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Lyme disease is the most common vector-borne disease in the United States. A cluster of children in Lyme, Connecticut, who had unexplained arthritis was reported by one of their parents in the mid-1970s. Investigation of this "epidemic" of arthritis led to the description of "Lyme" arthritis in 1976 and ultimately to the discovery of its bacterial etiology. Both the reported incidence of the disease and its geographic range have increased dramatically in recent years. Perhaps even more striking has been the increase in publicity about the illness in the consumer media, which has been accompanied at times by near-hysteria about both its risks and its complications. This publicity,combined with a very high frequency of misdiagnoses in people whose symptoms are due to other causes, has resulted in a degree of anxiety about Lyme disease (among both patients and physicians) out of proportion to the morbidity it causes.Lyme disease is caused by the spirochete Borrelia burgdorferi, a fastidious, microaerophilic bacterium that replicates very slowly and requires special media to grow in the laboratory. B burgdorferi is transmitted by ticks of the Ixodid species—in the United States, primarily Ixodes scapularis (previously called Ixodes dammini), the deer tick. Lyme disease occurs most commonly in areas where deer ticks are abundant and where the prevalence of B burgdorferi in these ticks is high (20% to 50%)—southern New England, southeastern New York, New Jersey, eastern Pennsylvania, eastern Maryland, Delaware, and parts of Minnesota and Wisconsin. Lyme disease is rare in the Pacific states because although Ixodes pacificus (the Western black-legged tick)can transmit B burgdorferi, very few (<2%) of these ticks are infected with the organism. People who have increased occupational,recreational, or residential exposure to tick-infested woodlands and fields(the preferred habitat of ticks) in endemic areas are at increased risk of developing Lyme disease.The life cycle of Ixodid ticks consists of three stages—larva, nymph, and adult—that occur during a 2-year period(Fig. 1). Each stage feeds only once. The adult female lays eggs in the spring, and the larvae emerge in the early summer. They overwinter and emerge the following spring as nymphs. In the fall, the nymphs molt and become adults. The adults spend the winter on an animal host, a favorite being the white-tailed deer (hence the name, the deer tick). In the spring, the females lay their eggs and die, completing the 2-year life cycle.Most larvae (98%) are not infected with B burgdorferi because transovarial transmission rarely occurs. The larvae feed on a wide variety of small mammals (such as Peromyscus leucopus, the white-footed mouse) that are important natural reservoirs for B burgdorferi and thereby may become infected. A tick can acquire infection with B burgdorferi at each stage in its life cycle, so the proportion of adult ticks that is infected is higher than that of either nymphs or larvae. However, most cases of Lyme disease occur after the bites of nymphal-stage ticks because they are more abundant than adult ticks, they are more difficult to detect due to their small size, and humans frequently enter tick-infested habitats at times of the year when they are prevalent.A number of factors are associated with the risk of transmission of B burgdorferi from ticks to humans. First, a tick has to be infected to transmit the organism. The proportion of infected ticks varies greatly both by geographic area and stage of tick in its life cycle. I pacificusoften feeds on lizards, which are not a competent reservoir for B burgdorferi. Consequently, only 1% to 3% of these ticks, even in the nymphal and adult stages, are infected with B burgdorferi. By contrast, I scapularis feeds on small mammals that are competent reservoirs for B burgdorferi. As a result,in endemic areas, rates of infection of I scapularis are approximately 2% for larvae, 15% to 30% for nymphs, and 30% to 50% for adults. Infection rates as high as 60% to 90% have been reported in selected areas.Lyme disease occurs throughout the world. In Europe, most cases are seen in the Scandinavian countries and in central Europe (especially Germany, Austria,and Switzerland), although cases have been reported throughout the continent. The incidence of Lyme disease varies tremendously from region to region and even within local areas. Information about the true incidence of the disease is complicated by reliance, in most instances, on passive reporting of cases as well as by the high frequency of misdiagnosis. Further, studies have indicated that as many as 50% of patients who develop serologic evidence of recent infection with B burgdorferi may be asymptomatic.In 1995, 11,603 cases of Lyme disease were reported