Bacterial infections can cause a variety of diseases. Scarlet fever is caused by Streptococcus pyogenes and presents with a characteristic rash. Tetanus is caused by Clostridium tetani and causes muscle spasms. Tuberculosis is caused by Mycobacterium tuberculosis and commonly affects the lungs, causing cough and weight loss. It can be diagnosed by smear or culture and treated with antibiotics.
Gingivitis is defined as the inflammation of gingival tissue.Gingival inflammation has two components: the acute
inflammatory component, with vasodilation, edema, and
polymorphonuclear infiltration, and the chronic inflammatory
component, with B and T lymphocytes and capillary
proliferation forming a granulomatous response.
Gingivitis is a form of gum disease characterised by reversible gingival inflammation without destruction of tooth-supporting tissues, periodontal ligament or bone
Gingivitis is defined as the inflammation of gingival tissue.Gingival inflammation has two components: the acute
inflammatory component, with vasodilation, edema, and
polymorphonuclear infiltration, and the chronic inflammatory
component, with B and T lymphocytes and capillary
proliferation forming a granulomatous response.
Gingivitis is a form of gum disease characterised by reversible gingival inflammation without destruction of tooth-supporting tissues, periodontal ligament or bone
Swollen lymph nodes usually occur as a result of infection from bacteria or viruses. Rarely, swollen lymph nodes are caused by cancer. Your lymph nodes, also called lymph glands, play a vital role in your body's ability to fight off infections. They function as filters, trapping viruses, bacteria and other causes of illnesses before they can infect other parts of your body. Common areas where you might notice swollen lymph nodes include your neck, under your chin, in your armpits and in your groin.
In some cases, the passage of time .Hard, swollen or tender lymph nodes
Itchy skin, Lump, or mass that can be felt beneath the skin, Rash
Redness, warmth or selling immune system disorders
Lupus — a chronic inflammatory disease that targets your joints, skin, kidneys, blood cells, heart and lungs
Rheumatoid arthritis — a chronic inflammatory disease targeting the tissue that lines your joints (synovium)
Cancers
Lymphoma — cancer that originates in your lymphatic system
Leukemia — cancer of your body's blood-forming tissue, including your bone marrow and lymphatic system
Other cancers that have spread (metastasized) to lymph nodes
Swollen lymph nodes usually occur as a result of infection from bacteria or viruses. Rarely, swollen lymph nodes are caused by cancer. Your lymph nodes, also called lymph glands, play a vital role in your body's ability to fight off infections. They function as filters, trapping viruses, bacteria and other causes of illnesses before they can infect other parts of your body. Common areas where you might notice swollen lymph nodes include your neck, under your chin, in your armpits and in your groin.
In some cases, the passage of time .Hard, swollen or tender lymph nodes
Itchy skin, Lump, or mass that can be felt beneath the skin, Rash
Redness, warmth or selling immune system disorders
Lupus — a chronic inflammatory disease that targets your joints, skin, kidneys, blood cells, heart and lungs
Rheumatoid arthritis — a chronic inflammatory disease targeting the tissue that lines your joints (synovium)
Cancers
Lymphoma — cancer that originates in your lymphatic system
Leukemia — cancer of your body's blood-forming tissue, including your bone marrow and lymphatic system
Other cancers that have spread (metastasized) to lymph nodes
ATYPICAL MYCOBACTERIAL INFECTIONS AND THEIR MANIFESTATIONSDR. MOHNISH SEKAR
Infections caused by nontuberculous mycobacteria (NTM) are increasing for several reasons, including diagnostic advances, increased awareness and a larger at-risk population. NTM pulmonary disease is surpassing tuberculosis (TB) in some low incidence areas.
Granulomatous diseases of the head & neckMammootty Ik
covers all the important granulomatous diseases of head and neck region with a brief and to-the-point description of pathogenesis, clinical features , differential diagnosis and management of each disorder
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
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
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.
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.
