Epidemiology: some basic concepts and definitions 1. Introduction A question frequently asked is, "What is epidemiology"?

There are many different definitions of the term. In the main, people attempting to define epidemiology have normally done so in the context of their o n particular interests or needs. A useful general definition is that given !y "ch a!e et al #$%&&', hich defines epidemiology as the study of disease in populations. It thus differs from the more conventional medical approaches to the study of disease that are normally concerned ith the study of disease processes in affected individuals. While the o!(ective of the latter is to find cures for diseases in individuals already affected, epidemiology is !asically concerned ith the reasons hy those individuals !ecame diseased in the first place. Inherent in the epidemiological approach is the !elief that the frequency of occurrence of a disease in a population is governed !y the interaction of a large num!er of different factors or determinants. The epidemiologist !elieves that !y studying these interactions it may !ecome possi!le to manipulate some of the determinants involved, and so reduce the frequency ith hich the disease in question occurs m a population. At this stage it is necessary to ascertain population and determinant. hat is meant !y the terms

A population can !e defined as the complete collection of individuals that have some particular characteristic#s' in common. )epending on the characteristic#s' !eing considered, a population can !e very large or very small. *or example, one may ish to study a particular disease in a particular cattle population in a particular country. That cattle population could consist of+ All the cattle in the country or All the dairy cattle in the country or All the dairy cattle of a certain !reed in the country etc. Another term often used in epidemiological studies is population at risk. This is usually a su!set of the original, defined population and comprises the total num!er of individuals in that original population that are considered capa!le of acquiring the particular disease or disease characteristic !eing studied. *or instance, e might !e interested in studying the frequency ith hich a!ortion occurs in a population of dairy cattle of a certain !reed in

a certain country. The population at risk ould not !e all the individual animals of that particular dairy !reed in that country, since this ould include males, steers and immature females, all of hich ould not or could not !e pregnant and therefore could not a!ort, It ould consist of female cattle of that !reed hich ere of !reeding age. -o ever, if the characteristic !eing studied as infection !y one of the infectious agents that can cause a!ortion, such as Brucella abortus, the population at risk ould have to include all calves, adult males, steers and immature females of the particular !reed in question, since all these individuals could potentially !ecome infected ith this organism. A determinant is any factor or varia!le that can affect the frequency ith hich a disease occurs in a population. )eterminants can !e !roadly classified as !eing either intrinsic or extrinsic in nature. Intrinsic determinants are physical or physiological characteristics of the host or disease agent #or intermediate host or vector, if present' hich are generally determined genetically. .xtrinsic determinants are normally associated ith some form of environmental influence on the host or disease agent #or intermediate host or vector, if present'. They may also include interventions made !y man into the disease process !y the use of drugs, vaccines, dips, movement controls and quarantines. The role of determinants in the disease process is discussed in more detail later on in this chapter. "ince the determinants of disease are often varied, the epidemiologist may have to dra on a num!er of different scientific disciplines and techniques if he is to study them. The epidemiological approach is, therefore, a holistic one and the "art" of epidemiology lies in the a!ility of the epidemiologist to coordinate the use of such disciplines and techniques in a disease investigation, and to produce from the results generated a composite and comprehensive picture of ho a particular disease maintains itself in nature. If e accept the premise that the frequency ith hich a disease occurs in a population is governed !y a large num!er of determinants, it ould !e expected that some of these, particularly the extrinsic ones, ould vary in space and time. It follo s, therefore, that disease is a dynamic process. The type and pattern of diseases in livestock differ from country to country, area to area, species to species and production system to production system. *urthermore, the range and importance of the disease pro!lems encountered may change dramatically over time ithin the criteria mentioned. The effective control of disease depends as much on a thorough understanding of the many complex factors that govern the changes taking place in a disease process as it does on the provision of veterinary inputs such as drugs, vaccines and dips.

