Why are there so many insects?

few reasons. Insects multiply very fast. Most females lay up to 200 eggs in a lifetime. A queen termite can lay more than 30,000 eggs a day! Insects can survive the most difficult conditions on Earth. You can find insects at the North and South Poles and at the equator, in deserts and in jungles, under the ground and high in the air—and almost everywhere in between. Insects are small. This means that each one needs little food and can easily hide from its enemies.

How many kinds of insects are there?

More than one million different species, or kinds. And scientists are still counting. Every year, experts find up to 10,000 new species. They think there may be as many as 30 million species yet to be discovered. At this rate, it will take another 1,000 years to locate and identify all the insect species in the world!

Who has been on Earth longer: insects or humans?

Insects, by far. The oldest insect fossils are at least 400 million years old. Compare that to the earliest humans. They appeared no more than four million years ago.

How many insects live in your backyard?

About 2,000 in every square yard (square meter) of soil. Suppose you dug up 1 square mile (2.6 km2) of land. You’d find more than five and onehalf billion insects. That is about the total number of people in the whole world! Scientists say insects outnumber people one million to one!

Are spiders insects?

No. Spiders belong to another group of small animals, called arachnids (uh-RAK-nidz). Other arachnids include ticks, mites, and scorpions. Unlike insects, spiders have eight legs and only two parts to their body. Also, they have neither wings nor antennae. So never call a spider an insect!

Are flies insects?

Yes. So are ants, bees, ladybugs, mosquitoes, butterflies, moths—and about one million other kinds of small animals. All adult insects have three parts to their body: head, thorax, and abdomen. The head has the eyes, mouth parts, and two antennae, or feelers. On the thorax most insects have six legs and either two or four wings. The abdomen is where the insect digests food and breathes. Even with these three parts, most insects are less than 1/4 inch (6.4 mm) long.

How do flies walk upside down?

Easily! Flies have tiny claws at the ends of their feet that grip the rough spots on ceilings, windows, or walls. Also, their feet have hairy pads covered with a sticky substance that helps them cling to any surface. It’s a little like walking with chewing gum on the bottom of your shoes.

Between the claws and the sticky stuff, flies can walk anywhere they want!

Aflatoxin Poisoning

Aflatoxin poisoning, like botulism poisoning, is a case of food poisoning . However, it is slightly different than the carcass - maggot cycle of botulism poisoning, wherein the wildlife are affected by feeding on toxin - containing insects. In the case of aflatoxin poisoning, the wildlife ingest plant products that contain high levels of afl atoxin. Like botulism, this disease is not truly infectious, but caused by a biotoxin.

So what is the role of insects in this disease? Aspergillus fungi develop in cereal grains when plants are stressed or damaged. Hot, dry weather is stressful to plants, as is damage by insects, hail, and early frost. The products normally affected by aflatoxin are cereal grains and oil seeds, particularly corn, rice, sorghum, cottonseed and peanuts. Insects also serve to move the fungus around from plant to plant in the field, or within stored grains as they feed. Even aflatoxin - free grain can become heavily contaminated if it is not stored properly after harvest. Insect infestation in stored grain causes increase in moisture levels within grain. Increased moisture levels facilitate growth of fungi including Aspergillus , and production of heat, which promotes more growth of Aspergillus , as optimal growth of this fungus occurs at 26 – 32 ° C.

How important is aflatoxin poisoning to free - ranging waterfowl? Following are some examples of poisoning in the USA. In the winter of 1977 – 1978, approximately 7500 ducks and geese were killed in Texas following ingestion of crop residue, with corn and rice recovered from the digestive tract of the dead birds containing 500 ppb of AFB 1 . Similarly, in 1998 – 1999 approximately 10,000 waterfowl died in Louisiana after eating affected corn. Corn intended for consumption by mature poultry is not allowed to have over 200 ppb of aflatoxin, so clearly these wild birds ingested too much aflatoxin. Survey of residual corn in farmers ’ fields, or planted for wildlife, has shown that such grain may contain high levels of aflatoxin. For example, 32% of the corn growing near the Mississippi Sandhill Crane National Wildlife Refuge was found to contain over 200 ppb of AFB 1 , and corn grown in southern Georgia and northern Florida to provide food for quail and other wildlife was found to contain up to 1200 ppb of AFB 1 . Corn used to feed deer in North Carolina and South Carolina was found to contain 750 ppb of AFB 1 , and even birdseed sold for home bird feeding has been found to contain aflatoxin.

Considerable potential exists for wildlife to be poisoned unintentionally by cultivated crops. Indeed, it is estimated that 25% of the world ’ s food supply of grains is contaminated with aflatoxin, with contamination being higher in developing than industrialized countries. Also, the rate of aflatoxin infection is higher in warm, wet production areas such as the southeastern USA, where phytophagous insects abound. Numerous species have been poisoned by afl atoxins, including fi sh, birds, and mammals. Young animals are more susceptible than old animals, and animals such as rats and rabbits that metabolize the metabolites rapidly are more susceptible than those that metabolize the aflatoxin slowly. Serious poisonings have involved snow geese, Chen caerulescens ; Ross ’ s geese, Chen rossi ; greater white - fronted geese, Anseralbifrons ; mallards, Anas platyrhynchos ; northern pintails, Anasacuta ; and ring - necked pheasants, Phasianus colchicus , among others.

Avian Botulism

Although bacteria are often transmitted when insects feed on their wildlife hosts, transmission of the toxin that causes avian botulism can occur in a different manner. Avian botulism is the most signifi cant disease of migratory birds, especially waterfowl and shorebirds. Not surprisingly, it was formerly called ‘ duck sickness. ’ The bacterial complex known as Clostridium botulinum produces protein neurotoxins that cause food poisoning when animals (or humans) eat toxin - laden food. There are several different neurotoxins produced by Clostridium , with type C 1 being most common among birds, though loons and gulls are typically affected by type E toxin. Although over 250 species of birds have been found to experience botulism poisoning (scavengers such as vultures and crows seem to be resistant), it is filter feeding, dabbling, and fish - eating birds that are especially likely to ingest toxin. Apparently, the poison originates with invertebrates and plants living under anaerobic (depleted of oxygen) conditions in marshes and mud flats, because these bacteria only develop under anaerobic conditions. Decomposing vertebrate carcasses also support high levels of toxin production, producing a secondary form of poisoning called the carcass - maggot cycle of botulism . Decomposing animals are a very suitable substrate for growth of Clostridium , as decomposition also generates anaerobic conditions and the high temperatures that favor bacterial growth and toxin production. The dead animals are not attractive to waterfowl, but these birds will readily ingest any mature fly larvae (maggots) that disperse from the carcass, and most maggots do move a considerable distance as they leave the carcass and search for dry pupation sites.

Maggots developing in carcasses can have very high levels of toxin, and cause death to birds that feed upon them. Thus, all that is needed to initiate a prolonged cycle of botulism poisoning is initial death of some animals following a storm, collision with power transmission lines, algal poisoning, or feeding on invertebrates or decaying plant material rich in Clostridium. The bacteria normally found within the bodies of animals in wet habitats are then free to multiply in their carcasses, which are then assimilated into blowflies, which are fed upon by other birds, which then die and become available to more blowflies. Thus, outbreaks of botulism can originate in several ways, and persist for long periods. It is important to note that the animals are not killed because they became infected with the Clostridium botulinum bacterium, they die after ingesting their chemical metabolites, which happen to be poisonous neurotoxins. Thus, Avian Botulism is not really an infectious disease, but a biotoxin, and not quite comparable to most bacterial diseases.

