Malaria is an infectious disease caused by Plasmodium parasites that are transmitted via mosquito bites. The document discusses the history and life cycle of malaria parasites, describing how they were first observed by Hippocrates and eventually their full life cycle was discovered in the late 19th/early 20th century. It also summarizes methods for diagnosing malaria, including examining blood smears under microscopy, rapid diagnostic tests, fluorescent microscopy using stains, and PCR to detect parasite genetic material.
To Present an up-to-date summary of the best microbiology practice related to malaria diagnostics
PGY-3, IAU Clinical Microbiology Residency
Dammam, KSA
Hookworm is one of the most important small intestinal nematodes causing iron deficiency anemia. This PPT illustrates hookworms associated with human diseases, life cycle, pathogenesis, laboratory diagnosis, treatment and prevention of hookworm infection.
Wuchereria Bancrofti, the adult worm or parasites and its embryo microfilariae . The studies of microbiology. Its about Introduction, morphology, life cycle, pathogenesis, diagnosis and treatment
To Present an up-to-date summary of the best microbiology practice related to malaria diagnostics
PGY-3, IAU Clinical Microbiology Residency
Dammam, KSA
Hookworm is one of the most important small intestinal nematodes causing iron deficiency anemia. This PPT illustrates hookworms associated with human diseases, life cycle, pathogenesis, laboratory diagnosis, treatment and prevention of hookworm infection.
Wuchereria Bancrofti, the adult worm or parasites and its embryo microfilariae . The studies of microbiology. Its about Introduction, morphology, life cycle, pathogenesis, diagnosis and treatment
Respiratory physiology and respiratory disordersMarvin Gonzaga
Respiratory physiology and respiratory disorders - The functions of the parts of the Respiratory System including common respiratory diseases *NOTE: some of the items in my Respiratory System Quiz Bowl http://www.slideshare.net/dylanerrolcross/respiratory-system-quiz-bowl can be found here
able of ContentsIntroductionObjectives of Giemsa stainPrincipleReagents UsedProcedureStaining procedure 1: Thin Film stainingStaining Procedure 2: Thick Film StainingResultsInterpretation/ConclusionApplications Giemsa stainAdvantagesLimitationsReferencesFour Charged in Plot to Kidnap an Iranian Journalist in New YorkIntroductionGiemsa stain was a name adopted from a Germany Chemist scientist, for his application of a combination of reagents in demonstrating the presence of parasites in malaria.It belongs to a group of stains known as Romanowsky stains. These are neutral stains made up of a mixture of oxidized methylene blue, azure, and Eosin Y and they performed on an air-dried slide that is post-fixed with methanol. Romanowsky stains are applied in the differentiation of cells, pathological examinations of samples like blood and bone marrow films and demonstration of parasites e.g malaria. There are four types of Romanoswsky stains:Giemsa stainJenner StainWright stainMay-Grunwald StainLeishman stainObjectives of Giemsa stainTo accurately prepare the Giemsa stain stock solutionTo stain and identify blood cellsTo differentiate blood cells nuclei from the cytoplasmPrincipleGiemsa stain is a gold standard staining technique that is used for both thin and thick smears to examine blood for malaria parasites, a routine check-up for other blood parasites and to morphologically differentiate the nuclear and cytoplasm of Erythrocytes, leucocytes and Platelets and parasites.Like any type of Romanowsky stains, it composed of both the Acidic and Basic dyes, in relation to affinities of acidity and basicity for blood cells. Azure and methylene blue, a basic dye binds to the acid nucleus producing blue-purple color. Eosin is an acidic dye that is attracted to the cytoplasm and cytoplasmic granules which are alkaline-producing red coloration. The stain must be buffered with water to pH 6.8 or 7.2, to precipitate the dyes to bind simple materials.Classically, Giemsa stain is a differential stain which is made up of a combination of reagents (Azure, Methylene blue, and Eosin dye) used widely in cytogenetics and histopathology for the diagnosis of:Malaria, spirochetes and other blood parasitesChlamydia trachomatis inclusion bodiesBorrelia sppYersinia pestisHistoplasma sppPneumocystis jiroveci cystsReagents UsedMethanolGiemsa powderGlycerinWater (Buffer)ProcedurePreparation of the Giemsa Stain Stock solution (500ml)Into 250ml of methanol, add 3.8g of Giemsa powder and dissolve.Heat the solution up to ~60oCThen, add 250ml of glycerin to the solution, slowly.Filter the solution and leave it to stand for about 1-2 months before use.Preparation of Working solutionAdd 10ml of stock solution to 80ml of distilled water and 10ml of methanolStaining procedure 1: Thin Film stainingOn a clean dry microscopic glass slide, make a thin film of the specimen (blood) and leave to air dry.dip the smear (2-3 dips) into pure methanol for fixation of the
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
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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
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
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.