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
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
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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
3. BACTERIA
2
Bacteria constitute a large domain or kingdom of
prokaryotic microorganisms. Typically a few
micrometres in length, bacteria have a wide range of
shapes, ranging from spheres to rods and spirals
5. Highly contagious systemic infection
Predominantly in children
β – hemolytic streptococci (Streptococcus pyogens)
Organisms produce an erythrogenic toxin
Attacks blood vessels, produces characteristic skin rash
Scarlet Fever (Scarlatina)
4
6. Clinical features
• The microorganism enters the body usually through pharynx
• Incubation period: 3-5 days
• Pharyngitis
• Tonsillitis
• Headache, chills, fever, vomiting.
• Sand paper skin
5
7. • Enlargement & tenderness of cervical lymph nodes
• Characteristic diffuse, bright scarlet skin rash which appears on
the 3rd day– “sun burn” with “goose pimples”
• When the rash is prominent in areas of skin folds – “Pastia
lines”
• Rash clears in 1 week followed by period of desquamation for
3 – 8 weeks.
6
8. Oral manifestations
Scattered petechiae on soft palate.
First 2 days – white coating on dorsal surface of tongue
through which only fungiform papillae seen (white strawberry
tongue)
By 4th or 5th day – white coating desquamates, reveals
erythematous dorsal surface with hyperplastic fungiform
papillae – (red strawberry tongue or raspberry tongue)
8
9. 11
Stomatitis Scarlatina- small punctate red macules appear on hard &
soft palate & uvula
o Congested mucosa of palate
o Fiery red colour throat
o Tonsils-swollen & grayish exudate
Complications:
Peritonsillar abscess
Rhinitis
Sinusitis
Otitis media
11. Tetanus (Lock-Jaw)
Acute infection of the nervous system
Causative organism: exotoxin of anaerobic gram +ve bacilli
“Clostridium tetani”.
Characterized by intense activity of motor neurons & results
in the severe muscle spasm.
13
Incubation period: 6-10 days
Can enter body through trauma
Pathogenesis- Tetanospasmin
12. Clinical features
Characterised by involvement of multiple muscles
Lock Jaw- Trismus due to spasm of masseter, rigid abdomen and
stiff proximal limb muscles.
Prolonged contraction of facial muscles results in grimace or
sneer called as Risus scardonicus.
Contraction of back muscles produces an arched back called
opisthotomus.
Spasms occur spontaneously/ slight stimulation
14
13. Other features- Dsyphagia, restricted chest movement, layrngeal
spasm leading to asphyxia.
Local Tetanus:
• Manifest as spasm of muscles near the wound
•Cephalic Tetanus- trismus and facial palsy
•Occur after head inury or ear infection
15
14. Treatment
Aim:
• To remove spores at the sites of the wound
• Prevent toxin production
• Neutralize unbound toxins
• Prevent muscular spams
• Antibiotics should be given to erradicate source of toxins:
• Penicillin 10-12 million units IV x 10 days
• Metronidazole 1g / 12hrs
17
15. Antitoxin:
• Injected to neutralize circulating toxin and unbound toxin within
wound.
• Human tetanus immunoglobin (TIG)
Prophylaxis
• Wound debridement and booster dose of TT
• ATS (Anti tetanus sera) 1500 units or TIG 250 units
• Active Immunization: 3 doses of triple vaccine in 1st year of life
• Booster dose – 5 to 10 year interval
16. Diphtheria
Acute Infectious and communicable disease
Skin and mucous membrane
Causative organism: Corynebacterium diphtheriae
Produces lethal exotoxin causing tissue necrosis.
Humans only reservoir
Characterised by local inflammation and grayish
pseudomembrane
Mode of spread: 1. Direct skin contact
2. Respiratory droplets
18
17. Clinical features
19
Incubation period: 2-5 days
Types of diphtheria: Tonsillar, Pharyngeal, Laryngeal
Clinically:
Malaise, headache, fever , Sore throat
Mild redness & edema of pharynx
Tender enlargement of lymph nodes
Edema of neck, submandibular region & anterior part of the
neck giving “bull neck” appearance
18. Oral manifestations
Oropharyngeal exudate – begins from one or both tonsils as
patchy, yellow white, thin film.(diphtheritic membrane)
Thickens to form adherent grayish green covering.
May develop patches of green or black necrosis.
Involve entire soft palate, uvula, larynx or trachea.
21
19. Laboratory Diagnosis
Direct Microscopy: smear stained with albert stain
show “Chinese Letter” or “Cuneiform Arrangement”.
