Chapter 16 Parasitosis
OBSERVATIONAL METHODS OF SPECIMEN
Parasitosis is an inflammatory disease caused by different kinds of parasites, which
invade into the human body, damaging the whole or certain parts of the body. Though
pathological changes involve different organs and tissues in different location where
parasites parasitize, they are characterized by the basic pathological changes of
inflammation, which are alteration, exudation and proliferation, and most of which is
chronic inflammation.
Macroscopically, there is necrosis caused by mechanical, toxic and allergenic
effects parasites, accompanying with epithelial and fibrotic proliferation caused by
injury repair. The parasitic bodies and eggs may be seen in lesions.
Microscopically, besides the nonspecific changes such as focal tissue necrosis,
epithelial and fibrotic proliferation, the parasitic bodies and eggs are the main
diagnostic criteria for the disease. In addition, dense eosinophilic infiltration and
inflammatory granuloma formation in focal tissue can be seen. The focal changes may
include one or two kinds of changes mentioned above.
AIMS
1.To grasp the characters and features of the pathologic change of intestinal
amoebiasis; to be acquainted with the morphological features of amoebiasis in
other organs.
2.To be acquainted with the basic pathological changes of schistosomiasis and the
pathological features of hepatic and intestinal schistosomiasis.
3.To
know
the
pathological
echinococcosis and filariasis.
features
of
clonorchiasis,
paragonimiasis,
CONTENTS
Amoebiasis
Gross specimen
Tissue section
Amoebiasis of the colon
Amoebiasis of the colon
Amoebic abscess of the liver
Schistosomiasis
Schistosomiasis of colon (Chronic)
Acute egg nodule
Schistosomiasis of the liver
Chronic egg nodule
Colonic schistosomiasis
Hepatic schistosomiasis
Clonorchiasis
Clonorchiasis
Echinococcosis
Echinococcus granulosus cyst of
the liver
Granulosus echinococcosis
Alveolar echinococcosis of the liver
Paragonimiasis
Paragonimiasis
Paragonimiasis
Filariasis
Elephantiasis of lower extremity
Subcutaneous filarial nodule
KEY POINTS OF SPECIMEN OBSERVATION
1. Amoebiasis
(ⅰ) Amoebiasis of the colon
Basic pathologic changes
(1) Gross morphology
◆
There are spherical, oval or irregular ulcers in different number and size on the
intestinal mucosa.
◆
There are undermined ulcerations on cut surface that are in flask shape (i.e. a
narrow neck and a broad base), surrounded by edematous mucosa of irregular
edge, with reddish-brown hemorrhage and necrosis.
◆
The mucosa between the ulcers is generally normal.
(2) Histopathology
◆
The mucosa and submucosa undergo colliquative necrosis, forming flask
shape ulceration. There is no apparent inflammatory reaction at the base of and
periphery of ulcer, with light congestion, edema, minor infiltration of
lymphocyte, phagocyte and plasma cell and hemorrhage.
◆
There are varies numbers of amoeboid trophozoites at the boundary of ulcers
and venules, characterized by the spherical-shape, 20 to 40µm in diameter (6
to 7 times of RBC), small and round nucleus and basophilic plasma, within
which there are vacuoles and phagocytized red blood cells, lymphocytes and
the debris, surrounded by tissue dissolving halo.
Specimen observation
Case abstract：Female, 26 years old. She had a low fever, abdominal distension, pain
and diarrhea for one week. Her stool is dark-red and, like jam accompanying with
stench. Physical examination: The right and lower abdomen tenderness (+) Feces
examination: Red blood cell (+++). There are amoebic trophozoites in it.
Gross specimen:： (Fig. 16-01) A segment of colon with dissected wall. There are
many spherical, irregular ulcers in different size on the colon mucosa. What is the
clinical manifestation of the patient? Why are the feces jelly-like?
Tissue section:： (Fig. 16-02a, b) Longitudinal dissected colonic wall. There are two
minor ulcers reaching the submucosa. Mucosa and submucosa tissue undergo necrosis
and form an ulcer in typical flask shape. Part of necrotic tissues has been ejected.
Structure of remaining tissue has been destroyed without normal cell morphology
accompanying with even purple-stain unstructured granular substance. At the
boundary between necrotic and normal tissue, inflammatory reaction is not mild, the
blood vessels enlarge and hyperemia. Certain lymphocytes and plasmocytes infiltrate.
Some large amebic trophozoite can be seen. Can we diagnose the disease only based
on detection of the small trophozoites in feces and tissues?