4. Ancient History of Malaria
• Malaria parasites have been with us since the
dawn of time. They probably originated in
Africa (along with mankind), and fossils of
mosquitoes up to 30 million years old, show
that the malaria vector, the malaria mosquito,
was present well before the earliest history.
5. Hippocrates and Malaria
• Hippocrates, a physician
born in ancient Greece,
today regarded as the
"Father of Medicine", was
the first to describe the
manifestations of the
disease, and relate them to
the time of year and to
where the patients lived.
6. History – Events on Malaria
• 1753- name of malaria was given.
• 1847-Meckel observed presence of pigment in
organs.
• 1880 - Charles Louis Alphose Lavern discovered
malarial parasite in wet mount. wins Nobel Prize in
1907
• 1883 - Methylene blue stain - Marchafava
• 1891 - Polychrome stain- Romanowsky
• 1898 - Roland Ross - Life cycle of parasite
transmission, wins Nobel Prize in 1902
• 1948 - Site of Exoerythrocytic development in Liver
by Shortt and Garnham
7. Major Developments in 20th Century
• 1955 - WHO starts world wide malaria
eradication programme using DDT
• 1970 – Mosquitos develop resistance to DDT
Programme fails
• 1976 – Trager and Jensen in vitro cultivation
of parasite
9. Introduction
• Malaria is probably one of the oldest diseases known to
mankind that has had profound impact on our history.
• It is a huge social, economical and health problem,
particularly in the tropical countries.
• Malaria is a vector-borne infectious disease caused by single-
celled protozoan parasites of the genus Plasmodium.
• Malaria is transmitted from person to person by the bite of
female mosquitoes.
12. What causes Malaria
• Malaria is caused by a parasite called
Plasmodium, which is transmitted via the bites
of infected mosquitoes. In the human body,
the parasites multiply in the liver, and then
infect red blood cells.
• Transmission of Malaria do not occur <160c
and >330c
• Do not occur > 2000 meters altitude.
13. Etiology of Malaria
• Five Species known to infect Man
1 Plasmodium vivax – Benign Tertian, Tertian
Malaria(Grassi and Feletti)
2 P.ovale - Ovale tertian Malaria(Stephens)
3 P.malariae – Quartan malaria (Laveran)
4 P.falciparum – Falciparum malaria or
Malignant Tertian malaria(Welch)
5 P. knowlesi (Sinton and Muller)
15. LIFE CYCLE OF MALARISA PARASITE
IN MAN IN MOSQUITO
• PRE ERYTHROCYTIC • GAMETOCYTE
SCHIZOGONY- • ZYGOTE
CRYPTOZOITES. • OOKINETE
• ERYTHROCYTIC CYCLE- • OOCYST
MEROZOITES.
• SPOROZOITE
• GAMETOGONY-
GAMETOCYTES
• EXOERYTHROCYTIC CYCLE-
PHANEROZOITES.
16. Period of Pre erythrocytic cycle
• 1 P.vivax 8 days
• 2 P.falciparum – 6 days
• 3 P.malariae - 13 – 16 days,
• 4 P.ovale 9 days
On maturation Liver cells ruputure
Liberate Merozoites into blood stream
17. Affinity of Parasite to Erythrocytes
• P.vivax Young red blood cells
• P.malariae Old red blood cells
• P.ovale Young red blood cells
• P.falciparum Infects all age groups
Also adhere to the endothelial lining of Blood
vessesl
Causes the obstruction, Thrombosis and Local
Ischemias
19. Trophozoites
• After invasion grow and
feed on hemoglobin
• Blue cytoplasm and red
nucleus, Called as
Signet ring appearance
• Hence called ring form
20. Schizont
• When the Trophozoite is fully developed
becomes compact.
• Malarial pigments are scattered through the
cytoplasm
• The Nucleus is large and lies at the periphery
starts dividing.
• Becomes Schizont
21. Exo Erythrocytic Schizogony
• Some Sprozoites do not undergo sporogony in
the first instance
• But go into resting stage called as
Hypnozoites,( hibernation )
• Within 2 years reactivate to form Schizonts
release Merozoites and attack red cell and
produce relapses
• Absent in P falciparum
22. Gametogony
• Merozoites differentiate into Male and female
gametocytes
• Macrogametocytes also called female gametocytes
• Microgametocyte also called as male gametocytes
• They develop in the red cells
• Found in the peripheral blood smears
• Microgametocyte of all species are similar in size
• Macro gametocytes are larger in size.
