Past Papers Qs and As

Special Aug 2016 (book 1 Dr Neethling, book 2 Prof Oldewage; 7Qs; 100 Marks)

Sup June 2016 (Dr Neethling; 8Qs; 100 Marks)

June 2014 (Dr JC Van Dyk; 6Qs; 80 Marks)

June 2016 (Dr Neethling; 8Qs; 100 Marks)

July 2014 (Dr JC Van Dyk; 5Qs; 75 Marks)

Sup July 2019 (Section A Dr Neethling, Section B Prof Oldewage; 7Qs; 100 Marks)

June 2019 (Section A Dr Neethling, Section B Prof Oldewage; 7Qs; 100 Marks)

Questions from Tutorial with Justine

 Special Aug 2016 Q1 (Book 1) AND June 2016 Q1

In regions where Leishmania donovani is prevalent, parents often crush sand flies into small
wounds on their children to help them develop immunity against infections by this parasite. With
the aid of a diagram, justify this statement by explaining the physiological process how increased
immunity is gained through this process. (15)

In the above Q, which part does she want? TH1 or TH2 or the whole thing? = she wants TH2. How do
you get immunity? For you to have immunity against it you have to have had developed antibodies,
so the Q wants the TH2 arm.

The parents catch sand flies, and they have no idea whether these sand flies are infected or not, but
they catch then and they crush them, and those crushed insects gets pushed into wounds that they
have created on these children. They rub it into that wound. So by having a wound already on the
skin they have already broken the skin barrier, so they have broken the innate immunity, and are
now introducing an invader whether it is the Leishmania or just the insect itself, they have
introduced the invader into the skin, this causes the child to have inflammation and all the other
responses such as fever, but ultimately antibodies are formed towards these antigens of the
sandflies and if the sandflies were infected with Leishmania antibodies towards the Leishmania will
also be formed, and the hope is that that sand fly is infected and that Leishmania was introduced to
the body and the children now then have antibodies against Leishmania.

The first 5/6 marks are explaining the body and how it has caused a reaction, so you have broken
the skin barrier and caused inflammation, and the innate immune system has now recognised the
threat and has called the NKs, and all the other immune responses, and then talk about the TH2
arm which is the antibody mediated response.

By doing this they have actively exposed their child to Leishmania the child has then been allowed to
develop antibodies for the Leishmania and can now if they get bitten naturally by a sand fly that is
carrying Leishmania, again that introduces Leishmania the body will then know how to fight it off
much faster.

Sup June 2016 Q1 AND June 2019 Q2 (Section A)

African sleeping sickness is only manageable by arsenical drugs and the prognosis is poor once the
central nervous system is involved. Discuss this statement by identifying the parasite (1), its
transmission (1), the symptoms and pathogenesis (6), and how this parasite manages to survive in
the host (7). [15]
The parasite that causes African Sleeping Sickness is Trypanosoma brucei gambiense for chronic
sleeping sickness and Trypanosoma brucei rhodesiense for acute sleeping sickness. For Trypanosoma
brucei gambiense it is transmitted by the Glossina sp. the tsetse fly, symptoms and pathogenesis are
a chancre at the site of inoculation, swollen lymph nodes at the neck, groin, and legs and at the base
of the skull called Winterbottom’s sign, there is intermittent fever, swelling increases and there is a
generalised pain, headache and weakness, there are also cramps and sleep walking occurs. Once it
invades the central nervous system (at which point it is chronic) the person becomes apathetic, with
a disinclination to work, and mental dullness, tremors in the hands tongue and trunk begin to occur,
there is a disturbance in coordination, paralysis and convulsions, and increased sleepiness, finally a
coma and death due to malnutrition, pneumonia, heart failure or falling while sleeping. For
Trypanosoma brucei rhodesiense it is transmitted by the Glossina sp. the tsetse fly, symptoms and
pathogenesis are a chancre at the site of inoculation, swollen lymph nodes at the neck, groin and
legs and at the base of the skull called Winterbottom’s sign, there is a constant fever, pain,
headache, weakness, and cramps, there is also rapid weight loss with heart involvement, death (due
to heart failure of keeping the fever so high for so long) occurs is a few months before any nervous
disorders can occur.

The parasite manages to occur so long n the host since it avoids the hosts immune system by using
antigenic variation. There is a successive dominance of each of a series of Variable Antigen Type
(VAT) over rime, in the remission the antibodies are destroying the trypanosomes, but before a
complete elimination the trypanosomes express a new variant-specific surface glycoproteins (VSG)
covers the organism surface coat, this serves as a barrier to antibodies and compliments that might
act against non-variant membrane proteins, the bloodstream trypanosomes actively internalise host
antibodies to create new Variant Antigen Type (VAT), thus the trypanosomes are able to avoid
detection and complete destruction within the host.

June 2014 Q1

Discuss the various mechanisms/processes involved in the innate immune response. (20)

Met with Dr Neethling after ST1, she implies that Innate immunity would not be asked in the
exam, rather Adaptive immunity will be asked, but she said not to ignore Innate as it makes up a
part of the Adaptive immunity.

Innate immunity is a mechanism of defence that does not depend on prior exposure to the antigen,
it is part of the body’s natural defence, it is antigen non-specific, it does not distinguish one potential
threat from another, it is the immunity that you are born with and is genetically coded in you.

There are seven defence mechanisms that are part of Innate immunity: Physical barrier,
Inflammation and Fever, as well as the following 4 that are cellular defences including Phagocytosis,
Immunological surveillance, interferons, and the Compliment system.

The Physical barrier is the first line of defence it is made up of the epithelium of the skin which when
unbroken blocks direct entry of antigens, sweat glands that secrete oils that contains IgA to
neutralise bacteria, Hair/ Feathers that blocks pathogens from reaching the skin, and the mucous
membranes of the respiratory tract, urinary tract, and gastro-intestinal tract, these have cilia that
help remove pathogens, the mucous contains anti-microbial chemicals and the stomach acid and
digestive enzymes kill or neutralise ingested microbes.

Inflammation is a localized response to the injury, when there is tissue damage, the tissues release
prostaglandins, proteins and potassium ions, this causes a change in the interstitial fluid and mast
cells release histamine and heparin which causes a dilation of the blood vessels causing an increase
in blood flow and vessel permeability, this helps the clotting factors and the compliment activation,
which in turn activates more phagocytes causing cytokines to stimulate fibroblasts to form scar
tissue which helps the tissue to be repaired.

July 2014 Q1

Discuss the antibody-mediated immune response and also refer to the specific cytokines involved.
(20)

TH2 is antibody mediated.

You have an antigen presenting cell, that secretes IL-1 (Interleukine-1) and activates T cells and B
cells, then there is an uncommitted Tcell which is traveling from the Bone marrow to the thymus.
When the uncommitted Tcell is exposed to the IL1 it then becomes a TH2 lymphocyte. The TH2
lymphocyte secretes IL4 which is a growth factor for B cells and suppresses the TH1 arm. This is on of
those that both supresses and activates. By the time that this starts to happen the TH1 arm has
gained some form of control which is why it does not matter that it is being suppressed.

