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INTRODUCTION: Venezuelan equine encephalitis virus has caused periodic epidemics and epizootics in the American continent since the 1920s. Such events have been profusely documented from the epidemiologic point of view, however, reports concerning the clinical features of this disease are rather scarce. OBJECTIVE: To analyze the clinical characteristics evidenced by Venezuelan equine encephalitis patients from Zulia state (western Venezuela) studied during the outbreak that occurred in Colombia and Venezuela in 1995. These cases, classified as complicated, were hospitalized at the Hospital Universitario de Maracaibo, state of Zulia, Venezuela. PATIENTS AND METHODS: The clinical charts of 313 Venezuelan equine encephalitis patients hospitalized during the period January 1st 1995-March 31st 1996 were reviewed. These cases accounted for 2.82% of 11,072 patients that were medically assisted during the outbreak. The following variables were analyzed: age, gender, signs and symptoms, contact history, complications and evolution. RESULTS: Intracranial hypertension signs became eloquent in 55.9% of these patients. Neurologic complications were represented by two cases of cerebellitis, two cases of meningoencephalitis and one case of encephalomyelitis. The mortality rate was 1.7%. CONCLUSION: Our results corroborate the benign evolutionary profile that is typical of this entity.

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Se describen las características clínicas de la Encefalitis Equina Venezolana (EEV) y la capacidad teratogénica de diversos Togavirus. Se destaca la similitud entre las alteraciones intrauterinas inducidas por el virus de la EEV y el de la rubeola. Se señalan las observaciones descritas en 1967 por Wenger sobre necrosis cerebral masiva en fetos de mujeres que presumiblemente habían padecido de encefalitis y se describe el desarrollo de un modelo experimental en ratas a finales de la década de 1970-1980. La patogenia de la infección intrauterina parece relacionada con alteraciones vasculares placentarias y del sistema nervioso central en ratas sobrevivientes a la infección viral; se destaca la similitud entre estos hallazgos y lesiones vasculates cerebrales en niÑos con síndrome de rubeola congénita. Se hace énfasis en la necesidad de estudios multidisciplinarios en las áreas endémicas de EEV como una vía para detectar secuelas del efecto del virus in utero. Finalmente se proponen algunos modelos experimentales en animales para esclarecer diversos aspectos sobre el efecto intrauterino provocado por el virus de la EEV

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The Venezuelan equine encephalomyelitis (VEE) is one the most serious viral infections of the nervous system. It has a wide geographic distribution and may give rise to sequela like mental retardation, amnesia, abortion, epilepsy and hidroanencephaly in infected humans and animals. The pathology of this infection is focused mainly in two tissues: lymphohematopoietic and nervous. The VEE virus has a special cytopathic activity on the nervous cells (glia and neurons) while the lesions produced in the myelin are probably a consequence of the immunological response of the host to the infection. The alterations produced by the VEE virus in different neuronal types can originate changes in the brain concentrations of several neurotransmitters and their receptors. Some biochemical modifications that have also been reported could be due to the cytopathic effect of the virus.

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Venezuelan equine encephalitis (VEE) virus has been implicated as producing alterations in glucose metabolism in animals. We performed oral glucose tolerance tests and measured serum immunoreactive insulin responses in 13 patients who were infected by VEE virus during an epidemic in 1969, in Zulia State, Venezuela. No significant alterations in the glucose tolerance test were found. Sera of 86 diabetic outpatients and 98 control individuals with normal glycemia at a local hospital were tested for antibodies to VEE virus by hemagglutination inhibition. No statistically significant difference was found between the two groups; 10.4% of the diabetic patients had detectable antibodies against VEE virus, compared to 7.1% of controls. Seventy-three percent of the diabetics with antibodies were individuals over 40 yr old, whose diabetes could be catalogued as insulin independent. The results of these studies indicate no relationship of VEE virus infection to subsequent diabetes.

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Rhesus monkey fetuses were inoculated with Venezuelan Equine Encephalitis (VEE) vaccine virus by the direct intracerebral route at approximately 100 days gestation to determine possible teratogenicity of the virus. Congenital micrencephaly, hydrocephalus and cataracts were found in all animals and porencephaly in 67 percent of the cases. The virus replicated in the brain and other organs of the fetus. VEE vaccine virus is teratogenic for non-human primates and must be considered a potential teratogen of man.

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Viral infections have been implicated in the induction of diabetes mellitus in man and laboratory animals. Since virus-specific immunofluorescence (FA) is detectable in hamster pancreas during the acute phase of Venezuelan encephalitis (VE), experiments were designed to correlate pathologic and virologic events with metabolic studies in VE-infected hamsters. Golden Syrian hamsters were inoculated s.c. in groups of four to 12 with 100,000 plaque-forming units (PFU) of the vaccine strain (TC-83) of VE or 1,000 PFU of the virulent Trinidad strain of VE. Ultrastructurally, during Trinidad infection, mature virions were associated with the cell surfaces and within pancreatic beta cells in contrast to absence of virus-related changes in TC-83-infected hamsters. Virus-specific-FA was noted in islet cells and acinar cells of Trinidad-infected hamsters. VE growth curves demonstrated viral replication in pancreas with both strains. Although ultrastructural and FA changes were much more prominent in Trinidad-infected hamsters in contrast to TC-83-infected hamsters during the first few days of illness, the rapid lethality of the Trinidad-infected group necessitated performing all metabolic studies in TC-83-strain-infected hamsters. Accordingly, for the metabolic studies, glucose tolerance tests (GTT) using 2 mg. or 5 gm./kg. glucose i.p. were performed in groups of hamsters acutely infected two days earlier with the TC-83 vaccine strain and in 24-day and 90-day convalescent hamsters after TC-83 vaccine strain. Samples were obtained for glucose and immunoreactive insulin (IRI) determinations. Glucose intolerance occurred in hamsters in each of the infected groups given 5 gm./kg. glucose except for the 90-day convalescent TC-83 group. Severely decreased IRI responses occurred in the 24-day and 90-day convalescent TC-83 hamsters following both 2- and 5-gm./kg. glucose. Pancreatic IRI content in 24-day convalescent TC-83 hamsters was within normal limits, suggesting a defect in IRI release from the beta cells at this stage of convalescence.

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The purpose of this study was the identification of possible sequelae of the infection of human individuals with Virus of Venezuelan Equine Encephalitis (VEE). Special emphasis was laid on exploring neurological, psychological and behavioural aspects and particularly on the search for a possible association of the disease with epileptic phenomena, brain damage and/or mental deficiency. A four-year period of observation was conducted on a sample of children from El Carmelo (Colombia) where an epidemic of VEE took place in 1967. A group of seven children who presented the encephalitic type of the illness and were hospitalized with symptoms of CNS involvement and a confirmed diagnosis of VEE constituted the index group. This group was compared with four control groups of children with matched demographic characteristics but separated according to whether they were ill at the time of the epidemic and whether they presented serological evidence of having been infected with VEE Virus. Evaluations were conducted at three points in time during the follow-up period and they included the following procedures: (1) Survey on personal background and behaviour (through a standard questionnaire dealing with all areas of functioning); (2) Complete paediatric examination, including a careful neurological check-up; (3) Psychological examination using intelligence tests; (4) Electro-encephalographic examination according to standard techniques, with the patient awake, asleep and under photic stimulation; (5) Bi-weekly home visits to keep a record on intercurrent illness throughout the observation period. Statistical analysis of results shows significant differences between the groups in regard to the distribution of abnormalities.

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