Konzo

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Thorkild Tylleskar - One of the best experts on this subject based on the ideXlab platform.

  • Abnormalities of somatosensory evoked potentials in Konzo – an upper motor neuron disorder
    Clinical Neurophysiology, 2020
    Co-Authors: Daniel Tshala-katumbay, Thorkild Tylleskar, Theodore Kazadi-kayembe, Peo Fallmar, K. Edebol Eeg-olofsson, T. Kayembe-kalula
    Abstract:

    Abstract Objective : To determine whether the somatosensory pathways are involved or not in Konzo. Methods : In 1998, 21 Konzo subjects (15 females and 6 males; mean age 21 years) underwent a SEP study with a two-channel-equipment (Medtronic Keypoint, Denmark) whereas in 2000, 15 subjects (7 females and 8 males; mean age 21 years) participated in a study with a 4-channel-equipment. Results : Most subjects (19/21 in 1998 and 12/15 in 2000) showed normal median SEPs. The remainders had no median cortical responses. All 21 subjects in 1998 and 9 out of 15 in 2000 showed abnormalities of tibial SEPs mainly consisting of absence of cortical responses, prolonged cortical latencies, and central sensory delay to the lumbar spine. Most subjects showed normal absolute latencies both at peripheral and spinal levels. The SEP findings did not correlate with the severity, neither the duration of Konzo, nor the experience or not of sensory symptoms at the onset of the disease. Conclusion : Our findings are not specific of Konzo. However, they suggest involvement of intracranial somatosensory pathways and point to similarities with other motor neuron diseases.

  • Konzo a distinct neurological disease associated with food cassava cyanogenic poisoning
    Brain Research Bulletin, 2019
    Co-Authors: Esperance Kashalaabotnes, Michael J Boivin, Daniel Okitundu, Dieudonne Mumba, Desire Tshalakatumbay, Thorkild Tylleskar
    Abstract:

    Abstract Epidemics of neurodegenerative diseases putatively caused by food toxins have been reported in the tropics with no clear understanding of their pathogenetic mechanisms. These diseases include the disease named Konzo that has been well documented in sub-Sahara Africa, mostly among children and women of childbearing age. Outbreaks of Konzo have occurred in the Democratic Republic of Congo, Mozambique, Tanzania, Central African Republic, Angola, Cameroun, and most recently in Zambia. The main clinical picture consists of a symmetrical, permanent and irreversible spastic paraparesis (motor neuron disease) with no signs of sensory or genitourinary impairments. Recently, cognitive impairments and neurodevelopmental delays have been reported among school-aged and very young children. The exact pathogenetic mechanisms of the disease remain unknown. Epidemiological studies consistently show an association between outbreaks of the disease and chronic dietary reliance on insufficiently processed cyanogenic cassava (manioc or tapioca). Biochemical and toxicological studies suggest that the metabolites of linamarin (α-Hydroxyisobutyronitrile β-D-glucopyranoside, the main cassava cyanogen), notably cyanide (mitochondrial toxin), thiocyanate (AMPA chaotropic agent), and cyanate (protein carbamoylating agent) may play an important role in the pathogenesis of Konzo. Experimental data suggest that thiol-redox and protein- folding mechanisms may also be perturbed. Factors of susceptibility including genetics, poor nutrition, poverty and dietary cyanogen exposure, or their interactions have been suggested. Serological studies have ruled out the role of retroviruses such as the human lymphotropic viruses HIV-I/II or HTLV-I/II. Because there is no cure for Konzo, prevention of the disease remains of paramount importance. Prospects for cognitive rehabilitation still need to be explored and tested.

  • molekylarantropologisk forskning om Konzo ad modum hans rosling
    Socialmedicinsk tidskrift, 2018
    Co-Authors: Thorkild Tylleskar
    Abstract:

    Hans Rosling hade en lysande forskarkarriar under 1980 och 1990-talen innan sin karriar som edutainer. Under tiden som lakare i Nacala i norra Mocambique stod han plotsligt mitt i en epidemi av en okand typ av spastisk forlamning, numera kallad Konzo. Detta blev startpunkten for en lang rad falt studier i flera afrikanska lander. Utmarkande for hans forskning var en extremt tvarvetenskaplig ansats som han kallade molekylarantropologi och dar han tog i bruk allt fran antropologi via medicin och kemi till jordbruksforskning. Omkring Konzo och kassava handledde han ett dussintal doktorander inom klinisk medicin, klinisk kemi, nutrition och agronomi. Han ordnade en tvar vetenskaplig kurs om kassava, kassavaodling och kassavatoxicitet i Uppsala 1990 och ett internationellt tvarvetenskapligt symposium i samma amnen i Nigeria 1994.

