This document discusses infections of the ear, nose, and throat. It describes the anatomy and defenses of the ear canal and middle ear. Common bacterial causes of otitis externa and media are Staphylococcus aureus and Streptococcus pneumoniae. Chronic or recurrent otitis media can lead to hearing loss or involve unusual pathogens like mycobacteria. The document also reviews the anatomy of the nasal cavity and paranasal sinuses. Fungal rhinosinusitis and mucormycosis are important infections of the sinuses.
2021 laboratory diagnosis of infectious diseases dr.ihsan alsaimarydr.Ihsan alsaimary
2021 laboratory diagnosis of infectious diseases
dr. ihsan alsaimary
university of basrah - college of medicine- DEPARTMENT OF MICROBIOLOGY
POBOX 696 ASHAR
BASRAH 42001
IRAQ
Src jbbr-21-125 Dr. ihsan edan abdulkareem alsaimary PROFESSOR IN MEDICAL M...dr.Ihsan alsaimary
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Src jbbr-20-120 Dr. ihsan edan abdulkareem alsaimary PROFESSOR IN MEDICAL M...dr.Ihsan alsaimary
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Doi10.18535ijmsciv7i11.06 Dr. ihsan edan abdulkareem alsaimary PROFESSOR I...dr.Ihsan alsaimary
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Assessment of immunomolecular_expression_and_prognostic_role_of_tlr7_among_pa...dr.Ihsan alsaimary
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Estimation of Dr. ihsan edan abdulkareem alsaimary PROFESSOR IN MEDICAL MICR...dr.Ihsan alsaimary
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Tolerance & autoimmunity and organ specific autoimmune diseasesdr.Ihsan alsaimary
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Pathogenesis of microbial infections dr. ihsan alsaimarydr.Ihsan alsaimary
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
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
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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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.
Are There Any Natural Remedies To Treat Syphilis.pdf
Ear, nose and throat infections dr.ihsan alsaimary
1. Ear, Nose and
Throat infections
Dr. Ihsan Edan Alsaimary
Dept.Microbiology , College Of Medicine-
University Of Basrah , Basrah- Iraq
ihsanalsaimary@gmail.com
2. Ear canal
Ear canal 2.5 cm sac.
Cartilaginous covered
by layers of sebaceous
and apocrine glands
and hair.
The glands produce a
thin layer of ceruman.
3. Defence mechanisms of ear
Outer ear
Hair
Ceruman
Internal ear
External bony part of the labyrinth has
perilymph
Internal membrane part contains endolymph
4. Antibacterial properties of ceruman
Contains lysozyme.
Contains saturated fatty
acids.
Has a pH of 6.9
Lateral epithelium
migration towards external
os mechanically cleans the
ear canal.
Insufficient ceruman
predisposes to ear
infection.
5. Perforation of tympanic
membrane due to
insertion of a 'q' tip. This
is likely to result in both
an otitis media and otitis
externa
7. Ear swabs
Culture of ear swabs
Used for OE not very useful for OM
unless fluid from the middle ear is
swabbed
Neonatal screening
8. Acute OE
Majority of infections are due to
bacteria – Staphylococcus aureus,
Pseudomonas aeruginosa,
anaerobes
Fungal infections account for only
10%
9. Acute OE
Acute localised OE usually caused by
Staph.aureus which causes furuncles or
pustule of a hair follicle.
Acute diffuse OE. Also called ‘swimmers
ear’ and is associated with hot humid
conditions. Polymicrobial infections usually
involving Staph.aureus, pseudomonas and
anaerobes.
10. Treatment of acute OE
Usually using topical rather than systemic
antibiotics unless there is significant
infection of the pinna and surrounding
tissues.
In less severe cases topical antibiotics and
steroid are all that is required. In more
severe cases suction of debris and
application of wicks or packs of antibiotic
and steroids are required.
Aminoglycosides such as neomycin or
11. Chronic otitis externa
External auditory canal with
Aspergillus overgrowth
manifesting as a cottony matrix
topped by small black balls.
Chronic OE is usually
caused by colonization
by coliforms or fungi
and is best treated by
topical cleansing
rather than antibiotic
treatment.
