This document discusses lymphatic filariasis, caused by parasitic roundworms transmitted by mosquitoes. It provides details on the life cycle and morphology of the parasites. Clinical manifestations range from asymptomatic microfilaremia to acute adenolymphangitis and chronic manifestations like lymphedema and elephantiasis. Pathogenesis involves blockage of lymph vessels by adult worms and inflammatory responses. Diagnosis is via blood smears to detect microfilariae and treatment aims to eliminate parasites and control symptoms.
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
Malaria(Plasmodium falciparum)- Epidemiology, Life Cycle, Prevention and Erad...Sarath
Malaria(Plasmodium falciparum)- Epidemiology, Life Cycle, Prevention and Eradication.
Contains Videos in two slides. So try using Power Point 2010.
My email : doc.sarathrs@gmail.com
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
Malaria(Plasmodium falciparum)- Epidemiology, Life Cycle, Prevention and Erad...Sarath
Malaria(Plasmodium falciparum)- Epidemiology, Life Cycle, Prevention and Eradication.
Contains Videos in two slides. So try using Power Point 2010.
My email : doc.sarathrs@gmail.com
LUMEN DWELLING FLAGELLATES - GIARDIA
REFS:
INTERNATIONALLY ACCEPTED BOOK OF MEDICAL PARASITOLOGY BY K. D. CHATTERJEE
TEXT BOOK OF MEDICAL PARASITOLOGY BY PANIKER
IMAGE SOURCES : FROM INTERNET
Leishmaniasis is caused by a protozoa parasite from over 20 Leishmania species. Over 90 sandfly species are known to transmit Leishmania parasites. There are 3 main forms of the disease:
Visceral leishmaniasis (VL), also known as kala-azar is fatal if left untreated in over 95% of cases. It is characterized by irregular bouts of fever, weight loss, enlargement of the spleen and liver, and anaemia. Most cases occur in Brazil, East Africa and in South-East Asia. An estimated 50 000 to 90 000 new cases of VL occur worldwide each year out of which only an estimated 25–45% are reported to WHO. In 2017, more than 95% of new cases reported to WHO occurred in 10 countries: Bangladesh, Brazil, China, Ethiopia, India, Kenya, Nepal, Somalia, South Sudan and Sudan.
Cutaneous leishmaniasis (CL) is the most common form of leishmaniasis and causes skin lesions, mainly ulcers, on exposed parts of the body, leaving life-long scars and serious disability or stigma. About 95% of CL cases occur in the Americas, the Mediterranean basin, the Middle East and Central Asia. In 2017 over 95% of new CL cases occurred in 6 countries: Afghanistan, Algeria, Brazil, Colombia, Iran (Islamic Republic of), Iraq and the Syrian Arab Republic. It is estimated that between 600 000 to 1 million new cases occur worldwide annually.
Mucocutaneous leishmaniasis leads to partial or total destruction of mucous membranes of the nose, mouth and throat. Over 90% of mucocutaneous leishmaniasis cases occur in Bolivia (the Plurinational State of), Brazil, Ethiopia and Peru.
Transmission
Leishmania parasites are transmitted through the bites of infected female phlebotomine sandflies, which feed on blood to produce eggs. The epidemiology of leishmaniasis depends on the characteristics of the parasite and sandfly species, the local ecological characteristics of the transmission sites, current and past exposure of the human population to the parasite, and human behaviour. Some 70 animal species, including humans, have been found as natural reservoir hosts of Leishmania parasites.
(WHO, 2019)
https://www.who.int/news-room/fact-sheets/detail/leishmaniasis
LUMEN DWELLING FLAGELLATES - GIARDIA
REFS:
INTERNATIONALLY ACCEPTED BOOK OF MEDICAL PARASITOLOGY BY K. D. CHATTERJEE
TEXT BOOK OF MEDICAL PARASITOLOGY BY PANIKER
IMAGE SOURCES : FROM INTERNET
Leishmaniasis is caused by a protozoa parasite from over 20 Leishmania species. Over 90 sandfly species are known to transmit Leishmania parasites. There are 3 main forms of the disease:
Visceral leishmaniasis (VL), also known as kala-azar is fatal if left untreated in over 95% of cases. It is characterized by irregular bouts of fever, weight loss, enlargement of the spleen and liver, and anaemia. Most cases occur in Brazil, East Africa and in South-East Asia. An estimated 50 000 to 90 000 new cases of VL occur worldwide each year out of which only an estimated 25–45% are reported to WHO. In 2017, more than 95% of new cases reported to WHO occurred in 10 countries: Bangladesh, Brazil, China, Ethiopia, India, Kenya, Nepal, Somalia, South Sudan and Sudan.
