This document provides information on Corynebacterium, including Corynebacterium diphtheriae which causes diphtheria. It discusses the morphology, cultural characteristics, biotypes, virulence factors, pathogenesis, clinical presentation, complications, laboratory diagnosis and epidemiology of C. diphtheriae. The key points are that C. diphtheriae is a gram-positive bacillus that produces a powerful exotoxin causing diphtheria, a serious infection of the upper respiratory tract, and immunization is important for control of the disease.
The genus Shigella exclusively infects human intestine.
Shigella dysenteriae is the causative agent of bacillary dysentery or shigellosis in humans.
It is a diarrheal illness which is characterized by frequent passage of blood stained mucopurulent stools.
The four important species of the genus Shigella are:
Shigella dysenteriae
Shigella flexneri
Shigella sonnei
Shigella boydii.
The PPT is mainly all about Mycobacterium Tuberculosis. Agents causing the disease Tuberculosis, pathogenesis, laboratory diagnosis, treatment and prophylaxis. It was made for both BSc and MSc students.
The genus Shigella exclusively infects human intestine.
Shigella dysenteriae is the causative agent of bacillary dysentery or shigellosis in humans.
It is a diarrheal illness which is characterized by frequent passage of blood stained mucopurulent stools.
The four important species of the genus Shigella are:
Shigella dysenteriae
Shigella flexneri
Shigella sonnei
Shigella boydii.
The PPT is mainly all about Mycobacterium Tuberculosis. Agents causing the disease Tuberculosis, pathogenesis, laboratory diagnosis, treatment and prophylaxis. It was made for both BSc and MSc students.
Aerobic Non-Spore-Forming Gram-Positive BacilliSijo A
Disease: listeriosis.
L. monocytogenes causes a variety of infections in neonates, pregnant women, and immunosuppressed patients.
CNS infections: meningitis, encephalitis, brain abscess, spinal cord infections.
Neonatal:
Early onset: Granulomatosis infantisepticum—in utero infection disseminated systemically that causes stillbirth.
Late onset: Bacterial meningitis.
Food poisoning, bacteremia.
Mode of transmission:
Direct contact: Human gastrointestinal tract, ingestion of contaminated food, such as meat and dairy products.
Endogenous strain: Colonized mothers may pass organism to fetus. Portal of entry is probably from gastrointestinal tract to blood and in some instances from blood to meninges.
Diphtheria is an infection caused by the bacterium Corynebacterium diphtheriae. Diphtheria causes a thick covering in the back of the throat. It can lead to difficulty breathing, heart failure, paralysis, and even death. CDC recommends vaccines for infants, children, teens and adults to prevent diphtheria. The presentation consists of basic concepts regarding the bacteria and its infection. It has explanation in detail about signs and symptoms of Diptheria
LEPROSY
CELLULITIS
IMPETIGO
LEPROSY REVISION NOTES FOR NEET PG AIIMS PREPARATION
WITH HIGH YIELD TOPICS BASED ON LECTURE NOTES AND PREVIOUS YEAR QUESTIONS
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This seminar consisits of description of various bacterial diseases along with their oral manifestations,diagnosis and treatment.an addition of suitable case reports for better understanding and associated disorders
A detailed description of sarcoidosis, pulmonary in specific but also covering the other systems. a rare entity in india or a better way to say, often an overlooked disease.
Tropical theileriosis or Mediterranean coast fever Ranjini Manuel
heileriases are a group of tickborne diseases caused by Theileria spp. A large number of Theileria spp are found in domestic and wild animals in tick-infested areas of the Old World. The most important species affecting cattle are T parva and T annulata, which cause widespread death in tropical and subtropical areas of the Old World. T lestoquardi, T luwenshuni, and T uilenbergi are important causes of mortality in sheep.
Adenoviridae is a group of medium sized, non-enveloped, double stranded DNA viruses that replicate and produce disease in the eye and in the respiratory, gastrointestinal and urinary tracts;
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
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
- 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
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.
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
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
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!
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
1. CORYNEBACTERIUM
A Presentation By
G. Prashanth Kumar
Department of Microbiology & Parasitology,
Faculty of Medicine, International Medical & Technological University,
Dar-Es-Salaam, Tanzania.
2. INTRODUCTION
• Corynebacteria / “Coryneform bacteria” – a group
of non-spore forming, gram- positive bacilli, tend
to be clubbed or irregularly shaped; (coryne =
club)
• Corynebacterium diphtheriae the causative agent
of Diphtheria is the major pathogen in this group.
• Other pathogenic corynebacteria are:
• C. Ulcerans: Diphtheria like lessions.
