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MICROBES BY OTHER NAMES
1372 DESFERRIOXAMINE AND SYSTEMIC YERSINIOSIS
SIR,-The report of Dr Davies and others (July 23, p 181) of ocular toxicity associated with intravenous desferrioxamine (DFX) prompts us to draw attention to another potential hazard of DFX
therapy. During the past few months, we encountered two patients with Yersinia enterocolitica septicaemia who were receiving DFX for chronic iron overload due to &bgr;-thalassaemia in one and chronic haemodialysis in the other. Although the relation between iron overload and systemic yersiniosis is well known, the influence of DFX on yersiniosis has not been investigated. Adult Balb/c mice in groups of five were injected intraperitoneally with 0 -5ml 10% (V/V) iron-dextran solution (’Imferon’) or dextran. The following day, mice received 5 mg DFX intraperitoneally (’Desferal’) or saline and 10-fold dilutions of a virulent, plasmidbearing strain of Yenterocolitica serotype 03.Mice were observed for 7 days and the median lethal dose (LDso) was determined.3DFX greatly enhanced the susceptibility of iron-overloaded mice to Y enterocolitica, reducing the LDso more than one million-fold, and similar results were obtained even in the absence of iron:
DFX is
of a family of iron-binding ligands, termed of microbial origin that compete successfully with transferrin for available iron.4 Y enterocolitica is unusual among enteric bacteria in that it produces no detectable siderophores, although it does have receptors for them and can thus utilise ferrioxamine as a growth promotor.5 Patients with iron overload are prone to infection with a variety of microorganisms.Yenterocolitica is of particular interest in this regard, since systemic infections with this organism are virtually unknown in patients with normal iron stores. The remarkable dependence of Y enterocolitica on iron can be explained by its inability to synthesise iron-binding compounds. Supply of exogenous siderophores, such as DFX, apparently enable bacteria to overcome this handicap and express much increased virulence for man as well as laboratory animals. one
siderophores,
Department of Microbiology, University of Melbourne, Parkville, Victoria 3052, Australia
pneumonic plague. At a London hospital in 1946, reporting on a urethral exudate from a medical student, I used the department’s customary brevity and wrote: "No neisseriae seen". The doctor in charge of student health stormed into the laboratory: "I’m not interested in these neezery or whatever they are you haven’t seen: I want to know if there are gonococci". I now realise that he was making a good point. Last year, a surgeon, examining in the primary FRCS examination, asked an Arab candidate to "talk to us about the clap bacillus". As she told him, he was as ignorant of the bacteriology of gonorrhoea as he was lacking in manners. I am aware that "microbe" is anathema to some microbiologists. One once wrote to me, "Have the goodness to refrain from using the word ’microbe’. I am sure you would not advocate referring to faeces as ...."-but why, Sir, should I blemish your pages by quoting his coprophrasia? Sandy Lodge Way, Northwood, Middlesex HA6 2AS 30
WM ST C. SYMMERS
R. M. ROBINS-BROWNE
J. K. PRPIC
MICROBES BY OTHER NAMES
SIR,-Sir James Howie’s letter (Oct 8, p 855) reminds me of occasions when use of formally correct names of microorganisms caused misunderstanding. A note of some of them may remind pathologists to use nomenclature understood by clinical colleagues. A child who lived on a dairy farm had enlarged cervical lymph nodes. The histological report read: "Acid-and-alcohol-fast bacilli present; consistent with Mycobacterium bovis". The child’s father, a surgeon farmer, replied: "Thank God it is not lymphadenoma, which is what I was afraid of. We are lucky it is not even TB". The name Mycobacterium bovis was not familiar to him: he knew this organism only as "the bovine type of tubercle bacillus". He had heard of atypical mycobacteria, which he believed to be rare and harmless, and took Mycobacterium bovis to be one of them. A senior colleague once objected to my referring to "tubercle bacilli" during a clinical discussion. "As a teacher," he said "you have a duty to 1. Robins-Browne
avoid colloquialism-the only permissible name for the organism I that causes tuberculosis is Mycobacterium tuberculosis. A retired consultant physician told me of one of his gaffes: he did so not so much in humility as in criticism of the inadequacy of a system of continuing education that had failed to teach him that Bacillus typhosus had been renamed. When he heard that Salmonella typhi had been grown from a stool of a patient he replied: "That’s grand-just food-poisoning. I really believed she had typhoid". As for plague, I was once asked to look at sections of an inguinal lymph node from a patient in a distant country. The pathologist who sent them suspected syphilis. The patient had been admitted with an acutely painful swelling in a groin, vomiting, and collapse. The clinical diagnosis was strangulated hernia but the surgeon, finding a mass of necrotic lymph nodes, changed his diagnosis to lymphadenitis of primary syphilis (a recognised simulant of strangulated hernia), even though there was no obvious chancre. The sections contained what looked to me like plague bacilli, so I asked the pathologist’s embassy to send him a signal. Feeling it unwise to use the word plague, I referred to Yersinia pestis. The pathologist was not familiar with the name Yersinia: by the time he had discovered that Yersinia pestis and what he knew as Pasteurella pestis were the same the patient had recovered-but three members of the staff of the hospital were gravely ill, and one died of
RM, Rabson AR, Koornhof HJ. Generalised infection with Yersinia enterocolitica and the role of iron. Contrib Microbiol Immunol 1979; 5: 277-82. 2. Prpic JK, Robins-Browne RM, Davey RB. Differentiation between virulent and avirulent Yersinia enterocolitica isolates by using congo red agar. J Clin Microbiol 1983; 18: 486-90. 3. Reed LJ, Meunch H. A simple method of estimating fifty per cent endpoints. Am J Hyg 1935; 27: 493-97. 4. Neilands JB. Microbial iron compounds. Annu Rev Biochem 1981; 50: 715-31. 5. Perry RD, Brubaker RR. Accumulation of iron by yersiniae. J Bacteriol 1979; 137: 1290-98. 6. Weinberg ED. Iron and infection. Microbiol Rev 1978; 42: 45-66.
