Streptococcus Enterococcus B Hemolysis 1. Main biological features a. Cell shape
ID: 147355 • Letter: S
Question
Streptococcus Enterococcus B Hemolysis
1. Main biological features
a. Cell shape, arrangement, Gram stain, endospores, capsule, unusual features.
2. Clinical Manifestations
a. List the diseases that are produced by this microorganism.
3. Mechanism of Disease
a. List of how the microorganism induces disease: Toxin, proteolysis, pyogenic, immunological mechanism or multiple mechanisms.
4. Transmission
a. How the microorganism is transmitted and who is at risk of acquiring the infection.
5. Prevention
a. List the most common prevention methods
b. Is there a vaccine?
6. Treatment
a. Is antimicrobial intervention necessary?
b. Have resistant strains been detected?
c. List the common methods of treatment (you don’t need to list drug names).
d. Prognosis – Mortality associated with the disease
Explanation / Answer
Hemolysis is the breakdown of red blood cells (RBC). A substance that causes hemolysis is a hemolysin. Brown (1919) introduced three terms alpha, beta and gamma to indicate three types of streptococci based on haemolytic reactions observed on blood agar plates. Beta-hemolysis is associated with complete lysis of red cells surrounding the colony.
Main biological features of Streptococcus Enterococcus B Hemolysis:
Streptococcus is a genus of gram-positive coccus (plural cocci), or spherical bacteria, Cell division in streptococci occurs along a single axis, so as they grow they tend to form pairs or chains that may appear bent or twisted. (Contrast with that of staphylococci, which divide along multiple axes, thereby generating irregular grape-like clusters of cells.). Group A streptococci have a hyaluronic acid capsule.
2. Clinical Manifestations and Mechanism of Disease:
Acute Streptococcus pyogenes infections may take the form of pharyngitis, scarlet fever (rash), impetigo, cellulitis, or erysipelas. Invasive infections can result in necrotizing fasciitis, myositis and streptococcal toxic shock syndrome. Patients may also develop immune-mediated sequelae such as acute rheumatic fever and acute glomerulonephritis. S agalactiae may cause meningitis, neonatal sepsis, and pneumonia in neonates; adults may experience vaginitis, puerperal fever, urinary tract infection, skin infection, and endocarditis. Viridans streptococci can cause endocarditis, and Enterococcus is associated with urinary tract and biliary tract infections. Anaerobic streptococci participate in mixed infections of the abdomen, pelvis, brain, and lungs.
4. Transmission: Group A -hemolytic streptococci are spread by respiratory secretions and fomites. The incidence of both respiratory and skin infections peaks in childhood. Infection can be transmitted by asymptomatic carriers. Acute rheumatic fever was previously common among the poor; susceptibility may be partly genetic.
5. Prevention:
a. Antibody to M protein gives type-specific immunity to group A streptococci. Antibody to erythrogenic toxin prevents the rash of scarlet fever. Immune mechanisms are important in the pathogenesis of acute rheumatic fever. Maternal IgG protects the neonate against group B streptococci.
b. Vaccines are under development.
6. Prompt penicillin treatment of streptococcal pharyngitis reduces the antigenic stimulus and therefore prevents glomerulonephritis and acute rheumatic fever. Vancomycin resistance among the enterococci is an emerging microbial threat. Vaccines are under development.