Cutaneous leishmaniasis (CL) is the most common form of leishmaniasis and causes skin lesions, mainly ulcers, on exposed parts of the body, leaving life-long scars and serious disability or stigma. About 95% of CL cases occur in the Americas, the Mediterranean basin, the Middle East and Central Asia. In 2017 over 95% of new CL cases occurred in 6 countries: Afghanistan, Algeria, Brazil, Colombia, Iran (Islamic Republic of), Iraq and the Syrian Arab Republic. It is estimated that between 600 000 to 1 million new cases occur worldwide annually.
Mucocutaneous leishmaniasis leads to partial or total destruction of mucous membranes of the nose, mouth and throat. Over 90% of mucocutaneous leishmaniasis cases occur in Bolivia (the Plurinational State of), Brazil, Ethiopia and Peru.
Transmission
Leishmania parasites are transmitted through the bites of infected female phlebotomine sandflies, which feed on blood to produce eggs. The epidemiology of leishmaniasis depends on the characteristics of the parasite and sandfly species, the local ecological characteristics of the transmission sites, current and past exposure of the human population to the parasite, and human behaviour. Some 70 animal species, including humans, have been found as natural reservoir hosts of Leishmania parasites.
(WHO, 2019)
https://www.who.int/news-room/fact-sheets/detail/leishmaniasis
Filarial worms are thread-like nematodes of which there are at least 8 species for which humans, especially in tropical regions, are the definitive host
A detailed description of HIV covering virology, morphology, pathogenesis, clinical stages and manifestations, laboratory diagnosis, and diagnostic strategy, and therapeutic options and prevention.
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Morphology, Life cycle, Clinical manifestations and laboratory diagnosis of E. histolytica from Clinical and Microbiological point of view for UG and PG Students.
Basic discussion on Clinical and Microbiological Aspects of Food Poisoning caused by various bacteria, viruses, protozoa, and Fungi along with their clinical and laboratory diagnosis and basic management.
Basic description of Infective Endocarditis from a Clinical and Microbiological point of view with description on Pathogenesis, Clinical Manifestations, Clinical and Laboratory diagnosis.
Basic description of Lyme disease from Microbiological and Clinical point of view with discussion on Pathology, Clinical Features and, Laboratory Diagnosis.
A basic description of Leishmania spp. along with Old and New world Leishmaniasis regarding Parasite morphology, Life Cycle, Pathogenesis, Clinical manifestations, Laboratory Diagnosis and Treatment.
Detailed description of malarial parasites especially P. falciparum with regards to their Morphology, Life cycle, Pathogenesis, Epidemiology, Clinical manifestations and complications and Laboratory diagnosis including modern methods and treatment.
Describes the basic properties and mechanisms of T cells and B cells in maintaining Immune Response against foreign antigens or infections and covers the UG and PG portion of immunology.
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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
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
2. Lecture Objectives
1. Introduction of filariasis
2. Parasitological description –Morphology and Life cycle
3. History of filariasis in ancient and modern times.
4. Epidemiology of filariasis and the burden of the disease.
5. Pathogenesis
6. Clinical spectrum of filarial diseases.
7. Laboratory diagnosis- Conventional and newer methods
8. Treatment of filariasis in short.
3. Introduction
Nematodes belonging to the superfamily Filarioidea are slender thread-like worms (Latin,
filum and thread), which are transmitted by the bite of blood-sucking insects.
The filarial worms reside in the subcutaneous tissues, lymphatic system, or body cavities of
humans.
The adult worm generally measures 80-100 mm in length and 0.25-0.30 mm in breadth; the
female worm being longer than the males.
The tail of the male worm has perianal papillae and unequal spicules but no caudal bursa.
The female worms are viviparous and give birth to larvae known as microfilariae. The
microfilariae released by the female worm, can be detected in the peripheral blood or cutaneous
tissues, depending on the species.
In some species, the microfilariae retain their egg membranes which envelop them as sheath.
They are known as sheathed microfilariae.
