Epidemiology of Vector-Borne Diseases

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COMPONENTS OF TRANSMISSION CYCLES

The components of a transmission cycle of an arthropodborne disease are (1) a vertebrate host which develops a level of infection with the parasite that is infectious to a vector, (2) an arthropod host or vector that acquires the parasite from the infected host and is capable of transmission, and (3) one or more vertebrate hosts that are susceptible to infection with the parasite after being fed upon by the vector (Fig. 2.1). Vector-borne parasites have evolved

Components of the transmission cycle of an anthroponosis such as malaria or louse-borne typhus. (Original by Margo Duncan)

mechanisms for tolerating high constant body temperatures and evading the complex immune systems of the vertebrate hosts as well as for tolerating variable body temperatures and avoiding the very different defensive mechanisms of the arthropod vectors. Asexual parasites, such as viruses and bacteria, employ essentially the same life form to infect both vertebrate and arthropod hosts, whereas more highly evolved heterosexual parasites, such as protozoa and helminths, have different life stages in their vertebrate and arthropod hosts. Some asexual parasites, such as the plague bacillus, intermittently may bypass the arthropod host and be transmitted directly from one vertebrate host to another.

Among sexually reproducing parasites, the host in which gametocyte union occurs is called the definitive host, whereas the host in which asexual reproduction occurs is called the intermediate host. Vertebrates or arthropods can serve as either definitive or intermediate hosts, depending upon the life cycle of the parasite. For example, humans are the definitive host for the filarial worm, Wuchereria bancrofti, because adult male and female worms mate within the human lymphatic system, whereas the mosquito vector, Culex quinquefasciatus, is the intermediate host where development occurs without reproduction. In contrast, humans are the intermediate host of the Plasmodium protozoan that causes malaria, because only asexual reproduction occurs in the human host; gametocytes produced in the human host unite only in the gut of the definitive mosquito host.

A disease is the response of the host to infection with the parasite and can occur in either vertebrate or arthropod hosts. Immunity includes all properties of the host that confer resistance to infection and play an important role in determining host suitability and the extent of disease or illness. Some species or individuals within species populations have natural immunity and are refractory to infection. Natural immunity does not require that the host have previous contact with the parasite, but it may be age dependent. For example, humans do not become infected with avian malaria parasites, even though infective Culex mosquito vectors feed frequently on humans. Conversely, mosquitoes do not become infected with the measles or poliomyelitis viruses that infect humans, even though these viruses undoubtedly are ingested by mosquitoes blood feeding on viremic hosts.

Individuals within populations become infected with parasites, recover, and in the process actively acquire immunity. This acquired immunity to the parasite ranges from transient to lifelong and may provide partial to complete permanent protection. A partial immune response may permit continued infection but may reduce the severity of disease, whereas complete protection results in a cure and usually prevents immediate reinfection.

Acquired immunity may be humeral and result in the rapid formation of antibodies, or it may be cellular and result in the activation of T cells and macrophages. Antibodies consist of five classes of proteins called immunoglobulins that have specific functions in host immunity. Immunoglobulin G (IgG) is most common, comprising over 85% of the immunoglobulins present in the sera of normal individuals. The IgGs are relatively small proteins and typically develop to high concentrations several weeks after infection; they may persist at detectable and protective levels for years. In contrast, IgMs are large macroglobulins that appear shortly after infection but decay rapidly. For the laboratory diagnosis of many diseases, serum samples typically are tested during periods of acute illness and convalescence, 2 to 4 weeks later. A fourfold increase in parasite-specific IgG antibody concentration in these paired sera provides diagnostic serological evidence of infection. The presence of elevated concentrations of IgM presumptively implies current or recent infection. T cells and macrophages are several classes of cells that are responsible for the recognition and elimination of parasites. In long-lived vertebrate hosts, acquired immunity may decline over time, eventually allowing reinfection.

Clinically, the host response to infection ranges from inapparent or asymptomatic to mildly symptomatic to acute. Generally it is beneficial for the parasite if the host tolerates infection and permits parasite reproduction and/or development without becoming severely ill and dying before infecting additional vectors.

THE VERTEBRATE HOST

One or more primary vertebrate hosts are essential for the maintenance of parasite transmission, whereas secondary or incidental hosts are not essential to maintain transmission but may contribute to parasite amplification. Amplification refers to the general increase in the number of parasites present in a given area. An amplifying host increases the number of parasites and therefore the number of infected vectors. Amplifying hosts typically do not remain infected for long periods of time and may develop disease. A reservoir host supports parasite development, remains infected for long periods, and serves as a source of vector infection, but it usually does not develop acute disease.

Attributes of a primary vertebrate host include accessibility, susceptibility, and transmissibility.

Accessibility. The vertebrate host must be abundant and fed upon frequently by vectors. Host seasonality, diel activity, and habitat selection determine availability in time and space to host-seeking vectors. For example, the avian hosts of eastern equine encephalomyelitis (EEE) virus generally begin nesting in swamps coincidentally with the emergence of the first spring generation of the mosquito vector, Culiseta melanura, thereby bringing EEE virus, susceptible avian hosts, and mosquitoes together in time and space. Diel activity patterns also may be critical. For example, larvae (microfilariae) of W. bancrofti move to the peripheral circulatory system of the human host during specific hours of the night that coincide with the biting rhythm of the mosquito vector, Cx. quinquefasciatus. Historically, epidemics of vector-borne diseases have been associated with increases in human accessibility to vectors during wars, natural disasters, environmental changes, or human migrations.

