Microbiology - Parasitology Exam Notes
1. What are Parasitic Diseases?
Host- parasite R/ship
- Symbiosis ;-living together’ – a close association between two organisms.
a. mutualism – both organisms are benefited (bacteria in bowel)
b. commensalism – one organism is benefited, the other is Unaffected.
c. Parasite;- An organism that is deriving its sustenance from another without giving something in
return .
Parasitology ;- The science or study of these host-parasite relationships
Vector;- ‘carrier’ of a parasite from one host to another .
The host;- The organism that provides food and/or protection
Types of host
a) definitive host – the host in which sexual maturity an reproduction takes place, [Link]
b) intermediate host – the host in which the parasite undergoes essential development. More than
one
intermediate host may be required by some parasites.
Humans sometimes serve as an intermediate host, [Link]
c) reservoir (carrier) host – the host harboring a parasite in nature – serving as a source of infection
for other susceptible hosts.
Reservoir hosts show no sign or symptom of disease;-
A number of parasites require more than one host to complete their life cycle
Major Types of Parasitic Diseases
- Nematodes – intestinal helminths (worms)
Cestodes – tapeworms
Trematodes – Schistosomiasis, flukes, etc.
Intestinal and Luminal Protozoa – Amebiasis, Giardiasis
Blood Protozoa – Malaria, African sleeping sickness, etc.
Arthropods &Ticks – Fleas, lice, ticks, etc.
Eradication, Elimination, and Control
Eradication;-A permanent reduction to zero of the worldwide incidence of infection
Elimination (interruption of transmission);- Reduction to zero of the incidence of infection by a
specific pathogen in a defined geographical area.
Control :- Reduction of disease incidence, prevalence, intensity,morbidity or mortality.
Continued intervention measured may be required
Endemic;- Regularly found among particular people or in a certain area
Main Strategy of the WHO roadmap
Provide coordinated guidance and technical assistance to governments and health programs to
eradicate, eliminate, or control.
Encourage coordination between pharmaceutical companies, healthcare agencies,
philanthropists (e. Bill Gates), universities to overcome neglected tropical diseases (NTDs).
- Outcome: a significate reduction in morbidity and transmission so that they are no longer a
public health problem.
1. Nematodes – Intestinal Helminths (worms)
Nematodes are cylindrical worms, hence the name roundworm
The mode of transmission varies with the type of worm
May involve ingestion of eggs or larvae.
Penetration by larvae
Bite of vectors
Ingestion of stages in the meat of intermediate hosts
Worms are often long-lived
Morphology described as a tube within a tube – the outer tube contains musculature and inner
tube contains the digestive tract
- Soil-transmitted helminth (worm) infections – Neglected Tropical
Disease
o Ascaris lumbricoides (roundworm) (NTD) – infects >1 billion
people
o Trichuris trichiura (whipworm) (NTD) – infects 795 million
o Ancylostoma duodenale and Necator americanes
(hookworms) (NTD) – infects 740 million
- Other examples of nematodes
o Enterobius vermicularis (pinworm),
o Trichinella spiralis (trichinosis),
o Strongyloides stercoralis (Cochin-china diarrhea),
o Dracunulus medinensis (fiery serpents) (NTD)
WHO Action on Soil-Transmitted Helminths – Control Strategies
- Morbidity to be controlled by delivering preventive chemotherapy
- Elimination and eradication will not be achieved until affected
populations have access to effective sanitation, and sewage
treatment, and disposal
- Treat once or twice a year – pre-school and school-age children
- Adults at high risk in certain occupations (e. tea-pickers, miners..)
