The Bubonic PlagueandRubellaA Comparison Ellen Perlow HS 5353 Epidemiology Dr. Wiginton Fall 2002 – Texas Woman’s University Dept. of Health Studies November 19, 2002 – http://www.a4access.org/epipaper.ppt Narrative at http://www.a4access.org/epipaper1102.doc This presentation is available in alternative formats upon request.
Bubonic Plague: Enzootic Agent: Bacterium:Yersinia pestisVector: Blood-sucking rat flea: Xenopsylla cheopisHosts: Rodents-rats/shrews, prairie dogs, etc. Environment: Rodent-friendly: food, garbage, unsanitary conditionsTransmission: a) Most common mode: bite of flea infected with Yersinia pestis bacterium; b) less frequently: direct contact with infectious body fluids or tissues while handling infected animal or c) inhaling infectious respiratory droplets or other infectious materials.
Types of Plague • Bubonic plague: most common form of U.S. cases: 80%-90%. Case Fatality Rate if not treated: 50%-60% • Septicemic plague: when Yersinia pestis invades and continues to multiply in the bloodstream; primary or secondary to bubonic plague. U.S. 1947-1977: 10% septicemic. Case fatality rate-50%. Complications: septic shock, consumptive coagulopathy, meningitis, coma. • Pneumonic plague: least common but most dangerous and fatal form - inhalation of infectious respiratory droplets. Incubation period: 1-3 days. Without treatment, death within 18 hours after onset of respiratory symptoms. (Centers for Disease Control and Prevention (1996). Prevention of plague: recommendations of the Advisory Committee on Immunization Practices (ACIP). Morbidity and Mortality Weekly Report, 45(RR-14): 1-15.
History of Bubonic Plague - 1 • Biblical times: circa 1000 B.C.E. • 1 Samuel 5: capture of Ark of Covenant from Israelites by Philistines at battle of Aphek followed by outbreak of what appears to have been the plague in five cities of the Philistines starting in Ashdod. (Septuagint/Vulgate: Philistines smitten with tumors … “and rats appeared in their land and death and destruction were throughout the cities.” (Griffin, J.P. (2000) Bubonic plague in Biblical times. [Letter]. Journal of the Royal Society of Medicine, 93, 449.)
History of Bubonic Plague - 2 • Summer 430 B.C.E.: Athens • Athens at war with Sparta • Sailors brought mysterious illness from Egypt. 1/3 population of Athens died. Pericles killed. • Changed history: Athens lost to Sparta. • Could have been typhus, smallpox, scarlet fever. (Giblin, J.C. (1995). When plague strikes: the Black Death, smallpox, AIDS. HarperCollins, 1-3.)
History of Bubonic Plague - 3 • 1346-1347: Black Sea/S. Ukraine • Epidemic: “Victims suffered from headaches, felt weak and tired, and staggered when they try to walk. By the third day, the lymph nodes in the sufferers’ groins, or occasionally their armpits, began to swell.” Swellings=buboes. In Greek. groin=boubon=disease name: Bubonic plague. • Also named “Black Death” “The Great Pestilence.” • Italian traders blamed. Infected, return to Sicily. Plague spread to Sicily, then mainland Italy. (Giblin, J.C. (1995). When plague strikes: the Black Death, smallpox, AIDS. HarperCollins, 11-12. Working Group on Civiliian Biodefense (2000). Plague as a biological weapon. JAMA, 283(17), 2281.)
History of Bubonic Plague - 4 • October 1347: Sicily -- Italy • Italian sailors ordered to stay on board. Did not know that carriers were black rats and fleas that lived in their hair. Plague spread to port of Messina, ports of mainland Italy, Milan, Florence, Venice ... • Splendid breeding ground: garbage, garbage … • Venice decree of quaranta giorni =quarantine of sailors on ships for 40 days • Literary references: Bocaccio’s Decameron. • By winter 1348-1349, 1/3-1/2 population of Italy killed. (Giblin, J.C. (1995). When plague strikes: the Black Death, smallpox, AIDS. HarperCollins, 13-20.)
