acquired immunity


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immunity

 [ĭ-mu´nĭ-te]
the condition of being immune; the protection against infectious disease conferred either by the immune response generated by immunization or previous infection or by other nonimmunologic factors. It encompasses the capacity to distinguish foreign material from self, and to neutralize, eliminate, or metabolize that which is foreign (nonself) by the physiologic mechanisms of the immune response.

The mechanisms of immunity are essentially concerned with the body's ability to recognize and dispose of substances which it interprets as foreign and harmful to its well-being. When such a substance enters the body, complex chemical and mechanical activities are set into motion to defend and protect the body's cells and tissues. The foreign substance, usually a protein, is called an antigen, that is, one that generates the production of an antagonist. The most common response to the antigen is the production of antibody. The antigen--antibody reaction is an essential component of the overall immune response. A second type of activity, cellular response, is also an essential component.

The various and complex mechanisms of immunity are basic to the body's ability to protect itself against specific infectious agents and parasites, to accept or reject cells and tissues from other individuals, as in blood transfusions and organ transplants, and to protect against cancer, as when the immune system recognizes malignant cells as not-self and destroys them.

There has been extensive research into the body's ability to differentiate between cells, organisms, and other substances that are self (not alien to the body), and those that are nonself and therefore must be eliminated. A major motivating force behind these research efforts has been the need for more information about growth and proliferation of malignant cells, the inability of certain individuals to develop normal immunological responses (as in immunodeficiency conditions), and mechanisms of failure of the body to recognize its own tissues (as in autoimmune diseases).
Immunological Responses. Immunological responses in humans can be divided into two broad categories: humoral immunity, which takes place in the body fluids (humors) and is concerned with antibody and complement activities; and cell-mediated or cellular immunity, which involves a variety of activities designed to destroy or at least contain cells that are recognized by the body as alien and harmful. Both types of responses are instigated by lymphocytes that originate in the bone marrow as stem cells and later are converted into mature cells having specific properties and functions.

The two kinds of lymphocytes that are important to establishment of immunity are T lymphocytes (T cells) and B lymphocytes (B cells). (See under lymphocyte.) The T lymphocytes differentiate in the thymus and are therefore called thymus-dependent. There are several types involved in cell-mediated immunity, delayed hypersensitivity, production of lymphokines, and the regulation of the immune response of other T and B cells.

The B lymphocytes are so named because they were first identified during research studies involving the immunologic activity of the bursa of Fabricius, a lymphoid organ in the chicken. (Humans have no analogous organ.) They mature into plasma cells that are primarily responsible for forming antibodies, thereby providing humoral immunity.
Humoral Immunity. At the time a substance enters the body and is interpreted as foreign, antibodies are released from plasma cells and enter the body fluids where they can react with the specific antigens for which they were formed. This release of antibodies is stimulated by antigen-specific groups (clones) of B lymphocytes. Each B lymphocyte has IgM immunoglobulin receptors that play a major role in capturing its specific antigen and in launching production of the immunoglobulins (which are antibodies) that are capable of neutralizing and destroying that particular type of antigen.

Most of the B lymphocytes activated by the presence of their specific antigen become plasma cells, which then synthesize and export antibodies. The activated B lymphocytes that do not become plasma cells continue to reside as “memory” cells in the lymphoid tissue, where they stand ready for future encounters with antigens that may enter the body. It is these memory cells that provide continued immunity after initial exposure to the antigens.

There are two types of humoral immune response: primary and secondary. The primary response begins immediately after the initial contact with an antigen; the resulting antibody appears 48 to 72 hours later. The antibodies produced during this primary response are predominantly of the IgM class of immunoglobulins.

A secondary response occurs within 24 to 48 hours. This reaction produces large quantities of immunoglobulins that are predominantly of the IgG class. The secondary response persists much longer than the primary response and is the result of repeated contact with the antigens. This phenomenon is the basic principle underlying consecutive immunizations.

The ability of the antibody to bind with or “stick to” antigen renders it capable of destroying the antigen in a number of ways; for example, agglutination and opsonization. Antibody also “fixes” or activates complement, which is the second component of the humoral immune system. Complement is the name given a complex series of enzymatic proteins which are present but inactive in normal serum. When complement fixation takes place, the antigen, antibody, and complement become bound together. The cell membrane of the antigen (which usually is a bacterial cell) then ruptures, resulting in dissolution of the antigen cell and a leakage of its substance into the body fluids. This destructive process is called lysis.
Cellular Immunity. This type of immune response is dependent upon T lymphocytes, which are primarily concerned with a delayed type of immune response. Examples of this include rejection of transplanted organs, defense against slowly developing bacterial diseases that result from intracellular infections, delayed hypersensitivity reactions, certain autoimmune diseases, some allergic reactions, and recognition and rejection of self cells undergoing alteration, for example, those infected with viruses, and cancer cells that have tumor-specific antigens on their surfaces. These responses are called cell-mediated immune responses.

The T lymphocyte becomes sensitized by its first contact with a specific antigen. Subsequent exposure to the antigen stimulates a host of chemical and mechanical activities, all designed to either destroy or inactivate the offending antigen. Some of the sensitized T lymphocytes combine with the antigen to deactivate it, while others set about to destroy the invading organism by direct invasion or the release of chemical factors. These chemical factors, through their influence on macrophages and unsensitized lymphocytes, enhance the effectiveness of the immune response.

Among the more active chemical factors are lymphokines, which are potent and biologically active proteins; their names are often descriptive of their functions: Ones that directly affect the macrophages are the macrophage chemotactic factor, which attracts macrophages to the invasion site; migration inhibitory factor, which causes macrophages to remain at the invasion site; and macrophage-activating factor, which stimulates the metabolic activities of these large cells and thereby improves their ability to ingest the foreign invaders.

Another factor, a protein called interferon, is produced by the body cells, especially T lymphocytes, following viral infection or in response to a wide variety of inducers, such as certain nonviral infectious agents and synthetic polymers.

A portion of the population of T lymphocytes is transformed into killer cells by the lymphocyte-transforming factor (blastogenic factor). These activated lymphocytes produce a lymphotoxin or cytotoxin that damages the cell membranes of the antigens, causing them to rupture.

In order to ensure an ample supply of T lymphocytes, two factors are at work: lymphocyte-transforming factor stimulates lymphocytes that have already undergone conversion to sensitized T lymphocytes, so that they increase their numbers by repeated cell division and clone formation; in the absence of antigens, transfer factor takes over the task of sensitizing those lymphocytes that have not been exposed to antigen.

