streptococci

Streptococci

Ass.prof. Nebras. Al-Dabagh
Streptococci are Gram-positive, nonmotile, nonsporeforming, catalase-negative cocci that occur in pairs or chains. Older cultures may lose their Gram-positive character. Most streptococci are facultative anaerobes, and some are obligate (strict) anaerobes. Most re quire enriched media (blood agar).
Classification
Streptococci are classified on the basis of :
1-colony morphology (hemolysis )
They are divided into three groups by the type of hemolysis on blood agar: ?-hemolytic (clear, complete lysis of red cells), ? hemolytic (incomplete, green hemolysis), and ? hemolytic (no hemolysis).
2- biochemical reactions
3- serologic specificity : Serologic grouping is based on antigenic differences in cell wall carbohydrates (groups A to V), in cell wall pili-associated protein,
4 - polysaccharide capsule .
Rebecca Lancefield developed the serologic classification scheme in 1933. ?-hemolytic strains possess group-specific cell wall antigens, most of which are carbohydrates. These antigens can be detected by immunologic assays and have been useful for the rapid identification of some important streptococcal pathogens.
Beta-hemolytic
Group A
Group A S. pyogenes (GAS) is the causative agent in a wide range of group A streptococcal infections
Toxins and enzymes of group A streptococci
Heamolysine : Beta hemolysis (?-hemolysis), sometimes called complete hemolysis, is a complete lysis of red cells in the media around and under the colonies: the area appears lightened (yellow) and transparent.
Streptolysin, an exotoxin, is the enzyme produced by the bacteria which causes the complete lysis of red blood cells. There are two types of streptolysin: Streptolysin O (SLO) and streptolysin S (SLS). Streptolysin O is an oxygen-sensitive cytotoxin, secreted by most Group A Streptococcus (GAS), and interacts with cholesterol in the membrane of eukaryotic cells (mainly red and white blood cells, macrophages, and platelets), and usually results in ?-hemolysis under the surface of blood agar.
Streptolysin S is an oxygen-stable cytotoxin also produced by most GAS strains which results in clearing on the surface of blood agar .
The biggest threat to GAS survival within the host is the neutrophil response and opsonin-mediated phagocytosis. The coiled-coil surface M protein and M-like proteins play major roles in the prevention of opsonophagocytosis of the bacterium.
Proteases
To prevent neutrophil activation and migration to the site of infection, GAS produces two proteolytic enzymes.
Group A streptococci make several DNA degrading enzymes (DNAase) whose contribution to pathogenesis . Previously they were regarded to be required for bacterial spread through purulent material

Disease caused by streptococcus pyogenes :
These infections may be noninvasive or invasive. The noninvasive infections tend to be more common and less severe. The most common of these infections include streptococcal pharyngitis (strep throat) and impetigo
The invasive infections caused by group A ?-hemolytic streptococci tend to be more severe and less common. This occurs when the bacterium is able to infect areas where it is not usually found, such as the blood and the organs. The diseases that may be caused include streptococcal toxic shock syndrome, necrotizing fasciitis, pneumonia, and bacteremia.
Additional complications may be caused by GAS, namely acute rheumatic feverand acute glomerulonephritis. Rheumatic fever, a disease that affects the joints, kidneys, and heart valves, is a consequence of untreated strep A infection caused not by the bacterium itself.
Rheumatic fever is caused by the antibodies created by the immune system to fight off the infection cross-reacting with other proteins in the body. This "cross-reaction" causes the body to essentially attack itself and leads to the damage above.
Prevention
S. pyogenes infections are best prevented through effective hand hygiene. No vaccines are currently available to protect against S. pyogenes infection, although research has been conducted into the development of one.
Difficulties in developing a vaccine include the wide variety of strains of S. pyogenes present in the environment and the large amount of time and number of people that will be needed for appropriate trials for safety and efficacy of the vaccine.
Treatment
The treatment of choice is penicillin, and the duration of treatment is around 10 days.
Antibiotic therapy (using injected penicillin) has been shown to reduce the risk of acute rheumatic fever. In individuals with a penicillin allergy, erythromycin, other macrolides, and cephalosporins have been shown to be effective treatments.
Treatment with ampicillin, amoxicillin/clavulanic acid, or clindamycin is appropriate if deep oropharyngeal abscesses are present, in conjunction with aspiration or drainage

