Lectures On BIOL 105 Parasitology 2018

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Lectures on Parasitology
Parasitology is the study of parasites, their hosts, and the relationship between them. It is an
applied field of biology dedicated to the study of the biology, ecology and relationships which
parasites are involved in with other organisms known as the host.
Branches of Parasitology
1. Medical Parasitology This is the science that deals with organisms living in the human
body (the host) and the medical significance of host-parasite relationship. It's also
concerned with the various methods of their diagnosis, treatment and finally their
prevention and control.
2. Veterinary parasitology The study of parasites that cause economic losses in agriculture
or aquaculture operations, or which infect companion animals. This is becoming
particularly important as emerging diseases threatens global food security. In Nigeria, a
number of studies have been conducted in fish parasitology and other vertebrates such as
Lizards and Cats with Zoonotic potential.
3. Structural parasitology This is the study of structures of proteins from parasites.
Determination of parasitic protein structures may help to better understand how these
proteins function differently from homologous proteins in humans. In addition, protein
structures may inform the process of drug discovery.
4. Quantitative parasitology Parasites exhibit an aggregated distribution among host
individuals, thus the majority of parasites live in the minority of hosts. This feature forces
parasitologists to use advanced biostatistical methodologies.
5. Parasite Ecology Parasites can provide information about host population ecology. In
fisheries biology, for example, parasite communities can be used to distinguish distinct
populations of the same fish species co-inhabiting a region. Additionally, parasites possess
a variety of specialized traits and life - history strategies that enable them to colonize hosts.
Understanding these aspects of parasite ecology, of interest in their own right, can
illuminate parasite -avoidance strategies employed by host.
6. Malariology This is an aspect of parasitology which focuses mainly on the study of
Protozon parasite, Plasmodium, its species, their biology, pathogenicity, epidemiology and
management of the parasitic infection.
7. Helminthology “Helminth” means worms. Hence as the name implies it is the study of
vermiform parasites ranging from trematodes to Cestodans, Nematodans and leeches.
8. Parasite Immunology This is an aspect which deals with parasite survival in host as well
as host susceptibility. This aspect is particularly important when formulating
concentrations of chemotherapeutic agents and vaccines.
The scope of Parasitology

As a biological discipline, the scope of parasitology is not determined by the organism or
environment in question, but by their way of life. This means it forms a synthesis of other
disciplines, and draws on techniques from fields such as cell biology, bioinformatics,biochemistry,
molecular biology, immunology, genetics,evolution and ecology. Thus parasitology covers a wide
range of topics which centre around parasites, their taxonomic positions, their structural and
physiological biology, life cycle patterns, ecology, pathenogenicity, diagnosis of infection as well
as management with chemotherapy and other contemporary techniques.
BIOL 105 Parasitology

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Parasitic Disease transmission
By virtue of their nature, parasites reside in their hosts, depend on their hosts for physiological and
nutritional ends and hence often result in adverse effects on their host. The parasite-host interaction
does not occur in isolation; rather it is affected by conditions known as risk factors. A risk factor
which must occur for a disease situation to arise is known as the necessary risk while the
organism/parasite which causes the disease is called an agent.The causal web is a simple triangle
which shows the inevitable link between the agent (parasite), the host and the environment. Often
times especially with parasitic infections, there may be a vector which links all components as
shown below.
Thus a number of factors predisposes a host to attack by a vector, affects vector viability and life
cycles and even how the host respond to parasitic infections/diseases. All these add up into the
concept of Epidemiology.
The concept of epidemiology
Epidemiology is the study of the disease pattern and distribution, within a defined community or
population. It is derived from the combination of Greek words Epi which means upon, demos
which means people and logy which means study. It is an interdisciplinary subject, involving
medicine, science, geography and statistics. Epidemiology is a quantitative science that evaluates
the occurrence, distribution, determinants of control of disease pattern in a defined population.
Thus in epidemiology, demographic and social characteristics of the host such as population
density, poverty etc. are important attributes in epidemiological studies. Physical, biological,
sociological and psychological variables are significant determinants of disease distribution and
patterns. They are considered as extrinsic factors. Demographic and social attributes of the
definitive host are significant factors in disease manifestation. The demographic factors include:
Age
Sex,
Race,
Population density etc.
Thus epidemiology is a scientific enquiry on disease occurrence. i.e the study of disease
distribution and its determinants. The unit of the study of epidemiology is a defined or identifiable
population. A population in this context is not always defined by geographical Vector boundries
rather by a number of other factors such as age, sex, occupation, ethnicity, religion, institution, etc.
Epidemiology is therefore the study of disease occurrence in populations-humans, plants, animals.
It is indeed an analytical arm of community and preventive medicine, utilizing statistics as a
working tool. It is integral to the management of public health and it aims to improve the health of
the population.
The aims of epidemiology includes to :
Determine the primary agent or ascertain causative factors
Understand the causation of disease, disorders or conditions
Determine the characteristics of the agent or causative factors
Define the mode of transmission
Define and determine contributing/confounding factors

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Identify and explain geographic disease patterns

Determine, describe and report the natural cause of disease, disability, injury and/or death
Determine suitable control measures
Determine preventive measures
Aid in planning and development of health services and
Provide administrative and planning data in public health management.
Measure of Epidemiology
There are a number of tools for measurement or description in epidemiology. These include:
 Prevalence: frequency of a disease at a particular time. Based on prevalence a disease
may be defined as endemic (maintain a relatively constant but moderate level of
occurrence), Hyper- endemic (persistently high and continuous level of occurrence),
epidemic (an outbreak or sudden occurrence of a disease with considerable intensity) or
Holoendemic ( high prevalence amongst children in a population).
 Epidemiological rate- morbidity rate, mortality rate, incidence rate, admission rate etc.
 Disease Burden (overall weight of effect of a disease) using DALY.
 Estimation of disease intensity using direct parasite count, indirect counting of eggs and
cysts in faeces, indirect measurement of levels of immunological responses to parasite antigens.
 Parasite dispersion estimation which may be under dispersion, random or over dispersion.
 Geographical distribution estimation using mapping techniques such as manual
cartographic maps, geographic information system and remote sensing.
Epidemiological studies may be descriptive, analytical (cohort, or case control), experimental

or rapid epidemiological assessment.
Disability Adjusted Life Years (DALYs)

In epidemiology, the disease burden on the economy is approached from the view that morbidity
from parasitic infection impairs productivity as a result of loss of valuable man- hour. This is
calculated using an index known as the Disability adjusted life years (DALYs).
DALYs is an health indicator which translates disabilities into years of healthy life lost, by giving
each disease state a disability weight ranging from zero (healthy) to 1 (death). It incorporates the
potential years of lost life as a result of death at a given age. It measures the burden of a disease of
a defined population and the effectiveness of interventions. They are valid indicators of population
heath.
In summary, DALYs can simply be defined as the number of health years of life lost due to
premature death or disability.
DALYs estimate of Common Parasitic Diseases

The table below shows the global estimates of parasitic disease effects using the DALYs tool.
Table 1: Global estimates of some parasitic diseases (WHO, 2002)

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The burden of various diseases over time, depends on many factors. Presently, some disease
burdens have continued to increase. For instance, increasing malaria burdens occur in some
countries of Africa due to factors such as drug resistance, frequent exposure of the non-immune
populations, the emergence of HIV/AIDS, climatic and environmental changes and the breakdown
of control programmes. Such increased parasite burden results in increased economic burden of
the population.
The economic burden of a disease is the totality of direct and indirect costs associated with the
infection. These include morbidity, loss of productivity, absenteeism and cost of health care in
the infected people, as well as the losses in agriculture and non- agricultural enterprises.
Reference:
http://www.nou.edu.ng/uploads/NOUN_OCL/pdf/pdf2/BIO%20411%20PARASITOLOGY.pdf
Types of Parasites
According to the nature of the host-parasite interactions and the environmental factors, the
parasite may be one of the following types:
1. An obligatory parasite that is completely dependent on its host and can’t survive without
it e.g. hookworms.
2. A facultative parasite that can change its life style between free-living in the environment
and parasitic according to the surrounding conditions. e.g. Strongyloides stercoralis.
3. An accidental parasite that affects an unusual host e.g. Toxocara canis (a dog parasite) in
man.
4. A temporary parasite that visits the host only for feeding and then leaves it. e.g. Bed bug
visiting man for a blood meal.
5. A permanent parasite that lives in or on its host without leaving it e.g. Lice.
6. An opportunistic parasite that is capable of producing disease in an immune-deficient
host (like AIDS and cancer patients). In the immuno-competent host, it is either found in
a latent form or causes a self-limiting disease e.g. Toxoplasma gondii.
7. A zoonotic parasite that primarily infects animals and is transmittable to humans. e.g.
Fasciola species (Assaf et al.,2004).
Types of Hosts
Hosts are classified according to their role in the life cycle of the parasite into:
1. Definitive host (DH) that harbours the adult or sexually mature stages of the parasite (or in
whom sexual reproduction occurs) e.g. man is DH for Schistosoma haematobium, while
female Anopheles mosquito is DH for Plasmodium species (malaria parasites).
2. Intermediate host (IH) that harbours larval or sexually immature stages of the parasite (or
in whom asexual reproduction occurs) e.g. man is IH of malaria parasites. Two

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intermediate hosts termed 1st and 2nd IH may be needed for completion of a parasite's life
cycle, e.g. Pirenella conica snail is the 1 st IH, while Tilapia (Bolty) fish is the 2nd IH for
Heterophyes heterophyes
3. Reservoir host (RH) harbours the same species and same stages of the parasite as man. It
maintains the life cycle of the parasite in nature and is therefore, a reservoir source of
infection for man. e.g. sheep are RH for Fasciola hepatica.
4. Paratenic or transport host in whom the parasite does not undergo any development but
remains alive and infective to another host. Paratenic hosts bridge gap between the
intermediate and definitive hosts. For example, dogs and pigs may carry hookworm eggs
from one place to another, but the eggs do not hatch or pass through any development in
these animals.
5. Vector is an arthropod that transmits parasites from one host to another, e.g. female sand
fly transmits Leishmania parasites ((Bogitsh al., 2005).
Types of Symbiotic Association:

