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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.
Cryptococcosis also called as Torulosis is a subacute or chronic fungal infection caused by Cryptococcus neoformans. It leads to compications such as fatal meningoencephalitis. It is an opportunistic infection in HIV-infected patients. The PPT discuss on the morphology of the fungus, pathogenesis, laboratory diagnosis and treatment.
Introduction
Disease
Important Properties
Transmission & Epidemiology
Risk factor of reactivation
Pathogenesis
Clinical Findings
Laboratory Diagnosis
Approaches to the diagnosis of latent infections
Treatment
Prevention
Introduction
Disease
Important Properties
Transmission & Epidemiology
Risk factor of reactivation
Pathogenesis
Clinical Findings
Laboratory Diagnosis
Approaches to the diagnosis of latent infections
Treatment
Prevention
The information about Leprosy is a basic content intended to share Students of Graduate and postgraduate in Life Sciences.
The up loader has no Commercial interests
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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
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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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
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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.
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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
2. Infection and Disease
Leprosy
Vedas
Bible
Fear and Social outcasts
Hansen 1868 - Identifies First microorganism.
Least understood and not cultured in artificial
medium
3. It is a disease of Historical importance.
World's oldest recorded disease
First described KUSHTA in ancient indian text
(sushruta samhita) in 600 B.C.
Stigmatized disease
Gerhard Henrick Armauer Hansen discovered
mycobacterium leprae hence leprosy is also called
hansen’s disease.
First bacterium to be identified capable of causing
human disease.
Cannot be cultivated on culture media.
More than 6-8 million cases of leprosy worldwide,
60% of which are in india.
What is Leprosy?
4. It is a chronic infectious disease caused by
M.leprae, an acid fast, rod shaped bacillus. It
mainly affects the skin, peripheral nerves,
and mucosa of the respiratory tract etc.,
It has left behind a terrifying image in
history and human memory of mutilation,
rejection and exclusion from society.
LEPROSY
5. Mycobacterium leprare
MORPHOLOGY
They are acid fast bacilli arranged singly, in parallel
bundles (like rolls of cigarette in a packet) or in
globular masses.
Appear as straight or curved rods
Size is 1 – 8 microns x 0.5 microns.
less acid fast than tubercle bacilli.
Live bacilli stain uniformly & appear solid.
Dead bacilli appear as fragmented with granules.
Intracellularly They appear as bundles of bacilli
bound together by lipid like substance THE GLIA.
These masses are known as GLOBI. Parallel rows
of globi Presents a cigar bundle appearance.
11. Ultrastructural characteristics of M. leprae
The ultrastructure of M. leprae is common in the
genus Mycobacterium. Electron microscopy has shown that
this bacillus has cytoplasm, plasma membrane, cell wall, and
capsule. The cytoplasm contains common structures in gram-
positive microorganisms.
The plasma membrane has a permeable lipid bilayer
containing interaction proteins, which are the protein surface
antigens.
The cell wall attached to the plasma membrane is composed
of peptidoglycans bound to branched chain polysaccharides,
consisting of arabinogalactans, which support mycolic acids,
and lipoarabinomannan (LAM), similarly to
other mycobacteria.
The cell wall has a characteristic phenolic glycolipid (PGL-1).
Its carbohydrate antigenic determinant has been synthesised.
This triglycerride binds to the basal lamina of schwann cells.
12. Resistance
Viable for 9 -16 days in warm humid
environment.
In moist soil for 46 days
Direct sunlight for two hours.
Ultraviolet light for 30 minutes.
13. Leprosy
A chronic granulomatous disease primarily
involving Skin, Peripheral nerves, Nasal
mucosa
Incubation period 3 -15 years.
Source of infection- nasal discharge & skin
lesions.
Portal of entry- inhalation of infectious aerosols,
through skin contact (damaged skin) and
prolonged close contact with infective paitents.
Principle target cell- schwann cell, resulting in
nerve damage causing manifestations of
leprosy (anesthesia and muscle paralysis).
14. Classification ( Madrid )
Lepromatous
Tuberculoid
Dimorphic/borderline
Indeterminate.
Type of disease is a reflection of the immune status of
the host.
Delayed hypersensitivity determines the response of
the host to infection and production of clinical type.
Lepromatous and tuberculoid are two extreme or polar
forms of leprosy.
Lepromatous leprosy- CMI is absent or deficient
Tuberculoid leprosy- CMI is intact.
Indeterminate- between the two, can acquire any form.
15. Borderline- Lesions clinically resemble
tuberculoid leprosy but bacteriologically
resemble lepromatous type.
Therefore the clinical type of leprosy is not
permanent and changes with chemotherapy
and alteration in immune status of the host.