History of Bubonic Plague - 5 • Sp. 1348: Marseilles-Avignon, France • Avignon: Pope’s home. Pilgrims unknowingly brought plague. • Feb.-May: 400 people/day, 1349: 50,000-Paris • Pope Clement: fire/humors (Hippocrates, Galen) • Church: no dissection, autopsies. Humors/miasmas theories of Hippocrates, Galen. • Attributed plague to imbalance of humors; miasmas. • Treatments: bloodletting at site of buboes, prayer. (Giblin, J.C. (1995). When plague strikes: the Black Death, smallpox, AIDS. HarperCollins, 21-25.)
History of Bubonic Plague - 6 • Summer 1349-1351: British Isles and Germany … early 1400s. • Plague killed up to 80% of some villages • Devastation led to vehement persecution and discrimination against people who were different • German Flagellant movement, 1st Holocaust, intense Anti-Semitism. Power of Church reduced (precursor to rise of Protestantism). • Epidemics in Europe about every 10 years to early 1400s. Europe lost ½ of population. (Giblin, J.C. (1995). When plague strikes: the Black Death, smallpox, AIDS. HarperCollins, 26-40.)
History of Bubonic Plague - 7 • 15th-16th-17th Centuries • Reform of Catholic Church ---Protestantism • Medicine: Practical courses in anatomy, surgery • Medical textbooks in European languages • Consumer health … Scientific method … Gutenberg (1456), Discovery of “America” (1492) • 1664-Fall 1665: Great Plague of London. 70,000 died. Thought to be person to person transmission. Quarantines in homes. (Giblin, J.C. (1995). When plague strikes: the Black Death, smallpox, AIDS. HarperCollins, 41-49.)
History of Bubonic Plague - 8 • 18th-19th Centuries • By 1750, bubonic plague faded out in western Europe, though still active in Mediterranean. • 1855: pandemic in interior of China, to Canton and Hong Kong. Killed >12 million people in India and China. • Medicine: Work of Pasteur, Koch with bacteria. • 1894: Kitasato and Dr. Alexandre E.J. Yersin isolated and described the cause of plague. Dr. Yersin received the credit: bacteria later named Yersinia pestis (Giblin, J.C. (1995). When plague strikes: the Black Death, smallpox, AIDS. HarperCollins, 49-50. Yancey, D. (1994). The hunt for hidden killers: ten cases of medical mystery. Brookfield, CT: Millbrook Press, 61-71.)
History of Bubonic Plague - 9 • 20th Century • 1900-1904: San Francisco outbreak: 121 cases,118 died • Person/person transmission: Asian immigrants isolated. • Quarantine did not work; scientists’ explanation accepted • Ships disinfected. Massive clean-up. Rats destroyed. • 1924-1925: Los Angeles outbreak: 40 cases, 38 died. • 1940s: Development of antibiotics. Plague treatable. • By 1949: New Mexico U.S. leader in # of plague cases • Threat if no antibiotics; 9/94-India: pneumonic plague • 1898-1920, 1991, 1995-1998: Madagascar epidemics • Dec. 1996 CDC MMWR Prevention of Plague Report (Giblin, J.C. (1995), 50-51; Boisier (2002)… Emerging Infectious Diseases; McClain, C. Of Medicine, Race and American Law-1900)
History of Bubonic Plague - 10 • 21st Century … Today as we speak • November 7, 2002: CNN.com: “Bubonic plague suspected in New York City [NYC] Visitors” • Nov. 9, 2002: New Mexico visitors to NYC diagnosed with bubonic plague still in hospital. • NYC’s first case of bubonic plague in a century. (CDC, 2002) • Couple suspected of contracting plague from rodents on their property (Robin, 2002) • Plague as biological weapon (U.S. Working Group on Civilian Biodefense, JAMA (5/3/2000): Recommendations
History of Bubonic Plague - 11 • 21st Century … Today as we speak, continued: • “According to the World Health Organization (WHO), as of May 27, 2002, the Malawian Ministry of Health has reported a total of 71 cases of bubonic plague in the district of Nsanje since the onset of the outbreak on April 16, 2002. The outbreak has affected 26 villages - 23 in the Ndamera area, 2 in Chimombo, and 1 village in neighboring Mozambique.” Centers for Disease Control and Prevention. National Center for Infectious Diseases. Travelers’ health: outbreak of bubonic plague in Malawi, as of May 27, 2002. Retrieved November 9, 2002, from http://www.cdc.gov/travel/other/plague-outbreak-malawi.htm.
