[On the occurrence of a variant of type 25 ECHO virus].
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By means of the excimer-forming lipid technique changes of membrane fluidity of human PMNs exposed to a chemoattractant (FMLP) and/or Echo virus, type 9, strain A. Barty has been investigated. It was shown that preincubation of PMNs with Echo 9 virus results in a viral dose-dependent decrease of membrane fluidity of granulocytes exposed to FMLP. The virus-induced rigidity of cell membrane causes obviously a disturbance in the aggregation of membrane particles to form receptors, and thus can lead to a failure of regular processing of chemotactic signals.
Preincubation (37 degrees C, 60 min) of human neutrophilic granulocytes with various concentrations of infectious ECHO virus, type 9, strain A. Barty resulted in virus-dose dependent inhibition of neutrophil chemotactic reactivity (Boyden-chamber assay) to chemoattractants (F-Met-Leu-Phen: zymosan-activated human serum). Other cellular functions-phagocytosis, increase of oxidative cell metabolism, intracellular killing of live staphylococci--remained intact. This selective inhibition of human neutrophilic chemotaxis was due to viral induced cytotoxicity or competitive inhibition of chemotactic cell surface receptors.
At Ste. Justine Hospital, Montreal, during the period 1957-61, ECHO 9 virus was isolated in 27 cases, in 20 of these during the summer of 1961. All had evidence of meningeal irritation, accompanied by fever and headache. Four of the 20 patients diagnosed during the summer of 1961 had convulsions; 12 presented with a rash; and two simulated meningococcemia. Of the 27 patients, two were paralyzed and one case was diagnosed as transverse myelitis. ECHO 9 virus was isolated from stools and from throat specimens in equal proportion; it was isolated from cerebrospinal fluid in only two instances. Pathogenicity for suckling mice was observed in two of 22 inoculated directly with the specimen material and in 10 of 11 inoculated with the cultured material.
The oral and parenteral infections of chimpanzees receiving echo Types 6 and 4 viruses successively are described. The two infections, spaced 2(1/2) months apart, and given by the same route in each animal, failed to induce overt disease. The inapparent infections were demonstrated by virus excretion in the throat and the stools and the development of neutralizing antibodies. Complement-fixing antibodies also appeared after Type 6 infection, but fell more rapidly than the neutralizing antibodies. After oral infection, echo-6 virus was found for equal periods in both the throat and feces, but echo-4 persisted in the throat for much longer periods than in the lower bowel. Almost no virus carriage occurred after parenteral inoculation. No true viremia was exhibited in any of the animals. One of the chimpanzees had neutralizing antibodies against Type 6 virus in its pre-inoculation serum. It responded extraordinarily to the Type 6 exposure, developing antibody levels of 1:50,000 to echo-6, of 1:1024 against the echo-6' variant, and of 1:64 against the echo 6'' variant. Although Type 4 antibodies developed after the exposure, they proved difficult to measure by ordinary methods. However, they could be satisfactorily assayed by the plaque reduction method. Three other chimpanzees fed echo-2, echo-3, and an untypable echo virus, respectively, yielded results confirming those established with Types 4 and 6.
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In October 1978, a 6 day-old child became ill in a maternity ward and died with clinical signs of septicemia. In quick succession, 6 other children fell ill with aseptic meningitis, 5 within the first 10 days post partum and one child 4 weeks old. From these 6 children virus was isolated at different times and from various sites (CSF, pharynx, rectum). 25 isolates were obtained. By cross-neutralization an antigenic variant of Echo virus 11 was identified. Since further isolations were unsuccessful the route of infection was reconstructed from environmental investigation and clinical and serological data in 49 people. A laboratory infection with the agent isolated gave additional opportunities for detailed virological and clinical observations.
A boy with agammaglobulinaemia diagnosed and treated from the age of 3 years 2 months developed encephalitis at 4 years 3 months. The illness showed a remitting but deteriorating course until death aged 6 years 5 months. Echo virus type 27 was isolated from the cerebrospinal fluid during the terminal illness. The virus was not isolated from five earlier cerebrospinal fluid samples nor was virus detected in a temporal lobe biopsy.
An infant with mononuclear pleocytosis, hypoglycorrhachia, and elevated protein in cerebrospinal fluid emphasizes the occasional difficulty in distinguishing viral and tuberculous meningitis at the time of presentation. Although the cerebrospinal fluid values were compatible with tuberculous meningitis, ECHO virus type 9 was grown from the spinal fluid.
The clinical records of 15 children admitted to Hospital Infantile de México Federico Gómez with diagnosis of viral meningitis were reviewed. They were part of 19 patients admitted with this diagnosis during a 5 week period (March 22 to April 30, 1992) and represent a significant increase of aseptic meningitis compared with the same periods of previous years at Hospital Infantile de Mexico and in Mexico City where there is an ongoing epidemic outbreak of this entity. All the patients studied had spinal fluid findings consistent with viral meningitis and in 4 of them on ECHO virus type 30 was isolated at the Enterovirus Section of the CDC, Atlanta Georgia USA.
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