SKIN CANCER AND THE ULTRAVIOLET SPECTRUM
SiR,-Your Nov 12 note (p 1152) discusses a study from the US National Cancer Institute on non-melanoma skin cancer. The incidence of this skin cancer is closely associated with exposure to ultraviolet radiation, ultraviolet B (UVB) exerting the greater effect. However, recent work has demonstrated that UVA can cause similar immunological changes in laboratory animals and man, which could result in an increased susceptibility to cancer (including non-melanoma skin cancer). Over the past 25 years major changes in lifestyle have led to substantial additional exposure to sunlight in terms of body area, intensity, and duration of exposure: sun-seeking activities have become commonplace, especially in the developed world. Such exposure is further augmented by the use of solaria and other sun substitutes where the predominant form of radiation received is in the UVA spectral range. This greatly increased and dedicated exposure to ultraviolet radiation is a major mechanism to the rising incidence of non-melanoma skin cancer. Amplification factors are mentioned in your article in relation to UVB intensity; however, the intentional exposure to sources other than sunlight will become a confounding factor in future calculations. As for the impact of chlorofluorocarbons on the ozone layer, the most recent international scientific review reported calculations which estimated that continued releases of these compounds could Streilein JW. Ultraviolet radiation produces selective immune incompetence.J Invest Dermatol 1983; 81: 85-86. 2. United Nations Environment Programme Co-ordinating Committee on the Ozone Layer. UNEP/CCOL (April, 1983).
1. Bergstresser PR,
SIR,-The report of Dr Davies and others (July 23, p 181) of ocular toxicity associated with intravenous desferrioxamine (DFX) prompts us to draw attention to another potential hazard of DFX
therapy. During the past few months, we encountered two patients with Yersinia enterocolitica septicaemia who were receiving DFX for chronic iron overload due to &bgr;-thalassaemia in one and chronic haemodialysis in the other. Although the relation between iron overload and systemic yersiniosis is well known, the influence of DFX on yersiniosis has not been investigated. Adult Balb/c mice in groups of five were injected intraperitoneally with 0 -5ml 10% (V/V) iron-dextran solution (’Imferon’) or dextran. The following day, mice received 5 mg DFX intraperitoneally (’Desferal’) or saline and 10-fold dilutions of a virulent, plasmidbearing strain of Yenterocolitica serotype 03.Mice were observed for 7 days and the median lethal dose (LDso) was determined.3DFX greatly enhanced the susceptibility of iron-overloaded mice to Y enterocolitica, reducing the LDso more than one million-fold, and similar results were obtained even in the absence of iron:
DFX is
of a family of iron-binding ligands, termed of microbial origin that compete successfully with transferrin for available iron.4 Y enterocolitica is unusual among enteric bacteria in that it produces no detectable siderophores, although it does have receptors for them and can thus utilise ferrioxamine as a growth promotor.5 Patients with iron overload are prone to infection with a variety of microorganisms.Yenterocolitica is of particular interest in this regard, since systemic infections with this organism are virtually unknown in patients with normal iron stores. The remarkable dependence of Y enterocolitica on iron can be explained by its inability to synthesise iron-binding compounds. Supply of exogenous siderophores, such as DFX, apparently enable bacteria to overcome this handicap and express much increased virulence for man as well as laboratory animals. one
siderophores,
Department of Microbiology, University of Melbourne, Parkville, Victoria 3052, Australia
pneumonic plague. At a London hospital in 1946, reporting on a urethral exudate from a medical student, I used the department’s customary brevity and wrote: "No neisseriae seen". The doctor in charge of student health stormed into the laboratory: "I’m not interested in these neezery or whatever they are you haven’t seen: I want to know if there are gonococci". I now realise that he was making a good point. Last year, a surgeon, examining in the primary FRCS examination, asked an Arab candidate to "talk to us about the clap bacillus". As she told him, he was as ignorant of the bacteriology of gonorrhoea as he was lacking in manners. I am aware that "microbe" is anathema to some microbiologists. One once wrote to me, "Have the goodness to refrain from using the word ’microbe’. I am sure you would not advocate referring to faeces as ...."-but why, Sir, should I blemish your pages by quoting his coprophrasia? Sandy Lodge Way, Northwood, Middlesex HA6 2AS 30
WM ST C. SYMMERS
R. M. ROBINS-BROWNE
J. K. PRPIC
