FIGURE 12.35 Section of horse brain (cerebrum) infected with eastern equine encephalomyelitis virus, showing neutrophil invasion around capillary, (Photo by J. D. Patterson.)

WEE viruses, immunization has reduced the frequency of horse cases.

Venezuelan equine encephalomyelitis (VEE) Complex

Encephalomyelitis in equids caused by viruses of the VEE complex occurs in northern South America, Central America, and Mexico. The epizootic viruses are transmitted by many species of mosquitoes (see Table IV) among horses, burros, and mules. These animals develop a viremia sufficient to infect the mosquitoes. Consequently, VEE epidemics can be maintained by transmission between mosquitoes and horses, differing in this regard from WEE and EEE, for which horses are largely dead-end hosts. An epidemic strain of VEE virus was first isolated in 1938 from a horse in Venezuela. In 1969, a large outbreak of VEE involving both equids and humans in Central America spread northward in the succeeding 2 years through Mexico, and in 1971 it spread across the border into Texas (Pan American Health Organization, 1972). Cases continued in Mexico through 1972. There were thousands of horse cases throughout this region during that time. Epizootic virus activity did not occur again in the region until an outbreak in Venezuela in 1992—1993 and in Chiapas, Mexico, in 1993. Another outbreak of VEE occurred in northern Colombia and Venezuela in 1995. The rapidity of spread of these outbreaks over large geographic areas is undoubtedly due to the role of both horses and birds as competent reservoir hosts. It is expedited by the evacuation of horses, already infected but not yet ill, away from an epizootic area.

Japanese encephalitis (JE) virus

Encephalitis caused by JE virus occurs in widespread parts of Asia, including Malaysia and Indonesia. In Japan, epizootics and epidemics have occurred in August and September in many years since the discovery of this disease in 1935 in that country. The virus was isolated from brain tissue of a horse in 1937. JE virus causes acute infection in horses and swine. It is particularly an economic problem because of the importance of swine as a food source and market commodity in rural Asia. Pigs develop viremia sufficient for mosquito transmission, therefore serving as important amplifying hosts, and may develop encephalitic symptoms. Transplacental infection causes stillbirth and abortion. Infected boars may become sterile.

Rift Valley fever (RVE) virus

This pathogen has caused epizootics of acute illness, elevated rates of abortion, and death in cattle, goats, and sheep in Egypt and parts of sub-Saharan Africa.

Outbreaks in Egypt and Mauritania were particularly noteworthy. The virus is both viscerotropic and neurotropic in these animals. Their viremias are of sufficient titer to infect mosquitoes. Disease outbreaks generally have involved thousands to hundreds of thousands of livestock cases, causing substantial economic losses.

Wesselsbron (WSL) virus

This is a flavivirus with distribution in parts of sub-Saharan Africa, Madagascar, and Thailand. It causes a disease similar to that of RVF in sheep and goats and also causes a mild illness in cattle. Infected ewes may abort their fetuses, and lambs suffer high mortality. Humans infected with Wesselsbron virus may develop a febrile illness with rash, fever, and myalgia. The virus is transmitted by Aedes species, including Ae. meintoshi and Ae. circum-luteolus in South Africa.

Fowlpox virus

This virus belongs to a group of poxviruses that infect vertebrates and invertebrates and are classified within the family Poxviridae. Among the poxviruses are those in the bird-infecting genus Avipoxvirus, such as fowlpox, ca-narypox, and pigeonpox viruses. Mosquitoes may mechanically transmit the avipox viruses by contamination of mouthparts and subsequent transfer of infectious virions to noninfected birds. Fowlpox is an important disease of domestic fowl, particularly chickens. It causes development of papules along the comb and beak. While probing these papules, mosquitoes may contaminate their mouthparts with virions. If disturbed during feeding, they may move to another animal to feed, thus transferring the virus to a new host. Another form of fowlpox virus is transmitted directly by droplets of pus containing the virus.