The bacilli look green and
Metacromatic granules appear bluish black
23
20. Treatment
Antidiphtheritic toxins (ADS) combined with
antibiotics – Once disease has developed
Erythromycin, procaine penicillin or i.v. penicillin
Prevention : By immunization of “diphtheria toxoid”
DPT vaccination (Diptheria toxoid, tetanus toxoid
and pertusis.
Given 3 doses from age of 3 years , interval of 4-6
weeks
Booster dose after 1 year.
24
21. Tuberculosis (Koch's disease)
(acid fast
It is an chronic granulomatous inflammation.
Causative organism: Mycobacterium tuberculosis
bacilli)..
Incidence: more common in poor countries of Africa, Latin
America &Asia.
• Mode of transmission: Small air borne droplets generated by
coughing, sneezing, talking of a person with tuberculosis.
Pulmonary TB is the chief form of the disease although it may
also occur in any part of the body including major organs such
as kidney, liver, bone etc..
25
23. Pathogenesis of Primary tuberculosis
Droplet spread & inhalation
Goes in to the lung alveoli
Engulfed by alveolar macrophages
Multiply within macrophages
Either host cells overcome bacteria, or vice versa
28
24. Clinical features
• Episodic fever, chills, fatigability, malaise.
• Gradual loss of weight
• Persistent cough with or with out hemoptysis.
• Night sweating, dyspnea.
30
25. Extra – pulmonary TB
• May involve lymph nodes, skin, skeletal system, CNS, kidneys
& GIT
Scrofula: Involvement of cervical lymph nodes
• Swelling, tenderness of lymph nodes.
• Involvement of TMJ
• Involved nodes may develop:
• Cold Abscess
• Lupus vulgaris –
• involvement of the skin
31
26. Oral manifestation
Do occur but are relatively uncommon (0.1%)
Lesions of oral mucosa are seldom primary, but they are
secondary to pulmonary diseases.
Organisms are carried in the sputum & enter the mucosal tissues
only if there is a break or a breach in the mucosal surface.
Organisms may be carried to the oral tissues by the
hematogenous route, deposited in the submucosa & may
proliferate & ulcerate the overlying mucosa.
33
27. Lesions may occur at any site in oral mucosa, but the tongue is the
most common site followed by palate, lips, buccal mucosa,
gingiva & frenum.
Usually the TB lesion is irregular, superficial or deep, painful ulcer
which tends to increase in size.
Less frequent –nodular, granular or firm leukoplakic areas
TB gingivitis – manifests as diffuse, hyperemic, nodular or
papillary proliferation of gingival tissues.
34
29. Diagnosis.
Staining of the smear prepared from sputum by Ziehl-Neelsen
stain
Chest radiograph
OPG
Fine needle aspiration of Lymph nodes
Bacterial culture in Lowenstein-Jensen media
Mantoux Test (Tuberculin test)
42
30. TUBERCULIN TEST
Mantoux Test:
•Hypersensitivity reaction to tubercular antigen
• Ten units of purified derivative in 0.1 ml normal saline
is injected intradermally in flexor aspect of the forearm.
• Test is positive if 2-4 days later there is inflammatory
reaction with surrounding erythema (not less than
5mm).
• Inference: Size of the inflammatory reaction
43
31. Treatment
• First line of drugs: Rifampicin, Isoniazid, Ethambutol,
Pyrazinamide, Sterptomycin
• Second line of drugs: Cycloserine, ethionamide, Amikacin,
Levofloxacin, Moxifloxacin
Regimen:
Initial phase ( 2 months): PYRAZINAMIDE + ETHAMBUTOL +
RIFAMPICIN+ ISONIAZID
Continuation phase (4 months): RIFAMPICIN+ ISONIAZID
44
32.
33. Directly Observed Therapy (DOT)
• Means that a Trained healthcare worker or other designated
individual (excluding a family member) provides the prescribed
TB drugs and watches the patient swallow every dose.
BCG Vaccine
•Prepared from the strain of attenuated live bovine tuberculosis
bacillus, Mycobacterium Bovis.
•80 % effective in preventing TB for 15 years
34. Leprosy(Hansen's Disease)
Chronic granulomatous infection.
