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PubMed2026

Upsurge of pneumococcal clade I-α/CC180 serotype 3 and its association with a LytA mutation linked to immune evasion and disease potential: an observational and experimental study.

BACKGROUND: Streptococcus pneumoniae serotype 3 is one of the most prevalent serotypes that cause invasive pneumococcal disease (IPD) in children and adults worldwide. Serotype 3 is associated with vaccine failures and breakthrough episodes in children vaccinated with 13-valent pneumococcal conjugate vaccine (PCV13). In this study, we aimed to investigate potential genetic mechanisms that could explain the increase in cases of serotype 3 IPD in Spain. METHODS: We analysed the epidemiology of serotype 3 causing IPD in Spain, during 2009-23, in different age groups. Molecular characterisation was performed by whole-genome sequencing. Host-pathogen interactions of the different lineages were evaluated in terms of interaction with lung epithelial cells, biofilm formation, and capsular polysaccharide production, using opsonophagocytosis assays and mouse models of pneumonia. We used Poisson regression models to compare incidence and chi-square test calculations to identify clonal variations across vaccine periods. FINDINGS: Genomic analyses confirmed the predominance of clade I-α/clonal complex (CC) 180 in Spain, which shows increased resistance to complement-mediated immunity and phagocytosis and enhanced potential to infect lung cells. In all isolates of this lineage, we observed a single amino acid substitution (166His→Tyr) in the crucial virulence factor LytA, which increased its enzymatic activity. On evaluating the phagocytosis of mutants without LytA of the two major lineages of serotype 3 (CC180 and CC260), LytA was responsible for the increased phagocytosis-evasion pattern of clade I-α/CC180. Evaluation of individuals with IPD caused by different serotype 3 genotypes confirmed a significant (p<0·05) association between cardiac and respiratory comorbidities and infection by sequence type 180/CC180, which showed the importance of CC180 in IPD. INTERPRETATION: Our findings confirm that PCV13 reduced IPD cases caused by the susceptible CC260 lineage until CC260 was replaced by the clade I-α/CC180 lineage, which has a higher potential to cause IPD and divert the host immune system. A key mutation on LytA protein was associated with this hypervirulent phenotype. Emerging lineages jeopardise the effectiveness of pneumococcal conjugate vaccines. FUNDING: Ministerio de Ciencia e Innovación, Instituto de Salud Carlos III, and PubMLST.

Animals↗

PubMed2006

Total and serotype-specific pneumococcal antibody titres in children with normal and abnormal humoral immunity.

A heptavalent pneumococcal conjugate vaccine (PCV-7) protects children against invasive pneumococcal disease. The aim of this study was to evaluate immunoglobulin subclass and serotype-specific pneumococcal antibody responses to vaccination in children with a history of recurrent or severe bacterial infections. Pneumococcal IgG, IgG1, IgG2 titres were assayed by ELISA, and nine serotype concentrations measured using a nonaplex bead assay in 145 children investigated for recurrent or severe infections. Children mounted an exclusively IgG1 response after vaccination with two doses of PCV-7 and a dose of 23 valent pneumococcal polysaccharide vaccine (PPV-23), with pneumococcal IgG2 antibody titres remaining low to negligible. Measurement of serotype-specific responses demonstrated that although PCV-7 specific serotype responses increased significantly post-vaccination, specific IgG against two of the serotypes not covered by PCV-7 but only by PPV-23 remained low. We conclude that in contrast to antibody response to natural infection with Pneumococcus or pneumococcal polysaccharide vaccines which are often of a IgG2 subclass, responses in children after PCV-7 are of IgG1 subclass. Serotype-specific IgG were useful in determining the protection against specific pneumococcal strains, and showed that the PPV-23 did not broaden protection against non-PCV-7 serotypes.

Adolescent↗

PubMed1993

Prolonged recovery of desiccated adenoviral serotypes 5, 8, and 19 from plastic and metal surfaces in vitro.

