Infection and Immunity
Infection and immunity involve interaction between the host (man) and the infecting microorganism. Based on their relationship to their hosts, microorganisms can be classified as saprophytes and Parasites.
Saprophytes are free-living microbes that subsist 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.
Parasite: Parasite may be defined as a microorganism, which lives on a living host and derives nutrition from the host, without any benefit to the host.
Commensal: Commensals (con, with; mensa, table, i.e. living together) live in complete harmony with the host body without causing any harm to it. The commensals constitute the normal bacterial flora of the body such as Staphylococcus epidermidis of skin and Escherichia coli of gastrointestinal tract. The commensals subsist on secretions, food residues or waste products of the body.
Opportunistic pathogens: Some commensals or saprophytes can produce disease when the body resistance is lowered; such organisms are termed as opportunistic pathogens.
Pathogens: A microorganism capable of producing disease is called pathogen. Majority of the pathogenic bacteria are heterotrophs.
Pathogenicity: Pathogenicity refers to the ability of a class of bacteria to produce disease.
Virulence: Virulence is a measure of the degree of pathogenicity and depends on invasiveness and toxigenecity of the organism.
The term infection and disease are often used synonymously when discussing hosp-parasite relationships. The difference between these terms is helpful to understand the development of the normal microflora, which represents a successful host-microorganism relationship.
Colonizer: A microorganism that makes contact with the host but does not cause the host to produce an immune response that would destroy it or cause an allergic response is called a Colonizer.
Infection: Microorganisms that make contact with the host and elicit an immune response (antibody production) are said to cause infection.
Disease: If the microorganism brings about an abnormal condition in the host, in addition to elicting antibodies, it is said to cause a Disease.
Infection: Infection may be defined as lodgement and multiplication of an infectious agent in the body. All infections do not invariably results in disease. Some infections may remain asymptomatic and others may lead to development of signs and symptoms after breakdown of host-parasite relationship in favour of the parasite. It is necessary to distinguish between the term infection and infectious disease. Infection does not always results in disease. In fact disease is but a rare consequence of infection, which is a common natural event.
Infection may be classified in various ways such as:
Primary infection: Initial infection with a parasite in a host is termed as primary infection.
Reinfection: Subsequent infections by the same parasite in the host are termed as reinfections.
Secondary infection: When a new parasite sets up an infection in a host whose resistance is lowered by a preexisting infectious disease, is termed as secondary infection.
Focal infection (focal sepsis): A localized site of infection from which bacteria and their products are spread to other parts of the body. Or. Indicates a condition where, due to infection or sepsis at localized sites such as appendix or tonsils, generalized effects are produced.
Cross infection: when in a patient already suffering from a disease a new infection is set up from an other host or another external source, it is termed as cross infection.
Nosocomial infections: Cross infections occurring in hospitals are called nosocomial infections.
Iatrogenic infection: It refers 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 form external sources, infections are classified as endogenous or exogenous, respectively. Based on the clinical effects of infections, they may be classified into different varieties.
Infection and immunity involve interaction between the host (man) and the infecting microorganism. Based on their relationship to their hosts, microorganisms can be classified as saprophytes and Parasites.
Saprophytes are free-living microbes that subsist 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.
Parasite: Parasite may be defined as a microorganism, which lives on a living host and derives nutrition from the host, without any benefit to the host.
Commensal: Commensals (con, with; mensa, table, i.e. living together) live in complete harmony with the host body without causing any harm to it. The commensals constitute the normal bacterial flora of the body such as Staphylococcus epidermidis of skin and Escherichia coli of gastrointestinal tract. The commensals subsist on secretions, food residues or waste products of the body.
Opportunistic pathogens: Some commensals or saprophytes can produce disease when the body resistance is lowered; such organisms are termed as opportunistic pathogens.
Pathogens: A microorganism capable of producing disease is called pathogen. Majority of the pathogenic bacteria are heterotrophs.
Pathogenicity: Pathogenicity refers to the ability of a class of bacteria to produce disease.
Virulence: Virulence is a measure of the degree of pathogenicity and depends on invasiveness and toxigenecity of the organism.
The term infection and disease are often used synonymously when discussing hosp-parasite relationships. The difference between these terms is helpful to understand the development of the normal microflora, which represents a successful host-microorganism relationship.
Colonizer: A microorganism that makes contact with the host but does not cause the host to produce an immune response that would destroy it or cause an allergic response is called a Colonizer.
Infection: Microorganisms that make contact with the host and elicit an immune response (antibody production) are said to cause infection.
Disease: If the microorganism brings about an abnormal condition in the host, in addition to elicting antibodies, it is said to cause a Disease.
Infection: Infection may be defined as lodgement and multiplication of an infectious agent in the body. All infections do not invariably results in disease. Some infections may remain asymptomatic and others may lead to development of signs and symptoms after breakdown of host-parasite relationship in favour of the parasite. It is necessary to distinguish between the term infection and infectious disease. Infection does not always results in disease. In fact disease is but a rare consequence of infection, which is a common natural event.
Infection may be classified in various ways such as:
Primary infection: Initial infection with a parasite in a host is termed as primary infection.
Reinfection: Subsequent infections by the same parasite in the host are termed as reinfections.
Secondary infection: When a new parasite sets up an infection in a host whose resistance is lowered by a preexisting infectious disease, is termed as secondary infection.
Focal infection (focal sepsis): A localized site of infection from which bacteria and their products are spread to other parts of the body. Or. Indicates a condition where, due to infection or sepsis at localized sites such as appendix or tonsils, generalized effects are produced.
Cross infection: when in a patient already suffering from a disease a new infection is set up from an other host or another external source, it is termed as cross infection.
Nosocomial infections: Cross infections occurring in hospitals are called nosocomial infections.
Iatrogenic infection: It refers 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 form external sources, infections are classified as endogenous or exogenous, respectively. Based on the clinical effects of infections, they may be classified into different varieties.
Inapparent infection: Is one where clinical effects are not apparent.
Sub-clinical infection: it is a synonoym of inapparent infection.
Atypical infection: Is one in which the typical or characteristic clinical manifestations of the particular infectious disease are not present.
Latent infections: Some parasites, following infections, may remain in the tissues in a latent or hidden form proliferating and producing clinical disease when the host resistance is lowered. This is termed latent infections.
Sources of infection: Infection may be acquired endogenously or exogenously.
Endogenous sources: This occurs with microorganisms of the host’s normal flora which behave as pathogens outside their habitat.
