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Bubonic plague in a child presenting with fever and altered mental status
CASE REPORT bubonic plague
Bubonic Plague in a Child Presenting With Fever and Altered Mental Status An 8-year-old Navajo boy presented to the emergency department with fever and altered mental status. Because the child lived in a plague-endemic area of the southwestern United States, antibiotics effective against Yersinia pestis were administered rapidly. Buboes were appreciated on physical examination, and the diagnosis of bubonic plague was confirmed by positive blood cultures. Characteristics and treatment of Yersinia pestis infection are discussed. The need for a high index of suspicion for the presence of plague in patients who present to the ED and who reside or have recently traveled in a plague-endemic area is emphasized. [Migden D: Bubonic plague in a child presenting with fever and altered mental status. A n n Emerg Med February 1990;19:207-2091]
INTRODUCTION
Douglas Migden, DO Gallup, New Mexico From the Emergency Department, Gallup Indian Medical Center, Gallup, New Mexico. Received for publication June 22, 1989. Accepted for publication July 31, 1989. Address for reprints: Douglas Migden, DO, Alaska Native Medical Center, PO Box 107741, Anchorage, Alaska 99510-7741.
The plague that ravaged medieval Europe is endemic in the southwestern United States. The case of a child with bubonic plague is presented and discussed. Mortality is significant when diagnosis and treatment are missed or delayed. 1 Emergency physicians should be familiar with characteristics of plague because the disease can result in rapid deterioration and death.
CASE REPORT An 8-year-old Navajo boy was brought to the emergency department after being found unresponsive on the hospital lobby restroom floor. His grandmother had taken him to the hospital to be evaluated for fever. He was alert and oriented when she saw him walk into the restroom. Bystanders alleged the child had a seizure in the restroom, but this could not be substantiated. On physical examination, the child was nonambulatory, in a fetal-like position, awake, uncooperative, and making incomprehensible sounds. Vital signs were rectal temperature of 40.8 C; pulse, 160; respirations, 32; and blood pressure, 120/80 m m Hg. Pupils were equal, round, and reactive to light, and the fundi were without papilledema or hemorrhage. Tympanic membranes and the 0ropharynx were normal. The neck was slightly stiff. Chest and abdominal examinations were unremarkable. Further neurologic examination was remarkable for nonpurposeful movement of all extremities and behavior that varied from being lethargic to somewhat combative. Small abrasions were noted perianally. No rashes or other skin lesions were noted. Laboratory evaluation revealed a leukocyte count of 16,600 m m '3 with 94% polymorphonuclear leukocytes, 4% bands, and 2% monocytes; hemoglobin, 11.0 g/dL; and hematocrit, 36.6%. Electrolytes, glucose, serum ammonia, coagulation studies, arterial blood gases, urinalysis, and liver function tests were essentially normal with the exception of a carbon dioxide of 18 mEq/L. A sepsis workup, including chest radiograph, blood and urine cultures, and lumbar puncture, was performed. Meningitis (pneumococcal and meningococcal) and plague were considered to be likely etiologies for the patient's presentation. Chloramphenicol 750 mg IV was administered in the ED. Acetaminophen 325 mg was given rectally. The chest radiograph and cerebrospinal fluid (CSF) analysis were unremarkable. The child was admitted to the pediatric service, placed in
19:2 February 1990
Annals of Emergency Medicine
207/155
BUBONIC PLAGUE Migden
