T uberculosis (TB) is one of the most prevalent zoonotic diseases worldwide and remains the leading cause of death from a single infectious agent (1). The causative pathogens of TB in humans and animals are a group of closely related acid-fast bacilli commonly known as the Mycobacterium tuberculosis complex (MTBC). One animal-adapted sublineage within the complex, M. microti, was fi rst isolated from fi eld voles (Microtus agrestis) that had granulomatous tuberculosis-like lesions (2). Although wild rodents, such as bank voles (Myodes glareolus), wood mice (Apodemus sylvaticus), and shrews (Sorex araneus), are considered to be primary reservoirs for M. microti, several other hosts have been identifi ed, including domestic and wild animals (3,4). Overall, cats (5,6), New World camelids ( 7), and free-ranging wild boar (8-10) seem to be prone to M. microti infections; humans (11-14) and other animal species, including pigs (15), goats (16), cattle (17,18), dogs ( 19), captive meerkats (20), squirrel monkeys (21), and ferrets ( 14), are most likely incidental hosts.This broad host range, however, highlights the pathogenic potential of M. microti and the need to reveal its virulence mechanisms. Comparative genomics studies have identifi ed >100 genes whose presence are facultative and differ among members of MTBC. Many of these genes occur in chromosomal regions of difference (RD) that have been deleted from certain species and that may confer differences in phenotype, host range, and virulence (22). Isolates of the animal-adapted ecotype defi ned as M. microti are characterized by the deletion of the RD1 mic in the RD1 region, which includes open reading frame coding for well-known virulence factors, such as early secreted antigenic target (ESAT) 6, locus tag Rv3875, and CFP-10, a culture fi ltrate protein encoded by the neighboring gene Rv3874 (23). Strains lacking RD1 are likely to be less virulent or pathogenic than other members of the MTBC possessing an intact locus (22). However, pulmonary and disseminated M. microti infections have been described in both immunocompromised and immunocompetent human patients in different countries in Europe (11,12,14,24). Until recently, reports of M. microti infections were geographically restricted to continental Europe and the United Kingdom. However, a recent study from South Africa revealed the presence of this Mycobacterium species in 1.9% of local human tuberculosis cases (25). These fi ndings highlight the potential of M. microti to cause clinical illness in immunocompetent patients and suggest that the pathogenicity of certain strains is higher than previously estimated.
T uberculosis (TB) is one of the most prevalent zoonotic diseases worldwide and remains the leading cause of death from a single infectious agent (1). The causative pathogens of TB in humans and animals are a group of closely related acid-fast bacilli commonly known as the Mycobacterium tuberculosis complex (MTBC). One animal-adapted sublineage within the complex, M. microti, was fi rst isolated from fi eld voles (Microtus agrestis) that had granulomatous tuberculosis-like lesions (2). Although wild rodents, such as bank voles (Myodes glareolus), wood mice (Apodemus sylvaticus), and shrews (Sorex araneus), are considered to be primary reservoirs for M. microti, several other hosts have been identifi ed, including domestic and wild animals (3,4). Overall, cats (5,6), New World camelids ( 7), and free-ranging wild boar (8-10) seem to be prone to M. microti infections; humans (11-14) and other animal species, including pigs (15), goats (16), cattle (17,18), dogs ( 19), captive meerkats (20), squirrel monkeys (21), and ferrets ( 14), are most likely incidental hosts.This broad host range, however, highlights the pathogenic potential of M. microti and the need to reveal its virulence mechanisms. Comparative genomics studies have identifi ed >100 genes whose presence are facultative and differ among members of MTBC. Many of these genes occur in chromosomal regions of difference (RD) that have been deleted from certain species and that may confer differences in phenotype, host range, and virulence (22). Isolates of the animal-adapted ecotype defi ned as M. microti are characterized by the deletion of the RD1 mic in the RD1 region, which includes open reading frame coding for well-known virulence factors, such as early secreted antigenic target (ESAT) 6, locus tag Rv3875, and CFP-10, a culture fi ltrate protein encoded by the neighboring gene Rv3874 (23). Strains lacking RD1 are likely to be less virulent or pathogenic than other members of the MTBC possessing an intact locus (22). However, pulmonary and disseminated M. microti infections have been described in both immunocompromised and immunocompetent human patients in different countries in Europe (11,12,14,24). Until recently, reports of M. microti infections were geographically restricted to continental Europe and the United Kingdom. However, a recent study from South Africa revealed the presence of this Mycobacterium species in 1.9% of local human tuberculosis cases (25). These fi ndings highlight the potential of M. microti to cause clinical illness in immunocompetent patients and suggest that the pathogenicity of certain strains is higher than previously estimated.
Summary Application of the cell culture neutralization (N) test demonstrates that representative strains of the 1963 A2 variant are antigenically homogeneous. Reaction patterns of individual antisera clearly show the differences between the 1957 strain and the current family of A2 viruses. None of these differences could be demonstrated by hemagglutination-inhibiting (HI) test alone. The analysis of the patterns of incidence of N antibody in recruit populations lends laboratory support to the epidemiologic descriptions of the progression of the 1963 epidemic across the United States. Despite the presence of considerable N antibody to both the 1957 and 1963 strains of virus, 47 cases of A2 virus infection were confirmed in 1963. The tenuous correlation between humoral antibody to influenza and immunity has been discussed.
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