- It is considered that ‘deworming school-age children is probably the
most economically efficient public health activity that can be
implemented in any low-income country where soil-transmitted
helminthes are endemic’
- In 2010, 711 million people worldwide received preventive
chemotherapy for at least one neglected tropical disease
WHO’s challenges and goals for prevention of neglected tropical diseases
- Preventive chemotherapy
o The large-scale delivery of single-dose, quality-assured
medicines, either alone or in combination, provided free of
charge and at regular intervals to prevent selected diseases
Innovative and intensified disease management
o Controlling through case management the diseases that are
difficult to diagnose and treat, and which in most cases
trigger severe clinical manifestations and complications
Vector control and pesticide management
o The safe and judicious management of public-health
pesticides to achieve vector control through integrated vector
management
Safe drinking-water, basic sanitation and hygiene services, and
education
o The prioritization of improved sanitation combined with the
delivery of preventive chemotherapy and health education to
sustain reductions in prevalence of many of these diseases
Zoonotic disease management
o The application of veterinary sciences and interventions to
protect and improve human health (also referred to as
veterinary public health)
Roadmap targets: WHO Action on Soil-Transmitted Helminths
- 600 million tablets of albendazole or mebendazole
- By 2015
o 50% of preschool children are regularly treated
o 100% of countries have an action plan
- By 2020
o 75% of preschool and school-aged children are regularly
treated
o 75% coverage of preschool and school-aged children in 100%
countries affected
Ascaris lumbricoides (roundworm)
- Background and epidemiology
o A soil-transmitted helminth
MICROBIOLGY – Sue V – Parasitology
The Americas, Central and Southern Africa, Southern
Asia, Indonesia, Australia, and Pacific Islands
o A. duodenale
Dominant species in the Mediterranean region and
northern Asia
- Morphology
o Adult – 11mm long
- Characteristics
o Enter through the foot – ‘hookworm foot’
- Life Cycle
o A different strategy for entry into human
o Eggs are released in the stool
o Larvae hatch in soil 1-2 days called rhabditiform
o Undergo two moults in the soil over a period of 51 days and
develop into infective filariform larvae ready to infect
humans
o Survive 3-4 weeks in this form
o Humans become infected when infective flariform larvae
penetrate skin, enter the bloodstream and move to the heart
and lungs, penetrate the alveoli of the lungs ascend to the
throat and are then swallowed
o Develop into adults in the lumen of the small intestine and
attach to the intestinal wall
o Live for 1-2 years
Symptoms
o Major symptoms are from blood loss as the hookworms
damage intestinal mucosa
o Anemia is common
o Loss of iron can retard growth and mental development
Diagnosis and Treatment
o Finding hookworm eggs in feces
o Mebendazole for 3 days is effective
Control
o Sanitation is the chief method of control – avoid contact with
infected fecal material
o Avoid walking barefoot in hookworm-infected areas
o Do not defecate in places other than latrines, toilets
o Do not use human excrement or raw sewage as manure or
fertilizer in agriculture
Dracunculus medinensis (Guinea worm)
- History
MICROBIOLGY – Sue V – Parasitology
o Known as a parasite of humans since about 1530 BC
o Persian physicians removed D. medinensis from patient
during 9th century
- Hosts
o Definitive: Humans
o Intermediate: Copepod
- Distribution
o As of 2005, Guinea worm disease only occurs in Africa, and
few remote villages in Rajasthan, India and Yemen.
o Only 9 countries are endemic:
Sudan, Ghana, Nigeria, Mali, Togo, Burkina Faso,
Ethiopia, Niger, and Ivory Coast
o >50% of all cases of Guinea worm disease are reported from
southern Sudan
o 3 million cases in the 1980s
- Morphology
o The adult female guinea worms is a long, slender worm ranging from 30-120cm length x 0.09-0
width
o Three mature guinea worms (size)
Gravid (carrying eggs) female > mature female >
mature male
- Characteristics
o Only helminthic parasite transmitted solely through water
But usually occurs during drought
Everyone is forced to drink from the same stagnant
water supplies or pay for a well
o Three conditions to be met before D. medinensis can complete
its life cycle
The skin of an infected individual must come in
contact with water
The water must contain the appropriate species of
microcrustacean
The water must be used for drinking
o Believed that parasites feed on blood due to the gut often
being filled with dark brown gut material
- Vector - Crustacean
Life Cycle
