11 rs [[leamine Oniectves Alter reading and studying this chapter, you should be blot: ‘ Define the terms soprophytes, parasite, commensel, pathogen. '¢ Describe classification of infections ‘¢ Deline and differentiate primary, secondary, oppor tunistic and reinfections. Infection and immunity involve interaction between the animal body (host) and the infecting microorganisms, MICROORGANISMS AND HOST Based on their relationship to their host they can be divided into saprophytes and parasites. A. Saprophytes B. Parasites A Saprophytes Saprophytes (from Greek sapros decayed; and phyton plant) are free-living microbes that live on dead or decaying organic matter. They are found in soil and water and play an important role in the degradation of ‘organic materials in nature. They are oflittlerelevance in infectious disease because they are generally incapable ‘of multiplying on living tissues. However, saprophytes, like Bacillus subtilis may cause infection sometimes when host resistance is lowered. B Parasites Parasites are microbes that can establish themselves and multiply in the hosts. There are many parasitic agent's ‘or organisms among the viruses, bacteria, fungi, plants, and animals. By convention, when the word parasite is used without quantification, it refers specifically to a protozoan or helminthic (nematode, trematode, cestode) ‘organisms. Parasite mirobes may be either pathogens or ‘commensal: Pathogens Pathogens (from eek path , disease, and gen, to pro- duce) are the microorganisms or agents, which are caps bie of producing disease in the host. Its ability to cause disease is called pathogenicity. Infection '¢ Name and define various types of carrier. 4 Discuss modes ol spreed of infection giving suitable examples lst toxins. ferences between: exolonies ond endo: ‘Types of Pathogens They are two types: Primary and opportunist pathogens. Primary (frank) pathogens Primary (frank) pathogens are the organisms, which are capable of producing disease in previously healthy in viduals with intact immunological defences. However, these bacteria may mare readily cause disease in in viduals with impaired defences 4b Opportunist pathogens Opportunist pathogens rarely cause disease in indi viduals with intact immunological and anatomical defences. These bacteria are able to cause disease only when such defences are impaired or compromised, as a result of congenital or acquired disease or by the use of immunosuppressive therapy or surgical techniques. Many opportunistic pathogens are part of the normal human flora, e.g. coagulase negative staphylococci and Escherichia coli Commensals Commensals (organisms of normal flora) are the micro ‘organisms that live in complete harmony with the host without causing any damage to it. Skin and mucous membranes are sterile at birth. The normal bacterial flora of the body consist largely of commensals. Many commensal: behave as facultative pathogens in that they can produce disease when the host resistance is lowered. INFECTION AND INFECTIOUS DISEASE isnecessary to distinguish between the term ‘infection’ and ‘infectious diseaseInfection The lodgement and multiplication of a parasite in or fon the tissues of a host constitute infection. It does not inwariably result in disease. In fact, disease is but a rare ‘consequence of infection, which is a common natural event Infectious disease ‘An infectious disease is any change from a state of health in a part or all of the host body is net capable of ‘carrying on its normal functions due to the presence of ‘an organism or its products. CLASSIFICATION OF INFECTIONS Infections may be classified in various ways. 1. Primary infection: Initial infection with a parasite ina host is termed primary infection i saeloaies eisezua hieere i inane in the host are termed reiafections 3, Secondary infection: When anew parasite sets up an infection in a host whose resistance is lowered by a preexisting infectious disease, this is termed secondary infection. 4 Local infection: The term Local infection (mone appropriately local sepsis) indicates a condition Where, due to infection or sepsis at localized sites such as appendix oF tonsils, generalized effects are produced. 5. Cross infection: When in a patient already sulfer- ing from a disease a new infection is set up from another host or another extemal source, it is termed cress infection 6 Nosocomial infections: Cross infections occurring n hospitals are called nosocomial infections (from reek nosoconion hospital). trogenie infection: The term iatrogenic infection relers to physician induced infections resulting, from investigative. therapeutic or other procedures. Depending on whether the source of infection is from the host's own body or from extemal sources, infections are classified as endogenous or exogenows, respectively. Based on the clinical effects of infes tions, they may be classified into different varieties & Inapparent infection: Inapparent infect where clinical effects are not apparent. 