Exogenous sources:
Man:
The commonest source of infection for human beings is the human beings themselves. The parasite may originate from a patient or a carrier. A Carrier is a person who harbors the pathogenic microorganism without suffering form any ill effect because of it. Several types of carriers have been identified. A healthy carrier is one who harbors the pathogen but has never suffered form the disease caused by the pathogen. While a convalescent carrier is one who has recovered form the disease and continues to harbor the pathogen in his body. Depending on the duration of carriage, carriers are classified as temporary and chronic carriers. The temporary carrier state lasts less than six months, while chronic carriage may last for several years and some times even for the rest of ones life. The term contact carrier is applied to a person who acquires the pathogen from a patient, while the term paradoxical carrier refers to a carrier who acquires the pathogen form another carrier.
Animals:
Many pathogens can infect both man and animals. Zoonoses are infections between vertebrate- animals and man. Many of those infections affect agridultural workers and veterinary surgeons. General public acquires infection through contaminated meat and milk. The infected animals serve as reservoir hosts. An epidemic occurring in animal is called epixootic (plague in rats), where as the term enzootic refers to endemic occurring in animals (Plague in rats and brucellosis in cattels).
Insects:
Blood sucking insects may transmit pathogens to human beings. The diseases so caused are called arthropod borne diseases. Insects such as mosquitoes, ticks, mites, flies, fleas and lice that transmit infections are called vectors. Transmission may be mechanical (transmission of dysentery or typhoid bacilli by the domestic fly). Such vectors are called mechanical vectors. In other instances, the pathogen multiplies in the body of the vector, often undergoing part of its developmental cucle in it. Such vectors are termed as Biological vectors (Aedes aegypti mosquito in yellow fever, Anopheles mosquito in malaria). Biological vectors transmit infection only after the pathogen 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.
Beside acting as a vector, some insects may also act as reservoir hosts. Infection is maintained in such insects by transovarial or transstadial passage.
Soil and water:
Some pathogens can survive in the soil for very long periods. Spores of tetanus bacilli may remain viable in the soil for several decades and serve as the source of infection. Fungi are also parasites such as roundworm and hookworm survive in the soil and cause human infections.
Water may act as the source of infection either due to contamination with pathogenic microorganisms (cholera vibrio, infective hepatitis virus) or due to the presence of aquatic vectors (Cyclops in guinea worm infection).
Food: Contaminated food may act as a source of infection. The presence of pathogens in food may be due to external contamination (food poisoning by staphylococcus) or due to pre-existent infection in meat or other animal products (salmonellosis).
Methods of transmission of infection
The routes of transmission may be by way of contact, vehicle, vector, air and transplacental. The infective agent has to find out a portal of entry for successful parasitism.
Contact: Infection may be acquired by contact, which may be direct or indirect. Direct contact refers to transmission of microorganisms from person to person by close personal association. Handshaking, kissing, sneezing, coughing and sexual contact represent the most usual ways that microorganisms are transferred by direct means. Sexually transmitted diseases such as syphilis and gonorrhea illustrate spread by direct contact. The term contagious disease had been used for diseases transmitted by direct contact. Where as infectious diseases are those signifying all other modes of transmission. This distinction is now not generally employed.
Sneezing and coughing may also be considered a method of direct spread, provided the individuals are within a few feet of each other. The microorganisms are expelled in droplets that are carried only a few feet and then drop to horizontal surface. Direct spread of this kind is characteristic of measles, a viral disease.
Indirect contact may be through the agency of fomites, which are inanimate objects such as clothing, pencils or toys that may be contaminated by a pathogen from one person and act as a vehicle for its transmission to another. Pencils shared by school children may act as fomites in the transmission of diphtheria and face towels in trachoma.
Inhalation:
Respiratory infections such as influenza and tuberculosis are transmitted by inhalation of the pathogen. Such microbes are shed by the patients into the environment, in secretions from the nose or throat during sneezing, speaking or coughing. Large drops of such secretions fall to the ground and dry there. Pathogens resistant to drying may remain viable in the dust and act as sources of infection. Small droplets, under 0.1 mm in diameter, evaporate immediately to become minute particles or droplet nuclei (usually 1-10 µm in diameter) which remain suspended in the air for long periods, acting as sources of infection.
Ingestion:
Intestinal infections are generally acquired by the ingestion of food or drink contaminated by pathogens. Infection transmitted by ingestion may be waterborne (cholera), foodborne (food poisoning), or handborne (dysentery). The importance of fingerborne transmission is being increasingly recognized, not only in the case of pathogens entering through the mouth, but also those that enter through the nose and eyes.
Inoculation:
pathogens, in some instances, may be inoculated directly into the tissues of the host. Tetanus spores implanted in deep wounds, rabies virus deposited subcutaneously by dog bite and arboviruses injected by insect vectors are examples. Infection by inoculation may be iatrogenic when unsterile syringes and surgical equipment are employed. Hepatitis B and the Human Immunodeficiency Virus (HIV) may be transmitted through transfusion of infected blood, or the use of contaminated syringes and needles, particularly among addicts of injectable drugs.
Insects:
Insects may act as mechanical or biological vectors of infectious diseases.
Congenital:
Some pathogens are able to cross the placental barrier and infect the ferus in utero. This is known as vertical transmission. This may result in abortion, miscarriage or stillbirth. Live infants may be born with manifestations of a disease, as in congenital syphilis. Intrauterine infection with the rubella virus, especially in the first trimester of pregnancy, may interfere with organogenesis and lead to congenital malformation. Such infections are known as teratogenic infections.
Iatrogenic and laboratory infections:
Infection may sometimes be transmitted during administration of injections, lumbar puncture and catheterization, if meticulous care in asepsis is lacking. Modern methods of treatment such as exchange transfusion, dialysis, and heart and transplant surgery have increased the possibilities for iatrogenic infections. Laboratory personnel handling infectious material are at risk and special care should be taken to prevent laboratory infection.
The outcome of an infection will depend on the interaction between microbial factors, which predispose to pathogenicity and host factors that contribute to resistance.
Factors predisposing to microbial pathogenicity:
The term pathogenicity and virulence refer to the ability of a microbe to produce disease or tissue injury but it is convenient to make a fine distinction between them. Pathogenicity is generally employed to refer to the ability of a microbial species to produce disease while the term virulence is applied to the same property in a strain of microorganism. Thus the species M. tuberculosis or polio virus is referred to as being pathogenic. The pathogenic species M. tuberculosis and the polio virus contain strains of varying degrees of virulence including those which are avirulent, such as the vaccine strains.
