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1.  A comparison of the distribution of Clostridium botulinum in soil and in lake mud. 
The Journal of Hygiene  1977;78(1):39-41.
In 1975, 25 soil samples were collected from the London area. Of these, 20 were obtained 200-300 yards from 20 lakes that had been shown in 1974 to contain mud contaminated with one or more of types of B, C, D, and E of clostridium botulinum. By means of a technique comparable with that use for the examination of mud, the 20 soil samples were found negative. The remaining 5 soil samples, obtained from sites that were not in close proximity to lakes, were also negative except for one that contained type B.
PMCID: PMC2129734  PMID: 319167
2.  Landfill sites, botulism and gulls. 
Epidemiology and Infection  1994;112(2):385-391.
Botulism due to Clostridium botulinum type C causes considerable mortality in gulls in the UK, and refuse disposal sites are suspected as a major source of toxin. C. botulinum types B, C and D were each found in 12 (63.2%) of 19 landfill sites examined. Type E was detected in only one (5.2%) and types A, F and G were not found. The prevalence of type C spores was much higher than that demonstrated in the UK environment by earlier surveys. The presence of these spores, together with the rotting organic matter and generated heat associated with landfill sites, undoubtedly leads to bacterial proliferation and toxigenesis. This is likely to result in botulism in scavenging gulls unless skilled landfill management prevents the ingestion of toxic material. Type D spores were previously shown to be rare in the UK environment and their high prevalence on landfill sites was therefore surprising. Four composite samples of refuse collected before distribution on a landfill gave negative results for C. botulinum and it seems likely that the gulls themselves play a major role in introducing contamination.
PMCID: PMC2271455  PMID: 8150012
3.  The production of Clostridium botulinum type A, B and D toxin in rotting carcasses. 
Epidemiology and Infection  1994;113(2):335-343.
Carrion is a major source of botulinal toxin for animals. A type D strain of Clostridium botulinum differed from type A and B strains in producing (1) much higher concentrations of toxin in putrefying mouse carcasses at several different temperatures over a period of 35 days, (2) toxicity that sometimes persisted in mouse carcasses for at least a year, and (3) mouse carcasses with exceptionally high oral toxicity. Fish carcasses were much less favourable than mouse carcasses for type D toxigenesis. The study, together with earlier studies on types C and E, indicated that carrion contaminated with C. botulinum type C or D is likely to be particularly dangerous for animals that may ingest it. This accords with the observation that carrion-transmitted botulism in animals is usually caused by type C or D.
PMCID: PMC2271544  PMID: 7925670
4.  Effect of disturbance of the gastrointestinal microflora on the faecal excretion of Fusobacterium necrophorum biovar A. 
Epidemiology and Infection  1993;110(2):333-337.
Oral pretreatment of mice with either a mixture of kanamycin and erythromycin or metronidazole to modify the gut microflora greatly enhanced the faecal excretion of Fusobacterium necrophorum biovar A given by mouth. This lends support to the suggestion that disturbance of the gastrointestinal microflora in animals such as cattle, which often carry the organism in the rumen, may lead to intestinal multiplication and faecal excretion, thereby providing a source of infection that may lead to necrobacillosis of the body surface.
PMCID: PMC2272254  PMID: 8472777
5.  The prevalence of Fusobacterium necrophorum biovar A in animal faeces. 
Epidemiology and Infection  1993;110(2):327-331.
Only a small proportion of animals tested were found to be excreting Fusobacterium necrophorum biovar A, the causative organism of necrobacillosis, in the faeces (3 of 69 wallabies, 1 of 66 deer, 2 of 81 cattle). The two positive cattle belonged to a single group of calves on a farm with a history of necrobacillosis and the litter underfoot also readily yielded biovar A organisms. All attempts to demonstrate biovar A in litter on other farms and in soil from an area populated by wallabies and deer failed. Ruminal contents from young beef cattle proved a fertile source of F. necrophorum biovar A, 15 of 18 animals giving a positive result. It is suggested that disturbance of the gastrointestinal microflora leads to intestinal multiplication and faecal excretion of the organism, which may then give rise to necrobacillosis of the body surface.
PMCID: PMC2272251  PMID: 8472776
6.  A sensitive method for isolating Fusobacterium necrophorum from faeces. 
Epidemiology and Infection  1991;106(2):311-317.
