Legionnaires’ disease is an acute bronchopneumonia produced by a gram-negative bacillus. It derives its name and notoriety from the peculiar, highly publicized disease that struck 182 people (29 of whom died) at an American Legion convention in Philadelphia in July 1976. This disease may occur epidemically or sporadically, usually in late summer or early fall. Its severity ranges from a mild illness, with or without pneumonitis, to multilobar pneumonia, with a mortality as high as 15%. A milder, self-limiting form (Pontiac syndrome) subsides within a few days but leaves the patient fatigued for several weeks. This form mimics Legionnaires’disease but produces few or no respiratory symptoms, no pneumonia, and no fatalities.
The causative agent of Legionnaires’ disease, Legionella pneumophila, is an aerobic, gram-negative bacillus that’s probably transmitted by an airborne route. In past epidemics, it has spread through cooling towers or evaporation condensers in air-conditioning systems. However, Legionella bacilli also flourish in soil and excavation sites. The disease doesn’t spread from person to person.
Legionnaires’ disease is most likely to affect:
❑ middle-age and elderly people
❑ immunocompromised patients (particularly those receiving corticosteroids, for example, after a transplant) or those with lymphoma or other disorders associated with delayed hypersensitivity
❑ patients with a chronic underlying disease, such as diabetes, chronic renal failure, or chronic obstructive pulmonary disease
❑ those with alcoholism
❑ cigarette smokers
❑ those on a ventilator for extended periods
The multisystem clinical features of Legionnaires’ disease follow a predictable sequence, although the onset of the disease may be gradual or sudden. After a 2- to 10-day incubation period, nonspecific, prodromal signs and symptoms appear, including diarrhea, anorexia, malaise, diffuse myalgias and generalized weakness, headache, and recurrent chills. An unremitting fever develops within 12 to 48 hours with a temperature that may reach 105° F (40.6° C). A cough then develops that’s nonproductive initially but eventually may produce grayish, nonpurulent, and occasionally blood-streaked sputum.
Other characteristic features include nausea, vomiting, disorientation, mental sluggishness, confusion, mild temporary amnesia, pleuritic chest pain, tachypnea, dyspnea, and fine crackles. Patients who develop pneumonia may also experience hypoxia. Other complications include hypotension, delirium, heart failure, arrhythmias, acute respiratory failure, renal failure, and shock (usually fatal).
The patient history focuses on possible sources of infection and predisposing conditions. Additional tests reveal:
❑ Chest X-ray shows patchy, localized infiltration, which progresses to multilobar consolidation (usually involving the lower lobes), pleural effusion and, in fulminant disease, opacification of the entire lung.
❑ Auscultation reveals fine crackles, progressing to coarse crackles as the disease advances.
❑ Abnormal findings include leukocytosis, increased erythrocyte sedimentation rate, an increase in liver enzyme levels (alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase), hyponatremia, decreased partial pressure of arterial oxygen and, initially, decreased partial pressure of arterial carbon dioxide. Bronchial washings and blood, pleural fluid, and sputum tests rule out other infections.
Antibiotic treatment begins as soon as Legionnaires’ disease is suspected and diagnostic material is collected; it shouldn’t await laboratory confirmation. Quinolone (ciprofloxacin, levofloxacin, moxifloxacin, or gatifloxacin) is commonly used, although a macrolide (azithromycin, clarithromycin, or erythromycin) may be prescribed for some patients. Supportive therapy includes administration of antipyretics, fluid replacement, circulatory support with pressor drugs, if necessary, and oxygen administration by mask, cannula, or mechanical ventilation.
❑ Closely monitor the patient’s respiratory status. Evaluate chest wall expansion, depth and pattern of respirations, cough, and chest pain. Watch for restlessness as a sign of hypoxemia, which requires suctioning, repositioning, or more aggressive oxygen therapy.
❑ Continually monitor the patient’s vital signs, oximetry or arterial blood gas values, level of consciousness, and dryness and color of lips and mucous membranes. Watch for signs of shock (decreased blood pressure, thready pulse, diaphoresis, and clammy skin).
❑ Keep the patient comfortable. Provide mouth care frequently. If necessary, apply soothing cream to the nostrils.
❑ Replace fluid and electrolytes, as needed. The patient with renal failure may require dialysis.
❑ Provide mechanical ventilation and other respiratory therapy, as needed. Teach the patient how to cough effectively, and encourage deep-breathing exercises. Stress the need to continue these until recovery is complete.
❑ Give antibiotic therapy as ordered, and observe carefully for adverse effects.
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Title: Professional Guide to Diseases (Eighth Edition)
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2005
ISBN: 1-58255-370-X
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