Beruflich Dokumente
Kultur Dokumente
Parasitic Diseases
Yoes Prijatna Dachlan
Faculty of Medicine
Universitas Airlangga
Tropical Medicine:
Parasitology
Parasitic diseases
Zoonosis
(Yoes Prijatna Dachlan, 2015)
Key facts
Schistosomiasis is an acute and chronic disease caused by parasitic worms.
People are infected during routine agricultural, domestic, occupational and
recreational activities which expose them to infested water.
Lack of hygiene and certain play habits of school-aged children such as swimming
or fishing in infested water make them especially vulnerable to infection.
Schistosomiasis control focuses on reducing disease through periodic, large-scale
population treatment with praziquantel; a more comprehensive approach including
potable water, adequate sanitation and snail control would also reduce transmission.
At least 261 million people required preventive treatment for schistosomiasis in
2013.
More than 40 million people were treated for schistosomiasis in 2013
Symptoms of schistosomiasis are caused by the bodys reaction to the worms eggs
Intestinal
schistosomiasis
Urogenital
schistosomiasis
Species
Geographical
distribution
Schistosoma mansoni
Schistosoma
japonicum
Schistosoma mekongi
Several districts of
Cambodia and the
Lao Peoples
Democratic Republic
Schistosoma
guineensis and
related S.
intercalatum
Schistosoma
haematobium
Schistosoma species
Egg
Delayed-type hypersensitivity
An inflammatory granuloma forms with epithelial,
giant, plasma and eosinophil cells and fibroblasts.
There is subsequent fibrosis and calcification.
(Yoes Prijatna Dachlan, 2013)
Intestinal amoebiasis
Intestinal amebiasis is caused by the protozoan Entamoeba histolytica
Most infection is asymptomatic; clinical manifestations include amebic dysentery
and extraintestinal disease. Symptoms range from mild diarrhea to severe
dysentery producing abdominal pain, diarrhea and bloody stools
Amebiasis occurs worldwide; the prevalence is disproportionately increased in
developing countries because of poor socioeconomic conditions and sanitation
levels
Extraintestinal manifestations include amebic liver abscess and other more rare
manifestations such as pulmonary, cardiac, or brain involvement
The parasite exists in two forms, a cyst stage (the infective form), and a
trophozoite stage (the form that causes invasive disease)
Pathogenesis:Lysis of target cells via a contact-dependent mechanism; lysis of
target cells via a contact-dependent mechanism; formation of amebapores, a
family
of small peptides that can form pores in lipid bilayers, resulting in cytolysis of
infected cells
Diagnosis: Diagnostic techniques include microscopy, antigen detection, serology,
molecular techniques, and colonoscopy with histological examination
(Yoes Prijatna Dachlan, 2015)
Entamoeba histolytica
NCD
Malnutrit
ion
AIDS
A long-term
immunosuppre
ssive therapy
IMMUNOCOMPROMIZED HOSTS
OPPORTUNISTIC INFECTIONS
Pneumocystis carini, Toxoplasma gondii,
Leishmania spp, Trypanosoma cruzi,Plasmodium
spp, Giardia lamblia, Schistosoma spp,
Cryptosporidium parvum, Cyclospora
(Yoes Prijatna Dachlan, 2015)
CLINICAL DISEASE
pragmatically divided into three
categories
Disease amongst children in endemic
areas
Disease in pregnant women
Disease in non-immune individuals
(English,M., & Newton, C.R.J.C., 2005)
(Yoes Prijatna Dachlan 2015)
Holoendemic
Cerebral Malaria
Hyperendemic
Mesoendemic
Severe Anemia
Cerebral Malaria
Renal Failure
Hipoendemic
Unstable
Severe Anemia
1
3 4 5
10
20
40
60
PREGNANT WOMEN
exhibit
susceptibility
to P. falciparum infection
The
risk
of
infecti
on
ThrTTT
PARITY
Kontrol
P.falciparum
sebelum terpapar
obat artemisinin
48 jam
P.falciparum
dipapar obat
artemisinin
(Lilik Maslachah, 2013)
(Yoes Prijatna Dachlan, 2013)
Malaria Control
Public health control measures are the first line of defence to
protect people living in malaria risk areas. The control
measures that are recommended depend on the level of
malaria risk in an area.
