Ebere C. Anyanwu

Critical control points of complementary food preparation and handling in eastern Nigeria

OBJECTIVE To investigate microbial contamination and critical control points (CCPs) in the preparation and handling of complementary foods in 120 households in Imo state, Nigeria. METHODS The Hazard Analysis Critical Control Point (HACCP) approach was used to investigate processes and procedures that contributed to microbial contamination, growth and survival, and to identify points where controls could be applied to prevent or eliminate these microbiological hazards or reduce them to acceptable levels. Food samples were collected and tested microbiologically at different stages of preparation and handling. FINDINGS During cooking, all foods attained temperatures capable of destroying vegetative forms of food-borne pathogens. However, the risk of contamination increased by storage of food at ambient temperature, by using insufficiently high temperatures to reheat the food, and by adding contaminated ingredients such as dried ground crayfish and soybean powder at stages where no further heat treatment was applied. The purchasing of contaminated raw foodstuffs and ingredients, particularly raw akamu, from vendors in open markets is also a CCP. CONCLUSION Although an unsafe environment poses many hazards for childrens food, the hygienic quality of prepared food can be assured if basic food safety principles are observed. When many factors contribute to food contamination, identification of CCPs becomes particularly important and can facilitate appropriate targeting of resources and prevention efforts.

Neurophysiological Effects of Chronic Indoor Environmental Toxic Mold Exposure on Children

The phenomenon of building-related diseases is attracting much research interest in recent years because of the extent to which it affects people with compromised immune systems, especially children. In this study, we reported the neurological findings in children who attended our Center because of chronic exposure to toxic molds. Clinical neurological and neurobehavioral questionnaires were administered with the cooperation of the childrens parents. The children then underwent a series of neurophysiological tests including electroencephalogram (EEG), brainstem evoked potential (BAEP), visual evoked potential (VEP), and somatosensory evoked potential (SSEP). The results showed high levels of abnormalities in the analysis of the subjective responses derived from the questionnaires. The EEG examination was abnormal in seven out of ten of the patients compared to the controls with only one in ten with episodes of bihemispheric sharp activity. In all the patients, there was frontotemporal theta wave ativity that seemed to indicate diffuse changes characteristic of metabolic encephalopathies. Also, there was highly marked 1 to 3 Hz delta activity that was asymmetrical in the right hemisphere of the brain in three out of ten patients. The waveforms of BAEP showed abnormalities in 90% of the patients with both 15’ and 31’ check sizes compared to none in the controls. There were significant delays in waveform V in a majority of the patients representing dysfunctional cognitive process and conductive hearing loss in both ears. VEP showed clear abnormalities in four in ten of the patients with P100 amplitudes and latencies decreased bilaterally. In all the patients, there was slowing of conduction in the right tibial at an average of 36.9 ms and there was significant decrease in amplitude of response at the proximal stimulation site. Sensory latencies obtained in the median, ulnar, and sural nerves bilaterally showed abnormalities in five out of ten compared to none in the controls. The median, ulnar, and sural sensory potentials were abnormal in six out of ten patients. There was prolongation of the median distal sensory latencies bilaterally at an average of 4.55 ms on the right and an average of 6.10 ms on the left as compared to the ulnars of 2.55 ms bilaterally. There was no abnormality in the controls. These findings represent evidence of diffuse polyneuropathy to which three patients demonstrated borderline slow motor conduction at an average of 41.1 ms. Overall, the objective neurophysiological measurements (EEG, BAEP, VEP, and SSEP) were abnormal, indicating significant neurological deficits in all the patients. Our findings revealed the extent to which toxic molds can affect the neurological and behavioral status of children. Further work should be encouraged in this regard.

Neurochemical changes in the aging process: implications in medication in the elderly.

Aging is an inevitable process in human development, which follows a time course thatcan be delayed, or hastened, by lifestyles, diseases and events. The factors that affectthe aging process can be delayed, but not prevented. This paper evaluates theneurochemical changes in the aging process and their relevance in the modality ofelderly medication. For clarity and understanding of the relevant neurobiochemicalprocess and effects, the neuroanatomical, physiological, and neurobehavioral changesare reviewed as they relate to medication in the elderly.

Evaluation of the Drug Treatment and Persistence of Onychomycosis

Onychomycosis is a common nail disease responsible for approximately 50% of diseases of the nail. It occurs more in the elderly, though several cases have been reported among children. Several factors influence, such as climate, geography, and migration. The two dermatophytes most commonly implicated in onychomycosis are Trichophyton rubrum and T. mentagrophytes, accounting for more than 90% of onychomycoses. Nonetheless, several other toxigenic molds have been implicated. For convenience, onychomycosis is divided into four major clinical presentations: distal subungal, which is the most common form of the disease; proximal subungal, which is the most common form found in patients with human immunodeficiency virus infection; superficial; and total dystrophic onychomycosis. Epidemiology of onychomycosis in adults and children is evaluated and the most common clinical symptoms addressed. Although the risk factors are discussed, the multifactorial nature of onychomycosis makes this inexhaustible. The diagnosis and treatments are difficult and the choice of appropriate antifungal drugs complex and require the knowledge of the chemical structures of the metabolites of the molds that cause onychomycosis and their interaction with the antifungal drugs. This is true because most of the antifungal drugs are derived from mold/fungal metabolism. Treatment with griseofulvin and amphotericin is displaced by the use of newer drugs from azole compounds, pyrimidines, and allylamines derivatives. Amorolfine, itraconazole, and ciclopirox nail lacquer solution 8 have gained support globally, but the side effects, drug resistance, and persistence of the disease are still a serious concern to the patients, just as economics and quality of life. Hence, the search for safer and more efficacious drug treatments are continuing.

