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Experimental Streptococcus bovis infections in pigeons.

Thirty pigeons were experimentally infected with Streptococcus bovis using an intravenous infection model. Ninety percent of the inoculated pigeons developed clinical disease. Disease signs included acute death, inability to fly, lameness, inappetence, emaciation, polyuria, and the production of slimy, green droppings. At necropsy, the septicemic character of the disease was evident. Typical lesions included extensive well-circumscribed areas of necrosis in the pectoral muscle, tenosynovitis of the tendon of the Musculus pectoralis profundus, and arthritis of the stifle, tibiotarsal, or shoulder joints. Focal myocardial necrosis also was seen. Meningitis and encephalitis occurred in the cerebrum and the cerebellum. Disease signs and lesions described here after experimental infection were similar to those in naturally occurring cases of S. bovis septicemia.

Animals↗

Serotype III Streptococcus agalactiae from bovine milk and human neonatal infections.

Streptococcus agalactiae (group B streptococcus [GBS]) causes invasive human infections and bovine mastitis. This study examined the genetic relationship between bovine and human serotype III GBS by using molecular techniques that classify human serotype III GBS into four distinct phylogenetic lineages. Bovine serotype III GBS were largely contained in two lineages, which are distinct from the two major lineages (restriction digest types III-2 and III-3) that infect human neonates. One of the bovine lineages closely resembles the human III-1 lineage, whose members occasionally cause human neonatal infections. The bovine strains in the other lineage characteristically have an initiation factor IF2 gene (infB) H allele and multilocus sequence types that are not found in human GBS strains. Evidence suggests that this "H allele" lineage is related to the human III-3 lineage. These results support the assertion that human and bovine GBS are largely unrelated and provide further insight into the genetic relation between human and bovine GBS.

Alleles↗

[Invasive infections by Streptococcus pyogenes].

Invasive infections by Streptococcus pyogenes continually increase both in France and in others industrialized countries. Because of the seriousness, the rapidity of the evolution and the epidemic potentialities, guidelines for managing these infections are requested by the Superior Council of Public Hygiene of France. The authors report herein a case of an adult stricken down by a violent evolution due to Streptococcus pyogenes. They point up how diagnosis, treatment and prophylaxis for family circle are difficult.

Diagnosis, Differential↗

Characterization of the Streptococcus pneumoniae NADH oxidase that is required for infection.

Streptococcus pneumoniae is an important human pathogen capable of causing serious infections. NADH oxidase, a factor necessary for infection, was previously identified as part of a signature-tagged mutagenesis screen of a S. pneumoniae clinical isolate, 0100993. The mutant, with a plasmid insertion disrupting the nox gene, was attenuated for virulence in a murine respiratory tract infection model. A complete refined nox deletion mutant was generated by allelic-replacement mutagenesis and found to be attenuated for virulence 10(5)-fold in the murine respiratory tract infection model and at least 10(4)-fold in a Mongolian gerbil otitis media infection model, confirming the importance of the NADH oxidase for both types of S. pneumoniae infection. NADH oxidase converts O(2) to H(2)O. If O(2) is not fully reduced, it can form superoxide anion (O2(-)) and hydrogen peroxide (H(2)O(2)), both of which can be toxic to cells. Bacterial cell extracts from the allelic-replacement mutant were found to lack NADH oxidase activity and the mutant was unable to grow exponentially under conditions of vigorous aeration. In contrast, the mutant displayed normal growth characteristics under conditions of limited aeration. The S. pneumoniae nox gene was cloned and expressed in E. coli. The purified His-tagged NADH oxidase was shown to oxidize NADH with a K:(m) of 32 microM, but was unable to oxidize NADPH. Oxidation of NADH was independent of exogenous FAD or FMN.

Alleles↗

[Effectiveness of the antibiotics chloramphenicol and rifampin in the treatment of Streptococcus pneumoniae-induced meningitis and systemic infections].

