See more
What is the colony morphology of Streptococcus?
Streptococci often have a mucoid or smooth colonial morphology, and S pneumoniae colonies exhibit a central depression caused by rapid partial autolysis. As S pneumoniae colonies age, viability is lost during fermentative growth in the absence of catalase and peroxidase because of the accumulation of peroxide.
What are the characteristics of Streptococcus pneumoniae?
Streptococcus pneumoniae are lancet-shaped, gram-positive, facultative anaerobic bacteria with more than 100 known serotypes. Most S. pneumoniae serotypes can cause disease, but only a minority of serotypes produce the majority of pneumococcal infections.
What is the Gram reaction morphology and arrangement of Streptococcus pneumoniae?
Streptococcus pneumoniae bacteria are gram-positive cocci arranged in chains and pairs (diplococci) on microscopic examination. A green, α-hemolytic, zone surrounds S. pneumoniae colonies on blood-agar plates.
How do you identify Streptococcus pneumoniae?
S. pneumoniae can be identified using Gram stain, catalase, and optochin tests simultaneously, with bile solubility as a confirmatory test. If these tests indicate that the isolate is S. pneumoniae, serological tests to identify the serotype can be performed.
What is Streptococcus pneumoniae known for?
Streptococcus pneumoniae is the most common cause of middle ear infections, sepsis (blood infection) in children and pneumonia in immunocompromised individuals and the elderly. It can also cause meningitis (inflammation of the coverings of the brain and spinal cord) or sinus infections.
What is Streptococcus pneumoniae common name?
Pneumococcal [noo-muh-KOK-uhl] disease is a name for any infection caused by bacteria called Streptococcus pneumoniae, or pneumococcus. Pneumococcal infections can range from ear and sinus infections to pneumonia and bloodstream infections. There are vaccines to help prevent pneumococcal disease.
What is the difference between pneumonia and Streptococcus pneumoniae?
Pneumonia is an inflammatory disease of the lung, responsible for high morbidity and mortality worldwide. It is caused by bacteria, viruses, fungi, or other microorganisms. Streptococcus pneumoniae, a gram-positive bacterium with over 90 serotypes, is the most common causative agent.
What is the shape of pneumonia?
pneumonia is a lancet-shaped, gram-positive, facultative anaerobic organism that typically occurs in pairs or short chains.
Is Streptococcus pneumoniae catalase positive or negative?
catalase-negativeAll streptococci are catalase-negative. S. pneumoniae strains are sensitive to the chemical optochin (ethylhydrocupreine hydrochloride). Optochin sensitivity allows for the presumptive identification of alpha-hemolytic streptococci as S.
What is size of Streptococcus pneumoniae?
It is microbiologically characterized as a gram-positive coccus, 0.5 to 1.25 μm (micrometres; 1 μm = 10−6 metre) in diameter, often found in a chain configuration and surrounded by a capsule consisting of complex carbohydrate (polysaccharide).
Does Streptococcus pneumoniae have flagella?
This bacteria is equipped with flagella referred to as antigen T. However, unlike the flagella observed in S. pneumoniae, the presence of the flagella in S. pyogenes causes decreased invasiveness and pathogenicity of the strain.
Why is it important to distinguish Streptococcus pneumoniae from other streptococci?
Reliable distinction of Streptococcus pneumoniae and viridans group streptococci is important because of the different pathogenic properties of these organisms.
What is the difference between pneumonia and Streptococcus pneumoniae?
Pneumonia is an inflammatory disease of the lung, responsible for high morbidity and mortality worldwide. It is caused by bacteria, viruses, fungi, or other microorganisms. Streptococcus pneumoniae, a gram-positive bacterium with over 90 serotypes, is the most common causative agent.
What are two strains of pneumococcus and the distinguishing characteristics of each?
Griffith used two strains of pneumococcus (Diplococcus pneumoniae) bacteria which infect mice – a type III-S (smooth) which was virulent, and a type II-R (rough) strain which was nonvirulent.
What group is Streptococcus pneumoniae?
The species S. pneumoniae belongs to the S. mitis group streptococci, which are part of the so-called viridans streptococci group, which also includes the S. salivarius, S.
How is Streptococcus pneumoniae distinguished from other streptococci that have the same hemolytic properties What additional tests are needed or performed?
S. pneumoniae can be differentiated from other α-hemolytic streptococci by its carbohydrate fermentation and solubility in bile. Type-specific identification is based on the polysaccharide capsule that surrounds the cell wall.
Where is Streptococcus pneumoniae found?
