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eMedicine Specialties > Emergency Medicine > Warfare - Chemical, Biological, Radiological, Nuclear and Explosives

CBRNE - Plague

Author: Demetres G Velendzas, MD, Attending Staff, Department of Emergency Medicine, Manchester Memorial Hospital, Eastern Connecticut Health Network
Coauthor(s): Susan E Dufel, MD, FACEP, Program Director, Associate Professor, Department of Traumatology and Emergency Medicine, Division of Emergency Medicine, University of Connecticut School of Medicine; Deirdre Cronin, MD, Resident Physician, Department of Emergency Medicine, University of Connecticut School of Medicine, Farmington
Contributor Information and Disclosures

Updated: Sep 22, 2009

Introduction

Background

The plague has caused more fear and terror than perhaps any other infectious disease in the history of humankind. It has laid claim to nearly 200 million lives and has brought about monumental changes such as the end of the Dark Ages and the advancement of clinical research in medicine.1

Although still debated by historians, the plague has been responsible for at least 3 great pandemics and multiple epidemics in history. The first spread occurred from the Middle East to the Mediterranean basin during the fifth and sixth centuries AD, killing approximately 50% of the population in these areas. The second pandemic afflicted Europe between the 8th and 14th centuries, destroying nearly 40% of the population. The third pandemic started in approximately 1855 in China, and, although it has been mostly controlled, it is still ongoing.

Alexandre Yersin isolated the plague bacillus, developed an antiserum to combat the disease, and postulated its connection with fleas and rats during the epidemic of 1894. The plague bacillus was named Yersinia pestis in his memory.2

Pandemics have succeeded in entrenching the plague in every major continent, with the possible exception of Australia. Unlike smallpox, the plague never will be eradicated. It lives in millions of animals and on billions of fleas that reside on them. It is a disease of the desert, the steppes, the mountains, and the forest.3

Although, the plague has been considered a disease of the Middle Ages, multiple outbreaks in India and Africa during the last 20 years have stoked fears of another global pandemic.4,5,2 One reason may be the climatic change brought about by global warming. This change is ideal for increasing the prevalence of Y pestis in the host population. A recent study has estimated a more than 50% increase in the plague host prevalence with an increase of 1 degree Centigrade of the temperature in spring.6 Another reason may be the increasing population explosion worldwide, which is bringing humans into ever-increasing contact with wildlife. Lastly, the dramatic population increase will contribute to conditions of overcrowding and poor sanitation—conditions ripe for plague hosts and vectors to flourish in.

Additionally, there has been significant concern over the return of plague as a potential biological weapon. In 1347, the Tartars catapulted bodies of plague victims over the city walls during the siege of Kaffa, and, in World War II, the Japanese dropped bombs containing fleas inoculated with Yersinia pestis to infect their enemies with the deadly illness. During the Cold War, the Soviets succeeded in aerosolizing the bacteria and in creating strains of multidrug-resistant Yersinia.7,8 Aerosolized Y pestis, causing primary pneumonic plague, has been recognized by bioterrorism experts as having one of the highest potentials as a bioterrorism agent due to its extremely high mortality, its high uptake into enzootic and epizootic animals as well as humans, and its ability to be spread over a large area. It has been classified as a Category A select agent by the CDC.1

Pathophysiology

The etiologic agent of the plague is Y pestis, a facultative anaerobic, intracellular, gram-negative bacillus. Significant genomic similarity and conservation of DNA sequences suggest Y pestis evolved from the less virulent Yersinia pseudotuberculosis.9

The organism can be transmitted from a host to a human via the bite of a vector (usually a flea), via close contact with infected tissue or body fluids, and via direct inhalation of aerosolized bacteria. Currently, the most common form of transmission involves the bite of an infected flea. More than 200 different rodents and species can serve as hosts.

The vector is usually the rat flea, Xenopsylla cheopis. Thirty different flea species have been identified as able to carry the plague bacillus. Other carriers of plague include ticks and human lice. A flea is shown in the image below.

Here a flea is shown with a blocked proventriculu...

Here a flea is shown with a blocked proventriculus, equivalent to the gastroesophageal region in man. In nature, this flea would develop a ravenous hunger because of its inability to digest the fibrinoid mass of blood and bacteria. Ensuing a biting of the nearest mammal results in clearing of the proventriculus through regurgitation of thousands of bacteria into the bite wound. Courtesy of United States Army Environmental Hygiene Agency.

