In this chapter medicine to increase appetite 60caps brahmi with visa, however treatment junctional rhythm cheap 60 caps brahmi free shipping, we will examine the role of those innate, nonadaptive defenses that form early barriers to infectious disease. The microorganisms that are encountered daily in the life of a normal healthy individual only occasionally cause perceptible disease. Most are detected and destroyed within minutes or hours by defense mechanisms that do not require a prolonged period of induction because they do not rely on the clonal expansion of antigen-specific lymphocytes: these are the mechanisms of innate immunity. The time course and different phases of an encounter with a new pathogen are summarized in. The innate immune mechanisms act immediately, and are followed by early induced responses, which can be activated by infection but do not generate lasting protective immunity. Only if an infectious organism can breach these early lines of defense will an adaptive immune response ensue, with the generation of antigen-specific effector cells that specifically target the pathogen, and memory cells that can prevent reinfection with the same microorganism. The power of adaptive immune responses is due to their antigen specificity, which we will be studying in the following chapters. However, they harness, and also depend upon, many of the effector mechanisms used by the innate immune system, which we will describe in this chapter. The effector mechanisms that remove the infectious agent (for example, phagocytes and complement) are similar or identical in each phase, but the first two phases rely on recognition of pathogens by germline-encoded receptors of the innate immune system, whereas adaptive immunity uses variable antigen-specific receptors that are produced as a result of gene rearrangements. Adaptive immunity occurs late, because the rare B and T cells specific for the invading pathogen must undergo clonal expansion before they differentiate into effector cells that can clear the infection. Whereas the adaptive immune system uses a large repertoire of receptors encoded by rearranging genes to recognize a huge variety of antigens (see Section 1-10), innate immunity depends upon germline-encoded receptors to recognize features that are common to many pathogens. In fact, as we will see, the mechanisms of innate immunity discriminate very effectively between host cells and pathogen surfaces, and this ability to discriminate between self and nonself, and to recognize broad classes of pathogens, contributes to the induction of an appropriate adaptive immune response. In the first part of the chapter we will consider the fixed defenses of the body: the epithelia that line the internal and external surfaces of the body, and the phagocytes that can engulf and digest invading microorganisms. As well as killing microorganisms, the activities of some of these phagocytes induce the next phase of the early response, and ultimately, if the infection is not cleared, the adaptive immune response. The second part of the chapter is devoted to a system of plasma proteins known as the complement system. This important element of innate immunity interacts with microorganisms to promote their removal by phagocytic cells. Next, we take a closer look at the receptors used by the immune system to recognize pathogens, and the last part of the chapter describes how the activation of phagocytic cells at the beginning of the innate immune response to infection leads to the induced or adaptive immune response. Microorganisms that cause pathology in humans and animals enter the body at different sites and produce disease by a variety of mechanisms. Many different infectious agents can cause pathology, and those that do are referred to as pathogenic microorganisms or pathogens. Invasions by microorganisms are initially countered, in all vertebrates, by innate defense mechanisms that preexist in all individuals and act within minutes of infection. Only when the innate host defenses are bypassed, evaded, or overwhelmed is an induced or adaptive immune response required. In the first part of this chapter we will describe briefly the infectious strategies of microorganisms before examining the innate host defenses that, in most cases, prevent infection from becoming established. Thus we will look at the defense functions of the epithelial surfaces of the body, the role of antimicrobial peptides and proteins, and the defense of body tissues by macrophages and neutrophils, which bind and ingest invading microorganisms in a process known as phagocytosis. Infectious agents must overcome innate host defenses to establish a focus of infection. Our bodies are constantly exposed to microorganisms present in the environment, including infectious agents that have been shed from infected individuals. Contact with these microorganisms may occur through external or internal epithelial surfaces: the respiratory tract mucosa provides a route of entry for airborne microorganisms, the gastrointestinal mucosa for microorganisms in food and water; insect bites and wounds allow micro-organisms to penetrate the skin; and direct contact between individuals offers opportunities for infection of the skin and reproductive mucosa. The epithelial surfaces of the body serve as an effective barrier against most microorganisms, and are rapidly repaired if wounded. Furthermore, most of the microorganisms that do succeed in crossing the epithelial surfaces are efficiently removed by innate immune mechanisms that function in the underlying tissues.