16. 1. lepromatous
Seen where host resistance is low.
Bacilli seen in large numbers as globi inside lepra cells or
extracellularly.
Known as MULTIBACILLARY disease.
Antibodies are produced, but they do not prevent bacterial
proliferation.
Skin lesions tend to be multiple and symmetrical, preferably located
in the colder areas of the body, characterized by hypochromic,
erythematous or bright brownish spots with indefinite borders.
As the disease progresses, lesions infiltrate forming plaques and
nodules (lepromas).
Nodules ulcerate and bacilli invade the mucosa of nose, mouth and
upper respiratory tract and are shed in nasal and oral secretions.
Mucous membranes, eyes, bones, joints, lymph nodes, blood
vessels, upper airways, teeth, and internal organs may be affected
Lepromin test is negative due to deficient CMI.
17. Clinical features
Lesions are large, diffuse and granulomatous
and multibacillary.
Diffuse sensory nerve involvement and
patchy anaesthesia is common.
Facial disfigurement is commonly observed.
Results in leonine facies.
paitents are anergic to lepromin.
19. Characteristics of clinical forms
Lepromatous leprosy: ichthyosiform appearance of the skin of the legs and
lepromas
Lepromatous leprosy:
infiltrated face and
madarosis
21. 2.Tuberculoid type
Localised form of the disease and Seen in
paitents with high degree of resistance.
CMI is intact and lepromin test is positive.
Skin lesions are few and sharply demarcated.
There is early neural involvement which
leads to deformities in hands and feet.
Bacilli are scanty in lesions. This is known as
Paucibacillary disease.
23. Characteristics of clinical forms
Tuberculoid leprosy: well-defined annular erythematous plaque on the dorsum of the
hand
Lepromatous leprosy: dry and barely
discernible hypochromic spots on the
arm
25. 3.Dimorphous/ Borderline type
Lesions clinically resemble tuberculoid leprosy
but bacteriologically resemble lepromatous
type.
Can shift to any spectrum depending on
chemotherapy or alterations in host resistance.
26. Characteristics of clinical forms
Borderline leprosy: polymorphic appearance of the lesions
Borderline leprosy:
brownish erythematous
plaques (foveal spots) in the
trunk
27. 4. Indeterminate type
There is early unstable tissue reaction not
characteristic of either lepromatous or
tuberculoid type.
Lesions heal spontaneously in some person
and in others it may progress to lepromatous
or tuberculoid type.
29. Ridley and Jopling
Classification
Based on clinical, histopathological and
immunological findings, Ridley and jopling
classified spectrum of leprosy into 5 types:
Tuberculoid (TT)
Borderline Tuberculoid (BT)
Borderline (BB)
Boderline lepromatous (BL)
lepromatous (LL)
30.
31.
32. WHO classification
Two Groups-
Paucibacillary & Multibacillary.
Paucibacillary (PB):
Includes al cases of tuberculoid types and
some cases of borderline type.
The number of M. leprae in the body is small
(less than 1 million) and a skin smear test is
negative.
The patient presents five or fewer skin lesions.
Most cases of leprosy are PB.
33. Multibacillary
Includes all cases of lepromatous type and
some cases of borderline type.
M. leprae can multiple in the body almost
without any check and is thus present in high
numbers.
The bacillus has likely spread to almost all
areas of skin and peripheral nerves.
A skin smear test is positive and the patient
presents more than five skin lesions.
34. EPIDEMIOLOGY
Exclusive human disease. Only source of infection is
patient.
Patient with untreated lepromatic leprosy my discharge
upto 8 x 10 bacilli in one nose blow.⁸
Asymptomatic infection is quite common in endemic
areas.
Not highly communicable. Incubation period is around 2 –
5 years.
6 to 8 million people are affected worldwide and 600,00
new cases are estimated annually, 60% of them of which
are in india
Mostly confined to underdeveloped areas of the tropics
and southern hemisphere (asia, africa, latin america and
the pacific)
35. More than 80% of the world cases are observed
in india, china, myanmar, indonesia, brazil,
nigeria, madagascar and nepal.
India has maximum prevalence with 13 of global
total. 90% cases are tuberculoid.
Odisha & bihar have highest prevalence ( > 5 per
1000 population) and haryana the least (< 0.1 per
1000)
36. Immunity
• Innate Immunity exists against lepra bacilli in
humans.
Infection induces both Humoral & Cellular immune
response.
Type of leprosy is determined by status of CMI.
CMI destroys the bacilli and determines the
recovery.
Adequate CMI can manifest with Tuberculoid
leprosy.
Deficient CMI develops lepromatous type of
disease.
