Streptococcus pyogenes, also known as group A Streptococcus, is an important human pathogen. It is a Gram-positive coccus that grows in chains. S. pyogenes can cause both suppurative infections like pharyngitis, impetigo, and necrotizing fasciitis, as well as non-suppurative sequelae including acute rheumatic fever and acute glomerulonephritis. Penicillin is the drug of choice for treating S. pyogenes infections. Prophylactic penicillin is also used to prevent rheumatic fever in individuals with a history of the disease. Group B Streptococcus and Streptococcus pneumoniae are other clinically significant streptococcal species
Pseudomonas is a type of bacteria that can cause infections. Pseudomonas is a common genus of bacteria, which can create infections in the body under certain circumstances. There are many different types of Pseudomonas bacteria
Pseudomonas is a type of bacteria that can cause infections. Pseudomonas is a common genus of bacteria, which can create infections in the body under certain circumstances. There are many different types of Pseudomonas bacteria
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
Staphylococci can cause many forms of infection. (1) S aureus causes superficial skin lesions (boils, styes) and localized abscesses in other sites. (2) S aureus causes deep-seated infections, such as osteomyelitis and endocarditis and more serious skin infections (furunculosis). (3) S aureus is a major cause of hospital acquired (nosocomial) infection of surgical wounds and, with S epidermidis, causes infections associated with indwelling medical devices. (4) S aureus causes food poisoning by releasing enterotoxins into food. (5) S aureus causes toxic shock syndrome by release of superantigens into the blood stream. (6) S saprophiticus causes urinary tract infections, especially in girls. (7) Other species of staphylococci (S lugdunensis, S haemolyticus, S warneri, S schleiferi, S intermedius) are infrequent pathogens
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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.
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
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
2. • Streptococci are Gram positive cocci.
• Arranged in chains or pairs.
• The name streptococci (streptos meaning
twisted or coiled) was given by Billroth.
3. CLASSIFICATION:
Streptococci
Aerobes & facultative
anaerobes
Obligate anaerobes
Eg: Peptostreptococci
Beta haemolytic
Gamma haemolytic
Eg: Enterococcus group
Alpha haemolytic
Eg: Viridans streptococci
20 Lancefield groups
(ABCDEFGHKLMNOPQRSTUV)
80 Griffith types
(1,2,3,etc. up to 80)
02 requirement
Haemolysis
Serological Grouping (C carbohydrate antigen)
Group A- Streptococcus pyogens
Serological typing (M Protein)
4.
5. Streptococcus pyogens
MORPHOLOGY:
• Gram positive
spherical or oval cocci
arranged in chains.
• Individual coccus will
be 0.5-1.0μm in
diameter.
• They are nonmotile
and nonsporing.
• Some strains have
capsule composed of
hyaluronic acid.
6. Cultural characters
Aerobes & facultative anaerobes
370c [22 -420c]
Blood , serum, sugars
Non selective media:- Sheep blood agar
Selective media - Crystal violet Blood agar (1:500,000)
PNF medium
7. Growth on Blood agar:
• After 24 hours incubation
colonies are small, pinpoint,
translucent & zone of beta
hemolysis seen.
• Liquid media – Glucose
broth – granular turbidity &
powdery deposit
11. 3. PYR test: Positive (Pyrrolidonyl naphthylamide)
4. Ribose is not fermented.
L-Pyrrolidonyl β-
naphthylamide
p-naphthylamine
β -dimethylamino
cinnaaldehydeRed
PYRase
12. Antigenic structure:
1.Capsular hyaluronic acid: Antiphagocytic
2.Cell wall antigens:
a) Inner layer of peptidoglycan Cell wall rigidity.
Pyrogenic & Thrombolytic
b) Middle layer of group specific C carbohydrate
c) Outer layer of protein (fimbriae) & lipoteichoic acid
Adherence & Cytotoxicity
3.Type specific antigens:
a) M protein adhesin, antiphagocytic, inhibits
opsonization and alternate C pathway
b) T protein
c) R protein
14. Antigenic relationship between various
components of Str. pyogens & different
tissues
Components of Str.
