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Mietzner, and M. Jawetz, Jawetz, Melnick, & Adelberg's Medical. Microbiology, McGraw-Hill, 26th edition, Jawetz, Melnick, & Adelberg's Medical Microbiology by Brooks GF, Butel JS, Morse SA,. Melnick JL, Jawetz E, Adelberg EA. 23rd edition. Lange Publication.

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Jawetz medical microbiology 26th edition pdf kickasstorrents

Опубликовано в Torentjes in hoorn instrument | Октябрь 2nd, 2012

jawetz medical microbiology 26th edition pdf kickasstorrents

Mietzner, and M. Jawetz, Jawetz, Melnick, & Adelberg's Medical. Microbiology, McGraw-Hill, 26th edition, Course Wise Content Details for torenttok.site Microbiology Programme 10th edition. Jawetz, Melnick, &Adelberg's Medical Microbiology by Carroll KC. torenttok.site › wp-content › uploads › /07 › MSc_. ENCARTA 2014 UTORRENT FOR MAC She has taken and confirm it. Repeat the above with Outlook Live. Directly from the user will be. Cons Users cannot them on your entre la parole live operating systems.

Sapremia: Presence of metabolic products of saprophytes in the blood. Source of Infection Human Being The commonest source of infection for human being is the human being. Human being gets the infection from either patient or a carrier. Carrier is a person who harbors the parasite, but himself does not suffer from the illness. There are six types of carriers. Healthy carrier is a person who harbors the pathogen, but has never suffered from the disease.

Convalescent carrier is a person who recovered from the disease, but continues to harbor the pathogen. Temporary carrier is a person, who harbors the parasite for less than 6 months. Contact carrier is a person, who acquires the pathogen from a patient. Paradoxical carrier is a person, who gets the pathogen from a carrier. Animals Animals may act as source of infection without suffering.

Such animals maintain the parasites in nature and acts as reservoir of human infections. The zoonotic diseases are bacterial, viral, parasitic and fungal. Bacterial: The diseases caused by bacteria are as follows: 1. Plague from rats. Brucellosis and tuberculosis from cows. Anthrax from sheep. Leptospirosis from dogs, pigs, sheep, cows and rodents. Psittacosis from parrots and other birds. Relapsing fever from rodent via ticks and lice. Salmonellosis from dogs, cats and poultry.

Viral: The diseases caused by virus are as follows: 1. Rabies from dogs. Japanese encephalitis from pigs. Lassa fever, hantavirus infection via rodents. Parasitic: The diseases caused by parasites are as follows: 1. African sleeping sickness from wild games via tsetse fly. Hydatid disease from dogs. Leishmaniasis from dogs via sand fly. Tapeworm infection from cattle, swine and rodents. Toxoplasmosis from cats, bats, rodents and domestic animals.

Fungal: The diseases caused by fungus are as follows: 1. Histoplasmosis from birds and bats. Ringworm Tinea from cats, dogs and other domestic animals. Insects Insects may transmit the pathogens to humans. Insects such as mosquitoes, ticks, lice and flies, which transmit the pathogens are known as vectors. Vectors may be: 1. Biological vectors, where pathogens multiply and undergo developmental cycle malaria, filaria, kala-azar, etc.

Mechanical vectors, which transmit infective parasite mechanically or passively by holding in their appendages, e. Besides vectors, some insects may also act as reservoir hosts e. Infection is maintained in such insects by transovarial passage. Soil and Water Some pathogens are able to survive in soil spores of tetanus and gas gangrene bacilli, Histoplasma capsulatum and water Vibrio cholerae, hepatitis A and E. Food Contaminated food material may act as source of infection food poisoning by Staphylococcus aureus, Bacillus cereus, E.

There may be also pre-existing infections of meat, milk, etc. Salmonella typhimurium, Mycobacterium tuberculosis. Methods of Transmission of Infection The methods of transmission of infection Fig. Contact transmission. Transmission by vehicles. Transmission by vectors. Contact Transmission Direct contact transmission: In horizontal transmission, individuals acquire pathogens by shaking hands, kissing, touching or by having sexual contact causes sexually transmitted disease STD such as acquired immunodeficiency syndrome AIDS.

Pathogens can also spread by touching genital herpes lesions and then touching the eyes and it also spreads from fecal matter to mouth by unwashed hands fecal-oral transmission. Indirect contact transmission: Occurs through fomites, non-living objects that can harbor and transmit infectious agents.

Droplet nuclei consist of dried mucus, which protects microorganisms embedded in it. These particles can be inhaled directly or can become airborne. Droplet transmission over a distance of less than 1 m is not considered airborne chickenpox, tuberculosis, influenza, measles, histoplasmosis. Foodborne transmission: Pathogens that are most likely transmitted in food are unhygienically cooked or refrigerated poorly. Foodborne pathogens cause gastroenteritis botulinum toxins, aflatoxin, staphylococcal poisoning, salmonellosis, listeriosis, toxoplasmosis, tapeworm infection, hepatitis A and E.

Transmission by Vehicles Transmission by Vectors Vehicle is a non-living carrier of an infectious agent from its reservoir to a susceptible host. Common vehicles are water, air and food. Blood and other body fluids, intravenous IV fluids can serve as vehicle for transmission.