Plague

Yersinia pestis affecting mammals is called plague, and is renowned for causing three pandemics that killed about 200 million people in past centuries. This disease, and its hosts and vectors, have had profound effects on human history. The first pandemic, known as the Justinian Plague , affected the Byzantine Empire, specifi cally Egypt, the Middle East, and Mediterranean Europe. It lasted from about 540 to 700 A.D. and caused about a 50% – 60% reduction in human populations in the affected area. The second pandemic, called the Black Death , occurred in the 1300s and killed about 75 million people, or about one - third of the people in Europe. The third (unnamed) pandemic started about 1855 in China, but was soon spread to seaports in many countries around the world. India was particularly affected, realizing about 12.5 million deaths in 20 years. It was during this outbreak that the bacterial cause of the disease was discovered. It was not until 1908 that the involvement of rats was established, though it was suspected for centuries because massive deaths of rats typically preceded the occurrence of disease in humans. Technically, the third pandemic has not been terminated as there are continuing cases, particularly in Vietnam, where up to 250,000 cases are estimated to have occurred in the second half of the 1900s. Thus, plague remains an occasional problem, especially in less developed countries. Plague outbreaks typically subside when most susceptible hosts perish, or surviving hosts develop immunity.

Among humans, this bacterium causes three forms of plague, based on the nature of the infection. Bubonic Plague is transmitted by fleas to the skin, swellings called buboes occur, and lymph nodes are commonly affected. Septicemic Plague occurs when the flea injects the bacilli directly into a capillary vein, and the infection becomes general rather than localized in the lymph system. Pneumonic Plague , is caused by transmission of the bacilli through coughing or sputum following involvement of the lungs.

Plague normally resides in wildlife, specifically rodents, and is transmitted by fl eas. Virtually all mammals can become infected with the pathogen, though susceptibility varies widely, and nearly all non - rodent and non - lagomorph species are considered to be incidental hosts. Maintenance of the plague at relatively low levels in wild rodents is sometimes referred to as Sylvatic Plague or Campestral Plague . In the USA, it persists at low levels in arid western rural environments but occasionally erupts to attain higher levels, even affecting humans in urban environments as far east as New York City. In the enzootic cycle the reservoir consists of 30 – 40 species of rodents, with birds, rabbits, carnivores, and primates unaffected. In urban areas, outbreaks usually involve urban rats. Outbreaks based on urban rat hosts is referred to as Murine Plague . Around the world, more than 200 species of rodents can be affected.

Lyme Disease

Lyme Disease, the clinical manifestation of Lyme borreliosis,
is a chronic, debilitating disease of humans,
and presently infects more humans than any other
tick - borne infection. Lyme borreliosis is caused by the
spirochaete Borrelia burgdorferi and is transmitted by hard ticks in the genus Ixodes . The important vector species vary geographically: I. scapularis and I. pacificus are the important species in the eastern and western regions of North America, respectively, whereas I. ricinus and I. persulcatus are the important species in Europe and Asia, respectively. Lyme disease now occurs in most temperate areas of the Holarctic region, and also from Australia and occasionally from South America and Africa. Lyme borreliosis has become increasingly important to humans in recent years due to increased contact between ticks borne on wildlife, and humans. Due to its increased prevalence, it is often designated an emerging pathogen.

The host range of Lyme borreliosis is impressive, with over 50 species of wild mammals known to support the pathogen. The important mammalian reservoirs in North America are eastern cottontail, Sylvilagus fl oridanus ; wood rats, Neotoma spp.; kangaroo rats, Dipodomys californicus ; white - footed mice, Permyscus leucopus ; eastern chipmunks, Tamias striatus ; black rat, Rattus rattus ; and Norway rat, Rattus norvegicus . In Europe, the important mammalian reservoirs include mountain hare, Lepus timidus ; squirrels, Sciurus spp.; wood mice, Apodemes sylvaticus ; yellow - necked mice, Apodemes fl avicollis ; bank voles, Clethrionomys glareolus ; and Eurasian hedgehog, Erinaceus europaeus . Also, a number of birds support the bacterium, including ring - necked pheasant, Phasianus colchicus ; wild turkey, Meleagris gallopavo ; Atlantic puffi n, Fratercula arctica ; house wren, Troglodytes aedon ; robin, Erithacus rubcula ; yellowthroat, Geothlypis trichas ; song sparrow, Melospiza melodia ; house sparrow, Passer domesticus ; and orchard oriole, Icterus spurious . Migratory birds are important in spreading the disease and ticks. Adult ticks feed on larger animals, and various deer are favored. Although the deer are not good hosts for the bacteria, they are important because they are the principal source of nutrition for ticks that are already infected with B. burgdorferi . Often overlooked is the potential role of lizards and other reptiles to support ticks. However, research in Hungary showed that lizards were common hosts for Ixodes ricinus . Further, Borrelia burgdorferi was found in several species of lizards. The Lyme disease cycle is shown diagrammatically in Fig. 8.2 .

Vectors of this disease are said to be three - host ticks because they take three blood meals, each from a separate vertebrate host. They feed as a larva, again as a nymph, and then as an adult. Fully fed (replete) female ticks detach from their fi nal host to oviposit, and larvae hatch from the eggs. Typically, larvae ingest the bacteria during their fi rst blood meal but are not capable of transmitting disease, whereas nymphs and adults developing from these infected larvae can infect new hosts. Nymphs and larvae usually feed on the same hosts; thus, nymphs are important in continuing the cycle because they inoculate vertebrate hosts that are fed upon by uninfected larval ticks. Rodents and some birds are persistently infected and fed upon by a high proportion of the immature tick population. In contrast, lizards and deer do not become persistently infected so do not act as such important reservoirs of the disease.

The primary site of infection is typically the skin, and a small infl ammatory response at the site is normal. The spirochaetes soon spread to the lymph, blood, heart, bone and other organs. Signs of infection generally are absent from naturally infected wildlife, and most wildlife seem to tolerate the infection, though some mice display neurological disturbances. In general, there is no impact of B. bergdorferi on wildlife populations. In contrast, skin rash, arthritis and cardiac disease are prevalent in humans following infection.

The key to protecting humans from Lyme disease is personal protection. Hikers should seek to avoid tick infested habitats, wear light clothing to enable detection of ticks, wear long pants and sleeves to minimize skin exposure, tuck pants into boots to keep ticks away from skin, use insect repellents, and search for and remove ticks regularly. Tick control is of limited value. Habitat modifi cation is useful if it decreases contact of humans with wildlife, and the ticks borne by wildlife.

Anaplasmosis

This disease is caused by rickettsiae in the genus Anaplasma , with A. marginale the best known, and found throughout the tropical and subtropical regions of the world. It is an infectious, but not contagious, disease of ruminant animals that is transmitted mostly by ticks, but to a much lesser degree by tabanid fl ies. The host range of Anaplasma is considerable, including deer, Odocoileus spp.; elk, Cervus elaphus ; giraffe, Giraffa camelopardalis ; pronghorn, Antilocapra americana ; American bison, Bison bison ; cape buffalo, Syncerus caffer ; Asian water buffalo, Bubalus bubalis ; wildebeest, Connochaetes spp.; bighorn sheep, Ovis canadensis ; and many African antelope species in addition to domestic cattle, sheep, and goats.