2. Intrinsic determinants of disease 2.1. Disease agents as determinants of disease Agents associated ith disease can !e categori/ed into t o !road groups+ 0 "1iving" agents, such as viruses, !acteria, rickettsia, proto/oa, helminths, arthropods etc. 0 "2on3living" agents, such as heat and cold, ater, nutrients, toxic su!stances etc. "ince infectious diseases of livestock are generally regarded as !eing of prime importance in Africa, the follo ing discussion is concerned principally ith the determinants associated ith the so3called living disease agents. In instances of infectious disease, the presence or a!sence of the aetiological agent is the main determining factor in the epidemiology of the disease. 4!viously, disease cannot occur in the a!sence of the agent, !ut, conversely, disease need not al ays result from the presence of the agent. This leads us to the important epidemiological distinction !et een infection and disease. Infection can !e defined as the invasion of a living organism, the host, !y another living organism, the agent. Disease can !e defined as a derangement in the function of the !ody of the host or any of its parts. 2.1.1. Infectivity, virulence and pathogenicity hole

Whether infection takes place or not may depend on a hole range of determinants, !oth intrinsic and extrinsic, hich affect the host and the agent #and the intermediate host or the vector, if present'. Infectivity is a measure of the a!ility of a disease agent to esta!lish itself in the host. This term can !e used qualitatively, hen an agent is referred to as !eing of lo , medium or high infectivity, or quantitatively. Attempts to quantify infectivity normally involve the use of a statistic kno n as I)56. This refers to the individual dose or num!ers of the agent required to infect 567 of a specified population of suscepti!le animals under controlled environmental condition. -aving !ecome infected, the host may or may not !ecome diseased, and this is again determined !y a range of intrinsic and extrinsic determinants affecting the agent and the host. T o terms 3 virulence

and pathogenicity 3 are often used to descri!e the a!ility of the agent to cause disease. Virulence can !e defined as a measure of the severity of a disease caused !y a specified agent. In its strict sense, virulence is a la!oratory term and is used to measure the varying a!ility of disease agents to produce disease under controlled conditions. It is often quantified !y a statistic kno n as 1)56 hich refers to the individual dose or num!ers of the agent hich ill kill 567 of a specified population of suscepti!le animals under controlled environmental conditions. Pathogenicity is an epidemiological term used to descri!e the a!ility of a particular disease agent of kno n virulence to produce disease in a range of hosts under a range of environmental conditions. 2.1.2. Host/agent relationships

The relationships !et een infection and disease are frequently dynamic in nature. They centre on the "!alance" that can !e achieved !et een the resistance mechanism of the host and the infectivity and virulence of the agent. )isease out!reaks caused !y the introduction of an agent into a suscepti!le host population hich has not !een previously exposed to that agent normally result in a disease of high pathogenicity ith commensurate severe losses in the host population. "uch a process is actually detrimental to the agent8s survival, since !y killing off the host population it adversely affects !oth its a!ility to reproduce and its chances of gaining access to ne suscepti!le hosts. An agent can therefore improve its chances of survival !y increasing its infectivity and decreasing its pathogenicity, and some agents have a natural tendency to do this under certain circumstances. "ince a commensal or parasitic relationship confers no !enefits to the hosts, they tend to develop means of resisting infection !y disease agents. While the agents, in order to survive, develop methods of circumventing the hosts8 defences. )isease agents normally have much shorter generation intervals and can multiply much more rapidly than their hosts, and therefore tend to evolve much quicker. This rapid evolution usually ena!les the agents to keep comforta!ly ahead of the hosts8 defence mechanisms. There are many mechanisms !y hich infectious agents can avoid or overcome the defences of the host. The t o mechanisms hose consequences are of particular importance in the field of livestock disease control are the carrier state and antigenic variation. Creation of the carrier state. The term "carrier" is used to descri!e an individual that is infected !y a disease agent and is capa!le of

disseminating that disease agent !ut sho s no sign of clinical disease. Three types of carrier state are recognised+ 0 The true carrier, hich is an infected individual capa!le of disseminating the infectious agent !ut hich never exhi!its clinical signs of disease. True carriers occur in various diseases, including salmonellosis. 0 The incubatory carrier, hich is an infected individual capa!le of disseminating the infectious agent hile the disease is still in the incu!atory stage. In foot3and3mouth disease, for instance, infected animals are most infectious $9 to 9: hours !efore the clinical signs of the disease appear. 0 The convalescent carrier, hich is an individual that continues to disseminate the infectious agent after the clinical signs of the disease have disappeared. ;onvalescent carriers occur in such diseases as contagious !ovine pleuropneumonia. Antigenic variation. "ome species of disease agent seek to evade the hosts8 defence mechanisms !y altering their antigenic characteristics. The most extreme case of antigenic variation occurs in trypanosomiasis, here infection in the host usually takes the form of a series of parasitaemias each one of hich involves a form of trypanosome antigenically different from the preceding one. This type of antigenic variation occurs during the course of a single infection. Another type of antigenic variation occurs in certain agents, such as the foot3and3mouth disease virus, that are highly infectious in nature and that depend for their survival on a continuous cycling through host populations of relatively long3lived animals. The a!ility to reinfect the same host at a later date is o!viously desira!le for the agent8s survival, and this is dependent on the generation of a relatively short3lived immunity com!ined ith the a!ility of the agent to undergo antigenic variation during its passage through the host population. In such circumstances there is a strong selection pressure for antigenic variants. The t o main types of variation are+ Antigenic drift, hich involves only minor changes in antigenicity, so that hosts previously infected ith the agent retain a certain degree of immunity to the drifted strain. Antigenic shift, hich involves a ma(or change in antigenicity, so that previously infected individuals possess little or no immunity to the shifted agent.