Tools for the control of malaria include:
Long lasting insecticide-treated nets
Indoor residual spraying
Intermittent presumptive treatment of malaria in infants,
young children and those attending school
Intermittent presumptive treatment for pregnant women
Access to effective treatment for children with a fever
Capacity to detect, prepare and respond to early warnings for
epidemics
Education and communication
(Yoes Prijatna Dachlan, 2015)
Indicative of partial
immunity
Asymptomatic
malaria parasitemia
A known phenomenon
in malaria endemic areas
with high year-round
transmision
RDT
A low level of
Plasmodium parasites,
asexual
or
gametocytes
Being detectable in
the blood without the
individual being ill
(2009)
Taenia solium
(PL Chiodini, AH Moody, DW Manser, 2001
Atl Medical Helminthol & Protozool)
EPIDEMIOLOGY
Approximately 50 million people worldwide are estimated to have
cysticercosis infection. Cysticercosis is endemic in many regions of
Central and South America, sub-Saharan Africa, India, Asia,
Indonesia (Bali, Papua, Pulau Samosir)
The prevalence of cysticercosis varies within these countries and is
often higher in rural or periurban areas where pigs are raised and
sanitary conditions are suboptimal
In some such communities the rate of epilepsy approaches 3 percent,
and 25 to 40 percent of these cases have evidence of cysticercosis
Cysticercosis is transmitted by ingestion of T. solium eggs shed in the
stool of a human tapeworm carrier (figure 1). Following ingestion,
embryos (oncospheres) hatch in the small intestine, invade the bowel
wall and disseminate hematogenously to brain, striated muscles,
liver, and/or other tissues
Over a period of three to eight weeks, tissue cysticerci develop; these
consist of membranous walls filled with fluid and an invaginated scolex
(Yoes Prijatna Dachlan, 2015)
Invaginated scolex
T. solium
scolex T. solium
(Muller R, Wakelin D,
2002, Worms and
human disease, 2nd ed)
Cystic lesion
Cerebral cysticercosis: this 44-year-old woman from Kenya had recent-onset epilepsy(Bannister B,
Gillespie S, Jones J, 2006, Infection. Microbiol. & Management, 3rd ed)
Clinical Diagnosis
In general, parenchymal cysts are associated with
seizures and headache, while extraparenchymal cysts
are associated with symptoms of elevated intracranial
pressure (eg, headache, nausea, and vomiting) and
may be accompanied by altered mental status
DIAGNOSIS
CLINIC
IMAGING
IMMUNOLOGIC DATA
EPIDEMIOLOGIC DATA
Radiographic imaging :
Computed tomographic (CT) scan
MRI (magnetic resonance imaging)
Deteksi cysticercus :
NCC dan extraNCC
cerebral cortex atau brainstem
SEROLOGY
ELISA
CFT
RIA
HEMMAGLUTANITION
IMMUNOBLOT
Toxoplasma gondii
Toxoplasma gondii is a protozoan parasite that can infect many animals,
including humans. Most infections are silent and have no ill effect on the patient
The acute phase of this infection lasts for less than around ten days. The parasite
causes a very strong type-1 response focused on the interferon-gamma secreted
by the T lymphocytes. This immune response limits the tissue extension of the
parasite, ensuring the survival of the host, but, paradoxically, also aiding the
survival of the parasite by converting it into a bradyzoite, an intracellular
quiescent resistant form persisting in the muscle and brain tissues
Protozoa: Toxoplasma
gondii
tachyzoite
Definitive host (DH) Toxoplasma gondii : domestic cats and their relatives).
1 Unsporulated oocysts are shed in the cats feces. Oocysts take 1-5 days to sporulate in the
environment and become infective
2 Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil,
water or plant material contaminated with oocysts
3 Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural
and muscle tissue and develop into tissue cyst bradyzoites
4 Cats become infected after consuming intermediate hosts harboring tissue cysts
5
may also become infected with tissue cysts after ingestion of sporulated oocysts in the
environment
Humans can become infected by:
In the human host, the parasites form tissue cysts, most commonly in skeletal
muscle, myocardium, brain, and eyes
Diagnosis of congenital infections can be achieved by detecting T. gondii DNA in amniotic fluid
Acute toksoplasmosis
Latent toksoplasmosis
Cutaneous toxoplasmosis
Skin lesions may occur (rarely): roseola, erythema multiformelike eruption, prurigo-like nodule, urticaria, maculopapula
EMERGING ZOONOSES
Indirect transmission : the infection of animal require
the presence of an intervening vector, or a specific
arthropod vector, and to carry it to human
vertebrate animals
Indirect transmission :
e.g.
West Nile,
Trypanosomiasis,
Plague
Vecto
r
Vecto
r
vertebrate animals
Direct transmission
Direct transmission
e.g. Lassa
Once across the species barrier,
some Lassa virus (Arenavirus) may
spread by human to human
~ genetic modification
External factors
(Shakespeare, M., 2009)
ling
d
n
a
h
Food
Farming practice
Global
ern
att
Mt
p
Ec
os
A
change
Warmi
ng
Closer
and
prolon
ged
contact
with
species
carrier
The
pathogen
must have
the
opportunity
to cross the
barrier
ys
te
m
The ability
of the
causative
agent to
cross
species
barrier
Pathogen
transmission
The pathogen
may adapt to
human
physiology
and
immunology
MODE of
TRANSMISSION
AEROSOL INHALATION
BLOOD, SALIVA
FAECES, URINE
Indirect spread may also involve animalassociated organic residues - Psittacosis in human
FOMITE CONTACT
ORAL OR PHYSICAL
CONTACT
PARASITIC VECTORS
SCRATCHES, BITES,
(Yoes Prijatna Dachlan PBL 30-3-
Toxocariasis
canis
VLM, OLM,CT
Humans acquire
knowlesi malaria
P. knowlesi is derived from ancestral parasite
population that existed prior to human settlement
in Southeast Asia, and underwent significant
population approximately 30,000 40,000 years
ago
Knowlesi malaria is primarily a zoonosis with wild
macaques as the reservoir hosts
On going ecological changes due to the
destruction of natural forests, may alter the
parasite, macaque and mosquito population
dynamics and lead the parasites to switch to
human as the preferred
hosts
(Lee K-S,
2011; Kakilaya, B.S., 2011)
TERIMAKASIH