Leishmaniasis is caused by a protozoa parasite from over 20 Leishmania species. Over 90 sandfly species are known to transmit Leishmania parasites. There are 3 main forms of the disease:
Visceral leishmaniasis (VL), also known as kala-azar is fatal if left untreated in over 95% of cases. It is characterized by irregular bouts of fever, weight loss, enlargement of the spleen and liver, and anaemia. Most cases occur in Brazil, East Africa and in South-East Asia. An estimated 50 000 to 90 000 new cases of VL occur worldwide each year out of which only an estimated 25–45% are reported to WHO. In 2017, more than 95% of new cases reported to WHO occurred in 10 countries: Bangladesh, Brazil, China, Ethiopia, India, Kenya, Nepal, Somalia, South Sudan and Sudan.
Cutaneous leishmaniasis (CL) is the most common form of leishmaniasis and causes skin lesions, mainly ulcers, on exposed parts of the body, leaving life-long scars and serious disability or stigma. About 95% of CL cases occur in the Americas, the Mediterranean basin, the Middle East and Central Asia. In 2017 over 95% of new CL cases occurred in 6 countries: Afghanistan, Algeria, Brazil, Colombia, Iran (Islamic Republic of), Iraq and the Syrian Arab Republic. It is estimated that between 600 000 to 1 million new cases occur worldwide annually.
Mucocutaneous leishmaniasis leads to partial or total destruction of mucous membranes of the nose, mouth and throat. Over 90% of mucocutaneous leishmaniasis cases occur in Bolivia (the Plurinational State of), Brazil, Ethiopia and Peru.
Transmission
Leishmania parasites are transmitted through the bites of infected female phlebotomine sandflies, which feed on blood to produce eggs. The epidemiology of leishmaniasis depends on the characteristics of the parasite and sandfly species, the local ecological characteristics of the transmission sites, current and past exposure of the human population to the parasite, and human behaviour. Some 70 animal species, including humans, have been found as natural reservoir hosts of Leishmania parasites.
(WHO, 2019)
https://www.who.int/news-room/fact-sheets/detail/leishmaniasis
LUMEN DWELLING FLAGELLATES - GIARDIA
REFS:
INTERNATIONALLY ACCEPTED BOOK OF MEDICAL PARASITOLOGY BY K. D. CHATTERJEE
TEXT BOOK OF MEDICAL PARASITOLOGY BY PANIKER
IMAGE SOURCES : FROM INTERNET
Leishmaniasis is caused by a protozoa parasite from over 20 Leishmania species. Over 90 sandfly species are known to transmit Leishmania parasites. There are 3 main forms of the disease:
Visceral leishmaniasis (VL), also known as kala-azar is fatal if left untreated in over 95% of cases. It is characterized by irregular bouts of fever, weight loss, enlargement of the spleen and liver, and anaemia. Most cases occur in Brazil, East Africa and in South-East Asia. An estimated 50 000 to 90 000 new cases of VL occur worldwide each year out of which only an estimated 25–45% are reported to WHO. In 2017, more than 95% of new cases reported to WHO occurred in 10 countries: Bangladesh, Brazil, China, Ethiopia, India, Kenya, Nepal, Somalia, South Sudan and Sudan.
Cutaneous leishmaniasis (CL) is the most common form of leishmaniasis and causes skin lesions, mainly ulcers, on exposed parts of the body, leaving life-long scars and serious disability or stigma. About 95% of CL cases occur in the Americas, the Mediterranean basin, the Middle East and Central Asia. In 2017 over 95% of new CL cases occurred in 6 countries: Afghanistan, Algeria, Brazil, Colombia, Iran (Islamic Republic of), Iraq and the Syrian Arab Republic. It is estimated that between 600 000 to 1 million new cases occur worldwide annually.
Mucocutaneous leishmaniasis leads to partial or total destruction of mucous membranes of the nose, mouth and throat. Over 90% of mucocutaneous leishmaniasis cases occur in Bolivia (the Plurinational State of), Brazil, Ethiopia and Peru.