Enhancement of virulence is known as exaltation and can be demonstrated experimentally by serial passage in susceptible hosts. Reduction of virulence is known as attenuation and can be achieved by passage through unfavourable hosts, repeated cultures in artificial media, growth under high temperature or in the presence of weak antiseptic, desiccation or prolonged storage in culture. Virulence is the sum total of several determinants, as follows:
Adhesion: The initial event in the pathogenesis of many infections is the attachment of the bacteria to body surfaces. This attachment is not a chance event but a specific reaction between surface receptors on host cells and adhesive structures on the surface of bacteria. These adhesive structures are called adhesins. Adhesins may occur as organized structures, such as fimbriae or fibrillae and pili, or as colonization factors. This specific adhesin may account for the tissue tropisms and host specificity exhibited by many pathogens. Adhesins serve as virulence factors and loss of adhesins often renders the strain avirulent. Adhesins aer usually made of protein and are antigenic in nature. Specific immunization with adhesins has been attempted as a method of prophylaxis in some infections, as for instance against E. coli diarrhea in calves and piglets and gonorrhea in human beings.
Invasiveness:Invasiveness refers to the ability of microorganisms to penetrate tissue. Highly invasive pathogens characteristically produce spreading or generalized lesions (e.g. streptococcal septicemia following wound infecton), while less invasive pathogens cause more localized lesions. Invasiveness is not always associated with virulence or vice versa. e.g. Clostridium tetani, the causative agent of tetanus, is not an invasive organism but is extremely virulent once it has infected the host because of the release of a potent toxin. Many viruses are capable of invading tissue but are not pathogenic to humans.
Toxigenicity: Bacteria produce two types of toxins namely exotoxins and endotoxins.
Exotoxins:
Exotoxins are heat labile proteins which are secreted by certain species of bacteria and diffuse readily into the surrounding medium. They are highly potent in minute amounts and constitute some of the most poisonous substances known. One mg of tetanus or botulinum toxin is sufficient to kill more than one million guinea pigs and it has been estimated that 3 kg of botulinum toxin can kill all the inhabitants of the world. Most exotoxins are highly antigenic that is they can stimulate the formation of antibodies (antitoxins) when injected into appropriate hosts. For this reasons exotoxins can be used to induce active immunity against toxin caused diseases such as diphtheria and tetanus. However, because many toxins are potent and lethal poisons, they cannot be injected into the human body without some modification of the toxin molecule. They can be modified chemically by phenol, formaldehyde and various acids. In its modified form the toxin is called a tosoid. When injected into the body toxoid have the ability to stimulate the formation of antibodies that neutralize the specific exotoxins from which they were derived and toxoid are not toxic to the host. Toxoids or incactivated virulent microorganisms use in immunization are referred to as vaccines.
Endotoxins:
Endotoxins are heat stable lipopolysaccharides (LPS) which form an integral part of the cell wall of Gram negative bacteria. Their toxicity depends on the lipid component (Lipid A). they are not secreated out side the bacterial cell and are released only by the disintegration of the cell wall. They cannot be toxoided. They are poor antigens and their toxicity is not completely neutralized by the homologous antibodies. They are active only in relatively large doses. They do not exhibit specific pharmacological activities. All endotoxins, whether isolatd from pathogenic or nonpathogenic bacteria, produce similar effects. Administration of small quantities of endotoxin in susceptible animals causes an elevation of body temperature manifestd within 15 minutes and lasting for several hours. The pyrogenic effect of fluids used for intravenous administration is usually dur to the presence of endotoxins from contaminant bacteria. Intravenous injections of large doses of endotoxin and massive gram negative septicemias cause endotoxic shock marked by fever, leucopenia, thrombocytopenia, significant fall in blood pressure, circulatory collapse and bloody diarrhea leading to death.
Communicability: The ability of a parasite to spread form one host to another is known as communicability. This property does not influence the production of disease in an individual host but determines the survival and distribution of a parasite in a community. A correlation need not exist between virulence and communicability. In fact a highly virulent parasite may not exhibit a high degree of communicability due to its rapidly lethal effect on the host. In general infections in which the pathogen is shed in secreations, as in respiratory or intestinal diseases, are highly communicable. In some instances, as in hydrophobia, human infection represents a dead end. There being an interruption in the spread of the pathogen to other hosts. Development of epidemic and pandemic diseases requires the strain of pathogen to possess high degrees of virulence and communicability.
Other bacterial products:
Some bacterial products other than toxins, though devoid of intrinsic toxicity, may contribute to virulence by ingibiting the mechanisms of host resistance. Pathogenic staphylococci produce a thrombin-like enzyme coagulase, which prevents phagocytosis by forming a fibrin barrier around the bacteria and walling off the lesion.
Fibrinolysins promote the spread of infections by breaking down the fibrin barrier in tissues. Hyaluronidases split hyaluronic acid which, is a component of intercellular connective tissue and thus facilitate the spread of infection along tissue spaces. Leucocidins damage polymorphonuclear leucocytes. Many pathogens produce hemolysins capable of destroying erythrocytes but their significance in pathogenicity is not clearly understood.
Bacterial appendages:
Capsulated bacteria are not readily phagocytosed. Some bacterial surface antigens such as the Vi and K antigens help the bacteria to withstand phagocytosis and the lytic activity of complement.
Characteristics differentiating Exotoxins from Endotoxins
Exotoxins Endotoxins
Generally produced by Gram positive bacteria Produced by Gram negative bacteria
They are protein in nature Lipopolysaccharide in nature
They are heat labile Heat stable
Actively secreated by cells; do no diffuse into surrounding medium
Sub-clinical infection: it is a synonoym of inapparent infection.
Atypical infection: Is one in which the typical or characteristic clinical manifestations of the particular infectious disease are not present.
Latent infections: Some parasites, following infections, may remain in the tissues in a latent or hidden form proliferating and producing clinical disease when the host resistance is lowered. This is termed latent infections.
Sources of infection: Infection may be acquired endogenously or exogenously.
Endogenous sources: This occurs with microorganisms of the host’s normal flora which behave as pathogens outside their habitat.
Exogenous sources:
Man:
The commonest source of infection for human beings is the human beings themselves. The parasite may originate from a patient or a carrier. A Carrier is a person who harbors the pathogenic microorganism without suffering form any ill effect because of it. Several types of carriers have been identified. A healthy carrier is one who harbors the pathogen but has never suffered form the disease caused by the pathogen. While a convalescent carrier is one who has recovered form the disease and continues to harbor the pathogen in his body. Depending on the duration of carriage, carriers are classified as temporary and chronic carriers. The temporary carrier state lasts less than six months, while chronic carriage may last for several years and some times even for the rest of ones life. The term contact carrier is applied to a person who acquires the pathogen from a patient, while the term paradoxical carrier refers to a carrier who acquires the pathogen form another carrier.
