Books on the topic 'Allergic response'

Food allergy is an immune response to food that can be classified as immunoglobulin (Ig)-E and non-IgE mediated. Milk, egg, peanut, tree nuts, and fish are among the most prevalent causes of food allergy. Mild reactions can include itchy rash, watering eyes, and nasal congestion while a severe reaction results in anaphylaxis. A detailed clinical history is essential when making a diagnosis, and skin prick testing and quantitative measurement of food-specific IgE antibodies can be helpful. Cow milk protein allergy causes a plethora of symptoms and frequently resolves spontaneously over the first 2 years of life; diagnosis is based mainly on clinical history. Food challenges have a pivotal role in the diagnosis of food allergy. Introduction of ‘allergic’ foods at 3–6 months alongside continuing breastfeeding may prevent allergy.

Exposure to contaminants in the home and all indoor spaces can cause disease, including chronic inflammation, allergy, and asthma. Controlling dust, which can contain mold spores, insect parts, fecal material, pet dander, skin fragments, packaging materials, dust mites, volatile cleaning agents, and carpet fragments, is essential for clean indoor air. Dust is a vector for chemical toxins and organic and inorganic materials, which are sources of inflammation. The triggered immune response plays a central role in the pathogenesis of asthma, allergy, and sinusitis. Controlling humidity is necessary to minimize mold and the infiltration of dust mites and other insects in the home.

The Immune System: A Very Short Introduction describes the immune system and how it works in health and disease. It focuses on the human immune system, considering how it evolved, and the basic rules that govern its behaviour. The immune system comprises a series of organs, cells, and chemical messengers that work together as a team to provide defence against infection. These components are discussed along with the critical signals that trigger them and how they exert their protective effects, including innate and adaptive responses. The consequences of too little immunity (immunodeficiency), caused for example by HIV/AIDS, and too much, leading to auto-immune and allergic diseases, are also considered.

This chapter discusses a collection of practical topics of relevance to the anaesthetist. Topics covered include herbal medicines, blood exposure incidents, target-controlled infusions, death on the table, dealing with a complaint, anaphylaxis follow-up, latex allergy, long-term venous access, enhanced recovery and cardiac output monitoring, depth of anaesthesia monitoring, neuromuscular blockade and reversal, evidence-based anaesthesia, and the Cochrane Collaboration. There is a section on military anaesthesia which includes damage control resuscitation, medical emergency response team, the Triservice Anaesthesia Apparatus, and military uses of total intravenous anaesthesia.

This chapter discusses a collection of practical topics of relevance to the anaesthetist. Topics covered include herbal medicines, blood exposure incidents, target-controlled infusions, death on the table, dealing with a complaint, anaphylaxis follow-up, latex allergy, long-term venous access, enhanced recovery and cardiac output monitoring, depth of anaesthesia monitoring, neuromuscular blockade and reversal, evidence-based anaesthesia, and the Cochrane Collaboration. There is a section on military anaesthesia which includes damage control resuscitation, medical emergency response team, the Triservice Anaesthesia Apparatus, and military uses of total intravenous anaesthesia.

Listeria monocytogenes is a intracellular bacterial pathogen that causes serious foodborne illness in humans. Among all infectious diseases caused by gastrointestinal pathogens, listeriosis has the highest mortality rate, likely because of its ability to cross the gastrointestinal barrier and cause sepsis and infection of other organs such as the brain and placenta. Infection of the placenta leads to fetal infection, and otherwise healthy pregnant women have a significantly increased incidence of listeriosis than the general population, likely due to changes in the maternal cell-mediated immune response during pregnancy. Clinical manifestations include miscarriage, stillbirth, preterm labor, and neonatal infection and death. Neonates develop early-onset sepsis or late-onset meningitis. Physicians must evaluate pregnant women and neonates with febrile illnesses for listeriosis, since prompt treatment with antibiotics can cure it. It is important to note that L. monocytogenes is resistant to cephalosporins. Ampicillin is the treatment of choice in patients without penicillin allergy.

Cystic fibrosis lung disease is characterized by chronic infection, inflammation and a progressive loss of lung function. Patients are also affected by recurrent episodes of increased respiratory symptoms, called exacerbations which have a detrimental effect on quality of life, the rate of lung function decline, and mortality. Early diagnosis and treatment is vital. Diagnosis relies on a combination of symptoms, examination findings, the results of laboratory tests, and lung function. Antibiotics are the mainstay of treatment but airway clearance, nutrition, and glucose homeostasis must also be optimized. Mild exacerbations are usually treated with oral antibiotics and more severe exacerbations with intravenous antibiotics. The choice of antibiotic is guided by the patient’s chronic pulmonary infections, the in-vitro antibiotic sensitivities, known antibiotic allergies, and the previous response to treatment. In patients with chronic Pseudomonas aeruginosa infection, antibiotic monotherapy is thought to increase the risk of resistance and treatment with 2 antibiotics is therefore suggested (usually a β‎-lactam and an aminoglycoside). Although there is a lack of evidence on the duration of treatment, most patients receive around 14 days. This can be altered according to the time taken for symptoms and lung function to return to pre-exacerbation levels. If patients are carefully selected and receive appropriate monitoring, home intravenous antibiotics can be as effective as in-patient treatment. They are also associated with decreased disruption to patients / family life, decreased risk of cross infection and decreased costs.

Trichinellosis is caused by nematodes of the genus Trichinella. These zoonotic parasites show a cosmopolitan distribution in all the continents, but Antarctica. They circulate in nature by synanthropic-domestic and sylvatic cycles. Today, eight species and four genotypes are recognized, all of which infect mammals, including humans, one species also infects birds, and two other species infect also reptiles.Parasites of the genus Trichinella are unusual among the other nematodes in that the worm undergoes a complete developmental cycle, from larva to adult to larva, in the body of a single host, which has a profound influence on the epidemiology of trichinellosis. When the cycle is complete, the muscles of the infected animal contain a reservoir of larvae, capable of long-term survival. Humans and other hosts become infected by ingesting muscle tissuescontaining viable larvae.The symptoms associated with trichinellosis vary with the severity of infection, i.e. the number of viable larvae ingested, and the time after infection. The capacity of the worm population to undergo massive multiplication in the body is a major determinant. Progression of disease follows the biological development of the parasite. Symptoms are associated first with the gastrointestinal tract, as the worms invade and establish in the small intestine, become more general as the body responds immunologically, and finally focus on the muscles as the larvae penetrate the muscle cells and develop there. Although Trichinella worms cause pathological changes directly by mechanical damage, most of the clinical features of trichinellosis are immunopathological in origin and can be related to the capacity of the parasite to induce allergic responses.The main source of human infection is raw or under-cooked meat products from pig, wild boar, bear, walrus, and horses, but meat products from other animals have been implicated. In humans, the diagnosis of infection is made by immunological tests or by direct examination of muscle biopsies using microscopy or by recovery of larvae after artificial digestion. Treatment requires both the use of anthelmintic drugs to kill the parasite itself and symptomatic treatment to minimize inflammatory responses.Both pre-slaughter prevention and post-slaughter control can be used to prevent Trichinella infections in animals. The first involves pig management control as well as continuous surveillance programmes. Meat inspection is a successful post-slaughter strategy. However, a continuous consumer education is of great importance in countries where meat inspection is not mandatory.

Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.