Questions: ①What are the pathological features of intestinal amoebiasis? What is
the clinical manifestation? ②If a patient suffered abdominal pain and diarrhea, what
diseases do you think of according to the pathological knowledge you have learned?
What are the similarities and differences in the pathological changes and clinical
manifestation respectively?
(ⅱ) Amoebic abscess of the liver
Basic pathologic changes
(1) Gross morphology
◆There
is single or numerous abscesses in the liver varying in size, within which
there are reddish-brown jelly-like content.
◆The
abscess has irregular shaggy necrotic inner wall, like torn cotton fiber.
◆The
wall of chronic abscess is thickened.
(2) Histopathology
◆There
are incomplete colliquative necrosis and minor inflammatory exudation at
the inner wall of the abscess, with pink-stain colliquative necrosis in the cavity.
◆The
amoeboid trophozoites may be seen in the margins of abscess.
◆The
wall of the chronic abscess is encapsulated by granulation tissue and fibrous
tissue.
Specimen observation
Case abstract：Patient is a female and 31 years old. She complained of fever and
occasional abdominal distension for a week. She got the amoebic dysentery 5 years
ago. Physical Examination: The liver enlarges. The lower section of liver reaches 3.6
cm from the dextral midclavicular line. Tenderness (+). Ultrasonic wave B: There is a
liquefied dark area which covers about 4.3cm×5.1 cm on the right lobe of liver.
Gross specimen: (Fig. 16-03) The liver is enlarged, with a 4.5cm×5.3cm abscess in
the right lobe on cut surface, content flowed out. The wall of the abscess is rough,
with unliqiufied necrosis attached, such as blood vessels, bile ducts and fibrous
connective tissue, showing the appearance of torn cotton fiber.
Questions: To distinguish the hepatic amoebic abscess and bacterial abscess
according to the character of inflammation and pathological change.
2. Schistosomiasis
(ⅰ) Acute egg nodule
Basic pathologic changes
(1) Gross morphology
The nodule appears yellowish–gray, with the diameter varying from 0.5 to 4mm.
(2) Histopathology (Fig. 16-04a,b)
◆
There are more or less mature eggs in the center of the nodule.
◆
There are flare-like eosinophilic radiant protrusions on the surface of eggs,
which is called Hoeppli phenomenon.
◆
Around the eggs is marked aggregation of eosinophils, which resembles
abscess. Thus it’s called eosinophlic abscess.
(ⅱ) Chronic egg nodule
Basic pathologic changes
Histopathology (Fig. 16-05)
◆
There are necrotic and calcified eggs at the center of the nodules.
◆
There is pseudotubercle or chronic egg granuloma formed by epitheloid-cells,
multinucleus giant cells, lymphocytes and fibroblasts around the eggs.
◆
The egg nodules transform into scary granuloma owing to further fibrosis.
(ⅲ) Schistosomiasis of the colon
Basic pathologic changes
(1) Gross morphology
◆
Acute stage: The colon is hyperemic, swelling, with mucosa necrosis,
shedding and formation of ulcers in various sizes in severe case.
◆
Chronic stage: There are irregular thickening and stiffness of the colonic wall,
accompanied by the formation of minute ulcers or inflammatory polyps.
(2) Histopathology
◆
Acute stage: The colon is hyperemia and swelling. Acute egg nodules may be
seen in every layer, especially in the submucosa, with mucosa necrosis,
shedding and formation of ulcers in severe case.
◆
Chronic stage: Chronic egg nodules may be seen in submucosa, surrounded by
proliferation of fibrous tissue accompanying with the formation of
inflammatory polyps.
Specimen observation
Case abstract: female, 45 years old. She suffered ache of left lower abdomen,
diarrhea for 13 years, abdominal distension for 4years, no exsufflation or defecation
for 3 days. Physical examination: pale eyelid, liver can’t be touched; spleen is located
at 1.5cm below left rib arch. Abdominal vein varicose, sign of ascites (+). Left lower
abdominal tenderness (+), local intestinal penstaltil wave can be seen with bowel
sound 23times/minute. Laboratory examination: moderate anemia. Feces examination:
existence of schistosome ovum. B-ultrasonic examination: hepatic cirrhosis,
splenomegaly.
Gross specimen: (Fig. 16-06) Colonic pipe has been dissected. Mucosal fold
disappear, polyposis emerge, and colonic wall is so obviously thickening that the
intestinal cavity become stenosis. To judge this case is in the acute or chronic stage.
How do the pathological changes develop?
