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Pneumocystis carinii infection in patients with chronic bronchial disease
range 15-120, median 60) IU/mL, with 16 (24, range 3-75-120, median 7-5) after the fifth vaccination (table). The difference between the mean titres after the fourth and fifth doses of vaccine is significant (Wilcoxon matched pairs-test p<0-001). Four doses of HDCV elicited levels of protective SRVNA2 (>0-5 IU/mL) in all vaccinees, indicating that a four-dose schedule of HDCV does not compromise the protection of those exposed to rabies, but it does substantially reduce (by 20%) the expense of HDCV vaccination. were
53
(SD 36,
compared
We thank Drs Sinasi Ozsoylu, suggestions and criticisms.
Ugur Dilmen,
and Mete
Toppare,
for
M, male; F, female; *mean (SD). Table : General characteristics among carriers and non-carriers of Pneumocystis carinii with chronic obstructive lung disease
*Mustafa Hasbahceci, Mehmet Kiyan, Ergul Eyol, Larry C Ewalt, Donald L Lodmell *Hacettepe University Hospital Department of Surgery, Central Campus Sihhiye, Ankara, Turkey, and Laboratory of Persistent Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana, USA
1 Trivedi CR. Profile of dog-bites, rabies and default in antirabic immunization at VSG Hospital, Ahmedabad. J Int Med Assoc 1981; 76: 134-36. 2 WHO Expert Committee on rabies. Eight Report. World Health Organization Technical Report Series, 1992; 824: 1-84. 3 Smith JS, Yaeger PA, Baer GM. A rapid reproducible test for determining rabies neutralizing antibody. Bull WHO 1973; 48: 535-41.
Pneumocystis carinii infection in patients with chronic bronchial disease SIR-Pneumocystis carinii is a major pulmonary pathogen in immunocompromised hosts, particularly in those with AIDS. Serological surveys have shown that the parasite has a world-wide distribution but with variations in its frequency and epidemiological pattern.’ Epidemiological surveys on the general population have been hindered, since serological testing cannot distinguish between past and current infections,’ and the use of invasive methods such as bronchoscopy was frequently necessary to establish a definitive diagnosis of pneumocystosis. For all these reasons, the precise epidemiology of P carinii infection still remains unknown. However, the increase in the frequency of AIDSrelated P carinii pneumonia has led to improved diagnostic techniques such as the high-yield, induced-sputum staining method and the high sensitivity and specificity of immunofluorescence with monoclonal antibodies.2 To obtain an approximation of the prevalence of P carinii carriers in the general population, our Department of Internal Medicine has evaluated a non-selected sample of patients with chronic obstructive lung disease (chronic sputum producers) who presented to our emergency area with worsening of their pulmonary disease. Standardised epidemiological and clinical studies were carried out and sputum samples were obtained from each patient included in the study at the time they arrived at hospital. The specimens were simultaneously assayed by four different methods in order to enhance the specificity of the study: toluidine blue 0 stain, modified Giemsa stain, methenamine silver stain, and immunofluorescence with mononuclear antibodies. Identification was considered as positive if P carinii was detected by all four techniques. Simultaneous sputum analysis of 50 patients with chronic bronchial disease by the four techniques identified five subjects (95% CI 3-17) as carriers of P carinii. There were no relevant differences in age or lymphocyte concentrations between carriers and non-carriers (table). Two infected patients had never been treated with corticosteroid whereas the other three had only inhaled this agent. All subjects
denied being at risk for HIV infection, and no other reason could be found for immunosuppression. A commercial enzyme immunoassay (Abbott Laboratories, USA) did not detect HIV-1 infection in either group. The prevalence in our sample of patients with chronic obstructive lung disease is similar to that of cases of P carinii pneumonia in HIV patients recorded at our hospital between 1989 and 1993 (13-2%). This finding indicates that the prevalence in the general population must be much the same and that cases of pneumonia in immunodepressed patients are due more to recurrence in chronic carriers than to new infections. The role of these chronic sputum producers in the transmission of P carinii is yet to be deduced. The high frequency of carriers could account for the recorded increase in the incidence of pneumonia caused by this organism in patients undergoing immunosuppressive producers or in those harbouring malignancies.3 Furthermore, this could explain some recent reports of P carinii pneumonia in those without predisposing diseases.4,5
*Enrique J Calderón, Carmen Regordán, Francisco J Medrano, Manuel Ollero, José M Varela *Department of Internal Medicine, and Microbiology Service, del Rocío University Hospital, 41013 Seville, Spain
Virgen
1
Smulian AG, Sullivan DW, Linke MJ, et al. Geographic variation in the humoral response to Pneumocystis carinii. J Infect Dis 1993; 167: 1243-47.