Animals:
Many pathogens can infect both man and animals. Zoonoses are infections between vertebrate- animals and man. Many of those infections affect agridultural workers and veterinary surgeons. General public acquires infection through contaminated meat and milk. The infected animals serve as reservoir hosts. An epidemic occurring in animal is called epixootic (plague in rats), where as the term enzootic refers to endemic occurring in animals (Plague in rats and brucellosis in cattels).
Insects:
Blood sucking insects may transmit pathogens to human beings. The diseases so caused are called arthropod borne diseases. Insects such as mosquitoes, ticks, mites, flies, fleas and lice that transmit infections are called vectors. Transmission may be mechanical (transmission of dysentery or typhoid bacilli by the domestic fly). Such vectors are called mechanical vectors. In other instances, the pathogen multiplies in the body of the vector, often undergoing part of its developmental cucle in it. Such vectors are termed as Biological vectors (Aedes aegypti mosquito in yellow fever, Anopheles mosquito in malaria). Biological vectors transmit infection only after the pathogen 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.
Beside acting as a vector, some insects may also act as reservoir hosts. Infection is maintained in such insects by transovarial or transstadial passage.
Soil and water:
Some pathogens can survive in the soil for very long periods. Spores of tetanus bacilli may remain viable in the soil for several decades and serve as the source of infection. Fungi are also parasites such as roundworm and hookworm survive in the soil and cause human infections.
Water may act as the source of infection either due to contamination with pathogenic microorganisms (cholera vibrio, infective hepatitis virus) or due to the presence of aquatic vectors (Cyclops in guinea worm infection).
Food: Contaminated food may act as a source of infection. The presence of pathogens in food may be due to external contamination (food poisoning by staphylococcus) or due to pre-existent infection in meat or other animal products (salmonellosis).
Methods of transmission of infection
The routes of transmission may be by way of contact, vehicle, vector, air and transplacental. The infective agent has to find out a portal of entry for successful parasitism.
Contact: Infection may be acquired by contact, which may be direct or indirect. Direct contact refers to transmission of microorganisms from person to person by close personal association. Handshaking, kissing, sneezing, coughing and sexual contact represent the most usual ways that microorganisms are transferred by direct means. Sexually transmitted diseases such as syphilis and gonorrhea illustrate spread by direct contact. The term contagious disease had been used for diseases transmitted by direct contact. Where as infectious diseases are those signifying all other modes of transmission. This distinction is now not generally employed.
Sneezing and coughing may also be considered a method of direct spread, provided the individuals are within a few feet of each other. The microorganisms are expelled in droplets that are carried only a few feet and then drop to horizontal surface. Direct spread of this kind is characteristic of measles, a viral disease.
Indirect contact may be through the agency of fomites, which are inanimate objects such as clothing, pencils or toys that may be contaminated by a pathogen from one person and act as a vehicle for its transmission to another. Pencils shared by school children may act as fomites in the transmission of diphtheria and face towels in trachoma.
Inhalation:
Respiratory infections such as influenza and tuberculosis are transmitted by inhalation of the pathogen. Such microbes are shed by the patients into the environment, in secretions from the nose or throat during sneezing, speaking or coughing. Large drops of such secretions fall to the ground and dry there. Pathogens resistant to drying may remain viable in the dust and act as sources of infection. Small droplets, under 0.1 mm in diameter, evaporate immediately to become minute particles or droplet nuclei (usually 1-10 µm in diameter) which remain suspended in the air for long periods, acting as sources of infection.
Ingestion:
Intestinal infections are generally acquired by the ingestion of food or drink contaminated by pathogens. Infection transmitted by ingestion may be waterborne (cholera), foodborne (food poisoning), or handborne (dysentery). The importance of fingerborne transmission is being increasingly recognized, not only in the case of pathogens entering through the mouth, but also those that enter through the nose and eyes.
Inoculation:
pathogens, in some instances, may be inoculated directly into the tissues of the host. Tetanus spores implanted in deep wounds, rabies virus deposited subcutaneously by dog bite and arboviruses injected by insect vectors are examples. Infection by inoculation may be iatrogenic when unsterile syringes and surgical equipment are employed. Hepatitis B and the Human Immunodeficiency Virus (HIV) may be transmitted through transfusion of infected blood, or the use of contaminated syringes and needles, particularly among addicts of injectable drugs.
Insects:
Insects may act as mechanical or biological vectors of infectious diseases.
Congenital:
Some pathogens are able to cross the placental barrier and infect the ferus in utero. This is known as vertical transmission. This may result in abortion, miscarriage or stillbirth. Live infants may be born with manifestations of a disease, as in congenital syphilis. Intrauterine infection with the rubella virus, especially in the first trimester of pregnancy, may interfere with organogenesis and lead to congenital malformation. Such infections are known as teratogenic infections.
Iatrogenic and laboratory infections:
Infection may sometimes be transmitted during administration of injections, lumbar puncture and catheterization, if meticulous care in asepsis is lacking. Modern methods of treatment such as exchange transfusion, dialysis, and heart and transplant surgery have increased the possibilities for iatrogenic infections. Laboratory personnel handling infectious material are at risk and special care should be taken to prevent laboratory infection.
The outcome of an infection will depend on the interaction between microbial factors, which predispose to pathogenicity and host factors that contribute to resistance.
Factors predisposing to microbial pathogenicity:
The term pathogenicity and virulence refer to the ability of a microbe to produce disease or tissue injury but it is convenient to make a fine distinction between them. Pathogenicity is generally employed to refer to the ability of a microbial species to produce disease while the term virulence is applied to the same property in a strain of microorganism. Thus the species M. tuberculosis or polio virus is referred to as being pathogenic. The pathogenic species M. tuberculosis and the polio virus contain strains of varying degrees of virulence including those which are avirulent, such as the vaccine strains.
Enhancement of virulence is known as exaltation and can be demonstrated experimentally by serial passage in susceptible hosts. Reduction of virulence is known as attenuation and can be achieved by passage through unfavourable hosts, repeated cultures in artificial media, growth under high temperature or in the presence of weak antiseptic, desiccation or prolonged storage in culture. Virulence is the sum total of several determinants, as follows:
Adhesion: The initial event in the pathogenesis of many infections is the attachment of the bacteria to body surfaces. This attachment is not a chance event but a specific reaction between surface receptors on host cells and adhesive structures on the surface of bacteria. These adhesive structures are called adhesins. Adhesins may occur as organized structures, such as fimbriae or fibrillae and pili, or as colonization factors. This specific adhesin may account for the tissue tropisms and host specificity exhibited by many pathogens. Adhesins serve as virulence factors and loss of adhesins often renders the strain avirulent. Adhesins aer usually made of protein and are antigenic in nature. Specific immunization with adhesins has been attempted as a method of prophylaxis in some infections, as for instance against E. coli diarrhea in calves and piglets and gonorrhea in human beings.
