HTLV-I and scabies in Australian Aborigines

1281

in

a

few

days. Serial chest radiographs showed resolution of the

interstitial lung disease. 8 weeks later, joint symptoms

were still for and the rash NSAIDs control, persisted requiring intermittently. White cell counts, ESR, and liver function tests had reverted to normal. Although human parvovirus B19 infection may cause acute polyarthritis in adults,8,9 other clinical features presented by our patient, including high spiking fever, the evanescent rash, interstitial lung disease, and high leukocytosis, made the diagnosis of adult Still’s disease more likely, and satisfied the criteria of Reginato et al.6 Viruses associated with adult Still’s disease include rubella, parainfluenza, and Epstein-Barr viruses, and echovirus 7 and cytomegalovirus.3-5,7,8 Increased serum ferritin is frequently encountered and may be of diagnostic valueand has been associated in a few patients with a virus-associated

haemophagocytic syndrome.5 The clinical spectrum of adult Still’s disease, especially the frequent occurrence of sore throat and lymphadenopathy with high fever, and its remittent nature in many cases, suggests that an infectious agent could trigger the disease in genetically predisposed patients. Human parvovirus B19 should be added to the list of

candidates. Service de Médecine Interne, Hôpital Louis Mourier, Université Paris VII, 92700 Colombes, France

J. POUCHOT H. OUAKIL M. L. DEBIN P. VINCENEUX

1. Harth M, Thompson JM, Ralph ED. Adult Still’s disease. Can Med Assoc J 1979; 120: 1507-10. 2. Huang SHK, De Coteau WE. Adult onset Still’s disease: an unusual presentation of rubella infection. Can Med Assoc J 1980; 122: 1275-76. 3. Ohta A, Yamguchi M, Tsunematsu T, et al. Adult Still’s disease: a multicenter survey of Japanese patients. J Rheumatol 1990; 17: 1058-63. 4. Wouters JMGW, van der Veen J, van de Putte LBA, de Rooij DJRAM. Adult onset Still’s disease and viral infections. J Rheumatol 1988; 47: 764-67. 5. Coffernils M, Soupart A, Pradier O, Feremans W, Nève P, Decaux G. Hyperferritinemia in adult onset Still’s disease and the hemophagocytic syndrome.

J Rheumatol 1992; 19: 1425-27. 6. Reginato AJ, Schumacher HR, Baker DG, O’Connor CR, Ferreiros J. Adult onset Still’s disease: experience in 23 patients and literature review with emphasis on organ failure. Semin Arthritis Rheum 1987; 17: 39-57. 7. White DG, Woolf AD, Mortimer PP, Cohen BJ, Blake DR, Bacon PA. Human parvovirus arthropathy. Lancet 1985; i: 419-21. 8. Reid DM, Reid TMS, Brown T, Rennie JAN, Eastmond CJ. Human parvovirusassociated arthritis: a clinical and laboratory description. Lancet 1985; i: 422-25.

Age (years) Complement resistance. infections in adults, we observed a much higher proportion of serum-resistant strains: resistant/intermediate versus sensitive was 156/17 in adults and 39/54 in children (p < 0 0001, test). Our results in younger children suggest that, with B catarrhalis as with other gram-negative bacteria, complement resistance is an important virulence factor.8

Eijkman-Winkler Institute for Medical and Clinical

Microbiology,

University Hospital, NL-3508 GA Utrecht, Netherlands

CEES HOL CEES M. VERDUIN ETIENNE VAN DIJKE JAN VERHOEF HANS VAN DIJK

1. Hager H, Verghese A, Alvarez S, Berk SL. Branhamella catarrhalis respiratory infections. Rev Infect Dis 1987; 9: 1140-49. 2. Catlin BW. Branhamella catarrhalis: an organism gaining respect as a pathogen. Clin 3.

Microbiol Rev 1990; 3: 293-330. Boyle FM, Georgiou PR, Tilse MH, McCormack JG. Branhamella (Moraxella) catarrhalis: pathogenic significance in respiratory infections. Med J Aust 1991; 154: 592-96.

