Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
71 Cards in this Set
- Front
- Back
|
Describe the physiology of Streptococcus.
|
Gram positive, Aerotolerant faciultative anaerobe, nonmotile, nonsporeforming, and fermentative.
|
|
|
What happens in alpha hemolyic species?
|
partial rupture of the blood cells in vivo. The iron in the blood cells turns green.
|
|
|
What happens in beta hemolytic species?
|
Complete rupture of the blood cell in vivo.
|
|
|
What happens in gamma hemolytic species?
|
no hemolysis, rarely cause disease.
|
|
|
What are Lancefield groupings?
|
Serological properties of the cell wall based on the carbohydrate signature. Useful for typing beta hemolytic species.
|
|
|
What is the group-A specific carbohydrate in S. pyogenes?
|
N-Acetyl glucosamine and rhamnose.
|
|
|
What type of hemolyte is S. pyogenes?
|
beta hemolytic
|
|
|
What are the three ways S. pyogenes uses to attach to a host?
|
Lipoteichoic acid, M protein, Protein F
|
|
|
Describe the M protein.
|
Anchored in the cytoplasmic membrane, protrudes through the cell wall, antigenetically variable being less variable closer to the membrane and more variable away from it.
|
|
|
What are the functions of M protein?
|
Virulence (strains without M protein are avirulent), protect against phagocytosis, attach to host cells.
|
|
|
What is Protein F?
|
Fibronectin binding protein that facilitates attachment in congruence with M protein.
|
|
|
What are the types of cells that S. pyogenes invades?
|
Although primarily extracellular pathogen, will invade respiratory epithelial cells. May aid in long-term maintenance of infection. (persistant pharyngitis)
|
|
|
What are the two enzymes that aid in tissue invasion?
|
Hyaluronidase and streptokinase
|
|
|
What is the debate with hyaluronidase and S. pyogenes?
|
It is thought to play a more important role in streptoccal invasion, and can possible break down its own capsule.
|
|
|
What is the role of streptokinase?
|
lyses blood clots?
|
|
|
How is evasion acheived?
|
avoiding opsonization and phagocytosis.
|
|
|
What are the three things S. pyogenes has to aid in evasion?
|
A capsule, M protein, and C5a peptidase.
|
|
|
What is the capsule of S. pyogenes made of?
|
hyaluronic acid.
|
|
|
What is the purpose of M protein?
|
Antigenic variability. There are so many M protein variables that one antibody is unlikely to protect against another. Also protects against opsonization. Destabilizes C3b when combined with factor H and prevents opsonization.
|
|
|
What is the role of C5a?
|
Agent produced during inflammation process that disrupts inflammation.
|
|
|
What causes streptococcal toxic shock syndrome?
|
Superantigens -- streptococcal pyrogenic exotoxins
|
|
|
What are the purposes of Streptolysin O and Streptolysin S?
|
To lyse red and white blood cells.
|
|
|
What is the mortality rate of Sreptococcal Toxic Shock Syndrome?
|
45%
|
|
|
What is the mortality rate of necrotizing fasciitis?
|
25%
|
|
|
What is pharyngitis?
|
Inflammation of the pharynx associated with Streptococcus pyogenes. Found in the colder months and is highly contagious.
|
|
|
What is impetigo?
|
Caused by S. pyogenes. Associated with warmer months. Highly contagious.
|
|
|
What does suppurative mean?
|
Active infections associated with pus
|
|
|
What is saquela?
|
Condition following as a consequence of a disease. Rheumatic fever and acute glomerulonephritis. Caused by S. pyogenes.
|
|
|
What results as a complication of pharyngitis?
|
Scarlet fever. Caused by S. pyogenes.
|
|
|
How does scarlet fever occur?
|
Complication of pharyngitis. Strain expresses pyrogenic exotoxins. Creates erythematous rash and strawberry tongue.
|
|
|
What is impetigo?
|
Strains causing pustular infection. Different than that causing pharyngitis. Caused by S. aureus or S. pyogenes
|
|
|
What is erysipelas?
|
Acute localized skin infection. Infection of breaks in the cutaneous barrier. Area is raised and differentiated from normal skin. Primarily affects the young and the old. Caused by S. pyogenes.
|
|
|
What is cellulitis?
|
Involves deeper tissue than erysipelas. Organism introduced through broken skin. More diffuse reddening. No distinct reddening between affected and uneffected areas. Caused by S. pyogenes
|
|
|
What is necrotizing fasciitis?
|
Gangrene, a deep subcutaneous infection. Organism is introduced through broken skin. Requires through antibiotic therapy and removal of infected tissue. Caused by S. pyogenes.
|
|
|
What is streptococcal toxic shock syndrome?
|
Similar to staphylococcal TSS except patients may have bacteremia and necrotizing fasciitis may occur. Sudden onset of shock and organ failure. Caused by S. pyogenes.
|
|
|
What is rheumatic fever?
|
Inflammation lesions of the hearts, joints, subcutaneous tissue and CN tissue. This will follow pharyngitis but not cutaneous infections. Caused by S. pyogenes
|
|
|
What is the leading cause of heart disease for people under 50?
|
Rheumatic fever.
|
|
|
What are all the non-suppurative, post-streptococcal sequelae?
|
rheumatic fever, acute glomerulonephritis,
|
|
|
What is acute glomerulonephritis?
|
Inflammation of the kidneys, follows pharyngitis or cutaneous infection, associated with certain strains of S. pyrogenes.