The isolation of Fusobacterium necrophorum present in small numbers in heavily contaminated material such as faeces or soil is hampered by the lack of an efficient selective medium and by the high minimum infective dose of the organism. A sensitive method for the detection and isolation of faecal strains of F. necrophorum type A was based on the subcutaneous injection of faeces, suspended (5% w/v) in broth culture of Actinomyces (Corynebacterium) pyogenes or Staphylococcus aureus to increase fusobacterial infectivity, into mice pretreated with clostridial antitoxins. When necrobacillosis developed F. necrophorum was identified microscopically in tissue from the advancing edge of the lesion and isolated on a partly selective medium. The enhancement of fusobacterial infectivity produced by A. pyogenes and by S. aureus was high, but the latter was slightly the more efficient, enabling as few as 80 F. necrophorum organisms/g of faeces to be detected. Use of the method showed that 3 of 16 wallabies had F. necrophorum in their faeces at the time of examination. Numerous epidemiological applications are suggested.
PMCID: PMC2271996  PMID: 2019300
7.  Necrobacillosis and immunity in mice. 
Epidemiology and Infection  1989;103(1):211-215.
The study arose from the recent finding that sub-lethal numbers of certain bacterial species greatly enhanced the infectivity of Fusobacterium necrophorum. A severe F. necrophorum infection in mice, cured with metronidazole, produced significant though slight resistance, which was demonstrable by challenge with a minute dose of F. necrophorum (less than 20 organisms) suspended in a sub-lethal dose of Escherichia coli (300 x 10(6) organisms) to enhance fusobacterial infectivity. In an earlier comparable experiment, challenge with F. necrophorum alone, in necessarily large doses (greater than or equal to 3 x 10(6) organisms), failed to demonstrate that a single cured fusobacterial infection gave rise to resistance; such an infection neither protected against the fatal necrobacillosis produced by challenge nor prolonged survival. A sub-lethal E. coli infection was also shown by challenge with a minute dose of F. necrophorum (less than 10 organisms), suspended in a sub-lethal dose of E. coli (152 x 10(6) organisms), to produce significant though slight protection against necrobacillosis. The degrees of resistance demonstrated were too slight to give any encouragement to the prospect of an effective necrobacillosis vaccine.
PMCID: PMC2249485  PMID: 2673823
8.  Factors affecting the toxicity of rotting carcasses containing Clostridium botulinum type E. 
Epidemiology and Infection  1988;100(3):399-405.
Mice killed shortly after receiving c. 2000 spores of a type E strain of Clostridium botulinum per os were incubated at one of five chosen temperatures together with bottles of cooked meat medium seeded with a similar inoculum. After incubation the rotting carcasses were homogenized. Sterile membrane filtrates of the homogenates (10%, w/v) and pure cultures were then titrated for toxicity. Some of the main findings were confirmed with two further type E strains. Toxicity produced at 37 degrees C was poor in both carcasses and cultures (200-20,000 mouse intraperitoneal LD/g or ml). It was good in both systems at 30 and 23 degrees C, usually reaching 20,000-200,000 LD/g or ml, and in carcasses occasionally more; at 30 degrees C maximal toxicity was reached more quickly in carcasses than in cultures. Prolonged incubation (36-118 days) at 30 or 23 degrees C resulted in complete loss of toxicity in virtually all carcasses but not in cultures. At 16 degrees C the development of toxicity in carcasses was strikingly greater than in cultures. At 9 degrees C neither system produced more than slight toxicity after prolonged incubation. Trypsinization increased the toxicity of cultures but not usually of carcasses. Unfiltered carcass homogenate (10%, w/v) with maximal intraperitoneal toxicity was harmless for mice by mouth in doses of 0.25 ml. These findings differed in important respects from those made earlier with a type C strain.
PMCID: PMC2249348  PMID: 3288491
9.  Clostridium botulinum type C in the Mersey estuary. 
The Journal of Hygiene  1982;89(3):507-511.
Nineteen of 98 samples of mud or sand taken from the Mersey estuary in 1981 contained Clostridium botulinum type C, the organism almost always responsible for botulism in water birds. In the Dungeon and Score Bank areas, where many dead and dying birds were found during the period September-December 1979, almost half the samples contained type C. Most of the positive samples were essentially muddy rather than sandy. The findings do not prove that botulism contributed to the 1979 mortality but are nonetheless thought-provoking, particularly because type C--unlike type B--is by no means ubiquitous in Britain. Type B was present in 12.2% of samples from the Mersey estuary.
PMCID: PMC2134233  PMID: 6759578
10.  Observations on the antigenic differences between the so-called SC and LC strains of Mycoplasma mycoides subsp. mycoides. 