Myxoma virus

This is a leporivirus and the causative agent of myxomatosis, an enzootic disease of lagomorphs in parts of South America and the western United States. It is transmitted mechanically by the bite of arthropods, principally fleas. These viruses produce dermal vascularized tumors. When mosquitoes, fleas, or black flies probe these tumors, the mouthparts become contaminated with virus particles. Later, if the mosquitoes probe another uninfected lagomorph, that animal may become infected. Natural infections of myxoma virus occur without acute disease in rabbits of the genus Sylvilagus in South America and California. However, Old World rabbits (Oryctolagus cuniculus) are highly susceptible to infection and generally die. Outbreaks of acute disease among domesticated Old World rabbits have been documented in South America and California.

Myxoma virus was introduced into Australia in the 1950s as a means of controlling introduced European rabbits, a pest in that country. The virus spread rapidly through the rabbit populations via mechanical transmission by fleas, mosquitoes, and other means and greatly reduced rabbit populations there. The mosquito vectors in Australia are Cx. annulirostris, An. annulipes, and Aedes species.

Many Plasmodium species infect animals other than humans, including reptiles, birds, rodents, and nonhuman primates.

The malarias of reptiles, also called saurian malarias, are caused by a group of 29 Plasmodium species. They infect a wide range of lizards and some snakes in 15 families (Telford, 1994). Vectors are biting midges, phlebotomine sand flies, and Culex mosquitoes. Haemoproteid and leu-cocytozooid malarias also occur in reptiles, but their vectors have not been established.

Malarial infection of birds is widespread geographically (Van Riper et al., 1994). Parasites in three common genera of hemosporine blood parasites of birds (Hepa-tocystis, Haemoproteus, and Leucocytozoon) are transmitted by biting midge, louse fly, and black fly vectors, respectively. The avian malarias in the genus Plasmodium are all mosquito-borne. Plasmodium species that infect birds have been important research models for studying malaria. Indeed, the original observations by Ronald Ross on the role of mosquitoes as malaria vectors were made with bird malaria.

Currently, about 30 species of avian Plasmodium are recognized. However, the taxonomic status of some species is uncertain and others remain to be described. Among the important species that cause disease in domestic fowl or wild birds are Plasmodium gallinaceum (sometimes called chicken malaria), P. hermansi (a parasite of wild and domestic turkeys in the United States), P. relictum, P. lophurae, P. cathemerium, P. circumflexum, and P. elongatum. As with human malarias, there is variation in life cycles and pathogenesis of the avian malarias. This variation is related to intrinsic qualities of the species and to variation in susceptibility among host species, age, and general health status.

A bird becomes infected after inoculation of sporozoites from an infective mosquito. Merogony occurs in bone marrow, in endothelial cells, and in the erythrocytes.

Avian Malarias

Nonhuman Malarias

Reptilian Malarias

In acute infections, these parasites may cause severe anemia, damage to bone marrow tissues, and other pathology that may result in death. Younger birds tend to be more susceptible to overt illness than older birds.

Although Anopheles mosquitoes can be competent laboratory vectors for some bird malarias, field and laboratory data show that culicines in the genera Culex, Culiseta, Aedes, and Ochlerotatus are the natural vectors. In Africa, Ae. aegypti is an important local vector of P.gal-linaceum to chickens. The impact of bird malaria on natural bird populations is poorly known. It was introduced into Hawaii along with exotic birds and Culex mosquitoes and is thought to be responsible for the reduction and extinction of native bird populations there. Bird malaria occasionally has been documented as the cause of morbidity and mortality among penguins in zoos.

Rodent Malarias

The 12 Plasmodium species infecting rodents, called rodent or murine malarias, all occur in Africa and Asia. The vectors are assumed to be Anopheles mosquitoes, but in most cases the vector species is unknown. P. berghei, P. vinckei, P. yoelli, P. chabaudi, and P. aegyptensis parasitize African murine rodents. The first two are transmitted by An. dureni in Zaire, and P. vinckei is transmitted by An. cinctus in Nigeria. P. atheruri infects the African brush-tailed porcupine (Atherurus africanus) and is transmitted by An. smithii. P. anomaluri, P. landauae, and P. pulmophilum occur in African flying squirrels (Anomalurus spp.); An. machardyi is the probable vector of the P. atheruri. The three species of Plasmodium found in Asian flying squirrels are P. booliati, P. watteni, and P. incertae. The significance of rodent malarias to the health and population dynamics of their natural hosts is largely unknown, although the prevalences of infection can be high. They have become important laboratory models for human malaria, particularly in host immunological responses, drug screening studies, and vaccine development. Cox (1993) provides a succinct review of the rodent malarias.

