240
CMV, 60% were infected with other viruses (apart from HIV) such as Epstein-Barr or hepatitis B virus, and 82% had verified
myocbacterial infection. Other bacterial infectious were also present in some patients. In contrast, only 30% of 44 AIDS patients with dementia due to brain tumour or toxoplasmosis were infected with CMV, only 18% had other viral infections, and only 11% had bacterial infections. The combination of CMV with mycobacteria was highly correlated (p < 005) with microglial and demyelinating encephalitis in these patients. More importantly, no other infectious agent or combination of agents differentiated between affected and non-affected patients; nor did patients with CMV infections only or patients with bacterial infections only develop encephalitis.’ These are precisely the results that one would expect from animal models of autoimmune encephalitis.2 It would therefore be interesting to know whether Power’s patients or others with demyelinisation and microglial nodules are also characterised by concurrent viral and bacterial infections. If this correlation holds up, vaccination against CMV, use of antiviral drugs such as acyclovir and ganciclovir, and BCG therapy or other antimicrobial prophylaxis may be effective in preventing or curing such encephalopathies, especially in high-risk groups such as transplant, cancer chemotherapy, and AIDS patients. Department of Physiology, Michigan State University, East Lansing, Michigan 48824, USA
ROBERT S. ROOT-BERNSTEIN
1. Root-Bernstein RS. Multiple-antigen-mediated autoimmunity (MAMA) in AIDS: a possible model for postinfectious autoimmune complications. Res Immunol 1990; 141: 321-39. 2. Westall FC, Root-Bernstein RS. Cause and prevention of postinfectious and postvaccinal neuropathies in light of anew theory of autoimmunity. Lancet 1986; ii: 251-52. 3. Schneck SA. Neuropathological features of human organ transplantation. J Neuropathol Exp Neurol 1965; 24: 415-29. 4. Morton R, Graham DI, Bnggs JD, Hamilton DNH. Principal neuropathological and general necropsy findings in 24 renal transplant patients. J Clin Pathol 1982; 34: 31-39. 5. Petito CK, Navia BA, Cho E-S, Jordan BD, George DC, Price RW. Vacuolar myelopathy pathologically resembling subacute combined degeneration in patients with acquired immunodeficiency syndrome. N EnglJ Med 1985; 312: 874-79 6. Navia BA, Jordan BD, Price RW. The AIDS dementia complex I: clinical features. Ann Neural 1986; 19: 517-35.
Falls among the elderly SIR,—Delmi and colleagues! suggest that malnutrition among the elderly may increase the risk of fracture after an accidental fall. the frequency of complications and deaths after hip fracture was significantly lower in those who received an oral dietary supplement. Dr Vellas and colleagues (Dec 8, p 1447) compared anthropometric and biological markers between non-fallers and fallers, and found an increased propensity to fall among malnourished elderly. A secondary nutritional deficiency state in the elderly may also take place during chronic illness, which may also increase risk offalls.2,3 We describe a case-control study to test whether falls among elderly are associated with chronic disease leading to death. The female residents of a nursing home were studied and 20 deaths (mean age, 89 years; none as a result of fracture or hypothermia) were recorded between November, 1988, and October, 1990. 44 mobile women (mean age 88), alive in October, 1990, and who lived in the nursing home at the same time as cases, formed the control group. Cases were observed for a mean of 14 months compared with 24 months for controls. Results of the analysis for both fallers/non-fallers and recurrent/ex and non-fallers FALLS AMONG PATIENTS WITH CHRONIC DISEASE
shown in the table. A woman who fell twice or more within 12 months of observation was classified as a recurrent faller. The frequency of falls per 12 person-months of observation in cases was 2-90 compared with 0-77 in controls (rate ratio =3-77, 95% CI are
2-47-5-77). Our study does not directly examine whether nutritional deficiences were responsible for observed differences in rates of falls between cases and controls. However, we do show that the risk of having two or more falls within 12 months of observation was significantly higher among those with chronic disease. Institute of Social and Preventive Medicine, University of Zurich, 8006 Zurich, Switzerland
MICHAL GOSTYNSKI
1. Delmi M, Rapin C-H, Bengoa J-M, et al Dietary supplementation in elderly patients with fractured neck of the femur. Lancet 1990; 335: 1013-16. 2. Gryfe CI, Amies A, Ashley MJ. A longitudinal study of falls in an elderly population I Incidence and morbidity. Age Ageing 1977; 6: 201-10. 3. Wild D, Nayak USL, Isaacs B How dangerous are falls in old people at home? Br Med J 1981; 282: 266-68.
