Public Health Importance

Fleas are of public health significance for several reasons. Many species are annoying biters that can cause considerable discomfort, sometimes leading to secondary infections of bite wounds. The bites of some species can cause dermatitis or allergic reactions. Allergic responses also can result from contact with, or inhalation of, flea products (e.g., larval exuviae). Females of the chigoe actually invade human skin tissue, especially of the feet and toes, and cause painful lesions that are prone to serious secondary infection. Other fleas are intermediate hosts of tapeworms that can parasitize humans. Fleas also serve as vectors of the causative agents of several important zoonotic diseases, such as murine typhus and plague (Table II).

Flea bites (Fig. 7.14) can cause intense irritation for several days. Bites are characterized by a tiny purplish spot, or purpura pulicosa, surrounded by slightly swollen skin called roseola pulicosa. The vast majority of flea bites experienced by humans are due to the cat flea. This flea is an unrelenting biter which generally attacks humans on the ankles (Fig. 7.14), although other parts of the body may be affected. Women tend to be more commonly bitten than men, suggesting a hormonal association between this species and human females. In addition to the annoyance it causes, Ctenocephalides felis is a proven vector of the causative agent of endemic typhus. The cat flea is discussed in more detail with respect to its veterinary importance.

The human flea also is an annoying biter of people in various parts of the world. The closely related P. simulans sometimes infests households and causes dermatitis in humans in western North America. Several other species of fleas may bite humans to the point of annoyance, including the dog flea, the sticktight flea, the northern rat flea, and several species of Xenopsylla, including the Oriental rat flea (Table I). Also, the squirrel flea Orchopeas howardi and some bird fleas belonging to the genus Ceratophyllus, including the European chicken flea, occasionally bite humans.

Members of households and adjacent premises harboring pets or domestic rodents can be especially prone to

or reappearing in different areas of Europe. London experienced a major epidemic in 1348, followed by another in 1665, with foci of the disease persisting in the city throughout this time period.

The third major pandemic of plague spread across the globe in the late 1800s after originating from a focus in China's Yunnan Province in 1855. From 1896 to 1948, this pandemic accounted for 12 million deaths in India alone. Several plague foci initiated during the peak of this pandemic still persist today. In the United States, for example, plague bacilli were introduced with infected ship-borne rats in 1899 in San Francisco and from there eventually spread to at least 14 western states and 2 Canadian provinces. Plague continues to persist in native rodents and fleas in most of these areas of western North America. Some researchers, however, contend that plague was already enzootic in North America prior to 1899 and that the apparent spread of the disease merely reflected intensified surveillance efforts. Accounts of plague include works by Stark etal. (1966), Bahmanyar and Cavanaugh (1976), Twigg (1978), Barnes (1982), Duplaix (1988), Mee (1990), Craven et al. (1993), Poland etui. (1994), Madon etui. (1997), and Goddard (1999).

Nucleotide sequencing of ribosomal RNA in T. pestis shows a correlation between the. geographical distribution of genetic strains, or biovars, of T. pestis and their spread during the three pandemics. There are three biovars of T. pestis: biovar Antiqua occurs in Africa, biovar Medievialis mainly in central Asia, and biovar Orientalis in Europe, Asia, Africa, North America, and South America.

Today plague occurs as fairly discrete foci in various parts of Asia, southern and northwestern Africa, South America, and western North America. Recent outbreaks have surfaced in Brazil, Democratic Republic of the Congo, Ecuador, India, Madagascar, Malawi, Mongolia, Peru, South Africa, Tanzania, and Vietnam. Globally, nearly 19,000 human cases of plague were reported to the World Health Organization from a total of 20 countries during 1984-1994. During 1970-1994, a total of 334 cases of indigenous plague were reported for the United States; the peak years were 1983 and 1984, with 40 and 31 cases, respectively (Craven etal., 1993). Eighty percent of cases in the United States have occurred in Arizona, New Mexico, or Colorado.

In addition to bites from infected fleas, plague infections can result from direct contact with moribund or dead mammals infected with T. pestis or, rarely, from inanimate objects harboring the pathogen. In such cases the pathogen typically enters the body through skin lesions. Inhalation infection also can occur from aerosolized T. pestis.

