Clinical presentation and diagnosis of influenza
The disease is characterized by an acute onset and the development of three main syndromes: intoxication, catarrhal, and hemorrhagic.
In the first days of the illness, high fever, chills, marked weakness, myalgia, and eyeball pain exacerbated by eye movement are typical. Subsequently, a dry cough develops, along with potential epistaxis, nausea, and vomiting. Examination reveals facial flushing, lip cyanosis, scleral injection, and oropharyngeal changes: hyperemia of the arches and posterior pharyngeal wall, and petechiae on the mucous membrane.
A detailed clinical diagnosis must reflect the degree of severity (mild, moderate, severe) and the presence of complications, such as infectious-toxic shock, acute cardiovascular or respiratory failure, hemorrhagic syndrome, or meningitis. To confirm the diagnosis, PCR and virological testing are performed, along with differential diagnosis against similar infections.
Principles of treatment for uncomplicated and severe forms
Most patients with an uncomplicated course can be managed on an outpatient basis. The mainstay of pathogenetic therapy is detoxification (abundant fluid intake) and symptomatic agents (antipyretics, mucolytics, vitamins to strengthen vascular walls). Etiotropic therapy (oseltamivir, zanamivir) should be initiated within the first 48 hours.
In severe forms, hospitalization is mandatory. Intensive care in the hospital setting includes parenteral detoxification with a glucose-potassium mixture, antioxidants, and glucocorticoids. When oxygenation parameters decline (PaO2 < 60 mm Hg, SpO2 < 90%), oxygen therapy is prescribed; if respiratory failure progresses, mechanical ventilation is initiated. Antibacterial drugs are used exclusively when bacterial complications supervene or when chronic infection foci are present.
Poisonous mushroom poisoning syndromes
In addition to viral infections, food-borne toxicoinfections and poisonings play a crucial role in the differential diagnosis of acute conditions.
- Phalloidin syndrome: Develops after ingestion of mushrooms containing thermostable toxins (amanitin, phalloin). Characterized by severe gastroenteritis (intractable vomiting, profuse bloody diarrhea) and rapid development of hepatorenal failure (anuria, jaundice, coma). Cardiovascular failure and acrocyanosis may occur.
- Muscarine syndrome: Latent period is short (1–6 hours). Characterized by profuse sweating, hypersalivation, bronchorhea, as well as colicky abdominal pain, vomiting, and diarrhea. Specific signs include pupillary constriction (miosis) and pronounced neurological disorders (confusion, delirium).
- Helvellic acid poisoning: Occurs upon ingestion of improperly cooked spring mushrooms. Symptoms include stomach pain, vomiting, and in severe cases, hemolytic jaundice, hemoglobinuria, and mydriasis, potentially progressing to coma amidst signs of cardiac weakness.
Influenza complications: clinical cases
A severe course may be complicated by secondary flora superinfection. For example, the development of secondary bacterial pleuropneumonia manifests as a secondary temperature spike on the 7th day of illness, increased cough (potentially with blood-streaked mucopurulent sputum), pleuritic chest pain on inspiration, and dullness to percussion.
Another formidable complication is acute respiratory distress syndrome (ARDS), accompanied by stage II–III acute respiratory failure. Patients exhibit severe dyspnea (orthopnea, tachypnea up to 50 breaths per minute), frothy pink sputum production, moist rales throughout both lung fields, marked arterial hypotension, and tachycardia.
Briefly: answers to topical questions
What are the main clinical forms of adenoviral infection?
The disease may present as:
- Rhinopharyngitis.
- Rhinopharyngotonsillitis.
- Pharyngoconjunctivitis.
- Keratoconjunctivitis.
Sources also note age-specific variants and rare forms:
- in early-age children — pharyngoconjunctivitis;
- in young children — gastroenteritis;
- rare forms — meningoencephalitis and hemorrhagic cystitis.
Which eye manifestations are most characteristic of adenoviral infection?
Adenoviral infection is most characteristically marked by the development of conjunctivitis and keratoconjunctivitis. A pathognomonic sign is pharyngoconjunctival fever, which represents a combination of pronounced catarrhal syndrome and conjunctivitis. In complicated cases, severe corneal inflammation develops, carrying a risk of vision loss.
What lymph node changes are typical for adenoviral infection?
Adenoviral infection is typically characterized by lymphadenopathy. Sources also note involvement of oropharyngeal lymphoid tissue, and less commonly, the intestine and abdominal lymph nodes. Additionally, hepatosplenomegaly is characteristic of adenoviral infection.
What are the main transmission routes of adenoviral infection?
Sources indicate the following for adenoviral infection:
- airborne (aerogenic) transmission;
- contact transmission.
For viral acute intestinal infections, whose pathogens include certain enteric adenoviruses, a fecal-oral mechanism of transmission is indicated. The entry portal for acute respiratory viral infections (ARVI) is the mucous membrane of the upper respiratory tract.
How does adenoviral infection clinically differ from influenza?
Adenoviral infection differs from influenza by the following features:
| Sign | Adenoviral infection | Seasonal influenza |
|---|---|---|
| Onset | Gradual | Acute |
| Course | Protracted, undulating | Acute |
| Leading clinical syndrome | Catarrhal | Intoxication |
| Severity of intoxication | Moderate; less pronounced than in influenza | Severe |
| Duration of intoxication | 8–10 days | 2–5 days |
| Catarrhal manifestations | Highly pronounced; combination of pronounced catarrhal syndrome and conjunctivitis is characteristic | Moderately pronounced, appearing later; influenza features nasal congestion, oropharyngeal hyperemia, dry cough, and a sensation of raw burning behind the sternum |
Lymphadenopathy and hepatosplenomegaly are also characteristic of adenoviral infection.
What is the incubation period for adenovirus infection?
The incubation period for adenovirus infection ranges from 4 to 14 days.
Which medications are used for the local treatment of adenoviral conjunctivitis?
Antiviral agents are used for the local treatment of adenoviral conjunctivitis:
- Interferon alfa-2a preparations — for example, Reaferon-EU.
- Combination drugs — Ophthalmoferon eye drops (interferon alfa-2a combined with the antihistamine diphenhydramine), which have a complex antiviral, anti-inflammatory, and local anesthetic effect.
- Nucleases — ribonuclease and deoxyribonuclease preparations.
How does the peripheral blood picture change in uncomplicated adenovirus infection?
The peripheral blood picture in uncomplicated adenovirus infection reveals neutrophilic leukocytosis (left shift of the leukocyte formula) and an accelerated erythrocyte sedimentation rate (elevated ESR).
To remember the indications for antibiotics in influenza, use the three "C" rule: Chronic respiratory diseases, Chronic foci of infection, Clearly confirmed bacterial complications.
Class and exam questions
When is etiotropic therapy prescribed for influenza?
Antiviral drugs (e.g., oseltamivir) are most effective when administered within the first 48 hours of symptom onset.
When are antibiotics indicated in influenza?
Antibiotic therapy is prescribed strictly for confirmed bacterial complications (e.g., pneumonia), as well as for patients with chronic respiratory diseases or other chronic foci of infection.
What are the criteria for discharging a patient after recovery from influenza?
Discharge of a convalescent patient is performed upon sustained clinical recovery and no earlier than the 3rd day of sustained normalization of body temperature.
What else to study on this topic
- Pathogenesis of hemorrhagic syndrome in severe viral infections
- Mechanism of action of direct and indirect mucolytic agents
- Differential diagnosis of infectious-toxic shock
- Features of acid-base balance (ABB) in acute respiratory failure
- Toxicodynamics of amatinin and mechanisms of liver damage in mushroom poisoning
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