Vaccines need to be highly immunogenic, capable of eliciting a robust immune response, while also being non-pathogenic.
Efforts to combat multiple infectious diseases through mixed vaccines have shown limitations.
Exceptions include successful responses from clostridial vaccines, notably in sheep diseases control.
Prepared from specific bacterial strains causing outbreaks, autogenous vaccines target particular infections.
Killed vaccines, while safe, offer shorter immunity duration compared to live vaccines. However, the immune response to killed vaccines can be prolonged when the antigens in the vaccines are combined with certain substances known as adjuvants.
Advances in genetic engineering have led to subunit, synthetic peptide, and vector virus vaccines.
Horses are commonly used to produce antisera for disease prevention due to the large serum volume they provide.
Animal Selection for Immune Sera Production: Various species like cattle, sheep, goats, dogs, and rabbits are utilized to produce specialized antisera. These animals undergo a series of injections with specific bacterial antigens or toxoids. After the injection regimen, their blood sera are tested for antibody levels. Upon reaching satisfactory levels, the animals are bled, and the sera are collected, stored, or concentrated using ammonium sulfate precipitation to obtain globulin fractions.
Duration of Passive Immunity: Passive immunity from hyperimmune serum lasts briefly in animals. The temporary immunity's duration may vary based on factors like homologous or heterologous antiserum administration. Homologous antiserum derived from the same species can provide immunity for 3-4 weeks, while heterologous antiserum may only be effective for about 1-3 weeks.
Prolonging Immunity: To extend the protective effect of passive immunity, multiple injections of hyperimmune sera at intervals are considered. However, caution is necessary, especially with heterologous sera, as they can trigger hypersensitive reactions in recipients.
Hypersensitive Reactions: Heterologous gamma-globulin can provoke hypersensitive reactions in recipients, leading to general anaphylactic or local Arthus reactions upon repeated doses. In contrast, homologous hyperimmune sera are less likely to induce hypersensitive reactions after multiple administrations.
Microbial Pathogens: Only a small fraction of bacteria, fungi, and viruses present in the environment can cause diseases by adapting to the body's conditions. These pathogens possess specific properties enabling them to resist the body's defense mechanisms and instigate disease development.
Pathogenicity: Pathogenicity refers to an organism's ability to cause disease in a host. Different strains of microorganisms within the same species exhibit varying pathogenic potentials, influencing their disease-causing abilities.
Virulence: Virulence characterizes a strain's capacity to induce disease under defined conditions. Variations in virulence levels among strains are associated with distinct properties of the organisms, such as toxin production or the presence of protective features like capsules.
Clostridium botulinum produces potent neurotoxins that are absorbed through the intestine after ingestion. Unlike tetanus toxin, botulinum toxin acts on all cholinergic nerve fibers, affecting both peripheral and autonomic nerves.
The alpha toxin from Clostridium oedematiens causes gelatinous edema and haemoconcentration by likely targeting blood vessel walls. Other toxins from this organism have various activities such as haemolytic and necrotizing effects.
The alpha toxin is associated with the lethal effects of Clostridium sépticum. Other toxins include beta toxin (deoxyribonuclease), gamma toxin (hyaluronidase), and delta toxin (haemolytic).
Clostridium welchii strains produce various toxins, including the alpha toxin with lecithinase, haemolytic, necrotizing properties. These toxins can cause edema, hemorrhage, necrosis, and shock by affecting capillaries and cell structures.
Clostridial toxins impact tissue cells in experimental settings. Antitoxins can neutralize these effects if administered early. Active immunization through vaccines can also help by producing antibodies before toxin exposure.
Staphylococci produce toxins with lethal, necrotic, and haemolytic effects, along with enterotoxins and enzymes like coagulase and hyaluronidase. These toxins facilitate bacterial spread in tissues.
Streptococci toxins include haemolysins, fibrinolysin, streptodornase, hyaluronidase, and an erythrogenic factor. These toxins collectively impair host defense mechanisms, aiding bacterial establishment in the body.
A toxin produced by Corynebacterium pyogenes can destruct red blood cells, proving lethal to rabbits and mice while causing necrosis in guinea pigs. The exact mechanisms behind these toxic reactions and their impact on the host's cellular defenses remain unclear.
In certain bacterial infections, organisms can enter the bloodstream, spreading rapidly to various body organs. For instance, in pyaemic infections, infected clots can dislodge and migrate to different body sites. Severe trauma or contaminated wounds may also introduce bacteria into blood vessels, leading to widespread distribution.
Acute infection with Bacillus anthracis showcases rapid bacterial multiplication overwhelming the body's defense mechanisms. The disease's pathogenesis involves three bacterial products, including a toxin causing edema and lethality.
Salmonella and Escherichia bacteria can induce significant bacteraemia during initial infection stages, especially in young animals. These organisms can enter the bloodstream, leading to severe bacteraemia, potentially fatal during acute generalized infections.
After primary infection establishment, the body's response and lesion development depend on the infecting microorganism and tissue characteristics. Granulomatous reactions, seen in chronic infections like tuberculosis, involve defensive and reparative responses within tissues.
Viral infections and immunological reactions are complex processes that involve interactions between pathogens and host immune responses. Understanding these mechanisms is crucial for developing effective treatment and prevention strategies.
Fungal infections in animals, specifically the pathogenesis of these infections, have historically received limited attention. Recent studies indicate that these infections are rare and typically occur under specific favorable conditions despite the prevalence of potentially pathogenic fungi on or within animal bodies.
Ringworm fungi, known as dermatophytes, can exist in the soil and easily come into contact with animal skin. These fungi target keratinized tissue and produce enzymes that digest keratin, leading to skin and hair infections. The initial stage involves hyphae penetrating hair follicles, causing mild tissue reactions like congestion and exudate formation.
Similar to dermatophytes, little research has been done on the pathogenesis of systemic mycotic infections in animals. Conditions that trigger pathogenic effects often involve changes in microbial morphology. Aspergillus species, for example, can transition into mycelia in active lesions, affecting various animal species.
Aspergillus infections can lead to allergic skin reactions, especially in rabbits, after exposure to spores. Likewise, Coccidioides immitis infections can cause skin eruptions. Moniliasis, caused by Candida albicans, involves toxin production and tissue penetration by mycelia.
Herd immunity refers to a group of animals' ability to resist infection collectively. Factors like frequency of contact and the number of susceptible individuals influence herd immunity, similar to individual immunity. Lack of herd immunity can result in increased disease occurrence in animal groups.
The zero-disease concept aims to eliminate specific diseases through vaccination and surveillance within a defined period. Achieving 100% vaccination in high-risk areas is crucial. This concept, successfully implemented in smaller countries, faces challenges in larger countries like India, where efforts are being made, such as for rinderpest eradication.
1. ما هي الفرق بين اللقاحات الحية والميتة؟ |
2. ما هو دور الأدجوفانتس في اللقاحات؟ |
3. ما هي آلية عمل اللقاحات الفرعية والببتيدات الاصطناعية واللقاحات المعدلة وراثياً؟ |
4. كيف يتم تحضير الأمصال فائقة الحصانة؟ |
5. ما هي الآليات الباثوجينية للعدوى البكتيرية وتأثيرات السموم الكلوستريدية؟ |
289 docs
|
|
Explore Courses for UPSC exam
|