In biology, the relationship between two organisms is mainly in the form of symbiosis, defined as
"life together", i.e., the two organisms live in an association with one another. Thus, there are at
least three types of relationships based on whether the symbiont has beneficial, harmful, or no
effects on the other (Todar, 2011).
1. Mutualism is a relationship in which both partners benefit from the association. Mutualism
is usually obligatory, since inmost cases hysiological dependence has evolved to such a
degree that one mutual cannot survive without the other (Swift, 2009). Blood-sucking
leeches cannot digest blood, and overcome that by harbouring certain intestinal bacterial
species to do the digestion for their hosts. At least 20% of insect species, as well as many
mites, spiders, crustaceans, and nematodes, are mutually infected with bacteria of genus
Wolbachia(Warren, 2003). Also, filarial nematodes such Wuchereria bancroftiand
Onchocerca volvulus which cause serious human diseases, are mutually infected with
Wolbachia, and they can be cured of their bacterial infections by treating patients with
antibiotics, but the worms die too (Rajan, 2003).
2. Commensalism: in which one partner benefits from the association, but the host is neither
helped nor harmed. Commensalism may be facultative, in the sense that the commensal
may not be required to participate in an association to survive (Swift, 2009). Humans
harbor several species of commensal protozoans, that colonize in the intestinal tract such
as Entamoeba dispar, Entamoeba hartmanni,Entamoeba moshkovskii, Entamoeba polecki,
Endolimax nana, Iodomoeba butschlii (Ortega, 2006).
3. Parasitism: in which one of the participants, the parasite, either harms or lives at the
expense of the host. Parasites may cause mechanical injury, such as boring a hole into the
host or digging into its skin or ot her tissues, stimulate a damaging inflammatory or immune
response. Most parasites inflict a combination of these conditions on their hosts (Taliaferro,
2009).

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Classification and General Characters of Human Parasites.

The most acceptable taxonomic classification of human parasites includes Endoparasites and
Ectoparasites. Endoparasites are sub-classified into Helminthic parasites (multicellular organisms)
and Protozoan parasites (unicellular organisms). Helminthic parasites are either flat worms
(Trematodes), segmented ribbon like worms (Cestodes) or cylindrical worms (Nematodes).
Parasites’ Life Cycles

Life cycles of parasites may be simple or complex. Parasites that are characterized by a simple or
direct life cycle have only one host and are described as monoxenous (e.g.life cycle of Ascaris
lumbricoides). The parasite generally spends most of its life in or on the host, and may reproduce
within the host. Because offspring must be transmitted to other hosts, however, the parasite or its
progeny must have some way of leaving the host, surviving in the external environment for some
period, and locating and infecting a new host. Parasites with simple life cycles have both parasitic
and free-living life stages. The proportion of the total life cycle spent in each stage varies according
to the parasite.
Parasites with more complex life cycles involving multiple hosts are described as having indirect
or heteroxenous life cycles (e.g. life cycle of Fasciola spp.). The primary or definitive host of a
heteroxenous species is the one in which adult parasites live and reproduce sexually. The
secondary or intermediate host (IH) is the host where immature life stages of the parasite live and
reproduce asexually. In many cases, the parasite passes through critical developmental stages in
the IH. The latter may also aid in transmitting parasites to their final host.Rat flea, for example, is
the IH for mammalian parasites such as the tapeworm; Hymenolepis diminuta . Some parasites are
transmitted directly from one host to another, often by insects, described as vectors. One
particularly effective vector for vertebrate parasites is the mosquito, which plays a role in
transmission of numerous parasites including heartworm, the viruses that cause yellow fever and
encephalitis, and Plasmodium , the protozoan that causes malaria
(http://www.mosquito.org/mosquito-borne-diseases).
Refereence:
Manar M.S. El-Tonsy. (n.d.). Introduction To Medical Parasitology.Parasitology Department,
Faculty of Medicine, Ain Shams University, Cairo, Egypt. Retrieved from:
http://www.eolss.net/sample-chapters/c03/e5-25-52.pdf
http://www.eolss.net/Eolss-sampleAllChapter.aspx
Protozoa
Protozoa are one-celled animals found worldwide in most habitats. Most species are free living,
but all higher animals are infected with one or more species of protozoa. Infections range from
asymptomatic to life threatening, depending on the species and strain of the parasite and the
resistance of the host.
Protozoa are microscopic unicellular eukaryotes that have a relatively complex internal structure
and carry out complex metabolic activities. Some protozoa have structures for propulsion or other
types of movement.

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On the basis of light and electron microscopic morphology, the protozoa are currently classified
into six phyla. Most species causing human disease are members of the phyla Sacromastigophora
and Apicomplexa.
The stages of parasitic protozoa that actively feed and multiply are frequently called trophozoites;
in some protozoa, other terms are used for these stages. Cysts are stages with a protective
membrane or thickened wall. Protozoan cysts that must survive outside the host usually have more
resistant walls than cysts that form in tissues.
Binary fission, the most common form of reproduction, is asexual; multiple asexual division occurs
in some forms. Both sexual and asexual reproduction occur in the Apicomplexa.
All parasitic protozoa require preformed organic substances—that is, nutrition is holozoic as in
higher animals.
Robert G. Yaeger.Chapter 77Protozoa: Structure, Classification, Growth, and Development

http://www.ncbi.nlm.nih.gov/books/NBK8325/
Balantidium coli
Balantidium coli is the largest protozoan parasite in humans and causes a disease called
balantidiasis. It belongs to the ciliophora phylum and is the only protozoan ciliate to infect humans.
It goes through two development phases; a cyst and a trophozoite. Trophozoites are 0.03–0.15
mm long and 0.025–0.12 mm wide. Their shape is either spherical or oblong. Their surface is
covered with cilia and are able to move around. Trophozoites have both a micronucleus and a
macronucleus, which both are normally visible. The macronucleus is bigger and sausage-shaped
whereas the micronucleus is less notable. Cysts are spherical and 0.04–0.06 mm in diameter. They
have a tough multilayered shell which protects them against stomach acid of the host, when
ingested. They are usually destroyed at a pH lower than five (normal pH of a healthy stomach is
about three). Some people are weakened by other diseases and thus the cysts are not killed. Unlike
trophozoites, cysts cannot reproduce and do not have any cilia for moving.
The life cycle of Balantidium coli begins, when a human eats food or water that has been
contaminated with infective cysts. If the cysts survive through the stomach, trophozoites are
formed in the small intestine. Trophozoites live in the cecum and the colon of the large intestine.
They live and feed in the lumen but sometimes penetrate the mucosa. They multiply by transverse
binary fission in the intestinal wall. Some trophozoites return to the lumen and encyst (transform
into cysts) once the feces dry up. The cysts are formed either in the large intestine or outside of the
body. If the feces get in contact with vegetables or drinking water, humans might ingest the cysts.

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About 1 % of the world's population is infected with balantidiasis. Most infections occur in
developing countries where feces are more likely to get in contact with food and drinking water.
In addition to humans, pigs and other animals carry the disease. People who raise pigs have bigger
risk of getting infected with balantidiasis.
Balantidiasis is often asymptomatic. But in some cases the patient might have diarrhea, weight
loss and dysentery. Dysentery is an inflammatory disorder of the intestine, particularly of the
colon, that causes severe diarrhea containing blood and/or mucus in the feces with stomach pain
and fever. Untreated dysentery cases can be fatal.
Diagnosis can be made by finding trophozoites from a stool or tissue

sample (collected during endoscopy). Cysts are rarely found.
Trophozoites are passed irregularly and quickly destroyed outside the
colon. For this reason many stool samples are usually required to
confirm the disease.

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Balantidiasis is treated with tetracycline according to the instructions of your health care provider.
Tetracycline is not recommended for pregnant women or children under 8 years old. If the drug is
not available, then iodoquinol and metronidazole can be used.
Balantidiasis infections can be prevented by following proper hygiene practices. Do not use
human feces as fertilizer in agriculture. Wash your hands after going to the toilet and before meal.
Only drink pure water. Wash vegetables and cook meat properly. Infective Balantidium coli cysts
are killed by heat.
http://www.parasitesinhumans.org/balantidium-coli.html
Entamoeba histolytica
Entamoeba histolytica is a protozoan parasite responsible for a disease called amoebiasis. It occurs
usually in the large intestine and causes internal inflammation as its name suggests (histo = tissue,
lytic = destroying). 50 million people are infected worldwide, mostly in tropical countries in areas
of poor sanitation. In industrialized countries most of the infected patients are immigrants,
institutionalized people and those who have recently visited developing countries.
Inside humans Entamoeba histolytica lives and multiplies as a trophozoite. Trophozoites are
oblong and about 15–20 µm in length. In order to infect other humans they encyst and exit the
body. The life cycle of Entamoeba histolytica does not require any intermediate host. Mature cysts
(spherical, 12–15 µm in diameter) are passed in the feces of an infected human. Another human
can get infected by ingesting them in fecally contaminated water, food or hands. If the cysts survive
the acidic stomach, they transform back into trophozoites in the small intestine. Trophozoites
migrate to the large intestine where they live and multiply by binary fission. Both cysts and
trophozoites are sometimes present in the feces. Cysts are usually found in firm stool, whereas
trophozoites are found in loose stool. Only cysts can survive longer periods (up to many weeks
outside the host) and infect other humans. If trophozoites are ingested, they are killed by the gastric
acid of the stomach. Occasionally trophozoites might be transmitted during sexual intercourse.

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Most Entamoeba histolytica infections are asymptomatic and trophozoites remain in the intestinal
lumen feeding on surrounding nutrients. About 10–20 % of the infections develop into amoebiasis
which causes 70 000 deaths each year. Minor infections (luminal amoebiasis) can cause
symptoms that include:
 gas (flatulence)
 intermittent constipation
 loose stools
 stomach ache
 stomach cramping.
Severe infections inflame the mucosa of the large intestine causing amoebic dysentery. The
parasites can also penetrate the intestinal wall and travel to organs such as the liver via bloodstream
causing extraintestinal amoebiasis. Symptoms of these more severe infections include:
 anemia

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 appendicitis (inflammation of the appendix)

 bloody diarrhea
 fatigue
 fever
 gas (flatulence)
 genital and skin lesions
 intermittent constipation
 liver abscesses (can lead to death, if not treated)
 malnutrition
 painful defecation (passage of the stool)
 peritonitis (inflammation of the peritoneum which is the thin membrane that lines the
abdominal wall)
 pleuropulmonary abscesses
 stomach ache
 stomach cramping
 toxic megacolon (dilated colon)
 weight loss.
To prevent spreading the infection to others, one should take care of personal hygiene. Always
wash your hands with soap and water after using the toilet and before eating or preparing food.
Amoebiasis is common in developing countries. Some good practices, when visiting areas of poor
sanitation:
 Wash your hands often.