History of Bubonic Plague - 12 • 21st Century, Controversy, Outbreaks, heightened interest, terrorism ... • How to prepare for terrorism via plague (especially pneumonic). (Don't miss smallpox/plague outbreaks: adapt strategies to track bioterrorism. ED management : the monthly update on emergency department management. 2002 Jan; 14(1): 1-3.) • History of Bubonic Plague: Was it really the plague, or scarlet fever, or ebola virus? ... Delta 32 gene mutation • Current Outbreaks: NYC …CDC Travelers’ Health Information on Plague (retrieved 11/9/2002): enzootic in wild rodent populations over large rural areas of the Americas, Africa, and Asia. Prophylactic measures: antibiotics, insect repellants … http://www.cdc.gov/travel/diseases/plague.htm; PBS...
Rubella / German Measles / Gregg’s Syndrome: Virus Agent: Togavirus, genus Rubivirus, RNA virus(isolated 1962 by Parkman and Weller) Transmission:Human to human respiratory transmission. Replication in nasopharynx and regional lymph nodes. Viremia (virus in bloodstream) 5-7 days after exposure with spread to tissues. Intrauterine: placenta, fetus affected during viremia.Centers for Disease Control and Prevention (2002). Rubella. Retrieved November 16, 2002, from http://www.cdc.gov/nip/publications/pink/rubella.pdf
History of Rubella - 1 • 1881: Officially recognized as a distinct clinical entity at international medical congress in London. Before that time, confusion as to whether it was a mild form of measles (rubeola) or scarlet fever, or both, and what it should be called. • The name “rubella”, first proposed in 1866, accepted. • In the next 60 years, little attention was paid to rubella since the disease was not considered serious and did not have serious complications. (Horstmann, Dorothy M. (1986, Oct. 11). The rubella story, 1881-1985. South African Medical Journal, Supplement, 60-63.)
History of Rubella - 2 • 1935: Epidemic of rubella, largely went unnoticed. • 1940: Large rubella epidemic in Australia. • 1941: Australian ophthalmologist Dr. Norman Gregg discovered relationship between maternal rubella during pregnancy and congenital “defects” in infants. • 1941: Dr. Gregg had observed in his practice in Sydney a rise in the number of infants born with cataracts. Found that the mothers of most of the infants had contracted rubella when they were in their first few months of pregnancy during the 1940 epidemic. • Dr. Gregg’s colleagues also noticed numerous infants being born with cataracts, as well as infants born who were small in size, had failure to thrive, cardiac abnormalities, and microphthalmia – an unnatural smallness of the eyes. • 1941: Dr. Gregg documented 78 cases of congenital rubella syndrome [CRS] and published a paper in the Transactions of the Ophthalmological Society of Australia (Horstmann, Dorothy M. (1986, Oct. 11). The rubella story, 1881-1985. South African Medical Journal, Supplement, 60-63; Cooper, L.Z. (1966). German measles. Scientific American 215(7): 30-37.)
