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A PLAGUE ON U.S.
CASE STUDY (1):
A middle aged couple was vacationing in New York City from their ranch in New
Mexico. After several days of enjoying the luxury of their hotel and seeing
the sights, they both began feeling ill. Their symptoms were similar, fever,
fatigue, myalgia and one-sided inguinal swelling. Two days later, on Nov. 5,
they went to an emergency room (ER) in a New York City hospital after consulting
with their physician in New Mexico and the doctor at the hotel.
On admission the 55 year-old man appeared sickest with chills, diaphoresis (sweating), and lower extremity cyanosis. He had tender left inguinal adenopathy with overlying edema. His temperature was 104º F., blood pressure - 78/50, WBC count - 24,000/µL (normal: 4,300 - 10,800/µL), Platelet count - 72,000/µL (normal: 130,000 - 400,000/µL). A blood culture was taken and after 24 hours a gram stain showed bipolar gram negative rods.
The 47 year-old wife had tender right inguinal and femoral adenopathy with overlying erythema and induration. Her temperature was 102.2º F, blood pressure - 120/72, WBC count - 9,500/µL, platelet count - 189,000/µL. Aspiration of the inguinal lymph nodes did not yield any material.
CASE STUDY QUESTIONS:
1. What is the most probable organism recovered from the blood culture?
2. Where did the couple most likely become infected?
3. What is the usual route of infection for this disease?
4. The causative organism is on the list of possible bioterrorist agents. Why
wasn't this episode considered to be a bioterrorist incident?
CASE DISCUSSION:
Subculture of the husband's blood culture grew organisms identified as Yersinia
pestis. This was confirmed on Nov. 6 by positive direct fluorescent antibody
to Y. pestis F1 antigen and polymerase chain reaction (PCR) performed
on the initial blood culture by the NYC Public Health Laboratory. His diagnosis
was acute septicemic plague.
Although no organisms were recovered from the wife, she was given a presumptive diagnosis of bubonic plague because of her clinical signs and symptoms and her husband's Y. pestis positive blood culture.
Both were given multiple antibiotics. The wife recovered without complications.
The husband developed acute renal failure, acute respiratory distress syndrome
and disseminated intravascular coagulation. He required hemodialysis and mechanical
ventilation and subsequently underwent bilateral foot amputations because of
ischemia.
After 6 weeks in the ICU he recovered and was discharged to a rehabilitation
facility.
During initial consultation with medical personnel the couple reported that routine surveillance conducted by the New Mexico Department of Health had identified Y. pestis in a dead wood rat on their New Mexico property. The hotel physician notified the ER about the arrival of two possible plague patients and the need for respiratory isolation pending the exclusion of pulmonary infection. Various New York State agencies as well as the CDC were contacted to facilitate diagnostic testing, coordinate public health response and assess the possibility of terrorism. After determining that the two plague cases were probably acquired naturally, the agencies held a press conference to reassure the public that the exposures had occurred in New Mexico, a known plague endemic area, and not in NYC.
One day after the patients were evaluated, New Mexico Department of Health and CDC investigated the couple's New Mexico property. Rodent traps were placed in and around the couple's home and along a nearby hiking trail where wood rat (Neotoma species) nests and rodent burrows were abundant. Five flea pools comprising 88 fleas were harvested from 41 trapped rodents. All fleas were cultured for Y. pestis and rodents were bled for culture. Y. pestis isolates from the husband's blood culture and from flea samples were compared by using pulsed-field gel electrophoresis (PFGE). The PFGE patterns of the isolate from the husband and from seven New Mexico flea pools, two obtained in July and five obtained during the November investigation, were indistinguishable.
Plague warning signs were placed at trailheads near the couple's property. Plague information pamphlets were distributed in the community and close neighbors were contacted directly to inform them of the risk for infection in the area. (1)
EPIDEMIOLOGY AND HISTORY OF PLAGUE
Plague, the scourge of the Middle-Ages, is a rodent-associated zoonosis transmitted
by the bite of fleas infected with Y. pestis. The organism is transmitted
from animal to animal and occasionally to humans. For eons it lived in the blood
of resistant wild rodents in northern Asia. During the Middle Ages plague began
to infect the domestic rats that infested towns and cities. After the rats died,
their fleas bit and infected the people. Bubonic plague (the Black Death) swept
the continent. Plague traveled by infected rats on ships sailing to various
ports and spread to Europe and England. The Black Death caused the death of
over half the population.
