Strep 1 Flashcards
slide 3 for the classification of stpah, strep and enterococci
gram—- and shape
gram positive cocci
arranged—-
linearily or in pairs or in chains
catalase?/respiration?/capsule?
negative/facultative anaerobe/some are encapsulated
motile? sporulating?/part of commensal flora?
non-motile/non-sporulating/may be part of commnesal flora
since strep are so diverse and heterp, one method of classification is not enough:
1) lancefield (based on cell wall carbs)
2) hemolysis
3) biochemical properties
lancefield group carb antigen is a —/ serological grouping into groups: ——
dimer of N-acetyl glucosamine and rhamnose: important for identification / A to H and K to U
method of lanecefield identification:
1) lysis of strep cells with enzyme to destry the cell wall
2) then we treat the sample wih antisera (antibody) specific to the C-antigen (precipitin test)
slide 11 to know the classification based on blood hemolysis and slide 12
slide 13: types of virulence factors 3and group A strep
strep pyogenes capsule is encaspsulated with—
hyaluronic acid so it’s a poor immunogen since GAS capsular hyaluronate is chemically similar to that found
in human connective tissue and no antibodies has been observed
virulence factors of GAS:
1)capsule: prevents oponized phagocytosis by neutrophiles or macrophages/ is nonantigenic since it’s chemically similar to tissues of hostso bacteria goes unrecognized by host and hides its antigens
2)M protein>120 serotype:next flaschard
3)lipoteichoic acid: mediate bactrial adherence to host epithethelial cells and mucosal surfaces
4)peptidoglycan: composed of polymers of repeating subunits of N acetylglucosamine and
N acetylmuramic acid. The peptidoglycan provides rigidity to the cell wall
explain the casue of antigenic drift and shift
Antigenic shift and antigenic drift are ways that pathogens (like viruses or bacteria) change over time to escape the immune system.
antigenic drift= small changes due to mutations
antigenic shift= big changes due to the swapping of genetic material between strains
what about the M protein as a virulence factor?
M protein (>120 serotype):
* is the major cause of antigenic shift and antigenic drift in the Group A streptococci
* M protein also binds fibrinogen from serum and blocks the binding of complement to
the underlying peptidoglycan—-inhibit phagocytosis so it uses firbrinogen to cover itself ta ma yeje 3leya l complement
* Antibody againt M protein is durable. (long lasting protection)
IP of GAS:
2-4 days
pharyngitiys caused by—is primaryily a disease of —
S.pyogenes/ a disease of children between the ages of 5 and 15
this pathogen is spread from person to person through—-/thete are coincidences where the organisms is inroudced into the —
respiratory droplets particulary duirng the winter months (crowding, daycare facilities)/spuerficical or deep tissues throygh a break in the skin
streptococcal diseases:
1) impetigo
2)rheumatic fever
3)cellulitis
4)scarlet fever (rash and lesions)
5)sore throat (strep pharyngitis or tonsilitis)
6) glumerulnphiritis
transmission of phrangitis:
droplets, saliva or nasal secretions
often a colonizer in——
asymptomatic perople (high in children)
symptoms of pharyngitis:
1-Sore throat (2-4 days post exposure),malaise, high grade fever, headache,
2-Lymphoid hyperplasia of the posterior portion of the pharynx
* enlarged tonsils
* Intense nasopharyngitis
* tonsillitis
* redness/edema of mucus membranes with purulent exudates (Purulent exudates refer to thick, pus-containing fluid that forms at the site of infection or inflammation.)
3- Lymph nodes enlarge
4-High CRP (C-reactive protein (CRP) is a protein made by the liver that increases in response to inflammation. )and WBC count
scarlet fever is a complication of ——. its—
phrayngitis/ it’s severe pharingitis/ skin infection and high grade fever
it’s characterized by —
red rash on trunk that may spread to extrimities after 24 hours of illness/Diffuse red spots over upper part of the chest-spread to remainder of the trunk, neck
and extremities, face flushed./pharyngitism, tonsilitism and hemorrhagic spots on the hard and soft palates (white
strawberry tongue)
it involves the acquisition of a —-
bacteriophage that mediate sthe production of a pyrogenic exotoxin
the rash disappaeras over the next——and is followed by
5-7 days / desquam,ation
impetigo is also known as ——
streptococcal pyoderma
common in—-that have—during—–/—-layer inftcion/it’s a CONFINED infection that affects exposed areas like—-/
kids/poor personal hygiene/warm ,moist summer monthns/superficial/arms and face and legs/
development
papule—vescile—crust
characterized by ——–
purulenty (pus) vesicles
colonization of the skin then—
develoment of impetigo in 10 days due to abrasions, trauma, insect bites
systemic signs of infections are–
uncommon
erisepelas usually happens—
post S. pyogenes resp or skin infection
lesions are raised above —
the level of skin/ they’re a salmon red color/clear demarcation between involved and uninvolved tissue
what about the lymphnodes?