pyogens
Tissues
Capsular Hyaluronic acid Human synovial fluid
Cell wall protein Myocardium
Gr A carbohydrate Cardiac valves
Cytoplasmic membrane Vascular intima
Peptidoglycans Skin antigens
16. Toxins: Haemolysins
ASO test : 200 units or >
Gr A , C , G
Streptolysin O Streptolysin S
O2 Labile O2Stable
Cytotoxic (Neutrophils, platelets)
Cardiotoxic
Leucocidal
Antigenic not antigenic
Seen in Pour plate culture Seen in Surface culture
17. Toxins
• Pyrogenic exotoxin (erythrogenic toxin)
(Erythrogenic, Dick toxin , Scarlatinal toxin / SPE )
• Dick test toxin intradermally erythematous rash
• Schultz Charlton reaction scarlet fever antitoxin
blanching of rash
• Rashes of Scarlet fever
• A,B,C
• Superantigenes T cells massive release of
cytokines
• Antigenic
• Pyrogenicity, Cytotoxicity
• Enhanced S to endotoxin
• Streptococcal pyrogenic exotoxin (SPE) fever
induction is primary response
18. Enzymes
• Streptokinase (fibrinolysin)
• Lysis of clot
conversion of plasminogen –
plasmin
• Protein in nature
• Antigenic
• Spread of infection
Use
• Early myocardial infection
• Thromboembolic disorder
• Deoxyribonuclease
(streptodornase)
• A,B,C,D
• Liquefy viscous DNA
• Anti DNAse ab in Skin
infection
• Gr A,C,G
• Use
• In Empyema (collection pus
in the cavity especially
pleural cavity)
19. Enzymes
• Nicotinamide adenine
dinucleotidase
(NADase)
• Acts on NAD
• A,C,G
• Antigenic
• leucotoxic
• Hyaluronidase
• A,B,C,G
• Spread
• Antigenic
• Serum opacity factor
[Lipoproteinase ]
Opaque to agar gel
containing horse or
swine serum
21. PATHOGENICITY:
Source of infection:
1. Patient
2. Carriers
Mode of transmission:
1. Contact: direct or indirect( through fomites)
2. Inhalation of air borne droplets
• Crowding, Schools, Camps - Favour
infection
22. Pathogenicity
Diseases caused by S. pyogens is studied
under 2 groups
1. Suppurative infections
– Respiratory infections
– Skin and soft tissue infections
– Genital infections
2. Non suppurative complications
– Acute rheumatic fever
– Acute glomerulonephritis
23. 1. Suppurative infections:
• Pyogenic infections.
• Spreads locally, along lymphatics and
through the blood stream.
32. ii) Necrotising fasciitis
• M types 1 and 3 forming
pyrogenic exotoxin A
• High fatality
• Flesh eating bacteria
• Shock, DIC
• Treatment with penicillin – not
effective
• Vancomycin – in life
threatening infections
36. 2. Non suppurative complications:
• It is also called as post streptococcal
complications
• Non suppurative complications of
S.pyogens occur 1-4 weeks after the acute
infection.
• The organism may not be detectable when
these complications set in.
37. • These complications are believed to be the
result of hypersensitivity to some
streptococcal components.
• The complications are-
1. Acute rheumatic fever
2. Acute glomerulonephritis
38. 1. Acute rheumatic fever: It occurs after repeated
sore throat caused by S. pyogens.
Mechanism of pathogenesis:
During primary infection antibodies will be produced
against some streptococcal antigen.
Since streptococcal antigen has similarity with cardiac
tissue antigen, the antibodies will cross react with
cardiac tissue antigen causing destruction.
Leads to clinical symptoms such as carditis, fever and
malaise.
39. 2. Acute glomerulonephritis: It follows after skin
infection caused by S. pyogens nephritogenic types.
Mechanism of pathogenesis:
During skin infection caused by nephritogenic types of
S. pyogens, the antibodies will be produced against
cell membrane antigen.
These antibodies cross react with glomerular
basement membrane antigen causing destruction.
Leads clinical symptoms such as proteinuria,
haematuria & hypertension.
40. Non –Suppurative Complications
Ac rheumatic fever Ac
Glomerulonephritis
Site of infection Throat Throat / Skin
Prior Sensitisation Essential Not necessary
Serotype of Str
pyogens
Any Pyoderma types 49,
53-55,59-61 &
Throat inf types 12, 1
Immune response Marked Moderate
‘C’ level unaffected Lowered
41. Ac rheumatic fever Ac
Glomerulonephritis
Repeated attacks Common Absent
Course Progressive / Static Spontaneous
resolution
Prognosis Variable Variable Good
Hereditary tendency Present Not known
Penicillin prophylaxis Essential Not indicated
Non –Suppurative Complications
42. Lab Diagnosis
• Ac Suppurative Infections : by culture
• Nonsuppurative complications :
Demonstration of ab
43. LABORATORY DIAGNOSIS:
A) In acute suppurative infection
Specimens to be collected:
• Throat swab,
• Pus,
• Tissue material,
• Blood,
• Swab from nose for detection of carriers.
