676
Of the 88
patients who were being regularly followed, 11 (13%) anti-HCV positive by ELISA (OD 1.4 [1’0]) at the initial visit. 2 of these were ELI SA negative in 1990, whereas 1 patient, who was initially negative, had become ELISA positive by 1990. The latter had no identifiable source of infection. 3 of these ELISA-positive samples were reactive by RIBA, 2 were indeterminate (1 RIBA C100-3 reactive, 1 RIBA 5-1-1 reactive), and 6 were non-reactive. This corresponds to about a 3% prevalence of anti-HCV positivity for the group as a whole. For 7 of the 11 patients ELISA-positive in 1990, serum was available for HCV RNA determination. None had detectable HCV-RNA. The table shows ELISA OD values to RIBA and PCR data for these 7 patients. We conclude that the frequency of apparent anti-HCV positivity in Italian patients with PBC is somewhat higher than in the general population.10 However, since none of the patients with PBC tested by PCR, unlike those with autoimmune chronic active hepatitis5 had detectable HCV-RNA in serum, it is unlikely that HCV plays a part in the pathogenesis of PBC. were
Istituto di Scienze Biomediche, Ospedale S. Paolo, 20142 Milan, Italy
E. BERTOLINI P. ZERMIANI P. M. BATTEZZATI S. BRUNO
Division of Gastroenterology, University of Modena, Modena
E. VILLA F. MANENTI
Blood Transfusion Centre,
Ospedale S Paolo, Milan
F. MARELLI G. A. MORONI
Department of Medicine, Ospedale S. Paolo, Milan
M. ZUIN M. PODDA
Department of Internal Medicine,
1. McFarlane IG, Smith HM, Johnson PJ, Bray GP, Vergani D, Williams R. Hepatitis C virus antibodies in chronic active hepatitis: pathogenic factor or false-positive result? Lancet 1990; 335: 754-57. 2. Theilmann L, Blazek M, Goeser T, Gmelin K, Kommerell B, Fiehn W. False-positive anti-HCV tests in rheumatoid arthritis. Lancet 1990; 335: 1346. 3. Weiner AJ, Truett MA, Rosenblatt J, et al. HCV testing in low-risk population. Lancet 1990; 336: 695. 4. Wong DC, Diwan AR, Rosen L, et al. Non-specificity of anti-HCV test for seroepidemiological analysis. Lancet 1990; 336: 750-51. 5. Magrin S, Craxi A, Fabiano C, et al. Are autoimmune chronic active hepatitis (CAH) and HCV-infection related diseases? J Hepatol (in press). 6. Housset C, Hirschauer C, Courouce AM, Calvo A, Degos F, Benhamou JP. High prevalence of false positive anti HCV tests in primary biliary cirrhosis. J Hepatol 1990; 11: S30. 7. Fusconi M, Lenzi M, Ballardini G, et al. Anti-HCV testing in autoimmune hepatitis
and primary biliary cirrhosis. Lancet 1990; 336: 823. 8. Chiaramonte M, Floreani A, Giacomini A, et al. Anti-HCV in primary biliary cirrhosis. Gut 1990; 31: A626. 9. Schrumpf E, Elgjo K, Fausa O, Haukenes G, Rollag H. The significance of anti-HCV antibodies measured in chronic liver disease. J Hepatol 1990; 11: S111 10. Sirchia G, Bellobuono A, Giovannetti A, Marconi M. Antibodies to hepatitis C virus in Italian blood donors. Lancet 1989; ii: 797.