4. Subclinical infections The term subclinical infection is often used as a synonym to inapparent infection, Atypical infection: Atypical infection is one in which the typical or characteristic clinical manifes tations of the particular infectious disease are not present Latent infection: Some parasites, following infec tion, may remain in the tissues ina latent or hidden form proliferating and producing clinical disease when the host resistance is lowered. This is termed latent infection aw. n, SOURCES OF INFECTION AL Human b B. Animals: C. Insects D. Soil and water E. Food ngs A. Human Beings The commonest source of infection for human beings is human beings themselves. The parasite may originate from patient orcarrier. Humans play a substantial role as microbial reservoirs. Humans serving as the microbial reservoir i. Indeed, the passage of a neonate from the sterile en- Vironment of the mother’s womb through the birth canal, which is heavily colonized with Various mi: ‘robial agents, isa primary example of one human directly acquiring microorganisms from another human serving as the reservoir. li, Acquisition of “strep” throat through touching, Hepatitis by blood transfusions iv. Gonorthea, syphilis, and (AIDS) acquired immune deficiency syndrome by sexual contact \. Tuberculosis by coughing; and the common cold through sneezing, Carrier A cartier is person who harbors the microorganisms without suffering from any il effect, because of i, There are several types of carriers 1. Convalescent cartier: A convalescent carrier is an individual who has recovered from the infectious disease but continues to harbor large numbers of the pathogen Healthy carrier: A healthy carrier isan indi who harbors the pathogen but isnot il 3. Incubatory carrier: An incubatory carrier is an ndividual who is incubating the pathogen in lange numbers but isnot yet il 4. Temporary carviers: Convalescent, healthy, and ncubatory carriers may harbor the pathogen for caly a brief period (hours, days, ar weeks) and lasts less than six months and then called casual, acute, transient or temporary carriers, Chronic carriers: They harbor the pathogen for Jong periods (months, years, oF life). 6. Contact carriers: The term contact carrier isapplied to a person who acquires the pathogen from a patient. 7. Paradoxical carrier: Paradoxical carrier refers to a ‘atrier Who acquires the pathogens from another carrier Carriers may be classified according to portal of exit of the infectious agent such as urinary carriers, intesti- nal carriers, respiratory carriers, nasal cartiers, etc idualB.Animals Reservoir Hosts Many pathogens are capable of causing infections in both human beings and animals. Therefore, animals may act as a source of infection of such organisms. These, animals serve to maintain the parasite in nature and act as reservoir and they are, therefore, called res- ervoir hosts. Zoonosis ‘The diseases and infections, which ate transmissible to rman from animals are called zoonosis, Humans contact the pathogens by several mechanisms. Examples of soonoti diseases: Bacterial Anthrax, brucellosis, Qfever, leptospirosis, bovine tuber -ealosis, bubonic plague, Salmonella food poisoning, Viral Rabies, yellow fever, cowpox, monkeypox Protozoal Leishmaniasis, toxoplasmosis, trypanosomiasis, babe- Helminthic Echinococcosis, teniasis,trichinellosis Fungal Microsporum canis, Trichophyton verrucestm, Cnsects Arthropodborne Diseases Biood-sucking insects such as mosquitoes, ticks, mites, flies, and lice may transmit pathogens to human beings and diseases so caused are called arthropodborne diseases Vectors Insects that transmit infections are called vectors. Vector- borne transmission can be of two types either mechani- ‘al (external) or biological (internal). i. Mechanical vector: The disease agent is transmit- ted mechanically by the arthropod. Carriage is pas- sive, with no growth of the pathogen during trans- Examples: Transmission of diarrhea, dysentery, typhoid, food poisoning and trachoma by the housefly, fi, Biological vectors: Biological vectors are those in whom the pathogens multiply or undergo devel- ‘opmental changes with or without multiplication, Biological vectors transmit infection only’ after the pathogen has multiplied in them sufficiently or has undergone a developmental cycle. The interval between the time of entry of the pathogen into the vector and the vector becoming infective is called the extrinsic incubation period. Examples: Aedes