strict isolation, and treated with 525 mg chloramphenicol IV (70 mg/kg/ day) and 1.5 g ampicillin W (200 rag/ kg/day), both every six hours. On the ward, his m e n t a l status improved markedly over the first seven hours after admission, and tender enlarged left axillary and left inguinal lymph nodes were noted on further physical e x a m i n a t i o n . Bubo a s p i r a t i o n attempts were unsuccessful. Two days after admission, blood cultures were r e p o r t e d as p o s i t i v e for Yersinia pestis. CSF cultures were negative. The child was discharged with a normal neurologic examination three days after admission and given oral chloramphenicol (500 mg four times a day for ten days) to take at home. He was afebrile and otherwise well when seen in the pediatric clinic two days after discharge. DISCUSSION H u m a n plague is an acute disease caused by Y pestis, a Gram-negative, p l e o m o r p h i c rod. I n f e c t i o n occurs primarily in rodents and most commonly is transmitted to h u m a n beings by the bite of an infected rodent flea. Other animals, including rabbits, dogs, cats, coyotes, foxes, bobcats, and badgers, also may be infected with the plague bacillus. 2 In addition, infection can occur from direct contact with the blood or tissues of an infected animal; it rarely occurs by inhalation of Y pestis in droplets aerosolized by an animal or h u m a n being with plague pneumonia. 3 Hum a n plague r e m a i n s e n d e m i c in m a n y parts of the world, including Southeast Asia, South America, and rural and s e m i r u r a l areas of the southwestern United States. 4 In the United States, plague can occur in any month; however, the maj o r i t y of c a s e s o c c u r f r o m M a y through September. Of the 299 human plague cases reported from 1956 through 1987, 173 (53.9%) occurred in New Mexico. The center of distribution in the Southwest includes the Navajo reservation, located in northwestern N e w Mexico, northeastern Arizona, and southern Utah. s T h e p r i m a r y c l i n i c a l f o r m s of plague are bubonic, septicemic, and p n e u m o n i c . Rarer f o r m s include meningeal, ophthalmic, pharyngeal, and cutaneous plague. 6 Bubonic plague, the most common t y p e of plague, r e s u l t s m o s t frequently from flea bite and occasion156/208
ally by direct c o n t a m i n a t i o n of an open skin lesion by plague-infected material. After percutaneous inoculation, a local infection, which is usually not of clinical significance, occurs; however, rarely a local bullous or ulcerated lesion develops at the inoculation site. Within one to six days, the infection spreads by the l y m p h a t i c s to the regional l y m p h nodes - most often inguinal or axillary. S y m p t o m s u s u a l l y d e v e l o p within two to six days and include sudden onset of severe malaise, headache, shaking chills, and pain in the affected lymph nodes, which may not be enlarged initially. C l i n i c a l p r o g r e s s i o n u s u a l l y is rapid with the bubo typically becoming very painful, large, and fluctuant. With the onset of fever, intermittent bacteremia frequently occurs and can result in a full-blown, Gram-negative sepsis. 6 The m o r t a l i t y rate for untreated b u b o n i c plague is 50% to 60%.3 Primary septicemic plague is characterized by septicemia in the absence of buboes, which either do not d e v e l o p or o c c u r in t h e d e e p e r lymphatics, undetectable by palpation. Again, symptoms are similar to other forms of Gram-negative sepsis. The absence of a bubo results in delayed and missed diagnosis. In a New Mexico study, p a t i e n t s w i t h septicemic plague visited a physician sooner and were hospitalized earlier than patients with bubonic plague. However, s e p t i c e m i c plague diagn o s i s was s l o w e r t h a n t h a t for bubonic plague, presumably because the presence of a bubo is such a significant diagnostic clue. 7 The mortality rate for u n t r e a t e d s e p t i c e m i c plague is almost 100%.s P n e u m o n i c plague occurs either primarily from aerosolized droplets (primary pneumonic plague) or secondarily from hematogenous spread to the lungs. P r i m a r y p n e u m o n i c plague has an incubation period of one to three days. Pneumonic plague is c h a r a c t e r i z e d by cough, bloody sputum, high fever, and chills. 6 Radiographic features include alveolar infiltrates, pulmonary nodules, and pleural effusions. 9 Survival is unlikely in patients with primary pneumonic plague if antibiotic therapy is not started within 18 hours of onset. 6 T h e m o r t a l i t y rate for u n t r e a t e d p n e u m o n i c plague is 100%. 3 No cases of pneumonic plague transmisAnnals of Emergency Medicine