History of Rubella - 3 1941: Discovery of association between maternal rubella and newborn’s differences - profound impact on the entire field of congenital disease. Rubella was the very first well defined teratogen: an agent that causes developmental differences. Dr. Gregg’s findings were confirmed in other studies in Europe, the U.S., New Zealand, and Australia. The studies showed that many children born with differences were correlated with their mothers having a history of rubella. (Horstmann, Dorothy M. (1986, Oct. 11). The rubella story, 1881-1985. South African Medical Journal, Supplement, 60-63. Parkman, P.D., Meyer, H.M., Jr., Hilleman, M.R. (1997, 2000). Vaccine developed for German measles, 1960-1969. DISCovering U.S. History. Gale Research. Retrieved September 16, 2002, from http://galenet.galegroup.com/servlet/SRCCE/. Cooper, L.Z. (1966). German measles. Scientific American 215(7): 30-37.)
History of Rubella - 4 1941-1961: For twenty years, scientists tried to isolate the rubella virus, using experimental animals, but without success. 1962: Drs. Parkman, Meyer, Hilleman at 3 laboratories – Walter Reed, Harvard, and NIH - isolated rubella virus. New standard of cooperation in medical research. Early 1960s: 40,000 and 45,000 cases of rubella per year. (Horstmann, Dorothy M. (1986, Oct. 11). The rubella story, 1881-1985. South African Medical Journal, Supplement, 60-63. Parkman, P.D., Meyer, H.M., Jr., Hilleman, M.R. (1997, 2000). Vaccine developed for German measles, 1960-1969. DISCovering U.S. History. Gale Research. Retrieved September 16, 2002, from http://galenet.galegroup.com/servlet/SRCCE/. Cooper, L.Z. (1966). German measles. Scientific American 215(7): 30-37.)
History of Rubella - 5 Spring 1964: Large epidemic of rubella in the United States. 7,000 fetal deaths, 20,000 babies born with congenital differences. Investigators discovered very different virologies of rubella intra-uterine infection and the post-natal infection. July 1966:Pediatrician Louis Z. Cooper publishes “German Measles,” Scientific American. By 1969, three rubella vaccines ready for licensing.: HPV77 DE5 (via monkey kidney cells and duck embryo tissue cultures), the Cendehill strain (via rabbit kidney cells), and the RA27/3 strain (isolated in human diploid cells). Rubella vaccines induce seroconversions in approximately 95% of susceptible individuals. The vaccine-induced infection is non-communicable. Viremia – the existence of viral particles in the bloodstream – occurs at such a low level that it is not easily detected. (Horstmann, Dorothy M. (1986, Oct. 11). The rubella story, 1881-1985. South African Medical Journal, Supplement, 60-63. Parkman, P.D., Meyer, H.M., Jr., Hilleman, M.R. (1997, 2000). Vaccine developed for German measles, 1960-1969. DISCovering U.S. History. Gale Research. Retrieved September 16, 2002, from http://galenet.galegroup.com/servlet/SRCCE/. Cooper, L.Z. (1966). German measles. Scientific American 215(7): 30-37.)
History of Rubella - 6 1969 - Beginning of rubella vaccination programs in US, UK, Australia,New Zealand. US/other nations different approaches: target populations for immunization. • U.S.: focus on children who had not yet reached puberty, both boys and girls, 1 year and older. Goal to protect the age group in which most infections occurred. This way, it was reasoned, women who are pregnant would avoid being exposed to the infection. For the U.S. approach, a very high herd immunity in the population most greatly affected – young children, was necessary. Identification and immunization of women of child-bearing age also was recommended. In the United Kingdom, Europe, and Australia, the immunization program begun in 1970 was limited to girls, usually between 10-14 years of age and to susceptible women. Thought that incidence of the congenital disease would not be reduced until the mid-1980s. (Horstmann, Dorothy M. (1986, Oct. 11). The rubella story, 1881-1985. South African Medical Journal, Supplement, 60-63. Parkman, P.D., Meyer, H.M., Jr., Hilleman, M.R. (1997, 2000). Vaccine developed for German measles, 1960-1969. DISCovering U.S. History. Gale Research. Retrieved September 16, 2002, from http://galenet.galegroup.com/servlet/SRCCE/. Cooper, L.Z. (1966). German measles. Scientific American 215(7): 30-37.)