Transmission
Leishmania parasites are transmitted through the bites of infected female phlebotomine sandflies, which feed on blood to produce eggs. The epidemiology of leishmaniasis depends on the characteristics of the parasite and sandfly species, the local ecological characteristics of the transmission sites, current and past exposure of the human population to the parasite, and human behaviour. Some 70 animal species, including humans, have been found as natural reservoir hosts of Leishmania parasites.
(WHO, 2019)
https://www.who.int/news-room/fact-sheets/detail/leishmaniasis
LUMEN DWELLING FLAGELLATES - GIARDIA
REFS:
INTERNATIONALLY ACCEPTED BOOK OF MEDICAL PARASITOLOGY BY K. D. CHATTERJEE
TEXT BOOK OF MEDICAL PARASITOLOGY BY PANIKER
IMAGE SOURCES : FROM INTERNET
This is the presentation on Trypanosomiasis that covers classification and diseases caused by Trypanosoma, its life cycle, Geographical distribution, Transmission, diagnosis and treatment and finally its scenario in India.
Some flow charts have been taken from published articles, that can be searched directly from net.
Visceral leishmaniasis is spread by sandfly bites. This type of leishmaniasis affects the internal organs, usually the spleen, liver and bone marrow.
Some people have no symptoms. For others, symptoms may include fever, weight loss and swelling of the spleen or liver.
coccidian parasite is a very important topic for pg entrance........so every important point about it have been discussed in detail......take a look at it...
A comprehensive description of leischmaniasis with its types, transmission, epidemiology, pathogenesis, prevention and control. It also includes details regarding lab diagnosis, disease agent, vector and host.
Malaria(Plasmodium falciparum)- Epidemiology, Life Cycle, Prevention and Erad...Sarath
Malaria(Plasmodium falciparum)- Epidemiology, Life Cycle, Prevention and Eradication.
Contains Videos in two slides. So try using Power Point 2010.
My email : doc.sarathrs@gmail.com
This is the presentation on Trypanosomiasis that covers classification and diseases caused by Trypanosoma, its life cycle, Geographical distribution, Transmission, diagnosis and treatment and finally its scenario in India.
Some flow charts have been taken from published articles, that can be searched directly from net.
Visceral leishmaniasis is spread by sandfly bites. This type of leishmaniasis affects the internal organs, usually the spleen, liver and bone marrow.
Some people have no symptoms. For others, symptoms may include fever, weight loss and swelling of the spleen or liver.
coccidian parasite is a very important topic for pg entrance........so every important point about it have been discussed in detail......take a look at it...
A comprehensive description of leischmaniasis with its types, transmission, epidemiology, pathogenesis, prevention and control. It also includes details regarding lab diagnosis, disease agent, vector and host.
Malaria(Plasmodium falciparum)- Epidemiology, Life Cycle, Prevention and Erad...Sarath
Malaria(Plasmodium falciparum)- Epidemiology, Life Cycle, Prevention and Eradication.
Contains Videos in two slides. So try using Power Point 2010.
My email : doc.sarathrs@gmail.com
Evaluation of infection course in mice induced by L. major in presence of pos...Nanomedicine Journal (NMJ)
Abstract:
An inoculation of virulent Leishmania major is known as leishmanization (LZ) which is proven to be the most effective control measure against Cutaneous Leishmaniasis (CL). However, using LZ is restricted due to various side effects such as uncontrolled lesion development. In the present research, the efficacy of cationic nanoliposomes containing CpG oligodeoxynucleotides (CpG ODN) as an improved adjuvant delivery system was studied to diminish the lesion development and infection course of L. major after inoculation into the mice. BALB/c mice were inoculated subcutaneously (SC) with L. major plus empty DSPC, DSPC (CpG ODN), DSPC (Non CpG ODN), empty DMPC, DMPC (CpG ODN), DMPC (Non CpG ODN) or HEPES buffer. The results showed that group of mice received DMPC (CpG ODN) nanoliposomes developed a significantly smaller lesion and showed minimum number of L. major in the spleen and draining lymph nodes. In addition, using DMPC (CpG ODN) liposomes resulted in a Th1 type of immune response with a preponderance of IgG2a isotype which is concurrent with the production of DMPC (CpG) induced IFN-γ in the spleen of the mice. Taken together, the results suggested that immune modulation using DMPC (CpG ODN) nanoliposomes might be a practical approach to improve the safety of LZ
Keywords:
DMPC (CpG ODN) nanoliposomes; CpG ODN; L. major; Leishmanization; Immune response
exposicion, dermatolotogia, jueves 6 de diciembre 2012, leishmaniasis, parasitosis. Gabriela Ycaza Zurita 6to año: facultad de ciencias medicas, escuela de medicina, universidad de guayaquil
Leishmaniasis is a wide array of clinical manifestations caused by parasites of the Trypanosomatida genus Leishmania. It is generally spread through the bite of phlebotomine sandflies, Phlebotomus and Lutzomyia, and occurs most frequently in the tropics and sub-tropics of Africa, Asia,
Visceral leishmaniasis (VL), also known as kala-azar, is the most severe form of leishmaniasis caused by the protozoan parasite Leishmania donovani and transmitted by the infected sandflies. It characterized by irregular bouts of fever, substantial weight loss, swelling of the spleen and liver, and anaemia.
