This document provides information on malaria epidemiology, causative organisms, life cycle, diagnosis and management in pregnancy. Some key points:
- Malaria affects over 40% of the world's population, with India contributing 70% of cases in Southeast Asia. It is a leading cause of infectious death.
- Plasmodium falciparum is the most dangerous species and a major cause of mortality. It is transmitted via the bite of infected Anopheles mosquitoes.
- Malaria in pregnancy leads to worse outcomes for both mother and baby, including higher mortality, anemia, low birth weight, stillbirth and neonatal mortality.
- Diagnosis involves blood smear microscopy, antigen detection tests and
For pregnant women diagnosed with uncomplicated malaria caused by chloroquine-resistant P. vivax infection, prompt treatment with artemether-lumfantrine (second and third trimesters) or mefloquine (all trimesters) is recommended. Doxycycline and tetracycline are generally not indicated for use in pregnant women
For pregnant women diagnosed with uncomplicated malaria caused by chloroquine-resistant P. vivax infection, prompt treatment with artemether-lumfantrine (second and third trimesters) or mefloquine (all trimesters) is recommended. Doxycycline and tetracycline are generally not indicated for use in pregnant women
Preeclampsia is a disorder that is unique to human pregnancy, and the only known cure for this complication is delivery. Preeclampsia affects approximately 4% to 5% of pregnancies . The Preeclampsia Foundation states that: “Globally, preeclampsia and other hypertensive disorders of pregnancy are a leading cause of maternal and infant illness and death. By conservative estimates, these disorders are responsible for 76,000 maternal and 500,000 infant deaths each year.” As is evident from the statement that, preeclampsia is a major contributor to maternal and fetal morbidity and mortality worldwide. In India, the incidence of preeclampsia is reported to be 8-10% among the pregnant women. According to a study, the prevalence of hypertensive disorders of pregnancy was 7.8% with preeclampsia in 5.4% of the study population in India
Preeclampsia is a disorder that is unique to human pregnancy, and the only known cure for this complication is delivery. Preeclampsia affects approximately 4% to 5% of pregnancies . The Preeclampsia Foundation states that: “Globally, preeclampsia and other hypertensive disorders of pregnancy are a leading cause of maternal and infant illness and death. By conservative estimates, these disorders are responsible for 76,000 maternal and 500,000 infant deaths each year.” As is evident from the statement that, preeclampsia is a major contributor to maternal and fetal morbidity and mortality worldwide. In India, the incidence of preeclampsia is reported to be 8-10% among the pregnant women. According to a study, the prevalence of hypertensive disorders of pregnancy was 7.8% with preeclampsia in 5.4% of the study population in India
An Obstetrics and gynecology presentation: A 20 years old single female undergraduate presents to the emergency unit with fever, lower abdominal pain and abnormal vaginal discharge of 5 days duration. Discuss her management
Menopause: Symptoms, Concerns, and Management StrategiesSummit Health
Presentation about menopause, including information about common symptoms such as hot flashes, sleeplessness, and weight gain as well as other physiologic changes such as bone loss and cardiovascular risks. Dr. Gibbons and Dr. Cummings will offer recommendations on treatment and management options that can help you navigate this important life transition.
A comprehensive guide to the management of hyperglycaemia in pregnancy aimed at the primary care physician and based on latest evidenced based criteria. Includes information from latest studies such as HAPO study and ACHOIS, and involves guidelines from the IADPSG, ADA, WHO and Malaysia.
dr jaideep malhotra talking on malaria in pregnancy at the MEDICAL DISORDERS WORKSHOP.....jam paccked halls at AICOG 2013 ................enjoy the presentation
Malaria in pregnancy by dr alka mukherjee nagpur m.s. indiaalka mukherjee
An estimated 125 million pregnancies per year are at risk of malaria around the world.1 For both mother and child, malaria is potentially life-threatening. MMV’s MiMBa strategy aims to raise the standard of care for pregnant women and their newborns affected by malaria.
Key elements of the MiMBa strategy include:
• Ensuring drug supplies for children and pregnant women;
• Generating data on existing compounds to inform on their use in pregnant women and neonates;
• Developing new antimalarial medicines to address the needs of pregnant women and neonates;
• Strengthening the capture of safety data from routine clinical use of antimalarial medicines during pregnancy;
• Advocating for changes in drug development that promote the safe inclusion of pregnant women into clinical studies, with the aim of generating data to support earlier access to innovative medicines for this population.