to the United States Centers for Disease Control and Prevention (CDC) by 43 states and the District of Columbia, which was the second highest number reported since surveillance began in 1982 (although it was an 11% decrease from the 13,043 cases reported in 1994)(Fig. 2). More than 75% of the reported cases occurred in just 63 counties(Fig. 3). In Connecticut, which has the highest incidence of Lyme disease in the United States, the reported annual incidence of Lyme disease in 1995 was 47.1/100,000 persons and varied from 7.5/100,000 persons in Hartford County to 129.7/100,000 persons in Wyndham County. In certain towns in which the disease is hyperendemic (eg, Lyme), the annual incidence may be as high as 1,000/100,000 persons or more. The incidence of Lyme disease is highest among children. The reported incidence among children 5 to 10 years of age in Connecticut in 1995 was 79/100,000 per year. Because not all cases of Lyme disease are reported, these figures undoubtedly are underestimates.B burgdorferi is transmitted when an infected tick inoculates the organism into the blood vessels of the skin of its host. The risk of transmission from infected deer ticks is related to the duration of feeding. It takes hours for the mouth parts of ticks to implant fully in the host and much longer (days) for the tick to become fully engorged. Experiments with animals have shown that nymphal-stage ticks must feed for 36 to 48 hours or longer and adult ticks must feed for 48 to 72 hours or longer before the risk of transmission of B burgdorferi from infected ticks becomes substantial. The duration of time that a tick has fed can be estimated from indices of engorgement derived from experiments with animals. Based on these indices, there is evidence that approximately 75% of persons who recognize that they have been bitten by a deer tick remove the tick fewer than 48 hours after it has begun to feed. Indeed, the majority of persons who develop Lyme disease do not recall a tick bite. Unrecognized tick bites probably are associated with greater risk because unrecognized ticks may feed longer. A history of a tick bite is an indication that the person is at risk and should not be assumed to be the only exposure.Like other spirochetes, B burgdorferi is a cylindrically shaped organism, and its cell membrane is covered by flagella and a loosely associated outer membrane. The three major outer-surface proteins,OspA, OspB, and OspC (which are highly charged basic proteins of molecular weights of about 31, 34, and 23 kd, respectively), as well as the 41-kd flagellar protein, are important targets of the immune response of humans. Differences in the frequency of certain clinical manifestations of Lyme disease in Europe and in the United States (eg, the greater frequency of neuritis in European patients) have been attributed to differences in the molecular structure of different strains of B burgdorferi.After B burgdorferi is inoculated by the tick into the skin, it begins to spread locally. The inflammation results in a single erythema migrans rash in approximately two thirds of patients who become symptomatic. Days to weeks later, the spirochete may disseminate via either the bloodstream or the lymphatics to many other sites, including the skin(almost 25% of patients develop multiple erythema migrans), eye, muscle,bone, synovial tissue, central nervous system, and heart. Although it may be possible to isolate the organism from cultures of tissue, the small numbers that are present and the fastidious nature of its in vitro growth makes recovery of the spirochete difficult. Nevertheless, B burgdorferi has been isolated from the blood or from tissue at all stages of the illness.The pathogenesis of the symptoms late in the course of Lyme disease appears to be related to long-term persistence of organisms in tissues. It is likely that relatively few organisms actually invade the host, but mediators of inflammation amplify the inflammatory response and lead to much of the tissue damage. The spirochete prefers cell surfaces, but it will adhere to a wide variety of cell types, which may explain why it can cause clinical manifestations in such a broad array of organ systems. Because the organism may persist in tissues for prolonged periods of time, symptoms may appear very late in the course of infection. The symptoms of Lyme disease are due to inflammation, mediated by interleukin-1 and other lymphokines, that is a direct result of the presence of the organism. However, in a small subset of patients who have refractory symptoms despite antimicrobial treatment (such as recurrent Lyme arthritis), the symptoms may have an immunogenetic basis. There is substantial evidence that patients who have a high prevalence of the HLA-DR2, DR3, and DR4 allotypes may be genetically predisposed to develop