History of Rubella - 7 1989 – Eradication of rubella: goal of Healthy People 2000. 1988-1991: Reduction in rubella cases 98% since pre-vaccination era. However, 2-3 fold increase in incidence of rubella since 1982 (JAMA, 1991) 1990: 1093 cases from 38 states,+DC. California: 4x. 2002: CDC: U.S. on verge of eradication of indigenous rubella. “Rubella occurs mainly among foreign-born Hispanic adults who are either unvaccinated or whose vaccination status is unknown…” 1998-2002: Controversy: MMR vaccine causes autism? November 7, 2002: Publication of Danish study showing no link between administration of MMR vaccine and autism. November 19, 2002: Threats due to lack of vaccination in other countries, threats due to terrorism? … Centers for Disease Control and Prevention. National Center for Health Statistics (1999). Healthy people 2000 progress review objective charts. Increase in rubella and congenital rubella. (1991, March 6). JAMA, The Journal of the American Medical Association, 265(9), 1076-1077.(Rubella almost eradicated in the United States. (2002, 5 February). Virus Weekly. Retrieved September 16, 2002 from, General Reference Center Gold. Madsen K. M., Hviid A., Vestergaard M., Schendel D., Wohlfahrt J., Thorsen P., Olsen J., Melbye M. (2000, November 7). A population-based study of measles, mumps, and rubella vaccination and autism. New England Journal of Medicine, 347, 1477-1482.
Symptoms of the Disease:Bubonic Plague – Symptoms • Bubonic plague: enlarged, tender lymph nodes (buboes), fever, chills, prostration, gastrointestinal symptoms • Septicemic plague: fever, chills, prostration, abdominal pain, shock and bleeding into skin and other organs • Pneumonic plague: fever, chills, cough and difficulty breathing; rapid shock and death if not treated early (Centers for Disease Control and Prevention. CDC plague fact sheet. Retrieved October 22, 2002, from http://www.cdc.gov/ncidod/dvbid/plague/facts.htm)
Symptoms of the Disease:Rubella Symptoms - 1 • “Rubella is a mild, highly contagious illness that is caused by a virus. It is characterized by a rash, swollen glands and, especially in adults, joint pain. The rash usually lasts about three days and may be accompanied by a low fever. Other symptoms such as headache, loss of appetite and sore throat are more common in infected adults and teenagers than in children. Sometimes there are no symptoms at all. • Rubella is caused by a different virus from the one that causes regular measles (rubeola). Immunity to rubella does not protect a person from measles, or vice versa.” National Institutes of Health. National Toxicology Program (NTP). Center for the Evaluation of Risks to Human Reproduction [CERHR]. Rubella (German measles) 5/24/02). Retrieved October 23, 2002, from http://cerhr.niehs.nih.gov/genpub/topics/rubella-ccae.html.
Symptoms of the Disease:Rubella – Symptoms - 2 • “Rubella is a mild illness which may present few or no symptoms. Symptoms may include a rash, slight fever, joint aches, headache, discomfort, runny nose and reddened eyes. The lymph nodes just behind the ears and at the back of the neck may swell, causing some soreness and/or pain. The rash, which may be itchy, first appears on the face and progresses from head to foot, lasting about three days. As many as half of all rubella cases occur without a rash. The incubation period for rubella is 12-23 days; in most cases, symptoms appear within 16-18 days.” (New York State Department of Health. Communicable disease fact sheet: rubella. Retrieved October 23, 2002, from http://www.health.state.ny.us/nysdoh/consumer/rubella.htm)
Symptoms of the Disease:Rubella – Symptoms - 3 • Rubella, lasts less than two weeks in children. • Symptoms: swollen glands, a low fever, transient three-day rash. • In women who are pregnant, the infection can pass to the developing fetus, especially during the first trimester of pregnancy, causing severe injuries to the fetus/newborn. • Approximately 15-20% of women who are pregnant who acquire German measles during the first trimester give birth to infants with heart defects (50%), deafness (50%), eye defects and blindness (40%), mental retardation (40%), blood defects such anemia and bleeding (30%), bone lesions, enlarged liver, enlarged spleen, and hand abnormalities. • About 10% of infants born with congenital rubella syndrome [CRS] die, while severe infections result in spontaneous abortion. • Greatest period of virulence: first two months of pregnancy. Studies show that 50% of women infected during the first month of pregnancy gave births to babies with a host of differences. If women infected in 3rd month, 10% of infants have these differences. Infection after 4th month cause less severe differences in the fetus. (Parkman, Meyer, & Hilleman, 1997, 2000).