sion among h u m a n beings have been d o c u m e n t e d in the U n i t e d States since 1925.1° Diagnosis is established by examination and culture of clinical specimens. Gram-, Wayson-, and fluorescent-antibody staining should be performed on bubo aspirate, sputum, and CSF. Blood cultures should be obtained from all suspected cases of plague. Plague serology can be used for retrospective diagnostic confirmation. 2 Antibiotics should be started as soon as possible, preferably after diagnostic s p e c i m e n s are collected. Streptomycin, tetracycline, or chloramphenieol are the drugs of choice. 2 Gentamicin is also appropriate treatment for patients suspected of having nonspecific G r a m - n e g a t i v e sepsis who reside in or have recently visited plague-endemic areas. Chloramphenicol should be given intravenously to hypotensive patients and also is the drug of choice in meningeal and ophthalmic plague because of its penetration into these tissues. 3 Patients with plague should be kept in strict isolation for 48 hours after initiation of appropriate antibiotic therapy. If pneumonia or draining lesions have not developed, isolation can be terminated. Plague pneumonia patients should be kept in respiratory isolation for the first four days of antibiotic therapy. 3 People who have had recent close contact w i t h a p n e u m o n i c plague case should receive prophylactic oral tetracycline (500 mg four times a day in a d u l t s ) or t r i m e t h o p r i m - s u l f a m e t h o x a z o l e if less t h a n eight years old or pregnant (unless near term), for seven daysJ 1 Contacts of nonpneumonic plague cases do not n e e d p r o p h y l a c t i c a n t i b i o t i c s . 12 However, contacts of nonpneumonic plague cases who may have been exposed to the same source of plague as the diagnosed patient and become febrile or develop other s y m p t o m s should be treated. In our case, appropriate therapy was administered rapidly as the patient presented with sepsis and lived in a p l a g u e - e n d e m i c area of rural New Mexico. However, a bubo was not noted on the initial physical examination, possibly as a consequence of the patient's altered mental status and uncooperative behavior. T h e case-fatality rate in people traveling between endemic and non19:2 February 1990
e n d e m i c areas is h i g h e r t h a n a m o n g n o n t r a v e l e r s (55% c o m p a r e d w i t h 18%), p r e s u m a b l y b e c a u s e of m i s s e d or d e l a y e d diagnoses.S, 1° T h e r e f o r e , emergency physicians in nonend e m i c areas s h o u l d h a v e a h i g h i n d e x of s u s p i c i o n f o r t h e p r e s e n c e of p l a g u e in s u c h travelers w h o p r e s e n t to t h e E D w i t h t e n d e r b u b o e s or sepsis. Patients who recently have b e e n i n a p l a g u e - e n d e m i c a r e a and p r e s e n t w i t h fever, l y m p h a d e n o p a thy, or b o t h b u t do n o t o t h e r w i s e appear s e r i o u s l y ill s h o u l d h a v e b l o o d c u l t u r e s d r a w n , r e c e i v e oral a n t i b i o t i c s ( t e t r a c y c l i n e [500 m g four t i m e s a d a y i n a d u l t s ] or t r i m e t h o p r i m s u l f a m e t h o x a z o l e if less t h a n e i g h t years old, for s e v e n days) and be ree v a l u a t e d in 24 h o u r s if t h e y are n o t hospitalized.
SUMMARY A case of b u b o n i c p l a g u e in a c h i l d w i t h fever and altered m e n t a l status is p r e s e n t e d a n d d i s c u s s e d . D e l a y e d a n d m i s s e d d i a g n o s e s of t h e m a j o r f o r m s of p l a g u e r e s u l t in s i g n i f i c a n t
19:2 February 1990
m o r t a l i t y . A w a r e n e s s by e m e r g e n c y p h y s i c i a n s of t h e c h a r a c t e r i s t i c s , treatment, and epidemiology of p l a g u e , e s p e c i a l l y t h e p o s s i b i l i t y of its e x i s t e n c e in p a t i e n t s w h o l i v e or recently have traveled in a plaguee n d e m i c area, s h o u l d r e s u l t i n increased survival.
