What is Streptococcus?

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Streptococcus is a genus of gram-positive cocci, or bacteria, with a thick peptidoglycan layer in their cell walls (gram-positive) that appear under the microscope as chains of two or more spherical cells (cocci). The streptococci can grow in low concentrations of oxygen or without oxygen and are distinguished from bacteria in the genus Staphylococcus in the laboratory by the production of the enzyme catalase by staph species.
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Definition

Streptococcus is a genus of gram-positive cocci, or bacteria, with a thick peptidoglycan layer in their cell walls (gram-positive) that appear under the microscope as chains of two or more spherical cells (cocci). The streptococci can grow in low concentrations of oxygen or without oxygen and are distinguished from bacteria in the genus Staphylococcus in the laboratory by the production of the enzyme catalase by staph species.

The streptococci are classified in a number of ways, including by the identity of molecules on the cell surface and by the presence and variety of hemolysin, or enzyme, that lyse red blood cells. Alpha-hemolytic species lyse red blood cells and oxidize hemoglobin to leave an opaque green residue on blood agar petri dishes. Beta-hemolytic species leave a transparent halo around colonies on blood agar petri dishes. Gamma-hemolytic species exhibit neither of these traits.

Natural Habitat and Features

Streptococci are a part of the normal microbiota of humans and other mammals. Some streptococci can cause infectious diseases. The progression from latency to infectious disease is not well understood, but scientists have investigated the possibility that virus-induced genetic changes in streptococcal species are responsible for the sudden appearance of “flesh-eating” disease, or necrotizing fasciitis.

Pathogenicity and Clinical Significance

S. pyogenes is a notable member of the beta-hemolytic streptococci. Pyogenes is an opportunistic pathogen widely distributed in humans. It causes acute bacterial pharyngitis, commonly known as strep throat, and infections of the skin and circulatory system. These bacteria are able to evade the human immune system though various means. That is, the cells are covered in hyaluronic acid, which is a component of human connective tissue and, therefore, non-immunogenic; and a series of proteins, M proteins, prevents the engulfment of bacterial cells by immune cells. Two toxins that destroy immune cells also cause beta-hemolysis of red blood cells.

Pyogenes strains that produce erythrogenic exotoxins, the extracellular proteins responsible for the scarlet fever rash, may produce one of three varieties. Exposure to one variety does not induce immunity to the others, so a person may have recurring infection. These toxins are not encoded on the bacterial chromosome, but on plasmids. Prompt antibiotic therapy of strep throat has reduced the incidence of scarlet fever.

Acute rheumatic fever and acute glomerulonephritis are also consequences of untreated strep throat. The symptoms of rheumatic fever occur about three to four weeks following strep throat and include pains in the joints and long-term damage to the heart, likely because of an autoimmune response. Glomerulonephritis is swelling of the kidneys following strep throat or a streptococcal skin infection.

Streptococcal impetigo is a localized skin infection caused by pyogenes. Erysipelas is an acute infection of the skin with fever. Strains that express the enzyme streptokinase may dissolve a blood clot to penetrate to deeper tissue. Infection of deep muscle and fat tissue, the lungs, and blood can be life-threatening. Necrotizing fasciitis (infection of muscle and fat tissue) kills about 20 percent of infected persons, and streptococcal toxic shock syndrome (an infection causing low blood pressure and shock and injury to the kidneys, liver, and lungs) kills up to 60 percent of infected persons.

Another beta-hemolytic species, agalactiae, is the major cause of meningitis, pneumonia, and infections of the bloodstream in newborns. The female genital tract is the natural habitat for agalactiae, with 25 to 35 percent of the female population being carriers. Newborns are infected at birth or during their stay in a hospital nursery. Antibiotic therapy of pregnant women who carry agalactiae prevents transmission to their fetuses at birth.

Most human cases of bacterial pneumonia are caused by alpha-hemolytic pneumoniae. This species grows as pairs of cocci coated in a thick carbohydrate capsule. Colonies on blood agar petri dishes are surrounded by transparent agar and a mucoid appearance. Pneumoniae is an inhabitant of the upper respiratory tract of up to 70 percent of the population. In immunocompromised hosts, such as many elderly persons, and in those with a viral infection, this strain causes pneumonia. The infection in the lungs results in fluid retention and difficulty in breathing. Recovery follows after five to six days, even without antibiotic treatment. An increase of circulating antibodies accompanies a decrease in the severity of the symptoms. Penicillin or erythromycin hastens recovery, while a few persons with pneumococcal-pneumonia, primarily the elderly, die even though they are being treated with antibiotics.

Spinal meningitis caused by pneumoniae had been the second leading cause of bacterial meningitis. This changed when a glycoconjugate vaccine was added to the infant immunization schedule in the United States and other countries.

Mutans, mitis, and sanguinis are alpha-hemolytic streptococci that are normal inhabitants of the human mouth. Mutans and mitis are found in dental plaque. S. mutans produces dextran from sucrose. Dextran is the sticky component of dental plaque that allows many bacterial species to stick to tooth surfaces. When bacteria grow on the teeth, they produce acid that contributes to the creation of cavities. Non-hemolytic species, also called gamma-hemolytic streptococci, are not human pathogens.

Drug Susceptibility

Streptococcal infections are treated primarily with antibiotics. Widespread incidence of resistance has not occurred to the extent that it has in the staphylococcal species. Multiply resistant strains have been documented, though. The treatment of strep throat has become more difficult because of antibiotic resistance of non-strep bacteria in the throat. Other bacteria can destroy penicillin and other beta-lactam antibiotics and, thus, shield sensitive pyogenes from their effect.

Bibliography

Brachman, Philip S., and Elias Abrutyn, eds. Bacterial Infections of Humans: Epidemiology and Control. 4th ed. New York: Springer, 2009. A college-level introduction that focuses on the mechanisms of pathogenicity.

Parker, James N., and Philip M. Parker, eds. The Official Patient’s Sourcebook on “Streptococcus pneumoniae” Infections. San Diego, Calif.: Icon Health, 2002. Draws from public, academic, government, and peer-reviewed research to provide a wide-ranging handbook for patients with pneumonia infections.

Tortora, Gerard J., Berdell R. Funke, and Christine L. Case. Microbiology: An Introduction. 10th ed. San Francisco: Benjamin Cummings, 2010. A great reference for those interested in exploring the microbial world. Provides readers with an appreciation of the pathogenicity and usefulness of microorganisms.

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