Download tropical diseases and clinical parasitology

The University of Medical Sciences
in Poznań
Department and Clinic of Tropical
and Parasitic Diseases
Head of the Department: Prof. Jerzy Stefaniak, MD, PhD
TROPICAL DISEASES AND CLINICAL PARASITOLOGY
Course for English Speaking Students
2012/2013
A Guide for the Students
Course coordinator:
Elżbieta Kacprzak, MD PhD
Karolina Mrówka, MD
Dear Students,
The head and the staff of the Department and Clinic of Tropical and Parasitic Diseases welcome all of
you to the lectures and exercises on clinical parasitology, including elements of tropical diseases and
international health. The course on clinical parasitology is the continuation of the basic course on
parasitology, being a part of microbiology and constitutes an essential part of the course on infectious and
parasitic diseases. The program was arranged to keep a balance between the theoretical knowledge and
practical skills. It is also concentrated on some selected syndromes and diseases, which we do accept as
the most important for a future general practitioner. The course on clinical parasitology includes:
 hours of lectures
 hours of practice in the ward
 hours of seminars on the case study and video presentations
 hours of the laboratory practice
 hours of individual study with help of a CD-ROM program on malaria.
The course ends with a test, if it is unsatisfactory it should be repeated at a later term.
At the end of the course the student is expected to:
 have a basic knowledge of the most important parasitic and tropical diseases

understand the pathological mechanisms responsible for the diseases as well as the most important
ways of the transmission of an infection

be able to choose the proper diagnosis procedures and treatment schedules

be prepared for broadening her/his practical knowledge in a self-study process and, of course

pass the examination in the US related to the infectious and parasitic diseases.
It is expected that the students will have their own white protective clothes, at least when approaching
patients and in the laboratory. Smoking and eating is not allowed in the Clinic. The lectures and the
seminars will be carried out in the Rydygier Auditorium. The other activities will be run in the
Department and Clinic of Tropical and Parasitic Diseases located in the main building of the University
Teaching Hospital No 2, Przybyszewskiego Street 49, on its second floor. Phone number to the Clinic is
8691-360 or 8691-363. The Rydygier Auditorium is located in the University Hospital No 2 on the first
floor, next to the hospital chapel.
The staff of the Department will be ready to help you in the learning process and to assist you in your
specific interest:
Jerzy Stefaniak, MD PhD Prof. – Head of the Department (tropical and parasitic diseases)
Elżbieta Kacprzak, MD PhD – Assistant (tropical diseases, travel medicine)
Małgorzata Paul, MD PhD – Assistant (European Network on Toxoplasmosis)
Łukasz Pielok, MD PhD – Assistant (echinococcosis)
Clinton Muoto, MD – Assistant (tropical diseases, Nigeria)
Karolina Mrówka, MD PhD student – Assistant
Zbigniew Pawłowski, MD PhD DTMH – Guest (tropical diseases, WHO expert)
Hanna Mizgajska, MD PhD – Guest, Head of Department of Biology and Environmental Protection,
University of Physical Education (toxocarosis)
Mateusz Cofta M.Sc, PhD student – Assistant (humanitarian aid)
Time table
The exact time-table and list of facilitators responsible for the lectures, seminars and exercises are
attached as an annex of the Guide.
Rules and principles at the Department
Note that all students have to wear protecting clothes and their own shoes during the exercises. Students
who will not wear protecting clothes and shoes will be not allowed to attend the seminars and exercises in
the Clinic.
It is strictly forbidden to bring any meal to the Clinic.
Jackets can be kept in the cloak-room next to the Rydygier Auditorium.
Any personal belongings can be kept in the Clinic in a special cupboard. The key for the cupboard is
available in the Clinic Secretary Room and should be given back after the exercises. The Clinic is not
responsible for the belongings deposited in the cupboard.
Students’ responsibility is to complete the course on clinical parasitology and tropical diseases and
to know evaluation rules.
1. Attendance at the clinical session, seminars and lectures is compulsory.
2. The students are allowed not to attend 3 hours of the course without any written excuse. Any longer
absence needs a written excuse. Without such excuse the student will be not allowed to write the test
exam. The written excuse has to be handed in to the Course Coordinator.
3. Students who miss more than one day of the program have to repeat the course with the other group.
4. All the students who attend the seminars, lectures and exercises need to get a sign from the facilitators
on the “Student Card”. The completed set of signatures from facilitators confirming activity of the
students during the course will be used to allow the student to participate in the test.
5. The Head of the Department will make the final evaluation of the student on the basis of the results of
the test, feedback given from the facilitators about the students’ activity during the course and
discussion on a topic chosen by the Professor.
6. The student who will not pass the test need to repeat the written exam before the final evaluation in
the term pointed by the Course Coordinator.