 Avoid eating raw food.
 Avoid eating raw vegetables or fruit that you did not wash and peel yourself.
 Avoid consuming milk or other dairy products that have not been pasteurized.
 Drink only bottled or boiled water or carbonated (bubbly) drinks in cans or bottles.
Natural water can be made safe by filtering it through an "absolute 1 micron or less" filter and
dissolving iodine tablets in the filtered water. "Absolute 1 micron" filters are found in
outdoor/camping supply stores. Micron = micrometer = 0.001 mm.
Amoebiasis is diagnosed by your health care provider under a microscope by finding cysts and
(rarely trophozoites) from a stool sample. The results are usually said to be negative, if Entamoeba
histolytica is not found in three different stool samples. But it still does not necessarily mean that
you are not infected because the microscopic parasite is hard to find and it might not be present
the particular samples. A blood test might also be available but is only recommended, if your health
care provider believes that the infection could have spread to other parts of the body. Trophozoites
can be identified under a microscope from biopsy samples taken during colonoscopy or surgery.
Entamoeba histolytica should be differentiated from the non-pathogenic Entamoeba dispar. The
two are morphologically identical and differentiation must be based on immunologic or
isoenzymatic analysis or molecular methods. They can be distinguished under a microscope, if
Entamoeba histolytica has ingested red blood cells. Entamoeba dispar is about 10 times more
common. If either one is found, then you are usually treated.

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If you are experiencing amoebiasis symptoms, you are treated with two antibiotics. The preferred
drugs are metronidazole or tinidazole immediately followed with paromomycin, diloxanide
furoate or iodoquinol. Asymptomatic intestinal amoebiasis is treated with paromomycin,
diloxanide furoate or iodoquinol.
Leishmania
Leishmania is a microscopic protozoon and is responsible for a disease called leishmaniasis.

Leishmaniasis is spread by sandflies and about 12 million people are infected worldwide. It causes
the most parasitic deaths after malaria.
The two most common forms are visceral and cutaneous leishmaniasis. There are about 500 000
new visceral leishmaniasis cases each year. More than 90 % of the visceral leishmaniasis
infections take place in Bangladesh, Brazil, India, Nepal and Sudan. The disease develops a few
months after the sandfly bite and causes:
 anemia
 enlarged liver and spleen
 fever
 weaker inflammatory response (due to the loss of phagocytes)
 weight loss.
There are about 1.5 million new cutaneous leishmaniasis cases each year. The disease causes
skin sores a few weeks after the bite. The sores vary in appearance and might or might not be
painful. A fully developed sore usually has a raised edge and a central crater. Some sores are
covered by crust tissue. Nearby lymph glands might swell up, if the sore is located further from
the heart than the glands. Over 90 % of the cutaneous leishmaniasis infections occur in Afganistan,
Algeria, Brazil, Iran, Iraq, Peru, Saudi Arabia and Syria.
Leishmania parasite has two separate life forms. In humans it mainly lives as amastigote which
does not have flagella to move around with. Inside insects Leishmania appears as promastigote
which has a flagellum and is able to move. When a sandfly infected with Leishmania feeds, the
parasites are transmitted to the biting area. Sandflies are smaller than regular mosquitoes and fly
very quietly. Their bite might be painless and might go unnoticed. Leishmania uses your white
cells as a hiding place so it lets a phagocyte eat itself. Neutrophil granulocytes are the first
phagocytes that arrive to the infected area. They immediately start consuming the Leishmania. To
prevent granulocytes from killing it, Leishmania releases special chemicals. These chemicals make
the granulocytes harmless and signal other immune defense cells that everything is under control.
The chemicals also prolong the life span of the neutrophil granulocyte from 6–10 hours to 2–3
days. Leishmania does this to get inside macrophages. This would not be possible without the
delay because it takes about 2 days for macrophages to arrive to the infected area. When the
macrophages finally arrive they do not see any parasites. They only find old neutrophil
granulocytes which are signaling the macrophages to go ahead and eat them. Since the parasites
are inside the granulocytes the macrophages cannot see them and will not bother using any killer
enzymes for the ingested granulocytes. This is because the granulocyte is signalling the
macrophage that "I'm too old to live so I'll release my own decomposing enzymes. You, my dear

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macrophage, you just go ahead and eat me and I'll destroy myself once I get inside you." This is
how the parasite gets inside a macrophage which have much longer life expectancy (up to many
months). So Leishmania has enough time to reproduce inside the host cell. As soon as the
macrophage is filled with Leishmania, it bursts and the parasites start looking for new hosts.
Diagnosis is done by doing lab tests. Depending on the particular Leishmania species and the
location of the infection, different treatment is used. There is a new drug sodium stibogluconate,
which might become the preferred medicine in the future. Currently it is not available in every
country.
Trypanosoma brucei
Sleeping sickness, African trypanosomiasis, is a deadly blood disease caused by two variates of
Trypanosoma brucei and transmitted by tsetse fly. Trypanosoma brucei rhodesiense causes East
African trypanosomiasis. 1000 new T. b. rhodesiense infections are reported to World Health
Organization annually. Trypanosoma brucei gambiense causes West African trypanosomiasis
(also known as Gambian sleeping sickness). More than 12 000 new infections are reported to the
WHO each year. The two subspecies do not overlap in geographic distribution. They infect
humans and tsetse flies (Glossina genus) in the woodlands, savannah and the dense vegetation
between Kalahari and Sahara deserts. Less than 1 % of tsetse flies carry the parasite. T.b.
rhodesiense is found in eastern and southeastern Africa. Over 95 % of the T.b. rhodesiense
infections occur in Malawi, Tanzania, Uganda, and Zambia. T.b. gambiense is found
predominately in central Africa and in some areas of West Africa. Over 95 % of the T.b. gambiense

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infections occur in Angola, Central African Republic, Chad, northern Uganda, Sudan, Republic of
the Congo and Democratic Republic of the Congo.
Trypanosoma brucei needs two hosts to live and reproduce. Its life cycle starts, when an infected
tsetse fly bites human skin. While it is feeding on blood, metacyclic trypomastigotes are
transmitted to the skin from the salivary glands of the fly. The parasites get into the bloodstream
by entering lymphatic or blood vessels. They travel in different body fluids (such as blood,
lymphatic or spinal fluid), transform into bloodstream trypomastigotes and multiply by binary
fission. The disease can be spread by another tsetse fly that drinks the infected blood. Inside the
fly the life cycle takes about three weeks. Ingested bloodstream trypomastigotes transform into
procyclic trypomastigotes in the fly's midgut and multiply. They transform into epimastigotes,
migrate to the salivary glands, then transform into metacyclic trypomastigotes and multiply once
again by binary fission.
Trypanosoma brucei is not killed by the immune system because it has a glycoprotein (VSG)
coating. The coating makes its cell membrane very thick and hard to recognize. It also changes
frequently its structure to always keep ahead of the immune response. T. b. rhodesiense and T. b.
gambiense are indistinguishable under a microscope. A trypomastigote is 14 to 33 µm long and
has a tiny kinetoplast located at the posterior end, a centrally located nucleus, an undulating
membrane, and a flagellum. Trypomastigotes are the only stage found in patients. Humans are the
main host for T. b., but it is sometimes found in animals.

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East African trypanosomiasis is more acute and progresses quicker than West African
trypanosomiasis. Symptoms can be minor in the beginning but usually become apparent within
the first months of the infection. African trypanosomiasis has three symptomatic stages, the last
one being the most dangerous eventually leading to death, if left untreated.
1. In 1–3 weeks after the bite a chancre (a red sore skin lesion) can develop on the bite area.
2. Several weeks or months later Trypanosoma parasites in the blood, spinal and lymphatic fluid
(hemolymphatic stage) can cause:
 anemia
 cardiac dysfunction
 pruritus (itching)
 fatigue
 fever
 headache
 muscle or joint pain
 skin rash
 splenomegaly (enlargement of the spleen)
 swelling of the lymph nodes (most prominently in the back of the neck and in the groin),
hands and face
 thrombocytopenia (low level of platelets, thrombocytes)
 weight loss.
 blackouts
 coma
 confusion and abnormal behaviour
 death (within months or years)
 insomnia (sleeping troubles)
 personality changes
 somnolence (extreme fatigue).
Your health care provider does the diagnosis by examining blood, lymph node or tissue aspirates
(fluid suction), bone marrow, chancre or cerebrospinal fluid under a microscope.
Treatment is based on symptoms and laboratory results. The drug choice depends on the infecting
species and the stage of infection. Pentamidine isethionate and suramin are usually used for
treating the hemolymphatic stage of West and East African Trypanosomiasis, respectively.
Melarsoprol is used for late disease with central nervous system involvement (infections by T.b.
gambiense or T. b. rhodiense). Hospitalization for initial treatment is often necessary. Periodic
follow-ups that include a spinal tap are required for two years.
Tsetse flies are common only in rural Africa, not in urban cities. Areas of heavy infestation
(endemic areas) should be avoided. Tsetse flies are attracted to bright colours, very dark colours

