Malaria is a life-threatening disease caused by Plasmodium parasites transmitted via mosquito bites. It is most prevalent in developing countries, especially sub-Saharan Africa. The most severe form is caused by P. falciparum. Symptoms include fever, chills, and flu-like illness. Diagnosis involves microscopy of blood smears or rapid diagnostic tests to detect parasites. Treatment depends on the Plasmodium species and disease severity, ranging from chloroquine for non-severe P. vivax to artemisinin-based combination therapy for P. falciparum. Prevention involves mosquito control and antimalarial drugs. Malaria poses a major global health challenge but can be controlled through
Malaria is a life-threatening disease caused by parasites that are transmitted to people through the bites of infected female Anopheles mosquitoes. It is preventable and curable.
Malaria is a life-threatening disease caused by parasites that are transmitted to people through the bites of infected female Anopheles mosquitoes. It is preventable and curable.
Introduction, epidemiology, global trends, Indian setting, pathogenesis, life cycle, clinical manifestations, investigations, treatment regimen, prevention.
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 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
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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
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.
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
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!
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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
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
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
3. INTRODUCTION
• Malaria comes from Italian words “mal” and “aria”
meaning bad air.
• Mostly in developing country
• Death occur mostly in infant and children
• Malaria is curable if effective treatment is started
early.
• Chloroquine was effective for treating all cases but
recently chloroquine resistant pf malaria .
4. ETIOLOGY
• Malaria is a potentially life threatening parasitic
disease caused by P.vivax, P.falciparum, P.malariae,
P.ovale,
• After 2004, P.knowlesi (primate malaria ) southeast
Asia.
• Transmitted by the infective bite of female
Anopheles mosquito
• Transmitted through blood transfusion, use of
contaminated needles and trans placentally
5. ETIOLOGY
• Malaria is one of the major public health problems of
the India.
• India reports around one million malaria cases
annually.
• P. falciparum and P. vivax are the most common
species causing malaria
• P.vivax is more prevalent in the plain areas, while P.
falciparum predominates in forested and hilly
areas….
6. EPIDEMIOLOGY
• According to the latest WHO data, 216 million malaria
cases worldwide.
• 445 000 people died of malaria in 2016.
• With over 90% of these deaths occurring in sub-saharan
Africa.
• All the others occurring in south-east asia and south
america.
• Almost all malaria deaths are caused by plasmodium
falciparum.
• Most of these deaths occur in african children younger
than 5 years.
9. • API : confirmed cases during one year X 1000
population under surveillance
• ABER: number of slides examined X 100
population
• SPR : % of slide +ve for malarial parasite irrespective
of species
• SFR : % of slide +ve for falciparum
11. SITUATION IN INDIA
• 0.8 million confirmed cases -(NVBDCP 2017)
• Out of which 533801 plasmodium falciparum 104
deaths
• 76238 cases of malaria till April 2018 ,42 thousand
falciparum cases, 3 deaths
14. PATHOGENESIS
• Complex life cycle of plasmodium
• Asexual life cycle in human (intermediate host)
Exoerythrocytic and erythrocytic
• Sexual life cycle in female anaphele(definitive host)
sporogonic cycle
15. LIFE CYCLE OF PLASMODIUM
PARASITE
SHOWING THE DIFFERENT STAGES IN THE MALARIA LIFE CYCLE
17. FOUR IMPORTANT PATHOLOGIC
PROCESS
• Fever ( erythrocytic rupture and release of
merozoites)
• Anemia( hemolysis ,sequestration of RBC in spleen ,
bone marrow suppression)
• Immunopathologic event(release of pro-
inflammatory event TNF
• Tissue anoxia ( cytoadherence )
18. • RBC containing Hb S resist malaria parasite growth
• RBC lacking Duffy blood group resist to P.vivax
• RBC containing Hb F and ovalocytes resistant to
p.falciparum.
19. CLINICAL MANIFESTATION
• Children are asymptomatic during initial phase-the
incubation period.
