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1. Draw the trophozoite stage of Giardia and describe how this organism causes disease.
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Giardia is intestinal parasite and it is non-invasive.
Once excystation occurs, trophozoites are releases and they uses their flagella to ‘swim’
to the microvilli covered surface of duodenum and jejunum where they attach to the
enterocytes using their adhesive disc.
Lectins present on the surface of Giardia binds to receptor present on surface of
enterocytes. This attachment process damage microvilli, which interfere with nutrition
absorption by villi.
Rapid multiplication of trophozoites eventually creates a physical barriers between the
enterocytes and intestinal lumen, further interfering with nutrition absorption. This
process leads to enterocytes damage, villi atrophy, crypt hyperplasia, intestinal
hyperpermeability and brush boarder damage that causes a reduction in disaccharide
enzyme secretion.
Lectins and other cytopathic substance secreted by parasite also causes indirect damage
to intestinal epithelium.
Trophozoites do not invade or penetrate surrounding tissue or enter blood stream. So,
infection is generally restricted to intestinal lumen.
Giardiasis results in decreased jejunal electrolyte water and glucose absorptiom, and
damages to intestinal epithelium leads to malabsorption of electrolyte and fluids,
resulting in osmotic diarrhea known as giardiasis.
2. Draw the trophozoite stage of Entamoeba and describe how this organism causes
disease.
Mode of infection:
 Faeco-oral route
 Ingestion of cyst contaminated foods and water
Virulence factors:
i. Cyst wall: cyst wall is resistant to low pH and gastric juice of stomach.
ii. Lectin: Surface of trophozoite contains lectin that is specific to lingards (N-acetylgalactosamine and galactose sugar) present in surface of intestinal epithelium.
iii. Ionophore like protein: It causes leakage of ions such as Na+, K+, Ca++ from target cells.
iv. Hydrolytic enzymes: Phosphatase, proteinease, glycosidase and RNase causes tissue
destruction and necrosis.
v. Toxin and haemolysin
Pathogenesis;
 The parasites express large number of virulence factors including lectin, lytic peptide,
cysteine, proteineases and phospholipase.
 Excystation of cyst in intestine releases 4 trophozoites which then colonizes the large
intestine. The binding of trophozoites with the colonic epithelium is a dynamic process
in the pathogenesis. After adherence trophozoite lyse the target cell by its ionophore like
protein that causes leakage of ions from cytoplasm. The proteolytic enzymes secreted by
the amoeba causes tissue destruction giving flask shaped amoebic ulcer, is a typical
feature of intestinal amoebiasis.
 Trophozoites penetrates the columnar epithelium of mucosa causing lysis and moves
deep inside till they reached submucosa layer and multiply rapidly. Ultimately amoeba
destroy considerable area of the submucosa leading an abscess formation which breaks
down to form ulcer. The ulcer is flask shaped with narrow neck and broad base. The
ulcer may be localized in ileo-caecal region or generalized throughout the large intestine.
 From intestine, the parasites may be carried to other vital organs such as liver, heart,
brain etc through blood circulation. Pulmonary and hepatic amoebic abscesses are
frequent and rarely cerebral, cutaneous and splenic amoebic abscesses.
3. What are some examples of roundworms studied in lab?
Ascaris lumbricoides
Hook worm
Pin worm
Trichinella
4. Draw a tapeworm scolex
5. How could a person become infected with roundworms or tapeworms?
Worms are mainly spread in small bits of poo from people with a worm infection. Some
are caught from food.
You can get infected by:
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touching objects or surfaces with worm eggs on them – if someone with worms
doesn't wash their hands
touching soil or swallowing water or food with worm eggs in it – mainly a risk
in parts of the world without modern toilets or sewage systems
walking barefoot on soil containing worms – only a risk in parts of the world
without modern toilets or sewage systems
eating raw or undercooked beef, pork or freshwater fish (like salmon or trout)
containing baby worms – more common in parts of the world with poor food
hygiene standards
6. Draw Trichinella and describe its portal of entry and pathogenesis.
Trichinellosis (trichinosis) is caused by nematodes (roundworms) of the
genus Trichinella. In addition to the classical agent T. spiralis (found worldwide in
many carnivorous and omnivorous animals), several other species of Trichinella are
now recognized, including T. pseudospiralis (mammals and birds worldwide), T.
nativa (Arctic
bears), T.
nelsoni (African
predators
and
scavengers),
and T.
britovi (carnivores of Europe and western Asia).