aegypti mosquito in yellow fever, Anopheles mosquito in malaria, Reservoir Hosts Resides acting as vectors, some insects may also act ax reservoir hosts (for example, ticks in relapsing fever and spotted fever). Infection is maintained in such insects by transovarial or transstadial passage. D. Soll and Water iSoil Some pathogens can survive in the soil for long periods. Examples 2. Spores of tetanus and gat gangrene: Spores of! tetanus and gas gangrene remain viable in the soil for several decades and serve as source of infec- tion. The human and animal intestine s thenormal habitat of these organisms and they enter the soil through their feces b. Fungi and parasites: Fungi (causing mycetoma, sporotrichosis, histoplasmosis) and parasites such. as roundworms and hookworms also survive in the soil and cause human infection, i. Water Water may act asthe source of infection either due to contamination with pathogenic microorganisms (Shige 1s, Salmonella, Vitro cholera, poliomyelitis virus, hepa tis virus) oF due the presence of aquatic vector (cyclops containing larvae of guinea worm infection. E. Food Contaminated food may act as source of infection of organisms causing food poisoning, gastroenteritis, diar thea and dysentery. There are two primary types of food-related diseases: foodborne infections and food intoxicants. MODES OF TRANSMISSION OF INFECTION _ ‘The aman host may acquive microbial agents by vari cus means referred toas the moves of ransmssion Patho- genic onganiama can apread from one host to another by 2 Variety of mechanisms. These include Contact Inhalation Ingestion Inoculation Insects Congenital Iatrogenic and laboratory infections 1. Contact Infection may be acquired by contact, which may be director indirect, 4 Direct contact Directcontact implies an actual physical interaction with the infectious source. Diseases transmitted by directee ‘Malaria, ilaria, viral encephalitis (e.g. Japanese encephalitis), viral fevers (e.g. dengue, ‘West Mle, viral hemorrhagic fevers (e.g. yellow fever, dengue hemorrhagic fever) ‘Typhoid and paratyphoid fever, diarthea, dysentery, cholera, gastroenteritis, amebiasis, helrmintnc infestations, poliomyelitis, conjunctWvitis, trachoma, anthrax, yaws, etc, Kala-azar, oriental sore, sand fy fever, oraya fever ‘Sleeping sickness Epidemic typhus, relapsing fever, trench fever, pedicutosis Bubonic plague, endemic typhus, chiggerosis, Hymenolepts diminuta Onchocerciass Chagas disease ‘Tick typhus, viral encephalitis, viral fevers, viralhemerrhagic fever, disease), tularemia, tick paralysis, human babesiosis 10. Soft tick Qlever, relapsing fever 11, Trombiculld mite ‘Scrub typhus, Rickettsialpox. 12, Itch-mte ‘Seabies 13, Cyclops 14, Cockroaches Enteric pathogens such as exchange transfusion, dialysis, and heart and transplant surgery have increased the possibilities for iatrogenic infections, These are known as iatrogenic ot physician-induced infections, Laboratory personnel handling infectious materialand doing mouth-pipetting, ave particularly at risk. FACTORS PREDISPOSING TO MICROBIAL \THOGENICITY. Pathogenicity and Virulence Pathogenicity Denotes the ability of a microbial species to cause di ‘ease. The term virulence (Latin virulent, from virus, poison) denotes the ability ofa strain ofa species to pro- duce disease. Virulence Virulence provides a quantitative measure of patho- genicity, oF the likelihood of causing disease, For exam- ple, encapsulated pneumococci are more virulent than onencapsulated peumococei, and Escherichia cli that ‘express Shiga-like toxins are more virulent than those that do not express these toxins. The virulence of a strain is not constant and may undergo spontaneous or induced variation Exaltation wancement of virulence is known as exaltation, This ‘can be induced by serial passage af a strain in an experi mental animal. Attenuation Reduction of virulence is known as attenuation and ‘ean be induced by passage through unfavorable hosts, repeated culture in artificial media, growth under high Guinea worm disease, fish tapeworm (D. (atum) temperature or inthe presence of weak antiseptic, des- {ecation, or prolonged storage in culture. Virutence Factors Virulence factors refer to the propertios (e.g ucts) that enable a microorganistn to establish it ce within a host ofa particular species and enhance its potential to cause disease. Virulence is determined by three characteristics of the pathogens: invasiveness, infectivity, and pathogenic potential. A major aspect of pathogenic potential is toxigenicty Determinants of Virulence ‘Transmissbility ‘Adhesion Invasiveness ‘Toxigeniity Avoidance of host defence mechanisms Enzymes Plasmids Bacteriophages Communicability Infecting dose Route of infection 1. Transmissibility The fist step of the infectious processis the entry of the microorganism into the host by one of several ports: the respiratory tract, gastrointestinal tract, urogenital tract, or through skin that has been cut, punctured, or burned. Once entry is achieved, the pathogen must overcome a diversity of host defenses before it can establish itself ‘These include phagocytosis, the acidic environments of the stomach and urogenital trict. and various hydrolyt- {c and proteolytic enzymes found in saliva, in stomach, and in the small intestine 1 3 4 5. 