Um alerta: celebridades científicas e médicas irão dominar a cena

Para quem considera que o jornalismo chegou ao fundo do poço com o livro publicado sobre o "caso Eloá"; e, para quem acha que se passou da conta no "caso Isabela Nardoni"; e, finalmente para aqueles que qualquer notícia sobre o caso "ex-qualquer coisa de Suzana Vieira" foi o limite do suportável, aguardem o pior.

Na área médica e científica, a situação caminha para a consagração de celebridades, sejam pessoas físicas ou jurídicas. Quem leu ministro afirmar que o centro de gravidade da ciência e tecnologia se moveu para hospitais privados sente o despautério. Quem viu presidente, ministros, governador e prefeito paparicando um centro de cardiologia de hospital privado sentiu a barra. Quem vê pesquisador mais interessado em aparecer em coluna social a publicar um artigo científico e, depois reclamar de bancas de julgamento sabe do que se trata. Quem lê blogue de cientista prometendo a cura dos males da humanidade também entende o problema sério com o qual nos deparamos.

Em breve, teremos o Datena criticando a escolha de projetos do Instituto Nacional de Ciência e Tecnologia, a Hebe Camargo indicando o seu candidato preferido para professor titular e, por aí caminharemos.

Ao invés, de estudar para um concurso acadêmico, o candidato será entrevistado no Jô Soares e, utilizará esse fato como ponto alto de seu currículo acadêmico.

Ao CAPES, sugiro que novos critérios sejam estabelecidos como menção em coluna social. A única dúvida: menção em Mônica Bérgamo (Folha) ou Sônia Racy (Estadão) devem ser consideradas ambas como Qualis A? Citação na Vejinha seria Qualis B, porque regional, mas em Veja, seria Qualis A, correto?

Ao CNPq e à FAPESP sugiro que pagamento de assessoria de imprensa (serviços de pessoa jurídica) seja permitido na solicitação de qualquer projeto, afinal não é justo que somente quem tem cônjuge rico possa ter seu esquema de promoção.

Porque o câncer não superará as doenças cardiovasculares no Brasil em 2020

A imprensa repercutiu essa apresentação o IARC afirmando que as mortes por câncer superarão as por doenças cardiovasculares em 2020. Não há um único estudo sobre o tema, trata-se de mera especulação , a não ser que na China e India, o hábito tabágico se espalha. Mas, o tabagismo também aumenta o número de mortes por doença cardiovascular.

No Brasil, esse quadro não acontecerá porque a prevalência:

1.de hipertensão é muito elevada quando comparada aos países europeus e EUA.

2. do tabagismo nunca foi elevada como na Europa, EUA e Ásia. 3. da obesidade e do diabetes está em elevação e, terá impacto na mortalidade cardiovascular como já se observa no EUA. O mais grave da afirmativa do IARC é desconhecer que o espectro das doenças cardiovasculares naõ se restringem à sindrome coronariana aguda e à doença cerebrovascular. Essas duas entidades clínicas são manifestações do fenômeno aterosclerótico-hipertensivo que evoluirá para acometer outros órgãos (rins, retina, córtex cerebral) e funções (renal, visual, cognitiva, auditiva).