Susceptibility. Once exposed, a primary host must be susceptible to infection and permit the development and reproduction of the parasite. Dead-end hosts either do not support a level of infection sufficient to infect vectors or become extremely ill and die before the parasite can complete development, enter the peripheral circulatory system or other tissues, and infect additional vectors. Ideal reservoir hosts permit parasites to survive in the peripheral circulatory system (or other suitable tissues) in sufficient numbers for sufficiently long time periods to be an effective source for vector infection. Asexual parasites, such as viruses and bacteria, typically produce intensive infections that produce large numbers of infectious organisms for relatively short periods during which the host either succumbs to infection or develops protective immunity. In the case of EEE virus, for example, 1 ml of blood from an infected bird may contain as many as 101~ virus particles during both day and night for a 2- to 5-day period; birds that survive such infections typically develop long-lasting, protective immunity. In contrast, highly evolved parasites produce comparatively few individuals during a longer period. W. bancrofti, for example, maintains comparatively few microfilaria in the bloodstream (usually < 10 microfilaria per cubic millimeter of blood), which circulate most abundantly in the peripheral blood during periods of the day when the mosquito vectors blood feed. However, because both the worms and the human host are long-lived, transmission is enhanced by repeated exposure rather than by an intense parasite presentation over a period of a few days. Infection with > 100 microfilaria per female mosquito may prove fatal for the vector; therefore, in this case, limiting the number of parasites that infect the vector may increase the probability of transmission.

Transmissibility. Suitable numbers of susceptible vertebrate hosts must be available to become infected and thereby maintain the parasite. Transmission rates typically decrease concurrently with a reduction in the number of susceptible (i.e., nonimmune) individuals remaining in the host population. The epidemic threshold refers to the number of susceptible individuals required for epidemic transmission to occur, whereas the endemic threshold refers to the number of susceptible individuals required for parasite persistence. These numerical thresholds vary depending on the immunology and dynamics of infection in the host population. Therefore, suitable hosts must be abundant and either not develop lasting immunity or have a relatively rapid reproductive rate, ensuring the rapid recruitment of susceptibles into the population. In the case of malaria, for example, the parasite elicits an immune response that rarely is completely protective, and the host remains susceptible to reinfection. In contrast, encephalitis virus infections of passerine birds typically produce lifelong protection, but bird life expectancy is short and the population replacement rate is rapid, ensuring the constant renewal of susceptible hosts.

THE ARTHROPOD VECTOR

Literally, a vectoris a “carrier” of a parasite from one host to another. An effective vector generally exhibits characteristics that complement those listed above for the vertebrate hosts and include host selection, infection, and transmission.

Host selection. A suitable vector must be abundant and feed frequently upon infective vertebrate hosts during periods when stages of the parasite are circulating in the peripheral blood or other tissues accessible to the vector. Host-seeking or biting activity during the wrong time or at the wrong place on the wrong host will reduce contact with infective hosts and reduce the efficiency of transmission. Patterns of host selection determine the types of parasites to which vectors are exposed. Anthropophagic vectors feed selectively on humans and are important in the transmission of human parasites. Anthropophagic vectors which readily enter houses to feed on humans or to rest on the interior surfaces are termed endophilic (literally, “inside loving”). Vectors which rarely enter houses are termed exophilic (i.e., “outside loving”). Zoophagic vectors feed primarily on vertebrates other than humans. Mammalophagic vectors blood feed primarily on mammals and are important in the maintenance of mammalian parasites. In contrast, ornithophagic vectors feed primarily on avian hosts and are important in the maintenance of avian parasites. There is a distinction between vectors attracted to a host and those which successfully blood feed on the host. Mammalophagic vectors therefore represent a subset of those mammalophilic vectors that are attracted to mammalian hosts.

Infection. The vector must be susceptible to infection and survive long enough for the parasite to complete multiplication and/or development. Not all arthropods that ingest parasites support parasite maturation, dissemination, and transmission. For example, the mosquito Cx. quinquefasciatus occasionally becomes infected with western equine encephalomyelitis (WEE) virus; however, because this virus rarely escapes the midgut, this species rarely transmits WEE virus. Some arthropods are susceptible to infection under laboratory conditions, but in nature they seldom feed on infected vertebrate hosts and/or survive long enough to allow parasite development. The transmission rate is the number of new infections per unit of time and is dependent upon the rate of parasite development to the infective stage and the frequency of blood feeding by the vector. Because many arthropod vectors are poildlothermic and contact their homeothermic vertebrate hosts intermittently, parasite transmission rates frequently are dependent upon ambient temperature. Therefore, transmission rates for many parasites are more rapid at tropical than at temperate latitudes, and at temperate latitudes they progress most rapidly during summer. The frequency of host contact and, therefore, the transmission rate also depend upon the life history of the vector. For example, epidemics of malaria in the tropics transmitted by a mosquito that feeds at 2-day intervals progress faster than epidemics of Lyme disease at temperate latitudes, where the spirochetes are transmitted to humans principally by the nymphal stage of a hard tick vector that may have one generation and one blood meal per life stage per year.