Two ecological forms of plague are recognized: urban plague, carried by domestic rats and their fleas in cities and towns, and wild-rodent plague (sylvatic plague, derived from the Latin silva, meaning trees; campestral plague; rural plague), maintained in several species of mammals (mainly rodents) and their fleas in rural areas away from human populations. Over 200 species of rodents and other mammals (e.g., certain carnivores) may serve as reservoir hosts of wild-rodent plague. In North America, ground squirrels, rock squirrels, chipmunks, and prairie dogs are particularly important, whereas in Asia, gerbils and susliks (ground squirrels) typically fill this role. Similarly, various gerbils and the peridomestic rat Mastomys natalensis are important reservoirs in parts of Africa. The sigmodontine rat Zygodontomys brevicauda is prevalent in most South American foci. Plague-infected tree squirrels have been found in some towns in the western United States. In an attempt to limit future spread, plague is presently one of only three internationally quarantinable infections.

In many plague-endemic regions, wild-rodent plague persists enzootically in discrete rodent populations. Under certain conditions, the disease can become epizootic and spread to commensal rats to trigger urban plague. Some populations of reservoir hosts are refractory to infection with T. pestis, while others are highly susceptible. This is reflected by large-scale die-offs in infected prairie dog {Cynomysspp.) towns in North America. Intermediate stages of susceptibility to plague exist between these two extremes in other reservoir populations. In most regions where plague persists there are distinctly different species of enzootic and epizootic rodent reservoir hosts. Most carnivores, especially felids, are susceptible to infection with T. pestis. The disease is often severe in domestic cats, which can serve as a source ofinfected fleas to households. Bites, scratches, or inhalation of infectious aerosols from infected cats also can disseminate T. pestis. Human plague cases acquired from domestic cats have increased in recent years in the United States.

Although the Oriental rat flea and other Xenopsylla species are important vectors of Y. pestis, there are at least 125 species of fleas that are capable of transmitting the pathogen. In North America, several flea species can transmit the plague bacterium to native rodents; Oropsylla montana (Fig. 7.2E) and perhaps Hoplopsyllus anoma-lus (Fig. 7.2G) are the more important among these. In Russia and northern Asia, fleas belonging to the genera Citellophilus, Neopsylla, and Ctenophthalmus are significant enzootic vectors within rodent communities. In addition, the widespread fleas P. irritans and N.fasciatus are capable of transmitting plague bacilli. Because X. cheopis survives poorly in cool climates, historical réévaluations suggest that, contrary to former dogma, P. irritans, rather than X. cheopis, may have been the principal flea vector of T. pestis in the great plague epidemics of northern Europe.

FIGURE 7.15 Blockage of midgut of Oriental rat flea (Xenopsytta cheopis) by mass of Yersinia pcstis, the causative agent of plague. (Courtesy of US Public Health Scrvice.)

A susceptible flea typically becomes infected after imbibing plague bacilli in its blood meal from an infected host. The bacterium invades the flea midgut, where under suitable conditions it multiplies rapidly, often culminating in complete blockage of the gut anterior to the proventricular spines. This proventricular blockage (Fig. 7.15) results from clumping of the bacteria 8-51 days after ingestion. Although some gut blockages may clear spontaneously, persistent blockage of the flea gut is central to efficient transmission of T. pcstis. Fleas with blockages are incapable of ingesting a blood meal from a host. Feeding attempts by these fleas result in the drawing of blood into the flea esophagus, followed by regurgitation of the blood meal into the host. This regurgitation is caused by the elastic recoil action of the esophagus when resistance from the proventricular blockage is reached. Infection results when plague bacilli are regurgitated with the blood meal into the host.

Fleas with gut blockages are hungry and make repeated, aggressive feeding attempts. This can result in the infection of several different hosts and amplification of an epidemic. A single T.pestisgene can determine whether or not proventricular blockage forms in infected X. cheopis, whereas another gene determines whether a flea midgut infection will develop. Unless the gut blockage clears, the infected flea ultimately succumbs to starvation, dehydration, or toxicity from bacterial metabolites, itself becoming a victim of plague. As with most other pathogens transmitted by fleas, plague bacilli do not pass through the gut wall of infected fleas to invade the hemocoel, salivary glands, or other organs.