In some other species of filarial nematodes, the egg membrane is ruptured and is known as
unsheathed microfilariae.
4. Introduction
Once the microfilariae are classified on the basis of sheath as "sheathed" or
"unsheathed", their further differentiation can be done on the characteristic
arrangement of nuclei.
Periodicity Depending on when the largest number of microfilariae occur in blood,
filarial worms can exhibit nocturnal, diurnal periodicity or no periodicity at all.
The basis of periodicity is unknown but it may be an adaptation to the biting habits of the
vector.
The life cycle of filarial nematodes is passed in two hosts: (1) definitive host is man and
(2) intermediate host are the blood-sucking arthropods.
The microfilariae complete their development in the arthropod host to produce the
infective larval stages.
These are transmitted to humans by arthropod, which are their vectors also during the
next feed.
Adult worms live for many years whereas microfilariae survive for 3-36 months.
5. Introduction
Eight species of filarial worms infect humans, of them six are pathogenic-
(1) Wuchereria bancrofti,
(2) Brugia malayi and
(3) B. timori cause lymphatic filariasis;
(4) Loa loa causes malabar swellings and allergic lesions;
(5) Onchocerca volvulus causes eye lesions and dermatitis;
(6) Mansonella streptocerca leads to skin diseases; and two of them,
(7) M. ozzardi and (8) M. perstans are virtually nonpathogenic.
Infection with any of the filarial worms may be called filariasis, but
Traditionally, the term filariasis refers to lymphatic filariasis caused by
Wuchereria or Brugia species.
6.
7.
8.
9.
10.
11. LYMPHATIC FILARIASIS-
Introduction
Lymphatic filariasis (LF) is the second most common mosquito-borne
disease globally.
LF infection occurs by exposure to mosquito bites. There are three parasites,
which cause human LF
Wuchereria bancrofti,
Brugia malayi, and
Brugia timori all of them are transmitted by Anopheles, Aedes, and
Culex.
W. bancrofti is responsible for more than 90% of infections globally,
B. malayi is mostly contributed to the transmission of the remainder.
12. LYMPHATIC FILARIASIS-
Introduction
The third parasite, B. timori, is common in a few countries in
Southeast Asia.
The most important filarial diseases for humans are lymphatic
filariases, in which the adult worms are found in the lymphatic system.
The lymphatic form of filariasis will be the focus of the site.
Lymphatic is also referred to sometimes as “elephantiasis.”
Elephantiasis is actually an extreme clinical feature of filariasis.
13. LYMPHATIC FILARIASIS-
History
Ancient Time
It is known that lymphatic filariasis occurred in the Nile region, and ancient artifacts
suggest that the disease may have been found as early as 2000BC.
A statue of Pharaoh Mentuhotep depicts swollen limbs, a characteristic of elephantiasis.
Artifacts from the Nok civilization in West Africa also show scrotal swelling, another
characteristic of elephantiasis.
The first reliable documentation of lymphatic filariasis symptoms is from an exploration
of Goa between 1588 and 1592 ( by writings of Jan Huygen Linschoten)
Recent Times
In 1863, French surgeon Jean-Nicolas Demarquay Microfilariae in fluid extracted
from a hydrocoele (another common symptom of lymphatic filariasis) firstly.
Three years later, Otto Henry Wucherer Microfilariae in urine.
14. LYMPHATIC FILARIASIS-
History
Timothy Lewis Microfilariae in both blood and urine.
The adult worm was discovered by Joseph Bancroft.
Patrick Manson in 1877 Pinpoint the microfilariae in mosquitoes.
In 1900, George Carmichael Low discovered microfilariae in the
proboscis of mosquitoes, and finally pinpointed the true mechanism of
transmission, which is attributed to infective bite from a mosquito
vector.
16. LYMPHATIC FILARIASIS-
Epidemiology
One of the most important infectious diseases worldwide Lymphatic
filariasis most common.
120M people in at least eighty countries are infected with the parasites
associated with lymphatic filariasis.
90% of this infection W. bancrofti.
1B people are estimated to be at risk for Infection.
25M men have the genital disease (hydrocele) and almost 15M, mostly
women, have lymphoedema or elephantiasis of the leg.
Many kinds of mosquitoes can transmit the parasite, depending on the
geographic area. For example, in AfricaAnopheles
AmericasCulex,
Aedes and Mansonia Pacific and Asia.