Causative organism: Mycobacterium leprae (AFB)
Slightly contagious disease.
Mostly documented in Brazil, Indonesia, Myanmar &
Nigeria
Modes of transmission: Direct contact, Materno fetal
transmission
Types: Paucibacilliary and Multibacillary
46
35. Clinical features
Tuberculoid lesions: (paucibacillary)
Small number of well circumscribed, hypopigmented skin lesions
Nerve involvement results in anesthesia of affected skin
Accompanied by loss of sweating.
Oral lesions are rare
47
36. Lepromatous lesions: (multibacillary)
Begins slowly with numerous, ill defined, hypopigmented
macules or papules.
With time, lesions become thickened
Hair on eyebrows & eyelashes often lost.
Nerve involvement – leads to loss of sweating
49
37. Oral manifestations
Facial involvement common
Skin enlargement leads to distorted facial features (leonine facies)
Nasal involvement – nose bleeds, stuffiness, loss of smell
Collapse of bridge of nose – pathognomonic
52
38. Small tumor like masses-“LEPROMAS” develop on the
tongue, lips & hard palate – break down & ulcerate.
Gingival hyperplasia with loosening of the teeth.
54
39. Histopathologic features
Paucibacillary type – granulomatous inflammation with well formed
clusters of epitheloid histiocytes, lymphocytes & giant cells.
Paucity of organisms – can be demonstrated only with acid fast
staining.
Multibacillary type – no well formed granulomas.
Sheets of lymphocytes mixed with vacuolated histiocytes called as
“Lepra cells”
56
50. Noma (Cancrum Oris, Gangrenous
Stomatitis)
It is a rapidly spreading gangrene of the oral & facial tissues.
Seen commonly in debilitated or nutritionally deficient
children.
Occurs chiefly in persons who are undernourished
61
Considered a 2o complication of systemic disease rather then a
primary disease.
Appears to originate as a specific infection by the Vincent’s
organism.
Fusobacterium, Prevotella intermedia, Borrelia
vincentii, Porphyromonas gingivalis
51. Clinical features
Begins as a small ulcer of the gingival mucosa.(NUG)
Rapidly spreads and involve the surrounding tissues of the
jaws, lips & cheeks by gangrenous necrosis.(NUS)
The over lying skin becomes inflamed, edematous & finally
necrotic.
Line of demarcation develops between healthy & dead tissue.
63
52. • Large masses of tissue may sloghout,
leaving the jaw exposed
• Commencement of the gangrene is denoted
by the appearance of blacking of the skin.
• Subcutaneous fat pad & buccal fat pad
undergo necrosis.
• Odor arises from the gangrenous
tissue which is extremely foul.
• Occasionally the tongue & palate are
involved.
53. Lesion not restricted by tissue planes.
Patients have high temperature during the course of the
disease.
They usually suffer from 2o infections and may die from
toxemia or pneumonia
65
54. Treatment
Systemic Antibiotics (penicillin & metronidazole)
Wound care
Correction of nutrition, hydration & electrolyte imbalance
68
55. Actinomycosis
Chronic granulomatous, suppurative & fibrosing disease.
Caused by anaerobic, gram+ve, non
acid fast, branched, filamentous
bacteria.
Actinomyces israelii most common causative agent,
A. viscosus second
It is characterized chiefly by the formation of abscesses
which tends to drain by the formation of sinus tracts.
69
56. Classification
Classified anatomically according to the location of the lesion
1) Cervico-facial Actinomycosis
55%
1) Abdominal Actinomycosis
25%
1) Pulmonary Actinomycosis
15%
70
57. Clinical features
May either be an acute, rapidly progressing infection or
slow progressing, chronic lesion.
Organism enters the tissue though the oral mucous
membrane.
May either remain localized in the mucous membrane itself
or might spread to involve the salivary glands, bones or skin
Swelling & induration of the tissues
Develop into one or more abscesses which later rupture to
liberate pus which contain “sulphur granules”.