Murphy TF, Sethi S. Bacterial infection in chronic obstructive pulmonary disease. Am Rev Respir Dis 1992; 146: 1067-83. 5. Rice PA. Molecular basis for serum resistance in Neisseria gonorrhoeae. Clin Microbiol 4.

Rev 1989; 2S: 112-17. 6. Vaneechoutte M, Verschraegen G, Claeys G, Weise B, van den Abeele A.

Respiratory

Moraxella (Branhamella) catarrhalis in adults and children and interpretation of the isolation of M catarrhalis from sputum. J Clin Microbiol 1990; 28: 2674-80. 7. Ejlertsen T. Pharyngeal carriage of Moraxella (Branhamella) catarrhalis in healthy adults. Eur J Clin Microbiol Infect Dis 1991; 10: 89. 8. Verduin CM, Hol C. Bootsma HJ, Verhoef J, Van Dijk H. Observations on constitutional reistance to infection. Immunol Today 1993; 14: 44-45. tract carrier rates of

Complement resistance in Branhamella (Moraxella) catarrhalis SIR,-Branhamella (Moraxella) catarrhalis is a gram-negative bacterium frequently found as a commensal of the nasopharynx in children,l and is the third major pathogen in upper respiratory tract infections of children and in lower respiratory tract infections of elderly people and patients with chronic obstructive pulmonary disease.l-4 Although resistance to complement-mediated lysis is an important virulence factor of gram-negative organisms,s nothing is known about the occurrence of complement resistance in B catarrhalis strains of different origin. We studied the frequency of serum complement resistance in 93 strains isolated from the nose or throat of 303 healthy children (age 4-13 years) and 179 cultures from sputum of adult patients with pulmonary B catarrhalis infections. Serum resistance was defined as survival of the bacteria during 3 h incubation in 50% human pooled serum.

We found

rate of B catarrhalis carriership, which 14% as age increased from 4 to 13 years. Normal values in adults do not exceed 5%."’ We observed a sharp decrease in complement-resistant strains with increasing age among the children, whereas the number of complement-sensitive strains increased up to age 9 years, and declined thereafter. Obviously, serum-sensitive strains have an advantage in colonising the nasopharynx of older children. In younger children (4-7 years), who are regularly more susceptible to upper respiratory tract infections, serum-resistant and intermediate strains predominated (figure). In the strains isolated from lower respiratory tract a

high

decreased from 40

to

HTLV-I and scabies in Australian

Aborigines

SIR,-Human T lymphotropic virus type I (HTLV-I) has been linked with adult T-cell leukaemia/lymphoma (ATLL) and with HTLV-1-associated-myeIopathy/tropicaI-spastic-paraparesis (HAM/TSP). It is transmissible by blood transfusion, intravenous drug use, perinatally, and sexually. HTLV-1 predisposes to chronic lichenified rashes in children due to non-pathogenic streptococci and staphylococci z Strongyloides stercoralis is a marker of HTLV-1 infection.3 These findings may reflect abnormal T-cell immunity,3 which is thought to be pathogenic in Norwegian scabies.4 In our Aboriginal community, chronic skin infestations caused by Sarcoptes scabiei, often resulting in Norwegian scabies, are commons Chronic suppurative skin and respiratory diseases are also common, usually without adequate explanation.5 These disorders have been ascribed to a non-specific immunological abnormality due to malnutrition, compounded5 by poor living conditions and personal and community hygiene. We have observed an association between Norwegian scabies and HTLV-I antibody in Aboriginal patients from our community. 24 full-blood Aboriginal inpatients with a range of illnesses that could have an immunological basis or be related to

1282

HTLV-I ANTIBODY RESULTS IN ABORIGINAL PATIENTS

Antibody cross-reactions with lipopolysaccharide from E coli 0157 after cholera vaccination SiR,—Strains of Escherichia coli serotype 0157:H7 are an important cause of haemolytic uraemic syndrome (HUS) in the UKl and North America.2 Patients infected with E coli 0157:H7

patient with chronic suppurative skin infection had equivocal western blot, but positive on other tests and is included as positive here. Exclusion of this patient will increase statistical evidence for association between Norwegian scabies and

*1

was

HTLV-I. WB pos=western blot positive.