• Pregnant women are especially susceptible to malaria infection. Without existing immunity, severe malaria can develop requiring emergency treatment, and pregnancy loss is common. In semi-immune women, consequences of malaria for the mother include anaemia while stillbirth, premature delivery and foetal growth restriction affect the developing foetus. Preventive measures include insecticide-treated nets and (in some African settings) intermittent preventive treatment. Prompt management of maternal infection is key, using parenteral artemisinins for severe malaria, and artemisinin combination treatments (ACTs) in the second and third trimesters of pregnancy. ACTs may soon also be recommended as an alternative to quinine as a treatment in the first trimester of pregnancy. Monitoring the safety of antimalarials and understanding their pharmacokinetics is particularly important in pregnancy with the altered maternal physiology and the risks to the developing foetus. As increasing numbers of countries embrace malaria elimination as a goal, the special needs of the vulnerable group of pregnant women and their infants should not be overlooked.
An infection is the invasion of an organism's body tissues by disease causing agents, their multiplication, and the reaction of host tissues to the infectious agents and the toxins they produce. An infectious disease, also known as a transmissible disease or communicable disease, is an illness resulting from an infection.
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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.
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.
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
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
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.
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.
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
Maxilla, Mandible & Hyoid Bone & Clinical Correlations by Dr. RIG.pptx
Malaria in pregnancy
1. EPIDEMIOLOGY
• 40 % of world’s population affected by Malaria.
(WHO)
• Of the 2.5 million reported cases in the South East
Asia, India alone contributes about 70% of the total
cases.
• >25million woman are at risk of malaria(WHO)
• Maiaria is 2nd most common cause of infectious
death after T.B.
• Deaths- Under estimated/Unknown,1.1 to 2.7 million
per year
• India most affected area are
UP,Bihar,Karnataka,Rajasthan MP
• Gender related mortality - Females more
2. Malaria in Pregnancy:
•Mutually aggravating
•Mortality is double
•Primigravidae - 60-70%
•Highest prevalence in second half.
•Plasmodium Falciparum – More common
3. Gravidity and malaria
• Primigravida have no pre-existing immunity to placental
parasites and are highly susceptible.
• In high transmission areas, primigravida develop
immunity to placental parasites and are protected in
subsequent pregnancies.
• In low transmission areas, multigravida are unexposed
and unprotected
4. CAUSATIVE ORGANISM
• Malaria vector borne disease caused by
protozoan plasmodium
1.P.falciparum(most dangerous account for
90%death d/t malaria)
2.P.vivax(most widely spread species)
3.P.malariae
4.P.ovale
5.P.knowlesi(malaria in macaques but can
infect human)
5. • Malaria transmitted by
mosquito female
Anopheles
1.Bite of infected
mosquito
2.Congenital infection
3.Blood transfusion
4.Contaminated needle
5.Organ transplantation
6. SOME FACTS ABOUT ANOPHELES
They choose their victim by odor.
Males are more frequently bitten.
Most common time of bite is late evening to early
morning with peak at midnight.
Stylets cut & proboscis probe for tiny blood vessels in
the skin. If it does not strike blood proboscis is withdrawn
and struck again at different angle.
They can fly for few Km.
Their life span is 2–3 weeks.
Human blood is needed to lay eggs and nourish eggs.
7. LIFE CYCLE OF PLASMODIUM
• Human - intermediate host(asexual cycle)
• Mosquito-definitive host(sexual cycle)
• Infective form for human-sporozoite(in
salivary gland of mosquito)
8. • P.vivax affect young RBC
• P.falciparum- all stages RBC
• P.malariae-old RBC
9.
10. Malaria in Pregnancy : Double
Trouble
• Malaria is more common in pregnancy
compared to the general population.
• Malaria in pregnancy tends to be more
atypical in presentation. This could be due
to the hormonal, immunological and
hematological changes of pregnancy.
• The parasiteamia tends to be 10 times higher.
• P. falciparum malaria in pregnancy being
more severe, the mortality is also double (13
%) compared to the non-pregnant population
(6.5%).
11. • During normal pregnancy, the cellular immune response
(Th1) is suppressed to prevent fetal rejection.
• Malaria stimulates the Th1 response intrauterine
growth retardation.
• Malaria stimulates expression of an HIV co-receptor
(CCR5) in the placenta.
• Generalised immunosuppression in pregnancy with
reduction in gamma globulin synthesis and inhibition of
reticulo endothelial system, resulting in
– Decrease in the levels of anti malarial antibodies and
loss of acquired immunity to malaria.