17.
18.
19. LYMPHATIC FILARIASIS-
Life Cycle
The extrinsic life cycle starts when the microfilariae are ingested with
the human blood by a bite of a mosquito.
The microfilariae migrate through the gut wall of the mosquito to
thoracic muscles where they become shorter and thicker, later develop
into the first-stage larvae (L1).
After 5–7 days, the L1 grow and develop to become the second stage
(L2), which is more active and finally by 10–11 days, they develop to
become the infective stage larvae (L3).
After maturity, most of the infective larvae (L3) move to the
mosquito’s proboscis, where they become ready to infect another
human.
20. LYMPHATIC FILARIASIS-
Life Cycle
When the mosquito bites the host, L3 is put on the skin surface and
after pulling the proboscis; they get into the wound and travel to the
lymphatics.
After about 9–10 days of entering, the L3 molt to become the fourth
stage larvae (L4).
The L4 stage needs several days to few months before it develops and
becomes an adult. In the human body, adult worms (male and female)
live in lymph vessels and lymph nodes.
After mating, the females produce numerous microfilariae, which
migrate into the lymphatic system and spread through the bloodstream
21.
22. LYMPHATIC FILARIASIS-
Parasite Morphology
Adult worm
The adults are whitish, translucent, thread-like worms with smooth cuticle
and tapering ends.
The female is larger (70-100 × 0.25 mm) than the male (25-40 x 0.1 mm).
The posterior end of the female worm is straight, while that of the male is
curved vertically and contains two spicules of unequal length.
Males and females remain coiled together usually in the abdominal and
inguinal lymphatics and in the testicular tissues.
The female worm is viviparous and directly liberates sheathed microfilariae
into lymph.
The adult worms live for many years, probably 10-15 years or more.
23. LYMPHATIC FILARIASIS-
Parasite Morphology
Microfilariae:
The microfilaria has a colorless, translucent body with a blunt head, and pointed
tail.
It measures 250-300 µm in length and 6-10 µm in thickness.
It can move forwards and backwards within the sheath which is much longer than
the embryo.
It is covered by a hyaline sheath, within which it can actively move forwards and
backwards as sheath is much longer than the embryo.
When stained with Leishman or other Romanowsky stains, structural details can
be made out.
Along the central axis of the microfilaria, a column of granules can be seen, which
are called somatic cells or nuclei.
24. LYMPHATIC FILARIASIS-
Parasite Morphology
The granules are absent at certain specific locations- a feature which helps in the
identification of the species.
The specific locations are as following
At the head end is a clear Space devoid of granules, called the cephalic space.
In Microfilaria bancrofti, the cephalic space is as long as it is broad, while in
Microfilaria malayi, it is longer than its breadth.
With vital a stains, a stylet can be demonstrated projecting from the cephalic
space.
The anterior half of the microfilaria, is an oblique area devoid of granules called
the nerve ring.
Approximately midway along the length of the microfilaria is the anterior V-spot,
which represents the rudimentary excretory system.
The posterior V-spot (tail spot) represents the cloaca or anal pore.
29. LYMPHATIC FILARIASIS-
Pathogenesis
• Infection caused by W. bancrofti is termed as wuchereriasis or bancroftian filariasis.
• The disease can present as:
Classical filariasis
Occult filariasis.
Classical filariasis:
It occurs due to blockage of lymph vessels and lymph nodes by the adult worms.
The blockage could be due to mechanical factors or allergic inflammatory reaction to
worm antigens and secretions.
The affected lymph nodes and vessels are infiltrated with macrophages, eosinophils,
lymphocytes and plasma cells.
The vessel walls get thickened and the lumen narrowed or occluded, leading to lymph
stasis and dilatation of lymph vessels.
30. LYMPHATIC FILARIASIS-
Pathogenesis
The worms inside lymph nodes and vessels may cause granuloma formation, with subsequent
scarring and even calcification.
Inflammatory changes damage the valves in lymph vessels, further aggravating lymph stasis.
Increased permeability of lymph vessel walls lead to leakage of protein-rich lymph into the
tissues.
This produces the typical hard pitting or brawny edema of filariasis.
Fibroblasts invade the edematous tissues, laying down fibrous tissue, producing the nonpitting
gross edema of elephantiasis.
Recurrent secondary bacterial infections cause further damage.