Insects act as mechanical vectors. House flies and other insects transmit pathogens passively on their feet and body parts. The pathogens do not multiply in the vector. Insects act as biological vectors who transmit pathogens actively, i. Waterborne transmission: Pathogens do not grow in pure water. Waterborne pathogens are transmitted in water contaminated with untreated or inadequate treated sewage.

Such indirect fecal-oral transmission occurs when pathogens from feces enter contaminated water and the sample is taken by another individual. Polioviruses, enteroviruses hepatitis A and E and several bacteria Vibrio cholerae, Shigella, Leptospira and Campylobacter are waterborne microbes that infect the digestive system and cause gastroenteritis.

Airborne transmission: Airborne microorganisms are mainly transmitted from soil, water, plants or animals. Pathogens are said to be airborne if they travel more than 1 m in air. Both, airborne pathogens and those that are suspended in droplets, have chance of reaching near hosts in a overcrowded locality.

Airborne pathogens fall to the floor and combine with dust particles to become suspended in aerosols. Dust particles can harbor many pathogens staphylococci, streptococci, bacterial and fungal spores. Pathogenicity is the capacity to produce disease. Mycobacterium tuberculosis frequently causes disease upon entering the host, where as Staphylococcus epidermidis cause disease rarely, when it enters into a host with poor defense.

Most infectious agents exhibit a degree of pathogenicity between these extremes. Virulence is the degree of pathogenicity. This term also refers to the intensity of the disease produced by pathogens and varies among different microbial species.

For example, Bacillus cereus causes mild gastroenteritis, where as rabies virus causes fatal neurological damages. Virulence also varies among members of main species. The virulence of a strain is not constant and may undergo spontaneous or induced variation. Enhancement of virulence is known as exaltation, which can be done by serial passage, the rapid transfer of the pathogen through susceptible animals several times. Presumably the microbe becomes better able to damage the host with each animal passage.

Reduction of virulence is known as attenuation, which can be achieved by: 1. Passage through unfavorable host. Repeated culture in artificial media. Growth under high temperature. Growth in the presence of week antiseptic solution. Prolonged storage in culture. Virulence is the sum total of several determinants as detailed below. Microbial Virulence Factors Virulence factors are structural or physiological characteristics that help the microorganisms to cause infection and disease.

Adhesion Once the bacteria enter the body of the host, the critical point in the production of bacterial disease is the organisms adherence or attachment to the host cell surface. If they did not adhere, they would be swept away by the mucus and other fluids that bathe the tissue surface. Adhesins are proteins or glycoproteins found on pili fimbriae and capsules.

Most adhesins that have been identified permit the pathogens to adhere only to receptors on certain host epithelial cells Table 2. Adherence to host epithelial cells may be the essential first step in the pathogenesis of many infectious diseases. Adherence allows the organisms to colonize and multiply at a rate faster than their removal, offers access to body tissues and cells and provides focus for elaboration of enzymes and toxins.

Adherence may also be nutritionally important. The interaction between bacteria and tissue cell surfaces in the adhesion process are complex. Several factors play important roles Figs 2. Surface hydrophobicity and net surface charge: Bacteria and host cells, commonly have a negative surface charges and therefore, have a repulsive electrostatic forces. In general, more hydrophobic the bacterial cell surface, the greater adherence to the host cell.

Binding molecules on bacteria ligands and host cell receptor interactions also play important role in adhesion. Invasiveness Invasion is the term commonly used to describe the entry of the bacteria into the host cells, implying an active role of the organism. Some bacteria such as pneumococci and streptococci release digestive enzymes that allow them to invade tissues rapidly and cause severe illness.

The examples of bacterial invasion have been noted in Table 2. The bacteria also make contact with membrane junction that form part of transport network between host cells. The bacteria use a Toxins produced by bacteria are generally classified into two groups, exotoxins and endotoxins. Toxigenicity Figs 2.

Surface molecules on a pathogen, called adhesins or ligands, bind specifically to complementary surface receptors; B. Selective attachment of a pathogenic strain of E. Bacteria adhering to the skin of a salamander. Neisseria gonorrhoeae Chlamydia trachomatis Opacity-associated proteins Oap enhance the invasion of the cells by Neisseria gonorrhoeae. Shigella species Invasion plasmid antigen IpaB, IpaC, IpaD Listeria monocytogenes Invade with the help of internalin protein, through coiling phagocytosis Exotoxins Exotoxins are heat-labile proteins, which are secreted by certain species of bacteria and diffuse readily into the surrounding medium Figs 2.

They are highly potent in minute amount, e. It has been estimated that 3 kg of botulinum toxin is sufficient enough to kill all the inhabitants of the world. Exotoxins are classified in Box 2. The toxin molecule is secreted as a single polypeptide molecule 62, MW. This native toxin is enzymatically divided into fragments, A and B.

Exotoxins are highly antigenic and can be toxoided by treatment with formaldehyde Fig. Endotoxins Endotoxins are heat stable, polysaccharideprotein-lipid complex, which form an integral part of the cell wall of gram-negative bacteria. They are not secreted into the medium, weakly antigenic, hence cannot be toxoided.

All endotoxins, whether from pathogenic or non-pathogenic have similar effects Table 2. Box 2. Based on site of action: 1. Cytotoxins, e. Enterotoxins, e. Neurotoxins, e. Cutaneous exotoxins, e. Pyrogenic exotoxin, e. Special toxins, e. Based on mechanism of action of exotoxins: 1.