Leishmaniasis is a vectorborne disease that is transmitted by sand flies and caused by obligate intracellular protozoa of the genus Leishmania. Human infection is caused by more than 20 species. These include the L. donovani complex with 2 species (L. donovani, L. infantum [also known as L. chagasi in the New World]); the L. mexicana complex with 3 main species (L. mexicana, L. amazonensis, and L. venezuelensis); L. tropica; L. major; L. aethiopica; and the subgenus Viannia with 4 main species (L. [V.] braziliensis, L. [V.] guyanensis, L. [V.] panamensis, and L. [V.] peruviana). The different species are morphologically indistinguishable, but they can be differentiated by isoenzyme analysis, molecular methods, or monoclonal antibodies.
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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
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
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!
- 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
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
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.
2. What is Kala-Azar
• Kala-azar means dark pigmentation which is
characteristic of cases of visceral
leishmaniasis. It is caused by Leishmania
donovani bodies and may be present either in
endemic, epidemic or sporadic forms. It is
widely prevalent in India in epidemic form in
states of Bihar, Assam and Bengal. Kala azar
found in East and North Africa is a disease of
young children and young adults, being more
common in males as compared to females.
2
5. KALA AZAR
• Leishmaniasis is a disease caused by protozoan
parasites of to the genus Leishmania and is
transmitted by the bite of sand fly.
• Human infection is caused by about 21 of 30
species that infect mammals. These include the L.
donovani complex with three species (L. donovani,
L. infantum, and L. chagasi
5
6. Pathogenesis
• Infections range from asymptomatic to progressive,
fully developed kala-azar.
• Incubation period is usually 2 – 4 months.
• Symptoms – Begins with low-grade fever and
malaise, followed by progressive wasting, anemia,
and protrusion of the abdomen from enlarged liver
and spleen.
• Fatal after 2 – 3 years if not treated.
• In acute cases with chills, fevers up to 104⁰ F and
vomiting; death may occur within 6 – 12 months.
• Immediate cause of death is usually an invasion of a
secondary pathogen that the body is unable to
combat.
6
7. Leishmaniasis is Neglected Disease
• Leishmaniasis is a globally important but
neglected disease, affecting
approximately two million people every
year. For most people, infection results in
a slow-to-heal skin ulcer. In others,
however, the parasite targets the liver,
spleen and bone marrow, leading to over
70,000 deaths annually.
7
8. The Parasite
• Phylum
• Order
• Family
• Genus
Sarcomastigophora
Kinetoplastida
Trypanosomatidae
Leishmania
8
10. CLASSIFICATION
Old world
leishmaniasis
• Leishmania donovani
• L.infantum
• L.tropica
• L.major
• L.aethiopica
New world
leishmaniasis
• L.braziliensis
• L.mexicana complex
• L.peruviana
• L.chagasi
10
11. • ALL the leishmania species are
morphologically identical to each other.
• These are distinguished by
• Intrinsic characters
• Biochemical characters
• Immunological characters
11
15. • Amastigotes (*)
of Leishmania
donovani in the
cells of a
spleen. The
individual
amastigotes
measure
approximately 1
μm in diameter.
15
16. Morphology and Life Cycle
• Amastigotes
measure 2-3
micrometers, with a
large nucleus and
Kinetoplast.