The written exam will be organized on the last day of the course. It will consist of 30 questions.
Any problems regarding organizational issues during the course should be reported to the Course
Coordinator.
List of recommended books:
1. Manson-Bahr P.E.C.: Manson Tropical Diseases, 21-th edition 2002.
2. Manal B.K., Wilkins E.G.L., Dundar E.M., Mayon-White R.T.: Lecture notes on infectious diseases,
1996.
3. Gillespie S.H., Person R.D.: Principles and practice of clinical parasitology, 2001.
4. Bell Dion R.: Lectures Notes on Tropical Medicine, 1990.
1. FIRST COURSE COORDINATOR: Elżbieta Kacprzak, MD PhD
2. FIRST COORDINATOR E-MAIL ADDRESS: [email protected]
3. SECOND COURSE COORDINATOR: Karolina Mrówka, MD
4. SECOND COORDINATOR E-MAIL ADDRESS: [email protected]
5. COURSE COORDINATOR CONSULTING HOURS: every Wednesday 11-13 pm (make an
appointment by writing an e-mail or calling 61-8-691-766)
6. DATES OF FINAL TESTS: Friday 5.10.2012, 12.10.2012, 7.12.2012, 14.12.2012, 18.01.2013,
15.02.2013, 1.03.2013, 24.05.1013;
7. DATES OF REPETITION TESTS: every Friday 1 and 2 weeks after the final test , which is: 12.
and 19.10.2012, 19. and 26.10.2012, 14. and 21.12.2012, 21. and 28.12.2012, 25.01. and 1.02.2013,
22.02 and 1.03.2013, 8. and 15.03.2013, 31.05 and 7.06.2013.
The staff of the Department and the Clinic of Tropical and Parasitic Diseases wish you to be
satisfied with your results after the final evaluation and further success in your medical career.
SCHEDULE OF THE COURSE
TROPICAL DISEASES AND CLINICAL PARASITOLOGY
Time
Subject
Facilitator
Room
Monday
09.00 - 09.45
09.45 - 11.15
11.15 - 12.00
12.00 - 12.30
12.30 - 14.00
14.00 - 14.45
12.30 - 14.45
Introduction to tropical diseases /seminar/
Malaria /seminar/
Trypanosomiases /seminar/
Lunch break
Group A: Malaria diagnosis in practice /exercise/
Group A: Diagnosis of intestinal parasitoses /exercise/
Group B: Tropical diseases in computer programs /exercise/
J. Stefaniak
K. Mrówka
M. Paul
Anaesthesiology Clinic
Anaesthesiology Clinic
Anaesthesiology Clinic
M. Paul, K. Mrówka
K. Mrówka, M. Paul
C. Muoto
Laboratory
Laboratory
Library Patomorphology
Tuesday
09.00 - 09.45
09.45 - 10.30
10.30 - 11.15
11.15 - 12.00
1230 - 12.30
12.30 - 14.00
14.00 - 14.45
12.30 - 14.45
Eosinophilia in parasitic diseases /seminar/
Trichinellosis /seminar/
Schistosomosis /seminar/
Tropical filarioses /seminar/
Lunch break
Group B: Malaria diagnosis in practice /exercise/
Group B: Diagnosis of intestinal parasitoses /exercise/
Group A: Tropical diseases in computer programs /exercise/
K. Mrówka
Ł. Pielok
C. Muoto
C. Muoto
Anaesthesiology Clinic
Anaesthesiology Clinic
Anaesthesiology Clinic
Anaesthesiology Clinic
M. Paul, K. Mrówka
K. Mrówka, M. Paul
C. Muoto
Laboratory
Laboratory
Library Patomorphology
Wednesday
09.00 - 10.30
10.30 - 10.45
10.45 - 11.30
11.30 - 12.15
12.15 - 13.00
13.00 - 13.30
13.30 - 15.00
Echinococcosis and alveococcosis /seminar/
Break
Toxoplasmosis /seminar/
Congenital toxoplasmosis /seminar/
Amoebosis /seminar/
Lunch break
Practice in the ward /exercise/
Ł. Pielok
Anaesthesiology Clinic
M. Paul
M. Paul
C. Muoto
Anaesthesiology Clinic
Anaesthesiology Clinic
Anaesthesiology Clinic
K. Mrówka, Ł. Pielok,
C. Muoto
Clinic
K. Mrówka, Ł. Pielok,
C. Muoto
Clinic
M. Paul
Ł. Pielok
M. Paul
Anaesthesiology Clinic
Anaesthesiology Clinic
Anaesthesiology Clinic
K. Mrówka, Ł. Pielok,
C. Muoto
Clinic
K. Mrówka, Ł. Pielok,