IL4 works on Bcells and changes them into plasma cells which then release specific antibodies. The
TH2 lymphocyte also secretes IL6 which is also an important growth factor for Bcells that are late in
differentiation (so they have not differentiated into a specific type of Bcell yet).

The TH2 lymphocyte also secretes IL5 which activates eosinophils. The eosinophil then becomes an
activated eosinophil which ten feeds back into the innate and feeds back into the TH1 arm.

The TH2 arm has 4 functions of the antibody in the host cell defence. The first is opsonisation, in
which a pathogen is coated with IgG to attract and enhance phagocytosis. The plasma cells release
the antibodies, which then go to coat the antigen and attract the macrophage to then phagocytise
that antigen. The second id Neutralisation in which antibodies bind to specific sites on body cells
where the bacteria or virus normally attach, thus preventing the attachment by blocking the bacteria
and viruses for attaching themselves. The third is Antibody dependant, cell mediated Cytotoxicity
(ADCC). The antibody is bound to the surface of an invader and may trigger contact killing of the
invader by host cells. So, they are either killed by Natural Killer cells (NKs) or cytolytic T lymphocytes
or Polymorphonuclear leukocytes (PMNs) trigger killing. The 4th is the Activation of Compliment. The
antibody is now bound to the antigen and the C1 complex binds to the antibody and activates the
chain reaction of C2 and C4 and C3 and all the others, the Classical pathway occurs on adaptive
immunity and is dependent on fixed antibody.

C1 binds to the antibody molecule already attached to the antigen and acts as an enzyme to catalyse
a series of reactions with other C2 and C3 proteins, C3b attaches to the antigen and attracts
phagocytes, stimulates phagocytosis and inflammation. It also triggers the release of C5 to C9
complexes. The C5-C9 form a membrane attack complex (MAC) which punctures the cell membrane
through fore formation like Natural Killer cells which leads to cell lysis.

Sup July 2019 Q1 (Section A)

The human body is remarkable in its ability to protect itself. Describe innate immunity with
the aid of sketches. [20]
Met with Dr Neethling after ST1, she implies that Innate immunity would not be asked in the
exam, rather Adaptive immunity will be asked, but she said not to ignore Innate as it makes up a
part of the Adaptive immunity.

June 2019 Q1 (Section A)

Discuss the process of acquired immunity, with emphasis on antibody mediated immunity.
Also explain how antibodies mediate the destruction of antigens. [12]

TH2 is antibody mediated.

You have an antigen presenting cell, that secretes IL-1 (Interleukine-1) and activates T cells and B
cells, then there is an uncommitted Tcell which is traveling from the Bone marrow to the thymus.
When the uncommitted Tcell is exposed to the IL1 it then becomes a TH2 lymphocyte. The TH2
lymphocyte secretes IL4 which is a growth factor for B cells and suppresses the TH1 arm. This is on of
those that both supresses and activates. By the time that this starts to happen the TH1 arm has
gained some form of control which is why it does not matter that it is being suppressed.

IL4 works on Bcells and changes them into plasma cells which then release specific antibodies. The
TH2 lymphocyte also secretes IL6 which is also an important growth factor for Bcells that are late in
differentiation (so they have not differentiated into a specific type of Bcell yet).

The TH2 lymphocyte also secretes IL5 which activates eosinophils. The eosinophil then becomes an
activated eosinophil which ten feeds back into the innate and feeds back into the TH1 arm.

The TH2 arm has 4 functions of the antibody in the host cell defence. The first is opsonisation, in
which a pathogen is coated with IgG to attract and enhance phagocytosis. The plasma cells release
the antibodies, which then go to coat the antigen and attract the macrophage to then phagocytise
that antigen. The second id Neutralisation in which antibodies bind to specific sites on body cells
where the bacteria or virus normally attach, thus preventing the attachment by blocking the bacteria
and viruses for attaching themselves. The third is Antibody dependant, cell mediated Cytotoxicity
(ADCC). The antibody is bound to the surface of an invader and may trigger contact killing of the
invader by host cells. So, they are either killed by Natural Killer cells (NKs) or cytolytic T lymphocytes
or Polymorphonuclear leukocytes (PMNs) trigger killing. The 4th is the Activation of Compliment. The
antibody is now bound to the antigen and the C1 complex binds to the antibody and activates the
chain reaction of C2 and C4 and C3 and all the others, the Classical pathway occurs on adaptive
immunity and is dependent on fixed antibody.

C1 binds to the antibody molecule already attached to the antigen and acts as an enzyme to catalyse
a series of reactions with other C2 and C3 proteins, C3b attaches to the antigen and attracts
phagocytes, stimulates phagocytosis and inflammation. It also triggers the release of C5 to C9
complexes. The C5-C9 form a membrane attack complex (MAC) which punctures the cell membrane
through fore formation like Natural Killer cells which leads to cell lysis.

Special Aug 2016 Q2 (Book 1)

A friend’s fish have started developing small greyish pustules of about 1cm on the skin and gills.
The fish seem to be producing more mucous than normal. Some of them have even died. It all
started when he caught a wild fish and added it to his aquarium. What parasite is affecting the
fish? (2) Make an annotated diagram explaining the life cycle of the parasite. (8) Explain how your
friend can rid his fish and aquarium of the parasite and how he can prevent this from happening
again. (3) How did the parasite cause some of the fish to die? (2). (15)

The parasite is Ichthyophthirius multifiliis, the lifecycle is 1 a pustule on the skin of the host bursts
releasing the trophozoite, 2 the trophozoite encysts in water and 3 the cyst undergoes division to
form tomites 4 the tomites are released from the cyst as ciliates. 5 the tomites attaches to the skin
and develops into a trophozoite.
The aquarium must be treated with a
very dilute formaldehyde or with
malachite green (this dyes everything
green), which can also be fed to the fish,
or with methylene blue (this dyes
everything blue), to prevent this from
happening again, when you get a new
fish place it in a quarantine tank, in which
you can see if it is infected, and if it is
treat with dilute formaldehyde,
malachite green or methylene blue, only
once you are sure that it is bot infected
you can put it in the main tank. The host
can die due to suffocation, the parasite
causes a white to grey pustules on the
skin, which causes the host to produce
excessive mucus in effort to scratch as
fish have no hands to scratch an itch with, the gills then become covered with the mucus and the
fish suffocates due to there not being oxygen entering the lungs.

Sup June 2016 Q2

Describe the life cycle of Ichthyophthirius multifiliis with the aid of sketches. [10]

Lifecycle of Ichthyophthirius multifiliis, 1 a pustule on the skin of the host

bursts releasing the trophozoite, 2 the trophozoite encysts in water and 3 the
cyst undergoes division to form tomites 4 the tomites are released from the
cyst as ciliates. 5 the tomites attaches to the skin and develops into a
trophozoite.