Transmission. Once infected, the vector must exhibit a high probability of refeeding on one or more susceptible hosts to ensure the transmission of the parasite. Diversion of vectors to nonsusceptible or dead-end hosts dampens transmission effectiveness. The term zooprophylaxis (literally, “animal protection”) arose to describe the diversion of Anopheles infected with human malaria parasites from humans to cattle, a dead-end host for the parasites. With zooprophylaxis the dead-end host typically exhibits natural immunity, in which host tissues are unacceptable to parasites and do not permit growth or reproduction. Alternatively, transmission to a dead-end host may result in serious illness, because the host-parasite relationship has not coevolved to the point of tolerance by the dead-end host. WEE virus, for example, can cause serious illness in humans, which are considered to be a dead-end host because they rarely produce a viremia sufficient to infect mosquitoes.

MODES OF TRANSMISSION

The transmission of parasites by vectors may be vertical or horizontal. Vertical transmission is the passage of parasites directly to subsequent life stages or generations within vector populations. Horizontal transmission describes the passage of parasites between vector and vertebrate hosts.

VERTICAL TRANSMISSION

Three types of vertical transmission are possible within vector populations: transstadial, transgenerational, and venereal transmission.

Transstadial transmission is the sequential passage of parasites acquired during one life stage or stadium through the molt to the next stage(s) or stadium. Transstadial transmission is essential for the survival of parasites transmitted by mites and hard ticks that blood feed once during each life stage and die after oviposition. Lyme disease spirochetes, for example, that are acquired by larval ticks must be passed transstadially to the nymphal stage before transmission to vertebrates.

Transgenerational transmission is defined as the vertical passage of parasites by an infected parent to its offspring. Some parasites may be maintained transgenerationally for multiple generations, whereas others require horizontal transmission for amplification. Transgenerational transmission normally occurs transovarially (through the ovary) after the parasites infect the ovarian germinal tissue. In this situation most of the progeny are infected. Other parasites do not actually infect the ovary and, although they are passed on to their progeny, transmission is not truly transovarial. This situation is usually less efficient and only a small percentage of the progeny are infected. Transgenerational transmission in vectors such as mosquitoes also must include transstadial transmission, because the immature life stages do not blood feed.

Venereal transmission is the passage of parasites between male and female vectors and is relatively rare. Venereal transmission usually is limited to transovarially infected males who infect females during insemination, which, in turn, infect their progeny during fertilization.

La Crosse virus (Fig. 2.2) is an example of a vertically maintained parasite where the arthropod host serves as the reservoir. This virus is maintained by transgenerational transmission within clones of infected Aedes triseriatus mosquitoes and is amplified by horizontal transmission among squirrels and chipmunks. Because this temperate mosquito rarely has more than two generations per year, La Crosse virus spends long periods in infected vectors and relatively short periods in infected vertebrate hosts. Females infected vertically or horizontally transmit their infection transovarially to first-instar larvae. These larvae transmit the virus transstadially through the four larval stadia and the pupal stage to the adults. These transgenerationally infected females then take a blood meal and oviposit infected eggs, often in the same tree hole from which they emerged. Some blood meal

Modes of transmission of a vertically maintained parasite, La Crosse encephalitis virus.

hosts become viremic and amplify the number of infected Ae. triseriatus females by horizontal transmission. Venereal transmission of the virus from transgenerationally infected males to uninfected females has been demonstrated in the laboratory and may serve to establish new clones of infected females in nature.

HORIZONTAL TRANSMISSION

Horizontal transmission is essential for the maintenance of almost all vector-borne parasites and is accomplished by either anterior (biting) or posterior (defecation) routes. Anterior-station transmission occurs when parasites are liberated from the mouthparts or salivary glands during blood feeding (e.g., malaria parasites, encephalitis viruses, filarial worms). Posterior-station (or stercorarian) transmission occurs when parasites remain within the gut and are transmitted via contaminated feces. The trypanosome that causes Chagas disease, for example, develops to the infective stage within the hindgut and is discharged onto the host skin when the triatomid vector defecates during feeding. Irritation resulting from salivary proteins introduced into the host during feeding causes the host to scratch the bite and rub the parasite into the wound. Louse-borne relapsing fever and typhus fever rickettsia also employ posterior-station modes of transmission.

There are four types of horizontal transmission, depending upon the role of the arthropod in the life cycle of the parasite: mechanical, multiplicative, developmental, and cyclodevelopmental.

Mechanical transmission occurs when the parasite is transmitted among vertebrate hosts without amplification or development within the vector, usually by contaminated mouthparts. Arthropods that are associated intimately with their vertebrate hosts and feed at frequent intervals have a greater probability of transmitting parasites mechanically. The role of the arthropod is essentially an extension of contact transmission between vertebrate hosts. Eye gnats, for example, have rasping, sponging mouthparts and feed repeatedly at the mucous membranes of a variety of vertebrate hosts, malting them an effective mechanical vector of the bacteria which cause conjunctivitis or “pink eye.” Mechanical transmission also may be accomplished by contaminated mouthparts if the vector is interrupted while blood feeding and then immediately refeeds on a second host in an attempt to complete the blood meal.

