625
from closed oyster beds in Mobile Bay, Alabama,
during routine
sampling.2 This strain differs in three ways from the toxigenic strain the estuaries of the northern Gulf Coast: it lacks the VcA-3 vibriophage and it has a different and haemolysin chromosomal restriction pattern.3This, the first report of this strain in US coastal waters, prompted an investigation into potential sources of the organism. Attention focused on maritime activities, primarily marine transportation, that might introduce V cholerae to the Gulf Coast. Non-endemic pathogenic species can be inadvertently introduced into a region when discharged with ballast tank waters and sediments of bulk cargo vessels (see International Maritime Organisation [IMO] guidelines on this matter, adopted July 4, 1991). Vessels from Latin America could carry V cholerae in their ballast water, bilge water, or sewage tanks. Ballast water is taken on to maintain a vessel’s stability while at sea and while onloading and offloading in port; it is routinely discharged when a ship enters or docks at a port, especially if cargo is to be taken on. Such discharges are a potential source of the cholera organism since ballast tanks may hold millions of gallons of water. (Holding tanks are used for sewage and waste water storage and it is illegal to discharge from holding tanks into Alabama water.) US Food and Drug Administration scientists, accompanied by US Coast Guard authorities, and with the permission of ships’ captains, collected samples of ballast water, bilge water, and sewage from marine sanitation devices and holding tanks from fourteen cargo ships docking in Gulf of Mexico ports at Mobile, Alabama, or at Gulfport or Pascagoula, Mississippi. Toxigenic V cholerae 01, biotype El Tor, serotype Inaba, was recovered from ballast, bilge, and sewage from three ships. Toxigenicity was confirmed by reversed passive latex agglutination and polymerase chain reaction with primers constructed at the Enteric Diseases Branch, US Centers for Disease Control. The three ships had last ports of call in Brazil, Colombia, and Chile. The presence of the organism was not related to the presence of faecal coliforms. Although these fmdings do not prove the source of the organism in Gulf Coast waters, they imply that ballast water could be a vehicle of transmission and that cargo ships may be responsible for the introduction of V cholerae 01 into the area. These findings also raise the question of the potential for global transfer of the organism. The introduction of non-indigenous and pathogenic species from ballast water has been recognised by the IMO as a global problem. IMO has adopted voluntary guidelines for the exchange of ballast water on the high seas to reduce the potential spread of pathogens, and the US Coast Guard requests shipping agents and ship owners to comply with these guidelines. Additional surveillance data may be required to ascertain the extent of this problem.
endemic
to
Biological Hazards Branch, Division of Seafood Research, FDA Office of Seafood, Dauphin Island, Alabama 36528, USA
SUSAN A. MCCARTHY R. MERRILL MCPHEARSON ANTHONY M. GUARINO
Shellfish Sanitation Branch, Division of Seafood Programs, Northeast Technical Services Unit, FDA Office of Seafood, North Kingstown, Rhode Island
JACK L. GAINES
1 Centers for Disease Control. Update: cholera: western hemisphere, and recommendations for treatment of cholera. MMWR 1991; 40: 562-65. 2. DePaola A, Capers GM, Motes ML, et al. Isolation of Latin American strain of Vibrio cholerae O1 from US Gulf Coast. Lancet 1992; 339: 624-25. 3 Wachsmuth IK, Bopp CA, Fields PI, Carrillo C. Difference between toxigenic Vibrio cholerae O1 from South America and US Gulf Coast. Lancet 1991; 337: 1097-98.