The Journal of Hygiene  1981;87(3):437-442.
The so-called SC (small colony) and LC (large colony) strains of Mycoplasma mycoides subsp. mycoides are said to be indistinguishable by the in vitro serological tests of generally used in mycoplasmology. In mice the immunity given by a single dose of killed LC-strain vaccine against challenge with SC strains is - unlike that given by SC-strain vaccine - only partial. When multiple doses of killed or living vaccines were given, the majority of 13 LC strains still failed to immunize completely against a SC strain. This suggests that, although some protective antigens are shared between both types of strain, at least one of importance is present in the SC strains but absent from the majority of LC strains. The difference between the protective-antigen content of SC and most LC strains is thus qualitative, and not merely quantitative.
PMCID: PMC2134135  PMID: 7031127
11.  Further studies on caprine and ovine mycoplasmas related to Mycoplasma mycoides subsp. mycoides 
The Journal of Hygiene  1980;85(2):247-256.
Nine caprine and ovine mycoplasma strains, said to be indistinguishable serologically from Mycoplasma mycoides subsp. mycoides (the causative organism of contagious bovine pleuropneumonia; CBPP) were examined in mice by (1) a mycoplasmaemia test, and (2) a cross-protection test. Of the nine strains, two from goats belonged to a small colony (SC) type; four caprine and three ovine strains belonged to a large colony (LC) type.
The two SC strains — like a single SC strain examined in an earlier study — were indistinguishable from genuine M. mycoides subsp. mycoides as isolated from CBPP. They produced mycoplasmaemia readily. In a cross-protection test, the two SC strains and a CBPP strain immunized completely against each other.
Of the seven LC strains, six — like six LC strains examined in an earlier study — were easily distinguished from genuine M. mycoides subsp. mycoides; except for one that was not tested, all were shown to lack the ability to produce mycoplasmaemia readily. In cross-protection tests all six strains immunized partially but not completely against a CBPP strain.
The seventh LC strain (Mankefår 2833) was exceptional: it produced mycoplasmaemia readily, resembling the SC strains in this respect. Like other LC strains, in cross-protection tests it protected only partially against a CBPP strain. Strain Mankefår 2833 was isolated in ca. 1965 by Brack from a Barbary sheep (Ammotragus lervia) in a German zoo.
The ability of Mankefår 2833 to produce mycoplasmaemia enabled it to be used as a challenge strain in cross-protection tests. For the purpose of such tests the collection of nine mycoplasma strains referred to above was augmented with six LC strains from an earlier study. Partial but not complete protection against Mankefår 2833 was produced by two caprine SC strains, one CBPP strain, and nine LC strains. Three further LC strains gave protection that may have been as strong as that produced by the homologous strain, but confirmatory experiments are needed. A strain of M. mycoides subsp. capri gave no protection against Mankefår 2833.
PMCID: PMC2133930  PMID: 7005327
12.  Differentiation of Mycoplasma mycoides subsp. mycoides from certain closely related caprine mycoplasmas by mycoplasmaemia and cross-protection tests in mice. 
The Journal of Hygiene  1979;82(3):407-418.
In recent years, mycoplasma taxonomists have found that numerous mycoplasma strains from goats are serologically indistinguishable from Mycoplasma mycoides subsp. mycoides, the causative agent of contagious bovine pleuropneumonia (CBPP), by routinely used tests, e.g. the metabolism- and growth-inhibition tests. As a result, such organisms are now openly referred to as M. mycoides subsp. mycoides. Seven of these so-called M. mycoides subsp. mycoides strains from goats were compared with two strains of M. mycoides subsp. mycoides from CBPP, and with one strain of M. mycoides subsp. capri, by means of two in-vivo tests, namely, (1) a test of the ability of each strain, injected intraperitoneally into mice, to produce mycoplasmaemia, and (2) a cross-protection test in mice. Of the seven strains, only one ('O goat') was indistinguishable from genuine M. mycoides subsp. mycoides; it also had small colonies resembling those of genuine M. mycoides subsp. mycoides. The other six were easily distinguished from genuine M. mycoides subsp. mycoides, and they produced large colonies. These six strains and others like them should no longer be given a name that fails to distinguish them from the causative agent of CBPP. Cross-protection tests showed that the seven goat strains referred to above differed from M. mycoides subsp. capri.
PMCID: PMC2130076  PMID: 376695
13.  Clostridium botulinum in aquatic environments in Great Britain and Ireland. 
The Journal of Hygiene  1978;80(3):431-438.