Cancer set to overtake heart disease as top global killer December 11, 2008 Lisa Nainggolan and Nick Mulcahy Aarhus, Denmark - Cancer is set to overtake cardiovascular disease to become the leading cause of death worldwide by 2010, according to a new report [1] from the International Agency for Research on Cancer (IARC), a division of the World Health Organization (WHO). President of the American Heart Association (AHA), Dr Tim Gardner, told heartwire he applauds the new report and looks forward to working with cancer organizations to tackle risk factors that increase the likelihood of both cancer and cardiovascular disease. According to the IARC report—which is a call to action asking governments to help fund cancer-prevention and research initiatives and international tobacco-control policies—the burden of cancer doubled globally between 1975 and 2000 and is set to double again by 2020 and nearly triple by 2030. The report—which was discussed at an event in Atlanta this week called Conquering Cancer: A Global Effort—says that low- and middle-income countries will experience the impact of higher cancer incidence and death rates more sharply than industrialized countries. The factors they have identified as predictive of an increase in cancer deaths are the very same factors that are going to result in more cardiovascular deaths, too. This is also true of heart disease—just last week, as reported by heartwire, researchers predicted that 85% of cardiovascular deaths worldwide would occur in low- and middle-income countries by 2030. However, the authors of this article stressed that there still exists "a window of opportunity" to prevent the epidemic from reaching its full potential and magnitude. Among the reasons stated by the IARC for the growing cancer burden is the adoption in less well-developed countries of "Western" habits, such as tobacco use and high-calorie, high-fat, and trans-fat diets. "Obviously, this new cancer report is an important prediction," Gardner told heartwire. "The risk and demographic factors they have identified as predictive of an increase in cancer deaths are the very same factors that are going to result in more cardiovascular deaths, too, so we are on the same track." US deaths from cancer and heart disease currently declining The news on cancer in developing countries is in contrast with another recent report that shows cancer incidence and death rates for men and women in the US continuing to decline [2]. The number-one and number-three killers in the US currently are coronary heart disease and stroke, respectively, says the AHA [3]. And while the nation has already made progress in reducing death rates from these two conditions, Gardner says that without a concerted effort to reduce some key risk factors, such as obesity and physical inactivity, "the momentum of reducing heart disease and stroke deaths will be lost. We will see our children developing heart disease earlier. This could reverse the progress in cardiovascular death rates that we have seen over the past decade." We are not jealous about our position in terms of heart disease being the number-one killer. "We are not jealous about our position in terms of heart disease being the number-one killer; it's a distinction none of us want to have," he added. "The AHA has been working for decades to move out of that 'top spot' of being the number-one killer. But unless we can do better in reducing some of these risk factors in the US, it may be a long time before we can shed the title of number one."Smoking is the easiest target Cigarette smoking accounts for nearly 440 000 of the more than 2.4 million annual deaths in the US, and there are catastrophic predictions for the number of deaths that will occur due to smoking in developing countries. In India, for example, new research published earlier this year forecasts that by 2010 around one million deaths per year there will be attributable to smoking. "Tobacco use is an enormous health burden across the globe and makes a significant contribution to deaths from both cancer and cardiovascular disease," Gardner adds. "We applaud the findings of the IARC report. We're very concerned about smoking rates in the US and newly developed countries, and we are really working very hard on trying to deal with that—the one risk factor that can most easily be targeted." Sources Leading US cancer organizations unite against the growing global cancer burden [press release]. December 9, 2008. Available at: http://www.eurekalert.org/pub_releases/2008-12/acs-luc120908.php. Jemal A, Siegel R, Ward E, et al. Cancer statistics, 2008. CA Cancer J Clin 2008; 58:71-96. American Heart Association. American Heart Association comment on the International Agency for Research on Cancer, World Cancer Report [press release]. December 11, 2008. Available at: http://americanheart.mediaroom.com/index.php?s=43&item=625.

Prevenção do Câncer de Próstata: melhor do que InCa e SBU

Abaixo, um artigo do New England Journal of Medicine bem melhor do que as opiniões enviesadas da Sociedade Brasileira de Urologia e "a posição firme e decidida" do Instituto Nacional do Câncer. Aliás, um dos momentos mais infelizes do ano, foi o protagonizado por ambos, Sociedade e Instituto.

Screening for Prostate Cancer among Men 75 Years of Age or Older. Michael Barry.