June 2014 Q2

Briefly discuss the pathogenesis, diagnosis, and treatment of an Echinococcus granulosus infection.
(10)

The pathogenesis is that the patient can be symptomless for up to 20 years, the nervous system is
affected which has clinical effects, it affects the bone marrow so growth is restricted sue to the
necrosis of bone which can cause spontaneous fractures, the hydatid cyst can cause sudden death if
ruptures due to anaphylactic shock. Diagnosis can only be via finding the hydatids which can only be
seen through X-ray or ultrasound or a CAT scan. Treatment is only possible via surgery, of removing
the cysts, the doctor first drains the cyst, then fills it with 10% formaldehyde, then drain the
formaldehyde, and finally removes the cyst, when surgery is not an option, Albendazole can be used.
 June 2016 Q2

Describe the life cycle of Plasmodium falciparum with the aid of sketches. (10)

Plasmodium falciparum lifecycle:

A female Anopheles mosquito bites the host – human- and sporozoites are injected into the blood
system. The sporozoites enter the liver cells, and undergo asexual schizogony a form of multiple
fission, to form merozoites which erupt from the liver cells and infect red blood cells (RBC0 where
they become motile trophozoites (an incubation period of 10-15 days can occur here) trophozoites
feed on haemoglobin and form an insoluble compound “hemozoin” which accumulates in the red
blood cells, and then in the liver, spleen, and other organs. The trophozoite matures into the signet
ring stage where it undergoes schizogony to form the schizont stage, the nuclear and cytoplasmic
material split during schizogony and then the products of trophozoite nuclear division acquire
cytoplasm forming merozoites again. The merozoites reproduce asexually and the red blood cells
burst releasing the merozoites and their wates products into the blood stream causing fever and
chills in the human, the merozoites then repeat this asexual cycle. Some trophozoites develop into
gametocytes in the blood which are ingested by the mosquito when it takes its next blood meal. The
gametophytes undergo gametogenesis to form the micro and macrogametes. The newly formed
gametes fuse in syngamy fusion (fertilisation or anisogametes), forming a motile ookinete in the
stomach of the mosquito. The ookinete penetrates the stomach wall forming an oocyte which
undergoes sporogony – multiple fission of zygotic oocytes) to form haploid sporozoites. This is an
asexual zygotic meiosis. This is the infective stage, the sporozoites undergo multiple sporogony and
the oocyte grows until it bursts releasing the sporozoites which then migrate to the salivary gland of
the mosquito, from here the sporozoites are then injected in to the next human that the mosquito
takes a blood meal from, beginning the cycle again.

July 2014 Q2

Discuss Giardia intestinalis infection in terms of pathogenesis, diagnosis and treatment. (15)
Many people are symptomless, symptoms can include an increased mucous production, diarrhoea,
dehydration, intestinal pein, flatulence, weight loss, fatty stool, there is no blood in the stool.
Diagnosis can be done by a faecal smear, and cysts or trophozoites must be identified. It is treated
with metronidazole or with quinacrine and al occupants of the house must be treated. The cysts are
highly contagious so there must alco be in increased of sanitation in the house.

Sup July 2019 Q2 (Section A)

A patient has been diagnosed with hydatidosis. Explain what the likely cause for this infection is (2).
Name the parasite that causes it (1). Discuss treatment options (3), and with the aid of diagrams,
describe the lifecycle of the parasite (9). [15]

A patient diagnosed with hydatidosis, is likely caused by humans eating infected tissue, that is
tissues infected with cysts, or by ingesting eggs from the faecal oral route. The parasite that causes
this is Echinococcus granulosis. Treatment is only possible via surgery, of removing the cysts, the
doctor first drains the cyst, then fills it with 10% formaldehyde, then drain the formaldehyde, and
finally removes the cyst, when surgery is not an option, Albendazole can be used. The lifecycle is as
follows: 1 adults in the intestine of the definitive host have a ripe gravid proglottids develop a
rupture in their wall releasing the eggs. 2 the
eggs are infective to intermediate host upon
ingestion, 3 the oncosphere penetrates the
intestinal wall and heads to the liver, lungs and
other sites, 4 the oncosphere metamorphoses
into a bladder worm called a unilocular hydatid,
5 the unilocular hydatids contain many
protoscolices which are infective to the
definitive host. 6 the definitive host eats the
infected tissue, 7 the scolex evaginates, 8 the
scolex attaches to the intestine and fully
develops. 9 the adults in the intestine of the
definitive host matures and finds a mate and the
female produces eggs.

Special Aug 2016 Q3 (Book 1) AND July 2014 Q3

Describe the life cycle of Echinococcus granulosis with the aid of sketches. (10)

The lifecycle is as follows: 1 adult in the intestine of the

definitive host have a ripe gravid proglottids develop a rupture
in their wall releasing the eggs. 2 the eggs are infective to
intermediate host upon ingestion, 3 the oncosphere penetrates
the intestinal wall and heads to the liver, lungs and other sites,
4 the oncosphere metamorphoses into a bladder worm called a
unilocular hydatid, 5 the unilocular hydatids contain many
protoscolices which are infective to the definitive host. 6 the
definitive host eats the infected tissue, 7 the scolex evaginates,
8 the scolex attaches to the intestine and fully develops. 9 the
adults in the intestine of the definitive host matures and finds a
mate and the female produces eggs.
 Sup June 2016 Q3 AND June 2016 Q3

On a camping trip, you purchase meat from a farmer who informs you that there have been
outbreaks of Taenia saginata and T. solium within the region, but he insists that only his livestock is
safe. As an experienced parasitologist, report the pathogenesis of these parasites to him and provide
him with a preventative method should he sell to other people. [10]

Taenia saginata’s (from beef) pathogenesis can be asymptomatic or can be mild to moderate with
the following: dizziness, abdominal pain, diarrhoea, headache, localised sensitivity to touch and
nausea, delirium, intestinal obstruction needing surgery, loss of appetite, allergic reaction,
psychological effects if the patients see worms in their underwear. Taenia solium’s (form pigs)
pathogenesis is cysticercosis, that is cysticerci in the subcutaneous connective tissues and a fibrous
capsule of host origin surrounding the metacestodes, the effect is dependant on the location, if on
the skeletal muscle, skin, or liver then there is little noticeable pathogenesis, if it is on the eye, ocular
cysticercosis there is irreparable damage. If it is on the brain, it causes a pressure can lead to
blindness, paralysis, disorientation or sudden onset of epilepsy, there is severe inflammation when it
is on the eye or brain since it cannot be treated. He should tell people to cook the meat that they get
from him very well to kill any parasites within the meat if there is any, and if the people start to
show symptoms as presents above, they should seek medical attention and treat with taenicides and
praziquantel and ensure that they recover the scolex preventing further strobilation.

