No description available.

A Síndrome Multissistêmica do Definhamento do Suíno (SMDS) é uma doença emergente e mundialmente distribuída, que tem trazido sérios prejuízos econômicos para a indústria suinícola. O Circovírus Suíno tipo 2 (PCV2), agente causal da doença, provoca lesões principalmente nos tecidos linfóides, e sugere-se que produza imunossupressão, predispondo o hospedeiro a infecções virais, bacterianas e fúngicas secundárias. Neste trabalho, é descrito um estudo da prevalência e bacteriologia das otites purulentas em suínos apresentando a SMDS, bem como em animais de baixo desenvolvimento e de crescimento normal. No total, foram examinados 385 suínos com idades entre 60 e 130 dias. De 242 animais com a SMDS, 57 (23,5%) apresentaram lesões purulentas no ouvido médio. Dentre 119 animais de baixo desenvolvimento, apenas 1 (0,7%) apresentou a lesão. Não foram detectadas lesões macroscópicas no ouvido médio dos 24 animais com crescimento normal (controles). Os agentes isolados com maior freqüência das lesões foram Arcanobacterium pyogenes, Streptococcus α– hemolíticos e Pasteurella multocida, encontrados em, respectivamente, 37 (43%), 32 (37,2%) e 24 (27,9%) dos 86 ouvidos submetidos à bacteriologia. A alta prevalência de lesões purulentas no ouvido médio de animais com a SMDS sugere que a infecção pelo PCV2 pode tornar o suíno mais suscetível às otites bacterianas. Por outro lado, a prevalência reduzida das lesões em suínos de baixo desenvolvimento sugere que a otite não representa uma causa importante de mau desempenho em suínos nas fases de crescimento e terminação. O isolamento do A. pyogenes, de Streptococcus α- hemolíticos e da P. multocida na maioria das lesões está de acordo com relatos anteriores, confirmando a importância desses organismos como agentes causais da otite média em suínos. / Postweaning Multisystemic Wasting Syndrome (PMWS) is an emerging disease disseminated globally that causes severe losses to the pig industry. Porcine circovirus type 2 (PCV2) is the causal agent of the disease and causes lesions mainly in lymphoid tissue and it is suggested that it can cause immunosuppression, predisposing the host to viral, bacterial and mycotic infections. In the present work we describe a study on prevalence and bacteriology of purulent otitis in pigs with PMWS, as well as in pigs with attrition and pigs with normal growth. A total amount of 385 animals were examined, with ages ranging from 60 to 130 days. Among 242 pigs with PMWS, 57 (23,5%) showed purulent lesions in the middle ear. Among 119 pigs with attrition, only 1 (0,7%) presented the lesion. In 24 control pigs, middle ear lesions were not detected. The agents most frequently isolated from the lesions were Arcanobacterium pyogenes, α–hemolytic Streptococci and Pasteurella multocida, found respectively in 36 (43%), 32 (37,2%) and 24 (27,9%) of 86 ears bacteriologically examined. The high prevalence of purulent lesions found in middle ear of PMWS affected pigs suggests that PCV2 infection can increase susceptibility of swine to bacterial otitis. On the other hand, the small prevalence of lesions in piglets with attrition suggests that otitis does not represent a significant cause for depressed growth in pigs from growing and finishing ages. The isolation of A. pyogenes, α-hemolytic Streptococci and P. multocida from most lesions agrees with previous reports, confirming the importance of these organisms as causal agents in the etiology of otitis media in pigs.

