15.5.3. Rickettsias and plague
Rickettsias are bacteria (Proteobacteria: Rickettsiales) associated with arthropods. The genus Rickettsia includes virulent pathogens of humans. R. prowazekii, which causes endemic typhus, has influenced world affairs as much as any politician, causing the deaths of millions of refugees and soldiers in times of social upheaval, such as the years of Napoleonic invasion of Russia and those following World War I. Typhus symptoms are headache, high fever, spreading rash, delirium, and aching muscles, and in epidemic typhus from 10% to 60% of untreated patients die. The vectors of typhus are lice (Box 15.3), notably the body louse, Pediculus humanus corporis. Infestation of lice indicates unsanitary conditions and in western nations, after years of decline, is resurgent in homeless people. Although the head louse (P. humanus capitis), pubic louse (Pthirus pubis), and some fleas experimentally can transmit R. prowazekii, they are of little or no epidemiological significance. After the rickettsias of R. prowazekii have multiplied in the louse epithelium, they rupture the cells and are voided in the feces. Because the louse dies, the rickettsias are demonstrated to be rather poorly adapted to the louse host. Human hosts are infected by scratching infected louse feces (which remain infective for up to two months after deposition) into the itchy site where the louse has fed. There is evidence of low level persistence of rickettsias in those who recover from typhus. These act as endemic reservoirs for resurgence of the disease, and domestic and a few wild animals may be disease reservoirs. Lice are also vectors of relapsing fever, a spirochete disease that historically occurred together with epidemic typhus.
Other rickettsial diseases include murine typhus, transmitted by flea vectors, scrub typhus through trombiculid mite vectors, and a series of spotted fevers, termed tick-borne typhus. Many of these diseases have a wide range of natural hosts, with antibodies to the widespread American Rocky Mountain spotted fever (Rickettsia rickettsii) reported from numerous bird and mammal species. Throughout the range of the disease from Virginia to Brazil, several species of ticks with broad host ranges are involved, with transmission through feeding activity alone. Bartonellosis (Oroya fever) is a rickettsial infection transmitted by South American phlebotomine sand flies, with symptoms of exhaustion, anemia, and high fever, followed by wart-like eruptions on the skin.
Plague is a rodent—flea—rodent disease caused by the bacterium Yersinia pestis, also known as Y. pseudotuberculosis var. pestis. Plague-bearing fleas are principally Xenopsylla cheopis, which is ubiquitous between 35°N and 35°S, but also include X. brasiliensis in India, Africa, and South America, and X. astia in south-east Asia. Although other species including Ctenocephalides felis and C. canis (cat and dog fleas) can transmit plague, they play a minor role at most. The major vector fleas occur especially on peri-domestic (house-dwelling) species of Rattus, such as the black rat (R. rattus) and brown rat (R. norvegicus). Reservoirs for plague in specific localities include the bandicoot (Bandicota bengalensis) in India, rock squirrels (Spermophilus spp.) in western USA and related ground squirrels (Citellus sp.) in south-east Europe, gerbils (Meriones spp.) in the Middle East, and Tatera spp. in India and South Africa. Between plague outbreaks, the bacterium circulates within some or all of these rodents without evident mortality, thus providing silent, long-term reservoirs of infection.
When humans become involved in plague outbreaks (such as the pandemic called the “Black Death” that ravaged the northern hemisphere during the 14th century) mortality may approach 90% in undernourished people and around 25% in previously well-fed, healthy people. The plague epidemiological cycle commences amongst rats, with fleas naturally transmitting Y. pestis between peri-domestic rats. In an outbreak of plague, when the preferred-host brown rats die, some infected fleas move on to and eventually kill the secondary preference, black rats. As X. cheopis readily bites humans, infected fleas switch host again in the absence of the rats. Plague is a particular problem where rat (and flea) populations are high, as occurs in overcrowded, unsanitary urban conditions. Outbreak conditions require appropriate preceding conditions of mild temperatures and high humidity that encourage build-up of flea populations by increased larval survival and adult longevity. Thus, natural variations in the intensity of plague epidemics relate to the previous year’s climate. Even during prolonged plague outbreaks, periods of fewer cases used to occur when hot, dry conditions prevented recruitment, because flea larvae are very susceptible to desiccation, and low humidity reduced adult survival in the subsequent year.
During its infective lifetime the flea varies in its ability to transmit plague, according to internal physiological changes induced by Y. pestis. If the flea takes an infected blood meal, Y. pestis increases in the proventriculus and midgut and may form an impassable plug. Further feeding involves a fruitless attempt by the pharyngeal pump to force more blood into the gut, with the result that a contaminated mixture of blood and bacteria is regurgitated. However, the survival time of Y. pestis outside the flea (of no more than a few hours) suggests that mechanical transmission is unlikely. More likely, even if the proventricular blockage is alleviated, it fails to function properly as a one-way valve, and at every subsequent attempt at feeding, the flea regurgitates a contaminated mixture of blood and pathogen into the feeding wound of each successive host.
