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PubMed2005

Impact of pneumococcal conjugate vaccine and the severity of winter influenza-like illnesses on invasive pneumococcal infections in children and adults.

BACKGROUND: Pneumococcal conjugate vaccine (PCV7), recommended in July 2000 for routine use in infants, has resulted in a reduction in the rate of invasive pneumococcal disease (IPD) in young children. We studied the impact of PCV7 and the possible contribution of the severity of influenza-like respiratory infection season on the rate of IPD on children and adults. METHODS: In 7 hospitals of a health system, episodes of IPD were identified by the microbiology laboratories during the 2-year period before July 2000 and the 4-year period after July 2000 during routine use of PCV7, and patient records were reviewed. Episodes of influenza-like illnesses during each winter in a local county were prospectively measured by reports from all acute care hospitals and episodes of absenteeism resulting from influenza-like illnesses from all schools. RESULTS: There were 720 patients with blood and/or cerebrospinal fluid isolates of Streptococcus pneumoniae. There were significant reductions in cases of IPD in children younger than 2 years, 68% reduction; children 2-4 years of age, 70%; adults 18-49 years of age, 42%; and adults older than 64 years, 30%. Annually, during the PCV7 period, there were significantly fewer episodes of influenza-like illnesses than during the pre-PCV7 years. CONCLUSIONS: PCV7 efficacy and resultant herd-type immunity resulted in a reduction in the rate of IPD not only in young children but also in young and elderly adults. Milder winter respiratory viral seasons may possibly have contributed to the observed reduction in the rate of IPD.

Adolescent↗
PubMed2001

Protection against bacteremic pneumococcal infection by antibody to pneumolysin.

Pneumolysin is an important virulence factor of Streptococcus pneumoniae. This study examined the hypothesis that human antibody to pneumolysin provides protection against pneumococcal infection. At the time of hospital admission, patients with nonbacteremic pneumococcal pneumonia had higher levels of serum anti-pneumolysin IgG than did patients with bacteremic pneumococcal pneumonia or uninfected control subjects. IgG levels rose significantly during convalescence in patients with bacteremic pneumonia, reaching levels observed in nonbacteremic patients. Purified human anti-pneumolysin IgG protected mice against intraperitoneal challenge with S. pneumoniae types 1 or 4 in a dose-related fashion; mice that received anti-pneumolysin IgG had a greater likelihood of surviving challenge and had negative blood cultures. Pneumolysin damages epithelial cells and inhibits phagocytic function of polymorphonuclear leukocytes. One hypothesis that might explain the study results is that, early in infection, IgG to pneumolysin blocks these effects in the alveoli, thereby protecting the host against bacteremic pneumococcal disease.

Animals↗
PubMed2004

Azithromycin compared with beta-lactam antibiotic treatment failures in pneumococcal infections of children.

OBJECTIVE: To determine whether treatment failures occurred more commonly with azithromycin than with beta-lactam antibiotics in children who developed invasive pneumococcal disease within 30 days of receiving prior antimicrobial therapy. METHODS: Retrospective review of medical records of children evaluated at Texas Children's Hospital between 1996 and 2002 who had received antimicrobials (azithromycin or a beta-lactam antibiotic) and developed invasive pneumococcal disease within 30 days. Treatment failure was defined as invasive pneumococcal infection that occurred while taking antimicrobials or within 3 days of stopping azithromycin treatment or 1 day of stopping beta-lactam treatment. Penicillin and azithromycin susceptibilities were determined and categorized according to National Committee for Clinical Laboratory Standards guidelines. RESULTS: We identified 21 and 33 children with similar demographic features who had developed invasive pneumococcal disease within 1 month of receiving azithromycin or a beta-lactam antibiotic, respectively. Eleven (52%) children in the azithromycin group and 11 (33%) in the beta-lactam group met the definition for treatment failures (P = 0.34). Eight treatment failures while receiving azithromycin were caused by pneumococci with the macrolide-resistant (M) phenotype, 2 with the macrolide-, lincosamide- and streptogramin B-resistant (MLSB) phenotype and 1 by a macrolide-susceptible organism. In the beta-lactam group 7 had a penicillin-resistant isolate, 3 had an intermediately susceptible isolate and 1 had a susceptible isolate. CONCLUSIONS: Our study suggests that treatment failures among patients who developed invasive disease within 30 days of receiving an antimicrobial occur as frequently in patients who receive beta-lactam antibiotics as in those who receive azithromycin. Furthermore macrolide resistant organisms are not more likely to be recovered after a macrolide treatment failure than a penicillin-nonsusceptible isolate being recovered after a beta-lactam treatment failure (P = 1.0).