Here a flea is shown with a blocked proventriculu...

Here a flea is shown with a blocked proventriculus, equivalent to the gastroesophageal region in man. In nature, this flea would develop a ravenous hunger because of its inability to digest the fibrinoid mass of blood and bacteria. Ensuing a biting of the nearest mammal results in clearing of the proventriculus through regurgitation of thousands of bacteria into the bite wound. Courtesy of United States Army Environmental Hygiene Agency.


Rodents resistant to the infection, such as wood rats, kangaroo roots, deer mice, grasshopper mice, and voles, form an enzootic stage that ensures the long-term survival of the bacillus. Occasionally, fleas transfer the bacteria to animals that are susceptible to plague such as ground squirrels (an infected squirrel is shown in the image below), prairie dogs, and chipmunks. In the event of large numbers of host animals dying off, hungry fleas search out new food sources. This is known as an epizootic stage and ensures the spread of the organism to new territory. A sylvatic stage occurs when humans are infected from wild animals. Carnivores with the exception of cats and black-footed ferrets have a fairly strong resistance profile, but they can be transfer vectors. Birds and hoofed animals are seldom infected, and reptiles and fish are resistant to plague.3

Rock squirrel in extremis coughing of blood-strea...

Rock squirrel in extremis coughing of blood-streaked sputum of pneumonic plague. Courtesy of Ken Gage, PhD, CDC, Fort Collins, CO.

Rock squirrel in extremis coughing of blood-strea...

Rock squirrel in extremis coughing of blood-streaked sputum of pneumonic plague. Courtesy of Ken Gage, PhD, CDC, Fort Collins, CO.


Virulent plague bacteria can survive dormant in soil, animal carcasses, grains, flea feces, buried bodies, and dried sputum.10,3

Three forms of the plague exist: bubonic plague, pneumonic plague, and septicemic plague. The bubonic form makes up approximately 80-95% of cases worldwide2 and is caused by deposition of the bacillus in the skin by the bite of an infected vector. If the vector is a flea, bacillus proliferates in the flea's esophagus, preventing food entry into the stomach. To overcome starvation, the flea begins a blood-sucking rampage. Between its attempts to swallow, the distended bacillus-packed esophagus recoils, depositing the bacillus into the victim's skin.

The bacillus invades nearby lymphoid tissue, producing the famous bubo, an inflamed, necrotic, and hemorrhagic lymph node. Spread occurs along the lymphatic channels toward the thoracic duct, with eventual seeding of the vasculature. Bacteremia and septicemia ensue. The bacillus potentially seeds every organ, including the lungs, liver, spleen, kidneys, and rarely even the meninges.

The most virulent form, pneumonic plague, results from direct inhalation of the bacillus, which occurs from close contact of infected hosts or from aerosolized bacteria such as may occur if used as a biological weapon. A severe and rapidly progressive multilobar bronchopneumonia ensues with subsequent bacteremia and septicemia. Secondary pneumonic plague is caused when an infected patient seeds his or her lungs and airways.

The third type of plague is a primary septicemic plague. This is hypothesized to occur when the bacillus is deposited in the vasculature, bypassing the lymphatics. Early dissemination with sepsis occurs but without the formation of a bubo. This usually is observed in bites to the oral, tonsillar, and pharyngeal area and is believed to occur because of the vascularity of the tissue and short lymphatic distance to the thoracic duct.

Frequency

United States

An average of 10-15 cases per year have been reported during the last few decades. One of the largest animal foci of the plague worldwide is found west of the 100th parallel, in states such as New Mexico, Arizona, Colorado, Utah, and California. Only one case of imported plague has been reported since 1926. Most cases occur during the wet, warmer months of the year.11 In 2006, 13 human plague cases were reported in the United States, the most since 1994.

International

From 1987-2001, the World Health Organization has reported an annual average of 38,876 cases of the plague with 2847 deaths worldwide. The number of actual cases is probably much higher, given the failure of many countries to diagnose and report the plague. Most cases occur in the developing countries of Africa and Asia. Recent outbreaks of the plague have occurred in Vietnam, India, Algeria, Madagascar, and the northeastern part of the Democratic Republic of the Congo.12 During 2000-2001, 95% of the world's cases occurred in Africa.2

The illustration below shows the distribution of the plague in 1998.
 

World distribution of plague, 1998. From the Cent...

World distribution of plague, 1998. From the Centers for Disease Control and Prevention (CDC), Atlanta, Ga.