Streptococcus pneumoniae, a common pathogen in pediatric infections, has become resistant to penicillin and make these infections difficult to treat. Rifampin and chloramphenicol have been recommended as alternative therapies, since they are less costly and more accessible to communities with limited resources. However, their use may be restricted by the differing levels of resistance found in target populations. The objective was to determine minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC) for chloramphenicol and rifampin in strains of S. pneumoniae. These strains were newly isolated from children under age 5 that had demonstrated systemic infections and meningitis. A subgroup of 107 isolates of S. pneumoniae was selected from 324 strains isolated during a period of 2 years (1994-1996). Among these isolates, 60 were penicillin-resistant and 47 were susceptible; 53 isolates were from children with meningitis. MIC and MBC for chloramphenicol and rifampicin were obtained by standard methods recommended by the National Committee for Clinical Laboratory Standards (NCCLS). S. pneumoniae ATCC strain 49619 served as the control. An isolate was considered susceptible to chloramphenicol when MIC = 4 microg/ml and resistant when MIC = 8 microg/ml. A strain was considered susceptible to rifampin when MIC = 1 microg/ml and resistant when MIC = 4 microg/ml. MBC was determined by recording the lower concentration of the antibiotic that inhibited 99.9% of the initial inoculum. Chloramphenicol resistance was found in 21% of the 107 isolates. In the group susceptible to penicillin, 11% were resistant to chloramphenicol and in the group resistant to penicillin 28% was resistant to chloramphenicol as well. MBC was found > 4 microg/ml in 28% of the isolates susceptible to penicillin and in 60% of the resistant isolates. No isolates were found resistant to rifampin. However, 2 penicillin resistant isolates showed CBM > 1 microg/ml to rifampin, and one with CIM = 1 microg/ml had a MBC to rifampicin of 16 microg/ml. Meningitis isolates showed higher CIM and CBM than the group of total isolates. These data suggest that chloramphenicol is not recommended for invasive infections caused by S. pneumoniae in Colombia. Rifampin is a more effective therapy in combination with other antibiotics for treatment of this kind of infections. Further studies are necessary to clarify the significance of low levels of MBC to rifampin found in some strains, since this may affect the efficacy of therapies that include this antibiotic.

Anti-Bacterial Agents↗

The demonstration by ribotyping of the stability of oral Streptococcus mutans infection over 5 to 7 years in children.

The distribution of serotypes and ribotypes of mutans streptococcal isolates obtained from seven unrelated children at 5 and at 10 or 12 yr of age was investigated. For ribotyping, chromosomal DNA from 5 to 13 isolates per subject was digested with restriction endonucleases EcoRI and HindIII. The DNA fragments were electrophoretically separated, blotted on to nylon membrane and hybridized to the plasmid pKK3535, which contains the rRNA operon of the Escherichia coli chromosome. The ribotypes were unique for each child. In five children only one ribotype and serotype (c, e or f) was found. In one child two serotypes (c and f) were found at baseline and only one (serotype c) in the follow-up sample. In one child the same serotype was not found in the baseline (serotype e) and in the follow-up (serotype c) samples. Every child except one had a ribotype that was identical to one found 5-7 yr later. The results suggest that, at the age of 5 yr, infection by Streptococcus mutans has already stabilized and the colonizing strain remains permanent.

Bacterial Typing Techniques↗

Effects of a Streptococcus equi infection--mediated nutritional insult during mid-gestation in primiparous Thoroughbred fillies. Part 1: placental and fetal development.