Pneumococcal bacteraemia in immunocompetent adults SIR,-Dr Eng and Dr Aronson (Nov 17, p 1266) describe two immunocompetent adults with pneumococcal bacteraemia
secondary to otitis media and bronchitis. What investigations were used to determine immunocompetence in these patients? Selective antibody deficiency against carbohydrate antigens, notably pneumococcal polysaccharide and Haemophilus influenzae type b capsular polysaccharide, is being increasingly recognised as an important form of primary antibody deficiency.’,2 These patients would pass off as being immunocompetent if investigation of humoral immunity was limited to total serum immunoglobulin and IgG subclass levels. Apart from serum electrophoresis in the first patient, Eng and Aronson do not provide information about humoral immunity. It would be difficult to justify humoral immunocompetence in these patients in the absence of data on specific antibody responses to pneumococcal polysaccharide. Department of Immunology, John Radcliffe Hospital, Oxford OX3 9DU, UK
S. A. MISBAH G. P. SPICKETT
1 Ambrosino DM, Siber GR, Chilmonczyk BA, et al. An immunodeficiency characterized by impaired antibody responses to polysaccharides. N Engl J Med 1987; 316: 790-93 2 Kumararatne DS, Joyce HJ, Hazlewood M, et al. Selective deficiency of anticarbohydrate antibody responses leading to infections with capsulated bacterial pathogens. In. Chapel HM, Levinsky R, Webster ADB, eds. Progress m immune deficiency III. Roy Soc Med Int Symp Ser. London Royal Society of Medicine, 1991: 132-33.
*** This letter has been shown to Dr Eng and Dr Aronson, whose reply follows.-ED. L. SIR,—The causes of immunodeficiency in patients with pneumococcal bacteraemia are varied.1,2 A systematic laboratory search for immunodeficiency was not done in the patients we reported. The patients, both over 40, were previously healthy and have remained so after their admissions (now, 13 and 8 months later, respectively). Neither patient had meningitis, pneumonia, otitis, or bronchitis before admission. They do not seem to have congenital or acquired immunodeficiency states.!-6 Besides a normal serum protein electrophoresis in the first patient, complement levels and serum immunoglobulin were normal. Both patients received short courses of antibiotics and have not relapsed. Patients with immunoglobulin subclass deficiency characteristically have recurrent infections.2,7 Immunoglobulin subclassification was not done because our patients had not had bacterial infections before. Therefore, we believe that all known causes of humoral immunodeficiency were unlikely in our patients. We
cannot
For A vs B, odds rano=2 55, 95% CI 0 83-7 78, Fisher’s exact test 0 162
(two-sided)
For A, vs A, + B, odds ratio (two-sided)
= 7 93, 95% CI 2-53-24-87; Fisher’s exact test 0 00123
measure
specific
responses
to
pneumococcal
in these two patients because no pre-vaccination serum remains. As a group, adults with no previous infections, who have a single episode of encapsulated bacteraemia from occult or superficial infections, have not been studied systematically with respect to their antibody response to carbohydrate antigens or to
polysaccharide
CMV, 60% were infected with other viruses (apart from HIV) such as Epstein-Barr or hepatitis B virus, and 82% had verified
myocbacterial infection. Other bacterial infectious were also present in some patients. In contrast, only 30% of 44 AIDS patients with dementia due to brain tumour or toxoplasmosis were infected with CMV, only 18% had other viral infections, and only 11% had bacterial infections. The combination of CMV with mycobacteria was highly correlated (p < 005) with microglial and demyelinating encephalitis in these patients. More importantly, no other infectious agent or combination of agents differentiated between affected and non-affected patients; nor did patients with CMV infections only or patients with bacterial infections only develop encephalitis.’ These are precisely the results that one would expect from animal models of autoimmune encephalitis.2 It would therefore be interesting to know whether Power’s patients or others with demyelinisation and microglial nodules are also characterised by concurrent viral and bacterial infections. If this correlation holds up, vaccination against CMV, use of antiviral drugs such as acyclovir and ganciclovir, and BCG therapy or other antimicrobial prophylaxis may be effective in preventing or curing such encephalopathies, especially in high-risk groups such as transplant, cancer chemotherapy, and AIDS patients. Department of Physiology, Michigan State University, East Lansing, Michigan 48824, USA
ROBERT S. ROOT-BERNSTEIN
1. Root-Bernstein RS. Multiple-antigen-mediated autoimmunity (MAMA) in AIDS: a possible model for postinfectious autoimmune complications. Res Immunol 1990; 141: 321-39. 2. Westall FC, Root-Bernstein RS. Cause and prevention of postinfectious and postvaccinal neuropathies in light of anew theory of autoimmunity. Lancet 1986; ii: 251-52. 3. Schneck SA. Neuropathological features of human organ transplantation. J Neuropathol Exp Neurol 1965; 24: 415-29. 4. Morton R, Graham DI, Bnggs JD, Hamilton DNH. Principal neuropathological and general necropsy findings in 24 renal transplant patients. J Clin Pathol 1982; 34: 31-39. 5. Petito CK, Navia BA, Cho E-S, Jordan BD, George DC, Price RW. Vacuolar myelopathy pathologically resembling subacute combined degeneration in patients with acquired immunodeficiency syndrome. N EnglJ Med 1985; 312: 874-79 6. Navia BA, Jordan BD, Price RW. The AIDS dementia complex I: clinical features. Ann Neural 1986; 19: 517-35.