6. 7. ‘ 9, 10. 02. Adhesion Adhesins The initial event in the pathogenesis is the attachment eria to body surfaces. This attachment is not 1 chance event but a specific reaction between surface ‘receptors on host cells and adhesive structures (ligands) fon the surface of bacteria, These adhesive structures are called adhes ‘Adhesions may occur as organized structures, such tors. Nonspecific surface properties of the bacterium, including surface charge and hydrophobicity, also con- tnbute to the initial stages of the adhesion process. Some bacteria (for example, Escherichia coll) use their pill toadhere to the surface of host cell. Group A strep- tococe have similar structures (fimbriae), A striking example of the importance of adhesion is that of Neis seria gonorrhoeae in which strains that lack pili are not pathogenic. If bacterium is invasive in nature, adhee- tence helps in penetrating host cells. Adhesins os Virulence Factors ‘Adhesins serve as virulence factors, and loss of adhes- ins often renders the strain avirulent, Adhesins are usu- ally made of protein and are antigenic in nature. Spe- cific immunization with adhesins has been attempted as a method of prophylaxis in some infections, as for instance against E, coll diarrhea in calves and piglets, and gonorrhea in human beings. 3. Invasiveness Invasiveness signifies the ability ofa pathogen tospread in the host tissues after establishing infection. For many disease-producing bacteria, invasion of the host's epi- thelium is central to the infectious process. Highly invasive pathogens characteristically produce spread- ing or generalized lesions (eg. streptococcal septicemia following wound infection), while less invasive patho- gens cause more localized lesions (e.g. staphylococeal abscess). Some pathogens though capable of causing serious of even fatal diseases lack invasiveness (e.g. the tetanus bacillus which remains confined to the site of entry and produces the disease by elaborating, a potent toxin), 4. Toxigenicity Some bacteria cause disease by producing toxins, of which there are two general types: the exotoxins and the endotoxins. Both gram-positive and gram-negative bacteria secrete the exotoxins, which are proteins. In contrast, the endotoxins, which are lipopolysaccha- rides, are not secreted, but instead are integral com- ponents of the cell walls of gram-negative bacteria (Table 112). Exotoxins Exotoxins are soluble 60 to 89°C which are secreted by certain species of bac- iv and diffuse readily into the surrounding medium. r ‘Those ore highly potent in minute amounts and include some of the most poisonous substances known. Wis estimated that as litle as one microgeam of tetanus exotoxin can killan adult human, One mg of tetanus or botulinum toxin is sufficient to kill more than one mil- lion guinea pigs and 3 kg of botulinum toxin can kill ll the inhabitants of the world. ‘Treatment with dilute formaldehyde destroys the toxic activity of most exotoxins, but does not affect their antigenicity. Formaldehyde—inactivated toxins, called toxoids, are thus useful in preparing vaccines. Exotoxin proteins are in many cases encoded by ‘genes carried on plasmids or temperate bacteriophag: ‘They exhibit specific tissue affinity and pharmaco- logical activities, each toxin producing a typical effect which can be made out by characteristic clinical mani- festations or autopsy appearances. ‘They are associated with specific diseases and have specific mechanisms of action. They are easily inactivated by formaldehyde, iodine, and other chemicals to form immunogenic toxoids. ‘They are unable to produce a fever in the host direct ly and often given the name of the disease they produce (e.g: the diphtheria toxin). Exotoxins ae generally formed by gram-positive bacteria but may alsobe produced by some gram-ne} tive organisms such as Shiga’s dysentery bacillus, chol- ra vibrio and enterotoxigentc E.coli, Endotoxins These are heat-stable, lipopolysaccharide (LPS) compo nents of the outer membranes of gram-negative bacter but not gram-positive bacteria, Theit toxicity depends upon the the component (lipid A). They are released into the host’s circulation