Plague entered California in 1899 on a ship from Hong Kong. (2) There had been two cases of plague on board, causing the ship to be quarantined at Angel Island. A search of the ship revealed 11 stowaways. The next day two of them were missing. Their bodies were found floating in the Bay and autopsy showed infection with the plague bacillus. When the ship was allowed to dock in San Francisco, rats escaped. Nine months later plague cases occurred in S.F.'s Chinatown. Political issues vied with scientific eradication and control efforts. City officials didn't want it known that plague was present and denied its occurrence. Even the governor refused to believe or to help with anti-plague efforts. Finally the U.S. Surgeon General got permission from President McKinley to pass anti-plague regulations. Commissions and Boards formed, fought with the governor, and were disbanded, underfunded, and reformed. Meanwhile additional plague cases occurred. Finally in April 1901 a clean-up campaign scoured Chinatown, halting the epidemic. The last case, in 1904, caused a fatality in a woman in Concord. There were 121 cases in San Francisco and 5 more in the Bay Area with 122 deaths.
Plague remained endemic in the city. After the 1906 earthquake the devastation and refugee camps fostered an increase in the rat population with proximity to people (3). Plague cases again occurred, but this time anti-plague measures, particularly rat control, were started early and halted the epidemic by 1909. With rat poison as well as a 5 cent per rat bounty, over 2 million rats were killed. Cleaning up unsanitary conditions eliminated rat hiding and nesting sites. This epidemic caused 160 cases with 77 deaths.
The elimination of plague cases in the Bay Area did not eliminate the plague bacillus. By this time the organism had become established in deer mice, Peromyscus and other resistant wild rodents. Y. pestis became firmly entrenched in the wild (sylvatic) rodent population in the Coastal Mountains and eventually spread to the Sierra Nevada and beyond. Today plague is endemic in resistant sylvatic rodents throughout the western 17 states (4).
Occasionally the organism spreads to more susceptible rodents, like ground squirrels or wood rats. Epizootic outbreaks kill large numbers in squirrel colonies, leaving infected, hungry fleas around the burrows. These sites are dangerous to hunters, campers and residents living nearby. When these die-offs of ground squirrels occur, public health workers close campgrounds or parks, put up warning signs and apply insecticides to kill the fleas.
Although transmission by infected fleas is the most common method of transmission, predators or scavengers can contract the disease by eating prey and hunters may become infected by handling or skinning infected game animals. Cats are very susceptible to plague. They are exposed by eating rodents infected with plague. Cats develop pneumonic plague and can pose a risk to their owners and to veterinarians.
During 1988-2002, a total of 112 human cases of plague were reported from 11 western states. Most of the cases were in Northern Arizona and New Mexico with sporadic cases occurring elsewhere. About 80% of these exposures occurred in environments around houses that provided abundant food and hiding places for plague-susceptible rodents (1). Such conditions were present around the home of the case study couple.
MANIFESTATIONS OF PLAGUE (5)
In addition to the bite of infected fleas, plague can be transmitted by eating
infected animals, exposure of infected meat or patient's suppurating lesions
through broken skin, or by inhalation of aerosolized plague bacteria. Cats are
very susceptible to plague. They are exposed by eating rodents infected with
plague. Cats develop pneumonic plague and can pose a risk to their owners and
to veterinarians.
There are three forms of plague in humans, bubonic, septicemic, and pneumonic.
Bubonic Plague: The incubation period for bubonic plague is usually 2-6 days. The symptoms include fever, chills, myalgias, arthralgias, sore throat and headache. Within 24 hours the patient notices tenderness and pain in one or more regional lymph nodes proximal to the site of inoculation of Y. pestis organisms. A lymphadenitis (bubo) develops. The bubo becomes very painful, swollen and hemorrhagic, finally appearing black, thus leading to the name, Black Death. Early treatment with appropriate antibiotics such as streptomycin or gentamicin usually results in alleviation of manifestations over 2 to 5 days. Untreated bubonic plague has a fatality rate of more than 50%.