It is apparent that the immune response brings about intensive activity at the site of invasion; it is not only the pathogen that is destroyed, but invariably, there is death or damage to some normal tissues.
Interactions Between the Two Systems. There are several areas in which the cellular and humoral systems interact and thereby improve the efficiency of the overall immune response. For example, a by-product of the enzymatic activity of the complement system acts as a chemotactic factor, attracting T lymphocytes and macrophages to the invasion site. In another example, although T lymphocytes are not required for the production of antibody, there is optimal antibody production after interaction between T and B lymphocytes.

For a discussion of abnormalities of the immune response system, see immune response.
Types of Immunity. An individual may be naturally immune to certain pathological conditions or may acquire immunity through either active or passive means.
Natural immunity is a genetic characteristic of an individual and is due to the particular species and race to which one belongs, to one's sex, and to one's individual ability to produce immune bodies. All humans are immune to certain diseases that affect animals of the lower species; males are more resistant to some disorders than are females, and vice versa. Persons of one race are more susceptible to some diseases than those of another race that has had exposure to the infectious agents through successive generations. One's individual ability to produce immune bodies, and thereby ward off pathogens, is influenced by one's state of physical health, one's nutritional status, and one's emotional response to stress.

In order for an individual to acquire immunity one's body must be stimulated to produce its own immune response components (active immunity) or these substances must be produced by other persons or animals and then passed on to the person (passive immunity). Active immunity can be established in two ways: by having the disease or by receiving modified pathogens and toxins. When an individual is exposed to a disease and the pathogenic organisms enter the body, the production of antibody is initiated. After recovery from the illness, memory cells remain in the body and stand ready as a defense against future invasion. It is possible, through the use of vaccines, bacterins, and modified toxins (toxoids), to stimulate the production of specific antibodies without having an attack of the disease. These are artificial means by which an individual can acquire active immunity.

Sometimes it is desirable to provide “ready-made” immune bodies, as in cases in which the patient has already been exposed to the antigen, is experiencing the symptoms of the disease, and needs reinforcements to help mitigate its harmful effects. Examples of conditions for which an individual may be given such passive immunity include tetanus, diphtheria, and a venomous snake bite. The patient is given immune serum, which contains gamma globulin, antibodies (including antitoxin) produced by the animal from which the serum was taken.

It is not always necessary that the patient actually suffer from the disease and exhibit its symptoms before passive immunity is provided. In some instances in which exposure to an infectious agent is suspected, immune bodies may be given to ward off a full-blown attack or at least to lessen its severity.

Another way in which immunity can be passively acquired is across the placental barrier from fetus to mother. The maternal antibody thus acquired serves as protection for the newborn until he can actively establish immunity on his own. Although humoral immunity can be acquired in this way, cellular immunity cannot.
Cell-mediated immunity. From Applegate, 2000.
acquired immunity specific immunity attributable to the presence of antibody and to a heightened reactivity of antibody-forming cells, specifically immune lymphoid cells (responsible for cell-mediated immunity), and of phagocytic cells, following prior exposure to an infectious agent or its antigens, or passive transfer of antibody or immune lymphoid cells (adoptive immunity).
adoptive immunity passive immunity of the cell-mediated type conferred by the administration of sensitized lymphocytes from an immune donor.
artificial immunity acquired (active or passive) immunity produced by deliberate exposure to an antigen, such as a vaccine.

ac·quired im·mu·ni·ty

resistance resulting from previous exposure of an individual in question to an infectious agent or antigen; it may be active and specific, as a result of naturally acquired (apparent or inapparent) infection or intentional vaccination (artificial active immunity); or it may be passive, being acquired through transfer of antibodies from another person or from an animal, either naturally, as from mother to fetus, or by intentional inoculation (artificial passive immunity).

acquired immunity

n.
Immunity obtained either from the development of antibodies in response to exposure to an antigen, as from vaccination or an attack of an infectious disease, or from the transmission of antibodies, as from mother to fetus through the placenta or the injection of antiserum.

acquired immunity

any form of immunity that is not innate and is obtained during life. It may be naturally or artificially acquired and actively or passively induced. Naturally acquired immunity is obtained by the development of antibodies resulting from an attack of infectious disease or by the transmission of antibodies from the mother through the placenta to the fetus or to the infant through colostrum and breast milk. Artificially acquired immunity is obtained by vaccination or by the injection of immune gamma globulin. Acquired immunity can be divided into cell-mediated immunity (T cells) and humoral immunity (B cells). Compare natural immunity. See also active immunity, passive immunity.

acquired immunity

(1) Any immune response to exogenous antigens.  
(2) Any compromise in immune function unrelated to inherited defects in the immune system.
(3) Immunity in which non-self antigens trigger an anti-self immune reaction after a period of sensitisation. Foreign antigens are then “attacked” by sensitised T cells, which are responsible for the so-called cellular immunity; plasma cells, B cells and other specialised immune cells act in concert with T cells to produce antibodies, the humoral immune response, which attach to the antigen, directing T-cell activity; antibodies also stimulate the release of nonspecific chemical mediators (e.g., complement, IFN, ILs), which enhance antigen destruction.

acquired immunity

Immunology
1. Adaptive immunity Any immune response to exogenous antigens or immunogens.
2. Secondary immunity Any compromise in immune function unrelated to inherited defects in the immune system. See AIDS.
3. Immunity in which non-self antigens trigger an antiself immune reaction after a sensitization period.

ac·quired im·mu·ni·ty

(ă-kwīrd' i-myū'ni-tē)
Resistance resulting from previous exposure of the individual in question to an infectious agent or antigen; it may be active, as a result of naturally acquired infection or vaccination; or passive, being acquired from transfer of antibodies from another person or from an animal, either from mother to fetus or by inoculation.

acquired

non-congenital

syndrome

aggregated objective signs, subjective symptoms and specific pathologies that typify specific conditions
  • acquired immunodeficiency syndrome; AIDS severe reduction in numbers of T4 lymphocyte helper (CD4) cells (due to infection with human immunodeficiency virus [HIV]) and resultant compromise of humoral and cell-mediated immunity; patients show lymphadenopathy, opportunistic infections (e.g. tinea and verrucae) and unusual infections (e.g. histoplasmosis, gastrointestinal tract candidiasis, Pneumocystis carnii pneumonia [PCP]), unusual malignancies (e.g. Kaposi's sarcoma), wasting diseases and presenile dementia

  • acute compartment syndrome; ACS increased lower-limb intracompartmental pressure on exercise (exercise expands muscles, increases intracompartmental pressures, inducing pain); treated initially by rest, immobilization, non-steroidal anti-inflammatory drugs; severe cases may require surgical decompression (fasciotomy)

