Streptococcaceae and Enterococcus species Flashcards
Based on hemolysis on 5% Sheep Blood Agar Medium
Smith and Brown’s Classification
denotes incomplete lysis of erythrocytes with reduction of hemoglobin and the formation of green pigment
α-hemolysis
Streptococci producing such pattern of hemolysis were later on described as “green streptococci”.
α-hemolysis
refers to the complete disruption of erythrocytes resulting to clearing of the blood around the bacterial growth.
β-hemolysis
signifies absence of hemolysis thereby no change is seen in the medium surrounding bacterial growth.
γ-hemolysis
Streptococci producing such pattern of hemolysis were later on described as “indifferent streptococci”.
γ-hemolysis
a small zone of intact erythrocytes immediately adjacent to bacterial colony is surrounded with a zone of complete erythrocyte hemolysis.
α’ (alpha prime)-hemolysis (wide zone of alpha hemolysis)
This type of hemolysis maybe confused with β-hemolysis.
α’ (alpha prime)-hemolysis (wide zone of alpha hemolysis)
Discovered by Rebecca Lancefield in the 1930s based on group-specific antigens which are either cell wall polysaccharides, AKA C-substance, (as in human group A, B, C, F, and G streptococci); or lipoteichoic acids as in the group D streptococci and Enterococcus species These antigens stimulated formation of antibodies with differing specificities.
Lancefield Classification
Typing with specific antiserum causing agglutination is generally done only for groups A, B, C, F, and G.
Lancefield Classification
Based on temperature for growth particularly at 10OC and 45OC.
Academic/ Bergey’s Classification
consists of streptococci that do not grow at both 10OC and 45OC.
Pyogenic group
includes streptococci which fail to grow at 10OC but can be recovered at temperatures up to 45OC.
Viridans group
are streptococci that grow at both 10OC and 45OC.
Enterococcus group
comprise of streptococci that are frequently recovered in dairy products, can grow at 10OC but fail to grow at 45OC.
Lactic group
Group A β-Hemolytic Streptococci (GAS): Streptococcus pyogenes: Habitat
human throat and skin
Group A β-Hemolytic Streptococci (GAS): Streptococcus pyogenes: Transmission
respiratory droplets or contact with cutaneous lesions.
The most common infection caused by S. pyogenes.
Pharyngitis or streptococcal sore throat
Although it may occur at any age, it occurs most frequently between the ages of 5 and 15 years.
Pharyngitis or streptococcal sore throat
Characterized by acute sore throat, malaise, fever, and headache
Pharyngitis or streptococcal sore throat
Typically involves the tonsillar pillars, uvula, and soft palate, which become red, swollen, and covered with a yellowwhite exudate. The cervical lymph nodes that drain this area may also become swollen and tender.
Pharyngitis or streptococcal sore throat
Usually self-limiting (illness resolves on its own even without medical intervention). Typically, the fever is gone by the third to fifth day, and other manifestations subside within 1 week.
Pharyngitis or streptococcal sore throat
Pharyngitis or streptococcal sore throat
Caused by lysogenized strains of S. pyogenes that produce pyrogenic exotoxins A - C
Scarlet Fever
Occurs in association with streptococcal pharyngitis
Scarlet Fever
The buccal mucosa, temples, and cheeks are deep red, except for a pale area around the mouth and nose (circumoral pallor).
Scarlet Fever
Punctate hemorrhages appear on the hard and soft palates, and the tongue becomes covered with a yellow-white exudate through which the red papillae are prominent (strawberry tongue).
Scarlet Fever
A diffuse red “sandpaper” rash appears on the second day of illness, spreading from the upper chest to the trunk and extremities.
Scarlet Fever
Circulating antibody to the toxin neutralizes its effects.
Scarlet Fever
Infection of superficial layers of skin
Streptococcal pyoderma (or impetigo)
Usually occurs in children ages 2-15 years old, with peak incidence in the 2- to 5- year age group.
Streptococcal pyoderma (or impetigo)
Characterized by the formation of papules that develop into vesicular lesions and evolve into pustules. These pustules break down over the next 5 to 7 days to form thick scabs.
Streptococcal pyoderma (or impetigo)
Lesions are often seen on the lower extremities and may also involve other pathogens such as S. aureus.