Anti-Bacterial Agents↗
PubMed1985

Combined IgG2, IgG4 and IgA deficiency: low C1q concentrations and the presence of excess C1r and C1s in an adult patient with recurrent pneumococcal infections.

The complement (C) profile was investigated in an adult patient with combined IgG2, IgG4 and IgA deficiency and recurrent pneumococcal infections. The analysis revealed no gross impairment of the classic and alternative pathways of C activation. However, the concentrations of circulating C1q were persistently decreased, and the sera contained an excess of C1r-C1s complexes, resembling the C1 aberrations previously found in children with recurrent acute otitis media. The concentrations of C4 in the patient were persistently low. This could be ascribed to partial C4 deficiency with lack of C4A variants. The patient's IgG and IgM antibody responses to pneumococcal capsular polysaccharides and to other bacterial carbohydrate antigens were very poor. Interestingly, pneumococcal C-polysaccharide (CPS) could be detected in serum obtained during infection-free periods. Since CPS has been shown to bind C1q without causing C1 activation, the possibility was considered that the C1 aberrations in serum were due to circulating CPS. After administration of intramuscular gammaglobulin to the patient, the serum C1q levels were observed to return to normal.

Adolescent↗
PubMed1997

[Splenic atrophy and fatal pneumococcal infection in inflammatory bowel disease].

Fatal pneumococcal disease occurred in a young woman with ulcerative colitis that had been quiescent for ten years. Howell-Jolly bodies were present in the peripheral blood smear. Severe atrophy of the spleen (weight 7 g) was discovered at autopsy. The evidence that hyposplenism is associated with inflammatory bowel disease is reviewed and it is suggested that these patients should undergo ultrasound examination and examination of blood smear for detection of functional hyposplenism. We conclude that pneumococcal vaccination should be considered for all patients with inflammatory bowel disease.

Adult↗
PubMed1979

[Severe pneumococcal infections of adults. 100 cases collected in three years (Claude Bernard Hospital, Paris) (author's transl)].

After retrospective in intensive care unit of 100 severe cases of pneumococcal infection in three years, the authors analyse the circumstances of onset (occurring in autumn of winter), the general status (without evident high risk population), the symptomatology (84% of meningitis, 30% of pneumonia), the origin of infection (essentialy otitis media in meningitis). The case fatality rate is 39%. Frequency of multiple visceral localisations and of bacteremias is emphasized.

Adolescent↗
PubMed2002

Characterization of the dihydrolipoamide dehydrogenase from Streptococcus pneumoniae and its role in pneumococcal infection.

In the present study, we have characterized the dihydrolipoamide dehydrogenase (DLDH) of Strepto-coccus pneumoniae and its role during pneumococcal infection. We have also demonstrated that a lack of DLDH results in a deficiency in alpha-galactoside metabolism and galactose transport. DLDH is an enzyme that is classically involved in the three-step conversion of 2-oxo acids to their respective acyl-CoA derivatives, but DLDH has also been shown to have other functions. The dldh gene was virtually identical in three pneumococcal strains examined. Besides the functional domains and motifs associated with this enzyme, analysis of the pneumococcal dldh gene sequence revealed the presence of an N-terminal lipoyl domain. DLDH-negative bacteria totally lacked DLDH activity, indicating that this gene encodes the only DLDH in S. pneumoniae. These DLDH-negative bacteria grew normally in vitro but were avirulent in sepsis and lung infection models in mice, indicating that DLDH activity is necessary for the survival of pneumococci within the host. The lack of virulence was not associated with a loss of 2-oxo acid dehydrogenase activity, as the wild-type pneumococcal strains did not contain activity of any of the known 2-oxo acid enzyme complexes. Instead, studies of carbohydrate utilization demonstrated that the DLDH-negative bacteria were impaired for alpha-galactoside and galactose metabolism. The DLDH mutants lost their ability to oxidize or grow with galactose or melibiose as sole carbon source and showed reduced oxidation and growth on raffinose or stachyose. The bacteria had an 85% reduction in alpha-galactosidase activity and showed virtually no transport of galactose into the cells, which can explain these phenotypic changes. The DLDH-negative bacteria produced only 50% of normal capsular polysaccharide, a phenotype that may be associated with impaired carbohydrate metabolism.