  • anterior tarsal syndrome; ATS deep peroneal nerve entrapment at anterior ankle/dorsal talonavicular joint, due to restriction of ankle dorsiflexion (e.g. tight boots; ski boots), or local soft-tissue trauma (e.g. dorsal tarsal exostoses); characterized by extensor hallucis longus weakness, dorsal foot paraesthesia and numbness of first intermetatarsal space (symptoms can be induced by deep peroneal nerve percussion as crosses the anterior aspect of the ankle joint, or by ankle joint plantarflexion whilst simultaneously dorsiflexing toes)

  • anterior tibial compartment syndrome ischaemic necrosis of anterior compartment muscle fibres, due to local arterial compression by engorged muscles, after unaccustomed exertion

  • anterior tibiotalar impingement syndrome anterior ankle pain at ankle dorsiflexion (e.g. at midstance, just before heel lift) due to inferior tibial/neck of talus exostosis

  • Apert's syndrome type Ia acrocephalosyndactyly, characterized by features of Carpenter's syndrome, with lesser digital (2-5) fusion into one mass, usually with a common mega-nail

  • Apert-Crouzon syndrome type IIa acrocephalosyndactyly characterized by features of Carpenter's syndrome with additional craniofacial dysostosis, maxillary hypoplasia, and 2-4 digit fusion

  • Bazex syndrome; acrokeratosis paraneoplastica keratoderma (i.e. erythema, scaling and irritation) of skin of ears, nose, hands and feet and later generalized hyperkeratosis in men with underlying internal malignancy; condition regresses when underlying malignancy is resolved

  • Behçet's syndrome chronic vasculitic disease of unknown cause; characterized by seronegative arthritis of knees and ankles, elbows and wrists, mouth ulcers, erythema nodosum, visual impairment and cerebrovascular accident

  • benign familial joint hypermobility syndrome; BFJHS generalized joint hypermobility, diagnosed as 2 major/1 major + 2 minor/4 minor criteria (see Table 1) in the absence of Ehlers-Danlos syndrome, Marfan's syndrome and osteogenesis imperfecta

  • Brocq-Lyell syndrome; toxic epidermal necrolysis severe, acute, systemic drug reaction characterized by hyperpigmented skin lesions and epidermal detachment

  • Brown-Séquard syndrome hemiparaplegia and hyperaesthesia, with ipsilateral loss of stereognosis and contralateral hemianaesthesia; due to unilateral spinal cord lesion

  • carpal tunnel syndrome pain, paraesthesia and loss of power of palmar muscles; associated with rheumatoid arthritis

  • Carpenter's syndrome; acrocephalopolysyndactyly oxycephaly, bradysyndactyly and polydactyly of the feet, with learning difficulties

  • Charcot's syndrome see intermittent claudication

  • chronic compartment syndrome; CCS; chronic exertional compartment syndrome exercise-induced fascial compartment pain; caused by compromised circulation and relative ischaemia of intracompartmental tissues, with long-term muscle and nerve dysfunction and damage; recalcitrant cases require surgical decompression through fasciotomy (see syndrome, acute compartment)

  • compartment syndrome see syndrome, acute compartment; syndrome, chronic compartment

  • complex regional pain syndrome; CRPS; chronic regional pain syndrome neuroinflammatory dysfunction, due to ion interaction of nociceptive C-fibre nerve endings, the sympathetic nervous system and spinal cord efferent motor nerves; characterized by vasomotor instability, hyperalgesia and impaired motor function; diagnosed from clinical presentation, symptoms reduction on administration of sympathetic nerve blockade, and intense, focal periarticular uptake of contrast medium in a delayed imaging-phase bone scan; treated by early, aggressive physical therapy to prevent contracture and muscle wasting, symptomatic relief by sympathetic nerve blockade, non-steroidal anti-inflammatory drugs, tricyclic antidepressants and anticonvulsant medication; immobilization is contraindicated

  • complex regional pain syndrome type 1; CRPS 1; reflex sympathetic dystrophy; Sudek's atrophy; allodynia sympathetic nervous system-mediated acute pain and vasomotor instability, triggered by minor or surgical trauma without obvious nerve injury; affects women more than men; pain is excessive and out of proportion to severity of initiating injury; diagnosis is based on clinical symptoms aided by bone scan, laser Doppler studies and thermography; patients may show anxiety, depression and disturbed sleep; condition is difficult to manage; patients suspected of CRPS 1 should have early referral to a pain clinic (see Table 2); presents in three stages:

    • stage 1 acute phase, lasting 2-3 months, with regional severe burning pain, warmth and swelling triggered by stress/light touch, bone demineralization, skin trophic changes

    • stage 2 dystrophic phase/Sudek's atrophy; lasting for several months; characterized by constant unrelenting pain, exacerbated by any stimulus, and tissue cyanosis, coolness and induration, and diffuse osteoporosis

    • stage 3 atrophic phase, characterized by reduced/absent/intractable pain, irreversible atrophy of skin/subcutaneous tissues, flexion contractures of foot, advanced osteoporosis with a 'ground-glass' appearance on X-ray of affected bone

  • complex regional pain syndrome, type 2; CRPS 2; causalgia; sympathetic pain syndrome persistent and severe skin paraesthesia/burning sensations; caused by trauma to peripheral sensory nerve fibres; symptoms, progress and treatment are similar to that of CRPS 1

  • Conn's syndrome primary aldosteronism; characterized by headaches, thirst, nocturia, polyuria, hypovolaemia, fatigue, hypertension, alkalosis, and potassium depletion

  • constrictive band syndrome intrauterine development of deep, tight, circumferential folds around leg/foot, and compromised limb development distal to band (e.g. autoamputation; marked oedema of distal tissues); thought to relate to strands of amniotic membrane enwrapping the developing limb

  • Cushing's syndrome raised blood cortisol (e.g. due to pituitary tumour; long-term steroid therapy); characterized by central obesity, moon-like facies, acne, skin striae, hypertension, decreased carbohydrate tolerance and tendency to diabetes, female amenorrhoea and hirsutism

  • Down's syndrome chromosomal disorder (trisomy 21) characterized by congenital short stature, broad short hands/feet, characteristic facies (pronounced epicanthic skin folds, flat hypoplastic face, short nose, enlarged tongue), transverse palmar crease, very dry skin, learning difficulties; formerly termed mongolism

    Edwards' syndrome trisomy 18, with congenital characteristic facies (micrognathia, low-set ears), rocker-bottom feet, severe learning difficulties; affected children often die in early childhood

