1148
calves, and prostatic plexus, and
a resolved pyogenic meningitis. The eighth cranial nerves were grossly intact and there was no intracerebral abscess formation. S suis type II is a porcine zoonosis caused by a group R streptococcus that is responsible for septicaemia, meningitis, and arthritis in young pigs and meningitis in man.1 Case reports’have documented the importance of exposure to, or close contact with, pigs or unprocessed pork. Presentation with bilateral perceptive nerve deafness is characteristic of this disease.’,4 Young pigs are probably infected via the nasopharynx,s but the portal of entry in man is uncertain. Arends and Zanen’ reported 19 of 30 patients infected with probable occupational wounds, and skin injury was documented in 13 of 44 cases recorded in Europe.3 Lacerations of the skin of the hands and arms could well increase the risk of transmission from infected meat. Our patient’s wife reported a recent laceration of his left forearm ten days before admission, the result of trauma from the sharp rib-end of a carcass. Similar injuries of the hand are common in abattoir workers.6 Although S suis meningitis is rare (3 per 100 000), the rate of this disease in abattoir workers in the Netherlands in 1968-84 was 1500 times that for other workers.’ We feel that people in daily contact with pigs or pork should be advised to use protective handwear, and work practices in the meat processing industry should be revised to keep such trauma to a minimum.
Departments of Medicine North Middlesex Hospital, London N18 1QX, UK
and
Microbiology,
D. CLARKE J. ALMEYDA I. RAMSAY Y. J. DRABU
1. Arends
JP, Zanen HC. Meningitis caused by Streptococcus suis in humans. Rev Infect Dis 1988; 10: 131-37. 2. Zanen HC, Engel HWB. Porcine streptococci causing meningitis and septicaemia in man. Lancet 1975; i: 1286-88. 3. Lutticken R, Temmen N, Hahn G, Bartelheimer EW Meningitis caused by Streptococcus suis: case report and review of the literature. Infection 1986; 14: 181-85. 4. Shneerson JM, Chattopadhyay B, Murphy MFG, Fawcett IW. Permanent perceptive
deafness due to Streptococcus suis type II Infection. J Laryngol Otol 1980; 94: 425-27. 5. Elliott SD, Alexander TJL, Thomas H. Streptococcal infection in young pigs. II. Epidemiology and experimental production of the disease J Hyg (Camb) 1966, 64: 213-20. 6. Fraser CAM, Ball LC, Moms CA, Noah ND. Serological characterization of group A streptococci associated with skin sepsis in meat handlers. J Hyg (Camb) 1977; 78: 283-96.
Hypoplastic left heart syndrome: some clues to its aetiology SIR,-Hypoplastic left-heart syndrome (HLHS) is exhibited by between 1 in 5000 and 1 in 10 000 newborn babies. Without surgery it is fatal.! Between 1985 and 1991 HLHS was the reason for about 40% of heart transplants on infants done at Loma Linda University Medical Center, California. The cause is probably multifactorial but we hypothesised that defective growth-factor production could contribute. We report here immunocytochemical studies on sections of heart removed from 15 infants with HLHS who had heart transplants at age 4 to 90 days. Staining was assessed relative to that seen in normal hearts of roughly the same age, which showed only mild immunoreactivity for all growth factors. Staining (scored as negative-to-mild, moderate, strong, or intense) was strong or intense in 11 cases for platelet-derived growth factor (PDGF)-BB, 7 cases for PDGF-AA, 7 cases for transforming growth factor (TFG )-et, and 2 cases for TGF-&bgr;3 (figure). Where growth factors were overexpressed staining was seen in both ventricles. TGF-&bgr;3’ while implicated in valve formationwas not inappropriately expressed among the hypoplastic left heart tissues we examined. PDGF-BB stimulates growth and inhibits differentiation of L6 myoblastswhich are comparable to cardiac myocytes.4 Thus, the high levels of this peptide found here within neonatal myocytes may be significant to the aetiology of some forms of congenital heart disease such as HLHS. The role ofTFG-ot in cardiogenesis is unknown but EGF (which has the same biological activity) is a powerful chronotropic and inotropic agent for cardiac
Immunocytochemical detection of growth factors. Sections of heart stained by standard immunocytochemical techniques and avidin-biotin complex (Dako) Top left: normal heart (14 weeks), showing lack of staining for PDGF-AA Top nght: strong staining for TG F:x in hypoplastic left ventricle. Bottom strong staining m hypoplastic left ventricle for PDG F-AA (left) and PDGF-BB (right).