Horizontal transmission of
hepatitis
B virus
SiR,—Dr Gill and colleagues (Jan 26, p 247) highlight their findings of high prevalence of hepatitis B markers in former far eastern prisoners-of-war (POWs). We too have done such a study, examining specimens taken from all POWs who presented to Royal Air Force hospitals for health screening during 1990. The patients had been held in various geographical locations throughout south-east Asia for variable periods of time. Our findings agree with those of Gill et al,l showing a similar rate of past infection with hepatitis B (44% of 107). However, 4 (3-7%) of our study group proved to be carriers of HBsAg, whereas none was in Gill and colleagues’ group. Investigation of the prevalence of hepatitis B infection in the British Armed Forces (unpublished data) indicate that past infection with and carriage of HBsAg is very rare, being even lower than that cited for selected UK populationsThis may reflect the smaller "at risk" groups within the military (ie, intravenous drug abusers, homosexuals), and a different ethnic profile, from that of the UK in general. From a practical viewpoint this means that the POW patients form a major group of patients within military hospitals in this country that is likely to pose a risk for hepatitis B transmission. Although they may be a small proportion of such
patients elsewhere, their importance in respect of infection control should not be forgotten. Pathology and Tropical Medicine, Halton, Aylesbury, Bucks HP22 5PG, UK RAF Institute of
A. D. GREEN
S. J. HARBOUR
GV, Bell DR, Vamdervelde EM. Horizontal transmission of hepatitis B virus amongst British 2nd World War soldiers in South-East Asia Postgrad Med J 1991, 67: 39-41. 2. Tedder RS, Cameron CH, Barbara JAJ, Howell D Viral hepatitis markers in blood donors with history of jaundice. Lancet 1980; i: 595-96. 1. Gill
Rickettsia conorii isolated from ticks introduced to northern France by a dog SiR,—A 53-year-old man presented in October, 1989,2 months after his return from a stay on the French Riviera, with a severe form of Mediterranean spotted fever. He had a widespread rash with black eschar on the anterior chest, pneumonia, lymphocytic meningitis, nephritis, hepatitis, and conjunctival injection. Serological tests, with immunofluorescence techniques, were positive with titres of 10 240 for IgG and 640 for IgM. After treatment with ofloxacin for 3 weeks he was cured. The time that had elapsed between the end of his stay on the French Riviera and the onset of clinical signs was too long for the infection to have been acquired while he was in that endemic area.’1 In November, 1989, the patient’s dogs, which had been on the French Riviera during that summer, were found to be seropositive for Rickettsia conorii (IgG titre 2560). In May, 1990, three ticks (Rhipicephalus sanguineus) were found on the dogs. After culture on primary chicken embryo cells and inoculation in guineapigs, R conorii was identified (Dr M. Tibon, Rickettsia Laboratory, Institute Pasteur, Paris). This observation confirms the possibility of Mediterranean spotted fever being "exported" from an endemic area (here southeastern France) via dogs carrying tick-bome R conorii.2,3 The mild 1989-90 winter and early spring probably helped dog ticks to survive.4-6 This form of Mediterranean spotted fever, with a seemingly uncharacteristic incubation period, may mislead the physician and delay the onset of specific treatment. When Mediterranean spotted fever is suspected, an unusual incubation period (more than 15 days) should not exclude the diagnosis.
Department of Infectious Diseases, University of Lille, Centre Hospitalier de Tourcoing 59208 Tourcoing, France
E. SENNEVILLE F. AJANA P. LECOCQ
C. CHIDIAC Y. MOUTON
1. Font-Creus B, Bella-Cueto F, Espero-Arenas E, et al Mediterranean spotted fever, a cooperative study of 227 cases. Rev Infect Dis 1985; 7: 635-42. 2. Lambert M, Dugernier T, Bigaignon G, Rahier J, Piot P. Mediterranean spotted fever in Belgium. Lancet 1984; ii: 1038 3. Peter O, Burgdorfer W, Aeschlimann A, Cuatelannat P. Rickettsia conoru isolated from Rhipicephalus sanguineus introduced m Switzerland on a pet dog. Z Parasit 1984. 70: 265-70 4. Esero-Arenas E, Font-Creus B, Bella-Cueto F, Segura-Porta F Climatic factors in resurgence of Mediteranean spotted fever. Lancet 1986; i 1333 5. Brouqui P, Toga B, Raoult D. La fièvre boutonneuse Méditerranéenne en 1988 Méd Mal Infect 1988; 6/7: 323-28. 6. Segura-Porta F, Font-Creus B. Resurgence of Mediterranean spotted fever in Spain Lancet 1982; ii. 280.