REASONS FOR PERFORMING STUDY: There is a paucity of information on factors that influence placental development in the horse. HYPOTHESIS: Changes in nutrition, particularly around the time of proliferative placental growth, can affect development of the placenta and fetal growth. OBJECTIVE: To investigate the effects of 2 planes of nutrition and an unforeseen infection-mediated nutritional insult on placental and fetal development in the mare. METHODS: Twenty maiden Thoroughbred fillies, age 3 or 4 years, mated to one Thoroughbred stallion, were maintained on either High or Moderate food intake throughout pregnancy. In mid-gestation all the mares unexpectedly became infected with Streptococcus equi and suffered varying degrees of weight loss as a consequence. Gross and stereological measurements of the placenta and measurements of foal birthweight, crown-rump length, ponderal index and plasma IGF-1 concentration were made at term. RESULTS: Gains in bodyweight during gestation were significantly higher in the High vs. the Moderate nutrition groups. Placental and fetal growth parameters were not influenced by the plane of nutrition. However, transient weight loss in mid-gestation from acutely reduced food intake resulted in morphological changes to the allantochorion and decreased foal birthweight. CONCLUSIONS: Excessive weight gain during gestation in maiden Thoroughbred fillies does not result in nutrient partitioning to the dam at the expense of the fetus. However, sudden weight loss in mid-gestation has detrimental effects on placental development which results in reduced fetal growth. POTENTIAL RELEVANCE: Clinicians should appreciate the likely effects of maternal infection and resulting weight loss on pregnancy outcome.

Animal Nutritional Physiological Phenomena↗

[Fatal maternal streptococcus A infection after cesarean section].

A case is reported of an infection with Streptococcus pyogenes, occurring 24 hours after an elective Caesarean section in a 30 year old woman. She worsened during the first 48 h, with shock (Pasys less than 70 mmHg, pH 7.28) as well as abdominal tenderness and guarding. Laparotomy revealed peritonitis, and subtotal hysterectomy was carried out. Gram positive cocci were found in the peritoneal exudate, with bacterial cultures yielding Streptococcus pyogenes. Histopathological examination of the specimen revealed necrosing endomyometritis with septic thrombophlebitis. During the immediate post-operative period, there were several prolonged episodes of circulatory arrest treated with dobutamine, adrenaline, and noradrenaline. Multiple organ failure occurred during the next five days, despite antibiotic therapy (vancomycin, tienamycin, amikacin) and intensive care. It included jaundice, thrombocytopaenia (10 G.l(-1] adult respiratory distress syndrome (ARDS). A further laparotomy was carried out because of abdominal and thigh cellulitis, with completion of the hysterectomy and bilateral salpingo-oophorectomy. Streptococcus pyogenes was still present in the peritoneal cavity. There followed an improvement, with a return to normal of the platelet count, haemodynamic stability such that vasoactive drugs were no longer needed, and a decrease in the degree of jaundice. However, the ARDS worsened, and the patient died 15 days after the Caesarean section. There have been recent reports of similar cases, suggesting an increase in the virulence of group A streptococci linked to a re-emergence of exotoxin A.

Adult↗

Changes in blood pH in rats after infection with Streptococcus pneumoniae.

Acid-base alterations in Streptococcus pneumoniae infection were studied in 80 male albino rats. Hematocrit and concentrations of plasma electrolytes, glucose, and total protein were also measured. At 3-h intervals throughout a 27-h study, four control and four infected rats were anesthetized with ether, and blood samples were taken. Arterial blood pH, Po2, and hematocrit increased in the infected group, whereas arterial Pco2, HCO3-, and venous Po2 decreased. Plasma K+ concentration increased slightly and glucose levels decreased in the infected rats as the sepsis progressed. No significant changes were observed in venous blood pH, HCO3-, and Pco2. Plasma Na+, Cl-, and total protein remained unchanged. The increase in arterial blood pH and decrease in arterial Pco2 and HCO3- indicated respiratory alkalosis, which was present in rats infected with S. pneumoniae.

Acid-Base Equilibrium↗

Both influenza-induced neutrophil dysfunction and neutrophil-independent mechanisms contribute to increased susceptibility to a secondary Streptococcus pneumoniae infection.

