Observations on the epidemiology of lumpy skin disease in Kenya.

Lumpy skin disease virus strains isolated in Kenya over a period of some 20 years have proved to be serologically identical. They were indistinguishable by indirect fluorescent antibody and serum neutralization test from the South African Neethling and West African serotypes. These two serological methods proved of value in studying the antibody responses to infection. While epizootic spread of LSD has occurred in Kenya, most cases are of a sporadic nature and are thought to be the result of accidental contacts with a maintenance cycle. There is evidence of antibody to LSD in the African buffalo (Syncerus caffer) in those areas where LSD is considered to be enzootic in Kenya, and also in small numbers of domestic cattle. No buffalo or bovine sera contained antibody to cowpox virus. An area enzootic for LSD is proposed and it is suggested that the maintenance cycle involves the buffalo. No antibody was found in the other wild ruminant species examined.     

Contraception and sickle cell disease

Although women with sickle cell disease have been found to have a delay in puberty of 2.3 years, there is no evidence that they are less fertile than women without hemoglobinopathy. Women with sickle cell disease therefore need adequate family planning advice to prevent unwanted pregnancy. The need for good and comprehensive advice is particularly important given the association among these women between pregnancy and increased maternal and fetal mortality and morbidity rates. Moreover, unwanted pregnancy rates among women with sickle cell disease have been reported as being in the range of 38-64%, and one study found that only 33% of a group of women with sickle cell disease used any form of contraception compared to 66% in a control group. Sickle cell disease is listed in the manufacturers' data sheets in the UK as a contraindication to the use of the majority of combined oral contraceptive pills, but there is little good evidence to support this restriction. In fact, women with the sickle cell trait have no particular added risks and can be offered the usual range of contraceptive methods. Evidence that the use of injectable progestagens may reduce the risk of crises, however, suggests that they should be recommended as a first option of contraception for these women. Good evidence exists that the injectables are safe and effective for women with sickle cell disease despite the adverse publicity which they have received. The IUD appears to be safe as are the common barrier methods, while the combined oral contraceptive pill is a convenient, effective, and reliable form of contraception which should continue to be prescribed for these women, albeit with caution.     

Osteoarticular manifestations of sickle cell disease

Sickle cell disease is a genetic chronic anemia caused by existence of abnormal haemoglobin. Osteo articular manifestations are often observed in the evolution of the disease, and in some cases, they inaugur the disease. Authors discuss physio-pathological mechanisms and describe main osteoarticular signs of sickle cell disease.     

Homocysteine elevation in sickle cell disease

OBJECTIVE: Ischemic complications are common in patients with sickle cell disease. Hyperhomocysteinemia is a risk factor for arteriosclerosis and venous thrombosis, and given the propensity of patients with sickle cell disease to develop ischemic complications, we hypothesized that they might have elevated plasma homocysteine concentrations. METHODS: Plasma concentrations of homocysteine, vitamin B12 and folate were measured in 49 adults with sickle cell disease and 16 normotensive Black controls. All subjects with sickle cell disease had been prescribed folic acid 1 mg by mouth daily. RESULTS: The median plasma concentration of homocysteine of subjects with sickle cell disease was approximately 1.5-fold higher than that of controls (p=0.0008). This difference persisted, even when subjects with renal insufficiency were excluded. Plasma folate levels were 1.5-fold higher in subjects with sickle cell disease than in controls (p=0.0498). There was no significant difference in plasma vitamin B12 concentrations between the two groups. There was no difference in plasma homocysteine concentrations between transfused and non-transfused sickle cell subjects. CONCLUSIONS: Patients with sickle cell disease have elevated plasma concentrations of homocysteine in spite of elevated plasma folate levels and vitamin B12 concentrations similar to those observed in controls. Based on these data, we hypothesize that the concentration of folate required to normalize plasma homocysteine levels in patients with sickle cell disease may be higher than that of normal controls and that patients with sickle cell disease have a higher nutritional requirement for folic acid than the general population.     

Cephalosporin-resistant pneumococci and sickle cell disease

Sickle cell anemia patients have 600 times the risk for invasive pneumococcal disease than their healthy peers. High-level cephalosporin resistance was described in the 1990s in healthy children from Tennessee, but its prevalence in sickle cell disease patients is unknown. Pneumococcal isolates from sickle cell disease patients from Tennessee were subjected to multilocus sequence typing to characterize antimicrobial drug-resistant strains. Twenty-one percent of strains were resistant to cefotaxime and penicillin. Of the 14 cephalosporin-resistant strains, 9 were sequence types previously described as highly cephalosporin resistant, while resistance was found for the first time in 3 clones: Maryland6B, ST660, and a novel clone, ST1753. High-level cephalosporin resistance exists in more settings than initially recognized, and its high prevalence in sickle cell disease patients may decrease the efficacy of third-generation cephalosporins in invasive pneumococcal disease.     

Human genome project and sickle cell disease

Sickle cell disease is one of the most common genetic blood disorders in the United States that affects 1 in every 375 African Americans. Sickle cell disease is an inherited condition caused by abnormal hemoglobin in the red blood cells. The Human Genome Project has provided valuable insight and extensive research advances in the understanding of the human genome and sickle cell disease. Significant progress in genetic knowledge has led to an increase in the ability for researchers to map and sequence genes for diagnosis, treatment, and prevention of sickle cell disease and other chronic illnesses. This article explores some of the recent knowledge and advances about sickle cell disease and the Human Genome Project.     

Acute chest syndrome in sickle cell disease

Acute chest syndrome (ACS) is a leading complication of sickle cell disease (SCD) with significant morbidity and mortality. ACS is the most common cause of death and the second most common cause of hospitalization in patients with SCD. Delineating the specific cause of ACS is often difficult, and multiple risk factors that precipitate ACS frequently coexist. The prominent risk factors include infection, hypoxia, bronchial hyperresponsiveness, the SCD genotype, and opioid use. The key to the successful treatment of ACS is early recognition and initiation of treatment without delay. The main goal is to prevent and treat acute respiratory failure and, thus, minimize irreversible lung damage. This review focuses on the risk factors, pathogenesis, clinical presentation, and management of ACS.     

Observations on the epidemiology of ephemeral fever in Kenya

Ephemeral fever antibody was found in domestic cattle in Kenya across a wide range of ecological zones, from highland forests and grasslands to desert and semidesert thorn scrub. Antibody was found in several species of game animals, notably waterbuck and buffalo, where over 50% of the samples showed antibody to EF. Evidence was obtained to show that the virus had been cycling in these wild ruminant populations between epizootics in domestic cattle.     

Iron status of children with sickle cell disease

BACKGROUND: Dietary iron requirements are unclear in children with SS-type sickle cell disease. METHODS: Iron status was assessed in 104 nontransfused African American children (aged 0.5 to 17.6 years) with sickle cell disease who receive no iron supplement. Dietary iron intake was not measured at the time of this study. RESULTS: Serum ferritin was normal or high in all children. Other hematologic and biochemical indicators of iron deficiency were in the normal range in most children. CONCLUSIONS: Unlike previous studies, this sample of children and adolescents did not show signs of iron deficiency.