o Humans become infected by drinking unfiltered water
containing copepods (small crustaceans) which are infected
with larvae of D. medinensis
o Following ingestion, the copepods die and release the larvae,
which penetrate the host stomach and intestinal wall and
enter the abdominal cavity and retroperitoneal space
o The worm molts again 20 days and 43 days post infection
o Females are fertilized by the third month
o After maturation into adults and copulation, the male worm
die and the females migrate into the subcutaneous tissues
towards the surface of the skin
o Approx. one year after infection, the female worm induces a
blister on the skin, generally on the distal lower extremity,
which ruptures
o When this lesion comes into contact with water, which the
patient seeks to relieve the local discomfort, the female worm
emerges and releases larvae
o The larvae are ingested by a copepod and after two weeks
(and two molts) have developed into infected larvae
MICROBIOLGY – Sue V – Parasitology
- Examples
o Wuchereria bancrofti and W. (Brugia) malayi (elephantiasis)
o Onchocerca volvulus (Blinding filariasis; river blindness)
o Loa loa (eye worm)
Wuchereria bancrofti (elephantiasis)
- Human pathogen, distributed in tropical areas worldwide
- 40 million people are estimated to be disfigured and incapacitated by
this disease - Infected individuals are generally incapacitated
- One of the major causes of disability worldwide
- Insect vector required for transmission - by mosquitos – making
control difficult
- Adult Filarial worms are around 10cm long
- The adult male and female worms reside in lymphatic where they
mate and produce large numbers of larvae, called microfilariae
- The microfilariae circulate in the blood stream where they can be
picked up by a biting mosquito
- Adult worms can live for many years, continuously producing
microfilariae and contributing to ongoing transmission of the disease
- Acquired by bite of a blackfly – insect-borne parasites are difficult to
control
- Symptoms
o Parasites are lodged in the lymphatic system
o Many people are asymptomatic and there is slow damage to
the lymphatic system
o Causes lymphedema – filarial worms obstruct the lymphatic
system and cause swelling – usually in legs, arms, breasts, and
genitalia
o Can be associated with high fever every 8-10 weeks
o Enlarged lymph nodes and inflammatory response to live and
dead parasites
- Diagnosis
o Presence of microfilaria in blood samples collected at night
- Treatment
o DEC (Diethylcarbamazine) for 14 days kills the adult worms
- Vector – mosquitos
- Life Cycle
o L3 larve form called filariform larvae enter the human body
during a mosquito bite
o They enter through the bite wound and migrate lymphatic
vessels and lymph nodes
o Take ~1 year to mature
o Adult females produce larvae called microfilaria (measuring
~250um)
o Microfilaria move actively in the lymphatic and blood system
o Mosquitos are infected during a blood meal
o 10-14 days traverse mosquito and become infective for man
in the mosquito
-
The Global Program to Eliminate Lymphatic Filariasis
(elephantiasis)
MICROBIOLGY – Sue V – Parasitology
o In 2008, 496 million people were treated in a mass drug
administration program
o China and Republic of Korea no longer an endemic problem
o There are 81 countries listed as endemic for lymphatic
filariasis
o 2 billion tablets of DEC have been donated to WHO by Eisai
for 2013-2020
o The drugs are safe and are given to everyone in each area –
this must be repeated for 4-6 years
o WHO estimates if levels of drug therapy are maintained then
elimination can occur in Pacific Islands (not Papua New
Guinea) by 2015
o By 2017, the goal is to have 70% of 81 endemic countries to
have stopped drug therapy and be in a surveillance stage
o By 2020, 100% of all endemic countries will be certified free
from disease
Onchocerca volvulus (Blinding filariasis; river blindness)
- Caused by a Helminth worm
MICROBIOLGY – Sue V – Parasitology
o The scolex (head) contains sucksers and hooks
o Proglottids form the ribbon-like body
o Eggs are produced in each proglottid
o Eggs are released when proglottids are broken down by
digestive enzymes in the host
o Each proglottid is 18x6cm
o Eggs are 35x45 micrometers
o Cestodes can have 3-3000 proglottids
Tenia solium (Pork Tapeworm) & T (Beef Tapeworm)
- Worldwide distribution – highest in developing countries
- As high as 10% in the developing world
- T. saginata are 4-6 meters long
- T. solium are 0 meters long
- Life Cycle
o Transmission occurs with feces contaminated – with eggs
that are eaten by cows or pigs
o Larval cyst called a cystercerci is ingested with poorly cooked
infected meat
o Larvae escape the cyst and pass to small intestine and attach
to the mucosa
