- Email: [email protected]
Monitoring of cyanocobalamin and hydroxocobalamin during treatment of cyanide intoxication
With Surmont and Liu, we emphasise the importance of attention to morphological details, particularly size, when observations do not fit geographical or travel history.
paying *G A
Jones, R J Hooper
Public Health
Laboratory,
Derriford
Hospital, Plymouth PL6 8DH, UK
Systolic propulsion of the eyeballs in tricuspid regurgitation with ischaemic heart disease was clinic with symptoms suggesting predominantly right-sided heart failure. Among the features on physical examination were gross distension of the jugular SIR-A 69-year-old referred to our
veins,
woman
blowing systolic murmur augmented by inspiration, peripheral oedema, and an enlarged liver with a pulsatile edge. Systolic propulsion of the eyeballs was readily seen upon sitting the patient up at 45 degrees, and looking straight across the curve of her eyes from either side. An echocardiogram with flow studies confirmed severe tricuspid regurgitation. After diuretic treatment, the patient’s symptoms improved, the jugular venous pressure fell, the tricuspid murmur became softer, and pulsation of the eyeballs disappeared. Local causes of systolic propulsion of the eyeballs, such as a
a fistula between the cavernous sinus and carotid artery, are unilateral. Thus, while this sign is little known and seldom reported, !,2 it may indicate severe tricuspid regurgitation. Furthermore, in these difficult economic times, this sign permits lucrative wagers with colleagues who generally disbelieve its existence until shown otherwise.
C David Naylor Epidemiology Unit, Sunnybrook Health Science Centre, University of Toronto, Ontario, Canada M4N 3M5 Clinical
Earnest DL, Hurst JW. Exophthalmos, stare, increase in intraocular pressure and systolic propulsion of the eyeballs due to congestive heart failure. Am J Cardiol 1970; 26: 351-54. 2 Allen SJ, Naylor CD. Pulsation of the eyeballs in tricuspid regurgitation. Can Med Assoc J 1985; 133: 119-20.
measured both hydroxocobalamin and cyanocobalamin with a method based on derivative spectrophotometry.’ The results of the hydroxocobalamin measurements, however, were not shown or discussed, although these data could have supported their theory that 5 g of hydroxocobalamin is capable of binding all available cyanide ions up to about 40 )JLmoI/L, a point at which all the hydroxocobalamin is used up. Limited information on both hydroxocobalamin and cyanocobalamin concentrations, measured under similar conditions, was published previously by Houeto and others.2 In this report, both of two fire victims with initial blood cyanide concentrations of 15 (JbmoI/L and 135 u.mol/L, strongly resembling patients seven and nine, respectively, were found to have high post-treatment hydroxocobalamin plasma concentrations, equivalent to or greater than 250 jjbmol/L. In the victim with low initial cyanide concentration, the cyanocobalamin concentration was reported to be lower than the hydroxocobalamin concentration. The inverse situation was seen in the patient with high initial cyanide. In both patients the sum of the initial and hydroxocobalamin cyanocobalamin concentrations, measured immediately after administration of the antidote, was around 500-600 jjbmol/L. Such values are more consistent with the administration of a dose of 3-714 mmol of hydroxocobalamin (5 g), than peak values of 300 u,moI/L. Although the relation between pretreatment blood cyanide concentrations and cyanocobalamin concentrations in plasma and urine are very useful, it remains to be proven that the binding capacity of a 5 g dose of hydroxocobalamin is saturated at pretreatment blood cyanide concentrations of around 40 jjLmol/L. *P Demedts, A Wauters, F Franck, H Neels Laboratory of Clinical Chemistry and Toxicology, AZ Middelheim, 2020 Antwerp, Belgium
1
Houeto P, Buneaux F, Galliot-Guilley M, Baud FJ, Levillain P. Determination of hydroxocobalamin and cyanocobalamin by derivative spectrofotometry in cyanide poisoning. J Anal Toxicol 1994; 18: 154-58.