Mud samples from aquatic environments in many parts of Great Britain and Ireland were collected, mainly in 1975 and 1976, and examined for Clostridium botulinum. The samples were taken from lakes, ponds, reservoirs, marshes, mudflats, streams, rivers and canals, and the sampling areas included a number of bird refuges and reserves. Of 554 samples 194 (35.0%) were positive and 167 (30.1%), 19 (3.4%), 6 (1.1%) and 15 (2.7%) contained types B, C, D and E respectively; 13 (2.3%) contained more than one type. Each type demonstrated was found in both fresh-and salt-water environments. Type B was widespread; types C, D and E were demonstrated in widely separated areas in England and Wales, and type C was found in both the north and south of Scotland. The results were compared with those reported earlier in respect of surveys in the London area, the Norfolk Boads and the Camargue (France).
PMCID: PMC2129799  PMID: 349077
14.  The low prevalence of Clostridium botulinum in the lakes, marshes and waterways of the Camargue. 
The Journal of Hygiene  1977;78(1):33-37.
Mud samples collected in June 1975 from the lakes, marshes and waterways of the Camargue were examined for Clostridium botulinum. The Grand Rhône and Petit Rhône were shown to contain types B and E, but of 44 samples taken from well distributed sites on the Ile de la Carmargue, only two (4-5%) were positive and these contained type E alone. The survey indicated a much lower prevalence of Cl. botulinum than any encountered in recent surveys of inland aquatic environments elsewhere.
PMCID: PMC2129731  PMID: 319166
15.  Letter: Fish farms and botulism. 
British Medical Journal  1975;3(5978):301-302.
PMCID: PMC1674207  PMID: 1097048
16.  Effect of sub-lethal treatment with formalin on the germination of Aspergillus fumigatus spores 
The Journal of Hygiene  1973;71(4):745-753.
Sub-lethal exposure of Aspergillus fumigatus spore suspensions to formalin resulted in prolongation by 1-22 days of the period of less than one day normally needed by spores to produce visible growth in Sabouraud's liquid medium at 37° C.; the degree of delay depended on the concentration of formalin and the duration of exposure, and was due to an increase in the germination-time of spores. The formalin concentration could be adjusted so as to affect the germination-time of almost all spores in a suspension without reducing viability. The effect on germination was not abolished by thorough washing or treatment with sodium sulphite. The spores of four different strains of A. fumigatus and of cultures aged 3 to 14 days reacted similarly to formalin treatment. Although of greatly reduced virulence for mice, affected viable spores were still capable of producing infection and death following intravenous inoculation, provided they were not eliminated by the host before germination occurred.
PMCID: PMC2130422  PMID: 4588774
17.  Pathogenicity of Fusobacterium necrophorum strains from man and animals. 
Epidemiology and Infection  1993;110(3):499-506.
Necrobacillosis occurs in man and animals. The typical forms of the disease in animals are caused by Fusobacterium necrophorum biovar A; biovar B strains are much less pathogenic. In this study the pathogenicity for mice of eight human isolates of F. necrophorum was compared with that of animal biovar A and B strains. By subcutaneous inoculation seven of the human strains differed from biovar A but resembled biovar B in (1) producing, at the most, mild local lesions that rapidly healed, and (2) showing no enhancement of infectivity when suspended in sub-lethal doses of Staphylococcus aureus broth culture. The eighth human strain (A2433) resembled biovar A but differed from biovar B in (1) producing severe lesions, and (2) showing greatly enhanced infectivity in the presence of S. aureus. Nonetheless, strain A2433 differed from biovar A, both in the nature of the lesions produced and in its failure to cause severe general signs of illness and rapidly fatal infection. By intravenous inoculation one of two biovar B strains and all except one of the eight human strains produced purulent lesions, often severe, in the liver and elsewhere, but infection was not usually associated with general signs of illness. In contrast, intravenous injection of a biovar A strain gave rise to a rapidly fatal infection, with severe lesions in the liver or elsewhere. The results suggest that the term 'necrobacillosis' as used in human and veterinary medicine refers to diseases that differ in important respects.
PMCID: PMC2272280  PMID: 8519315
18.  Further observations on enhancement of the infectivity of Fusobacterium necrophorum by other bacteria. 
Epidemiology and Infection  1991;106(2):305-310.