C. Muoto
Clinic
M. Cofta
K. Mrówka
M. Paul
K. Mrówka
M. Paul
Anaesthesiology Clinic
Anaesthesiology Clinic
Anaesthesiology Clinic
Anaesthesiology Clinic
Anaesthesiology Clinic
15.00 - 15.15 Break
15.15 - 16.45 Practice in the ward /exercise/
Thursday
09.00 - 10.30
10.30 - 11.15
11.15 - 12.00
12.00 - 12.30
12.30 - 14.00
Leishmaniases /seminar/
Cysticercosis /seminar/
Cases of tropical diseases /seminar/
Lunch break
Practice in the ward /exercise/
14.00 - 14.15 Break
14.15 - 15.45 Practice in the ward /exercise/
Friday
09.00 - 09.45
09.45 - 10.30
10.30 - 11.15
11.15 - 12.00
12.00 - 12.45
12.45 - 13.00
13.00 - 14.30
Report from Polish Medical Center in Tanzania /seminar/
Cholera: an example of epidemic disease /seminar/
Review (case presentation) /seminar/
Test
Discussion on the test answers /seminar/
Break
Summary, oral exam and closing session
J. Stefaniak, E. Kacprzak Clinic, Professor Office
ASCARIDOSIS
1. ETIOLOGICAL AGENT:
 parasitic nematode Ascsaris Lumbricoides
 parasites in small intestine
2. CLINICAL SYMPTOMS:
 alimentary system: diarrhea/constipation, bowel obstruction, appendicitis, cholelithiasis
 respiratory system: cough, dyspnoe – ascaris pneumonitis
 allergic symptoms: asthma, chronic urticaria
3. DIAGNOSIS:
 stool examination (eggs)
 duodenal endoscopy
 eosinophilia (during larvae migration)
4. TREATMENT: albendazole, mebendazole (SINGLE DOSE)
TRICHUROSIS
1. ETIOLOGICAL AGENT
 parasitic nematode (Trichuris trichiura – Whip worm)
 parasites in large intestine
2. CLINICAL SYMPTOMS:
 haemorrhagic colitis
 prolapse of anus
 growth inhibition in children
3. DIAGNOSIS:
 stool examination (eggs)
4. TREATMENT: albendazole, mebendazole for 3 day
HOOKWORMS INVASION
1. ETIOLOGICAL AGENT:
 nematode: Necator Americanus, Ancylostoma Duodenale
 parasites in a small intestine
2. CLINICAL SYMPTOMS: SYNDROM OF MIGRATING SKIN LARVAE, anemia
3. DIAGNOSIS:
 stool examination (eggs)
 duodenal endoscopy
 eosinophilia (during larvae migration)
4. TREATMENT: albendazole, mebendazole for 5 days
TAENIASES
1. ETIOLOGICAL AGENT :
 Taenia saginata (unarmed tapeworm), Taenia solium (armed tapeworm)
 parasites in small intestine (jejunum)
 way of invasion: eating raw or undercooked meat
2. CLINICAL SYMPTOMS:
 weakness
 lost of weight
 stomachache
 nausea
 increased/decreased appetite
 expelling gravid proglottids
3. DIAGNOSIS:
 stool examination (PROGLOTTIDS)
4. TREATMENT: praziquantel
5. SEQUELAE OF T. SOLIUM INVASION: cysticercosis
TRICHINELLOSIS
1. ETIOLOGICAL AGENT:
 parasitic nematode of the genus Trichinella (8 species and 3 genotypes):
encapsulated and non encapsulated species
 occurs on all continents except Antarctica
 circulates in cycles of sylvatic and synantropic animals
 animal reservoir: mammals (carnivorous and omnivorous), birds (T. pseudospiralis),
reptiles
 way of invasion: eating raw or undercooked meat
Species
T. spiralis
T. nativa
Genotype Host
T1
Mammals
T2
Mammals
T6
Mammals
Distribution
T3
Mammals
T8
Mammals
Cosmopolitan
Arctic and subarctic regions of America, Europe and Asia
Arctic and subarctic regions of America
Temperate areas of Europe and Asia, Northern and Western
Africa
South Africa and Namibia
T4
Mammals and birds
Cosmopolitan
T. nelsoni
T5
T9
T7
Temperate areas of North America
Japan
Eastern and Southern Africa
T. papuae
T10
T. zimbabwensis
T11
Mammals
Mammals
Mammals
Mammals and
reptiles
Mammals and
reptiles
T. britovi
T.