cells.While overexpression of TFG-x may contribute to abnormal development of the heart it is also possible that it modulates some aspect of cardiovascular physiology in HLHS. We found overexpression of PDGF and TGF-rx in myocytes associated with HLHS in both ventricles. If these factors are associated with the aetiology of HLHS why is it only the left side of the heart that fails to develop? One explanation is that they are expressed globally in an attempt to rectify the deformity. We thank Prof C.-H. Heldin (Uppsala, Sweden) for the gift of PDGF antisera. This work was supported in part by the Research Endowment Trust of St Thomas’ Hospital, London. We thank Norwich Eaton Ltd for their support. UMDS,
Guy’s Hospital, London SE1, UK
Department of Pathology, Immunology Center, and Department of Surgery, Loma Linda, University Medical Centre,
P. B.
J. BURTON
Loma, Linda, California
A. HAUCK S. L. NEHLSEN-CANNARELLA G. A. GUSEWITCH
Oncogene Science Inc, Uniondale, NY
C. M. SORENSEN
Department of Surgery, Division of Cardiothoracic Surgery, Loma Linda University Medical Center, Loma Linda, California 92354, USA
1.
S. R. GUNDRY L. L. BAILEY
Bailey LL, Nehlsen-Cannarella SL, Doroshow RW, et al. Cardiac allotransplantation in new-boms as therapy for hypoplastic left-heart syndrome. N Engl J Med 1986; 315: 949-51.
JD, Dagle JM, Walder JA, Weeks DL, Runyan RB. Epithelial mesenchymal embryonic cardiac endothelial cells is inhibited by a modified antisence oligodeoxynucleotide to transforming growth factor &bgr;3. Proc Natl Acad
2. Potts
transformation of
Sci USA 1991, 88: 1516-20. Jin P, Sejersen T, Ringerts NR. Recombinant platelet-denved growth factor BB stimulates growth and inhibits differentiation of rat L6 myoblasts. J Biol Chem 1991, 266: 1245-49 4. Schneider MD, Parker TG. Cardiac myocytes as targets for the action of peptide growth factors. Circulation 1990; 81: 1443-56. 5. Nair BG, Rashed HM, Patel TB. Epidermal growth factor stimulated rat cardiac adenylate cyclase through a GTP-binding regulatory protein. Biochem J 1989, 264: 3.
563-71.
calves, and prostatic plexus, and
a resolved pyogenic meningitis. The eighth cranial nerves were grossly intact and there was no intracerebral abscess formation. S suis type II is a porcine zoonosis caused by a group R streptococcus that is responsible for septicaemia, meningitis, and arthritis in young pigs and meningitis in man.1 Case reports’have documented the importance of exposure to, or close contact with, pigs or unprocessed pork. Presentation with bilateral perceptive nerve deafness is characteristic of this disease.’,4 Young pigs are probably infected via the nasopharynx,s but the portal of entry in man is uncertain. Arends and Zanen’ reported 19 of 30 patients infected with probable occupational wounds, and skin injury was documented in 13 of 44 cases recorded in Europe.3 Lacerations of the skin of the hands and arms could well increase the risk of transmission from infected meat. Our patient’s wife reported a recent laceration of his left forearm ten days before admission, the result of trauma from the sharp rib-end of a carcass. Similar injuries of the hand are common in abattoir workers.6 Although S suis meningitis is rare (3 per 100 000), the rate of this disease in abattoir workers in the Netherlands in 1968-84 was 1500 times that for other workers.’ We feel that people in daily contact with pigs or pork should be advised to use protective handwear, and work practices in the meat processing industry should be revised to keep such trauma to a minimum.
Departments of Medicine North Middlesex Hospital, London N18 1QX, UK
and
Microbiology,
D. CLARKE J. ALMEYDA I. RAMSAY Y. J. DRABU
1. Arends
JP, Zanen HC. Meningitis caused by Streptococcus suis in humans. Rev Infect Dis 1988; 10: 131-37. 2. Zanen HC, Engel HWB. Porcine streptococci causing meningitis and septicaemia in man. Lancet 1975; i: 1286-88. 3. Lutticken R, Temmen N, Hahn G, Bartelheimer EW Meningitis caused by Streptococcus suis: case report and review of the literature. Infection 1986; 14: 181-85. 4. Shneerson JM, Chattopadhyay B, Murphy MFG, Fawcett IW. Permanent perceptive
deafness due to Streptococcus suis type II Infection. J Laryngol Otol 1980; 94: 425-27. 5. Elliott SD, Alexander TJL, Thomas H. Streptococcal infection in young pigs. II. Epidemiology and experimental production of the disease J Hyg (Camb) 1966, 64: 213-20. 6. Fraser CAM, Ball LC, Moms CA, Noah ND. Serological characterization of group A streptococci associated with skin sepsis in meat handlers. J Hyg (Camb) 1977; 78: 283-96.
