Plague

On August 2, 1996, a young man, age 18, with fever, pain, diarrhea, and tenderness in his left groin, was seen at a local outpatient clinic in Flagstaff, Arizona. He was treated with a nonsteroidal antiinflammatory medication and sent home. The next day he had difficulty breathing and collapsed while taking a shower. Brought to a hospital emergency room, he was pronounced dead on arrival. On August 8, cultures of blood samples taken in the emergency department were positive for Yersinia pestis, the plague bacillus.

On August 17, 1996, a 16-year-old girl in western Colorado had pain followed by numbness in her left armpit. Fever, chills, and vomiting occurred over the following 2 days. At a local hospital she was treated for chest pain as she said she had fallen from a trampoline. An appointment with a neurologist was scheduled, and she was sent home. On August 21, she was found semiconscious at home and was taken back to the hospital. Within an hour of arrival she went into respiratory arrest, and was transferred to another hospital with a diagnosis of respiratory distress syndrome and possible meningitis. Her condition rapidly deteriorated. She died later that day. On August 23, blood and spinal fluid cultures obtained on August 21, were positive for Y. pestis [37].

Five cases of human plague were reported in the United States in 1996, two of which resulted in deaths. On average, 10-20 cases per year are the expectation, occurring mostly in young people under 20, with highest rates are among the Navajo. Others at risk are hunters and veterinarians. Although an ancient affliction, plague remains one of the world's most feared diseases, and appears to be too complex to be eradicated. This zoonotic disease has reservoirs on nearly every continent and has the uncanny ability to overwhelm host immune systems. Obviously plague is a perfect choice as a bioweapon, even though its spread is preventable and the illness curable if diagnosed rapidly and appropriate treatment instituted. Nevertheless, the devastation attributed to bubonic and pneumonic plagues dwarf that of most other diseases. Estimates put the death toll at 200 million.

Plague is primarily a disease conveyed among wild rodents. We humans can become infected when entering rodent territory, as illustrated in Figure 3.4 . The infection is easily transmitted from rodent to human by the bite of an infected flea that picked up the bacterium from its rodent host, while taking a blood meal and then taking another blood meal from a human and disgorging bacteria into the bite site. Intimately involved in the affair are rodent, flea,

Figure 3.4. Cycles of transmission and sequence of events leading to infection and possible outbreaks of bubonic and pneumonic plagues. (Figure shows fleas carrying Yersinia pestis bacteria, obtained from wild rodents, disgorging the bacteria while taking a blood meal from an unsuspecting individual.)

Figure 3.4. Cycles of transmission and sequence of events leading to infection and possible outbreaks of bubonic and pneumonic plagues. (Figure shows fleas carrying Yersinia pestis bacteria, obtained from wild rodents, disgorging the bacteria while taking a blood meal from an unsuspecting individual.)

Figure 3.5. 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. (Figure adapted from the Centers for Disease Control, Atlanta.)

Figure 3.5. 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. (Figure adapted from the Centers for Disease Control, Atlanta.)

bacterium, and human—far too complex to even contemplate eradication. Plague can also be acquired by direct contact with infected animal carcasses or by inhalation of contaminated airborne droplets.

Plague exists in three forms: bubonic, pneumonic, and septicemic. Bubonic is the classic and most common type, that produced the infamous Black Death of the fourteenth and seventeenth centuries. After a flea, most often the oriental rat flea, Xenopsylla cheopis (Fig. 3.5), ingests Yersinia pestis from its rodent host, yersinia produces a chemical, coagulase, that clots ingested blood in the flea' s proventriculus, an organ between its esophagus and stomach, which blocks passage of the next blood meal into the flea's stomach. With this blockage, fleas requrgitate Y. pestis into the wound site of the bite they made while attempting to feed. It 's quite ingenious. Between 25,000 and 100,000 bacteria are sent into the wound site. Those bacteria now migrate to regional lymph nodes, where many are engulfed and destroyed by polymorphonuclear leukocytes—a type of phagocyte. But those that remain viable in the lymph nodes induce inflammation and edema, which cause painful, swollen buboes (the lymph nodes) in armpits and groin, hence bubonic (from the Greek boubon ' meaning groin). Swollen buboes are timeless indicators of bubonic plague. No other infectious disease produces that manifestation. The "blackness" of the Black Death refers to, and is the aftereffect of, subcutaneous hemorrhages forming dark patches on the skin as blood oxidizes and turns purple-brown to black. But that is not the end of it. The bacteria can also enter the bloodstream, initiating septicemia and systemic shock, which, if not treated promptly and appropriately, is deadly.

Pneumonic plague is a rare but deadly form of plague that is spread via respiratory droplets in close contact (between 2 and 5 feet) with an infected person. The illness progresses rapidly from fever and flulike symptoms to an overwhelming pneumonia with heavy coughing and production of bloody sputum. Especially serious is the fact that the majority of cases in the United States were spread by droplets from infected domestic cats. Veterinarians have been at unusually high risk [38].

Yersinia pestis is so highly infective that no more than 100-500 microbial cells are required to produce illness; and, of course, it is contagious. Edema and respiratory lung congestion are common symptoms followed by respiratory collapse, if not rapidly treated with antibiotics. Mortality approaches 50%. There is little doubt that this form of plague would be a terrorist's choice.

Most human plague occurs as a result of contact between rodents (many kinds) and people. However, human outbreaks are often preceded by epizootics, with large numbers of deaths among susceptible animals, which can signal an alert that human involvement could follow, which is often the case with teenagers who walk through rodent-infested areas, get bitten or scratched, or inhale airborne organisms.

As a bioweapon in today's world, the choice would not be fleas, even though they were used effectively by the Japanese during World War II. Weaponized, airborne Y. pestis would be the choice. During the 1950s and 1960s the United States and Russia developed procedures for aerosolizing Y. pestis, further enhancing its infectivity and virulence. Among its many attributes is the fact that in the early stages of dispersal and consequent illness it would be mis-diagnosed, leading to a high and rapid death rate. The fact that it is communicable would sharply increase infections. Perhaps of even greater concern, plague can trigger fear and panic that would be difficult to contain. As a bio-weapon, physicians would be faced with severe and rapidly progressing pneumonia. Many similar cases would occur over several days. Buboes, of course, would be absent, and the illness would be occurring in urban rather than in rural areas, and there would be no indication of prior epizootics. Together these factors could catch people unaware and unprepared, permitting numbers of deaths before a correct diagnosis was made and appropriate treatment instituted. Indeed, here again, surprise is on the side of the bad guys.

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