Invasiveness:Invasiveness refers to the ability of microorganisms to penetrate tissue. Highly invasive pathogens characteristically produce spreading or generalized lesions (e.g. streptococcal septicemia following wound infecton), while less invasive pathogens cause more localized lesions. Invasiveness is not always associated with virulence or vice versa. e.g. Clostridium tetani, the causative agent of tetanus, is not an invasive organism but is extremely virulent once it has infected the host because of the release of a potent toxin. Many viruses are capable of invading tissue but are not pathogenic to humans.
Toxigenicity: Bacteria produce two types of toxins namely exotoxins and endotoxins.
Exotoxins:
Exotoxins are heat labile proteins which are secreted by certain species of bacteria and diffuse readily into the surrounding medium. They are highly potent in minute amounts and constitute some of the most poisonous substances known. One mg of tetanus or botulinum toxin is sufficient to kill more than one million guinea pigs and it has been estimated that 3 kg of botulinum toxin can kill all the inhabitants of the world. Most exotoxins are highly antigenic that is they can stimulate the formation of antibodies (antitoxins) when injected into appropriate hosts. For this reasons exotoxins can be used to induce active immunity against toxin caused diseases such as diphtheria and tetanus. However, because many toxins are potent and lethal poisons, they cannot be injected into the human body without some modification of the toxin molecule. They can be modified chemically by phenol, formaldehyde and various acids. In its modified form the toxin is called a tosoid. When injected into the body toxoid have the ability to stimulate the formation of antibodies that neutralize the specific exotoxins from which they were derived and toxoid are not toxic to the host. Toxoids or incactivated virulent microorganisms use in immunization are referred to as vaccines.
Endotoxins:
Endotoxins are heat stable lipopolysaccharides (LPS) which form an integral part of the cell wall of Gram negative bacteria. Their toxicity depends on the lipid component (Lipid A). they are not secreated out side the bacterial cell and are released only by the disintegration of the cell wall. They cannot be toxoided. They are poor antigens and their toxicity is not completely neutralized by the homologous antibodies. They are active only in relatively large doses. They do not exhibit specific pharmacological activities. All endotoxins, whether isolatd from pathogenic or nonpathogenic bacteria, produce similar effects. Administration of small quantities of endotoxin in susceptible animals causes an elevation of body temperature manifestd within 15 minutes and lasting for several hours. The pyrogenic effect of fluids used for intravenous administration is usually dur to the presence of endotoxins from contaminant bacteria. Intravenous injections of large doses of endotoxin and massive gram negative septicemias cause endotoxic shock marked by fever, leucopenia, thrombocytopenia, significant fall in blood pressure, circulatory collapse and bloody diarrhea leading to death.
Communicability: The ability of a parasite to spread form one host to another is known as communicability. This property does not influence the production of disease in an individual host but determines the survival and distribution of a parasite in a community. A correlation need not exist between virulence and communicability. In fact a highly virulent parasite may not exhibit a high degree of communicability due to its rapidly lethal effect on the host. In general infections in which the pathogen is shed in secreations, as in respiratory or intestinal diseases, are highly communicable. In some instances, as in hydrophobia, human infection represents a dead end. There being an interruption in the spread of the pathogen to other hosts. Development of epidemic and pandemic diseases requires the strain of pathogen to possess high degrees of virulence and communicability.
Other bacterial products:
Some bacterial products other than toxins, though devoid of intrinsic toxicity, may contribute to virulence by ingibiting the mechanisms of host resistance. Pathogenic staphylococci produce a thrombin-like enzyme coagulase, which prevents phagocytosis by forming a fibrin barrier around the bacteria and walling off the lesion.
Fibrinolysins promote the spread of infections by breaking down the fibrin barrier in tissues. Hyaluronidases split hyaluronic acid which, is a component of intercellular connective tissue and thus facilitate the spread of infection along tissue spaces. Leucocidins damage polymorphonuclear leucocytes. Many pathogens produce hemolysins capable of destroying erythrocytes but their significance in pathogenicity is not clearly understood.
Bacterial appendages:
Capsulated bacteria are not readily phagocytosed. Some bacterial surface antigens such as the Vi and K antigens help the bacteria to withstand phagocytosis and the lytic activity of complement.
Characteristics differentiating Exotoxins from Endotoxins
Exotoxins Endotoxins
Generally produced by Gram positive bacteria Produced by Gram negative bacteria
They are protein in nature Lipopolysaccharide in nature
They are heat labile Heat stable
Actively secreated by cells; do no diffuse into surrounding medium
diffuse into surrounding medium Form part of cell wall;
Often are high molecular weight Low molecular weight components
Action of exotoxin is often enzymic No enzymic action
Shows specific pharmacological effect Effect is non-specific; action common to all endotoxins.
Often are high molecular weight Low molecular weight components
Action of exotoxin is often enzymic No enzymic action
Shows specific pharmacological effect Effect is non-specific; action common to all endotoxins.
for each exotoxins
Exotoxins have specific tissue affinities
No specific tissue affinity
Active in very minute doses
Active only in very large doses
Highly antigenic in nature
They are weakly antigenic
Exotoxins can be toxioded
Cannot be toxioded
Action specifically neutralized by antibody
Neutralization by antibody is ineffective
Infecting dose: Successful infections require that an adequate number of bacteria should gain entry into the host. The dosage may be estimated as the minimum infecting dose (MID) or minimum lethal dose (MLD).
MID: The minimum number of bacteria required to produce clinical evidence of infection in susceptible animal under standard conditions.
MLD: The minimum number of bacteria required to cause death of susceptible animal under standard conditions.
As animals exhibit considerable individual variation in susceptibility, these doses are more correctly estimated as statistical expressions, ID50 and LD50, as the dose required for infecting or killing 50 per cent of the animals tested under standard conditions.
