Bio

PROF. KABIRA WANJIKU M.

Personal Information

Publications


2018

Kabira, WM.  2018.  Changing the Mainstream Celebrating Women’s Resilience. Changing the Mainstream Celebrating Women’s Resilience.

2016

Kabira, WM.  2016.  So Near yet so far. . American Journal of Arts and Humanities, 1, A1-A11.

2015

Kabira, WM.  2015.  Rural Women’s Perspectives on Marriage and Related Issues: Analysis of Personal Narratives from Kenyan Women. Path ways to African Feminism and Development, Journal of the African Women Studies Centre, University of Nairobi.
Kabira, WM.  2015.  Why hearing the Voices of Kenyan Women is Important for a More Just Future. . The Conversation-Africa Pilot (https://theconversation.com/why-hearing-the-voices-of-kenyan-women-is-important-for-a-more-just-future-47638).
Kabira, WM.  2015.  Creating Women’s Knowledge: A Case Study of Three African Women Writers. Eastern African Literary and Cultural Studies, Routledge Taylor & Francis Group .

2014

Kabira, WM.  2014.  Food Security Score for Kenya, Pathways to African Feminism and Development. Journal of the African Women Studies Centre, University of Nairobi.
Kabira, WM.  2014.  Validating Women’s Knowledge and Experiences. Pathways to African Feminism and Development ,Journal of the African Women’s Studies Centre, University of Nairobi..
Kabira, WM.  2014.  Food Security Score for Kenya, Pathways to African Feminism and Development. Journal of the African Women Studies Centre, University of Nairobi.

2013

  2013.  Our Second Homecoming: Voices from African Women. The Nairobi Journal of Literature, Journal of the Department of Literature University of Nairobi..
Kabira, WM.  2013.  Women’s Experiences as Sources of Public and Legitimate Knowledge: Constitution Making in Kenya. Pathwaysto African Feminism and Development, Journal of the African Women Studies CentreUniversity of Nairobi..

2012

2010

Kabira, WM.  2010.  “A Time of Harvest: Women and Constitution Making in Kenya-1992-2010” . University of Nairobi Press.
and Njogu, KWMW.  2010.  “Reclaiming my Dreams: Oral Narratives,” by W.M. Kabira and W. Njogu,. University of Nairobi Press.

2007

2005

Kabira, WM.  2005.  “Letter to Mariama Ba,” by W.M. Kabira, . University of Nairobi Press .