-more prone for malarial infection and the parasitemia
tends to be much higher.
12. Change in placenta
• Placenta is the preferred site of
sequestration and development of
malarial parasite.
• Intervillous spaces are filled with
parasites and macrophages, interfering
with oxygen and nutrient transport to the
foetus.
• Villous hypertrophy and fibrinoid
necrosis of villi
• All the placental tissues exhibit malarial
pigments
14. CLINICAL FEATURES
FEVER
• Stage 1-Cold stage
• Chills for 15 mt to 1 hour
• Caused due to rupture from the host red cells escape
into Blood
• Preset with nausea, vomitting,headache
– Stage 2-Hot stage
• Fever may reach upto 400
c may last for several hours
starts invading newer red cells.
• Stage 3-Sweating stage
Patent starts sweating, concludes the episode.
Cycles are frequently Asynchronous
Paroxysms occur every 48 – 72 hours
In P.malariae pyrexia may last for 8 hours or more and
temperature my exceed 410C
15. • Interval between fever
• 48hrs -Malaria tertiana (P.vivax,P.ovale)
• 72hrs -Malaria quartiana(P.malariae)
• Irregular high grade fever(P.falciparum)
16. • Anemia :
– In developing countries, where malaria is most
common, anemia is a common feature of pregnancy.
– Malnutrition and helminthiasis are the commonest
causes of anemia.
– In such a situation, malaria will compound the
problem.
» Anemia may even be the presenting feature
of malaria and therefore all cases of anemia
should be tested for M.P.
– Anemia as a presenting feature is more common in
partially immune multigravidae living in hyper
endemic areas.
17. ANAEMIA
• Malaria can cause or aggravate anaemia due to:
– Hemolysis of parasitised red blood cells.
– Increased demands of pregnancy.
– Profound hemolysis can aggravate folate deficiency.
• Anemia due to malaria is more common and
severe between 16-29 weeks.
• It can develop suddenly, in case of severe
malaria with high grades of parasitemia.
• Pre existing iron and folate deficiency can exacerbate the anemia of
malaria and vice versa.
18. • Splenomegaly :
– Enlargement of the spleen may be variable.
• Complications :
– Complications tend to be more common and more severe in
pregnancy.
– A patient may present with complications of malaria or they may
develop suddenly.
– Acute pulmonary edema,
– hypoglycemia
– anemia are more common in pregnancy.
– Jaundice, convulsions, altered sensorium, coma, vomiting /
diarrhoea and other complications may be seen.
20. ACUTE PULMONARY EDEMA
• Acute pulmonary oedema is also a more common complication of
malaria in pregnancy compared to the non-pregnant population.
• It may be the presenting feature or can develop suddenly after
several days. It is more common in 2nd
and 3rd
trimesters.
• It can develop suddenly in immediate post-partum period. This
is due to
– Auto transfusion of placental blood with high proportion of
parasitised RBC’s
– Sudden increase in peripheral vascular resistance after delivery.
• It is aggravated by pre existing anaemia and hemodynamic
changes of pregnancy.
• Acute pulmonary oedema carries a very high mortality.
21. HYPOGLYCEMIA
• This is another complication of malaria that is
peculiarly more common in pregnancy.
• The following factors contribute to hypoglycemia:
– Increased demands of hypercatabolic state and
infecting parasites.
– Hypoglycaemic response to starvation.
– Increased response of pancreatic islets to secretory
stimuli (like quinine) leads to hyperinsulinemia and
hypoglycemia..
22. • Hypoglycaemia in these patients can remain
asymptomatic and may not be detected,
because:
– all the symptoms of hypoglycemia are also caused by
malaria viz. tachycardia, sweating, giddiness etc.
– Some patients may have abnormal behaviour,
convulsions, altered sensorium, sudden loss of
consciousness etc.
– These symptoms of hypoglycemia may be easily
confused with cerebral malaria.
– Therefore, in all pregnant women with falciparum
malaria, particularly those receiving quinine,
blood sugar should be monitored every 4-6 hours.
