A continuing high incidence of subacute sclerosing panencephalitis (SSPE) in the Eastern Highlands of Papua New Guinea.

The aims of this descriptive study were to confirm the high incidence of subacute sclerosing panencephalitis (SSPE) previously reported from Papua New Guinea (PNG) and to relate SSPE to previous measles vaccination and measles illness. From February 1997 to April 1999 we diagnosed a total of 55 patients with SSPE at Goroka Base General Hospital in Eastern Highlands Province (EHP) of PNG. The diagnosis was based on high cerebrospinal fluid and serum measles virus antibody titres with progressive neurological disorder and myoclonic jerks. Of these 55 patients 42 were from EHP, including 32 whose onset was in the 2-year period 1997-1998. The annual incidence of SSPE in EHP in these 2 years was 98 per million population under 20 years of age, the highest ever reported. This incidence was more than ten times higher than the highest incidence in the prevaccine era reported from elsewhere. The mean age of onset of SSPE was 7.7 years (range 2.8-14.8 years) and the interval between measles and the onset of SSPE, where known, had a mean of 5.9 years and a range of 2.5-11.1 years. Among the SSPE patients 19 had a documented history of measles vaccination. Eight of these 19 also had documentation of previous measles illness; of these, seven were vaccinated after the development of measles and one was vaccinated 20 days before measles illness. Two non-SSPE children received vaccination twice which was documented and subsequently developed measles which was also substantiated by documentation. Two patients with SSPE yielded amplified nucleotide sequences of measles virus that were different from any of the vaccine strains. We found no evidence to implicate measles vaccination in the development of SSPE.

[Transient pure red cell aplasia in an adult with acute parvovirus B19 infection: observation of PVB19 DNA by polymerase chain reaction, viral antibody and erythroid cells in the bone marrow].

A 35-year-old female was referred to our hospital for fever and anemia. Physical examination was unremarkable. Complete blood count revealed microcytic hypochromic anemia and reticulocytopenia. The bone marrow cellularity was normal. Some giant pronormoblasts were seen but other erythroid cells were absent. No stainable iron was seen. Parvovirus B19 (PVB19) DNA was detectable by polymerase chain reaction. Anti-PVB19 IgM-antibody was also positive in the serum on admission. Antibodies against rubella, measles, mumps, EB virus and HBs were negative and HBs antigen was also negative. Thus the diagnosis of iron deficiency anemia complicated with pure red cell aplasia secondary to PVB19 infection was made. The PVB19 DNA was still positive on days 6 and 11, suggesting that PVB19 virus persists as long as 3 weeks after the onset of PVB19 infection. However, the erythroid cells had recovered by day 6 after admission suggesting that the development of IgM antibody successfully protected the erythroid cells from infection by the residual PVB19. Hence, careful observation for PVB19 DNA and the antibody may be necessary if immunodeficient patients developed anemia of unknown etiology.