Prostate-cancer screening with the prostate-specific antigen (PSA) test remains one of the most controversial issues in modern medicine. The U.S. Preventive Services Task Force (USPSTF), an independent group of experts supported by the Agency for Healthcare Research and Quality under a mandate from Congress, recently revised its recommendations regarding prostate-cancer screening. The USPSTF concluded that "the current evidence is insufficient to assess the balance of benefits and harms of prostate cancer screening in men younger than age 75 years," but it now "recommends against screening for prostate cancer in men age 75 years or older."1 In its 2002 statement, the task force did not recommend for or against screening in either age group. The implication of the new recommendation for medical practice is that clinicians should discuss the potential benefits and known harms of screening with men between 50 and 74 years of age, but not necessarily with older men. Why change the recommendation for men 75 or older, at least given the continuing dearth of evidence from randomized trials that addresses the tradeoff between the benefits and harms of prostate-cancer screening in men of any age? The task force believes that at least a moderate amount of evidence now makes it possible to conclude that the known harms of screening outweigh the possible benefits for this age group. This statement does not imply that prostate cancer is an unimportant problem among men 75 or older; in fact, as the statement acknowledges, 71% of deaths due to prostate cancer — almost 20,000 annually in the United States — occur after the age of 75. Moreover, it does not mean that no men 75 or older could possibly benefit from screening. After all, there are relatively healthy men in their late 70s and even early 80s harboring high-grade cancers that are likely to kill them; early detection and attempted curative treatment might prevent these men from dying from prostate cancer. So why not continue to offer screening after the age of 74? First, the effectiveness of attempted curative treatment for prostate cancer among men 75 or older appears to be low or negligible. In the only published randomized trial comparing the effect of radical prostatectomy with a strategy of "watchful waiting" for men with clinically localized prostate cancer, the benefit of radical prostatectomy was statistically significant but small, with an absolute difference of 5.4 percentage points in the rate of death due to prostate cancer at 12 years (which has not widened with continued follow-up). This difference means that about 18 radical prostatectomies would have to be performed to prevent a single death from prostate cancer over a 12-year period.2 However, in subgroup analyses at both 10 and 12 years of follow-up, even this level of effectiveness appeared to be confined to men 65 years of age or younger. Men 75 or older were not enrolled, presumably because they were considered less likely to benefit from surgery. It is important to note that less than 10% of subjects in this Scandinavian trial had their prostate cancer diagnosed through screening. The long average lag time between a detectable increase in the PSA level — 5 to 10 years — and the development of clinical cancer, as well as the possibility of overdiagnosis associated with PSA screening, suggests that an even smaller benefit may be seen in the U.S. Prostate Cancer Intervention versus Observation Trial (PIVOT), in which about three quarters of participants had their cancer diagnosed through PSA screening. Results from PIVOT are expected in 2010. As in the Scandinavian trial, men 75 or older were not enrolled. The effect of competing hazards would also attenuate the benefit of screening and attempted curative treatment for men 75 or older. Given the slow growth of most prostate cancers and the resultant long lead times between detectability and clinical disease, men may need to live much longer than 10 years to reap the benefits of PSA screening — and of course, preventing a death from prostate cancer does not bestow immortality. For example, out of 1000 75-year-old male nonsmokers, 19 would be expected to die of prostate cancer over the next 10 years, whereas 430 would be expected to die of other causes.3 Even if a few of the deaths from prostate cancer could be prevented within this time frame, the effect on overall mortality would be small. And fewer older men than younger men would still be alive beyond 10 years to reap any delayed benefits of screening; for example, life expectancy for men surviving to the age of 85 is about 6 years. Whereas the benefits of screening attenuate with age, the harms increase. PSA levels are strongly age-dependent, so at any given PSA threshold, older men will have substantially higher risks of both requiring a prostate biopsy and being diagnosed with prostate cancer. For example, about 6% of men in their 60s, 21% in their 70s, and 28% in their 80s would be expected to have a PSA level above 4.0 ng per liter,4 a common threshold for considering a prostate biopsy. Regular PSA screening roughly doubles the risk that men will have to face a diagnosis of prostate cancer over the next 10 years, but many of these cancers would never present clinically. Given that the risk of prostate cancer is also age-related, this effect will be greatest among older men. And finally, the risks of both postoperative death and complications of radical prostatectomy are age-related, escalating after the age of 75.5 Given the unfavorable trade-off between the possible benefits and known risks of prostate-cancer screening after the age of 74, I believe the USPSTF recommendation is sound. As with all guidelines, clinical judgment should be used in its application. For example, given the relationship between self-rated health and life expectancy, a clinician might consider having a discussion about PSA screening with (not simply testing) men in their late 70s who rate their own health as "excellent" but discontinue screening discussions at the age of 75 if self-rated health is "good," at the age of 70 if self-rated health is "fair," and at the age of 65 if self-rated health is "poor." These thresholds roughly correspond to a remaining life expectancy of 10 years, a threshold below which other guidelines — for example, those from the American Cancer Society — have recommended against screening. Any threshold, of course, is inevitably somewhat arbitrary. Considering the ongoing controversies surrounding prostate-cancer screening, evidence from randomized trials about benefit and harms would be welcome indeed. The large, ongoing trials of PSA screening in the United States (the Prostate, Lung, Colorectal, and Ovarian, or PLCO, Cancer Screening Trial), Europe (the European Randomized Study of Screening for Prostate Cancer, or ERSPC), and the United Kingdom (Prostate Testing for Cancer and Treatment, or Protect) will eventually help to resolve some of these controversies — the first two trials should produce results over the next 5 years. However, none of the findings from these trials will bear directly on the question of whether screening is appropriate for men 75 or older, since men in this age group were excluded from all three. Population-based studies of PSA testing in the United States have shown fairly high levels of screening among men in their late 70s and even in their 80s. The new recommendations from the USPSTF should prompt clinicians and patients to think twice, or even three times, before ordering PSA tests for cases in which screening is especially likely to do more harm than good.