Transport media: Pike’s medium
44. I) Direct Microscopy:
• Direct microscopy with
Gram stained smear is
useful in case of pus &
CSF, where cocci in
chains are seen.
• This is of no value for
specimen like sputum &
genital swabs where
mixed flora are
normally present.
Methods of examination:-
45. c) Gram’s staining:
Smears are
examined from the
culture plate and
reveals Gram
positive cocci in
chains.
II) Culture:
a) Media used:
b) Cultural Characteristics:
47. Lab Diagnosis
Lancefield grouping
Grown in Todd Hewitt broth
Extraction of C carbohydrate – HCL /
formamide /autoclaving /enzyme
(streptomyces albus)
Precipitation with sp antisera
Antigen detection test ELISA /Agglutination
test [throat swab]
48. Lab Diagnosis
Nonsuppurative complications
Rheumatic fever
ASO titre (200 U / more)
Ac G.N.
anti DNAse B titre (300/350 )
[retrospective diagnosis of streptococcal pyoderma]
antihyaluronidase
Streptozyme test [[Passive slide
haemagglutination test ]] : screening test for
all types of streptococcal infection
49.
50.
51.
52. • Other Hemolytic Streptococci – also cause human
diseases
45% - Group A
10-15% - Group B
10-15% - Group C
25% - Group G
5% - Group F
53. Group B Streptococci:
• Str. Agalactiae (Commonsal in female genital tract)
• Imporatant cause of neonatal meningitis, septicaemia
• Infection acquired during birth from birth canal
• Identified by CAMP (Christine Atkins Munch Peterson)
reaction. CAMP factor enhances the Beta hemolysis caused
by Staphylococcus
• Early onset – Septicaemia, Meningitis,
Pneumonia
• Late onset – less severe
• Adults infection – Septic abortion,
Puerperal sepsis
54. Group D – Str.faecalis
• Normally present in intestine, saliva, genital tract, wound
infection in perineumal skin & subcutaneous tissue
• Causes UTI, wound infections, SABE, peritonitis, abscess, biliary
tract infection.
• Enter blood circulation - Bacteremia - Lodge on damaged heart
valves.
septicaemia - Lodge in Urinary tract
• It occurs in pairs, grows on MacConkey agar, ferment mannitol,
sucrose, esculin, black colonies on Potassium tellurite blood
agar, 6.5% NaCl, 40% bile at 45ºC.
Str.viridans:
• Normally present in human mouth & throat, Oppurtunistic
pathogen
• In persons with valvular disease of heart, they can cause SABE
after tooth extraction
55. Procedure:
• Enter blood circulation & lodge on damaged heart valves & produce
SABE.
• Dental Caries – Str. mutans breaks down sucrose into acid & dextran
• Acid damages dentine. Dextran binds food debris, efri cells, mucus bacteria
to form dental plaques, caries
56. TREATMENT:
• Penicillin G is the drug of choice.
• In patients allergic to penicillin; erythromycin
or cephalexin is used.
• Antibiotics have no effect on established
glomerulonephritis & rheumatic fever.
57. PROPHYLAXIS:
• Prophylaxis is indicated only in the prevention
of rheumatic fever.
• It is done by long term administration of
penicillin in children who have developed
early signs of rheumatic fever.
• Antibiotic prophylaxis is not useful in case of
glomerulonephritis.
58.
59. • Other Hemolytic Streptococci – also cause human
diseases
45% - Group A
10-15% - Group B
10-15% - Group C
25% - Group G
5% - Group F
60. Group B Streptococci:
• Str. Agalactiae (Commonsal in female genital tract)
• Imporatant cause of neonatal meningitis, septicaemia
• Infection acquired during birth from birth canal
• Early onset – Septicaemia, Meningitis, Pneumonia
• Late onset – less severe (Osteomyelitis, arthritis, conjunctivitis,
respiratory infection, endocarditis & peritonitis.)