Q fever: from deer to
dog to man
SIR,-Cattle, sheep, and goats are the main reservoirs of Coxiella burnetii in man.1 Human infection commonly takes place when an infected animal gives birth, since high concentrations of the organism are found in the products of conception.2We now report the first outbreak of Q fever after exposure to a deer and an infected pregnant dog. In late November, 1989,7 members (A-G) of a family from New Brunswick became ill with headache, fever, myalgia, fatigue, sweats, and a mild non-productive cough. 6 had multiple small round opacities on chest radiography. 6 had a greater than four-fold rise in phase II antibody titre to C burnetii antigen with the indirect immunofluorescence test (IFA). The seventh family member had a
Of the 88
patients who were being regularly followed, 11 (13%) anti-HCV positive by ELISA (OD 1.4 [1’0]) at the initial visit. 2 of these were ELI SA negative in 1990, whereas 1 patient, who was initially negative, had become ELISA positive by 1990. The latter had no identifiable source of infection. 3 of these ELISA-positive samples were reactive by RIBA, 2 were indeterminate (1 RIBA C100-3 reactive, 1 RIBA 5-1-1 reactive), and 6 were non-reactive. This corresponds to about a 3% prevalence of anti-HCV positivity for the group as a whole. For 7 of the 11 patients ELISA-positive in 1990, serum was available for HCV RNA determination. None had detectable HCV-RNA. The table shows ELISA OD values to RIBA and PCR data for these 7 patients. We conclude that the frequency of apparent anti-HCV positivity in Italian patients with PBC is somewhat higher than in the general population.10 However, since none of the patients with PBC tested by PCR, unlike those with autoimmune chronic active hepatitis5 had detectable HCV-RNA in serum, it is unlikely that HCV plays a part in the pathogenesis of PBC. were
Istituto di Scienze Biomediche, Ospedale S. Paolo, 20142 Milan, Italy
E. BERTOLINI P. ZERMIANI P. M. BATTEZZATI S. BRUNO
Division of Gastroenterology, University of Modena, Modena
E. VILLA F. MANENTI
Blood Transfusion Centre,
Ospedale S Paolo, Milan
F. MARELLI G. A. MORONI
Department of Medicine, Ospedale S. Paolo, Milan
M. ZUIN M. PODDA
Department of Internal Medicine,
1. McFarlane IG, Smith HM, Johnson PJ, Bray GP, Vergani D, Williams R. Hepatitis C virus antibodies in chronic active hepatitis: pathogenic factor or false-positive result? Lancet 1990; 335: 754-57. 2. Theilmann L, Blazek M, Goeser T, Gmelin K, Kommerell B, Fiehn W. False-positive anti-HCV tests in rheumatoid arthritis. Lancet 1990; 335: 1346. 3. Weiner AJ, Truett MA, Rosenblatt J, et al. HCV testing in low-risk population. Lancet 1990; 336: 695. 4. Wong DC, Diwan AR, Rosen L, et al. Non-specificity of anti-HCV test for seroepidemiological analysis. Lancet 1990; 336: 750-51. 5. Magrin S, Craxi A, Fabiano C, et al. Are autoimmune chronic active hepatitis (CAH) and HCV-infection related diseases? J Hepatol (in press). 6. Housset C, Hirschauer C, Courouce AM, Calvo A, Degos F, Benhamou JP. High prevalence of false positive anti HCV tests in primary biliary cirrhosis. J Hepatol 1990; 11: S30. 7. Fusconi M, Lenzi M, Ballardini G, et al. Anti-HCV testing in autoimmune hepatitis
and primary biliary cirrhosis. Lancet 1990; 336: 823. 8. Chiaramonte M, Floreani A, Giacomini A, et al. Anti-HCV in primary biliary cirrhosis. Gut 1990; 31: A626. 9. Schrumpf E, Elgjo K, Fausa O, Haukenes G, Rollag H. The significance of anti-HCV antibodies measured in chronic liver disease. J Hepatol 1990; 11: S111 10. Sirchia G, Bellobuono A, Giovannetti A, Marconi M. Antibodies to hepatitis C virus in Italian blood donors. Lancet 1989; ii: 797.