Rarely caused by
syphilis or leprosy
12. Malignant otitis externa
Malignant external otitis with pus
draining from the necrotic ear canal
and underlying osteomyelitic bone.
Life threatening condition
affecting diabetics, the
immunocompromised and
elderly.
Severe necrotizing infection of
soft tissues, bones, blood
vessels and cartilage with risk
of neurological involvement
and facial paralysis.
The patient requires hospital
admission and treatment with
high dose antibiotics, surgery
to debride dead tissue and
occasionally hyperbaric
treatment.
13. Non-bacterial cause of OE
Ramsey Hunt Syndrome –
Herpes Zoster Oticus. Severe
otalgia, facial paralysis and
varicelliform rash over the
pinna. Treated with antivirals.
14. Otitis media
Occurs between the ear drum and the inner
ear and includes the eustachian tube.
It is defined by the accumulation of fluid in
the middle ear with symptoms of acute
infection.
Serous OM or Sterile OM does occur and is
often attributed to an allergy or radiation
treatment.
15. Acute Otitis media
Usually caused by migration of bacteria from the
naso-pharynx up the eustachian tube and into the
ear.
Common disease of children (80% - 90% by the
age of 2 years old) with frequent recurrence of
infection. The highest incidence rate is between 6-
24 months old.
This is because up to the age of seven years the
eustachian tube is relatively short, and more
horizontal than in older children & adults.
It is important to treat as it can lead to hearing loss
and affect the speech and behaviour of children.
16. Acute OM (pathogens)
Often viral – RSV and parainfluenzae
Can lead to bacterial infections usually due
to S.pneumoniae, H.influenzae and
Moraxella species.
Less commonly S.pyogenes, S.aureus,
enterobactericaea and anaerobic Gram
negative non-sporing rods such as
Prevotella, Fusobacteria, Porphyromonas
and Bacteroides .
17. Chronic OM
Caused by perforation of the tympanic membrane
or problems with immune function.
Very destructive and persistent and can result in
loss of hearing. May be associated with
mastoiditis.
Commonly caused by pseudomonades and
S.aureus including MRSA. Anaerobes and fungi
are found in a quarter of cases. More likely to be
polymicrobial than acute OM.
Can be caused by viruses – RSV, Influenza,
enteroviruses & rhinoviruses. Other unusual bacteria
Alloiococcus otitidis - Gram positive cocci
Turicella otitidis – Gram positive bacilli
18. Mycobacterium OM
Mycobacterium tuberculosis
Incidence 0.04% - 0.9%
Can get to ear by haematogenous route,
regurgitation through the eustachian tube,
through previously existing tympanic
membrane perforations, or direct extension
of a nasopharyngeal site of infection.
19. Evaluation of patient
History of contact with TB.
Culture and staining of ear fluid for AAFB.
Chest X Ray, urinalysis and sputum
Microscopy & culture for AAFB.
LP if CNS involvement suspected.
Treatment
6 – 9 month treatment with isoniazid,
rifampicin and pyrazinamide.
20. Parasites
Ascaris worms have
been found in the
middle ear causing
chronic OM after
migrating from the
naso-pharynx via the
eustachian tube.
21. Treatment of OM
Oral antibiotics.
Surgical treatment by
Myringotomy. Allow
fluids to drain out can
be used with
Tympanostomy tubes.
22. Myringitis
Inflammation of the tympanic
membrane
Myringitis can be caused by bacteria
such as S.pneumoniae, M.
pneumoniae, H.influenzae or viruses
such as Herpes zoster and influenza.
Bacterial infections are usually treated
with antibiotics.
24. Nose
External region is composed of a framework
of bone & cartilage overlain with skin and
lined with mucous membrane. The external
nares lead to a vestibule lined with skin
bearing hairs for coarse filtering.
Inner nasal cavity lies above the mouth and
communicates with the pharynx via 2
internal nares. 4 paranasal sinuses also open
into this cavity. The inner nose is also lined
by a mucous membrane which secretes
mucous. Its walls are thrown into a series of
25. Pharynx
Muscular and lined with a mucous
membrane.