16
and moving vehicles. Check for tsetse flies before entering the car. Tsetse flies are day biters. They
can bite through thin clothing and the bite is usually very painful. Permethrin-impregnated clothing
and use of DEET repellent (spray) can reduce the risk of getting bitten. Wear long-sleeved shirts
and pants made of medium-weight material in neutral colours that blend in with the background
environment. Avoid thickets because during the hottest period of the day tsetse fly rests in bushes.
Use insect repellent. Even though insect repellents are not effective against flies, they are effective
in preventing other insects (such as malaria-carrying Anopheles mosquitoes) from biting.
http://www.parasitesinhumans.org/trypanosoma-brucei-sleeping-sickness.html
Plasmodium falciparum
Plasmodium falciparum is the Plasmodium species responsible for 85 % of the malaria cases. The
three less common and less dangerous Plasmodium species are: P. ovale, P. malariae and P. vivax.
Malaria infects over 200 million people annually, mostly in poor tropical and subtropical countries
of Africa. It is the deadliest parasitic disease killing over one million people each year. 90 % of
the deaths occur south of the Sahara desert and most are under five-year-old children. In addition
to Africa, malaria occurs in South and Southeast Asia, Central and South America, the Caribbean
and the Middle East. Even within tropical and subtropical areas, malaria does not usually occur at
high altitudes (over 1500 meters), during colder seasons, in countries of successful malaria
programs or in deserts.
Life cycle
Malaria is carried by Anopheles mosquitoes. Of the over 400 Anopheles species, only 30–40 can
transmit malaria. The infection starts, when a female mosquito injects (in her saliva) "sporozoites"
(one form of P. falciparum) into human skin while taking a blood meal. A sporozoite travels (in
the bloodstream) into the liver where it invades a liver cell. It matures into a "schizont" (mother
cell) which produces 30000–40000 "merozoites" (daughter cells) within six days. The merozoites
burst out and invade red blood cells. Within two days one merozoite transforms into a trophozoite,
then into a schizont and finally 8–24 new merozoites burst out from the schizont and the red cell
as it ruptures. Then the merozoites invade new red cells. P. falciparum can prevent an infected red
cell from going to the spleen (the organ where old and damaged red cells are destroyed) by sending
adhesive proteins to the cell membrane of the red cell. The proteins make the red cell to stick to
small blood vessel walls. This poses a threat for the human host since the clustered red cells might
create a blockage in the circulation system.
A merozoite can also develop into a "gametocyte" which is the stage that can infect a mosquito.
There are two kinds of gametocytes: males (microgametes) and females (macrogametes). They get
ingested by a mosquito, when it drinks infected blood. Inside the mosquito's midgut, male and
female gametocytes merge into "zygotes" which then develop into "ookinetes." The motile
ookinetes penetrate the midgut wall and develop into "oocysts." The cysts eventually release
sporozoites, which migrate into the salivary glands where they get injected into humans. The
development inside a mosquito takes about two weeks and only after that time can the mosquito
transmit the disease. P. falciparum cannot complete its life cycle at temperatures below 20 °C.

17
Symptoms
After being bitten by an infected mosquito, symptoms usually begin within 10–30 days. Malaria
can be uncomplicated or severe. Symptoms of uncomplicated malaria might include:
 chills
 diarrhea
 fever
 headaches
 muscle pain
 nausea
 sweating
 vomiting
 weakness.
Some less noticeable manifestations:
 enlargement of the spleen or liver

 increased breathing frequency
 mild anemia
 mild jaundice (yellowish eye whites and skin).

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The disease can turn into severe malaria, if there are serious organ failures or abnormalities in the
bloodstream or metabolism. Symptoms of severe malaria might include:
 breathing difficulties
 coma
 confusion
 death
 focal neurologic signs
 seizures
 severe anemia.
Some less noticeable manifestations:
 abnormalities in blood coagulation

 hemoglobin in the urine
 high acidity of the blood
 hypoglycemia (low blood glucose)
 low blood pressure
 kidney failure.
During pregnancy malaria can lead to premature baby delivery or delivery of a low-birth-weight
baby. The infant can get the parasite from the mother and develop the disease. Central nervous
system involvement (cerebral malaria) can cause (especially in small children) blindness, deafness,
speech difficulty, paralyses and trouble with movements.
Diagnosis
Malaria is usually diagnosed by examining a blood sample under a microscope. There are also test
kits that detect antigens of P. falciparum in the patient's blood. These immunologic tests are known
as rapid diagnostic tests (RDTs). RDTs can detect two different malaria antigens, one for P.
falciparum and the other is found in all four human malaria species. RDTs usually show results in
about 20 minutes. It is a good alternative to microscopy, when reliable microscopic diagnosis
cannot be done. RDT might not detect some infections, if there are not enough malaria parasites
in the patient’s blood. A negative RDT result can be followed up by microscopy. If a patient with
positive RDT result is not responding to treatment, another blood sample should be taken. This
time using microscopy to determine whether the medicine was appropriate for the Plasmodium
species.
Diagnosis can be challenging for many reasons:
 Some health workers in developing countries are insufficiently trained and supervised.
 The microscopes and reagents might be of poor quality and the supply of electricity
might be unreliable.
 Some health workers save blood samples until a qualified person is available to perform
the microscopy. This delay results sometimes as incorrect diagnosis.

19
 Many malaria endemic communities do not have the proper diagnostic tools such as
microscopes and RDTs.
Treatment
Most malaria deaths occur in rural areas. Quick progression from illness to death can be prevented
by fast and effective medication. Patients who have uncomplicated malaria can visit a nearby
hospital to get treated and then go home to rest. In emergency cases rectal artesunate drug can be
given as a first line treatment (if they cannot be treated orally). Patients with severe malaria can be
hospitalized for many days. When treating a malaria patient, the following should be taken into
account:
 age and size of the person (to give the correct amount of medication)
 drug allergies or other medications taken by the patient
 health condition, when starting the treatment
 where the person was infected (what Plasmodium species is likely to be responsible and
what drug is needed).
P. falciparum and P. vivax have been confirmed to be resistant (in some areas) to many antimalarial
drugs. For example, chloroquine resistant strain of P. falciparum has spread to most endemic areas.
Listed below are some drugs that are usually recommended by national malaria control programs.
They might not be effective in many parts of the world due to drug resistant strains.
 artemesinin-containing combination treatments (for example, artemether-lumefantrine,

artesunate-amodiaquine)
 atovaquone-proguanil
 chloroquine
 doxycycline
 mefloquine
 quinine
 sulfadoxine-pyrimethamine.
Primaquine, is used as an adjunct against certain Plasmodium species. It is active against the
dormant liver forms (hypnozoites which are rare/nonexistent with P. falciparum). Primaquine is
not recommended for people who are deficient in glucose-6-phosphate dehydrogenase or for
pregnant women. Treating all people simultaneously in a population can prevent major malaria
epidemics. Unfortunately it can also increase drug resistance of the parasite and complications in
those who are glucose-6-phosphate dehydrogenase deficient.
Prevention
Insecticide-treated bed nets may reduce deaths of children under 5 years up to 20 % (according to
trials in several African communities). Anopheles mosquitoes usually feed during the night so you
can protect yourself by sleeping under a bed net. If everyone in a community has a bed net, the
occurrence of malaria can be reduced. Bed nets are usually made of polyester but sometimes

20
cotton, polyethylene, or polypropylene is used instead. All bed nets are treated with pyrethroid
insecticides, which have are low health risks to humans but are toxic to insects even at low doses.
Pyrethroids do not rapidly wear off, unless exposed to sunlight or washed. "Long-lasting
insecticide-treated bed nets" maintain effective levels of insecticide for three years or more. Bed
net donations can be made through organizations such as Nothing But Nets and Malaria No More.
The price of one bed net is only a few US dollars (which is often too expensive for people in
developing countries).
Many malaria-carrying mosquitoes are endophilic, meaning that they typically rest inside the
house after taking a blood meal. Indoor Residual Spraying of the walls and other surfaces can
kill them reducing the chances that infected mosquitoes spread the disease from one household to
another.
Humans living in areas where malaria is common can become partially immune. Travelers, young
children, women having their first or second pregnancy and those who are weakened by other
diseases (such as AIDS) have little to no immunity against malaria. Recommendations for
pregnant women living in malaria endemic areas:
 Eat iron and folate supplements to prevent anemia.

 Get a curative dose of an antimalarial drug at least twice during pregnancy (starting from
the second trimester).
 Sleep under an insecticide-treated bed net.
The number of mosquitoes may be controlled by eliminating mosquito larvae before they reach
adulthood. Rainfall forms water puddles where mosquitoes lay their eggs and aquatic larvae
develop into adults in a few days. Draining or removal of small puddles can reduce the number of
mosquitoes near populations. Chemical insecticides can also be applied but might harm the
environment. Other methods applied to water:
 insect growth regulators

 oil that suffocates the aquatic larvae
 toxins from the bacterium Bacillus thuringiensis var. israelensis (Bti).
Additional personal protection methods include:
 glass windows (a well-constructed house)

 repellent
 white or light-colored clothes covering most of the body.
http://www.parasitesinhumans.org/plasmodium-falciparum-malaria.html
Trematodes
Fasciola hepatica
Fasciola hepatica is a parasitic fluke that lives in the liver. In addition to humans it infects cows
and sheep. It is known as the common liver fluke and causes a disease called fascioliasis.

21
The life cycle of Fasciola hepatica starts when a female lays eggs in the liver of an infected human.
Immature eggs are discharged in the biliary ducts and taken out in the feces. If landed in water, the
eggs become embryonated and develop larvae called miracidia. A miracidium invades an aquatic
snail and develops into cercaria, a larva that is capable of swimming with its large tail. The cercaria
exits and finds aquatic vegetation where it forms a cyst called metacercaria. A human eats the raw
freshwater plant containing the cyst. The metacercaria excysts in the first part of the small intestine,
duodenum. It then penetrates the intestinal wall and gets into the peritoneal cavity. It finds the liver
and starts eating liver cells. This happens only a few days after the initial contact with the parasite.
Usually the larva spends a few weeks just browsing and eating the liver. Then it relocates to the
bile duct where it begins its final stage and becomes an adult. It takes about three months for the
metacercaria to develop into an adult. Adults are about 3 cm long and 1 cm wide. Adult females
can produce up to 25000 eggs per day.
In the chronic phase of fascioliasis adults in the large biliary ducts cause liver inflammation and
obstruction of the biliary fluid. During the migration of the larvae (this acute phase of the disease
lasts many weeks) symptoms include:
 diarrhea
 eosinophilia (high number of white blood cells)
 fever
 nausea
 stomach ache
 vomiting.
Fasciola hepatica is found in areas where cattle and sheep are raised.
Fasciola hepatica is identified from eggs in a stool sample. The eggs are very similar to those of
Fasciolopsis buski. Early stage of the infection can be diagnosed from a blood sample, if
antibodies are found. Fascioliasis is treated with triclabendazole drug.