23. CEREBRAL MALARIA
Needs Intensive care
1. ABC of coma care
2. Prompt institution of antimalarials
3. Treatment of hyperpyrexia
4. Management of other complications
5. Treatment of associated infections
24. Effect of malaria on foetus
Malaria in pregnancy detrimental to foetus
due to-
a.high grade fever
b.placental insufficiency
c.hypoglycemia
d.anaemia
25. • There is interesting fact that primigravidas
may develop more clinical symptoms of
malaria, woman with higher immunity may
not demonstrate sympt. but they may
have more placental burden so more fetal
complications
26. Resulting in-
• Spontaneous abortion
• Premature birth
• I.U.G.R.
• Still birth
• Low birth weight
• Congenital malaria<5%(b/c of protection
by maternal IgG) more with P.malariae
• Perinatal and neonatal mortality 15%-70%
(P.vivax 15.7%,P.falciparum 33%)
29. DIAGNOSIS
• High level of awareness
• Peripheral blood smear (Gold standard)
thick smear: rapid diagnosis
thin : species identification
• other advantages
If negative : repeat blood test 6 hourly for 6 times
• Antigen detection techniques : (PfHPR-2)
• Fluorescent staining
• PCR based assay
• Antibody test
• Placental blood smear
• Currently available rapid diagnotic tests are as follows-
• Histidine rich protein two (HRP 2) – asexual stages &
young gametocyte of Pfalciparum
• Parasite lactate dehydrogenas – for all 4 types
• Plasmodium aldolase – for all four types
30. sample collection-any time irrespective to
fever but before administration of
antimalarial drugs
Advantage:-
• can diagnose 5-
10parasites/ml
• identificatin of species
&stage of parasite
• parasite density
• malarial pigment in
neutrophils
&monocyte
• Disadvantage:-
• time consuming
• skilled technician
• in mixed infection one
species suppress
32. • parasites are not detected at
times in peripheral smear :-
a. sequestration deep vascular bed
b. partially treated patients
c. prophylactic antimalarial t/t
d. inexperienced technician
e. poor quality staining
33. RAPID DIAGNOSTIC TEST
Currently available rapid diagnotic tests are as follows-
Histidine rich protein two (HRP 2) – asexual stages & young gametocyte of
Pfalciparum
Parasite lactate dehydrogenas – for all 4 types
Plasmodium aldolase – for all four types
WHO- A MINIMUM STANDARD OF 95% SENSITIVITY FOR P.FALCIPARUM DENSITIES
OF 100 PARASITES/L OF BLOOD AND A SPECIFICITY OF 95%
HRP-II with parasite density 100/ml of blood -90% - with 10/ml -75%
HRP-II remain positive for 1-3wk.
p LDH remain positive for 5 days.
34. Antigen detection tests
Principle: dipstick antigen capture assay employs a monoclonal
antibody detecting the Pf.HRP-2 antigen in the blood
Rapid, simple, sensitive test
Species specificity Optimal Assay
Control
Plasmodium pan specific
monoclonal antibody
P. falciparum
specific
monoclonal
antibody
35. Antibody detection (not for acute infection)
a.RIA
b.ELISA
=
Antigen-antibody
complex
Patient’s serum
contains specific
and non-specific
antibodies
+
Antigen
36. QBC TEST
Spinning blood in a specialised capillary tubes in
which parasite DNA is stained with acridine
orange.
Detected by ultraviolet microscope
PCR TEST:-
SENSITIVE CAN IDENTIFY DIFFERENT SPECIES
WITHin 48-72 hrs but expensive
38. MANAGEMENT
Management of malaria in pregnancy
involves the following three aspects and
equal importance should be attached to
all the three.
• Treatment of malaria
• Management of complications
• Management of labour
39. TREATMENT OF MALARIA
• Treatment of malaria in pregnancy should be energetic, anticipatory and
careful.
• Energetic:
• Don't waste any time.
• It is better to admit all cases of P. falciparum malaria.
• Assess severity- General condition, pallor, jaundice, BP,
temperature, hemoglobin, Parasite count, SGPT, S. bilirubin, S. creatinine,
Blood sugar.
• Anticipatory:
• one should always be looking for any complications by regular
monitoring.
• Monitor maternal and fetal vital parameters 2 hourly.
• RBS 4-6 hourly; hemoglobin and parasite count 12 hourly; S.
creatinine; S. bilirubin and Intake / Output chart daily.
40. • Careful:
• The physiologic changes of pregnancy pose special problems
in management of malaria.
• Certain drugs are contraindicated in pregnancy or may cause
more severe adverse effects. All these factors should be taken
into consideration while treating these patients.
• Choose drugs according to severity of the disease/ sensitivity
pattern in the locality.
• Avoid drugs that are contraindicated.