– P.falcirum :9-14 days
– P.vivax :12-17 days
– P.ovale :16-17 days
– P.malariae:18-40 days
21. CLINICAL FEATURES
• Fever is the cardinal symptom of malaria.
intermittent with or without periodicity or
continuous.
• Many cases have chills and rigors.
• Non-specific & mimic like viral , enteric fever.
• Suspected in patients residing in endemic
• Recently visited endemic
22. • All clinically suspected malaria cases should be
investigated immediately by microscopy
and/or Rapid Diagnostic Test (RDT).
23. CONGENITAL MALARIA
• By all four species
• In endemic areas important cause of abortion, still
birth, premature births and IUGR.
• Placenta may be black in colour d/t malaria pigment
• Maternal t/t is inadequate to cure fetus
24. Congenital malaria
• CLINICAL MANIFESTATIONS(mc b/w 10 and 30
days of age)
• Fever
• Irritability
• Poor feeding
• Vomiting
• FTT
• Pallor
• Jaundice
• Hepatosplenomegaly
27. Clinical Diagnosis
• Signs and symptoms are nonspecific
• History of high grade fever with or without chills
• Headache, back pain, myalgia and abdominal pain
• Pallor, abnormal bleeding and Jaundice
• Respiratory distress, pulmonary edema and
circulatory collapse
• Impaired consciousness
• Splenomegaly (common), hepatomegaly
• Anemia, thrombocytopenia
29. Parasite detection
Thick blood film
• Used for screening of parasites.
• 5-10 parasites/µL
Thin blood film
• Species & stages of parasites
• 200 parasites/µL
• Percentage of infected erythrocytes
30. The Malaria Parasite
• Three developmental
stages seen in blood
films:
– Trophozoite
– Schizont
– Gametocyte
31. Different stain for microscopy
• Giemsa stain ( superior stain )
• Leishman stain
• Field’s stain( quick method of staining thick
without fixation)
32. Microscopy
Advantages
• Low direct costs
• High sensitivity
• Differentiation between plasmodium species
• Determination of parasite densities
• Ability to monitor response to therapy
34. QUANTITATIVE BUFFY COAT TEST
(QBC)
• Involve staining of centrifuged and
compressed red cell layer with acridine
orange and examination under UV light
source.
• Fast, easy, more sensitive
• Need special equipment, costly, more false
positivity d/t staining artifacts, not able to
differciate the parasite
35. Rapid Diagnostic Tests
• Immunochromatographic tests that detect
parasite specific antigen in a finger prick blood
sample
• NVBDCP supplies RDT kits for detection of P.
falciparum at locations where microscopy
results are not obtainable within 24 hours of
sample collection
36. Type of RDT-
• Based on
1. Histidine-Rich Protein 2 (HRP2)
2. Parasite specific lactate dehydrogenase
(pLDH)
3. Aldolase ( not used )
37. Criteria for selection of RDT
Recommendations are
i. For Pf:
Sensitivity and Specificity should be minimum
95% at parasite density level of 200 asexual
parasites/ul of blood
ii. For Pv:
Sensitivity: ≥75% at density of 200 parasites/ul
Specificity : ≥ 90%
39. Advantages
• Quick to perform (in practice, about 20 minutes)
• Sensitive in detecting P.falciparum, which causes
severe malaria
• Does not require skilled laboratory technicians
and can be used by health workers and non
health personnel after a few hours of training
• Does not require electricity or laboratory
equipment
40. False Negative result
– Insufficient parasites to register a positive result
– RDT kit damaged
– Illness by another species of malaria parasite
which RDT is not designed to detect
41. False Positive Result
– Dead parasite
– persistence of malaria gametocytes
– individuals with high immunity
42. Rapid Diagnostic Test
• Negative RDT should not preclude treatment
in a strongly suspected case, especially in
severe clinical disease
• RDTs do not quantitate P. falciparum
parasitemia
• Pf HRP-2 based kits may show positive result
up to three weeks after successful treatment
and parasite clearance.