2
3 4
5
Peglow SL, Smulian AG, Linke MJ, et al. Serologic responses to Pneumocystis carinii antigens in health and disease. J Infect Dis 1990; 161: 296-306. Varthalitis I, Aoun M, Daneau D, Meunier F. Pneumocystis carinii pneumonia in patients with cancer. Cancer 1993; 71: 481-85. Jacobs JL, Libby DM, Winter RA, et al. A cluster of Pneumocystis carinii pneumonia in adults without predisposing illnesses. N Engl J Med 1991; 324: 246-50. Cano S, Capote F, Pereira A, Calderón E, Castillo J. Pneumocystis carinii pneumonia in patients without predisposing illness: acute episode and follow-up of five cases. Chest 1993; 104: 376-81.
Protracted fever
debility
and
fatigue after
acute
Q
SiR-The conventional view of acute Q fever is that it is an unpleasant, often severe, febrile illness but one from which patients make an uneventful recovery except for a minority who subsequently develop chronic endocarditis, chronic hepatitis, or osteitis. Experience in Adelaide since 1980 and more recently Australia-wide suggests that this view is incorrect. In 1982, Maddocks (unpublished) found that 64% of 109 laboratory-verified Q fever patients, in two south Australian abattoir-associated outbreaks, were still unwell 6-12 months after the acute attack with inappropriate fatigue, night sweats, pain in the muscles and joints, mood changes, interrupted, unrefreshing sleep patterns, and loss of libido. 977
53
(SD 36,
compared
We thank Drs Sinasi Ozsoylu, suggestions and criticisms.
Ugur Dilmen,
and Mete
Toppare,
for
M, male; F, female; *mean (SD). Table : General characteristics among carriers and non-carriers of Pneumocystis carinii with chronic obstructive lung disease
*Mustafa Hasbahceci, Mehmet Kiyan, Ergul Eyol, Larry C Ewalt, Donald L Lodmell *Hacettepe University Hospital Department of Surgery, Central Campus Sihhiye, Ankara, Turkey, and Laboratory of Persistent Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana, USA
1 Trivedi CR. Profile of dog-bites, rabies and default in antirabic immunization at VSG Hospital, Ahmedabad. J Int Med Assoc 1981; 76: 134-36. 2 WHO Expert Committee on rabies. Eight Report. World Health Organization Technical Report Series, 1992; 824: 1-84. 3 Smith JS, Yaeger PA, Baer GM. A rapid reproducible test for determining rabies neutralizing antibody. Bull WHO 1973; 48: 535-41.