1
Authors’
of
Monitoring cyanocobalamin and hydroxocobalamin during treatment of cyanide intoxication SiR-Houeto and colleagues (Sept 2, p 605), describe the monitoring of cyanocobalamin and hydroxocobalamin in fire victims with suspected cyanide poisoning and given a fixed dose of hydroxocobalamin intravenously. Although this approach seems to offer many advantages over the measurement of blood cyanide concentrations, some seems justified. According to Houeto and coscepticism workers’ hypothesis, the amount of cyanocobalamin formed in patients with cyanide inhalation exposure and given 5 g hydroxocobalamin can rise in relation to the initial blood cyanide level up to a concentration around 300 mol/L. The cyanide-binding capacity of the antidote seems to be saturated at pretreatment blood cyanide concentrations exceeding 40 mol/L. Hydroxocobalamin is known to be an antidote with high affinity for cyanide, forming cyanocobalamin on a molar basis. The recorded differences between the pretreatment blood cyanide levels and the initial plasma cyanocobalamin concentrations are therefore difficult to explain, unless cyanide is rapidly extracted from tissue. A plasma cyanocobalamine concentration of 40 fLmol/L, found in a patient with a negative initial blood cyanide test, is even more surprising. Furthermore, Houeto and colleagues 1706
reply
SiR-We
agree with Demedts and colleagues’ in vitro, hydroxocobalamin binds cyanide on a molar basis to form cyanocobalamin. However, the situation in vivo is not easily extrapolated because the tissue distribution of the three products-cyanide, hydroxocobalamin, and cyanocobalamin-would certainly affect the ability of hydroxocobalamin to bind cyanide. Another report has shown that the protein binding of hydroxocobalamin is important and much more so than that of cyanocobalamin.’ We confirm that patients seven and nine in our Lancet article are those reported in the description of the method of measurement of cobalamins by
fully assumption that,
spectrophotometry.2 Our
results obtained with spectrophotometric and others obtained with high-performance liquid chromatography’ showed that maximum measured plasma cyanocobalamin concentrations can greatly exceed the corresponding blood cyanide concentrations. These data support the hypothesis that hydroxocobalamin acts very rapidly by inducing an extracellular redistribution of cyanide into the intravascular space. Such a mechanism of action is known for digitalis-specific and colchicine-specific immunotherapy; data from our laboratory (S Borron, unpublished) suggest that the methaemoglobin-forming agent, sodium nitrite, acts in a similar manner. Furthermore, with respect to the maximum measured concentration of cyanobalamin and limited binding capacity measurements
of the 5 g hydroxocobalamin dose regimen, our results are reinforced by the findings of Astier and Baud.’ Despite the blood cyanide concentrations of up to 260 fLmol/L, including three cases of pure cyanide ingestion and four of smoke inhalation, the maximum measured concentration of cyanocobalamin did not exceed 275 fLmol/L. These patients were also treated with a 5 g dose of hydroxocobalamin. In our own study we outlined that in patient eight, who received a second 5 g dose, the maximum measured concentration of cyanocobalamin went from 288 jjbmoI/L after the first dose to 544 limol/L after 10 g. Because of the rapidity of formation of cyanocobalamin, the rate of administration of hydroxocobalamin can obviously greatly alter the maximum measured concentration of cyanocobalamin. We suggest that a study of in-vivo binding capacity would be useful. *P
other cases of occupational asthma due this contention. Fidias E Leon-S Department of Neurology, University of Alabama Birmingham, AL 35294, USA 1 2
at
to
moulds,2 supports
Birmingham,
UAD Station,
Sherson D, Hansen I, Sissgaard T. Occupationally related respiratory symptoms in trout-processing workers. Allergy 1989; 44: 336-41. Klaustermeyer WB, Bardana EJ, Hale C. Pulmonary hypersensitivity to Alternaria and Aspergillus in baker’s asthma. Clin Allergy 1977; 7: 227-33.
3 4
Leon-S FE. Bacteria no! Fungus yes!. J Clin Epidemiol 1995; 48: 1183-84. Leon-S FE, Zaninovic V. Sindrome de neuromicotoxicosis humana: la otra posibilidad en enfermedades neurodegeneratives. Acta Neurol Col
(in press). 5
Baur X, Frauhman
G, Haug B, Raache B, Reiher W, Weiss W. Role of aspergillus amylase in baker’s asthma. Lancet 1986; i: 43.