Damage to the cell membrane, e. Alteration of cell function, e. Lethal action, e. Endotoxins exert their effects, when gramnegative bacteria die and their cell walls undergo lysis, thus liberating the endotoxins. Antibiotics used to treat diseases caused by gram-negative bacteria can lyse the bacterial cells; this reaction releases endotoxin and may lead to an immediate worsening of the symptoms, but the condition usually improves as the endotoxin breaks down.

Exotoxins are produced inside, mostly in gram-positive bacteria as part of their growth and metabolism. They are then released into the surrounding medium; B. Endotoxins are part of the outer portion of the cell wall of gram-negative bacteria. They are liberated when the bacteria die and the cell wall breaks apart. Table 2. Another consequence of endotoxin is the activation of clotting factor Hageman factor causing formation of small blood clots. These blood clots obstruct capillaries. At the same time lipopolysaccharide acts on plasminogen, producing plasmin, which acts on clots and breakdown fibrin clot.

There is re- 15 duction in fibrinogen, accumulation of fibrin breakdown products that brings about disseminated intravascular coagulation. Pyrogenicity of endotoxin is believed to occur when gram-negative bacteria are ingested by phagocytes and degraded in the vacuoles, the lipopolysaccharides LPS of the bacterial cell wall is released. These endotoxins activate macrophage to produce interleukin-1 IL-1 , endogenous pyrogen, Fig.

A proposed model for the mechanism of action of diphtheria toxin DNA, deoxyribonucleic acid; mRNA, messenger ribonucleic acid. IL-1 induces the hypothalamus to release lipids called prostaglandins, which reset the thermostat in the hypothalamus at higher temperature.

The result is fever. Aspirin and acetaminophen reduces fever by inhibiting the synthesis of prostaglandins Figs 2. Shock refers to life-threatening fall of blood pressure. Shock caused by gram-negative bacteria is called septic shock or endotoxic shock. Hence there is a drop in blood pressure resulting in shock. The hemolymph blood of the Atlantic coast horseshoe crab Limulus polyphemus contains white blood cells WBCs called amebocytes, which have large amount of protein lysate that cause clotting.

In the presence of endotoxin, amebocytes in the crab hemolymph lyse and liberate their clotting protein. As a result there will be clot formation in positive test. Rabbit pyrogenicity test: This test is done on rabbit, a pyrogen sensitive mammal to know the pyrogenic effect of endotoxin. The sample of solution suspected to be contaminated with LPS of gram-negative bacilli is injected intravenously into the ear veins of adult rabbits.

The rectal temperature of the animal is monitored before and after the IV injection of solution. If the solution contains endotoxin, the rectal temperature of the animal will be higher than normal indicating the pyrogenic effect of endotoxin. Enzymes and Other Bacterial Products The virulence of some bacteria is thought to be aided by the production of enzymes, hemolysin, cytocidin, etc.

Coagulase is an enzyme produced by S. Coagulase helps in deposition of fibrin on the surface of Staphylococcus, which protect them from being phagocytosed. Figs 2. A macrophage ingests a gram-negative bacterium; B. The bacterium is degraded in a vacuole, releasing endotoxins that induce the macrophage to produce interleukins IL-1 ; C. IL-1 is released by the macrophage into the bloodstream through which it travels to the hypothalamus of the brain; D.

Collagenase and lecithinase produced by Clostridium perfringens facilitates the spread of gas gangrene. Hemolysins and leukocidins of S. Other hemolysin producers are Streptococcus pyogenes and Clostridium perfringens. One of the better known kinase is fibrinolysin streptokinase , which breaks down fibrin and dissolves the clot formed by the body to help in spreading infection. Immunoglobulin IgA1 proteases produced by Neisseria gonorrhoeae, N.

Inhibition of Phagocytosis Microorganisms have managed to develop a mechanism for inhibiting every step in the normal phagocytic process Figs 2. Inhibition of chemotaxis Several bacterial toxins are able to inhibit the migration of leukocyte towards chemoattractants e. Cholera toxin of Vibrio cholerae, enterotoxin of E. Some microbial surface components such as the hyaluronic acid capsule of S. Inhibition of attachment of phagocytes The bacterial capsule is by far the most important ubiquitous antiphagocytic substance 17 e.

The mechanism by which encapsulation confers resistance to phagocytosis may include decreased binding of serum opsonins; inaccessibility of ligands IgG and C3b required for phagocytic binding and decreased hydrophobicity of the bacterial surface. It should be noted that the presence of anticapsular antibody overcomes the antiphagocytic effect of the capsules. Numerous other structural components are antiphagocytics.

Examples include the protein A of S. Inhibition of lysosome fusion Microorganisms can escape from phagocytosis by inhibiting the fusion of the lysosome with the phagosome e. Legionella pneumophila, Chlamydia psittaci, Toxoplasma gondii, M. Resistance to killing in a phagolysosome Facultative or obligate intracellular parasites must be able to resist killing by developing the ability to resist either the oxygen-dependent or oxygen-independent antimicrobicidal actions of the phagolysosome enzymes.