BACKGROUND: Prevention of the spread of epidemic keratoconjunctivitis (EKC) at eye care facilities (doctors' offices, clinics, hospitals) has been a major public health goal for ophthalmology for more than 50 years. The authors explored a potentially contributing attribute of the adenovirus serotypes that cause EKC. Specifically, they investigated the capacity of different clinical and laboratory ocular serotypes (AD8, 19, and 5) to survive for extended periods of time in a desiccated state. METHODS: Twenty microliters containing 2000 plaque-forming units of different ATCC laboratory adenoviral ocular serotypes (AD8, 19, and 5) and clinical isolates (AD8 Cray, AD19 Kowalski, and AD5 McEwen) were inoculated onto 7-mm plastic disks and 6-mm aluminum foil disks and were allowed to completely desiccate. At weekly intervals up to 7 weeks, eight desiccated virus-inoculated plastic or metal disks per serotype were added to tissue culture medium, and the amount of recoverable virus was determined by plaque assay on A549 cells. RESULTS: Ocular adenoviral serotypes AD8, 19, and 5 could be recovered up to 49 days from plastic, and 35 to 49 days from metal. Sufficient virus concentrations (> 100 plaque-forming units/disk) to be clinically infectious were recovered up to 28 days. Differences in recovery among serotypes (AD19 > AD5, AD8) were demonstrated, but laboratory and clinical isolates of the same serotype were usually comparable. CONCLUSIONS: Ocular isolates of adenovirus that cause EKC are much harder than previously suspected, and the capacity to survive in a desiccated state may possibly play some role in office-based mini-epidemics of EKC.

Adenoviruses, Human↗

PubMed2000

A gene cluster for the synthesis of serotype d-specific polysaccharide antigen in Actinobacillus actinomycetemcomitans.

The serotype d antigen of Actinobacillus actinomycetemcomitans consists of D-glucose, D-mannose, and L-rhamnose in a molar ratio of 1:2:1. A gene cluster involved in the synthesis of serotype-specific polysaccharide antigen was cloned from the chromosomal DNA of A. actinomycetemcomitans IDH 781 (serotype d). This cluster consisted of 12 open reading frames. Insertional inactivation of six genes in this cluster resulted in loss of ability of A. actinomycetemcomitans IDH 781 cells to produce the polysaccharide. Comparing the structure of the gene cluster with similar clusters from other serotypes of A. actinomycetemcomitans, showed that eight genes are unique to serotype d; the other four genes are involved in the biosynthesis of dTDP-L-rhamnose. These results suggest that the synthesis and structure of serotype d-specific polysaccharide of A. actinomycetemcomitans is quite different from those of other serotype strains.

Actinobacillus↗

PubMed2002

Detection of antibodies to Actinobacillus pleuropneumoniae serotype 12 in pig serum using a blocking enzyme-linked immunosorbent assay.

The objective was to develop a blocking enzyme-linked immunosorbent assay (ELISA) for detection of antibodies to Actinobacillus pleuropneumoniae (Ap) serotype 12 in pig serum. Lipopolysaccharide (LPS) from Ap serotype 12 was purified and used as antigen in the assay. Antibodies to the LPS antigen in samples of pig serum were detected by inhibition of the binding of polyclonal rabbit antibodies raised against Ap serotype 12. The assay was evaluated against sera from experimentally infected pigs, from pig herds naturally infected with Ap and from herds declared free of Ap serotype 12 infection. The blocking ELISA showed no cross-reaction when tested with sera from pigs experimentally infected with 12 other serotypes of Ap biotype 1. The sensitivity and specificity of the blocking ELISA on the herd level was evaluated by testing sera from pig herds naturally infected with Ap serotypes 2 and/or 12 and from herds declared free of infection with Ap. The Ap serotype 12 blocking ELISA showed a herd sensitivity of 0.77 (95% confidence interval, 0.62-0.88) and a herd specificity of 1.00 (0.95-1.00) with a cut-off value at 40% relative absorbance or 60% inhibition. The assay may be used advantageously as a confirmatory test in serological surveillance programmes for Ap infections in SPF systems for pig production.