June 2014 Q3

People infected by Enterobius vermicularis lose sleep due to the parasites’ activity. Discuss this
statement by referring to the life cycle and associated pathology of the parasite. (15)

Lifecycle of Enterobius vermicularis:

1 the gravid female deposits the eggs on the perianal folds

(which can be tested with a perianal swab) and the larvae
mature within the eggs, 2 self-innoculation occurs after
touching the area or contaminated surfaces and linens and
then touching mouth and eggs are ingested, 3 the eggs hatch
in the small intestine,4 the adults establish themselves in the
lumen of the cecum, 5 the gravid female migrates to the
perianal region and deposits her eggs beginning the cycle
again. The pathology it is usually asymptomatic, but in heavy
infections there can be damage to the intestinal wall and
damage because of the eggs being deposited, the
microscopical sores in the mucosa can cause secondary
infections with bacteria, there is itching which causes
scratching allowing the bacteria to feed and for secondary
infections to occur, which causes more itching. It also causes
sleeplessness, loss of appetite, weight loss, and nightmares in
children. This is mostly due to the psychological effect of waking up in the morning and finding that
there are worms in the patients under wear, it can also be since the females lay their eggs in the
early morning when the child is sleeping which can cause discomfort and nightmares which in turn
also causes sleeplessness.
 Sup July 2019 Q3 (Section A)

Describe the lifecycle by Entamoeba hystolitica and refer to the pathology inflicted by this parasite.
[15]
1 ingestion of mature cysts in faecal contaminated food water of
hands, 2 excystation occurs in the small intestine,3 trophozoites
are released which migrate to the large intestine, the trophozoites
multiply and produce cysts, 4 cysts are passed in the faces they
have walls to protect against the external environment, this is the
infective stage. A this is a non-invasive infection the trophozoite
remain confined to the intestinal lumen and individual are
asymptomatic arrives and cyst passers (the initial disease is
intermittent diarrhoea cramps vomiting malaise, it hydrolyses and
invades tissue, a galactose specific membrane lectin produces an
inflammatory response, intestinal lesion can be 1st in the cecum,
appendix or the upper colon, the numbers increase in ulcers which
causes mucosal destruction and necrosis, there can also be an
ameboma which is an obstruction. Older lesions have bacteria
which break through the muscularis mucosae into the submucosa
into the muscle and into the serosa which causes extra-intestinal
diseases). B intestinal disease the trophozoites invade the
intestinal mucosa. C extra intestinal disease (his is hepatic amoebiasis which is liver lesions or
pulmonary amoebiasis which are lung lesions, they can be on the brain, skin, penis, kidneys,
adrenals, spleen, or pericardium but the last 4 are rare.), the trophozoites invade though the
bloodstream to the liver brain and lungs, transmission can also occur through faecal exposure during
sexual contact. (There can also be acute amoebic dysentery which causes headaches fever and
severe abdominal cramps there will also be prolonged straining at still with no results, there will be
liquid faeces with blood, and death from peritonitis or cardiac failure and exhaustion.)

June 2019 Q3 (Section A)

Describe the lifecycle of Entamoeba hystolitica. How would you confirm this infection in a
patient? How is it treated? [15]

1 ingestion of mature cysts in faecal contaminated food water of hands, 2

excystation occurs in the small intestine,3 trophozoites are released
which migrate to the large intestine, the trophozoites multiply and
produce cysts, 4 cysts are passed in the faces they have walls to protect
against the external environment, this is the infective stage. A this is a
non-invasive infection the trophozoite remain confined to the intestinal
lumen and individual are asymptomatic arrives and cyst passers. B
intestinal disease the trophozoites invade the intestinal mucosa. C extra
intestinal disease, the trophozoites invade though the bloodstream to
the liver brain and lungs, transmission can also occur through faecal
exposure during sexual contact.

Trophozoites or cysts are demonstrated in stool on a wet mount that is

fixed and stained, it is treated with metronidazole, it can also be treated
with Tetracycline and diiodohydroxyquin or with ornidazole and
tinidazole to cure hepatic abscesses.
 Special Aug 2016 Q4 (Book 2) AND Sup July 2019 Q5 (Section B) AND June 2019 Q5 (Section B)

Discuss Strongyloides stercoralis with reference to the following: biology (3), epidemiology (4),
pathogenesis (8), diagnosis (3) and treatment (2). (20)

Strongyloides stercoralis biology it is not often found in the respiratory system, pancreas, and gall
bladder, it has a buccal capsule that is small, long and cylindrical oesophagus without a basal
bulbous, the rhabditiform larvae are shorter and slower, vulva is about 1/3rd of the body length and
distinguished by prominent genital primordium, eggs are ovular and released in the lumen or
submucosa. The female anchors herself with er mouth in the mucosa of the intestine and bores
anteriorly into the sub mucosa, she produces dozens of partially embryonated eggs daily that are
released into the lumen or the sub mucosa, there are 2 types of larvae the free living and the
infective that enters the skin or becomes ingested by the host. The epidemiology is through contact
with infected soil/ water specifically in the tropics, it is also common in areas where there is poor
sanitation. There are 3 stages of pathogenesis, the first is the entering stage there is a slight swelling
and severe itching there is often a secondary infection caused by bacteria causing a skin infection.
The second stage is migration through the lungs this causes damage to the lung tissue which causes
and increased immunological reaction, and when they develop in the lungs there is a severe burning
in the chest and a dry cough TB reactivated. The 3rd stage is ingestion when the parasite enters the
intestinal mucosa and develops into an adult, then eggs are produces which causes an intense
burning pain and tissue brakes off the intestine and there can be a bacterial infection because of this
which causes inflammation and septicaemia and even death. Diagnosis demonstrates adults or
larvae in faeces, but the larvae is difficult to identify, Treat with Thiabendazole.

Sup June 2016 Q4

You are buying a guest house from a person who had the guest house standing vacant for 18
months. Using your knowledge of parasitology explain how you will go about cleaning the house and
furniture before you re-open the business. Explain which parasites may be contracted and give a
short but convincing explanation of the expected pathology if you should take short cuts. Refer to at
least 5 (five) taxonomic groups [15]
To clean the house, you must thoroughly sanitise all surfaces with a strong acid, and wash all
curtains extremely well, at least twice at a temperature that is above 90 degrees Celsius, to destroy
any tick or mite eggs that may have been deposited there, as well as any eggs of Enterobius
vermicularis.

If the house had been vacant for 18 months there may have been squatters who inhabited the house
and perhaps if the toilets did not flush there may be sewerage found in odd places in the house, this
means that there could be Giardia intestinalis on surfaces that were in contact with the faecal
matter, since the cysts can survive for several months, if you take short cuts in cleaning then Giardia
can be contracted causing an increased mucus production as well as diarrhoea and dehydration,
intestinal pain, flatulence wight loss and fatty stool.

Bugs can also fly into the house if left vacant so there could have been conenose bugs flying around
and defecating on surfaces, this means that there could be Trypanosoma cruzi (if the house is in
South America) that if the faces is touched then the human will be infected and if the area is not
cleaned well some symptoms will be acute local inflammation, swelling or regional lymph nodes,
anaemia, loss of strength chills and even heart failure.

Enterobius vermicularis, has many eggs that can stand for long periods of time that can infect bed
linen clothes curtains, carpets and couches, the eggs are viable in the environment for up to 1 week
so if there were squatters evicted recently there could be Enterobius vermicularis if the bedding or
curtains are shaken the eggs could be come airborne and the eggs could then be inhaled causing
infection, it is usually asymptomatic however if there are heavy infections the symptoms could be
microscopical sores in the mucosa leading to secondary infection, there could be itching, in children
there could be sleeplessness, loss of appetite, nightmares and weight loss.