Route of infection: Some bacteria, such as streptococci, can initiate infection whatever be the mode of entry. Others can survive and multiply only when introduced by the optimal routes. Cholera vibrio are infective orally bur are unable to cause infection when introduced subcutaneously. This difference is probably related to modes by which different bacteria are able to initiate tissue damage and establish themselves. Bacteria also differ in their in their sites of election in to the host body after introduction into tissues. They also differ in their ability to produce damage of different organs in different species of animals. e.g. Tubercle bacilli injected into rabbits cause lesions mainly in the kidney and infrequently in the liver and spleen, but in guinea pigs the lesions are mainly in the liver and spleen, the kidneys being spared.
The reasons for such selective multiplication in tissues are largely obscure, though they may be related to the presence in tissues of substances that may selectively hinder or favour their multiplication.
Types of infectious diseases: Infectious diseases may be localized or generalized. Localised infections may be superficial or deep seated, Generalized infection involve the spread of the infecting agent from the site of entry by contiguity, through the bloodstream. Circulation of bacteria in the blood is known as bacteremia. Transient bacteremia is a frequent event even healthy individuals and may occur during chewing, brushing or teeth or straining at stools. The bacteria are immediately mopped up by phagocytic cells and are unable to initiate infection. Bacteremia of greater severity and longer duration is seen during generalized infections as in typhoid fever.
Septicemia is the condition where bacteria circulate and multiply in the blood, form toxic products and cause high, swinging type of fever.
Pyemia is a condition where pyogenic bacteria produce septicemia with multiple abscesses in the internal organs such as the spleen, liver and kidney.
Depending on their spread in the community infectious diseases may be classified into different types:
Endemic diseases are those, which are constantly present in a particular area. Typhoid fever is endemic in most parts of India.
Epidemic deseases are those which spreads rapidly, involving many persons in the area at the same time.
Pandemic is an epidemic that spreads through many areas of the world involving very large numbers of people within a short period.
Prosodemic diseases are those which spread by direct person to person contact, hence evolve very slowly, such creeping or smouldering epidemics are refered as prosodemic diseases (e.g. cerebrospinal fever).
IMMUNITY
Def: Immunity refers to the resistance exhibited by the host towards injury caused by microorganisms and their products. Protection against infectious diseases is only one of the consequences of the immune response, which in its entirety is concerned with the reaction of the body against any foreign antigen.
Classification of Immunity: Immunity against infectious diseases if of different types. It can be classified as follows:
Immunity can be broadly of two types (i) Innate or Native immunity and (ii) Acquired immunity.
Innate immunity: it is the resistance to infections that an individual possess by virtue of his genetic and constitutional make up. It is not affected by prior contact with microbes or immunization. It may be nonspecific (when it indicates a degree of resistance to infections in general) or specific (when the resistance to a particular pathogen is concerned).
Innate immunity may be considered at three different levels (i) species, (ii) race and (iii) individual. i.e. Innate immunity is species specific, race specific and individual specific.
(i) Species immunity refers to the total or relative refractoriness to a pathogen, shown by all members of a species. i.e. Animals of same species exhibit uniform pattern of susceptibility to infections, (e.g. B. anthracis infects human but not chicken, birds are immune to tetanus).
The mechanism of species immunity is not clearly understood but may be due ot the physiological and biochemical differences between tissues of different species may be responsible for species-specific immunity. This has been proved by pasteur’s experiment on anthrax in frogs, which are naturally resistant to the disease but become susceptible when their body temperature is raised is raised from 25°C to 35°C.
(ii) Racial immunity: With in a species, different races may show differences in the susceptibility to infections. This is known as racial immunity. e.g. High resistance of Algerian sheep to anthrax. Such racial differences are known to be genetic in origin and by selection and inbreeding, it is possible to develop at will race that possess high degrees of resistance or susceptibility to various pathogens. It has been reported that the people of Negroid origin in the USA are more susceptible than the Jews to tuberculosis. An interesting instance of genetic resistance to plasmodium falciparum malaria is seen in some part of Africa and the Mediterranean coast. A hereditary abnormality of red cells (sickling), prevalent in the area, confers immunity to infection by the malarial parasite and may have evolved from the survival advantage conferred by it in a malarial environment.
(iii) Individual immunity: Resistance to infection varies with different individuals of the same species and the race. Thus, certain individuals may be found within a highly susceptible population, who unaccountably cannot be infected by some microorganisms even though they have no previous contact with the same. The individual immunity is commonly observed in endemic outbreaks.
Factors influencing innate immunity:
There are several factors, which influences the level of innate immunity such as age, hormonal influence, nutrition etc.
IMMUNITY
Innate (natural) Acquired (Specific)
i. Species: Birds immune to tetanus
ii. Racial: Algerian sheep immune to anthrax
iii. Individual: Seen in endemic area
Active
No specific tissue affinity
Active in very minute doses
Active only in very large doses
Highly antigenic in nature
They are weakly antigenic
Exotoxins can be toxioded
Cannot be toxioded
Action specifically neutralized by antibody
Neutralization by antibody is ineffective
Infecting dose: Successful infections require that an adequate number of bacteria should gain entry into the host. The dosage may be estimated as the minimum infecting dose (MID) or minimum lethal dose (MLD).
MID: The minimum number of bacteria required to produce clinical evidence of infection in susceptible animal under standard conditions.
MLD: The minimum number of bacteria required to cause death of susceptible animal under standard conditions.
As animals exhibit considerable individual variation in susceptibility, these doses are more correctly estimated as statistical expressions, ID50 and LD50, as the dose required for infecting or killing 50 per cent of the animals tested under standard conditions.
Route of infection: Some bacteria, such as streptococci, can initiate infection whatever be the mode of entry. Others can survive and multiply only when introduced by the optimal routes. Cholera vibrio are infective orally bur are unable to cause infection when introduced subcutaneously. This difference is probably related to modes by which different bacteria are able to initiate tissue damage and establish themselves. Bacteria also differ in their in their sites of election in to the host body after introduction into tissues. They also differ in their ability to produce damage of different organs in different species of animals. e.g. Tubercle bacilli injected into rabbits cause lesions mainly in the kidney and infrequently in the liver and spleen, but in guinea pigs the lesions are mainly in the liver and spleen, the kidneys being spared.
The reasons for such selective multiplication in tissues are largely obscure, though they may be related to the presence in tissues of substances that may selectively hinder or favour their multiplication.
Types of infectious diseases: Infectious diseases may be localized or generalized. Localised infections may be superficial or deep seated, Generalized infection involve the spread of the infecting agent from the site of entry by contiguity, through the bloodstream. Circulation of bacteria in the blood is known as bacteremia. Transient bacteremia is a frequent event even healthy individuals and may occur during chewing, brushing or teeth or straining at stools. The bacteria are immediately mopped up by phagocytic cells and are unable to initiate infection. Bacteremia of greater severity and longer duration is seen during generalized infections as in typhoid fever.