2004

2001

1999

M., PROFKABIRAWANJIKU.  1999.  Reclaiming Women. East African Medical Journal 68(9): 714-9. : AIDS 24(6):891-7 Abstract
Department of Infectious Disease Epidemiology, Imperial College School of Medicine, London, UK. Previous attempts to determine the interactions between filariasis transmission intensity, infection and chronic disease have been limited by a lack of a theoretical framework that allows the explicit examination of mechanisms that may link these variables at the community level. Here, we show how deterministic mathematical models, in conjunction with analyses of standardized field data from communities with varying parasite transmission intensities, can provide a particularly powerful framework for investigating this topic. These models were based on adult worm population dynamics, worm initiated chronic disease and two major forms of acquired immunity (larval- versus adult-worm generated) explicitly linked to community transmission intensity as measured by the Annual Transmission Potential (ATP). They were then fitted to data from low, moderate and moderately high transmission communities from East Africa to determine the mechanistic relationships between transmission, infection and observed filarial morbidity. The results indicate a profound effect of transmission intensity on patent infection and chronic disease, and on the generation and impact of immunity on these variables. For infection, the analysis indicates that in areas of higher parasite transmission, community-specific microfilarial rates may increase proportionately with transmission intensity until moderated by the generation of herd immunity. This supports recent suggestions that acquired immunity in filariasis is transmission driven and may be significant only in areas of high transmission. In East Africa, this transmission threshold is likely to be higher than an ATP of at least 100. A new finding from the analysis of the disease data is that per capita worm pathogenicity could increase with transmission intensity such that the prevalences of both hydrocele and lymphoedema, even without immunopathological involvement, may increase disproportionately with transmission intensity. For lymphoedema, this rise may be further accelerated with the onset of immunopathology. An intriguing finding is that there may be at least two types of immunity operating in filariasis: one implicated in anti-infection immunity and generated by past experience of adult worms, the other involved in immune-mediated pathology and based on cumulative experience of infective larvae. If confirmed, these findings have important implications for the new global initiative to achieve control of this disease.
M., PROFKABIRAWANJIKU.  1999.  Our Mothers Footsteps Ed. Wanjiku Kabira and Patricia Ngurukie CCGD. East African Medical Journal 68(9): 714-9. : AIDS 24(6):891-7 Abstract
Department of Infectious Disease Epidemiology, Imperial College School of Medicine, London, UK. Previous attempts to determine the interactions between filariasis transmission intensity, infection and chronic disease have been limited by a lack of a theoretical framework that allows the explicit examination of mechanisms that may link these variables at the community level. Here, we show how deterministic mathematical models, in conjunction with analyses of standardized field data from communities with varying parasite transmission intensities, can provide a particularly powerful framework for investigating this topic. These models were based on adult worm population dynamics, worm initiated chronic disease and two major forms of acquired immunity (larval- versus adult-worm generated) explicitly linked to community transmission intensity as measured by the Annual Transmission Potential (ATP). They were then fitted to data from low, moderate and moderately high transmission communities from East Africa to determine the mechanistic relationships between transmission, infection and observed filarial morbidity. The results indicate a profound effect of transmission intensity on patent infection and chronic disease, and on the generation and impact of immunity on these variables. For infection, the analysis indicates that in areas of higher parasite transmission, community-specific microfilarial rates may increase proportionately with transmission intensity until moderated by the generation of herd immunity. This supports recent suggestions that acquired immunity in filariasis is transmission driven and may be significant only in areas of high transmission. In East Africa, this transmission threshold is likely to be higher than an ATP of at least 100. A new finding from the analysis of the disease data is that per capita worm pathogenicity could increase with transmission intensity such that the prevalences of both hydrocele and lymphoedema, even without immunopathological involvement, may increase disproportionately with transmission intensity. For lymphoedema, this rise may be further accelerated with the onset of immunopathology. An intriguing finding is that there may be at least two types of immunity operating in filariasis: one implicated in anti-infection immunity and generated by past experience of adult worms, the other involved in immune-mediated pathology and based on cumulative experience of infective larvae. If confirmed, these findings have important implications for the new global initiative to achieve control of this disease.
M., PROFKABIRAWANJIKU.  1999.  Our Secret Lives - Kabira Wanjiku and Akinyi Nzioki, Phoenix Publishers. East African Medical Journal 68(9): 714-9. : AIDS 24(6):891-7 Abstract
Department of Infectious Disease Epidemiology, Imperial College School of Medicine, London, UK. Previous attempts to determine the interactions between filariasis transmission intensity, infection and chronic disease have been limited by a lack of a theoretical framework that allows the explicit examination of mechanisms that may link these variables at the community level. Here, we show how deterministic mathematical models, in conjunction with analyses of standardized field data from communities with varying parasite transmission intensities, can provide a particularly powerful framework for investigating this topic. These models were based on adult worm population dynamics, worm initiated chronic disease and two major forms of acquired immunity (larval- versus adult-worm generated) explicitly linked to community transmission intensity as measured by the Annual Transmission Potential (ATP). They were then fitted to data from low, moderate and moderately high transmission communities from East Africa to determine the mechanistic relationships between transmission, infection and observed filarial morbidity. The results indicate a profound effect of transmission intensity on patent infection and chronic disease, and on the generation and impact of immunity on these variables. For infection, the analysis indicates that in areas of higher parasite transmission, community-specific microfilarial rates may increase proportionately with transmission intensity until moderated by the generation of herd immunity. This supports recent suggestions that acquired immunity in filariasis is transmission driven and may be significant only in areas of high transmission. In East Africa, this transmission threshold is likely to be higher than an ATP of at least 100. A new finding from the analysis of the disease data is that per capita worm pathogenicity could increase with transmission intensity such that the prevalences of both hydrocele and lymphoedema, even without immunopathological involvement, may increase disproportionately with transmission intensity. For lymphoedema, this rise may be further accelerated with the onset of immunopathology. An intriguing finding is that there may be at least two types of immunity operating in filariasis: one implicated in anti-infection immunity and generated by past experience of adult worms, the other involved in immune-mediated pathology and based on cumulative experience of infective larvae. If confirmed, these findings have important implications for the new global initiative to achieve control of this disease.
M., PROFKABIRAWANJIKU.  1999.  Affirmative Action . East African Medical Journal 68(9): 714-9. : AIDS 24(6):891-7 Abstract
Department of Infectious Disease Epidemiology, Imperial College School of Medicine, London, UK. Previous attempts to determine the interactions between filariasis transmission intensity, infection and chronic disease have been limited by a lack of a theoretical framework that allows the explicit examination of mechanisms that may link these variables at the community level. Here, we show how deterministic mathematical models, in conjunction with analyses of standardized field data from communities with varying parasite transmission intensities, can provide a particularly powerful framework for investigating this topic. These models were based on adult worm population dynamics, worm initiated chronic disease and two major forms of acquired immunity (larval- versus adult-worm generated) explicitly linked to community transmission intensity as measured by the Annual Transmission Potential (ATP). They were then fitted to data from low, moderate and moderately high transmission communities from East Africa to determine the mechanistic relationships between transmission, infection and observed filarial morbidity. The results indicate a profound effect of transmission intensity on patent infection and chronic disease, and on the generation and impact of immunity on these variables. For infection, the analysis indicates that in areas of higher parasite transmission, community-specific microfilarial rates may increase proportionately with transmission intensity until moderated by the generation of herd immunity. This supports recent suggestions that acquired immunity in filariasis is transmission driven and may be significant only in areas of high transmission. In East Africa, this transmission threshold is likely to be higher than an ATP of at least 100. A new finding from the analysis of the disease data is that per capita worm pathogenicity could increase with transmission intensity such that the prevalences of both hydrocele and lymphoedema, even without immunopathological involvement, may increase disproportionately with transmission intensity. For lymphoedema, this rise may be further accelerated with the onset of immunopathology. An intriguing finding is that there may be at least two types of immunity operating in filariasis: one implicated in anti-infection immunity and generated by past experience of adult worms, the other involved in immune-mediated pathology and based on cumulative experience of infective larvae. If confirmed, these findings have important implications for the new global initiative to achieve control of this disease.