Tissue section: (Fig. 16-07a,b) A large amount of fibrous tissue proliferates in the
submucous layer. Many chronic egg nodules come into existence in submucosa and
other layers. There are dead eggs in the center of the nodule, the shells of ovum is
broken or calcified, and foreign body granuloma can be seen around it. To judge these
tubercles are acute or chronic egg nodules.
Questions: What colonic diseases manifest the symptom of dysentery, and what are
their pathological features respectively?
(ⅳ) Schistosomiasis of the liver
Basic pathologic changes
(1) Gross morphology
◆
Acute stage: The liver is slightly enlarged, with numerous gray or
yellowish-gray nodules from the size of millet to soybean.
◆
Chronic stage: The liver is shrunk with hard texture, rough surface and
shallow stripe, forming the bulgy lobular architecture and the bulky node in
severe case. There is often massive fibrosis around major portal tracts, which
is know as Symmers’ pipestem fibrosis.
(2) Histopathology
There are acute or chronic egg nodules in the portal space, within which sees
◆
proliferation of fibrous tissue, whereas the maintaining of lobular architecture.
Specimen observation
Case abstract: patient, male, 45, suffered splenomegaly for 2 years accompanying
with abdominal distension over 20 days. He was diagnosed as acute schistomosiasis 8
years ago; hepatitis attack record denied Physical examination: Anemia face,
abdominal protruding, abdominal wall varicosis, spleen oversized, ascites (+).
Ultrasonic B: hepatic cirrhosis, 7.8mm below echo ranging of portal vein wall,
splenomegaly, 2500ml ascites.
Gross specimen: (Fig. 16-08) The liver decreases in size and becomes hard in
consistency. Vast fibrous tissue proliferate along truck and branch of portal vein in
branch distribution, which is known as pipestem hepatocirrhosis.
Tissue section: (Fig. 16-09a, b, c, d) Normal liver tissues are separated into big
patches by proliferative fibrous tissue around portal area and portal vein, without
pseudolobule formation. There are some unevenly distributed schistosoma egg
nodulars in portal area. In tubercula, necrosis and calcification are noticeable.
Cholangio hyperplasia and chronic cell infiltration also can be seen.
Questions: ① What are the morphological differences between schistosomiasis
cirrhosis and portal cirrhosis of the liver? ② How does the portal hypertension
caused by schistosomiasis cirrhosis of the liver?
3. Clonorchiasis
Basic pathologic changes
(1) Gross morphology
◆
The liver is enlarged, firm and rough, with gray dilated protruded bile duct.
◆
Bile ducts dilated to cyst form, with distinct thick wall on the cut surface.
◆
There are numerous bodies of Clonorchis in some bile ducts.
(2) Histopathology
◆
There are bodies and eggs of Clonorchis in the bile ducts.
◆
Biliary epithelium and submucosa gland proliferate. Epitheliums are papilloid
or adenomatous proliferation or suffered atypical proliferation.
Specimen observation
Case abstract: male, 22. She was fond of raw fish, suffering abdominal distension for
one year, accompanying with pain in liver zone, anorexia, and diarrhea occasionally,
no hepatitis attack record. Physical examination: thin, slight anemia, swollen liver,
1.5cm below xiphoid process, moderate consistency. Ultra-sonic B: slight
hepatomegaly. Blood test: white blood cell 10×109 / L, eosinophilic granulocyte
19.8%.
Gross specimen: The liver is slightly enlarged, with the thickening dilated ducts filled
with
bile on cut
surface. When the
liver is
pressed, the
translucent
sunflower-seed-shape adult worm in ducts may be seen.
Tissue section: (Fig. 16-10a,b) There are bodies and eggs of clonorchias in the dilated
ducts, epithlium and periductal fibrous tissue proliferate accompanying infiltration of
lymphocytes and eosinophils. Hepatic cells are compressed and atrophy.
Questions: What the diagostic evidences of Clonorchiasis? How does it lead to the
cholangiocarcinoma?
4. Echinococcosis
(ⅰ) Echinococcus granulosus cyst of the liver (Hydatid disease)
Basic pathologic changes
(1) Gross morphology
◆There
are various size of spherical or irregular cysts in the liver, the wall of cyst
is translucent, gray, like sheet jelly.
(2) Histopathology
◆
There are myriads of scolices, fertile cysts and daughter cysts in the hydatid
cysts.
◆
The wall of the cyst is composed of germinal layer (single or plural cellular
lining), chitinous layer (red laminated structure) and the fibrous capsule.
◆
Necrosis and calcification of the capsule may be observed.
◆
The liver cells around the cyst undergo atrophy and degeneration.
