Streptococcus pyogenes
Streptococcus pyogenes.jpg
S. pyogenes bacteria at 900x magnification
Scientific classification
Kingdom: Eubacteria
Phylum: Firmicutes
Class: Bacilli
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Species: S. pyogenes
Binomial name
Streptococcus pyogenes
Rosenbach 1884
Streptococcus pyogenes is a species of Gram-positive bacteria. These bacteria are aerotolerant and an extracellular bacterium, made up of non-motile and non-sporing cocci. As expected with a streptococci, it is clinically important in human illness. It is an infrequent, but usually pathogenic, part of the skin microbiota. It is the predominant species harboring the Lancefield group A antigen, and is often called group A streptococcus (GAS). However, both Streptococcus dysgalactiae and the Streptococcus anginosus group can possess group A antigen. Group A streptococci when grown on blood agar typically produces small zones of beta-hemolysis, a complete destruction of red blood cells. (A zone size of 2–3 mm is typical.) It is thus also called group A (beta-hemolytic) streptococcus (GABHS), and can make colonies greater than 5 mm in size.[1]
Like other cocci, streptococci are round bacteria. The name is derived from Greek words meaning chain(Strepto) of berries (coccus) and pus(pyo)-forming(genes), because streptococcal cells tend to link in chains of round cells (see image) and a number of infections caused by the bacterium, produce pus. Streptococci are can be catalase positive or negative.[2] S. pyogenes can be cultured on blood agar plates. Under ideal conditions, it has an incubation period of 1 to 3 days.[3]
An estimated 700 million GAS infections occur worldwide each year. While the overall mortality rate for these infections is 0.1%, over 650,000 of the cases are severe and invasive, and have a mortality rate of 25%.[4] Early recognition and treatment are critical; diagnostic failure can result in sepsis and death.[5][6]
Streptococcus pyogenes
Streptococcus pyogenes.jpg
S. pyogenes bacteria at 900x magnification
Scientific classification
Kingdom: Eubacteria
Phylum: Firmicutes
Class: Bacilli
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Species: S. pyogenes
Binomial name
Streptococcus pyogenes
Rosenbach 1884
Streptococcus pyogenes is a species of Gram-positive bacteria. These bacteria are aerotolerant and an extracellular bacterium, made up of non-motile and non-sporing cocci. As expected with a streptococci, it is clinically important in human illness. It is an infrequent, but usually pathogenic, part of the skin microbiota. It is the predominant species harboring the Lancefield group A antigen, and is often called group A streptococcus (GAS). However, both Streptococcus dysgalactiae and the Streptococcus anginosus group can possess group A antigen. Group A streptococci when grown on blood agar typically produces small zones of beta-hemolysis, a complete destruction of red blood cells. (A zone size of 2–3 mm is typical.) It is thus also called group A (beta-hemolytic) streptococcus (GABHS), and can make colonies greater than 5 mm in size.[1]
Like other cocci, streptococci are round bacteria. The name is derived from Greek words meaning chain(Strepto) of berries (coccus) and pus(pyo)-forming(genes), because streptococcal cells tend to link in chains of round cells (see image) and a number of infections caused by the bacterium, produce pus. Streptococci are can be catalase positive or negative.[2] S. pyogenes can be cultured on blood agar plates. Under ideal conditions, it has an incubation period of 1 to 3 days.[3]
An estimated 700 million GAS infections occur worldwide each year. While the overall mortality rate for these infections is 0.1%, over 650,000 of the cases are severe and invasive, and have a mortality rate of 25%.[4] Early recognition and treatment are critical; diagnostic failure can result in sepsis and death.[5][6]
Bordetella (Gram-Negative Rod Related to the Respiratory Tract)Syeda Maryam
In this presentation, we are discussing Bordetella Pertussis, its important properties, EPIDEMIOLOGY, PATHOGENESIS, Several factors that play a role in the pathogenesis, Pertussis toxin production,
adenylate cyclase production, Tracheal
cytotoxin, Whooping cough, its CLINICAL FINDINGS, THE CLASSIC PICTURE OF WHOOPING
COUGH IN YOUNG CHILDREN, it's LABORATORY DIAGNOSIS, TREATMENT, PREVENTION, KILLED VACCINE, and ACELLULAR VACCINE.