• Corynebacteria Causing Superficial skin infections:
C. minutissimum and C. tenuis.
• Diphtheriods: Normal commensals in throat, skin
and conjunctiva.
3. HISTORY
• Hippocrates provided the first clinical description
of diphtheria in the 4th century B.C.
• Bretonneu (1821), a French army surgeon,
described the unique clinical characteristics of
the disease, and used the term ‘dipht`erie’ to
signify the tough leathery pseudomembrane that
occurs in oropharynx and some times in
nasopharynx;
(diphtheros = leather)
4. HISTORY
• The bacterium that caused diphtheria was first
described by Klebs in 1883, and was cultivated by
Loeffler in 1884, who applied Koch's postulates and
properly identified Corynebacterium diphtheriae as
the agent of the disease.
• In 1884, Loeffler concluded that C. diphtheriae
produced a soluble toxin, and thereby provided the
first description of a bacterial exotoxin.
• Roux and Yersin (1888) discovered the diphtheria
exotoxin and established its pathogenic effects.
• The antitoxin was described by von Behring(1890).
6. MORPHOLOGY
• Slender Gram-positive rods, pleomorphic; easily
decolousised;
• 0.6-0.8μ diameter and 3-6 μ length;
• Irregular swelling at one or both ends (‘club
shaped’);
• Non-capsulate, Non-sporing and nonmotile
• Granules containing polymetaphosphate are seen in
the cells;
• Take up bluish purple color against lightly stained
cytoplasm, when stained with Loeffler’s Methylene
Blue, and hence called ‘Metachromatic granules’;
• Also called, ‘volutin granules’ or ‘Babes Ernst
granules’;
• They are often situated at poles- ‘polar bodies’
7. MORPHOLOGY
• Special stains for
demonstrating the
granules :
– Albert’s stain
– Neisser’s stain
– Ponder’s stain
• The bacilli are arranged in
pairs, palisades or small
groups; the bacilli lie at
various angles to each other,
resembling the letters, V or L;
• This is called, “Chinese letter
pattern” or “cuneiform
pattern”;
8. CULTURAL CHARACTERISTICS
• Aerobe and facultative anaerobe;
• Optimum temperature is 370C
• Growth scanty on ordinary media;
• Enrichment with: blood, serum or egg is
necessary for good growth;
• Potassium tellurite(0.04%) acts as a ‘selective
agent’, as it inhibits growth of most oral
commensals and retards the growth of Candida
albicans and S.aureus;
9. MEDIA FOR CULTIVATION
• Blood agar
• Loeffler’s serum slope
• Tellurite blood agar
• Hoyle’s tellurite lysed-blood agar
• Tinsdale’s medium (cystine added to tellurite
containing agar)
10. COLONY CHARACTERISTICS
• Blood agar : small,
granular and gray with
irregular edges;
Hemolysis may or may
not present;
• Loeffler’s serum slope:
– Very rapid growth;
– Colonies in 6-8 hrs
– Initially circular white
opaque colonies and
acquire yellowish tint on
incubation
11. COLONY CHARACTERISTICS
• Tellurite blood agar:
– Growth slow; colonies seen after 48 hrs;
– The colonies are brown to black with a brown-
black halo because the tellurite is reduced to
metallic tellurium;
– Staphylococcus also produce such colonies
A diagrammatic representation
12. COLONY CHARACTERISTICS
• Tinsdale’s medium (also
contain cystine in
addition to tellurite):
– Grey black colonies with
dark brown haloes
indicate C.diphtheriae
and C.ulcerans (these
contain cystinase)
13. BIOTYPES
• McLeod and Anderson classified diphtheria
bacilli, based on the colony characteristics on
Tellurite medium and other properties like
biochemical reactions and severity of disease;
• 3 biotypes :
– gravis
– intermedius
– mitis
• 4th biotype : belfanti has also been described
14. Feature gravis intermedius mitis
Morphology
shot rods,
few granules
some degree of
pleomorphism
long barred forms
poor granulation
Pleomorphism
long curved
prominent granules
Pleomorphism
Colony on
tellurite blood
agar (48 hrs)
Daisy head colony
(flat colony with raised
dark centre and crenated
edge; radial striations)
Frog's egg colony
(dull granular centre
with glistening
periphery and
lighter ring near edge)
Poached egg colony
(shiny , flat with central
elevation)
Consistency of
the colonies
Brittle
not easily emulsifiable intermediate
soft, buttery
easily emulsifiable
Hemolysis Variable nonhemolytic hemolytic
Glycogen/
starch
fermentation
Positive Negative Negative
15. OTHER FEATURES OF VARIOUS BIOTYPES
• The gravis and mitis are associated with high
case fatality rates;
• Paralytic complications more with gravis;
• Hemorrhagic complications –gravis and
intermdius;
• Obstruction to air passage - mitis
• mitis – endemic ; gravis and intermedius-
epidemic
16. BIOCHEMICAL REACTIONS
• Hiss serum sugars – for testing fermentation
reactions;
• Ferment- glucose, galactose, maltose and
dextrose; but not lactose, sucrose, mannitol;
• Proteolytic activity is absent;
• Do not hydrolyse urea;
• Do not form phosphatase;
• Produce cystinase (halo on Tinsdale’s medium)
17. RESISTANCE
• Cultures remain viable for 2-3 wks at 25-300C
• Destroyed by heat
• Resistant to light, desiccation or freezing;
• Easily destroyed by antiseptics
• Susceptible to – Penicillin, erythromycin and
broad spectrum antibiotics;
19. VIRULENCE FACTORS
• Virulent strains of diphtheria bacilli produce a
very powerful exotoxin.