  • neuropsychological effects of Konzo a neuromotor disease associated with poorly processed cassava
    Pediatrics, 2013
    Co-Authors: Michael J Boivin, Daniel Okitundu, Marie Therese Sombo, Dieudonne Mumba, Guy Makila Mabe Bumoko, Thorkild Tylleskar, Connie Page, Jean Jacques Muyembe, Desire Tshalakatumbay
    Abstract:

    BACKGROUND: Konzo is an irreversible upper-motor neuron disorder affecting children dependent on bitter cassava for food. Although the neuroepidemiology of Konzo is well characterized, we report the first neuropsychological findings. METHOD: Children with Konzo in the Democratic Republic of Congo (mean age 8.7 years) were compared with children without Konzo (mean age 9.1 years) on the Kaufman Assessment Battery for Children, second edition (KABC-II), and the Bruininks-Oseretsky Test of Motor Proficiency, second edition (BOT-2). Both groups were also compared with normative KABC measures from earlier studies in a nearby nonKonzo region. RESULTS: Using a Kruskal-Wallis test, children with Konzo did worse on the KABC-II simultaneous processing (visual-spatial analysis) ( K [1] = 8.78, P = .003) and mental processing index (MPI) ( K [1] = 4.56, P = .03) than children without Konzo. Both Konzo and nonKonzo groups had poorer KABC sequential processing (memory) and MPI relative to the normative group from a nonKonzo region ( K [2] = 75.55, P K [1] = 83.26, P P CONCLUSIONS: Motor proficiency is dramatically affected, and both children with and without Konzo have impaired neurocognition compared with control children from a nonoutbreak area. This may evidence a subclinical neurocognitive form of the disease, extending the human burden of Konzo with dramatic public health implications.

  • cassava food toxins Konzo disease and neurodegeneration in sub sahara africans
    Neurology, 2013
    Co-Authors: Daniel Tshalakatumbay, Michael J Boivin, Thorkild Tylleskar, K. T. Kazadi, M Banea, N. Mumba, L Okitundu, J J Muyembetamfum
    Abstract:

    Endemoepidemic neurodegenerative diseases putatively caused by food toxins have been reported around the globe with no clear understanding of their pathogenetic mechanisms. These diseases include the amyotrophic lateral sclerosis/parkinsonism dementia complex among the Guamanians; neurolathyrism among Europeans, Indians, and populations of the Horn of Africa; and tropical ataxic neuropathy or Konzo among sub-Sahara Africans.1,2 We focus on the molecular determinants of susceptibility to Konzo, a poorly known self-limited and irreversible upper motor neuron disease (spastic paraparesis) highly prevalent in Congo-Kinshasa, Mozambique, Tanzania, Central African Republic, Angola, and Cameroon. The main clinical picture consists of a symmetrical, permanent, and irreversible spastic paraparesis with no signs of sensory or genitourinary impairments.2,3 Severely affected individuals may present with a tetraparesis and pseudobulbar signs. The disease Konzo was named after a fetish used by the “Yaka” population of Congo-Kinshasa. The World Health Organization has adopted the following epidemiologic criteria for the disease: 1) an abrupt onset (<1 week) of weakness in legs and a nonprogressive course of the disease in a formerly healthy person, 2) a symmetrical spastic abnormality when walking and/or running, and 3) bilaterally exaggerated knee and/or ankle jerks without signs of disease of the spine.

Desire Tshalakatumbay - One of the best experts on this subject based on the ideXlab platform.

  • Konzo a distinct neurological disease associated with food cassava cyanogenic poisoning
    Brain Research Bulletin, 2019
    Co-Authors: Esperance Kashalaabotnes, Michael J Boivin, Daniel Okitundu, Dieudonne Mumba, Desire Tshalakatumbay, Thorkild Tylleskar
    Abstract:

    Abstract Epidemics of neurodegenerative diseases putatively caused by food toxins have been reported in the tropics with no clear understanding of their pathogenetic mechanisms. These diseases include the disease named Konzo that has been well documented in sub-Sahara Africa, mostly among children and women of childbearing age. Outbreaks of Konzo have occurred in the Democratic Republic of Congo, Mozambique, Tanzania, Central African Republic, Angola, Cameroun, and most recently in Zambia. The main clinical picture consists of a symmetrical, permanent and irreversible spastic paraparesis (motor neuron disease) with no signs of sensory or genitourinary impairments. Recently, cognitive impairments and neurodevelopmental delays have been reported among school-aged and very young children. The exact pathogenetic mechanisms of the disease remain unknown. Epidemiological studies consistently show an association between outbreaks of the disease and chronic dietary reliance on insufficiently processed cyanogenic cassava (manioc or tapioca). Biochemical and toxicological studies suggest that the metabolites of linamarin (α-Hydroxyisobutyronitrile β-D-glucopyranoside, the main cassava cyanogen), notably cyanide (mitochondrial toxin), thiocyanate (AMPA chaotropic agent), and cyanate (protein carbamoylating agent) may play an important role in the pathogenesis of Konzo. Experimental data suggest that thiol-redox and protein- folding mechanisms may also be perturbed. Factors of susceptibility including genetics, poor nutrition, poverty and dietary cyanogen exposure, or their interactions have been suggested. Serological studies have ruled out the role of retroviruses such as the human lymphotropic viruses HIV-I/II or HTLV-I/II. Because there is no cure for Konzo, prevention of the disease remains of paramount importance. Prospects for cognitive rehabilitation still need to be explored and tested.