admission and before streptokinase therapy, was correlated significantly with fibrinogen (r=046, p =0-0001).As expected, MPV was also correlated with platelet number (r=0’46, p 0 0001). MPV and indirect measurements of infarct size were not significantly associated: peak creatine kinase (r = 0-02), QRS score (r=032), and ejection fraction (r = 0-02). In addition MPV was not a predictor of single-vessel or triple-vessel disease. The nature of the association between platelet reactivity and ischaemic heart disease is controversial. Our data and those of Martin et al suggest that there may be a dynamic relation between MPV and fibrinogen, and that at the time of an acute event MPV is no longer an independent risk factor for outcome of MI. It is important to determine at what point in convalescence the relation between MPV and fibrinogen is lost and what factors released before and during coronary thrombosis are determinants of platelet size.2.3 These fmdings underline the importance of platelet reactivity in coronary thrombosis and of developing therapeutic strategies to control the haemostaticplatelet axis in the prevention and treatment of myocardial infarction. =
Newham General Hospital, London E13 8RU, UK
1. Hirsh J. Hyperreactive platelets and complications of coronary artery disease. N Engl J Med 1987; 316: 1543-44. 2. Fuster V, Chesebro JH. Mechanisms of unstable angina. N Engl J Med 1986; 315: 1023-25. 3. Kristensen SD, Bath PMW, Martin JF. Differences in bleeding time, aspirin sensitivity and adrenaline between acute myocardial infarction and unstable angina. Cardiovasc Res 1990; 24: 19-23.
Mupirocin-resistant Staphylococcus aureus SIR,-We would comment on your correspondence about mupirocin resistance (Jan 4, p 56). First, whereas two levels of mupirocin resistance were originally described, high-level transferable and low level, we now know there to be a spectrum of so-called resistance. We have examined 181 Staphylococcus aureus isolates of known epidemiological backgrounds from three countries. We found a continuum of mupirocin minimum inhibitory concentrations (MICs) at inocula of 10’ colony-forming units per spot. Several isolates had MICs of 128-512 mg/1, intermediate
to those described previously. In one patient mixed populations were found with MICs of 16 and 1024 mg/1. We are investigating these isolates further to determine the genetic and resistance mechanisms. Disc susceptibility testing to a 5 ng mupirocin disc, as recommended,l was less helpful than with a 200 ug disc, in that organisms with MICs of 32 mg/1 or more produced
of inhibition. Second, judgment of failure of a therapeutic topical agent such as mupirocin is difficult because factors other than resistance may be relevant and have been largely ignored in published accounts. These include reinfection from other patients on a ward or in a clinic and recolonisation from other sites, such as via stool or throat. It is unreasonable to blame such failure on the agent per se. Indeed, nasal mupirocin may be very effective at eradicating throat carriage,2 but this remains to be confirmed by proper controlled studies. In view of the ability of staphylococci to reach stepwise very high levels of resistance to the agentit may be advisable to maintain the highest levels of mupirocin possible on the skin, and perhaps we should reconsider application, as originally recommended, of three, or even four, times a day and not twice a day, as advocated by Rode and co-workers (Jan 4, p 56).
no zones
Platelet size and outcome after myocardial infarction SIR,-Professor Martin and colleagues (Dec 7, p 1409) add further support to the hypothesis that platelet reactivity may be associated with outcome in myocardial infarction by demonstrating that mean platelet volume (MPV) is an independent risk factor for recurrent infarction. We have investigated haematological indices in 68 patients with acute myocardial infarction who were eligible for thrombolytic therapy with streptokinase. MPV, at the time of
K. RANJADAYALAN V. UMACHANDRAN A. D. TIMMIS C. N. GUTTERIDGE
Division of Hospital Infection, Central Public Health Laboratory, London NW9 5HT, UK
B. COOKSON H. FARRELLY M-F. PALEPOU R. GEORGE
Phillips I, Andrews JM, Bndson E, et al. A guide to sensitivity testing J Antimicrob Chemother 1991; 27 (suppl D): 40 2. Cookson BD, Phillips I. Methicillin-resistant staphylococci J Appl Bacteriol 1990; 69 (suppl 19): 55-70. 3. Slocombe B, Perry C. The antimicrobial activity of mupirocin—an update on resistance J Hosp Infect 1991; 19 (suppl B): 19-25 1.