Antigenic shifts are of particular significance hen the control of a disease is !eing attempted !y vaccination, since in effect they represent the introduction of a ne agent against hich the existing vaccine is likely to confer little or no immunity. The capacity of parasites to evolve rapidly has important implications in other areas of disease control. The very act of introducing a control measure or disease treatment may, in itself, create conditions here!y a strong pressure is exerted on the agent population to select strains hich are resistant to the measures or treatments imposed. The evolution of such resistant strains ill, in turn, (eopardise the effectiveness of the control measure or treatment. <esistant strains of agents are most likely to develop hen the measures or treatments are carried out on a ide scale !ut improperly 3 as, for example, in the case of anti!iotic resistance arising through the idespread, unsupervised use of anti!iotics !y livestock producers. 4ther terms used to further define host=agent relationships include+ Incubation period, hich is the period of time that elapses from the infection of the host !y the agent to the appearance of clinical symptoms. Prepatent period, hich is the period !et een the infection of the host !y the agent and the detection of the agent in the tissues or secretions of the host. Period of communicability, hich is the period of time during hich an infected host remains capa!le of transmitting the infective agent. 2.1.3. Methods of transmitting infectious agents

Ascertaining the means !y hich disease agents are transmitted is a ma(or o!(ective in epidemiological studies, since once the mechanisms !y hich a particular disease is transmitted are understood, it may !ecome possi!le to introduce measures to prevent transmission from taking place. There are three main ays !y hich disease agents are transmitted from infected to suscepti!le hosts. An agent may !e transmitted through contact !et een infected and suscepti!le individuals, or it may !e conveyed !et een these individuals !y means of an inanimate o!(ect or via another animal serving as a vector or intermediate host. These methods of transmission are not mutually exclusive> the same disease agent may !e transmitted !y more than one of the follo ing ays.

Contact transmission. In contact transmissions the agent is conveyed !et een hosts through direct physical contact, as in the case of venereally transmitted diseases such as vi!riosis or trichomoniasis, or through indirect contact. In cases of indirect contact the agent is normally contained in the excretions, secretions or exhalations of the infected host i.e. in the faeces, urine, milk, saliva, placenta and placental fluids, or as aerosols or droplets in the !reath. "uscepti!le hosts contract the infection either !y direct exposure to these or through exposure to su!stances contaminated !y them. )iseases spread in this fashion include rinderpest, foot3and3mouth disease, 2e castle disease, and contagious !ovine pleuropneumonia. ;ontact transmissions can !e further distinguished according to hether they occur hori/ontally !et een individuals of the same generation or vertically !et een individuals of different generations. In vertical transmissions the infectious agent is usually passed from dam to offspring either in the uterus or through the colostrum. The main factors determining hether or not transmission takes place in contact3transmitted diseases are+ 3 The a!ility of the agent to survive in the environment. <inderpest virus, for example, is easily destroyed in the environment, so contact !et een infected and suscepti!le individuals must !e close and immediate for transmission to take place, hereas, under certain circumstances, foot3 and3mouth disease can spread !et een idely separated stock. 3 The extent of the contact that occurs !et een infected and suscepti!le individuals of the host populations and their mo!ility ithin these populations. The control of livestock movements is, therefore, a vital factor in the control of contact3transmitted diseases hich, in Africa, normally occur more frequently during the dry season hen livestock movements are at their highest. Vehicular transmission. In vehicular transmission the agent is transferred !et een infected and suscepti!le hosts !y means of an inanimate su!stance or o!(ect #sometimes called fomite', such as ater, foodstuffs, !edding materials, veterinary equipment and pharmaceuticals, or on the skin, hair or mouthparts of animals. In contrast to indirect transmission, the survival time of the agent in or on the vehicle is usually prolonged. This means, in effect, that vehicular transmission can take place over greater distances and over longer time periods. -ygiene, disinfection