43. 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
44. Polymerase Chain Reaction
• Detect parasite DNA
• Highly sensitive
• Very useful for detecting mixed infection,
particularly at low parasite density
• Identify drug resistance
• May have use in epidemiological investigations
• Not routinely available
• Differentiate b/w p.knowlesi and p.malaria , cant
be done by microscopy.
47. Uncomplicated malaria
• Defined as symptomatic malaria without signs
of severity or evidence (clinical or lab) of vital
organ dysfunction.
• Signs and symptom nonspecific
• Suspected clinically on basis of fever or history
of fever
48. TREATMENT
• Treatment of P. vivax malaria :
• Confirmed P. vivax cases should be treated with
chloroquine in full therapeutic dose of 25 mg/kg as
per the age-wise dosage schedule :
NO. OF TABLETS
AGE DAY 1
(10 mg /Kg)
DAY 2
(10 mg/Kg)
DAY 3
(5 mg/Kg)
< 1 YEARS 1/2 1/2 1/4
1-4 YEARS 1 1 1/2
5-8 YEARS 2 2 1
9-14 YEARS 3 3 1 1/2
>15 YEARS 4 4 2
49. Prevention of relapse
• P. vivax or P. ovale parasites remain
dormant in the liver cells in the form of
hypnozoites which can later cause a
relapse.
• For its prevention, primaquine should be
given at a dose of 0.25 mg/kg body
weight daily for 14 days under
supervision.
• Primaquine is contraindicated in
pregnant women, infants and known
G6PD deficient patients.
50. • Primaquine can lead to hemolysis in G6PD deficiency. Caution
should be exercised before administering primaquine in areas
known to have high prevalence of G6PD deficiency. Patient
should be advised to stop primaquine immediately if develops any
of the following symptoms and should report to the doctor
immediately:
(i) dark coloured urine
(ii) yellow conjunctiva
(iii) bluish discolouration of lips
(iv) abdominal pain
(v) nausea
(vi) vomiting
(vii) breathlessness
51. Treatment of Uncomplicated P. falciparum
malaria
• Artemisinin Combination Therapy (ACT) should be given to all the
confirmed P. falciparum cases found positive by microscopy or RDT.
• This is to be accompanied by single dose of primaquine (0.75 mg/kg
body weight) on Day 2.(0.25 mg/kg –WHO, G-6PD screening not
required)
• ACT consists of an artemisinin derivative combined with a
longacting antimalarial (amodiaquine, lumefantrine, mefloquine,
piperaquine or sulfadoxine-pyrimethamine).
• The ACT recommended in the National Programme all over India
except northeastern states is artesunate (4 mg/kg body weight)
daily for 3 days and sulfadoxine (25 mg/kg body weight) –
pyrimethamine (1.25 mg/kg body weight) [AS+SP] on Day 0.
52.
53. • In the northeastern states (Arunachal Pradesh, Asom,Manipur,
Meghalaya, Mizoram, Nagaland, and Tripura), due to the recent
reports of late treatment failures to the current combination of AS+SP
in P. falciparum malaria, the presently recommended ACT in national
drug policy is fixed dose combination (FDC) of Artemether-
lumefantrine (AL).
• Although the ACT used in the national programme in NE states
is AL and rest of India is AS+SP, the other fixed dose combinations
registered for marketing in India are artesunate-amodiaquine,
artesunate-mefloquine and arterolane-piperaquine (for adults
only) and can be used for treatment of uncomplicated P. falciparum
or mixed infections.
54.
55. Treatment of malaria in pregnancy
The ACT should be given for treatment of P. falciparum malaria
in second and third trimesters of pregnancy, while quinine is
recommended in the first trimester. Plasmodium vivax malaria
can be treated with chloroquine.
Treatment of mixed infections
Mixed infections with P. falciparum should be treated as
falciparum malaria. Since AS+SP is not effective in vivax malaria,
other ACT should be used. However, anti-relapse treatment
with
primaquine can be given for 14 days, if indicated.