Houeto, J R Hoffman, M Imbert, P Levillain, F J Baud
Laboratoire et Réanimation Toxicologique, Hôpital Fernand Widal, 75475 Paris, France
Streptococcus suis as threat to pig-farmers 1
2
FJ. Simultaneous determination of hydroxocobalamin and its cyanide complex cyanocobalamin in human plasma by high-
and abattoir workers
performance liquid chromatography. Application to pharmacokinetic studies after high-dose hydroxocobalamin as an antidote for severe cyanide poisoning. J Chromatogr 1995; 667: 129-35. Houeto P, Buneaux F, Galliott-Guilley M, Baud FJ, Levillain P. Determination of hydroxocobalamin by derivative spectrophotometry in cyanide poisoning. J Anal Toxicol 1994; 18: 154-58.
and colleagues, in their Nov 11 describe a farmer with due to commentary, meningitis suis. is often a This commensal Streptococcus microorganism in pigs but can lead to disease in these animals (meningitis, bronchopneumonia, arthritis, endocarditis, and sepsis). They suggest that S suis produces only a purulent meningitis in man, very occasionally with a fatal outcome. However, arthritis, pneumonia, endophthalmitis, and endocarditis are also seen.’ More important is the fact that S suis can lead to a fulminant sepsis.!,2 Bungener and Bialek3 described an abattoir worker with chills and high fever who died of septic shock 4 h after hospital admission. Blood culture revealed S suis type II and numerous bacteria were found in the small vessels of many organs at necropsy. There was no meningitis but there were many fresh cuts and abrasions on the hands. We reported4 a 26-year-old pig farmer who had abdominal pain with diarrhoea and vomiting a few hours before admission. On arrival the patient had high fever and hypotension. There were no meningeal signs. The skin of the finger tips was split. Despite immediate fluid and antibiotic therapy, the patient developed multiple organ failure with adult respiratory distress syndrome, cardiac failure, intravascular coagulation, rhabdomyolysis, and acute renal failure. The shock proved to result from septicaemia with S suis type II. The patient recovered completely after intensive therapy. S suis infection is a zoonosis. Human beings usually develop meningitis. Septic shock is rare but fulminant and commonly fatal.’" Early recognition in pig farmers and abattoir personnel is of utmost importance. In addition to therapy for shock, immediate intravenous penicillin is mandatory. Infection could possibly be prevented by prompt disinfection of skin injuries in persons at risk.
Astier A, Baud
Salmon, ventilation, and mycotoxin inhalation SiR-Douglas and colleagues (Sept 16, p 737) report that occupational asthma was present in workers at a factory processing salmon with the ventilation system enclosed and that it decreased "after fitting an exhaust ventilation system". Sherson and colleagues’ reported a similar situation and the respiratory problems they described were thought to be caused by a bacterial endotoxin present in the environment. Interestingly, the clinical pictures resemble respiratory problems associated with the grain industry, poultry-processing, and silo unloading, and can also be compared with old-book disease, sick-building syndrome, and baker’s asthma, among other, all of which are thought to be promoted by closed environments.’-’ It is important to emphasise that closed environments not only affect the biologically respirable dust-containing bacterial endotoxins but also allow moulds to grow easily. 3,-1 Penicillium, asperqillus, and alternaria are most commonly found, and some have the capability of producing mycotoxins such as ochratoxins, tricothecens, and aflatoxins. These have been found both in the air of closed places and in patients with occupational asthma.’,2 Even though Douglas and colleagues record a direct correlation between IgE and cigarette consumption, it is noteworthy that Baur and co-workers5 also found IgEmediated sensitisation in their patients, but they thought that this was attributable to the allergenic effects of Aspergillus amilase. It should be remembered that moulds and their related mycotoxins can produce type I and type III hypersensitiVity,2 as well as immunodeficiency in exposed individuals.’ This fact is very important because mycotoxins might act as an important cofactor not only in occupational asthma but also in allowing other pathogenic to act retroviruses, microorganisms, including there was an the fact that opportunistically.4 Finally, in from of transferred improvement high symptoms people to low exposure areas in Douglas’ study, as also described in
