how flukes are important, parasites for human.Most discoveries made between 1874 1918 • Discovered in Brazil in 1850 by Diesing • First described in Bengal tigers housed in zoos in Hamburg and Amsterdam in 1877 • Coenraad Kerbert named the parasite after the manager of the zoo G.F Westerman • Sidney Ringer discovered the parasite in a human in a Portuguese man during an autopsy in 1879 • Rudolf Luekart found that the parasite found in the tiger is the same as the parasite that caused hemoptysis in Formosa and Japan • 1916 1922 Japanese workers discovered the life cycle in the snail.

1. LUNG FLUKE
DR. VEERENDRA MARAVI
JR-2 , DEPT OF MICROBIOLOGY

2. CONTENTS
◦ INTRODUCTION
◦ HISTORY
◦ MARPHOLOGY
◦ GEOGRAPHICAL DISTRIBUTION
◦ EPIDEMIOLOGY
◦ LIFE CYCLE OF PARAGONIMUS WESTERMANI
◦ PATHOLOGY
◦ CLINICAL MANIFESTATION
◦ LABORATORY DIAGNOSIS
◦ TREATMENT
◦ CANTROL AND PREVENTION
◦

3. INTRODUCTION
◦Paragonimus westermani is known as lung fluke that
infects human cause paragonimiasis.
◦ Infections are most common in eastern Asia and in
South America.
◦ Paragonimiasis present as a sub-acute to chronic
inflammatory disease of the lung.
◦Discovered by Coenraad Kerbert in 1878

4. ◦Scientific name: Paragonimus westermani
◦Order: Plagiorchiida
◦Phylum: Platyhelminthes
◦Domain: Eukaryota
◦Family: Paragonimidae
◦Kingdom: Animalia

5. HISTORY
 Discovered in Brazil in 1850 by Diesing ;- “Distoma Rude”.
 Naterer first detected the lung fluke in 1828.
 Cornerad Kerbert detected flukes in the lungs of a Bengal tiger
in 1878 and named Distoma westermani, (zoo manager G.F Westerman)
 Both Manson and von Baelz in 1880 reported finding eggs in
the sputum of humans.
 Yokogawa in 1915 and Nakagawai in 1916 completely
described the life cycle.
1899, the name Paragonimus westermani has been used

6. • Morphology (Adult)
◦ The adult worm is hen egg shaped Size: 7.5 - 12 mm long, 4-6 mm
broad and about 3-5 mm thick.
◦ Adults worms live in the lungs, usually in pairs in cystic spaces that
communicate with bronchi.
◦ Its anterior end is slightly broader than the posterior end.
◦ The ventral sucker in situated near about the middle of the body.
◦ Life span of the adult worm is about 6 to 7 years
◦ The excretory vesicle is large and extends from the posterior extremity
to the anterior region, dividing the body into two equal halves:
unbranch intestinal caeca and Caudal region.

7. Morphology of P. westermani

8. Morphology (Egg)
◦Golden brown in colour
◦oval in shape
◦flattened opercula
◦80 -120 μm by 50 -60 μm in
size
◦Contain an un segmented ovum
surrounded by yolk cell

9. Human Pargonimiasis

10. Geographical Distribution Source:-WHO 2015 ‘a’

11. Epidemiology
◦ It is estimated that 20 million are infected with Paragonimus
westermani
◦ It is endemic in China, Korea, Japan, the Philippines, and Taiwan
Japan, Korea, Formosa, China, Manchuria, the Philippine Islands
and India
◦ Infection is also found in parts of tropical West Africa, from the
Congo and Nigeria, especially from Southern Cameron
◦ Rare in the US but it is found in Missouri

12. ◦India: Paragonimiasis is endemic in North East states of India. Many
cases are reported from Manipur with a prevalence of 6.7%.
◦ Earlier, P. westermani was thought to be the causative agent of
paragonimiasis in Manipur.
◦ According to the recent studies, P. heterotremus may be the
responsible for paragonimiasis in Manipur

13. ◦Humans contract the infection through ingestion of
raw, undercooked, pickled, or wine-soaked crabs or
crayfish .
◦Also become infected by the ingestion of uncooked
meat from wild animals, such as wild boar.

14. ◦The migrating larvae in this meat may pass through the
intestinal wall and continue their developmental cycle
when eaten.
◦Raw juice from crushed crayfish used as a home remedy
for the treatment of measles has been a significant
source of infection and may be a cause of cerebral
paragonimiasis in children .