chronic recurrent Lyme arthritis long after the bacteria have been killed.The clinical manifestations of Lyme disease generally are divided into two stages: early and late. Early Lyme disease often is subdivided further into early localized and early disseminated disease. The usual clinical manifestations of the different stages of Lyme disease are shown in Table 1. The skin is the initial target organ for infection by B burgdorferi. The first clinical manifestation is the typical annular rash, erythema migrans. It usually occurs 7 to 14 days after the tick bite, although its onset has been reported as few as 3 days and as many as 4 weeks later. The rash may be uniformly erythematous(Fig. 4)or it may appear as a target lesion with variable degrees of central clearing(Fig. 5). Occasionally there may be vesicular or necrotic areas in the center of the rash. The rash may be itchy, painful, or asymptomatic and may be accompanied by systemic symptoms, such as fever, myalgia, headache, or malaise. If the patient is not treated, the rash gradually expands (hence,the name "migrans"), sometimes to more than 1 ft in diameter. It will persist for at least 1 to 2 weeks and usually for longer. Approximately two thirds of children who have Lyme disease will have single erythema migrans.A substantial proportion of children (nearly 25%) in the United States who are acutely infected with B burgdorferidevelop multiple erythema migrans lesions, a manifestation of early disseminated disease that occurs approximately 3 to 10 weeks after initial infection. The secondary skin lesions, which may develop several days or even weeks after the first lesion, are smaller than the primary lesion. Fever and myalgia usually accompany the rash. Patients also may complain of headache, neck pain, or malaise, and conjunctivitis and regional lymphadenopathy may develop. Occasionally, when the erythema migrans rash resolves, new evanescent lesions, which usually are small (1 to 3 cm)erythematous annular lesions, appear and disappear over several weeks. These lesions may appear at different sites but generally do not expand.At this stage of the illness, aseptic meningitis may occur, although it is rare (about 1% of all patients). DNA of B burgdorferi has been found in the cerebrospinal fluid of patients at this stage of the illness. Focal neurologic manifestations, specifically cranioneuropathies, also may occur. Seventh-nerve palsy (facial palsy) is relatively common, affecting about 3% of children, and may be the presenting as well as the only manifestation of Lyme disease. The palsy usually lasts from 2 to 8 weeks before complete resolution (with or without treatment). Rarely, the palsy may resolve only partially or not at all. Bannworth syndrome (meningopolyneuritis)has been reported more commonly as a manifestation of Lyme disease in Europe. Encephalitis, with or without focal neurologic signs, occasionally occurs.Arthritis is the classic manifestation of late Lyme disease, occurring in about 7% of affected children. Patients who have arthralgia, a common, nonspecific symptom that frequently is present among patients who have early Lyme disease as well as those who do not have Lyme disease,should be differentiated from those who have objective evidence of synovitis(eg, an effusion), which is the hallmark of late Lyme disease. The arthritis occurs weeks to months after the initial infection. Primarily the large joints, especially the knee (which is affected in more than 90% of the cases), are involved. Although the affected joint is swollen and tender, the patient usually does not experience the exquisite pain that is typical of acute bacterial arthritis. Joint swelling generally resolves within 1 to 2 weeks (although it may last for several weeks) before recurring, often in other joints. Although the large joints are involved most commonly, any joint, including small ones, may be affected. If untreated, the episodes of arthritis often increase in duration, sometimes lasting for months. However,the disease usually resolves eventually, even in patients who are untreated and who have had many recurrences of arthritis. Most patients will not have a history of erythema migrans because those who have the rash usually are treated with antimicrobials and do not develop late manifestations of disease.Late central nervous system manifestations of Lyme disease(sometimes termed tertiary neuroborreliosis) rarely have been reported in children. In adults, chronic demyelinating encephalitis, polyneuritis, and impairment of memory have been attributed to Lyme disease, although there is controversy about the frequency with which such late manifestations occur,especially among patients who have been treated. Other very rare manifestations of late Lyme disease include acrodermatitis chronica atrophicans (a chronic, atrophic