SiR-Perseghin
*A K M Bartelink, E
van
Kregten
Departments of *Intensive Care and Microbiology, Eemland Hospital, 3816 CP Amersfoot, Netherlands
1 2 3 4
Kay R, Cheng AF, Tse CY. Streptococcus suis infection in Hong Kong. Q J Med 1995; 88: 39-47. Zanen HC, Engel HWB. Porcine streptococci causing meningitis and septicaemia in man. Lancet 1975; i: 1286-88. Bungener W, Bialek R. Fatal Streptococcus suis septicemia in an abattoir worker. Eur J Clin Microbiol Infect Dis 1989; 8: 306-08. Kregten E van, Jaarsveld B van, Rozenberg-Arska M, Bartelink A. Fulminant sepsis with Streptococcus suis type 2. In: Orefici G, ed. New perspectives on streptococci and streptococcal infections. Stuttgart: Gustav Fisher Verlag, 1992: 39-40. 1707
paying *G A
Jones, R J Hooper
Public Health
Laboratory,
Derriford
Hospital, Plymouth PL6 8DH, UK
Systolic propulsion of the eyeballs in tricuspid regurgitation with ischaemic heart disease was clinic with symptoms suggesting predominantly right-sided heart failure. Among the features on physical examination were gross distension of the jugular SIR-A 69-year-old referred to our
veins,
woman
blowing systolic murmur augmented by inspiration, peripheral oedema, and an enlarged liver with a pulsatile edge. Systolic propulsion of the eyeballs was readily seen upon sitting the patient up at 45 degrees, and looking straight across the curve of her eyes from either side. An echocardiogram with flow studies confirmed severe tricuspid regurgitation. After diuretic treatment, the patient’s symptoms improved, the jugular venous pressure fell, the tricuspid murmur became softer, and pulsation of the eyeballs disappeared. Local causes of systolic propulsion of the eyeballs, such as a
a fistula between the cavernous sinus and carotid artery, are unilateral. Thus, while this sign is little known and seldom reported, !,2 it may indicate severe tricuspid regurgitation. Furthermore, in these difficult economic times, this sign permits lucrative wagers with colleagues who generally disbelieve its existence until shown otherwise.
C David Naylor Epidemiology Unit, Sunnybrook Health Science Centre, University of Toronto, Ontario, Canada M4N 3M5 Clinical
Earnest DL, Hurst JW. Exophthalmos, stare, increase in intraocular pressure and systolic propulsion of the eyeballs due to congestive heart failure. Am J Cardiol 1970; 26: 351-54. 2 Allen SJ, Naylor CD. Pulsation of the eyeballs in tricuspid regurgitation. Can Med Assoc J 1985; 133: 119-20.
measured both hydroxocobalamin and cyanocobalamin with a method based on derivative spectrophotometry.’ The results of the hydroxocobalamin measurements, however, were not shown or discussed, although these data could have supported their theory that 5 g of hydroxocobalamin is capable of binding all available cyanide ions up to about 40 )JLmoI/L, a point at which all the hydroxocobalamin is used up. Limited information on both hydroxocobalamin and cyanocobalamin concentrations, measured under similar conditions, was published previously by Houeto and others.2 In this report, both of two fire victims with initial blood cyanide concentrations of 15 (JbmoI/L and 135 u.mol/L, strongly resembling patients seven and nine, respectively, were found to have high post-treatment hydroxocobalamin plasma concentrations, equivalent to or greater than 250 jjbmol/L. In the victim with low initial cyanide concentration, the cyanocobalamin concentration was reported to be lower than the hydroxocobalamin concentration. The inverse situation was seen in the patient with high initial cyanide. In both patients the sum of the initial and hydroxocobalamin cyanocobalamin concentrations, measured immediately after administration of the antidote, was around 500-600 jjbmol/L. Such values are more consistent with the administration of a dose of 3-714 mmol of hydroxocobalamin (5 g), than peak values of 300 u,moI/L. Although the relation between pretreatment blood cyanide concentrations and cyanocobalamin concentrations in plasma and urine are very useful, it remains to be proven that the binding capacity of a 5 g dose of hydroxocobalamin is saturated at pretreatment blood cyanide concentrations of around 40 jjLmol/L. *P Demedts, A Wauters, F Franck, H Neels Laboratory of Clinical Chemistry and Toxicology, AZ Middelheim, 2020 Antwerp, Belgium
1
Houeto P, Buneaux F, Galliot-Guilley M, Baud FJ, Levillain P. Determination of hydroxocobalamin and cyanocobalamin by derivative spectrofotometry in cyanide poisoning. J Anal Toxicol 1994; 18: 154-58.