22

23
http://www.parasitesinhumans.org/fasciola-hepatica-liver-fluke.html
Schistosoma
Schistosomiasis (also known as snail fever or bilharzia) is caused by blood flukes from the genus
Schistosoma. More than 200 million people are infected worldwide. Mostly in freshwaters where
there are many snails which are the intermediate host. There are five main species infecting
humans: Schistosoma mansoni, S. haematobium, S. japonicum and two geographically localized
species S. intercalatum and S. mekongi.
Schistosoma requires the use of two hosts to complete its life cycle. Depending on the Schistosoma
species their eggs are shed either in the feces or urine of an infected human. Eggs can survive up
to a week in dry land. If the feces end up in water, larvae called miracidia hatch and start finding
certain species of freshwater snails. When they find a snail they penetrate its foot and transform
into sporocysts (another larval form). These primary sporocysts multiply asexually into secondary
sporocysts and travel to the snail's hepatopancreas. They multiply asexually producing hundreds
of cercariae (another larval form). (The process from sporocyst to cercaria takes a few months.)
Cercariae exit the snail and start waiting in the water. They can survive about 48 hours in
favourable conditions. When they sense that human skin is near, they quickly swim and attach
with suckers. They find a suitable spot (usually a hair follicle) and penetrate the skin using special
enzymes. As they enter they transform into schistosomulae (another larval form). Only head parts
enter, they leave tails behind. Each schistosomula stays a few days in the skin and then enters the
bloodstream through dermal lymphatic vessels or blood venules. They travel in the bloodstream
to get to specific blood veins. In humans Schistosoma reaches fertility in 6–8 weeks. The newly
developed adult females and males find each other and pair up. Adult blood flukes are 1–2 cm
long. Males make a gynaecophoric channel for the longer and thinner females to reside. The worm
pair then travel to rectal or mesenteric veins. They attach to the venous wall with oral and ventral
suckers and can live for many years. Females lay eggs on the endothelial lining of the venous
capillary walls at the rate of 300–3000 eggs per day depending on the Schistosoma species. Some
eggs are flushed by circulating blood ending up causing inflammation in organs such as liver or
lungs. Most eggs however travel to the lumen of the intestinal tract (S. japonicum and S. mansoni)
and of the ureters and bladder (S. haematobium), thus exiting the body in the feces or urine. Mature
eggs produce special enzymes and can penetrate many membranes such as rectal veins or intestinal
wall. The eggs get out of the body and the cycle starts again.

24
Schistosoma species can migrate around and are not bound to just one location. But each species
has a preferred location. For example, S. japonicum resides more frequently in the veins that drain
the small intestine. S. mansoni is found more often in the veins that drain the large intestine. S.
haematobium occurs usually in the venous plexus of bladder, but can also be found in the rectal
venules.
The first symptoms are a rash or itch during the first few days. Within two months chills, cough,
diarrhea, fatigue, fever and muscle aches can occur. Usually however during the first few weeks
schistosomiasis is asymptomatic. The disease is worse for children who can develop anemia,
learning difficulties and malnutrition. After years of infection eggs inflame organs such as the
liver, bladder and lungs. If eggs end up in the brain or spinal cord, they can cause paralysis, seizures
or inflammation of the spinal cord.
Diagnosis is done from a stool or urine sample by microscopic examination. You need to provide
your health care provider with the samples. Eggs can be present in the feces in infections of all
Schistosoma species and in the urine in infections of S. haematobium and S. japonicum. Tissue
biopsy (bladder or rectal biopsy) can also be used in finding eggs, if stool or urine samples are
negative. It takes about two months for the parasite to mature into reproducing adult and only after
that time will there be eggs present.
Schistosomiasis is treated with praziquantel according to the advice of your health care provider.
For infections caused by S. mansoni oxamniquine can be used in areas where praziquantel is less
effective.

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Geographic distribution
 Africa: all freshwater in sub-Saharan and southern Africa, also in the Nile River valley in
Egypt
 Caribbean: Antigua, Dominican Republic, Guadeloupe, Martinique, Montserrat, Saint
Lucia (low risk)
 South America: Brazil, Suriname, Venezuela
 Southern China
 Southeast Asia: Cambodia, central Indonesia, Laos, Mekong delta and Philippines
 The Middle East: Iran, Iraq, Saudi Arabia, Yemen.
Avoid freshwater lakes, rivers or streams in areas where schistosomiasis occurs. Drying your skin
with a towel immediately after swimming might sweep some larval blood flukes away. Swimming
in the salty ocean and in chlorinated swimming pools is quite safe. Human feces should be
prevented of getting into water to prevent snails from getting infected. In addition to humans
Schistosoma species infect many animals such as cats, dogs, horses, pigs, rodents and goats.
http://www.parasitesinhumans.org/schistosoma-blood-flukes.html
Paragonimus westermani
Human lung fluke, Paragonimus westermani, infects 22 million people in Africa, Asia and South
and Central America. Southeast Asia in particular is affected because raw seafood is very
popular there. Humans get infected with the disease, paragonimiasis, by eating raw crabs or fish
that are carrying the parasite. Even properly cooked sushi can cause infection, if the cook or
waiter is careless when preparing the food. In Asia about 80 % of freshwater crabs are infected
with the lung fluke.

26
Life cycle of a lung fluke begins, when the female lays eggs that are carried out from the human
lungs in the sputum by the motion of microvilli. Then the eggs are taken through the
gastrointestinal tract and out of the body. If the feces get in contact with water, then after two
weeks larvae called miracidia hatch and start to grow. A miracidium finds a snail and penetrates
its skin. In 3–5 months miracidium develops further and produces another larval form called
cercaria. The cercaria crawls out of the snail to find fresh water crayfish (a lobster-like creature)
or crabs. It finds its way to the muscles of the crab and starts forming a cyst. Within two months it
transforms into metacercaria which is the resting form of cercaria. If a human eats this infected
crab raw, the metacercaria cyst gets into the stomach. Once inside the beginning of the small
intestine, duodenum, the metacercaria excysts and penetrates the intestinal wall. It continues
through abdominal wall and diaphragm into the lungs where it forms a capsule and develops into
an adult. Male and female lung worms reproduce and the cycle starts again.
Sometimes lung fluke larvae accidentally travel to the brain or other organs and reproduce there.
But because the secretion of the eggs from the brain is blocked the life cycle will not happen. If
the worm goes to the spinal cord instead of the lungs, the host might become paralyzed. If it infects
the heart, the host could die.
Lung flukes cause pain and severe coughing (there might be some blood, too). Paragonimiasis
diagnosis is done by looking at sputum (slime from the lungs), to see if there are any lung fluke
eggs. Feces can be examined, too. Alternatively X-rays and biopsies can be taken. Paragonimiasis
is usually treated with a drug called praziquantel.
Salting food does not kill the parasite, cooking and freezing will. After ingestion it takes about
three mEonths for the lung fluke to start laying eggs. The host might stay infected up to 20 years.

27

28
adult
egg
Adult lung flukes are 4–6 mm wide, 3–5 mm thick and 7–12 mm long. They are red-brown looking
almost like a coffee bean. They hold on to tissue with two suckers. The oral sucker is in the front
and just before the center of its lower body is the ventral sucker.
In addition to humans, Paragonimus westermani infects other carnivores such as felids (cats etc.),
canids (dogs etc.), rodents (rats etc.), weasels and pigs.
http://www.parasitesinhumans.org/paragonimus-westermani-lung-fluke.html
Cestodes
Taenia saginata
Taenia saginata is a large tapeworm that causes an infection called taeniasis. It is commonly
known as the beef tapeworm or cattle tapeworm because it uses cows as intermediate hosts.
Humans are the only definitive hosts. Taeniasis occurs worldwide and is relatively common in
Africa, Eastern Europe, Latin America and the Philippines.
The life cycle of Taenia saginata starts, when eggs are passed in the feces of an infected human in
a container called a proglottid or a tapeworm segment. They can survive a few months out in the
environment. If a cow (the intermediate host) feeds on contaminated vegetation, it ingests mature
eggs or gravid proglottids. In the small intestine larvae called oncospheres hatch, penetrate the
intestinal wall, enter the bloodstream and migrate to muscle tissue (rarely to liver or other organs),
where they encyst into cysticerci. The tiny cysticerci can survive for years and still be infective
when humans eat the meat. If the beef is not cooked properly, cysticerci excyst in the small
intestine and develop into adults within two months. Adults attach to the intestinal wall with their
scolex using four suckers. The scolex has a pear-shaped and cup-like appearance reaching 1–2 mm

29
in diameter. It is attached to the neck which starts to produce proglottids that make up the flat,
long, segmented body also known as strobila. The proglottids mature and grow bigger as they get
further from the neck. They are about 16–20 mm long and 5–7 mm wide and each proglottid has
its own reproductive organs. They absorb nutrients through their membranes and produce up to
100 000 eggs per day. Proglottids break off from the tail and move with stool out of the human
body. A full-grown Taenia saginata is whitish in colour and has about 1000–2000 proglottids and
about six of them detach every day. The eggs usually stay inside the proglottids until they are out
in the environment. When the proglottid dries up, it ruptures and releases the eggs. The eggs are
embryonated, walnut brown and about 35 micrometers in diameter having a 6-hooked oncosphere
inside its thick shell. If the feces land on grazing ground for cattle, a cow might accidentally ingest
proglottids or eggs. Taenia saginata can live up to 25 years. It can grow up to 5 meters but in some
cases can reach lengths of over 10 meters (coiled in the intestinal tract).
The disease is often asymptomatic. Taeniasis caused by Taenia saginata is more noticeable than
taeniasis caused by Taenia solium (although T. solium is overall more dangerous because of the
risk of cysticercosis). Heavy infection of Taenia saginata can cause some of the following
symptoms:

30
Migrating proglottids can cause:
 inflammation of the appendix)

 inflammation of the bile duct)
 unpleasant surprise when seen in the feces.
Your health care provider makes the Taenia saginata diagnosis by identifying eggs or
proglottids. Eggs and proglottids start appearing in the stool sample after three months of the
start of the infection. During the first three months antibody detection methods can be used to
find antibodies from a blood sample. All Taenia species have similar eggs so identification can
only be done at the genus level. For educational purposes the specific species can be identified
by examining gravid proglottids. The diagnosis can also be done during an endoscopic
examination.
Treatment is traditionally done with an oral drug called praziquantel. It causes paralysis of the
worm by opening its membrane calcium channels. Then through peristaltic movements the
tapeworm is defecated out. Alternatively niclosamide can be used. Both drugs have some side
effects (especially praziquantel) that are similar to actual tapeworm infection symptoms.
Endoscopic treatment is available in some areas. In the endoscopic treatment a drug is injected
straight to the small intestine. This causes all nearby tapeworms to detach and come out whole. If
the scolex (and neck) is left behind, it might produce new segments.
To prevent infection:
 Cook beef at or above 60 °C until it is no longer pink inside. Alternatively freeze the
meat at or below -5 °C for a few days.
 Prevent cattle from eating in areas, where vegetation might be contaminated with humans
feces.

