PARASITOLOGY

PATHOLOGICAL EFFECT OF THE PARASITE UPON THE HOST

n1837 Ciliated larvae from F. hepaticawere observed by Freidich Creplin

n1852 Fluke eggs do not cause an infection, as shown by Simonds

n1875 Cercariae are released from Lymnaea truncatulaand seen to climb up vegetation,

possibly to encyst. This was noted by David Weinland, who speculated that they may be

ingested by sheep

n1882 Development in snail noted by Rudolf Leukart

n1882 Algernon Thomas observed that miracidia developed into sporocysts within the

snail and that rediae are produced from the sporocyst. He also showed that rediae can

reproduce and that cercariae with tails are formed in the rediae. He also suggested that

cercariae encysted on the grass

n1914 True migration pathway through the definitive host demonstrated by Dimitry Szinitzin

7.5.7. 3The disease fascioliasis
Two species of Fasciola(F. hepaticaand F. gigantica) infect humans. The disease has been
reported in 56 countries and highest of the recent outbreaks occurred in Bolivia, Peru,
Portugal and Egypt. The damage caused by the infection increases the possibility of liver
cancer.

n Symptoms: Loss of weight; accumulation of fluids in the abdomen due to liver dam-

age; ‘bottle-jaw’ or collection of fluid in the lower jaw; diarrhoea; lethargy followed
by death.
n The extent of the disease depends upon the number of challenging metacercariae.

Ingestion of 200–800 metacercariae causes chronic disease; 800–1,500 causes sub-

acute disease and 800–4,000 causes acute disease. Ingestion of 100 or more adult

flukes is usually lethal.

Entry into the liver causes acute traumatic hepatitis. The outer capsule (Glisson’s
capsule) becomes irregular and fibrosed due to fluke migration. At 10 days post-
infection there is an inflammatory response in some sub-capsular regions of the liver
close to penetration sites. Migration through the hepatic tissue leaves a trail of necrotic
tracts. The migratory tunnels can cause haemorrhagic lesions surrounded by an extens-
ive gathering of neutrophils, eosinophils, lymphocytes, macrophages and hepatocytes.
However, the leukocytes never seem to be close to the parasite.
During chronic and secondary infections neutrophils are replace by eosinophils. The
increase in weight of the lymph nodes and particular swellings of the follicles suggest that
there is an increase in lymphocyte activity, possibly B cells.
Toxic products, possibly metabolic waste, are released by the parasite and could be
the possible cause of some of the liver tissue necrosis. This damage is in addition to the
mechanical damage caused by the parasite’s migratory activities, such as peri-portal
fibrosis accompanied by bile duct proliferation. The fibrosis leads to a distortion of the
hepatic architecture.
The fluke’s entry into the bile ducts produces new symptoms such as hyperplastic
cholangitis (proliferation and size increase of the bile ducts) and secretion of large
amounts of proline by the parasite, which irritates the ducts. Expansion of the bile duct
occurs resulting in an exudation and emigration of cells into the surrounding tissues
(lamina propria and surrounding adventitia). In some advanced cases granuloma-like