Septicemic Plague: Septicemic plague occurs when host defenses are breached and the plague bacillus enters and multiplies in the bloodstream. It is a progressive, overwhelming infection. Gastrointestinal symptoms frequently occur with nausea, vomiting, diarrhea and abdominal pain. Multifocal hepatic and splenic necrosis is common. Diffuse myocarditis and respiratory distress syndrome may occur. DIC, renal shutdown, hypotension with shock are preterminal events. If not treated early with appropriate antibiotics, septicemic plague can be fatal.
Pneumonic Plague: Primary pneumonic plague occurs from directly inhaling Y. pestis. Secondary develops from a bubonic or septicemic plague infection. The incubation period is 1-3 days for naturally occurring primary; 2-6 days for intentionally disseminated pneumonic plague. The initial symptoms occur suddenly with chills, fever, headache, myalgias, weakness, and dizziness. Pulmonary signs, cough, sputum, chest pain, tachypnea and dyspnea develop on the second day of illness. Transmission of plague to contacts is a grave risk of pneumonic plague. It is most frequently fatal of the plague forms. If treatment is not instituted within 18 hours after onset of symptoms the fatality rate is close to 100%. Unfortunately most pneumonic plague cases are not diagnosed and treated within this time. Even the treated cases had a fatality rate of over 40% in the U.S. during the last half of the 20th century.The overall fatality rate for all types of plague in the U.S. since 1950 has been 16%. Most of these deaths were due to delay in seeking or instituting treatment, misdiagnosis, and incorrect treatment.
LABORATORY IDENTIFICATION OF YERSINIA PESTIS
Yersinia pestis is a gram-negative, non-motile, fermentative rod. It
stains easily with gram stain and appears as single or short-chained pleomorphic
gram-negative, fat rods. It may not have a bipolar appearance on gram stain.
To show the bipolar characteristic, use Wayson, Giemsa, or Wright's stain. Cultures
grow better at 28o than at 35o; grow slowly, and must be incubated longer for
optimum growth. On blood agar the colony has a fried egg appearance. On clear
medium there is a skirt around the young colony. There is a lot of capsular
material that forms strings with a loop. Although it ferments glucose and mannitol,
it is relatively inert. It is a non-lactose fermenter on MacConkey agar and
is oxidase and urease negative. It can be identified by various automated bacteriologic
test systems, but some may give erroneous interpretations.
Confirmation is by direct fluorescent antibody testing or antigen capture enzyme-linked immunosorbant assay.
Confirmatory testing of the patient's disease includes culture or a fourfold or greater change in antibody titer between acute and convalescent sera.
DIFFERENTIATION OF NATURALLY OCCURRING PLAGUE FROM BIOTERRORIST RELEASE OF PLAGUE
| Naturally occurring plague | Bioterrorist plague |
| Patient in or from a plague endemic area | May occur in a non-plague endemic area |
| Lymph node swelling indicating infection from a flea bite, i.e., bubonic plague type | Pneumonic plague is most common |
| Usually individual or few cases | May involve many cases |
REPORTING/APPROPRIATE ACTION (6,7)
The following is a generalized response to a possible bioterrorist agent. The
CDC and individual states have web sites that give information for procedures
and reporting.
SUMMARY
Plague is a disease caused by the organism, Yersinia pestis. There
are three types of disease, bubonic, septicemic and pneumonic. It is a zoonosis
and usually transmitted by the bite of an infected flea (bubonic) but may be
transmitted by eating infected animals, by contact through broken skin with
infected animals or patient's suppurating lesions, or by inhalation of aerosolized
bacteria, either in infectious body fluids, or intentionally produced.
Plague is endemic in 17 Western sates. It is maintained in resistant sylvatic
rodents but can occasionally be spread to susceptible rodents such as ground
squirrels.
When plague occurs in humans in the U.S., bioterrorism must be ruled out. Characteristics
of bioterrorism spread include pneumonic expression, occurrence in non-endemic
areas and multiple cases.
PLAGUE REFERENCES
Review Questions - Course #056-958 - A PLAGUE ON U.S.
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