pseudospiralis
T. murrelli
Papua New Guinea
Africa South of the Sahara
2. LIFE CYCLE:
ENTERAL PHASE:
muscle tissues are ingested in the stomach and larvae are released – – larvae penetrate
the intestinal mucosa of the small intestine – – larvae reach adult stage within 48 h post
infection – – male and female mate – – female worm releases new borne larvae (NBL)
in lymphatic vessels after next 5-6 days
PARENTERAL PHASE:
new borne larvae reach striated muscles and penetrate the muscle cell – – larvae grow to
infective stage in nurse-cell (former muscle cell) – – after a period of time nurse-cell
calcifies
3. SYMPTOMS:
ACUTE PHASE:
 diarrhoea
 fever
 periorbital and facial oedema
 conjunctival and subungunal haemorrhages
 myalgia
CHRONIC PHASE:
 general discomfort
 chronic pain of muscles
 persistent formications
 numbness
 sweating
 impaired muscle strength and coordination
 IgG in serum
 bioelectric muscle disturbances
 inflamatory cells in muscles
COMPLICATIONS (within first 2 weeks of symptoms):
 cardiological
 neurological
 ocular
 respiratory
 digestive
4. DIAGNOSIS:
 interview: time and frequency of consumption of infected meat, time of onset of
symptoms, way meat’s been treated, consumption of alcohol
 physical examination
 non specific blood tests: leucocytosis, eosinophilia, elevated muscle enzymes,
electrolytes disturbances (hypokalaemia), hypoproteinemia, hypoalbuminemia
 specific blood tests: serological test
 muscle biopsy (trichinoscopy, artificial digestion)
5. TREATMENT:
 antihelmintics (albendazol, mebendazol, pyrantel)
 glucocortycosteroids
 pain killers
 fluids and electrolytes infusion
7. PREVENTION: meat inspection, and hygiene and legislation
ECHINOCOCCOSIS
1. Echinococcosis is a zoonotic disease caused by tapeworm Echinococcus granulosus.
2. Adult form, reaching up to 17mm in length, lives in the small intestine of the canine, which
are the definitive hosts.
3. Herbivores becomes intermediate hosts by ingesting echinococcal eggs, containing larvae,
which penetrate the wall of the intestine and form a hydatid cyst in liver (70%) lungs (20%)
or other organs.
4. Hydatid cysts are composed of the pericyst (host’s fibrotic tissue) and endocyst (parasite’s
germinal layer), producing protoscolices - invasive forms for the canine.
5. Life cycle of the Echinococcus granulosus
6. WHO classification of the hydatid cysts in the liver in US imaging
7. DIAGNOSIS:
 anamnesis (contact with dogs, breeding sheeps etc.), symptoms (absent for years)
 imaging techniques: US, CT, MRI
 serological tests: ELISA (70%), Western- blot (98%)
 Fine Needle Aspiration Biopsy (FNAB) - protoscolices, antigen 5
8. TREATMENT:
 albendazol chemotherapy up to 90 days
 surgery with albendazol antihelmintic cover
 PAIR (Puncture Aspiration Injection Reaspiration)
 watch and wait
9. PREVENTION:
 treatment of the affected dogs
 avoiding feeding dogs on raw offal
 washing hands, raw vegetables and fruits
 avoiding contact with soil without protecting gloves
ALVEOCOCCOSIS
1. Alveooccosis is a rare zoonotic disease caused by tapeworm Echinococcus multilocularis.
2. Adult form of the tapeworm, lives in the small intestine of the foxes, which are the
definitive hosts.
3. Herbivores, rodents, and accidentally people become intermediate hosts by ingesting
invasive eggs, containing larvae, which penetrate the wall of the intestine and settle down in
the liver in 99% of cases. Primary locations in lungs, brain or other organs are very rare,
though, the spillage of the process may occur.
4. Liver space occupying lesion in alveococcosis is usually irregular, grows in an infiltrative
way, affecting neighbouring tissues. Massive necrosis and calcifications are present; no
protoscolices are produced in humans.
5. Life cycle of the Echinococcus multilocularis.
6. DIAGNOSIS:
 anamnesis (contact with foxes, living next to forest, eating blueberries, mushrooms
etc.) symptoms (absent for years, rarely sudden onset with cachexia, jaundice,
ascites, loss of weight; symptoms similar to primary liver neoplasm)
 imaging techniques: US, CT, MRI (lesions often indistinguishable with hepatoma)
 serological tests: ELISA (70%), Western-blot (98%)
 histopathology (PAS)
7. TREATMENT:
 albendazol chemotherapy, lifelong
 surgery with albendazol antihelmintic cover
 prognosis is poor
8. PREVENTION:
 avoiding foxes
 washing hands, raw vegetables and fruits
 avoiding contact with soil without protecting gloves
MALARIA
1. ETIOLOGICAL AGENT :
 intracellular protozoa (erythrocytes, hepatocytes)
 Plasmodium vivxt, P. ovale, P. malariae, P. falciparum, P. knowlesi
 way of invasion: bite of mosquito (Anopheless spp.)