Pneumocystis carinii infection in patients with chronic bronchial disease SIR-Pneumocystis carinii is a major pulmonary pathogen in immunocompromised hosts, particularly in those with AIDS. Serological surveys have shown that the parasite has a world-wide distribution but with variations in its frequency and epidemiological pattern.’ Epidemiological surveys on the general population have been hindered, since serological testing cannot distinguish between past and current infections,’ and the use of invasive methods such as bronchoscopy was frequently necessary to establish a definitive diagnosis of pneumocystosis. For all these reasons, the precise epidemiology of P carinii infection still remains unknown. However, the increase in the frequency of AIDSrelated P carinii pneumonia has led to improved diagnostic techniques such as the high-yield, induced-sputum staining method and the high sensitivity and specificity of immunofluorescence with monoclonal antibodies.2 To obtain an approximation of the prevalence of P carinii carriers in the general population, our Department of Internal Medicine has evaluated a non-selected sample of patients with chronic obstructive lung disease (chronic sputum producers) who presented to our emergency area with worsening of their pulmonary disease. Standardised epidemiological and clinical studies were carried out and sputum samples were obtained from each patient included in the study at the time they arrived at hospital. The specimens were simultaneously assayed by four different methods in order to enhance the specificity of the study: toluidine blue 0 stain, modified Giemsa stain, methenamine silver stain, and immunofluorescence with mononuclear antibodies. Identification was considered as positive if P carinii was detected by all four techniques. Simultaneous sputum analysis of 50 patients with chronic bronchial disease by the four techniques identified five subjects (95% CI 3-17) as carriers of P carinii. There were no relevant differences in age or lymphocyte concentrations between carriers and non-carriers (table). Two infected patients had never been treated with corticosteroid whereas the other three had only inhaled this agent. All subjects
denied being at risk for HIV infection, and no other reason could be found for immunosuppression. A commercial enzyme immunoassay (Abbott Laboratories, USA) did not detect HIV-1 infection in either group. The prevalence in our sample of patients with chronic obstructive lung disease is similar to that of cases of P carinii pneumonia in HIV patients recorded at our hospital between 1989 and 1993 (13-2%). This finding indicates that the prevalence in the general population must be much the same and that cases of pneumonia in immunodepressed patients are due more to recurrence in chronic carriers than to new infections. The role of these chronic sputum producers in the transmission of P carinii is yet to be deduced. The high frequency of carriers could account for the recorded increase in the incidence of pneumonia caused by this organism in patients undergoing immunosuppressive producers or in those harbouring malignancies.3 Furthermore, this could explain some recent reports of P carinii pneumonia in those without predisposing diseases.4,5
*Enrique J Calderón, Carmen Regordán, Francisco J Medrano, Manuel Ollero, José M Varela *Department of Internal Medicine, and Microbiology Service, del Rocío University Hospital, 41013 Seville, Spain
Virgen
1
Smulian AG, Sullivan DW, Linke MJ, et al. Geographic variation in the humoral response to Pneumocystis carinii. J Infect Dis 1993; 167: 1243-47.
2
3 4
5
Peglow SL, Smulian AG, Linke MJ, et al. Serologic responses to Pneumocystis carinii antigens in health and disease. J Infect Dis 1990; 161: 296-306. Varthalitis I, Aoun M, Daneau D, Meunier F. Pneumocystis carinii pneumonia in patients with cancer. Cancer 1993; 71: 481-85. Jacobs JL, Libby DM, Winter RA, et al. A cluster of Pneumocystis carinii pneumonia in adults without predisposing illnesses. N Engl J Med 1991; 324: 246-50. Cano S, Capote F, Pereira A, Calderón E, Castillo J. Pneumocystis carinii pneumonia in patients without predisposing illness: acute episode and follow-up of five cases. Chest 1993; 104: 376-81.
Protracted fever
debility
and
fatigue after
acute
Q
SiR-The conventional view of acute Q fever is that it is an unpleasant, often severe, febrile illness but one from which patients make an uneventful recovery except for a minority who subsequently develop chronic endocarditis, chronic hepatitis, or osteitis. Experience in Adelaide since 1980 and more recently Australia-wide suggests that this view is incorrect. In 1982, Maddocks (unpublished) found that 64% of 109 laboratory-verified Q fever patients, in two south Australian abattoir-associated outbreaks, were still unwell 6-12 months after the acute attack with inappropriate fatigue, night sweats, pain in the muscles and joints, mood changes, interrupted, unrefreshing sleep patterns, and loss of libido. 977