Amino Acid Sequence↗
PubMed1981

Complement in pneumococcal infections with varying degrees of severity.

Complement component levels (Clq, Cls, C4, C3, factor B and properdin) and C1 subcomponent complexes (C1r-C1s, C1-r-C1-, C1-r-C1-s-C1 inactivator, 1A) were studied in 16 adults with pneumococcal infections varying severity. Patients with fulminant disease and signs of septic shock showed pronounced hypocomplementemia. In patients with pneumococcal pneumonia or meningitis elevated levels of C1-r-C1-s-C1- IA complexes indicated activation of C1, despite normal levels of C1q, C1s, C4 and C3. Moderately decreased properdin values suggested involvement of the alternative pathway. In adults with pneumococcal otitis no changes in the complement profile was found. In contrast, pronounced aberrations of the C1 subcomponents were earlier demonstrated in children with otitis.

Adolescent↗
PubMedDate not supplied

Royal Society of Tropical Medicine and Hygiene Meeting at Manson House, London, 12 December 1996. HIV and pneumococcal infection in Africa. Microbiological aspects.

By the 1930s several studies had shown that Streptococcus pneumoniae was an important pathogen in Nairobi (Kenya) and various risk factors for infection were recognized, including seasonally cold conditions, overcrowding and recent arrival in the city. Research into pneumococcal disease declined with the arrival of penicillin but recently interest has been rekindled by recognition of the pneumococcus as a human immunodeficiency virus (HIV)-associated pathogen and by the emergence of antibiotic resistance. The pneumococcus and its association with HIV were studied during the course of the Wellcome Trust/Kenya Medical Research Institute HIV Programme in Nairobi (1988-1993). There were generally high rates of pneumococcal disease. The pneumococcus (with tuberculosis and salmonellosis) was a major HIV-related pathogen. One study showed HIV seropositivity to confer a relative risk of 17.8 for pneumococcal infection. Recurrent infection accounted for a large proportion (25%) of disease episodes in a longitudinally studied cohort of HIV patients. There were higher pneumococcal carriage rates in HIV-positive than in HIV-negative patients (28% vs. 16%, P = 0.003). High rates of resistance were found to penicillin (25%). Molecular characterization of penicillin-resistant strains identified 11 separate clones, showing great genetic diversity in a small sample of isolates, and there was evidence of horizontal spread of penicillin-binding protein genes between separate lineages. Molecular characterization of isolates from patients with recurrent disease suggested that both relapse and reinfection might occur. There was molecular evidence of transfer of capsular genes between clones (serotype switching). The overall spectrum of serotypes resembled those reported elsewhere, most serotypes being included in the 23-valent vaccine. Higher numbered serotypes were associated with respiratory tract source and antibiotic resistance. Various methods were used to show 82% concordance between pernasal and blood isolates in pneumonia cases. HIV-seropositive patients were more prone to infection with penicillin- and tetracycline-resistant organisms than seronegative patients (penicillin, 27% vs. 7%; tetracycline, 40% vs. 17%), a difference reflected by different serotype profiles in the 2 groups. These studies highlight the importance of the pneumococcus as an HIV-related pathogen in one part of Africa. The high rates of antibiotic resistance are a cause of concern. There should be continued monitoring of resistance patterns, and assessments of the significance of pneumococcal disease made elsewhere in Africa are to be encouraged.

Cohort Studies↗
PubMed2004

Host-pathogen interaction during pneumococcal infection in patients with chronic obstructive pulmonary disease.

Acute exacerbation is a frequent complication of chronic obstructive pulmonary disease (COPD). Recent studies suggested a role for bacteria such as Streptococcus pneumoniae in the development of acute exacerbation. For this study, we investigated the following in COPD patients: (i) the epidemiology of pneumococcal colonization and infection, (ii) the effect of pneumococcal colonization on the development of exacerbation, and (iii) the immunological response against S. pneumoniae. We cultured sputa of 269 COPD patients during a stable state and during exacerbation of COPD and characterized 115 pneumococcal isolates by use of serotyping. Moreover, we studied serum immunoglobulin G (IgG) antibody titers, antibody avidities, and functional antibody titers against the seven conjugate vaccine serotypes in these patients. Colonization with only pneumococci (monocultures) increased the risk of exacerbation, with a hazard ratio of 2.93 (95% confidence interval, 1.41 to 6.07). The most prevalent pneumococcal serotypes found were serotypes 19F, 3, 14, 9L/N/V, 23A/B, and 11. We calculated the theoretical coverage for the 7- and 11-valent pneumococcal vaccines to be 60 and 73%, respectively. All patients had detectable IgG levels against the seven conjugate vaccine serotypes. These antibody titers were significantly lower than those in vaccinated healthy adults. Finally, on average, a 2.5-fold rise in serotype-specific and functional antibodies in S. pneumoniae-positive sputum cultures was observed during exacerbation. Our data indicate that pneumococcal colonization in COPD patients is frequently caused by vaccine serotype strains. Moreover, pneumococcal colonization is a risk factor for exacerbation of COPD. Finally, our findings demonstrate that COPD patients are able to mount a significant immune response to pneumococcal infection. COPD patients may therefore benefit from pneumococcal vaccination.