HTLV-1 infection were tested for antibody to HTLV-1. All had one or more of the following clinical conditions: Norwegian scabies, scabies, chronic infected skin lesions, recurrent chest infections, bronchiectasis, unexplained abnormal liver function tests, seronegative arthropathy, neurological disease, and unexplained renal abnormalities. No patient had ATLL or HAM/TSP. When appropriate, patients also had other tests, including plasma electrophoresis, immunoglobulin subclassification, B-cell and T-cell surface markers, HIV antibody, alpha-1 antitrypsin, and anti-nuclear antibody. Apart from polyclonal gammopathies in 5 patients, no other laboratory immunological abnormalities were detected. An additional 6 patients were tested for HTLV-I antibody, including 1 part-Aboriginal patient with end-stage Hodgkin’s lymphoma and Norwegian scabies, and 5 white patients. All 6 were HTLV-I seronegative. HTLV-1 antibody was tested in serum by a passive particle agglutination test (Serodia). Positive results were confirmed by western blot (HTLV1-2 version 2.3, Diagnostic Biotech) and enzyme immunoassay (HTLV-I,

Cambridge Biotech). 5 of 5 Aboriginal patients with Norwegian scabies had unequivocal laboratory evidence of HTLV-I infection, but only 6 of 19 others were seropositive (p=00187, Fisher’s exact test). Although not a case-control study, no significant differences in sex or age distribution were noted between patients with and without Norwegian scabies (table). However, in those with Norwegian scabies (all HTLV-1 antibody positive), younger patients and males were more predominant, which contrasts with epidemiological evidence and further implies that Norwegian scabies and HTLV-I are associated. Overall seroprevalence was 46% but patients were selected for testing because of other possible HTLV-I associated illnesses, which is the likely explanation for this high rate. Previous studies in local Aborigines show an HTLV-1 seroprevalence of 14% .7 We believe uncharacterised immunological defects caused by HTLV-I explain the occurrence of Norwegian scabies in our patients. We conclude that Norwegian scabies is associated with HTLV-1 infection, and suggest that in communities with a high seroprevalence of HTLV-I that Norwegian scabies may be a marker of infection. We thank the staffs of the South Australian HIV Reference Laboratory and the National HIV Reference Centre, Fairfield, Victoria, for the relevant virological studies.

Department of Medicine, Springs Hospital, Springs, Northern Territory 0870, Australia

Alice Alice

L. C. MOLLISON S. T. H. Lo G. MARKING

Anonymous. Virus diseases: human T lymphotropic virus type I, HTLV-I. Wkly Epidemiol Rec 1989; 49: 382-83. 2. LaLegranade L, Hanchard B, Fletcher V, et al. Infective dermatitis of Jamaican children, a marker for HTLV-I infection. Lancet 1990; 336: 1345-47. 3. Nakada K, Kohakura M, Komoda H, et al. High incidence of HTLV-I antibody in carriers of Strongyloides stercoralis. Lancet 1984; i: 633. 4. Burkhart CG. Scabies: an epidemiologic reassessment. Ann Intern Med 1983; 98: 1.

498-503. 5. Gracey M. Annie B. Cunningham lecture: nutrition and infections in Australian Aboriginal children. Aust NZ J Med 1991; 21: 921-27. 6. Blattner WA. Epidemiology of HTLV-I and associated diseases. In: Blatmer WA, ed. Human retrovirology: HTLV-I New York: Raven Press, 1990: 251-65. 7. Bastian I, Hinuma Y, Doherty RR. HTLV-I amongst Northern Temtory Aborigines. Med J Aust (in press).