• The ‘virulence’ of diphtheria bacilli is due to
their capacity to-
– Establish infection and growing rapidly
– Quickly elaborate an exotoxin
• Avirulent strains are common among
convalescents , contacts and carriers,
particularly those with extra-faucial infection
20. DIPHTHERIA TOXIN
• The pathognomonic effects are due to the
toxin;
• Almost all the gravis and intermedius strains
and 80-85% of mitis strains are toxigenic
• Toxin is a protein;
• Mol. Wt.: 62,000
• Two fragments, A and B;
• Extremely potent :
– 0.1 μg lethal to guinea pig
• Inactive when released
21. Toxin – mechanism of action
• Fragment B : binds to a cell surface receptor
and helps in transport of toxin into the cell;
• After entering the cell, A subunit is released ;
• A subunit catalyses the transfer of ‘adenosine
diphosphate ribose (ADPR)’ from NAD+
• ADPR binds with the elongation factor EF 2
• “ADPR-EF2” complex is inactive protein
synthesis stops abruptly necrotising and
neurotoxic effects of the toxin;
22.
23. PATHOGENICITY
• Commonest site of infection: Upper respiratory
tract (fauces, larynx,nose)
• Ocassionally, other cutaneous or
mucocutaneous areas ( otitic/conjunctival/
genitovulval/vaginal/ prepucial/skin)
• Faucial diphtheria is the commonest type;
• Sore throat is frequently the presenting
symptom;
24. PATHOLOGY
• After infection, the bacilli multiply on the
mucous membrane or skin abrasion;
• The toxigenic strains start producing toxin;
• Diphtheria is a ‘toxemia’;
• The bacteria confine to the site of entry but
the exotoxin is absorbed into the mucus
membrane and causes destruction of
epithelium and a superficial inflammatory
response;
25. PATHOLOGY
• The toxin causes local necrotic changes;
• The resulting fibrinous exudate, together with
the epithelial cells, leucocytes, erythrocytes
and bacteria constitute : “pseudomembrane”
• Any effort to remove it will tear off capillaries
beneath it and cause bleeding;
• Mechanical complications are due to
pseudomembrane and systemic effects are
due to the toxin;
26. Toxin-systemic absorption
• The bacilli continue to produce the toxin;
• The toxin is absorbed systemically and damages
heart muscle, liver, adrenals etc.;
• The toxin also cause nerve damage, especially of
soft palate(palatine) and eye muscles (ciliary);
• Toxin absorption is negligible in case of skin
infection with toxigenic strains;
• Nontoxigenic strains can also produce local
disease but systemic effects are absent;
27. CLINICAL DISEASES
• Incubation period : usually 3-4 days;
• Acute infection : in the form of –
– Membranous tonsillitis
– Nasal infection
– Laryngeal infection
– Skin infection –uncommon;
28. CLINICAL DISEASES
• Characteristic feature is :
‘wash –leather’ eleveted
greyish greeen
membrane in the tonsils
with a well defined edge
surrounded by a zone of
inflammation;
30. CLASSIFICATION BASED ON CLINICAL SEVERITY
• Malignant or hypertoxic:
– ‘Bull neck’ due to marked adenitis in neck;
– Severe toxemia
– Circulatory failure
– Death
– Paralytic squealae in survivors
• Septic : ulceration, cellulitis and gangrene
around pseudomembrane;
• Hemorrhagic: bleeding from the edge of
pseudomembrane, epistaxis, purpura etc.