15. ◦ Habitat: Adult worm live in respiratory tract (lung) of man.
◦ Definitive Hosts: Man and Domestic animals
(usually host in Asia are the tiger & leopard)
◦ Intermediate Host:
First Host:
A fresh water snail of the genus Melania
Second Host:
A fresh water crayfish or a crab

17. Life cycle of Paragonimus westermani
◦ The eggs are excreted unembryonated in the sputum, or alternately
they are swallowed and passed with stool.
◦ In the external environment, the eggs become embryonated , and
miracidia hatch and seek the first intermediate host, a snail, and
penetrate its soft tissues .
◦ Miracidia go through several developmental stages inside the snail
:sporocysts , rediae , with the latter giving rise to many cercariae , which
emerge from the snail.
◦ The cercariae invade the second intermediate host, a crustacean such as
a crab or crayfish, where they encyst and become metacercariae . This is
the infective stage for the mammalian host.

18. ◦ Human infection with P. westermani occurs by eating inadequately
cooked or pickled crab or crayfish that harbor metacercariae of the
parasite .
◦ The metacercariae excyst in the duodenum, penetrate through the
intestinal wall into the peritoneal cavity, then through the abdominal
wall and diaphragm into the lungs, where they become encapsulated
and develop into adults (7.5 to 12 mm by 4 to 6 mm). The worms can
also reach other organs and tissues, such as the brain and striated
muscles, respectively.
◦ However, when this takes place completion of the life cycles is not
achieved, because the eggs laid cannot exit these sites. Time from
infection to oviposition is 65 to 90 days.

19. ◦Infections may persist for 20 years in humans.
Animals such as pigs, dogs, and a variety of feline
species can also harbor Paragonimus westermani

21. Second intermediate
hosts for Paragonimus
spp.
(Upper, left) Crab; (right);
metacercaria. (Lower)
Crayfish.

22. Mode of Infection-
◦ Eating raw, undercooked or
◦pickled crustaceans such as crab or crayfish
◦ Spitting, a habit in Asian countries.
◦ Cultures that eat raw crustaceans.

23. Possible means of acquiring infection with Paragonimus spp.

24. PATHOLOGY
◦ When humans ingest raw infected crustaceans, larval flukes develop in
the small intestine, penetrate the intestinal wall into the peritoneal
cavity 30 minutes to 48 hours after excysting .
◦ They then migrate into the abdominal wall or liver, where they undergo
further development. Approximately 1 week later, adult flukes re-enter
from the abdominal cavity and penetrate the diaphragm to reach the
pleural space and lungs . Flukes mature, a fibrous cyst wall develops
around them, and then egg deposition starts 5 -6 weeks after infection.
◦ The symptoms of the early stages of this disease appear to be few with
some people

25. PATHOLOGY
◦ The worms finally get into the lung parenchyma and induce acute
exudative pneumonitis and haemorrhage .
◦ They gradually mature and are encysted, thereby producing zones of
active inflammation with exudate and of collagenous fibrous tissue. The
worms are found usually in pairs.
◦ When grown up, these worms are often found inside the bronchial
lumen lined with bronchial epithelia of squamous metaplastic character .
◦ The cysts consist of the parasite and of dense collagenous connective
tissue including various inflammatory cells and eosinophils

26. PATHOLOGY
◦ Once the parasite is in the lung or another organ, the worm stimulates
an inflammatory response that eventually coats tissue.
◦ If worms enter the CSF of the spinal cord, it can result in partial or total
paralysis.
◦ There have also been fatal cases of Paragonimiasis by infection of the
heart.
◦ Cerebral cases may result in cerebral cysticercosis (fluid filled cysts
surrounding the worm ).
◦ The adult worm , as it move around , cause lesions by mechanical
damage.
◦ The eggs may couse granulomatous reaction which may soften to form
cavities, the wall of which is compose of fibrous granuloma tissue (
Epithelioid cell, Lymphocyte, Plasma cell, eosinophils , Gaints cell and
fibroblast.)

27. Clinical Manifestation
Pulmonary paragonimiasis
◦ Chronic cough,
◦ Haemoptysis ,
◦ Stimulating a case of bronchiectasis , Bronchitis .
◦ chest pain with dyspnoea and fever.
◦ Pleural effusion and pneumothorax are possible complications. others
may remain asymptomatic for weeks to months between periods of
hemoptysis.
◦ As the cysts rupture, a cough develops, with increased production of
viscous blood-tinged sputum (rusty sputum, which may have a foul fish
odor) with chest pain.

28. Paragonimus westermani egg in the lung (crosssection).

29. Cerebral Disease
worms found in the brain usually contain eggs.
◦ migrate from ruptured lung cysts
◦ The worms eventually encapsulated cause necrosis within the brain
tissue.
◦ May couse cerebral hemorrhage, edema, and meningitis. associated
lung lesion or a history of lung disease. Symptoms include fever,
headache, nausea, vomiting, visual disturbances, motor weakness,
localized or generalized paralysis .
◦ May exhibit personality changes, possible disorientation,
◦ May decline in cognitive function. Depending on the central nervous
system location.