A Síndrome Multissistêmica do Definhamento do Suíno (SMDS) é uma doença emergente e mundialmente distribuída, que tem trazido sérios prejuízos econômicos para a indústria suinícola. O Circovírus Suíno tipo 2 (PCV2), agente causal da doença, provoca lesões principalmente nos tecidos linfóides, e sugere-se que produza imunossupressão, predispondo o hospedeiro a infecções virais, bacterianas e fúngicas secundárias. Neste trabalho, é descrito um estudo da prevalência e bacteriologia das otites purulentas em suínos apresentando a SMDS, bem como em animais de baixo desenvolvimento e de crescimento normal. No total, foram examinados 385 suínos com idades entre 60 e 130 dias. De 242 animais com a SMDS, 57 (23,5%) apresentaram lesões purulentas no ouvido médio. Dentre 119 animais de baixo desenvolvimento, apenas 1 (0,7%) apresentou a lesão. Não foram detectadas lesões macroscópicas no ouvido médio dos 24 animais com crescimento normal (controles). Os agentes isolados com maior freqüência das lesões foram Arcanobacterium pyogenes, Streptococcus α– hemolíticos e Pasteurella multocida, encontrados em, respectivamente, 37 (43%), 32 (37,2%) e 24 (27,9%) dos 86 ouvidos submetidos à bacteriologia. A alta prevalência de lesões purulentas no ouvido médio de animais com a SMDS sugere que a infecção pelo PCV2 pode tornar o suíno mais suscetível às otites bacterianas. Por outro lado, a prevalência reduzida das lesões em suínos de baixo desenvolvimento sugere que a otite não representa uma causa importante de mau desempenho em suínos nas fases de crescimento e terminação. O isolamento do A. pyogenes, de Streptococcus α- hemolíticos e da P. multocida na maioria das lesões está de acordo com relatos anteriores, confirmando a importância desses organismos como agentes causais da otite média em suínos. / Postweaning Multisystemic Wasting Syndrome (PMWS) is an emerging disease disseminated globally that causes severe losses to the pig industry. Porcine circovirus type 2 (PCV2) is the causal agent of the disease and causes lesions mainly in lymphoid tissue and it is suggested that it can cause immunosuppression, predisposing the host to viral, bacterial and mycotic infections. In the present work we describe a study on prevalence and bacteriology of purulent otitis in pigs with PMWS, as well as in pigs with attrition and pigs with normal growth. A total amount of 385 animals were examined, with ages ranging from 60 to 130 days. Among 242 pigs with PMWS, 57 (23,5%) showed purulent lesions in the middle ear. Among 119 pigs with attrition, only 1 (0,7%) presented the lesion. In 24 control pigs, middle ear lesions were not detected. The agents most frequently isolated from the lesions were Arcanobacterium pyogenes, α–hemolytic Streptococci and Pasteurella multocida, found respectively in 36 (43%), 32 (37,2%) and 24 (27,9%) of 86 ears bacteriologically examined. The high prevalence of purulent lesions found in middle ear of PMWS affected pigs suggests that PCV2 infection can increase susceptibility of swine to bacterial otitis. On the other hand, the small prevalence of lesions in piglets with attrition suggests that otitis does not represent a significant cause for depressed growth in pigs from growing and finishing ages. The isolation of A. pyogenes, α-hemolytic Streptococci and P. multocida from most lesions agrees with previous reports, confirming the importance of these organisms as causal agents in the etiology of otitis media in pigs.

A Síndrome Multissistêmica do Definhamento do Suíno (SMDS) é uma doença emergente e mundialmente distribuída, que tem trazido sérios prejuízos econômicos para a indústria suinícola. O Circovírus Suíno tipo 2 (PCV2), agente causal da doença, provoca lesões principalmente nos tecidos linfóides, e sugere-se que produza imunossupressão, predispondo o hospedeiro a infecções virais, bacterianas e fúngicas secundárias. Neste trabalho, é descrito um estudo da prevalência e bacteriologia das otites purulentas em suínos apresentando a SMDS, bem como em animais de baixo desenvolvimento e de crescimento normal. No total, foram examinados 385 suínos com idades entre 60 e 130 dias. De 242 animais com a SMDS, 57 (23,5%) apresentaram lesões purulentas no ouvido médio. Dentre 119 animais de baixo desenvolvimento, apenas 1 (0,7%) apresentou a lesão. Não foram detectadas lesões macroscópicas no ouvido médio dos 24 animais com crescimento normal (controles). Os agentes isolados com maior freqüência das lesões foram Arcanobacterium pyogenes, Streptococcus α– hemolíticos e Pasteurella multocida, encontrados em, respectivamente, 37 (43%), 32 (37,2%) e 24 (27,9%) dos 