CT Epidemiologia 21/03/16: complicações neurológicas associadas as Arboviroses (Chikungunya e Zika)

A congenital abnormality of calves, suggestive of a new type of arthropod-borne virus infection.

About 1000 calves with a congenital disease were born in Kagoshima prefecture, Japan, between October 1990 and October 1991, the peaks of the epidemic being in March and July 1991. Of 85 abnormal calves examined pathologically and serologically, 70 appeared to have been suffering from a viral disease. Of these 70 animals, 17 had lesions bearing some resemblance to those of the diseases produced by Akabane, Chuzan, Aino, bluetongue and bovine viral diarrhoea-mucosal disease viruses-diseases known to occur in Kagoshima-but serum samples contained no antibodies to these viruses or to infectious bovine rhinotracheitis virus. This suggested the occurrence of a new type of viral infection in southern Japan. Six of the 17 calves were born dead and the others manifested clinical signs such as weakness, difficulty in sucking, inability to stand, vertigo, opisthotonus, staggering and weak eyesight or blindness. They were of small size and showed domed head, scoliosis, arthrogryposis, maxillary retraction, sunken eye, cataracts, and irregularities and defects of the teeth. At necropsy, almost all cases showed hydranencephaly, and many had cerebral defects and cerebellar hypoplasia or agenesis. Both cerebral and cerebellar lesions were seen in six cases, two of which showed a hypoplastic defect of the brain stem. Histopathological examination of the affected organs revealed gliosis, loss of cerebral parenchyma resulting from dilation of the ventricles, perivascular cuffing with round cells such as lymphocytes and plasma cells, proliferation of blood vessels, thick-walled blood vessels in the brain stem, dilation of mesencephalic aqueducts, cerebellar cortical dysplasia, decreased nerve cells in the ventral horn of the spinal cord, and myodysplasia of skeletal muscle.

Akabane disease in cattle: congenital abnormalities caused by viral infection. Spontaneous disease.

Akabane disease, an infectious disorder causing congenital abnormalities in calves, was studied in naturally affected calves between 1972 and 1974 in Japan. The animals included one three-month fetus from which a strain of Akabane virus (OBE-1) was isolated, and a total of 177 stillborn or premature fetuses and deformed or infirm newborn calves that died within a few days of birth. The three-month fetus had nonpurulent encephalomyelitis in the undifferentiated central nervous system, characterized by necrosis of the nerve tissue and endothelial proliferation in the encephalitic process; and polymyositis in the myotubule phase with parenchymal degeneration and cellular infiltrates in the skeletal muscle. The full-term fetuses and newborn calves had nonpurulent encephalomyelitis in the early stage of the epizootic. In the middle to late stages, a dysplastic muscular change which we call runt-muscle disease was seen simultaneously with a decrease in number of ventral horn neurons in the spinal cord and arthrogryposis in the legs. Cystic cavities and thick vascular walls sometimes were seen in the central nervous system in these stages. Hydranencephaly was prominent in the late stage.

Akabane disease in cattle: congenital abnormalities caused by viral infection. Experimental disease.

Nonpurulent encephalomyelitis and polymyositis were primary lesions of cattle and goats experimentally infected with Akabane virus. Two caprine fetuses, two months old, were infected placentally and examined 11 days after inoculation; twin caprine fetuses, three months old, were inoculated intramuscularly through the dam's uterus and examined nine days after inoculation. Both lesions were seen in each fetus. Reactive proliferation of immature endothelial cells was a significant encephalitic change. Myositic changes included parenchymal degeneration and cell infiltration in fetuses in the myotubule phase and the beginning of the myofiber phase. Only nonpurulent encephalomyelitis was seen in six calves 14 days to one year old, inoculated intracerebrally and examined six to 47 days after inoculation. Nerve-cell degeneration, neurological mobilization, and perivascular cuffs were typical encephalitic changes in the calves. Five fetuses were infected transplacentally and had polymyositis alone. The four bovine fetuses, two to six months old, were examined nine to 18 days after inoculation, and one caprine fetus, one month old, was examined 11 days after inoculation. Neither encephalomyelitis nor polymyositis was seen in four calves under one year old that were inoculated intravenously.

Congenital abnormalities in newborn lambs after infection of pregnant sheep with Akabane virus.

Akabane virus (a Bunyavirus) has been associated with epizootics of congenital deformities in cattle, sheep, and goats. Experimental studies using mouse-adapted virus inoculated intravenously into pregnant sheep gave an inapparent infection. Neutralizing antibodies were detected on day 5, and peaks in the titer were seen at days 10 and 48. Ewes infected at day 30 to 36 of pregnancy produced five (31% incidence) deformed lambs. Sera from four of these possessed neutralizing antibodies to Akabane virus before ingesting colostrum. Two lambs had arthrogryposis, hydranencephaly, kyphosis, scoliosis, and brachygnathia; one had micrencephaly; and the other two had porencephaly. The two lambs with arthrogryposis and hydranencephaly also had extensive lesions in other tissues. In the spinal cord there was a marked decrease in the number of ventral horn neurones and a depletion of myelin. Skeletal muscles showed marked atrophy. The medulla of the thymus possessed large Hassall's corpuscles and a reduced number of thymocytes in the cortex. It would appear that the pathogenic effects of Akabane virus are related to the gestational age (30 to 36 days) at which the fetus is infected. Akabane virus can now be included in the growing list of teratogenic viruses and provides an interesting system for studying such congenital diseases.