56. Few available fixed dose combinations
• CHLOROQUINE –TABLETS-100 ,150 ,300 mg BASE (150 mg
base=250 mg phosphate salt or 200 mg sulfate salt)
⮚ Syrup- 50 mg base=5ml
• ACT combinations available :
⮚ Falcigo plus kit –artesunate 50 mg + mefloquine 250 mg
⮚ Larinate 200 kit- artesunate 200 mg + sulphadoxine 500
mg+pyrimethamine 25 mg (larinate 50,100 also avialable)
⮚ Larinate –MF :artesunate 200 mg +mefloquine 250 mg
⮚ Tab. Lumerax-20 DT, Combither ,,ARH-L (Artemether 20 mg +
lumefantrine120 mg) , lumerax -40 and 80 also available.
⮚ Syp- lumerax-20/120/ 5 ml
⮚ Syp- lumether-40/240/ 5 ml
• Primaquine –tablets;7.5 and 15 mg
57. Treatment based on clinical criteria without
laboratory confirmation
All the efforts should be made to diagnose malaria either by
microscopy or RDT. However, special circumstances should be
addressed as mentioned below:
● If RDT for only P. falciparum is used, negative cases showing
signs and symptoms of malaria without any other obvious
cause for fever should be considered as ‘clinical malaria’ and
treated with chloroquine in full therapeutic dose of 25 mg/kg
body weight over three days. If a slide result is obtained later,
the treatment should be completed according to species.
● Suspected malaria cases not confirmed by RDT or microscopy
should be treated with chloroquine in full therapeutic dose.
58. General recommendations for the management of
uncomplicated malaria
• Avoid starting treatment on an empty stomach. The first
dose should be given under observation.
• Dose should be repeated if vomiting occurs within half an
hour of antimalarial intake.
• The patient should be asked to report back, if there is no
improvement after 48 hours or if the situation deteriorates.
• The patient should also be examined and investigated for
concomitant illnesses.
59. TREATMENT FAILURE/DRUG RESISTANCE
• After treatment patient is considered cured if
he/she does not have fever or parasitaemia till
Day 28.
• Some patients may not respond to treatment
which may be due to drug resistance or
treatment failure, especially in falciparum
malaria.
60. Early treatment failure (ETF):
Development of danger signs or severe malaria
on Day 1, 2 or 3, in the presence of
parasitaemia;
⮚ Parasitaemia on Day 2 higher than on Day 0,
irrespective of axillary temperature;
⮚ Parasitaemia on Day 3 with axillary
temperature >37.5°C;
⮚ and Parasitaemia on Day 3, >25% of count on
Day 0.
61. Late clinical failure (LCF):LATE TRAETMENT FAILURE
Development of danger signs or severe malaria in the presence
of parasitaemia on any day between Day 4 and Day 28 (Day
42) in patients who did not previously meet any of the criteria
of early treatment failure;
The presence of parasitaemia on any day between Day 4 and
Day 28 (Day 42) with axillary temperature >37°C in patients who
did not previously meet any of the criteria of early treatment
failure.
62. Late parasitological failure (LPF):
Presence of parasitaemia on any day between Day 7 and Day
28 with axillary temperature <37.5°C in patients who did not
previously meet any of the criteria of early treatment failure or
late clinical failure.
Such cases of falciparum malaria should be given alternative
ACT or quinine with Doxycycline.
Doxycycline is contraindicated in pregnancy, lactation and in
children up to 8 years.
Treatment failure with chloroquine in P. vivax malaria is rare in
India.