Streptococcal pyoderma (or impetigo)
An infection of the dermis and subcutaneous tissues
Erysipelas
Organism enters through a small wound or incision on the face or extremities
Erysipelas
Characterized by edema and erythematous (red) lesion that is hot, and often vesicular with rapidly advancing, well-demarcated edges
Erysipelas
Infection usually occurs on the face and commonly in association with a history of streptococcal sore throat.
Erysipelas
Pain, and systemic manifestations, such fever and lymphadenopathy are evident.
Erysipelas
An acute, rapidly spreading infection of the skin and subcutaneous tissues.
Cellulitis
Occurs following streptococcal infection of preexisting lesions (i.e. mild trauma, burns, wounds, or surgical incisions).
Cellulitis
Symptoms include pain, tenderness, swelling, and erythema particularly occurring within the affected area.
Cellulitis
Cellulitis:
Differentiated from erysipelas by two clinical findings:
In cellulitis, the lesion is not raised, and the line between the involved and uninvolved tissue is indistinct.
Consists of extensive and very rapidly spreading necrosis of the skin, tissues, and fascia.
Necrotizing fasciitis (streptococcal gangrene)
Organism enters at the site of localized trauma or previous surgery, or via hematogenous seeding of subcutaneous muscles and soft tissue.
Necrotizing fasciitis (streptococcal gangrene)
Affected tissues become gangrenous, with sloughing of devitalized tissues and extensive subcutaneous tissue necrosis.
Necrotizing fasciitis (streptococcal gangrene)
Group A streptococci that cause necrotizing fasciitis are termed “flesh-eating bacteria”.
Necrotizing fasciitis (streptococcal gangrene)
Bacteria other than S pyogenes can also cause necrotizing fasciitis.
Necrotizing fasciitis (streptococcal gangrene)
Occurs in women following child birth (either by vaginal or abdominal/Csection) or abortion.
Puerperal fever
Organisms colonizing the genital tract or from an obstetrical personnel invade the upper genital tract, causing endometritis, lymphangitis, bacteremia, necrotizing fasciitis, and streptococcal toxic shock syndrome.
Puerperal fever
Intrapartum (occuring during pregnancy) transmission of group A streptococci, may lead to severe and often fatal group A streptococcal disease in the neonate.
Puerperal fever
Manifestations in the neonate include septicemia, jaundice, and cellulitis, or stillbirth.
Puerperal fever
May result from streptococcal infection of traumatic or surgical wounds.
Bacteremia or Sepsis
Can be rapidly fatal.
Bacteremia or Sepsis
Can also occur with skin infections, such as cellulitis and rarely pharyngitis.
Bacteremia or Sepsis
Are non-suppurative sequelae that occur weeks after GAS infection in the throat and/or skin.
Post Streptococcal Diseases
Inflammation of the glomeruli of the kidneys caused by the M strains of S. pyogenes (nephritogenic).
Acute Glomerulonephritis (AGN)
Begins 1 to 4 weeks after streptococcal pharyngitis or 3 to 6 weeks after skin infection; primarily a disease of childhood.
Acute Glomerulonephritis (AGN)
May be initiated by deposition and accumulation of antigenantibody complexes on the glomerular basement membrane
Acute Glomerulonephritis (AGN)
Signs symptoms: dark, smoky urine (due to blood and proteins) edema, hypertension, and urea nitrogen retention.
Acute Glomerulonephritis (AGN)
Majority recover completely while some develop chronic glomerulonephritis with kidney failure, and a few die
Acute Glomerulonephritis (AGN)
Considered as the most serious sequela of S. pyogenes because it results in damage to heart muscle and valves.
Rheumatic fever (RF)
Occurs 1–4 weeks after S. pyogenes pharyngitis
Rheumatic fever (RF)
Is an autoimmune disease, i.e., antibodies formed against streptococcal antigens cross react with the molecules of the host that trigger inflammation and injury of tissues (of the heart, joints, CNS)
Rheumatic fever (RF)
Signs and symptoms: fever, malaise, arthritis, carditis, chorea (neurologic disorder characterized by involuntary jerky movements), and skin nodules
Rheumatic fever (RF)
Pathologic processes of S. pyogenes infection can extend to the heart. The cross-reaction between streptococcal-induced antibodies and heart proteins have a gradual destructive effect on atrioventricular valve. Scarring and deformation change the capacity of the valves to close and shine the blood properly leading to Rheumatic Heart Disease.
Rheumatic fever (RF)
Has a marked tendency to be reactivated by recurrent streptococcal infections in contrast with nephritis.
Rheumatic fever (RF)