Case histories of insect- or arachnid-caused human illness.

Insects, arachnids, and other medically important arthropods affect human health directly by bites, stings, and blisters, and indirectly by disease transmission. In this paper, three widely divergent cases of insect- or arachnid-caused human illness are presented--a spider bite, a mosquito-borne disease case, and an imaginary mite problem. Some key references are included for each topic, as well as editorial comment to add perspective.

Experimental infection of young broiler chickens with eastern equine encephalitis virus and Highlands J virus.

Two-week-old broiler chickens were experimentally infected with either eastern equine encephalitis (EEE) virus or Highland J (HJ) virus. Mortality rates were 24/30 (80%) in EEE-virus-inoculated chickens and 2/30 (7%) in HJ-virus-inoculated chickens. Chickens inoculated with EEE virus exhibited severe depression and somnolence on days 1-6 postexposure (PE), with 17/30 birds dying during this period. After day 6 PE, EEE-virus-inoculated chickens exhibited abdominal distention, depression, and growth retardation, and an additional seven chickens died. Pathologic changes in EE-virus-inoculated chickens dying on days 1-6 PE consisted of multifocal necrosis in the heart and liver, as well as lymphoid depletion and necrosis in the thymus, spleen, and bursa of Fabricius. Ascites, pericardial effusion, and right ventricular dilatation of the heart were the predominant lesions in chickens dying after day 6 PE. No clinical signs were observed in sham-inoculated controls or in most HJ-virus-inoculated chickens. Ascites, pericardial effusion, and multifocal myocardial necrosis were observed in 2/30 HJ-virus-inoculated chickens that died or were euthanatized after development of clinical signs. These findings indicate that both EEE virus and HJ virus are pathogenic for young chickens.

Localized eastern equine encephalitis in Santiago del Estero Province, Argentina, without human infection.

In 1981, a localized epizootic of Eastern Equine Encephalitis (EEE) occurred in irrigated areas of four counties in the province of Santiago del Estero, Argentina. The diagnosis was confirmed by serology, and there was no evidence of involvement of Western or Venezuelan equine encephalitis viruses. The overall incidence of equine encephalitis was estimated 17%, the case-fatality rate at 61% and the inapparent: apparent infection ratio less than or equal to 2.9:1. This is the first localized epizootic defined in Argentina and the first in which EEE has been found as the sole etiologic arbovirus. This posed the possibility to look for human infection in the area. In spite of a careful surveillance, no evidence of human disease or infection was found, differing from the situation in USA where EEE virus is a public health problem. Nevertheless vector/s and vertebrate hosts involved in the transmission cycle in Argentina remain unknown, precluding at present speculations on the potential human risk.

Localized Eastern equine encephalitis in Santiago del Estero province, Argentina, without human infection

Se documenta una epizootia de encefalitis equina del este (EEE) localizada en una zona irrigada de cuatro departamentos de la Privincia de Santiago del Estero, Argentina, en 1981. La incidencia de casos equinos fue estimada en 17% con una tasa de casos fatales del 61% y una relación de infección inaparente: aparente de < ou = 2,9:1. El diagnóstico para el virus EEE fue confirmado por pruebas serológicas y no se encontró evidencia de casos por virus de las encefalitis del oeste o Venezuela. Esta es la primera epizootia circunscripta a una pequeña área geográfica que se ha definido en Argentina y la primera en que el virus EEE se ha encontrado como único arbovirus etiológico. Su reconocimiento brindo la posibilidad de buscar la infección humana, pero no se encontró clara evidencia de enfermedad o infección. Esto se atribuyó a la baja densidad de población humana rural, aunque no se descartaron otros factores ecológicos. La serología en otros animales no permitió determinar los huéspedes vertebrados y no se estudiaron los vectores por lo cual el ciclo de transmisión continúa desconocido, impidiendo especular sobre el riesgo potencial del virus EEE para el hombre en Argentina

Localized Eastern equine encephalitis in Santiago del Estero province, Argentina, without human infection

Se documenta una epizootia de encefalitis equina del este (EEE) localizada en una zona irrigada de cuatro departamentos de la Privincia de Santiago del Estero, Argentina, en 1981. La incidencia de casos equinos fue estimada en 17% con una tasa de casos fatales del 61% y una relación de infección inaparente: aparente de < ou = 2,9:1. El diagnóstico para el virus EEE fue confirmado por pruebas serológicas y no se encontró evidencia de casos por virus de las encefalitis del oeste o Venezuela. Esta es la primera epizootia circunscripta a una pequeña área geográfica que se ha definido en Argentina y la primera en que el virus EEE se ha encontrado como único arbovirus etiológico. Su reconocimiento brindo la posibilidad de buscar la infección humana, pero no se encontró clara evidencia de enfermedad o infección. Esto se atribuyó a la baja densidad de población humana rural, aunque no se descartaron otros factores ecológicos. La serología en otros animales no permitió determinar los huéspedes vertebrados y no se estudiaron los vectores por lo cual el ciclo de transmisión continúa desconocido, impidiendo especular sobre el riesgo potencial del virus EEE para el hombre en Argentina (AU)

[Effect of immunosuppressants on the enhanced sensitivity of white mice to the eastern equine encephalitis virus]. / Vliianie immunosupressantov na povyshenie chuvstvitel'nosti belykh myshei k virusu vostochnogo éntsefalomielita loshadei.