• Amastigotes mainly
live within cells of
the RE system, but
have been found in
nearly every tissue
and fluid of the
body.
16
17. Life cycle
• The organism is transmitted by the
bite of several species of blood-feeding
sand flies (Phlebotomus)
which carries the promastigote in
the anterior gut and pharynx. It
gains access to mononuclear
phagocytes where it transform into
amastigote and divides until the
infected cell ruptures.
17
19. Life cycle
• The released organisms infect other
cells. The sand-fly acquires the
organisms during the blood meal,
the Amastigote transform into
flagellate Promastigote and multiply
in the gut until the anterior gut and
pharynx are packed. Dogs and
rodents are common reservoirs. 19
23. • Pallor in hands of a
visceral
leishmaniasis
patient.
23
24. Laboratory diagnosis
• Blood counts: Anaemia, neutropenia, thrombocytopenia
• A/G ratio reversed (n-4.5:2, in kala-azar-2.8:4)
• Parasitological Diagnosis
• PBF
• Needle biopsy/aspiration
• Culture
• Animal inoculation
• Immunological tests
• Non-specific tests
• Aldehyde tests
• Antimony test
• A:G Complement fixation test with W.K.K antigen
24
25. • Immunological tests
• Non-specific test
• Aldehyde test
• Antimony test
• Complement fixation test with W.K.K antigen
• Specific tests
• Direct agglutination test(DAT)
• Indirect haemagglutination test (IHA)
• Indirect fluorescent antibody test(IFAT)
• ELISA
25
26. Parasitological diagnosis:
Specimen :
Bone marrow aspirate
Splenic aspirate
Lymph node aspiration
Tissue biopsy
Microscopy – PBF, Buffy coat smear
Culture
Animal inoculation- golden hamester
26
28. L. donovani bodies
L. donovani bodies may be
demonstrated in buffy
coat preparations of
blood and bone
marrow aspirate.
PBF is made with straight
leucocytic edge
Aspirates taken from
enlarged lymph nodes
show parasites in 60
percent of cases.
28
29. Culturing of the Parasite
• Organisms can be
cultured in Nicolle-
NovyMcneal (NNN
media) media from
clinical specimens
obtained from
splenic or bone
marrow aspirates.
29
30. Cultivation
• NNN medium-Biphasic media- 2 parts of salt
agar+1 part of defibrinated rabbit blood,
melted & cooled to 48⁰C ice, inoculated into
water of condensation, incubated at 22-25⁰C
for the 21 days.
• Hockmeyer medium- Insect cell culture
medium+ foetal calf serum+ penicillin+
streptomycin( detected after 2-3 d)
• Schneider Dorsophila Medium
30
31. Promastigote in culture in NNN
medium (magnification 100×)
NNN culture medium
Promastigotes growing in culture medium Bone marrow aspirate -“rosette” of
extra-cellular Promastigotes (Giemsa stain31).
32. Immunological Diagnosis:
• Specific serologic tests:
• Direct Agglutination Test (DAT),
• ELISA,
• IFAT,
• CFT for detection of antibodies
• Rapid immunochromatic test(ICT): By using
rk39Ag
• Molecular Methods: PCR & RT-PCR.
32
33. Direct agglutination test
• Direct agglutination test
(DAT) based on
agglutination of the
trypsinized whole
promastigotes is useful
in endemic regions. Its
sensitivity ranges from
91-100% and specificity
from 72 to 100%.
33
34. ELISA
• ELISA is an important
sero diagnostic tool
for leishmaniasis. It
is a highly sensitive
test and its
specificity depends
upon the antigen
used.
34
35. Chromatographic strip test
• A ready to use immuno
chromatographic strip
test based on rk 39
antigen has been
developed as a rapid test
for diagnosis of kala azar.
An important limitation of
this test is the presence
of antibodies in healthy
controls hailing from
endemic regions.
35
36. • Non specific serological tests for
hypergammaglobinemia
• Napier’s Aldehyde test: Patient’s sera is mixed
with a drop of 40% formalin in a test tube.
Positive test is indicated by jellification.
