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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvOTY3NDk1LW92ZXJ2aWV3\nDrugs & Diseases > Pediatrics: General Medicine\nPediatric Plague\nAuthor: Vinod K Dhawan, MD, FACP, FRCPC, FIDSA; Chief Editor: Russell W Steele, MD more...\nSections Pediatric Plague\nFurther Inpatient Care\nInpatient & Outpatient Medications\nPlague, a zoonotic disease caused by the gram-negative bacterium Yersinia pestis, is transmitted to humans by the bites of infected fleas (eg, Xenopsylla cheopis), scratches from infected animals, inhalation of aerosols, or consumption of food contaminated with Y pestis. [1, 2] No disease has impacted civilization as deeply as the plague. As many as 200 million people have died from this disease.\nThe first pandemic, known as the Justinian plague (AD 541-544), began in Egypt and spread throughout the Middle East and Mediterranean areas. Eventually, the entire known world was affected. By the 8th century, plague receded into scattered endemic areas.\nThe second pandemic began in 1347, when traders from central Asia introduced plague into ports of Sicily. This became the first epidemic, known as the Black Death, which killed over one third of the population of Europe. Later, following the Great Plague of London (1665), the disease subsided.\nThe third pandemic began in Hong Kong in 1894 and continues to the present. Alexandre Yersin discovered the plague bacillus, Y pestis, and effective antibiotics were introduced in the early 1940s; however, plague remains endemic in much of the world. [3, 4]\nExamples of findings are shown in the images below.\nEcchymoses at the base of the neck in a girl with plague. The bandage is over the site of a prior bubo aspirate. These lesions are probably the source of the line from the children's nursery rhyme, \"ring around the rosy.\" Courtesy of Jack Poland, PhD, Centers for Disease Control and Prevention (CDC), Fort Collins, Colo.\nAcral necrosis of the nose, the lips, and the fingers and residual ecchymoses over both forearms in a patient recovering from bubonic plague that disseminated to the blood and the lungs. At one time, the patient's entire body was ecchymotic. Reprinted from 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.\nAcral necrosis of the toes and residual ecchymoses over both forearms in a patient recovering from bubonic plague that disseminated to the blood and the lungs. At one time, the patient's entire body was ecchymotic. Reprinted from 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.\nThe classic mode of transmission to humans is a flea bite (see the image below).\nPictured is a flea with a blocked proventriculus, which is equivalent to the gastroesophageal region in a human. In nature, this flea would develop a ravenous hunger because of its inability to digest the fibrinoid mass of blood and bacteria. If this flea were to bite a mammal, the proventriculus would be cleared, and thousands of bacteria would be regurgitated into the bite wound. Courtesy of the United States Army Environmental Hygiene Agency.\nAlternately, broken skin serves as a portal when tissue or blood of an infected animal is handled (skinning or evisceration of infected animals). Competency of the flea to serve as vector for transmission of plague to humans depends on its willingness to feed on a human host and its tendency to regurgitate intestinal contents during a blood meal. Fleas from sylvatic rodents feed on humans only reluctantly. However, the Oriental rat flea (Xenopsylla cheopis) is an effective vector because of its tendency to regurgitate and to feed on nonrodent hosts (see the image below).\nMale Xenopsylla cheopis (oriental rat flea) engorged with blood. This flea is the primary vector of plague in most large plague epidemics in Asia, Africa, and South America. Both male and female fleas can transmit the infection. Image courtesy of the Centers for Disease Control and Prevention (CDC).\nWhen the flea takes a blood meal from an infected rodent, stomach enzymes cause a clot to form, blocking the flea's proventricularis. At its next attempt to feed, unable to swallow due to the blockage, the flea regurgitates plague bacilli into the bite wound.\nThe organisms invade the lymphatics and travel to regional lymph nodes, causing inflammation (see the image below).