ENCEPHALITIS IN EXPERIMENTAL COXSACKIE B-3 INFECTION

1961 ◽  
Vol 7 (2) ◽  
pp. 175-184 ◽  
Author(s):  
E. Irene Grodums ◽  
George Dempster
Keyword(s):  
Anatomical Distribution ◽  
The Past ◽  
B Virus ◽  
Group B ◽  
Old Mice ◽  
The Brain ◽  
Standard Prototype ◽  
Experimental Disease ◽  
Coxsackie B ◽  
Coxsackie Group

A study has been made of the vulnerability of various parts of the brain in experimental Coxsackie B-3 virus infection. The standard prototype Coxsackie B-3 virus and a stock of inbred albino mice have been used for this purpose. The sites of greatest susceptibility have been precisely defined by thorough examinations of the whole brain and it has been observed that in 7- to 12-day-old mice the lesions are confined to sensory centers.Furthermore, observations have been made upon the effects of various factors such as the age at the time of inoculation, the state of myelination in different parts of the brain, and the route of inoculation. The complete resistance of the cerebellum to damage in spite of multiplication of virus in this site is of considerable interest.In the past little attention has been paid to the anatomical distribution of the brain lesions caused by the Coxsackie group B virus. It would seem to be profitable to direct attention to the features of the experimental disease in view of our lack of basic information regarding many non-fatal illnesses which affect the brain.

EXPERIMENTAL COXSACKIE B-3 INFECTION IN THE HIBERNATING SQUIRREL AND BAT

1961 ◽  
Vol 7 (4) ◽  
pp. 587-594 ◽  
Author(s):  
George Dempster ◽  
E. Irene Grodums ◽  
W. A. Spencer
Keyword(s):  
Ground Squirrel ◽  
Adult Mouse ◽  
Brown Fat ◽  
Young Mouse ◽  
B Virus ◽  
Group B ◽  
First Time ◽  
The Brain ◽  
Coxsackie B ◽  
Coxsackie Group

It has been shown for the first time that Coxsackie B-3 virus will infect hibernating mammals such as the ground squirrel and the bat, in both the hibernating and nonhibernating states. Pathological changes in the heart and brown fat of squirrels in hibernation were comparable with those observed in mice. In squirrels the brain appeared to be relatively resistant, although the region of the olfactory bulb was often involved. Although no lesions were observed in bats killed in hibernation, a few died with meningoencephalitis. Viraemia was observed in both species and found to be more persistent in the bat.Biochemical studies were conducted upon the normal brown fat of the different species, and it was interesting to find that whereas the morphology and lipid content (total lipid and phospholipid) of the young mouse, adult squirrel, and adult bat were very similar, the corresponding characters of adult mouse brown fat showed marked differences. The significance of the resemblance of young mouse brown fat to that found in the hibernating mammal is being assessed further in the light of the function of the brown fat and its susceptibility to Coxsackie group B virus infection.

THE PATHOGENESIS OF COXSACKIE GROUP B VIRUSES IN EXPERIMENTAL INFECTION

1962 ◽  
Vol 8 (1) ◽  
pp. 105-113 ◽  
Author(s):  
E. Irene Grodums ◽  
George Dempster
Keyword(s):  
Inflammatory Cell ◽  
Host Population ◽  
Adult Mice ◽  
Age Factor ◽  
Group B ◽  
Experimental Findings ◽  
Heart Lesions ◽  
Old Mice ◽  
The Brain ◽  
Coxsackie Group

The experimental findings show that in mouse-adapted strains of different Coxsackie group B types of virus, distinctly varied patterns of pathogenesis exist. In the particular host population under study, both of the B-3 strains examined are peculiarly cardiotropic for 17-day-old mice and adult mice. In contrast, the B-1 strain, while mildly cardiotropic for sucklings, neither propagates nor produces lesions in the 17-day weanlings. The age factor does not seem to have any effect upon two strains of B-5 viruses which show the same degree of moderate cardiotropism in sucklings and weanlings.It can be seen from observations made upon the brown fat that lesions are produced in adult mice with all but B-2 virus. Interpretation of the heart lesion, however, is complicated by the appearance of heart lesions in control animals of this age. These heart lesions were not observed in the control sucklings or weanlings. In spite of this, there is evidence that the B-3 virus induces specific heart lesions in adult mice.It would appear that the B-2, B-4, and the Kita strain of B-5 provoke a marked inflammatory cell response in the brain which distinguishes them from the other strains.