logical and clinical aspects of bubonic plague. West J Med 1986;144:447-451. 5. Barnes AM, Quan TJ, Beard ML, et ah Plague in American Indians, 1956-1987. MMWR 1988; 37:11-16. 6. Poland JD, Barnes AM: Plague, in Steele Ji: (ed): CRC Handbook Series in Zoonoses, Section A: Bacterial, Rickettsial, and Mycotic Dis eases. Boca Raton, Florida, CRC Press, 1979, vol
1, p 515-559. The author thanks Michael Clayton, MD, Karen Carlson, MD, Gary Criddle, RN, James Grabman, MD, Larry Crook, MD, Brad Selden, MD, Bruce Tempest, MD, and Nellie Beilke for their help in patient care and manuscript review or preparation.
REFERENCES 1. Mann JM, Schmid GP, Stoesz PA, et ah Peripatetic plague. JAMA 1982;247:47-48. 2. Sewell CM {ed): New Mexico Health and Environment Department Epidemiology Report: Human Plague in New Mexico. Santa Fe, New Mexico Health and Environment Department, April 1988. 3. Welty TK: Plague. A m Faro Physician 1986; 33:159-164. 4. Ganem DE: Plasmids and pestilence - Bio-
Annals of Emergency Medicine
7. Hall HI:, Montes JM, Mann JM: Septicemic plague in New Mexico. J Infect Dis 1987; 155:113-118. 8. Cantey JR: Plague in Vietnam: Clinical observations and treatment with kanamycin. Arch Intern Med 1974;133:280-283. 9. Alsofrom DJ, Mettler I:A Jr, Mann JM: Radiographic manifestations of plague in New Mexico, 1975-1980: A review of 42 proved cases. Radiology 1981;139:561-565. 10. Plague - South Carolina. MMWR 1983; 32:417-418. 11. Poland JD: Plague, in Corm HR (ed): Conn's Current Therapy, ed 35. Philadelphia, WB Saunders, 1983, p 47-49. 12. Welty TK, Grabman J, Kompare E, et ah Nineteen cases of plague in Arizona - A spectrum including ecthyma gangrenosum due to plague and plague in pregnancy. West J Med 1985;i42:641-646.
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Bubonic Plague in a Child Presenting With Fever and Altered Mental Status An 8-year-old Navajo boy presented to the emergency department with fever and altered mental status. Because the child lived in a plague-endemic area of the southwestern United States, antibiotics effective against Yersinia pestis were administered rapidly. Buboes were appreciated on physical examination, and the diagnosis of bubonic plague was confirmed by positive blood cultures. Characteristics and treatment of Yersinia pestis infection are discussed. The need for a high index of suspicion for the presence of plague in patients who present to the ED and who reside or have recently traveled in a plague-endemic area is emphasized. [Migden D: Bubonic plague in a child presenting with fever and altered mental status. A n n Emerg Med February 1990;19:207-2091]
INTRODUCTION
Douglas Migden, DO Gallup, New Mexico From the Emergency Department, Gallup Indian Medical Center, Gallup, New Mexico. Received for publication June 22, 1989. Accepted for publication July 31, 1989. Address for reprints: Douglas Migden, DO, Alaska Native Medical Center, PO Box 107741, Anchorage, Alaska 99510-7741.
The plague that ravaged medieval Europe is endemic in the southwestern United States. The case of a child with bubonic plague is presented and discussed. Mortality is significant when diagnosis and treatment are missed or delayed. 1 Emergency physicians should be familiar with characteristics of plague because the disease can result in rapid deterioration and death.