\nAfter the femoral lymph nodes, the next most commonly involved regions in plague are the inguinal, axillary, and cervical areas. This child has an erythematous, eroded, crusting, necrotic ulcer at the presumed primary inoculation site in the left upper quadrant. This type of lesion is uncommon in patients with plague. The location of the bubo is primarily a function of the region of the body in which an infected flea inoculates plague bacilli. Courtesy of Jack Poland, PhD, Centers for Disease Control and Prevention (CDC), Fort Collins, Colo.\nLarge, tender lymph nodes are termed buboes and give the bubonic form of plague its name. If the infection is not contained at this site, the organisms may be further spread via the bloodstream to organs such as lungs, spleen, liver, kidneys, and meninges. Bacteremia without the appearance of buboes is considered septicemic plague. Pneumonic plague occurs when pneumonia results from either hematogenous spread (secondary pneumonic plague) or inhalation (primary pneumonic plague) of organisms transmitted from animals or other humans.\nPlague is considered endemic in all western and southwestern states. [5] Most human cases in the United States occur in two regions:\n· Northern New Mexico, northern Arizona, and southern Colorado\n· California, southern Oregon, and far western Nevada\nReported cases of human plague in US 1970-2012. Courtesy of the CDC.\nMost cases of plague are acquired in rural areas. Native Americans who reside on reservations are at increased risk for acquisition of the disease. Ground squirrels and prairie dogs serve as major enzootic foci (see the image below). [6]\nRock squirrel in extremis coughing blood-streaked sputum related to pneumonic plague. Courtesy of Ken Gage, PhD, Centers for Disease Control and Prevention (CDC), Fort Collins, Colo.\nDogs and cats are susceptible to plague. Domestic animals, cats in particular, have been responsible for human cases.\nBetween 1900 and 2012, 1006 confirmed or probable human plague cases occurred in the United States. Over 80% of United States plague cases have been the bubonic form. During 2001–2012, the annual number of human plague cases reported in the United States ranged from one to 17 (median = three cases). [7, 8]\nHowever, plague activity increased during 2015. In a CDC report published on August 25, 2015, a total of 11 cases of human plague had been reported since April 1, 2015. [9] Affected patients were residents of six states: Arizona (two), California (one), Colorado (four), Georgia (one), New Mexico (two), and Oregon (one). The two cases in Georgia and California residents were linked to exposures at or near Yosemite National Park in the southern Sierra Nevada Mountains of California. It is unclear why the number of cases in 2015 is higher than usual.\nPlague reached a worldwide maximum of 5419 cases (274 fatal) in 1997, and the incidence has declined since that time. [10] In 2003, 9 countries reported 2118 cases (182 fatal) to the World Health Organization (WHO). [11] Algeria reported cases of human plague for the first time in 50 years. India and Indonesia also recently reported cases after a 30-year to 50-year quiescent period. Almost all of the cases reported in the last 20 years have occurred among people living in small towns and villages or agricultural areas rather than in larger towns and cities. Between 1,000 and 2,000 cases each year are reported to the World Health Organization (WHO), though the true number is likely much higher. Occurrence is thought to be underreported. [12, 13] Currently, about 95% of the world’s human plague cases now occur in the African region, including Madagascar. [14] World distribution of plague is shown below.\nWorldwide distribution of plague cases 2000-2009. Courtesy of the CDC.\nMortality is approximately 16%, which increases to 40-70% in untreated cases. [15] Practitioners must maintain a high index of suspicion for plague, especially with patients exposed to animals or fleas in endemic areas. The most common complications are secondary septicemia, pneumonia, and meningitis. Polyarthritis, lung abscesses, and superinfection of lymph nodes also rarely occur.