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Streptococcus pneumoniae is commonly known for its alpha/beta hemolytic activity. It is also a gram-positive bacterium.

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Streptococcus pneumoniae, or pneumococcus, is a Gram-positive, alpha-hemolytic (under aerobic conditions) or beta-hemolytic (under anaerobic conditions), facultative anaerobic member of the genus Streptococcus. They are usually found in pairs ( diplococci) and do not form spores and are nonmotile. As a significant human pathogenic bacterium S. pneumoniae was recognized as a major cause of pneumonia in the late 19th century, and is the subject of many humoral immunity studies.

S. pneumoniae resides asymptomatically in healthy carriers typically colonizing the respiratory tract, sinuses, and nasal cavity. However, in susceptible individuals with weaker immune systems, such as the elderly and young children, the bacterium may become pathogenic and spread to other locations to cause disease. It spreads by direct person-to-person contact via respiratory droplets and by autoinoculation in persons carrying the bacteria in their upper respiratory tracts. It can be a cause of neonatal infections.

S. pneumoniae is the main cause of community acquired pneumonia and meningitis in children and the elderly, and of sepsis in those infected with HIV. The organism also causes many types of pneumococcal infections other than pneumonia. These invasive pneumococcal diseases include bronchitis, rhinitis, acute sinusitis, otitis media, conjunctivitis, meningitis, sepsis, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscess.

S. pneumoniae can be differentiated from the viridans streptococci, some of which are also alpha-hemolytic, using an optochin test, as S. pneumoniae is optochin-sensitive. S. pneumoniae can also be distinguished based on its sensitivity to lysis by bile, the so-called "bile solubility test". The encapsulated, Gram-positive, coccoid bacteria have a distinctive morphology on Gram stain, lancet-shaped diplococci. They have a polysaccharide capsule that acts as a virulence factor for the organism; more than 90 different serotypes are known, and these types differ in virulence, prevalence, and extent of drug resistance.

In 1881, the organism, known later in 1886 as the pneumococcus for its role as a cause of pneumonia, was first isolated simultaneously and independently by the U.S. Army physician George Sternberg and the French chemist Louis Pasteur.

The organism was termed Diplococcus pneumoniae from 1920 because of its characteristic appearance in Gram-stained sputum. It was renamed Streptococcus pneumoniae in 1974 because it was very similar to streptococci.

S. pneumoniae played a central role in demonstrating that genetic material consists of DNA. In 1928, Frederick Griffith demonstrated transformation of life turning harmless pneumococcus into a lethal form by co-inoculating the live pneumococci into a mouse along with heat-killed virulent pneumococci. In 1944, Oswald Avery, Colin MacLeod, and Maclyn McCarty demonstrated that the transforming factor in Griffith's experiment was not protein, as was widely believed at the time, but DNA. Avery's work marked the birth of the molecular era of genetics.

The genome of S. pneumoniae is a closed, circular DNA structure that contains between 2.0 and 2.1 million base pairs depending on the strain. It has a core set of 1553 genes, plus 154 genes in its virulome, which contribute to virulence and 176 genes that maintain a noninvasive phenotype. Genetic information can vary up to 10% between strains. The pneumococcal genome is known to contain a large and diverse repertoire of antimicrobial peptides, including 11 different lantibiotics.

Transformation

Natural bacterial transformation involves the transfer of DNA from one bacterium to another through the surrounding medium. Transformation is a complex developmental process requiring energy and is dependent on expression of numerous genes. In S. pneumoniae, at least 23 genes are required for transformation. For a bacterium to bind, take up, and recombine exogenous DNA into its chromosome, it must enter a special physiological state called competence.

Competence in S. pneumoniae is induced by DNA-damaging agents such as mitomycin C, fluoroquinolone antibiotics ( norfloxacin, levofloxacin and moxifloxacin), and topoisomerase inhibitors. Transformation protects S. pneumoniae against the bactericidal effect of mitomycin C. Michod et al. summarized evidence that induction of competence in S. pneumoniae is associated with increased resistance to oxidative stress and increased expression of the RecA protein, a key component of the recombinational repair machinery for removing DNA damages. On the basis of these findings, they suggested that transformation is an adaptation for repairing oxidative DNA damages. S. pneumoniae infection stimulates polymorphonuclear leukocytes (granulocytes) to produce an oxidative burst that is potentially lethal to the bacteria. The ability of S. pneumoniae to repair the oxidative DNA damages in its genome, caused by this host defense, likely contributes to this pathogen's virulence. Consistent with this premise, Li et al. reported that, among different highly transformable S. pneumoniae isolates, nasal colonization fitness and virulence (lung infectivity) depend on an intact competence system.