World distribution of plague, 1998. From the Cent...

World distribution of plague, 1998. From the Centers for Disease Control and Prevention (CDC), Atlanta, Ga.


Mortality/Morbidity

  • Bubonic plague has a 1-15% mortality rate in treated cases and a 40-60% mortality rate in untreated cases.
  • Septicemic plague (primary or secondary) has a 40% mortality rate in treated cases and 100% mortality rate in untreated cases.
  • Pneumonic plague (primary or secondary) has 100% mortality rate if not treated within the first 24 hours of infection.

Sex

More than 50% of cases of plague occur in males.

Age

Approximately 50% of cases occur in persons younger than 20 years.

Clinical

History

In general, after an incubation period of 1-6 days, the history suggests a severe and rapidly progressive sepsis.

  • Recent travel in the Southwestern and Pacific Coast regions of the United States, particularly in New Mexico, Arizona, California, and Utah, should raise suspicion of a fleabite. Although imported plague is rare, similar suspicion should exist for any recent travel to endemic areas outside the United States. Fewer than 10% of patients recall a prior fleabite.
  • Close contact with any potentially infected host or rural environment should raise suspicion for the plague. Historically, the rat has been believed to be the main plague host; however, currently in the United States, the ground and rock squirrels are the most common hosts. In recent years, the domestic cat has emerged as a prominent host that transmits the plague to veterinarians.13
  • A sudden increase in the incidence of severe pneumonia in previously healthy individuals should raise concern for pneumonic plague possibly deployed as a bioterrorism weapon.
  • Symptoms14,2
    • Fever
    • Chills
    • Myalgias
    • Sore throat
    • Headache
    • Weakness
    • Malaise
    • Enlarged, painful, swollen lymph node
    • Abdominal pain - Only presenting symptom more common in a patient presenting with septicemic plague (primary blood-borne plague) versus one presenting with bubonic plague
    • Nausea, vomiting (bloody at times)
    • Constipation, diarrhea, and black or tarry stools
    • Gastrointestinal complaints (may precede a bubo)
    • Cough, which may be productive of bloody sputum
    • Shortness of breath
    • Stiff neck (if meningitic infiltration by plague bacillus has occurred)

Physical

In general, after an incubation period of 1-6 days, the plague presents with the physical findings of severe and rapidly progressive sepsis with or without features of pneumonia. Multiple organ involvement occurs. Pneumonic plague may present only as a severe pneumonia.

  • Temperature of 37-40.9°C, tachycardia, tachypnea, and hypotension, if in late septic shock
  • Inguinal bubo (60%), axillary (30%), cervical (10%), or epitrochlear (10%) (Bubo is usually no greater than 5 cm, extremely tender, erythematous, and surrounded by a boggy hemorrhagic area; patient often flexes, abducts, and externally rotates the hip near an involved inguinal node to reduce pain at the site.) Children are more likely to have a cervical or submandibular bubo.2 Images below show a bubo and a necrotic ulcer.

    • A suppurative, bubo of the femoral lymph node (sh...

      A suppurative, bubo of the femoral lymph node (shown here), the most common site of the erythematous, tender, swollen, nodes in a plague victim. The next most common lymph node regions involved are the inguinal, axillary, and cervical areas. The child in the image below has an erythematous, eroded, crusting, necrotic ulcer at the presumed primary inoculation site on the left upper quadrant. This type of lesion is uncommonly found in patients with plague. Bubo location is primarily a function of the region of the body in which an infected flea inoculates plague bacilli. Courtesy of Jack Poland, PhD, CDC, Fort Collins, CO.

      A suppurative, bubo of the femoral lymph node (sh...

      A suppurative, bubo of the femoral lymph node (shown here), the most common site of the erythematous, tender, swollen, nodes in a plague victim. The next most common lymph node regions involved are the inguinal, axillary, and cervical areas. The child in the image below has an erythematous, eroded, crusting, necrotic ulcer at the presumed primary inoculation site on the left upper quadrant. This type of lesion is uncommonly found in patients with plague. Bubo location is primarily a function of the region of the body in which an infected flea inoculates plague bacilli. Courtesy of Jack Poland, PhD, CDC, Fort Collins, CO.


    • A suppurative, bubo of the femoral lymph node, sh...