Occult fllariasis:
It occurs as a result of hypersensitivity reaction to microfilarial antigens, not directly due to
lymphatic involvement.
Microfilariae are not found in blood, as they are destroyed by the allergic inflammation in the
tissues.
31.
32.
33. LYMPHATIC FILARIASIS-
Clinical Manifestations
The most common presentations of lymphatic filariasis are
Symptomatic (subclinical) microfilaremia,
Acute adenolymphangitis (ADL) and
Chronic lymphatic disease.
Most of the patients appear clinically asymptomatic but virtually all of them have
subclinical disease including
Microscopic hematuria or proteinuria,
Dilated lymphatics (visualized by imaging) and in men with W. bancrofti
infection,
Scrotal lymphangiectasia [Lymphangiectases represent superficial lymphatic
dilatation caused by a wide range of scarring processes. Lymphangiectasia occurs
as a consequence of lymphatic damage by an external cause, leading to obstruction
of local lymphatic drainage.] (detected by ultrasound).
34. LYMPHATIC FILARIASIS-
Clinical Manifestations
Acute adenolymphangitis is characterized by
High fever,
Lymphatic inflammation (lymphangitis and lymphadenitis) and
Transient local edema.
Fever is of high grade, sudden in onset, associated with rigors and last for 2 or 3
days.
Lymphangitis is inflamed lymph vessels seen as red streaks underneath the skin.
Lymphatics of the testes and spermatic cord are frequently involved, with
epididymo-orchitis and funiculitis.
Acute lymphangitis is usually caused by allergic or inflammatory reaction to
filarial infection, but may often be associated with streptococcal infection also.
35. LYMPHATIC FILARIASIS-
Clinical Manifestations
Lymphadenitis
Inflammation of lymph nodes.
Most common affected lymph nodes being inguinal nodes followed by
axillary nodes.
The lymph nodes become enlarged, painful and tender.
Lymphedema
This follows successive attacks of lymphangitis and usually starts as
swelling around the ankle, spreading to the back of the foot and leg.
It may also affect the arms, breast, scrotum, vulva, or any other part of body.
Initially, the edema is pitting in nature, but in course of time, becomes
hard and nonpitting.
36. LYMPHATIC FILARIASIS-
Clinical Manifestations
Lymphangiovarix
Dilatation of lymph vessels commonly occurs in the inguinal, scrotal, testicular and abdominal
sites.
The lymphangitis and lymphadenitis can involve both the upper and lower extremities but
involvement of genital lymphatic occurs exclusively with W. bancrofti infection.
The genital involvement Funiculitis, Epididymitis and Hydrocele formation.
Hydrocele:very common manifestation of filariasis.
Accumulation of fluid occurs due to obstruction of lymph vessels of the spermatic cord and also
by exudation from the inflamed testes and epididymis.
The fluid is usually clear and straw colored but may sometimes be cloudy, milky, or hemorrhagic.
The hydrocele may be unilateral or bilateral and is generally small in size in the early stage, but
may occasionally assume enormous proportions in association with elephantiasis of the scrotum.
The largest reported hydrocele weighed over 100 kilograms.
37. LYMPHATIC FILARIASIS-
Clinical Manifestations
Lymphorrhagia
Rupture of lymph varices leading to release of lymph or chyle and resulting in
Chyluria,
Chylous diarrhea,
Chylous ascites and
Chylothorax, depending on the involved site.
Elephantiasis
Repeated leakage of lymph into tissues first results in lymphedema, then to elephantiasis, in which there is
Nonpitting brawny edema
Growth of new adventitious tissue
Thickened skin, cracks, and fissures
Secondary bacterial and fungal infections, commonly seen in leg but may also involve other parts of body.
38. LYMPHATIC FILARIASIS-
Clinical Manifestations
Occult filariasis:
Massive eosinophilia (30-80%)
Hepatosplenomegaly
Pulmonary symptoms like dry nocturnal cough, dyspnea and asthmatic
wheezing.
Arthritis,
Glomerulonephritis,
Thrombophlebitis,
Tenosynovitis, etc.
Classical features of lymphatic filariasis are absent.
Meyers Kouwenaar syndrome is a synonym for occult filariasis.