\nSepticemic plague\nMortality ranges from 30-50% for patients with septicemic plague and increases to nearly 100% in untreated cases. This high mortality rate reflects the difficulty in diagnosis, given the disease's similarity to gram-negative bacterial sepsis. Diagnosis is often made postmortem.\nPneumonic plague\nThe fatality rate of untreated pneumonic plague approaches 100%. The last reported case of person-to-person transmission occurred during a plague epidemic in Los Angeles in 1924. Since then, cases of primary pneumonic plague have been acquired chiefly from infected cats.\nHuman plague cases and deaths in US 2004-2014. Courtesy of the CDC.\nPlague occurs in both men and women. It is slightly more common among men.\nPlague has occurred in people of all ages, although, 50% of cases occur in people ages 12–45.\nButler T. Plague into the 21st century. Clin Infect Dis. 2009 Sep 1. 49(5):736-42. [Medline].\nWilliamson ED. Plague. Vaccine. 2009 Nov 5. 27 Suppl 4:D56-60. [Medline].\nPrentice MB, Rahalison L. Plague. Lancet. 2007 Apr 7. 369(9568):1196-207. [Medline].\nRocca P. The modern plague. Del Med J. 2007 May. 79(5):189-90. [Medline].\nBen Ari T, Gershunov A, Gage KL, et al. Human plague in the USA: the importance of regional and local climate. Biol Lett. 2008 Dec 23. 4(6):737-40. [Medline]. [Full Text].\nThiagarajan B, Bai Y, Gage KL, Cully JF Jr. Prevalence of Yersinia pestis in rodents and fleas associated with black-tailed prairie dogs (Cynomys ludovicianus) at Thunder Basin National Grassland, Wyoming. J Wildl Dis. 2008 Jul. 44(3):731-6. [Medline].\nAdams DA, Jajosky RA, Ajani U, Kriseman J, Sharp P, Onwen DH, et al. Summary of notifiable diseases--United States, 2012. MMWR Morb Mortal Wkly Rep. 2014 Sep 19. 61 (53):1-121. [Medline].\nKugeler KJ, Staples JE, Hinckley AF, Gage KL, Mead PS. Epidemiology of human plague in the United States, 1900-2012. Emerg Infect Dis. 2015 Jan. 21 (1):16-22. [Medline].\nKwit N, Nelson C, Kugeler K, Petersen J, Plante L, Yaglom H, et al. Human Plague - United States, 2015. MMWR Morb Mortal Wkly Rep. 2015 Aug 28. 64 (33):918-9. [Medline].\nCleri DJ, Vernaleo JR, Lombardi LJ, et al. Plague pneumonia disease caused by Yersinia pestis. Semin Respir Infect. 1997 Mar. 12(1):12-23. [Medline].\nWorld Health Organization. Human plague in 2002 and 2003. Wkly Epidemiol Rec. 2004 Aug 13. 79(33):301-6. [Medline].\nGupta ML, Sharma A. Pneumonic plague, northern India, 2002. Emerg Infect Dis. 2007 Apr. 13(4):664-6. [Medline].\nJosko D. Yersinia pestis: still a plague in the 21st century. Clin Lab Sci. 2004 Winter. 17(1):25-9. [Medline].\nNeerinckx S, Bertherat E, Leirs H. Human plague occurrences in Africa: an overview from 1877 to 2008. Trans R Soc Trop Med Hyg. 2010 Feb. 104(2):97-103. [Medline].\nHuman plague: review of regional morbidity and mortality, 2004-2009. Wkly Epidemiol Rec. 2009 Feb 5. 85(6):40-5. [Medline].\nPiarroux R, Abedi AA, Shako JC, Kebela B, Karhemere S, Diatta G, et al. Plague epidemics and lice, Democratic Republic of the Congo. Emerg Infect Dis. 2013 Mar. 19(3):505-6. [Medline]. [Full Text].\nRunfola JK, House J, Miller L, Colton L, Hite D, Hawley A, et al. Outbreak of Human Pneumonic Plague with Dog-to-Human and Possible Human-to-Human Transmission--Colorado, June-July 2014. MMWR Morb Mortal Wkly Rep. 2015 May 1. 64 (16):429-34. [Medline].\nMittal V, Bhattacharya D, Rana UV, Rai A, Pasha ST, Kumar A, et al. Prompt laboratory diagnosis in timely containment of a plague outbreak in India. J Commun Dis. 2006 Dec. 38(4):317-24. [Medline].\nRussell P, Nelson M, Whittington D, et al. Laboratory diagnosis of plague. Br J Biomed Sci. 1997 Dec. 54(4):231-6. [Medline].\nTomaso H, Jacob D, Eickhoff M, et al. Preliminary validation of real-time PCR assays for the identification of Yersinia pestis. Clin Chem Lab Med. 2008. 46(9):1239-44. [Medline].\nCrook LD, Tempest B. Plague. A clinical review of 27 cases. Arch Intern Med. 1992 Jun. 152(6):1253-6. [Medline].\nPlague: Resources for Clinicians. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/plague/healthcare/clinicians.html. October 5, 2015; Accessed: March 30, 2016.\nStevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014 Jul 15. 59 (2):e10-52. [Medline].\nWeir E. Plague: a continuing threat. CMAJ. 2005 Jun 7. 172(12):1555. [Medline].\nWang X, Zhang X, Zhou D, Yang R. Live-attenuated Yersinia pestis vaccines. Expert Rev Vaccines. 