86 ouvidos submetidos à bacteriologia. A alta prevalência de lesões purulentas no ouvido médio de animais com a SMDS sugere que a infecção pelo PCV2 pode tornar o suíno mais suscetível às otites bacterianas. Por outro lado, a prevalência reduzida das lesões em suínos de baixo desenvolvimento sugere que a otite não representa uma causa importante de mau desempenho em suínos nas fases de crescimento e terminação. O isolamento do A. pyogenes, de Streptococcus α- hemolíticos e da P. multocida na maioria das lesões está de acordo com relatos anteriores, confirmando a importância desses organismos como agentes causais da otite média em suínos. / Postweaning Multisystemic Wasting Syndrome (PMWS) is an emerging disease disseminated globally that causes severe losses to the pig industry. Porcine circovirus type 2 (PCV2) is the causal agent of the disease and causes lesions mainly in lymphoid tissue and it is suggested that it can cause immunosuppression, predisposing the host to viral, bacterial and mycotic infections. In the present work we describe a study on prevalence and bacteriology of purulent otitis in pigs with PMWS, as well as in pigs with attrition and pigs with normal growth. A total amount of 385 animals were examined, with ages ranging from 60 to 130 days. Among 242 pigs with PMWS, 57 (23,5%) showed purulent lesions in the middle ear. Among 119 pigs with attrition, only 1 (0,7%) presented the lesion. In 24 control pigs, middle ear lesions were not detected. The agents most frequently isolated from the lesions were Arcanobacterium pyogenes, α–hemolytic Streptococci and Pasteurella multocida, found respectively in 36 (43%), 32 (37,2%) and 24 (27,9%) of 86 ears bacteriologically examined. The high prevalence of purulent lesions found in middle ear of PMWS affected pigs suggests that PCV2 infection can increase susceptibility of swine to bacterial otitis. On the other hand, the small prevalence of lesions in piglets with attrition suggests that otitis does not represent a significant cause for depressed growth in pigs from growing and finishing ages. The isolation of A. pyogenes, α-hemolytic Streptococci and P. multocida from most lesions agrees with previous reports, confirming the importance of these organisms as causal agents in the etiology of otitis media in pigs.

Les espèces réactives de l’oxygène (ERO) contrôlent plusieurs aspects de la carcinogenèse, étant donné leur capacité àpromouvoir la prolifération mais aussi à induire la sénescence et l’apoptose. Dans les stades avancés de cancer, les EROpeuvent également participer au développement de l’atrophie musculaire, engendrant une détérioration de la qualité de viedes patients. L’activité physique (AP), connue pour augmenter les défenses antioxydants de l’organisme et lasupplémentation en antioxydants sont considérées comme deux stratégies susceptibles de moduler la croissance tumorale, d’améliorer la performance physique et de réduire les effets secondaires liés à la maladie et aux traitements anticancéreux. Néanmoins, plusieurs questions restent aujourd’hui sans réponse. En effet, bien que l’AP puisse réduire la progression du cancer du sein, du colon et de la prostate, son impact sur les cancers se développant au sein du muscle (ex : le liposarcome), donc soumis aux contractions musculaires répétées, reste méconnu. En utilisant des approches in vivo et in vitro, nous avons démontré que maintenir une AP régulière accélère la croissance du liposarcome intramusculaire, probablement, via la réduction des taux circulants d’insuline et l’inhibition de la voie « P38 MAPK-P21 ». Pour les patients ne pouvant pas pratiquer d’AP, la consommation d’antioxydants pourrait être un moyen de réduire les ERO tumorales et musculaires et ainsi être prometteuse. Toutefois, les études actuelles restent très controversées. Nos travaux ont montré dans un modèle murin de cachexie cancéreuse que des doses nutritionnelles d’un produit antioxydant commercialisé en France, étaient suffisantes pour accélérer la croissance de la tumeur colique, favoriser la perte de masse corporelle totale et musculaire et engendrer la mort prématurée des souris. L’ensemble de nos résultats suggère que la pratique d’AP et la consommation en antioxydants peuvent induire des effets différents selon le type de tumeur et leur implantation, nécessitant une prise en charge individualisée des patients. En effet, (1) les patients atteints d’un LS intramusculaire devraient éviter de pratiquer une AP durant la période préopératoire mais ces résultats doivent être confirmés par une étude clinique, (2) les patients avec un stade avancé de cancer