from closed oyster beds in Mobile Bay, Alabama,
during routine
sampling.2 This strain differs in three ways from the toxigenic strain the estuaries of the northern Gulf Coast: it lacks the VcA-3 vibriophage and it has a different and haemolysin chromosomal restriction pattern.3This, the first report of this strain in US coastal waters, prompted an investigation into potential sources of the organism. Attention focused on maritime activities, primarily marine transportation, that might introduce V cholerae to the Gulf Coast. Non-endemic pathogenic species can be inadvertently introduced into a region when discharged with ballast tank waters and sediments of bulk cargo vessels (see International Maritime Organisation [IMO] guidelines on this matter, adopted July 4, 1991). Vessels from Latin America could carry V cholerae in their ballast water, bilge water, or sewage tanks. Ballast water is taken on to maintain a vessel’s stability while at sea and while onloading and offloading in port; it is routinely discharged when a ship enters or docks at a port, especially if cargo is to be taken on. Such discharges are a potential source of the cholera organism since ballast tanks may hold millions of gallons of water. (Holding tanks are used for sewage and waste water storage and it is illegal to discharge from holding tanks into Alabama water.) US Food and Drug Administration scientists, accompanied by US Coast Guard authorities, and with the permission of ships’ captains, collected samples of ballast water, bilge water, and sewage from marine sanitation devices and holding tanks from fourteen cargo ships docking in Gulf of Mexico ports at Mobile, Alabama, or at Gulfport or Pascagoula, Mississippi. Toxigenic V cholerae 01, biotype El Tor, serotype Inaba, was recovered from ballast, bilge, and sewage from three ships. Toxigenicity was confirmed by reversed passive latex agglutination and polymerase chain reaction with primers constructed at the Enteric Diseases Branch, US Centers for Disease Control. The three ships had last ports of call in Brazil, Colombia, and Chile. The presence of the organism was not related to the presence of faecal coliforms. Although these fmdings do not prove the source of the organism in Gulf Coast waters, they imply that ballast water could be a vehicle of transmission and that cargo ships may be responsible for the introduction of V cholerae 01 into the area. These findings also raise the question of the potential for global transfer of the organism. The introduction of non-indigenous and pathogenic species from ballast water has been recognised by the IMO as a global problem. IMO has adopted voluntary guidelines for the exchange of ballast water on the high seas to reduce the potential spread of pathogens, and the US Coast Guard requests shipping agents and ship owners to comply with these guidelines. Additional surveillance data may be required to ascertain the extent of this problem.
endemic
to
Biological Hazards Branch, Division of Seafood Research, FDA Office of Seafood, Dauphin Island, Alabama 36528, USA
SUSAN A. MCCARTHY R. MERRILL MCPHEARSON ANTHONY M. GUARINO
Shellfish Sanitation Branch, Division of Seafood Programs, Northeast Technical Services Unit, FDA Office of Seafood, North Kingstown, Rhode Island
JACK L. GAINES
1 Centers for Disease Control. Update: cholera: western hemisphere, and recommendations for treatment of cholera. MMWR 1991; 40: 562-65. 2. DePaola A, Capers GM, Motes ML, et al. Isolation of Latin American strain of Vibrio cholerae O1 from US Gulf Coast. Lancet 1992; 339: 624-25. 3 Wachsmuth IK, Bopp CA, Fields PI, Carrillo C. Difference between toxigenic Vibrio cholerae O1 from South America and US Gulf Coast. Lancet 1991; 337: 1097-98.