Bordetella (Gram-Negative Rod Related to the Respiratory Tract)Syeda Maryam
In this presentation, we are discussing Bordetella Pertussis, its important properties, EPIDEMIOLOGY, PATHOGENESIS, Several factors that play a role in the pathogenesis, Pertussis toxin production,
adenylate cyclase production, Tracheal
cytotoxin, Whooping cough, its CLINICAL FINDINGS, THE CLASSIC PICTURE OF WHOOPING
COUGH IN YOUNG CHILDREN, it's LABORATORY DIAGNOSIS, TREATMENT, PREVENTION, KILLED VACCINE, and ACELLULAR VACCINE.
Pharyngitis (or sore throat) - most common upper respiratory tract infections (URTI).
Viral pharyngitis - vast majority of cases – self-limited.
Bacteria - important etiologic agents of pharyngitis, require specific antibiotic treatment - can lead to serious complications and sequelae
Streptococcus pyogenes
Corynebacterium diphtheriae
Rare causes
Other β-hemolytic streptococci (group C and G)
Arcanobacterium hemolyticum
Fusobacterium necrophorum
Mycoplasma pneumoniae
Neisseria gonorrhoeae
Size – 0.5-1 m.
Shape – oval /elliptical.
Arrangement – in chains esp. in liquid culture media. (upto 50 cocci in a chain).
Divide in one plane.
Daughter cells do not seperate.
Gram positive
Cultures older than log phase may lose gram reaction.
Capsule –
Hyaluronic acid (group A, C). Nonimmunogenic.
Polysaccharide (group B, D ).
Nonmotile.
Nonsporing.
L-forms – cell-wall deficient, require thiol & pyridoxal for growth. Found in blood (due to antibiotics).
Aerobes & facultative anaerobes.
22-42°C; opt.37.
pH for growth –opt. 7.4.
Capnophilic – 10% CO2.
Fastidious; need blood / serum / sugar.
Liquid medium (e.g. Todd-Hewitt broth) – granular turbidity + powdery deposits.
Blood agar –
0.5-1mm, circular, low convex, -hemolytic.
Matt colonies – pathogenic
Glossy colonies – nonpathogenic.
Selective medium –
Crystal violet (1:500,000) in B.A.
Catalase – ve
Sugar fermentation –
Glucose, lactose, maltose, trehalose - . (constitutive enzymes).
Other sugars & alcohols - ,(inducible enz.).
*Ribose sugars – not fermented.
*Pyrolidonyl naphthalamide hydrolysis (PYR) - +ve (differentiates gr. A from other groups).
Delicate organism
Survives in dust in dark for many weeks.
Susceptible to heat , 54°C x 30 min.
Susceptible to common antiseptics.
Resistant to –
Crystal violet (1mg/litre) – for isolation of gr A.
Nalidixic acid (15mg/litre) for isolation of & Colistin (10mg/litre) gr. B
Bacitracin sensitive – differentiates gr. A from other hemolytic
Hyaluronic acid capsule-nonantigenic, antiphagocytic, thrombolytic.
Innermost cell wall layer peptidoglycan (NAG-NAM)
Cell-wall CHO – Group sp. Ag. Todd-Hewit growth →
Extraction by –
HCl (Lancefield)
Formamide (Fuller)
Enzyme of Streptomyces albus (Maxted)
Autoclave (Rantz & Randall).
Capillary pptn /ring pptn
M protein –
Acid extraction & Serotyping.
100 M-types.
T protein –
Typing by slide agglutination with trypsinised RBCs.
R protein –
Present in gr. B, C, G & some serotypes of gr. A (23, 28, 48).
. Antigenic cross-reactions
Capsular hyaluronic acid synovial fluid.
Cellwall CHO cardiac valves.
Cellwall peptidoglycan skin.
Cyto. membrane vascular intima & cardiac muscle.
M protein* - reqd. for invasive infection.
Receptor for fibrinogen, factor H, IgG.
Capsule - antiphagocytic
Group CHO Ag’-invasive properties.
Protein F- binds fibronectin on epi. Surface
Lipoteichoic acid loosely binds strepto’ to epi surface. F prtn, M prtn secur
Gram-positive cocci include Staphylococcus (catalase-positive), which grows clusters, and Streptococcus (catalase-negative), which grows in chains. The staphylococci further subdivide into coagulase-positive (S. aureus) and coagulase-negative (S. epidermidis and S. saprophyticus) species. Streptococcus bacteria subdivide into Strep. pyogenes (Group A), Strep. agalactiae (Group B), enterococci (Group D), Strep viridans, and Strep pneumonia.
Gram-positive bacilli (rods) subdivide according to their ability to produce spores. Bacillus and Clostridia are spore-forming rods while Listeria and Corynebacterium are not. Spore-forming rods that produce spores can survive in environments for many years. Also, the branching filament rods encompass Nocardia and actinomyces.