o Worm develops over 3-4 months proglottids of the body
develop
o Adult can live in the small intestine for as long as 25 years
o Eggs or proglottids release in stool
Symptoms
o Light infections remain asymptomatic
o Heavier infections – abdominal discomfort, vomiting, and
diarrhea
Diagnosis
o Recovery of eggs or proglottids in stool or from the perianal
area
Treatment
o Praziquantel
Control
o Cysticerci do not survive temperatures <10 degrees C and >50
degrees C
Cysticerosis – neglected tropical disease
- Affecting areas of the world with poor sanitation
MICROBIOLGY – Sue V – Parasitology
- Embryonated eggs ingested by Human
- Ocosperes hatch and circulate
- May develop in any organ including brain and eyes
- Major cause of epilepsy - ~29% of people with epilepsy in some part
of the world have cysticercosis
- Cerebral cysticercosis can be as high as 1 per 1000
- Auto-infection is common – someone with a tapeworm infects
themselves with eggs from their tapeworm
- Number of active Cysticercosis cases with epilepsy/neurological
disorder
o Africa – 0.31-4 million
o India – ~1 million
o Latin America – 0 – 1 million
o Mexico – 144,433
- A clear strategy for controlling this disease worldwide is still in
progress
- Elimination of cysticercosis requires improvements in sanitary
conditions, especially prevention of open defecation
- Chemotherapy for humans, pig husbandry and pig treatment
combined with vaccination using a newly developed recombinant
vaccine
- A validated strategy for the control and elimination of Taenia solium
taeniasis/cysticercosis will be available by 2015; and interventions
for control and elimination scaled up in selected countries in Africa,
Asia, and Latin America by 2020
- Chemotherapy for humans, pig husbandry and pig treatment
combined with vaccination using a newly developed recombinant
vaccine for pigs
Treatment
o Human cysticercosis is difficult to treat
o Long courses with praziquantel and/or albendazole, as well
as supporting therapy with corticosteroids and/or antiepileptic drugs, and possibly surgery
Control
o Wash hands with soap and warm water after using the toilet
and before handling food
o Teach children the important of washing hands to prevent
infection
o Wash and peel all raw vegetables and fruits before eating
o Avoid raw vegetables and fruits that cannot be peeled when
traveling in developing countries
Life Cycle
Trematodes – Flukes
MICROBIOLGY – Sue V – Parasitology
- High risk population categories:
o School age children
Children between age 6-15
Swim and play in nearby lakes or irrigation channels
Spend long hours in the water where their entire
bodies are exposed
o Women
Carry out household work of collecting water,
washing clothes, utensils etc.
Particularly important when pregnant
o Fishermen/irrigation workers
Occupations involving contact with water – more
exposed to infection and should be treated as a highrisk group
- Control Strategies (WHO)
o Over 200 million people require treatment for schistosomiasis
yearly
o In 2012, more than 35 million people were treated for
schistosomiasis – 83% were Sub-Saharan African
o Praziquantel is available free of change to a few high-disease
burden least developed countries (LDC)
o Studies in China and Egypt show that mass treatment in
infected areas without individual diagnosis can give
significant impacts on infection
o Treatment several times during childhood is likely to prevent
disease in adulthood and reduced requirements for
praziquantel
o Even with this generous drug donation – this is not enough to
eliminate the disease
o WHO targets
By 2015, Schistosomiasis eliminated from Eastern
Med, Caribbean, Indonesia, and Mekong River Basin
By 2020, selected countries in Africa will have
eliminated Schistosomiasis
Helminths – Social and economic impact of parasitic worm diseases
- Incapacitate people so they are unable to work
- Families and children suffer poverty and malnutrition due to patient
unable to work
- Impairs physical growth
- Children are weak and suffer general malaise
- Education suffers
Modes of Infection
- Contaminative
o Where personal hygiene and community sanitation is lacking.
Cysts or eggs remain infective for long periods in
contaminated soil
- Soil or water-borne
o Difficult to control
o Children eat dirt, which can contain eggs, etc.
o Certain larvae can penetrate skin of bare feet or enter skin in
infested water
o Education and sanitary control of waste is best means of
prevention
- Food-borne
o Inadequately cooked beef, pork, fish, shell fish, and some
vegetables can be sources of infection
- Arthropod-borne
o The most difficult of all to control; often produces disease that
are fatal.
o More commonly found in moist tropical areas of world
o Mosquitoes transmit malaria, etc.