|
|
|
Describe S. agalictiae.
|
Group specific carbohydrate (Rhamnose, RAG, galactose), Narrow zone of beta hemolysis, and capsular polysaccharide (not composed of hyaluronic acid)
|
|
|
Describe the epidemology of S. agalictiae.
|
Colonize in the lower GI tract. Genital acquisition likely from rectal site. Most common cause of meningitis and septicemia in newborns.
|
|
|
Describe the early onset clinical disease of S. algalactiae and how it's transmitted.
|
The early onset is a neonatal disease that includes bacteremia, pneumonia, and meningitis. It's transmitted from mother to child.
|
|
|
Describe the late onset clinical disease of S. algalactiae and how it's transmitted.
|
Bacteremia and meningitis, and it's transmittes in ways other than from mother to child.
|
|
|
Describe the clinical diseases of S. algalactiae other than later and early onset.
|
Infections in pregnant women, which occur during or immediately after pregnancy and infection in the elderly which occur with a high mortality rate.
|
|
|
Describe the physiology and structure of S. pneumoniae.
|
alpha hemolytic, virulent strains have capsule, lipoteichoic and teichoic acid that contain choline.
|
|
|
Describe the function of choline in S. pneumoniae.
|
Choline serves as a binding site for choline binding proteins which enable attachment on the outside of the cell.
|
|
|
Name some examples of choline binding proteins.
|
Pneumococcal surface adhesin A (PsaA), Pneumococcal surface protein A (PspA), and autolysins (including LytA, LytB, and LytC)
|
|
|
Where does initial colonization of S. pneumoniae occur?
|
in the nasopharynx.
|
|
|
How does S. pneumoniae attach?
|
via pneumococcal surface adhesin A
|
|
|
What normal host factors prevent spread of the pathogen S. pneumoniae?
|
normal movement of the ciliae and mucous prevent movement to the lungs, sinuses, and middle ear.
|
|
|
What are two things that help S. pneumoniae invade?
|
predisposing factors, such as respiratory infection. Also Pneumolysin is a toxin that damages ciliated cells, thus preventing clearance and facilitating invasion.
|
|
|
What is the role of pneumolysin and where is it located?
|
Toxin that damages cilia and aids in the spread of S. pneumoniae. kills phagocytes. Located in bacterial cytoplasm, therefore it must be released before it is activated (requires breakdown of cell wall).
|
|
|
How does S. pneumoniae evade phagocytosis?
|
Caspule, pneumococcal protein A-->prevent complement opsonization, and pneumolysin
|
|
|
Describe how S. pneumoniae causes disease.
|
S .pneumonia causes inflammation via autolysins releasing cell wall components and activating the complement. Pneumolysin destroys host phagocyte cells and mediates more inflammation. This inflammation allows the bacteria to spread and directs tissue damage along the way.
|
|
|
What is the purpose of autolysins in S. pneumoniae?
|
to release their cell wall components in order to activate the complement.
|
|
|
Who are most at risk for S. pneumoniae and why?
|
Young children because they do not have the caspsullary antibodies and the elderly because they have a weakened immune system.
|
|
|
When is the incidence of S. pneumoniae highest?
|
in the colder months.
|
|
|
Describe pneumonia.
|
Caused by S. pneumoniae, often preceded by other viral respiratory tract infections, bacteria multiply in the alveolar spaces of lungs causing inflammation and tissue damage.
|
|
|
What are the clinical diseases of S. pneumoniae?
|
Meningitis, Ostis media, Sinusitis, mastoiditis, occult bacteremia, sepsis with hemorrhegic shock, pneumonia, arthritis, peritonitis
|
|
|
Describe sinusitis and otitis media.
|
Otitis media is a middle ear infection. they are often preceded by a viral respiratory tract infection. Can be cause by S. pneumoniae.
|
|
|
Describe meningitis.
|
S. pneumoniae is the leading cause of meningitis. Mortality associated with S. pneumonia is higher than for all other causes of bacterial meningitis.
|
|
|
Describe bacteremia associated with S. pneumoniae.
|
Not associated with sinusitis or ostitis Meida. 25-30% patients with pneumonia develop bacteremia
|
|
|
Describe some factors to identify streptococci bacterium.
|
fermentative, catalase negative, gram positive, fermentative.
|
|
|
Describe how to identify S. pyogenes.
|
Beta hemolytic, Lancefield group A, Bacitracin sensitive, Streptolysin O antibodies.
|
|
|
Describe how to identify S. agalactiae.
|
Beta hemolytic, Lancefield Group B, Hydrolysis of hippurate, positive CAMP
|
|
|
Describe how to identify S. pneumoniae.
|
Alpha hemolytic, soluble in bile, and Optochin sensitive.
|
|
|
Describe the CAMP test.
|
S. agalactiae produces a CAMP factor that acts synergistically with S. aureus beta toxin. This produces a characteristic zone of hydrolysis in the shape of an arrowhead.
|
|
|
How do you treat S. pyogenes?
|
Penicillin.
|
|
|
How do you treat S. agalactiae?
|
Penicillin, pregnant women should be treated and tested as necessary.
|
|
|
How do you treat S. pneumoniae?
|
Penicillin, although resistance is developing.
|
|
|
Describe the vaccine for S. pneumoniae.
|
For 23 serotypes. Not very immunogenic, but it is improving with by conjugation with protein.
|