produce serum antibodies to the lipopolysaccharide of this organism, and serodiagnosis provides valuable evidence of infection, especially in the later stages of disease when E coli 0157 cannot be isolated from patients’ faeces.3 Antibody-antigen crossreactions have been demonstrated between the lipopolysaccharides of E coli 0157 and bacteria such as Yersinia enterocolitica, Brucella abortus, and certain strains of Citrobacter freundii:’-6 These crossreactions must be taken into consideration when interpreting the results of serological tests. Rabbit serum antibodies against the lipopolysaccharide from Vibrio cholerae 01-Inaba reacted with that of E coli 0157. Rabbit serum antibodies against the lipopolysaccharide of E coli 0157 reacted with the homologous lipopolysaccharide only.’ Similarly, serum antibodies from patients with HUS caused by E coli 0157 also reacted with the lipopolysaccharide of E coli 0157 but not with that of V cholerae 01-Inaba. This observation suggested that patients with a history of cholera or individuals vaccinated with V cholerae might produce antibodies that would react with the lipopolysaccharide of E coli 0157 in serological tests. To investigate this possibility, sera from 9 healthy volunteers with no history of cholera or HUS but immunised with Cho/Vac cholera vaccine (Wellcome) were tested for serum antibodies to the lipopolysaccharide from E coli 0157 with a routine procedure established in our laboratory. Sera are diluted in phosphatebuffered saline and tested with an enzyme-linked immunosorbent assay (ELISA) based on E coli 0157 lipopolysaccharide; values under 0-4 are considered antibody negative and sera with values over 0-7 are considered antibody positive. Sera giving ELISA values under 0-7 but over 0-4 are tested by the more definitive method of immunoblotting. 5 of the 9 volunteers’ sera gave ELISA values between 0-4 and 0-7, and contained antibodies reacting with E coli 0157 lipopolysaccharide by immunoblotting. By established criteria, these results would have been considered indicative of infection with E coli 0157. We concluded that interpretation of the results of serological tests needs to take into account the medical history of patients, especially those vaccinated against cholera. The serological response of patients with a history of cholera to the lipopolysaccharide of E coli 0157 is unknown. Laboratory of Enteric Pathogens, Central Public Health Laboratory, Colindale, London NW9 5HT, UK

H. CHART B. ROWE

1. Kleanthos H, Smith HR, Scotland SM, et al. Haemolytic uraemic syndrome in the British Isles, 1985-1988; association with verocytotoxin-producing Escherichia coli. Part 2: microbiological aspects. Arch Dis Child 1990; 65: 722-27. 2. Karmali MA. Infection by verocytotoxin-producing Escherichia coli. Clin Microbiol Rev 1989; 2: 15-38. 3. Chart H, Smith HR, Scotland SM, Rowe B, Milford DV, Taylor CM Serological identification of Escherichia colt 0157:H7 infection m haemolytic uraemic syndome. Lancet 1991; 337: 138-40. 4. Chart H, Cheasty T, Cope D, Rowe B. The serological relationship between Yersima enterocolitica 09 and Escherichia coli 0157 using sera from patients with yersiniosis and haemolytic uraemic syndrome. Epidemiol Infect 1991; 107: 349-56. 5. Chart H, Okubadejo OA, Rowe B. The serological relationship between Escherichia coli 0157 and Yersinia enterocolitica 09 using sera from patients with brucellosis. Epidemiol Infect 1991; 108: 77-85. 6. Chart H, Willshaw GA, Cheasty T, Rowe B. Structure and antigenic properties of Citrobacter freundii lipopolysaccharides. J Appl Bacteriol (in press) 7. Chart H, Cheasty T, Georgiou T, Rowe B. Antigenic cross-reactions between Erchertehia coli 0157, Vibrio cholerae (Inaba) and group N Salmonella. Serodiag Immunother Infect Dis (in press).

Halofantrine resistance in African countries SIR,-Professor Brasseur and colleagues (April 3, p 901) account rapid emergence of Plasmodium falciparum resistance to halofantrine, contrasting with the absence of resistance to mefloquine in the Congo, by high drug-pressure from halofantrine. With the same micro-isotopic test with results expressed in ICo (the for the