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.