64. SEVERE MALARIA
Severe malaria is characterized by one or more of the following
features :
• Impaired consciousness/coma
• Repeated generalized convulsions
• Renal failure (Serum Creatinine >3 mg/dl)
• Jaundice (Serum Bilirubin >3 mg/dl)
• Severe anaemia (Hb <5 g/dl) ,In > 12 years old patients < 7 gm %
• Pulmonary oedema/acute respiratory distress syndrome
• Hypoglycaemia (Plasma Glucose <40 mg/dl , treatment threshold
for < 5 year-54 mg/dl)
65. Severe malaria
• Metabolic acidosis
• Circulatory collapse/shock (Systolic BP <80 mm Hg, <70 mmHg in
children)
• Abnormal bleeding and Disseminated intravascular coagulation (DIC)/
Haemoglobinuria
• Hyperpyrexia (Temperature >106°F or >42°C) (NVBDCP)
• Hyperparasitaemia (>5% parasitized RBCs , WHO- > 10 %)
• Prostration (WHO)
66. Diagnosis of severe malaria cases negative on microscopy
Microscopic evidence may be negative for asexual parasites in
patients with severe infections due to sequestration and partial
treatment. Efforts should be made to confirm these cases by
RDT
or repeat microscopy. However, if clinical presentation
indicates
severe malaria and there is no alternative explanation these
patients should be treated accordingly.
67. Specific antimalarial treatment of severe
malaria
• Artesunate: 2.4 mg/kg body weight i.v. or i.m. given on
admission (time=0), then at 12 and 24 hours, then once a
day(Care should be taken to dilute artesunate powder in
5%Sodium bi-carbonate provided in the pack).
• Artemether: 3.2 mg/kg body weight i.m. given on admission
then 1.6 mg/kg body weight per day.
68. • Quinine: 20 mg quinine salt/kg body weight on admission
(i.v. infusion in 5% dextrose/dextrose saline over a period
of 4 hours) followed by maintenance dose of 10 mg/kg body
weight 8 hourly; infusion rate should not exceed 5 mg/kg
body weight per hour.
Loading dose of 20 mg/kg body weight should not be given, if the
patient has already received quinine.
NEVER GIVE BOLUS INJECTION OF QUININE.
If parenteral quinine therapy needs to be continued beyond 48
hours, dose should be reduced to 7 mg/ kg body weight 8 hourly.
( WHO -10mg/kg 12 hrly )
69. FOLLOW ON TREATMENT
• Once the patient can tolerate oral therapy or
after at least 24 hours of parenteral therapy,
further follow-uptreatment should be as
below:
• Patients receiving artemisinin derivatives
should get full course of oral ACT. However,
ACT containing mefloquine should be avoided
in cerebral malaria due to neuropsychiatric
complications.
• Patients receiving parenteral quinine should
also betreated with full course of oral ACT.
70. • In first trimester of pregnancy, parenteral
quinine is the drug of choice.
• If quinine is not available, artemisinin derivatives
may be given to save the life of mother. In second
and third trimester, parenteral artemisinin
derivatives are preferred
73. Severe malaria due to P. vivax
• In recent years, increased attention has been
drawn to severe malaria caused by P. vivax.
• Some cases have been reported in India,
and there is reason to fear that this problem may
become more common in the coming years.
• Severe malaria caused by P. vivax
should be treated like severe P. falciparum
malaria, however, primaquine should be given for
14 days for preventing relapse as per guidelines
after the patient recovers from acute illness and
can tolerate primaquine.
74. SIDE EFFECTS OF ANTIMALARIALS
• Artemether:
– Dizziness, reticulocytopenia, neutropenia, elevated
liver enzymes, prolonged QT interval, bradycardia
• Artesunate:
– GI disturbances, cough, rash, arthralgia, delayed
hemolysis
• Chloroquine:
– Pleuritis, headache, hepatitis, widening of QRS and QT
interval, nausea, vomiting, retinopathy, keratopathy,
hair loss
75. SIDE EFFECTS OF ANTIMALARIALS
• Mefloquine:
– Hepatitis, polyneuropathy, skin rashes, C/I in
cerebral malaria
• Primaquine:
– Hypertension, cardiac arrythmia
• Sulfadoxine-pyrimethamine:
– SJS, TEN, Erythema multiforme, C/I in
documented megaloblastic anaemia d/t folate
deficiency
77. CHEMOPROPHYLAXIS
• Chemoprophylaxis is recommended for travellers,
migrant labourers and military personnel exposed to
malaria in highly endemic areas.