follow: {ng bacterial cell lysis, ‘They are toxic only at high doses (milligram per kilo- gram amounts) They cannot be toxoided ‘They are poor antigens and weakly immunogenic and their toxicity is not completely neutralized by the homologous antbodies. ‘They do not exhibit specific pharmacological activi- ties. They are generally similar, despite source. ‘All endotoxins, produce similar effects whether iso- Inted from pathogenic oF nonpathogenic bacteria ‘Administration of small quantities of endotoxin in susceptible animals causes an elevation of body tem- perature manifested within 15 minutes and lasting for several hours. The pyrogenic effect of fluids used for intravenous administration is usually due to the pres- ence of endotoxins from contaminant bacteria. They are usually capable of producing general systematic effects. Intravenous injections of large doses of endotoxin and massive gram-negative septicemias cause endotoxic shock marked by fever, leukopenia, thrombocytopenia, significant fall in blood pressure, circulatory collapse ind bloody diarthea leading to death (Table 11.2).1. Proteins 2. Heat-labile (inactivated at 60-80%) 3. Actively secreted by the cells; diffuse into the sur rounding medium “4. Readily separable trom cuttures by physical means ‘such as filtration 5. Action often enzymic 6. Specific pharmacological effect for each exotoxin Specific tissue affinities ‘rghiy toxic ang fatal in microgram quantities 9. Highly antigenic 10. Action specifically neutralized by antibody 11, Usually do not produce fever 12, Produced by both gram-positive bacteria and gram- negative bacteria Frequently controlled by extrachromosomal genes (eg. plasmids) Disease, e.g. Botullem, diphtheria, tetanus 13, 14. 5. Avoidance of Host Defence Mechanisms Bacteria also have evolved many mechanisms 10 evade host defenses. Several of these evasive mecha- nisms are now discussed. a. Capsules Some bacteria such as Streptococcus pnewmeniae, Neisse- ria meningitidis, and Haemophilus influenzae can produce a slippery mucoid capsule that prevents the phagocyte from effectively contacting the bacterium, and noncap- sulate variants usually exhibit much reduced virulence. , Streptococcal M protein Other bacteria evade phagocytosis by producing spe- alized surlace proteins such as the M protein on Strep- ftococcus pyogenes. Resistance to killing by phagocytic cells Some bacteria have evolved the ability to survive inside neutrophils, monocytes, and macrophages. These path- fogens not only survive within macrophages and other phagocytes, but may actually multiply intracellulary. Difierent organisms use different strategies for survival i. Toescape from thephagosome before itmerges with the lysosome, as seen with Listeria menocylogenes, Shigella, and Ricketsia i. To prevent phagolysosome fusion, e.g. in Mycobac- terium tuberculosis, probably at least partly because ofits waxy external layer. fil, Production of catalase by Staph. aureus and N. -govorrlueae is thought to protect these organisms from such toxic products. Lpopolysaccharide on outer membrane. Lipid A por- tion is toxic 2. Heat-stable 3. Ferm integral part af the cell wall; do net diffuse into ‘surrounding medium 44. Obtained onty by call ysis 5. Noenzymic action Nonspecific action ofall endotoxins 7. No Specific tissue affinities '8. Moderate toxicity. Active only in very large doses 9. Weakly antigenic: 10. Neutralization by antibody ineffective 11, Usually produce fever by release of intertukin-t 12, Produced by gram-negative bacteria only ‘Synthesized directly by chromosomal genes 14, Gram-negative infections, meningococcemia Antigen Variation in surface antigen composition during the course of infection provides a mechanism of avoidance of specific immune responses directed at those antigens. Examples i. Pathogenic Neisseria ii, The borrelia generate antigenic variation. Other bacteria show strain-specific antigenic varia- bility such as group A streptococci 75 antigenically. distinct serotypes of M proteins. ¢ Serum resistance To survive in the blood, bacteria must be able to resist Isis as a result of deposition of complement on the bacterial surface. Some gram-negative bacteria can longthen the 0 chains in their lipopolysaccharide to prevent complement activation. {f Siderophore and iron acquisition Many bacteria produce these low molecular weight compounds called siderophores that can acquire iron from the host's iron binding proteins. This property enhances the virulence. 