Biomedical subjects
Publications and source records attributed to D I Simpson.
A hospital outbreak of haemorrhagic fever took place in Dubai in November, 1979. The index case died in the casualty department shortly after admission. There were five secondary cases among hospital staff, two of whom died. When, 3 months after this outbreak, a patient with symptoms characteristic of haemorrhagic fever was admitted, immediate barrier nursing prevented further secondary cases.
During the 1976 Ebola virus outbreak in Sudan, the investigations team gained the impression that fewer haemorrhagic manifestations and few fatalities occurred during the later stages of the epidemic after the virus had undergone several generations in man. This impression was also noted in guinea pigs experimentally infected with Sudanese and Zairean strains of Ebola virus. The virulence of the Sudanese isolates was less intense than isolates emanating from Zaire. Similar findings were seen in monkeys; a Zairean isolated produced fatal infections, whereas monkeys inoculated with a Sudan strain generally recovered. Two monkeys, which had recovered from Sudanese strain infections and had developed high levels of antibody detectable by immunofluorescence, were challenged with the Zairean strain. Both developed viraemias and died. The mechanisms of this "failed protection" are discussed.
In a study conducted on the Kano Plain, Kenya, virus isolation attempts were made on ixodid ticks collected, over a 14-month period, from livestock held in family enclosures (bomas) before releasing the animals for daily foraging. 8735 Amblyomma variegatum (Fabricius) were tested, 98.6% of which were taken from cattle, yielding 36 strains of Dugbe (DUG), four strains of Nairobi sheep disease (NSD), three strains of Bhanja (BHA), one strain of Thogoto (THO) and five strains of virus which could not be characterized. 6549 Rhipicephalus spp. ticks were collected (60.3% from cattle). NSD, DUG and BHA viruses were each isolated twice from ticks taken from cattle. One BHA virus strain was recovered from ticks from a sheep. One strain recovered from ticks on cattle could not be characterized.
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An epidemic of yellow fever (YF) occurred in the Gambia between May 1978 and January 1979. Retrospective case-finding methods and active surveillance led to the identification of 271 clinically suspected cases. A confirmatory or presumptive laboratory diagnosis was established in 94 cases. The earliest serologically documented case occurred in June 1978, at the extreme east of the Gambia. Small numbers of cases occurred in August and September. The epidemic peaked in October, and cases continued to occur at a diminishing rate through January, when a mass vaccination campaign was completed. The outbreak was largely confined to the eastern half of the country (MacCarthy Island and Upper River Divisions). In nine survey villages in this area (total population 1,531) the attack rate was 2.6--4.4%, with a mortality rate of 0.8%, and a case fatality rate of 19.4%. If these villages are representative of the total affected region, there may have been as many as 8,400 cases and 1,600 deaths during the outbreak. The disease incidence was highest in the 0- to 9-year age group (6.7%) and decreased with advancing age to 1.7% in persons over 40 years. Overall, 32.6% of survey village inhabitants had YF complement-fixing (CF) antibodies. The prevalence of antibody patterns indicating primary YF infection decreased with age, in concert with disease incidence. The overall inapparent:apparent infection ratio was 12:1. In persons with serological responses indicating flaviviral superinfection, the inapparent:apparent infection ratio was 10 times higher than in persons with primary YF infection. Sylvatic vectors of YF virus, principally Aedes furcifer-taylori and Ae. luteocephalus are believed to have been responsible for transmission, at least at the beginning of the outbreak. Eighty-four percent of wild monkeys shot in January 1979 had YF neutralizing antibodies, and 32% had CF antibodies. Domestic Aedes aegypti were absent or present at very low indices in many severely affected villages (see companion paper). In January, however, aegypti-borne YF 2.5 months into the dry season was documented by isolation of YF virus from a sick man and from this vector species in the absence of sylvatic vectors. Thus, in villages where the classical urban vector was abundant, interhuman transmission by Ae. aegypti occurred and continued into the dry season. A mass vaccination campaign, begun in December, was completed on 25 January, with over 95% coverage of the Gambian population. A seroconversion rate of 93% was determined in a group of vaccinees. This outbreak emphasizes the continuing public health importance of YF in West Africa and points out the need for inclusion of 17D YF vaccination in future programs of multiple immunication.