• Avoid over / under dosing of drugs
• Avoid fluid overload / dehydration
• Maintain adequate intake of calories.
41. MANAGEMENT OF MALARIA IN PREGNANCY
• Treatment depends on -
a.severity of disease
b.getational age
• WHO recommended -in endemic area t/t
should started within 24hrs after 1st
symptom.
a.uncomplicated malaria -OPD basis t/t
b.complicated malaria-Hospitalisation
42. • DOC in pregnancy(WHO)
a. All trimester
1st line- chloroquine,quinine
2nd line -artesunate,artemether.arteether
b.2nd &3rd trimester
pyrimethamine+sulphadoxine,mefloquine
NIMR GUIDLINE 2010
• Quinine in 1st trimester
• chloroquine for P.vivax
• ACT for t/t of P.falciparum in 2nd &3rd trimester
• ACT containing mefloquine should avoided in cerebral
malaria d/t neuropsychiatric complication
43. Drugs contraindicated in pregnancy
• Tetracycline
– Cause abnormalities of skeletal and muscular growth, tooth
development, lens/cornea
• Doxycycline
– Risk of cosmetic staining of primary teeth is undetermined
– Excreted into breast milk
• Primaquine
– Harmful to newborns who are relatively Glucose-6-Phosphatase-
Dehydrogenase (G6PD) deficient
• Halofantrine
– No conclusive studies in pregnant women
– Has been shown to cause unwanted effects, including death of
the fetus, in animals
44. DRUGS
• Chloroquine:
– 600mg (base) start, 300mg after 6 hours, 24 hours & 48 hours
• Quinine:
– IV - 20mg/kg infusion over 4 hours, repeat 8 hourly.
– Maintenance: 10mg over 4 hours, 8 hourly.
Follow with oral medication after clinically stable.
• Oral – 600mg 8hourly ( maximum 2 gm / day) for 7 days.
• Presently fixed dose combinations of
• Artesunate + amodiaquine
• Blister pack of artesunate +mefloquine
45. Artemisinin compounds(rapid
Schizonticidal)
• Artesunate(Falcigo):
– Oral-100mg BD on day 1, then 50mg BD for 4-6 days (Total
dose 10mg/kg).
– IM / IV-120mg on Day 1 followed by 60mg daily for 4 days. In
severe cases an additional dose of 60mg after 6 hours on Day 1.
• Artemether(Larither):
– Six amp (480mg) IM in 5 / 3 days
– 80mg BD X3 days
• Arteether(Emal inj):
– One amp (150mg) IM / day for3 consecutive days.
46. UNCOMPLICATED MALARIA
• Oral quinine 600mg 8hrly for 7days
OR
• Chloroquine 10mg/kg f/b 10mg/kg at
24 hrs & 5mg/kg at 48 hrs
• Avoid starting t/t on empty stomach
• 1st dose given under observation
• repeat dose if vomitting within 30min
• ask to report back if no improvement/deteriorate
47. COMPLICATED MALARIA
• Signs of uncomplicated malaria, plus:
• Dizziness
• Breathlessness
• Sleepy/drowsy
• Confusion/coma
• Sometimes fits, jaundice, severe dehydration
48. COMPLICATED MALARIA
• Artesunate i.v. 2.4mg/kg at 0,12,24hrs f/b
daily when pt able to take orally
artesunate2mg/kg daily for 7days
• Quinine i.v.20mg/kg in D5% over 4hrs f/b
10mg/kg over 4hrs 8hrly (max dose of
quinine 1.4gm) when pt able to take orallly
quinine 600mg tds for 7 days
49. DRUG RESISTANCE
• Resistance of P. falciparum to antimalarial drugs is an ever
increasing problem
• WHO recommends these combinations,incase of drug
resistance.
• Artemether–lumefantrine,
• Artesunate– amodiaquine,
• Artesunate–mefloquine,
• Artesunate–sulfadoxine–pyrimethamine, area dependent
• Dihydroartemisinin–piperaquine.
