Porth's Essentials of Pathophysiology, 4e

543

Respiratory Tract Infections, Neoplasms, and Childhood Disorders

C h a p t e r 2 2

Hemagglutinin

Viral envelope

Neuraminidase

Nucleoprotein

B

Polymerase

RNA

A

C FIGURE 22-2. Influenza type A virus. (A) Model of the RNA influenza A virus, showing the hemagglutinin and neuraminidase envelope glycoproteins that provide access to host cells. (B) Negative-stained transmission electron micrograph (TEM) depicting the ultrastructural details of a number of influenza viral particles, or “virions.” (C) TEM revealing ultrastructural features of the 1918 influenza pandemic virus virions. (B and C from the Centers for Disease Control and Prevention Public Health Image Library. Nos. 8432, 8996. B courtesy of F.A. Murphy; C courtesy of Cynthia Goldsmith.)

If the virus spreads to the lower respiratory tract, the infection can cause severe shedding of bronchial and alveolar cells. In addition to compromising the natural defenses of the respiratory tract, influenza infection pro- motes bacterial adhesion to epithelial cells. Manifestations In the early stages, the symptoms of influenza often are indistinguishable from other viral infections. There is an abrupt onset of fever and chills; malaise; muscle aching; headache; profuse, watery nasal discharge; nonproductive cough; and sore throat. 15–17 One distinguishing feature of an influenza viral infection is the rapid onset, sometimes in as little as minutes, of profound malaise. The symp- toms of uncomplicated rhinotracheitis usually peak by days 3 to 5 and disappear by days 7 to 10. Weakness, cough, and malaise may persist for weeks after clinical resolution of influenza. Young children with influenza viral infection can have initial symptoms mimicking bac- terial sepsis with high fevers and febrile convulsions. Viral pneumonia occurs as a complication of influ- enza, most frequently in the elderly or in persons with cardiopulmonary disease, but has been reported in pregnant women and in healthy, immunocompetent people. 18 It typically develops within 1 day after onset of influenza and is characterized by rapid progression

of fever, tachypnea, tachycardia, cyanosis, and hypo- tension. The clinical course of influenza pneumonia progresses rapidly. It can cause hypoxemia and death within a few days of onset. Survivors often develop dif- fuse pulmonary fibrosis. Secondary complications typically include sinusitis, otitis media, bronchitis, and bacterial pneumonia. 15 Persons who develop secondary bacterial pneumonia usually report that they were beginning to feel better when they experienced a return of fever, shaking chills, pleuritic chest pain, and productive cough. The most common causes of secondary bacterial pneumonia are S. pneumoniae, S. aureus, H. influenzae, and M. catarrhalis. This form of pneumonia commonly produces less cya- nosis and tachypnea and is usually milder than primary influenza pneumonia. Influenza-related deaths can result from pneumonia as well as exacerbations of cardiopul- monary conditions and other disease. Reye syndrome (fatty liver with encephalitis) is a rare complication of influenza, particularly in young children who have been given aspirin as an antipyretic agent. 15 Diagnosis andTreatment Diagnosis is based on symptoms such as sudden onset of fever, cough, weakness, and myalgias. The probability of influenza varies with the prevalence of the disease in