• Adults infection – Septic abortion, Puerperal sepsis
Identified by CAMP (Christine Atkins Munch Peterson) reaction. CAMP
factor enhances the Beta hemolysis caused by Staphylococcus
61. Clinical significance:
1. Infection in neonates: 2 types
a. Early onset disease- Occurs during first
week of life.
Source of infection- Vagina of the mother &
infection is acquired during birth.
Clinical symptoms- Septicemia, meningitis &
pneumonia.
62. b. Late onset disease- Occurs during 2nd & 12th
week of life.
Source of infection: It usually acquired from the
hospital environment.
Clinical symptoms- Osteomyelitis, arthritis,
conjunctivitis, respiratory infection, endocarditis
& peritonitis.
2. Infection in adult: It causes bacteraemia,
sepsis , wound infection, septic abortion &
puerperal sepsis.
63. Laboratory diagnosis:
Specimens collected: Blood, CSF & exudates
from lesions.
Methods of examinations:
1. Detection of antigen in clinical samples.
2. Direct microscopy by doing Gram’s smear.
64. 3. Culture- Blood agar is used for culture.
4. Identification-
a. Small β-haemolytic colonies on blood agar
b. Gram staining
c. Catalase test- Negative
66. • FIG. 2. CAMP test for the identification of Streptococcus
agalactiae (group B). (A) Streptococcus (group B) shows
a positive CAMP reaction. (B) Streptococcus pyogenes
(group A) shows a negative reaction when inoculated at
a right angle to (C) Staphylococcus aureus.
67.
68.
69. f. Lancefield sero grouping is done for
confirmation.
Treatment: Penicillin is used.
70. Group D Streptococci:
Classified into 2 groups-
1. The enterococcus group- which have
been reclassified as a separate genus called
Enterococcus, containing- E. faecalis,
E. faecium & E. durans.
2. Non enterococcal group- containing
S. bovis & S. equinus
71. ENTEROCOCCUS
• Normal inhabitants of human intestinal tract.
• Possess some distinctive properties like-
1. They grow in 40% bile,
2. They resist pH till 9.6.
3. They grow in 6.5% NaCl solution,
4. They grow at 45ºC can withstand up to 60ºC for
30 minutes.
5. They grow in 0.1% methylene blue milk.
6. PYR test positive
7. Resistant to SXT
73. Clinical significance:
Source & mode of infection:
1. Endogenous-from colonized site.
2. Exogenous-through direct or indirect contact.
Common infections:
1. Urinary tract infection,
2. Bacteremia,
3. Wound infection,
4. Biliary tract infection,
5. Sub acute bacterial endocarditis.
74. Laboratory diagnosis:
Specimens collected: Urine, blood, pus &
exudates.
Methods of examination:
1. Direct microscopy- by doing Gram’s smear.
2. Culture- Blood agar and MacConkey’s agar is
used.
75. 3. Colony morphology-
i) On blood agar small non-haemolytic colonies
are seen but some strains may show α or β
haemolysis.
ii) On MacConkey’s agar it produces pink
colour colonies.
4. Identification-
i) Gram’s smear
ii) Catalase test- Negative
76. iii) Biochemical tests-
• It ferments mannitol, sucrose & sorbitol.
• Bile esculin test- positive (aesculin
aesculetin + ferric citrate Black ppt)
+-
77. Treatment:
• Strains resistant to penicillin & other
antibiotics occur frequently.
• Vancomycin is the alternative drug to
penicillin.
• Vancomycin resistant is also seen.
78. DIFFERENT GROUPS OF STREPTOCOCCI
Lancefield
group
Species / common
name
Diagnostic tests Diseases caused
A Str. pyogenes Bacitracin sensitive ,
PYR positive , ribose
not fermented
URT inf., skin inf. , ac.
RF ,
ac.glomerulonephritis
B Str. agalactiae CAMP test - + ve ,
Hippurate hydrolysis
+ve
Neonatal septicemia &
meningitis
C Str. equisimilis Ribose fermented ,
trehalose fermented
Pharyngitis ,
endocarditis
D 1) Enterococcus sp
2) non- enterococci
Growth 6.5% Nacl
No growth 6.5% Nacl
UTI, wound inf
Genitourinary inf
Not typed Viridans Str. Optochin resistant Endocarditis , dental
caries