Because of the high organism burden in patients with disseminated disease treatment ingrown toenail order brahmi 60 caps on line, cultures of respiratory specimens medicine natural cheap brahmi 60 caps fast delivery, blood, bone marrow, and tissue are of value. Growth of the mycelial form in culture is slow, and once isolated, the identification must be confirmed by conversion to the yeast phase or by use of exoantigen testing or nucleic acid hybridization. As with the other dimorphic pathogens, cultures of Histoplasma must be handled with care in a biosafety cabinet. Serologic diagnosis of histoplasmosis employs tests for both antigen and antibody detection (see Table 64-2). Detection of Histoplasma antigen in serum and urine by enzyme immunoassay has become very useful, particularly in diagnosing disseminated disease (see Tables 64-2 and 644). The sensitivity of antigen detection is greater in urine specimens than in blood and ranges from 21% in chronic pulmonary disease to 92% in disseminated disease. Serial measurements of antigen may be used to assess response to therapy and for establishing relapse of the disease. This infection is also known as South American blastomycosis and is the major dimorphic endemic fungal infection in Latin American countries. Primary paracoccidioidomycosis usually occurs in young people as a self-limited pulmonary process. Reactivation of a primary quiescent lesion may occur years later, resulting in chronic progressive pulmonary disease with or without involvement of other organs. White colonies become apparent in 3 to 4 weeks, eventually taking on a velvety appearance. The mycelial form is nondescript and nondiagnostic: hyaline septate hyphae with intercalated chlamydoconidia. Specific identification requires conversion to the yeast form or exoantigen testing. The variability in size and number of blastoconidia and their connection to the parent cell are identifying features (see Figure 64-13). Epidemiology Paracoccidioidomycosis is endemic throughout Latin America but is more prevalent in South America than Central America (see Figure 64-2). The highest incidence is seen in Brazil, followed by Colombia, Venezuela, Ecuador, and Argentina. All patients diagnosed outside of Latin America previously had lived in Latin America. The ecology of the endemic areas includes high humidity, rich vegetation, moderate temperatures, and acid soil. These conditions are found along rivers from the Amazon jungle to small indigenous forests in Uruguay. The portal of entry is thought to be either by inhalation or traumatic inoculation (Figure 64-14), although even this is poorly understood. Although infection occurs in children (peak incidence 10 to 19 years), overt disease is uncommon in both children and adolescents. Estrogen-mediated inhibition of the mold-toyeast transition may account for the 15: 1 male/female ratio of clinical disease. Most patients with clinically apparent disease live in rural areas and have close contact with the soil. Depression of cell-mediated immunity correlates with the acute progressive form of the disease. A subacute disseminated form is seen in younger patients and immunocompromised individuals with marked lymphadenopathy, organomegaly, bone marrow involvement, and osteoarticular manifestations mimicking osteomyelitis. Adults most often present with a chronic pulmonary form of the disease marked by respiratory problems, often as the sole manifestation. The disease progresses slowly over months to years, with persistent cough, purulent sputum, chest pain, weight loss, dyspnea, and fever. Although 25% of patients exhibit only pulmonary manifestations of the disease, the infection can disseminate to extrapulmonary sites in the absence of diagnosis and treatment.
Given the destructive effects of complement medicine organizer box effective brahmi 60caps, and the way in which its activation is rapidly amplified through a triggered-enzyme cascade treatment renal cell carcinoma generic 60 caps brahmi, it is not surprising that there are several mechanisms to prevent its uncontrolled activation. As we have seen, the effector molecules of complement are generated through the sequential activation of zymogens, which are present in plasma in an inactive form. The activation of these zymogens usually occurs on a pathogen surface, and the activated complement fragments produced in the ensuing cascade of reactions usually bind nearby or are rapidly inactivated by hydrolysis. These two features of complement activation act as safeguards against uncontrolled activation. Even so, all complement components are activated spontaneously at a low rate in plasma, and activated complement components will sometimes bind proteins on host cells. The potentially damaging consequences are prevented by a series of complement control proteins, summarized in. As we saw in discussing the alternative pathway of complement activation (see Section 2-9) many of these control proteins specifically protect host cells while allowing complement activation to proceed on pathogen surfaces. The complement control proteins therefore allow complement to distinguish self from nonself. The small fragment of C2, C2a, is further cleaved into a peptide, the C2 kinin, which causes extensive swelling the most dangerous being local swelling in the trachea, which can lead to suffocation. The large activated fragments of C4 and C2, which normally combine to form the C3 convertase, do not damage host cells in such patients because C4b is rapidly inactivated in plasma. Furthermore, any convertase that accidentally forms on a host cell is inactivated by the mechanisms described below. The thioester bond of activated C3 and C4 is extremely reactive and has no mechanism for distinguishing an acceptor hydroxyl or amine group on a host cell from a similar group on the surface of a pathogen. A series of protective mechanisms, mediated by other proteins, has evolved to ensure that the binding of a small number of C3 or C4 molecules to host cell membranes results in minimal formation of C3 convertase and little amplification of complement activation. We have already encountered most of these mechanisms in the description of the alternative pathway. The first catalyze the cleavage of any C3b or C4b that does bind to host cells into inactive products. The complement-regulatory enzyme responsible is the plasma serine protease factor I; it circulates in active form but can only cleave C3b and C4b when they are bound to a cofactor protein. In these circumstances, factor I cleaves C3b, first into iC3b and then further to C3dg, thus permanently inactivating it. Microbial cell walls lack these protective proteins and cannot promote the breakdown of C3b and C4b. Instead, these proteins act as binding sites for factor B and C2, promoting complement activation. The importance of factor I can be seen in people with genetic factor I deficiency. Because of uncontrolled complement activation, complement proteins rapidly become depleted and such people suffer repeated bacterial infections, especially with ubiquitous pyogenic bacteria. Complement activation is regulated by a series of proteins that serve to protect host cells from accidental damage. These act on different stages of the complement cascade, dissociating complexes or catalyzing the enzymatic degradation of covalently bound complement proteins. Stages in the complement cascade are shown schematically down the left side of the figure, with the control reactions on the right. C3b is bound in both the fluid phase and at cell membranes by a cofactor protein called factor H (see Section 2-9). Factor H is an important complement regulator at cell membranes, and at first sight it is not obvious how factor H can distinguish C3b bound to host cells or to a pathogen. However, the carbohydrate content of the cell membranes of bacterial pathogens differs from that of their hosts and this is the basis for the protective effect of factor H. Factor H has affinity for the terminal sialic acids of host cell membrane glycoproteins and this increases the binding of factor H to any C3b deposited on host cells. In contrast, factor H has a much lower affinity for C3b deposited on the cell walls of many bacteria, and factor B binds in preference, resulting in amplification of complement activation on bacterial cell surfaces.