Streptococcus pneumoniae are found worldwide. Found in primates, livestock and felines. They are the part of normal flora of upper respiratory tract infection in humans. Mostly found in throat and nasal passage. They infection mostly children in winter seasons. They are Mesophilic, 30 to 35°C.
What is the diameter of a pili?
They are non-sporing and non-motile bacteria. May have pili for adherence. They are 0.5 x 1.25 µm in diameter. They are mostly found in pairs (diplococci). Also found singly and in short chains isolated from body liquids. They are lancet-shaped or bullet-shaped. They are capsulated.
How many serotypes are there in Streptococcus pneumoniae?
There are 100 known serotypes of Streptococcus pneumoniae, the bacteria that cause pneumococcal disease. Streptococcus pneumoniae are lancet-shaped, gram-positive, facultative anaerobic bacteria with 100 known serotypes. Most S. pneumoniae serotypes can cause disease, but only a minority of serotypes produce the majority of pneumococcal infections.
How many people are carriers of pneumococci?
The bacteria may be isolated from the nasopharynx of 5–90% of healthy persons, depending on the population and setting: 5–10% of adults without children are carriers. 20–60% of school-aged children may be carriers.
How to identify Streptococcus pneumoniae?
Identification of Streptococcus pneumoniae from culture depends on observation of the morphologic characteristics of both the bacteria and the colonies, as well as on three other main phenotypic characteristics, including catalase negativity, bile solubility, and optochin susceptibility. Suscepti bility to optochin is a mainstay for the identification of pneumococci due to the ease of performance of the test, the basis of which is optochin’s inhibition of the pneumococcal ATPase, a characteristic that is not generally shared by other viridians streptococci [2]. However, the emergence of optochin-resistant variants [3] has brought into question the validity of using this sole test for the presumptive identification of pneumococci. The specificity of the bile solubility test remains high, and it is the most accurate single test for the identification of S. pneumoniae [3]. The bile solubility phenotype is due to the activation of the major autolytic enzyme (an N -acetylmuramyl- l -alanine amidase encoded by the lytA gene), which can also be achieved by sodium deoxycholate. A few pneumococcal isolates were found to be insoluble in sodium deoxycholate, which has been ascribed to alterations in the major autolysin [4], but the overwhelming majority of pneumococci remain bile soluble, making it an extremely accurate test for pneumococcal identification.
What are the surface proteins of Streptococcus pneumoniae?
Streptococcus pneumoniae expresses different families of surface-exposed proteins, distinguished by their mode of attachment to the cell: lipoproteins, choline-binding proteins, LPxTG-anchored proteins, the pneumococcal histidine triad family proteins, and non-classical surface proteins. These proteins have diverse roles in the interaction of the pneumococcus with its host, such as adhesion to epithelial cells and extracellular matrix proteins, substrate transport, immune evasion, and bacterial fitness. Here we will focus on a subset of surface proteins of S. pneumoniae, namely those whose predicted function in pneumococcal pathogenesis is not directly related to cellular adhesion.
How to identify CPS?
The identification of the pneumococcal CPS by the Quellung effect or Neufeld test, using specific rabbit sera, is a proven technique that has been used since the early days of pneumococcal serotyping [9]. However, this technique requires specific expertise, so more recently, the Statens Serum Institut has made a latex agglutination test available, which allows a more streamlined procedure for serotyping pneumococci [11]. To further simplify this process, several “genetic serotyping” schemes have been developed to identify particular characteristics of the cps loci. In spite of the multitude of approaches, those more widely adopted are based on PCR amplification of specific serogroup or serotype genes [12,13]. In fact, both conventional and real-time PCR procedures have been developed, and a great diversity of schemes have been proposed to accommodate the differences in prevalence of the various serotypes in different geographic regions [13–15]. Although genetic serotyping has made serotyping available to a greater number of laboratories and has helped to clarify unclear reactions, phenotypic methods remain the gold standard for pneumococcal serotyping [15], and reflecting this, hybrid approaches involving both PCR and monoclonal antibodies have also been developed [16]. Perhaps the clearest examples of this are isolates in which the capsular locus contains point mutations or insertions leading to the absence of expression of a CPS (van der Linden and Ramirez, unpublished data) but that would be assigned a serotype according to genetic serotyping schemes.
What is the etiological diagnosis of pneumonia?
Etiological Diagnosis of Pneumococcal Infections. Pneumococci are a leading cause of pneumonia and an important cause of meningitis, bacteremia, sepsis, otitis media, rhinitis, and sinusitis [1]. Classically, the etiological diagnosis of these infections has been done by growing the microorganism from suitable patient samples.