S. pneumoniae is part of the normal upper respiratory tract flora. As with many natural flora, it can become pathogenic under the right conditions, typically when the immune system of the host is suppressed. Invasins, such as pneumolysin, an anti phagocytic capsule, various adhesins, and immunogenic cell wall components are all major virulence factors. After S. pneumoniae colonizes the air sacs of the lungs, the body responds by stimulating the inflammatory response, causing plasma, blood, and white blood cells to fill the alveoli. This condition is called pneumonia.

Pneumonia is the most common of the S. pneumoniae diseases which include symptoms such as fever and chills, cough, rapid breathing, difficulty breathing, and chest pain. For the elderly, they may include confusion, low alertness, and the former listed symptoms to a lesser degree.

Pneumococcal meningitis is an infection of the tissue covering the brain and spinal cord. Symptoms include stiff neck, fever, headache, confusion, and photophobia.

Sepsis is caused by overwhelming response to an infection and leads to tissue damage, organ failure, and even death. The symptoms include confusion, shortness of breath, elevated heart rate, pain or discomfort, over-perspiration, fever, shivering, or feeling cold.

Due to the importance of disease caused by S. pneumoniae, several vaccines have been developed to protect against invasive infection. The World Health Organization recommends routine childhood pneumococcal vaccination; it is incorporated into the childhood immunization schedule in a number of countries including the United Kingdom, the United States, and South Africa.

Interaction with Haemophilus influenzae

Historically, Haemophilus influenzae has been a significant cause of infection, and both H. influenzae and S. pneumoniae can be found in the human upper respiratory system. A study of competition revealed S. pneumoniae overpowered H. influenzae by attacking it with hydrogen peroxide. However, in a study adding both bacteria to the nasal cavity of a mouse within 2 weeks, only H. influenzae survives; further analysis showed that neutrophils exposed to dead H. influenzae were more aggressive in attacking S. pneumoniae.

Diagnosis is generally made based on clinical suspicion along with a positive culture from a sample from virtually any place in the body. S. pneumoniae is, in general, optochin sensitive, although optochin resistance has been observed.

The recent advances in next-generation sequencing and comparative genomics have enabled the development of robust and reliable molecular methods for the detection and identification of S. pneumoniae. For instance, the Xisco gene was recently described as a biomarker for PCR-based detection of S. pneumoniae and differentiation from closely related species.

Atromentin and leucomelone possess antibacterial activity, inhibiting the enzyme enoyl-acyl carrier protein reductase, (essential for the biosynthesis of fatty acids) in S. pneumoniae. Optochin sensitivity in a culture of Streptococcus pneumoniae

Resistant pneumococcal strains are called penicillin-resistant pneumococci ( PRP), penicillin-resistant Streptococcus pneumoniae ( PRSP), Streptococcus pneumoniae penicillin resistant ( SPPR) or drug-resistant Strepotococcus pneumoniae ( DRSP). Until the year 2000 out of 60,000 yearly cases 40% and out of the 30,000 cases in the year 2015 30% of the infections were resistant to one or more antibiotics.

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Streptococcus pneumoniae , or pneumococcus, is a Gram-positive, alpha-hemolytic (under aerobic conditions) or beta-hemolytic (under anaerobic conditions), facultative anaerobic member of the genus Streptococcus . They are usually found in pairs ( diplococci) and do not form spores and are nonmotile. As a significant human pathogenic bacterium S.

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Kingdom: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Species: S. pneumoniae

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Often living asymptomatically in healthy individuals.  However, it is the main cause of pneumonia and meningitis in children and elderly.  Additionally, the bacterium can cause a number of other pneumoncoccal infections. [Link]

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By vaccination of children less than 2 years old with PCV7/PCV13 caused the incident rate of conjuctivitis to decline.  This reveals that pneumoccous-NTHi interaction has a large role to play in the infection process. Herd immunity is key in lowering rate of infection.

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BACKGROUND:

Bacterial conjunctivitis is most commonly caused by nontypeable Haemophilus influenzae (NTHi), followed by Streptococcus pneumoniae. No population-based data on the impact of pneumococcal conjugate vaccines (PCVs) on the incidence of bacterial conjunctivitis have been published. We assessed rate dynamics of overall, pneumococcal and NTHi conjunctivitis in children aged 2-23 months in southern Israel before and after PCV implementation.

METHODS:

This is a 12-year prospective, population-based surveillance, from July 2004 through June 2017. Our medical center serves a captive population of ~30,000 children <2 years, and its Clinical Microbiology Laboratory processes >80% of all community-derived cultures, enabling incidence calculation. PCV7/PCV13 were implemented in the national immunization program in July-2009/November-2010, respectively. Pneumococci, NTHi, Moraxella catarrhalis and Streptococcus pyogenes were considered pathogens. Continuous annual incidences and incidence-rate ratios comparing the PCV13 period (2015-2017) to the pre-PCV period (2004-2008) were calculated.