Anaplasma infect erythrocytes (red blood cells) exclusively, causing anemia and reduced hemoglobin concentrations due to damage to the erythrocytes. However, although domesticated ruminants are quite susceptible to infection, wild ruminants are quite resistant. In either type of ruminant, survivors that have been exposed to acute anaplasmosis usually regain normal hematologic parameters, and possess antibodies for some time.

Cattle, and to a lesser degree sheep, are affected by anaplasmosis. Wild ruminants, though substantially immune, play a major role in maintenance and spread of the disease. As noted previously, ticks are largely responsible for inoculating domesticated livestock, and when wild and domesticated animals share the same pastures, the wild animals become a problem for ranchers. Only where effective tick vectors are absent is the problem diminished.

Tularemia

The bacterium Francisella tularensis affects primarily lagomorphs (rabbits and hares) and rodents in the northern hemisphere, especially western North America, central Europe, and the former USSR, but also in Asia and Africa. However, it has a broad host range, affecting 190 species of mammals and 23 species of birds in addition to a few amphibians and numerous invertebrates. Among the more important hosts in North America are hares, Lepus spp.; New World rabbits, Sylvilagus spp.; water voles, Arviocola sp.; muskrat, Ondatra zibithecus ; American beaver, Castor canadensis ; lemmings, Lemmus spp.; voles, Microtus spp.; hamster, Cricetus cricetus ; and red - backed voles, Myodes spp. In Europe, the disease is common among European brown hare, Lepus europaeus ; varying hare, Lepus timidus ; common vole, Microtus arvalis ; house mouse, Mus musculus ; common shrew, Sorex araneus ; and others. Birds are relatively resistant, though gallinaceous game bird species such as grouse, as well as hawks, owls, and some waterfowl are susceptible.

Francisella tularensis is a highly infectious agent that enters the body in several ways, but primarily via inoculation by blood - feeding arthropods. Other routes of infection include inhalation of aerosols or handling and ingestion of contaminated water or meat. Among the important arthropod vectors are mosquitoes, fleas, tabanid flies, and ticks. A number of ticks from several genera are associated with transmission. Tularemia is primarily an acute disease, infecting the blood and causing infl ammation and necrosis in wildlife. The liver, spleen, bone marrow, and lungs are affected.

In western North America, various host and vector systems are evident. In the eastern USA, cottontail rabbit, Sylvilagus fl oridanus , is infected by ticks and biting fl ies, with tularemia serving as a regulatory mechanism for rabbit populations. In Canada and northern USA, however, muskrat, Ondatra zibethicus, and American beaver, Castor canadensis , are most affected, with the disease apparently water - borne. In both cases, humans are also at risk, both from tick bites and from handling rabbits. The effect on wildlife populations, especially beaver, is signifi cant in North America. In Europe, a different pattern occurs, with the vertebrate host primarily hares and the vector primarily mosquitoes.

Tularemia is rarely a problem for domesticated animals, though cats, dogs, horses, and sheep are occasionally affected. However, it is an issue for humans in areas where tularemia occurs. In some cases, it is advisable to delay the hunting season until cold weather reduces the density of ticks, and the probability of human infection. Also, trappers handling wildlife need to be aware of the risk. Finally, wildlife managers need to be sensitive to the population shifts due to incidence of tularemia, and may need to adjust harvest quotas in furbearers.

Bacteria

Bacteria are small, but not nearly so small as viruses. They are single - celled organisms. Bacteria are prokaryotes , which means that they do not have a cell nucleus or other membrane - bound organelles. They contain a single chromosome with double - stranded DNA. Some bacteria are saprophytic, and others are parasites. Some survive for years under adverse environmental conditions. Traditionally, they are divided into one of two groups based on their staining characteristics when exposed to the ‘ gram stain. ’ Bacteria that stain blue are said to be gram - positive; bacteria that stain pink are said to be gram - negative. Bacteria multiply rapidly in infected organisms, but can be eliminated by the host’s immunological system. Rickettsiae are small, gram - negative, intracellular bacteria that cannot live outside the cell, so unlike many bacteria they cannot be cultured on artifi cial media. They are variable in form but often rod - shaped, have DNA, RNA, and cell walls. Due to their small size, they were once thought to be viruses or positioned somewhere between viruses and bacteria. They are found in one family (Rickettsiae) and several genera (e.g., Rickettsia , Ehrlichea , and Anaplasma ). They are natural parasites of certain arthropods (lice, fleas, ticks, mites) and mammals, and cause many important diseases in humans and animals. Spirochaetes are also gram - negative bacteria, but are motile and free - living. Table 8.2 shows some bacteria that involve wildlife and insects.

The role of insects in transmitting bacteria is quite important for some diseases, but not for others. For example, avian cholera is a very important disease of birds, affecting over 190 species around the world, and sometimes causing massive death in both wild and domestic birds. About 35 species of ducks, geese and swans are susceptible, though this is the most susceptible group, with fewer than 10 species known to be susceptible in each of the following: wading birds, gallinaceous birds, doves and pigeons, woodpeckers, shorebirds, hawks and eagles, and owls. Transmission occurs principally by inhalation of aerosols (droplets), or ingestion of contaminated food or water. However, insects such as chewing lice, poultry mites, soft ticks, and tabanid flies have been shown to harbor and transmit the bacterium. Likewise, avian tuberculosis can be found in fowl tick ( Argas persicus ) and its feces, so it is implicated in mechanical transmission, though this is thought to be of little consequence as compared to direct contact among birds and contamination of food and water. In some cases, such as with heartwater, long - distance relocation of wildlife by humans can result in movement of the disease, and the ticks that vector it effectively, because the host animals are not sufficiently screened prior to transport.

Hemorrhagic Disease

This disease is caused both by bluetongue virus and epizootic hemorrhagic disease virus, with the results of infection referred to collectively as hemorrhagic disease. These are similar orbiviruses in the family Reoviridae, and exist as many strains that differ in pathogenicity. Biting midges (Diptera: Certatopogonidae) of the genus Culicoides are the only known vectors of this disease, though many different species are involved around the world.

The name ‘ bluetongue ’ is based on the tendency of the tongue and mucosal membranes to turn blue, a result of cyanosis. This also can occur with epizootic hemorrhagic disease infection. Other common signs of infection include an arched back, lameness, and painful or cracked hooves in affected animals. Affected animals can appear disoriented, weak and staggering, or asymptomatic but followed by sudden death. Death may result from congestion of the lungs, necrosis, and internal hemorrhaging. The digestive tract and the organs are typically involved, including the kidneys, thymus, spleen, and lymph nodes. Reproduction is also affected, resulting in aborted or stillborn animals, particularly livestock. Because the viruses can be transmitted in semen, mandatory testing of semen is required prior to artifi cial insemination. Thus, economic loss results from the disease in livestock, the inability to export semen to countries that lack the disease, and from reduced abundance of wildlife.