How do bacterial pathogens influence host signaling?
The induction of host signal transduction cascades by bacterial pathogens contributes directly to their virulence. In addition to the pore-forming cytolysin pneumolysin, several surface-exposed proteins of Streptococcus pneumoniae are also potent modulators of complex host signaling pathways. These pneumococcal surface proteins either directly mediate adhesion of pneumococci to specific cell surface receptors or recruit extracellular matrix or serum components as molecular bridges for binding to cellular receptors. In turn, adhesion triggers and subverts host signal transduction cascades to promote pneumococcal translocation across tissue barriers and dissemination within host tissues. This chapter summarizes the current knowledge of how pneumolysin and major adhesins manipulate host signaling pathways. The chapter will provide a structured overview of the signaling profiles induced by pneumococci, focusing on the receptors required and comparing the key signaling molecules and intracellular responses involved.
How does Streptococcus pneumoniae survive?
To survive in the human population, Streptococcus pneumoniae has evolved to colonize the mucosal surfaces of the upper respiratory tract. From there, the pneumococcus can then successfully spread to other susceptible hosts. The success of the pneumococcus in surviving and persisting in the human population is clearly demonstrated by the approximately 1.9–5.8 billion people estimated to be colonized with S. pneumoniae at any given time (inferred from [1,2] ). Despite the fact that the pneumococcus is notorious for its ability to cause severe invasive disease, the majority of colonized individuals will not develop clinical symptoms. This strongly suggests that colonization actually represents the primary selective force for pneumococcal evolution and implies that many of the host–pathogen interactions observed during pneumococcal disease must be viewed within the context of asymptomatic colonization. In this chapter we will discuss the dynamics and mechanisms of pneumococcal colonization of the upper respiratory tract and subsequent transmission to a new host. Although we will also briefly touch upon how pneumococcal colonization perturbs mucosal homeostasis and how this affects immune signaling, disease development, and bacterial clearance, these aspects are primarily discussed in other chapters.
What is the role of pneumococci in the evolution of the pathogen?
Research on Streptococcus pneumoniae has revealed key aspects in the study of infectious diseases and pathogen evolution, but pneumococci remain a major cause of morbidity and mortality. New insights into the pathogenic mechanisms of this species confirmed the key role of the capsular polysaccharide but have also identified the important functions played by proteins in the interaction with the host. The capacity of pneumococci to exchange DNA is central in the adaptation to human-imposed selective pressures and our understanding of the mechanisms underlying competence is raising new questions about the evolution of these bacteria. A greater knowledge of the biology of pneumococci resulted in new diagnostic tests that together with a revision of the breakpoints defining resistance to penicillin and the advent of conjugate vaccines, are changing our understanding of the burden of pneumococcal disease and our approaches to prevent and treat infections by this important pathogen.
How to diagnose pneumonia?
The diagnosis of the causative organism for pneumonia can be obtained through a variety of means including blood cultures, sputum analysis, and urinary antigens. The routine collection of blood cultures has been controversial in the literature. Recently the Centers for Medicaid and Medicare Services and the Joint Commission on Accreditation of Healthcare Organizations have noted that routine collection of blood cultures is no longer a core measure that is being tracked. Also, the American College of Emergency Physicians (ACEP) made a grade B recommendation against the routine collection of blood cultures in patients admitted with CAP. Further sources note that blood cultures should be obtained in those admitted to the intensive care unit, those with leukopenia, cavitary lesion, severe liver disease, alcohol abuse, asplenia or pleural effusions. When blood cultures are positive, the majority show S. pneumoniabut rarely change clinical management.
How common is S pneumoniae?
Although S. pneumoniae pneumonia can occur in all populations, it is more common in patients older than 65 years, younger than 2 years, those who smoke, abuse alcohol, have asthma or COPD, or are asplenic. The overall rate of confirmed S. pneumoniaeinfection in the United States is 5.16 to 6.11 cases/100,000 in adults with the rate for those older than 65 years being 36.4/100,000 and infants younger than 1 year being 34.2/100,000. [7][8][9] World Health Organization estimated that 1.6 million deaths in 2005 including 1 million children less than 5 years of age, occurred due to streptococcus pneumoniae. It is a common co-infection in influenza patients and affects the morbidity and mortality in such patients.
What is the most common pathogen to cause CAP?
