Plague
Plague: Excerpt from Professional Guide to Diseases (Eighth Edition)
Plague, also known as the black death, is an acute infection caused by the gram-negative, nonmotile, nonsporulating bacillus Yersinia pestis (formerly called Pasteurella pestis).
Plague occurs in several forms. Bubonic plague, the most common, causes the characteristic swollen, and sometimes suppurating, lymph glands (buboes) that give this infection its name. Other forms include septicemic plague, a severe, rapid systemic form, and pneumonic plague, which can be primary or secondary to the other two forms. Primary pneumonic plague is an acutely fulminant, highly contagious form that causes acute prostration, respiratory distress, and death — in many cases within 2 to 3 days after onset.
Without treatment, mortality is about 60% in bubonic plague and approaches 100% in both septicemic and pneumonic plagues. With treatment, mortality is approximately 18% for all forms of plague, largely due to the delay between onset and treatment and the patient's age and physical condition.
Causes and incidence
Plague is usually transmitted to humans through the bite of a flea from an infected rodent host, such as a rat, squirrel, prairie dog, or hare. (See Carrier of bubonic plague.) Occasionally, transmission occurs from handling infected animals or their tissues. Bubonic plague is notorious for the historic pandemics in Europe and Asia during the Middle Ages, which in some areas killed up to two-thirds of the population. This form is rarely transmitted from person to person. However, the untreated bubonic form may progress to a secondary pneumonic form, which is transmitted by contaminated respiratory droplets (coughing) and is highly contagious. In the United States, the primary pneumonic form usually occurs after inhalation of Y. pestis in a laboratory.
Sylvatic (wild rodent) plague remains endemic in South America, the Near East, central and Southeast Asia, north central and southern Africa, Mexico, and western United States and Canada. In the United States, its incidence has been rising, a possible reflection of different bacterial strains or environmental changes that favor rodent growth in certain areas. Plague tends to occur between May and September; between October and February it usually occurs in hunters who skin wild animals. One attack confers permanent immunity.
Signs and symptoms
The incubation period, early symptoms, severity at onset, and clinical course vary in the three forms of plague. In bubonic plague, the incubation period is 2 to 8 days. The milder form begins with malaise, fever, and pain or tenderness in regional lymph nodes, possibly associated with swelling. Lymph node damage (usually axillary or inguinal) eventually produces painful, inflamed, and possibly suppurative buboes. The classic sign of plague is an excruciatingly painful bubo. Hemorrhagic areas may become necrotic; in the skin, such areas appear dark — hence the name “black death.”
This infection can progress extremely rapidly. A seemingly mildly ill person with only fever and adenitis may become moribund within hours. Plague may also begin dramatically, with a sudden high fever of 103° to 106° F (39.4° to 41.1° C), chills, myalgia, headache, prostration, restlessness, disorientation, delirium, toxemia, and staggering gait. Occasionally, it causes abdominal pain, nausea, vomiting, and constipation followed by diarrhea (frequently bloody), skin mottling, petechiae, and circulatory collapse.
In primary pneumonic plague, the incubation period is 2 to 3 days followed by a typically acute onset, with high fever, chills, severe headache, tachycardia, tachypnea, dyspnea, and a productive cough (first mucoid sputum, later frothy pink or red).
Secondary pneumonic plague, the pulmonary extension of the bubonic form, complicates about 5% of cases of untreated plague. A cough producing bloody sputum signals this complication. Both the primary and secondary forms of pneumonic plague rapidly cause severe prostration, respiratory distress and, usually, death.
Septicemic plague usually develops without overt lymph node enlargement. In this form, the patient shows toxicity, hyperpyrexia, seizures, prostration, shock, and disseminated intravascular coagulation (DIC). Septicemic plague causes widespread nonspecific tissue damage — such as peritoneal or pleural effusions, pericarditis, and meningitis. It's rapidly fatal unless promptly and correctly treated.
Diagnosis
Because plague is rare in the United States, it's commonly overlooked until after the patient dies or multiple cases develop. Characteristic buboes and a history of exposure to rodents in known endemic areas strongly suggest bubonic plague.
CONFIRMING DIAGNOSIS Stained smears and cultures of Y. pestis obtained from a needle aspirate of a small amount of fluid from skin lesions confirm this diagnosis.
Postmortem examination of a guinea pig inoculated with a sample of blood or purulent drainage allows isolation of the organism. Other laboratory findings include a white blood cell count of over 20,000/µl with increased polymorphonuclear leukocytes and hemoagglutination reaction (antibody titer) studies. Diagnosis should rule out tularemia, typhus, and typhoid.
In pneumonic plague, diagnosis requires a chest X-ray to show fulminating pneumonia and stained smear and culture of sputum to identify Y. pestis. Other bacterial pneumonias and psittacosis must be ruled out. Stained smear and blood culture containing Y. pestis are diagnostic in septicemic plague. However, cultures of Y. pestis grow slowly; so, in suspected plague (especially pneumonic and septicemic plagues), treatment should begin without waiting for laboratory confirmation. For a presumptive diagnosis of plague, a fluorescent antibody test may be ordered.
Treatment
Antimicrobial treatment of suspected plague must begin immediately after blood specimens have been taken for culture and should'nt be delayed for laboratory confirmation. Generally, treatment consists of large doses of streptomycin, the drug proven most effective against Y. pestis. Other effective drugs include gentamicin, doxycycline, tetracycline, and chloramphenicol. Penicillins are ineffective against plague.
In both septicemic and pneumonic plagues, life-saving antimicrobial treatment must begin within 18 hours of onset. Supportive management aims to control fever, shock, and seizures and to maintain fluid balance.
After antimicrobial therapy has begun, glucocorticoids can combat life-threatening toxemia and shock; diazepam relieves restlessness; and, if the patient develops DIC, treatment may include heparin.
Special considerations
❑Patients with bubonic plague require standard precautions.
❑Use an approved insecticide to rid the patient and his clothing of fleas. Carefully dispose of soiled dressings and linens, feces, and sputum. If the patient has pneumonic plague, wear a mask and follow droplet precautions. Handle all exudates, purulent discharge, and laboratory specimens with gloves. For more information, consult your infection control officer.
❑Give drugs and treat complications as ordered.
❑Treat buboes with hot, moist compresses. Never excise or drain them because this could spread the infection.
❑When septicemic plague causes peripheral tissue necrosis, prevent further injury to necrotic tissue. Avoid using restraints or armboards, and pad the bed's side rails.
❑For patients with pneumonic plague, obtain a history of patient contacts so that they can be quarantined for 7 days of observation. Administer prophylactic tetracycline or chloramphenicol, as ordered.
❑Report suspected cases of plague to local public health department officials so they can identify the source of infection.
❑To help prevent plague, discourage contact with wild animals (especially those that are sick or dead), and support programs aimed at reducing insect and rodent populations. Recommend immunization with plague vaccine to travelers to, or residents of, endemic areas, even though the effect of immunization is transient.
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Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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