Upper nasopharynx. Receives air from the
internal nares and also communicates, via 2
openings of the eustacian tubes, with the
ears. This is also the site of the adenoids.
Oropharynx. Lies behind the mouth and is a
common passage way for the respiratory and
digestive tracts. The 2 pairs of tonsils are
found here.
Lower laryngopharynx. The digestive and
26. Larynx
This connects the pharynx and
trachea. The epiglottis, a cartilage
overlying the larynx, moves like a
trapdoor to close off the remainder
of the respiratory tract during
swallowing of food.
28. Colonization resistance
Normal flora Respiratory pathogens that
can be carried
Transient colonisation
α haemolytic streptococci S. pyogenes Enterobacteriaceae
Neisseria species S. pneumoniae Pseudomonades
Diphtheroids H. influenzae Candida
Anaerobic cocci C. diphtheriae
Fusobacteria
Bacteroides
Micrococci
29. Nose swabs
Nasal carriage
S.aureus including MRSA
Lancefield group A streptococci
C. diphtheriae
Epistaxis – S.aureus carriage
30. Sinuses
Frontal sinuses (in the forehead)
Maxillary sinuses (behind the cheek
bones)
Ethmoid sinuses (between the eyes)
Sphenoid sinuses (behind the eyes)
31.
32.
33. Sinusitis
Sinusitis, nasal discharge.
Looking for: S.pneumoniae,
H.influenzae but may be caused by
‘S.milleri’ group and anaerobes
especially if the condition is chronic.
Nose swabs are no good. Pus, antral
wash outs, nasopharyngeal swabs or
ethmoid biopsies needed.
35. Mucormycosis
Most infections are life-threatening, and risk
factors, such as diabetic ketoacidosis and
neutropaenia, are present in most cases.
Severe infection of the facial sinuses, which
may extend into the brain, is the most
common presentation.
Successful treatment requires correction of
the underlying risk factor or factors,
antifungal therapy with amphotericin B, and
aggressive surgery.
Mucormycosis carries a very high mortality
36. Fungal balls
Sphenoidal and maxillary fungal
balls
Non-invasive
Headaches
Can lead to recurrent bacterial
infections and central nervous
system complications
37. Sphenoid fungal balls
Computed tomography scan of
the sinuses.
Axial view of sphenoid sinus
showing opacity, small
hyperdensities (white arrow) and
osteosclerosis (black arrow) of
the bone wall
Photography of the fungus ball, or truffle.
39. Rarely seen nasal infections
Rhinoscleroma
Caused by Klebsiella
rhinoscleromatis. Rare
form of chronic
granulomatous nasal
infection affecting nasal
passages and sinuses and
can include the larynx and
pharynx. Progressive –
tumour-like growths.
Found in Eastern Europe,
Latin America, Central
Africa and South East
Asia.Hebra nose
40. Rhinoscleroma
Endemic to North and Central Africa, Central and
South America and Southeast Asia.
Rhinoscleroma has been identified as an
opportunistic infection that can occur in patients
with HIV infections
There are three histologic stages of development of
rhinoscleroma. In the catarrhal stage, the mucosa
contains non-specific inflammatory changes with
neutrophils, cellular debris and granulation tissue.
In the proliferative stage, there is an intense
infiltrate of plasma cells and large foamy
histiocytes termed "Mikulicz cells" which contain
numerous rod-shaped bacteria within their
41. Rhinoscleroma
Diagnosis is usually made by the identification of
the Mikulicz cells in tissue biopsy. The bacteria
may be seen in H&E stained sections, but are
more easily identified with PAS, Geimsa or
Warthin-Starry stains.
Therapy is with traditional antimicrobial therapy -
streptomycin, tetracycline and trimethoprim-
sulfamethoxazole which may successfully treat
early lesions. Prolonged high dose oral
ciprofloxacin has been successful in achieving
resolution in patients with extensive disease.
Surgical debridement may be necessary in cases of
airway obstruction.
42. Rarely seen nasal infections
Ozaenia
Chronic atrophic rhinitis.
Can destroy the mucosa –
characterized by purulent, chronic
foul smelling nasal discharge.