Horizontal transmission of
hepatitis
B virus
SiR,—Dr Gill and colleagues (Jan 26, p 247) highlight their findings of high prevalence of hepatitis B markers in former far eastern prisoners-of-war (POWs). We too have done such a study, examining specimens taken from all POWs who presented to Royal Air Force hospitals for health screening during 1990. The patients had been held in various geographical locations throughout south-east Asia for variable periods of time. Our findings agree with those of Gill et al,l showing a similar rate of past infection with hepatitis B (44% of 107). However, 4 (3-7%) of our study group proved to be carriers of HBsAg, whereas none was in Gill and colleagues’ group. Investigation of the prevalence of hepatitis B infection in the British Armed Forces (unpublished data) indicate that past infection with and carriage of HBsAg is very rare, being even lower than that cited for selected UK populationsThis may reflect the smaller "at risk" groups within the military (ie, intravenous drug abusers, homosexuals), and a different ethnic profile, from that of the UK in general. From a practical viewpoint this means that the POW patients form a major group of patients within military hospitals in this country that is likely to pose a risk for hepatitis B transmission. Although they may be a small proportion of such
patients elsewhere, their importance in respect of infection control should not be forgotten. Pathology and Tropical Medicine, Halton, Aylesbury, Bucks HP22 5PG, UK RAF Institute of
A. D. GREEN
S. J. HARBOUR
GV, Bell DR, Vamdervelde EM. Horizontal transmission of hepatitis B virus amongst British 2nd World War soldiers in South-East Asia Postgrad Med J 1991, 67: 39-41. 2. Tedder RS, Cameron CH, Barbara JAJ, Howell D Viral hepatitis markers in blood donors with history of jaundice. Lancet 1980; i: 595-96. 1. Gill
Rickettsia conorii isolated from ticks introduced to northern France by a dog SiR,—A 53-year-old man presented in October, 1989,2 months after his return from a stay on the French Riviera, with a severe form of Mediterranean spotted fever. He had a widespread rash with black eschar on the anterior chest, pneumonia, lymphocytic meningitis, nephritis, hepatitis, and conjunctival injection. Serological tests, with immunofluorescence techniques, were positive with titres of 10 240 for IgG and 640 for IgM. After treatment with ofloxacin for 3 weeks he was cured. The time that had elapsed between the end of his stay on the French Riviera and the onset of clinical signs was too long for the infection to have been acquired while he was in that endemic area.’1 In November, 1989, the patient’s dogs, which had been on the French Riviera during that summer, were found to be seropositive for Rickettsia conorii (IgG titre 2560). In May, 1990, three ticks (Rhipicephalus sanguineus) were found on the dogs. After culture on primary chicken embryo cells and inoculation in guineapigs, R conorii was identified (Dr M. Tibon, Rickettsia Laboratory, Institute Pasteur, Paris). This observation confirms the possibility of Mediterranean spotted fever being "exported" from an endemic area (here southeastern France) via dogs carrying tick-bome R conorii.2,3 The mild 1989-90 winter and early spring probably helped dog ticks to survive.4-6 This form of Mediterranean spotted fever, with a seemingly uncharacteristic incubation period, may mislead the physician and delay the onset of specific treatment. When Mediterranean spotted fever is suspected, an unusual incubation period (more than 15 days) should not exclude the diagnosis.
Department of Infectious Diseases, University of Lille, Centre Hospitalier de Tourcoing 59208 Tourcoing, France
E. SENNEVILLE F. AJANA P. LECOCQ
C. CHIDIAC Y. MOUTON
1. Font-Creus B, Bella-Cueto F, Espero-Arenas E, et al Mediterranean spotted fever, a cooperative study of 227 cases. Rev Infect Dis 1985; 7: 635-42. 2. Lambert M, Dugernier T, Bigaignon G, Rahier J, Piot P. Mediterranean spotted fever in Belgium. Lancet 1984; ii: 1038 3. Peter O, Burgdorfer W, Aeschlimann A, Cuatelannat P. Rickettsia conoru isolated from Rhipicephalus sanguineus introduced m Switzerland on a pet dog. Z Parasit 1984. 70: 265-70 4. Esero-Arenas E, Font-Creus B, Bella-Cueto F, Segura-Porta F Climatic factors in resurgence of Mediteranean spotted fever. Lancet 1986; i 1333 5. Brouqui P, Toga B, Raoult D. La fièvre boutonneuse Méditerranéenne en 1988 Méd Mal Infect 1988; 6/7: 323-28. 6. Segura-Porta F, Font-Creus B. Resurgence of Mediterranean spotted fever in Spain Lancet 1982; ii. 280.
Q fever: from deer to
dog to man
SIR,-Cattle, sheep, and goats are the main reservoirs of Coxiella burnetii in man.1 Human infection commonly takes place when an infected animal gives birth, since high concentrations of the organism are found in the products of conception.2We now report the first outbreak of Q fever after exposure to a deer and an infected pregnant dog. In late November, 1989,7 members (A-G) of a family from New Brunswick became ill with headache, fever, myalgia, fatigue, sweats, and a mild non-productive cough. 6 had multiple small round opacities on chest radiography. 6 had a greater than four-fold rise in phase II antibody titre to C burnetii antigen with the indirect immunofluorescence test (IFA). The seventh family member had a