The role of Coxsackie Group B virus infections in sporadic myopericarditis

1971 ◽  
Vol 82 (6) ◽  
pp. 750-758 ◽  
Author(s):  
Clyde H. Koontz ◽  
C.George Ray
Keyword(s):  
Virus Infections ◽  
B Virus ◽  
Group B ◽  
Coxsackie Group

Coxsackie Group B virus and primary myocardial disease in infants and children

1974 ◽  
Vol 88 (3) ◽  
pp. 311-314 ◽  
Author(s):  
Prapit Sudhas Na Ayuthya ◽  
Jidbhong Jayavasu ◽  
Boonchob Pongpanich
Keyword(s):  
Infants And Children ◽  
Myocardial Disease ◽  
B Virus ◽  
Group B ◽  
In Infants And Children ◽  
Coxsackie Group

Fatal Coxsackie B2 Infection In One Dizygous Twin

PEDIATRICS ◽  
1973 ◽  
Vol 52 (4) ◽  
pp. 604-605
Author(s):  
George A. Nankervis ◽  
Leonard P. Rome
Keyword(s):  
Fatal Case ◽  
White Female ◽  
Dizygotic Twin ◽  
Significant Morbidity ◽  
Birth Canal ◽  
The Past ◽  
B Virus ◽  
Coxsackie B Virus ◽  
Transplacental Infection ◽  
Coxsackie B

Devastating coxsackie B virus infection has been reported in a number of neonates during the past several years.1-4 Although transplacental infection may occur, characteristically the viral infection is acquired during passage through the birth canal or shortly thereafter. The neonate is usually asymptomatic until 4 to 5 days of age when the onset of lethargy, poor feeding, and temperature instability are noted. Significant morbidity or mortality frequently ensues. This report describes a fatal case of neonatal coxsackie B2 infection in one dizygotic twin. CASE REPORT E. D. was the first of twins delivered to a 29-year-old gravida 3, para 2, white female after 37 weeks' gestation.

PASSIVE NEUTRALIZING ANTIBODIES IN EXPERIMENTAL COXSACKIE B-1 VIRUS INFECTION

1964 ◽  
Vol 10 (1) ◽  
pp. 53-61
Author(s):  
E. Irene Grodums ◽  
George Dempster
Keyword(s):  
Neutralizing Antibodies ◽  
Brown Fat ◽  
Microscopical Examination ◽  
Severe Damage ◽  
Virus Inoculation ◽  
Challenge Virus ◽  
Before And After ◽  
Old Mice ◽  
The Brain ◽  
Coxsackie B

Passive neutralizing antibodies specific to Coxsackie B-1 virus are transmitted from immune mice to the litters both before and after birth.Before birth the antibodies are transmitted via the mother"s blood; their presence could not be detected by the age of 17 days. After birth, the antibodies apparently are transmitted by milk. The ND50 of these antibodies is maintained if the litter is suckled by an immune mother.Although the immune 4-day-old litters survive after intracerebral inoculation and there are no signs of paralysis or other severe damage to the CNS, the brain lesions on microscopical examination appear to be as extensive as in the non-immune controls. The brain tissues of the immune mice are spared if the virus is introduced by the subcutaneous route.The damage observed in the interscapular brown fat in either the immune 4- or the 17-day-old mice, irrespective of the route of virus inoculation, is considerably reduced or minimal, if the presence of the passive antibody can be demonstrated in the blood.When the offspring are born of and suckled by an immune mother, the multiplication of the Coxsackie B-1 virus in the brown fat appears to be completely blocked, and there is no evidence of an immediate antigenic stimulus by the challenge virus.

scholarly journals Coxsackie group B virus infection and acute diarrhoea occurring among children in Costa Rica.

1966 ◽  
Vol 41 (220) ◽  
pp. 636-641 ◽  
Author(s):  
W. Pelon ◽  
V. M. Villarejos ◽  
J. S. Rhim ◽  
F. J. Payne
Keyword(s):  
Costa Rica ◽  
Virus Infection ◽  
Acute Diarrhoea ◽  
B Virus ◽  
Group B ◽  
Coxsackie Group
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