There can also be Cimex lectularis which are bugs that feed on the host they are cannibals so they
can survive for long times without a host by eating others of their kin, they do not naturally transmit
any disease but they can transmit hepatitis B, if the house was not sanitised properly then they can
be a nuisance and the host can suffer form loss of sleep, the sores can be infected and they feed on
blood which can cause there to be a haemoglobin deficiency s well as an iron deficiency, they can
also cause anaemia due to loss of blood.

Ticks and mites are also common as they can live for long periods of time up to 21 years, and if the
beds and floors are not cleaned sufficiently then they can cause anaemia from the blood loss when
feeding, dermatosis if they leave mouth parts in the skin after feeding and being pulled out
incorrectly, the can also lead to secondary infections since they leave an open wound after feeding
leaving the area open to bacteria or fungal or virus infection.

June 2014 Q4

Parasites in the class Monogenea are well adapted, in terms of reproduction, for their parasitic
lifestyle. Discuss this statement with reference to the biology of Gyrodactylus sp. (5)

Gyrodactylus sp. are viviparous with a sequential polyembryony they have no distinct ovary, the Egg
Cell Formation Region (ECFR) is posterior to the uterus the oocytes develop and sperm is stored and
the layer of cells in the chamber in the ovary the ECFR and the uterus show syncytium and the young
develop into sub adults with a juvenile inside and another inside that thus having a Russian doll
effect, only once the juvenile is born can the egg be formed in the ovary and fertilized thus being
oviparous and so massive infections can develop quickly.

June 2016 Q4

You are appointed as a biologist at a municipality. The sewage works is often out of order resulting
in the dumping of sewage into the drinking water. Motivate from a parasitological perspective to
your employer why this situation is intolerable. Use 5 examples to represent all phyla studied during
this course to substantiate your response. Explain how a parasite may be contracted and give a short
but convincing explanation of the expected pathology. (20)
There are many infections that can come from the water if sewage is dumped into drinking water,
since many eggs of parasites within humans are deposited in the intestine and colon of humans and
passed out of the human with excretion. If there is sewage in the drinking water, then even if the
water is purified there will still be eggs within the wates so ingestion of the eggs will result in
infection of humans by the parasites.

Clonorchis sinensis has eggs that are passed in faeces, if there is poor sanitation then they will also
be in the drinking water, this means that if the drinking water is contaminated and the eggs are
ingested the human will begin to show symptoms such as excess mucus production, the ducts near
the liver, gall bladder and pancreas become surrounded by eosinophils and mononuclear white
blood cells causing the ducts to become fibrous, this causes the liver cells to atrophy and become
necrotic and causes jaundice.
Giardia intestinalis cysts within the water since they are passed in the faeces will be in the
contaminated water and will cause the human to become infected and will cause an increased
mucus production as well as diarrhoea and dehydration, intestinal pain, flatulence wight loss and
fatty stool.

[needs more]

July 2014 Q4

The pathogenesis associated with the Ancylostomidae can generally be divided into three phases.
Discuss this statement in detail. (15)

The pathogenesis associated with the Ancylostomidae can generally be divided into three phases:
Phase 1 is the cutaneous phase, Migration/ lung phase is the second and the third is the intestinal
phase.

Cutaneous phase: there is little damage as it penetrates the skin via cracks or hair follicles. The
penetration of the skin causes an immunological reaction and pyogenic bacteria enters the wound
casing a ground itch.

Migration/ lung phase; each worm migrates from the stomach through the lungs to be coughed up,
the migration of each worm causes bleeding (haemorrhage) sometimes there is a dry cough and a
sore throat, but it is usually asymptomatic, in severe cases there can be pneumonitis.

Intestinal phase: the parasite attaches to the mucosa with the buccal capsule and teeth and move
around taking up more blood than needed this causes an iron deficiency and anaemia, sometimes
there is abdominal pain and loss of appetite and geophagy (eating of soil).

June 2019 Q4 (Section A)

With the aid of sketches, describe the lifecycle of Diplozoon sp. [8]

The egg hatches into an oncomiracidium with 2

clamps, it feeds and grwos until it develops into a
Diporpa with 2 clams, it then develops into a sub-
adult diporpa with 4 clamps. The Diplozoon then
finds a mate and begins to fuse at the genital pore,
it then completes its fusion forming a diporpa with
6 to 8 clamps, at this stage it then can sexualy
mature into an adult with 6 – 8 clamps and it
begins to produce eggs, which then go on to hatch
repeating the cycle again. Once fused they are
fused for life as their intestines join, and they
become one organism.

Special Aug 2016 Q5 (Book 2) (ST2 Q1 2021)

 Make an annotated drawing of the life cycle of Haemonchus contortis (8). Discuss the pathology
caused by the parasite (7). (15)

The pathology is such that it infects sheep and goats when they step on stool or they stem on
infected soil, or on infected grass. The parasite burrows into the skin of the foot, by cutting the skin
or by entering near a hair follicle. When they cut into the skin, they cause a red mark on the skin
which causes swelling due to the immune system trying to fix the damaged skin. They migrate to the
blood and nymph vessels and enter the lungs of the host. The host coughs up the parasite and
swallows them back down into the stomach. Due to their cuticle, they are able to withstand the
gastric juices and not be digested. They then move into the intestine and attach to the host in the
intestine. Theys suck the blood from the intestine as wall as any food that enters the intestine to be
absorbed. Due to this, that they eat the blood, they cause oedema in the host and an iron deficiency,
this causes light-headedness and the inability to concentrate causing the host to collapse. They also
eat the food of the host making the host lose weight and become anaemic since they are not getting
the nutrition that they need. The eyelid if looked at (the bottom of the eye) becomes a milky white
colour due to the lack of blood and the throat enlarged. It also reproduces within the host and the
eggs when they exit the host’s anus can cause an itching when the female adult moves to the anus
to deposit the eggs. Headache, stomach pains and intestinal pains are also common due to the
parasite moving within the host.

Sup June 2016 Q5

List the effect of ticks and mites and their hosts and provide examples of each. [10]
Anaemia – blood loss due to feeding.

Dermatosis – from mouth parts remaining in the bite wound after the organism leaves or is pulled
off, or from saliva and causing secondary infection.
Paralysis – bitten near the base of the skull and toxic secretions.

Otoacariasis – infection in the ear canal.

Infections – transmission of bacteria (Rickettsia africae), viruses (Hyalomma marginatum), or

parasites (Haemaphysalis elliptica).

[Probably need more examples]

June 2014 Q5

Compare the Ceratopogonidae with the Culicidae with regards to their mode of feeding. Explain the
role of the different mouth parts. (10)

Family Culicidae (mosquitos) are solenophages and penetrate the individual capillaries and feed on
the blood, females feed by inserting their fascicle into a blood vessel and pump blood into the food
channel, males lack mandibular stylets and do not feed on blood only on plant juice. The fascicle
consists of 6 stylets: 2 mandibles for piercing, 2 maxillae for piercing, a hypopharynx for saliva that
has anticoagulants and an labrum-epipharynx within an elongated labium with the tip the labella for
drawing up food.

