CHAPTER 1: PARASITOLOGY
exam: 5 open questions where you have to link al the chapters. Questions like “what can
you attract by drinken water” or something. De 6th question is about recognising a
microscopic and macroscopic pathogen. You don’t have to draw lifecycles, but you
should know the mechanisms.
definition and classification
parasitism is a way of symbiosis
= “living” together of 2 or more species, we have 3 different kinds of symbiosis
symbiosis kind dependance damage
mutualism 2-way dependance partial no
commensalism (=feeding 1-way dependance no (no): sometimes
together, like bacteria in the gut) commensals can
become dangerous,
if the bacteria in the
gut travel to the
liver f.e.
parasitism 1-way yes yes!!
- 50% of all animal species are parasitic: this is because we have a lot of insects
and insects are almost always parasitic
- 100% of animals and plants become parasitized: only viruses cannot become
parasitized
- several parasites per host species
- different hosts for one parasite species
parasitology
= study of parasitic symbiosis. We will focus on protozoa, helminths (tapeworms,
flatworms, roundworms) and arthropods (bedbugs, thicks, head lice..)
definitions
obligate parasitic stage required with cycle. The life cycle of the parasite
required a host. f.e: tsetse fly
facultative independent, non-parasitic cycle possible.
- f.e: mosquitos, they can easily live on nectar instead of blood
from humans
- f.e: STH (soil transmitted helminths) are nematodes that can
survive in the soil but can also survive in the skin if you walk on
1
, your bare feet with it
permanent total cycle on the host, like lice
temporary part of the cycle on the host, like ticks
incidental relatively rare in this particular host
- f.e: the haring worm, normally in sea mammals but if you eat a
poorly cooked fish, it can infect and cause problems. Human is
an accidental host
erratic abnormal location within the host
stenoxene high-host specificity
- f.e: pinworms in humans (aarswormen)
euryxene low host specificity
- f.e: toxoplasmosis can infect cattle, lambs, cats, mice, humans…
homoxene one host within the cycle (direct cycle), this is a simple life cyle
- f.e: trichomona vaglinalis, this is a permanent infection that
transfers from human to human
heteroxene more hosts within the cycle (indirect cycle), this is a complex cycle,
sometimes even 5 hosts in the life cycle
definitive the host in which the parasite reaches the adult stage, sexual
multiplication happens inside that host
intermediate a host in which you find the larval stage (with development, you have
different morphological phases)
paratenic a host in which you find the larval stage (without development, just
waiting for another host to pick the larva up)
vector active role in transmission (you have biological or mechanical
transmission)
prepatent period between infection and the host becoming infectious, so the
period moment the eggs release in the stool for example
patent period infectious period (production of eggs, larvae)
endo-parasite lives within the host
ecto-parasite lives on the host
meso-parasit lives in external cavities like mouth, ear, sinuses, genitals..
e - f.e: tricholoma vaginalis
reservoir the host which is the normal biotope of the parasite
zoonosis vertebrate animal is the source of infection for man
2
,some parasites have a complex life cycle
- 1 to 4 successive hosts
- inclusion of invertebrate and vertebrate hosts
- alternation between ‘terrestrial’ and ‘aquatic’ biotopes
- horizontal en vertical (mother → child like toxoplasmose) transmission options
- if we look at the life cycle, we should know the epidemiology, clinical
disease+diagnosis and a design of preventive and curative control
adaptations for establishment in the host
=adaptations they make to infect, survive and reproduce
= each time it infects another host, it should adapt to another organism
morphological making adaptations in size, form, locomotion, attachment, sensory
function, digestive system…²
biological increase of reproductive potential: egg production, hermaphroditism,
parthenogenesis, loss of seasonality, short-pre adult life, survival,
inclusion of asexual multiplication, inclusion of secondary and
tertiary hosts
immunological absorption of ‘host’ antigen, antigenic variation, immunologic
‘sanctuary’ sites (parasite lives inside an immunological cells or they
cross barriers like BBB or eye, these places are immunoprivileged
disruption of host immunity, ‘masking’ surface antigens
biological energy metabolism (aerobe, microaerophilic), uptake of nutrients,
increase of transporter systems
parasite-host infections
= infection mechanisms
- passive: via food, via direct contact
- active: vectors, specific adaptations of infective larvae
- vertical transmission ‘rarely)
survial and immunity → see
immunology course → very
complex, we won’t go into detail
3
, pathogenesis depends on…
parasite host
- species/strain - age
- infection pressure - nutritional status
- localization - immune status
- stage - physiological condition
↓↓↓
1. wasting, spoliation
2. formation of toxic products: fe: toxic products by malaria
3. immunosuppression leads to opportunistic infections
4. allergy and hypersensitivity, helminths can lead to anaphylactic shock
5. mechanical damage (pressure, obstruction, migration)
6. irritation on skin or organs and tis
clinical signs
- subclinical: most frequent, the patient shows no symptoms. This is good for the
patients but bad for the environment because they can still transmit the disease
- clinical: depend on the parasite load, on your specific immunity and some hosts
are more susceptible then others.