CASE REPORT An 8-year-old Navajo boy was brought to the emergency department after being found unresponsive on the hospital lobby restroom floor. His grandmother had taken him to the hospital to be evaluated for fever. He was alert and oriented when she saw him walk into the restroom. Bystanders alleged the child had a seizure in the restroom, but this could not be substantiated. On physical examination, the child was nonambulatory, in a fetal-like position, awake, uncooperative, and making incomprehensible sounds. Vital signs were rectal temperature of 40.8 C; pulse, 160; respirations, 32; and blood pressure, 120/80 m m Hg. Pupils were equal, round, and reactive to light, and the fundi were without papilledema or hemorrhage. Tympanic membranes and the 0ropharynx were normal. The neck was slightly stiff. Chest and abdominal examinations were unremarkable. Further neurologic examination was remarkable for nonpurposeful movement of all extremities and behavior that varied from being lethargic to somewhat combative. Small abrasions were noted perianally. No rashes or other skin lesions were noted. Laboratory evaluation revealed a leukocyte count of 16,600 m m '3 with 94% polymorphonuclear leukocytes, 4% bands, and 2% monocytes; hemoglobin, 11.0 g/dL; and hematocrit, 36.6%. Electrolytes, glucose, serum ammonia, coagulation studies, arterial blood gases, urinalysis, and liver function tests were essentially normal with the exception of a carbon dioxide of 18 mEq/L. A sepsis workup, including chest radiograph, blood and urine cultures, and lumbar puncture, was performed. Meningitis (pneumococcal and meningococcal) and plague were considered to be likely etiologies for the patient's presentation. Chloramphenicol 750 mg IV was administered in the ED. Acetaminophen 325 mg was given rectally. The chest radiograph and cerebrospinal fluid (CSF) analysis were unremarkable. The child was admitted to the pediatric service, placed in
19:2 February 1990
Annals of Emergency Medicine
207/155
BUBONIC PLAGUE Migden
strict isolation, and treated with 525 mg chloramphenicol IV (70 mg/kg/ day) and 1.5 g ampicillin W (200 rag/ kg/day), both every six hours. On the ward, his m e n t a l status improved markedly over the first seven hours after admission, and tender enlarged left axillary and left inguinal lymph nodes were noted on further physical e x a m i n a t i o n . Bubo a s p i r a t i o n attempts were unsuccessful. Two days after admission, blood cultures were r e p o r t e d as p o s i t i v e for Yersinia pestis. CSF cultures were negative. The child was discharged with a normal neurologic examination three days after admission and given oral chloramphenicol (500 mg four times a day for ten days) to take at home. He was afebrile and otherwise well when seen in the pediatric clinic two days after discharge. DISCUSSION H u m a n plague is an acute disease caused by Y pestis, a Gram-negative, p l e o m o r p h i c rod. I n f e c t i o n occurs primarily in rodents and most commonly is transmitted to h u m a n beings by the bite of an infected rodent flea. Other animals, including rabbits, dogs, cats, coyotes, foxes, bobcats, and badgers, also may be infected with the plague bacillus. 2 In addition, infection can occur from direct contact with the blood or tissues of an infected animal; it rarely occurs by inhalation of Y pestis in droplets aerosolized by an animal or h u m a n being with plague pneumonia. 3 Hum a n plague r e m a i n s e n d e m i c in m a n y parts of the world, including Southeast Asia, South America, and rural and s e m i r u r a l areas of the southwestern United States. 4 In the United States, plague can occur in any month; however, the maj o r i t y of c a s e s o c c u r f r o m M a y through September. Of the 299 human plague cases reported from 1956 through 1987, 173 (53.9%) occurred in New Mexico. The center of distribution in the Southwest includes the Navajo reservation, located in northwestern N e w Mexico, northeastern Arizona, and southern Utah. s T h e p r i m a r y c l i n i c a l f o r m s of plague are bubonic, septicemic, and p n e u m o n i c . Rarer f o r m s include meningeal, ophthalmic, pharyngeal, and cutaneous plague. 6 Bubonic plague, the most common t y p e of plague, r e s u l t s m o s t frequently from flea bite and occasion156/208