devraient être vigilants quant à l’utilisation de suppléments antioxydants ; une telle pratique pouvant avoir des répercussions dangereuses sur leur santé. / Reactive oxygen species (ROS) control several aspects of carcinogenesis as they can either promote tumor growth andprogression or senescence and apoptosis. In advanced stages of cancer, ROS can also drive the development of other cancerrelated complications like, muscle wasting. Physical activity (PA) and antioxidant supplementation have been proposed as two adjuvant strategies to better control tumor growth, ameliorate performance and alleviate secondary symptoms related to cancer itself or to the heavy anticancer therapies. However, several issues remain to be elucidated. First of all, although PA could reduce colon, breast and prostate cancer growth and progression, its impact remains unknown on orthotopic intramuscular tumors like liposarcoma, which directly affect the musculoskeletal apparatus and reduce physical function. Secondly, given the limitedness of PA application in some advanced stages of cancer, patients may increase their dependency on nutritional and antioxidant complements as an alternative strategy, but such practice has spark a lot of polemic and inconsistent results. In this thesis, we have addressed the effectiveness of PA and antioxidants in two distinct animal models of cancer. Using in vivo and in vitro approaches, we found that voluntary PA accelerated the growth of intramuscular liposarcoma tumors and exacerbated skeletal muscle dysfunction, mainly, by decreasing circulating insulin levels and the subsequent activation of the tumor suppressor pathway “P38 MAPK-P21”. We also demonstrated that nutritional doses of commercial antioxidants enhanced colon tumor growth, total body/skeletal muscle weight loss and caused premature death of mice. Such mechanism was due to selective changes in oxidative damage profiles, which decreased in tumor but increased in skeletal muscle, in a way driving tumor growth and skeletal muscle wasting/dysfunction. Clinically, it seems that (1) patients with intramuscular liposarcoma may, at least, not increase their levels of PA or undergo hospital-supervised exercise program, during the preoperative period; until the confirmation of our findings with clinical data and (2) patients with advanced stages of cancer must be very careful against the use of antioxidants as it could lifethreatening. Accordingly, health agencies in France, Europe and USA prohibit the use of synthetic antioxidant supplements without dietary counseling by a cancer patient’s physician and/or nutritionist.

No description available.

Porcine circovirus type 2 (PCV2) is the primary causative agent of postweaning multisystemic wasting syndrome (PMWS), whereas the ubiquitous porcine circovirus type 1 (PCV1) is nonpathogenic for pigs. Since its initial detection in a Canadian commercial swine herd in 1991, PMWS has been detected in all swine producing regions of the world and is now a serious economic problem to the swine industry. The objectives of this dissertation were to biologically, genetically and experimentally characterize both PCV1 and PCV2, to identify the genetic determinant(s) for virulence and replication, and to develop an effective genetically-engineered vaccine against PCV2 infection and PMWS. The genetic heterogeneity of PCV2 and PCV1 isolates from different geographic origins were determined. We found that, although PCV1 and PCV2 genomes were very conserved, some minor genomic variation exists among PCV1 isolates and PCV2 isolates. The nonpathogenic PCV1 and pathogenic PCV2 share only about 76% nucleotide sequence identity but have similar genomic organization. The highest sequence variability among PCV isolates is found in the immunogenic ORF2 capsid gene. Based on the sequence data in this dissertation, a universal polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay was developed that is capable of detecting all known PCV isolates and differentiating between infections by nonpathogenic PCV1 and pathogenic PCV2. In order to study the structural and functional relationship of PCV genes and to develop a genetically-engineered vaccine, we constructed infectious DNA clones of both PCV1 and PCV2. By using the PCV2 infectious clone, we showed that pigs can be infected by direct intrahepatic injection of PCV2 infectious DNA clone. The pathological lesions and clinical disease associated with PCV2 infection were more definitively characterized by using the infectious DNA clone. We found that PCV2 is the primary but not the sole causative agent of PMWS, as the