Actinobacillus Infections↗

PubMed2005

Epidemiological differences among pneumococcal serotypes.

The bacterial species Streptococcus pneumoniae consists of 90 immunologically distinct serotypes, of which some possess distinct epidemiological properties. Certain serotypes are much more likely to be associated with nasopharyngeal colonisation than to cause invasive disease. Compared with transient or infrequent colonisers, serotypes carried at high rates by young children may rapidly elicit age-associated natural immunity to invasive disease. Other serotypes seem to be of disproportionate importance as causes of disease in very young infants, in older children, in immunocompromised individuals, or in elderly people. Some serotypes seem to be associated with particular disease syndromes, such as complicated pneumonias in children, or with higher rates of hospitalisation in children or mortality in adults, or are consistently responsible for outbreaks in certain populations. Since pneumococcal conjugate vaccines are directed at specific serotypes, national immunisation advisory committees may wish to consider these serotype-specific properties when considering which vaccine formulation to introduce into a national programme.

Humans↗

PubMed2003

Diversity of Mannheimia haemolytica and pasteurella trehalosi serotypes from apparently healthy sheep and abattoir specimens in the highlands of Wollo, North East Ethiopia.

The prevalence and serotypic diversity of Mannheimia [Pasteurella] haemolytica and Pasteurella trehalosi from nasal swabs, sera and abattoir specimens from sheep in the highlands of Wollo, North East Ethiopia was investigated. Prevalence rates of 83% and 75% of these microorganisms were found in the serum samples and nasal swabs, respectively, from apparently healthy sheep. In a local abattoir, 205 lungs were investigated, 34% of which showed pneumonia, from which samples were collected from 51 lungs and the same number of corresponding tonsils. Mannheimia and Pasteurella species were isolated from 59% of these pneumonic lungs and 69% of the respective tonsils. M. haemolytica serotypes accounted for 41 (59%) and P. trehalosi for 11 (32%) of the isolates from the abattoir specimens. The majority (67%) of isolates from nasal swabs were P. trehalosi, M. haemolytica being isolated f rom 4 (13%) of the swabs. M. glucosida was isolated only from the tonsils. The predominant serotypes of the isolates from both the nasal swabs and the abattoir specimens were M. haemolytica A1 (17%) and P. trehalosi T4 (16%) and T3 (13%). P. trehalosi T15 was less commonly encountered, while M. haemolytica A9 and A13 were not isolated. Studies on sera from 100 sheep indicated that antibodies against M. haemolytica serotype A1 (14%) were most common, followed by A5 and A8 (each 10%) and A9 and P. trehalosi T3 (each 9%) and T4 (8%). Antibodies against M. glucosida or serotype All occurred in 2% of the sera. Multiple serotypes were common in all types of samples. The importance of including in vaccines the most prevalent serotypes involved in the pneumonia of sheep in the area is discussed.

Animals↗

PubMed2002

Bacterial colonization and invasion in pigs experimentally exposed to Streptococcus suis serotype 2 in aerosol.

A recently developed porcine model for aerogenous infection with Streptococcus suis serotype 2 was applied in a study of the phases of bacterial colonization and initial invasion. Eighteen pigs were exposed to aerosolized S. suis serotype 2 after pre-exposure to mild acetic acid in aerosol. The animals were killed consecutively within the first six days after challenge. After death, all animals were necropsied and examined by bacteriology, histopathology, and immunohistochemistry. Systemic infection was established in four out of 18 animals exposed to S. suis serotype 2. All systemically infected animals developed clinical signs and lesions typical of the infection. In four additional animals, subclinical infection was demonstrated by re-isolation of S. suis from the palatine tonsil. However, in all 18 challenged animals, immunohistochemistry demonstrated S. suis serotype 2 antigen in the palatine and/or nasopharyngeal tonsils. In all four systemically infected animals, S. suis serotype 2 antigen was also found in the mandibular lymph node. These observations point towards the tonsils as possible portals of entry for S. suis serotype 2 with subsequent lymphogenous spread. Thus, the present findings parallel the proposed pathogenesis for S. suis serotype 1 infection in pigs.

