fever, a complication that develops more frequently in children with S. pyogenes pharyngitis than in adults with the same infection.

Rheumatic fever represents different sets of clinical manifestations with onset of symptoms several days to five weeks after streptococcal throat infection. Patients with rheumatic fever first have a fever, and painful swelling of several joints such as the knees, elbows, or wrists. Severe rheumatic fever can result in damage to the heart valves.


  • Pharyngitis is common all over the world
  • Pharyngitis due to S. pyogenes is usually a disease of children between 5 and 15 years of age.
  • In the temperate climate zone, it is most common during winter and early spring.
  • Viruses are the most common cause of pharyngitis,
  • With a few ins and outs (e.g. diphtheria), pharyngitis is benign and self-limiting.
  • Viral pharyngitis is acquired by contact from person to person and after contact with infectious objects.
  • S. pyogenes is transmitted by contact from person to person.


In viral pharyngitis, the viruses come in contact with the nasopharyngeal mucosal cells and replicate in those cells. Host damage is usually damage to the cells in which the virus replicates.

In bacterial pharyngitis, S. pyogenes is captured by mucosal epithelial cells using M protein, lipotechoic acid, and fibronectin-binding protein (F protein). It has a capsule composed of hyaluronic acid that prevents phagocytosis by host macrophages. Since the hyaluronic acid of the bacterial capsule is identical to the host’s hyaluronic acid, it facilitates the survival of the bacterium by covering the bacterial antigens.

Extracellular factors produced by S.pyogenes during infection include proteases and hyaluronidase. These extracellular factors help bacteria invade the mucosa. Direct spread to other sites may occur, but is now relatively rare with respect to antibiotic therapy.

Non-suppurative lesions resulting in rheumatic fever and glomerulonephritis may still occur after S.pyogenes throat infections. Several bacterial antigens of S.pyogenes are believed to share epitopes with cardiac and renal tissue Autoimmune reaction occurs in some patients after the production of an immune response to these cross-reactive bacterial antigens and damages the patient’s heart and kidneys. Note: Rheumatic fever and glomerulonephritis may occur after an episode of pharyngitis; glomerulonephritis itself can also occur after a skin infection (e.g., impetigo).


Throat virus cultures are rarely performed due to the mild nature of the disease and the cost of culturing the pathogen itself. There are fewer cases of bacterial throat infection (compared to viral pharyngitis); however, delaying treatment of S.pyogenes pharyngitis for more than 9 days after the onset of symptoms increases the possibility of developing rheumatic fever and suppurative complications (e.g., peritonsillar abscess, mastoiditis).

Therefore, strategies for diagnosing acute pharyngitis are primarily aimed at identifying patients with S.pyogenes pharyngitis, who require antimicrobial therapy, as well as avoiding unnecessary treatment of patients diagnosed with acute viral pharyngitis.

The best way to determine the etiological agent is a throat swab and its planting on agar, where beta hemolytic colonies, negative catalase, ie. gram positive cocci sensitive to bacitracin (bacitracin test).

Cultures are not necessary and the diagnosis of all cases of pharyngitis, and this is especially true for adults. If the patient has clinical and epidemiological features of pharyngitis (cough, conjunctivitis, diarrhea,…) suggesting viral pharyngitis, no further testing is required. If there are suggestions on the bacterial etiology, it is necessary to make a culture.

Children under the age of 18 are more likely to develop S.pyogenes pharyngitis, and are more likely to develop suppurative and non-suppurative complications if left untreated. Therefore, it is necessary to work cultures. If the test is positive, it is necessary to give penicillin.

Rheumatic fever is a non-suppurative complication of S.pyogenes pharyngitis and resembles a number of other diseases affecting the joints (e.g., rheumatoid arthritis, SLE, serum sickness). The side table lists the diagnostic criteria for S.pyogenes pharyngitis.

Therapy and prevention

All patients with acute pharyngitis should be given appropriate doses of antipyretics, analgesics, and supportive care.

Viral pharyngitis

It is treated with analgesics (eg paracetamol). The patient should be encouraged to drink fluids to avoid dehydration. Susceptible persons should be warned to limit contact with an infected person.