full spectrum of clinical PMWS was not reproduced by the infectious PCV2 DNA clone although pathological lesions characteristic of PMWS were reproduced. A chimeric vaccine was constructed by cloning the immunogenic capsid gene of the pathogenic PCV2 into the genomic backbone of the non-pathogenic PCV1 virus. We showed that the resulting chimeric PCV1-2 vaccine virus, retained the non-pathogenic nature of PCV1 but induced a protective immune response against a wild-type PCV2 challenge. In vaccinated pigs, the chimeric PCV1-2 vaccine reduced PCV2 viremia length and serum virus loads and reduced pathological lesions such as lymphoid depletion (LD) and histiocytic replacement (HR) in lymphoid tissues, inflammation and discoloration of the lymph nodes. The amounts of PCV2 antigen and PCV2 genomic copy loads in lymph node tissues were also significantly reduced. Our results indicated that the attenuated chimeric PCV1-2 virus induces protective immunity against PCV2 infection and thus could serve as an effective vaccine against PCV2 and PMWS. To improve the safety of the vaccine, we attempted to identify the genetic determinant(s) for PCV2 virulence. An isolate of PCV2 was serially passaged for 120 times in PK-15 cells. After 120 passages, a total of two amino acid mutations were identified in the capsid protein of the passage 120 virus (VP120), P110A and R191S. Compared to other known PCV1 and PCV2 sequences, the two amino acid mutations in PCV2 VP120 are unique. The VP120 virus was biologically characterized in vitro and experimentally characterized in specific-pathogen-free (SPF) pigs. The two amino acid mutations resulted in an enhanced replication ability of PCV2 VP120 in PK-15 cells and an attenuated phenotype in infected pigs. The P110A and R191S mutations in the capsid protein either alone or collectively are likely important for PCV2 virulence and replication. In summary, we genetically characterized PCV2 isolates from different geographic regions and developed a PCR-RFLP assay. We constructed and characterized infectious DNA clones of PCV1 and PCV2, and developed a genetically engineered vaccine against PCV2 infection. We also identified the genetic determinants for PCV2 virulence and replication. The vaccine developed in this study, when it becomes available, will help the swine industry control this important pathogen. / Ph. D.

Yes / The aryl hydrocarbon receptor (AHR) mediates the toxic effects of dioxin (2, 3, 7, 8-tetrachlorodibenzo-p-dioxin; TCDD), which includes thymic atrophy, steatohepatitis, and a lethal wasting syndrome in laboratory rodents. Although the mechanisms of dioxin toxicity remain unknown, AHR signaling in hepatocytes is necessary for dioxin-induced liver toxicity. We previously reported that loss of TCDD-inducible poly(adenosine diphosphate [ADP]-ribose) polymerase (TIPARP/PARP7/ARTD14), an AHR target gene and mono-ADP-ribosyltransferase, increases the sensitivity of mice to dioxin-induced toxicities. To test the hypothesis that TIPARP is a negative regulator of AHR signaling in hepatocytes, we generated Tiparpfl/fl mice in which exon 3 of Tiparp is flanked by loxP sites, followed by Cre-lox technology to create hepatocyte-specific (Tiparpfl/flCreAlb) and whole-body (Tiparpfl/flCreCMV; TiparpEx3−/−) Tiparp null mice. Tiparpfl/flCreAlb and TiparpEx3−/− mice given a single injection of 10 μg/kg dioxin did not survive beyond days 7 and 9, respectively, while all Tiparp+/+ mice survived the 30-day treatment. Dioxin-exposed Tiparpfl/flCreAlb and TiparpEx3−/− mice had increased steatohepatitis and hepatotoxicity as indicated by greater staining of neutral lipids and serum alanine aminotransferase activity than similarly treated wild-type mice. Tiparpfl/flCreAlb and TiparpEx3−/− mice exhibited augmented AHR signaling, denoted by increased dioxin-induced gene expression. Metabolomic studies revealed alterations in lipid and amino acid metabolism in liver extracts from Tiparpfl/flCreAlb mice compared with wild-type mice. Taken together, these data illustrate that TIPARP is an important negative regulator of AHR activity, and that its specific loss in hepatocytes is sufficient to increase sensitivity to dioxin-induced steatohepatitis and lethality. / This work was supported by Canadian Institutes of Health Research (CIHR) operating grants (MOP-494265 and MOP-125919), CIHR New Investigator Award, an Early Researcher Award from the Ontario Ministry of Innovation (ER10-07-028), an unrestricted research grant from the DOW Chemical Company, the Johan Throne Holst Foundation, Novo Nordic Foundation and the Norwegian Cancer Society to J.M.