and control over the distri!ution of likely vehicles of transmission are important factors in the control of vehically transmitted diseases. ;ertain agents may take the opportunity to reproduce themselves during vehicular transmission. This occurs in the transmission of food3 !orne !acteria, such as salmonella and coliforms, and underlines the importance of strict hygiene in the handling of foodstuffs and livestock feeds, since a small initial contamination may eventually result in the gross contamination of a hole !atch of food or feed. Vectors and intermediate hosts. ;onfusion frequently arises !et een the terms "vector", "intermediate host" and "definitive host". The latter t o terms are essentially parasitological terms and descri!e the different types of hosts that are !iologically necessary in the lives of agents ith relatively complicated life cycles. 0 A definitive host is a host in of its development. hich the agent undergoes a sexual phase

0 An intermediate host is a host in phase of its development.

hich the agent undergoes an asexual hile intermediate hosts can

The definitive host is usually a verte!rate, !e either verte!rates or inverte!rates.

0 A vector is an inverte!rate animal that actively transmits an infectious agent !et een infected and suscepti!le verte!rates. .ssentially, vectors can transmit infectious agents in t o ays. They can serve as a vehicle here!y the infectious agent is conveyed from one host to another ithout undergoing a stage of development or multiplication. This is kno n as mechanical transmission. Alternatively, the infectious agent can undergo some stage of development or multiplication in the vector 3 this is kno n as biological transmission 3 and in this case the vector is serving either as an intermediate or definitive host, depending on hich stage of the development cycle of the agent takes place ithin it. ?erte!rate intermediate hosts play the same role in the transmission of their disease agents as !iological vectors. In mechanical transmission the agent is carried on the skin or mouthparts of the vector from an infected to a suscepti!le host. The survival time of the agent in or on the vector is usually short, and as a result the transmission of the agent has to !e accomplished rapidly. The carriers are normally inged haematophagous insects, and transmission

usually takes place hen suscepti!le and infected hosts are in close proximity and hen large num!ers of vectors are present. In !iological transmission, since the agent develops in the vector, a period of time elapses !et een the acquisition of the infectious agent !y the vector and its !ecoming infective. 4nce it has !ecome infective, the vector may remain so, normally for a considera!le period if not the rest of its life. This provides more than a single opportunity for disease transmission. In addition, vectors may !e a!le to pass the agent on to their o n offspring transovarially. ransovarial transmission ena!les an infectious agent to !e maintained in a vector population through many generations ithout that population having to !e reinfected, and, as such, the vector population remains a continuous source of risk. If transovarial transmission does not occur, at least one stage in each generation of the vector must !ecome infected !efore transmission of the agent can take place. Arthropod vectors that undergo metamorphosis have the capacity to pass an agent from one developmental stage to the next. This is kno n as transtadial transmission. @sually in transtadial transmission, one developmental stage !ecomes infected ith the disease agent and the follo ing stage transmits it. If different developmental stages feed on different host species, transtadial transmission can provide a mechanism for an inter3species transmission of disease agents. 2.2. Host determinants

The main intrinsic determinants in the host hich can influence the frequency of occurrence of infection and disease are species, !reed, age and sex. 2.2.1. Species suscepti ilities and natural reservoirs

Aost disease agents are capa!le of infecting a range of animal species, !oth verte!rate and inverte!rate. The severity of the disease resulting from such infections may, ho ever, vary !et een the species concerned. While certain host species may !e refractory to infection ith certain disease agents, e.g. equines to the foot3and3mouth disease virus, very fe disease agents are in fact restricted to one host species. The multi3species suscepti!ility to disease agents is particularly important if the species concerned are a!le to maintain the disease agent ithin their populations i.e. to function as natural reservoirs of infection. The failure of programmes aimed at controlling a certain