Multiplicative (or propagative) transmission occurs when the parasite multiplies asexually within the vector and is transmitted only after a suitable incubation period is completed. In this case, the parasite does not undergo metamorphosis and the form transmitted is indistinguishable from the form ingested with the blood meal. St. Louis encephalitis (SLE) virus, for example, is not transmitted until the virus replicates within and passes through the midgut, is disseminated throughout the hemocoel, and enters and replicates within the salivary glands. However, the form of the virus does not change throughout this process.

Developmental transmission occurs when the parasite develops and metamorphoses, but does not multiply, within the vector. Microfilariae of W. bancrofti, for example, are ingested with the blood meal, penetrate the mosquito gut, move to the flight muscles, where they molt twice, and then move to the mouthparts, where they remain until they are deposited during blood feeding. These filarial worms do not reproduce asexually within the mosquito vector; i.e., the number of worms available for transmission is always equal to or less than the number ingested.

Cyclodevelopmental transmission occurs when the parasite metamorphoses and reproduces asexually within the arthropod vector. In the life cycle of the malaria parasite, for example, gametocytes that are ingested with the blood meal unite within the mosquito gut and then change to an invasive form that penetrates the gut and forms an asexually reproducing stage on the outside of the gut wall. Following asexual reproduction, this stage ruptures and liberates infective forms that move to the salivary glands, from where they are transmitted during the next blood meal.

The extrinsic incubation period is the time interval between vector infection and parasite transmission when the parasite is away from the vertebrate host. The intrinsic incubation period is the time from infection to the onset of symptoms in the vertebrate host. Repeated lag periods of consistent duration between clusters of new cases at the onset of epidemics were first noticed by early epidemiologists who coined the term extrinsic incubation. These intervals actually represent the combined duration of extrinsic and intrinsic incubation periods.

The duration of the extrinsic incubation period is typically temperature dependent. The rate of parasite development normally increases as a linear degree-day function of ambient temperature between upper and lower thresholds. After being ingested by the mosquito vector, WEE virus, for example, must enter and multiply in cells of the midgut, escape the gut, be disseminated throughout the hemocoel, and then infect the salivary glands, after which the virus may be transmitted by bite. Under hot summer conditions, this process may be completed within 4 days, and the vector mosquito, Cx. tarsalis, is capable of transmitting the virus during the next blood meal. In contrast, under cooler spring conditions transmission may be delayed until the third blood meal. Some parasites may increase the frequency of vector blood feeding and thereby enhance transmission. The plague bacillus, for example, remains within and eventually blocks the gut of the most efficient flea vector, Xenopsylla cheopis. Regurgitation occurs during blood feeding, causing vector starvation and, therefore, transmission at progressively more closely spaced intervals before the vector succumbs to starvation.

TRANSMISSION CYCLES

Transmission cycles vary considerably depending upon their complexity and the role of humans as hosts for the parasite. A vector-borne anthroponosis is a disease resulting from a parasite that normally infects only humans and one or more anthropophagic vectors (Fig. 2.1). Malaria, some forms of filariasis, and louse-borne typhus are examples of anthroponoses with transmission cycles that involve humans and host-specific vectors. Humans serve as reservoir hosts for these parasites, which may persist for years as chronic infections. Vectors of anthroponoses selectively blood feed upon humans and are associated with domestic or peridomestic environments. Widespread transmission of an anthroponosis with an increase in the number of diagnosed human cases during a specified period of time is called an epidemic. When human cases reappear consistently in time and space, transmission is said to be endemic.

Zoonoses are diseases of animals that occasionally infect humans. Likewise, ornithonoses are diseases of wild birds that are transmitted occasionally to humans. In most vector-borne zoonoses, humans are not an essential component of the transmission cycle, but rather become infected when bitten by a vector that fed previously on an infected animal host. Although humans frequently become ill, they rarely circulate sufficient numbers of parasites to infect vectors and thus are termed dead-end hosts. The enzootic transmission cycle is the basic, or primary, animal cycle (literally “in animals”). When levels of enzootic transmission escalate, transmission may become epizootic (an outbreak of disease among animals). Transmission from the enzootic cycle to dead-end hosts is called tangential transmission (i.e., at a tangent from the basic transmission cycle). Often different vectors are responsible for enzootic, epizootic, and tangential transmission. Bridge vectors transmit parasites tangentially between different enzootic and dead-end host species. Human involvement in zoonoses may depend on the establishment of a secondary amplification cycle among vertebrate hosts inhabiting the peridomestic environment.

WEE virus is a zoonosis that exemplifies primary and secondary transmission cycles and tangential transmission to man and equines (Fig. 2.3). In California, WEE virus amplification occurs in a primary enzootic transmission cycle that consists of several species of passerine birds and Cx. tarsal# mosquitoes. In addition to birds, Cx. tarsalis blood feed on a variety of mammals, including rabbits. Rabbits, especially jackrabbits, develop sufficient viremia to infect some Cx. tarsalis and Ae. melanimon mosquitoes, thereby initiating a secondary zoonotic transmission cycle. WEE virus activity in the secondary Aedes-rabbit cycle usually has been detected after

Components of the transmission cycles of a zoonosis such as western equine encephalomyelitis (WEE) virus. (Original by Margo Duncan)

amplification in the primary Cx. tarsalis-bird cycle. Both Cx. tarsalis and Ae. melanimon transmit the virus tangentially to humans and equines, which are dead-end hosts for the virus.