50. VIVAX MALARIA
• Chloroquine sensitive
chloroquine base 10mg/kg OD for 2 days f/b
5mg/kg on day 3
• Chloroquine resistant
Quinine salt 10mg/kg BD for 7days
or
Mefloquine 15mg/kg single dose
or
Artesunate 4mg/kg in divided loading dose
f/b 2mg/kg OD for 6 days
51. FALCIPARUM MALARIA
• Chloroquine sensitive
Chloroquine base 10mg/kg OD for 2days f/b 5mg/kg on
day 3
• Chloroquine Resisant
sulfadoxine(500mg)/pyrimethamine(25mg) 3tab single dose
or
Quinine salt 10mg/kg TDS for 7days
or
quinine salt 10mg/kg TDS for 3 days+
sulfadoxine/pyrimethamine 3 tab single dose on 1st day
52. MANAGEMENT OF COMLICATION OF
MALARIA
• Acute Pulmonary Oedema:
– Careful fluid management; back rest; oxygen; diuretics; ventilation if needed.
• Hypoglycaemia:
– 25-50% Dextrose, 50-100 ml I.V., followed by 10% dextrose continuous infusion.
– If fluid overload is a problem, then Inj. Glucagon 0.5-1 mg can be given intra
muscularly.
– Blood sugar should be monitored every 4-6 hours for recurrent hypoglycemia.
• Anemia:
– Packed cells should be transfused if haemoglobin is <5 g%.
• Rnal failure:
• Reenal failure could be pre-renal due to unrecognised dehydration or renal due to severe
parasitemia.
– Treatment involves careful fluid management, diuretics, and dialysis if needed.
• Septicaemic shock(ALGID MALARIA)
– Secondary bacterial infections like urinary tract infection, pneumonia
etc. are more common in pregnancy associated with malaria. .
– Treatment involves administration of 3rd generation cephalosporins,
fluid replacement, monitoring of vital parameters and intake and output.
• Exchange transfusion:
– Exchange transfusion is indicated in cases of severe falciparum malaria
to reduce the parasite load.
– It is especially useful in cases of very high parasitemia (helps in
clearing) and impending pulmonary oedema (helps to reduce fluid load).
53. • Radical Cure:-
for prevention of relapse of P.vivax
Tab chloroquine 300mg/wk untill stoppage
of lactation,complete therapeutic t/t given
at that time chloroquine & primaquine
given for 14 days
• Mixed infection :-
std therapy for uncomplicated/complicated
malaria f/b course of primaquine
54. DURING LABOUR
• Careful monitoring of maternal &fetal
parameters because fetal distress
common and remained unrecognised
• All efforts should made to bring temp.
under control by cold
sponging,antipyretics
55. MALARIA CONTROL DURING PREGNANCY
• Antenatal care & health education
• Intermittent preventive treatment
• Use of insecticide treated net
• case management of malarial disease
56. Intermittent preventive treatment
INTERMITTENT PRESUMTIVE TREATMENT
• Based on an assumption that every pregnant woman in
a malaria-endemic area is infected with malaria
• Recommends that every pregnant women receive at
least two treatment doses of an effective antimalarial
drug
• Sulfadoxine-pyrimethamine (SP) currently considered
the most effective drug for IPT
sp should avoid during first 16weeks
57. Doses for IPT
• Chloroquine: - 300mg base, administered once
every week.
• Pyrimethamine-25mg + Sulphadoxine-500mg: -
One tablet once weekly.
• Mefloquine: -250mg weekly.
– Dose may have to be increased in the last trimester,
in view of the accelerated clearance of the drug.
• Proguanil: - 150-200mg / day.
58. Chemoprophylaxis during pregnancy
• Malaria being potentially fatal to both the mother and the
foetus, this should be an important part of antenatal care
in areas of high transmission.
– All pregnant women, who remain in the malarial endemic area :
during their pregnancy, should be protected with
chemoprophylaxis.
• Choice of anti malarials for chemo prophylaxis
– Chloroquine being the safest drug in pregnancy, should be the
first choice
– In areas with known resistance to Chloroquine
• Pyrimethamine + Sulpha, Mefloquine or Proguanil can be
used.
• But these drugs should be started only after 1st trimester
only.
59. Doses for chemoprophylaxis
• Chloroquine: - 300mg base, administered once
every week.
• Pyrimethamine-25mg + Sulphadoxine-500mg: -
One tablet once weekly.
• Mefloquine: -250mg weekly.
– Dose may have to be increased in the last trimester,
in view of the accelerated clearance of the drug.
• Proguanil: - 150-200mg / day.
60. VACCINE
• Malaria vaccines in development.
• No licensed vaccine against malaria
currently exists
• The parasite has evolved a series of
strategies that allow it to confuse, hide,
and misdirect the human immune system.
• The parasite changes through several life
stages even while in the human host,
presenting a different subset of molecules
for the immune system to combat at each
stage.