disease in one species has often !een !lamed on the presence of natural reservoir species, !ecause they can reintroduce the infectious agent. When investigating the potential of a certain species to act as a natural reservoir of a particular disease agent, and the implications this ould have on disease control policy, the follo ing considerations need to !e !orne in mind+ Infection !ith the disease agent. Although it may !e possi!le to infect a certain host species ith a disease agent under la!oratory conditions, this may only !e achieva!le !y using a method of transmission that does not occur naturally #e.g. intracere!ral inoculation'. If this is the case, that particular host species is unlikely to play a significant role in the epidemiology of the disease. Ability of a host species to maintain a disease agent. It may prove possi!le to demonstrate that a particular host species can !e infected !y a certain disease agent and that that infection can !e accomplished !y a natural means of transmission. A further question then needs to !e asked, namely, is that species capa!le of maintaining the agent ithin its populations for significant periods of time? If this is not the case, then although that particular species may !e involved in the localised spread of the disease agent during an out!reak, it ill not serve as a continuous source of infection. As such, the importance of that species in the overall epidemiology of the disease may !e reduced, and it may !ecome possi!le to contemplate a disease control programme in hich control measures do not have to !e applied to that particular host species. In rinderpest control, for example, it has proved possi!le to control and perhaps even eradicate the disease !y concentrating control measures solely on cattle populations, in spite of the presence of species of ild game hich are also suscepti!le to the disease. ransmission from the natural reservoir. .ven if a species can function as a natural reservoir for a particular disease agent, transmission from that reservoir to domestic livestock may only occur rarely and in certain, clearly defined circumstances. If this is the case, the reservoir species is unlikely to cause a ma(or pro!lem in the initial control of the disease in question. -o ever, hen the frequency of occurrence of the disease has !een reduced to a lo level, and eradication of the disease !ecomes a possi!ility, the implications of the presence of reservoir host species for the success of the proposed eradication programme may have to !e re3 assessed. 2.2.2. !reed suscepti ilities

Within a host species, ide ranges of suscepti!ility to a particular disease are often o!served !et een different !reeds. In Africa, for example, certain !reeds of cattle, horses, sheep and goats are more tolerant of trypanosomiasis than others. Bos taurus !reeds of cattle are generally more suscepti!le to ticks and tick3!orne diseases than Bos indicus. It is important, ho ever, to distinguish !et een the differences in suscepti!ility that are genuinely related to !reed or species and the differences that may arise as a result of previous exposure to infection. Within !reeds too, differences in suscepti!ility to the same disease agent have !een noted !et een strains or families. This has led, in recent years, to the development of !reeding programmes designed to select for disease resistance. "elective !reeding has !een pioneered in the poultry industry here a large num!er of different "lines" of poultry have !een developed that are resistant to such diseases as Aarek8s disease, salmonellosis, and even vitamin ) and manganese deficiencies. Bigs, too, can !e selected for their resistance to atrophic rhinitis and some forms of coli!acillosis. There are !reeding programmes in Australia selecting for tick resistance in cattle, and in Creat Dritain there is increasing evidence that a similar approach could !e adopted for the control of certain forms of mastitis and meta!olic disorders in high3 yielding dairy cattle. In Africa, trypanotolerant !reeds of livestock are receiving increasing attention as a possi!le solution to the trypanosomiasis pro!lem m certain areas. Dreeding for disease resistance is pro!a!ly most applica!le as a disease control option in instances here particular disease agents are u!iquitous in the environment, or of non3infectious diseases caused !y multi3causal determinants, or here other methods of control have proved unsatisfactory. )ifferences in species or !reed suscepti!ility to disease must !e taken into account hen introducing ne !reeds or species into ne environments. The ne !reed or species may !e exposed to disease agents to hich the local !reeds or species are resistant !ut to hich the ne !reed or species is highly suscepti!le. ;onversely, the imported !reed or species may itself introduce a ne disease agent to hich it is resistant !ut to hich local !reeds or species are suscepti!le. This factor has !ecome the cause for much concern in recent years given the rapid development of international transport facilities here!y livestock and their products can easily !e conveyed from one part of the orld to another. *urthermore, !ecause of improvements in the disease investigation and diagnostic facilities of many veterinary services, disease agents are !eing identified that cause little or no disease in indigenous livestock populations !ut hich have the potential to cause a severe pro!lem in the more suscepti!le livestock populations of other

countries should these agents !e imported. Dluetongue is an example of a disease hich has attained prominence in this ay. 2.2.3. "ge suscepti ilities

)ifferences in suscepti!ility to disease are often seen !et een different age groups. *or example, young animals are generally less suscepti!le to tick3!orne diseases than older animals. There is, ho ever, often a pro!lem in distinguishing !et een true age resistance in young animals and passive resistance occasioned !y the transfer of maternal anti!odies via the placenta or in the colostrum. A false impression of age suscepti!ility may also !e created hen a highly infectious disease occurs frequently in a population. It may, for instance, appear that only young individuals are affected !y the disease in question. This may not !e due to a difference in age suscepti!ility !ut simply !ecause the older individuals, ho had !een infected previously, represent a surviving and immune population. 2.2.#. Se$ associations in disease