INTERSEASONAL MAINTENANCE

An important aspect of the ecology of vector-borne parasites is the mechanism(s) by which they persist between transmission seasons or outbreaks. Parasite transmission typically is most efficient when weather conditions are suitable for vector activity and population growth. In temperate latitudes, overwintering of parasites becomes problematic when vertebrate or arthropod hosts either enter a winter dormancy or migrate. Similar problems face tropical parasites when transmission is interrupted by prolonged dry or wet seasons. The apparent seasonality that is characteristic of most vector-borne parasites may be due to either the periodic amplification of a constantly present parasite or to the consistent reintroduction of parasites following focal extinction.

Mechanisms of parasite maintenance during periods of unfavorable weather include the following:

Continued transmission by vectors. During periods of unfavorable weather, vectors may remain active and continue to transmit parasites, although transmission rates may be slowed by cold temperature or low vector abundance. In temperate latitudes with cold winters, transmission may continue at a slow rate, because the frequency of blood feeding and rate ofparasite maturation in the vector is diminished. In tropical latitudes, widespread transmission may be terminated during extended dry seasons that reduce vector abundance and survival. In both instances, transmission may be restricted spatially and involve only a small portion of the vertebrate host population. Human infections during adverse periods usually are highly clumped and may be restricted to members of the same household.

Infected vectors. Many vectors enter a state of dormancy as non-blood-feeding immatures or adults. Vertically infected vectors typically remain infected for life and therefore may maintain parasites during periods when horizontal transmission is interrupted. California encephalitis virus, for example, is maintained during winter and drought periods within the transovarially infected eggs of its vector, Ae. melanimon. Infected eggs of this floodwater mosquito may remain dormant and infected for up to several years and are able to withstand winter cold, summer heat, and extended dry periods. Inundation of eggs during spring or summer produces broods of adult mosquitoes that are infected at emergence. Similarly, vectors that inhabit the nests of migratory hosts such as cliff swallows often remain alive and infected for extended periods until their hosts return.

Infected vertebrate hosts. Parasite maintenance may be accomplished by infected reservoir hosts that either continue to produce stages infective for vectors or harbor inactive stages of the parasite and then relapse or recrudesce during the season when vectors are blood feeding. Adult filarial worms, for example, continue to produce microfilariae throughout their lifetime, regardless of the population dynamics or seasonality of the mosquito vector. In contrast, some Korean strains of vivax malaria overwinter as dormant stages in the liver of the human host and then relapse in spring, concurrent with the termination of diapause by the mosquito vector(s).

Alternatively, parasites may become regionally extinct during unfavorable weather periods and then are reintroduced from distant refugia. Two possible mechanisms may allow the reintroduction of parasites:

Migratory vertebrate hosts. Many bird species overwinter in the tropics and return to temperate or subarctic breeding sites each spring, potentially bringing with them infections acquired at tropical or southern latitudes. It also is possible that the stress of long flights and ensuing reproduction triggers relapses of chronic infections. In addition, many large herbivores migrate annually between summer (or wet) and winter (or dry) pastures, bringing with them an array of parasites. Rapid longrange human or commercial transportation is another possible mode for vector and parasite introduction. The seasonal transport of agricultural products and the movements of migratory agricultural workers may result in the appearance of seasonality.

Weather fronts. Infected vectors may be carried long distances by prevailing weather fronts. Consistent weather patterns, such as the sweep of the southeastern monsoon from the Indian Ocean across the Indian subcontinent, may passively transport infected vectors over hundreds of kilometers. The onset of WEE virus activity in the north central United States and Canada has been attributed to the dispersal of infected mosquitoes by storm fronts.

VECTOR INCRIMINATION

To understand the epidemiology of vector-borne disease, it is essential to establish which arthropod(s) is/are the primary vector(s) responsible for parasite transmission. Partial or incomplete vector incrimination has resulted in the misdirection of control efforts at arthropod species that do not play a substantial role in either enzootic maintenance or epidemic transmission. Vector incrimination combines field and laboratory data that measure field infection rates, vector competence, and vectorial capacity.

Infection rates. The collection of infected arthropods in nature is an important first step in identifying potential vectors, because it indicates that the candidate species feeds on vertebrate hosts carrying the parasite. Infection data may be expressed as a percentage at one point in time or an infection prevalence (i.e., number of vectors infected/number examined x 100). The more commonly employed infection rate refers to infection incidence and includes change over a specified time period. When the infection prevalence is low and arthropods are tested in groups or pools, data are referred to as a minimum infection rate (number of pools of vectors positive/ total specimens tested/unit of time x 100 or 1000). Minimum infection rates are relative values with ranges delineated by pool size. For example, minimum infection rates of vectors tested in pools consisting of 50 individuals each must range from 0 to 20 per 1000 females tested.