The Neurological Significance of Abnormal Natural Killer Cell Activity in Chronic Toxigenic Mold Exposures

Toxigenic mold activities produce metabolites that are either broad-spectrum antibiotics or mycotoxins that are cytotoxic. Indoor environmental exposure to these toxigenic molds leads to adverse health conditions with the main outcome measure of frequent neuroimmunologic and behavioral consequences. One of the immune system disorders found in patients presenting with toxigenic mold exposure is an abnormal natural killer cell activity. This paper presents an overview of the neurological significance of abnormal natural killer cell (NKC) activity in chronic toxigenic mold exposure. A comprehensive review of the literature was carried out to evaluate and assess the conditions under which the immune system could be dysfunctionally interfered with leading to abnormal NKC activity and the involvement of mycotoxins in these processes. The functions, mechanism, the factors that influence NKC activities, and the roles of mycotoxins in NKCs were cited wherever necessary. The major presentations are headache, general debilitating pains, nose bleeding, fevers with body temperatures up to 40° C (104°F), cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, vertigo/dizziness, and in some cases, seizures. Although sleep is commonly considered a restorative process that is important for the proper functioning of the immune system, it could be disturbed by mycotoxins. Most likely, mycotoxins exert some rigorous effects on the circadian rhythmic processes resulting in sleep deprivation to which an acute and transient increase in NKC activity is observed. Depression, psychological stress, tissue injuries, malignancies, carcinogenesis, chronic fatigue syndrome, and experimental allergic encephalomyelitis could be induced at very low physiological concentrations by mycotoxin-induced NKC activity. In the light of this review, it is concluded that chronic exposures to toxigenic mold could lead to abnormal NKC activity with a wide range of neurological consequences, some of which were headache, general debilitating pains, fever, cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, and seizures.

Photosensitive epilepsy beyond adolescence: is freedom from photosensitivity age-dependent?

Patients with photosensitive epilepsy (PSE) are said to lose photosensitivity with age. That is, they do not suffer from photosensitive epileptic seizures after the third decade of life. This claim seems to be an over generalised statement and does not take into account all other important confounding factors that determine the duration and process of neurological illnesses. Hence, there are contradictions pertaining to age of freedom of photosensitivity in epilepsy and in epilepsy with photosensitivity. Often patients are declared free from epileptic activity; however, some of these patients are still found to have seizures a few years later. This paper assesses the freedom photosensitivity in 58 PSE patients to ascertain validity of the claim that patients lose their photosensitivity with age. Thirty-nine of the 58 patients (67%) were female whilst (33%) were male, giving a female/male ratio of 3:1. The average age of onset of photosensitivity was 7 years. Of all the cases studied forty-one (71%) had a family history of photosensitive epilepsy, while seventeen (29%) had no family history of photosensitive epilepsy. Proof of photosensitivity in all the patients was determined by persistent EEG abnormalities including occipital spike and wave discharges. Results show that photosensitivity persisted beyond adolescence; hence, there was no specific age limit of freedom from photosensitivity in patients, especially in those with family history of photosensitive epilepsy. However, those patients who were having regular antiepileptic medication and/or were taking adequate preventive measures had a temporary period of freedom from sensitivity which lasted 1-4 years. These findings suggest that freedom from photosensitivity is not age-dependent, especially in those patients with family history of photosensitive epilepsy.

Impacts of extraction methods in the rapid determination of atrazine residues in foods using supercritical fluid chromatography and enzyme-linked immunosorbent assay: microwave solvent vs. supercritical fluid extractions.

It is an accepted fact that many food products that we eat today have the possibility of being contaminated by various chemicals used from planting to processing. These chemicals have been shown to cause illnesses for which some concerned government agencies have instituted regulatory mechanisms to minimize the risks and the effects on humans. It is for these concerns that reliable and accurate rapid determination techniques are needed to effect proper regulatory standards for the protection of peoples nutritional health. This paper, therefore, reports the comparative evaluation of the extraction methods in the determination of atrazine (commonly used in agricultural as a herbicide) residues in foods using supercritical fluid chromatography (SFC) and enzyme-linked immunosorbent assay (ELISA) techniques. Supercritical fluid extraction (SFE) and microwave solvent extraction (MSE) methods were used to test samples of frozen vegetables, fruit juice, and jam from local food markets in Houston. Results showed a high recovery percentage of atrazine residues using supercritical fluid coupled with ELISA and SFC than with MSE. Comparatively, however, atrazine was detected 90.9 and 54.5% using SFC and ELISA techniques, respectively. ELISA technique was, however, less time consuming, lower in cost, and more sensitive with low detection limit of atrazine residues than SFC technique.