Escape from phagolysosome into cytoplasm: Some parasites can lyse the phagolysosomal membrane and escape into the cytoplasm. Escape from Host Immune Response By antigenic variation Organisms may evade the immune response by modifying their surface antigens. The best example of antigenic variation is that of African trypanosomiasis.

This disease is characterized by repeated episodes of bloodstream invasion and remission. The trypanosomes are able to circumvent the effects of these antibodies by changing the antigens present on their surface coat. Schematic diagram of the steps in phagocytosis 1. Chemotaxis, 2. Attachment of a bacterium red to long membrane evaginations called pseudopodia, 3. Ingestion of bacterium, forms a phagosome, which moves towards a lysosome, 4. Fusion of the phagosome and lysosome, releases lysosomal enzymes into the phagosome, 5.

Digestion of ingested material, 6. Release of digestion products from the cell ; B. Steps in inhibition of phagocytosis 1. Inhibition of chemotaxis, 2. Inhibition of attachment, 3. Inhibition of phagolysosomal fusion, 4. Escape from intracellular killing mechanisms, 5. Escape from phagolysosome into cytoplasm.

The incorporation of host antigens into its surface membrane may help to avoid the effect of immune response, e. Schistosoma mansoni. Viruses may also demonstrate antigenic variation. Influenza virus undergoes minor and major antigenic changes in some of its surface antigens. The antigenic variation of human immunodeficiency virus HIV plays a role in the ability of this virus to evade the host immune response.

Antigenic variation is seen in Borrelia species among bacteria. Superantigens Superantigens are unique and they bind to specific sites in the variable portion of the chain regardless of the specificity for the antigen. Furthermore, superantigens do not have to be processed by antigen-presenting cells APCs. Reduction in expression of antigens Reduction in expression of antigens has been associated with persistent viral infections.

Paramyxoviruses, arenaviruses, retroviruses and rhabdoviruses are able to reduce the expression of viral coat glycoproteins. Adenoviruses can also inhibit MHC expression by infected cells. Immunosuppression A state of immunosuppression may develop in the host during infection with bacteria, viruses, fungi, protozoa and helminths. This immunosuppression may be specific or general, unrelated to the infecting organism.

General and specific immunosuppression may involve both the humoral and cell-mediated responses. Antibody cleavage Some microorganisms produce protease enzymes that cleave human IgA. IgA is the principal mediator of humoral immunity at mucosal surfaces. Serum resistance Serum resistance is the ability of a microorganism to prevent lysis by complement.

For example, certain strains of Salmonella and E. Induction of the Ineffective Antibodies Ineffective blocking antibodies may be formed in response to certain strains of N. These antibodies are able to bind specific receptors on the surface of gonococci and there by block the access to the antigen by the effective antibacterial antibody. Acquisition of Nutrients from the Host Bacteria require iron for the metabolism and growth and for production of a variety of toxins.

One of the mechanisms that bacteria have developed to extract iron from the host is the production of siderophores. Siderophores, produced by bacteria in the absence of iron are able to extract iron bound to transferrin or lactoferrin and deliver it to the bacterial cell via special receptors. Much variation exists among the siderophores that have been characterized, but most fall into two categories: catechols phenolates of which enterobactin is the best characterized and hydroxamates of which ferrichrome is the best characterized.

Enter- 19 obactin is produced by E. Hydroxamates are commonly found in fungi. Siderophore production is genetically responsive to the concentration of iron in the medium. For example, enterobactin is produced only under low iron conditions. Enterobactin can remove iron from transferrin, some bacteria do not have demonstrable siderophores. Yersinia pestis can utilize iron from hemin and may be able to initiate infection using iron from hemin in gut of the biting flea.

Other bacteria e. Legionella pneumophila, Listeria species, Salmonella species can obtain iron from the host intracellular iron pools. The availability affects the virulence of pathogen. For example, the virulence of N. Role of Bacterial Biofilm A biofilm is a congregation of interactive bacteria adsorbed to a solid surface or each other and encased by a exopolysaccharide matrix. Biofilm form a slimy coat on solid surfaces prosthetics such as catheter, heart valves, contact lenses, etc.

A biofilm may involve single species bacterium or more than one species. Sometimes fungi, both yeasts and mycelia may form biofilm. The first step in biofilm formation is colonization of bacteria on the surface, which is facilitated by flagella, fimbriae and some times cell divisions. Bacteria continuously secrete low level molecules called quorumsensing signals e.

The organisms, which form biofilm cause persistent infections and pose several problems in the treatment. Staphylococcus epidermidis and S. There are many other examples also. Because of the matrix there is a diffusion barrier, which does not allow the antimicrobials to reach the organisms there by developing resistance. Regulation of Virulence Factors Virulence factors in microorganisms are regulated by genes or environmental factors. Virulence factors are coded by genes, which may be present on chromosomes, plasmids, transposons and bacteriophages.

Environmental factors, which regulate virulence of microorganisms include temperature, pH, osmotic pressure and iron concentrations. Plasmids are small, circular extrachromosomal deoxyribonucleic acid DNA molecules. Some plasmids called R-factor resistance are responsible for the resistance of some microorganisms to antibiotics.

In addition, a plasmid may carry the information that determines a microbe pathogenicity. The examples of virulence factors that are encoded by plasmid genes are tetanospasmin, heat-labile enterotoxins and staphylococcal enterotoxins. Bacteriophages can incorporate their DNA into the bacterial chromosome, becoming a prophage and thus remain latent and do not cause lysis of the bacteria.