It is important to distinguish between infected hosts harboring a parasite and infective hosts capable of transmission. In developmental and cyclodevelopmental vectors, the infective stages may be distinguished by location in the vector, morphology, or biochemical properties. Distinguishing infective from noninfective vectors is difficult, if not impossible, with viral or bacterial infections, because the parasite form does not change. The ability to transmit may be implied by testing selected body parts, such as the cephalothorax, salivary glands, or head. With some tick pathogens, however, parasite movement to the mouthparts does not occur until several hours after attachment. As mentioned previously, the transmission rate is the number of new infections per time period. When standardized per unit of population size, the transmission rate may be expressed as an incidence. The annual parasite incidence is the number of new infections per year per 1000 population.

The entomological inoculation rate is the number of potentially infective bites per unit of time. This frequently is determined from the human or host biting rate and the proportion of vectors that are infective and is calculated as bites per human per time period x infectivity prevalence.

Vector competence is defined as the susceptibility of an arthropod species to infection with a parasite and its ability to transmit this acquired infection. Vector competence is determined quantitatively by feeding the candidate arthropod vector on a vertebrate host circulating the infective stage of the parasite, incubating the bloodfed arthropod under suitable ambient conditions, refeeding the arthropod on a noninfected susceptible vertebrate host, and then examining this host to determine if it became infected. Because it often is difficult to maintain natural vertebrate hosts in the laboratory and control the concentration of parasites in the peripheral circulatory system, laboratory hosts or artificial feeding systems frequently are used to expose the vector to the parasites. Susceptibility to infection may be expressed as the percentage of arthropods that became infected among those blood feeding. When the arthropod is fed on a range of parasite concentrations, susceptibility may be expressed as the median infectious dose required to infect 50% of blood-fed arthropods. The ability to transmit may be expressed either as the percentage of feeding females that transmitted or the percentage of hosts that became infected.

Failure of a blood-fed arthropod to become infected with or transmit a parasite may be attributed to the presence of one or more barriers to infection. For parasites transmitted by bite, the arthropod midgut provides the most important barrier. Often parasites will grow in a nonvector species if they are inoculated into the hemocoel, thereby by-passing this gut barrier. After penetrating and escaping from the midgut, the parasite then must multiply and/or mature and be disseminated to the salivary glands or mouthparts. Arthropod cellular or humeral immunity may clear the infection at this point, creating a dissemination barrier. Even after dissemination to the salivary glands, the parasite may not be able to infect or be transmitted from the salivary glands due to the presence of salivary gland infection or salivary gland escape barriers, respectively.

For parasites transmitted at the posterior station, vector competence may be expressed as the percentage of infected vectors passing infective stages of the parasite in their feces.

The concept of vectorial capacity summarizes quantitatively the basic ecological attributes of the vector relative to parasite transmission. Although developed for mosquito vectors of malaria parasites and most easily applied to anthroponoses, the model provides a framework to conceptualize how the ecological components of the transmission cycle of many vector-borne parasites interact.

Vectorial capacity is expressed by the formula:

C= ma2(pn)/(-lnP),

where C is the vectorial capacity as new infections per infection per day, ma is the bites per human per day, a is the human biting habit, P is the probability of daily survival, and n is the extrinsic incubation period (in days).

The biting rate (ma) frequently is estimated by collecting vectors as they attempt to blood feed and is expressed as bites per human per day or night (e.g., 10 mosquitoes per human per night). The human biting habit (a) combines vector feeding frequency and host selection. The feeding frequency is the length of time between blood meals and frequently is expressed as the inverse of the length of the gonotrophic cycle. Host selection patterns are determined by testing blood-fed vectors to determine what percentage fed on humans or the primary reservoir. Therefore, if the blood feeding frequency is 2 days and if 50% of host-seeking vectors feed on humans, a = (1/2 days) x (0.5) = 0.25. In this example, ma 2 = 10 bites/human/night x 0.25 = 2.5; a is repeated because infected vectors must refeed to transmit.

The probability of the vector surviving through the extrinsic incubation period of the parasite, pn, requires information on the probability of vector survival (P) and the duration of the extrinsic incubation period (n). P is estimated either vertically, by age-grading the vector population, or horizontally, by marking cohorts and monitoring their death rate over time. In Diptera, P may be estimated vertically from the parity rate (proportion of parous females per number examined). In practice, P = (parity rate) 1/~, where g is the length of the gonotrophic cycle. The extrinsic incubation period may be estimated from ambient temperature from data gathered during vector competence experiments by testing the time from infection to transmission for infected vectors incubated at different temperatures. Continuing our example, if P = 0.8 and n = 10 days, then the duration of infective life is Pn/(-lnP) = 0.81~ x 0.8) = 0.48. Therefore C = 2.5 x 0.48, or 1.2 parasite transmissions per infective host per day.

SURVEILLANCE

The number of cases of most vector-borne diseases typically varies over both time and space. Information on the number of cases can be gathered from morbidity and mortality records maintained by state or national governmental agencies for the human population. Morbidity data are records of illness, whereas mortality data are records of the cause of death. These data vary greatly in their quality and timeliness, depending upon the accuracy of determining the cause of illness or death and the rapidity of reporting. In the United States, the occurrence of confirmed cases of many vector-borne diseases, including yellow fever, plague, malaria, and encephalitis, must by law be reported to municipal health authorities. However, infections with many arthropod-borne parasites, including Lyme disease and the mosquito-borne encephalitides, frequently are asymptomatic or present variable clinical symptoms and therefore remain largely undiagnosed and underreported. The frequency of case detection and accuracy of reporting systems are dependent on the type of surveillance employed and the ability of the medical or veterinary community to recognize suggestive symptoms and request appropriate confirmatory laboratory tests. In addition, some laboratory tests vary in their specificity and sensitivity, thus complicating the interpretation of laboratory results. Cases may be classified as suspect or presumptive, based on the physician’s clinical diagnosis, or confirmed, based on a diagnostic rise in specific antibodies or the direct observation (or isolation) of the parasite from the case. Surveillance for clinical cases may be active or passive.