Specimen observation
Case abstract: Male, 34, herdsman. He suffered abdominal distension and pain
accompanying with fever over one month. Physical examination: body temperature
38.2℃,swollen liver, right to midclavicular line, 4.8cm below the rib. Laboratory
Blood test: white blood cell 1.1×109 / L, eosinophilic granulocyte 20%. Ultra-sonic B:
occupancy pathological change in right lobe of the liver 6.5×7cm2, skin test of
echinococcus(+).
Gross specimen: (Fig. 16-11) There are numerous daughter cysts in various size in
the cystic bulge.
Tissue section: (Fig. 16-12) The cyst is composed of the inner layer of germinal and
the outer layer of chitinous, within which there are scolices.
Questions: How did the patient suffer this disease, and what is the consequence if the
cyst ruptures into the abdominal cavity?
(ⅱ) Alveolar echinococcosis
Basic pathologic changes
(1) Gross morphology
◆
There are hard, gray bulge on the surface of the liver.
◆
There are numerous aggregative small cysts, separated by fibrous tissue,
showing the sponge-look appearance on the cut surface.
◆
The content of the cyst is similar to comedones in appearance, or jelly-like
when necrosis.
(2) Histopathology
◆
There are numerous different size of cysts in the liver.
◆
The wall of the cyst is red-stained chitinous ectocyst, with rare germinal layer.
◆
There are infiltration of eosinophils and granuloma formation around the cyst.
◆
There are atrophy, degeneration and coagulative necrosis of hepatic cells
around the cyst.
Specimen observation
Tissue section: (Fig. 16-13) The chitinous ectocyst is visible in the cysts, while the
germinal layer and scolices are absent. There is proliferation of fibrous tissue around
the cysts. Hepatic cells in left inferior corner suffered coagulative necrosis.
Questions What complications can the disease lead to?
5. Paragonimiasis
Basic pathologic changes
Penetration and parasitism of the fluke in the body cavity (thoracic cavity and
◆
abdominal cavity) result in fibrinous or sera-fibrinous inflammation, where the
eggs can be observed.
◆
Burrows and tunnels are formed by penetration of fluke, which leads to
hemorrhage and necrosis. Flukes and eggs can be found in the tunnel or burrow,
surrounded by eosinophils, accompanying with fibrous tissue proliferation and
formation of Charcot-Leyden crystals.
◆
Fluke can lead to focal necrosis and inflammatory reaction accompanied with
sponge-look cysts formation.
Specimen observation
Case abstract: Male, 36 years old, a worker in forestry.. He has had low fever and a
headache for more than 3 months; pain in the chest, cough and hemoptysis for 10 days.
He expectorated something like rotten peach pulp this morning. Physical examination:
body temperature:38.2℃, dropsy in both thoracic cavities. X-ray： A lot of cystic
shadows can be seen in the lower lung field of two lungs. Blood Routine: WBC 40×
109/L, acidophilic granulocytes 42%. Examination of the sputum detachment: bugs’
ova can be found.
Gross specimen: Numerous irregular cysts in different size may be observed on the
cut surface of the lungs. Some cysts are connected to the dilated bronchus; some
bronchus is cystiform dilation.
Tissue section: (Fig. 16-14a,b,c)
(a) A fluke in the dilated pulmonary bronchus, with eggs in fluke;
(b) The head of the fluke;
(c) Eggs excreted from the fluke, surrounded by necrotic and inflammatory cells.
Questions What is the clinical manifestation of Paragonimiasis? What are the
complications of the disease?
6. Filariasis
(ⅰ) Elephantiasis of lower extremity
Basic pathologic changes
(1) Gross morphology
(Fig. 16-15)The lower extremities are swollen, with the skin thickening, rough
◆
and firm, deep wrinkled, resemble the skin of elephant.
(2) Histopathology
◆
The epidermis is covered by excessive keratinization, under which are swollen
spinous cells. The dermis and the connective tissue are highly proliferated,
whereas the vanishing of elastic fiber.
◆
Proliferation, thickening and obstruction of lymphatic epithelium in the dermis
can be observed.
◆
There is minor infiltration of lymphocytes, plasma cells and eosinophils
around the lymphatics and vessels.
Questions What is the formation process of lower extremity Elephantiasis? Can the
lymphoedema develop to Elephantiasis or not?
(ⅱ) Subcutaneous filarial nodule
Basic pathologic changes
◆There
are degenerated and necrotic adult worms and microfilariae in the center of
the node, infiltrated with eosinophils, surrounded by fibrous tissue, multinuclear
giant cells, lymphocytes and plasma cells, showing the appearance of tubercle.