? – hemolytic Streptococci
It includes:
1. Viridans streptococci
2. Streptococcus pneumoniae

Viridans streptococci
This microorganism has low virulence and often colonize in the URT. They considered as commensal of the mouth and they can act as opportunistic pathogen and attack tissue. It is associated with dental caries and they are the leading cause of subacute bacterial endocarditis (SBE) following dental extraction it include

Streptococcus mitis
Streptococcus mutans
Streptococcus sangius
Streptococcus salivaris
These lack group specific carbohydrate in their cell wall.
S. mutans plays a major role in tooth decay, metabolizing sucrose to lactic acid using the enzyme glucansucrase. The acidic environment created in the mouth by this process is what causes the highly mineralized tooth enamel
. S. mutans is one of a few specialized organisms equipped with receptors that improve adhesion to the surface of teeth. Sucrose is used by S. mutans to produce a sticky, extracellular, based polysaccharide that allows them forming plaque.
S. mutans produces dextran via the enzyme dextransucrase (a hexosyltransferase) using sucrose as a substrate in the following reaction:
n sucrose ? (glucose)n + n fructose
Sucrose is the only sugar that S. mutans can use to form this sticky polysaccharide.
It is believed that Streptococcus mutans acquired the gene that enables it to produce biofilms through horizontal gene transfer with other lactic acid bacterial species, such as Lactobacillus.
S. mutans acquired the ability to increase the amount of carbohydrates it could metabolize, and consequently more organic acid was produced as a byproduct. This is significant in the formation of dental caries because increased acidity in the oral cavity amplifies the rate of demineralization of the tooth, which leads to carious lesions.
Cardiovascular disease
S. mutans is implicated in the pathogenesis of certain cardiovascular diseases, and is the most prevalent bacterial species detected in extirpated heart valve tissues, as well as in atheromatous plaques, with an incidence of 68.6% and 74.1%, respectively.
Prevention and treatment
Practice of good oral hygiene including daily brushing, flossing and the use of appropriate mouthwash can significantly reduce the number of oral bacteria and inhibit their proliferation. Oral bacteria often live in plaque, a kind of biofilm, hence mechanical removal of plaque is the most effective way of getting rid of harmful oral bacteria, as bacterial biofilms are notoriously resistant to antibiotics and antimicrobial rinses . However, there are some remedies used in the treatment of oral bacterial infection, in conjunction with mechanical cleaning.
Streptococcus pneumoniae

Also called Diplococcus pneumoniae or pneumococcus. -Normal inhabitant of the upper respiratory tract (URT) of human i.e. 40%-70% of normal individuals are carriers of these bacteria. - No animal reservoir, i.e. transmission is from infected to normal persons by direct route. - some times may cause important human diseases such as pneumonia, bronchitis, sinusitis, otitis media and less frequently invades blood stream producing bacteremia, and the most important complication of bacteremia includes: meningitis and septic arthritis.

Characteristics
Gram positive young culture
- Lancet shaped diplococci, the adjacent sides are blunt, while the distal sides (ends) are pointed, capsulated possessing a polysaccharide capsule. Facultative anaerobic.
-don’t grow on simple laboratory media (fastidious) i.e. requires enriched media.
- On blood agar they produce small colonies surrounding by ? type of hemolysis.

Antigenic structure of Diplococcus pneumoniae

1. Capsular polysaccharide (specific soluble substance SSS)
- large polysaccharide polymers (pneumococcal capsule).
- hydrophilic gel on the surface of the organism.
- Antigenic (once injected into human body it produces
antibodies) and type- specific.
- Pneumococci are differentiated into 80 serological types on
basis of capsular polysaccharide.
2.Somatic portion of pneumococci:
(Somatic means everything except capsule)
- Contains M- protein antigen that is characteristic for each type.
- M-protein antigen of pneumococci play no role in their virulence.
- Also contains Group specific carbohydrates which:
Pathogenicity:?In adults types 1-8 are the most important because 75% of pneumococcal pneumoniae are caused by these types. 50% of all pneumococcal bacteremia are fatal. Types: 6, 12, 19, 23 are the most important because they are responsible for all pneumococcal infection in children.

