BACTE- STREP

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Trisha

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GEN CHARACTERISTICS
Gram (+) spherical in shape arranged in chains or in pairs.
All streptococci are gram + in chains or pairs except S. pneumoniae which is gram + diplococci
Catalase-negative
They cannot breakdown hydrogen into oxygen and water
Non-motile
Non spore-former
Facultative anaerobe
○ They can grow in both the presence or absence of oxygen
Some species are Capnophilic (high CO2)
Growth is more pronounced on Blood Agar Plate (BAP), poor on Nutrient Agar Plate (NAP)
Small and somewhat transparent
GRAM POSITIVE
Cell wall structure
The streptococci produce a typical gram-positive cell wall consisting of a thick Peptidoglycan & teichoic acid
Most Streptococci, except for many of the viridans group, have a Common antigenic C carbohydrate which is a polysaccharide in nature that can be used to classify an isolate serologically
LANCEFIELD CLASSIFICATION
● Serological method for classifying Streptococci into one of the 20 groups designated by letter.
● based on the presence of a group specific Carbohydrate antigen known as C polysaccharide.
Group A: S. pyogenes
Group B: S. agalactiae
Beta hemolytic
complete lysis
Examples of beta hemolytic bacteria are Group A, beta-hemolytic Streptococci such as the S. pyogenes and Group B, beta hemolytic Streptococci, which is the S. agalactiae
Alpha hemolysis
partial lysis of RBC; greenish-gray or brownish discoloration of agar
S. pneumoniae (alpha-hemolytic), causes serious pneumonia and other deadly infectious diseases.
Clinically significant strep:
S. Pyogenes
antigenic structure: group a polysaccharide
virulence factors: helps S. Pyogenes infect humans
M protein (M1-M80)
Protein F
Lipoteichoic acid- Together with M protein, the Protein F and Lipoteichoic acid secures attachment of streptococci to the oral mucosal cells.
Hyaluronic acid capsule
Toxins and enzymes- SLO, SLS, DNASE
Antibodies can be measured in the Antistreptolysin O Test to determine whether an individual has had a recent infection with S. pyogenes
STREPTOCOCCAL PYROGENIC TOXINS (Spes)
Formerly known as erythrogenic toxins because of the ability to damage the plasma membrane of blood capillaries under the skin and produce red skin rash (scarlet fever)
These toxins are known as superantigens because of their ability to produce strong immune reaction
Clinical infections
Pharyngitis
aka strep or sore throat
s/sx: sore throat, malaise, fever, and headache
2. Scarlet fever
caused by temperate bacteriophage t12 that produce SPE
tongue becomes strawberry red
dick test
Clinical infections
Skin or pyodermal infxns
impetigo -> progress to whipping lesions
2. Erysipelas
uncommonly seen infxns of the skin
plainly demarcated
3. Cellulitis
deeper invasion by streptococci
serious and life threatening
gangrene
Necrotizing Fasciitis
result of trauma such as burns and lacerations
caused by flesh-eating strep
invasive infxn; necrosis of skin, subcutaneous fat, fascia
Necrotizing fasciitis
NF may be categorized as
○ Type 1 NF - polymicrobial infection (aerobic and anaerobic)
○ Type 2 NF - group A strep meaning it is a pure colony.
○ Type 3 NF - gas gangrene or clostridial myonecrosis.
STREPTOCOCCAL TOXIC SHOCK SYNDROME
leads to bacteremia, and severe multisystem infection
condition in which the entire organ system collapses, leading to death
patients are often bacteremic and have NF
streptococcal pyrogenic exotoxin (SpeA)- functions as superantigens
SLO and various cell wall antigens- contributes to toxic shock
POST STREPTOCOCCAL SEQUELAE
Rheumatic fever
occurs after the primary infection with Streptococcus biogenesis
Complications of untreated pharyngitis
fever and inflammation of the heart, joints, blood vessels and subcutaneous tissues
most serious result: chronic, progressive damage to the heart valves.