Questions: What are the changes of the skin after the formation of the node?
CASE DISCUSSION
Case One
Case abstract. A 36-year-old male, Mongolian, herdsman, has suffered pain in right
upper abdominal quadrant for half a year, skin and mucosa jaundice for a week. Half a
year ago he felt dull pain in the right upper abdominal quadrant without distinct
causes, but received no treatment, hospitalized for aggravation of pain, yellowish
stained sclera and urine seven days ago. No hepatitis history admitted.
Physical examination. Yellowish stained sclera, deep palpation pain in the RUQ,
liver enlargement of 3.6cm beneath the midclavicular line and 4.2cm beneath the
xiphoid process. Laboratory examination: WBC: 9.2×109/L, with eosinophils 6.4%.
TBIL: 18.6mol/L. DBIL: 45.6mol/L. Casoni test (+). GRA: 79%. EISA (+).
Ultrasound examination: 3.8cm×4.3cm spherical homogenous dark area in the right
lobe of the liver, clear-cut, common bile duct dilated to 6.2 in diameter. X-ray
examination: The right diaphragm arises. PTC examination: Left and right hepatic
duct, common hepatic duct and common bile duct are visible and a blastocele to the
right side of the gallbladder is visible, which connect to gallbladder.
Exploratory laparotomy. There is a 4.2cm×4.7cm cyst in the right lobe of the liver.
There are spherical translucent hydrated cysts in different size in the bile duct, drown
with the bile mixture. The cyst in the right lobe is connected to the common bile duct.
Undergo surgical removal of the cyst.
Discussion.
1. Make the clinical diagnosis according to the features of clinical and
pathological changes.
2. What is the cause and development of the disease?
Case two
Case abstract. A 40-year-old male, peasant, has suffered liver enlargement and pain
in upper abdominal quadrant for 3 months, aggravation of pain for 5 days,
accompanied by low fever, palpitation, vomiting and diarrhea.
The patient felt dull pain in the upper abdomen without distinct causes 3 months
ago, and was examined by a clinic and diagnosed as hepatomegaly and hepatitis.
There were low fever, palpitation and aggravation of abdominal pain and no obvious
improvement after treatment, accompanied by nausea, vomiting and diarrhea 5 days
before. The patient had denied diagnostic hepatitis history. After receiving the
examinations of ultrasound, ECG and x-ray, the patient looked pale, with cold
extremities and low blood pressure, and died for cease of heartbeat.
Physical examination. Orthopnea, shortness of breathe while lying flat, weak heart
sound, pulse 48/min, blood pressure 60/40mmHg, coarse breath sound, liver enlarged
to 3 fingers beneath the xiphoid process, clear-cut. Ultrasound: 12cm×10cm dark
area in the middle of the left lobe, with clearly defined border. ECG: sinus rhythm 112
/min, normal. X-ray: right diaphragm arises.
Autopsy record.
The pericardial enlarged distinctively, with the volume of 17cm×15.5cm×10.8cm,
contained with 1350ml dark red liquid. The liver weighs 850g, 5.2cm beneath the
xiphoid process. There is a 13.2cm×11.3cm×10.2cm spherical abscess in the middle
of the left lobe, with reddish brown pus inside. The liver tissue and diaphragm muscle
are thin above the abscess, which is adhered and connected with the apex pericardium.
Numerous round ulcers of different size may be seen on the mucosa of cecum and
ascending colon, 0.8 to 2.5cm in diameter, with undermined edge. Lymph nodes in
mesentery are enlarged and soft, 1.2 to 2.3cm in diameter.
Microscopically, amoeboid trophozoites are visible in the liver abscess and tissue
around the colonic ulcer.
Discussion.
1. What is the pathological diagnosis, and what does it depend on?
2. What is the cause of the death?
3. What is the cause and development of the disease?
PRACTICE REPORT
1. Illustrate the histological morphology of intestinal amebiasis and hepatic
unliocular echinococcosis.
2. Describe the histological features of acute schistosomiasis egg nodules,
chronic schistosomiasis egg nodules, and hepatic clonorchiasis; describe the
gross morphology of hepatic cirrhosis of schistosomiass and elephantiasis of
lower extremity.
3. Write speech outline for case discussion.
QUESTIONS FOR REVIEW
1. Summarize the pathological similarities and differences among schistosomiasis,
clonorchiasis and paragonimiasis.
2. What are the characteristics of hepatic cysts caused by parasites?
(Inner Mongolia University for Nationalities Tao Chun)