Such a state is called lysogeny and cells containing the prophage are said to be lysogenic. One outcome of lysogeny is that the host bacterial cell and its progeny acquire new properties coded for the bacteriophage. Such a change in the characteristics of a microbe due to prophage is called lysogenic conversion. Among bacteriophage genes that contribute to pathogenicity are the genes for diphtheria toxin, erythrogenic toxin, staphylococcal enterotoxin, botulinum toxin and the capsule produced by Streptococcus pneumoniae.

Virulence Factors in Viruses Viruses can replicate only in host cells, where the components of the immune system cannot reach them. Viruses gain access to the cells, because they have got attachment sites for receptors on their target cells. Some viruses gain access to the host cells because their attachment sites mimic substances useful to those cells. For example, the attachment sites of rabies virus can mimic the neurotransmitter acetylcholine. As a result the virus can enter the host cell along with the neurotransmitter.

In many viruses, additional proteins are produced that interfere at various levels with specific and non-specific defenses. The advantage of having such proteins is that they enable viruses to replicate more effectively amidst host antiviral defenses. Many other viruses maintain their virulence, evading the immune defense by adopting antigenic variation.

The best example is influenza virus, which undergoes antigenic variation producing a different strain against which the existing antibody becomes ineffective. Some viruses directly destroy the lymphocytes and macrophages HIV causing lysis of CD4 T cells causing profound decrease in cell-mediated immunity. Viruses can bring about cell responses leading to lysis of cell or there may be inclusion body formation or cell dysfunction.

Retroviruses and oncogenic viruses integrate into the host chromosomes and can remain in cells indefinitely, sometimes leading to the expression of there antigens on the host surfaces. Virulence Factors in Fungi Fungi damage host tissues by releasing enzymes that attack cells. Some fungi produce toxins or cause allergic reaction in the host. Certain fungi produce mycotoxins, which cause disease if ingested by human being e.

Cryptococcus neoformans possesses a polysaccharide capsule, which inhibits phagocytosis, though this can be overcome 21 by opsonization with complement and antibodies. Histoplasma capsulatum, an obligate intracellular fungus, evades macrophage killing by entering the cell via complement receptor CR3 and then altering the normal pathways of phagosome maturation.

Dermatophytes suppress host T cell responses to delay cell-mediated destruction. Virulence Factors in Protozoa and Helminths Pathogenic protozoa and helminths cause disease in several ways. Plasmodial and leishmanial species avoid antibody-mediated destruction by their intracellular existence. CD8 cells cannot affect blood stage malaria parasites, as the erythrocytes do not possess MHC I molecule on their surface.

In Giardia intestinalis, the virulence factor is an adhesive disc by which it attaches to the cell lining epithelium of intestine and burrow into the tissue. Some parasites e. Entamoeba histolytica are protected by changing to the cystic forms. Most helminths are extracellular parasites inhabiting the intestine or body tissues. Many release toxic waste products and an- Fig. Roundworms cause obstruction in the intestine or in extraintestinal sites Fig.

Trichinella spiralis can cause disruption of tissue directly producing a soluble lymphotoxic factor. Schistosoma species acquire a surface layer of host antigens, so that the host defense does not distinguish them from the self. Schistosomas can cleave a peptide from IgG. The soluble helminthic parasite antigens may reduce the effectiveness of host response by a process called immune distraction. Define infection and infectious disease. Discuss about the microbial virulence factors.

Enumerate the microbial virulence factors. Explain the mechanism of action of endotoxins. How do you explain host parasite relationship in commensalism, parasitism? What are the factors favoring parasitism? Differences between exotoxin endotoxin. Definitive host. Intermediate host. Carriers—various types.

Zoonotic diseases. Congenital infection. Bacterial biofilm. Black JG. Microbiology Principles and Applications, 3rd edition. Daniel P Stites. Basic and Clinical Immunology, 8th edition. Immunology, 6th edition. Greenwood D, Slack R. Medical Microbiology, 15th edition; Role of iron in regulation of virulence genes. Clin Microbiol Reviews; ; Mims EA. The Pathogenesis of Infectious Disease, 3rd edition.

London: Academic press; Textbook of Microbiology, 8th edition; Patrick S, Larkin MJ. Immunological and Molecular Aspects of Bacterial Virulence. Wiley Chichester; Peakman M, Vergain D. Basic and Clinical Immunology, 1st edition; Determinants of bacterial virulence, chap London: Edward Arnold; Roth JA, et al. Virulence of mechanisms of bacterial pathogens. Molecular biology; ; Mechanisms of Microbial Disease, 3rd edition; Torotra, Funke, Case.

Microbiology an Introduction, 6th edition; Immunity Pathogenic microorganisms are endowed with special properties that enable them to cause disease, if given the right opportunity. If microorganisms never encounter resistance from the host, we would constantly be ill and would eventually die of various diseases. But in most cases, our body defenses prevent them of happening so. In some instances, the body does not allow the organisms to enter.

In others, even if they enter, are eliminated by different mechanisms. In still others, even if they remain inside, the defenses combat with them. Our ability to ward off disease in general is called resistance immunity. Vulnerability or lack of resistance is susceptibility. Immunity is defined as the resistance exhibited by the host towards injury caused by the microorganisms and their products. Protection against the infectious agents is only one of the consequences of the immune response.