  • Ehlers-Danlos syndrome; Ehlers-Danlos diseases I-X hereditary connective tissue disorder characterized by collagen abnormality, marked generalized skin and blood vessel laxity, and joint hypermobility; skin is readily traumatized and heals slowly; see syndrome, hypermobility

  • Franconi's syndrome a form of anaemia associated with renal tubule dysfunction; adult Franconi's syndrome shows synostosis with osteomalacia, and acquired Franconi's syndrome is associated with multiple myeloma

  • Giles de la Tourette syndrome motor incoordination characterized by verbal, facial or limbic tics

  • Gorlin's syndrome multiple naevus-like basal cell carcinomata, causing small pits and depressions of palmar and plantar skin

  • Guillain-Barré syndrome; acute inflammatory polyneuropathy; acute idiopathic polyneuritis; infectious polyneuritis; postinfective polyneuropathy sudden-onset, acute, postviral polyneuritis; presents as distal pain, muscular weakness/flaccidity, paraesthesia; spreads proximally over 14-21 days; severe cases show spinal nerve involvement, with respiratory failure and limb paralysis (patient will require life support and anticoagulation to prevent deep-vein thrombosis); spontaneous recovery occurs over several weeks/months; some residual neuromotor effects may persist

  • Haglund's syndrome prominence of posterior superior lateral area of calcaneum, retrocalcaneal bursitis, Achilles tendon thickening and Achilles tendinitis; diagnostic rearfoot radiographic features include positive parallel pitch lines, loss of retrocalcaneal recess (indicating retrocalcaneal bursitis), Achilles tendon thickening, loss of distinct interface between Achilles tendon and pre-Achilles fat pad

  • heel pain syndrome see heel pain

  • heel spur syndrome see heel spur

  • Howel-Evans syndrome familial palmoplantar keratoderma, with increased risk of oesophageal cancer

  • Hurler's syndrome; lipochondrodystrophy; dysostosis multiplex autosomal-recessive inherited generalized lipid disturbance and mucopolysaccharoidosis, affecting cartilage, bone, skin, subcutaneous tissues, brain, liver and spleen; characterized by short stature, shortness of neck, trunk and digits, kyphosis, reduced joint mobility, learning difficulties, characteristic facies (so-called gargoylism) and visual impairment

  • hypermobility syndrome; joint hypermobility syndrome disordered collagen (types 1 and 3) structure, with associated decreased tensile strength of skin/structural tissues; characterized by generalized joint hypermobility, easy bruising, impaired healing, increasing incidence of joint/soft-tissue pain, joint dislocation and osteoarthritis; a presenting feature of benign familial joint hypermobility syndrome (BFJHS) (see Table 3), Ehlers-Danlos syndrome, Marfan syndrome and osteogenesis imperfecta

  • iliotibial band syndrome; ITBS; iliotibial band friction syndrome; ITBFS overuse-associated, friction-induced inflammation of ITB and associated bursa, where ITB moves over lateral femoral condyle (Gerdy's tubercle); due to repeated knee flexion and extension, especially in athletes/cyclists; presents as ITB pain at heel strike progressing to constant ITB pain; early-stage treatment includes a daily stretching programme (see Table 4) and application of heat (pre-exercise) and ice (postexercise) (see Table 5)

  • joint hypermobility syndrome see syndrome, hypermobility

  • lobster-claw syndrome extreme form of ectrodactyly; characterized by absence of third and fourth rays

  • Korsakoff's syndrome confusion and severe memory impairment with confabulation and Wernicke's syndrome, associated with chronic alcoholism

  • Lyell's syndrome drug-induced, acute skin sensitivity reaction; characterized by acute erythema, urticaria, vasculitis, purpura, marked exfoliation (peeling), flaccid bullae formation, subepidermal separation/detachment

  • Marfan's syndrome familial, autosomal-dominant, congenital changes in mesodermal and ectodermal tissues; characterized variably by musculoskeletal changes (e.g. increased height, excessive limb length, arachnodactyly; generalized tissue laxity and joint hypermobility), visual effects, and cardiovascular effects (e.g. aortic aneurysm)

  • medial tibial stress syndrome; MTSS; tibial fasciitis; shin splint muscle fatigue, reduced shock absorption, traction enthesiopathy and periostitis along anterior and posterior medial lower one-third of tibia (see Table 6) secondary to overuse/underpreparation for exercise; exacerbated by exercising on hard surfaces, especially in individuals who pronate excessively; treated by muscle-strengthening exercises, pre-exercise flexibility programme, modification of overall sports exercise programme (see Table 7), in conjunction with gait analysis, orthoses and correct shoe selection

  • Morquio's syndrome; type IV mucopolysaccharoidosis severe skeletal dysplasia including spine/thorax deformity, irregular epiphyses but normal shaft length of long bones, enlarged joints, flaccid ligaments, waddling gait and urinary abnormalities, due to autosomal-recessive error of mucopolysaccharide metabolism

  • Morton's syndrome congenital shortening of first metatarsal with apparent shortening of hallux and associated metatarsalgia

  • Munchausen's syndrome repeated fabrication of illness/symptoms of illness

  • Munchausen's syndrome by proxy repeated reporting of spurious illness/symptoms of illness by one person about another

  • musculoskeletal pain syndrome see polymyalgia rheumatica

  • nail-patella syndrome; hereditary arthrodysplasia autosomal-dominant abnormality of finger/toenails, absent/hypoplastic patella, defects of head of radius and iliac horns, and iris discoloration

  • nephrotic syndrome peripheral oedema, albuminuria, reduced plasma albumin (hypoalbuminaemia), refractory bodies in urine and raised blood cholesterol

  • nerve entrapment syndromes local nerve trunk compression (e.g. tibial, medial calcaneal lateral, first lateral branch of calcaneal, lateral plantar, high tibial, popliteal, deep peroneal, superficial, saphenous, sural or medial common hallucal nerves), as in tarsal/carpal tunnel syndromes, plantar digital neuritis, Morton's neuroma; characterized by distressing distal dermatomal sensory (e.g. pain and paraesthesia) and/or motor symptoms (e.g. muscle atrophy) (see Table 8)

  • Nievergelt-Pearlman syndrome rare autosomal-dominant bone disease causing lower-limb 'rhomboidal' tibia/fibula (crura rhomboidei), joint dysplasias, genu valgum, club foot, deformed toes; more common in males

  • overlap syndromes see mixed connective tissue diseases

  • patellofemoral joint syndrome see syndrome, runner's-knee

  • peroneal cuboid syndrome loss of rearfoot eversion due to long-standing peroneal tendon dysfunction/tendinitis; characterized by plantar pain from cuboid to first metatarsal