30. ◦ May also include paraplegia, sensory loss, or vision problems
◦ Specific sites can include the cerebral cortex, cerebellum,
basal ganglia, medulla oblongata, and spinal cord .
◦ When a worm dies, the lesion cavity becomes filled with
necrotic material.
◦ Cerebral paragonimiasis can be difficult to differentiate from
brain disease caused by other parasites

31. Paragonimiasis in Other Body Sites
◦ Ulcers or abscesses can also occur in the skin or subcutaneous tissue.
◦ Involvement of the mastoid area has been seen in P. africanus
◦ The skin is one of the common sites for ectopic paragomiasis may
seen in children. lesion is amigratory subcutaneous nodule that
appears on anterior , often migrating through the abdominal chestwall
◦ wall to the pelvic region or lower limbs
◦ Worm may invade any organ or tissue except bone.

32. ◦ Other body sites that have been infected include the breast, lymph
nodes, heart, pericardium, mediastinum , kidneys, adrenal gland,
omentum, bone marrow, stomach wall, bladder, spleen, pancreas, and
reproductive organs.
◦ Ectopic lesions are usually caused by worm migration.
◦ Dissemination of eggs to other body sites can also be responsible for the
extra pulmonary pathology

33. LABORATORY DIAGNOSIS
Sample specimen
Sputum
Stool
Gastric aspired
Pleural fluid
Washing
Tissue material

34. Microscopic Examinations
◦1. Sputum examination:
(1) Alkali digestive method (10%NaOH)
(2) Direct sputum smear
◦2. Stool examination:
(1) Alkali digestion
(2)Sedimentation method
(3) Direct faecal smear
◦3.Biopsy Materials by Staining Gimsa stains

35. Paragonimus eggs may be confused with Diphyllobothrium latum eggs, because of
similarities in their size and shape. Paragonimus eggs have opercular shoulders and
a marked thickening at the abopercular end.
Photographs (upper)
Drawings (lower)
(A )Diphyllobothrium latum egg
( B)Paragonimus westermani egg

36. KEY POINTS—LABORATORY DIAGNOSIS
◦ The wet preparation can be examined using the 10× (low-power)
objective; these eggs are large enough.
◦ The wet preparation should not be so thick that the eggs are obscured
by normal stool debris.
◦ In light infections, multiple stool and sputum specimens may be
needed before the eggs are detected.
◦ Not to add too much iodine to the wet preparation, or the eggs will
stain very darkly.
◦ The sedimentation concentration method should be used; because the
eggs do not float in the zinc sulfate flotation concentration method.

37. Immunological Test
◦Non specific Test:
1.Intradermal skin test
2.complement fixation test
◦Specific Test
1. Indirect haemagglutination test
2.ELISA

38. Molecular Technique
PCR technique
◦ Conventional PCR
◦ Real Time PCR
◦ DNA Hybridization
n

39. Imaging Technology
1.Chest X Ray –
Noduler,cystic and infiltrative in the middle and lower
lungs similar to TB, Bronchiectasis
2. CT scan of Chest -pulmonary lesions

41. Treatment
◦ Praziquantel Oral,
1.Causes severe spasms and paralysis of the worms muscles
2. Not for pregnant women. A/E- Stomach pains, dizziness,fever,
nausea, vomiting, headache
3. Better tolerated than Bithionol
◦ Bithionol-
use is limited due to side effects
◦ Triclabendazole-
If other drugs failed

42. CONTROL & PREVENTION
◦ Fully cook shellfish
◦ Heat water to 55° C for 5 minutes
◦ Freeze Fish - 20° C for 7 days
-35° C for 15 hours
◦ Make spitting illegal
◦ Use
Moluskicide to control snail population
Maintain the hygiene and sanitation

43. References
◦ 1. Garcia LS. Diagnostic Medical Parasitology. Washington, DC: ASM Ptess; 2019.
◦ 2. Sastry AS, Bhat S, Mishra D, Garcia LS, Sistla S. Essentials of Medical Parasitology.
New Delhi, India: Jaypee Brothers Medical Publishers (P) Ltd; 2019.
◦ 3. CDC - Paragonimiasis [Internet]. Centers for Disease Control and Prevention; 2023
[cited 2023 Nov 23]. Available from:
https://www.cdc.gov/parasites/paragonimus/index.html#:~:text=Paragonimus%20is%
20a%20lung%20fluke,to%20the%20central%20nervous%20system.

44. THANKYOU