S.pyogenes pharyngitis

It requires the use of antimicrobial agents, in addition to the therapies mentioned for acute viral pharyngitis. Antibiotics have been shown to limit the spread (e.g., peritonsillar abscesses, cervical lymphadenitis, mastoiditis); prevent the development of acute rheumatic fever (if given within 9 days of symptoms); improve clinical signs and symptoms (if given within 2 days of symptoms); they quickly reduce infectivity and reduce the transmission of bacteria from person to person and speed up recovery. Penicillin is the antibiotic of choice, and erythromycin for patients allergic to penicillin.

Rheumatic fever

Treatment includes antimicrobial drugs to eliminate S.pyogenes from the pharynx and anti-inflammatory drugs to suppress the clinical manifestations of the disease. Recurrence of rheumatic fever is more likely in patients who have had a previous episode of S.pyogenes pharyngitis.

Patients who have recovered from rheumatic fever should be protected with chemoprophylaxis in the form of a monthly dose of penicillin, and this chemoprophylaxis should be given throughout childhood. If permanent damage to the heart occurs, chemoprophylaxis should continue to be given for life.



Diphtheria is a bacterial disease that is rarely seen today due to a successful universal vaccine. Vaccination does not affect the ability of bacteria to colonize the oropharynx, but rather induces the production of antibodies to inhibit diphtheria toxin.


Corynebacterium diphtheriae is a gram positive stick that is irregularly stained by Gram. Only strains of C. diphtheriae that have beta phage, i.e., a toxin-producing lysogenic bacteriophage, can cause diphtheria.


Diphtheria results in pharyngeal pain, formation of pseudomembranes seen on the tonsils and posterior wall of the oropharynx, regional lymphadenopathy (“bull neck pictured right”), edema of surrounding tissues, bad breath, low-grade fever, and cough. Respiratory obstruction and tachypnea, stridor and cyanosis may occur. The toxin can cause damage to the cranial nerves and heart, causing neurological abnormalities (e.g., palatine paresis, difficulty swallowing, nasal fluid regurgitation), and myocarditis.


  • The disease occurs worldwide. however, in vaccinated areas very rarely (eg only 1 or 2 cases per year occur in the US)
  • The largest epidemic in recent history occurred in the former Soviet Union in 1994. year, with over 48,000 cases of diphtheria and over 1,700 deaths.
  • C. diphtheriae can colonize the oropharynx and skin of persons immune to the disease without causing the disease, and thus C. diphtheriae maintains its population.
  • Humans are the only known reservoir of C. diphtheriae.
  • The most common cause of death is heart damage due to diphtheria toxin.
  • C. diphtheriae is transmitted by droplets and skin contact. Healthy carriers and patients in the incubation phase are the best carriers.


C. diphtheriae colonizes the oropharynx and remains localized on mucosal surfaces. Only C. diphtheriae lysogens for bacteriophages carrying the toxin gene can cause diphtheria. Damage to the pharynx is caused by a toxin that kills mucosal cells by adenosine diphosphate ribosylation of elongation factor II and termination of protein synthesis.

The inflammatory response to cell death and dead cells is produced by pseudomembranes. Thotoxin can also bind to and damage heart cells and nerve cells. Major complications of diphtheria are myocarditis and damage to the cranial nerves. Myocarditis is more important than the two complications and causes the highest mortality. The cranial nerves are most sensitive to the toxin, resulting in difficulty swallowing and nasal fluid regurgitation.

There is also a cutaneous form of diphtheria – a cut in the skin can open the way for C. dipheriae to enter the subcutaneous tissue, leading to a chronic ulcer that does not heal, and has a gray membrane. Rarely, exotoxin production leads to tissue degeneration and death.


The diagnosis of diphtheria includes observation of pseudomembranes and bleeding after removal of the membrane, and severe cervical lymphadenopathy. Neurological abnormalities such as palate paresis, difficulty swallowing, and nasal fluid regurgitation are important signs for a correct diagnosis of diphtheria. An oropharyngeal swab should be taken and a culture made. Whether a strain produces a toxin can be deduced, for example, from PCR.

Treatment and p revenge

A patient with diphtheria should be hospitalized, placed in isolation, and treated immediately with a toxin antiserum. The most important task is to provide an antiserum to neutralize the toxic effects of diphtheria toxin. Another urgent task is antimicrobial therapy with penicillin or erythromycin. The patient should also be vaccinated to ensure immunity to the disease.


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