1
Authors’
of
Monitoring cyanocobalamin and hydroxocobalamin during treatment of cyanide intoxication SiR-Houeto and colleagues (Sept 2, p 605), describe the monitoring of cyanocobalamin and hydroxocobalamin in fire victims with suspected cyanide poisoning and given a fixed dose of hydroxocobalamin intravenously. Although this approach seems to offer many advantages over the measurement of blood cyanide concentrations, some seems justified. According to Houeto and coscepticism workers’ hypothesis, the amount of cyanocobalamin formed in patients with cyanide inhalation exposure and given 5 g hydroxocobalamin can rise in relation to the initial blood cyanide level up to a concentration around 300 mol/L. The cyanide-binding capacity of the antidote seems to be saturated at pretreatment blood cyanide concentrations exceeding 40 mol/L. Hydroxocobalamin is known to be an antidote with high affinity for cyanide, forming cyanocobalamin on a molar basis. The recorded differences between the pretreatment blood cyanide levels and the initial plasma cyanocobalamin concentrations are therefore difficult to explain, unless cyanide is rapidly extracted from tissue. A plasma cyanocobalamine concentration of 40 fLmol/L, found in a patient with a negative initial blood cyanide test, is even more surprising. Furthermore, Houeto and colleagues 1706
reply
SiR-We
agree with Demedts and colleagues’ in vitro, hydroxocobalamin binds cyanide on a molar basis to form cyanocobalamin. However, the situation in vivo is not easily extrapolated because the tissue distribution of the three products-cyanide, hydroxocobalamin, and cyanocobalamin-would certainly affect the ability of hydroxocobalamin to bind cyanide. Another report has shown that the protein binding of hydroxocobalamin is important and much more so than that of cyanocobalamin.’ We confirm that patients seven and nine in our Lancet article are those reported in the description of the method of measurement of cobalamins by
fully assumption that,
spectrophotometry.2 Our
results obtained with spectrophotometric and others obtained with high-performance liquid chromatography’ showed that maximum measured plasma cyanocobalamin concentrations can greatly exceed the corresponding blood cyanide concentrations. These data support the hypothesis that hydroxocobalamin acts very rapidly by inducing an extracellular redistribution of cyanide into the intravascular space. Such a mechanism of action is known for digitalis-specific and colchicine-specific immunotherapy; data from our laboratory (S Borron, unpublished) suggest that the methaemoglobin-forming agent, sodium nitrite, acts in a similar manner. Furthermore, with respect to the maximum measured concentration of cyanobalamin and limited binding capacity measurements
of the 5 g hydroxocobalamin dose regimen, our results are reinforced by the findings of Astier and Baud.’ Despite the blood cyanide concentrations of up to 260 fLmol/L, including three cases of pure cyanide ingestion and four of smoke inhalation, the maximum measured concentration of cyanocobalamin did not exceed 275 fLmol/L. These patients were also treated with a 5 g dose of hydroxocobalamin. In our own study we outlined that in patient eight, who received a second 5 g dose, the maximum measured concentration of cyanocobalamin went from 288 jjbmoI/L after the first dose to 544 limol/L after 10 g. Because of the rapidity of formation of cyanocobalamin, the rate of administration of hydroxocobalamin can obviously greatly alter the maximum measured concentration of cyanocobalamin. We suggest that a study of in-vivo binding capacity would be useful. *P
other cases of occupational asthma due this contention. Fidias E Leon-S Department of Neurology, University of Alabama Birmingham, AL 35294, USA 1 2
at
to
moulds,2 supports
Birmingham,
UAD Station,
Sherson D, Hansen I, Sissgaard T. Occupationally related respiratory symptoms in trout-processing workers. Allergy 1989; 44: 336-41. Klaustermeyer WB, Bardana EJ, Hale C. Pulmonary hypersensitivity to Alternaria and Aspergillus in baker’s asthma. Clin Allergy 1977; 7: 227-33.
3 4
Leon-S FE. Bacteria no! Fungus yes!. J Clin Epidemiol 1995; 48: 1183-84. Leon-S FE, Zaninovic V. Sindrome de neuromicotoxicosis humana: la otra posibilidad en enfermedades neurodegeneratives. Acta Neurol Col
(in press). 5
Baur X, Frauhman
G, Haug B, Raache B, Reiher W, Weiss W. Role of aspergillus amylase in baker’s asthma. Lancet 1986; i: 43.