Since secondary Streptococcus pneumoniae infections greatly increase the mortality of influenza infections, we determined the relative roles of neutrophil-dependent and -independent mechanisms in increased susceptibility to S. pneumoniae during influenza infection. Mice infected with influenza for 6 days, but not 3 days, showed a significant increase in susceptibility to S. pneumoniae infection compared to mice not infected with influenza. There was significant neutrophil accumulation in the lungs of S. pneumoniae-infected mice regardless of whether or not they were infected with influenza for 3 or 6 days. Depletion of neutrophils in these mice resulted in increased susceptibility to S. pneumoniae in both the non-influenza-infected mice and mice infected with influenza for 3 days but not in the mice infected with influenza for 6 days, indicating that a prior influenza infection of 6 days may compromise neutrophil function, resulting in increased susceptibility to a S. pneumoniae infection. Neutrophils from the lungs of mice infected with influenza for 3 or 6 days exhibited functional impairment in the form of decreased phagocytosis and intracellular reactive oxygen species generation in response to S. pneumoniae. In addition, neutrophil-depleted mice infected with influenza for 6 days were more susceptible to S. pneumoniae than neutrophil-depleted mice not infected with influenza, indicating that neutrophil-independent mechanisms also contribute to influenza-induced increased susceptibility to S. pneumoniae. Pulmonary interleukin-10 levels were increased in coinfected mice infected with influenza for 6 days but not 3 days. Thus, an influenza infection of 6 days increases susceptibility to S. pneumoniae by both suppression of neutrophil function and by neutrophil-independent mechanisms such as enhanced cytokine production.

Animals↗

Perinatal infections with Streptococcus pneumoniae.

Perinatal infections with Streptococcus pneumoniae although rare, have caused morbidity and mortality in both neonatal and puerperal patients. To determine the incidence of proven pneumococcal sepsis in these patient groups, blood culture records from 1977 to 1989 were reviewed. Of 89 parturient patients with true positive blood cultures, two (2.2%) were positive for the pneumococcus, whereas of 240 infants with positive blood cultures, three (1.25%) grew pneumococcus. The incidence of maternal pneumococcal sepsis was 0.04/1000 live births, and that of the neonates, 0.06/1000, and the overall rate for sepsis in these two groups was 1.7 and 4.7/1000 live births, respectively. In three mother-infant pairs, the identical pneumococcal serotypes, 7, 18, and 23, were isolated from both mother and infant. Birthweights and gestational ages of the infants ranged from 2330 to 3730 gm and 34 to 40 weeks, respectively. Respiratory distress and poor peripheral perfusion were the predominant clinical signs in the infants with sepsis and became apparent from shortly after birth until 5 days of life. Pyrexia, poor general condition, and leukocytosis characterized the mothers with sepsis. All patients survived following antibiotic and supportive care. Our epidemiologic survey confirms the rareness of perinatal pneumococcal infection and the ability of these organisms to cause morbidity in both mothers and infants.

Adult↗

Incidence and clinical presentation of invasive neonatal group B streptococcal infections in Germany.

OBJECTIVE: Streptococcus agalactiae (group B Streptococcus) is an important cause of morbidity and mortality in newborn infants. So far, there have been no published data on the incidence, morbidity, and mortality of invasive neonatal group B Streptococcus infections in Germany. METHODS: A prospective active surveillance study involving all of the pediatric hospitals, which reported their cases to the German Pediatric Surveillance Unit, and all of the microbiological laboratories serving pediatric hospitals, which reported their cases to the Laboratory Sentinel Group at Robert Koch Institute Berlin, was conducted between 2001 and 2003. Capture-recapture analysis was used to evaluate the completeness of reported neonatal invasive group B Streptococcus infections. RESULTS: We collected and analyzed data from 347 and 360 infants with invasive group B Streptococcus infection during the first 3 months of life, as reported by pediatricians to the German Pediatric Surveillance Unit and microbiologists to the Robert Koch Institute Berlin, respectively. Using capture-recapture analysis, we calculated an incidence of 0.47 per 1000 live births. Nearly 60% of the infants suffered from early-onset disease, and 16% of these presented with meningitis. In contrast, 61.8% of infants with late-onset disease presented with meningitis. Prematurity was present in 22.4% of early-onset disease and 39.7% of late-onset disease cases, respectively. A high proportion of infants suffered from sequelae because of group B Streptococcus infection at the time of discharge from the hospital. Most common sequelae were hydrocephalus and cerebral seizure. Case fatality rate was 4.3%. CONCLUSIONS: This study, which is the first to provide information on the current national incidence and morbidity of invasive group B Streptococcus infection in Germany, demonstrates remarkable country-specific variation in comparison with other European countries, which gather data in a similar fashion. Therefore, the importance of country-specific prevention guidelines has to be stressed.