Background: Highly Active Antiretroviral Treatment (HAART) has reduced the frequency of weight loss/wasting associated with HIV infection. However, weight loss remains a problem, even in the HAART era. Objectives: This study was carried out to assess weight change in a cohort of HIV-infected women on HAART in Rwanda, from 2005 to 2008, and to identify factors that predict weight loss in this cohort. Methods: Data from a cohort of 449 HIV-positive women on HAART enrolled in the Rwanda Women’s Inter-association Study and Assessment (RWISA), starting in May 2005, and followed at six monthly intervals until December 2008, were analysed. The outcome assessed in this study was change in weight, measured in kilograms at 6, 12 and 24 months after HAART initiation. Nutritional status was recorded and laboratory measurements (weight, height and CD4 cell count) were taken prior and after HAART initiation. All covariates were time dependent, except for the history of weight loss which was recorded at baseline only. Generalized Estimating Equation (GEE) using the linear link (Gaussian [normal]), exchangeable covariance structure and robust standard error was used to assess the factors associated with changes in weight (weight loss or weight gain) and to control for potential confounders. Results: Prior to HAART initiation, the mean weight of the study participants was 53.1 kg (SD 9.5). The mean BMI was 21.3 kg/m2 (SD 3.6) and the mean CD4 cell count was 222.9 cells/μL (SD 120.6) [47.6% had CD4 cell counts <200 cells/μL, 52.2% had CD4 cell counts ≥200 cells/μL]. Overall, the participants gained weight from baseline to 12 months after HAART initiation. The mean weight change was 1.9 kg (SD 7.8) (p<0.001) 6 months after HAART initiation, 2.9 kg (SD 5.9) (p <0.001) 12 months after HAART initiation, and 2.4 kg (SD 6.5) (p <0.001) 24 months after HAART initiation. Six months after HAART initiation, 48.3% of participants had gained weight, and 21.0% had lost weight. Twelve months after HAART initiation, 56.9% had gained weight, and 18.3% had lost weight, Twenty-four months after HAART initiation, 56.6% had gained weight, and 22.6% had lost weight. Participants with CD4 cell counts ≤ 200 cells/μL at baseline gained more weight than those with CD4 cell counts > 200 cells/μL at 6, 12 and 24 months after HAART initiation. Participants who were underweight (BMI <18.5 kg/m2) at baseline gained more weight than other participants three months after HAART initiation. Time-dependent diarrhoea for more than two weeks and a CD4 cell count of 200 - 350 cells/μL were significantly associated with weight loss (p≤ 0.05). Others factors, such as time-dependent education level (completion of secondary school), marital status (married legally and status other than married legally or widowed), and increases in CD4 cell counts, were associated with weight gain (p≤ 0.05). Conclusion: Although the majority of participants gained weight during the first 12 months of being on HAART, a significant proportion of participants lost weight while on HAART. The findings on the predictors of weight change in HIV-positive women on HAART can be used to promote weight gain in women who start HAART. Clinicians who take care of HIV-infected patients on HAART should pay attention to those who lose weight, and those who present with diarrhoea or with CD4 cell counts of <350 cells/μL at follow-up visits, since these factors are associated with weight loss in the HAART era.