EEE virus infection could be induced in white mice whose natural resistance to this virus had been reduced by immunosuppressive drugs such as: Adreson, Cyclophosphan and hydrocortisone.

Main Drain virus as a cause of equine encephalomyelitis.

Main Drain virus, which is thought to be transmitted normally among rabbits and various rodents by its natural vector, Culicoides variipennis, was isolated repeatedly from brain tissue of a sick horse from Sacramento County, California, and was implicated as the causative agent. Signs of illness were incoordination and ataxia, stiff neck, head pressing, inability to swallow, fever, and tachycardia.

Melioidosis with acute meningoencephalomyelitis in a horse.

A case of acute meningoencephalomyelitis caused by infection with Pseudomonas pseudomallei is described. Clinically there was inability to stand, opisthotonus, facial paralysis and nystagmus, rapidly progressing to violent struggling. Gross examination revealed malacia and haemorrhage in the medulla oblongata and adjacent spinal cord. Microscopically there were disseminated focal neutrophilic accumulations in affected areas, perivascular cuffing with mononuclear cells and lymphocytes and marked oedema. Intracellular bacteria were identified in sections stained by the Giemsa method.

Evidence for Sarcocystis as the etiologic agent of equine protozoal myeloencephalitis.

Equine protozoal myeloencephalitis (EPM) was diagnosed in 10 horses. By electron microscopy, schizonts were found in intact host cells of the spinal cords or, more frequently, free in the extracellular spaces. Developmental stages of schizonts differed morphologically, and the late stage of schizogony was characterized by endopolygeny. These findings permitted tentative identification of the protozoon as a Sarcocystis sp. Free merozoites were present in the extracellular spaces or in cells of the spinal cord. Pericytes of capillaries were most frequently parasitized by merozoites were present in the extracellular spaces or in cells of te spinal cord. Pericytes of capillaries were most frequently parasitized by merozoites, but the cytoplasm of neurons, macrophages, intravascular and tissue neutrophils, and axons of myelinated nerve fibers also contained these organisms. The presence of parasites in the cytoplasm of tissue and circulating neutrophils suggest that this putative Sarcocystis sp. may have a hematogenous phase of infection.

Equine leucoencephalomalacia (ELEM): a study of Fusarium moniliforme as an etiologic agent.

Signs and lesions characteristic of equine leucoencephalomalacia were produced in one of two donkeys given corn cultured with Fusarium moniliforme Sheldon. Gross and histopathologic lesions of the cerebrum included an extensive necrotic cavitation within one cerebral hemisphere, disruption and rarefication of the subcortical white matter, prominent perivascular hemorrhage, and some mononuclear cell perivascular cuffing. Another donkey and three rabbits fed the cultured corn did not develop characteristic signs or lesions of the toxicosis. Chick bioassay studies indicated that the cultured corn which produced the disease did not contain a monovalent salt of moniliformin.

Pheasant susceptibility at different ages to Eastern encephalitis virus from various sources in Massachusetts.

Thirteen isolates of Eastern encephalitis (EE) virus recovered from various hosts in Massachusetts differed significantly in pathogenicity for pheasants, 21 days old or older, inoculated subcutaneously with graded doses of virus. Among the least pathogenic were two isolates from Culiseta melanura mosquitoes, and among the most pathogenic isolates was one of pheasant origin. Nine-day-old pheasant chicks were highly susceptible to EE virus. Mortality did not appear to be totally dose-related, for inocula larger than an infecting dose did not increase mortality substantially.

Encephalitis caused by louping ill virus in a group of horses in Ireland.

An outbreak of LI infection in a group of free range horses is described. Three of 4 horses displayed signs of CNS disturbance and 2 of these died after illnesses ranging from 2-12 days duration. In both cases a variable degree of viral polioencephalomyelitis was observed. A virus antigenically indistinguishable from a reference strain of LI virus was isolated from the brain and cervical cord of a 3 y.o. draft mare. Serum samples obtained from 3 of the horses contained HI, CF, precipitating and neutralising antibodies to LI virus, with a rise in antibody titre being demonstrated in 2 animals.

Equine viral encephalitis.

The most important neurotropic viral infections of the horse are the arthropod-borne encephalitides. These include Venezuelan encephalitis (VE), eastern encephalitis (EE) and western encephalitis (WE), which are found in the Americas, and Japanese B encephalitis which occurs in the Far East. All the viruses cause encephalitis in man. Between 1969 and 1972 an epidemic of VE occurred in Central America. In 1971 the disease was reported in Texas, where it was brought under control by the vaccination of susceptible horses with an attenuated live virus vaccine and by the reduction of the mosquito population with insecticides sprayed from aircraft. A high titre viraemia occurs with VE virus in the horse and epidemics are maintained by a mosquito/horse cycle; infection of man and other species is incidental. EE and WE have been recognised as separate diseases since 1933 and in the U.S.A. horses are protected by routine vaccination. Epidemics of these diseases are routine vaccination. Epidemics of these diseases are now uncommon. In contrast with VE, both EE and WE viruses are maintained by a bird/mosquito cycle. The viraemia in the horse is generally considered insufficient to infect mosquito vectors; the horse is a "dead end host". Several species of mosquito can act as vectors of VE, WE and EE. The extension of other arthropod-borne diseases to areas originally outside their geographical distribution (e.g. bluetongue in sheep) serves to illustrate the potential of VE, WE and EE to cause disease on other continents.