III.Causative Agents and how they were determined:The Bubonic Plague and Rubella
Causative Agent – Bubonic Plague (Bacterium Yersinia pestis) - 1 Source: CDC Public Health Image Library, Image # 2117 URL: http://phil.cdc.gov/Phil/detail.asp?id=2117 (image in public domain) CDC Description: “Yersinia (Pasteurella) pestis causes plague in animals and humans. People usually get plague from being bitten by a rodent flea that is carrying the plague bacterium, or by handling an infected animal. “
Causative Agent – Bubonic Plague(Bacterium Yersinia pestis) - 2 • Plague is an infectious disease of animals and humans caused by the bacteriumYersinia pestis. The fundamental but separate works by Yersin and Kitasato in 1894 on the discovery of the etiologic agent of plague in Hong Kong opened the way for investigating the disease and how it is spread. Kitasato and Yersin described, within days of each other’s findings, the presence of bipolar staining organisms in the swollen lymph node (bubo), blood, lungs, liver and spleen of dead patients. (Bibel et al., 1976).
Causative Agent – Bubonic Plague(Bacterium Yersinia Pestis) - 2 • Cultures isolated from patient specimens were inoculated into a variety of laboratory animals, including mice. These animals died within days after injection, and the same bacilli as those found in patient specimens were present in the animal organs. Though both investigators reported their findings, Yersin was accepted as the primary discoverer of the organism now named after him, Yersinia pestis
Causative Agent – Bubonic Plague(Bacterium Yersinia pestis) - 3 • Yersin had recorded that rats were affected by plague not only during plague epidemics but also often preceding such epidemics in humans. In fact, plague was designated, in local languages, as a disease of the rats: villagers in China, India and Formosa (Taiwan) described that when hundreds and thousands of rats lie dead in and out of houses, plague outbreaks in people soon followed (Gross, 1995).
Causative Agent – Bubonic Plague(Bacterium: Yersinia pestis) - 4 • Simond described transmission of plague in 1898. Persons who became ill did not have to be in close contact with each other to acquire the disease. Simond observed residents of China and Formosa being frightened of dead rats and viewing these rats as a risk for developing plague. Simond suspected that the flea might be an intermediary factor in the transmission of plague. People were infected with plague only if they were in contact with recently dead rats. They were not infected if they touched rats that were dead for more than 24 hours. Simond demonstrated that the rat flea (Xenopsylla cheopis) transmitted the disease in an experiment in which a healthy rat, separated from direct contact with a recently plague-killed rat, died of plague after the infected fleas jumped from the first rat to the second. Centers for Disease Control and Prevention. Division of Vector-Borne Infectious Diseases. The plague: natural history. Retrieved October 22, 2002 from: http://www.cdc.gov/ncidod/dvbid/plague/history.htm
Causative Agent – Rubella(Togavirus, genus Rubivirus) Source: CDC Public Health Image Library, Image # 269 URL: http://phil.cdc.gov/Phil/detail.asp?id=269 CDC Description: “Transmission electron micrograph of rubella virus” (1981) [image in public domain]
Causative Agent – Rubella (Togavirus, genus Rubivirus) - 1 • Rubella as a separate entity not identified until 1881. Thought to be scarlet fever or measles. • Identity and severity discounted until 1941 since mild symptoms. • 1941: Dr. Norman McAlister Gregg in Australia discovered maternal-fetus intrauterine transmission. • General agreement that rubella caused by virus based on its incubation period (12-23 days), clinical course (symptoms appear 16-18 days), and lack of response to antibiotics. (Cooper, 1966, 32. NYS Dept. of Health, 2002, Rubella, 2002) • 1941-1961: Unsuccessful attempts using experimental animals to isolate rubella virus. The rubella epidemic (1960s). (1998, 2000). American Decades CD-ROM. Gale Research. Retrieved November 15, 2002, from Student Resource Center College Edition database, http://galenet.galegroup.com/servlet/SRCCE.