39. LYMPHATIC FILARIASIS-
Clinical Manifestations
Tropical pulmonary eosinophilia
This is a manifestation of occult filariasis which Presents with
Low-grade fever,
Loss of weight, and
Pulmonary symptoms such as dry nocturnal cough, dyspnea and asthmatic wheezing.
Children and Young adults are more commonly affected in areas of endemic filariasis including
the Indian subcontinent.
There is a marked increase in eosinophil count (>3000 µm - ≥ 50,000 µm).
Chest X-ray shows mottled shadows similar to miliary tuberculosis.
It is associated with a high level of serum immunoglobulin E (IgE) and filaria antibodies.
Serological tests with filarial antigen are usually strongly positive.
The condition responds to treatment with diethylcarbamazine (DEC), which acts on
microfilariae.
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45. LYMPHATIC FILARIASIS-
Laboratory Diagnosis
The diagnosis of filariasis depends on
Clinical features,
History of exposure in endemic areas and
Laboratory findings.
Demonstration of microfilaria
Microfilaria can be demonstrated in blood, chylous urine, exudate of
lymph varix and hydrocele fluid.
Peripheral blood is the specimen of choice.
The method has the advantage that the species of the infecting filaria can be
identified from the morphology of the microfilaria seen.
It is also the method used for carrier surveys.
46. LYMPHATIC FILARIASIS-
Laboratory Diagnosis
In India and other areas, where the prevalent filarial species is nocturnally
periodic, it is best to collect "night blood" samples between 10 pm and 4
am.
Microfilaria can be demonstrated in unstained as well as stained
preparations and in thick as well as thin smears.
Unstained film
Examination under the low power microscope shows the actively motile
microfilariae lashing the blood cells around.
The timing of blood collection is critical and should be based on the
periodicity of the microfilariae.
The examination may be conveniently made the next morning as
microfilariae retain their viability and motility a for a day or 2 at room
temperature.
48. LYMPHATIC FILARIASIS-
Laboratory Diagnosis
Stained film
A "thick and thin" blood smear is prepared on a clean glass slide and dried.
The thick part of the smear is dehemoglobinized by applying distilled water.
The smear is fixed in methanol and stained with Giemsa, Leishman, or
polychrome methylene blue stains.
Microfilariae may be seen under the low power microscope in the thick film.
The morphology of microfilariae can be studied in thin film.
The microfilaria of W. bancrofti are sheathed and appear smooth curves in stained
smear and are 298 µm long and 7.5-10 µm in diameter.
By using a micropipette for taking a known quantity of blood (20-60 mm") for
preparing the smear and counting the number of microfilariae in the entire stained
smear, microfilaria counts can be obtained.
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53. LYMPHATIC FILARIASIS-
Laboratory Diagnosis
Concentration techniques
Knot's concentration technique:
Anticoagulated blood (1 mL) is placed in 9 mL of 2% formalin and centrifuged 500 x g
for 1 minute.
The sediment is spread on a slide to dry thoroughly.
The slide is stained with Wright or Giemsa stain and examined microscopically for
microfilariae.
Nucleopore filtration:
In the filtration methods used at present, larger volumes of blood, up to 5 mL, can be
filtered through millipore or nucleopore membranes (3 µm diameter).
The membranes may be examined as such or after staining, for microfilariae.
The filter membrane technique is much more sensitive, so that blood can be collected
even during day time for screening.
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57. LYMPHATIC FILARIASIS-
Laboratory Diagnosis
The disadvantages of the technique are the cost and the need for venipuncture.
Diethylcarbamazine provocation test
A small dose of DEC (2 mg per kg body weight) induces microfilariae to appear in
peripheral blood even during day time.
For surveys, blood samples can be collected 20-50 minutes after the administration of one
100 mg tablet of DEC to adults.
Other specimens: Microfilaria may be demonstrated in centrifuged deposits of
Lymph,
Hydrocele fluid,
Chylous urine or
Other appropriate specimens.
Usually 10-20 mL of the first early morning urine is collected for examination and
demonstration.
58. LYMPHATIC FILARIASIS-
Laboratory Diagnosis
BiopsyAdult filarial worms can be seen in sections of biopsied lymph nodes,
but this is not employed in routine diagnosis.
Skin testIntradermal injection of filarial antigens (extracts of microfilariae,
adult worms and third-stage larvae of B. malayi or of the dog filaria Dirofilaria
immitis) induce an immediate hypersensitivity reaction.