Germany↗

Influenza A virus-infected hosts boost an invasive type of Streptococcus pyogenes infection in mice.

The apparent worldwide resurgence of invasive Streptococcus pyogenes infection in the last two decades remains unexplained. At present, animal models in which toxic shock-like syndrome or necrotizing fasciitis is induced after S. pyogenes infection are not well developed. We demonstrate here that infection with a nonlethal dose of influenza A virus 2 days before intranasal infection with a nonlethal dose of S. pyogenes strains led to a death rate of more than 90% in mice, 10% of which showed necrotizing fasciitis. Infection of lung alveolar epithelial cells by the influenza A virus resulted in viral hemagglutinin expression on the cell surface and promoted internalization of S. pyogenes. However, treatment with monoclonal antibodies to hemagglutinin markedly decreased this internalization. Our results indicate that prior infection with influenza A virus induces a lethal synergism, resulting in the induction of invasive S. pyogenes infection in mice.

Animals↗

Disease severity in acute bacterial rhinosinusitis is greater in patients infected with Streptococcus pneumoniae than in those infected with Haemophilus influenzae.

BACKGROUND: Streptococcus pneumoniae and Haemophilus influenzae are the most common causative pathogens in acute bacterial rhinosinusitis. A post hoc pooled analysis of four multinational Phase III clinical trials was conducted to compare disease severity in acute bacterial rhinosinusitis caused by S. pneumoniae or H. influenzae. METHODS: Patients were evaluated for acute bacterial rhinosinusitis clinician-assessed symptom severity and radiologic findings (total opacity, mucosal thickening, and air-fluid levels on maxillary sinus x-rays). Specimens for bacteriologic identification were collected by maxillary sinus tap, or by selective middle meatal cultures (sinus aspirates or swabs). RESULTS: Compared with patients infected with H. influenzae (n = 106), patients infected with S. pneumoniae (n = 143) showed a statistically significant higher incidence of severe disease (39.2% vs 23.6%, P = 0.0097) and total opacity (46.2% vs 29.2%, P = 0.0085). Mucosal thickening (47.6% vs 56.6%, P = 0.1616) and air-fluid levels (49% vs 56.6%, P = 0.2500) were comparable between the two groups. CONCLUSIONS: In acute bacterial rhinosinusitis, infection with S. pneumoniae is associated with more severe clinical symptoms and radiographic total opacification findings than infection with H. influenzae.

Acute Disease↗

The role played by tumor necrosis factor during localized and systemic infection with Streptococcus pneumoniae.

Tumor necrosis factor (TNF) has been proposed as a major mediator of host resistance in murine models of Streptococcus pneumoniae infection; in humans, anti-TNF therapies have been implicated in increased susceptibility to pneumococcal infection. Here, we use nonlethal (serotype 6B) and lethal (serotype 3) S. pneumoniae, neutralizing monoclonal antibodies to TNF, and TNF gene-deficient mice to reexamine the role played by TNF in antistreptococcal responses. After nonlethal challenge, primary resistance and all examined parameters of the cellular inflammatory response occurred independently of TNF activity. After lethal challenge, TNF deficiency resulted in more-rapid death but did not affect lung inflammation. However, the livers of the TNF gene-deficient mice, but not of the control mice, exhibited extensive signs of systemic disease. TNF, therefore, is dispensable for a complete cellular pulmonary inflammatory response to S. pneumoniae infection but enhances survival from disseminated lethal infection, at least in part by delaying systemic organ damage.

Animals↗

[Clinical relevance of the Streptococcus milleri group in head and neck infections].