Primate Malarias

The nonhuman primate malarias are caused by a group of 25 Plasmodium species, many of which are closely related to the human malarias (Collins and Aikawa, 1993). Seven of them infect lemurs in Madagascar and are poorly known. All 18 others have life cycles similar to those of the human malarias. Most have a tertian periodicity, but two species (P. brasilianum and P. inui) are quartan and one (P knowlesi) is quotidian; i.e., it has a periodicity of 1 day. Probably all are transmitted by Anopheles mosquitoes, but for 10 of them the vector species are unknown.

Of the 18 well-known primate malaria species, 13 occur in southern or southeastern Asia, where macaques, langurs (leaf monkeys), gibbons, and orangutans are the vertebrate hosts. These plasmodia include P. pitheci in the orangutan, the first nonhuman primate malaria to be described; P. knowlesi, a macaque parasite that has become an important laboratory model for development of human vaccines; and P cynomolgi, a parasite of macaques and langurs that serves as an important model for human P. vivax malaria. The vectors of these Asian primate malarias include An. hackeri, An. dirus, An. balabacensis, An. elegans, and An. introlatus.

Three primate malarias occur in Africa, where P gonderi infects mangabeys and mandrills and P reichenowi and P schwetzi infect chimpanzees and gorillas. Their natural vectors are unknown. Two Plasmodium species infect nonhuman primates in South America. P simium infects howler monkeys and woolly spider monkeys in Brazil. It is similar to the human parasite P malariae. P. brasilianum infects a wide range of New World monkeys in the family Cebidae, including howler monkeys, spider monkeys, woolly spider monkeys, titis, capuchins, woolly monkeys, bearded sakis, and squirrel monkeys. It is similar to the human parasite P vivax. Both South American species are transmitted by An. cruzii, which also is an important vector of human malaria in parts of South America. The larvae inhabit water-filled leaf axils of bromeliad plants at heights of 5 m or more, where the adults are likely to encounter arboreal primates.

Many species of Anopheles are competent laboratory vectors of primate malarias, including An. stephensi, An. maculatus, An. ga-mbiae, and An. dirus, which serve as vectors of human malaria. P knowlesi can infect humans experimentally and can be transmitted by the bite of An. dirus to other humans. P. cynomolgi has infected laboratory workers, and experimental studies showed that mosquito transmission from monkeys to humans, and from humans to humans, can occur. P brasilianum also infects humans. Human malaria due to infection with P brasilianum and P simium possibly occurred as a zoonosis in the New World prior to the arrival of Europeans, with An. cruzii acting as the vector. Alternatively, these two simian parasites might be derived from human Plasmodium species to which they are closely related. Coatney et al. (1971) reviewed the infectivity of nonhuman primate malarias to humans, and Collins and Aikawa (1993) reviewed the primate malarias.

Dog heartworm is caused by the mosquito-borne filarial nematode Dirofilaria immitis, a member of the family

Dog Heartworm

FIGURE 12.36 Dirofilaria immitis adults in right ventricle of dog heart. (Photo from H. D. Newson.)

FIGURE 12.36 Dirofilaria immitis adults in right ventricle of dog heart. (Photo from H. D. Newson.)

Onchocercidae (Boreham and Atwell, 1988). Adult D. immitis occupy the right ventricle of the canine heart and the pulmonary arteries (Fig. 12.36). The worms are 12—31 cm long and form aggregations of up to 50 or more individuals. In large aggregations, infection may extend to the right atrium. Contrary to popular belief, heartworm disease in dogs is not simply a consequence of a heavy worm burden in the ventricle resulting in impedance of blood flow. Rather, it is the result of deleterious changes in the endothelium and integrity of the walls of the pulmonary arteries, leading to pulmonary hypertension and right ventricular hypertrophy. These pathologic changes cause decreased cardiac output to the lungs, weakness, lethargy, chronic coughing, and ultimately congestive, heart failure. Dogs may die if left untreated.