Hemorrhagic disease affects wild and domestic ruminants in many parts of the world, including temperate and tropical areas. In the USA, disease is most prevalent in the western and southeastern states. Cattle and sheep are especially susceptible to infection, especially in North America. Most sheep and cattle remain asymptomatic, however. Hemorrhagic virus is reported to cause clinical disease in such North American species as white - tailed deer, Odocoileus virginianus ; pronghorn, Antilocapra americana ; bighorn sheep, Ovis canadensis ; elk, Cervus elaphus ; mountain goat, Oreamnos americanus ; and American bison, Bison bison . Hemorrhagic disease is particularly lethal to white - tailed deer and pronghorn. Though much less of a problem thus far, many African species seem to be susceptible to infection, including greater kudu, Tragelaphus strepsiceros ; muntjac, Muntiacus reevsi ; Grant ’ s gazelle, Gazella granti ; gemsbok, Oryx gazella ; sable antelope, Hippostragus niger ; African buffalo, Syncerus caffer ; ibex, Capra ibex ; and others. Antibodies to bluetongue virus have been found in carnivores in Africa, including wild dog, Lycaon pictus ; lion, Panthera leo ; cheetah, Acinonyx jubatus ; spotted hyena, Crocuta crocuta ; and others. It is possible that these carnivorous animals were infected by preying on infected ungulates.

Yellow Fever

Yellow Fever is found in the Americas, Europe and Africa, but is strangely absent from Asia. Formerly, it was quite important in both North and South America, including some cool - weather cities. Currently, it seems to be increasing in importance in Africa, making it not an emerging pathogen, but a re - emerging pathogen. This disease originated in Africa, and likely was introduced to the western hemisphere by the slave trade. In the 1600s – 1800s it caused epidemics in North American cities, including New Orleans, Philadelphia, New York, and Boston in the USA, and Halifax in Canada. Epidemics also occurred in Ireland, Wales, Spain, Uruguay, and Chile. It decimated Napoleon’s army in Haiti in 1802, causing the French to scale back their territorial ambitions in the New World. Yellow Fever virus was the first virus that was shown to be transmitted by a mosquito.

Yellow Fever cycles in both urban and forested (sylvan) environments, though the important hosts and vectors vary among locations. Primates (including grivet, Chlorocebus aethiops ; mangabeys, family Cercopithecidae; bush babies, family Galagidae; baboons, Papio spp.; and chimpanzees, Pan spp.) are the important wild hosts, and yellow fever can be fatal to howler monkeys, Alouatta spp; squirrel monkeys, Saimiri spp.; spider monkeys, Ateles spp.; and owl monkeys, Aotus spp. Typically, infection of monkey populations causes reduction in their density and collapse of the yellow fever epidemic, so the disease moves slowly through the population over a large area, returning after the population is replenished. Mortality among monkeys is much less common in Africa than in the Americas. Other animals such as the anteaters Tamandua tetradactyla and Cyclopes didactylus ; kinkajou, Potos flavus ; and various rodents may be involved as hosts, but their importance is uncertain.


Affected animals display fever, vomiting, pain, dehydration, and prostration, and sometimes hemorrhage including renal failure and death. Human infection produces similar maladies, including liver damage (resulting in jaundice, hence the name ‘ yellow fever ’ ), and up to 75% of affected humans die.

The mosquito Aedes aegypti is often called the yellow fever mosquito due to its association with yellow fever, particularly in urban situations. Aedes aegypti is particularly dangerous due to its affinity for houses, where it enters and feeds while the inhabitants sleep. Although eliminated from South America in the 1930s and 1940s, A. aegypti has recovered and now poses a significant threat to South American urban areas due to its association with yellow fever. In sylvan (forested) sites of the Americas, other Aedes spp., Haemagogus spp., and Sabathes chloropterus are the important vectors. In Africa, other Aedes spp. and Dicermyia spp. transmit the virus among monkeys and to people. Antimosquito programs have brought yellow fever under control in many urban areas, but in rural areas it remains a threat. It is sometimes referred to as ‘ woodcutter ’ s disease ’ due to its association with forested environments and the people who work there.

St. Louis Encephalitis

This virus is common throughout the western hemisphere, and until West Nile Virus was introduced to New York in 1999 it was the mosquito - transmitted disease agent of greatest medical importance in North America. St. Louis Encephalitis is transmitted by Culex mosquitoes in North America. Birds are generally considered to be the most important hosts for amplification of the virus, with the disease transmission cycle typically described as mosquito - bird - mosquito. Nestling birds are considered to be particularly susceptible to infection, possibly because they are confined to the nest and less able to defend themselves from biting mosquitoes. They also display less immunity and display higher levels of viremia than do adults of the same species. Among the birds known to be suitable hosts of St. Louis Encephalitis are northern cardinal, Cardinalis cardinalis ; American robin, Turdus migratorius ; northern bobwhite, Colinus virginianus ; blue jay, Cyanocitta cristata ; northern mockingbird, Mimus polyglottos ; and mourning dove, Zenaidura macroura . In urban environments birds such as the house sparrow, Passer domesticus ; house fi nch, Carpodacus mexicanus ; and European starling, Sturnus vulgaris , are important in virus amplifi cation. Birds inoculated with the virus by mosquitoes quickly develop viremia, allowing other mosquitoes to contract the disease by feeding on the blood of the infected bird, although the virus disappears equally quickly as the birds recover from infection. Thus, the ‘ window of opportunity ’ for mosquitoes is quite short, and disease spread occurs mostly when mosquitoes are very abundant. Outbreak of the disease dissipates as the birds become resistant to the virus. Unlike some other mosquito - borne arboviruses such as Eastern Equine Encephalitis and West Nile Virus, St. Louis Encephalitis does not adversely affect the bird hosts.

Other vertebrates are suspected to be hosts in the southeastern USA, where antibodies were found in Virginia opossum, Didelphis virginiana ; northern raccoon, Procyon lotor ; cotton mouse, Peromyscus gossypinus ; and nine - banded armadillos, Dasypus novemcinctus. Elsewhere, antibodies were found in big brown bat, Eptisicus fuscus ; little brown bat, Myotis lucifugus ; coyote, Canis latrans ; red fox, Vulpes vulpes ; striped skunk, Mephitis mephitis ; jackrabbits, Lepus spp.; deer mouse, Peromyscus maniculatus ; yellow - bellied marmot, Marmota fl aviventris ; and many other vertebrates. The presence of antibodies, though suggestive, does not by itself prove that an animal is an important host because the concentration of virus may be inadequate for successful infection of mosquitoes, or the host may not be attractive to mosquitoes that are important in the spread of disease to humans. A few mammals have been shown experimentally to develop viremia adequate for spread of the virus, including wood rat, Neotoma mexicana ; Audobon ’ s cottontail rabbit, Sylvilagus audubonii ; young (but not old) cotton rat, Sigmodon hispidus ; and least chipmunk, Eutamias minimus .

In Central and South America, the disease is transmitted by at least seven genera of mosquitoes. As in North America, birds seem to be the most important hosts, but the St. Louis Encephalitis virus has also been found in other vertebrates such as vesper mouse, Calomys musculinus ; grass mouse, Akodon arviculoides ; a rice rat, Oryzomys nigripes ; southern opossum, Didelphis marsupialis ; howler monkey, Alouatta nigerrina ; a spider monkey, Atles panisicus ; a three - toed sloth, Bradypus tridactylus ; various bats, and others. Whether or not these non - bird vertebrates are important in disease cycling is not evident, but at the very least these animals provide mosquitoes with blood meals, enhancing mosquito survival and reproduction.