71
58. o Skin over these abscesses is purplish red in color.
o These abscess areas after rupturing do heal but due to
chronicity of the disease , by the time one abscess heal the
other abscess is ready to rupture & perforate the skin
surface.
o Thus the patient over a period of time shows scars and
disfigurement of skin.
o The induration of soft tissues my get extended to
the underlying bones (maxilla & mandible)
o Mandible is more commonly involved than maxilla, if at
all maxilla is involved it may also involve cranium.
72
59. Histopathology
Granulomatous inflammation showing central abscess
formation, which shows typical bacterial colonies.
Colonies appear to be floating in a sea of PMNL’s with
giant cells & macrophages around the periphery.
The individual colony appear round or lobulated, made up
of a meshwork of filaments in a rosette pattern.
Filaments stain with hematoxylin, but shows eosinophilia
of the peripheral club shaped end of the filaments (ray
fungus)
75
60. Treatment
Chronic fibrosing cases – Antibiotics along with
drainage and excision of sinus tracts.
Mild Cases:
Oral Penicillin V 3-4 g/day or 4million units i.m daily
If allergic to penicillin – Tetracycline 500mg/6hrs
In case of Cervicofacial actinomycosis- 5- 6 weeks
Deep seated – 12 months
Severe Cases:
Penicillin 20 million unit IV for 2-6 weeks followed
by Oral dose for for 6- 12 months
77
61. Syphilis (Lues)
Syphilis is a sexually transmitted chronic infection caused by
Treponema pallidum
Characterized by an incubation period of about 2 to 6 weeks.
Infection goes through a classic evolution characterized by 3 stages
- Primary syphilis
- Secondary syphilis
- Tertiary syphilis
78
62. Etiology
The usual mode of transmission is through
- sexual intercourse
- secretions by intimate contacts
- transplacental transmissions
Pathogenesis:
T. pallidum gains entry through the intact mucosa or through
microscopic abrasions in the skin.
From here it enter the blood and lymphatics to eventually produce
systemic infections.
79
63. Classification
80
The disease is generally classified into two:
Acquired syphilis
Congenital syphilis
Acquired Syphilis
Is acquired from an infected person
It can be either through
▫ Sexual contact with an infected partner
▫ Careless handling of the infected patients by the health
professionals
64. Manifests in three stages:
1. Primary syphilis
2. Secondary syphilis
3. Tertiary (late) syphilis
82
65. Primary Syphilis
Develops at the site of inoculation approximately 3 weeks after
infection
Clinical symptoms appear at the site of inoculation
▫ male and female genitalia
▫ extra genital site like-fingers, oral region, perianal region.
(at these sites the spirochetes undergo rapid replication and
enter into the lymphatics or blood stream)
83
66. non -
Characteristic primary lesion of syphilis is called “Chancre”
It is a solitary, painless, indurated, nontender,
hemorrhagic, ulcerated or eroded lesion.
Chancre starts as a dull red macule or papule, which later on
becomes eroded or ulcerated and produces regional
lymphadenopathy
Resolves within 3 - 8 weeks
84
67. Oral manifestations
Chancre occurs on the lips, tongue, palate, gingiva, uvula and tonsils
May be painful due to secondary infection and are highly contagious
in nature
Chancres are ulcerated, indurated lesions covered by a grayish white
membrane
Often mistaken for an early carcinoma
85
68. Secondary Syphilis
Also called Metastatic Stage
Appears in about 6-8 weeks after the appearance of the primary
chancre
Occurs due to the generalized hematogenous dissemination of the
infection in the body
Characterized by skin lesions, mucosal lesions, few constitutional
symptoms and generalized lymphadenopathy
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69. Skin lesions occur in the form of nodular, flat- papillary
(condyloma lata) or pustular lesions.
Circinate (coin-like) lesions on the face & skin are
characteristic of secondary syphilis.
Areas of hyperpigmentations may be seen on the palms and
soles.
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70. Oral manifestations
The secondary lesions are mucocutaneous in nature and they
usually occur 6 to 8 weeks after the primary infection.
The oral lesions in this stage are called "mucous patches”;
commonly seen over the tongue, gingiva, tonsils, larynx, pharynx
and cheek, etc.
These patches are characterized by multiple, flat, irregular or
circular, slightly raised, painless, round erosions.
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71. Covered by a thin yellowish-grey (glistening) slough; surrounded
by a painful erythematous halo
Multiple mucous patches in the oral cavity coalesce together and
from “snail track” like ulcers.