31
Taenia solium
The pork tapeworm, Taenia solium, is the most harmful tapeworm in humans. Taenia solium
infection is acquired either from human feces that contains Taenia solium eggs or from uncooked
pork which contains larval cysts. If larvae are ingested, they mature into adults in the small
intestine. This infection type is called taeniasis and is often asymptomatic. If eggs are ingested,
the resulting disease is cysticercosis. It gets its name from larval Taenia solium called cysticercus.

32
Both diseases are common in Africa, Asia, South America and Southern Europe. Taeniasis is rare
in Muslim countries since people there do not consume pork.
Taeniasis
Taenia solium, as its Latin name suggests, uses pigs as intermediate hosts for its larval stage. A
pig gets infected with cysticercosis. If a human eats pork without cooking it, the dormant larva
excysts in the bowel. The larva matures into an adult tapeworm which absorbs nutrients from the
passing food.
The flat body of an adult Taenia solium consists mostly of segments, proglottids. Pork tapeworm
is attached to the intestinal wall with its head, the scolex. Its head has four suckers and two rows
of hooks. It has a neck that produces the segments which grow bigger as they move towards the
rectum. They absorb nutrients from the surrounding food. Each segment produces eggs that remain
inside it until the segment is passed out in the feces. The segment is less than 1 cm long and 2 cm
wide and contains up to 50000 eggs. Taenia solium grows up to 7 meters. A full grown pork
tapeworm consists of 1000 segments and sheds six gravid proglottids per day. The segments are
detached from the tail. Out in the nature they can be accidentally eaten by pigs or humans.
Taeniasis diagnosis is made by an endoscopic examination or by finding segments (or eggs) from
the feces. Taeniasis is usually treated with niclosamide or endoscopic removal.
Cysticercosis
Microscopic tapeworm eggs are ingested by a human or pig due to poor hygiene. Tiny larvae called
oncospheres hatch in the small intestine. They penetrate the intestinal wall and enter the
bloodstream. They travel to muscles or other tissue such as the liver or the brain. Lastly,
oncospheres transform into cysticerci and encyst. The smallest cysticerci are 0.5–1.5 cm long
whereas the biggest forms are 20 cm long. About 60 % of patients with cysticercosis have
cysticerci in the central nervous system which is called neurocysticercosis. Cysticerci molt into
adults only in the intestine. Immune system does not recognize the cysts. They can live in the tissue
for many years without causing any symptoms. Eventually they get old and their shell structures
start to leak causing an inflammatory response. Common symptoms include: muscle spasms,
dizziness, headaches and seizures. Major cysticerci infections can lead to a sudden death.
As the cysticerci die, the infected areas, lesions, shrink. The swelling goes down and symptoms
start to go away. The area of the organ where they sited will be covered with fibrosis. Vital
functions of the organ may be lost. If oncospheres travel to the eyes the developed cysticerci can
float in the eye and cause disturbed or blurry vision. Infection in the eyes can also cause swelling
or detachment of the retina.
The definitive host, human, can get infected with the same tapeworm over and over again. This
autoinfection can occur in two ways. In some rare cases the mature segments dissolve too early
releasing the eggs. It can happen, if the large intestine is not working properly. This retro-peristalsis
reverses the direction of the stool and the gravid proglottids are carried back to the stomach. The
larvae hatch and cause cysticercosis. Another way to autoinfect oneself with cysticerci is to scratch

33
the anus and then put fingers into the mouth. This too requires that some microscopic eggs have
been released from the segments before exiting the body. Normally the segments stay intact in the
colon.
Cysticercosis diagnosis is possible from Magnetic Resonance Imaging scans or X-rays. The cysts
resemble tumours so the diagnosis is not foolproof. Cysticercosis is generally treated with
albendazole in combination with anti-inflammatory drugs. Drug treatment is not necessary, if the
cysticerci are already dead. Surgical removal is possible, if the location of the cyst is known. All
cases of cysticercosis are not treated. The decision of whether or not to treat neurocysticercosis is
based upon symptoms and the number of cysticerci found in the brain. If only one is found,
treatment is often not given.

34
Nematodes
Ascaris lumbricoides
Ascaris lumbricoides, giant roundworm, is the most common parasitic worm in humans.
According to some estimates 25 % of humans are infected with the disease, ascariasis. Ascariasis
occurs worldwide, mostly in tropical and subtropical countries. It has highest prevalence in areas
of poor sanitation and where human feces are used as fertilizer.
The life cycle of Ascaris lumbricoides takes about three months. Ascariasis starts, when Ascaris
lumbricoides eggs are accidentally swallowed. They can be acquired from dirty fingers, water or
food that has been contaminated with feces of an infected human. Larvae hatch from the eggs,
penetrate the intestinal wall and enter the bloodstream. They stop at pulmonary arteries and stay
in the lungs for two weeks. They break into the alveoli and travel up the respiratory system to the
throat to be swallowed again. The migration is needed for the larvae to develop into adults. Adult
worms attach themselves to the intestinal wall ready to mate. Adults survive by eating food
digested by the host and live up to 2 years. A female produces about 200 000 microscopic eggs
per day that are passed in feces. The eggs fertilize into infective stage within a few weeks in the
right conditions in the soil. Unfertilized eggs are not infective. The eggs are very resistant to
chemicals, extreme temperatures and other rough conditions and can survive for months. Adult
females are 20–35 cm long and 3–6 mm in diameter. Male worms are a little smaller reaching 15–
30 cm in length and 2–4 mm in width.

35
Ascariasis can be asymptomatic, if there are only a few worms. If there are tens or hundreds of
worms, symptoms might include:
 diarrhea
 fever
 nausea
 stomach ache
 slower growing of a child or a teen
 vomiting
 weakness.
Unlike many other human roundworms, Ascaris lumbricoides does not usually feed on blood.
When larvae migrate through the lungs, the following pulmonary symptoms may occur:
 breathing difficulty
 cough and/or coughing up blood
 eosinophilic pneumonitis.
If you happen to vomit or defecate an adult Ascaris lumbricoides, take the worm to your health
care provider for diagnosis. Usually however, the diagnosis is done by examining your feces for

36
the presence of Ascaris lumbricoides eggs. Your health care provider asks you to provide stool
samples for testing.
Ascariasis is usually treated for 1–3 days with ascaricides medicine prescribed by your health care
provider. Some common drugs are albendazole, ivermectin, nitazoxanide and mebendazole, which
kills roundworms by preventing them from absorbing nutrients. You may be asked to provide
additional stool samples 1–2 weeks after the treatment to confirm that the worms are dead.
To prevent new infections:
 Avoid touching soil that might be contaminated with human feces.

 When traveling to areas where hygiene and sanitation are poor, avoid food and water that
might be contaminated with soil.
 Wash hands with water and soap before eating or preparing food.
 Wash, peel or cook all fruits and vegetables before eating.
Enterobius vermicularis
Human pinworm, Enterobius vermicularis, is the most common parasitic worm infection in the
United States and Western Europe. Pinworms are easily transmitted from human to human and are
particularly common in children. Luckily the disease, enterobiasis, causes only anal itching.
Enterobius vermicularis does not need an intermediate host to complete its life cycle. Humans get
infected by accidentally swallowing or inhaling microscopic pinworm eggs. Once inside the first
part of the small intestine, duodenum, pinworm larvae hatch from the eggs. The larvae are only
about 0.15 mm long but grow very fast. They migrate towards the ending of the small intestine as
they mature into adults. Adults are white, thin worms. Males are 0.2 mm thick and 2–5 mm long
whereas females are 0.5 mm thick and 8–13 mm long. Life expectancy for males is seven weeks
whereas females live 5–13 weeks. The males usually die after the pinworms have mated in the last
part of the small intestine, ileum. The gravid (pregnant) female resides at the beginning of the large
intestine, colon, eating whatever food passes through the intestinal tract. Female pinworm reaches
fertility within four weeks. She swims at the rate of 12 cm per hour towards the rectum. During
sleep when body temperature is low and there is less movement the female pushes out from the
anus and lays eggs on the outside skin. The eggs get stuck on skin, underwear or bedding and
become infective within a few hours. Eggs survive up to three weeks on clothing, sheets or other
objects. After the female has laid 11000–16000 eggs it dies.

37
Sometimes pinworms lay eggs inside the colon. If the eggs are not taken out in the feces the larvae
might have enough time to hatch. This can only happen in the large intestine or rectum and only if
enough oxygen is present. The larvae migrate back up the intestinal tract and develop into adults.
This is very rare but happens every now and then.
Diagnosis is made by identifying pinworms or their eggs. Worms can sometimes be seen on the
skin around the anus 2–3 hours after falling asleep. Eggs can be collected using a transparent
cellophane tape by pressing the sticky side of the tape to the anal skin. The eggs stick to the tape
which can be placed on a slide and examined under a microscope by a doctor. Bathing or having
a bowel movement can remove eggs from the skin. So this test should be done immediately after
waking up. It needs to be repeated on the following two mornings to increase the chance of finding
pinworm eggs.
Enterobiasis can be treated with either prescription or over-the-counter medications. A health care
provider should be consulted before treating a suspected infection. Some common drugs against
pinworms are albendazole and mebendazole. The drugs kill larvae and adults but not the eggs. To
get rid of all pinworms another dose needs to be taken after two weeks to kill the newly hatched