ally by direct c o n t a m i n a t i o n of an open skin lesion by plague-infected material. After percutaneous inoculation, a local infection, which is usually not of clinical significance, occurs; however, rarely a local bullous or ulcerated lesion develops at the inoculation site. Within one to six days, the infection spreads by the l y m p h a t i c s to the regional l y m p h nodes - most often inguinal or axillary. S y m p t o m s u s u a l l y d e v e l o p within two to six days and include sudden onset of severe malaise, headache, shaking chills, and pain in the affected lymph nodes, which may not be enlarged initially. C l i n i c a l p r o g r e s s i o n u s u a l l y is rapid with the bubo typically becoming very painful, large, and fluctuant. With the onset of fever, intermittent bacteremia frequently occurs and can result in a full-blown, Gram-negative sepsis. 6 The m o r t a l i t y rate for untreated b u b o n i c plague is 50% to 60%.3 Primary septicemic plague is characterized by septicemia in the absence of buboes, which either do not d e v e l o p or o c c u r in t h e d e e p e r lymphatics, undetectable by palpation. Again, symptoms are similar to other forms of Gram-negative sepsis. The absence of a bubo results in delayed and missed diagnosis. In a New Mexico study, p a t i e n t s w i t h septicemic plague visited a physician sooner and were hospitalized earlier than patients with bubonic plague. However, s e p t i c e m i c plague diagn o s i s was s l o w e r t h a n t h a t for bubonic plague, presumably because the presence of a bubo is such a significant diagnostic clue. 7 The mortality rate for u n t r e a t e d s e p t i c e m i c plague is almost 100%.s P n e u m o n i c plague occurs either primarily from aerosolized droplets (primary pneumonic plague) or secondarily from hematogenous spread to the lungs. P r i m a r y p n e u m o n i c plague has an incubation period of one to three days. Pneumonic plague is c h a r a c t e r i z e d by cough, bloody sputum, high fever, and chills. 6 Radiographic features include alveolar infiltrates, pulmonary nodules, and pleural effusions. 9 Survival is unlikely in patients with primary pneumonic plague if antibiotic therapy is not started within 18 hours of onset. 6 T h e m o r t a l i t y rate for u n t r e a t e d p n e u m o n i c plague is 100%. 3 No cases of pneumonic plague transmisAnnals of Emergency Medicine
sion among h u m a n beings have been d o c u m e n t e d in the U n i t e d States since 1925.1° Diagnosis is established by examination and culture of clinical specimens. Gram-, Wayson-, and fluorescent-antibody staining should be performed on bubo aspirate, sputum, and CSF. Blood cultures should be obtained from all suspected cases of plague. Plague serology can be used for retrospective diagnostic confirmation. 2 Antibiotics should be started as soon as possible, preferably after diagnostic s p e c i m e n s are collected. Streptomycin, tetracycline, or chloramphenieol are the drugs of choice. 2 Gentamicin is also appropriate treatment for patients suspected of having nonspecific G r a m - n e g a t i v e sepsis who reside in or have recently visited plague-endemic areas. Chloramphenicol should be given intravenously to hypotensive patients and also is the drug of choice in meningeal and ophthalmic plague because of its penetration into these tissues. 3 Patients with plague should be kept in strict isolation for 48 hours after initiation of appropriate antibiotic therapy. If pneumonia or draining lesions have not developed, isolation can be terminated. Plague pneumonia patients should be kept in respiratory isolation for the first four days of antibiotic therapy. 3 People who have had recent close contact w i t h a p n e u m o n i c plague case should receive prophylactic oral tetracycline (500 mg four times a day in a d u l t s ) or t r i m e t h o p r i m - s u l f a m e t h o x a z o l e if less t h a n eight years old or pregnant (unless near term), for seven daysJ 1 Contacts of nonpneumonic plague cases do not n e e d p r o p h y l a c t i c a n t i b i o t i c s . 12 However, contacts of nonpneumonic plague cases who may have been exposed to the same source of plague as the diagnosed patient and become febrile or develop other s y m p t o m s should be treated. In our case, appropriate therapy was administered rapidly as the patient presented with sepsis and lived in a p l a g u e - e n d e m i c area of rural New Mexico. However, a bubo was not noted on the initial physical examination, possibly as a consequence of the patient's altered mental status and uncooperative behavior. T h e case-fatality rate in people traveling between endemic and non19:2 February 1990
e n d e m i c areas is h i g h e r t h a n a m o n g n o n t r a v e l e r s (55% c o m p a r e d w i t h 18%), p r e s u m a b l y b e c a u s e of m i s s e d or d e l a y e d diagnoses.S, 1° T h e r e f o r e , emergency physicians in nonend e m i c areas s h o u l d h a v e a h i g h i n d e x of s u s p i c i o n f o r t h e p r e s e n c e of p l a g u e in s u c h travelers w h o p r e s e n t to t h e E D w i t h t e n d e r b u b o e s or sepsis. Patients who recently have b e e n i n a p l a g u e - e n d e m i c a r e a and p r e s e n t w i t h fever, l y m p h a d e n o p a thy, or b o t h b u t do n o t o t h e r w i s e appear s e r i o u s l y ill s h o u l d h a v e b l o o d c u l t u r e s d r a w n , r e c e i v e oral a n t i b i o t i c s ( t e t r a c y c l i n e [500 m g four t i m e s a d a y i n a d u l t s ] or t r i m e t h o p r i m s u l f a m e t h o x a z o l e if less t h a n e i g h t years old, for s e v e n days) and be ree v a l u a t e d in 24 h o u r s if t h e y are n o t hospitalized.