Many vertebrates have become viremic, some consistently, but disease is not apparent in wildlife. In humans, the virus ranges from unapparent infection to coma and fatal encephalitis. However, only about 1% of infections are clinically apparent and most remain undiagnosed. Different strains of the virus exist, and they differ in their ability to cause disease. The young and elderly are more often affected, but typically it is a more severe ailment in the elderly than in the young. St. Louis Encephalitis inflicts neurological damage such as memory loss, paralysis, and deterioration of fine motor skills in humans. The damage is limited to the brain and spinal cord. 

West Nile Virus

West Nile Virus has long been present in Africa, the Middle East, southern Europe, India and southern Asia. It was introduced to the western hemisphere in 1999, in New York, USA, and quickly spread through much of North America, attaining the Pacific coast in 2002. The source of the virus in North America is unknown, but several species of Eurasian birds occasionally migrate to North America, especially to the eastern seaboard of North America, and some may have been infected while in Europe. Among the occasional visitors to North America are Eurasian wigeon, Anas penelope ; green - winged teal, Anas crecca ; ruff, Philomachus pugnax ; little gull, Larus minutus ; and black - headed gull, Larus ridibundus . Alternatively, some seabirds are carried by tropical storms annually from Africa to North America, so this is a possible route of introduction. Birds such as cattle egret, Bubulcus ibis ; black - headed gull, Larus ridibundus ; yellow - legged gull, Larus cachinnans ; little egret, Egretta garzetta ; and gray heron, Ardea cinerea are possibilities. Finally, pet, zoo and domestic birds routinely pass through commercial airports such as J.F. Kennedy International Airport in New York, and could be a source of the virus. Epidemics in humans have occurred in Africa and Europe in addition to North America, and infection can cause fever, myalgia, rash, and encephalitis in some victims. In recent years it has become the most important arbovirus in North America. Its importance is likely to diminish as wildlife and humans develop resistance following exposure to the virus.

West Nile Virus is transmitted to birds principally by ornithophilic (bird - feeding) mosquitoes, although it has been found in other animals, and of course in humans. It also can be transmitted by organ transplant, blood transfusion, transplacental, and transmammary. Wild birds are the primary hosts, with ulex spp. being especially important vectors, and with humans and horses being accidental or ‘ dead - end ’ hosts that do not contribute to continued transmission. Domestic birds, except for geese, generally do not develop sufficient viremia to allow transmission. Domestic geese develop the necessary viremia to amplify transmission, and also suffer mortality. Migratory birds are important in the dissemination of West Nile Virus in temperate regions, and in North America the virus can persist during the winter in southern climates from Florida to California and then be reintroduced to northern areas annually.

In North America, West Nile Virus has become a major mortality factor of corvid birds. American crows, Corvus brachyrhynchos , are especially likely to perish when infected. Crows, blue jays, Cyanocitta cristata , black - billed magpie, Pica pica , and other species of Corvidae account for about 80% – 90% of the infected birds in most dead - bird surveys. Other birds that seem to have suffered signifi cant declines in abundance include American robin, Turdus migratorius ; tufted titmouse, Baeolophus bicolor ; house wren, Troglodytes aedon; chickadee, Poecile spp.; and eastern bluebird, Sialia sialis . However, some other birds seem to be quite susceptible, including various owls and raptors. The mortality of birds in the western hemisphere is much higher than typically occurs in the eastern hemisphere, likely due to the increased virulence in the native birds of the western hemisphere. It appears that most of the birds adversely affected are peridomestic (species that are often found in association with human habitations).

Although corvid birds regularly test positive for West Nile Virus, and often die, this does not mean that they are the most important species in maintaining the virus or enhancing dispersal in North America. American crows, for example, though very susceptible, typically comprise a small proportion of the bird community in an area, rarely exceeding 10%. Also, birds differ greatly in their attractiveness to mosquitoes, which affects the transmission potential. Field studies in the eastern USA have shown that American robin, Turdus migratorius , is highly preferred, being fed upon 16 times more often than if mosquitoes displayed no preference, and that virus antibodies are present in over 40% of the robins, documenting exposure to the virus. Importantly, it was estimated that nearly 60% of the infected mosquitoes became infected by feeding on virus - infected robins. In contrast, house sparrow, Passer domesticus , is avoided by mosquitoes and less than 20% showed evidence of exposure. Fish crow, Corvus ossifragus , also is highly selected by mosquitoes and fed upon more often than would be expected. However, their low level of abundance, like that of American crow, precludes them from being important in the epidemiology of the virus. Thus, variability in host - feeding behavior by mosquitoes, host suitability for virus amplification, and bird host abundance all interact to affect disease potential.

An assessment of birds important in introducing West Nile Virus to Europe from Africa, amplifying the virus, and enhancing its spread, suggested that perhaps 100 of the 300 bird species considered may play a role in West Nile epidemiology. Among the potentially important species are cattle egret, Bubulcus ibis ; gulls, Larus spp.; barn swallow, Hirundo rustica ; house martin, Delichon urbica ; common swift, Apus apus; common nightingale, Luscinia megarhynchos ; crows, Corvus spp.; blackcap, Sylvia atricapilla ; and European starling, Sturnus vulgaris . Further research will certainly show that not all are equally important. As in North America, Culex spp. mosquitoes seem most important in disease transmission.

West Nile Virus is not limited to birds, though it is best known as a pathogen of birds. Among other animals infected are eastern fox squirrel, Sciurus niger ; black bear, Ursus americanus ; white - tailed deer, Odocoileus virginianus ; and American alligator, Alligator mississippiensis . It is likely that the list of non - bird hosts will grow as the disease becomes further established in North America.

Avian Pox

This widespread disease, also known as fowl pox and bird pox, affects a large number of bird families and is found throughout the world. Infection causes localized proliferation of epithelial cells and production of lesions. In many cases it is only a mild affliction, and does not result in death. However, when the eyelids or mucous membranes of the oral or respiratory cavities are affected, mortality among infected birds can be high. It is a greater problem when population densities of birds are high, as among flocking birds and in zoos. There are a number of strains involved in this disease. It is most abundant in warm and moist regions, and occurs most commonly when mosquitoes are numerous, as they vector the disease.

Distribution and prevalence of this disease are determined by a number of factors, including weather, vector abundance, host abundance, and the strains present. It is a slow - developing disease that is manifested in the presence of pox lesions (wart - like growths) on the unfeathered portions (legs, feet, and skin around the eyes and beak) of the bird. Affected birds also display weakness, vision and breathing problems, difficulty in swallowing, emaciation, and reduced egg production. Secondary infections are common. Among wild birds, it occurs most commonly in upland game birds, songbirds, marine birds, occasionally in raptors and rarely in waterfowl. Avian pox is transmitted mechanically by mosquitoes and other biting arthropods, by direct contact among birds, and by inhalation of virus particles. In remote island locations where exposure to avian pox is limited, exposure of native indigenous fauna has resulted in high levels of bird mortality. Also, among wild populations of northern bobwhite, Colinus virginianus , and wild turkey, Meleagris gallopavo , in the southeastern USA, avian pox is regarded as a serious problem. For many bird species, it is not a major issue. Management involves eliminatanding mosquitoes and their breeding sites, eliminating
infected birds, and in the case of domestic birds, by disinfecting feeders, watering devices, and cages.