1998

Kabira, WM, Wasamba P.  1998.  Reclaiming women's space in politics. Website
M., PROFKABIRAWANJIKU.  1998.  Contesting Social Death, KOLA Publications Ed. Kabira, Masheti and Obote, KOLA Publications. East African Medical Journal 68(9): 714-9. : AIDS 24(6):891-7 Abstract
Department of Infectious Disease Epidemiology, Imperial College School of Medicine, London, UK. Previous attempts to determine the interactions between filariasis transmission intensity, infection and chronic disease have been limited by a lack of a theoretical framework that allows the explicit examination of mechanisms that may link these variables at the community level. Here, we show how deterministic mathematical models, in conjunction with analyses of standardized field data from communities with varying parasite transmission intensities, can provide a particularly powerful framework for investigating this topic. These models were based on adult worm population dynamics, worm initiated chronic disease and two major forms of acquired immunity (larval- versus adult-worm generated) explicitly linked to community transmission intensity as measured by the Annual Transmission Potential (ATP). They were then fitted to data from low, moderate and moderately high transmission communities from East Africa to determine the mechanistic relationships between transmission, infection and observed filarial morbidity. The results indicate a profound effect of transmission intensity on patent infection and chronic disease, and on the generation and impact of immunity on these variables. For infection, the analysis indicates that in areas of higher parasite transmission, community-specific microfilarial rates may increase proportionately with transmission intensity until moderated by the generation of herd immunity. This supports recent suggestions that acquired immunity in filariasis is transmission driven and may be significant only in areas of high transmission. In East Africa, this transmission threshold is likely to be higher than an ATP of at least 100. A new finding from the analysis of the disease data is that per capita worm pathogenicity could increase with transmission intensity such that the prevalences of both hydrocele and lymphoedema, even without immunopathological involvement, may increase disproportionately with transmission intensity. For lymphoedema, this rise may be further accelerated with the onset of immunopathology. An intriguing finding is that there may be at least two types of immunity operating in filariasis: one implicated in anti-infection immunity and generated by past experience of adult worms, the other involved in immune-mediated pathology and based on cumulative experience of infective larvae. If confirmed, these findings have important implications for the new global initiative to achieve control of this disease.
M., PROFKABIRAWANJIKU.  1998.  Understanding Oral Literature, Ed. Kabira, Masheti and Obote; University of Nairobi Press. East African Medical Journal 68(9): 714-9. : AIDS 24(6):891-7 Abstract
Department of Infectious Disease Epidemiology, Imperial College School of Medicine, London, UK. Previous attempts to determine the interactions between filariasis transmission intensity, infection and chronic disease have been limited by a lack of a theoretical framework that allows the explicit examination of mechanisms that may link these variables at the community level. Here, we show how deterministic mathematical models, in conjunction with analyses of standardized field data from communities with varying parasite transmission intensities, can provide a particularly powerful framework for investigating this topic. These models were based on adult worm population dynamics, worm initiated chronic disease and two major forms of acquired immunity (larval- versus adult-worm generated) explicitly linked to community transmission intensity as measured by the Annual Transmission Potential (ATP). They were then fitted to data from low, moderate and moderately high transmission communities from East Africa to determine the mechanistic relationships between transmission, infection and observed filarial morbidity. The results indicate a profound effect of transmission intensity on patent infection and chronic disease, and on the generation and impact of immunity on these variables. For infection, the analysis indicates that in areas of higher parasite transmission, community-specific microfilarial rates may increase proportionately with transmission intensity until moderated by the generation of herd immunity. This supports recent suggestions that acquired immunity in filariasis is transmission driven and may be significant only in areas of high transmission. In East Africa, this transmission threshold is likely to be higher than an ATP of at least 100. A new finding from the analysis of the disease data is that per capita worm pathogenicity could increase with transmission intensity such that the prevalences of both hydrocele and lymphoedema, even without immunopathological involvement, may increase disproportionately with transmission intensity. For lymphoedema, this rise may be further accelerated with the onset of immunopathology. An intriguing finding is that there may be at least two types of immunity operating in filariasis: one implicated in anti-infection immunity and generated by past experience of adult worms, the other involved in immune-mediated pathology and based on cumulative experience of infective larvae. If confirmed, these findings have important implications for the new global initiative to achieve control of this disease.

1997

Kabira, WM; Gachukia, EW; MFO.  1997.  The effect of women's role on health: The paradox . Website
Kabira, WM.  1997.  The oral artist. Website

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