Aerosols↗

PubMed1986

A comparison of serotyping, BRENDA-typing and incompatibility grouping, and toxin testing of haemolytic Escherichia coli isolated from piglets before and after weaning.

Before weaning, some young pigs in a research piggery excreted in their faeces a weakly haemolytic non-enterotoxigenic serotype of Escherichia Coli. After weaning, all of the pigs excreted strongly haemolytic Escherichia coli of known enteropathogenic serotypes (0-138 and 0-139). The 0-138 serotype produced vero cell toxin, whilst the 0-139 serotype elaborated heat labile enterotoxin. Haemolytic enterotoxigenic E. Coli were also recovered from three-week-old unweaned piglets with so-called ;milk scours; and from pigs with post-weaning diarrhoea on two local commercial piggeries. Selected haemolytic isolates were compared using serotyping, bacterial restriction endonuclease DNA analysis (BRENDA) and incompatibility grouping. The three typing methods divided most of the isolates into the same groupings; the exceptions were two isolates with the same BRENDA pattern and incompatibility group, but with different H-serotypes, and eleven isolates with the same serotype and BRENDA pattern but which showed differences in colony compatibility such that they were divided into five subgroups of a single incompatibility type.

Journal Article↗

PubMed1997

Spread of the serotype 23F multidrug-resistant Streptococcus pneumoniae clone to South Korea.

Thirty-eight antibiotic-resistant isolates of Streptococcus pneumoniae recovered in a hospital in Seoul, Korea, between February 1990 and March 1992 were analyzed for serotype, antibiotic susceptibility patterns, and chromosomal relatedness using pulsed-field gel electrophoretic (PFGE) analysis of SmaI chromosomal digests. Most of the isolates were from sputum samples, and a few strains were from otitis media and meningitis. The great majority of isolates (34 of 38, or 89%) were multiresistant, sharing virtually identical, elevated minimal inhibitory concentration (MIC) values (microgram/ml) for penicillin (1-2), chloramphenicol (12-25), tetracycline (25-30), and sulfamethoxazole/trimethoprim (> 100). Twenty of the isolates were also resistant to erythromycin, and all isolates were also considered to be resistant to ceftriaxone and cefotaxime (1-2) according to the new breakpoint definitions. The most frequent serotypes were 23F (17 of 38) and 19F(14 of 38); 2 belonged to serotype 15B and 1 of 24F. Of the remaining 4 isolates (2 serotype 3, 1 type 6B, and 1 type 9V) all were resistant to tetracycline and sulfamethoxazole/trimethoprim and with the exception of 1 of the type 3 strains, were also resistant to chloramphenicol. Eleven of the 14 serotype 19F isolates shared a relatively homogeneous PFGE pattern, which was indistinguishable from the PFGE pattern shown by most (12 of 17) of the 23F isolates. The PFGE pattern of these 19F and 23F isolates was also indistinguishable from the PFGE pattern shown by representative multiresistant capsular type 23F isolates from Croatia, Portugal, and New York City and the findings document the extensive geographic spread of this multidrug-resistant S. pneumoniae clone. The data also suggests in vivo capsular transformation of the multiresistant clone from serotype 23F to serotype 19F.

DNA Fingerprinting↗

PubMed2004

Pharmacology of botulinum neurotoxin serotype A.