In these associations the clinical signs of disease are associated ith sexual attri!utes, as in the case of diseases of the reproductive tract, rather than ith the fact that males may !e more suscepti!le than females or vice versa. "ometimes, too, one particular sex may !e regarded !y farmers as !eing of greater value than the other and ill therefore receive a correspondingly greater amount of care and attention hen sick. 2.3. %$trinsic determinants of disease

.xtrinsic determinants of disease are important in epidemiology in that they can have effects on the host, on the agent, and on the interactions !et een the host and the agent. They can also affect any intermediate hosts or vectors involved in the transmission of a disease, and thus determine the type and extent of the disease transmission taking place. There are three ma(or extrinsic determinants. The first t o are climate and soils, hich, !y interacting in a variety of ays, affect the environment of the host, the agent, and the intermediate host or vector, if they are present. The third ma(or factor is man, ho, uniquely among animals, has the a!ility to modify !oth the environment in hich he lives and the environment in hich he keeps his livestock. 2.3.1. &limate

When considering climate as a determinant of disease, a distinction is normally made !et een the macroclimate or eather, and the microclimate. The term microclimate refers to the actual climatic conditions prevailing in the specific, restricted environment here the host, agent, vector or intermediate host actually live. While man is as yet largely incapa!le of deli!erately manipulating macroclimates, he can control and manipulate microclimates to some extent. "acroclimates. A large num!er of different factors com!ine to make up the microclimate. "ome of these factors #heat, cold, rainfall, ind, humidity etc' can act as disease agents in their o n right, either individually or in com!inations. As such they can cause disease in young and ne !orn animals hich are particularly sensitive to heat, cold and dehydration. In older animals they tend to act more as indirect determinants of disease in that they can produce either alone or in com!inations ith other managemental and nutritional determinants 3 "stress" conditions in the host, hich may lo er its resistance !oth to infection and, if infection takes place, to disease. Aacroclimates can also affect the a!ility of a disease agent, or its intermediate host or vector, to survive in the environment. If the effects of eather on disease agents and their intermediate hosts or vectors are kno n, it may !e possi!le to predict hen host populations are at a particular risk of contracting disease and there!y to implement appropriate control measures at strategic times. This approach has !een used ith success in the control of such diseases as helminthiasis, ticks and tick3!orne diseases, trypanosomiasis, foot3and3mouth disease, and in mineral and other nutritional deficiencies. "icroclimates. While macroclimates can have a direct effect on microclimates, the study of macroclimates alone can frequently !e misleading in achieving an understanding of the epidemiology of a disease. <egions here existing macroclimatic conditions might !e thought unsuita!le for the transmission of a disease may, in fact, contain limited areas here the microclimatic conditions are suita!le for the survival of the disease agent and its vector or intermediate host. #An example may !e a ater hole or an irrigated pasture in an arid environment'. "uch areas often provide enhanced conditions for disease transmission, since they may prove attractive to livestock, particularly at those times of the year hen the macroclimate is at its most severe. If the host and the agent #and the vector or intermediate host, if they exist' are in close contact, the transmission of disease can !e effected rapidly and easily. Thus, in arid areas, the transmission of such diseases as helminthiasis and trypanosomiasis may in fact take place during the dry season hen the hosts, the agent and the vector are all concentrated around permanent ater sources. -igh contact rates in

these areas also favour the introduction and transmission of rinderpest, foot3and3mouth disease and contagious !ovine pleuropneumonia. 2.3.2. Soils

Dy interacting ith climate, soils determine vegetation and the environment in hich the livestock are kept. The main effect of vegetation is on nutrition. "oils therefore act indirectly as determinants of disease !y causing starvation, if there is little or no vegetation, or nutritiorial im!alances such as protein, energy, vitamin or mineral deficiencies. Aalnutrition can !e the direct cause of disease, or it can stress the host and thus increase its suscepti!ility to infection and disease from other sources. "oils can also have an effect on the a!ility of the agent to survive in the environment, through such factors as aterlogging, p- etc. 2.3.3. Man

Aan is often a!le to create favoura!le, artificial microclimates for livestock rearing !y providing such inputs as housing, ater supplies, irrigation etc. @nfortunately, this often results in the creation of conditions favoura!le for the survival of disease agents and their intermediate hosts or vectors. This means that, !y altering the environment, man can alter the determinants of the diseases present in that environment. The changes in determinants ill favour some diseases and !e detrimental to others. Thus changes in systems and methods of production ill result in changes in the relative importance of the diseases present, ith perhaps some ne diseases !eing introduced and others disappearing. The epidemiologist should !e alert to such changes and should attempt to predict the likely effect that these ill have on the overall disease picture, so that potentially dangerous situations can !e averted or controlled. Aan is also a!le to interfere directly in the disease process through the use of drugs, vaccines, movement controls, quarantines etc. Among the main tasks of the epidemiologist is the investigation of the efficacy such measures, as ell as to design ays in hich they can !e used most efficiently and to monitor the effects of their introduction on disease incidence. 2.#. Descri ing disease events in populations