But, the diagnostic value of the skin test is very limited due to the high rate of
false-positive and negative reactions.
Imaging techniques
Ultrasonography High frequency ultrasonography (USG) of scrotum and
female breast coupled with Doppler imaging may result in identification of motile
adult worm (filaria dance sign) within the dilated lymphatics.
Adult worm may be visualized in the lymphatics of the spermatic cord in up to
80% of the infected men with microfilaria associated with W. bancrofti.
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60. LYMPHATIC FILARIASIS-
Laboratory Diagnosis
Radiology Dead and calcified worms can be detected occasionally by X-ray.
In tropical pulmonary eosinophilia (TPE), chest X-ray shows mottled appearance resembling
military tuberculosis.
Intravenous urography, retrograde pyelography, lymphangiography and lymphoscintigraphy may
be used to demonstrate abnormal lymphatic urinary fistula.
Serodiagnosis (Demonstration of antibody)
Complement fixation,
Indirect hemagglutination (IHA),
Indirect fluorescent antibody (IFA),
Immunodiffusion and
Immunoenzyme tests have been described.
Indirect immunofluorescence an ELISA detect antibodies in over 95% of active cases and 70% of
established elephantiasis.
62. LYMPHATIC FILARIASIS-
Laboratory Diagnosis
Demonstration of circulating antigen
Highly sensitive and specific test for detection of specific circulating filarial antigen (CFA) have
been developed for detection of recent bancroftian filariasis.
Trop-bio test semiquantitative sandwich ELISA for detection of CFA in serum or plasma
specimen.
Immunochromatographic test (ICT) is a new and rapid filarial antigen test that detects soluble
W. bancrofti antigens using monoclonal antibody (ADI2) in the serum of infected humans.
Both assay have sensitivities of 93-100% and specificities approaching 100%.
Specific IgG4 antibody against W. bancrofti antigen WbSXP-1 have been used to develop
ELISA for detecting circulating filarial antigen in sera of patients with filariasis.
There is however, extensive cross-reactivity between filarial antigens and antigens of other
helminths, including intestinal roundworm, thus interpretation of serological findings can be
difficult.
Advantages: Antigen detection tests are more sensitive than microscopy and can differentiate
between current and past infections.
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64. LYMPHATIC FILARIASIS-
Laboratory Diagnosis
Molecular diagnostic technique
Polymerase chain reaction (PCR) can detect filarial deoxyribonucleic acid
(DNA) from patient's blood,
only when circulating microfilaria are present in peripheral blood but not in
chronic carrier state.
Usually the test provides sensitivities that are up to tenfold greater than
parasitic detection by direct examination and is 100% specific.
Recently LAMP technique has also been used.
Indirect evidences
Eosinophilia (5-15%) is a common finding in filariasis. Elevated serum IgE
levels can also be seen.
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66. LYMPHATIC FILARIASIS-
Treatment
Diethylcarbamazine is the drug of choice.
It is given orally in a dose of 6 mg/kg body weight daily for a period of 12 days amounting to a
total of 72 mg of DEC per kg of body weight.
Following treatment with DEC severe allergic reaction (Mazzotti reaction) may occur due to death
of microfilariae.
It kills both microfilaria and adult worm.
Antihistamines or corticosteroids may require to control the allergic phenomenon.
The administration of DEC can be carried out in three ways:
l. Mass therapy
In this approach, DEC is given to almost everyone in community irrespective of whether they have
microfilaremia disease manifestation or no signs of infection except those under 2 years of age,
pregnant women and seriously-ill patients.
67. LYMPHATIC FILARIASIS-
Treatment
The dose recommended is 6 mg/kg body weight.
In some countries it is used alone and in some, with albendazole or ivermectin.
Mass therapy is indicated in highly endemic areas.
2. Selective treatment
Diethylcarbamazine is given only to those who are microfilaria-positive.
In India, the current strategy is based on detection and treatment of human carriers and filarial
cases.
The recommended dose in the Indian program is DEC 6 mg/kg of body weight daily for 12 doses,
to be completed in 2 Weeks.
In endemic areas, treatment must be repeated every 2 years.
3. Diethylcarbamazine medicated salts
Common salt medicated with 1-4 gram of DEC per kg has been used for filariasis control in
Lakshadweep island, after an initial reduction in prevalence had been achieved by mass or
selective treatment of microfilaria carriers.