Houeto, J R Hoffman, M Imbert, P Levillain, F J Baud
Laboratoire et Réanimation Toxicologique, Hôpital Fernand Widal, 75475 Paris, France
Streptococcus suis as threat to pig-farmers 1
2
FJ. Simultaneous determination of hydroxocobalamin and its cyanide complex cyanocobalamin in human plasma by high-
and abattoir workers
performance liquid chromatography. Application to pharmacokinetic studies after high-dose hydroxocobalamin as an antidote for severe cyanide poisoning. J Chromatogr 1995; 667: 129-35. Houeto P, Buneaux F, Galliott-Guilley M, Baud FJ, Levillain P. Determination of hydroxocobalamin by derivative spectrophotometry in cyanide poisoning. J Anal Toxicol 1994; 18: 154-58.
and colleagues, in their Nov 11 describe a farmer with due to commentary, meningitis suis. is often a This commensal Streptococcus microorganism in pigs but can lead to disease in these animals (meningitis, bronchopneumonia, arthritis, endocarditis, and sepsis). They suggest that S suis produces only a purulent meningitis in man, very occasionally with a fatal outcome. However, arthritis, pneumonia, endophthalmitis, and endocarditis are also seen.’ More important is the fact that S suis can lead to a fulminant sepsis.!,2 Bungener and Bialek3 described an abattoir worker with chills and high fever who died of septic shock 4 h after hospital admission. Blood culture revealed S suis type II and numerous bacteria were found in the small vessels of many organs at necropsy. There was no meningitis but there were many fresh cuts and abrasions on the hands. We reported4 a 26-year-old pig farmer who had abdominal pain with diarrhoea and vomiting a few hours before admission. On arrival the patient had high fever and hypotension. There were no meningeal signs. The skin of the finger tips was split. Despite immediate fluid and antibiotic therapy, the patient developed multiple organ failure with adult respiratory distress syndrome, cardiac failure, intravascular coagulation, rhabdomyolysis, and acute renal failure. The shock proved to result from septicaemia with S suis type II. The patient recovered completely after intensive therapy. S suis infection is a zoonosis. Human beings usually develop meningitis. Septic shock is rare but fulminant and commonly fatal.’" Early recognition in pig farmers and abattoir personnel is of utmost importance. In addition to therapy for shock, immediate intravenous penicillin is mandatory. Infection could possibly be prevented by prompt disinfection of skin injuries in persons at risk.
Astier A, Baud
Salmon, ventilation, and mycotoxin inhalation SiR-Douglas and colleagues (Sept 16, p 737) report that occupational asthma was present in workers at a factory processing salmon with the ventilation system enclosed and that it decreased "after fitting an exhaust ventilation system". Sherson and colleagues’ reported a similar situation and the respiratory problems they described were thought to be caused by a bacterial endotoxin present in the environment. Interestingly, the clinical pictures resemble respiratory problems associated with the grain industry, poultry-processing, and silo unloading, and can also be compared with old-book disease, sick-building syndrome, and baker’s asthma, among other, all of which are thought to be promoted by closed environments.’-’ It is important to emphasise that closed environments not only affect the biologically respirable dust-containing bacterial endotoxins but also allow moulds to grow easily. 3,-1 Penicillium, asperqillus, and alternaria are most commonly found, and some have the capability of producing mycotoxins such as ochratoxins, tricothecens, and aflatoxins. These have been found both in the air of closed places and in patients with occupational asthma.’,2 Even though Douglas and colleagues record a direct correlation between IgE and cigarette consumption, it is noteworthy that Baur and co-workers5 also found IgEmediated sensitisation in their patients, but they thought that this was attributable to the allergenic effects of Aspergillus amilase. It should be remembered that moulds and their related mycotoxins can produce type I and type III hypersensitiVity,2 as well as immunodeficiency in exposed individuals.’ This fact is very important because mycotoxins might act as an important cofactor not only in occupational asthma but also in allowing other pathogenic to act retroviruses, microorganisms, including there was an the fact that opportunistically.4 Finally, in from of transferred improvement high symptoms people to low exposure areas in Douglas’ study, as also described in
SiR-Perseghin
*A K M Bartelink, E
van
Kregten
Departments of *Intensive Care and Microbiology, Eemland Hospital, 3816 CP Amersfoot, Netherlands
1 2 3 4
Kay R, Cheng AF, Tse CY. Streptococcus suis infection in Hong Kong. Q J Med 1995; 88: 39-47. Zanen HC, Engel HWB. Porcine streptococci causing meningitis and septicaemia in man. Lancet 1975; i: 1286-88. Bungener W, Bialek R. Fatal Streptococcus suis septicemia in an abattoir worker. Eur J Clin Microbiol Infect Dis 1989; 8: 306-08. Kregten E van, Jaarsveld B van, Rozenberg-Arska M, Bartelink A. Fulminant sepsis with Streptococcus suis type 2. In: Orefici G, ed. New perspectives on streptococci and streptococcal infections. Stuttgart: Gustav Fisher Verlag, 1992: 39-40. 1707