  • indice global des signes neurologiques du Konzo marqueur clinique de multiples facteurs de susceptibilite et de gravite des troubles neurocognitifs chez l enfant en milieu Konzo
    African Journal of Neurological Sciences, 2018
    Co-Authors: Daniel Okitundu Luwa Eandjofono, Michael J Boivin, Guy Bumoko Makilamabe, Jean Jacques Tamfummuyembe, Marietherese Sombo Ayanne, Jeanpierre Mayambu Banea, Dieudonne Mumba Ngoy, Desire Tshalakatumbay
    Abstract:

    Objectif : Quantifier la deterioration neurologique observee dans le Konzo eu egard aux multiples deficiences incriminees dans sa pathogenie. Methodes : Une etude transversale a ete entreprise aupres de 123 enfants Konzo et 87 non-Konzo (4-17 ans) en 2011 a Kahemba, Congo-Kinshasa. L’indice global de signes neurologiques du Konzo (IGSNK) etait etudie en relation avec le niveau socio-economique familial evalue par le HOME, les performances cognitives au KABC-II et motrices au BOT-2, les taux seriques des isoprostanes, oligoelements, et l’albuminemie et triglyceridemie mesures respectivement par LC-MS/MS, ICP-MS, et automate Piccolo. Les tests de χ2, de Mann-Whitney et Kruskal-Wallis, ou la correlation r de Spearman ont ete appliques au seuil de signification de 0,05. Resultats : L’augmentation de l’indice global des signes neurologiques du Konzo etait associee a la severite de la maladie (p < 0,001), le niveau socioeconomique familial (r = – 0,25 ; p < 0,001, la triglyceridemie (r = 0,55 , p = 0,001) et les 8,12-IsoProstaneF2-VI seriques (r = 0,33 , p= 0,06),), l’albuminemie (r = – 0,44 , p = 0,010 ) , la cupremie ( r = – 0,36 , p= 0,048), le selenium serique (r = – 0,57, p = 0,001) ; en plus de l’habilite motrice globale (r = -0,861 ; p < 0,001) et l’indice global de fonctionnement cognitif (r = – 0,44 ; p = 0,002). Conclusion : L’indice global des signes neurologiques du Konzo parait etre un bon marqueur clinique de multiples deficiences (pauvrete socio-familiale, malnutrition, stress oxydatif) incriminees dans la severite du Konzo. Mots cles : malnutrition, niveau socio-economique familial, stress oxydatif, Konzo, intoxication cyanhydrique, troubles moteurs et cognitifs Konzo global neurological index: a clinical marker of susceptibility and severity of neurocognitive deficits in children living in Konzo-affected areas Objective : To quantify the extent of neurological deficits in Konzo in a context of multiple factors incriminated in its pathogenesis. Methods : A cross-sectional study was carried out to assess 123 children with and 87 presumably healthy controls (4-17 years) in 2011 in kahemba, congo-kinshasa. A Konzo global neurological index (KGNI) was constructed and assessed in relation to socio-economic status (assessed using the home questionnaire),  cognitive and motor performances at the KABC-II and BOT-2, respectively; serum isoprostanes (measured by LC/MS-MS), trace elements (by ICP-MS), albumin and triglycerides (by automated Piccolo). The chi-square, Mann-Whitney and Kruskal-Wallis tests as well as the Spearman r coefficients were used at the 0.05 level of statistical significance. Results : A higher KGNI was significantly associated with the severity of Konzo (p < 0.001), poor socio-economic status (r = – 0.25, p < 0.001), elevated serum triglycerides (r = 0.55, p = 0.001), 8,12-isoprostane F2-VI (r = 0.33, p = 0.06), hypoalbuminemia (r = – 0.44, p = 0.010), low serum concentrations copper (r = – 0.36, p = 0.048) or selenium (r = – 0.57, p = 0.001);in addition to poor scores at the BOT-2 testing (r = -0.86; p < 0.001) and KABC-II testing for cognition (r = – 0.44; p = 0.002). Conclusion : The Konzo global neurological index appears to be a good clinical marker of disease susceptibility factors (poor socio-economic status, malnutrition, oxidative stress) incriminated in the severity of Konzo. Key words : malnutrition, socio-economic status, oxidative stress, cyanide intoxication, neurocognition

  • cognitive and motor performance in congolese children with Konzo during 4 years of follow up a longitudinal analysis
    The Lancet Global Health, 2017
    Co-Authors: Michael J Boivin, Daniel Okitundu, Bumoko Makilamabe, Marie Therese Sombo, Dieudonne Mumba, Alla Sikorskii, Banea Mayambu, Desire Tshalakatumbay
    Abstract:

    Summary Background Konzo is an irreversible upper-motor neuron disorder affecting children dependent on bitter cassava for food. The neurocognitive ability of children with Konzo over time has yet to be fully documented. Methods We did a longitudinal study in a Konzo outbreak zone continuously affected by Konzo since 1990, in the district of Kahemba, southern Bandundu Province, Congo. We enrolled children with a record of neurological diagnosis of Konzo in Kahemba town. For all study children with Konzo enrolled in the final sample for the baseline assessment, a neurological exam was done by neurologists to confirm Konzo diagnosis using the 1996 WHO criteria at 2 years and 4 years. In the initial baseline sample for each child with Konzo, we attempted to get consent from a comparison child without Konzo (1996 WHO criteria) within 2 years of age, from a neighbouring household who met inclusion criteria. The neuropsychological assessments were the Kaufman Assessment Battery for Children, second edition (KABC-II), and the Bruininks-Oseretsky Test of Motor Proficiency, second edition (BOT-2). Findings Data collection occurred between Oct 12, 2011, and Aug 14, 2015, in the town of Kahemba. 123 children from the Congo with Konzo and 87 presumably healthy children without Konzo from neighbouring households were enrolled. The planned assessments were completed by 76 children with Konzo and 82 children without Konzo at 2-year follow-up, and by 55 children with Konzo and 33 children without Konzo at 4-year follow-up. Boys with Konzo did worse than those without Konzo on the KABC-II Learning (p=0·0424) and on the Mental Processing Index (MPI; p=0·0111) assessments at 2-year follow-up, but girls did not. These differences observed in boys might have been caused by stunting. At 4-year follow-up, the difference in KABC-II MPI score between boys or girls with or without Konzo was not significant. Both boys and girls with Konzo had lower scores on BOT-2 than children without Konzo at both follow-up times (p Interpretation Motor and cognitive performance continues to be significantly impaired in boys with Konzo at 2-year follow-up compared with boys without Konzo. Because these impairments are associated in part with exposure to poorly processed cassava as measured by urinary thiocyanate, interventions are urgently needed to ensure improved processing of cassava to detoxify this food source. Funding US National Institutes of Health.

  • lower serum levels of selenium copper and zinc are related to neuromotor impairments in children with Konzo
    Journal of the Neurological Sciences, 2015
    Co-Authors: G M M Bumoko, Michael J Boivin, Daniel Okitundu, Jean Jacques Muyembe, N H Sadiki, A Rwatambuga, K P Kayembe, Mumba D Ngoyi, Jean Pierre Banea, Desire Tshalakatumbay
    Abstract:

    Abstract We assessed the relationship between key trace elements and neurocognitive and motor impairments observed in Konzo, a motor neuron disease associated with cassava cyanogenic exposure in nutritionally challenged African children. Serum concentrations of iron, copper, zinc, selenium, and neurotoxic lead, mercury, manganese, cadmium, and cobalt were measured in 123 Konzo children (mean age 8.53 years) and 87 non-Konzo children (mean age 9.07 years) using inductively coupled plasma mass spectrometry (ICPMS). Concentrations of trace elements were compared and related to performance scores on the Kaufman Assessment Battery for Children, 2nd edition (KABC-II) for cognition and Bruininks–Oseretsky Test, 2nd edition (BOT-2) for motor proficiency. Children with Konzo had low levels of selenium, copper, and zinc relative to controls. Selenium concentration significantly correlated with serum 8,12-iso-iPF2α-VI isoprostane (Spearman r = 0.75, p

  • Konzo neurology of a permanent and non progressive motor neuron disorder associated with food cassava toxicity
    2014
    Co-Authors: Daniel Okitundu, Dieudonne Mumba, Desire Tshalakatumbay
    Abstract:

    Epidemics of neurodegenerative diseases putatively caused by food toxins have been reported under the tropics with no clear understanding of their pathogenetic mechanisms. These diseases include the disease named Konzo, which has been well documented in sub-Saharan Africa, mostly among children and women of childbearing age. Konzo is highly prevalent in Congo-Kinshasa, Mozambique, Tanzania, Central African Republic, Angola, and Cameroun. The main clinical picture consists of a symmetrical, permanent and irreversible spastic paraparesis (motor neuron disease) with no signs of sensory or genitourinary impairments. Impaired cognition is possible but yet to be elucidated. The exact pathogenetic mechanisms of the disease remain unknown. Serological studies rule out the role of retroviruses such as the human lymphotropic viruses HIV-I/II or HTLV-I/II. Epidemiological studies consistently show an association between outbreaks of the disease and chronic dietary reliance on foodstuffs derived from insufficiently processed cyanogenic cassava (aka manioc or tapioca). Biochemical and toxicological studies suggest that the metabolites of linamarin (α-hydroxyisobutyronitrile β-d-glucopyranoside, the main cassava cyanogen), notably cyanide (mitochondrial toxin), thiocyanate (AMPA chaotropic agent), and cyanate (protein carbamoylating agent) may be important players in the pathogenesis of Konzo. Experimental data suggest that thiol-redox and protein-folding mechanisms may also be perturbed. Factors of susceptibility including genetics, poor nutrition, and environmental exposures, or their interaction, have yet to be elucidated. There is no cure for Konzo. Prevention of the disease remains of paramount importance.

Michael J Boivin - One of the best experts on this subject based on the ideXlab platform.