Mais uma vez, as vitaminas não contam

Uma vez mais, a perspectiva de prevenção do câncer com uso de vitaminas não consegue ser provado em dois ensaios clínicos publicados em JAMA, hoje. Vitamins E and C in the Prevention of Prostate and Total Cancer in Men: ThePhysicians' Health Study II Randomized Controlled Trial JAMA http://jama.ama-assn.org/cgi/content/abstract/2008.862v1?etoc Effect of Selenium and Vitamin E on Risk of Prostate Cancer and Other Cancers: The Selenium and Vitamin E Cancer Prevention Trial (SELECT) http://jama.ama-assn.org/cgi/content/abstract/2008.864v1?etoc Editorials: Randomized Trials of Antioxidant Supplementation for Cancer Prevention:First Bias, Now Chance--Next, Cause http://jama.ama-assn.org/cgi/content/full/2008.863v1?etoc

Esperança em nova vacina para malária

A Hopeful Beginning for Malaria Vaccines. William E. Collins, Ph.D., and John W. Barnwell, M.P.H., Ph.D. An effective human malaria vaccine has been sought for over 70 years, with little success.1 A successful malaria vaccine used in conjunction with other control interventions would help reduce and eventually eliminate the considerable global disease burden caused by malaria. Many different antigens have been identified as potential targets for malaria-vaccine development. One of these, the repetitive sequence of four amino acids in the circumsporozoite antigen on the surface of the sporozoite of Plasmodium falciparum, arguably the most important of the human malarias, is the basis for the RTS,S vaccine.2 This vaccine was subjected to extensive studies involving human volunteers, the results of which indicated a potential protective efficacy of about 40% when the vaccine was used in combination with an effective adjuvant therapy.3,4 Subsequently, a number of field studies have indicated that in endemic areas, this vaccine could have a rate of efficacy of about 30% against clinical disease and about 40% against new cases of infection.5,6 This is the first candidate malaria vaccine to show significant protection in laboratory- and field-based clinical studies. The evaluation of the safety and efficacy of malaria vaccines in infants and children is of utmost importance because most deaths and illness from malaria occur in these age groups, in areas of moderate-to-high transmission. In this issue of the Journal, Abdulla et al.7 describe their safety and immunogenicity trial in which the RTS,S vaccine was used in combination with the AS02D adjuvant (ClinicalTrials.gov number, NCT00289185 [ClinicalTrials.gov] ). The RTS,S/AS02D vaccine had a reasonable safety profile as compared with the control hepatitis B vaccine, and anticircumsporozoite-antibody titers were detectable in more than 98% of the infants receiving the RTS,S/AS02D vaccine. In this trial, RTS,S was given along with other vaccines for children (a vaccine containing diphtheria and tetanus toxoids, whole-cell pertussis vaccine, and conjugated Haemophilus influenzae type b vaccine), according to the Expanded Program on Immunization (EPI) schedule. There was no interference with immune responses to the EPI vaccines. This result suggests that it will be feasible to provide RTS,S together with other routine children's vaccines, making its delivery in endemic areas much easier and less costly. During the 6-month period after immunization, the incidences of malarial infection and clinical disease in the RTS,S group were reduced by 65% and 59%, respectively. There was a correlation between a reduced risk of infection and increased circumsporozoite antibody titers. There was no association, however, between a reduction in the incidence of clinically active malaria and an increased circumsporozoite-antibody titer. Also in this issue, Bejon et al.8 report on a phase 2b safety and efficacy trial of the RTS,S vaccine combined with the AS01E adjuvant, in children 5 to 17 months of age (NCT00380393 [ClinicalTrials.gov] ). The RTS,S/AS01E vaccine was associated with fewer severe adverse events than the control rabies vaccine. Overall, there was an unadjusted rate of efficacy of 60% against all episodes of P. falciparum clinical malaria, with anticircumsporozoite-antibody titers detectable in more than 99% of the recipients of the RTS,S/AS01E vaccine. However, as in the trial by Abdulla et al., there was no evidence that protection against clinical disease was correlated with anticircumsporozoite titers in children vaccinated with RTS,S/AS01E. The AS01E adjuvant used by Bejon et al. was developed to enhance the immune response to the circumsporozoite target antigen and, it was hoped, provide greater efficacy than the AS02D adjuvant used by Abdulla et al. and in earlier clinical studies of RTS,S. A comparison of the two articles reveals that the mean circumsporozoite antibody titers among the children receiving the RTS,S/AS01E vaccine were approximately 10 times that among those receiving the RTS,S/AS02D vaccine. However, although the overall mean antibody titers were lower with the AS02D adjuvant, both in the trial by Abdulla et al. and in a previous trial involving infants in Mozambique,9 the protection against infection and clinical disease was similar to that in the trial of AS01E by Bejon et al. In the studies by Abdulla and Bejon and their colleagues, the efficacy against clinical disease did not differ whether AS01E or AS02D was used as an adjuvant, but the efficacy with either is greater than the 30% rate reported in a previous trial.6 Whether the higher antibody