discussion about nematode,
their form, general characteristics, life cycle, discussion about their host.
diseases caused by nematodes
and discussion about different class of nematodes.
2. FORM, FUNCTION
• SHAPE AND BODY STRUCTURE
1. SYMMETRY: BILATERAL
2. BODY CAVITY: PSEUDOCOEL
3. BODY SHAPE: THREAD LIKE, NON SEGMENTED,
CYLINDRICAL BODY
4.SIMPLE DIGESTIVE SYSTEM
5. PROTECTIVE CUTICLE
6. PARASITISM
7. NERVOUS SYSTEM CONSISTS OF NERVE RING
8. NO CIRCULATORY SYSTEM
9. REPRODUCTION GENERALLY SEXUAL AND
GONOCHORISTIC
6. CLASSIFICATIONThey are divided into two classes
distinguished by differences in sensory
and excretory system.
1. Class Enoplea
-Subclass Dorylaimia
Amphids are well developed .Excretory
system are found in
single,ventral,glandular cells or entirely
absent. Mostly free-living and some are
parasiitic on plants and animals.
Orders –
Trichurida,Dioctophymatida,Muspiceida,Me
7. Trichuris trichiura
-”Whipworm”
-Most common gastrointestinal parasites
of human
-Eggs posses plugs
-Have stichosome esophagus
-Male have coiled posterior ends.
-Pathogenesis- Trichuriasis
10. Class Rhabditea
-Subclass Rhabditia
Amphids are generally poorly
developed. Phasmids are present .
Excretory system with one or two
lateral canals,with or without
associated glandular cells .Both free
living and parasitic.
Orders-
Rhabditida,Strongylida,Ascaridida,Ox
yurida,Spirurida.
12. MORPHOLOGY
•Because of their great size, abundance, and
cosmopolitan distribution, these nematodes
may well have been the first parasites known
to humans.
•These species are characterized by, in addition
to their great size, having three prominent
lips, each with a dentigerous ridge, and no
interlabia or alae.
•Male ( 15 cms to 31 cms) and females (20
cms to 49 cms) are of different size.
14. Biology of Ascaris
•Ascaris lumbricoides, a roundworm, infects
humans when an ingested fertilised egg
becomes a larval worm (called rhabditiform
larva) that penetrates the wall of
the duodenum and enters the blood stream.
From there, it is carried to the liver and heart,
and enters pulmonary circulation to break free
in the alveoli, where it grows and molts. In
three weeks, the larva passes from
the respiratory system to be coughed up,
swallowed, and thus returned to the small
intestine, where it matures to an adult male
15. Pathogenesis
•Little damage is caused by penetration of
intestinal mucosa by newly hatched worms.
•Infection with Ascaris lumbricoides often
causes no symptoms.
• Infections with a large number of worms
may cause abdominal pain or intestinal
obstruction. Adults feed on the contents of
the small intestine and in heavy infections this
may compound problems in malnourished
individuals (especially children).
17. Diagnosis and Treatment
DIAGNOSIS — The diagnosis of ascariasis is
usually made via stool microscopy. Other forms
of diagnosis are
through eosinophilia, imaging, ultrasound,
or serology examination.
TREATMENT — Treatment consists of choosing
the right drugs, therapy, follow-up,
and supportive care for each patient.
PREVENTION — Prevention of reinfection poses a
substantial problem since Ascaris parasites are
abundant in soil. Good sanitation to prevent fecal
contamination of soil is required. An education
program advising against the use of human feces
as a fertilizer is also needed in some areas. Soil
treatments have been attempted but are
19. MORPHOLOGY
MOST SPECIES ARE RATHER STOUT, AND THE
ANTERIOR END IS CURVED DORSALLY, GIVING THE
WORM A HOOKLIKE APPEARANCE
THE BUCCAL CAPSULE IS LARGE AND HEAVILY
SCLEROTIZED AND USUALLY IS ARMED WITH
CUTTING PLATES, TEETH, LANCETS, OR A DORSAL
CONE. LIPS ARE REDUCED OR ABSENT.
THE ESOPHAGUS IS STOUT, WITH A SWOLLEN
POSTERIOR END, GIVING IT A CLUB SHAPE
20. MORPHOLOGY
MALES HAVE A CONSPICUOUS COPULATORY
BURSA, CONSISTING OF TWO BROAD LATERAL
LOBES AND A SMALLER DORSAL LOBE, ALL
SUPPORTED BY FLESHY RAYS
FEMALES HAVE A SIMPLE, CONICAL TAIL. THE
VULVA IS POSTEQUATORIAL, AND TWO OVARIES
ARE PRESENT. ABOUT 5% OF THE DAILY OUTPUT OF
EGGS IS FOUND IN THE UTERI AT ANY ONE TIME;
THE TOTAL PRODUCTION IS SEVERAL THOUSAND
PER DAY FOR AS LONG AS NINE YEARS.