 life cycle:
2. CLINICAL SYMPTOMS (benign/malignant malaria):
 weakness
 cold
 chils
 fever
 sweats
 splenomegaly
 hepatomegaly
 cerebral malaria: headache, impairment of consciousness, seizures, hypertonicity,
opistothonos, disconjugate gaze, nystagmus, lack of reflexes
 pulmonary insufficiency
 cardiovascular collapse
 acute kidney failure
 DIC
3. DIAGNOSIS:
 microscopy of thick and thin blood smear
 immunochromatographic test
 serological test
 PCR
 histopathological examination of liver samples (hemozoine)
4. TREATMENT:
 chloroquine
 mefloquine
 artemisine
 quinine
 PRIMAQUINE
5. PREVENTION:
 bed-nets
 repellents
 chemoprophylaxis
 mechanoprophylaxis
VISCERAL LEISMANIOSIS
1. ETIOLOGICAL AGENT :
 intracellular protozoa (macrophages)
 Leismania infantum (Mediterranean, Middle East, Central Asia, China),
L. donovani (East Africa, India), L. chagasi (Central and South America)
 way of invasion: bite of sand fly (Phlebotomus spp., Lutzomyia spp.)
2. CLINICAL SYMPTOMS:
 weakness
 lost of weight
 two-fold fever
 splenomegaly
 pancytopenia
 hepatomegaly
 lymphadenopathy
 depigmentation/hyperpigmentation of skin
3. DIAGNOSIS:
 microscopy of samples from spleen, bone marrow and lymph nodes (amastigota)
 buffy coat, blood smear (amastigota)
 culture on NNN medium (promastigota)
 serological test
 PCR
 urine antigen test (K26 & K23)
4. TREATMENT:
 pentavalent antimonials
 amphotericin B
 pentamidin
 miltefosine
 paramomycin
5. COMPLICATIONS: death rate 50-95%
6. PREVENTION:
 bed-nets
 repellents
CUTANEUOS & MUCOCUTANEOUS LEISMANIOSIS
1. ETIOLOGICAL AGENT :
 Old World: Leishmania tropica, L. eatiopica, L. major, New World: L. brasilensis,
L. guyanensis, L. panamensis
 clinical forms: cutaneus (CL), diffuse cutaneus (DCL), recidivans (LR),
mucocutaneus (ML)
 90% of CL in Afghanistan, Brazil, Iran, Peru, Saudi Arabia, Syria, 90% of ML Bolivia,
Brazil, Peru
 way of invasion: bite of sand fly (Phlebotomus spp., Lutzomyia spp.)
2. CLINICAL SYMPTOMS:
 CL: skin ulcer
 ML: granulomatous lesions in mucosa and cartilages of naso-oropharyngeal cavity
and ears
3. DIAGNOSIS:
 microscopy/histopathology/PCR/culture on NNN medium of samples from edge of
ulcer
 skin test (Montenegro test)
4. TREATMENT:
 ketoconazole/itraconazole/fluconazole
 topical amphotericin B
 paramomycin ointment
 heat treatment/cryotherapy
 pentavalent antimonials (intralesional in CL, intravenous in MCL)
AFRICAN TRYPANOSOMIASIS
1. ETIOLOGICAL AGENT :
 intracellular protozoa (macrophages)
 Trypanosoma brucei gambiense (West&Central Africa), T. brucei rhodensiense
(East&Southern Africa)
 way of invasion: bite of tse-tse fly (Glossina spp.)
2. CLINICAL SYMPTOMS:
 trypanosomal chancre
 local lymphadenopathy
 parasitaemia: fever, joint pain, pruritus, splenomegaly, Winterbottom sign
 CNS involvement: behavioral changes, psychiatric disorders, sleep disorders, speech and
motor function disturbations, tremor and spasticity of muscles
 weakness
 lost of weight
 death
3. DIAGNOSIS:
 microscopy of blood smear and CSF
 microscopy of samples from lymph nodes, bone marrow and chancre
(trypanosomes)
 card agglutination test
4. TREATMENT:
 suramin
 melarsoprol
 pentamidine
5. PREVENTION:
 bed-nets
 fly traps
AMERICAN TRYPANOSOMIASIS
1. ETIOLOGICAL AGENT :
 Trypanosoma cruzi
 way of invasion: bite of Triatoma spp. bug (rubbing feaces into wound or conjunctiva)
2. CLINICAL SYMPTOMS: acute/chronic
 chagoma
 Romana sign
 fever
 local lymphadenopathy
 splenomegaly
 hepatomegaly
 cardiac damage
 encepahalitis
 cardiac diseases: cardiomyopathy, heart rythm disturbances
 megacolon/megaoesophagus
3. DIAGNOSIS:
 microscopy of blood smear (trypomastigota)
 culture
 xenodiagnosis
 serological test
4. TREATMENT:
 nifurtinox
 benznidazole
5. PREVENTION:
 avoiding contact with soil
IMMUNOLOGICAL AND MOLECULAR DIAGNOSIS OF PARASITIC AND TROPICAL
INFECTIONS
Objectives:
1) To understand advantages and pitfalls related to serological diagnosis;
2) Discussion on the relationship between the clinical activity of infection and immunological
response of the patient;
3) Interpretation of serological results in patients returning from tropical countries;
4) To present detailed recommendations for the application of immunological and molecular
methods in the most common parasitic and tropical diseases.