Gram-positive organisms have a thicker peptidoglycan cell wall compared with gram-negative bacteria. It is a 20 to 80 nm thick polymer while the peptidoglycan layer of the gram-negative cell wall is 2 to 3 nm thick and covered with an outer lipid bilayer membrane.
Bloodstream infection mortality rates have increased by 78% in just two decades[1]. Gram-positive organisms have highly variable growth and resistance patterns. The SCOPE project (Surveillance and Control of Pathogens of Epidemiologic Importance) found that gram-positive organisms in those with an underlying malignancy accounted for 62% of all bloodstream infections in 1995 and 76% in 2000 while gram-negative organisms accounted for 22% and 14% of infections for these years.[2]
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
How to Give Better Lectures: Some Tips for Doctors
Streptococci
1. STREPTOCOCCUS
It is gram positive cocci which are arranged in chains. They are part of normal human flora.
CLASSIFICATION –
A. Alpha haemolytic streptococci
B. Beeta haemolytic streptococci
C. Gamma or non haemolytic streptococci
MORPHOLOGY –
- Spherical or oval
- Diameter 0.5 to 1 micro meter
- Non motile
- Non sporing
- Capsule - group A & C (hyaluronic acid), group B&D (polysaccharide)
CULTURE –
- Aerobes & facultative anaerobes
- Temp – 22 – 42 degree
- Optimal temp. – 37 degree
- Grow poor in nutrient agar
- Good growth occur in media containing blood, sugar or serum.
- Crystal violet blood agar medium is used for isolation of strept. Pyrogenes.
- Colony – circular, small 0.5 to 1 mm pin point, semitransparent, low convex, wide zone of
beeta haemolysis.
BIOCHEMICAL REACTIONS –
- Catalase – negative
- Failure to ferment ribose which is useful to differentiate from staphylococcus.
- Hydrolysis of pyrrolidoniyl naphthalamide (PYR TEST)
- Several sugars are fermented by it producing acid without gases.
- Resistance to SXT antibiotics
ANTIGENIC STRUCTURE –
- Capsule hyaluronic acid
- Group specific polysaccharide antigen
- Type specific antigen
2. M – protein
T & R protein
Other associated factors
TOXINS -
- Haemolysins – it produce two type of haemolysins, streptolysin ‘O’ & ‘S’. they are produced
by group A, C and G. streptolysin O is oxygen and heat labile. It lyses red cells and it is also
cytotoxic for neutrophils and cardiac tissue. Streptolysin S is oxygen stable haemolysin and
is responsible for the haemolysis seen around colonies of streptococci on the surface of
blood agar plate. It also have leucocidal action.
- Pyrogenic exotoxin – This toxin is responsible for the rash of scarlet fever. It is only
produced by lysogenic strain of group A streptococci. Three types A,B and C have described.
Types A and C are coded for by bacteriophage genes but type B gene is chromosomal. It
causes pyrogenecity cytotoxicity and enhancement of susceptibility to endotoxin.
ENZYMES –
- Streptokinase
- Hyalurinodase
- NADase
- Deoxyribonuclease
PATHOGENESIS –
Streptococcus Lesions
Str. Pyogenes
(1) Pyogenic infections
Respiratory infections Acute tonsillitis or pharyngitis, scarlet fever
Skin infections Infections of wounds, burns and skin lesions,
erysipelas, impetigo
Genital infections Puerperal sepsis
Deep infections Bone and joint infections, lymphadenitis,
septicaemia, abscess in internal organs
(2) Non suppurative complications Rheumatic fever, acute glomerulonephritis
Group B streptococci Neonatal infections (septicemia & meningitis)
Enterococcus faecalis Urinary tract infections
Endocarditis
Viridans srteptococci Endocarditis
Dental caries
3. LAB DIAGNOSIS –
1. Specimen – Swab, Pus, Blood and CSF
2. Collection & transport – collected in sterile container, transported in Pikes transport
medium.
3. Gram staining of smear - Gram positive cocci which are arranged in chains.
4. Culture, colony, morphology and staining – culture in blood agar. for others see above.
5. Biochemical reactions – see above
6. Lancefield grouping – haemolytic streptococci are grouped serologically by lancefield
technique. It is done for definite classification and epidemiological studies. It depends on C
carbohydrate which is specific for each group. C carbohydrate is extracted from the cell wall
of streptococci and grouping done by a precipitation test with group antisera.
7. Antigen detection test – Elisa and agglutination test are used.
TREATMENT – PENICILLIN G
See differentiating features of acute rheumatic fever & acute glomerulonephritis.