The first priority in investigating the epidemiology of a disease is to descri!e accurately the nature of the pro!lem !eing investigated. ;omprehensive and accurate description of disease pro!lems often provides valua!le insights into the epidemiology of the disease !eing

investigated and allo s hypotheses a!out likely determinants to !e formulated. A description of a disease pro!lem should specify the disease and the population at risk, give information on the distri!ution of events in time and space, and include an attempt to quantify disease events. Disease diagnosis. If the disease is infectious in nature, the disease agent involved should also !e identified. *or the disease agent to !e infectious it must fulfil Eoch8s postulates that+ 3 The agent should !e present in all cases of the disease> 3 It can !e isolated and gro n in pure culture> and 3 It should !e capa!le of producing the disease hen innoculated into healthy animals. 4ne of the pro!lems associated ith these postulates is that they do not take into account the differences !et een different strains of agents, particularly in their virulence, pathogenicity, and infectivity, hich may !e important in the epidemiology of the disease. We shall have more to say on the pro!lems of disease diagnosis in ;hapter :. Populations at ris#. These can !e identified !y studying the distri!ution of the disease ithin host populations !y species, !reed, age and sex. )escriptions of population densities and movements are also of great value, particularly hen the disease is transmitted !y contact. Distribution of disease events in time and space. This generally involves looking for the "clustering" of disease events in time, space or !oth. The clustering of disease events in space can often !e demonstrated !y the use of conventional mapping techniques. This type of clustering may indicate the presence of a particular determinant or determinants #e.g. a vector, a mineral deficiency etc' in an area. It should !e remem!ered, ho ever, that clustering in space occurs naturally in the case of contact 3 transmitted diseases, and that it may also !e a function of host3 population density. The clustering of disease events in time may indicate that the host population as exposed to a common source of the disease or its determinant. 4ut!reaks of diseases transmitted !y such vehicles as ater or foodstuffs frequently exhi!it clustering in time, as in the case of food poisonings. "easonal clustering of disease events often indicates the influence of climatic determinants in some form or other.

The distri!ution of disease events in populations in time and space can !e descri!ed !y three !asic descriptive terms. These are+ endemic, epidemic and sporadic. An endemic disease is a disease that occurs in a population ith predicta!le regularity and ith only minor deviations from its expected frequency of occurrence. In endemic diseases, disease events are clustered in space !ut not in time. 2ote that a disease may !e endemic in a population at any frequency level, provided that it occurs ith predicta!le regularity. Additional terms can !e used to descri!e endemic diseases according to their frequency of occurrence. Thus+ $yperendemic is an endemic disease that affects a high proportion of the population at risk. "esoendemic is an endemic disease that affects a moderate proportion of the population at risk. $ypoendemic is an endemic disease that affects a small proportion of the population at risk. An epidemic disease is a disease that occurs in a population in excess of its normally expected frequency of occurrence. In an epidemic disease, disease events are clustered in time and space. 2ote that a disease may !e epidemic even at a lo frequency of occurrence, provided that it occurs in excess of its expected frequency. A pandemic is a large epidemic affecting several countries or even one or more continents. A sporadic disease is a disease that is normally a!sent from a population !ut hich can occur in that population, although rarely and ithout predicta!le regularity. Aany epidemics of infectious disease occur in a regular, cyclical fashion over a prolonged period of time. This is !ecause ith an increasing frequency of occurrence of the disease in a host population, the num!er of suscepti!le hosts decreases as individuals ithin that population !ecome infected, and then either die or recover and !ecome immune to reinfection. As the num!er of suscepti!le hosts decreases, so does the opportunity for disease transmission. This, in turn, means that the frequency of occurrence of ne cases of the disease declines. A period of time then elapses during hich ne suscepti!le individuals are !orn into the host population. The num!er of suscepti!le hosts in the population thus increases, and the opportunities for the disease agent to find a suscepti!le host are enhanced. As a result the frequency of

occurrence of the disease may increase and a ne place.