Family Ceratopogonidae (biting midges/ sand flies) are temophages and lacerate the skin and feed
on a pool of blood. The females feed on blood and both sexes feed on plant nectar. The fascicle is
made up of 6 parts: 2 flattened, blade-like mandibles with serrations for cutting, 2 narrow maxillae
with serrations for piercing, 1 hypopharynx for saliva that has anticoagulants, and 1 labrum-
epipharynx to draw up the food.

June 2016 Q5

List the taxonomic groups of mites. Explain the characteristics used to define these groups. Use
sketches were applicable. (15)
Mites:

Order Mesostigmata – has respiratory spiracles (stigmata) behind the 3rd coxae.

Order Prostigmata – spiracles are located between the chelicerae or on the dorsum of the
hysterososoma.
Order Astigmata – lack tracheal systems and respire through the tegument, they also lack claws
which are replaced with sucker-like structures on the pre-tarsi.

July 2014 Q5 (last Q)

Parasitic crustaceans of fish have specific morphological adaptations/features for adhesion to their
fish hosts. Discuss this statement by referring to the different examples you have studied. (10)

Lernaea cyprinacae anchors to their hosts by means of an anchor that is an outgrowth of the head,
which grows into the flesh of their host.

Ergasilus sp. the females attach to the hosts gills using their antennae which is long and ends in a
large claw, the antennae encircle the gill filament holding on to the gills extremely tightly clamping
on to not fall off.

Caligus sp. as an adult have a large cephalothorax with two lunules for attachment, the
cephalothorax along with the protopods allows for it to form a vacuum and attach to the hosts skin,
gills, or tail. As a chalimus it can attach to a host with a frontal filament.

Argulus sp. have sucking structures on the ventral side near the anterior end to help for attachment
to the host,
Succulina sp. as an adult grows dendric-like processes that ramify through the tissue s of the host to
obtain nutrition and to attach to the host.

Lironeca sp. burrows under the scales of the host and the skin of the host grows and surrounds the
parasite, they can also attach to the tongue of the fish and then begin to act as the tongue since the
tongue atrophies.

Sup June 2016 Q6

Discuss the adaptations present in Lernaea with regard to the morphology and life strategies [10]

Lernaea has adapted to a parasitic lifestyle in terms of morphology and life strategies by a massive
reduction in the locomotory appendages to very small appendages, it also has developed ana
attachment structure that is an anchor-like outgrowth that protrudes form the head and grows into
the skin of the host embedding the female there so that it can produce, the egg sacs are attached to
the end of the body so that there can be more eggs produced than if the eggs were to be kept in the
body since the body I so small, it produces a large number of eggs. The egg sacs appear about 23
days after hatching so there is a quick turn over from the time of hatching to the time of producing
eggs. The thorax segmentation becomes blurred, and the female can survive for up to a month
producing eggs and feeding on the host. The male dies about 24 hours after fertilisation as he has
fulfilled his purpose of fertilising the females. There are 3 nauplial stages and 5 copepod stages and
only after the 5the copepod stage is there sexual dimorphism.

June 2014 Q6 (last Q)

A chicken farmer complains that hundreds of his chicks are dying after being listless and producing
bloody diarrhoea. The disease is caused by a unicellular organism. Identify the parasite and diagnose
the disease, discuss the life cycle, and refer to the pathology. Also suggest treatment. (20)

Eimeria tenella is the unicellular parasite that causes

this to happen within the chickens on the farm, the
disease is called Coccidiosis occurring in the intestinal
ceca of chickens and causes a high mortality in young
birds. The disease can be diagnosed if the birds show
bloody diarrhoea due to the schizonts disrupting the
capillaries which causes haemorrhaging, sloughing of
the epithelium when the merozoite is released the
tissue is destroyed, the cecum is obstructed by
clotting blood which causes necrosis and death. It can
be treated with prophylactic drugs against coccidiosis
but once the infection is established there are no
drugs to cure it, rather the farmer must quarantine
the healthy chicks and destroy the infected chicks and
then sanitise the area to prevent the healthy chicks
becoming infected.

1 sporozoite breaks out of sporont in the intestine of

the host and enters the epithelium, 2 the sporozoite develops into 1st generation schizont. 3 the
schizont develops merozoites, 4 merozoites break out of host cell, 5 merozoites enter new intestinal
cells to form 2nd generation schizont. 6 merozoites develop macrogametes by gametogony. 7
merozoites develop macrogametes by gametogony, 8 merozoites enter new intestinal cells to
produce the 3rd generation schizonts, 9 2nd and 3rd generation merozoites enter new intestinal
epithelial cells to form microgametocytes. 10 microgametes released from microgametocytes, 11
microgametes fertilize macrogametes, 12 develop into zygotes which develop heavy walls to
become oocytes, 13 oocytes break out of host cells and pass through the faeces, 14 oocytes
sporulates, 15 sporont forms 4 sporoblasts each forms a sporocyst containing 2 sporozoites. 1
sporozoite breaks out of sporont in the intestine of the host and enters the epithelium, and the cycle
continues.

June 2016 Q6

Discuss the adaptations present in Sacculina with regard to the morphology and life strategies. (10)

Sacculina sp. starts off life as a nauplius stage with no mouth then undergoes 4 moults, the 5ht stage
called the cyprid, the females attach to the crab with her antennules, and the swimming legs are
shed, and the remaining larva are known as kentrogon made up only of undifferentiated cell mass,
which is then injected into the hemocoel of the crab at any spot when the cuticle is thin. The
embryonated cell mass attaches to the midgut of the host and begins to grow, it releases a hormone
that makes the host think that it is carrying its own babies so the host starts to become more female
like if it is a male or even more female like if it is already a female or even more male like if it is a
female, the host treats it as its own babies and feeds the parasite and keep sit safe. The male crabs
begin to look more feminine and become broader and have a more completely segmented
abdomen, there are alterations in the pleopods towards toe female type, externa is in the same
position and size as the egg mass of the crab, and the crab protects and grooms the parasite, the
parasite releases pheromones that stimulates the larval releasing behaviour of the host crab.