Myxomatosis

This viral disease of New World rabbits is transmitted by mosquitoes, black flies, fleas, lice, and mites. The virus adheres to the mouthparts of the arthropods as they probe the epidermis. Once the mouthparts are contaminated, the virus can be inoculated into another host during a later probe. The virus does not replicate in the vector. The natural hosts of the myxoma virus are the jungle rabbit, Sylvilagus brasiliensis , in South and Central America and S. bachmani in California, USA. It has only mild effects on New World rabbits, causing cutaneous fi broma (relatively harmless wart - like skin blemishes) but not a systemic disease. However, the myxoma virus is quite deadly to Old World rabbits, Oryctolagus spp. Infected European rabbits display a bedraggled appearance, with partially or completely swollen eyelids, discharge from the conjunctiva and nose, and swollen ears and head. Nodules measuring up to 1 cm in diameter may be found anywhere on the body. In addition to being almost blind, affected animals frequently are in respiratory distress.

In 1950, myxoma virus was introduced to Australia to reduce the population of European rabbits that had been deliberately but regrettably introduced, and where they had few natural enemies. The rabbits in Australia have caused the extinction of numerous animals and plants, and caused extensive soil erosion due to overgrazing. The virus quickly reduced the population of rabbits from 600 million to 100 million, but the rabbit populations have recovered partly as disease resistance has developed. Recently another virus, rabbit calicivirus, has been introduced to attempt population suppression in Australia. Myxomatosis was also introduced to France, where it spread rapidly throughout Europe, causing significant decreases in rabbit populations, and populations of some of the predators that fed upon them. Overall, the reduction in rabbit abundance is estimated at 30% – 40% in Australia to 50% – 70% in Great Britain. Vaccine is used in Europe to provide protection of rabbits from the virus; both live attenuated virus vaccines and inoculation with rabbit fibroma virus (which is innocuous to European rabbits) are used. In many respects, rabbit fibroma virus can generally be considered the eastern North American equivalent of myxoma virus, and is often seen in eastern cottontails, Sylvilagus floridanus , but with few serious effects.

The Nature of Parasitism

Organisms that live in association with another animal are usually referred to as a host and symbiont, and the relationship is referred to as symbiosis . In the case of wildlife disease, the microparasites (e.g., viruses, bacteria, and fungi) or macroparasites (e.g., protozoa, helminths, and arthropods) are the symbionts , and the wildlife (but in some cases livestock and humans) are the fi nal or defi nitive hosts. In the examples here, arthropods are often intermediate hosts. The nature of symbiosis varies, with the most common types:

• Mutualism . The host and symbiont are dependent on one another, and the relationship is mutually probeneficial. The microbial fl ora found in the digestive system of ruminants is a good example of mutual dependency.

• Commensalism . The host provides the habitat and food for the symbionts, which live without benefit or harm. In this case, the symbionts are dependent on the host, but the host does not depend on the symbiont. Many microbial parasites of wildlife have co - evolved with their normal hosts and cause no measurable harm, so under normal conditions they qualify as commensals. However, this relationship can shift when the host is stressed, and under these conditions may cause injury.

• Parasitism . The host supplies physiological support for the symbiont by providing habitat and sustenance, and often transport, and the symbiont is harmful to the host. The symbionts discussed here are parasites of wildlife to some degree, and sometimes to livestock, pets or humans. Their effect on wildlife may be severe or mild, and sometimes nearly imperceptable. There are several forms of parasitism, with parasitism classifi ed according to where the parasites are found, their temporal occurrence, and their relationship with their host. Some major forms of parasitism include:

• Ectoparasites . These organisms live on the external surface of the host, or cavities that open directly onto the surface. Foremost among the ectoparasites are the arthropods, such as lice, mites, and ticks.
• Endoparasites . These live within the body of the host, including the digestive system, lungs, liver, tissues, cells and freely in the body cavity. Viruses, bacteria, fungi, protozoa, tapeworms, and nematodes are good examples of endoparasites.
• Temporary parasites. These visit the host only briefl y, usually for food. Bloodsucking arthropods are a good example of such parasites.
• Stationary parasites . These spend a definite period of development in association with the host, either on or in it. Some are periodic parasites , leaving to spend another portion of their life in a non - parasitic mode. Examples of this include ticks and botflies. Others are permanent parasites , spending all of their life on a host except for a brief period when transferring from host to host. The viruses, bacteria, protozoa and helminths are examples of this (although in some cases they may persist for long periods, in the absence of a suitable host, in a resting stage).
• Incidental or aberrant parasites . These are parasites that occur only occasionally in a host, usually because there are behavioral or ecological barriers that keep the parasite from the prospective host.
• Obligate parasites . These parasites cannot continue with their life cycle unless they have access to a certain host (or hosts). Most of the parasites discussed here have a certain host or a restricted range of hosts to which they must gain access.
• Facultative parasites . These are parasites that do not require a certain host, but sometimes are found in association with it.

Parasites display many adaptations that make it possible to have a symbiotic relationship with their host. Although they have the same basic nutritional requirements as the host, the symbiont must have adaptations that allow them to enter or attach to a new host after they have escaped from their old host. The tarsal adaptations of lice that allow them to cling to the body hairs of their host are a readily visible adaptation, as are the hooks and suckers of helminths living in association with the host ’ s digestive tract. The symbiont must also escape the host, or at least its progeny must escape, in order to fi nd new hosts. The avenue of escape may be direct , as when eggs, immature stages of nematodes, or body segments (proglottids) of tapeworms are released from the host’s anus. Escape may also be indirect , as when an arthropod feeds on the blood of a host, takes up the symbiont, and transports it. Symbionts escaping both directly and indirectly may have one or more additional hosts that provide transport, maintenance, or an opportunity for propagation.

Organisms with direct escape from the old host and direct transmission to the new host can be said to have a direct life cycle . Those with indirect escape and indirect transmission can be said to have an indirect life cycle . The latter condition is more complicated, as host, symbiont, vector, and environment must all coincide for infection and development to occur. Here we are concerned mostly with disease organisms with an indirect life cycle, and specifically those that involve arthropods.

Cause Of Disease

It can be quite diffi cult to determine the cause of a disease. Factors that are thought to be causative factors of disease are called putative factors because their occurrence is often correlated with presence of the disease, but eventually evidence of their association is necessary before a cause and effect relationship is confirmed. The cause of a disease is often called the etiologic agent . It is also common to discuss the sign or clinical sign to indicate objective evidence that a disease is present, such as hair loss. It is unusual to use the term symptom with respect to diseases of animals, as this is a subjective assessment such as pain or lack of energy, and is something that cannot be communicated to humans by animals. It is interesting to note that entomologists have developed slightly different terminology than have wildlife biologists when describing diseases; entomologists use ‘ sign ’ to indicate physical manifestations of disease, and ‘ symptom ’ to indicate changes in behavior or function attributed to disease.

In some cases, criteria have been established to defi ne whether or not a cause and effect relationship exists between a disease and a putative cause. Often, healthy animals are exposed to a putative cause; if the disease develops, causation is considered to be proved. For infectious disease agents, it is necessary to prove Koch ’ s Postulates to establish the relationship between a disease and its putative cause. The rules of Koch ’ s postulates are:

• the putative agent must be found in every case of the occurrence of disease;
• the putative agent must not be associated with the absence of disease;
• the putative agent must multiply in the host when provided the opportunity;
• the putative agent must be capable of being re - isolated from experimental inoculated individuals.