PURPOSE: An historical perspective on the discovery and development of botulinum neurotoxin for commercial use, the differences between various botulinum toxin serotypes and commercially available products, and the structure, mechanism of action, pharmacologic effects, and immunogenicity of botulinum toxin type A are discussed. SUMMARY: Botulinum toxin was discovered several centuries ago, but its medical uses have only recently been explored. There are several botulinum toxin serotypes that differ in composition and molecular weight. The protein component of the macromolecular structure that has pharmacologic activity requires enzymatic activation, and the required enzyme varies by serotype. All serotypes interfere with muscle contraction by inhibiting acetylcholine release into the synaptic space at the neuromuscular junction, although the intracellular target varies by serotype. An antinociceptive effect may be mediated by a similar mechanism involving inhibition of pain mediator release. The effects of botulinum toxin usually are only temporary because collateral axonal sprouts that can release acetylcholine develop. The protein load and immunogenicity vary among the commercially available botulinum toxin products. The smallest protein load and longest dosing interval should be used to minimize resistance. Alternating among different serotypes is not an effective strategy for preventing or overcoming resistance because cross-resistance can occur. CONCLUSION: All botulinum toxin serotypes and products cause temporary muscle paralysis, yet vary in important ways that may affect their clinical use.

Botulinum Toxins, Type A↗

PubMed2001

VP5 and the N terminus of VP2 are not responsible for the different pathotype of serotype I and II infectious bursal disease virus.

Two serotypes have been identified in infectious bursal disease virus (IBDV), a member of the family BIRNAVIRIDAE: A reverse genetics system was used for generation of chimeras in genome segment A of the two serotypes, in which the complete viral VP5 gene and 3' noncoding region (NCR), or parts thereof, were exchanged. The engineered viruses were characterized in vitro and in vivo in comparison to serotype I and II IBDV. Our results show that IBDV chimeras exhibit a different phenotype in cell culture compared to the wild-type viruses. In in vitro-cultivated bursal-derived cells, chimeric viruses infected B lymphocytes, as does serotype I IBDV. Surprisingly, serotype II virus was also able to infect in vitro-cultivated bursal cells, but these were neither B lymphocytes nor macrophages. After infection of susceptible chickens all chimeras replicated in the bursa of Fabricius (BF), and three chimeric viruses caused mild depletion of bursal cells. In contrast, after infection of chickens with a chimeric IBDV containing exchanged VP5 as well as 3'-NCR, no depletion was detectable. The serotype II strain did not replicate in the BF nor did it cause depletion of bursal cells. Thus, the origin of VP5 does not explain the different pathotype of IBDV serotype I and II.

3' Untranslated Regions↗

PubMed2004

Molecular identification and characterization of two proposed new enterovirus serotypes, EV74 and EV75.

Sequencing of the gene that encodes the capsid protein VP1 has been used as a surrogate for antigenic typing in order to distinguish enterovirus serotypes; three new serotypes were identified recently by this method. In this study, 14 enterovirus isolates from six countries were characterized as members of two new types within the species Human enterovirus B, based on sequencing of the complete capsid-encoding (P1) region. Isolates within each of these two types differed significantly from one another and from all other known enterovirus serotypes on the basis of sequences that encode either VP1 alone or the entire P1 region. Members of each type were > or =77.2 % identical to one another (89.5 % amino acid identity) in VP1, but members of the two different types differed from one another and from other enteroviruses by > or =31 % in nucleotide sequence (25 % amino acid sequence difference), indicating that the two groups represent separate new candidate enterovirus types. The complete P1 sequences differed from those of all other enterovirus serotypes by > or =31 % (26 % amino acid sequence difference), but were highly conserved within a serotype (<8 % amino acid sequence difference). Phylogenetic analyses demonstrated that isolates of the same serotype were monophyletic in both VP1 and the capsid as a whole, as shown previously for other enterovirus serotypes. This paper proposes that these 14 isolates should be classified as members of two new human enterovirus types, enteroviruses 74 and 75 (EV74 and EV75).

Capsid Proteins↗

PubMed1989

[Epidemiological survey of group A hemolytic streptococci isolated in Osaka during the 21-year period between 1967 and 1987. Part I. Annual change of epidemic serotype].

