BRUCELLOSIS IN TEREKEKA COUNTY, CENTRAL EQUATORIA STATE, SOUTHERN SUDAN.

OBJECTIVES To identify factors associated with Brucellosis in patients attending Terekeka Health Facility, Terekeka County, Central Equatoria State, Southern Sudan and to evaluate the utility of the rapid test kit Euracil®. DESIGN A facility based case-control study. SETTING Terekeka Health Facility, Terekeka County, Central Equatoria State, Southern Sudan. SUBJECTS Cases were patients presenting at the Terekeka Health Facility with clinical symptoms suggestive of Brucellosis and tested positive for Brucellosis by rapid antigen test while controls were selected from individuals attending Terekeka Health facility with health problems unrelated to brucellosis or febrile illness. RESULTS A total of fifty eight cases with clinical symptoms suggestive of and tested positive for Brucellosis by rapid antigen test presented. A total of 116 consented controls were recruited into the study. Males accounted for 52% of the cases and 53% of the controls. The mean age was 31 years for both groups. Cases without formal education were 84% while 40% had no source of income, 20% of the cases and 14% of the controls were cattle keepers while 5% of the cases and 13% of the controls were students. In multivariate analysis there were many factors associated with Brucellosis like consumption of raw meat, living with animals at the same place, raising of goats, farm cleaning contact, eating of aborted and wild animals. Logistic regression revealed two factors associated with the disease; consumption of raw milk (OR=3.9, P-value 0.001, 95% CI 1.6666-9.0700) was a risk factor while drinking boiled milk was protective (OR = 0.09, p-value 0.000, 95% CI, 0.1-0.2). CONCLUSIONS The main age-groups affected were 20-30 years with males being affected more than females. Drinking of raw milk was significantly associated with Brucellosis while drinking boiled milk was protective. There should be active public health education on the benefits of boiling milk before consumption. Further studies to elucidate the extent and epidemiology of brucellosis in humans and animals in Southern Sudan are recommended.

[1]  C. Rooryck,et al.  Genetic basis of oculocutaneous albinism , 2009 .

[2]  S. Courrier,et al.  A novel mutation (delAACT) in the tyrosinase gene in a Cameroonian black with type 1A oculocutaneous albinism. , 2006, Journal of dermatological science.

[3]  Georgios Pappas,et al.  The new global map of human brucellosis. , 2006, The Lancet. Infectious diseases.

[4]  H. Shimizu,et al.  Oculocutaneous albinism type 4 is one of the most common types of albinism in Japan. , 2004, American journal of human genetics.

[5]  C. Summers,et al.  Tyrosinase gene mutations in oculocutaneous albinism 1 (OCA1): definition of the phenotype , 2003, Human Genetics.

[6]  M. Refai Incidence and control of brucellosis in the Near East region. , 2002, Veterinary microbiology.

[7]  M. Ramsay,et al.  Identification of P gene mutations in individuals with oculocutaneous albinism in sub‐Saharan Africa , 2000, Human mutation.

[8]  L. Wang,et al.  [Study on the characteristics of brucellosis on the Baicaopo Pasture]. , 1998, Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi.

[9]  J. Bothwell Pigmented skin lesions in tyrosinase‐positive oculocutaneous albinos: a study in black South Africans , 1997, International journal of dermatology.

[10]  M. Ramsay,et al.  Rufous oculocutaneous albinism in southern African Blacks is caused by mutations in the TYRP1 gene. , 1997, American journal of human genetics.

[11]  P. Lund Distribution of oculocutaneous albinism in Zimbabwe. , 1996, Journal of medical genetics.

[12]  M. Ramsay,et al.  An intragenic deletion of the P gene is the common mutation causing tyrosinase-positive oculocutaneous albinism in southern African Negroids. , 1995, American journal of human genetics.

[13]  S. Kidson,et al.  An ultrastructural study of melanocytes and melanosomes in the skin and hair bulbs of rufous albinos. , 1993, Pigment cell research.

[14]  M. Farrall,et al.  The tyrosinase-positive oculocutaneous albinism locus maps to chromosome 15q11.2-q12. , 1992, American journal of human genetics.

[15]  U. Francke,et al.  Homozygous tyrosinase gene mutation in an American black with tyrosinase-negative (type IA) oculocutaneous albinism. , 1991, American journal of human genetics.

[16]  R. Aquaron Oculocutaneous albinism in Cameroon. A 15-year follow-up study. , 1990, Ophthalmic paediatrics and genetics.

[17]  T. Jenkins,et al.  Albinism and skin cancer in Southern Africa , 1989, Clinical genetics.

[18]  T. Jenkins,et al.  The Response of Black Mothers to the [ill]irth of an Albino Infant , 1987 .

[19]  R. Lewis,et al.  Brown Ocuuiocutaneous Albinism: Clinical, Ophthalmological, and Biochemical Characterization , 1985 .

[20]  T. Jenkins,et al.  Prevalence of albinism in the South African negro. , 1982, South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde.

[21]  H. Stannus ANOMALIES OF PIGMENTATION AMONG NATIVES OF NYASALAND.A CONTRIBUTION TO THE STUDY OF ALBINISM , 1913 .

[22]  T. Jenkins,et al.  Cultural Influences on the Perception of Genetic Disorders in the Black Population of Southern Africa , 1997 .

[23]  W. Oetting,et al.  Molecular basis of type I (tryrosinase‐related) oculocutaneous albinism: Mutations and polymorphisms of the human tyrosinase gene , 1993 .

[24]  C. Magos,et al.  [Seroepidemiology of brucellosis in Mexico]. , 1992, Salud publica de Mexico.

[25]  J. I. Phillips,et al.  Red or rufous albinism in southern Africa. , 1990, Ophthalmic paediatrics and genetics.

[26]  A. Okoro Albinism in Nigeria. A clinical and social study. , 1975, The British journal of dermatology.