      A suppurative, bubo of the femoral lymph node, shown in the image above, is the most common site of the erythematous, tender, swollen, nodes in a plague victim. The next most common lymph node regions involved are the inguinal, axillary (shown here), and cervical areas. The child in this photo has an erythematous, eroded, crusting, necrotic ulcer at the presumed primary inoculation site on the left upper quadrant. This type of lesion is uncommonly found in patients with plague. Bubo location is primarily a function of the region of the body in which an infected flea inoculates plague bacilli. Courtesy of Jack Poland, PhD, CDC, Fort Collins, CO.

      A suppurative, bubo of the femoral lymph node, sh...

      A suppurative, bubo of the femoral lymph node, shown in the image above, is the most common site of the erythematous, tender, swollen, nodes in a plague victim. The next most common lymph node regions involved are the inguinal, axillary (shown here), and cervical areas. The child in this photo has an erythematous, eroded, crusting, necrotic ulcer at the presumed primary inoculation site on the left upper quadrant. This type of lesion is uncommonly found in patients with plague. Bubo location is primarily a function of the region of the body in which an infected flea inoculates plague bacilli. Courtesy of Jack Poland, PhD, CDC, Fort Collins, CO.

  • Dermatologic findings
    • A maculopapular lesion may be found at the site of the fleabite; however, such lesions commonly are found at autopsy implying that, in the United States, the diagnosis often is not determined until it is too late.
    • Acral cyanosis, ecchymosis (shown in the image below), petechiae, and digital gangrene are seen with Y pestis septicemia (from disseminated intravascular coagulation [DIC]).

    • Ecchymoses at the neck base of a girl with plague...

      Ecchymoses at the neck base of a girl with plague. Bandage is over the site of a prior bubo aspirate. These lesions probably gave rise to the title line of the children's nursery rhyme "Ring around the rosy." Courtesy of Jack Poland, PhD, CDC, Fort Collins, CO.

      Ecchymoses at the neck base of a girl with plague...

      Ecchymoses at the neck base of a girl with plague. Bandage is over the site of a prior bubo aspirate. These lesions probably gave rise to the title line of the children's nursery rhyme "Ring around the rosy." Courtesy of Jack Poland, PhD, CDC, Fort Collins, CO.

    • The medieval epithet "Black Death" is thought to have originated from the deeply cyanotic skin, ecchymoses, and/or acral necrosis associated with terminal septicemic and pneumonic plague.
    • The initially rose-colored purpuric lesions most likely gave rise to the child's nursery rhyme "Ring Around the Rosy."
      • "Ring around the rosy" - Rose-colored purpuric macules (may be caused by the Y pestis enzyme that acts alternately as a plasminogen activator or coagulase at various temperatures or may be due to DIC)
      • "Pocket full of posies" - Sweet-smelling flowers that those tending the sick would carry to ward off the stench of disease
      • "Ashes, ashes" - Impending mortality or "A-choo, a-choo" - The sneezing and coughing of pneumonic plague
      • "All fall down" - Death
    • Rare cases of ecthyma gangrenosum–like lesions and carbuncles due to blood-borne Y pestis have been described.
  • Diffuse crackles, diffuse areas of dullness to percussion (secondary to patchy consolidation of pneumonic plague), and hemoptysis
  • Diffuse abdominal tenderness, with or without guarding, splenomegaly, hematochezia, or heme-positive stools
  • Nuchal rigidity and diffuse muscle and joint tenderness
  • Various degrees of mental status changes, ranging from mild confusion or agitation to delirium and coma
  • Seizures
  • Bleeding from any body site or cavity (eg, hematemesis, hematochezia, hemoptysis)
  • Gangrene and necrosis (shown in the images below) of areas such as the digits, penis, and nares (ascribed to peripheral thrombosis secondary to DIC)

    • Acral necrosis of nose, lips, fingers (shown here...

      Acral necrosis of nose, lips, fingers (shown here) and toes (image below) and residual ecchymoses over both forearms in a patient recovering from bubonic plague that disseminated to blood and lungs. At one time, the patient's entire body was ecchymotic. Reprinted from McGovern TW, Friedlander AM. Plague. In: Sidell FR, Takafuji ET, Franz DR, eds. Medical Aspects of Chemical and Biological Warfare. Chapter 23 in: Zajtchuk R, Bellamy RF, eds. Textbook of Military Medicine. Washington, DC: US Department of the Army, Office of the Surgeon General, and Borden Institute; 1997: 493. Government publication, no copyright on photos.

      Acral necrosis of nose, lips, fingers (shown here...