  • polycystic ovary syndrome see syndrome, Stein-Leventhal

  • Raynaud's syndrome concomitant Raynaud's disease (always affecting hands, and frequently feet) in patients with connective tissue disorders, characterized by generalized digital cyanosis, localized painful vasculitic lesions of dorsal forefoot (30% of cases) and apices of toes (20-25% of cases); subcutaneous calcinosis (20% of cases) may masquerade as a seed corn

  • Reiter's syndrome urethritis, iridocyclitis, arthritis, plantar enthesiopathy and heel spur formation, often triggered by earlier gastrointestinal Escherichia coli infection or exposure to a sexually transmitted disease (e.g. Chlamydia trachomatis); more common in human leukocyte antigen (HLA) B27 tissue-type males; see keratoderma blenorrhagicum

  • restless-leg syndrome overwhelming need to move the lower limbs constantly; characteristic of chronic renal failure; thought to be triggered by accumulation of metabolites and uraemia

  • Reye's syndrome cerebral oedema and death (in 50% of cases, usually children), provoked by aspirin therapy; aspirin is proscribed for children less than 16 years old

  • Riley-Day syndrome; familial dysautonomia autosomal-dominant complete indifference to pain; also characterized by orthostatic hypotension, hyperhidrosis and hyporeflexic/absent deep tendon reflexes, pes cavus and trophic plantar ulceration

  • Roussy-Levy syndrome; hereditary areflexic dystasia; Charcot-Marie-Tooth (CMT) disease type II essential tremor, sensory ataxia, poor coordination and judgement of movement, kyphoscoliosis and distal muscle atrophy (especially peronei); autosomal-dominant inherited disease similar to CMT disease type 1, but developing in early childhood

  • runner's-knee syndrome mild lateral subluxation of patella in patellar groove; due to an increase in Q angle (i.e. >15°), often in association with excessive foot pronation, tibial varum, internal tibial torsion, weakened quadriceps group, malposition of vastus medialis, hard running surfaces or faulty sports shoes, leading to uneven pressure on anterolateral surface of femoral condyle and local pain; often affects female runners; treated by prescription orthoses to reduce torque, torsion and knee joint stress

  • scalded-skin syndrome scaled/peeling appearance of skin overlying areas of infection, or associated with adverse drug reactions

  • 'second-class travel' syndrome pulmonary thromboembolism due to prolonged periods of inactivity, e.g. passengers (who have been static for > 4 hours during long-haul intercontinental air flights) develop deep-vein thrombosis; the clot detaches, passing through venous circulation and heart, to block the pulmonary artery; characterized by sudden collapse and death; passengers on long-haul flights are advised to undertake leg muscle exercises regularly throughout the duration of the flight, wear 'antithrombotic' elasticated hosiery and consider medication with aspirin in the weeks before long-haul flight

  • sinus tarsi syndrome sensation of unsteadiness when walking on gravel/uneven ground and ongoing pain in lateral tarsal area just distal to and level with lateral malleolus, subsequent to inversion sprain/excess rearfoot pronation (e.g. as in rearfoot rheumatoid arthritis); local symptoms are exacerbated by heel inversion/eversion; treated by non-steroidal anti-inflammatory drugs, local immobilization, orthoses or steroid injection

  • SjÖgren's syndrome; sicca syndrome; keratoconjunctivitis sicca oral mucous membranes dryness, loss of lacrimal secretion, facial telangiectasias (i.e. butterfly rash), bilateral parathyroiditis (in younger women), strongly associated with rheumatoid arthritis and Raynaud's phenomenon

  • Stein-Leventhal syndrome; polycystic ovary syndrome multiple ovarian cyst formation, with associated menstrual abnormalities, infertility, enlarged ovaries, insulin resistance, obesity, acne, evidence of masculinization (e.g. hirsuitism) and increased tendency to type 2 diabetes mellitus; responds to treatment with oral contraceptive pill and/or metformin

  • Stevens-Johnson syndrome widespread bullous erythema multiforme of skin/mucous membranes; due to hypersensitivity/drug reaction

  • talar compression syndrome posterior ankle pain when foot is maximally plantarflexed at ankle joint; due to compression of posterior tubercle of talus on posterior margin of distal end of tibia; note: similar condition occurs with os trigonum, which impinges on posteroinferior margin of tibia (see Table 9)

  • tarsal tunnel syndrome; TTS pain, paraesthesia and numbness in sole of foot; due to tibial nerve compression within tarsal tunnel; associated with excess foot pronation or rearfoot rheumatoid arthritis; symptoms reproduced by tapping the skin overlying distal medial malleolar area (Tinel's sign positive); conservative treatment includes valgus filler pads, cobra pads and medial heel wedges, or control of excessive rearfoot pronation with moulded cushioned orthoses worn with bespoke shoes, together with non-steroidal anti-inflammatory drugs and/or disease-modifying antirheumatic drugs; surgical treatment includes decompression procedures to free posterior tibial nerve and excise local fibrous structures (see tarsal tunnel)

  • distal tarsal tunnel syndrome isolated entrapment of medial/lateral plantar nerves; medial plantar nerve is compressed between navicular tuberosity and belly of abductor hallucis longus, causing 'jogger's foot'; first branch of lateral plantar nerve (Baxter's nerve) may be entrapped as it courses laterally between bellies of abductor hallucis and quadratus plantae (flexor accessories) muscles (see Table 10)

  • proximal tarsal tunnel syndrome entrapment of posterior tibial nerve/its branches deep to flexor retinaculum; due to excessive subtalar joint pronation (with narrowing of tarsal tunnel, e.g. in rheumatoid foot) due to entrapment within attachments of flexor retinaculum, compression by an enlarged abductor hallucis muscle belly, enlarged navicular tuberosity, accessory navicular, presence of os tibialis externum, ischaemic compromise of posterior tibial nerve, or varicosities within tarsal tunnel

  • trisomy 21 syndrome see syndrome, Down's

  • Turner's syndrome sex-chromosome (XO) abnormality affecting 1:2500 females, with characteristic morphology (web neck, short stature), infantilism and amenorrhoea, coarctation of aorta and peripheral oedema; feet are oedematous, short and broad, show excess subtalar joint pronation and hyperextended halluces; nails tend to involution, and affected subjects are prone to ingrowing nails

  • Werner's syndrome autosomal-recessive condition characterized by scleroderma-like skin, cataracts, progeria (premature senility), hypogonadism and diabetes mellitus