28. Malaria Blood Smear
• Prepare smears as soon as possible after
collecting venous blood to avoid
• Changes in parasite morphology
• Staining characteristics
• Take care to avoid fixing the thick smear
• Risk of fixing thick when thin is fixed with
methanol if both smears on same slide
• Let alcohol on finger dry to avoid fixing
thick
• Be careful if drying with heat
29. Collection of Blood Smears
1. 4.
The second or third Slide must always be
finger is usually grasped by its edges.
selected and
cleaned.
2. 5.
Puncture at the side Touch the drop of
of the ball of the blood to the slide
finger. from below.
3.
Gently squeeze
toward the puncture
site.
30. Preparing thick and thin films
1. 4.
Touch one drop of Carry the drop of blood
blood to a clean to the first slide and hold
slide. at 45 degree angle.
2. 5.
Spread the first Pull the drop of blood
drop to make a 1 across the first slide in
cm circle. one motion.
3. 6.
Touch a fresh drop Wait for both to
of blood to the edge dry before fixing
of another slide. and staining.
34. Plasmodium falciparum
Infected erythrocytes: normal size
M I
Gametocytes: mature (M)and
immature (I) forms (I is rarely
Rings: double chromatin dots; accole forms;
seen in peripheral blood)
multiple infections in same red cell
Schizonts: 18-32 merozoites
(rarely seen in peripheral blood)
Trophozoites: compact
(rarely seen in
peripheral blood)
35. Plasmodium vivax
Infected erythrocytes: enlarged up to 2X; deformed; (Schüffner’s dots)
Rings Trophozoites: ameboid; deforms the erythrocyte
Schizonts: 12-24 merozoites Gametocytes: round-oval
37. Plasmodium malariae
Infected erythrocytes: size normal to decreased (3/4X)
Trophozoite: Trophozoite: Schizont:
compact typical 6-12 merozoites(rosette like);
band form coarse, dark pigment
38. Species Differentiation on Thin Films
Feature P. falciparum P. vivax P. ovale P. malariae
Enlarged infected RBC + +
Infected RBC shape round round, oval, round
distorted fimbriated
Stippling infected RBC Maurer Schuffner Schuffner Ziemann
dots dots dots dots
Trophozoite shape Small ring, large ring, large ring, small ring,
accoleform amoeboid compact compact
Chromatin dot often double single large single
Mature schizont rare, 18-32 12-24 8-12 6-12
merozoites merozoites merozoites merzoites
Gametocyte crescent shape large, large, compact,
round round round
39. Species Differentiation on Thin Films
P. falciparum P. vivax P. ovale P. malariae
Rings
Trophozoites
Schizonts
Gametocytes
40. Species Differentiation on Thick Films
Feature P. falciparum P. vivax P. ovale P. malariae
Uniform trophozoites +
Fragmented trophozoites ++ +
Compact trophozoites + +
Pigmented trophozoites +
Irregular cytoplasm + +
Stippling (“RBC ghosts”) + +
Schizonts visible very rarely often often often
Gametocytes visible occasionally usually usually usually
41. Calculating Parasite Density - 1
• Using 100X oil immersion lens, select area
with 10-20 WBCs/field on Thick smear
• Count the number of asexual parasites
and white blood cells in the same fields on
thick smear
• Count ≥ 200 WBCs
• Assume WBC is 8000/µl (or count it)
parasites/µl = parasites counted X WBC count/µl
WBC counted
42. Calculating Parasite Density - 2
• Count the number of parasitized and
nonparasitized red blood cells (RBCs) in
the same fields on thin smear
• Count 1000 RBCs (fewer RBCs if
parasitemia is high)
Number of parasite in 1 µl
Of blood = RBC IN million/cmm X Parasite %
43. Estimating Parasite Density
Alternate Method
• Count the number of asexual parasites
per high-power field (HPF) on a thick
blood film
+ 1-10 parasites per 100 HPF
++ 11-100 parasites per 100 HPF
+++ 1-10 parasites per each HPF
++++ > 10 parasites per each HPF
45. High Power
• Ring shaped trophozites • White eccentric “food
• The intraerythrocytic vacuole” in a ring form.
trophozoites multiply by binary • Very transient stage in Malaria.
fission or schizogony, forming Very rarely seen.
two to four separate
merozoites. .
46. the famous Maltese Cross
• Presence of 4 daughter merozoites in a tetrad is
pathomnemonic.
• However, rarely seen.
• Never seen in malaria.