6. Enzymes. Many species of bacteria produce tissue-degrading enz- ymes that play important roles inthe infection process. i. Coagulase: Coagulase is produced by S. aureus. ‘This thrombin-like enzyme prevents phagocytosis, by forming a fibrin barrier around thebacteria and. walling off the lesion. ii, Lecithinase-C and collagenase: C. perfringens pro- duces lecithinase-C and collagenase. Lecithinase- variation€ damages cell membranes by splitting lecithin to phosphorylcholine and diglyceride while col- lagenase degrades collagen, the major protein of fibrous connective tissue thus promoting spread of infection in tis Hyaluronidases: Hyaluronidases split hyaluronic acid which is a component of intercellular connec: tive tissue and thus facilitate the spread of infection along, tissue spaces iv. Streptokinase (fibrinolysin); Many hemolytic treptococei produce streptokinase (fibrinalysin) Finolysins promote the spread of infections by ‘breaking down the fibrin barrier in tissues ¥. Cytolysins: These include, hemalysins capable of destroying erythrocytes and leukocidins damage polymorphonuclear leukocytes. a. Streptolysin O and streptolysin § are produced by gioup A streptococci b. Most strains of Staphylococens aureus produce hemolysins & Escherichia coli strains that cause urinary tract infections. produce hemolysins whereas those strains that are part of normal gastrointestinal flora may or may not produce hemolysins Igh 1 proteases: These enzymes specifically cleave immunoglobulin IgA which protects at mucosal surfaces. tis an important virulence factor of N. gonorrhoeae, N. meningitidis, H. influencae, S. pnew Imonia, somestrains of Prevotelia melaninogenica and some streptococci associated with dental caries, 7.Plasmids Plasmids ate extrachomosomal DNA segments that ‘carry genes for antibiotic resistance known as R-fac- tors. Multiple drug resistance (R) plasmids increase the severity of clinical disease by their resistance to antibi otic therapy’ ‘Genes coding for some virulence characteristics may bbe plasmidborne. Surface antigens responsible for the colonization of intestinal mucosa by E.coli and entero- toxin production by E. coli and Staph. aureus are exams ples of plasmidborne virulence factors. 8. Bacteriophages ‘Tho classical example of phage directed virulence is seen in diphtheria. All the strains of C. diphtheriae pro- duce exotoxin only when they are lysogenized with a bacteriophage called betaphage. In diphtheria baci, the gene for toxin production is present in beta or other tor+ corynephages. The elimination of this phage abol- inhes the tonigenicty ofthe bacillus ‘9. Communicability The ability of a microbe to spread from one host to another is known as communicability. This property determines the survival and distribution of a parasite ina community but does not influence the production ‘of disease in an individual host, A correlation need not st between virulence and communicability. In fact, high degree of communicablity may not be exhibited by a highly virulent parasite due to its rapidly lethal effect on the host. In general, infectionsinwhichthe pathogenisshedin secretions, as in respiratory or intestinal disease highly communicable. In some instances infection reps sents a dead end, as in hydrophobia, there being, an interruption in the spread af the pathogen to other hosts. Cecurrence of epidemic and pandemic diseases requires that the pathogen should possess high degree of virulence and communicabiity 10. Infecting Dose ‘Adequate number of bacteria is required for successful infections. The dosage may be estimated as the mini- mum infecting dose (MID) or minimum lethal dose (MLD, Minimum Infecting Dose (MID) Minimum number of bacteria required to produce lin «al evidence of infection in a susceptible animal under standard conditions i called minimum infective dose (MID), Minimum Lethal Dose (MLD) MLD is a minimum number of bacteria that produce death in the animal under standard conditions. ‘Asanimals exhibit considerable individual variation {in susceptibility, these doses are more correct ed as statistical expressions, ID5) and LD50 as required to infect or kil 50 percent of the animals tested under standard conditions 11, Route of Infection Some bacteria can initiate infection whatever be the mode of entry such as streptococci. Certain bacteria are infective when introduced through optimal route, for example, cholera vibrios can produce lesion only when administered by oral route, but unable to cause infection when introduced subcutaneously. However, Staphylococcus aureus can cause lesion whatever may be the portal of entry. Probably this difference is related to modes by which different bacteria are able to initiate tis- sue damage and establish themselves. Bacteria after introduction into tissues also differ in their sites of election in the host body. They also differ in the ability to produce damage of different organs in different species of animals. Lesions are caused