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Between December 1976 and September 1977 the Seychelles group of islands in the Indian Ocean was struck by an extensive epidemic of dengue fever. The peak of the epidemic was in the last week of February. Type 2 dengue virus was isolated from patients and mosquitos. Aedes albopictus was the sole vector. The clinical picture was that of classical dengue. Haemorrhagic fever and the shock syndrome were not observed.Absenteeism from schools and offices, anamnestic questioning, and prevalence of antibodies in sera collected after the epidemic was over, indicated that approximately 75% of the population had been infected. Serological evidence was obtained of an epidemic of dengue in the islands more than 40 years earlier. This was confirmed by archival records.
A strain of Marburg virus and two strains of Ebola virus grown in Vero cells were compared by electron microscopy. The outer coat of the Marburg virion appeared to be more resistant to erosion by negative staining techniques than that of the Epbola strains. Marburg virus commonly produced "torus" forms and short filaments; the Zaire strain of Ebola produced extensive branched forms and very long filaments; the Sudan strain of Ebola produced shorter, less branched structures but very many aberrant forms. The mechanism for the production of these aberrant forms is described.
The development of Marburg virus and the Sudanese and Zaire strains of Ebola virus in Vero cells as visualized by electron microscopy is described. Despite differences in timing, all three strains appear to pass through identical stages of development. Initially there is a large increase in nucleolus material, and viral precursor material arranges itself in spirals and then into tubes. The cells fill with core material, which passes to the plasmalemma, which often proliferates. Each virion passes through the plasmalemma, acquiring a coat of host material. The formation of torus forms is discussed; the branched appearance that is often seen is believed to be an aberrant form. The reasons for this view are put forward.
Two plaque variants of Chikungunya (CHIK) virus were serologically compared with O'nyong nyong (ONN) virus in order to elucidate the reported one way antigenic relationships between the two viruses. Three different hypotheses are examined and evidence is shown to support one of them. Comparison of some biological properties of the viruses showed ONN to be distinct in some respects. All viruses and variants were found to replicate in Anopheles gambiae cells.
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Rift Valley fever virus isolates from the 1977 outbreak in Egypt were studied at an ultrastructural level. The particles measured 90 to 110 nm in diam. using negative staining and sectioning techniques, with a core component of 80 to 85 nm. The surface of the virions was calculated to be covered by approx. 160 sub-units. The particles were found in smooth endoplasmic reticular systems, which were made up of either multi-tubular complexes, or of a single large vacuole. The majority of these membrane systems were found to be unassociated with Golgi apparatus. Inclusion bodies were found within the host cell nuclei (made up of rods and fine granules) and in the cytoplasm (aggregates of fine or coarse granules). The possible relationship of these structures to virus replication is discussed.
Antigenic relationships among seven California group strains were studied by a plaque-reduction neutralization test (PRNT). Cross-reactions occurred in most cases but three subgroups were noted: (1) the major serogroup contained the viruses of California encephalitis, LaCrosse, Snowshoe Hare and Trahyna (including the Lumbo strain) whereas (2) Jamestown Canyon and (3) Trivittatus viruses were distinct. There was no significant difference between the PRNT results in mammalian (PS) cells incubated at 37 degrees C and amphibian (XTC-2) cells incubated at 28 degrees C. Trivittatus virus failed to produce plaques in XTC-2 cells.
The family Rhabdoviridae comprises approximately 75 viruses infecting vertebrates, invertebrates and plants. The main characteristics of the member viruses are: (i) the viruses infecting vertebrates and invertebrates are bullet-shaped and the viruses infecting plants are usually bacilliform; (ii) the viruses have particle lengths varying from 130 to 380 nm and widths varying from 60 to 95 nm; (iii) the viruses possess unit-membrane envelopes from which protrude spikes 5 to 10 nm long; (iv) the viruses have precisely coiled helical nuecleocapsids with a diameter of approx. 50 nm; (v) most of the viruses which have been studied contain 5 proteins; the prototype, vesicular stomatitis virus, contains proteins designated L (large), G (glycoprotein), N (nucleoprotein), NS (nonstructural) and M (matrix); N or NS is phosphorylated in most members which have been studied; (vi) the viruses contain single-stranded RNA which is transcribed into several messenger RNA species with sizes corresponding to the structural proteins; (vii) the nucleocapsid contains the RNA-dependent RNA polymerase and is infectious; and (viii) many of the viruses produce morphologically distinct defective-interfering (T) particles.
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