Trichinellosis is acquired by ingesting meat containing cysts (encysted larvae) After
exposure to gastric acid and pepsin, the larvae are released. from the cysts and invade
the small bowel mucosa where they develop into adult worms. (female 2.2 mm in
length, males 1.2 mm; life span in the small bowel: 4 weeks). After 1 week, the females
release larvae. that migrate to the striated muscles where they encyst Trichinella
pseudospiralis, however, does not encyst. Encystment is completed in 4 to 5 weeks and
the encysted larvae may remain viable for several years. Ingestion of the encysted
larvae perpetuates the cycle. Rats and rodents are primarily responsible for maintaining
the endemicity of this infection. Carnivorous/omnivorous animals, such as pigs or
bears, feed on infected rodents or meat from other animals. Different animal hosts are
implicated in the life cycle of the different species of Trichinella. Humans are
accidentally infected when eating improperly processed meat of these carnivorous
animals (or eating food contaminated with such meat).
7. Draw Trypanosoma and describe its life cycle, including the vector involved.
Life Cycle:
The life cycle of most trypanosomes species is digenetic. Man and domestic animals serve as
primary host and blood-sucking insect, the tsetse fly serve as the intermediate host. Man and
domestic animals becomes infected by the bite of tsetse fly. The injected parasite undergo
prepatent period of active multiplication in lymph, intercellular spaces and tissue cells. Finally
the parasite invades blood. It undergoes extensive multiplication.
During multiplication it changes shape of its body several times but finally changes into normal
trypanosomes. At this stage, it is ready for transmission into the intermediate host. After
sometime the pararits disappear completely from the blood due to formation of antibodies in
host body. In pathogenic forms, the parasites invade vital organs from the blood causing serious
disease.
In invertebrate host also, the parasite undergo extensive multiplication in stomach. Ultimately
they migrate into salivary glands. When tsetse fly bites the skin of vertebrate host for its bloodmeal, if pours a drop of saliva into the wound to prevent blood coagulation. With the drop of
saliva
numerous
trypanosomes
are
inoculated
into
the
blood
of
final
host.
CHARACTERISTIC
SKELETAL MUSCLE
Initiation of muscle
contraction
Acetylcholine released
somatic motor neurons.
Source of Ca2_ for contraction
Sarcoplasmic reticulum
Regulator proteins
relaxation
Duration
contraction
of
CARDIAC MUSCLE
SMOOTH MUSCLE
Cardiac muscle tissue
contracts when stimulated
by its own autorhythmic
fibers.
Smooth muscle fibers
contract in response to
nerve impulses, hormones,
and local factors.
Troponin and tropomyosin.
Sarcoplasmic reticulum and
interstitial fluid.
Troponin and tropomyosin.
Sarcoplasmic reticulum and
interstitial fluid.
Calmodulin and myosin light
chain for contraction kinase.
Ca2_ level in the cytosol
drops, tropomyosin
covers the myosinbinding sites, and the
muscle
fiber relaxes.
Ca2_ level in the cytosol
drops, tropomyosin
covers the myosinbinding sites, and the
muscle
fiber relaxes.
relax in response to
action potentials from
the autonomic nervous
system,
stretching,
hormones, or local
factors such as changes
in pH, oxygen and
carbon dioxide levels,
temperature, and ion
concentrations.
Fast.
Cardiac muscle tissue
remains contracted 10 to
15 times longer than
skeletal muscle tissue due
to prolonged delivery of
Ca2_ into the sarcoplasm.
The
duration
of
contraction and relaxation
of smooth muscle is longer
than in skeletal muscle
since it takes longer for
Ca2_ to reach the filaments.
by
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