It had already been shown with a single virulent strain (A42) of Fusobacterium necrophorum that suspension of the fusobacteria in sub-lethal doses of broth cultures of other bacteria reduced the minimum infective dose (greater than 10(6) organisms) for mice by subcutaneous inoculation, sometimes to less than 10 organisms. The present study extended the known range of bacteria with strong infectivity-enhancing properties to include Bacillus cereus, Klebsiella oxytoca and Staphylococcus aureus; and those with weaker effect to include Bacillus subtilis, 'Bacteroides melaninogenicus', Clostridium sporogenes, Pasteurella haemolytica, and Proteus mirabilis. The study also showed that five further virulent strains of F. necrophorum closely resembled A42 in respect of striking susceptibility to infectivity enhancement by Escherichia coli. Actinomyces (Corynebacterium) pyogenes and S. aureus. One further strain (A6) of F. necrophorum resembled A42 in respect of strong infectivity enhancement by A. pyogenes, S. aureus, B. cereus and K. oxytoca but differed from it and the other five strains in being only slightly affected by E. coli. This work was a necessary prelude to the development of a method, based on infectivity enhancement, for the detection and isolation of F. necrophorum present in small numbers in heavily contaminated material such as faeces.
PMCID: PMC2272010  PMID: 1902184
19.  Experimental observations on the pathogenesis of necrobacillosis. 
Epidemiology and Infection  1990;104(1):73-78.
Earlier studies showed that the minimum infective dose (greater than 10(6) organisms) of a virulent strain of Fusobacterium necrophorum could be greatly reduced by suspending the fusobacteria in sub-lethal doses of cultures of other bacteria such as Escherichia coli before inoculating mice subcutaneously. In the present study the infective dose of the same strain of F. necrophorum was reduced by a factor of greater than 10(3) by suspending the fusobacteria in sub-lethal doses of 5% homogenate of gaur or wallaby faeces. Sterile faecal filtrate had no such effect. The sites of low grade infection produced by the prior subcutaneous injection of E. coli culture or gaur faecal suspension were susceptible to superinfection by doses of F. necrophorum far below those required to infect normal tissue. This work helps to explain the production of necrobacillosis by the faecal contamination of small wounds. It proved impossible, however, to produce necrobacillosis in mice by the subcutaneous injection of faecal suspensions from 33 farm cattle. This suggests that the proportion of cattle with virulent F. necrophorum in their faeces is low.
PMCID: PMC2271731  PMID: 2307186
20.  The production of Clostridium botulinum toxin in mammalian, avian and piscine carrion. 
Epidemiology and Infection  1989;102(3):467-471.
Mice, birds (chicks, quail) and fish (rudd, goldfish) killed shortly after receiving 1300-2000 spores of Clostridium botulinum per os were incubated, usually at 23 degrees C for 7 days. A 10% (w/v) homogenate of each rotting carcass was then prepared, sterilized by membrane filtration, and assayed for toxin. In mouse carcasses a type C strain of C. botulinum usually produced greater than 2 X 10(5) mouse intraperitoneal LD/g; in fish carcasses it usually produced less--often much less--than 2 X 10(4) LD/g. Avian carcasses appeared to be intermediate between those of mice and fish in their ability to support toxigenesis. A type E strain of C. botulinum, unlike type C, produced toxin equally well in fish and mouse carrion, usually at a concentration of between 2 X 10(4) and 2 X 10(5) LD/g.
PMCID: PMC2249455  PMID: 2661255
21.  Factors affecting the toxicity of rotting carcasses containing Clostridium botulinum type C. 
Epidemiology and Infection  1987;98(3):345-351.
Mice killed shortly after receiving 1300-3000 spores of Clostridium botulinum type C per os were incubated at one of four chosen temperatures together with bottles of cooked meat medium seeded with a similar inoculum. After incubation the rotting carcasses were homogenized. Sterile membrane filtrates of the homogenates (10-20.8%, w/v) and pure cultures were then titrated for toxicity. A temperature of 37 degrees C produced less toxicity in most carcasses than in cultures. At 30 degrees C, however, toxicity (often 2 X 10(5) to 2 X 10(6) mouse intraperitoneal LD/g or ml) was roughly similar in both systems, and some carcasses and cultures were still toxic (2 X 10(4) to 2 X 10(5) LD/g or ml) after 349 days. Surprisingly, at 23 degrees C, through greatly reduced in the cultures, toxicity was high in many carcasses for at least 28 days. Little or no toxin was produced in either system at 16 degrees C. Unfiltered homogenates (17.8-22.5%, w/v; dose 0.25 ml per os) of toxic carcasses incubated at 30 degrees C for 7 days invariably produced death from botulism, often within as little as 4 h, but a 1 in 10 dilution produced less than 100% mortality.