Active surveillance involves active case detection in which health workers visit communities and seek out and test suspect cases. In malaria control programs, for example, a field worker visits every household biweekly or monthly and collects blood films from all persons with a current or recent fever. Fever patients are treated with antimalarial drugs presumptively, and these suspected cases are confirmed by detection of malaria parasites in a blood smear. Confirmed cases are revisited and additional medication administered, if necessary. This surveillance provides population infection rates regardless of case classification criteria.

Most surveillance programs rely on passive surveillance, which utilizes passive case detection to identify clinical human or veterinary cases. In this system, individuals seeking medical attention at primary health care organizations, such as physicians’ offices, hospitals, and clinics, are diagnosed by an attending physician who requests appropriate confirmatory laboratory tests. However, because many arthropod-borne diseases present a variety of nonspecific symptoms (e.g., headache, fever, general malaise, arthralgia), cases frequently may be missed or not specifically diagnosed. In mosquito-borne viral infections the patient often spontaneously recovers, and cases frequently are listed under fevers of unknown origin or aseptic (or viral) meningitis without a specific diagnosis. In a passive case-detection system, it is the responsibility of the attending physician to request laboratory confirmation of suspect clinical cases and then to notify the regional public health epidemiologist that a case of a vector-borne disease has been documented.

The reporting system for clinical cases of vector-borne diseases must be evaluated carefully when interpreting surveillance data. This evaluation should take into account the disease, its frequency of producing clinically recognizable symptoms, the sensitivity and specificity of confirmatory laboratory tests, and the type and extent of the reporting system. Usually programs that focus on the surveillance of a specific disease and employ active case detection provide the most reliable epidemiological information. In contrast, broad-based community health care systems that rely on passive case detection typically produce the least reliable information, especially for relatively rare vector-borne diseases with nonspecific symptoms.

Diseases that are always present or reappear consistently at a similar level during a specific transmission season are classified as endemic. The number of cases in a population is expressed as incidence or prevalence. Population is defined as the number of individuals at risk from infection in a given geographical area at a given time. Incidence is the number of new cases per unit of population per unit of time. Incidence data are derived from two or more successive samples spaced over time. Prevalence is the frequency of both old and new infections among members of a population. Prevalence typically is determined by a single point in time estimate and frequently is expressed as the percentage of the population tested that was found to have been infected.

The level of parasite endemicity in a population may be graded as hypoendemic (low), mesoendemic (medium), or hyperendemic (high), depending upon the incidence of infection and/or the immune status of the population. In malaria surveys, for example, the percentage of children with palpable spleens and the annual parasite incidence are used to characterize the level of endemicity. In endemic disease, the percentage of individuals with sera positive for IgG-class antibodies typically increases as a linear function of age or residence history, whereas in hypoendemic disease with intermittent transmission, this function is disjunct, with certain age groups expressing elevated positivity rates. The occurrence of an extraordinarily large number of human infections or cases is termed an epidemic. Health agencies, such as the World Health Organization, typically monitor incidence data to establish criteria necessary to classify the level of endemicity and to decide when an epidemic is under way. A geographically widespread epidemic on a continental scale is called a pandemic.

Serological surveys(or serosurveys) are a useful epidemiological tool for determining the cumulative infection experience of a population with one or more parasiteand host-related factors affecting the efficiency or risk of transmission, and reinfection rates. When coupled with morbidity data, serosurveys provide information on the ratio of apparent to inapparent infections. Random sampling during serosurveys representatively collects data on the entire population and may provide ecological information retrospectively by analysis of data collected concurrently with each serum sample. This information may assign risk factors for infection, such as sex, occupation, and residence history, or it may help in ascertaining age-related differences in susceptibility to disease. Stratified sampling is not random and targets a specific cohort or subpopulation. Although stratified samples may have greater sensitivity in detecting rare or contiguously distributed parasites, the data are not readily extrapolated to infection or disease trends in the entire population. Repeated serological testing of the same individuals within a population can determine the time and place of infection by determining when individuals first become seropositive, i.e., serologically positive with circulating antibodies against a specific parasite. This change from seronegative to seropositive is called a seroconversion.

Forecasting the risk of human infection usually is accomplished by monitoring environmental factors, vector abundance, the level of transmission within the primary and/or amplification cycles, and the numbers of human or domestic animal cases. As a general rule, the accuracy of forecasting is related inversely to the time and distance of the predictive parameter from the detection of human cases. Surveillance activities typically include the time series monitoring of environmental conditions, vector abundance, enzootic transmission rates, and clinical cases.

Environmental conditions. Unusually wet or warm weather may indicate favorable conditions for vector activity or population increases, concurrently increasing the risk of parasite transmission. Parameters frequently monitored include temperature, rainfall, snow pack (predictive of vernal flooding), and agricultural irrigation schedules.