Though Koch ’ s postulates are generally acceptable in ascribing cause and effect relationships, in many cases disease results from many stressors, including some abiotic factors. Thus, disease may be expressed only when a combination of events or factors occurs. Commonly, disease has primary and secondary causes, or situations that predispose an animal to disease. For example, it is easy to imagine how poor diet or adverse weather could interact with microbial pathogens by weakening the host ’ s ability to fend off infection. Some diseases are latent , which means that the potential for expression of the disease is present, but expression is suppressed and the animal is not contagious until triggered by something in the animal ’ s biology or environment. Indeed, it is not uncommon for an animal to be infected (to have the disease - causing organism within its body), but for there to be no apparent dysfunction (lacking disease). The lack of detectable dysfunction can be due to inherent resistance (the same pathogen in another population or species induces expression of disease) or by the condition or vigor of the animal, which suppresses disease expression.

For noninfectious diseases (those lacking an infectious agent that can be spread from host to host) such as exposure to pesticides, it is not possible to apply Koch ’ s postulates. In these cases, we must be content with exposing healthy animals to the stressor and observing the animal ’ s response, or by searching for chemical residues in animals suffering from disease. This is not always satisfactory, as it is difficult to know the appropriate dose to test. Also, though it is easy to assess acute toxicity caused by high doses because the animal ’ s response is usually rapid, it can be diffi cult to assess the effects of chronic toxicity caused by low doses applied over a long period. Low doses can interact with host metabolism, such as the hormonal system of the animal, or with other agents such as microbial pathogens, and it can be difficult to identify the true factor responsible for poor animal performance.

Disease Transmission

Wildlife disease agents can be transmitted vertically or horizontally. Vertical transmission refers to transmission of a disease agent from parent to offspring. Horizontal transmission refers to transmission of a disease agent from animal to animal, independent of their parental relationship. Horizontal transmission is the most common method of disease spread. It can result from several actions, including:

• skin to skin contact between members of the same species;
• airborne transmission of droplets containing disease agents;
• contact with secretions and excretions, including residual fecal materials;
• contact with genital and sexual materials;
• discharge from lesions;
• contact with infected carcasses;
• ingestion of contaminated water and food;
• transmission by other species.

Here we discuss only the latter means of disease transmission, transmission by other species, and specifically by arthropods. Because another species is involved in the transfer from host to host, it is considered to be a form of indirect transmission . Not surprisingly, direct transmission is defi ned as the transfer of a disease agent (pathogen) from one host to another without the involvement of another species. Transmission of an infective stage of a disease agent to a host can occur in various ways. Passive transmission occurs when the host is contaminated or infected accidentally through ingestion of food, water, or an infected arthropod; this occurs with many nematodes. Active transmission occurs when the disease agent actively penetrates the bodies of their host after gaining contact with them; this occurs with hookworms. Finally, inoculative transmission occurs when a vector such as a mosquito injects the disease agent into the new host during the process of blood feeding, as occurs with the protozoa causing malaria.

The importance of arthropod transmission as a means of disease spread varies greatly among diseases. For some wildlife diseases it is the only means or most important form of transmission, but for other diseases it is less important or arthropod transmission does not occur. It is useful to note that transmission of disease agents by arthropods is not completely independent of the other routes of horizontal transmission. Arthropods can be associated with food and carrion, for example, and wildlife could contract a disease from an insect or by feeding on contaminated food. Nevertheless, because an arthropod (serving as a ‘ vector ’ ) is involved in the transmission or transport process, such diseases are called vector - borne.

Vectors differ in their ability to acquire disease agents and to infect hosts ( vector competence ). Insects usually are short - lived, and acquire and transmit disease agents quickly, with the incubation period in the vector lasting perhaps a few days. Insects may be quite mobile, and typically take many small blood meals. In contrast, ticks are more long - lived, and incubation may require months. Ticks lack wings, so they are much less mobile, and normally take few but large blood meals.

Differences in vectorial capacity or vector competence are due to several factors. There are genetic variants among a single species of disease agent, for example, that differ in their ability to be acquired or transmitted. The vectors also differ in susceptibility to oral infection and effi ciency of transmission, population structure (density, longevity, etc.), host preference, and geographic distribution. Also, the vertebrate hosts differ in susceptibility, which may be manifested in the ability of the host to develop concentrations adequate to infect the vector, population structure (availability of susceptible stages), immune status (prior exposure may confer immunity), and overlap in space and time with the vectors. Often, the suitability of a host animal to produce adequate concentration of the disease agent, or the ability of the disease agent to replicate in the vector, determines the ability of the vector to acquire and transmit the agent. Disease concentration thresholds seemingly exist, especially with mosquitoes, below which transmission does not occur. Thus, certain hosts or vectors are more important in disease transmission cycles. With tick vectors, however, the concentration of disease agent within the host seems to be less important, as ticks can infect one another while feeding together on the same host. Such ‘ co - feeding ’ infection occurs with only minimal or incomplete systemic infection, and usually the ‘ donor ’ and ‘ recipient ’ ticks must be feeding in proximity.

Disease Hosts

There are several types of hosts for disease agents. Understanding the different types is important for understanding disease biology and epidemiology. A reservoir host (usually simply called ‘ reservoir ’ ) is an animal that harbors a disease agent. Reservoir hosts must be able to support the disease in the absence of other species, providing a means of long - term persistence. The reservoir host must be able to provide the disease agent to other species, allowing spread of the disease. The reservoir host usually is not seriously affected by the disease, though there may be signs of infection. Primary or definitive hosts are species in which the disease agent passes the adult, sexual, or multiplicative stage of the life cycle. The primary hosts can also be the reservoir hosts. Intermediate hosts are animal species that the disease agent passes through during the immature or nonsexual phase of the disease life cycle. Amplifier hosts are animals in which the disease agent abundance is increased without severely affecting the host. Incidental , aberrant , or unnatural hosts are not the normal hosts for a disease, and although in some cases they are not susceptible, in other cases they are extremely susceptible, displaying overt signs of infection. These are also called dead - end hosts or dilution hosts because they may perish or not support high concentrations of the disease agent, proving to be unsuitable for uptake of the disease agent by a vector.

Diseases normally have an environment or habitat where they persist in a relatively stable way. Here the environment (or host) and the disease agent are co - evolved, allowing both to co - exist and neither to eliminate the other. The modifi cation of habitat, or the movement of new wildlife, livestock or humans into an environment where a disease has evolved a stable relationship with its host can upset the balance and allow establishment of new disease - host relationships. In such situations, wildlife, livestock and humans can prove to be various types of host, and arthropods can prove to be vectors and/or intermediate hosts.

Virulence In Wildlife

The ability of a disease agent to cause impairment or dysfunction in an animal is called virulence or pathogenicity . These terms are synonymous, and can be used to describe the effects of any type of disease, but generally are used in the context of infectious diseases. Virulence and pathogenicity can be measured in terms of host mortality, reproduction, and altered life history. High virulence can occur as a coincidental by - product of infection, or it can be adaptive (beneficial) to the infectious agent.