Parasitic damage to host
- Trauma – damage to tissues, intestine, liver, eye
- Lytic action – activity of enzymes elaborated by organism
- Tissue response – localized inflammation, eosinophilia
- Blood loss – heavy infection with hookworm may cause anemia
- Secondary infections – weakened host susceptible to bacterial
infection, etc.
MICROBIOLGY – Sue V – Parasitology
Kinetoplastida Parasites (Protozoan parasite)
- All neglected tropical diseases
o Trypanosoma brucei – Trypanosomiasis (African sleeping
sickness)
o Trypanosoma cruzi – Chagas disease
o Leishmani sp. – Leishmaniasis
- Complex life cycles alternating between a mammalian host and
insect vector
African Sleeping Sickness (Trypanosomiasis) – Trypanosoma brucei
- African trypanosome cell types
o Trypomastigote
o Epimastigote
- Two major forms infect humans
T. brucei rhodesiense
T. brucei gambiense
Insect vector
Glossina moritans
Glossina palpalis
Geographical range
East & Central Africa
West & Southern Africa
Transmission cycle
Ungulate-fly-human
Human-fly-human
Disease progression
Rapid progression to
Slow progression (1
death
year)
Asymptomatic carriers Rare
Common
o Trypanosoma brucei. rhodesiense
A rapidly progressing disease restricted to the eastern
third of the continent
o Trypanosoma brucei. gambiense
A slowly developing disease predominant in the
western and central regions of Africa
Accounts for ~95% of cases
o 100% fatal without treatment, ~10,000 per year die from the
disease
o A WHO neglected tropical disease
Life Cycle
o The infective, metacytic form of the trypanosome is injected
during a bite by the tsetse fly
o The organism transforms into the trypomastigote dividing
bloodstream form
o Trypomastigotes can traverse the walls of blood and lymph
capillaries into the connective tissues
o Can cross the choroid plexus (BBB) into the brain and
cerebrospinal fluid
o The organism can be transmitted through blood transfusion
o Differentiates into a non-dividing ‘stumpy’ form that can
survive in the tsetse fly vector
Sleeping sickness
o Trypanosomes multiply in the tissue around the initial bite
site
MICROBIOLGY – Sue V – Parasitology
Antigenic Variation
o Occurs in viruses, bacteria, and eukaryotic parasites
o Trypanosomes are covered with a dense surface coat
o This is composed of VSG (variable surface glycoprotein)
o Variant specific antisera strongly react with VSG
o Surface coats from different clones are antigenically distinct
Antibodies cannot gain access to other surface molecules
o VSG dimers form a densely packed surface coat
o Other (non-variant) proteins like transferrin receptor or
hexose transporter are hidden in this coat
o Antibodies only raised against VSG
Trypansomes harbor ~1000 different VSG genes
-
o The genomic organization of trypanosomes is complex with
20 chromosomes and 100 mini chromosomes
o 6-10% of the total DNA is coding for VSGs (~1000 genes)
o Many (but not all) VSG genes are present on the 100 mini
chromosomes
o Only one is expressed at a time
o The parasite can switch between VSG variants, drawing
from a very large repertoire of VSG genes (>1500)
VSGs are expressed from telomeric expression sites
o Active VSG genes are found in expression sites
o Genes are read in (~20) expression sites like tapes in a tape
recorder but only one recorder is playing at a time
Life Cycle Stages in Humans have VSG
Introduction to antigen variation
o Acquired Immunity
Depends on antibody-antigen interaction
o Antigenic Variation
Exists as a system employed by various
micropathogens to evade acquired immunity and
required the continuous expression of antigenic
MICROBIOLGY – Sue V – Parasitology
variants that have not been encountered by that
host’s immune system
o The African trypanosome, Trypanosoma brucei, a classic
paradigm for parasite antigenic variation
o Vaccines are impossible to produce due to antigenic
variance
Chagas Disease (American trypanosomiasis) – Trypanosoma cruzi
- Single celled protozoan parasite
- Causes American tyrpanosomiasis or Chagas disease
- WHO neglected tropical disease
- Central and South America, stretching from parts of Mexico to
Argentina
- 7-8 million people infected by the parasite, 50 million are at risk
- Endemic in 21 Latin American countries