sclerotic lesion of the skin) and borrelia lymphocytoma, a localized, subcutaneous nodular lesion that usually occurs in either the earlobe or the breast.In the largest prospective study of children who had Lyme disease(a community-based study of 201 children in Connecticut), the initial manifestations of disease were: single erythema migrans (66%),multiple erythema migrans (23%), arthritis (7%), facial palsy (3%), aseptic meningitis (1%), and carditis(0.5%). Erythema migrans was more likely to occur on either the head or neck in younger children and on the extremities in older children,a finding similar to that recently reported from Europe. Only about one third of the children who had a single erythema migrans rash had positive serology for B burgdorferi at the time of presentation compared with almost 90% of the children who had multiple erythema migrans.More than 25% of the children had early disseminated Lyme disease at the time that they presented to a physician, and 89% had either single or multiple erythema migrans.Because clinical syndromes caused by congenital infection have been recognized with other spirochetal infections such as syphilis, the possible transmission of B burgdorferi from an infected pregnant woman to her unborn fetus has been of concern. Although case reports have been published in which B burgdorferi has been identified from several abortuses and from a few live-born children who had congenital anomalies, the placentas, abortuses, and tissues from affected children did not show histologic evidence of inflammation. In addition, no consistent pattern of congenital malformations (as would be expected in a"syndrome" due to congenital infection) has been identified. In two small longitudinal studies conducted by the CDC of pregnant women who developed Lyme disease, the adverse outcomes could not be attributed to infection with B burgdorferi. Furthermore, sero-surveys conducted in endemic areas found no difference in the prevalence of congenital malformations among the offspring of women who had serum antibodies against B burgdorferi and those who had no such antibodies.To assess the prevalence of clinically significant neurologic disorders attributable to congenital infection with B burgdorferi, two investigators conducted a survey of all pediatric neurologists in areas of the United States in which Lyme disease is endemic (Connecticut, Rhode Island, Massachusetts, New York, New Jersey, Wisconsin, and Minnesota). Of the 162 respondents to the survey (92%), none had seen a child who had a clinically significant neurologic disorder attributable to congenital Lyme disease or whose mother had Lyme disease during her pregnancy.There is no definitive evidence that B burgdorferi causes congenital disease, although the existence of such a syndrome also has not been excluded. If it does exist, congenital Lyme disease must be extremely rare. Finally, it should be noted that transmission of Lyme disease through breastfeeding never has been documented.The diagnosis of Lyme disease, especially in the absence of the characteristic rash, may be difficult because the other clinical manifestations of disease are not specific. Seventh-nerve palsy due to Lyme disease is indistinguishable from idiopathic Bell palsy, and Lyme arthritis may mimic either septic arthritis or pauciarticular juvenile rheumatoid arthritis. The clinical manifestations of Lyme meningitis may be difficult to distinguish from those of viral meningitis. Even the diagnosis of erythema migrans can be difficult because the rash initially may be confused with nummular eczema, granuloma annulare, an insect bite,ringworm, or cellulitis. However, the relatively rapid expansion of erythema migrans helps to distinguish it from these other conditions.Routine laboratory tests rarely are helpful in diagnosing Lyme disease because the associated abnormalities are nonspecific. The peripheral white blood cell count may be either normal or elevated. The erythrocyte sedimentation rate usually is elevated. The white blood cell concentration in joint fluid in patients who have Lyme arthritis may range from 25,000 to 125,000/mL, often with a preponderance of polymorphonuclear cells. When the central nervous system is involved, there usually is a with a of the of for B burgdorferi is and patients must an such as a or a to tissue or fluid for such tests are indicated only in rare including the that are on of of B burgdorferi have not been shown to be to be clinically studies in that is very Consequently, laboratory of Lyme disease usually on the of antibodies to B burgdorferi in the is well that the and of tests for Lyme disease The of is much than that of tests by that and the in the A study of the was conducted by the of and in with the In this and the CDC the (as by to of antibodies against B