Streptococcus pneumoniaeis the bacterium that has historically been the most common pathogen to cause CAP worldwide. In the era before antibiotics, S. pneumoniaewas estimated to be the cause of 95% of all cases of pneumonia. Currently, however, S. pneumoniae accounts for up to 15% of pneumonia cases in the United States and 27% of cases worldwide today. Blood cultures are positive in only 20% to 25% of all pneumonia cases that are caused by S. pneumonia making it a challenging diagnosis for the clinician. [1][2][3]
When is pneumonia most common?
Pneumococcal infections are present throughout the world and are most common during the winter and early spring months. IS. pneumoniae is prevalent in large part due to its colonizing ability in the nasopharynx. Almost 40%-50% healthy children and 20%-30% of healthy adults are carriers.[6] With childhood conjugate vaccination for Streptococcus pneumoniae, the colonization frequency has decreased.
What are the factors that affect the virulence of pneumonia?
S. pneumoniahas several virulence factors that allow it to cause infections in humans. A polysaccharide capsule interferes with phagocytosis by inhibiting the binding of complement C3b to the cell’s surface. Pneumococcal proteins also play a large role in the virulence of the bacteria. IgA1 protease interferes with host defense at mucosal surfaces, and neuraminidase prevents the attachment to epithelial cells. Other proteins that act in the virulence of S. pneumoniainclude pneumolysin, pneumococcal surface protein A, and autolysin. Lastly, pili allow for the adherence of the organism to cellular surfaces and play a role in host inflammation.
Is S pneumonia gram positive?
S. pneumoniais a lancet-shaped, gram-positive, facultative anaerobic organism that typically occurs in pairs or short chains. Encapsulated S. pneumonia is pathogenic for humans, and the capsular polysaccharide is the basis for which the organism is classified. As of 2011, a total of 92 separate serotypes have been isolated.
Does smoking cigarettes increase the risk of pneumococcal infection?
Cigarette smoking has been found to increase the risk of pneumococcal infection in otherwise healthy people. Therefore smoking cessation should be encouraged. Good nutrition, healthy environment and avoidance of daycare attendance decrease the frequency of acquiring the infection.
Where is Streptococcus pneumoniaeis found?
Streptococcus pneumoniaeis found predominantly in the mucus layer overlying the epithelial surface of the upper respiratory tract. Inflammation (indicated by the presence of neutrophils), which is induced by the pore-forming toxin pneumolysin or by co-infection with influenza virus or other respiratory viruses, stimulates secretions and increases shedding. By contrast, agglutinating antibodies such as anti-capsule immunoglobulin G (IgG) and IgA1 decrease shedding unless they are cleaved by the human IgA1-specific pneumococcal protease. Capsule type and amount also influence mucus association and numbers of shed bacteria.
How does Streptococcus pneumoniaeas affect the host?
Streptococcus pneumoniaeas a complex relationship with its obligate human host. On the one hand, the pneumococci are highly adapted commensals, and their main reservoir on the mucosal surface of the upper airways of carriers enables transmission. On the other hand, they can cause severe disease when bacterial and host factors allow them to invade essentially sterile sites, such as the middle ear spaces, lungs, bloodstream and meninges. Transmission, colonization and invasion depend on the remarkable ability of S. pneumoniaeto evade or take advantage of the host inflammatory and immune responses. The different stages of pneumococcal carriage and disease have been investigated in detail in animal models and, more recently, in experimental human infection. Furthermore, widespread vaccination and the resulting immune pressure have shed light on pneumococcal population dynamics and pathogenesis. Here, we review the mechanistic insights provided by these studies on the multiple and varied interactions of the pneumococcus and its host.
What are the functions of Streptococcus pneumoniaecolonization?
Key functions that enable Streptococcus pneumoniaecolonization are: establishing the first contact with the epithelium and epithelial receptors, interaction with the complement system, mucus degradation, metal binding, impairment of neutrophil activity and the pro-inflammatory effects of the toxin pneumolysin (Ply). The pneumococcal enzymes Neuraminidase A (NanA), β-galactosidase (BgaA) and β-N-acetylglucosaminidase (StrH) degrade mucus and thereby inhibit mucociliary clearance. Furthermore, the LytA (autolysin)-facilitated release of Ply damages the epithelium and reduces ciliary beating. Negatively charged capsular polysaccharide (CPS) inhibits bacterial mucus entrapment. CPS and several pneumococcal proteins, including pneumococcal surface protein A (PspA), choline-binding protein A (CbpA), enolase (Eno) and pneumococcal histidine triad protein (Pht), directly and indirectly block complement deposition. PspA also binds to lactoferrin to acquire iron and blocks the antimicrobial effect of apolactoferrin. Endopeptidase (PepO), which is released from the pneumococcal surface, binds to C1q and thereby depletes complement components. Pneumococcal CbpE impairs neutrophil recruitment by degrading platelet-activating factor (PAF), a host-derived inflammatory phospholipid. CbpA interacts with factor H interactions to facilitate adherence and subsequent internalization of S. pneumoniaevia cell glycosaminoglycans. CbpA also binds to polymeric immunoglobulin receptor (PIGR) to promote adherence. The zinc metalloprotease ZmpA (also known as immunoglobulin A1 protease) subverts mucosal humoral immunity by cleaving IgA1. Phosphorylcholine (ChoP) on teichoic acid mimics host PAF and allows binding to its receptor. Piliated strains express an ancillary pilus subunit tip adhesin called RrgA. Other S. pneumoniaeadhesins include enolase (Eno) and adherence and virulence protein A (PavA). PAFR, platelet-activating factor receptor.