- About 50,000 people die each year from the disease
- Transmission
o Latin America and South America where the vector is found
o Triatomine bugs live in walls, roofs of homes
o Active at night and bite exposed areas of skins whist humans
are sleeping
o Human migration leading to cases worldwide
o 4 ways
Food contaminated with triatomine feces
Blood transfusion from infected donors (blood
screening is necessary to avoid transmission)
Infection from mother to baby
Organ transplant
- Life Cycle
Vertebrate host cell invasion and infection persistence
o Flagellated metacyclins enter host cells
o Differentiate into amastigotes once invaded and divides
o Either egress from cells as amastigotes and re-infect local
cells OR differentiate into flagellated trypomastigotes within
host cells then egress and enter the bloodstream
o Triatomine bug hides inside any nucleic ell in the body
Symptoms
o Primary lesion:
Called a chagoma, appearing at the site of infection
Usually found on the face, eyelids, cheeks, lips or the
conjunctiva, but may occur on the abdomen or limbs
o Acute stage:
Appears 7-14 days after infection
Restlessness, sleeplessness, malaise, increasing
exhaustion, chills, fever, bone and muscle pains
Death occurs in 5-10% of infants
o Chronic stage:
Cardiac arrhythmia is common
MICROBIOLGY – Sue V – Parasitology
o Cutaneous leishmaniasis caused by Leishmania tropica
90% of cutaneous leishmaniasis cases occur in
Afghanistan, Brazil, Iran, Peru, Saudi Arabia and
Syria
Produces a papule (sore), 1-2 weeks (or as long as 1-2
months) after the bite
The papule gradually grows to form a relatively
painless ulcer
The ulcer heals in 2-10 months, even if untreated but
leaves a disfiguring scar
Disease may disseminate in the case of depressed
immune function
o Mucocutaneous leishmaniasis – L. braziliensis, L. mexicana
The initial symptoms of mucocutaneous leishmaniasis
are the same as those of cutaneous leishmaniasis
Later the organism can metastasize and the lesions
spread to mucoid (oral, pharyngeal, and nasal) tissues
Leads to destruction of the area and causes severe
deformity
o Visceral leishmaniasis – Leishmania donovani (most serious
disease)
Found in mononuclear phagocytic cells of spleen, liver,
lymph nodes, bone marrow, intestinal mucosa, and
other organs
Gets taken up by the macrophage and hides inside it –
the irony – macrophage is supposed to protect you
1-4 months after infection occurrence of fever, with
daily rise to 38-40 degrees C, accompanied by chills
and sweating
Spleen and liver progressively become enlarged
Skin develops hyper-pigmented granulomatous areas
(kala-azar means black disease)
Chronic disease renders patients susceptible to other
infections
Untreated disease results in death
- Visceral Leishmaniasis and HIV
o Leishmaniasis suppresses the immune system and increases
the onset of AIDS
o HIV infection increases the risk of developing active VL by
between 100 and 2320 times
o In southern Europe, up to 70% of cases of visceral
leishmainiasis in adults are associated with HIV infection
Leishmania sp. live inside macrophages
o Macrophages phagocytose parasites for destruction
o In macrophages destruction of a foreign antigen occurs when
lysosomes fuse with foreign antigen
o Leishmania parasites form a parasitophorous vacuole
o This vacuole is resistant to lysosomal damage
o Parasites continue to divide and eventually the cell burst
open
Diagnosis
o Cutaneous & mucocutaneous leishmaniasis isolation of the
organisms from the lesion aspirate or biopsy
o Visceral leishmaniasis – identification of amastigotes in a
blood smear
Treatment
o Pentostam or amphotericin B
o A course of intravenous injections
Control Strategies
o Controlling epidemics e. recent one in South Sudan (20092011)
o 25000 cases and caused more than 700 deaths
o Kept the mortality rate to show 5% compared with 35% in
the epidemic that occurred during the 1990s
o Better access to medicines – in December 2011, WHO signed
an agreement for the donation of 445,000 vials of liposomal
amphotericin B to treat visceral Leishmaniasis
o Regional elimination – 100% case-detection and elimination
in the Indian subcontinent by 2020
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