titers associated with the use of AS01E might translate into a longer duration of protective efficacy for the RTS,S vaccine remains to be demonstrated. The correlation of reduced incidence of infection with higher antibody levels is encouraging and intuitive, given the biologic basis of infection. Correlations between antibody levels and protection against disease are more difficult to reconcile in the context of the biologic features of malaria and the target of this vaccine. In humans, there are two main developmental stages of the malaria life cycle: the exoerythrocytic stage in the liver, involving the sporozoite and hypnozoite, and the erythrocytic stage in the blood, involving the merozoite. Immunity acquired against one form of the malaria parasite does not operate against other forms. Sporozoites — the target of RTS,S — are injected into humans through mosquito bites, infect hepatocytes, and initiate the development of other liver-stage parasites. One sporozoite produces thousands of merozoites that parasitize erythrocytes to initiate the blood stage of infection, which in turn produces the clinical disease of malaria. Thus, if immune responses generated by "leaky" pre-erythrocytic vaccines such as RTS,S fail to block just a single sporozoite from invading or developing in the hepatocyte, then a blood-stage infection will follow, and typical paroxysmal fevers and, perhaps, severe malarial disease will manifest. Although the results of Abdulla et al. and Bejon et al. are promising, the baseline incidence of malaria was low in each study area. Evaluations of vaccine-efficacy studies can be complicated by the introduction of insecticide-treated bed nets and artemisinin-based combination drug treatments through ongoing control programs across sub-Saharan Africa.10 Recent reports indicate that, in some areas in which malaria is endemic, such as in the Gambia in West Africa and Kenya and Tanzania in East Africa, there have been dramatic reductions in the malarial disease burden.11,12 However, as the RTS,S vaccine heads into phase 3 trials in 2009, large areas across Africa still have moderate-to-intense malaria transmission. Malaria transmission of yet higher intensity, with greater and more continuous assault by mosquito-injected sporozoites, could affect the efficacy of this vaccine.6 This is the first malaria vaccine to reach this stage of development, and it will be essential to learn how it performs in areas of more intense transmission. Only then will we have a clear idea of what effect it will have on the well-being of children in Africa and elsewhere and its role in malaria control. It is, indeed, a hopeful beginning. No potential conflict of interest relevant to this article was reported. Source Information From the Malaria Branch, Division of Parasitic Diseases, Centers for Disease Control and Prevention, Atlanta. The opinions expressed in this article are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention. This article (10.1056/NEJMe0808983) was published at www.nejm.org on December 8, 2008. It will appear in the December 11 issue of the Journal. References Druilhe P, Barnwell JW. Pre-erythrocytic stage malaria vaccines: time for a change in path. Curr Opin Microbiol 2007;10:371-378. [Medline] Gordon DM, McGovern TW, Krzych U, et al. Safety, immunogenicity, and efficacy of a recombinantly produced Plasmodium falciparum circumsporozoite protein-hepatitis B surface antigen subunit vaccine. J Infect Dis 1995;171:1576-1585. [ISI][Medline] Stoute JA, Slaoui M, Heppner DG, et al. A preliminary evaluation of a recombinant circumsporozoite protein vaccine against Plasmodium falciparum malaria. N Engl J Med 1997;336:86-91. [Free Full Text] Kester KE, McKinney DA, Tornieporth N, et al. Efficacy of recombinant circumsporozoite protein vaccine regimens against experimental Plasmodium falciparum malaria. J Infect Dis 2001;183:640-647. [CrossRef][ISI][Medline] Bojang KA, Milligan PJ, Pinder M, et al. Efficacy of RTS,S/AS02 malaria vaccine against Plasmodium falciparum infection in semi-immune adult men in The Gambia: a randomised trial. Lancet 2001;358:1927-1934. [CrossRef][Medline] Alonso PL, Sacarlal J, Aponte JJ, et al. Efficacy of the RTS,S/AS02A vaccine against Plasmodium falciparum infection and disease in young African children: randomised controlled trial. Lancet 2004;364:1411-1420. [CrossRef][Medline] Abdulla S, Oberholzer R, Juma O, et al. Safety and immunogenicity of RTS,S/AS02D malaria vaccine in infants. N Engl J Med 2008;359:2533-2544. [CrossRef] Bejon P, Lusingu J, Olotu A, et al. Efficacy of RTS,S/AS01E vaccine against malaria in children 5 to 17 months of age. N Engl J Med 2008;359:2521-2532. [CrossRef] Aponte JJ, Aide P, Renom M, et al. Safety of the RTS,S/AS02D candidate malaria vaccine in infants living in a highly endemic area of Mozambique: a double blind randomised controlled phase I/IIb trial. Lancet 2007;370:1543-1551. [CrossRef][Medline] Snow RW, Guerra CA, Mutheu JJ, Hay SI. International funding for malaria control in relation to populations at risk of stable Plasmodium falciparum transmission. PLoS Med 2008;5:e142-e142. [Medline] Ceesay SJ, Casals-Pascual C, Erskine J, et al. Changes in malaria indices between 1999 and 2007 in The Gambia: a retrospective analysis. Lancet 2008;372:1545-1554. [Medline] O'Meara WP, Bejon P, Mwangi TW, et al. Effect of a fall in malaria transmission on morbidity and mortality in Kilifi, Kenya. Lancet 2008;372:1555-1562. [Medline]