Hypoplastic left heart syndrome: some clues to its aetiology SIR,-Hypoplastic left-heart syndrome (HLHS) is exhibited by between 1 in 5000 and 1 in 10 000 newborn babies. Without surgery it is fatal.! Between 1985 and 1991 HLHS was the reason for about 40% of heart transplants on infants done at Loma Linda University Medical Center, California. The cause is probably multifactorial but we hypothesised that defective growth-factor production could contribute. We report here immunocytochemical studies on sections of heart removed from 15 infants with HLHS who had heart transplants at age 4 to 90 days. Staining was assessed relative to that seen in normal hearts of roughly the same age, which showed only mild immunoreactivity for all growth factors. Staining (scored as negative-to-mild, moderate, strong, or intense) was strong or intense in 11 cases for platelet-derived growth factor (PDGF)-BB, 7 cases for PDGF-AA, 7 cases for transforming growth factor (TFG )-et, and 2 cases for TGF-&bgr;3 (figure). Where growth factors were overexpressed staining was seen in both ventricles. TGF-&bgr;3’ while implicated in valve formationwas not inappropriately expressed among the hypoplastic left heart tissues we examined. PDGF-BB stimulates growth and inhibits differentiation of L6 myoblastswhich are comparable to cardiac myocytes.4 Thus, the high levels of this peptide found here within neonatal myocytes may be significant to the aetiology of some forms of congenital heart disease such as HLHS. The role ofTFG-ot in cardiogenesis is unknown but EGF (which has the same biological activity) is a powerful chronotropic and inotropic agent for cardiac
Immunocytochemical detection of growth factors. Sections of heart stained by standard immunocytochemical techniques and avidin-biotin complex (Dako) Top left: normal heart (14 weeks), showing lack of staining for PDGF-AA Top nght: strong staining for TG F:x in hypoplastic left ventricle. Bottom strong staining m hypoplastic left ventricle for PDG F-AA (left) and PDGF-BB (right).
cells.While overexpression of TFG-x may contribute to abnormal development of the heart it is also possible that it modulates some aspect of cardiovascular physiology in HLHS. We found overexpression of PDGF and TGF-rx in myocytes associated with HLHS in both ventricles. If these factors are associated with the aetiology of HLHS why is it only the left side of the heart that fails to develop? One explanation is that they are expressed globally in an attempt to rectify the deformity. We thank Prof C.-H. Heldin (Uppsala, Sweden) for the gift of PDGF antisera. This work was supported in part by the Research Endowment Trust of St Thomas’ Hospital, London. We thank Norwich Eaton Ltd for their support. UMDS,
Guy’s Hospital, London SE1, UK
Department of Pathology, Immunology Center, and Department of Surgery, Loma Linda, University Medical Centre,
P. B.
J. BURTON
Loma, Linda, California
A. HAUCK S. L. NEHLSEN-CANNARELLA G. A. GUSEWITCH
Oncogene Science Inc, Uniondale, NY
C. M. SORENSEN
Department of Surgery, Division of Cardiothoracic Surgery, Loma Linda University Medical Center, Loma Linda, California 92354, USA
1.
S. R. GUNDRY L. L. BAILEY
Bailey LL, Nehlsen-Cannarella SL, Doroshow RW, et al. Cardiac allotransplantation in new-boms as therapy for hypoplastic left-heart syndrome. N Engl J Med 1986; 315: 949-51.
JD, Dagle JM, Walder JA, Weeks DL, Runyan RB. Epithelial mesenchymal embryonic cardiac endothelial cells is inhibited by a modified antisence oligodeoxynucleotide to transforming growth factor &bgr;3. Proc Natl Acad
2. Potts
transformation of
Sci USA 1991, 88: 1516-20. Jin P, Sejersen T, Ringerts NR. Recombinant platelet-denved growth factor BB stimulates growth and inhibits differentiation of rat L6 myoblasts. J Biol Chem 1991, 266: 1245-49 4. Schneider MD, Parker TG. Cardiac myocytes as targets for the action of peptide growth factors. Circulation 1990; 81: 1443-56. 5. Nair BG, Rashed HM, Patel TB. Epidermal growth factor stimulated rat cardiac adenylate cyclase through a GTP-binding regulatory protein. Biochem J 1989, 264: 3.
563-71.