31. Bull neck : due to cervical adenitis and
edema of neck
32. COMPLICATIONS
• Asphyxia : due to mechanical obstruction
Emergency tracheostomy may be necessary;
• Acute circulatory failure
• Myocarditis
• Postdiphtheritic paralysis-
palatine(soft palate) and ciliary ( eye muscles)
nerves
Recovery – spontaneous and complete
• Septic : pneumonia and otitis media
• Relapse : in about 1% of cases
33. LABORATORY DIAGNOSIS
• This is to confirm the clinical impression and
for epidemiological purpose;
• Specific treatment must never be delayed for
laboratory reports, if the clinical picture is
strongly suggestive of diphtheria;
• Any delay may be fatal…!
• Laboratory diagnosis consists of the isolation
of the organism and demonstration of it’s
toxicity;
34. LABORATORY DIAGNOSIS
• Specimens :
– Swabs from – nose, throat or other suspected
lesions;
• Smear examination: Gram stain
– shows beaded rods in typical arrangement;
– Difficult to differentiate from some commensal
corynebacteria normally found in throat;
– Albert’s stain or Neisser’s stain is useful for
demonstrating the granules;
35. Numbers of large-sized Gram-positive rods are
embedded within the pseudomembrane (Gram).
LABORATORY DIAGNOSIS
36. LABORATORY DIAGNOSIS : CULTURE
• If the swabs can not be inoculated promptly, they
should be kept moistened with serum;
• Inoculate on :
– Loeffler’s serum slope
– Tellurite blood agar or Tinsdale medium
– Blood agar ( for differentiating Staphylococcal or
Streptococcal pharyngitis that simulate
diphtheria);
• Tellurite medium is particulary useful for isolating the
organism from – convalescents, contacts or carriers;
37. LABORATORY DIAGNOSIS : CULTURE
• Processing :
– Serum slope may show growth in 4-8 hrs but if
negative may need to be incubated for 24 hrs;
– Smear may show ‘diphtheria-like’ organisms;
– By about 48 hrs, Tellurite plates will yield growth;
– The isolate must be submitted for – ‘Virulence tests’
or ‘Toxigenicity tests’ before the bacteriological
diagnosis is complete;
38. VIRULENCE TESTS
• In vivo methods:
– Subcutaneous test
– Intracutaneous test
• In vitro methods:
– Elek’s gel precipitation test
– Tissue culture test
39. SUBCUTANEOUS TEST
Emulsify the growth form an overnight culture
of Loeffler’s serum slope in 2-4 ml broth
0.8 ml injected subcutaneously
Into two guinea pigs
Protected with
500 IU of antitoxin
18-24 hrs previously
Unprotected
Die in 4 days if the strain is
Virulent; autopsy shows
Characteristic features
Remain healthy
Disadvantage : Death of the animal
Control animal
Test animal
40. INTRACUTANEOUS TEST
0.1 ml of emulsion broth inoculated
intracutaneously in to two guinea pigs
Control animal Test animal
Should receive 500 IU
Of antitoxin previous day
Give 50 IU of antitoxin
Intraperitoneally
4 hrs after skin test
(To prevent death)
Inflammatory reaction
Progress to necrosis in 48-72 hrs
NO CHANGE
41. INTRACUTANEOUS TEST
• Animal does not die;
• Rabbits may also be used;
• As many as 10 strains can be tested
simultaneously;
42. Elek’s gel precipitation test
• In vitro test;
• A rectangular strip of filter paper is saturated
with the diphtheria antitoxin(1000 units/ml);
• This strip is placed on : agar plate with 20%
horse serum, while the medium is setting;
• The cultures to be tested are streaked at right
angles to the filter paper strip;
• A positive and negative control should be put;
44. After incubation – line of precipitation can be observed
Where the toxin and antitoxin meet at optimum conc.
The lines of precipitation will indicate that
the test strain is toxigenic
P T N
45. Tissue culture test
• Bacteria incorporated into an agar overlay of
cell culture monolayers;
• The toxin, if produced, diffuses into the cells
below and kills them;
46. EPIDEMIOLOGY
• Mainly a disease of childhood(pediatrics) in endemic
areas – uncommon below 1st year; peaks at 5.
• In nature, C.diphtheriae occurs in the respiratory
tract, in the wounds or in the skin of the infected
persons or carriers;
• Transmission is by-
– Droplet dissemination from cases or carriers
– Direct contact
– Occasionally, fomites;
• Nasopharyngeal or cutaneous carriage of toxigenic or
nontoxigenic strains can persist for life in healthy
people;
47. PROPHYLAXIS
• Diphtheria can be controlled by immunisation;
• Types of immunisation available for
diphtheria:
– Active
– Passive
– combined
• The objective of immunisation is to increase
protective levels of antitoxin in circulation;
48. Active immunisation
• Emil von Behring initiated immunisation for
diphtheria in children in 1913 using toxin –antitoxin
mixtures; (TAT)
• These preparations were hazardous;
• Danysz phenomenon: if the equivalent amounts of
toxin and antitoxin were mixed all at once, the final
preperation was nontoxic. But, if the same amount of
toxin was added in instalments, the resultant mixture
was toxic;
• In 1929, Ramon introduced ‘toxoid’.