Vector abundance. Standardized sampling at fixed sites and time intervals can be used to compare temporal and spatial changes in vector abundance that are useful in detecting an increased risk of parasite transmission. Extraordinary increases in vector abundance and survival may forecast accurately increased enzootic transmission and, to a lesser extent, epidemics.

Enzootic transmission rates. Monitoring the level of parasite infection in vector or vertebrate populations provides direct evidence that the parasite is present and being actively transmitted (Fig. 2.4). The level of transmission usually is directly predictive of the risk of human or domestic animal involvement. Enzootic transmission activity may be monitored by vector infection rates, vertebrate-host infection rates, sentinel seroconversion rates, and clinical cases.

Vector infection rates. Sampling vectors and testing them for parasites determines the level of infection in the vector population (Fig. 2.4, C and D). When vectors are tested individually, prevalence data are expressed as percentages; e.g., 10 females infected per 50 tested is a 20% infection rate. When combined with abundance estimates, infection rates also may be expressed as infected vectors per sampling unit per time interval; 100 bites per human per night x 0.2 infection rate – 20 infective bites per human per night. These data provide an index of the transmission rate. When infection rates are low and vector populations large, vectors usually are tested in lots or pools. It is statistically advantageous to keep the pool size constant and thus keep the chance of detecting

Mosquito-borne encephalitis surveillance in southern California. (A) Coop with 10 sentinel chickens; (B) Taking blood sample from chicken; (C) Hanging mosquito trap on permanent standard (components from left to right are trap motor and fan assembly with collecting carton, dry-ice bait in a Styrofoam container, and battery); (D) Sorting mosquito collections by species to estimate relative abundance.

infection the same. Because there may be more than one infected vector per pool, infection rates are expressed as a minimum infection rate = positive pools/total individuals tested x 100 or 1000.

Vertebrate-host infection rates. Introduced zoonoses, such as sylvatic plague in North American rodents, frequently produce elevated mortality that may be used to monitor epizootics of these parasites over time and space. In contrast, endemic zoonoses rarely result in vertebrate host mortality. Testing reservoir or amplifying hosts for infection is necessary to monitor the level of enzootic parasite transmission. Stratified sampling for these parasites (directly by parasite isolation or indirectly by seroprevalence) usually focuses on the young of the year to determine ongoing transmission. For example, examining nestling birds for viremia can provide information on the level of enzootic encephalitis virus transmission.

Monitoring the incidence of newly infected individuals in a population over time is necessary to detect increased transmission activity. Because many parasites are difficult to detect or are present only for a limited time period, sampling frequently emphasizes the monitoring of seropositivity. Monitoring the IgM antibody, which rises rapidly after infection and decays relatively quickly, can indicate the level of recent infection, whereas monitoring the IgG antibody documents the population’s historical experience with the parasite. Sampling, marldng, releasing, recapturing, and resampling wild animals is most useful in providing information on the time and place of infection in free-roaming animal populations.

Sentinel seroconversion rates. Sentinels typically are animals that can be monitored over time to quantify the prevalence of a parasite. Trapping wild animals or birds is labor intensive, and determining seroprevalence may provide little information on the time and place of infection, especially if the host has a large home range. To circumvent this problem, caged or tethered natural hosts or suitable domestic animals of known infection history are placed in sensitive habitat and repeatedly bled to detect infection. A suitable sentinel should be fed upon frequently by the primary vector species, be easy to diagnose when infected, be unable to infect additional vectors (i.e., not serve as an amplifying host), not succumb to infection, and be inexpensive to maintain and easy to bleed or otherwise sample for infection. Chickens, for example, are useful sentinels in mosquito-borne encephalitis virus surveillance programs (Fig. 2.4, A and B). Flocks of seronegative chickens are placed at farmhouses and then bled weekly or biweeldy to determine seroconversions to viruses such as WEE or SLE. Because the chickens are confined and the date of seroconversion known, the time and place of infection is determined, while the number seroconverting estimates the intensity of transmission.

Clinical cases. Detecting infection among domestic animals may be an important indication that an epizootic transmission is under way and that the risk of human infection has become elevated. Domestic animals often are more exposed to vectors than are humans and thus provide a more sensitive indication of parasite transmission. Clinical human cases in rural areas in close association with primary transmission cycles may be predictive of future epidemic transmission in urban settings.

Vector-borne diseases frequently affect only a small percentage of the human population, and therefore vector control remains the intervention method of choice. Control programs attempt to maintain vector abundance below thresholds necessary for the transmission of parasites to humans or domestic animals. When these programs fail, personal protection by repellents or insecticideimpregnated clothing, bed nets, or curtains is often the only recourse. Vaccination may be a viable alternative method of control for specific vector-borne diseases, if the vaccine imparts lasting immunity as in the case of yellow fever virus. However, many parasites, such as malaria, have evolved to the point where infection elicits a weak immune response that provides only shortterm and marginal protection. The need for continued revaccination at short intervals severely limits their global usefulness, especially in developing countries. Although breakthroughs in chemotherapy have been useful in case management, it remains the mandate of the medical/ veterinary entomologist to devise strategies which combine epidemiological and ecological information to effectively reduce or eliminate the risk of vector-borne diseases.

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