lymphtaic involvemet and lymophnode enlargment
systemic signs:
chills, leukocytosis, fever
occurs most commonly in— or — and always caused —
younger kids or older adults and always caused GAS
where on the body do they occur?
face and the legs
cellulitis is —-
skin and deeper subcutaneus infection. deeeper than ersipelas
acute spreading inflammation of —
burns, wounds or surgical treatment, mild trauma
usualy group– strep but also group — in recet rports
A, G
associated with —
burns wounds and surgical incisions
what about the lymphnode?
lymphnode enlargment
systemic signs:
leukocytosis, fever, chills, malaiasem bacteremia
lesion is not —or —
raised or demarcated
risk:
parenteral injection, parents with impaired lymphatic drainage
necrtizing fascitis is also known as
streptococcal gangrene
sreptocoocal gangrene is
rapidly spreaidng deep in the subcutaneous infection
results in the —
extensive destrcution of muscle and fat (flesh eating bacteria)
it can start due to a —
a small break in the skin (minor cut or trauma vesicular viral infection (A vesicular viral infection refers to a viral infection that causes the formation of blisters (vesicles), burn, surgery).
systemic symptoms develop:
toxicity, multi organ failure and death are the hallmarks of this disease
streptococcal toxic shock syndrome: due to M serotypes – or -. strains produce ——
1 or 3/pyrogenic exotxoins including SpeA and SpeC
we often see: —at the site of infection
soft tissue inflammatiom:
phase 1:Pain, fever, chills, malaise, nausea, vomiting, and diarrhea. Hypotention my
occur/early nechrotizing fascitis.
phase 2: tachycardia, persistent fever, and severe pain at the site of nechrotizing
fascitis.
phase 3:appearncae of purple bullae in skin is a bad prognosis pain intesnisfies as disease progresses to shock and organi failure (death can occur within 48 hours of hospitalization, high mortality rate=30%)
populations at risk:
HIV positive, cancer, pulmonary disease, alcoholic patients, IV drug abuse, DM, and Varicella Zoster Virus (VZV)
other diseases:
bacterimia and sepsis(due to surgical wouds). may be rapidly fatal due to STSS and may be seconday to necrotizing fascitis
autoimmune diseases:
1) rheumatic fever
2)
rehumatic fever / is a complication of —-
antibody produced against strep M protein cross recats with human cells/ pharyngitis
rehmautic fever is characterized by inflammation in the—
1) heart: Heart: pancarditis (endocarditis, pericarditis, myocarditis) along with arthralgia (joint pain)
2) joints: antabodis againat strep hyaluronic acid cross reacts with
connective tissue proteoglycans)
3) subcuatnaeous tissue: sub cutaneous nodules
the common age is —and time is —
school age children/fall-winter seasonality
diagnosis:
(+) Throat culture for strep. Pyogenes
Increased ASO-Titer (Anti-Streptolysin O) ASO-T test
Along with clinical manifestations
acute rheumatic heart diseasse:
beta hemolytice streptococcus: Streptococcal M protein
cross reacts with Cardiac
myosin and Sarcolemma
ACUTE GLOMERULONEPHRITIS
is a sequelae of both pharyngeal and pyodermal streptococcal infections
acute glomerunpheritis is seondary to—
skin infection characterized by deposition of antigeb-antibdy complex in the glomerulus cauisng bloody urine to develop and portein in urine, abnormal kidney markers
treatment: s pyogenes is very sensitive to—. for patients with a penicillin allergy.