The life cycle of D. immitis involves canids and mosquitoes. Dogs become infected by the bite of a mosquito whose labium carries third-stage larvae. These larvae break out of the labium while it is bent during feeding and are deposited onto the dog's skin, along with a small droplet of mosquito hemolymph from the ruptured labium, Only about 10% of the larvae successfully enter the skin, generally through the hole made by the mosquito's fascicle. They remain in situ subcutaneously, where they molt to fourth-stage larvae. The larvae then migrate to other subcutaneous, adipose, or muscle tissues and molt again to a fifth-stage larva. These worms, now approximately 18 mm long, enter the venous circulation and become established in the heart and pulmonary arteries. Generally, the fifth-stage larvae reach the heart at about 70—90 days after infection.

In the heart and pulmonary arteries, the fifth-stage larvae develop into sexually mature adults. After mating, at 6—7 months, the females begin to release into circulation the microfilariae, active embryonic life stages about 300 ¡xm long and 7 /¿m wide. The microfilaremia varies considerably, from 1,000 to 100,000 microfilariae per milliliter. It is nocturnally subperiodic, with peak concentrations occurring in the peripheral blood in the evening. Some dogs never develop microfilaremia, even though they support D. immitis adults and may have patent disease. These dogs are said to have occult infections.

Mosquitoes become infected with D. immitis when they imbibe blood from a microfilaremic dog. In an average blood meal of 5 /¿I, a mosquito may ingest between 5 and 500 microfilariae. Within 48 hr of ingestion, microfilariae migrate posteriorly in the midgut lumen to the Malpighian tubules and then into the distal cells of these tubules, where they develop intraceilularly to "sausage forms" or first-stage larvae, taking about 4 days at 26°C. Some remain trapped in the midgut. If more than a few begin to develop in the tubules, the mosquito is likely to be killed. The first-stage larvae molt to the second stage at about 8—10 days after ingestion. As they continue to grow they cause swelling and distention of the Malpighian tubules. At 12—14 days after ingesdon, they molt to the third stage. These forms break out of the Malpighian tubules and migrate through the hemolymph to the head and base of the mouthparts, then into the interior of the labium. The mosquito is then infective. The rate of these developmental processes is temperature dependent and varies with factors affecting competence for parasite development.

Vectors of D. immitis differ with geographic region; many mosquito species in several genera are competent to transmit it. Grieve et al. (1983) listed 20 species field-caught in the United States, in the genera Aedes, Ochlero-tatus, Psorophora, Anopheles, and Culex, in which infective-stage larvae of D. immitis have been detected.

Other Filarial Nematodes of Animals

Other species of Dirofilaria infect mammals. These include D. ursi, a bear parasite transmitted by the black fly Simulium venustum; D. roemeri, a wallaroo (a type of small kangaroo) parasite transmitted by the horse fly Dasybasis hebes; and the following mosquito-transmitted Dirofilaria species: Dirofilaria repensm canids; D. caryn-odes and D. magnilarvatum in monkeys; D. scapiceps in rabbits; D. tenuis in raccoons; and D. subdermata in porcupines.

In addition to Dirofilaria species, a large number of filarial nematodes in other genera of the Onchocercidae infect wild and domestic animals. Vectors include mosquitoes and a wide range of other blood-feeding Diptera, lice, fleas, mites, and ticks. The mosquito-borne oncho-cercid nematodes include species in the following genera: Aproctella, Breinlia, Brugia, Cardiofilaria, Conispicu-lum, Dirofilaria, Deraiophoronema, Folyella, Loiana, Molinema, Pelecitus, Oswaldofilaria, Saurositus, Skrjabi-nofilaria, Waltonella, and Wuchereria (Anderson, 1992; Bain and Chabaud, 1986; Hawking and Worms, 1961; Lavoipierre, 1958). Brugia pahangi of jirds (Meriones) is an important laboratory organism for studies on filariasis. B. malayi develops in the peritoneal cavity of gerbils, providing a laboratory infection model.