  • Wernicke's syndrome; Wernicke-Korsakoff syndrome; Wernicke's encephalopathy brainstem ischaemia causing nystagmus and other ocular effects, tremors and ataxia, mental confusion, hypothermia and hypotension; more common in chronic alcoholics

  • Wolff-Parkinson-White syndrome congenital atrioventricular interconnection causing tachycardia and characteristic electrocardiogram pattern

  • yellow-nail syndrome see nail, yellow

Table 1: The major and minor diagnostic criteria of benign familial joint hypermobility syndrome (BFJHS)
Major criteria
Current/historic Brighton score of 4/9
Arthralgia for >3/12 in four or more joints
Minor criteria
Current/historic Brighton score of 1, 2 or 3/9 (0, 1, 2, 3/9 if >50 years old)
Arthralgia for minimum of 3 months in 1-3 joints, or back pain for minimum of 3 months, or spondylosis/spondylolysis/spondylolisthesis
Dislocation/subluxation of > one joint, or one episode of simultaneous dislocation/subluxation of more than one joint
Three or more lesions of soft-tissue rheumatism (e.g. spondylitis, tenosynovitis, bursitis)
Marfanoid habitus (i.e. tall, slim physique, span:height ratio >1.3, upper:lower segment ratio <0.89, arachnodactyly [+Steinberg/wrist signs])
Abnormal skin: striae, hyperextensibility, thin skin, papyraceous scarring
Eye signs: drooping eyelids, myopia, antimongoloid slant
Varicose veins or hernia or uterine/rectal prolapse

Note: BFJHS is diagnosed in the presence of two major criteria, or one major and two minor criteria, or four minor criteria (adapted from Grahame R, Bird HA, Child A, Dolan AL, Fowler-Edwards A, Ferrell W, Gurley-Green S, Keer R, Mansi E, Murray K, Smith E. The British Society Special Interest Group on Heritable Disorders of Connective Tissue Criteria for the Benign Joint Hypermobility Syndrome. "The Revised (Brighton 1998) Criteria for the Diagnosis of the BJHS". Journal of Rheumatology 2000; 27:1777-1779).

Table 2: Features of complex regional pain syndrome
PhaseFeatures
Acute phase (duration: 2-3 months)
Reversible
Severe burning pain, warmth, swelling and joint stiffness within a limb: not confined to a dermatome or myotome
Bone demineralization
Symptoms (exacerbated by limb dependence, contact or stress) persist for 2-3 months
Chronic phase (duration: several months)
Reversible
Pain continues
The limb becomes cool, firm and cyanotic
Radiographs show diffuse osteoporosis
Digits develop flexure contractures
Persists for several months
Atrophic phase
Irreversible
Pain diminishes or becomes intractable
Skin and subcutaneous tissues become atrophic
Flexion contractures in foot become fixed
Osteoporosis becomes advanced; bone has a 'ground-glass' appearance
Table 3: The major and minor diagnostic criteria of benign familial joint hypermobility syndrome (BFJHS)
Major criteria
Current/historic Brighton score of 4/9
Arthralgia for >3/12 in four or more joints
Minor criteria
Current/historic Brighton score of 1, 2 or 3/9 (0, 1, 2, 3/9 if >50 years old)
Arthralgia for minimum of 3 months in 1-3 joints, or back pain for minimum of 3 months, or spondylosis/spondylolysis/spondylolisthesis
Dislocation/subluxation of > one joint, or one episode of simultaneous dislocation/subluxation of more than one joint
Three or more lesions of soft-tissue rheumatism (e.g. spondylitis, tenosynovitis, bursitis)
Marfanoid habitus (i.e. tall, slim physique, span:height ratio >1.3, upper:lower segment ratio <0.89, arachnodactyly [+Steinberg/wrist signs])
Abnormal skin: striae, hyperextensibility, thin skin, papyraceous scarring
Eye signs: drooping eyelids, myopia, antimongoloid slant
Varicose veins or hernia or uterine/rectal prolapse

Note: BFJHS is diagnosed in the presence of two major criteria, or one major and two minor criteria, or four minor criteria (adapted from Grahame R, Bird HA, Child A, Dolan AL, Fowler-Edwards A, Ferrell W, Gurley-Green S, Keer R, Mansi E, Murray K, Smith E. The British Society Special Interest Group on Heritable Disorders of Connective Tissue Criteria for the Benign Joint Hypermobility Syndrome. "The Revised (Brighton 1998) Criteria for the Diagnosis of the BJHS". Journal of Rheumatology 2000; 27:1777-1779).

Table 4: Iliotibial band-stretching regime
Muscle groupAction (hold for 5-10 seconds; repeat ×5, three times a day)
Hip abductorStand erect, legs straight, feet together; stretch trunk (on frontal plane) towards the unaffected leg
Iliotibial bandLie on a bench on the unaffected side, with the unaffected hip and knee slightly flexed, in order to maintain balance; flex the affected hip and straighten the affected knee so that the affected leg hangs off the bench; allow the iliotibial band of the affected leg to be stretched by gravitational pull
Lie on a bench on the affected side with the affected leg in line with the body and the hip and knee locked; flex the unaffected (upper) leg; place the hands on the bench immediately under the shoulder and push the trunk upwards as far as possible to apply stretch to the lateral area of the affected leg
Upper iliotibial bandStand erect; with affected leg behind normal leg; stretch trunk (on frontal plane) towards unaffected side
Lower iliotibial bandStand erect as above, with the knee of the affected leg slightly flexed and hips rotated (on transverse plane) towards affected leg; stretch trunk (on frontal plane) towards the unaffected side
Iliotibial band and hamstringsStand erect, with the affected leg behind the normal leg so that the knee of the affected leg rests on the posterior aspect of the non-affected knee; rotate the trunk (on transverse plane) away from the affected leg and attempt to touch the heel of the affected leg
Table 5: Treatment regime for iliotibial band syndrome
VisitAction
1Examination
Including Nobel's and Ober's tests, and excluding other causes of knee joint pain
Gait analysis - walking and running
Check for presence of tibial varum, tibial torsion, uncompensated rearfoot varus and limb length discrepancy (include shoe wear pattern)
Instigate the iliotibial band stretching regime (see Table 11), with a quadriceps- and adductor-strengthening programme
Ice massage to painful area at lateral aspect of knee Advise reduction in athletic activity
2Commence physical therapies, e.g. cortisone iontorphoresis or ultrasound and ice massageStabilizing orthoses and/or foot and ankle taping, ± heel lift
Continue stretching programme ± massage
Non-steroidal anti-inflammatory (10-day course of 400 mg ibuprofen qds)
Stop all athletic activity if pain does not resolve
3Magnetic resonance imaging/computed tomographic scan to knee joint areaRefer to orthopaedics

Most cases will resolve with one treatment; more severe cases will require a second visit and some will require orthopaedic referral.