Coincidental virulence offers no adaptive advantage to the causative agent; thus, virulence may be viewed as simply an accident. Coincidental virulence is  commonly seen in new or novel associations. Infectious diseases that have coevolved a relatively benign relationship with wildlife, for example, can be highly virulent to domestic animals or newly introduced wildlife because they have not had opportunity to evolve a relationship that benefi ts both the host and parasite. One - sided relationships favoring either the host or disease agent are not advantageous to the disease agent. In cases where the host is favored, the disease agent may be fully suppressed and not able to reproduce and spread to new hosts. On the other hand, relationships favoring the disease may result in premature death of the host, also resulting in failure of the disease to spread to new hosts. An example of coincidental virulence occurs with elaeophorosis, a nematode disease of wildlife. The nematodes are transmitted to wildlife by the bite of horsefl ies (Diptera: Tabanidae) but usually cause no harm to their normal host in western North America, mule deer ( Odocoileus hemionus ). The same nematode, when transmitted to abnormal hosts such as elk, Cervus elaphus ; moose, Alces alces ; white - tailed deer, Odocoileus virginianus ; or bighorn sheep, Ovis canadensis ; can cause disease. High virulence of infectious diseases originating with wildlife but adversely affecting humans and livestock is most often coincidental.

Disease In Wildlife

Whether they are infectious or parasitic, disease agents of wildlife share a common evolutionary pattern: all disease - causing organisms extract nutrients from their hosts. However, if they extract too much too quickly they jeopardize their own survival and ability to reproduce. For their progeny to survive, the parasite has to mature, reproduce, and either be transmitted to another host or be put in an environment where they (or their progeny) can likely fi nd another host. Natural selection favors organisms that are successful in this pursuit; they are most fit.

When disease becomes unusually abundant, this is usually called an epizooti c , epidemic , or outbreak. An exceptionally widespread epidemic is called a pandemic . In contrast, when the disease is at a low or normal level (not readily observable) it is said to be enzootic or endemic . Unfortunately, conservation biologists and biogeographers often use the term ‘ endemic ’ to refer to organisms that are native to an area, so this term has more than one meaning, a confusing situation. Native organisms are better referred to as indigenous . When diseases are capable of spreading from one individual to another, they are said to be contagious . Diseases that are new or increasing in prevalence are called emerging pathogens . For example, West Nile virus (see also discussion of West Nile virus, Chapter 8 ) fi rst attained the western hemisphere in 1999. Because it was new, it was viewed as an emerging pathogen. Initially, it caused epizootics among some forms of wildlife, particularly some avifauna. In most areas where it has occurred for a few years it has fallen to an enzootic state due to mortality among the most susceptible hosts and development of resistance among others. However, it will certainly cause an epizootic again at some time in the future as resistance diminishes, a new more virulent form of the virus evolves, or as the number of vectors increases. West Nile virus may be viewed as an emerging pathogen as it gains access to areas where it has not occurred previously, but it will never be an indigenous species in the western hemisphere.

Disease is often considered to consist of the effects of infective and parasitic organisms, but in fact disease is much more encompassing than that. The defi nition of disease can be expanded to include nearly anything that causes an impairment of the host animal. This includes (in addition to parasites) environmental factors like nutrition, toxicants, weather, inherited abnormalities, and combinations of these factors. Thus, when assessing disease in wildlife, it is important to consider that:
• disease is not measured by deaths of individuals, but
by impairment of performance. Wildlife populations
can go into decline due to decreased reproduction and
longevity, but with no noticeable increase in
mortality.
• disease is caused not only by extrinsic factors such as parasites, but also by intrinsic factors such as inherited physiological processes.
• disease may be the result of factors acting individually, or in concert with other factors. Indeed, several functions may be impaired simultaneously, none very noticeably, but collectively very important to fi tness of the organisms. Often, parasitic organisms are held in check by immune responses or general vigor of the host, but when stressed by lack of food or cold weather, the animals will succumb to the parasite.

In addition, it is useful to understand that disease can be brought about by the host ’ s physiological response to a disease agent, not simply by the direct effect of the disease agent. For example, invasion of a host by a microbial parasite may eventually cause injury, but disease develops initially as the host ’ s immune system recognizes the presence of the foreign bodies and responds with elevated body temperatures and increased numbers of white blood cells. The host animal may be less alert and unable to feed or hunt while responding metabolically to this invasion. Thus, although many animals have immune systems designed to thwart invasion or minimize feeding, it comes at a physiological cost.

Insect Body Regions

The principal body regions of insects are the head, thorax and abdomen (Fig. 2.3 ). Each region, or functional unit, is called a tagma (plural, tagmata ), and the process of the individual segments functioning as a unit is called tagmosis . The presence of these three body regions is not always apparent, however. The head may be small or hidden from view when examined from above, or the front wings may cover both the thorax and abdomen, giving the impression that there is only a single large segment. Alternatively, when viewed from below it is evident that insects consist of quite a large number of segments, some of which are fused. Even after fusion, it usually is possible to recognize three thoracic segments and about 11 abdominal segments. The six segments that fused to form the head are mostly unrecognizable. Legs, wings, and antennae are the appendages that are most evident on the tagmata, but often mouthparts and cerci can be seen.

Molting

The problem with being encased in a fairly rigid integument is that growth is severely limited. A certain amount of growth can occur because of the elastic nature of the intersegmental membranes. However, to allow signifi cant increase in size, the insect must shed its old cuticle (the nonliving part of the integument) and produce a new, larger body covering. Insects accomplish this by producing a new, larger but soft integument beneath their old rigid body covering, then shedding the old one and expanding to accommodate the new larger integument. This process is regulated by hormones, particularly ecdysone (this is discussed further under glandular systems, below).

The epithelial cells produce the cuticle, so this area of the integument is central to the entire molting process. The fi rst important step in molting is called apolysis , which is the separation of the epidermis from the old cuticle. The space that is created between the epidermis and the old cuticle during apolysis is called the exuvial space , a region where molting fl uid is secreted by the epidermal cells. After apolysis, the epidermal cells begin to secrete the new cuticle. First deposited is the outer layer of the epicuticle, then the inner epicuticle is formed. This is followed by secretion of the procuticle. Thus, the new cuticle is produced starting with the outer layers and working inward. Now the molting fl uid is activated, which digests the old endocuticle. Up to 90% of the cuticle is digested by protease and chitinase enzymes, and recycled to help construct a new procuticle. After all the layers are in place, the insect produces a layer of wax that is secreted through pore canals onto the surface of the new epicuticle. This protects the insect from desiccation. Finally, the insect sheds its old cuticle, called the exuviae , in a process called ecdysis . Ecdysis is a tricky process, as the insect must escape from its old covering. Often it anchors the old integument and crawls out, and may use gravity to aid in its escape by hanging from a branch (Fig. 2.2 ). However, it must split the old cuticle somewhere that will allow escape, often in the head region. After it fi rst escapes the old integument it is white or pale in color, and soft - bodied; such insects are said to be teneral . Finally, the molting insect must expand its body size while the new cuticle dries and hardens, because once it hardens not much more growth is possible until the next molt. So insects swallow air or water, and expand their body to swell to its maximum size while their body cover hardens. Slowly the insect cuticle hardens and darkens during a chemical process called sclerotization , which cross - links the proteins to create a new rigid exoskeleton. After this physical expansion and sclerotization, insects have some opportunity to add body tissue before they need to molt again.