49. Active immunisation - toxoids
• Two preparations of toxoid are available:
– Formol toxoid
– Adsorbed toxoid
• Formal toxoid : prepared by incubating the
toxin with formalin for 3-4 weeks;
• Adsorbed toxoid : purified toxoid is adsorbed
onto an adjuvant, either aluminium phosphate
or aluminium hydroxide; this is more
immunogenic;
50. Active immunisation - toxoids
• Adsorbed toxoid –given as IM injections
• Recommended vaccines:
– As a trivalent preperation : DPT (adsorbed
Diphtheria/Pertusis/Tetanus)
– Adsorbed Diphtheria/Tetanus (DT)
– Adsorbed low dose diphtheria vaccine for adults (d)
– Adsorbed Tetanus/low dose diphtheria vaccine(Td)
for adults;
– A quadraple vaccine containing DPT+inactivated
polio vaccine is also available;
51. Active immunisation- schedules
• Primary immunisation:
– 3 doses of DPT begening at 4th week of age, 8th and
12th week under Routine Immunization
schedule(Govt. of Tanzania)
• Booster (DPT) at 15-18 months of age;
– Further booster, as ‘DT’ at – 5 years of age;
• Dosage : 0.5 ml
– 10-25 Lf units of toxoid - recommended for
children
52. Active immunisation- schedules
• Contraindications:
– Acute febrile illness : postpone till recovery
– Severe local or systemic reaction to pertusis
component of DPT are likely; if they occur,
immunise with DT; acellular pertusis vaccine can be
added if the reaction is a local one;
53. Passive Immunisation
• Using antitoxin or
ADS(Antidiphtheritic serum);
• As an emergency measure when
susceptibles are exposed to
infection;
• Subcutaneous administration of
500-1000 units of antitoxin or
ADS(Antidiphtheritic serum);
• Risk of hypersensitivity as horse
serum used;
Historical engraving showing
how the medicinal serum was
obtained from
immunized horses.
54. Combined immunisation
• Administration of first dose of toxoid on one
arm, while ADS is given on the other arm, to
be continued by full course of active
immunisation;
• All cases that received prophylactic ADS
should receive combined immunisation;
55. TREATMENT
• Specific measure : prompt administration of antitoxin
to neutralize the circulating toxin;
– Dose: 20,000-1,00,000 units
– Half the dose given IV
– Antitoxin treatment is generally not indicated for
cutaneous diphtheria
• Antibiotics : Penicillin or Erythromycin for 14 days;
• Complete bed rest;
• Supportive therapy and treatment of complications
• Erythromycin: for treatment of carriers.
57. C.ULCERANS
–Resembles gravis biotype of C.diphtheriae
–Liquify gelatin, ferment trehalose slowly,
does not reduce nitrates;
–Produce two types of toxins;
–Guinea pigs: lesions similar to those of
C.diphtheirae;
–Cause infection in cows;
–Human infections may be transmitted
through cow’s milk;
–Diphtheria antitoxin is protective;
58. OTHER CORYNEBACTERIA
• Arcanobacterium(C.hemolyticum):
– pharyngitis and skin ulcers
• C.jakeium:
– cutaneous and blood stream infections in
immunocompromised; multi resistant;
• C.pseudotuberculosis: Preisz Nocord bacillus
– Pseudotubeculosis in sheep and lymphadenitis in
horses;
• C.minutissimum:
– Erythrasma, affecting axilla and groin
• C.tenuis: pigmented nodules around axillary and pubic
hair shafts.
• C.parvum: an immunomodulator agent
59. DIPHTHEROIDS
• Resemble C.diphtheriae and mistaken for them;
• Common commensals of nose, throat, nasopharynx,
skin, urinary tract and conjunctiva
• Produce no exotoxin;
• Stain more uniformly, few or no metachromatic
granules and tend to be arranged in palisades;
• Can produce disease in immunocompromised;
• Have been isolated in infections such as endocarditis
of prosthetic valves, lung abscess and UTI;
• Sensitive to Vancomycin;
• Ex. C.pseudodiphtheriticum – throat
• C.xerosus : conjunctival sac