2013 Jun. 12(6):677-86. [Medline].\nDennis DT, Chow CC. Plague. Pediatr Infect Dis J. 2004 Jan. 23(1):69-71. [Medline].\nLigon BL. Plague: a review of its history and potential as a biological weapon. Semin Pediatr Infect Dis. 2006 Jul. 17(3):161-70. [Medline].\nDattwyler RJ. Community-acquired pneumonia in the age of bio-terrorism. Allergy Asthma Proc. 2005 May-Jun. 26(3):191-4. [Medline].\nWright stain peripheral blood smear of patient with septicemic plague demonstrating bipolar, safety pin staining of Yersinia pestis. Although Wright stain often demonstrates this characteristic appearance, Giemsa and Wayson stains most consistently highlight this pattern. Courtesy of Jack Poland, PhD, Centers for Disease Control and Prevention (CDC), Fort Collins, CO.\nInguinal bubo on upper thigh of a person with bubonic plague. Image courtesy of the Centers for Disease Control and Prevention (CDC).\nYersinia pestis bacteria on fluorescent antibody test. Image courtesy of the Centers for Disease Control and Prevention (CDC).\nStreptomycin 1 g twice daily IM\nGentamicin 5 mg/kg once daily, or 2 mg/kg loading dose followed by 1.7 mg/kg every 8 hours IM or IV\nLevofloxacin 500 mg once daily IV or po\n400 mg every 8-12 hours\n500-750 mg twice daily po\nDoxycycline 100 mg twice daily or 200 mg once daily IV or po\nMoxifloxacin 400 mg once daily IV or po\nChloramphenicol 25 mg/kg every 6 hours IV\nStreptomycin 15 mg/kg twice daily (maximum 2 g/day) IM\nGentamicin 2.5 mg/kg/dose every 8 hours IM or IV\nLevofloxacin 10 mg/kg/dose (maximum 500 mg/dose) IV or po\n15 mg/kg/dose every 12 hours (maximum 400 mg/dose)\n20 mg/kg/dose every 12 hours (maximum 500 mg/dose) po\nWeight < 45 kg: 2.2 mg/kg twice daily (maximum 100 mg/dose)\nWeight ≥ 45 kg: same as adult dose\nIV or po\nChloramphenicol (for children > 2 years) 25 mg/kg every 6 h (maximum daily dose, 4 g) IV\nVinod K Dhawan, MD, FACP, FRCPC, FIDSA Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Infectious Diseases, Rancho Los Amigos National Rehabilitation Center\nVinod K Dhawan, MD, FACP, FRCPC, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, Royal College of Physicians and Surgeons of Canada\nRobert D Schremmer, MD Associate Professor, Department of Pediatrics, University of Missouri-Kansas City School of Medicine; Attending Physician, Division of Emergency Medical Services, Children's Mercy Hospital and Clinics\nRobert D Schremmer, MD is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics\nMary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference\nRussell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation\nRussell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association\nJosé Rafael Romero, MD Director of Pediatric Infectious Diseases Fellowship Program, Associate Professor, Department of Pediatrics, Combined Division of Pediatric Infectious Diseases, Creighton University/University of Nebraska Medical Center\nJosé Rafael Romero, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, New York Academy of Sciences, Pediatric Infectious Diseases Society\nLeslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine\nLeslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society\nencoded search term (Pediatric Plague) and Pediatric Plague\nTropical Myeloneuropathies\nTropical Sprue\nEndomyocardial Fibrosis\nCutaneous Larva Migrans\nVaccinations, Travel\nMiliaria\nAinhum\nEbola Just 'A Plane Ride Away'\nTravel health: Keeping Up-to-Date With The Risks of Insect-Borne Disease\nCDC Clarifies Diagnostic Testing for Individuals Who Could Have Either Dengue or Zika\nInfant Outcomes of Zika in Pregnancy: New Data\nAccording to Pediatricians\nCommon Chemicals May Play a Role in Childhood Obesity\nVaping: It's All a Smokescreen\nDiscussing Death With Children: A Developmental Approach\nSaybie, Believed to Be World's Tiniest Baby Ever to Survive, Goes Home\nSome Dietary Supplements Tied to Severe Outcomes in Youth\n2001 /viewarticle/914153 News\nNews Tropical Skin Conditions on the Rise, Difficult to Detect\nNews New WHO Regional Chief Must Battle Lifestyle Conditions, Tropical Diseases\nNews FDA OKs Triclabendazole (Egaten) for Neglected Tropical Disease Fascioliasis\nPractice Guideline Neurocysticercosis Clinical Practice Guidelines (2018)"