Adult↗
PubMed2004

Pneumococcal infections in HIV infected adults--clinical features, reasons behind the association and future hopes for prevention.

Streptococcus pneumoniae is the most important bacterial cause of pneumonia and meningitis among adults world wide. It is a particularly common cause of these infections and also bacteraemia among HIV infected adults with rates of disease increasing to more than 100 times the normal as HIV infection progresses to AIDS. This article briefly describes the common presentations and outcomes of pneumococcal disease (PD) in HIV infected adult inpatients in Malawi. Factors underlying susceptibility to pneumococcal infection in HIV infected adults are then reviewed, along with the effectiveness of current vaccines. Finally, novel approaches that will be needed to combat PD in HIV afflicted parts of the world are suggested.

AIDS-Related Opportunistic Infections↗
PubMed2006

Role of the property of C-reactive protein to activate the classical pathway of complement in protecting mice from pneumococcal infection.

C-reactive protein (CRP) is not an acute-phase protein in mice, and therefore, mice are widely used to investigate the functions of human CRP. It has been shown that CRP protects mice from pneumococcal infection, and an active complement system is required for full protection. In this study, we assessed the contribution of CRP's ability of activating the classical pathway of complement in the protection of mice from lethal infection with virulent Streptococcus pneumoniae type 3. We used two CRP mutants, Y175A and K114A. The Y175A CRP does not bind C1q and does not activate complement in human serum. The K114A CRP binds C1q and activates complement more efficiently than wild-type CRP. Passively administered, both CRP mutants and the wild-type CRP protected mice from infection equally. Infected mice injected with wild-type or mutant CRP had reduced bacteremia, resulting in lower mortality and increased longevity compared with mice that did not receive CRP. Thus, the protection of mice was independent of CRP-mediated activation of the classical pathway of complement. To confirm that human CRP does not differentiate between human and mouse complement, we analyzed the binding of human CRP to mouse C1q. Surprisingly, CRP did not react with mouse C1q, although both mutant and wild-type CRP activated mouse C3, indicating species specificity of CRP-C1q interaction. We conclude that the mouse is an unfit animal for exploring CRP-mediated activation of the classical complement pathway, and that the characteristic of CRP to activate the classical complement pathway has no role in protecting mice from infection.

Animals↗
PubMed2001

Visualizing pneumococcal infections in the lungs of live mice using bioluminescent Streptococcus pneumoniae transformed with a novel gram-positive lux transposon.

Animal studies with Streptococcus pneumoniae have provided valuable models for drug development. In order to monitor long-term pneumococcal infections noninvasively in living mice, a novel gram-positive lux transposon cassette, Tn4001 luxABCDE Km(r), that allows random integration of lux genes onto the bacterial chromosome was constructed. The cassette was designed so that the luxABCDE and kanamycin resistance genes were linked to form a single promoterless operon. Bioluminescence and kanamycin resistance only occur in a bacterial cell if this operon has transposed downstream of a promoter on the bacterium's chromosome. S. pneumoniae D39 was transformed with plasmid pAUL-A Tn4001 luxABCDE Km(r), and a number of highly bioluminescent colonies were recovered. Genomic DNA from the brightest D39 strain was used to transform a number of clinical S. pneumoniae isolates, and several of these strains were tested in animal models, including a pneumococcal lung infection model. Strong bioluminescent signals were seen in the lungs of the animals containing these pneumococci, allowing the course and antibiotic treatment of the infections to be readily monitored in real time in the living animals. Recovery of the bacteria from the animals showed that the bioluminescent signal corresponded to the number of CFU and that the lux construct was highly stable even after several days in vivo. We believe that this lux transposon will greatly expand the ability to evaluate drug efficacy against gram-positive bacteria in living animals using bioluminescence.

Amoxicillin↗