burgdorferi in of (with and to which the were The of the results in the laboratory with different as well as the of the results from different the were The of the of the from to and from to The investigators that with these for Lyme disease will result in a high rate of This is consistent with other reports of the of most tests for Lyme disease.The of Western the of serologic for Lyme disease. from the on of Lyme Disease in that a when tests for Lyme a either an or an and that result is positive or a Western to the If the or the is an is not The a of the concentration of antibodies against B burgdorferi. The about the of the that antibodies against of the spirochete are Most the presence of antibodies against at least either three or proteins of B least one of which is a more molecular outer for the to be tests are not for the diagnosis of early localized Lyme disease because only a of patients who have single erythema migrans will have a positive of tests very on the prevalence of the infection among patients who are because many including have the that nonspecific symptoms (eg, or may be manifestations of Lyme disease, parents of children who have only nonspecific symptoms frequently for Lyme disease tests for Lyme disease on such patients). Lyme disease will be the cause of the nonspecific symptoms in very of these children. However, because the of even tests for Lyme disease rarely 90% to of the tests in children who have no or symptoms of Lyme disease will be the majority of these will be Nevertheless, Lyme disease frequently is on these and such children often are treated with a patient has a positive serologic for antibodies to B burgdorferi, it is possible that Lyme disease may not be the cause of that In to the that the result is positive (a common the patient may have been infected with B burgdorferi and the symptoms may be to the infection. serum antibodies to B they may persist for many years despite treatment and clinical In addition, because a substantial proportion of people who become infected with B burgdorferi never develop symptoms, there will be a rate in endemic areas of When patients who had Lyme disease asymptomatic and untreated or clinically and develop any of symptoms and are for antibodies against B symptoms may be attributed to Lyme disease because of the positive should not tests for Lyme disease either for patients who have not been in endemic areas or for those who only nonspecific In the highly of certain proteins of B burgdorferi will become for in which will be more than for the treatment of children who have Lyme have been from studies of no clinical of treatment have been conducted among children. younger than years of age should not be treated with because it may cause of also is results with have been There is for new because the results of treatment with or have been so such as arthralgia, and myalgia may persist after a course of treatment for Lyme disease has been These nonspecific symptoms, which may accompany or more symptoms and of Lyme disease but almost never are the presenting resolve over several weeks. There is evidence that such symptoms are related to persistence of B burgdorferi, and there is no evidence that of antimicrobials their Because antibodies against B burgdorferi persist even after treatment of symptoms, there is no to tests of against B is a that Lyme disease is difficult to and that chronic recurrences are In the for treated children is The most common for treatment is the patient actually does not have Lyme In a of children who were treated for erythema all were well and none had developed symptoms of late disease at a of more than 3 years later. In a prospective study of 201 children who had Lyme disease had either early localized or early disseminated all were clinically at a of years later. The long-term for patients who are treated for late Lyme disease also is Although arthritis does especially among patients who have the or most children who are treated for Lyme arthritis are Indeed, long-term of children with Lyme disease before its cause was recognized of either were not treated with antimicrobials or were treated years after the onset of indicated that the arthritis multiple even in children who never were treated. of investigators tests on children to 4 years after they were treated and found no evidence of any long-term of the infection. Other investigators who are a community-based study of the long-term outcomes of persons who have Lyme disease have found no evidence of impairment of normal in children 4 to 10 years after endemic areas it is very common for children to be bitten by deer bites often However, the risk of Lyme disease is 1% to even in areas in which Lyme disease is of the it is highly Consequently, the of antimicrobial (the of which is for persons who have been bitten by a deer