POST STREPTOCOCCAL SEQUELAE
Glomerulonephritis or Acute Glomerulonephritis
Sometimes occur after a cutaneous or pharyngeal infection
It is more common in children than in adults
Pathogenesis: Immunologically mediated, where in antibodies are not removed, It is postulated that these antigen antibody complexes deposit/accumulate in the glomeruli of the kidney’s nephron
Inflammation of the glomeruli and nephrons, which obstruct the blood flow to the kidney and leads to hypertension and low urine output
Glomerulonephritis/Acute glomerulonephritis- Treatment
Penicillin – drug of choice
Erythromycin – for patients who are allergic of penicillin
Prophylactic doses of penicillin are given to patients with a history of rheumatic fever to prevent recurrent infection that might cause additional damage to heart valves
Cephalosporin
Bacitracin
Necrotizing fasciitis – surgical removal of nonviable tissues and infecting bacteria may be done to eliminate or prevent the additional infection that may occur because of these tissues
S. agalactiae
Antigenic structure:
All strains of S. agalactiae have the group B specific antigen – an acid stable polysaccharide located in the cell wall; The only specie that expresses group B antigen
PRECIPITIN TEST- which identifies the presence of proteins found on the surface of cell walls of bacteria. These type of specific antigens are detected using this test
S. agalactiae- Virulence factors
CAPSULE - An important virulence factor because it prevents phagocytosis.
SIALIC ACID – the most important component of the capsule and is a critical virulence determinant. Studies with mutant strains of S. agalactiae showed that the loss of capsular sialic acid was associated with loss of virulence.
Other virulence factors of S. agalactiae
CAMP Factor
Neuraminidase
DNAse
Hyraluronidase
Protease
CLINICAL INFECTIONS
Early Onset Infection
Affects <7days old
Accounts for about 80% of the clinical cases in newborns
Caused by vertical transmission of the organism from the mother
Colonization of the vagina and rectal area of Group B Streptococcus is found in 20-30 percent of pregnant women. Thus women are being screened before they deliver babies.
CLINICAL INFECTIONS: cont
2. Late Onset Infection
Affects at least 7 days old
Between one week and 3 months after birth
Usually presents as meningitis
Uncommonly associated with obstetric complications
The organism is rarely found on the vagina
Mortality rate is less compared to early onset
STREPTOCOCCUS DYSGALACTIAE subsp. equisimilis
Upper RT, Vagina, and skin of humans. Uncommon to domestic animals.
The spectrum of infections resembles S. pyogenes
○ Upper Respiratory Tract InfectionS
○ Skin Infections
○ Soft Tissue Infections
○ Invasive Infections (EX: Necrotizing fasciitis)
Streptococcus equi subsp. zooepidemicus
animal pathogen rarely isolated from human
associated with AGN and rheumatic fever infections
Streptococcus pneumoniae
AKA: Pneumococcus
Isolated from a variety of infections
C substance – antigen on its Cell Wall.
C-reactive protein (CRP) – a beta globulin in human serum, reacts with C substance to form a precipitate. This is a chemical reaction and not an antigen-antibody combination. The amount of CRP increases during inflammation and infection.
Diseases: Pneumonia, sinusitis, otitis media, bacteremia, and meningitis.
Most frequently encountered isolate in children younger than 3 years old with recurrent otitis media
No.1 cause of Bacterial Pneumonia
Virulence factors of S. pneumoniae
Capsule
greatest virulence factor
Laboratory strains that have lost the ability to produce a capsule are non-pathogenic. In addition, Opsonization of the capsule renders the organism a virulent.
2. Toxins produced
hemolysin
immunoglobulin a protease
neuraminidase
hyaluronidase
Clinical Infections in S. pneumoniae
Pneumococcal Pneumonia
Sinusitis (inflammation of nasal sinuses) and otitis media (inflammation of the middle ear)
Bacteremia and endocarditis
Pneumococcal Meningitis
Lobar pneumonia
Bacterial meningitis