The four overlapping aims of mosquito control are to prevent mosquito bites, keep mosquito populations at acceptable densities, minimize mosquito-vertebrate contact, and reduce the longevity of female mosquitoes. All of these actions minimize the annoying and harmful effects of bites and blood loss and interrupt pathogen transmission. The eradication of either mosquito species or their associated diseases is no longer viewed as a viable objective, except in small, isolated regions or in the case of recent invasions. Two exemplary failures of the eradication approach, on a grand scale, were the World Health Organization's global malaria eradication program and the Pan American Health Organization's attempt to eradicate Ae. aegypti from the Western Hemisphere. A notable exception was the successful elimination of the African immigrant An. gambiae from Brazil. The more realistic objective of modern mosquito control programs is integrated pest management to reduce mosquito abundance and disease prevalence, using prudent combinations of methods.

Personal protection is the most direct and simple approach to prevention. Outdoor exposure can be avoided during peak mosquito activity, and window screens can prevent mosquito entry into houses and animal shelters. Head nets reduce annoyance and prevent bites about the face and neck. Bed nets, impregnated with synthetic pyrethroid and strung over beds at night, repel mosquitoes and kill those that land on the nets. Impregnated mesh suits with hoods work similarly and can be worn over clothing. Other insecticidal devices create a repellent smoke or vapor that reduces mosquito attack in the immediate vicinity. Chemical repellents applied to skin or clothing prevent mosquitoes from landing or cause them to leave before probing. The most common one is N, N-diethyl-m-toluamide, or DEET.

Organized control provides efficient, area-wide mosquito management at local, regional, or national levels. In the United States, mosquito programs typically are county-level abatement districts. These focus on the control of nuisance and vector species, but they often also participate in surveillance for mosquito-borne disease pathogens. National organizations are usually parts of ministries of health and coordinate their disease and vector control efforts at that level. Especially in developing countries, there is now increasing emphasis on community cooperation, low technology, sustainability, and the integrated use of a variety of control tools that are adapted to local customs, conditions, and resources.

Habitat modification is a traditional and reliable tool in mosquito management. Adult resting places can be rendered unsuitable by harborage alteration. Changes in larval habitat that prevent oviposition, hatching, or larval development are called source reduction. Water is altered or eliminated in a variety of ways. This includes plastic foam beads that provide a floating barrier over latrine water, underground sewage lines, land drainage through ditches or underground tile pipes, waste tire shredding, trash-container disposal and natural container elimination, lids for water-storage barrels, vegetational changes in ponds, altered flow of tidal water through salt marshes, and water-level manipulation in reservoirs and rice fields. Each method is designed to interfere with specific features of a mosquito's natural history. Through appropriate application of ecological principles and an intimate knowledge of mosquito behavior and life cycles, desirable natural wetlands and newly created ones can be modified to minimize mosquito production while benefitting other wildlife.

Biological control of mosquitoes by predators or parasites has been studied extensively and has been reviewed by Chapman (1985), Beaty and Marquardt (1996), and others. Aerial predators, such as dragonflies, birds, and bats, receive much attention but do not specialize in adult mosquitoes and have little if any effect on their densities. Most efforts have been directed at the larval stage. Aquatic predators, both naturally occurring and introduced, include the mosquito fish (Gambusia affinis) and killifish (Fundulus spp.). Other fish, such as grass carp, e.g., Tilapia and Cyprinus, remove aquatic vegetation that provides harborage for larvae. Invertebrate predators include the predatory mosquito Toxorhynchites, several families of aquatic bugs and beetles, predatory copepods, hydras, and turbellarian flatworms; however, none has been implemented with great success. There have been attempts to develop the use of parasites and pathogens of mosquito larvae as control agents, including the nematode Romanomermis culicivorax; protozoans such as the cilia tes Lambornella and Tetrahymena; the gre-garine sporozoan Ascogregarina; and the microsporidian

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