Possible clinical signs:
GI - anorexia (loss of weight, one of the best signs that there are
problems because loss of body weight is an important sign of
infection
- diarrhea
- constipation
- vomiting
- anemia (also in a lot of infections seen)
respiratory - anorexia
- sneezing
- coughing
- dyspnea
- tachypnea
reproduction - sterility
- abortion
- congenital disorders
CNZ - anorexia
- convulsions
- paralysis
vascular - anorexia
- edema
4
exam: 5 open questions where you have to link al the chapters. Questions like “what can
you attract by drinken water” or something. De 6th question is about recognising a
microscopic and macroscopic pathogen. You don’t have to draw lifecycles, but you
should know the mechanisms.
definition and classification
parasitism is a way of symbiosis
= “living” together of 2 or more species, we have 3 different kinds of symbiosis
symbiosis kind dependance damage
mutualism 2-way dependance partial no
commensalism (=feeding 1-way dependance no (no): sometimes
together, like bacteria in the gut) commensals can
become dangerous,
if the bacteria in the
gut travel to the
liver f.e.
parasitism 1-way yes yes!!
- 50% of all animal species are parasitic: this is because we have a lot of insects
and insects are almost always parasitic
- 100% of animals and plants become parasitized: only viruses cannot become
parasitized
- several parasites per host species
- different hosts for one parasite species
parasitology
= study of parasitic symbiosis. We will focus on protozoa, helminths (tapeworms,
flatworms, roundworms) and arthropods (bedbugs, thicks, head lice..)
definitions
obligate parasitic stage required with cycle. The life cycle of the parasite
required a host. f.e: tsetse fly
facultative independent, non-parasitic cycle possible.
- f.e: mosquitos, they can easily live on nectar instead of blood
from humans
- f.e: STH (soil transmitted helminths) are nematodes that can
survive in the soil but can also survive in the skin if you walk on
1
, your bare feet with it
permanent total cycle on the host, like lice
temporary part of the cycle on the host, like ticks
incidental relatively rare in this particular host
- f.e: the haring worm, normally in sea mammals but if you eat a
poorly cooked fish, it can infect and cause problems. Human is
an accidental host
erratic abnormal location within the host
stenoxene high-host specificity
- f.e: pinworms in humans (aarswormen)
euryxene low host specificity
- f.e: toxoplasmosis can infect cattle, lambs, cats, mice, humans…
homoxene one host within the cycle (direct cycle), this is a simple life cyle
- f.e: trichomona vaglinalis, this is a permanent infection that
transfers from human to human
heteroxene more hosts within the cycle (indirect cycle), this is a complex cycle,
sometimes even 5 hosts in the life cycle
definitive the host in which the parasite reaches the adult stage, sexual
multiplication happens inside that host
intermediate a host in which you find the larval stage (with development, you have
different morphological phases)
paratenic a host in which you find the larval stage (without development, just
waiting for another host to pick the larva up)
vector active role in transmission (you have biological or mechanical
transmission)
prepatent period between infection and the host becoming infectious, so the
period moment the eggs release in the stool for example
patent period infectious period (production of eggs, larvae)
endo-parasite lives within the host
ecto-parasite lives on the host
meso-parasit lives in external cavities like mouth, ear, sinuses, genitals..
e - f.e: tricholoma vaginalis
reservoir the host which is the normal biotope of the parasite
zoonosis vertebrate animal is the source of infection for man
2
,some parasites have a complex life cycle
- 1 to 4 successive hosts
- inclusion of invertebrate and vertebrate hosts
- alternation between ‘terrestrial’ and ‘aquatic’ biotopes
- horizontal en vertical (mother → child like toxoplasmose) transmission options
- if we look at the life cycle, we should know the epidemiology, clinical
disease+diagnosis and a design of preventive and curative control
adaptations for establishment in the host
=adaptations they make to infect, survive and reproduce
= each time it infects another host, it should adapt to another organism
morphological making adaptations in size, form, locomotion, attachment, sensory
function, digestive system…²
biological increase of reproductive potential: egg production, hermaphroditism,
parthenogenesis, loss of seasonality, short-pre adult life, survival,
inclusion of asexual multiplication, inclusion of secondary and
tertiary hosts
immunological absorption of ‘host’ antigen, antigenic variation, immunologic
‘sanctuary’ sites (parasite lives inside an immunological cells or they
cross barriers like BBB or eye, these places are immunoprivileged
disruption of host immunity, ‘masking’ surface antigens
biological energy metabolism (aerobe, microaerophilic), uptake of nutrients,
increase of transporter systems
parasite-host infections
= infection mechanisms
- passive: via food, via direct contact
- active: vectors, specific adaptations of infective larvae
- vertical transmission ‘rarely)
survial and immunity → see
immunology course → very
complex, we won’t go into detail
3
, pathogenesis depends on…
parasite host
- species/strain - age
- infection pressure - nutritional status
- localization - immune status
- stage - physiological condition
↓↓↓
1. wasting, spoliation
2. formation of toxic products: fe: toxic products by malaria
3. immunosuppression leads to opportunistic infections
4. allergy and hypersensitivity, helminths can lead to anaphylactic shock
5. mechanical damage (pressure, obstruction, migration)
6. irritation on skin or organs and tis
clinical signs
- subclinical: most frequent, the patient shows no symptoms. This is good for the
patients but bad for the environment because they can still transmit the disease
- clinical: depend on the parasite load, on your specific immunity and some hosts
are more susceptible then others.
Possible clinical signs:
GI - anorexia (loss of weight, one of the best signs that there are
problems because loss of body weight is an important sign of
infection
- diarrhea
- constipation
- vomiting
- anemia (also in a lot of infections seen)
respiratory - anorexia
- sneezing
- coughing
- dyspnea
- tachypnea
reproduction - sterility
- abortion
- congenital disorders
CNZ - anorexia
- convulsions
- paralysis
vascular - anorexia
- edema
4