Streptococcus constellatus, S. intermedius, and S. anginosus, the 3 species of the S. milleri group, form part of the normal flora commonly found in the mouth, throat, and gastrointestinal and genital tracts. This group has become known as an important pathogen in infections and abscesses, but data on the anatomical distribution of these species is lacking in relation to clinical significance. We obtained 275 strains of the S. milleri group from different departments at our hospital over the last 3 years, including 54 strains from dental surgery, 47 from internal medicine, 44 from otolaryngology (head and neck), 43 from surgery, 32 from gynecology, 17 from urology, 16 from dermatology, 11 from brain surgery, 6 from pediatrics, 3 from orthopedics, and 2 from opthalmology. The 44 strains from head and neck were found in 42 patients,--23 with primary infection and 19 with secondary infection induced by cancer treatments. The primary infection group included 4 deep neck abscesses, 1 peritonsillar abscess, 5 tonsillitis, 4 paranasal sinusitis, 3 congenital aural fistula infections, 2 dental infections, 2 paranasal sinus cysts, 1 supprative parotitis, and 1 postoperative wound infection. The secondary infection group included 7 postoperative wound infections, 3 postoperative pulmonary infections, 3 laryngitis and pharyngitis, 3 terminal pneumonias, and 3 infections of the local recurrence site. The S. milleri group was the only isolated organism in 13 cases (56.5%) of primary infection and in 5 (26.3%) of secondary infection. Among other organisms from the primary infection group, no so-called major pathogens were found. Antimicrobial susceptibility tests of the S. milleri group showed that 50% were resistant to CCL and 33% to CTM. ABPC, CPDX, and CFDN were also found to be less sensitive, although no resistant strains were detected. To adequately culture the S. milleri group, incubation in air containing carbon dioxide or in an anaerobic atmosphere is required, and differentiation of the 3 requires biochemical reactivity tests. Since not all facilities use identical techniques in routine bacteriological examination, a considerable number of the S. milleri group could be missed in unknown species of alpha-,beta-, and gamma-streptococci and culture-negative cases. With antibiotics now being used widely, normal flora such as the S. milleri group may have become an important pathogen in head and neck infections due to an imbalance between organisms and host defense.

Humans↗

[Three interesting pediatric cases with penicillin-resistant Streptococcus pneumoniae infection].

Since penicillin-resistant Streptococcus pneumoniae first recognized in 1967, the rate of penicillin-resistant strains has been increasing worldwide. There have been up to 50% from pediatric specimens in Japan. We reported three pediatric cases with penicillin G resistant Streptococcus pneumoniae infection to show some important clue from these cases for clinical practice against resistant pneumococcal infection. The first case was a typical acute mastoiditis, although we have experienced only masked mastoiditis recently. The second case was meningitis with septicemia, which did not show any abnormality in the first obtained cerebrospinal fluid. The third case was recurrent bronchitis in a child with cerebral palsy. The minimum inhibition concentrations of these isolated strains were 0.25 microgram/ml in the second case an 2.0 microgram/ml in the first and third cases.

Adolescent↗

Streptococcus suis infection.

A recent outbreak of Streptococcus suis infection associated with the slaughter, preparation or consumption of pigs in Sichuan, China has led to concerns that similar outbreaks could occur in other Asian countries. Although the pig farming industry is flourishing in Taiwan, reports of S. suis infection remain rare. We report 2 cases of S. suis meningitis successfully treated with ceftriaxone and penicillin. Previous reports of S. suis infection from the English literature are reviewed and the clinical data of cases reported in Asian and European countries are summarized. In Europe, there was good correlation between clinical disease and porcine contact, while few cases in Asia reported this association. Meningitis remained the most common presentation of infection in both areas (84.6% and 75.2%, respectively), followed by sepsis (15.4% and 18.6%, respectively), which had a higher mortality rate, particularly for splenectomized patients. Other clinical presentations included enteritis, arthritis, endocarditis, pneumonia, spondylodiscitis, endophthalmitis, uveitis and peritonitis. Deafness was a distinct sequelae (50.5% in Europe and 51.9% in Asia) after recovery from S. suis infection, especially in patients with meningitis. Not all commercial identification systems for streptococci could offer adequate speciation for S. suis. When viridans group streptococci are isolated from patients with meningitis and sepsis, prompt and correct identification of isolates to the species level should be performed, especially in areas with a high prevalence of S. suis diseases.

Adolescent↗