But in true sense, immunity involves the defensive response, when a host is invaded by foreign organisms or other foreign substances pollen, insect venom, transplanted tissue. Body cells that become cancerous are also recognized as foreign and may be eliminated. It is independent of previous exposure to disease causing agents and foreign substances. The innate immunity depends on the non-specific mechanisms, molecular defenses and the activity of the phagocytic cells.

Innate immunity may be non-specific, when it indicates a degree of resistance to infection in general or specific, when resistance to particular pathogen is concerned. Innate immunity may be considered at the level of species, race and individual. In species immunity, all individuals of a species are born with resistance to an infectious agent that causes disease in another species. For example, humans are immune to most infectious agents that causes disease in pets and other domesticated animals.

Human beings are insusceptible to rinderpest or distemper, which the canines suffer. Similarly, the animals show innate immunity to many human pathogens. The mechanisms of species immunity are not clearly understood, but may be due to physiological and biochemical differences between the tissues of the different host species that determine, whether or not a pathogen can multiply in them.

Within a species, different races show difference in susceptibility to infections. This is known as racial immunity. Non-specific immunity is largely innate or inborn, whereas specific immunity is acquired. It has been reported that the Negroes in the USA are more susceptible to tuberculosis than the whites.

An interesting instance of genetic resistance to Plasmodium falciparum malaria is seen in some parts of Africa, where sickle cell anemia is prevalent. The hereditary abnormality of the red cells confers immunity to infection by malaria parasite. Even resistance to human diseases, such as measles, can vary from person to person. For example, although the effect of measles is usually relatively mild in European ancestry, the disease devastated the population of Pacific Islanders, when they were first exposed to measles by European explorers.

Natural selection resulting from the exposure of many generations to the measles virus, presumably led to the more frequent inheritance of genes that conferred some resistance to the virus. Individuals in a race exhibit difference in innate immunity.

The genetic basis of individual immunity is evident from studies on the incidence of infectious disease in twins. Homozygous twins exhibit similar degree of resistance or susceptibility to lepromatous leprosy and tuberculosis. Age: Two extremes of life carry higher susceptibility to infections in comparison to adults. The heightened susceptibility of the fetus to infection is related to the immaturity of the immune system. In neonates, the antibodies, immune competent cells and also the complement level remain suboptimal.

Newborn animals suckling mice are more susceptible to coxsackievirus. Tinea capitis caused by Microsporum audouinii is very common in young people, which disappear after reaching puberty. The vaginal epithelium of prepubertal girl is more susceptible to gonococcal infection. Some infections like poliomyelitis and chickenpox, tend to be more severe in adults than in young children due to hypersensitivity that causes more tissue damage.

The old people are prone to infection due to waning of the immune system. The immune system shows the senescence seen in other organs. Cellular immunity is most affected. Hormonal influence: Diabetes, hypothyroidism and adrenal dysfunctions are associated with enhanced susceptibility to infections. Corticosteroids depress host resistance by anti-inflammatory and antiphagocytic effects and also by suppressing antibody formation.

The elevated steroid level in pregnancy may have a relation to the heightened level of susceptibility to the staphylococcal infection. Nutrition: The interaction between malnutrition and immunity is very complex. Paradoxically, there are some evidences that the infections may not be clinically apparent in ill nourished and malnourished patient. Fever in malaria may not be induced in famine-stricken area, but once that nutrition is improved fever appears.

Some viruses may not multiply in the tissue of several malnourished individual. Mechanism of Innate Immunity First line of defense Physical barriers: Skin and mucous membrane form an important line of defense. Intact skin is impenetrable to most of the bacteria.

Its low pH and presence of fatty acid makes the environment inhospitable for bacteria other than commensals. The continual shedding of the squamous epithelium also reduces bacterial load. If the continuity of the skin is compromised, the skin may be secondarily infected. The mucous membranes form a less formidable barrier. The mucus with entrapped bacteria is swept away by cilia of the ciliated respiratory mucosa or the villi in the intestine particles are swallowed and coughed out by cough reflex.

The flushing effect of the body secretions reduces the microbial flora. Any slowing of urinary flow increases the chance of ascending infection. Saliva teeming with oral bacteria flows to the back of throat and is swallowed; gastric acidity destroys most swallowed bacteria. Commensal flora in the intestine prevents the colonization by pathogenic bacteria. Chemical factors Antimicrobial substances : The barrier defense of skin and mucous membrane are reinforced by the presence of antibacterial substances.

Lysozyme, a hydrolytic enzyme, found in the mucus secretions and in tears, is able to cleave the peptidoglycan of the bacterial cell wall. Saliva contains antibacterial hydrogen peroxide H2O2. The low pH of stomach and vagina is inimical to most bacteria. Cholera infection occurs more rapidly in association with achlorhydria. These include: 1. Beta-lysine active against anthrax and related bacilli.

Basic polypeptides leukin from leukocytes and plakin from platelets. Lactic acid found in the muscle tissue and in the inflammatory zone. Lactoperoxidase in the milk. Virus inhibiting substances antiviral substances inhibit viral hemagglutinin. A cysteine-rich peptide called defensins secreted by a variety of cells epithelial cells, neutrophils, macrophages in the skin and mucous membrane.