admission and before streptokinase therapy, was correlated significantly with fibrinogen (r=046, p =0-0001).As expected, MPV was also correlated with platelet number (r=0’46, p 0 0001). MPV and indirect measurements of infarct size were not significantly associated: peak creatine kinase (r = 0-02), QRS score (r=032), and ejection fraction (r = 0-02). In addition MPV was not a predictor of single-vessel or triple-vessel disease. The nature of the association between platelet reactivity and ischaemic heart disease is controversial. Our data and those of Martin et al suggest that there may be a dynamic relation between MPV and fibrinogen, and that at the time of an acute event MPV is no longer an independent risk factor for outcome of MI. It is important to determine at what point in convalescence the relation between MPV and fibrinogen is lost and what factors released before and during coronary thrombosis are determinants of platelet size.2.3 These fmdings underline the importance of platelet reactivity in coronary thrombosis and of developing therapeutic strategies to control the haemostaticplatelet axis in the prevention and treatment of myocardial infarction. =
Newham General Hospital, London E13 8RU, UK
1. Hirsh J. Hyperreactive platelets and complications of coronary artery disease. N Engl J Med 1987; 316: 1543-44. 2. Fuster V, Chesebro JH. Mechanisms of unstable angina. N Engl J Med 1986; 315: 1023-25. 3. Kristensen SD, Bath PMW, Martin JF. Differences in bleeding time, aspirin sensitivity and adrenaline between acute myocardial infarction and unstable angina. Cardiovasc Res 1990; 24: 19-23.
Mupirocin-resistant Staphylococcus aureus SIR,-We would comment on your correspondence about mupirocin resistance (Jan 4, p 56). First, whereas two levels of mupirocin resistance were originally described, high-level transferable and low level, we now know there to be a spectrum of so-called resistance. We have examined 181 Staphylococcus aureus isolates of known epidemiological backgrounds from three countries. We found a continuum of mupirocin minimum inhibitory concentrations (MICs) at inocula of 10’ colony-forming units per spot. Several isolates had MICs of 128-512 mg/1, intermediate
to those described previously. In one patient mixed populations were found with MICs of 16 and 1024 mg/1. We are investigating these isolates further to determine the genetic and resistance mechanisms. Disc susceptibility testing to a 5 ng mupirocin disc, as recommended,l was less helpful than with a 200 ug disc, in that organisms with MICs of 32 mg/1 or more produced
of inhibition. Second, judgment of failure of a therapeutic topical agent such as mupirocin is difficult because factors other than resistance may be relevant and have been largely ignored in published accounts. These include reinfection from other patients on a ward or in a clinic and recolonisation from other sites, such as via stool or throat. It is unreasonable to blame such failure on the agent per se. Indeed, nasal mupirocin may be very effective at eradicating throat carriage,2 but this remains to be confirmed by proper controlled studies. In view of the ability of staphylococci to reach stepwise very high levels of resistance to the agentit may be advisable to maintain the highest levels of mupirocin possible on the skin, and perhaps we should reconsider application, as originally recommended, of three, or even four, times a day and not twice a day, as advocated by Rode and co-workers (Jan 4, p 56).
no zones
Platelet size and outcome after myocardial infarction SIR,-Professor Martin and colleagues (Dec 7, p 1409) add further support to the hypothesis that platelet reactivity may be associated with outcome in myocardial infarction by demonstrating that mean platelet volume (MPV) is an independent risk factor for recurrent infarction. We have investigated haematological indices in 68 patients with acute myocardial infarction who were eligible for thrombolytic therapy with streptokinase. MPV, at the time of
K. RANJADAYALAN V. UMACHANDRAN A. D. TIMMIS C. N. GUTTERIDGE
Division of Hospital Infection, Central Public Health Laboratory, London NW9 5HT, UK
B. COOKSON H. FARRELLY M-F. PALEPOU R. GEORGE
Phillips I, Andrews JM, Bndson E, et al. A guide to sensitivity testing J Antimicrob Chemother 1991; 27 (suppl D): 40 2. Cookson BD, Phillips I. Methicillin-resistant staphylococci J Appl Bacteriol 1990; 69 (suppl 19): 55-70. 3. Slocombe B, Perry C. The antimicrobial activity of mupirocin—an update on resistance J Hosp Infect 1991; 19 (suppl B): 19-25 1.