PMCID: PMC2235363  PMID: 3297745
22.  Observations on experimental inactivated vaccines for contagious bovine pleuropneumonia. 
The Journal of Hygiene  1986;97(2):305-315.
In two trials the efficacy of inactivated vaccines against contagious bovine pleuropneumonia was tested by exposing vaccinated cattle to droplet infection provided by close contact with experimentally infected 'donors'. Complete protection was given by an extreme form of vaccination in which a heavy suspension of killed Mycoplasma mycoides subsp. mycoides emulsified with Freund's complete adjuvant was given in two large doses. 'Mouse-protective antibody' (MPA) was also produced, i.e. serum transferred to mice 2-4 h before intraperitoneal challenge prevented the development of mycoplasmaemia. However, the study did not answer the question 'Is MPA protective for cattle?'. No protection was given by a milder form of vaccination in which a lighter suspension of killed mycoplasmas emulsified with Freund's incomplete adjuvant was given in a comparatively small dose on a single occasion.
PMCID: PMC2083532  PMID: 3782785
23.  The adverse effect of dilution on the infectivity of Fusobacterium necrophorum culture. 
The Journal of Hygiene  1986;96(2):199-203.
Dilution had an adverse effect on the infectivity of 24 h cultures of a strain of Fusobacterium necrophorum, which became apparent at or near the minimum lethal dose. Thus in mice inoculated subcutaneously the mortality produced by 0.01 ml of undiluted culture was almost invariably greater than that produced by 0.1 ml of a 1 in 10 dilution. The explanation appeared to lie in the increased physical separation of bacterial cells that was the inevitable consequence of dilution.
PMCID: PMC2129643  PMID: 3517155
24.  The weak immunogenicity of Fusobacterium necrophorum. 
The Journal of Hygiene  1985;95(1):59-68.
Three of four extreme methods of immunization completely failed to protect mice against challenge with the homologous strain of Fusobacterium necrophorum. Unsuccessful vaccines included (1) broth culture killed by mild heat and emulsified with Freund's complete adjuvant, and (2) a homogenate of heavily infected mouse brains, inactivated by mild heat and given in two doses. Also unsuccessful as a method of immunization was the production of a severe subcutaneous infection with F. necrophorum, followed by curative treatment with metronidazole. Slight but significant protection against subcutaneous challenge resulted, however, from two such infections given in rapid succession. It would appear that the main virulence factors of F. necrophorum are only weakly immunogenic, and the experiments give little encouragement to the prospect of an effective necrobacillosis vaccine.
PMCID: PMC2129521  PMID: 3894509
25.  A study of F38-type and related mycoplasmas by mycoplasmaemia and cross-immunization tests in mice. 
The Journal of Hygiene  1984;93(3):465-473.
In vivo methods were used to study the F38-type mycoplasma in parallel with related mycoplasmas. Three of five strains of 'bovine serogroup 7' with an unknown history of subculture produced mycoplasmaemia in mice inoculated intraperitoneally. A strain of 'bovine serogroup L' also produced mycoplasmaemia, but no evidence of similar ability could be found for single strains of Mycoplasma capricolum, M. equigenitalium and M. primatum, or for two strains of the F38-type mycoplasma. In cross-immunization tests a bovine serogroup 7 strain (NCTC 10133) and a strain ('Blenheim') of the SC (small colony) type of M. mycoides subsp. mycoides were used for the purpose of challenge. Cross-protection was described as 'complete' or 'partial', depending on whether it was as great as, or less than, that produced by homologous vaccine. Although strain NCTC 10133 protected strongly, possibly completely, against Blenheim, and Blenheim gave partial protection against NCTC 10133, challenge with NCTC 10133 and Blenheim gave strikingly different results. Thus (1) F38-type strains, M equigenitalium and M. primatum all gave partial cross-protection against NCTC 10133 but not against Blenheim, (2) NCTC 10133, unlike Blenheim, was seldom susceptible to partial cross-protection by LC (large colony) strains of M. mycoides subsp. mycoides, and (3) three SC strains - which would have protected completely against Blenheim - protected only partially against NCTC 10133. NCTC 10133 and Blenheim were similar, however, in that M. capricolum and M. mycoides subsp. capri failed to cross-protect against them both.
PMCID: PMC2129469  PMID: 6392418

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