Highly contagious.
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72. Latent Syphilis
Called the Hidden Stage
Begins when the Secondary symptoms disappear
The bacteria begins to infest the bone marrow, lymph glands, vital
organs, and the central nervous system
It may last up to a month or a lifetime
1/3 of the cases left untreated proceed to tertiary stage
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73. Tertiary (Late) Syphilis
Occurs about 5-10 years after the primary infections and it affects
nearly every organs of the body
It mainly affects skin, mucous membrane, CNS & CVS
Typical lesions of tertiary syphilis is called " Gumma",
Localized, chronic granulomatous lesion having either nodular or
ulcerated surface.
Often appears as a "punched-out" ulcer, having vertical walls and a
dull red granulomatous base with an irregular outline.
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74. Tertiary Syphilis :Oral manifestations
Gumma are commonly seen on the hard and soft palate, lips and
tongue
This stage is not contagious.
Lesions begin as firm, small, pale, nodular masses in the midline
of the palate.
They frequently ulcerate by central necrosis and have a punched-
out edge with a wash-leather floor.
The ulcers are either single or multiple and are mostly painless.
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75. Tongue may be diffusely involved with gummata
Appear large, lobulated & irregularly shaped. (interstitial glossitis)
Diffuse atrophy & loss of papillae – syphilitic glossitis
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76. Congenital Syphilis
Congenital syphilis is a rare entity that occurs in children born of an
infected mother.
The condition occurs due to transplacental infection with
Treponema pallidum during fetal development
Congenital infection is associated with several adverse
outcomes, including:
Perinatal death
Premature delivery
Low birth weight
Congenital anomalies
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77. Clinical manifestations after birth are divided
arbitrarily into:
- Early Congenital syphilis (<=2 years of age)
- Late Congenital syphilis ( >2 years of age)
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78. Clinical Manifestations of Early Congenital
syphilis
Maculopapular rash
Hepatosplenomegaly
Jaundice due to the hepatitis
Anemia
Lymphadenopathy
Mucous patches
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79. Clinical Manifestations of Late Congenital
syphilis
Frontal bossing
Short maxilla
High -arched palate
Saddle nose
Mulberry molars
Hutchinson's incisors
Higoumenaki's sign
Enlargement of clavicle adjacent to the sternum
Relative prognathism of mandible
Interstitial keratitis
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Rhagades
Premature perioral fissuring
Saber shin
Anterior bowing of tibia as a result of periostitis
Eighth nerve deafness
Scaphoid scapulae
Concavity of vertebral border of the scapulae
Clutton's joint
Painless synovitis and enlargement of joints, usually the knee
81. Hutchinson's triad
Described by Sir Jonathan Hutchinson in 1858.
Defined the following three pathognomonic diagnostic features
Hutchinson's teeth
Ocular interstitial keratitis
Eighth nerve deafness
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82. Hutchinson's teeth
The infection alters the formation of both the anterior teeth
(Hutchinson's incisors) and the posterior dentition (Mulberry
molars, Fournier's molars, Moon's molars).
Hutchinson's incisors - exhibit their greatest mesiodistal width in
the middle third of the crown.
The incisal third tapers to the incisal edge
Resulting tooth resembles a straight - edge screwdriver.
The incisal edge often exhibits a central hypoplastic notch.
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83. Mulberry molars - taper toward the occlusal surface with a
constricted grinding surface.
The occlusal anatomy is abnormal
Numerous disorganized globular projections that resemble the
surface of a mulberry
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84. Demonstation Of Treponemes
DARK GROUND MICROSCOPY: Treponema pallidum
appears as a slender, spiral organism showing
rotational as well as flexion and extension movements
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85. Laboratory Tests
Detection
microscopy
Bacterial culture in artificial media.
Serological tests
Wasserman reaction, Khan test, Venereal disease research laboratory
(VDRL) test
ELISA
Western blot
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of bacteria in smear by dark ground illumination
86. Treatment
Penicillin will cure a person that has had syphilis for less than a
year.
Blood tests should check to make sure the infection has been
eliminated.
Tertiary syphilis is incurable as it has damaged body organs.
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