epidemic may take

When assessing the efficacy of measures introduced to control epidemics, an attempt should !e made to distinguish !et een a decline in the frequency of occurrence of the disease due to a control measure, and a natural decline in the epidemic cycle. .pidemics can !e prevented if the level of immunity in the host population can !e sustained. It is important, therefore, in instances here the control of an infectious disease is !eing attempted !y vaccination, that coverage !e maintained in the. host population even hen the disease is occurring rarely. %uantification of disease events. Any description of a disease pro!lem should include an attempt at quantification. The methods !y hich disease events in populations are quantified are descri!ed ''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''''' (H") IS &*+,I,-. -ave you ever ished you could have a clone of yourself to do home ork hile you hit the skate park or ent out ith your friends? Imagine if you could really do that. Where What exactly is cloning? ;loning is the creation of an organism that is an exact genetic copy of another. This means that every single !it of )2A is the same !et een the t o, Fou might not !elieve it, !ut there are human clones among us right no . They eren8t made in a la!, though+ they8re identical t ins, created naturally. Delo , e8ll see ho natural identical t ins relate to modern cloning technologies. -o is cloning done? ould you start?

Fou may have first heard of cloning hen )olly the "heep sho ed up on the scene in $%%&. ;loning technologies have !een around for much longer than )olly, though. -o does one go a!out making an exact genetic copy of an organism? There are a couple of ays to do this+ artificial em!ryo t inning and somatic cell nuclear transfer. -o do these processes differ?

1. "rtificial %m ryo )/inning Artificial em!ryo t inning is the relatively lo 3tech version of cloning. As the name suggests, this technology mimics the natural process of creating identical t ins. In nature, t ins occur (ust after fertili/ation of an egg cell !y a sperm cell. In rare cases, hen the resulting fertili/ed egg, called a /ygote, tries to divide into a t o3celled em!ryo, the t o cells separate. .ach cell continues dividing on its o n, ultimately developing into a separate individual ithin the mother. "ince the t o cells came from the same /ygote, the resulting individuals are genetically identical. Artificial em!ryo t inning uses the same approach, !ut it occurs in a Betri dish instead of in the mother8s !ody. This is accomplished !y manually separating a very early em!ryo into individual cells, and then allo ing each cell to divide and develop on its o n. The resulting em!ryos are placed into a surrogate mother, here they are carried to term and delivered. Again, since all the em!ryos came from the same /ygote, they are genetically identical. 2. Somatic &ell ,uclear )ransfer "omatic cell nuclear transfer, #";2T' uses a different approach than artificial em!ryo t inning, !ut it produces the same result+ an exact clone, or genetic copy, of an individual. This as the method used to create )olly the "heep. What does ";2T mean? 1et8s take it apart+ "omatic cell+ A somatic cell is any cell in the !ody other than the t o types of reproductive cells, sperm and egg. "perm and egg are also called germ cells. In mammals, every somatic cell has t o complete sets of chromosomes, hereas the germ cells only have one complete set. 2uclear+ The nucleus is like the cell8s !rain. It8s an enclosed compartment that contains all the information that cells need to form an organism. This information comes in the form of )2A. It8s the differences in our )2A that make each of us unique. Transfer+ Aoving an o!(ect from one place to another. To make )olly, researchers isolated a somatic cell from an adult female sheep. 2ext, they transferred the nucleus from that cell to an egg cell

from hich the nucleus had !een removed. After a couple of chemical t eaks, the egg cell, ith its ne nucleus, as !ehaving (ust like a freshly fertili/ed /ygote. It developed into an em!ryo, hich as implanted into a surrogate mother and carried to term. The lam!, )olly, as an exact genetic replica of the adult female sheep that donated the somatic cell nucleus to the egg. "he as the first3ever mammal to !e cloned from an adult somatic cell. -o does ";2T differ from the natural ay of making an em!ryo?

The fertili/ation of an egg !y a sperm and the ";2T cloning method !oth result in the same thing+ a dividing !all of cells, called an em!ryo. "o hat exactly is the difference !et een these methods? An em!ryo is composed of cells that contain t o complete sets of chromosomes. The difference !et een fertili/ation and ";2T lies in here those t o sets originated. In fertili/ation, the sperm and egg !oth contain one set of chromosomes. When the sperm and egg (oin, the resulting /ygote ends up ith t o sets 3 one from the father #sperm' and one from the mother #egg'. In ";2T, the egg cell8s single set of chromosomes is removed. It is replaced !y the nucleus from a somatic cell, hich already contains t o complete sets of chromosomes. Therefore, in the resulting em!ryo, !oth sets of chromosomes come from the somatic cell.