Septicemia is the condition where bacteria circulate and multiply in the blood, form toxic products and cause high, swinging type of fever.
Pyemia is a condition where pyogenic bacteria produce septicemia with multiple abscesses in the internal organs such as the spleen, liver and kidney.
Depending on their spread in the community infectious diseases may be classified into different types:
Endemic diseases are those, which are constantly present in a particular area. Typhoid fever is endemic in most parts of India.
Epidemic deseases are those which spreads rapidly, involving many persons in the area at the same time.
Pandemic is an epidemic that spreads through many areas of the world involving very large numbers of people within a short period.
Prosodemic diseases are those which spread by direct person to person contact, hence evolve very slowly, such creeping or smouldering epidemics are refered as prosodemic diseases (e.g. cerebrospinal fever).
IMMUNITY
Def: Immunity refers to the resistance exhibited by the host towards injury caused by microorganisms and their products. Protection against infectious diseases is only one of the consequences of the immune response, which in its entirety is concerned with the reaction of the body against any foreign antigen.
Classification of Immunity: Immunity against infectious diseases if of different types. It can be classified as follows:
Immunity can be broadly of two types (i) Innate or Native immunity and (ii) Acquired immunity.
Innate immunity: it is the resistance to infections that an individual possess by virtue of his genetic and constitutional make up. It is not affected by prior contact with microbes or immunization. It may be nonspecific (when it indicates a degree of resistance to infections in general) or specific (when the resistance to a particular pathogen is concerned).
Innate immunity may be considered at three different levels (i) species, (ii) race and (iii) individual. i.e. Innate immunity is species specific, race specific and individual specific.
(i) Species immunity refers to the total or relative refractoriness to a pathogen, shown by all members of a species. i.e. Animals of same species exhibit uniform pattern of susceptibility to infections, (e.g. B. anthracis infects human but not chicken, birds are immune to tetanus).
The mechanism of species immunity is not clearly understood but may be due ot the physiological and biochemical differences between tissues of different species may be responsible for species-specific immunity. This has been proved by pasteur’s experiment on anthrax in frogs, which are naturally resistant to the disease but become susceptible when their body temperature is raised is raised from 25°C to 35°C.
(ii) Racial immunity: With in a species, different races may show differences in the susceptibility to infections. This is known as racial immunity. e.g. High resistance of Algerian sheep to anthrax. Such racial differences are known to be genetic in origin and by selection and inbreeding, it is possible to develop at will race that possess high degrees of resistance or susceptibility to various pathogens. It has been reported that the people of Negroid origin in the USA are more susceptible than the Jews to tuberculosis. An interesting instance of genetic resistance to plasmodium falciparum malaria is seen in some part of Africa and the Mediterranean coast. A hereditary abnormality of red cells (sickling), prevalent in the area, confers immunity to infection by the malarial parasite and may have evolved from the survival advantage conferred by it in a malarial environment.
(iii) Individual immunity: Resistance to infection varies with different individuals of the same species and the race. Thus, certain individuals may be found within a highly susceptible population, who unaccountably cannot be infected by some microorganisms even though they have no previous contact with the same. The individual immunity is commonly observed in endemic outbreaks.
Factors influencing innate immunity:
There are several factors, which influences the level of innate immunity such as age, hormonal influence, nutrition etc.
IMMUNITY
Innate (natural) Acquired (Specific)
i. Species: Birds immune to tetanus
ii. Racial: Algerian sheep immune to anthrax
iii. Individual: Seen in endemic area
Active
Passive
Natural Artificial Natural Artificial
Follows clinical Induced by vaccination Tranplacental passage Injection
or subclinical IgG of preformed infections antibody
Age: Two extreme of life, i.e. fetus and old person carry high susceptibility of infectious diseases. In the former, the immune apparatus is immature whereas in the latter there is gradual waning of their immune response. The fetus in uterus is protected by the placental barrier form maternal infection. Certain pathogens, e.g. Rubella, Cytomegaloviruses and Toxoplasma gondii cross the placental barrier leading to congential malformation.
Hormonal influence: Certain hormonal disorders such as diabetes mellitus, hypothyroidism and adrenal dysfunction influence susceptibility to infection. In diabetes there is high incidence of staphylococcal sepsis partly due to altered metabolism and elevated level of carbohydrates in tissues. The susceptibility to infection is increased in both hypo and hyper adrenal states. Corticosteroids depress the host resistance by suppression of the inflammatory response and inhibiting antibody formation.
Nutrition: In general, malnutrition predisposes to bacterial infection such as gram-negative bacterial septicemia. Tuberculosis, herpes virus infection, measles and candidiasis. Cell mediated immunity and antibody response to T lymphocyte dependent antigens are primarily reduced in malnutrition.
ACQUIRED IMMUNITY
Resistance acquired by an individual during lifetime is called as acquired immunity. Acquired immunity is of two types: active and passive.
Active acquired immunity:
Active immunity is the resistance induced in an individual after effective contact with an antigen. It follows either natural infection or vaccination. Here the immune system actively participates in producing antibodies and often cell mediated immunity also. Active immunity develops slowly over a period of days or weeks but persists for a long time, usually for years.
Types of Active Immunity:
Active immunity may be acquired either naturally or artificially.
(i) Natural active acquired immunity: It is acquired by natural infection by the organisms. In large majority of the cases this occurs by sub clinical infections after repeated exposure to small doses of the infecting organism, which pass unnoticed. Such immunity is usually long lasting. Sub clinical attacks by pathogenic microbes play important role in preventing epidemics, e.g. poliomyelitis, tuberculosis. Some of these follow overt infections, for example person recovering from an attack of small pox develops natural active immunity.
(ii) Artificial active acquired immunity: It is the resistance produced by vaccination. The vaccines are preparations of live, attenuated or killed microorganisms, or their antigens or active materials derived from them (toxoids). The commonly employed vaccines are as follows:
Bacterial vaccines: (i) Live BCG, anthrax, plague and brucella vaccines. (ii) Killed TAB for enteric fever, autovaccine.
Viral vaccines: (i) Live- small pox, measles, influenza, mumps and Sabin poliomyelitis vaccine. (ii) Killed- Salk vaccine for poliomyelitis.
Bacterial products: Toxoids for tetanus and diphtheria.
Attenuation of live vaccine is done by ageing of culture, cultivation at high temperature (anthrax bacilli grown at 42°C), passage through animals of different species (variola virus through rabbit and calf), drying (rabies), by continued cultivation in presence of antagonistic substance (BCG) and by repeated subculture in artificial media (streptococci).