  • Clinical and biological characterization of Konzo forms in children in Kahemba/Democratic Republic of Congo
    Journal of the Neurological Sciences, 2019
    Co-Authors: J. Mbusa Kombi, Michael J Boivin, D Mukeba L Kahemba, J Banea P Mayambu, J. Muyembe Tamfum, D. Mumba Ngoy, D. Tshala Katumbay, D. Okitundu Luwa E. Andjafono
    Abstract:

    Background Clinical and biological characteristics of three forms of Konzo severity are still poorly documented. Objective Identify clinical as well biological and evolutive characteristics of three clinical patterns of Konzo and associated disorders of other organs. Methods A literature review was undertaken in PubMed, Global Science.Org and Google scholar. In addition, data from 213 children including 124 cases and 89 controls from the NIH-DRC Konzo project were used in the retrospective study. Sociodemographic factors, somatic, neurological and neuropsychological assessment data as well as biomarkers of malnutrition and cyanide intoxication were the variables of interest. Results The age of the children was higher in the severe form and lower in the mild form. Konzo disease severity was related to socio-economic distress, malnutrition and micronutrient deficiency (selenium, zinc and copper). Patellar and ankle exaggerated reflexes were more common in mild form thus ankle clonus, speech articulation disorders and Lhermitte sign were more frequent in moderate form. Socio-emotional, visual disorders and ankylosis had high frequency in severe form. Moderate form had shorter enzymatic detoxification rate thus higher urinary thiocyanate levels as well as some neurocognitive performances. Heart rate increased significantly with Konzo severity regardless of age. Frequently, severe form evolved towards mild form and vice versa. Conclusion Characteristics of three Konzo clinical patterns within children suggest different models of adaptation to cyanide intoxication that require in-depth studies.

  • clinical and biological characterization of Konzo forms in children in kahemba democratic republic of congo
    Journal of the Neurological Sciences, 2019
    Co-Authors: Mbusa J Kombi, Michael J Boivin, Tshala D Katumbay, D Mukeba L Kahemba, J Banea P Mayambu, Muyembe J Tamfum, Mumba D Ngoy, Okitundu Luwa D E Andjafono
    Abstract:

    Background Clinical and biological characteristics of three forms of Konzo severity are still poorly documented. Objective Identify clinical as well biological and evolutive characteristics of three clinical patterns of Konzo and associated disorders of other organs. Methods A literature review was undertaken in PubMed, Global Science.Org and Google scholar. In addition, data from 213 children including 124 cases and 89 controls from the NIH-DRC Konzo project were used in the retrospective study. Sociodemographic factors, somatic, neurological and neuropsychological assessment data as well as biomarkers of malnutrition and cyanide intoxication were the variables of interest. Results The age of the children was higher in the severe form and lower in the mild form. Konzo disease severity was related to socio-economic distress, malnutrition and micronutrient deficiency (selenium, zinc and copper). Patellar and ankle exaggerated reflexes were more common in mild form thus ankle clonus, speech articulation disorders and Lhermitte sign were more frequent in moderate form. Socio-emotional, visual disorders and ankylosis had high frequency in severe form. Moderate form had shorter enzymatic detoxification rate thus higher urinary thiocyanate levels as well as some neurocognitive performances. Heart rate increased significantly with Konzo severity regardless of age. Frequently, severe form evolved towards mild form and vice versa. Conclusion Characteristics of three Konzo clinical patterns within children suggest different models of adaptation to cyanide intoxication that require in-depth studies.

  • Konzo a distinct neurological disease associated with food cassava cyanogenic poisoning
    Brain Research Bulletin, 2019
    Co-Authors: Esperance Kashalaabotnes, Michael J Boivin, Daniel Okitundu, Dieudonne Mumba, Desire Tshalakatumbay, Thorkild Tylleskar
    Abstract:

    Abstract Epidemics of neurodegenerative diseases putatively caused by food toxins have been reported in the tropics with no clear understanding of their pathogenetic mechanisms. These diseases include the disease named Konzo that has been well documented in sub-Sahara Africa, mostly among children and women of childbearing age. Outbreaks of Konzo have occurred in the Democratic Republic of Congo, Mozambique, Tanzania, Central African Republic, Angola, Cameroun, and most recently in Zambia. The main clinical picture consists of a symmetrical, permanent and irreversible spastic paraparesis (motor neuron disease) with no signs of sensory or genitourinary impairments. Recently, cognitive impairments and neurodevelopmental delays have been reported among school-aged and very young children. The exact pathogenetic mechanisms of the disease remain unknown. Epidemiological studies consistently show an association between outbreaks of the disease and chronic dietary reliance on insufficiently processed cyanogenic cassava (manioc or tapioca). Biochemical and toxicological studies suggest that the metabolites of linamarin (α-Hydroxyisobutyronitrile β-D-glucopyranoside, the main cassava cyanogen), notably cyanide (mitochondrial toxin), thiocyanate (AMPA chaotropic agent), and cyanate (protein carbamoylating agent) may play an important role in the pathogenesis of Konzo. Experimental data suggest that thiol-redox and protein- folding mechanisms may also be perturbed. Factors of susceptibility including genetics, poor nutrition, poverty and dietary cyanogen exposure, or their interactions have been suggested. Serological studies have ruled out the role of retroviruses such as the human lymphotropic viruses HIV-I/II or HTLV-I/II. Because there is no cure for Konzo, prevention of the disease remains of paramount importance. Prospects for cognitive rehabilitation still need to be explored and tested.

  • Troubles socio-émotionnels de l’enfant en milieu Konzo, un syndrome paralytique de nature épidémique associé à une intoxication cyanhydrique d’origine alimentaire en Afrique sub-saharienne
    The Pan African medical journal, 2018
    Co-Authors: Daniel Okitundu Luwa E-andjafono, Michael J Boivin, Marie Therese Sombo Safi Ayanne, Dieudonne Mumba Ngoyi, Jean Pierre Banea Mayambu, Guy Bumoko Makila-mabe, Jean Jacques Tamfum-muyembe, Daniel Tshala-katumbay
    Abstract:

    Introduction the aim of this study was to describe the socioemotional profile of children living in Konzo-affected areas, an epidemic toxico-nutritional palsy in sub-Saharan Africa.