PhD, Faculty of Health Sciences, University of the Witwatersrand / Background: In low- to middle-income countries, rising levels of overweight and obesity are a result of multiple transitions, in particular, a nutrition transition. Consequently, in these countries, metabolic diseases are contributing increasingly to disease burden, despite the persisting burden of undernutrition and infectious diseases. Understanding the patterns and factors associated with persistent undernutrition and emerging obesity in children and adolescents, and concomitant risk for metabolic disease, is therefore of criticial importance. This should contribute to public health policy on interventions to prevent adult disease. Aims: To better understand the double burden of malnutrition in a poor, high HIV prevalent, transitional society in a middle-income country; In so doing, to inform policies and interventions to address the double burden of malnutrition. Methods: A cross-sectional growth survey was conducted in 2007 targeting 4000 children and adolescents 1-20 years of age living in rural South Africa. The survey was nested within the ongoing Agincourt Health and Socio-demographic Surveillance System, which acted as the sampling frame and also provided data for explanatory variables. Anthropometric measurements were performed on all participants using standard procedures. In addition, HIV testing was done on children aged 1 to 5 years and Tanner pubertal assessment was conducted among adolescents 9-20 years. A one-year follow-up of HIV positive children included a matched control group of HIV negative counterparts. Data collection involved both quantitative and qualitative methods. Growth z-scores were used to determine stunting, underweight and wasting and were generated using the 2006 WHO growth standards for children up to five years and the 1977 NCHS/WHO reference for older children. Overweight and obesity were determined using the International Obesity Task Force cut-offs for BMI for children aged up to 17 years and adult cut offs of BMI =25 and =30 kg/m2 for overweight and obesity respectively for adolescents 18 to 20 years. Waist circumference cut-offs of =94cm for males and =80cm for females, and waist-to-height ratio of 0.5 for both sexes, were used to determine central obesity and hence metabolic disease risk in ix adolescents. Descriptive analysis described patterns of nutritional status by age, sex, pubertal stage and HIV status. Linear and logistic regression was done to determine predictors of nutrional outcomes. A p-value of <0.05 was considered statistically significant. Results: Prevalence of undernutrition, particularly stunting, was substantial: 18% among children aged 1-4 years, with a peak of 32% in children at one year of age. Stunting and underweight were also substantial in adolescent boys, with underweight reaching a peak of 19% at 14 years of age. Concurrently, the prevalence of combined overweight and obesity, almost non-existent in boys, was prominent among adolescent girls, increasing with age, and reaching a peak of 25% at 18 years. Risk for metabolic disease using waist circumference cut-offs was substantial among adolescents, particularly girls, increasing with sexual maturation, and reaching a peak of 35% at Tanner stage 5. Prevalence of HIV in children aged 1-4 years was 4.4%. HIV positive children had poorer nutritional outcomes than that of HIV negative children in 2007. The impact of paediatric HIV on nutritional status at community level was, however, not significant. Significant predictors of undernutrition in children aged 1-4 years, documented at child, maternal, household and community levels, included child’s HIV status, age and birth weight; maternal age; age of household head; and area of residence. Significant predictors of overweight/obesity and risk for metabolic disease in adolescents aged 10-20 years, documented at individual/child and household levels included child’s age, sex and pubertal development; and household-level food security, socio-economic status, and household head’s highest education level. There was a high acceptance rate for the HIV test (95%). One year following the test, almost all caregivers had accepted and valued knowing their child’s HIV status, indicating that it enhanced their competency in caregiving. Additionally, nutritional status of HIV positive children had improved significantly within a year of follow-up. Conclusions: The study describes co-existing child stunting and adolescent overweight/obesity and risk for metabolic disease in a society undergoing nutrition transition. While likely that this profile reflects changes in nutrition and diet, variation in infectious disease burden, physical activity patterns, and social influences need to be investigated. The findings are critical in the wake of the rising public health importance of metabolic diseases in low- to middle-income countries, despite the unfinished agenda of undernutrition and infectious diseases. Clearly, policies and interventions to address malnutrition in this and other transitional societies need to be double-pronged. In addition, gender-biased nutritional patterns call for gender-sensitive policies and interventions. The study further documents a significant role of paediatric HIV on nutritional status, and the potential for community-based paediatic HIV testing to ameliorate this. Targeted early paediatric HIV testing of exposed or at risk children, followed by appropriate health care for infected children, may improve their nutritional status and survival.