Sup July 2019 Q6 (Section B)

Describe the lifecycle of Sacculina, describe the various effects on the host. [15]

Sacculina sp. starts off life as a nauplius stage with no mouth then undergoes 4 moults, the 5ht stage
called the cyprid, the females attach to the crab with her antennules, and the swimming legs are
shed, and the remaining larva are known as kentrogon made up only of undifferentiated cell mass,
which is then injected into the hemocoel of the crab at any spot when the cuticle is thin. Migrate to
a site just dorsal of the ventral nerve chord and grow. The central mass contains female gonads
which press against the host’s hypodermis in the ventral cephalothorax preventing cuticle
secretions, the cuticle breaks open and the gonadal mass becomes external called the externa.
Further development of the host ceases, the externa attracts one or more male cyprids and extrude
a spine covers larva called trichogon into the receptacles of the female, and spermatogenesis occurs,
reproduction is called crypotgenochorism and the parasites releases larvae. The embryonated cell
mass attaches to the midgut of the host and begins to grow, it releases a hormone that makes the
host think that it is carrying its own babies so the host starts to become more female like if it is a
male or even more female like if it is already a female or even more male like if it is a female, the
host treats it as its own babies and feeds the parasite and keep sit safe. The male crabs begin to look
more feminine and become broader and have a more completely segmented abdomen, there are
alterations in the pleopods towards toe female type, externa is in the same position and size as the
egg mass of the crab, and the crab protects and grooms the parasite, the parasite releases
pheromones that stimulates the larval releasing behaviour of the host crab.
 June 2019 Q6 (Section B)

Parasitic Copepoda have adapted to their existence by changing both their morphology and
biology. Please discuss this statement by referring to at least three examples you have studied. [15]

Lernaea sp. has adapted to a parasitic lifestyle in terms of morphology and life strategies by a
massive reduction in the locomotory appendages to very small appendages, it also has developed
ana attachment structure that is an anchor-like outgrowth that protrudes form the head and grows
into the skin of the host embedding the female there so that it can produce, the egg sacs are
attached to the end of the body so that there can be more eggs produced than if the eggs were to be
kept in the body since the body I so small, it produces a large number of eggs. The egg sacs appear
about 23 days after hatching so there is a quick turn over from the time of hatching to the time of
producing eggs. The thorax segmentation becomes blurred, and the female can survive for up to a
month producing eggs and feeding on the host. The male dies about 24 hours after fertilisation as he
has fulfilled his purpose of fertilising the females. There are 3 nauplial stages and 5 copepod stages
and only after the 5the copepod stage is there sexual dimorphism. The female is the only one that
parasitises the host fish as the males die after fertilisation.

Ergasilus sp. has adapted to a parasitic lifestyle in terms of morphology and life strategies with their
enlarged antennae modified for prehesion and with sensory antennules, the 3rd segment claws are
opposable, and the female usually attaches to the host with their antennae which ends in a sharp
claw, they encircle the gill filament and they can swim reasonably well if removed from the gills,
their 1st legs are adapted for feeding with blade-like spines to hep them feed on the mucus. The
females produce large amounts of eggs in egg sacs off the edge of the body that enables them to
produce large amounts of eggs.

Caligus sp. has adapted to a parasitic lifestyle in terms of morphology and life strategies by having no
free-living stages and being larger than the free-living groups, they also can attach to the gills, skin,
fins and moth of the host. They have a large cephalothorax and one thoracic segment, a large genital
segment and a small un-segmented abdomen. Prehesion is using the antennae and the maxillipeds.
2 lunules on the cephalothorax are also for adhesion to the host. The arrangement of the
cephalothorax and the protopods helps to form a vacuum for attachment to the host, they feed
through suction with a tubular mouth type spiphonostome and the mandibular tips have sharp
cutting blades that are used for piercing and tearing off bits of host tissue to be sucked up by the
siphonostome. The mandible tips are within the siphonostome.

Special Aug 2016 Q7 (Book 2) (last Q)

Discuss the effect of sanitation on contamination with round worms. Refer to specific examples
studied in this course. Explain in each case the minimum requirements. (10)

Sanitation is needed to prevent parasitic round worms.

Trichuris trichiura has eggs that are passed in faeces, the eggs are lemon-shaped with 2 opercula on
each side, it has a very strong shell that can resist acid and other strong disinfectants, in order to be
rid of the eggs proper sanitation is requires and the dumping of nightsoil should not be carried out,
the stool should be properly dealt with. If a human is infected the eggs are ingested via the fecal oral
route or by eating contaminated food or water, the eggs are ingested and hatch in the intestine in
the crypts of Lieberkuhn and move to the lumen of the ileocecal are. The entire are needs to be
sanitised and proper disposal of stool should be installed in the area.
Trichinella spiralis is transmitted when humas eat undercooked or raw pork, the food should be
either cooker very well, or the food can be frozen for 20 days below -15 degrees Celsius as this will
destroy the larvae (but not the eggs). Mebendazole is used to treat it if there is improper sanitation.

Strongyloides sp. is transmitted when the host is inContact with infected soil or water specifically in
the tropics, and is very common in areas with poor sanitation, thus it is important to have sanitation
and proper removal and disposal of faecal matter from the area, do not use night soil to fertilise the
plants without the proper precautions to not touch the soil or the surrounding area with bare skin,
or just do not use night soil at all.

Necator americanus and Ancylostoma duodenale are infective in their filiform larval stage, sanitation
is required with strong disinfectants in the toilets as well as not returning to the same place for toilet
needs, salt and or urine are effective in stopping the development of this round worm so the use of
urine is possible to be used as a form of sanitation for this parasite, being cautious not to be infected
by any parasites that may be within the urine.

Haemonchus contortus is infective in the egg stage that is ingested, since the eggs have a thin shell,
they are easily disinfected with acids or other disinfectants.

Ascaris lumbricoides is infective in the egg stage which has an incredibly strong shell that is viable for
up to a year and protects the embryo from 2% formalin, potassium dichromate, 50% hydrochloric
acid, nitric acid, and sulfuric acid. The infection can occur from eating dirt and other soiled fingers
and toys, from night soil , cockroaches, bank notes and via the placenta from mother to child, if
found in an area, proper sanitation needs to occur, with the disinfection of the entire house, school
or area where the eggs are found, children should be watched carefully and stopped from placing
dirty toys or fingers in their mouths, and produce grown in fields using night soil must be properly
washed before sale and again before use. Dogs must be do-wormed wafter they are born to prevent
further infection of children from infected pets.

Enterobius vermicularis has eggs that are infective and can be found on clothes, bed linen, curtains
and carpets, the eggs are viable for up to 1 week in a cool damp environment, when the eggs have
been dried, they can be shaken off whatever they are on in the process of cleaning and can be
inhaled. In the sanitation process clean all surfaces and wash all linen, curtains, ensure that a mask is
worn when doing clothes and linens, if possible, leave the infected area untouched for more than a
week, so that the eggs will become not viable, and then sanitise the area with the correct
disinfectants.

Wurchereria bancrofti is infective in the filariform larvae stage, and is transmitted via mosquitos
Anopheles, Aedes, and Culex the best way is to sanitise the area from the mosquitos and to destroy
the breeding habitats of the mosquitoes.

Sup June 2016 Q7

Discuss the pathology of Enterobius vermicularis (12). Indicate how the life cycle of the parasite co-
ordinates with the pathology (6). Describe treatment of patients with an infection (2). [20]
Pathogenesis is usually asymptomatic with heavy infections damaging the intestinal wall because of
the eggs being deposited, there are microscopical sores in the mucosa, and secondary infections
with bacteria, the itching causes scratching ang the scratching causes feeding which causes
secondary infections and more scratching. They migrate to the vagina and encyst in the peritoneum,
they cause in children nervousness, sleeplessness, loss of appetite, nightmares, and weight loss.
 The eggs are laid on the perianal
folds, and the larvae within the eggs
mature within 4-6 hours, 2 the
embryonated eggs are ingested by
the human via faecal oral route, 3
the larvae hatch in the small
intestine and 4 mature into adults in
the cecum. 5 gravid females migrate
to the perianal region at night to lay
eggs.