47. Fluorescent Microscopy
• Modification of light microscopy
• Fluorescent dyes detect RNA and DNA that is
contained in parasites
• Nucleic material not normally in mature RBCs
• Kawamoto technique
– Stain thin film with acridine orange (AO)
– Requires special equipment – fluorescent
microscope
– Nuclei of malaria parasites floresce bright
green and cytoplasm red.
– Staining itself is cheap
– Sensitivities around 90%
48.
49. Quantitative Buffy Coat (QBC ®)
• Useful for screening large numbers of samples
• Quick, saves time
• Requires centrifuge, special stains
• Malaria parasite floresce green yellow against
dark red –black background.
• 3 main disadvantages
– Species identification and quantification difficult
– High cost of capillaries and equipment
– Can’t store capillaries for later reference
52. Malaria Serology – antibody detection
• Immunologic assays to detect host
response
• Antibodies to asexual parasites appear
some days after invasion of RBCs and may
persist for months
• Positive test indicates past infection
• Not useful for treatment decisions
53. Malaria Serology – antibody detection
• Valuable epidemiologic tool in some settings
• Useful for
– Identifying infective donor in transfusion-
transmitted malaria
– Investigating congenital malaria, esp. if mom’s
smear is negative
– Diagnosing, or ruling out, tropical splenomegaly
syndrome
– Retrospective confirmation of empirically-treated
non-immunes
54. Target antigens for malaria RDT
pLDH HRP2
Pf-only
Pf and pan-specific bands Persists after parasite death
Closely reflects parasite
viability Aldolase
Pan-specific
Asexual and sexual stages
Closely reflects parasite viability
? Potential for monitoring
treatment efficacy
Pv, Po, Pm-specific Mabs
developed
70. Potential applications for RDTs.
Diagnosis in Confirmation of
remote areas dubious
microscopy
diagnosis
Rapid outbreak
investigation
and surveillance
Laboratory-based
screening / diagnosis
71. Polymerase Chain Reaction (PCR)
• Molecular technique to identify parasite
genetic material
• Uses whole blood collected in
anticoagulated tube or directly onto filter
paper
72. Polymerase Chain Reaction (PCR)
• Threshold of detection
– 5 parasites/µl
• Definitive species-specific diagnosis now
possible
• Can identify mutations – try to correlate to drug
resistance
• Parasitemia not quantifiable
• May have use in epidemiologic studies
• Requires specialized equipment, reagents, and
training
73. PCR: identification of malaria species
Lane S: Molecular base pair
standard (50-bp ladder). Black
arrows :size of standard bands.
Lane 1: P. vivax (size: 120 bp).
Lane 2: P. malariae (size: 144 bp).
Lane 3: P. falciparum (size: 205 bp).
Lane 4: P. ovale (size: 800 bp).
74. Comparison of methods for diagnosing Plasmodium
infection in blood
PARAMETER MICROSCOPY PCR FLUORESCENCE Dipstick HRP-2 Dipstick pLDH, ICT-Pf/Pv
Sensitivity
50 5 50 >100 >100
(parasites/micol)
P.f good, others P. falciparum and P.vivax good P.o
Specificity All species All species P. falciparum
difficult and P.m only Pldh
prarasite density crude
Yes No No crude estimation
or parasitemia estimation
time for result 30-60 min 24 hr 30-60 min 20 min 20 min
skill level High High Moderate Low Low
QBC apparatus
PCR or direct
equipment Microcsope Kit only Kit only
appratus fluorescence
microscope
cost /test Low High moderate/low Moderate Moderate
75. Hame jindgi apni kamiyo ko door karne ke bajay.
Bhagwan ne jo hame khubiya di hai unka upyog
karne me gujarni chahiye.
SPEAKER-DR. NARMADA PRASAD
TIWARI
76. a consequence was natural selection for
sickle-cell disease
, thalassaemias, glucose-6-phosphate
dehydrogenase
deficiency, ovalocytosis, elliptocytosis and
loss of the Gerbich antigen (glycophorin C)
and the Duffy antigen on
the erythrocytes because such blood
disorders confer a selective advantage
against malaria infection (balancing
selection).[7] The three major types of
inherited genetic resistance (sickle-cell
disease, thalassaemias, and glucose-6-
phosphate dehydrogenase deficiency)
were present in the Mediterranean world by
the time of the Roman Empire, about 2000
years ago.[8]
77. The term 'miasma' was coined
by Hippocrates of Kos who used it to
describe dangerous fumes from the ground
that are transported by winds and can
cause serious illnesses.[13] The name
malaria, derived from ‘mal’aria’ (bad air
in Medieval Italian). This idea came from
the Ancient Romans who thought that this
disease came from the horrible fumes from
the swamps