During the 21-year period between 1967 and 1987, a total of 6157 strains of group A streptococci isolated in Osaka were type-classified by T-agglutination method. The results were summarized as follows. 1. Sixteen serotypes were differentiated by the T-method during the course of investigation. The most common serotype was T-12 (37.1%), followed by T-4 (13.4%) and T-1 (10.4%). 2. The most dominant serotype was T-12 during 1968-1978, and other relatively frequent serotypes were T-4 in 1971, T-1 in 1972 and T-3 in 1974 throughout the period. Though T-12 was the main serotype in the isolates thereafter, other serotypes such as T-4 in 1979 and T-3 in 1985 also became prevalent, and they occupied the highest percentage. But they declined rapidly, and their duration period was relatively short. After 1976, no definite serotype showed the long-term epidemics, while several types (T-3, T-4 and T-12) showed short-term epidemics lasting a few years. 3. Group A streptococci were isolated most frequently from the patients aged 4-8 years, whereas the isolation rates were extremely lower from the 0- to 2-year-old children. Therefore, younger children seemed to have something which made it difficult to be infected with group A streptococci.

Adolescent↗

PubMed2001

Influence of patient age on Streptococcus pneumoniae serotypes causing invasive disease.

All clinical S. pneumoniae specimens isolated from patients with invasive or sterile-site infections admitted to one regional general hospital in southern Chile were collected during a 5-year period (February 1994 to September 1999). A total of 247 strains belonging to 50 serotypes were isolated in this survey: 69 in patients under 5 years of age, 129 in patients 5 to 64 years old, and 49 from patients 65 years and older. Eight serotypes were identified in all age groups, while all other serotypes were found exclusively in one age group or in patients over 4 years of age. Serotype 3 was never found in patients under 5 years old, and serotype 14 was not found in patients >64 years of age. There was no difference in the serotypes causing infection in each one of the 5 years of the survey. Our results suggest that both bacterial virulence factors and host factors play an important role in the selection of S. pneumoniae serotypes causing invasive infection. Possible host factors include age-related differences in the immune response. Comparative studies with other areas of the world may help to further understanding of our observations in southern Chile.

Adolescent↗

PubMed2006

Role of RpoS in fine-tuning the synthesis of Vi capsular polysaccharide in Salmonella enterica serotype Typhi.

Regulation of the synthesis of Vi polysaccharide, a major virulence determinant in Salmonella enterica serotype Typhi, is under the control of two regulatory systems, ompR-envZ and rscB-rscC, which respond to changes in osmolarity. Some serotype Typhi strains exhibit overexpression of Vi polysaccharide, which masks clinical detection of lipopolysaccharide O antigen. This variation in Vi polysaccharide and O antigen display (VW variation) has been observed since the initial studies of serotype Typhi. In this study, we report that rpoS plays a role in this increased expression in Vi polysaccharide. We constructed a variety of isogenic serotype Typhi mutants that differed in their expression levels of RpoS and examined the role of the rpoS product in synthesis of Vi polysaccharide under different osmolarity conditions. Vi polysaccharide synthesis was also examined in serotype Typhi mutants in which the native promoter of the rpoS was replaced by an araCP(BAD) cassette, so that the expression of rpoS was arabinose dependent. The RpoS(-) strains showed increased syntheses of Vi polysaccharide, which at low and medium osmolarities masked O antigen detection. In contrast, RpoS(+) strains showed lower syntheses of Vi polysaccharide, and an increased detection of O antigen was observed. During exponential growth, when rpoS is unstable or present at low levels, serotype Typhi RpoS(+) strains overexpress the Vi polysaccharide at levels comparable to those for RpoS(-) strains. Our results show that RpoS is another regulator of Vi polysaccharide synthesis and contributes to VW variation in serotype Typhi, which has implications for the development of recombinant attenuated Salmonella vaccines in humans.