  • troubles socio emotionnels de l enfant en milieu Konzo un syndrome paralytique de nature epidemique associe a une intoxication cyanhydrique d origine alimentaire en afrique sub saharienne
    The Pan African medical journal, 2018
    Co-Authors: Daniel Okitundu Luwa Eandjafono, Michael J Boivin, Guy Bumoko Makilamabe, Marie Therese Sombo Safi Ayanne, Dieudonne Mumba Ngoyi, Jean Jacques Tamfummuyembe, Jean Pierre Banea Mayambu, Daniel Tshalakatumbay
    Abstract:

    Introduction: the aim of this study was to describe the socioemotional profile of children living in Konzo-affected areas, an epidemic toxico-nutritional palsy in sub-Saharan Africa. Methods: we evaluated the socioemotional profile of 210 children, 123 with Konzo and 87 presumed to be healthy (4-17 years) based on a structured interview conducted with their parents during an epidemioclinic survey of Konzo in Congo-Kinshasa in 2011. Neurocognitive profile was identified by the KABC-II, the BOT-2 and the global neurological symptom index of Konzo. Associative tests were carried out by using chi-square test, logistic regression and, where applicable, generalized linear model, at the significance threshold of 0.05. Results: in general, irritability, physical violence or inhibition with or without sadness were found in 46.0%, 30.2%, 18.7% of children respectively, with an increased risk of Konzo (OR = 2.6; CI95%: 1.4-4.8; p = 0.001). Socioemotional disorder was associated with underweight (OR: 0.49; CI95%: 0.31-0.78; p = 0.002) and with an elevated global neurological symptom index of Konzo (OR: 1.33; CI 95%: 1.1-1.63; p = 0.019); furthermore it exacerbated cognitive impairment in children with Konzo (interaction neurological status-socioemotional disorders D = 6.297; p = 0.013). High cognitive performances were observed in children without Konzo but with socioemotional disorders. The average concentration (standard deviation ± SD) of urinary thiocyanate was higher (554.8 ± 371.6 µmol/l) among children with Konzo associated with socioemotional disorders. Conclusion: children living in Konzo-affected areas have socioemotional disorders. Their psychopathological status and the effect of Konzo on cognition require in-depth studies.

Hans Rosling - One of the best experts on this subject based on the ideXlab platform.

  • geographical and seasonal association between linamarin and cyanide exposure from cassava and the upper motor neurone disease Konzo in former zaire
    Tropical Medicine & International Health, 1997
    Co-Authors: Jean Pierre Baneamayambu, Thorkild Tylleskar, Nahimana Gitebo, Nunga Matadi, Mehari Gebremedhin, Hans Rosling
    Abstract:

    Geographical and seasonal association between linamarin and cyanide exposure from cassava and the upper motor neurone disease Konzo in former Zaire

  • Konzo and ebola in bandundu region of zaire
    The Lancet, 1997
    Co-Authors: M Banea, Thorkild Tylleskar, Hans Rosling
    Abstract:

    Vol 349 • March 1, 1997 621 confirmed that before the outbreaks of Konzo in the dry season, shortcuts were taken in the soaking of cassava because of increased sales, especially in 1992. The outbreak in 1995 was also preceded by such shortcuts, prompted by a sudden build-up of traders in Popokabaka after a military road block had been set up east of the road to Popokabaka; the road was blocked between May 12 and 23, because of an outbreak of Ebola in Kikwit. Similarly, in 1996, there was intensive trading and shortcuts were taken in the soaking of cassava. We found that urine samples from 160 (75%) of 213 randomly selected villagers from the catchment area had urinary thiocyanate concentrations of 300 μmol/L or more, indicating increased high exposure to cyanide. Our findings suggest that intensive trading, shortcuts in the soaking of cassava, and subsequent exposure to cyanide have a causative role in Konzo. We believe that the promotion of safe processing can prevent the disease. The recurrence of Konzo in Popokabaka may reflect an increase in trading close to Kinshasa because of poor road maintenance in Zaire, but the temporal relation of the outbreak and the statements from the population suggest that the road block also contributed to this recurrence. This link between the road block and the outbreak of Konzo constitutes an additional risk of such military action. We question whether such military action against impoverished people threatened by epidemics is at all effective. Medical advisers should defend the basic human rights of these people. Because securing essential medical care, preventive services, and food security can stop diseases such as Ebola, trypanosomiasis, and Konzo, which are all increasing because of the social collapse in Bandundu, the poorest region in Zaire.