Klebsiella ozaenae thought to be
the causative organism.
43. Rarely seen nasal infections
Rhinosporidiosis
Originally thought to be
fungus
It is a novel aquatic
protistan parasites
Mesomycetozoea
(DRIP clade)that infects
fish & amphibians as well
as man. Found in Eastern
Europe, South East Asia,
Central Africa & Latin
America.
Section of human nasal polyp stained
with periodic acid-Schiff (PAS) showing
Rhinosporidium seeberi cysts.
44. Rhinosporidiosis
Slow growing tumour like masses –
usually leading to unilateral obstruction
and polyp formation.
Diagnosis is by staining of tissue
biopsies.
Treatment by surgical excision
although relapses are common (10%).
Antimicrobial therapy ineffective.
46. Tonsillitis/pharyngitis
Streptococcus pyogenes
Scarlet fever
Non-suppurative post streptococcal sequelae:- Rheumatic
Fever. Glomerulonephritis.
Occur 2 -3 weeks after infection
Lancefield groups C & G
Vincents organisms
Viral – EBV, CMV, Enteroviruses, Adenovirus, Herpes
simplex, influenza viruses
Non-toxigenic Corynebacterium diphtheriae
Arcanobacterium haemolyticum
Candida
Neisseria gonorrhoeae
H. parainfluenzae
47. S. Pyogenes
Determinants of pathogenicity
Lipoteichoic acid Mediates adherence to bucchal mucosa,
complexes with M protein and binds to
fibronectin
M Protein Anti-phagocytic
Pyrogenic exotoxin (erythrogenic toxin)
A, B and C
All phage mediated.Dermal reactivity thought
to be a hypersensitivity reaction
Streptolysin O Extracellular
Oxygen labile
Antigenic
Membrane injury to cells
Streptolysin S Cell bound
Oxygen stable
Leucotoxic (after ingestion) to cell
NADase Especially produced by nephritogenic
strains (eg M12)
DNAase
A, B, C and D
Antigenic
48. Association of M types with disease
M type Pharyngitis Pyoderma
1 +++ ?
2 0 +++
3 ++ +/-
4 +++ +/-
12 ++++ +/-
25 ++ +/-
49 ++ ++++
55 0 +++
57 0 ++
49. Scarlet fever
Sore throat, fever, bright red tongue and fine
pinkish-red rash on the body that feels like
sandpaper to touch. It may start in one
place, but soon spreads to many parts of the
body, commonly the ears, neck, chest,
elbows, inner thighs and groin.
The rash does not normally spread to the
face, but the cheeks become flushed and the
area just around the mouth stays quite pale.
Streptococcal pyrogenic exotoxin A (SPE A)
(scarlet fever toxin)
Associated with M types:1, 3, 4, 6, 18, and 22
50. S. Pyogenes
Non-suppurative sequelae
Rheumatic fever
Causes arthritis, carditis, Sydenham chorea,
erythema marginatum and sub-cutaneous
nodules
Associated with phayngitis attack 3-4 weeks
previously
Common in children 6 -15 years old
Thought to be caused by antibody cross
reactivity. Characteristic rheumatic
granulomata develop in the connective
tissues and heart – Aschoff’s nodules.
Repeated attacks lead to valvular disease
51. S. Pyogenes
Non-suppurative sequelae
Acute glomerulonephritis
7-14 days post pharyngitis (or 14 -21
days post pyoderma)
Immune complexes in renal tubules
Associated with M types: 12 from
pharyngeal strains but 49 from
pyoderma
Clinical symptoms – Oedema, oliguria,
52. Complications of throat infections
Quinsy
Lemierre’s disease – infection of
the jugular vein which can lead to
septicaemia. Caused by
Fusobacterium necrophorum.
Epiglottitis – Haemophilus
influenzae
53. Fusobacterium necrophorum
Recurrent or persistent sore throat
3 -5 days anaerobic incubation on
supplemented blood plates such as
Fastidious Anaerobic Agar.
MAST-ID ring resistant to
vancomycin & sensitive to
kanamycin & colistin.
