CASE 4
A 75 year-old female residing in a nursing home developed the sudden onset of fever to 101o F, headache and malaise in December. Over the next two days, she had increasing difficulty breathing and was transferred to a medical facility where a diagnosis of pneumonia was made by chest x-ray. Her 2 year old grandson had visited her three days prior to the onset of symptoms. He became ill the day after the visit with cough, rhinorrhea and vomiting. The woman had not received an influenza vaccine that year; her physician deferred the vaccine because the patient had an upper respiratory infection. The woman was treated with antibiotics and oxygen. She gradually recovered. After she was discharged, the clinical virology laboratory isolated influenza B virus from a pharyngeal swab.
BACKGROUND
Influenza B virus (a negative strand RNA virus with a segmented genome).
Influenza viruses have a predilection for the respiratory tract, and viremia is rarely detected. They multiply in ciliated respiratory epithelial cells, leading to functional and structural ciliary abnormalities. This is accompanied by a switch-off of protein and nucleic acid synthesis in the affected cells, the release of lysosomal hydrolytic enzymes, and desquamation of both ciliated and mucus-producing epithelial cells. There is, thus substantial interference with the mechanical clearance mechanism of the respiratory tract. The process of cell death results in the cleavage of complement components, leading to localized inflammation. Early in infection, the primary chemotactic stimulus is directed toward mononuclear leukocytes, which constitute the major cellular inflammatory component. The respiratory epithelium may not be restored to normal for 2 to 10 weeks after the initial insult.
The virus particles are also toxic to tissues. This toxicity can be demonstrated by inoculating high concentrations of inactivated virions into mice, which produces acute inflammatory changes in the absence of viral penetration or replication within cells.
Other host cells functions are also severely impaired, particularly during the acute phase of infection. They include chemotactic phagocytic, and intracellular killing functions of polymorphonuclear leukocytes and perhaps of alveolar macrophage activity.
The net result of these effect, is that on entry into the respiratory tract, the viruses cause cell damage, especially in the respiratory epithelium, which elicits an acute inflammatory response and impairs mechanical and cellular host responses. This damage renders the host highly susceptible to invasive bacterial superinfection. In vitro studies also suggest that bacterial pathogens such as staphylococci can more readily adhere to the surfaces of influenza virus-infected cells. Recovery from infection begins with interferon production, which limits further virus replication, and with rapid generation of natural killer cells. Shortly thereafter, class I major histocompatibility complex (MHC)-restricted cytotoxic T cells appear in large numbers to participate in the lysis of virus-infected cells and, thus, in initial control of the infection. This is followed by the appearance of local and humoral antibody along with an evolving, more durable cellular immunity. Finally, there is repair of tissue damage.
Case 4