An acute bronchopneumonia, legionnaires’ disease is produced by a fastidious, gram-negative bacillus. 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 fever) 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.
Causes
The cause of legionnaires’ disease, Legionella pneumophila, is an aerobic, gram-negative bacillus that’s probably transmitted by an airborne route. With 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.
Predisposing Factors:
Legionnaires’ disease is more common in men than in women and is most likely to affect:
Although signs and symptoms of legionnaires’ disease emerge in a predictable sequence, onset of the disease may be gradual or sudden.
- middle-aged to elderly people
- immunocompromised people (particularly those receiving a corticosteroid, for example, after a transplant) or those with lymphoma or other disorders ssociated with delayed hypersensitivity
- patients with a chronic underlying disease, such as diabetes, chronic renal failure, or chronic obstructive pulmonary disease
- alcoholics
- cigarette smokers (three to four times more likely to develop legionnaires’ disease than nonsmokers).
Although signs and symptoms of legionnaires’ disease emerge in a predictable sequence, 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 myalgia and generalized weakness, headache, recurrent chills, and an unremitting fever, which develops within 12 to 48 hours with a temperature as high as 105° F (40.6° C). A cough then develops that is initially nonproductive but eventually may produce grayish, nonpurulent and, occasionally, blood-streaked sputum.
Other characteristic signs and symptoms include nausea, vomiting, disorientation, mental sluggishness, confusion, mild temporary amnesia, pleuritic chest pain, tachypnea, dyspnea, fine crackles and, in 50% of patients, bradycardia. 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).
Diagnosis
The patient history focuses on possible sources of infection and predisposing conditions. In addition, a 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 test findings include leukocytosis, an 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.
Definitive tests include direct immunofluorescence of respiratory tract secretions and tissue, a culture of L. pneumophila, and indirect fluorescent antibody testing of serum comparing acute samples with convalescent samples drawn at least 3 weeks later. A urine specimen for L. pneumophila antigen may also be performed. A convalescent serum showing a fourfold or greater rise in antibody titer for Legionella confirms this diagnosis.
The patient history focuses on possible sources of infection and predisposing conditions. In addition, a 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 test findings include leukocytosis, an 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.
Definitive tests include direct immunofluorescence of respiratory tract secretions and tissue, a culture of L. pneumophila, and indirect fluorescent antibody testing of serum comparing acute samples with convalescent samples drawn at least 3 weeks later. A urine specimen for L. pneumophila antigen may also be performed. A convalescent serum showing a fourfold or greater rise in antibody titer for Legionella confirms this diagnosis.
Treatment
Erythromycin is the drug of choice, but if it’s ineffective alone or contraindicated, rifampin can be used with it or as an alternative.
Supportive therapy includes administration of an antipyretic, fluid replacement, circulatory support with vasopressor drugs if necessary, and oxygen administration by mask, cannula, or mechanical ventilation
Erythromycin is the drug of choice, but if it’s ineffective alone or contraindicated, rifampin can be used with it or as an alternative.
Supportive therapy includes administration of an antipyretic, fluid replacement, circulatory support with vasopressor drugs if necessary, and oxygen administration by mask, cannula, or mechanical ventilation
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