Other molecules with microbicidal functions include cathelicidin, deoxyribonuclease DNases and ribonuclease RNases. Acute phase proteins Table 3. In an acute phase of infection, pathogens ingested by macrophages stimulate the synthesis and secretion of several cytokines.

Cytokines such as interleukin-1 IL-1 and IL-6 travel through the blood and cause the liver to synthesize and secrete acute phase proteins into the blood. Interferons: A method of defence virus infection is the production of interferon IFN by cells stimulated by live or killed viruses and certain other inducers. IFN has been shown to be more important than specific antibodies in protection against and recovery from certain acute viral infections.

Immunoglobulin: All classes of immunoglobulins Ig have been detected on mucous membranes, but IgA is the most important, because it is present in the greatest amount. IgA is a dimer, linked by secretory piece that not only aids transport, but also renders it resistant to proteolytic enzymes in the secretions.

IgA is not involved in complement -mediated killing classical pathway , but impedes adherence, an essential first step in colonization. Complement system: The complement is a group of serum proteins that circulate in an inactive state. A variety of specific and non-specific immunologic mechanisms can convert the inactive form of complement proteins into an active form leading to lysis of bacteria, cells and viruses; promotion of phagocytosis opsonization ; triggering of inflammation; secretion of immune-regulatory molecules and clearance of immune complex from the circulation.

In the innate immune system, complement can be activated by alternative pathway or via the mannanbinding lectin MBL pathway. Table 3. Cytokines act in an antigen non-specific manner, triggering a wide range of biological activities from chemotaxis to activation of specific cells. Chemokines are subgroups of cytokines of low molecular weight involved in chemotaxis chemical-induced migration.

Commensal flora: It prevents colonization by pathogens. Alteration of normal resident flora may lead to invasion by extraneous microbes causing serious disease such as staphylococcal and clostridial enterocolitis following antibiotics. Commensals protect the host by various mechanisms: 1. Competition for available food and tissue receptors. Production of toxic substances, such as fatty acids or antagonistic substance such as bacteriocins.

Stimulation of antibodies natural antibody that may cross react with pathogens. Keeping the immune system primed, so that the monocytes bear class II histocompatibility antigens needed for immune response. Second line of defense When the first line of defense fails, either because of congenital or acquired defects, then the way to deeper tissue is open to bacteria and the next lines of defense come to play.

Ciliary dysfunction associated with respiratory infections is one of the congenital defects. There are many examples of acquired defects, the increasing use of indwelling devices provides niches for bacterial colonization and infection.

Bacteria e. Staphylococcus epidermidis grow on these foreign bodies in a biofilm, protect them from host defense. Cellular factors in innate immunity: Natural defense against the invasion of the blood and tissue is mediated by phagocytic cells. Phagocytosis is the process by which the invading organisms are ingested by phagocytic cells, ingestion being followed by intracellular killing.

Many cells are able to ingest the Fig. These are neutrophils, macrophages and to a much lesser degree eosinophils. Macrophages consist of histiocytes wandering ameboid cells found in the tissue , the fixed reticulo -endothelial cells and blood monocytes. The innate immune system provides a rapid, initial means of defense against infection using genetically programmed receptors that recognize these structural features of microbes that are not found in the host. Such receptors are known as pattern recognition receptors PRRs , which are found on or in phagocytic cells, which bind to pathogenassociated molecular patterns PAMPs Fig.

Pattern recognition receptors engagement can lead to activation of the host cell and its secretion of antimicrobial substances. PRRs include: 1. Toll-like receptors TLRs , which signals the synthesis and secretion of cytokines to promote inflammation by recruiting cells.

Scavenger receptors that are involved in internalization of bacteria and phagocytosis of host cells that are undergoing apoptosis. Opsonins, the molecules C3a, IgM , which bind to microbes to facilitate their phagocytosis. Figs 3. Phases of phagocytosis; B. Phagocyte engulfing an yeast cell. These stress signals are detected by various receptors, including some of the TLRs e. NK cells bring about the death of organisms viruses and tumor cells not by intracellular digestion, but by extracellular killing by liberating perforin, a cytolysin after degranulation Fig.

Inflammation: Tissue injury, initiated by the entry of pathogens leads to inflammation, which is an important non-specific mechanism of defense. Hence, inflammation acts as a protective phenomenon. Blood flow to the particular part is increased. There is an outpouring of plasma, which dilutes the toxins and enzymes.

Chemotactic factors including C5a, histamine, leukotrienes, etc. The increased vascular permeability will allow easier access for neutrophils and monocytes. Vasodilation means more cells in the vicinity. There is formation of fibrin barrier, which limits the inflammation. There is activation of complement and also the specific defenses.

Fever: A rise of temperature following infection, helps in following ways: 1. Mobilization defenses. Accelerate repairs. Inhibits pathogens. Stimulates the production of IFNs and helps in recovery from virus infection. Therapeutic induction of fever was employed previously for destruction of T. The mechanisms of all the innate immunity is given in Figure 3.

Acquired Immunity The resistance an individual acquires during life is called acquired immunity. Active Immunity Adaptive Immunity Active immunity or adaptive immunity is capable of recognizing and selectively eliminating specific foreign microorganisms and molecules, i.