MICROBES BY OTHER NAMES
SIR,-Sir James Howie’s letter (Oct 8, p 855) reminds me of occasions when use of formally correct names of microorganisms caused misunderstanding. A note of some of them may remind pathologists to use nomenclature understood by clinical colleagues. A child who lived on a dairy farm had enlarged cervical lymph nodes. The histological report read: "Acid-and-alcohol-fast bacilli present; consistent with Mycobacterium bovis". The child’s father, a surgeon farmer, replied: "Thank God it is not lymphadenoma, which is what I was afraid of. We are lucky it is not even TB". The name Mycobacterium bovis was not familiar to him: he knew this organism only as "the bovine type of tubercle bacillus". He had heard of atypical mycobacteria, which he believed to be rare and harmless, and took Mycobacterium bovis to be one of them. A senior colleague once objected to my referring to "tubercle bacilli" during a clinical discussion. "As a teacher," he said "you have a duty to 1. Robins-Browne
avoid colloquialism-the only permissible name for the organism I that causes tuberculosis is Mycobacterium tuberculosis. A retired consultant physician told me of one of his gaffes: he did so not so much in humility as in criticism of the inadequacy of a system of continuing education that had failed to teach him that Bacillus typhosus had been renamed. When he heard that Salmonella typhi had been grown from a stool of a patient he replied: "That’s grand-just food-poisoning. I really believed she had typhoid". As for plague, I was once asked to look at sections of an inguinal lymph node from a patient in a distant country. The pathologist who sent them suspected syphilis. The patient had been admitted with an acutely painful swelling in a groin, vomiting, and collapse. The clinical diagnosis was strangulated hernia but the surgeon, finding a mass of necrotic lymph nodes, changed his diagnosis to lymphadenitis of primary syphilis (a recognised simulant of strangulated hernia), even though there was no obvious chancre. The sections contained what looked to me like plague bacilli, so I asked the pathologist’s embassy to send him a signal. Feeling it unwise to use the word plague, I referred to Yersinia pestis. The pathologist was not familiar with the name Yersinia: by the time he had discovered that Yersinia pestis and what he knew as Pasteurella pestis were the same the patient had recovered-but three members of the staff of the hospital were gravely ill, and one died of
RM, Rabson AR, Koornhof HJ. Generalised infection with Yersinia enterocolitica and the role of iron. Contrib Microbiol Immunol 1979; 5: 277-82. 2. Prpic JK, Robins-Browne RM, Davey RB. Differentiation between virulent and avirulent Yersinia enterocolitica isolates by using congo red agar. J Clin Microbiol 1983; 18: 486-90. 3. Reed LJ, Meunch H. A simple method of estimating fifty per cent endpoints. Am J Hyg 1935; 27: 493-97. 4. Neilands JB. Microbial iron compounds. Annu Rev Biochem 1981; 50: 715-31. 5. Perry RD, Brubaker RR. Accumulation of iron by yersiniae. J Bacteriol 1979; 137: 1290-98. 6. Weinberg ED. Iron and infection. Microbiol Rev 1978; 42: 45-66.
SKIN CANCER AND THE ULTRAVIOLET SPECTRUM
SiR,-Your Nov 12 note (p 1152) discusses a study from the US National Cancer Institute on non-melanoma skin cancer. The incidence of this skin cancer is closely associated with exposure to ultraviolet radiation, ultraviolet B (UVB) exerting the greater effect. However, recent work has demonstrated that UVA can cause similar immunological changes in laboratory animals and man, which could result in an increased susceptibility to cancer (including non-melanoma skin cancer). Over the past 25 years major changes in lifestyle have led to substantial additional exposure to sunlight in terms of body area, intensity, and duration of exposure: sun-seeking activities have become commonplace, especially in the developed world. Such exposure is further augmented by the use of solaria and other sun substitutes where the predominant form of radiation received is in the UVA spectral range. This greatly increased and dedicated exposure to ultraviolet radiation is a major mechanism to the rising incidence of non-melanoma skin cancer. Amplification factors are mentioned in your article in relation to UVB intensity; however, the intentional exposure to sources other than sunlight will become a confounding factor in future calculations. As for the impact of chlorofluorocarbons on the ozone layer, the most recent international scientific review reported calculations which estimated that continued releases of these compounds could Streilein JW. Ultraviolet radiation produces selective immune incompetence.J Invest Dermatol 1983; 81: 85-86. 2. United Nations Environment Programme Co-ordinating Committee on the Ozone Layer. UNEP/CCOL (April, 1983).
1. Bergstresser PR,