38
larvae. All family members should be treated at the same time. If children are in close contact with
other children, like in kindergarten, then there is a possibility that other families are infected, too.
The least embarrassing way to handle the situation is to only tell the kindergarten teacher. She will
inform the other parents that their children might have pinworms and should be treated with the
drug.
To prevent new infections always keep fingers out of your mouth and nose. Keep fingernails short
and do not bite your nails. Wash your hands after using the toilet and before eating or preparing
food. Change clothing, towels, and sheets frequently and wash them in hot water, especially during
and after pinworm treatment. If you have pets, keep them clean. The human pinworm, Enterobius
vermicularis, does not infect other animals but pets can carry eggs in their fur.
Hookworms
Hookworms are bloodsucking roundworms living in the small intestine. Some common names for
hookworm infections are: ancylostomiasis, necatoriasis, Egyptian chlorosis, tunnel disease,
miners' anemia and brickmaker's anemia. Hookworms are the second most common human worms
(the most common is Ascaris lumbricoides). There are thousands of hookworm species but only
two of them target humans. Necator americanus (necatoriasis) and Ancylostoma duodenale
(ancylostomiasis) infect over one billion people around the globe mostly in tropical and
subtropical climates. Necatoriasis predominates in the Americas (North, Central and South
America) and Australia, whereas ancylostomiasis occurs in the Middle East, southern Europe and
North Africa.
Necator americanus is gray-pink in colour. Male is 5–9 mm and female 10 mm long and about 0.5
mm thick. Usually they live a few years but can live up to 15 years. Females produce up to 10 000
eggs per day. Necator americanus is very similar to Ancylostoma duodenale. Ancylostoma
duodenale males are 5–10 mm and females 10 mm or more in length and 0.5 mm thick. They live
only about six months. Females produce up to 30 000 eggs per day.
The hookworm larvae that start the infection are less than a millimeter long. These third stage, L3,
larvae called filariform live on warm moist soil that has been contaminated with infected human
feces. Upon touch, a tiny filariform larva attaches to the skin and penetrates it. It burrows through
tissue until it reaches a blood vessel or lymphatic duct. It travels in the bloodstream to the small
pulmonary capillaries. It breaks into the lung alveoli and is taken towards the bronchus and trachea
by the movement of microvilli. It is coughed up to the throat and swallowed through the esophagus
to the stomach. After passing the stomach it hooks into the intestinal mucosa in the small intestine
and starts sucking blood. The arrival to the small intestine takes about a week. Then within a few

39
weeks it develops into an adult and is ready to mate. The produced eggs exit the body in the feces.
Rhabditiform (first stage, L1) larvae hatch in the feces or in warm, moist, sandy soil within two
days. They feed on organic matter and grow rapidly. They molt twice within 10 days to become
filariform (third stage, L3) larvae that are infective. Filariform larvae can survive up to four weeks
in the right conditions (warmth, moisture, shade).
Although most hookworm larvae travel straight to the small intestine, sometimes larval
Ancylostoma duodenale migrate to muscle tissue and become dormant. These sleeping larvae make
up a reserve that can cause infection years after treatment. According to some reports filariform
larvae of Ancylostoma duodenale can cause infection, if ingested. So in theory it is possible to get
infected by accidentally swallowing contaminated dirt. Necatoriasis on the other hand always
requires migration through the lungs.
Infected humans are more often adult men who work barefoot on fields. Hookworm infection is
the most problematic for women and children. Women lose blood with menstrual flow once a
month. They also need extra nutrients for babies. In some developing countries 30 % of pregnant
women are infected with hookworms. Their newborn babies might have low birth weights or even
die. When a woman gives birth, she excretes certain hormones into the bloodstream. The sleeping
larvae (only Ancylostoma duodenale) in the muscles wake up and find their way into the mammary
glands. When the mother breastfeeds her baby, the child gets infected, too.

40
Hookworms can cause some of the following symptoms:
 anemia (pale skin etc.) and protein deficiency caused by blood loss
 constipation
 congestive heart failure
 decreased rate of growth and mental development in children (caused by protein and iron
deficiency)
 diarrhea
 dizziness
 dyspnea (shortness of breath)
 excessive coughing during larvae migration
 fatigue (tiredness)
 fever
 loss of appetite
 nausea
 rash or sore and itchy feet after larval invasion
 stomach or chest pain
 vomiting
 weight loss.
Diagnosis of an intestinal hookworm infection is done by identifying hookworm eggs from a stool
sample under a microscope. Another stool sample after treatment is often required to make sure
all hookworms are dead. The infection is usually treated for 1–3 days with medication prescribed
by your health care provider. Some good drugs against hookworms are benzimidazoles such as
albendazole and mebendazole. The drugs are effective and appear to have only few side effects.
Iron supplements may also be prescribed to cure anemia. Despite of all efforts, the infection might
still continue due to awakened dormant larvae or new infections.
Hookworm infection is rarely lethal. In fact, hookworms have been used to cure autoimmune
diseases. In helminthic therapy hookworms are voluntarily swallowed. The parasitic infection
prevents the overly active immune system from destroying tissue focusing only on the foreign
organisms.
Human feces should not be used as fertilizer in agriculture. Do not walk barefoot or touch soil in
areas where hookworms are common. Also if you have cats or dogs, treat them with anti worm
pills regularly.
Cutaneous larva migrans
Animal hookworms Ancylostoma braziliense and Ancylostoma caninum normally parasitize only
dogs and cats. In humans they cause a skin condition called cutaneous larva migrans, creeping
eruption or ground itch. In the canine (or feline) intestine a female hookworm releases eggs into
the stool. The feces land on soil, and rhabditiform larvae hatch and evolve into filariform. The
filariform larvae burrow into human skin and start migrating in the epidermis. They cannot usually
breach the subcutaneous layer and live only up to a few months. They can migrate several
centimeters per day causing itchy red lesions and vesicles on the skin.

41
Cutaneous larva migrans is usually diagnosed from the signs and symptoms without laboratory
tests. There are no serologic tests for animal hookworm infections for humans. Cutaneous larva
migrans is a self-limiting infection and does not always require treatment. Severe cutaneous larva
migrans infections can be treated with albendazole and surgical removal.
Sometimes larval Ancylostoma caninum is able to penetrate the lower skin layer and migrate to
the small intestine, causing eosinophilic enteritis. It is possible that it can also migrate to the eye
and cause diffuse unilateral subacute neuroretinitis (DUSN). At the early stage of DUSN it
might cause vitritis, visual loss, mild papilledema, and consecutive crops of multiple, evanescent,
deep, gray-white, retinal lesions. After several months there might be widespread, diffuse and focal
depigmentation of the pigment epithelium, retinal arterial narrowing, severe visual loss, optic
atrophy, and electroretinographic changes.

42

43
http://www.parasitesinhumans.org/hookworms.html
http://www.parasitesinhumans.org/hookworms.html
Arthropods
Cimex lectularius
Bedbugs are skin parasites that live inside or near beds and feed on blood during the night. The
most common bedbug species is Cimex lectularius. Bedbugs remain in the same room as long as
there is constant blood supply. They can survive a few years without feeding but normally eat
every week, if the human host is present.
Bedbugs are flat and can easily hide in the wall or under the mattress. Adults are 1–3 mm wide
and 4–5 mm long wingless brown bugs. They crawl towards the meal by following heat and
carbon dioxide. They penetrate skin with two hollow tubes. The other is for drinking blood while
the other injects anticoagulants and pain relieving anesthetics. After feeding for a few minutes a
bedbug returns to its hiding place.
Bite marks might take up to a week to appear depending on the sensitivity of the host's skin. The
bites are often in a sequence or a clump. One bedbug can leave a number of sore red spots, if it
has to drill many holes before finding a blood vein. It also bites many times, if interrupted by a
touch or movement. If the bedbug is not disturbed, there might only be one red spot. Spots can
be found anywhere on the body. If bites are always found in a certain area, the hideout might
become easier to find.
Some chemical sprays are effective against adult bedbugs but powerless against eggs. The
preferred treatment for an apartment is to use heat. New heating methods are effective against
most domestic bugs and safe for delicate furniture. (See the link below for the heat method
video.) High temperature of at least 45 °C is applied to trouble areas. A fabric steamer is handy
for small items. Treating with other methods is effective, if the bugs are inside removable objects
such as mattresses. In addition to heat, freezing a few days at -20 °C kills most parasites. The
best treatment for a human is to stay away from bedbugs. If the bedbugs cannot be killed, there
are a few ways to keep them away. Two-sided adhesive tape can be applied to bed legs to stop
the bugs from crawling up into the bed. There are also some chemical powders that can be
applied on the floor around the bed legs that kill bugs that walk over it. Moving out of the house
is the best way as long as furniture and other objects are treated with heat or frost. A temporary
vacation is not long enough because bedbugs can survive years without eating. Bags should be
kept closed, when not in use on a vacation to stay clear from any additional bugs. Used clothes
that are bought from flea markets should be washed immediately. You might want to avoid using
other people's clothes or letting pets in the house.

44
Life Cycle of Bed Bug

Adults and all nymphal stages of Cimex spp. need to take blood meals from warm-blooded hosts,
which are typically humans for C. lectularius and C. hemipterus, although other mammals and
birds can be utilized in the absence of a human host. Female bed bugs lay about five eggs daily
throughout their adult lives in a sheltered location (mattress seams, crevices in box springs, spaces
under baseboards, etc). Eggs hatch in about 4-12 days into first instar nymphs which must take
a blood meal before molting to the next stage. The bugs will undergo five nymphal stages ( ,
, , , ), each one requiring a blood meal before molting to the next stage, with the fifth stage
molting into an adult . Nymphs, although lacking wing buds, resemble smaller versions of the
adults. Nymphs and adults take about 5-10 minutes to obtain a full blood meal. The adults may
take several blood meals over several weeks, assuming a warm-blooded host is available. Mating
occurs off the host and involves a unique form of copulation called 'traumatic insemination'
whereby the male penetrates the female’s abdominal wall with his external genitalia and
inseminates into her body cavity. Adults live 6-12 months and may survive for long periods of
time without feeding.

45
http://www.parasitesinhumans.org/cimex-lectularius-bedbug.html
Dermatobia hominis
The human botfly, Dermatobia hominis, belongs to the Oestroidea family. There are about 150
botfly species but only Dermatobia hominis uses man as a host. The larvae of these huge hairy
flies are parasitic living inside the skin.
Human botfly lays eggs on the skin. When a larva inside the egg detects warmth, it hatches and
penetrates the skin. It develops deep inside the skin and breaths through a special tube which has
an opening at the wound spot. After feeding for two months the botfly comes out and drops off.
On the soil it will take another week to become an adult botfly.
Botfly can also use a vector to carry the eggs. It can catch smaller flies and lay eggs under their
wings. When these smaller flies fly on the skin, they are rarely noticed. When the tiny larvae
inside the eggs recognize human warmth, they hatch and burrow into the skin. If the carrier fly is
killed by a smack, the mother botfly would still be safe and could lay new eggs some other time.
In this case only the carrier fly takes the risk of delivering the eggs.
The proper way to get rid of an almost mature larva inside the skin is to suffocate it. If you do
not have access to a doctor, you can cover its breathing hole with nail polish or adhesive tape.
The removal of the dead larva is done by pulling carefully with pliers or pincers.