Lepromatous leprosy patient have large number of
CD 8+ lymphocytes in contrast to tuberculoid
lesions which contain CD 4+ cells.
37. Lepra reactions
Lepra reactions occur in 30-50% of patients with
leprosy. They may occur before, or more often, after
the start of treatment and are induced by medicines,
stress and surgical procedures.
There are 3 main types of reaction.
Lepra type I (reversal) reaction
Lepra type I (reversal) reaction often affects those with
borderline shifting toward tuberculoid type, as the cell-
mediated immune system improves in the first few
months of drug treatment or for some other reason
such as pregnancy.
Type 1 reactions result in fever, red swollen skin, and
tender peripheral nerves.
Treatment requires oral corticosteroids and
nonsteroidal anti-inflammatories.
38. Lepra type II reaction
Lepra type II reaction is also called erythema
nodosum leprosum (ENL).
It affects those with borderline lepromatous or
lepromatous leprosy and is a humoral (antibody-
antigen) reaction to immune complexes.
Tends to occur few months after institution of
chemotherapy.
ENL presents as painful red nodules (lumps),
which can blister or ulcerate, accompanied by
fever, malaise, joint pain, nerve pain, eye disease
and involvement of other organs.
40. Lepromin Test
Mitsuda in 1919 – skin test – delayed hypersensitivity.
Lepromin (antigen) is boiled extract of lepromatous tissue in
isotonic saline – rich in lepra bacilli.
Mordern antigens are prepared from armadillo derived lepra
bacilli (lepromin A) and standardised ( 4 x 10 bacilli per ml).⁷
Injection of 0.1 ml of lepromin in an individual causes a
biphasic reaction.
Events in the reaction Biphasic reaction -
Early or Fernandez Reaction – erythema and induration of
10-30 mm diameter appears 24 – 48 hours, remains for 3 –
5 days, like tuberculin reaction, little significant.
41. Late Mitsuda reaction
Mitsuda reaction occurs after 1 – 2 weeks,
prominent after 3 - 5 weeks with diameter of 3-
5 mm.
Skin reaction consists of an indurated nodule.
Histology of nodule shows nfiltration with
Lymphocytes ,Epitheloid cells and giant cells.
Indicates CMI
Positive mitsuda reaction indicates resistance
to leprosy.
42. Significance of Lepromin Test
Test is not employed for Diagnosis of leprosy.
Classification of leprosy- test is negative in
lepromatous leprosy but positive in tuberculoid
leprosy.
Effectiveness of CMI
To asses the prognosis and response to
therapy. Positive test indicates good
response /recovery while Negative indicates
Bad prognosis.
To assess the resistance of individuals to
leprosy
43. Diagnosis of Leprosy
Diagnosis must therefore be made by doing a
biopsy, in which a small piece of skin is taken
to analyse for the leprosy bacterium.
Early diagnosis is very important because it
can prevent permanent deformities and
disability.
For routine examination specimen are
collected from nasal mucosa, skin lesions and
ear lobules.
44. 1. Specimens
Nasal smear
Skin smear
Slit skin smear
Nerve biopsy
2. MICROSCOPY
Diagnosis consists of demonstration of acid fast
bacilli in the lesions.
Smears are stained by Z.N staining technique.
5% sulphuric acid is used as decoloriser.
45. Smear Examination
1 + (1 -10 bacilli / 100 fields)
2 + (1-10 bacilli / 10 fields)
3 + (1 – 10 bacilli / one field)
4 + (10 – 100 bacilli / one field)
5 + (100 - 1000 bacilli /field)
6 + (> 1000 bacilli /field)
Number of Bacilli seen in each field is
recorded as Bacillary index.
46. The bacteriological index (BI)
This is an expression of the extent of
bacterial loads. It is calculated by counting six
to eight stained smears under the 100 x oil
immersion lens.
Indicates the Prognosis of the Disease.
Total score in all smears / Number of
smears
Eg 16/8 =2
So the index is 2
47. The Morphological index (MI)
This is calculated by counting the numbers of
solid-staining acid-fast rods. Only the solid-
staining bacilli are viable.
48. 3. Culture
Mouse foot pad
Armadillo
4. Serology
Detection of antibody against M.leprae
phenolic glycolipid antigen is a specific
diagnostic test.
49. Treatment of Leprosy
Multidrug regime
Paucibacillary lesions:-
Rifampicin 600 mg / once month
Dapsone 100 mg/day for 6 months
Multibacillary lesions:-
Rifampicin 600 mg / once month
Dapsone 100 mg/day
Clofazimine 50 mg daily
Continue for two years.
50. Other Drugs for Leprosy
Ethionamide
Prothionamide.