Table 6: Iliotibial band-stretching regime
Muscle groupAction (hold for 5-10 seconds; repeat ×5, three times a day)
Hip abductorStand erect, legs straight, feet together; stretch trunk (on frontal plane) towards the unaffected leg
Iliotibial bandLie on a bench on the unaffected side, with the unaffected hip and knee slightly flexed, in order to maintain balance; flex the affected hip and straighten the affected knee so that the affected leg hangs off the bench; allow the iliotibial band of the affected leg to be stretched by gravitational pull
Lie on a bench on the affected side with the affected leg in line with the body and the hip and knee locked; flex the unaffected (upper) leg; place the hands on the bench immediately under the shoulder and push the trunk upwards as far as possible to apply stretch to the lateral area of the affected leg
Upper iliotibial bandStand erect; with affected leg behind normal leg; stretch trunk (on frontal plane) towards unaffected side
Lower iliotibial bandStand erect as above, with the knee of the affected leg slightly flexed and hips rotated (on transverse plane) towards affected leg; stretch trunk (on frontal plane) towards the unaffected side
Iliotibial band and hamstringsStand erect, with the affected leg behind the normal leg so that the knee of the affected leg rests on the posterior aspect of the non-affected knee; rotate the trunk (on transverse plane) away from the affected leg and attempt to touch the heel of the affected leg
Table 7: Grades and characteristics of medial tibial stress syndrome (MTSS)
GradeCharacteristic
1Pain on palpation of the anteromedial (or posteromedial) area of tibial crest
No pain during activity or exercise
2Pain after activity or exercise
No pain during activity or exercise
3Pain during activity or exercise
Pain after activity or exercise
4Pain and discomfort during normal walking
Continual pain during activity or exercise
Table 8: Phased treatment approach to medial tibial stress syndrome (MTSS)
PresentationTreatment
Phase 1: acute phaseCessation of exercise activity until all pain resolves RICE(P)
Phase 2: rehabilitation phaseDeep compartment muscle exercise to strengthen the deep fascial-bone interface and reduce tension on the deep fascial insertion, in order to decrease pain and swelling and prevent fascial scarring
Phase 3: functional phaseUse of antipronatory/functional orthoses, strapping or taping in order to strengthen the fascial-bone interphase and prevent further excessive tension on the tibia
Phase 4: return to activityPhased and gradual return to normal levels of activity
Table 9: Presentations of nerve trunk irritation in the foot
Neuroma/lesionInvolved nerveLocation
Proximal tarsal tunnel syndromeBranches of the posterior tibial nerveMedial ankle area
Distal tarsal tunnel syndrome Jogger's footMedial plantar nerveBetween navicular tuberosity and belly of abductor hallucis
Distal tarsal tunnel syndrome Baxter's neuritisLateral plantar nerveBetween bellies of abductor hallucis, quadratus plantae and abductor digiti quinti minimi
Joplin's neuromaMedial plantar nerve properMedial area of first metatarsal head
Houser's neuromaFirst plantar intermetatarsal nerveBetween 1 and 2 metatarsals
Heuter's neuromaSecond plantar intermetatarsal nerveBetween 2 and 3 metatarsals
Morton's neuromaThird plantar intermetatarsal nerveBetween 3 and 4 metatarsals
Islen's neuromaFourth plantar intermetatarsal nerveBetween 4 and 5 metatarsals
Table 10: Accessory bones in the foot
Accessory bone in the footLocation
Os tibiale externum (accessory navicular)Within tibialis posterior tendon, adjacent to proximal part of navicular tuberosity
Os trigonumPosterior margin of talus
Os peroneumWithin peroneus longus tendon, adjacent to inferior lateral border of cuboid/calcaneocuboid joint
Os vesalianumAdjacent to fifth metatarsal base
Os intermetatarseumBetween bases of first and second metatarsals
Os interphalangeusWithin insertion of flexor hallucis longus tendon, adjacent to plantar area of hallux interphalangeal joint
Table 11: Presentations of nerve trunk irritation in the foot
Neuroma/lesionInvolved nerveLocation
Proximal tarsal tunnel syndromeBranches of the posterior tibial nerveMedial ankle area
Distal tarsal tunnel syndrome Jogger's footMedial plantar nerveBetween navicular tuberosity and belly of abductor hallucis
Distal tarsal tunnel syndrome Baxter's neuritisLateral plantar nerveBetween bellies of abductor hallucis, quadratus plantae and abductor digiti quinti minimi
Joplin's neuromaMedial plantar nerve properMedial area of first metatarsal head
Houser's neuromaFirst plantar intermetatarsal nerveBetween 1 and 2 metatarsals
Heuter's neuromaSecond plantar intermetatarsal nerveBetween 2 and 3 metatarsals
Morton's neuromaThird plantar intermetatarsal nerveBetween 3 and 4 metatarsals
Islen's neuromaFourth plantar intermetatarsal nerveBetween 4 and 5 metatarsals

acquired immunity,

n noninnate immunity obtained during a person's lifetime either by developing anti-bodies in response to an infection (naturally acquired immunity) or by vaccination (artificially acquired immunity).

ac·quired im·mu·ni·ty

(ă-kwīrd' i-myū'ni-tē)
Resistance due to previous exposure of the individual in question to an infectious agent or antigen; may be active, due to naturally acquired infection or vaccination; or passive, acquired from transfer of antibodies from another person or animal, either from mother to fetus or by inoculation.

immunity

1. the condition of being immune; security against a particular disease; nonsusceptibility to the invasive or pathogenic effects of microorganisms or helminth parasites or to the toxic effect of antigenic substances. Called also functional or protective immunity.
2. responsiveness to antigen that leads to more rapid binding or elimination of antigen than in the nonimmune state; it includes both humoral and cell-mediated immunity (below).
3. the capacity to distinguish foreign material from self, and to neutralize, eliminate or metabolize that which is foreign (non-self) by the physiological mechanisms of the immune response.
The mechanisms of immunity are essentially concerned with the body's ability to recognize and dispose of substances which it interprets as foreign and sometimes harmful to its well-being. When such a substance enters the body, complex chemical and mechanical activities are set into motion to defend and protect the body's cells and tissues. The foreign substance, usually a protein, is called an antigen, that is, one which generates the production of an antagonist. The most readily recognized response to the antigen is the production of antibody. The antigen-antibody reaction is an essential component of the overall immune response. Of equal or greater importance to antibody, particularly for some antigens, is the development of so-called cell-mediated immune response, which involves clonal expansion of specifically reactive T lymphocytes including cytotoxic T lymphocytes (Tc lymphocytes) which play a major role in eliminating the foreign antigens that are cell associated.
Immunological responses in animals can be divided into two broad categories: humoral immunity, which refers to the production of antibody which becomes part of the body fluids (humors), especially serum, and cell-mediated or cellular immunity, which involves a variety of activities designed to destroy or at least contain cells that are recognized by the body as expressing foreign antigens on their cell surface, e.g. viral antigens. Both types of response are mediated by lymphocytes that originate in the bone marrow as stem cells and later are converted into mature cells having specific properties and functions.