Laboratory diagnosis of parasitic and tropical infections can be definitively made by a direct
identification of parasites in blood, stool specimens, body fluids or biopsy material. Such identification is
not generally possible in diseases, in which parasites are located deep in host tissues and invasive
techniques with an incontestable risk to the patients may be necessary to obtain biological material for
analysis. The detection of specific anti-parasite antibodies in a circulation or systemic fluids in an
immunocompetent host can be very useful as an indicator of immunological response of the patient to the
contact with parasite antigens. The positive result of a serological test is a marker of an exposure to the
parasite at some indeterminate time only and it necessitates the more detailed differentiation between the
current and past infection stage. The presence of specific immunoglobulin M (IgM) and/or IgA antibodies
speaks in favour of recent infection, similarly to an increasing level of IgG of a low avidity. The kinetics
of specific antibodies is variable and it depends on the infectious agent, intensity of invasion,
pathogenecity of the strain and immunological status of the patient; some of parasitic and exotic
infections induce persistent immunity when low IgG values are synthesized for many years or all the
patient’s life long (toxoplasmosis, visceral leishmaniosis). When IgG result is negative, the determination
of specific IgE, especially in helminth invasions of tissues may be required. Commercially available
immunodiagnostic kits based on Enzyme-Linked ImmunoSorbent Assay (ELISA) are widely used for
diagnosing toxocarosis, toxoplasmosis, echinococcosis, trichinellosis, and cysticercosis. The presence of
antibodies to Echinococcus requires more specialistic differentiation between echinococcosis and
alveococcosis using ELISA or Western blotting with E. multilocularis-specific antigens (Em2plus,
Em18). Indirect haemagglutination assay (IHA) is a test of choice for serodiagnosis of extra-intestinal
amoebosis. The indirect immunofluorescence assay (IFA) is helpful in a diagnosis of malaria in cases
with a low level of parasitaemia and no exposure to the Plasmodium prior to recent travel in
hyperendemic areas. Specific antigen detection assays using stool specimens (coproantigens, fecal
antigens) are recommended in infections with Cryptosporidium parvum, Entamoeba histolytica, Taenia
spp., Giardia intestinalis and microsporidia.
Rapid tests for antigens using monoclonal antibodies to P. falciparum histidine-rich protein-2 (HRP2) may be useful at the primary health level in malaria-endemic areas where microscopy is often
unavailable. Confirmation of the ocular or cerebral location of parasites is based on the detection of the
local synthesis of specific antibodies in intra-ocular or cerebrospinal fluid, respectively by
immunoblotting/comparative immunological profiles (toxoplasmosis, toxocarosis). Molecular biology
methods should be performed in reference centers to improve diagnosis of some parasitic infections when
laboratory information is unavailable through traditional techniques or immunological response of the
patient is impaired (strongyloidosis, cerebral toxoplasmosis). Analysis of parasite nucleic acids is strongly
recommended in patients suspected of malaria, leishmaniosis, Chagas’ disease, echinococcosis,
microsporidiosis and congenital toxoplasmosis.
CONGENITAL TOXOPLASMOSIS – PREVENTION AND TREATMENT
Objectives:
1) To demonstrate the seroepidemiological data of different countries in relation to the
potential risk of primary Toxoplasma gondii infection during pregnancy;
2) To understand the principles of national screening programmes for toxoplasmosis in
pregnant women and neonates;
3) Presentation of the variability in clinical expression of congenital T. gondii infection in
foetuses and newborns;
4) To understand the diagnostic criteria for a final confirmation of congenital infection;
5) Discussion on the intensive, long-term anti-parasitic treatment of congenital Toxoplasma
infection;
6) Practical demonstration of pathognomonic signs and symptoms of clinically overt congenital
toxoplasmosis (transfontanel US, CT scan, eye fundus).