Virulence Markers
Streptococcus pneumoniae associated with Polysaccharide capsule which may prevent or delay phagocytosis. Non capsulated pneumococci are avirulent (nonpathogenic).
Inhalation these bacteria continuously but they are phagocytized this indicates that reparatory mucosa posses a great natural resistant to streptococci. In some individuals such bacteria colonize in the mucosa of URT and these become carriers. If resistance becomes low, the bacteria invade the lung producing pneumonia.

Predisposing Factors:

Viral infection , abnormality of respiratory tract. trauma of pharynx. Allergy , cough reflex, some change in movement of cilia , long bed rest. from lung they may invade the blood stream producing bacteremia.
Pathophysiology
Bacteria typically enter the lung with inhalation, though they can reach the lung through the bloodstream if other parts of the body are infected. Often, bacteria live in parts of the upper respiratory tract and are continuously being inhaled into the alveoli. Once inside the alveoli, bacteria travel into the spaces between the cells and also between adjacent alveoli through connecting pores. This invasion triggers the immune system to respond by sending white blood cells responsible for attacking microorganisms (neutrophils) to the lungs. The neutrophils engulf and kill the offending organisms but also release cytokines that result in a general activation of the immune system. This results in the fever, chills, and fatigue common in bacterial and fungal pneumonia. The neutrophils, bacteria, and fluid leaked from surrounding blood vessels fill the alveoli and result in impaired oxygen transportation.
Bacteria often travel from the lung into the blood stream (bacteremia) and can result in serious illness such as sepsis and eventually septic shock, in which there is low blood pressure leading to damage in multiple parts of the body including the brain, kidney, and heart. They can also travel to the area between the lungs and the chest wall, called the pleural cavity.
Treatment
Antibiotics are the treatment of choice for bacterial pneumonia and ventilation (oxygen supplement) as supportive therapy. The antibiotic choice depends on the nature of the pneumonia, the microorganisms most commonly causing pneumonia in the geographical region, and the immune status and underlying health of the individual. In the United Kingdom, amoxicillin is used as first-line therapy in the vast majority of patients acquiring pneumonia in the community, sometimes with added clarithromycin. In North America, where the "atypical" forms of community-acquired pneumonia are becoming more common, clarithromycin, azithromycin, or fluoroquinolones as single therapy, have displaced the amoxicillin as first-line therapy. Local patterns of antibiotic-resistance should always be considered when initiating pharmacotherapy.
Enterococci ( group D streptococci )
Enterococci are Gram-positive cocci that often occur in pairs (diplococci) or short chains, and are difficult to distinguish from streptococci on physical characteristics alone. Two species are common commensal organisms in the intestines of humans: E. faecalis (90-95%) and E. faecium (5-10%).
Enterococci are facultative anaerobic organisms, i.e., they are capable of cellular respiration in both oxygen-rich and oxygen-poor environments. Though they are not capable of forming spores, enterococci are tolerant of a wide range of environmental conditions: extreme temperature (10-45°C), pH (4.5-10.0) and high sodium chloride concentrations.
Enterococci typically exhibit gamma-hemolysis on sheep s blood agar.
Pathology
Important clinical infections caused by Enterococcus include urinary tract infections, bacteremia, bacterial endocarditis and meningitis. Sensitive strains of these bacteria can be treated with ampicillin, penicillin and vancomycin. Urinary tract infections can be treated specifically with nitrofurantoin, even in cases of vancomycin resistance.
From a medical standpoint, an important feature of this genus is the high level of intrinsic antibiotic resistance. Some enterococci are intrinsically resistant to ?-lactam-based antibiotics (penicillins, cephalosporins, carbapenems), as well as many aminoglycosides In the last two decades, particularly virulent strains of Enterococcus that are resistant to vancomycin (vancomycin-resistant Enterococcus, or VRE) have emerged in nosocomial infections of hospitalized patients, especially in the US.