Metabolism of Mycotoxins, Intracellular Functions of Vitamin B12, and Neurological Manifestations in Patients with Chronic Toxigenic Mold Exposures. A Review

This paper evaluates the possible reasons for consistent vitamin B12 deficiency in chronic toxigenic mold exposures and the synergistic relationships with the possible mycotoxic effects on one-carbon metabolism that lead to the manifestations of clinical neuropathological symptomology. Vitamins are first defined in general and the nutritional sources of vitamin B12 are evaluated in particular. Since patients with chronic exposures to toxigenic molds manifest vitamin B12 deficiencies, the role of mycotoxins in vitamin B12 metabolism is assessed, and since vitamin B12 plays important biochemical roles in one-carbon metabolism, the synergistic effects with mycotoxins on humans are reviewed. An outline of the proposed mechanism by which mycotoxins disrupt or interfere with the normal functions of vitamin B12 on one-carbon metabolism is proposed. The overall functions of vitamin B12 as a source of coenzymes, in intracellular recycling of methionine, in methionine synthase reaction, in the prevention of chromosome breakage, in methylation, and in maintaining a one-carbon metabolic balance are reviewed. Signs, symptoms, and clinical neurological indications of vitamin B12 deficiency are also cited. By implication and derivation, it is likely that the interruption of the structure and function of vitamin B12 would in turn interfere with the one-carbon metabolism leading to the neurological manifestations. This review is an attempt to formulate a basis for an ongoing research investigation on the subject.

Assessing the Health Effects of Long-Term Exposure to Insecticide-Treated Mosquito Nets in the Control of Malaria in Endemic Regions

Malaria is a protozoan disease caused in humans by the genus Plasmodium of which four species are known: P. falciparum, P. vivax, P. ovale, and P. malariae. It is transmitted through the bite of infected female mosquitoes of the genus Anopheles. Malaria is endemic in tropical and subtropical regions of the world. It is characterized by extreme exhaustion associated with paroxysms of high fever, sweating, shaking chills, and anemia. Approximately 40% of the worlds population, mostly those living in the poorest nations, are at risk. Much of the deaths due to malaria occur in Africa, mostly among children. The search for prevention and control interventions that are effective and sustainable remains an abiding challenge for national governments and international health agencies. To this end, the World Health Organization and several nongovernmental organizations are investing in the use of insecticide-treated mosquito nets (ITMNs) as a viable option. Trials of ITMNs in the 1980s and 1990s showed that they reduce deaths in young children by an average of 20% and multilateral agencies, spearheaded by Roll Back Malaria (RBM), seek to have 60% of the populations at risk sleeping under ITMNs by 2005. All pesticides are toxic by nature and present risks of adverse effects that depend on toxicity of the chemical and the degree of exposure. While there is agreement that ITMNs can be effective in reducing malaria morbidity and mortality under field trials, a number of factors relating to their sustainability and contribution to health improvement in less-developed countries have yet to be determined. In particular, the adverse effects associated with their long-term use and misuse has yet to be fully evaluated. Although this paper examines potential neurotoxic and neurobehavioral effects of long-term use of ITMNs and discusses priority public health actions for protecting the health of users, it forms the basis for further research.

Biochemical Changes in the Serum of Patients with Chronic Toxigenic Mold Exposures: A Risk Factor for Multiple Renal Dysfunctions

This paper analyzes and presents the biochemical abnormalities in the sera of patients presenting with chronic mycosis in order to investigate the relationship with the risks of multiple renal disorders. The study population (n = 10) consisted of six females and four males (mean age 36.3 years) exposed by toxic molds in their homes and offices for an average of 2.8 years. The control group comprised ten people, five males and five females (mean age 35.9 years) without any known exposures to toxic molds. Blood samples were obtained from both the patients and the controls and were processed using specific biochemical methods that included enzyme-linked immunoabsorbent assay (ELISA). There were biochemical abnormal concentrations in creatinine, uric acid, phosphorus, alkaline phosphotase, cholesterol, HDH, SGOT/AST, segmented neutrophils, lymphocytes, total T3, IgG and IgA immunoglobulins with significant differences between patients and controls. These abnormalities were consistent with multiple renal disorders. The major complaints of the mycosis patients were headaches, pulmonary symptoms, allergic reactions, memory loss, skin rashes, blurred vision symptoms, fatigue, and runny nose. These findings were depictive of a strong association of chronic mycosis with abnormal renal indicators. It was concluded that, although this research was a pilot investigation, based on the overall results, people exposed to chronic indoor environmental toxic molds were at risk of multiple renal complications.