tick is not a tick is tests such as the is not although it may important The for infection of humans of either a positive or a result is The may be positive even only very few organisms are Furthermore, the no about either the of the or the duration of both of which may be of the risk of In addition, and results are more to Lyme disease is to (such as long when tick-infested areas and to for and remove ticks after time in such areas. may but they may be from the skin, and frequently or in large may significant especially in have to develop an against Lyme disease. against outer A against Lyme disease in animal proteins have been developed and are being in in humans. Because the spirochete in ticks and in stages of illness but not at the time of initial infection in is that the by the tick blood during before it inoculates the spirochete into humans. of B burgdorferi occurs in the tick. Even the is found to be it likely will be because the risk of disease is in most and outcomes among persons who the disease are rare. that other are being

IntroductionAntibiotic prophylaxis with a single dose of doxycycline after a tick bite is one of the tools for preventing Lyme disease, which is becoming increasingly prevalent in Quebec. The aim of this work was to revisit this practice in adults and children younger than 8 years of age.MethodsTo assess the safety and absolute risk reduction (ARR) of doxycycline for preventing Lyme disease in contraindicated populations, two systematic reviews were conducted with a re-analysis of the original efficacy data. A knowledge mobilization framework was used to consider the scientific, contextual, and experiential evidence, taking into account information on patients’ and clinicians’ experiences.ResultsA single dose of doxycycline prescribed within 72 hours of being bitten by a tick (Ixodes scapularis) could prevent cutaneous manifestation of Lyme disease (ARR -2.8%, 95% confidence interval: -11.7–6.1; p = 0.06), without serious side effects, provided that the bite occurred in a geographical region where at least 25 percent of nymph and 50 percent of adult ticks are infected with the disease. However, the level of evidence was low and its generalizability to other contexts was doubtful. The decision to prescribe antibiotic prophylaxis may be based more on the fear of Lyme disease, rather than on effectiveness data and the real risk of contracting Lyme disease.ConclusionsIt may be challenging for clinicians to discuss Lyme disease prophylaxis with patients and their families in contexts where people are fearful of the disease, and the risk of contracting it from a tick bite is uncertain. Decision aids that provide scientific evidence on the real risk of developing Lyme disease after a tick bite, particularly in Quebec, can promote informed decisions based on patient preferences and values by supporting discussion between clinicians and patients.

This paper studies the phase equilibria in the La/sub 2/O/sub 3/-Y/sub 2/O/sub 3/ system in a wide range of temperatures (1350-2450 degrees C) and concentrations (0-100 mole % Y/sub 2/O/sub 3/). The phase-field boundaries were determined by the method of annealing and quenching with the help of DTA, during the course of which the samples were heated in an inert atmosphere up to 2450 degrees C. The phase composition of the samples was investigated by x-rays and petrographic analysis. The phase diagram of the system was constructed, for which the existence of wide regions of solid solutions based on A-, B-, C-, H-, and X-forms of rare-earth-element oxides, the decrease in the phase-transformation temperature of La/sub 2/O/sub 3/ and Y/sub 2/O/sub 3/ upon introducing a second element, and the presence of a compound of the perovskite structure with a region of homogeneity, formed by a solid-state reaction at 1585 degrees C, are typical.

Erythema multiforme and persistent erythema as early cutaneous manifestations of Lyme disease

Lyme Borreliosis

This review is focused on the role of infectious agents in the development of some lymphoma entities. Associations involving bacterial infections mostly regard marginal zone B-cell lymphomas of mucosa-associated lymphoid tissue (MALT)-type. Some paradigmatic examples of these associations include the Helicobacter pylori-related gastric MALT lymphoma and the more recently reported links between Chlamydophila psittaci and ocular adnexal MALT lymphomas and Borrelia burgdorferi and cutaneous MALT lymphomas. The well-documented association between Epstein-Barr virus infection and related lymphoproliferative disorders are analysed as an example of lymphotropic virus with tumourigenic activity. Molecular, biological and clinical features as well as therapeutic implications of these associations are analysed and future perspectives in this field are discussed.