Bacterial Proteins↗

PubMed2005

Characterization of the antibody response to the receptor binding domain of botulinum neurotoxin serotypes A and E.

Clostridium botulinum neurotoxins (BoNTs) are the most toxic proteins for humans. The current clostridial-derived vaccines against BoNT intoxication have limitations including production and accessibility. Conditions were established to express the soluble receptor binding domain (heavy-chain receptor [HCR]) of BoNT serotypes A and E in Escherichia coli. Sera isolated from mice and rabbits immunized with recombinant HCR/A1 (rHCR/A1) from the classical type A-Hall strain (ATCC 3502) (BoNT/A1) and rHCR/E from BoNT serotype E Beluga (BoNT/E(B)) neutralized the homologous serotype of BoNT but displayed differences in cross-recognition and cross-protection. Enzyme-linked immunosorbent assay and Western blotting showed that alpha-rHCR/A1 recognized epitopes within the C terminus of the HCR/A and HCR/E, while alpha-rHCR/E recognized epitopes within the N terminus or interface between the N and C termini of the HCR proteins. alpha-rHCR/E(B) sera possessed detectable neutralizing capacity for BoNT/A1, while alpha-rHCR/A1 did not neutralize BoNT/E. rHCR/A was an effective immunogen against BoNT/A1 and the Kyoto F infant strain (BoNT/A2), but not BoNT serotype E Alaska (BoNT/E(A)), while rHCR/E(B) neutralized BoNT/E(A), and under hyperimmunization conditions protected against BoNT/A1 and BoNT/A2. The protection elicited by rHCR/A1 to BoNT/A1 and BoNT/A2 and by rHCR/E(B) to BoNT/E(A) indicate that immunization with receptor binding domains elicit protection within sub-serotypes of BoNT. The protection elicited by hyperimmunization with rHCR/E against BoNT/A suggests the presence of common neutralizing epitopes between the serotypes E and A. These results show that a receptor binding domain subunit vaccine protects against serotype variants of BoNTs.

Amino Acid Sequence↗

PubMed2005

The Salmonella enterica serotype Typhimurium lpf, bcf, stb, stc, std, and sth fimbrial operons are required for intestinal persistence in mice.

Salmonella enterica serotype Typhimurium causes human infections that can frequently be traced back through the food chain to healthy livestock whose intestine is colonized by the pathogen. Little is known about the genes important for intestinal carriage of S. enterica serotype Typhimurium in vertebrate animals. Here we characterized the role of 10 fimbrial operons, agf, fim, lpf, pef, bcf, stb, stc, std, stf, and sth, using competitive infection experiments performed in genetically susceptible (BALB/c) and resistant (CBA) mice. Deletion of agfAB, fimAICDHF, lpfABCDE, pefABCDI, bcfABCDEFG, stbABCD, stcABCD, stdAB, stfACDEFG, or sthABCDE did not reduce the ability of S. enterica serotype Typhimurium to colonize the spleen and cecum of BALB/c mice 5 days after infection. Similarly, deletion of agfAB, fimAICDHF, pefABCDI, and stfACDEFG did not result in reduced recovery of S. enterica serotype Typhimurium from fecal samples collected from infected CBA mice over a 30-day time period. However, S. enterica serotype Typhimurium strains carrying deletions in lpfABCDE, bcfABCDEFG, stbABCD, stcABCD, stdAB, or sthABCDE were recovered at significantly reduced numbers from the feces of CBA mice. There was a good correlation (R(2) = 0.9626) between competitive indices in the cecum and fecal samples of CBA mice at 30 days after infection, suggesting that the recovery of S. enterica serotype Typhimurium from fecal samples closely reflected its ability to colonize the cecum. Collectively, these data show that six fimbrial operons (lpf, bcf, stb, stc, std, and sth) contribute to long-term intestinal carriage of S. enterica serotype Typhimurium in genetically resistant mice.

Animals↗