• Chopra’s antimony test: Positive test is by
formation of profuse flocculation when
patient ‘ sera is mixed with 4% urea stilbamine
solution.
36
37. 37
Skin test ( leishmanin test or Montenegro
test) It is a delayed hypersensitivity skin test
for survey of populations and follow-up after
treatment - 0.2 ml(6-10 million/ml of killed
promastigotes in 0.5% phenol saline)
injected—erythema ≥ 5mm→ +ve after 6-8
weeks of cure.
38. The leishmanin skin test (LST) or MST (Montenegro skin test)
PROBLEMS:
A positive leishmanin skin test
•Reference standards -antigens & performance (reading)- not developed.
•Most antigens, crude extracts of parasites, neither sensitive nor specific.
•Positivity not demonstrable until 5 months after the acute phase of VL-20%
• May or may not be positive for PKDL.
•Persistence of the lesions has been frequently associated with non reactivity in the
LST and high levels of anti-leishmanial antibodies.
38
39. Treatment:
• Pentavalent antimony (Pentostam)
• Amphotericin B
• Miltefosine
• Interferon
Treatment of complications:
• Anemia
• Bleeding
• Infections etc.
39
40. Control
• Vector control
• Reservoir control
• Treatment of active cases
• Vaccination
40
41. Management of Kala-azar Patients
• It includes both supportive and curative. All
patients of Kala azar should preferably be
hospitalized. Any infection complicating the
disease be treated by use of proper
antibiotics. Nutrition must be maintained.
Cases with severe anemia may require blood
transfusions. Pentavalent antimony
compounds are the drug of choice. Sodium
antimony gluconate (Pentostam) is the most
commonly used drug.
41
42. Kala-azar prevention:
• Multipronged approach is needed.
• Sand-flies are extremely sensitive to
insecticides & vector control through
insecticide spray is very important.
• Mosquito nets or curtains treated
with insecticides will keep out the
tiny sand-flies.
42
43. Kala-azar prevention:
• In endemic areas with zoonotic transmission,
infected or stray dogs should be destroyed.
• In areas with anthroponotic transmission,
early diagnosis & treatment of human
infections, to reduce the reservoir & control
epidemics of VL, is extremely important.
• Serology is useful for screening of suspected
cases in the field.
• No vaccine is currently available .
43
46. Post Kala Azar Dermal
Leishmanoid
Normally develops <2 years after recovery
Recrudescence
Restricted to skin
Rare but varies geographically(10% of cases
in India and 3% of cases in Africa)
46
47. PKDL
•L.donovani
•Non ulcerative skin lesin.
•Late sequale of VL.
•1-2 years after recovery fron VL.
•Currently, PKDL is reported to occur in only 1% of Indian VL
patient.
Nodular skin lesions in PKDL
•3 major representations-
(i) Erythematous indurated lesions on the butterfly area of
face;
(ii) Multiple symmetrical hypopigmented macules with
irregular margins that may coalesce, having generalized
distribution to the extremities and trunk; and
(iii) Combination of papules, nodules and plaques.
47
48. Fig. Clinical presentation in PKDL (A) PKDL nodular and popular lesions on face and
hypopigmented macules on neck in a patient
with polymorphic presentation (B) hypopigmented macules on trunk in a patient with macular
PKDL. (C) Erythematous and indurated
lesions over the butterfly area of face. 48
49. Complications of PKDL
1. Blindness due to corneal involvement.
2. Recently, nerve involvement in Indian PKDL reportd.
• Nowadays – reported from South America, Europe & India.
• Recurrence of VL following PKDL reported.
• LD bodies rich nodular skin lesions -sole reservoir to disseminate in
absence of zoonotic transmission.
49
50. Grey areas in PKDL
1. The factors of parasite/host origin -drive the parasite to shift from viscera to dermis. --It is
not known it is the residual parasite after VL infection, attributed to altered immune status or
is introduced upon re-infection by sandfly vector.
Antimony therapy for PKDL patients needs to be continued for much longer duration than
for VL patients (4 months instead of 4 wk for VL).
• Recently-High interleukin-10 (IL-10) levels in skin & peripheral blood.
-High level of C reactive protein in plasma of patients with VL
Predictive of the subsequent development of PKDL.
50