  • Konzo an epidemic spastic paraparesis in africa is not associated with antibodies to htlv 1 hiv of hiv gag encoded proteins
    Journal of Acquired Immune Deficiency syndomes and Human Retrovirology, 1996
    Co-Authors: Thorkild Tylleskar, M Banea, Blenda Bottiger, Gunnel Biberfeld, Hans Rosling
    Abstract:

    Konzo, an epidemic spastic paraparesis in Africa, is not associated with antibodies to HTLV-1, HIV of HIV-gag-encoded proteins

  • dietary determinants of a non progressive spastic paraparesis Konzo a case referent study in a high incidence area of zaire
    International Journal of Epidemiology, 1995
    Co-Authors: Thorkild Tylleskar, G Nahimana, M Banea, N Bikangi, L A Persson, Hans Rosling
    Abstract:

    Background. Konzo is an upper motor neuron disease in Africa, characterized by an abrupt onset of a permanent but non-progressive spastic paraparesis. It is named after the local designation in the first report from Zaire. Konzo has been attributed to a metabolic insult from the combined effect of high cyanide and low sulphur intake from several weeks of exclusive consumption of insufficiently processed bitter cassava roots. Methods. The association between insufficient soaking of cassava roots and Konzo is assessed in a matched case-referent study with multivariate conditional logistic regression including 57 case-referent pairs from a rural high incidence community of Zaire. Results. In the multivariate analysis short processing of cassava in the form of only 2 nights soaking yielded an odds ratio of 11.0 (95% confidence interval 1.7-73) when controlling for poverty-related factors and diet. We also show a dose-response relationship for insufficient cassava soaking, both unadjusted and adjusted for potential confounders. Conclusions. This study supports a causal relationship between insufficient processing of bitter cassava and Konzo.

  • Konzo a distinct disease entity with selective upper motor neuron damage
    Journal of Neurology Neurosurgery and Psychiatry, 1993
    Co-Authors: T Tylleskar, W P Howlett, H T Rwiza, S M Aquilonius, E Stalberg, B Linden, A Mandahl, H C Larsen, G R Brubaker, Hans Rosling
    Abstract:

    Two Tanzanian patients with Konzo were severely disabled by a non-progressive spastic paraparesis, since the sudden onset during an epidemic six years earlier. At the time of onset they had a high dietary intake of cyanide from exclusive consumption of insufficiently processed bitter cassava roots. MRI of brain and spinal cord were normal but motor evoked potentials on magnetic brain stimulation were absent, even in the only slightly affected upper limbs. Other neurophysiological investigations were largely normal but the more affected patient had central visual field defects. Konzo is a distinct disease entity with selective type upper motor neuron damage.

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  • soil nutrient adequacy for optimal cassava growth implications on cyanogenic glucoside production a case of Konzo affected mtwara region tanzania
    PLOS ONE, 2019
    Co-Authors: Matema L E Imakumbili, E Semu, J M R Semoka, A Abass, Geoffrey Mkamilo
    Abstract:

    Soils in areas affected by Konzo (a cassava cyanide intoxication paralytic disorder) are predominantly infertile and probably unable to supply cultivated cassava with the nutrients it needs to achieve optimal growth. Soil nutrient supply in these areas could also be influencing cyanogenic glucoside production in cassava, however there is hardly any knowledge on this. An assessment of soil nutrient levels on crop fields in Konzo-affected areas was therefore carried out to determine their adequacy for optimal cassava growth. Konzo-affected Mtwara region of Tanzania, was used as a case study. Whether soil nutrient supply influences cyanogenic glucoside production in cassava cultivated in Konzo-affected areas and how it could be doing this, was additionally investigated. To investigate this, correlations between total hydrogen cyanide (HCN) levels (a measure of cyanogenic glucoside content) in cassava roots and various soil nutrient levels on crops fields were carried out. This was followed by an investigation of relationships between cases of cassava cyanide intoxication and soil nutrient levels on crop fields from which the consumed toxic cassava roots had been harvested. Cases of cassava cyanide intoxication were used as a proxy for high cyanogenic glucoside levels in cassava roots. Logistic regression analysis was used in the latter investigation. Other important non-nutrient soil chemical characteristics, like pH and soil organic carbon, were also included in all analysis performed. The results revealed that most soil nutrients known to have reducing effects on cassava cyanogenic glucosides, like potassium (mean = 0.09 cmol/kg, SD = 0.05 cmol/kg), magnesium (mean = 0.26 cmol/kg, SD = 0.14 cmol/kg) and zinc (mean = 1.34 mg/kg, SD = 0.26 mg/kg) were deficient on several crop fields. The results also showed that cyanogenic glucosides in cassava roots could be increased with the increased supply of sulphur in soils in bitter cassava varieties (rs = 0.593, p = 0.032), and with the increased supply of P in soils in all cassava varieties (rs = 0.486, p = 0.026). The risk of cassava cyanide intoxication occurring (and thus high cyanogenic glucoside levels in cassava) was found to be likely increased by cultivating cassava on soils with high pH (X2 = 8.124, p = 0.004) and high iron (X2 = 5.740, p = 0.017). The study managed to establish that cassava grows under conditions of severe nutrient stress and that soil nutrient supply influences cyanogenic glucoside production in cassava cultivated in Konzo-affected areas of Mtwara region. Despite the multiple soil nutrient deficiencies on crop fields, low soil fertility was however not the only probable cause of increased cyanogenic glucosides in cassava, as high soil nutrient levels were also found to be potential contributors.