46
http://www.parasitesinhumans.org/dermatobia-hominis-human-botfly.html
Sarcoptes scabiei
Scabies is caused by a tiny mite called Sarcoptes scabiei. It gets its name from the Latin word
scabere which means to scratch. Sarcoptes scabiei is a skin parasite causing severe itching and
infections. There are at least 300 million cases every year worldwide. All ages of men and
women especially in crowded and unhygienic conditions are at risk.
Sarcoptes scabiei goes through four stages in its life cycle: egg, larva, nymph and adult. The life
cycle starts, when an adult female gets in contact with your skin. It crawls to crevices such as
elbows, feet, fingers and genital area. It penetrates the skin and burrows a tunnel. It can slice skin

47
with its sharp front legs and mouthparts. The other legs it uses for holding on to the skin with
suckers on each leg. It has eight legs in total. It takes about 30 minutes for it to burrow into the
skin. It then continues to drill horizontally across the skin laying eggs along the way. The tunnels
are usually shaped in a zigzag on the skin surface. It lays 2–3 eggs per day for two months. Then
it dies. Six-legged larvae hatch from the eggs within a few days. They find hair follicles where
they feed and molt into eight-legged nymphs. In order for the nymph to become an adult male it
molts once. This takes about ten days. To become a female it has to molt twice which takes about
17 days. Since the nymph has more time to eat and grow the females are larger than males.
Female Sarcoptes scabiei is 0.25–0.35 mm wide and 0.30–0.45 mm long. Males are about half of
that size. Mature female and male mate only once. The sperm keep the female fertile for the
whole two months that it lays eggs. Males do not usually burrow into the skin but only crawl and
feed on it.
The movement of Sarcoptes scabiei and eggs inside the tunnels cause local inflammation. This
allergic reaction causes very intense rashes. People who have never been exposed to scabies

48
develop allergic response within six weeks. Those who have had scabies previously will get the
rash within a few days. On average there are only a few fertile female mites per infected person.
These kind of infections can be harmless and the victim might not even notice it.
Scabies spreads easily through skin-to-skin contact. Mites can also crawl long distances. If you
scratch an infected area, they get inside your fingernails. Then if you touch common objects like
laptops, the mites can drop there and infect others.
Diagnosis is done by finding mites or their tunnels. The infected area is usually scratched so
much that the common s-pattern is not shown clearly. The tunnel can be revealed with ink or
topical tetracycline solution. Your doctor applies it on your skin and then sweeps it off with an
alcohol pad. Living mites can be identified under a microscope.
To get rid of Sarcoptes scabiei you need to wash your whole body with Sulfuric soap for a few
days. To relief itching during the treatment period use antihistamines such as chlorpheniramine.
Your entire home needs to be washed. If you have pets, wash them too and have them checked
by a vet. Common objects such as computer keyboards can be frozen at -20 °C for a few days to
kill the mites.
People who already have other diseases and thus weakened immune systems can develop
crusted scabies (also known as Norwegian scabies). It is characterized by thousands of mites
causing severe itching and rash. Norwegian scabies is treated with oral dose of Ivermectin which
has some severe unwanted side effects.
http://www.parasitesinhumans.org/sarcoptes-scabiei-scabies.html
Reference:
Bognot, F.L., Goce, E.E., Mergal, Z.F. & Munos D.S. (2015).Laboratory Manual in Microbiology
and Parasitology for Allied Medical Courses 2nd Edition. C & E Publishing Inc. 839 Edsa,
South Triangle, Quezon City
Cowan, M.K. & Talaro, K.P. (2006). Microbiology A Systems Approach. McGraw-Hill
Companies, Inc. 1221 Avenue of the Americas, New York, NY10020
Manar M.S. El-Tonsy. (n.d.). Introduction To Medical Parasitology.Parasitology Department,

Faculty of Medicine, Ain Shams University, Cairo, Egypt. Retrieved from:
http://www.eolss.net/sample-chapters/c03/e5-25-52.pdf

49
Parasites in Humans. Find the Nastiest Parasites in Humans. Retrieved from

http://www.parasitesinhumans.org/sarcoptes-scabiei-scabies.html
Parasitology. National Open University of Nigeria. School of Science and Technology. Retrieved
from http://www.nou.edu.ng/uploads/NOUN_OCL/pdf/pdf2/BIO%20411%20 PARASI
TOLOGY.pdf
Glossary
Risk factor - A risk factor is any attribute, characteristic or exposure of an individual that increases the
likelihood of developing a disease or injury. Some examples of the more important risk factors
are underweight, unsafe sex, high blood pressure, tobacco and alcohol consumption, and unsafe
water, sanitation and hygiene.
Vector - an organism, typically a biting insect or tick, that transmits a disease or parasite from one animal
or plant to another.
Domain: Eukaryota
(unranked): Sar
Superphylum: Alveolata
Phylum: Ciliophora
Class: Litostomatea
Order: Vestibuliferida
Family: Balantiididae
Genus: Balantidium
Species: B. coli
Domain: Eukaryota
(unranked): Amoebozoa
Subphylum: Conosa
Infraphylum: Archamoebae
Genus: Entamoeba
Species: E. histolytica

50
Domain: Eukaryota
(unranked): Excavata
Phylum: Euglenozoa
Class: Kinetoplastida
Order: Trypanosomatida
Genus: Leishmania

51
Kingdom: Excavata
Phylum: Euglenozoa
Class: Kinetoplastea
Order: Trypanosomatida
Genus: Trypanosoma
Species: T. brucei
Domain: Eukaryota
(unranked): SAR
Superphylum: Alveolata
Phylum: Apicomplexa
Class: Aconoidasida
Order: Haemosporida
Family: Plasmodiidae
Genus: Plasmodium
Species: P. falciparum

52
Kingdom: Animalia
Phylum: Platyhelminthes
Class: Trematoda
Subclass: Digenea
Order: Echinostomida
Suborder: Distomata
Family: Fasciolidae
Genus: Fasciola
Species: F. hepatica
Kingdom: Animalia
Class: Trematoda
Subclass: Digenea
Order: Strigeidida
Family: Schistosomatidae
Genus: Schistosoma

53
Kingdom: Animalia
Class: Trematoda
Order: Plagiorchiida
Family: Troglotrematidae
Genus: Paragonimus
Species: P. westermani
Kingdom: Animalia
Class: Cestoda
Order: Cyclophyllidea
Family: Taeniidae
Genus: Taenia
Species: T. saginata

54
Kingdom: Animalia
Class: Cestoda
Order: Cyclophyllidea
Family: Taeniidae
Genus: Taenia
Species: T. solium
Kingdom: Animalia
Phylum: Nematoda
Class: Secernentea
Order: Ascaridida
Family: Ascarididae
Genus: Ascaris
Species: A. lumbricoides
Kingdom Animalia
Phylum Nematoda
Class Rhabditea
Order Oxyurata
Family Oxyuridae
Genus Enterobius
Species vermicularis

55
Kingdom: Animalia
Phylum: Nematoda
Class: Secernentea
Order: Strongylida
Family: Ancylostomatidae
Genus: Necator
Species: N. americanus
Kingdom: Animalia
Phylum: Nematoda
Class: Secernentea
Order: Strongylida
Genus: Ancylostoma
Species: A. duodenale

56
Kingdom: Animalia
Phylum: Nematoda
Class: Secernentea
Order: Strongylida
Genus: Ancylostoma
Species: braziliense
Kingdom: Animalia
Phylum: Arthropoda
Class: Insecta
Order: Hemiptera
Suborder: Heteroptera
Infraorder: Cimicomorpha
Superfamily: Cimicoidea
Family: Cimicidae

57
Kingdom: Animalia
Phylum: Arthropoda
Class: Insecta
Order: Diptera
Family: Oestridae
Subfamily: Cuterebrinae
Genus: Dermatobia
Species: D. hominis
Kingdom: Animalia
Phylum: Arthropoda
Class: Insecta
Order: Hemiptera
Suborder: Heteroptera
Infraorder: Cimicomorpha
Superfamily: Cimicoidea
Cimicidae
Family:
Latreille, 1802
Cimex lectularius

58
Kingdom: Animalia
Phylum: Arthropoda
Class: Insecta
Order: Diptera
Family: Oestridae
Subfamily: Cuterebrinae
Genus: Dermatobia
Species: D. hominis
Kingdom: Animalia
Phylum: Arthropoda
Class: Arachnida
Subclass: Acari
Order: Sarcoptiformes
Family: Sarcoptidae
Genus: Sarcoptes
Species: S. scabiei

59

Lectures On BIOL 105 Parasitology 2018

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1

The scope of Parasitology

BIOL 105 Parasitology

Parasitic Disease transmission

The concept of epidemiology

BIOL 105 Parasitology

Identify and explain geographic disease patterns

Epidemiological studies may be descriptive, analytical (cohort, or case control), experimental

Disability Adjusted Life Years (DALYs)

DALYs estimate of Common Parasitic Diseases

BIOL 105 Parasitology

BIOL 105 Parasitology

Types of Symbiotic Association:

BIOL 105 Parasitology

Classification and General Characters of Human Parasites.

Parasites’ Life Cycles

BIOL 105 Parasitology

Robert G. Yaeger.Chapter 77Protozoa: Structure, Classification, Growth, and Development

BIOL 105 Parasitology

Diagnosis can be made by finding trophozoites from a stool or tissue

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

 appendicitis (inflammation of the appendix)

 Wash your hands often.

BIOL 105 Parasitology

Leishmania is a microscopic protozoon and is responsible for a disease called leishmaniasis.

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

Some less noticeable manifestations:

 enlargement of the spleen or liver

BIOL 105 Parasitology

Some less noticeable manifestations:

 abnormalities in blood coagulation

Diagnosis can be challenging for many reasons:

BIOL 105 Parasitology

 artemesinin-containing combination treatments (for example, artemether-lumefantrine,

BIOL 105 Parasitology

 Eat iron and folate supplements to prevent anemia.

 insect growth regulators

Additional personal protection methods include:

 glass windows (a well-constructed house)

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

Migrating proglottids can cause:

 inflammation of the appendix)

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology

BIOL 105 Parasitology