Toxoplasma gondii infection acquired during pregnancy by a non-immune woman constitutes a
risk of fetal transmission with potentially serious damages and sequelae for a fetus or newborn. Most
infections in the mother cause non-specific symptoms if any, and most infections are recognized
accidentally by only serological testing. The clinical pattern of congenital Toxoplasma infection varies
from an asymptomatic presentation to a clinically overt disease of a fetus or neonate with a risk of late
development of new complications until adolescence and early adult life. Psychomotor retardation and
secondary eye lesions leading to severe vision impairment, including blindness may pose significant
health problems in young people during the developmental period. The great majority of infants born
with toxoplasmosis are asymptomatic or have the disease that is not detected by the routine neonatal
examination at birth, but careful ophthalmologic examination may reveal evidence of chorioretinitis in
otherwise asymptomatic infants. The ability of the parasite to cross the placenta depends on the
anatomic characteristics of the placenta, which change with the stage of gestation. The total maternalfetal transmission rate is about 30% throughout all pregnancy, but varies from 6% at 13 weeks to 72%
at 36 weeks. Foetuses infected in early pregnancy are of a higher risk of manifesting clinical signs of
infection. Infections in the first trimester and early second trimester may lead to spontaneous abortion,
stillbirth or severe neonatal disease with a pathognomonic triad of clinical symptoms
(retinochoroiditis, intracranial calcifications, dilatation of lateral ventricles). Neurological sequelae
include seizures, developmental delay, enlargement of ventricular system or microcephalus, prominent
intracranial calcifications and rarely deafness. Brain calcifications are frequently periventricular, and
when they involve the aqueduct of Sylvius, with a subsequent hydrocephalus.
Approximately 75% of clinically apparent congenital toxoplasmosis manifests as visual impairment
caused by bilateral retinochoroiditis.
The final diagnosis is based on a detection of the parasites in amniotic fluid, fetal or neonatal blood or
body tissues, and the evidence of specific IgM and/or IgA antibodies in neonatal period, rising IgG
titres within the first 12 months of life or persistently positive IgG beyond the first year of life with or
without clinical signs of the classic triad (!).
The strategic approach for preventing congenital toxoplasmosis is strictly related to the incidence of
primary infection during pregnancy in a given area, resulting from the absence of specific antibodies in
women in the childbearing age group (susceptibility to infection). There are three available methods
for a prevention of Toxoplasma infection in the population at risk:
1)
Health education of pregnant women;
2)
Preconceptional serological screening of all women at procreative age, mandatory in France
and Austria, and strongly recommended in majority of European countries;
3)
Perinatal screening by using cord blood samples or neonatal screening based on peripheral
blood from newborns taken on Guthrie cards (PKU cards), practiced in New England,
Denmark, Poland, Sweden, and Brazil.
Long-term and intensive anti-parasitic treatment during the first year of life reduces the risk of late
retinochoroiditis or secondary neurological signs from > 85% to 5-8%. Impaired psychomotor
development may be improved by early treatment starting from the neonatal period.
TOXOPLASMOSIS – EPIDEMIOLOGY, CLINICAL EXPRESSION, DIAGNOSIS AND
TREATMENT
Objectives:
1) To understand the potential risk factors of Toxoplasma gondii infection and main transmission
routes in a human population in different countries;
2) Presentation of various clinical forms of acquired toxoplasmosis from the asymptomatic
infection to the clinically overt disease in immunocompetent and immunocompromised
patients;
3) To demonstrate the diagnostic possibilities for a confirmation of Toxoplasma infection,
including immunological criteria of recently acquired toxoplasmosis;
4) Discussion on clinical recommendations to anti-parasitic therapy in patients infected with
Toxoplasma;
5) Slide presentation of T. gondii developmental stages and clinical symptoms or signs due to
toxoplasmosis.
Toxoplasmosis is a protozoan infection caused by the obligate intracellular parasite Toxoplasma gondii.
The distribution of T. gondii is world-wide in all continents except Antarctica. The infection is usually
acquired orally or transplacentally, rarely by inoculation in a laboratory accident, by blood or leukocytes
transfusion, or less commonly through organ transplantation (bone marrow, heart, lungs). The disease may
also occur as the result of the recrudescence of the latent infection in immunocompromised individuals.
Humans may be infected either by eating the meat of animals containing infective tissue cysts or by inhaling
or ingesting sporulated oocysts excreted in the feces of domestic/wild cats from contaminated soil. The
relative risk of infection in the Europe, USA and Canada is considered to be higher from ingestion of
undercooked meat, but in societies with little meat in the diet oocysts are more important.
Most individuals positive for T. gondii antibodies have no history of a clinical syndrome that was
diagnosed as toxoplasmosis, leading to the supposition that most primary infections are asymptomatic or
unrecognized. The most common recognized finding is cervical lymphadenopathy, usually painless and
sometimes accompanied by low-grade fever. Toxoplasmic lymphadenitis may be evident for weeks, and
may need to be distinguished from lymphoma. The other common presentations is a mononucleosis–like
syndrom, which is characterized by fever, headache, malaise, lymphadenopathy, hepatosplenomegaly,
myalgia and lymphocytosis. The more severe manifestations of toxoplasmosis in persons with normal
immune function are rare and include pneumonitis, myocarditis, meningoencephalitis or polymyositis. The
most frequent condition predisposing to systemic toxoplasmosis is advanced HIV disease. Persons with
persistently less than 100 CD4+ T cells/l are at risk for reactivation of the previous infection.