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Thus medicine encyclopedia buy 60 caps brahmi fast delivery, the clinical syndrome produced by an allergic reaction depends critically on three variables: the amount of allergenspecific IgE present; the route by which the allergen is introduced; and the dose of allergen treatment under eye bags cheap 60caps brahmi visa. If an allergen is introduced directly into the bloodstream or is rapidly absorbed from the gut, the connective tissue mast cells associated with all blood vessels can become activated. Disseminated mast-cell activation has a variety of potentially fatal effects: the widespread increase in vascular permeability leads to a catastrophic loss of blood pressure; airways constrict, causing difficulty in breathing; and swelling of the epiglottis can cause suffocation. It can occur if drugs are administered to people who have IgE specific for that drug, or after an insect bite in individuals allergic to insect venom. Some foods, for example peanuts or brazil nuts, can cause systemic anaphylaxis in susceptible individuals. This syndrome can be rapidly fatal but can usually be controlled by the immediate injection of epinephrine, which relaxes the smooth muscle and inhibits the cardiovascular effects of anaphylaxis. The most frequent allergic reactions to drugs occur with penicillin and its relatives. In people with IgE antibodies against penicillin, administration of the drug by injection can cause anaphylaxis and even death. Great care should be taken to avoid giving a drug to patients with a past history of allergy to that drug or one that is closely related structurally. Penicillin acts as a hapten (see Section 9-2); it is a small molecule with a highly reactive -lactam ring that is crucial for its antibacterial activity. Thus, penicillin acts both as the B-cell antigen and, by modifying self peptides, as the T-cell antigen. When penicillin is injected intravenously into an allergic individual, the penicillinmodified proteins can cross-link IgE molecules on the mast cells and cause anaphylaxis. The dose and route of allergen administration determine the type of IgE-mediated allergic reaction that results. There are two main anatomical distributions of mast cells: those associated with vascularized connective tissues, called connective tissue mast cells, and those found in submucosal layers of the gut and respiratory tract, called mucosal mast cells. In an allergic individual, all of these are loaded with IgE directed against specific allergens. The overall response to an allergen then depends on which mast cells are activated. Allergen in the bloodstream activates connective tissue mast cells throughout the body, resulting in the systemic release of histamine and other mediators. Subcutaneous administration of allergen activates only local connective tissue mast cells, leading to a local inflammatory reaction. Inhaled allergen, penetrating across epithelia, activates mainly mucosal mast cells, causing smooth muscle contraction in the lower airways; this leads to bronchoconstriction and difficulty in expelling inhaled air. Mucosal mast-cell activation also increases the local secretion of mucus by epithelial cells and causes irritation. Similarly, ingested allergen penetrates across gut epithelia, causing vomiting due to intestinal smooth muscle contraction and diarrhea due to outflow of fluid across the gut epithelium. Food allergens can also be disseminated in the bloodstream, causing urticaria (hives) when the food allergen reaches the skin. Many people have mild allergies to inhaled antigens, manifesting as sneezing and a runny nose. This is called allergic rhinitis, and results from the activation of mucosal mast cells beneath the nasal epithelium by allergens such as pollens that release their protein contents, which can then diffuse across the mucus membranes of the nasal passages. Allergic rhinitis is characterized by intense itching and sneezing, local edema leading to blocked nasal passages, a nasal discharge, which is typically rich in eosinophils, and irritation of the nose as a result of histamine release. A similar reaction to airborne allergens deposited on the conjunctiva of the eye is called allergic conjunctivitis. Allergic rhinitis and conjunctivitis are commonly caused by environmental allergens that are only present during certain seasons of the year. For example, hay fever is caused by a variety of allergens, including certain grass and tree pollens. A more serious syndrome is allergic asthma, which is triggered by allergen-induced activation of submucosal mast cells in the lower airways. This leads within seconds to bronchial constriction and increased secretion of fluid and mucus, making breathing more difficult by trapping inhaled air in the lungs. Patients with allergic asthma often need treatment, and asthmatic attacks can be life-threatening. Although allergic asthma is initially driven by a response to a specific allergen, the subsequent chronic inflammation seems to be perpetuated even in the apparent absence of further exposure to allergen.
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