  • farmers perceptions on the causes of cassava root bitterness a case of Konzo affected mtwara region tanzania
    PLOS ONE, 2019
    Co-Authors: Matema L E Imakumbili, E Semu, J M R Semoka, A Abass, Geoffrey Mkamilo
    Abstract:

    In areas where Konzo (a cassava cyanide related paralytic disorder) persists, the agronomic factors causing increased cyanogenic glucoside levels in cassava, during periods without water stress, are hardly known. However, through their assessment of cassava root toxicity, using its bitter taste, farmers may have noticed factors unrelated to water stress that additionally influence the cyanogenic glucoside content of cassava cultivated in these areas. Increased cassava root bitterness is often associated with an increase in cyanogenic glucoside levels, making it a good indicator of changes in root cyanogenic glucoside content. Bitter cassava varieties that are preferentially planted by people living in most Konzo-affected areas, are an additional known contributor to high cyanogenic glucosides. It is water stress that further increases the inherent toxicity of the planted bitter cassava varieties. Using Konzo-affected Mtwara region in Tanzania as a case study, a household survey was carried out to identify the overlooked agronomic factors that additionally influence cyanogenic glucoside levels in cassava cultivated in Konzo-affected areas. A total of 120 farmers were interviewed and they mentioned a number of factors unrelated to water stress, as agronomic factors that influenced cassava root bitterness and hence cyanogenic glucoside production in cassava. The mentioned factors included; certain soil characteristics (14.2%), plant age at harvest (7.5%), poor weeding (0.8%), piecemeal harvesting (0.8%), and branch pruning (0.8%). The revealed factors constitute permanent environmental characteristics and crop management practices commonly used by farmers living in Konzo-affected Mtwara region in Tanzania. The revealed factors could be contributing to increased cyanogenic glucoside levels in cassava, during periods without water stress in areas where Konzo persists.

  • soil nutrient adequacy for optimal cassava growth implications on cyanogenic glucoside production a case of Konzo affected mtwara region tanzania
    bioRxiv, 2018
    Co-Authors: Matema L E Imakumbili, E Semu, J M R Semoka, A Abass, Geoffrey Mkamilo
    Abstract:

    Soils in areas affected by Konzo (a cassava cyanide intoxication paralytic disorder) are predominantly infertile and probably unable to supply cassava the nutrients it needs to achieve optimal growth. The soil nutrient levels in these areas, could also be influencing cyanogenic glucoside production in cultivated cassava, however there is hardly any knowledge on this. An assessment of soil nutrient levels on cassava fields in Konzo-affected areas was therefore carried out to determine their adequacy for optimal cassava growth and how this influences cassava cyanogenic glucoside production. Konzo-affected Mtwara region, in Tanzania, was used as a case study area. Correlations between total hydrogen cyanide (HCN) levels in cassava roots and various soil nutrient levels on cassava fields were carried out and relationships between cyanide intoxication and soil nutrient levels on fields from which toxic cassava roots had been harvested were also investigated. The results showed that cassava grows under conditions of severe nutrient stress in the region. Soil nutrients found to be deficient on most fields, like potassium (mean = 0.09, SD = 0.05 cmol/kg), magnesium (mean = 0.26, SD = 0.14 cmol/kg) and zinc (mean = 1.34, SD = 0.26 mg/kg), are known to reduce cyanogenic glucoside levels in cassava roots when adequate in soils. Cyanogenic glucoside levels in cassava roots however increased by high levels soil phosphorous (rs = 0.486, p = 0.026 for all varieties) and sulphur (rs = 0.593, p = 0.032 and rs = 0.714, p = 0.047; for bitter and sweet cassava varieties, respectively) on these soils. The likelihood of cassava cyanide intoxication was also increased on fields with high pH and iron levels. High levels of sulphur and phosphorus, to very high levels of iron occurred on some fields. How soil nutrient supply influences cassava cyanogenic glucoside production in the Konzo-affected areas was established.

  • farmers perceptions on the causes of cassava root bitterness in Konzo affected areas of mtwara region tanzania
    bioRxiv, 2018
    Co-Authors: Matema L E Imakumbili, E Semu, J M R Semoka, A Abass, Geoffrey Mkamilo
    Abstract:

    The agronomic factors influencing increased cyanogenic glucoside levels, particularly in bitter cassava varieties during periods without water stress, in areas where Konzo (a cassava cyanide related paralytic disorder also called spastic paraparesis) persists, are hardly known. However, through their assessment of bitter taste, farmers may have noticed factors unrelated to water stress and variety type that additionally influence cassava root cyanogenic glucoside content in these environments. Bitterness in cassava is usually associated with high cyanogenic glucoside levels. Using some Konzo-affected areas in Mtwara region of Tanzania as a case study, a survey was thus carried out to identify the factors, hitherto overlooked, that may additionally influence cyanogenic glucoside levels in cassava. A total of 120 farmers were interviewed. A number of factors unrelated to water stress and variety type that could be additionally influencing cyanogenic glucoside production in cassava plants were mentioned. The mentioned factors included nutrient poor soils, plant age at harvest, weeds, piecemeal harvesting, and branch pruning; the factors, respectively, constituted 14.2%, 7.5%, 0.8%, 0.8%, and 0.8% of the total responses given. The revealed factors constitute permanent environmental characteristics and commonly used crop management practices by farmers living in Konzo-prone Mtwara region of Tanzania that could be additionally resulting in high cyanogenic glucoside levels in cassava, regardless of water stress.

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