Falls among the elderly SIR,—Delmi and colleagues! suggest that malnutrition among the elderly may increase the risk of fracture after an accidental fall. the frequency of complications and deaths after hip fracture was significantly lower in those who received an oral dietary supplement. Dr Vellas and colleagues (Dec 8, p 1447) compared anthropometric and biological markers between non-fallers and fallers, and found an increased propensity to fall among malnourished elderly. A secondary nutritional deficiency state in the elderly may also take place during chronic illness, which may also increase risk offalls.2,3 We describe a case-control study to test whether falls among elderly are associated with chronic disease leading to death. The female residents of a nursing home were studied and 20 deaths (mean age, 89 years; none as a result of fracture or hypothermia) were recorded between November, 1988, and October, 1990. 44 mobile women (mean age 88), alive in October, 1990, and who lived in the nursing home at the same time as cases, formed the control group. Cases were observed for a mean of 14 months compared with 24 months for controls. Results of the analysis for both fallers/non-fallers and recurrent/ex and non-fallers FALLS AMONG PATIENTS WITH CHRONIC DISEASE
shown in the table. A woman who fell twice or more within 12 months of observation was classified as a recurrent faller. The frequency of falls per 12 person-months of observation in cases was 2-90 compared with 0-77 in controls (rate ratio =3-77, 95% CI are
2-47-5-77). Our study does not directly examine whether nutritional deficiences were responsible for observed differences in rates of falls between cases and controls. However, we do show that the risk of having two or more falls within 12 months of observation was significantly higher among those with chronic disease. Institute of Social and Preventive Medicine, University of Zurich, 8006 Zurich, Switzerland
MICHAL GOSTYNSKI
1. Delmi M, Rapin C-H, Bengoa J-M, et al Dietary supplementation in elderly patients with fractured neck of the femur. Lancet 1990; 335: 1013-16. 2. Gryfe CI, Amies A, Ashley MJ. A longitudinal study of falls in an elderly population I Incidence and morbidity. Age Ageing 1977; 6: 201-10. 3. Wild D, Nayak USL, Isaacs B How dangerous are falls in old people at home? Br Med J 1981; 282: 266-68.
Pneumococcal bacteraemia in immunocompetent adults SIR,-Dr Eng and Dr Aronson (Nov 17, p 1266) describe two immunocompetent adults with pneumococcal bacteraemia
secondary to otitis media and bronchitis. What investigations were used to determine immunocompetence in these patients? Selective antibody deficiency against carbohydrate antigens, notably pneumococcal polysaccharide and Haemophilus influenzae type b capsular polysaccharide, is being increasingly recognised as an important form of primary antibody deficiency.’,2 These patients would pass off as being immunocompetent if investigation of humoral immunity was limited to total serum immunoglobulin and IgG subclass levels. Apart from serum electrophoresis in the first patient, Eng and Aronson do not provide information about humoral immunity. It would be difficult to justify humoral immunocompetence in these patients in the absence of data on specific antibody responses to pneumococcal polysaccharide. Department of Immunology, John Radcliffe Hospital, Oxford OX3 9DU, UK
S. A. MISBAH G. P. SPICKETT
1 Ambrosino DM, Siber GR, Chilmonczyk BA, et al. An immunodeficiency characterized by impaired antibody responses to polysaccharides. N Engl J Med 1987; 316: 790-93 2 Kumararatne DS, Joyce HJ, Hazlewood M, et al. Selective deficiency of anticarbohydrate antibody responses leading to infections with capsulated bacterial pathogens. In. Chapel HM, Levinsky R, Webster ADB, eds. Progress m immune deficiency III. Roy Soc Med Int Symp Ser. London Royal Society of Medicine, 1991: 132-33.
*** This letter has been shown to Dr Eng and Dr Aronson, whose reply follows.-ED. L. SIR,—The causes of immunodeficiency in patients with pneumococcal bacteraemia are varied.1,2 A systematic laboratory search for immunodeficiency was not done in the patients we reported. The patients, both over 40, were previously healthy and have remained so after their admissions (now, 13 and 8 months later, respectively). Neither patient had meningitis, pneumonia, otitis, or bronchitis before admission. They do not seem to have congenital or acquired immunodeficiency states.!-6 Besides a normal serum protein electrophoresis in the first patient, complement levels and serum immunoglobulin were normal. Both patients received short courses of antibiotics and have not relapsed. Patients with immunoglobulin subclass deficiency characteristically have recurrent infections.2,7 Immunoglobulin subclassification was not done because our patients had not had bacterial infections before. Therefore, we believe that all known causes of humoral immunodeficiency were unlikely in our patients. We
cannot
For A vs B, odds rano=2 55, 95% CI 0 83-7 78, Fisher’s exact test 0 162
(two-sided)
For A, vs A, + B, odds ratio (two-sided)
= 7 93, 95% CI 2-53-24-87; Fisher’s exact test 0 00123
measure
specific
responses
to
pneumococcal
in these two patients because no pre-vaccination serum remains. As a group, adults with no previous infections, who have a single episode of encapsulated bacteraemia from occult or superficial infections, have not been studied systematically with respect to their antibody response to carbohydrate antigens or to
polysaccharide