Key environmental parameters influence the establishment of plague foci throughout the world. For example, X. cheopis is principally a denizen of drier habitats, and it is in these zones that the major plague foci have persisted. Where environmental factors tend to keep the

FIGURE 7.16 Plague patient with enlarged axillary lymph node, or bubo, characteristic of bubonic plague. (Courtesy of US Public Health Service.)

number of flea species in a given area low, plague is generally absent or rare. If the ambient temperature exceeds 28°C, plague-infected fleas often can clear their guts of blockages, and the disease does not develop to epidemic proportions.

There are three recognized clinical types of plague infection: bubonic, septicemic, and pneumonic plague. The most common of these is bubonic plague, which usually results from the bites of infected fleas but can result from handling infectious mammalian carcasses. This type of plague is characterized by grossly enlarged, tender, peripheral lymph nodes called buboes (singular bubo). They usually occur in the axillary or inguinal region (Fig. 7.16) and are typically teeming with plague bacilli.

In septicemic plague the pathogen initially bypasses or overwhelms the peripheral lymph nodes and invades deeper recesses of the body. Although internal buboes may develop, they are not easily detected. Instead, the bloodstream is invaded rapidly by the bacterium, and capillary walls start to leak, often turning the skin black. The absence of external buboes to aid diagnosis, coupled with swift invasion of the blood, make this form of plague especially severe, with many patients succumbing to fatal septicemia.

The most life-threatening form of the disease is pneumonic plague, in which patients have a lung infection of T. pestis and can cough or sneeze viable bacteria into the air. Inhalation of T, pestis by susceptible individuals results in the pulmonary form of this disease. Also, bubonic or septicemic plague can progress to pneumonic plague. Without prompt and aggressive medical attention, pneumonic plague is invariably fatal; some untreated patients die within a day of inhaling the pathogen. The severe pathogenicity of T. pestis is largely caused by endotoxins and exotoxins released by the dividing bacilli.

Flea-transmitted infection typically results in classic bubonic plague, in which buboes develop after an incubation period of 2—6 days. Accompanying symptoms are severe headache, fever, and shaking chills. Without treatment, most patients deteriorate rapidly, with a typical mortality rate of 50-60%. Septicemic plague is a particularly dangerous form of the disease because the incubation time is only 2—5 days and external buboes are absent. Pneumonic plague has a very short incubation period (1—3 days) and may spread rapidly from one victim to another. Overwhelming pneumonia characterized by coughing, bloody sputum, chills, and fever usually result in death within 3 days unless specific medication is administered within 15-18 hr of the onset of symptoms. Pneumonic plague spreads directly, and usually rapidly, from person to person without the involvement of flea vectors. In some cases, humans have contracted pneumonic plague after inhaling aerosolized bacilli expelled by infected household cats. Accurate diagnosis is important in identifying plague-infected patients. Various biochemical, serological, chromatographic, and staining tests, or lysis with a specific bacteriophage, are typically employed to detect T. pestis or specific antibody directed against it in humans, animals, or fleas. DNA probes and polymerase chain reaction (PCR) techniques used to amplify specific nucleotide sequences of T. pestis are becoming routine screening tools in many public health laboratories. A fiberoptic biosensor also has been developed to detect a specific antigen of T. pestis.

The treatment of plague patients usually involves immediate hospitalization, isolation, and administration of broad-spectrum antibiotics. Formalin-inactivated plague vaccines are available. They are not, however, totally effective. None is currently protective against pneumonic plague in humans, and most must be administered in multiple doses or at regular intervals to ensure protection.

Efforts to control plague typically involve removal of wild-rodent reservoir hosts and/or their fleas. In areas of potential plague activity, samples of rodent blood and tissues often are collected in order to monitor plague in reservoir host populations. Fleas also can be collected and screened for T. pestis. If samples are positive, then rodent and flea control measures should be considered.

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