RESULTS:

Disease caused by PCV13 serotypes declined by 93%, without significant replacement with non-PCV13 serotypes. Rates of pneumococcal, NTHi and overall culture-positive episodes declined by 59%, 41% and 42%, respectively, while rates of culture-negative and other pathogens episodes did not change significantly. An overall reduction in all submitted cultures rates of 35% was observed. This pattern was seen across all ages, including 2-5 month old infants.

CONCLUSIONS:

PCV7/PCV13 implementation resulted in a marked and significant decline in pneumococcal, NTHi and overall conjunctivitis rates in children <2 years. The impact on NTHi episodes alludes to the role of pneumococcus-NTHi interaction in conjunctivitis. The impact in infants <6 months suggests herd protection.

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s. pneumoniae
        ;conjunctivitis;nontypeable h. influenzae;pneumococcal conjugate vaccine

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BACKGROUND: Bacterial conjunctivitis is most commonly caused by nontypeable Haemophilus influenzae (NTHi), followed by Streptococcus pneumoniae. No population-based data on the impact of pneumococcal conjugate vaccines (PCVs) on the incidence of bacterial conjunctivitis have been published. We assessed rate dynamics of overall, pneumococcal and NTHi conjunctivitis in children aged 2-23 months in southern Israel before and after PCV implementation.

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Capnocytophaga gingivalis - Wiki Article

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Capnocytophaga gingivalis - Wiki Article

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C. gingivalis is a gram negative bacteria that can typically be found in the oropharyngeal tract of most mammals. Often referred to as an opportunistic pathogen.
[Link to Wiki Article]

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Capnocytophaga gingivalis and Strptococcus pneumoniae are distantly related.  The closest relative on this phylogenetic tree is Anaerococcus prevotii.

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C. gingivalis is apart of the genus Capnocytophaga.  Interestingly, this genus varies immensely in shape and size, which is completely dependent on the strain.  This bacterium can cause a condition called alveolar bone loss, which can lead to complete tooth loss. [Link]

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Studies were done to determine if Acute Exacerbations of Chronic Pulmonary Disease (AE-COPD) had origins in the pathogenic bacteria that are located in dental plaque biofilms. The study concluded that biofilms do harbor bacteria that contribute to the cause of AE-COPD. C. gingivalis was one of these harbored bacteria within the biofilm.

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BACKGROUND AND OBJECTIVE:

Acute exacerbations of chronic obstructive pulmonary disease (AE-COPD) are leading causes of mortality in hospital intensive care units. We sought to determine whether dental plaque biofilms might harbor pathogenic bacteria that can eventually cause lung infections in patients with severe AE-COPD.

MATERIAL AND METHODS:

Paired samples of subgingival plaque biofilm and tracheal aspirate were collected from 53 patients with severe AE-COPD. Total bacterial DNA was extracted from each sample individually for polymerase chain reaction amplification and/or generation of bacterial 16S rDNA sequences and cDNA libraries. We used a metagenomic approach, based on bacterial 16S rDNA sequences, to compare the distribution of species present in dental plaque and lung.

RESULTS:

Analysis of 1060 sequences (20 clones per patient) revealed a wide range of aerobic, anaerobic, pathogenic, opportunistic, novel and uncultivable bacterial species. Species indistinguishable between the paired subgingival plaque and tracheal aspirate samples (97-100% similarity in 16S rDNA sequence) were dental plaque pathogens (Aggregatibacter actinomycetemcomitans, Capnocytophaga sputigena, Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola) and lung pathogens (Acinetobacter baumannii, Klebsiella pneumoniae, Pseudomonas aeruginosa and Streptococcus pneumoniae). Real-time polymerase chain reaction of 16S rDNA indicated lower levels of Pseudomonas aeruginosa and Porphyromonas gingivalis colonizing the dental plaques compared with the paired tracheal aspirate samples.

CONCLUSION:

These results support the hypothesis that dental bacteria may contribute to the pathology of severe AE-COPD.

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BACKGROUND AND OBJECTIVE: Acute exacerbations of chronic obstructive pulmonary disease (AE-COPD) are leading causes of mortality in hospital intensive care units. We sought to determine whether dental plaque biofilms might harbor pathogenic bacteria that can eventually cause lung infections in patients with severe AE-COPD.

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In creation of this Padlet, I realized how interconnected various different bacteria are in maintaining homeostasis within the body.  Both of the bacteria I studied are considered opportunistic pathogens that react when their is an imbalance in oral microbiota.  The creation of the phylogenetic tree allowed me to appreciate how distantly bacterium can evolve.  The common ancestor that two bacteria share can still differ in many ways to the bacteria we see today.  It is important to study microbiology to understand how bacteria interact within our bodies so that we can develop treatments to counteract any pathogens we may encounter. Even if those pathogens are common residents within our oral microbiota.
Two PadletsI found interesting were [DJ Singh] and [Taylor Evans]