The sleeplessness, nervousness, and

nightmares is due to the feeling of
the females migrating to the perianal
folds to deposit her eggs.

Demonstration of the eggs or worms

in the peri-anal area during the night
or early morning suing a sticky tape
adhesive technique for diagnosis and
mebendazole also known as Vermox
is used to treat and repeated in 10 days, the entire family must be treated at the same time.

June 2016 Q7

Discuss the pathology of Wurchereria bancrofti (6). Indicate how the life cycle of the parasite co-
ordinates with the pathology (3). Describe treatment of patients with elephantiasis (1). (10)

The pathology of Wurchereria bancrofit is in 3 parts: Incubation, Acute or chronic inflammation and
3 the obstructive phase (chronic lymph edema).

1: Incubation there is no symptoms,

2: Acute or chronic inflammation when the female releases the microfilaria there is an intense
lymphatic inflammation in the lower part of the body. This causes a fever, cold fever, toxaemia, and
the area swollen and painful which may be red, the sudden enlargement of the reproductive organs
(orchitis) there is a proliferation of cells lining the lymph and abscesses form and dead worms and
bacteria are present.

3: obstruction phase (chronic lymph edema) the lymph drainage is prevented and there is lymph in
the urine as well as blood, there is scar formation in the lymph because of connective tissue
deposits, the worms become calcified and it is suspected that secondary bacterial infection
contributes to inflammation, granulomatous infiltration and in some cases collagenous
encapsulation with intense inflammation.

Treatment can be chemical with castor oil or carbon tetrachloride, mebendazole has been effective
in the case of one child. Swollen appendages must be tightly bandaged, it is important to control the
intermediate host, once all the worms have dies symptoms may gradually decrease, casual
infections do not lead to elephantiasis (repeated infections)
 Sup July 2019 Q7 (Section B) (last Q)

Describe the life cycle of an Anopheles fenustus with the aid of drawings (10). Discuss how the
parasite adapted for its parasitic lifestyle (5). [15]

The female adult lays singular eggs

that have floats in the surface of
the water, the egg hatches into the
larvae that lies parallel to the
surface of the water and breathed
through a rudimentary breathing
tube, the larva then moults into a
pupa with a large head and a tail
that is slightly curled beneath its
head. The pupa then become an
adult and there is sexual
dimorphism between the adults,
the male fertilises the female, and the female then goes to lay eggs on the surface of the water
repeating the cycle.

The Anopheles funesus is adapted to a parasitic life as it has eggs that are able to float on water
enabling the larvae when born to live in the water, the larvae have a breathing tube that enables
them to breath while in the water, the adults are soundless when they fly so as not to alert their
prey that they are approaching. The maxillary palps are the same length as the probiscus to help for
feefding. They are able to breed in minimal amounts of water and they are homophilic.

June 2019 Q7 (Section B) (last Q) AND Special Aug 2016 Q6 (Book 2)

Describe the lifecycle of Pediculus humanis with the aid of drawings (10). Discuss how the
parasite maintains its position on the host during all life stages (5). [15]
In the egg, the egg is cemented to the hairs of the animal ensuring that they will not fall off. The
larva is born with claws on the ends of their feet, to help them clamp on to the hair as soon as they
are hatched, to make sure that they are not going to fall off the host as soon as they are hatched.
The nymph and adult stages also have claws on their legs to clamp on to the hairs of the host to
ensure that they do not fall off the host.

Sup June 2016 Q8 (last Q) AND June 2016 Q8 (last Q)

Describe the adaptations towards a parasitic existence that is expressed by Cimex lectularis. Describe
both the basic morphological adaptations (2), including mouthparts (5) as well as life strategies (3)
[10]
Cimex lectularis are small wingless bug that feeds on blood, they are dorsoventrally flattened, and
the appendages are not adapted to adhesion rather to running fast, so that they can go to a host,
feed, and get away quickly to prevent being killed. They can survive long periods of starvation and
cannibalism is common. Females lay 200 to 500 eggs, eggs hatch in about 10 days and there are 5
nymphal instars each needing a blood meal, it takes from 38-128 days from egg to maturity. Their
mouth parts are adapted for sucking blood, they have mouth parts that cut through the skin,
injecting anticoagulants and painkillers. The bug pierces the skin with the rostrum which is made of
the maxillae and mandibles which have been modified into elongated shapes. The right and left
maxillary stylets are connected at their midline and a section at the centreline forms a large food
channal and a smaller salivary channel. The entire mandibular and maxillary bundle pierces the skin.

The tips of the right and left maxillary stylets are not the same; the right is hook-like and curved, and
the left is straight. The right and left mandibular stylets extend along the outer sides of their
respective maxillary stylets and do not reach anywhere near the tip of the fused maxillary stylets.
The stylets are retained in a groove in the labium, and during feeding, they are freed from the
groove as the jointed labium is bent or folded out of the way; its tip never enters the wound.

The mandibular stylet tips have small teeth, and through alternately moving these stylets back and
forth, the insect cuts a path through tissue for the maxillary bundle to reach an appropriately sized
blood vessel. Pressure from the blood vessel itself fills the insect with blood in three to five minutes.
The bug then withdraws the stylet bundle from the feeding position and retracts it back into the
labial groove, folds the entire unit back under the head, and returns to its hiding place.[29] It takes
between five and ten minutes for a Cimex to become completely engorged with blood. In all, the
insect may spend less than 20 minutes in physical contact with its host and does not try to feed
again until it has either completed a moult or, if an adult, has thoroughly digested the meal.

Copulation is a traumatic insemination the male copulatory appendage (paramere) curves to the left
and the aedeagus (penis) is small and located above the paramere base. The praramere stabs into a
notch (paragenital sinus) which is located on the female’s 5th abdominal sternite. The sperm enter
the hemocoel to the seminal conceptacles (like the spermathecae) and finally to the ova. The male
mates with females repeatedly and homosexual behaviour is common, interbreeding occurs
between species producing sterile eggs.

Questions from Tutorial with Justine

Discuss the adaptions in organisms which enable them to be successful as parasites by referring to
examples.

Discuss the characteristics of the lifecycles of Anopheles, Culex and Aedes that makes them good
vectors for parasites.

Discuss the roles flies play as vectors of diseases.

Discuss Ancylostoma duodenale with respect to the following: morphology (3), lifecycle and
pathogenesis (8) as well as treatment (4)

Describe the lifecycle of an Anopheles female with the aid of sketches, explaining the genus
specific/ diagnostic characteristics of each stage (i.e., characteristics different from Culex and
Aedes) also state the importance of water during each stage.

Distinguish morphological differences between the two hookworm species that were studied.

The motuth parts of parasitic insects are specifically adapted for their mode of feeding. Explain the
statement above with the aid of drawings.

Ticks and mites are important vectors for a variety of diseases. Discuss this statement by referring
to appropriate examples.

Describe the morphology of Tabanus, Musca and Stomoxys and explain how the morphology
facilitate the transmission of pathogens and parasites. List the pathogens and parasites that are
transmitted.

Describe the effects of ticks (Ixodida) on their host.