Colonies fluoresce green under UV
(300-412 nm)
54. Diphtheria
Diphtheria is an upper
respiratory tract illness
characterized by sore throat,
low fever, and an adherent
membrane (called a
pseudomembrane on the
tonsils, pharynx, and/or nasal
cavity.
Diphtheria toxin produced by
C. diphtheriae, can cause
myocarditis, polyneuritis, and
other systemic toxic effects. A
milder form of diphtheria can
be restricted to the skin.
58. Diphtheria
Gel diffusion test (ELEK plate) for C.diphtheria
toxin.
Outer strains are non-toxigenic, those in the
centre show toxin production. The anti-toxin
had been absorbed with non-toxic proteins
obtained from a non-toxigenic culture and thus
behaved as a monospecific antiserum. The
intersection of the bands with the bacterial
growth is removed some distance from the
piece of filter paper impregnated with
antiserum because horse anti-toxin has been
employed, which inhibits the precipitin
reaction in the region of antibody excess. Note
that the lines of precipitate generated by the 2
toxigenic strains merge to form arcs, indicating
that the toxins elaborated are immunolog
ically identical. (King et al, Am. J. Pub. Health,
1949, 39, 1314).
59. The Diphtheria Toxin
(DTx) Monomer. A (red)
is the catalytic domain; B
(yellow) is the binding
domain which displays the
receptor for cell
attachment; T (blue) is the
hydrophobic domain
responsible for insertion
into the endosome
membrane to secure the
release of A. The protein is
illustrated in its "closed"
configuration.
60. Oral thrush
Overgrowth of
Candida albicans due
to:
Broad spectrum
antibiotic therapy
Impaired immunity –
eg leukaemia,
lymphoma, AIDS
Diabetes
61. Whooping cough
The first recorded
outbreaks were in the 16th
century
B. pertussis was isolated
in pure culture in 1906 by
Jules Bordet and Octave
Gengou
The term whoop
originates from the
inflammation and
swelling of the laryngeal
structures that vibrate
when there is a rapid
inflow of air during
inspiration. Jules Bordet
62. Vaccines
Historically, the whooping cough vaccine has been
administered as a merthiolate-killed bacterial cell
suspension which is part of the DTP vaccine
Children are vaccinated at two, three and four months and
again before they start school
Immunity is not lifelong and older teenagers and adults are
still susceptible to whooping cough
Unfortunately, about 20% of the children that receive the
whole cell vaccine experience mild side effects. About 0.1%
of infants experience convulsions soon after receiving the
vaccine and in a very small number of cases (1 in 150,000?)
severe or irreversible brain damage may occur.
Acellular pertussis has fewer side effects than the whole cell
vaccine
63. Methods for detection
Culture
Direct immunofluorescence
PCR
Serology
B. pertussis can only be recovered for
the first 3 weeks of infection
PCR can be of use for a further 3 weeks
Serology
64. Pernasal swab
With the patient's head
immobilized, a swab
should be gently
inserted into the nostril
until it reaches the
posterior nares and is
then left in place for a
few seconds. The
tickling sensation of
the swab usually
induces a cough.
67. 1-Colonisation stage
Catarrhal stage. Fever & cough, worse at
night. ‘Runny nose’ and sneezing.
Organism readily isolated from pharyngeal
cultures.
Severity and duration of illness can be
reduced by antibiotic treatment
(erythromycin).
Adherence mechanisms - Filamentous
Haemagglutinin (FHA), a fimbrial like
structure and cell bound Pertussis Toxin
68. 2-Toxaemic stage
Spasmodic (Paroxysmal) stage.
Paroxysms of coughing followed by
inspiratory whoop.
Apnoic attacks & cyanosis.
B.pertussis rarely recovered.
Antimicrobial agents no effect on
progress of disease.
69. 3-Recovery stage
Gradual abatement of disease
The cough is very persistent, long after
infection is past and may last for 2 or 3
months. It was called 'the 100 days' cough'.
Complications:
Bronchopneumonia (commonly with H.
influenzae or S. pneumoniae.
Atelectasis leading to bronchiectasis.
Convulsions leading to brain damage.