Toxoplasmic encephalitis in AIDS is caused by a disruption of latent cysts in the central nervous system.
Other immunosuppressed persons at high risk are those treated for solid organ transplantation, especially
those without anti-T. gondii antibodies who have been given organs from T. gondii-positive donors.
Hodgkin’s disease and other lymphoma have been found to predispose to severe Toxoplasma infection.
In immunocompetent patients, toxoplasmic lymphadenitis is a self-limiting disease. Active
toxoplasmosis in immunocompromised patients (encephalitis, pneumonitis, disseminated infection) requires
therapy until symptoms resolve and for 4-6 weeks thereafter. Secondary prophylaxis or maintenance therapy
should be continued for the duration of immunosuppression.
TOXOCARA SPP. EGGS IN THE ENVIRONMENT AND ITS PUBLIC HEALTH IMPLICATIONS
Toxocara spp. is the most frequent nematode transmitted from animals to humans. It causes
zoonosis with variety of symptoms that commonly persist for 6-24 months as visceral infection (VLM Visceral Larva Migrans) or ocular infection often with permanent loss of visual acuity (OLM - Ocular
Larva Migrans). It is predominantly a disease of young children (2-7 years) but increasingly recognized in
adults. VLM results from the migration of Toxocara spp. larvae in the tissues of abnormal hosts such as
humans. Initially most larvae pass through the liver and lungs. This process may be associated with signs of
decreased appetite, abdominal pain, fever, hepatomegaly, coughing, wheezing and asthma. At this time it is
also usually characterized by an eosinophilia, increased WBC count, hypergammaglobulinaemia and
increase in level of antibodies to anti - A and anti - B blood group antigen. When subsequent exposure to T.
canis eggs can be avoided, the disease is self limiting. However if exposure persists or intensifies, other
organs can be invaded and the disease can be life threatening (invasion of myocardium or brain).
OLM results from the migration of larvae (single or more) in the eye. The presenting complains often
include loss of vision strabismus, leucocoria, a fixed pupil or a red eye. Sometimes the infection is
subclinical and it is only detected during a routine eye examination. The typical fundiscopic findings include:
either posterior retinochoroiditis with a hazy defined mass lesion associated with overlying inflammatory
cells in the vitreous or a peripherial intraretinal granuloma in an otherwise clinically normal eye.
Among people toxocarosis is a direct consequence of soil contamination with pets (dogs and cats)
and foxes faeces containing eggs of Toxocara spp. Seroprevalence surveys indicate that 3% to 7% of
healthy adults and 15% to 23% of children have antibodies to Toxocara.
Toxocarosis in the definitive host
In Poznan region toxocarosis was the most common parasitosis in dogs and cats with the prevalence
of 32% and 39% respectively. So, cats probably, disseminate in the environment more eggs than dogs. The
potentially important source of infection can also constitute T. canis in foxes especially when growing
number of the effected animals live more often close to the households. Specific hosts spread eggs in the
environment which become infective after about 20 days.
Toxocara spp. in paratenic hosts
Paratenic hosts can considerably support transmission of toxocarosis. Rat, mouse, hamster, guinea
pig, rabbit, sheep, pig, lamb, chicken are the examples of paratenic hosts of Toxocara spp. When larvae of
the parasite invade the brain it can change the behaviour of the hosts. Mice for example are more active, nor
afraid of the predator etc. The reaction of paratenic hosts for such infection facilitates transmission infection of definitive hosts.
Toxocara spp. eggs in the environment
Toxocara spp. eggs have thick and complex shell layers that protect them from the influence of
environmental factors. So, in favourable conditions - in the shadow, with proper temperature, enough
humidity and amount of oxygen - the eggs can stay alive in soil for several years, although the majority of
them perish during the first 6 months. The massive reproduction of Toxocara spp. (20 000 eggs for day) and
extreme resistance of eggs to adverse conditions contribute the cumulating of their infective stage in soil.
Among ecological factors important for successful completion of T. canis and T. cati life cycles there are
activity of biological vectors and the remaining of the eggs near the surface of the ground (after one year in loose sand soil - the eggs were found only in 3 cm thick layer). Moreover earthworms are the important
biological vector which support transmission of toxocarosis; living Toxocara spp. eggs are carried with
earthworms castings from deeper layers to the surface of the ground.
Toxocara spp. eggs were found in different countries of the world, in the soil of public and private
places such as: city backyards, country yards, playgrounds, parks.