• Short-term chemoprophylaxis (less than 6 weeks)
Doxycycline: 100 mg daily in adults and 1.5 mg/kg
body weight for children more than 8 years old. The
drug should be started 2 days before travel and
continued for 4 weeks after leaving the malarious
area
78. Long-term chemoprophylaxis (more than 6 weeks)
• Mefloquine: 5 mg/kg body weight (up to 250 mg) weekly and
should be administered two weeks before, during and four weeks
after leaving the area.
Mefloquine is contraindicated in cases with history of convulsions,
neuropsychiatric problems and cardiac conditions
79. Malaria control strategies
1. Early case Detection and Prompt Treatment
(EDPT)
2. Vector Control
3. Community Participation
4. Environmental Management & Source
Reduction Methods
80. Early case Detection and Prompt
Treatment
• EDPT is the main strategy of malaria control - radical
treatment is necessary for all the cases of malaria to
prevent transmission of malaria.
• Chloroquine is the main anti-malaria drug for
uncomplicated malaria.
• Drug Distribution Centres (DDCs) and Fever Treatment
Depots (FTDs) have been established in the rural areas
for providing easy access to anti-malarial drugs to the
community.
• Alternative drugs for chloroquine resistant malaria are
recommended as per the drug policy of malaria
81. Vector Control
• Chemical Control
– Use of Indoor Residual Spray (IRS) with insecticides
recommended under the programnme
– Use of chemical larvicides like Abate in potable water
– Aerosol space spray during day time
– Malathion fogging during outbreaks
• Biological Control
– Use of larvivorous fish in ornamental tanks, fountains
etc.
82. Mosquito control
measures
Anti larval
environmental
Chemical
(mineral oil,paris green,
fenthion,chlorpyrifos
Biological
Antiadult
Residual spray
(DDT,
malathion,lindane,OMX##
)
Space
spray(pyrithrim)
Genetic control
Personal
protection
Mosquito net
Repellant.(DEET)
Screening with
copper and
bronze
83. Personal Prophylatic Measures
• Use of mosquito repellent creams, liquids,
coils, mats etc.
• Screening of the houses with wire mesh
• Use of bednets treated with insecticide
• Wearing clothes that cover maximum surface
area of the body
84. Community Participation
• Sensitizing and involving the community for
detection of Anopheles breeding places and
their elimination
• NGO schemes involving them in programme
strategies
85. Environmental Management &
Source Reduction Methods
• Source reduction i.e. filling of the breeding
places
• Proper covering of stored water
• Channelization of breeding source
87. Malaria vaccine
• More than 30 P. falciparum malaria vaccine
candidates are at either advanced preclinical or
clinical stages of evaluation.
• Only the RTS,S/AS01 vaccine has completed Phase
3 evaluation and received a positive regulatory
assessment.
• WHO has developed a set of principles to ensure
the quality, safety, and efficacy of recombinant
vaccines targeting pre-erythrocytic and blood
stage malaria parasites.
88. • The vaccine has been recommended by WHO
for pilot introduction in selected areas of 3
African countries
• The vaccine will be made available through
routine immunization programmes to young
children living in selected areas in Ghana,
Kenya and Malawi. At least 360 000 children
in the selected areas will be vaccinated.
89. TAKE HOME MESSAGE
• Malaria is a potentially life threatening parasitic
disease and fortunately treatable.
• Acc to WHO 216 million malaria cases reported and
about 4.5 lakh deaths.
• India .8 million confirmed cases & 104 death in 2017.
• Classical sign & symptom may not be present
paediatric age group.
• All suspected malaria cases should promptly
investigated by RDT & microscopy.
90. • Empirical treatment should only be given if
illness could not be explained by any cause
and if high index of suspicion of malaria
• Anti malarial treatment once started should
be completed.
• Test using ab detection & PCR are not useful
for diagnosis
• Antibody detecting rapid diagnostic tests are
banned in India.
91. • Suspected severe malaria cases should receive
pre referral treatment depending upon the
availability
• Children < 20 kg BW should receive high dose
artesunate( 3mg/kg BW)