Journal of Paediatrics and Child HealthVolume 14, Issue 3 p. 139-140 Editorial CommentFree Access Nebulized Bronchodilator Therapy in Asthma L. I. Landau, L. I. LandauSearch for more papers by this author L. I. Landau, L. I. LandauSearch for more papers by this author First published: September 1978 https://doi.org/10.1111/jpc.1978.14.3.139Citations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume14, Issue3September 1978Pages 139-140 ReferencesRelatedInformation

Journal of Paediatrics and Child HealthVolume 9, Issue 4 p. 246-247 CONCEPTS OF AUTISM: A REVIEW LORNA WING, Corresponding Author LORNA WING from Institute of Psychiatry, London 1. Psychiatrist.Reprint Requests LORNA WING, Social Psychiatry Unit Institute of Psychiatry, De Crespigny Park, London, S.E.5, 8AF.Search for more papers by this author LORNA WING, Corresponding Author LORNA WING from Institute of Psychiatry, London 1. Psychiatrist.Reprint Requests LORNA WING, Social Psychiatry Unit Institute of Psychiatry, De Crespigny Park, London, S.E.5, 8AF.Search for more papers by this author First published: December 1973 https://doi.org/10.1111/j.1440-1754.1973.tb02227.xCitations: 2 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume9, Issue4December 1973Pages 246-247 RelatedInformation

Journal of Paediatrics and Child HealthVolume 35, Issue 1 p. 110-113 Book Reviews First published: 29 July 2003 https://doi.org/10.1046/j.1440-1754.1999.t01-1-00350.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume35, Issue1February 1999Pages 110-113 RelatedInformation

Journal of Paediatrics and Child HealthVolume 55, Issue 10 p. 1286-1286 Heads Up Virtual reality reduces pain from needles First published: 19 October 2019 https://doi.org/10.1111/jpc.14629 edited by Craig Mellis (craig.mellis@sydney.edu.au) Reviewer: Professor David Isaacs, david.isaacs@health.nsw.gov.au, Children's Hospital at Westmead, Sydney Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume55, Issue10October 2019Pages 1286-1286 RelatedInformation

Journal of Paediatrics and Child HealthVolume 24, Issue 3 p. 203-203 Free Access BREAST-FEEDING A. MACKENZIE, A. MACKENZIE Department of Gastroenterology Royal Children's Hospital Parkville, Vic. 3052Search for more papers by this author A. MACKENZIE, A. MACKENZIE Department of Gastroenterology Royal Children's Hospital Parkville, Vic. 3052Search for more papers by this author First published: June 1988 https://doi.org/10.1111/j.1440-1754.1988.tb00327.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume24, Issue3June 1988Pages 203-203 RelatedInformation

Journal of Paediatrics and Child HealthVolume 30, Issue 4 p. 374a-375 Free Access PAEDIATRICS IN THE ASIA-PACIFIC REGION M. GRACEY, M. GRACEY Principal Medical Advisor Aboriginal Health Policy and Programs Branch Health Department of Western Australia East Perth, WA 6004 AustraliaSearch for more papers by this authorH. B. WONG, H. B. WONG Principal Medical Advisor Aboriginal Health Policy and Programs Branch Health Department of Western Australia East Perth, WA 6004 AustraliaSearch for more papers by this author M. GRACEY, M. GRACEY Principal Medical Advisor Aboriginal Health Policy and Programs Branch Health Department of Western Australia East Perth, WA 6004 AustraliaSearch for more papers by this authorH. B. WONG, H. B. WONG Principal Medical Advisor Aboriginal Health Policy and Programs Branch Health Department of Western Australia East Perth, WA 6004 AustraliaSearch for more papers by this author First published: August 1994 https://doi.org/10.1111/j.1440-1754.1994.tb00675.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume30, Issue4August 1994Pages 374a-375 ReferencesRelatedInformation

Journal of Paediatrics and Child HealthVolume 59, Issue 4 p. 703-703 Case Images Thickened nails First published: 13 April 2023 https://doi.org/10.1111/jpc.1_16057Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. Volume59, Issue4April 2023Pages 703-703 RelatedInformation