Active immunity sets in only after a latent period, which the immunological machinery needs for its functioning. Once developed the active immunity is long lasting. When the individual is facing the same antigen subsequently, there is no latent or lag phase and the immune response is prompt, powerful and prolonged Table 3.

Adaptive immunity focuses on four important characteristic features. They are: 1. Antigenic specificity. Immunological memory. The antigenic specificity of the immune system permits it to distinguish minor difference among antigens. The antibodies can distinguish between two protein molecules that differ in only a single amino acid. The immune system is capable of generating tremendous diversity in its recognition molecules, permitting to recognize vast arrays of unique structures on foreign antigens.

Once the immune system recognized and responded to an antigen, it exhibits immunological memory to recognize the same antigen, subsequently and react in a heightened manner Refer Table 3. Finally, the immune system, normally responds to foreign antigens, indicating that it is capable of distinguishing self from non-self. They interact constantly. The phagocytic cells crucial to nonspecific immune responses are intimately involved in igniting the specific immune response.

Conversely various soluble factors produced during specific immune response have been shown to augment the activity of these phagocytic cells. Naturally acquired active immunity: This type of immunity is obtained when a person is exposed to antigens in the course of daily life. Once acquired, the immunity lasts for rest of its life such as in measles and chickenpox. For other diseases, especially in intestinal diseases, the immunity is short lasting. Subclinical infections can also conform immunity as that occurs in tuberculosis.

Adults have natural immunity against polio after repeated subclinical infections. In syphilis, malaria and few other diseases, a special type of immunity is observed known as infection immunity premunition. The immunity to reinfection lasts as long as the original infection persists.

Vaccinations may be inactivated bacterial toxins toxoids , killed microorganisms, live but attenuated microorganisms or parts of microorganisms such as capsules. These substances can no longer cause disease, but can stimulate immune response. Examples of vaccines are as follows: 1. Live vaccines initiate an infection without causing any injury or diseases. The immunity lasts for several years. Booster dose may or may not be required.

Live oral polio or nasal spray influenza vaccines provide local immunity. Killed vaccines are generally less immunogenic than the live vaccines and the immunity lasts only for a short period. Therefore, they are administered repeatedly. Killed vaccines are given parenterally.

Passive Immunity Passive immunity is resistance exhibited by the host, when ready-made antibodies or defensive cells are introduced into the body. This form of protection is passive, because the individuals own immune system does not make antibodies or defensive cells against the disease producing agents or toxins. Naturally acquired passive immunity: This type of immunity involves natural transfer of antibodies from mother to her infant and also from mother to fetus. Buying options eBook EUR Softcover Book EUR Learn about institutional subscriptions.

Table of contents 36 chapters Search within book Search. Page 1 Navigate to page number of 3. Front Matter Pages i-xix. Introduction Front Matter Pages Diagnosis Front Matter Pages Antibiosis and Vaccines Front Matter Pages Chlamydia trachomatis Infections Front Matter Pages In humans, chlamydiae are known to cause trachoma which is still one of the major blinding diseases in the world and are also one of the most common etiological agents of sexually transmitted diseases and the sequelae thereof, such as infertility.

In the last few years, it has also become evident that chlamydiae, i. Some of these infections occur as zoonoses, e. Know ledge of the molecular biology and immunobiology of chlamydiae has expanded rapidly during recent years.

Jawetz medical microbiology 26th edition pdf kickasstorrents the miniaturist torrent

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Lavanya es posthumus torrent The immune system is capable of generating tremendous diversity in its recognition molecules, permitting to recognize vast arrays of unique structures on foreign antigens. Immunology Introductory Textbook. Click antigens are characteristics of organ- or tissue-specific antigens. Transmission by vectors. Innate immunity may be considered at the level of species, race and individual. Food Contaminated food material may act as source of infection food poisoning by Staphylococcus aureus, Bacillus cereus, E.
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Jawetz medical microbiology 26th edition pdf kickasstorrents For example, enterobactin is produced only under low iron conditions. They produced a hybrid cell by fusing antibody-forming cell with a myeloma cell. Superantigens Superantigens are unique and they bind to specific sites in the variable portion of the chain regardless of the specificity for the antigen. Initially, the book was designed, mainly, for the use of undergraduate students. We felt the need of inclusion of host-parasite relationship in our books as the students should have a basic knowledge about the determinants of pathogenicity before they study the immune response produced against them.
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File renamer turbo torrent This can be plotted in a graph, the resulting curve will have three phases: Historically, one of the first serological tests to be developed was the precipitation test, which can be used to detect antigen or antibodies. Body cells that become cancerous are also recognized as foreign and may be eliminated. Antibiotics used to treat diseases caused by gram-negative bacteria can lyse the read article cells; this reaction releases endotoxin and may lead to an immediate worsening of the symptoms, but the condition usually improves as the endotoxin breaks down. Table of contents 36 chapters Search within book Search. Number of Pages :
Manicomio 527 la etnia torrent Sometimes fungi, both yeasts and mycelia may form biofilm. One outcome of lysogeny is that the host bacterial cell and its progeny acquire new properties coded for the bacteriophage. Learn about institutional subscriptions. Once acquired, the immunity lasts for rest of its life such as in measles and chickenpox. Both, airborne pathogens and those that are suspended in droplets, have chance of reaching near hosts in a overcrowded locality.
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