Causative Agent – Rubella (Togavirus, genus Rubivirus) - 2 • 1960-1962: Isolation of virus at 3 labs: Drs. Paul Parkman and Edward L. Buescher, Walter Reed Army Institute for Research; Drs. Thomas Weller and Franklin Neva at Harvard University; Drs. John L. Sever and Gilbert M. Schiff at the National Institutes of Health [NIH]. Upon moving to NIH, Dr. Parkman worked with Dr. Harry M. Meyer on finding a way to curb the growth of the virus. They were responsible for developing the first test – the hemaglutination-inhibition test - that could determine a person’s immunity to the rubella virus. This test could provide results in three hours, rather than the three weeks required via an older testing method. • Investigators discovered very different virologies of the rubella intra-uterine infection and the post-natal infection just in time for 1963-1965 major U.S. rubella epidemic. The rubella epidemic (1960s). (1998, 2000). American Decades CD-ROM. Gale Research. Retrieved November 15, 2002, from Student Resource Center College Edition database, http://galenet.galegroup.com/servlet/SRCCE. Cooper, 1966).
IV. How Diseases Spread: The Bubonic PlagueandRubella
How Disease Spread Bubonic Plague - 1 • Zoonotic infectious disease spread principally by reservoir of infected rats, shrews, prairie dogs, and other mammals. • Vector: Rat flea Source: CDC (in public domain) URL: http://www.cdc.gov/ncidod/ dvbid/plague/cheob6x4.htm CDC Description: Male 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.
How Disease Spread:Bubonic Plague - 2 • People usually bitten by rodent flea carrying the plague bacterium, Yersinia pestis, or by handling an infected animal. • Homes, places of work have flea-infested rats. Even with modern antibiotics, infected person is not treated promptly, the disease can cause illness or death. • Wild rodents in certain areas around world infected with plague. Outbreaks in people still occur in rural communities or in cities usually associated with infected rats, fleas that live in the home. • (Centers for Disease Control and Prevention. CDC Plague Home Page, 2002)
How Disease Spread:Bubonic Plague - 3 • In U.S., last urban plague epidemic: 1924-25: Los Angeles. Since then, in U.S., mostly scattered cases in rural areas (10-15 persons/year). • Globally, the World Health Organization: 1,000 to 3,000 cases of plague every year. • North America, plague in certain animals and their fleas: Pacific Coast to Great Plains, S.W. Canada to Mexico. • U.S. most human cases: 1) northern New Mexico, northern Arizona, and southern Colorado; and 2) California, southern Oregon, far western Nevada. • Also in Africa, Asia, and South America (see map). • (Centers for Disease Control and Prevention. CDC Plague Home Page, 2002)
How Disease Spread:Bubonic Plague - 4 • Natural cycle in its enzootic environment, involving small mammals and fleas without human involvement. • Quiescent periods, during which few or no human cases are detected, may last for years, leading to mistaken declarations of plague eradication. • However long the silent periods last, plague may suddenly reappear. The combination of false assurance of its eradication, and the failure of public health vigilance, sets the stage for the panic that may ensue when enzootic plague changes from its natural cycle into rodent and flea populations near where people live. • Poor sanitation, overcrowding, high numbers of rodents are conditions that enhance urban plague transmission. • Centers for Disease Control and Prevention. Division of Vector-Borne Infectious Diseases. The plague: natural history. Retrieved October 22, 2002 from: http://www.cdc.gov/ncidod/dvbid/plague/history.htm
How Disease Spread:Bubonic Plague - 5 • Controversy as to whether etiology was the same for all outbreaks of the plague: • “Because of the limits inherent in historical sources on ancient plague epidemics, many questions concerning their etiology and epidemiology remain unanswered. Molecular biology tools and the use of dental pulp as a preserved source of bacterial DNA enabled us to demonstrate that Yersinia pestis was the etiologic agent of the 1347 European Black Death and of two additional epidemics in 1590 and 1722 in southern France.” • (Drancourt, M. & Raoult, D. (2002, January). Molecular insights into the history of plague. Microbes and Infection / Institut Pasteur, 4(1): 105-9.)