21. BIOLOGY OF HOOKWORM
HOOKWORMS MATURE AND MATE IN THE SMALL
INTESTINE OF THEIR HOST
SPECIES INFECTING HUMANS CANNOT BE
DIAGNOSED RELIABLY BY THEIR EGGS ALONE
EGGS REQUIRE WARMTH, SHADE, AND
MOISTURE FOR CONTINUED DEVELOPMENT
JUVENILES LIVE IN THE FECES, FEEDING ON
FECAL MATTER, AND MOLT THEIR CUTICLE IN
TWO TO THREE DAYS
22. BIOLOGY OF HOOKWORM
WHEN THE GROUND SURFACE IS DRY, THEY
MIGRATE A SHORT DISTANCE INTO THE SOIL,
FOLLOWING THE RETREATING WATER. UNDER
IDEAL CONDITIONS, THEY CAN LIVE FOR SEVERAL
WEEKS.INFECTION OCCURS WHEN WORM CONTACT A
HOST’S SKIN AND BURROW INTO IT, AND THEY
SECOND STAGE JUVENILES, WHICH ALSO HAVE A
RHABDITIFORM ESOPHAGUS, CONTINUE TO FEED
AND GROW AND, AFTER ABOUT FIVE DAYS, MOLT
TO THE THIRD STAGE, WHICH IS INFECTIVE TO A
HOST. SECOND-STAGE CUTICLE MAY BE RETAINED
AS A LOOSEFITTING SHEATH UNTIL PENETRATION
OF A NEW HOST, OR IT MAY BE LOST EARLIER
23.
24.
25.
26. Diagnosis, Symptoms and
Treatment
Symptoms
•abdominal pain
•colic, or cramping
and excessive
crying in infants
•intestinal cramps
•nausea
• fever
•blood in stool
•a loss of appetite
Treatment & Prevention
•Albendazole,
Mebendazole
•wearing shoes
when you walk
outdoors, especially
in areas that might
have feces in the
soil
•drinking safe water
•properly cleaning
Diagnosis:
The standard method for diagnosing the
presence of hookworm is by identifying
hookworm eggs in a stool sample using a
microscope
28. Wuchereria bancrofti
• Definitive Host: Humans
• Intermediate Host: Mosquitoes (especially night-feeding
mosquitoes)
• Species: Anopheles, Aedes, Culex, Mansonia
• Morphology:
• Males:
• 40 mm long & 100 μm wide
• Fingerlike tail
• Females:
• 6-10 cm long & 300 μm wide
• They are viviparous
• Their vulva is near the level of the middle of
29.
30. Geographic
Distribution• Its infection is mainly found in the tropical
region, pacific islands and sometimes in the
Caribbean.
• West and south parts of Africa
• Egypt
• Southern Asia
• Western Pacific islands
• Northeastern coast of Brazil
• Guyana
• Caribbean island of Hispaniola
32. 1. The mosquito takes a blood meal,
transferring the L3 larva into the skin.
2. The L3 larva grow into adults in the lymph
ducts.
3. The adults reproduce, producing sheathed
microfilariae; the microfilariae migrate into
the blood and lymph channels
4. A mosquito takes a blood meal, ingesting the
microfilariae.
5. Once in the mosquito, the sheath of the
microfilariae is sloughed off. The microfilariae
then penetrates the midgut of the mosquito,
making its way into the thoracic muscles.
6. L1 larvae form
7. L3 larvae form
8. The L3 larvae are the infective stage,
33. • High levels of microfilaria in the blood
• No symptoms present
• Inflammatory (Acute) Phase:
• Inflammatory responses happen in response to
antigens from adult worms
• Lymphedema—swelling due to blockage of lymph
vessels
• Orchitis—inflammation of the testes
• Epididymitis—inflammation of the spermatic cord
• Obstructive Phase:
• Lymph varices—enlarged lymph vessels
(synonymous with varicose veins)
• Lymph scrotum— enlarged lymph vessels in the
scrotum
• Chyluria—lymph in urine (milky and sometimes
bloody urine)
• Elephantiasis—enlargement of limbs and thickening
35. Pathogenesis
• 6-12 months must pass before the
microfilariae mature and reproduce
• Once a person is infected, microfilariae can be
produced for up to ten years.
• There are 3 phases of infections:
asymptomatic, inflammatory (acute), and
obstructive.
36. Diagnosis• Thick blood smear
• Juveniles must be present in peripheral
blood
• Polymerase chain reaction (PCR)
• Distinguishes between other similar species
• Ultrasonography
• Detects vigorous movement of adults
known as “filaria dance sign”
• X-rays
• Detects dead, calcified worms
37. Treatment
• Primary drug of choice: diethylcarbamazine
(DEC)
• Eliminates microfilaria from the blood and
(if administered correctly) kills adult worms
• Ivermectin
• Albendazole & Mectizan
• Application of pressure bandages
38. Control
• Administration of Albendazole & Mectizan to
control the spread of the disease.
• There are currently no vaccines
• Elimination of common mosquito breeding
grounds
• Fallen coconuts
• containers filled with stagnant water
• Marshy and swampy areas.
• They hope to eradicate it by year 2020; so far,
the diseased population has declined
significantly