penicillin, oral cephalosprin can be used
mix of staph aureus and s pyogenes:
ocaxillin or vancomyocin
prevention:
1)Drainage and aggressive surgical debridement must be promptly initiated in
patients with serious soft-tissue infections
2) Persistent oropharyngeal carriage of S. pyogenes can occur after a complete
course of therapy
—- is the only species that carries the group B antigen
S. agalactiae
there are 3 serologic markers:
(1) The group-specific cell wall polysaccharide B antigen (Lancefield grouping
antigen; composed of rhamnose, N-acetylglucosamine, and galactose)
(2)Nine type-specific capsular polysaccharides (Ia, Ib, and II to VIII), serotypes Ia,
III, and V most commonly associated with colonization and disease
(3)Surface proteins (the most common is the c antigen).
virulence factors of GBS:
1) capsule: 1a, 3 and 5 are knwon to cause disease the most. go to slide 36
2)others: pore forming hemolysin/cytolysin promoting invasion and cell injury induce apoptosis and cell injury
bel entercoccus l feacelis hene —-while feaceium hene—
nonhemolytci/ alpha hemolytic
which capsular polysaccharides are most associated with colonization and disease?
1a, 3 and 5
what capsualr polysac contain sialic acid which—-
1a, 1b and 2/ prevents complemnet activation
group B strep colonize the—-
lower GI tract and the genoutritary tract
risk of transmission:
1) at birh: heavy colonization on monther
2) premature delivery (weaker immune systems)
3)prolonged membrane repture (the water breaks too early and labor doesn’t happen soon after) so the baby is exposed to the bacteria
4)colonization with subsequent development of disease in the neonate can occur in utero, at birth or during first few months of life
early onset vs late onset GBS disease
early=infant is infected as it passes through birth canal. in this case, baby becomes ill between birth and 6 days of life
(most often first 24 hours of life)
late onset=baby becomes infected after delivery by coming into contact with people who carry the GBS germ. In this case
symptoms appear later, when the baby is 7 days to 3
months or more old. Late-onset disease may be
acquired from an exogenous source (e.g., mother,
another infant)
Early-Onset Neonatal Disease (Disease in infants younger
than 7 days of age )
- in utero contraction
-lethargy, hypotenion, abnormal temp, poor feeding, (few hours after birth)
-penumonia, bacterimina or meningitis
-indisnguishable from sepsis caused by other pathogens
-Meningitis may be unapparent CSF testing for all neonates
-low mortality however neurological sequleae like blondess and deafness and severe mental retardation
Late Onset Neonatal Disease (disease appearing between 1 week
and 3 months of life)
Manifestation: Bacteremia with meningitis
osteomyelitis, septic arthritis, and cellulitis
accompanying bacteremia
low mortality rate but 50% neurological complications
infections in pregnant women:
1) endometritis: infection lining the uterus
2) wound infection and UTI’s (during or immediately after pregnancy)
men and nonpregnant women with group B
strep infections are genreally infecting older individuals and ave debilitating underlying conditions :Diabetes mellitus
Liver disease or history of alcohol abuse
Neurologic impairment Malignancy
Renal failure
Cardiovascular disease or heart failure
Pulmonary disease
Urologic disease
Peripheral vascular disease
what does it cause in these men and nonpregnant women?/ mortality is —in this population
bacterimina, penumonia, bone and joint infections, endocarditis , skin and soft tissue infections may occur/ higher
treatment: paper
prevention:
- it is recommended that all pregnant women should be screened for
colonization with group B streptococci at 35 to 37 weeks of
gestation
-Chemoprophylaxis should be used for all women who are either
colonized or at high risk
Laboratory diagnosis of
group A and B streptococcus—
group A specimens:—
group B specimens:—
1) beta hemolytic + catalase negative
2)Group A: throat, skin lesions (purulent material).blood and throat culture
3) urogenital material: cultire in CNA may be done to suppress growth of other organisms/
it forms—chains in clinical specimens and —chains in cultures
short/long
slide 44 and 45 and 46and 48
bacitracin is used to—
diffrentiate group A from B since A is susceptibe while B is resistant
PYR test measures the–
PYR IS an enzyme btw
-
hydrolyss of L-pyrrolidoyl beta naphthylamide and release of beta naphthylamine which in the prescence of p-dimethyl aminoccinamldehye forms a red compound
a positive PYR test allows for the —
positive identification of group A strep and also enterococcus species
hyppurate hydrolysis
IDK KAFE TILL 54
This test is an additional presumptive test used to aid in the identification of GBS. The bacteria produce the enzyme hippurate hydrolase which hydrolyzes sodium hippurate to
form benzoic acid and glycine.