In killed vaccine the organism are killed by heat, formalin, phenol, alcohol, ultraviolet light and photodynamic inactivation. These are preserved in phenol, alcohol, N-merthiolate. Toxoid are preparations of bacterial exotoxins inactivated by formaline (formal toxoid) or by alum (APT). they retain immunogenecity but not toxigenecity.
Passive acquired immunity:
The resistance that is induced in the recipient by transfer of antibodies preformed against infective agent or toxin in another host, is called passive immunity. The immune system plays no active role and the protective mechanism comes into force immediately after transfer of antibodies (immune serum). Passive protection is short lasting only for days or weeks. It is useful when instant immunity is required. Passive immunity is of two types: Natural and Artificial.
Natural passive acquired immunity:
It is the resistance passively transferred from the mother to foetus and infant, e.g. transfer of maternal antibody to foetus transplacentally and to infant through milk (colostrum).
Artificial passive acquired immunity
It is the resistance passively transferred to a recipient by the parenteral administration of antibodies. Passive administration of antibody is very useful in some clinical conditions.
Differences between active and passive immunity
Active immunity Passive immunity
Produced actively by the immune system of host Received passively by the host and the hosts immune system does not participate
Induced by infection or by contacts with immunogen i.e. vaccines Conferred by introduction of ready made antibodies
Immune response is durable and effective Immune response is short lived and less effective
Immunity develops only after a period of lag period Immunity effective immediately. No lag period Immunological memory is present
No immunological memory.
Natural Artificial Natural Artificial
Follows clinical Induced by vaccination Tranplacental passage Injection
or subclinical IgG of preformed infections antibody
Age: Two extreme of life, i.e. fetus and old person carry high susceptibility of infectious diseases. In the former, the immune apparatus is immature whereas in the latter there is gradual waning of their immune response. The fetus in uterus is protected by the placental barrier form maternal infection. Certain pathogens, e.g. Rubella, Cytomegaloviruses and Toxoplasma gondii cross the placental barrier leading to congential malformation.
Hormonal influence: Certain hormonal disorders such as diabetes mellitus, hypothyroidism and adrenal dysfunction influence susceptibility to infection. In diabetes there is high incidence of staphylococcal sepsis partly due to altered metabolism and elevated level of carbohydrates in tissues. The susceptibility to infection is increased in both hypo and hyper adrenal states. Corticosteroids depress the host resistance by suppression of the inflammatory response and inhibiting antibody formation.
Nutrition: In general, malnutrition predisposes to bacterial infection such as gram-negative bacterial septicemia. Tuberculosis, herpes virus infection, measles and candidiasis. Cell mediated immunity and antibody response to T lymphocyte dependent antigens are primarily reduced in malnutrition.
ACQUIRED IMMUNITY
Resistance acquired by an individual during lifetime is called as acquired immunity. Acquired immunity is of two types: active and passive.
Active acquired immunity:
Active immunity is the resistance induced in an individual after effective contact with an antigen. It follows either natural infection or vaccination. Here the immune system actively participates in producing antibodies and often cell mediated immunity also. Active immunity develops slowly over a period of days or weeks but persists for a long time, usually for years.
Types of Active Immunity:
Active immunity may be acquired either naturally or artificially.
(i) Natural active acquired immunity: It is acquired by natural infection by the organisms. In large majority of the cases this occurs by sub clinical infections after repeated exposure to small doses of the infecting organism, which pass unnoticed. Such immunity is usually long lasting. Sub clinical attacks by pathogenic microbes play important role in preventing epidemics, e.g. poliomyelitis, tuberculosis. Some of these follow overt infections, for example person recovering from an attack of small pox develops natural active immunity.
(ii) Artificial active acquired immunity: It is the resistance produced by vaccination. The vaccines are preparations of live, attenuated or killed microorganisms, or their antigens or active materials derived from them (toxoids). The commonly employed vaccines are as follows:
Bacterial vaccines: (i) Live BCG, anthrax, plague and brucella vaccines. (ii) Killed TAB for enteric fever, autovaccine.
Viral vaccines: (i) Live- small pox, measles, influenza, mumps and Sabin poliomyelitis vaccine. (ii) Killed- Salk vaccine for poliomyelitis.
Bacterial products: Toxoids for tetanus and diphtheria.
Attenuation of live vaccine is done by ageing of culture, cultivation at high temperature (anthrax bacilli grown at 42°C), passage through animals of different species (variola virus through rabbit and calf), drying (rabies), by continued cultivation in presence of antagonistic substance (BCG) and by repeated subculture in artificial media (streptococci).
In killed vaccine the organism are killed by heat, formalin, phenol, alcohol, ultraviolet light and photodynamic inactivation. These are preserved in phenol, alcohol, N-merthiolate. Toxoid are preparations of bacterial exotoxins inactivated by formaline (formal toxoid) or by alum (APT). they retain immunogenecity but not toxigenecity.
Passive acquired immunity:
The resistance that is induced in the recipient by transfer of antibodies preformed against infective agent or toxin in another host, is called passive immunity. The immune system plays no active role and the protective mechanism comes into force immediately after transfer of antibodies (immune serum). Passive protection is short lasting only for days or weeks. It is useful when instant immunity is required. Passive immunity is of two types: Natural and Artificial.
Natural passive acquired immunity:
It is the resistance passively transferred from the mother to foetus and infant, e.g. transfer of maternal antibody to foetus transplacentally and to infant through milk (colostrum).
Artificial passive acquired immunity
It is the resistance passively transferred to a recipient by the parenteral administration of antibodies. Passive administration of antibody is very useful in some clinical conditions.
Differences between active and passive immunity
Active immunity Passive immunity
Produced actively by the immune system of host Received passively by the host and the hosts immune system does not participate
Induced by infection or by contacts with immunogen i.e. vaccines Conferred by introduction of ready made antibodies
Immune response is durable and effective Immune response is short lived and less effective
Immunity develops only after a period of lag period Immunity effective immediately. No lag period Immunological memory is present
No immunological memory.
Subsequent challenge with booster dose is more effective Subsequent administration of a ntibody is less effective due to immune elimination.
After antigenic stimulus negative phase may occur No negative phase
Serves no purpose in immunodeficient hosts Applicable in immunodeficient hosts.
Used for prophylaxis to increase body resistance Used for treatment of acute infections.
After antigenic stimulus negative phase may occur No negative phase
Serves no purpose in immunodeficient hosts Applicable in immunodeficient hosts.
Used for prophylaxis to increase body resistance Used for treatment of acute infections.
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