      Acral necrosis of nose, lips, fingers (shown here) and toes (image below) and residual ecchymoses over both forearms in a patient recovering from bubonic plague that disseminated to blood and lungs. At one time, the patient's entire body was ecchymotic. Reprinted from McGovern TW, Friedlander AM. Plague. In: Sidell FR, Takafuji ET, Franz DR, eds. Medical Aspects of Chemical and Biological Warfare. Chapter 23 in: Zajtchuk R, Bellamy RF, eds. Textbook of Military Medicine. Washington, DC: US Department of the Army, Office of the Surgeon General, and Borden Institute; 1997: 493. Government publication, no copyright on photos.


    • Acral necrosis of nose, lips, fingers (image abov...

      Acral necrosis of nose, lips, fingers (image above) and toes (shown here) and residual ecchymoses over both forearms in a patient recovering from bubonic plague that disseminated to blood and lungs. At one time, the patient's entire body was ecchymotic. Reprinted from McGovern TW, Friedlander AM. Plague. In: Sidell FR, Takafuji ET, Franz DR, eds. Medical Aspects of Chemical and Biological Warfare. Chapter 23 in: Zajtchuk R, Bellamy RF, eds. Textbook of Military Medicine. Washington, DC: US Department of the Army, Office of the Surgeon General, and Borden Institute; 1997: 493. Government publication, no copyright on photos.

      Acral necrosis of nose, lips, fingers (image abov...

      Acral necrosis of nose, lips, fingers (image above) and toes (shown here) and residual ecchymoses over both forearms in a patient recovering from bubonic plague that disseminated to blood and lungs. At one time, the patient's entire body was ecchymotic. Reprinted from McGovern TW, Friedlander AM. Plague. In: Sidell FR, Takafuji ET, Franz DR, eds. Medical Aspects of Chemical and Biological Warfare. Chapter 23 in: Zajtchuk R, Bellamy RF, eds. Textbook of Military Medicine. Washington, DC: US Department of the Army, Office of the Surgeon General, and Borden Institute; 1997: 493. Government publication, no copyright on photos.

  • Pharyngitis culture positive for Y pestis has been seen in endemic areas in household contacts of those with bubonic plague. These patients also have associated cervical lymphadenopathy.

Causes

The etiologic agent is Y pestis, a facultative anaerobic, intracellular, gram-negative bacillus. The following are some epidemiologic factors that suggest an increased likelihood of infection with the plague:3

  • Rural or nonurban residency, especially in geographic areas with known plague foci
  • Contact with sick animals, small rodents, or other possible hosts
  • Wilderness activities (eg, camping, hiking, sleeping on ground, hunting)
  • Fleabite
  • Recent plague in the community
  • Occupation as a veterinarian
  • Summer months
  • Sudden influx of previously healthy patients with severe pneumonia, especially if geographically clustered

More on CBRNE - Plague

Overview: CBRNE - Plague
Differential Diagnoses & Workup: CBRNE - Plague
Treatment & Medication: CBRNE - Plague
Follow-up: CBRNE - Plague
Multimedia: CBRNE - Plague
References

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Further Reading

Contributor Information and Disclosures

Author

Demetres G Velendzas, MD, Attending Staff, Department of Emergency Medicine, Manchester Memorial Hospital, Eastern Connecticut Health Network
Demetres G Velendzas, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Susan E Dufel, MD, FACEP, Program Director, Associate Professor, Department of Traumatology and Emergency Medicine, Division of Emergency Medicine, University of Connecticut School of Medicine
Susan E Dufel, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Deirdre Cronin, MD, Resident Physician, Department of Emergency Medicine, University of Connecticut School of Medicine, Farmington
Disclosure: Nothing to disclose.

Medical Editor

Dan Danzl, MD, Chair, Department of Emergency Medicine, Professor, University of Louisville Hospital
Dan Danzl, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Kentucky Medical Association, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eric L Weiss, MD, DTM&H;, Director of Stanford Travel Medicine, Medical Director of Stanford Lifeflight, Assistant Professor, Departments of Emergency Medicine and Infectious Diseases, Stanford University School of Medicine
Eric L Weiss, MD, DTM&H; is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Robert G Darling, MD, FACEP, Clinical Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine; Associate Director, Center for Disaster and Humanitarian Assistance Medicine
Robert G Darling, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Association of Military Surgeons of the US
Disclosure: Nothing to disclose.

 
 
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