PLOS: doenças negligenciadas nos Estados Unidos

Neglected Infections of Poverty in the United States of America Peter J. Hotez. Department of Microbiology, Immunology, and Tropical Medicine, The George Washington University and Sabin Vaccine Institute, Washington, D.C., United States of America Abstract In the United States, there is a largely hidden burden of diseases caused by a group of chronic and debilitating parasitic, bacterial, and congenital infections known as the neglected infections of poverty. Like their neglected tropical disease counterparts in developing countries, the neglected infections of poverty in the US disproportionately affect impoverished and under-represented minority populations. 1The major neglected infections include the helminth infections, toxocariasis, strongyloidiasis, ascariasis, and cysticercosis; the intestinal protozoan infection trichomoniasis; some zoonotic bacterial infections, including leptospirosis; the vector-borne infections Chagas disease, leishmaniasis, trench fever, and dengue fever; and the congenital infections cytomegalovirus (CMV), toxoplasmosis, and syphilis. These diseases occur predominantly in people of color living in the Mississippi Delta and elsewhere in the American South, in disadvantaged urban areas, and in the US–Mexico borderlands, as well as in certain immigrant populations and disadvantaged white populations living in Appalachia. Preliminary disease burden estimates of the neglected infections of poverty indicate that tens of thousands, or in some cases, hundreds of thousands of poor Americans harbor these chronic infections, which represent some of the greatest health disparities in the United States. Specific policy recommendations include active surveillance (including newborn screening) to ascertain accurate population-based estimates of disease burden; epidemiological studies to determine the extent of autochthonous transmission of Chagas disease and other infections; mass or targeted treatments; vector control; and research and development for new control tools including improved diagnostics and accelerated development of a vaccine to prevent congenital CMV infection and congenital toxoplasmosis.