How Disease Spread:Bubonic Plague - 6 • Controversy as to whether etiology was the same for all outbreaks of the plague: The primary hypotheses raised by the author, a medieval historian, are that: • the Black Death of the 13th and 14th centuries was not the same disease as the rat-based bubonic plague of the 19th century whose Yersinia pestis agent was first cultured in Hong Kong in 1894; • Unlike populations of Western Europe who adapted to the pathogen of the Black Death at least for the first hundred years, humans do not have immunity for the modern bubonic plague. • The hypotheses are based on the findings that the two diseases were different in their signs, symptoms, and epidemiologies. ... • (Cohn, S.K., Jr. (2002, June). The Black Death: end of a paradigm. American Historical Review, 107(3): 703-738. Retrieved October 27, 2002, from Ebscohost database.)
How Disease Spread:Rubella - 1 • Rubella caused by togavirus that is spread from person to person when an infected person coughs or sneezes. • Rubella also spread by direct contact with the nasal or throat secretions of an infected person. If a pregnant woman gets rubella during the first 3 months of pregnancy, her baby is at risk of having serious birth defects or dying. • Highly contagious. High herd immunity required, 85-90% National Coalition for Adult Immunization. (2002). Facts about rubella for adults. Retrieved October 23, 2002, from http://www.nfid.org/factsheets/rubellaadult.html
How Disease Spread:Rubella - 2 • Congenital rubella being highly contagious also increases its virulence because affected newborns can infect others with the virus up to a year after birth. • In a hospital setting, newborns with congenital rubella syndrome [CRS] can infect hospital personnel, other newborns, and other women who are pregnant and visitors to the hospital, very much compounding the spread of the virus. Parkman, P.D., Meyer, H.M., Jr., Hilleman, M.R. (1997, 2000). Vaccine developed for German measles, 1960-1969. In DISCovering U.S. History. Gale Research. Retrieved September 16, 2002, from Student Resource Center College Edition database at http://galenet.galegroup.com/servlet/SRCCE/
Mechanisms of Containment:Bubonic Plague - 1 • OPPORTUNITIES • Increased self-sufficiency of state and county public health labs • Expanded active surveillance through carnivore serosurveys and application of geographic information systems (GIS) to surveillance programs • Increased education of public and health professionals • Collaborative applied research on plague prevention and control with other federal, state, and local health agencies, including application of GIS to surveillance Centers for Disease Control and Prevention. CDC plague fact sheet. Retrieved October 22, 2002, from http://www.cdc.gov/ncidod/dvbid/plague/facts.htm
Mechanisms of Containment:Bubonic Plague - 2 • RESEARCH • Ecology-based prevention and control strategies • Improved diagnostic reagents and methods • Development of potential vaccine candidates • Risk factor identification using landscape ecology and epidemiology CDC (2002). CDC plague fact sheet. Retrieved October 22, 2002, from http://www.cdc.gov/ncidod/dvbid/plague/facts.htm • PRACTICE • People refrain from contact with rodents, especially if population known to be infected • People use insect repellant when outside in areas with potential for having vectors and/or hosts. • People wear proper attire to protect selves.