mainly in the kidney and infrequently in the liver and spleen ‘hen tubercle bacilli injected into rabbits but in guinea Pigs the lesions are mainly in the liver and spleen, the kidneys being spared. The reasons are largely obscure for such selective multiplication in tissues, though they may be related to the presence in tissues of substances that may selectively hinder or favor their multiplication. ‘TYPES OF INFECTIOUS DISEASES may be localized or generalized Infectious A.Localized Localized infections may be superficial or deep-seated,B.Generalized Generalized infection involves the spread of the infect- ing agent from the site of entry by contiguity, through tissue spaces or channels, along the lymphatics or through the bloodstream (bacteremia) which leads to dissemination of organisms, 1, Bacteremia Circulation of bacteria in the blood is known as bvcte- ‘emia, Transient bacteremia is a frequent event even in healthy individuals and may occur during chewii brushing of teeth or straining at stools. The bacteria are immediately mopped up by phagocytic cells and are unable to initiate infection. Bacteremia of greater sevee~ ity and longer duration is seen during generalized infoc- tions as in typhoid fever. 2 Septicemia Itis the condition where bacteria circulate and multiply inthe blood, form toxic products and cause high, swing? ing type of fever. 3, Pyemia Itis condition where pyogenic bacteria produce septice- ‘mia with multiple abscesses in internal organs such as the spleen, liver and kidney. EPIDEMIOLOGICAL TERMINOLOGY Depending on the spread of infectious diseases in com- munity, they may be classified as endemic. epidemic, and pandemic. 1, Endemic ‘The disease which is constantly present in a pasticul area, eg. typhoid feveris endemic in most parts of Ind 2. Epidemic ‘The disease that spreads rapidly, involving many pee sons ina particular area at the same time, i called epi demic disease, eg, meningococcal meningitis, In the cold countries influenza causes annual winter epidem- 3, Pandemic IRisanepidemic that spreads through many area ofthe world involving very large number of persons within a short period, eg. cholera, influenza and enteroviral con- Junetivitis, Epidemics vary in the rapidity of spread. Waterborne diseases such as cholera and hepatitis may cause explo- sive outbreaks, while diseases which spread by person- toxperson contact evolve more slowly. Such creeping or smouldering epidemics, as that of cerebrospinal fever, are termed prosodemic diseases, Be KNOW MORE Infection ‘Humans and microorganisms inhabit the same planet, and their paths cross in many and varied ways so that {nteractionsare inevitable. Serum Resistance In the enterobacteriacene, resistance is primarily due to the composition of the ipopoysaccharide (LPS) present | inthe bacterial outer membrane. Others such as Neisseria _gonorrhocae generate serum resistance. OKO S aT | * Infection and immunity involve interaction be- tween the animal body (host) and the infecting mi- croorganisms. ‘Parasites are microbes that ean establish themselves and multiply in the hosts, Parasite mizobes may be either pathogens or commensals: Infection Infections may be classified in various ways: Sources of Infection: 1. Human beings—from a patient or cartier; 2. Animals;3. Insects; 4. Soil and water; 5. Water, 6, Food Modes of Transmission of Infection 1. Contact; 2. Inhalation; 3. Ingestion; 4. Inoculation, 5 Insects; 6, Congenital;7. latrogenic and laboratory infec tions. Determinants of Virulence 1 Transmissibility;2. Adhesion; 3. Ivasiveness;4. Toxi- genicity; 5. Enzymes; 6. Plasmids; 7. Bacteriophages; 8. Communicability; 9. Infecting; dose; 10. Route of infec tion, ‘Types of Infectious Diseases A. Localized infections may be superficial or deep: seated B. Generalized infection 1, Bacteremia; 2. Septicemia; 3. tyemia IMPORTANT QUESTIONS 1, Describe in detail the sources of infections to hus mans beings. 2. What are the various modes of spread of infection? Deseribe each in brie! giving suitable examples 3, Describe the factors determining microbial patho- enicity and virulence. 4. Distinguish between exotoxins and endotoxins in a tabulated form. FURTHER READING Mims CA. The Pathogenesis of Infectious Disease, rd edn London Academic Prins 1947. Toxton IR, Arbuthoot JP. Determinants of bacterial virulence, ‘Chap. 13 In: Topley and Wilson's Princes of Backology Virology and Immun, 8th eda. Vo. Landon: Edward Arnold 1990 Kelman DA, Falkow S: A molecular perspective of microbial ‘pathogenicity. In: Mandell, Donglas and practice of inter- tious diseases, Sth ed. Mandell GL, Bennett JE, Dolan R tox) Churchill Livingstone 2500 Sayer AA, Whit DD. ceria! Fthogeenis A Nols ETE Approach men Soc frac Poe Wt