How does S pneumoniae affect the nasopharynx?
As noted above, induction of pro-inflammatory chemokines and cytokines, upregulation of target receptors and damage to the respiratory epithelium caused by viral infection of the URT increases bacterial loads in the nasopharynx. This facilitates bacterial transmission but also increases the likelihood of penetration of host tissues and progression to localized or invasive disease. Progression to invasive disease is more likely in young children, elderly people and patients with specific lifestyle traits and comorbidities. There are also marked differences in the capacity of specific S. pneumoniaestrains to cause invasive disease, which is unsurprising given the vast genetic and phenotypic heterogeneity of this bacterium. S. pneumoniaefactors and pathways that contribute to tissue adherence and invasion are outlined in Fig. 4.
What is the purpose of Streptococcus pneumoniae?
This carriage is the prerequisite for both transmission to other individuals and invasive disease in the carrier. Carriers can shed S. pneumoniaein nasal secretions and thereby transmit the bacterium. Dissemination beyond its niche along the nasal epithelium, either by aspiration, bacteraemia or local spread, can lead to invasive diseases, such as pneumonia, meningitis and otitis media.
What is the source of S pneumoniaespread between hosts and the first step towards invasive disease?
Nasopharyngeal carriage is the source of S. pneumoniaespread between hosts and the first step towards invasive disease. Several bacterial factors are required for S. pneumoniaeto colonize and persist on the mucosal surface at a density and duration that is sufficient for transmission to occur (Fig. 3). For example, S. pneumoniaeexpresses two enzymes, peptidoglycan-N-acetylglucosamine deacetylase (PgdA) and attenuator of drug resistance (Adr), that modify its peptidoglycan and render it resistant to the lytic effects of lysozyme, which is abundant on the mucosal surface of the URT33. The main features that facilitate colonization are adherence to host cells and tissues, subversion of mucosal innate and adaptive immunity, and evasion of clearance by mucociliary flow.
Is S. pneumoniae gram positive?
S. pneumoniae may occur intracellularly or extracellularly as gram-positive lanceolate diplococci, but can also occur as single cocci or in short chains of cocci. S. pneumoniae is a fastidious bacterium, growing best at 35-37°C with ~5% CO2 (or in a candle-jar). It is usually cultured on media that contain blood, but can also grow on a chocolate agar plate (CAP). On a blood agar plate (BAP), colonies of S. pneumoniae appear as small, grey, moist (sometimes mucoidal), colonies and characteristically produce a zone of alpha-hemolysis (green) (Figure 1). The alpha-hemolytic property differentiates this organism from many species, but not from the commensal alpha-hemolytic (viridans) streptococci. Differentiating pneumococci from viridans streptococci is difficult as young pneumococcal colonies appear raised, similar to viridans streptococci. However, once the pneumococcal culture ages 24-48 hours, the colonies become flattened, and the central portion becomes depressed, which does not occur with viridans streptococci (Figure 2). A microscope (30-50X) or a 3X hand lens can also be a useful tool in differentiating pneumococci from viridans streptococci. Prior to identification and characterization testing procedures, isolates should always be inspected for purity of growth and a single colony should be re-streaked, when necessary, to obtain a pure culture. For the following identification and characterization procedures, it is essential to test alpha-hemolytic colonies that are less than a day old, typically grown overnight at 35-37°C with ~5% CO2 (or in a candle-jar).
Is serotyping necessary for pneumococci?
Although serotyping of pneumococci is not usually necessary for a clinical response, capsular serotype determination is a critical component of successful pneumococcal disease surveillance efforts. Effective current multivalent vaccines target combinations of key serotypes. Determination of serotype distributions associated with disease in certain regions provides information regarding the potential usefulness of applying existing vaccines and is also critical for assessing vaccine impact.