acquired immunity
antigen specific immunity attributable to the production of antibody and of specific immune T lymphocytes (responsible for cell-mediated immunity), following exposure to an antigen, or passive transfer of antibody or immune lymphoid cells (adoptive immunity).
active immunity
that which follows exposure to an antigen; acquired immunity attributable to the presence of antibody or of immune lymphoid cells formed in response to antigenic stimulus. Called also adaptive immunity.
adoptive immunity
passive immunity of the cell-mediated type conferred by the administration of sensitized lymphocytes from an immune donor to a naive recipient.
artificial immunity
includes acquired (active) immunity produced by deliberate exposure to an antigen, such as a vaccine or the administration of antibody (passive).
cellular immunity
dependent upon T lymphocytes which are sensitized by first exposure to a specific antigen. Subsequent exposure stimulates the release of a group of substances known as lymphokines, such as interferon, and interleukins as well as direct killing by cytotoxic T lymphocytes.
functional immunity
see immunity (above).
humoral immunity
mediated by antibodies formed by antigen-specific B lymphocytes. Each B lymphocyte has monomeric IgM receptors which capture specific antigen, initiating production of the specific immunoglobulins. B lymphocytes activated by the presence of their specific antigen undergo transformation, lymphocyte blastogenesis, whereby they become metabolically active, divide, and some mature to plasma cells, which are major producers of antibodies. Some cells revert to small lymphocytes, 'memory' cells, and the expanded clone of these cells, on re-exposure to the antigen, undergo further lymphocyte blastogenesis, leading to further increased antibody production and numbers of memory cells.
There are two types of humoral immune response: primary and secondary. The primary response begins immediately after the inital contact with an antigen; the resulting antibody, predominantly IgM, appears 48 to 72 hours later. The secondary response occurs within 24 to 48 hours and produces large quantities of predominantly IgG. The secondary response persists much longer than the primary response and is the result of repeated contact with the antigens.
innate immunity, native immunity, natural immunity
natural immunity resulting from the genetic makeup of the host, before exposure to an antigen.
maternal immunity
that acquired by the neonate by transplacental transfer of immunoglobulins or from ingestion of colostrum or via the yolk sac in the case of birds. The placentation of all agricultural animals precludes trans-placental transfer of immunoglobulin. Passive transfer of maternal immunity is effected by the transfer of immunoglobulilns present in high concentration in the first milk, colostrum, through the intestine of the newborn. The success of this transfer is dependent upon the time after birth that colostrum is ingested (physiologically 24-36 hours, but effectively for adequate transfer, 8 hours after birth) and on the mass of immunoglobulin ingested which is determined by the concentration of immunoglobulin in colostrum and the amount of colostrum ingested.
Failure of passive transfer results in a significant increase in risk for neonatal disease. Neonates that fail to acquire serum concentrations of IgG1 greater than 10 mg/ml are at significantly higher risk of septicemic, enteric and respiratory disease. Failure of passive transfer occurs as a result of neonates sucking the dam or acquiring colostrum by artificial feeding too late in the absorptive process, or by receiving too little colostrum or receiving colostrum with low immunoglobulin concentration. See also passive immunity (below) and colostral immunoglobulin.
natural immunity
see innate immunity (above).
passive immunity
the transfer of antibodies from a donor in which they were produced to a recipient for temporary immunity. Can be in the form of serum or colostrum or yolk. Significant transplacental transfer of antibodies is found in primates, but does not occur in domestic animals. Passive immunity in domestic mammals comes via the colostrum, with its high concentration of antibodies, and the more than normally pervious epithelium of the neonate's intestinal epithelium. In birds maternal antibody is transferred to the yolk, from where the developing chick embryo absorbs it from about day 11 of incubation. See also passive immunization.
protective immunity
see immunity (above).
References in periodicals archive ?
In their article--"Impact of Acquired Immunity and Dose-Dependent Probability of Illness on Quantitative Microbial Risk Assessment," published in Risk Analysis, the journal of the Society for Risk Analysis--Havelaar and Swart looked at four illustrative scenarios of exposure: (1) low frequency, low dose exposure (recreational water); (2) low frequency, high dose exposure (consumption of raw chicken liver); (3) high frequency, low dose exposure (direct contact with sheep and goats, i.
The protective effect of the trait is highest during the first 12 months, after the loss of passively acquired immunity and before specific protection mechanisms are developed.
By comparing the projected incidence using the Lyme disease transmission model to actual incidence of Lyme disease, we could assess the overall importance of factors missing from the basic model, such as the effects of inflammatory reactions against tick salivary proteins and acquired immunity to the spirochetal pathogen.
Though the team had warned British authority in 1940 that a yellow fever epidemic threatened in areas in which the population had no acquired immunity, no program of vaccinations was initiated, In the resulting (preventable) epidemic in the Nuba mountains, 40,000 Sudanese came down sick with the disease, with a mortality rate of nearly l0%.
Most of the 44 per cent who tested positive had contracted swine flu, although some had acquired immunity from a previous bout of flu, or had been vaccinated.
His research interests include neurotropic parasitic nematodes and acquired immunity to these infections.
It works by stimulating local innate and acquired immunity, producing 80%-100% clearance of AK lesions in 2-12 months in various studies and case reports.
105) our demonstration of a black resistance to yellow fever that could not be explained by acquired immunity.
The preclinical data suggested that talabostat can suppress tumor growth in the absence of acquired immunity and can act synergistically with docetaxel to decrease tumor growth and increase survival.
A strategy for monitoring the interaction between bacterial communities and viruses is to sequence specific bacterial DNA elements that confer acquired immunity against viral attack, called clustered regularly interspaced short palindromic repeats (CRISPRs).
The need for such vaccines is on the rise because sanitation in some developing countries is improving, and that means the naturally acquired immunity now prevalent in those countries will diminish, according to a press report from the National Institute of Allergy and Infectious Diseases.
To support his contention, in his response he makes an analogy with acquired immunity to malaria.

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