SUMMARY A case of b u b o n i c p l a g u e in a c h i l d w i t h fever and altered m e n t a l status is p r e s e n t e d a n d d i s c u s s e d . D e l a y e d a n d m i s s e d d i a g n o s e s of t h e m a j o r f o r m s of p l a g u e r e s u l t in s i g n i f i c a n t
19:2 February 1990
m o r t a l i t y . A w a r e n e s s by e m e r g e n c y p h y s i c i a n s of t h e c h a r a c t e r i s t i c s , treatment, and epidemiology of p l a g u e , e s p e c i a l l y t h e p o s s i b i l i t y of its e x i s t e n c e in p a t i e n t s w h o l i v e or recently have traveled in a plaguee n d e m i c area, s h o u l d r e s u l t i n increased survival.
logical and clinical aspects of bubonic plague. West J Med 1986;144:447-451. 5. Barnes AM, Quan TJ, Beard ML, et ah Plague in American Indians, 1956-1987. MMWR 1988; 37:11-16. 6. Poland JD, Barnes AM: Plague, in Steele Ji: (ed): CRC Handbook Series in Zoonoses, Section A: Bacterial, Rickettsial, and Mycotic Dis eases. Boca Raton, Florida, CRC Press, 1979, vol
1, p 515-559. The author thanks Michael Clayton, MD, Karen Carlson, MD, Gary Criddle, RN, James Grabman, MD, Larry Crook, MD, Brad Selden, MD, Bruce Tempest, MD, and Nellie Beilke for their help in patient care and manuscript review or preparation.
REFERENCES 1. Mann JM, Schmid GP, Stoesz PA, et ah Peripatetic plague. JAMA 1982;247:47-48. 2. Sewell CM {ed): New Mexico Health and Environment Department Epidemiology Report: Human Plague in New Mexico. Santa Fe, New Mexico Health and Environment Department, April 1988. 3. Welty TK: Plague. A m Faro Physician 1986; 33:159-164. 4. Ganem DE: Plasmids and pestilence - Bio-
Annals of Emergency Medicine
7. Hall HI:, Montes JM, Mann JM: Septicemic plague in New Mexico. J Infect Dis 1987; 155:113-118. 8. Cantey JR: Plague in Vietnam: Clinical observations and treatment with kanamycin. Arch Intern Med 1974;133:280-283. 9. Alsofrom DJ, Mettler I:A Jr, Mann JM: Radiographic manifestations of plague in New Mexico, 1975-1980: A review of 42 proved cases. Radiology 1981;139:561-565. 10. Plague - South Carolina. MMWR 1983; 32:417-418. 11. Poland JD: Plague, in Corm HR (ed): Conn's Current Therapy, ed 35. Philadelphia, WB Saunders, 1983, p 47-49. 12. Welty TK, Grabman J, Kompare E, et ah Nineteen cases of plague in Arizona - A spectrum including ecthyma gangrenosum due to plague and plague in pregnancy. West J Med 1985;i42:641-646.
209/157