Journal of Paediatrics and Child HealthVolume 36, Issue 2 p. 196-198 Free Access Letters to the Editor First published: 24 December 2001 https://doi.org/10.1046/j.1440-1754.2000.0473d.xCitations: 1AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat 15 October 1999 Dear Editor, PRENATAL CARE APPLICATIONS Two recent cases, one in New South Wales (NSW), Australia and the other in England, UK, have examined the care and protection issues for a child born to a mother who is HIV-1 positive In the NSW case, 1 the Department of Community Services made an application to the Supreme Court rather than to the Children’s Court, as it acknowledged that powers under the Children (Care and Protection) Act 1987 only existed once a child was born. The Supreme Court agreed that it held sufficient power to make orders to protect a child who was not yet born. In its application, the Department of Community Services argued that the chances of the child not contracting HIV-1 would be significantly enhanced if the child was born by Caesarian section, the child received AZT serum within the first 24 h of life, and the child was not breast-fed. In the circumstances, it was not necessary for the court to make an order on the way the mother gave birth. Subsequent to the birth, the court did grant a permanent injunction to prohibit the mother breast-feeding as the Judge found that ‘there is such a risk of irreparable injury that the grant of an injunction is justified’. The circumstances were similar in the later English case, 2 except that the child welfare authority did not become aware of the child until she was 4-months-old. The mother was HIV-1 positive, refused treatment, refused an elective Caesarean section and insisted on breast-feeding the child. An order was sought and granted under the English equivalent of section 23 (NSW) Children (Care and Protection) Act 1987, for the child to be tested for HIV-1. If the tests were positive then, because of the lateness of action, it would be necessary for the authority to seek court orders for medical treatment without parental consent and, possibly, care orders for the removal of the child from its mother. These applications would have serious implications for the future well-being of the child. The decisions are important in demonstrating the need to act promptly, and the range of powers which may be available to a court or a child welfare agency both outside and within existing care and protection legislation. R BEST Director, Legal Services D SMITH Team Leader, Child Law Legal Services Department of Community Services Ashfield, NSW Australia REFERENCES 1 Department of Community Services vs. A baby (unreported 9 July 1999 per Austin J, NSW Supreme Court), re: Baby A (unreported 26 July 1999 per Young J, NSW Supreme Court). Google Scholar 2 BrahamsD. Court order for HIV-1 test for baby. Lancet 1999; 367: 884. CrossrefWeb of Science®Google Scholar Citing Literature Volume36, Issue2April 2000Pages 196-198 ReferencesRelatedInformation

Journal of Paediatrics and Child HealthVolume 51, Issue 6 p. 649-649 Heads UpFree Access Millennium Development Goals First published: 02 June 2015 https://doi.org/10.1111/jpc.12922 edited by Craig Mellis (craig.mellis@sydney.edu.au) AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat The Millennium Development Goals were set by the United Nations in 2000, adopted by 189 countries, and set goals to be achieved by 2015, including the eradication of extreme poverty and improvements in child mortality, maternal health and primary education. A supplement of Archives of Diseases in Childhood describes progress.1 Deaths in <5-year-old children fell from 12.7 million in 1990 to 6.3 million in 2013, meaning 17 000 fewer children die every day. Enrolment in primary education in developing countries rose from 82% in 1999 to 90% in 2010, although this still leaves 57 million age-eligible children out of school. John Vince from Papua New Guinea (PNG) reports on Oceania.2 Although mortality rates remain higher in Aboriginal and Torres Strait Islanders than the rest of the population, their rates fell by almost 50% from 2002 to 2012. The proportion of gross national product allocated to health varied from 3% in PNG (equivalent to US$35–40) to 14% in Kiribati. Infectious diseases (pneumonia, meningitis, diarrhoeal diseases, malaria, tuberculosis) are the leading causes of child mortality in the low-income countries. Immunisation rates are suboptimal, and pneumococcal conjugate vaccines are only given in Australia and New Zealand. Malnutrition affects 11–18% of children in PNG, Solomon Islands and Vanuatu. Progress has been made in all countries of Oceania, often despite formidable obstacles. References 1Beattie RM et al. Arch. Dis. Child. 2015; 100 (Suppl. 1): s1. CrossrefPubMedWeb of Science®Google Scholar 2Vince JD. Arch. Dis. Child. 2015; 100 (Suppl. 1): s63– 65. CrossrefPubMedWeb of Science®Google Scholar Reviewer: David Isaacs, david.isaacs@health.nsw.gov.au Volume51, Issue6June 2015Pages 649-649 ReferencesRelatedInformation