INFEKSI TORCH PADA

DEWASA

DR. NELDA APRILIA SALIM, SpPD

Divisi tropik dan infeksi Penyakit Dalam FK
Unsri/RSMH Palembang
2020
TOXOPLASMOSIS
• Disebabkan parasit Toxoplasma gondii
• Zoonosis ditularkan hewan
• Toksoplasmosi kongenital 
– Infeksi pada bayi baru lahir
– penularan lewat plasenta
– Dari ibu yang terinfeksi toksoplasma
– Bayi biasanya asimptomatik
– Manifestasi lanjut bervariasi: korioretinitis,
strabismus, epilepsi, retardasi psikomotor
 Epidemiologi
• Prevalensi anti T.gondii positif pd manusia:
– Indonesia: 2-63%
– Eskimo: 1%
– El Salvador: 90%
• Prevalensi nti T.gondii positif pada hewan:
– Kucing 25-73%
– Babi 11-36%
– Kambing 11-61%
– Anjing 75%
– Ternak lain: <10%
 Epidemiologi
• Prevalensi anti T.gondii:
– Umur >>
– ♀=♂
– Dataran tinggi >> rendah
– Daerah tropik >>
• Keadaan toksoplasmosis dipengaruhi:
– Kebiasaan konsumsi daging kurang matang
– Hewan peliharaan kucing
– Tikus, burung berkeliaran  buruan kucing
– Lipas, lalat >>>
– Cacing tanah>>
 Siklus hidup
• Host definitif: Family Felidae (kucing rumah dan sejenisnya)
1. Kotoran kucing mengandung ookistayang tidak tersporulasi.
Dalam 1-5 hari ookista mengalami sporulasi  infektif
2. Host intermedia: tikus atau burung terinfeksi ookista bila
termakan tanah atau air yg mgdg ookista
3. Ookista berubah menjadi takizoit segera setelah tertelan, dan
menempati jaringan syaraf dan otot untuk berkembang menjadi
kista bradizoit jaringan
4. Kucing terinfeksi kembali jika memakan host intermediate yg
mgdg kista bradizoit jaringan
5. Hewan ternak untuk konsumsi manusia dapat terinfeksi bila
termakan ookista sporulasi yg infektif
Penularan Toxoplasma pd manusia
• Akuisita: bila makan daging mentah atau kurang matang 
daging mengandung kista jaringan atau takizoit Toksoplasma,
atau air minum, buah dan sayur yg terkontaminasi ookista nfektif.
Jalur lain: bila ookista yang dikeluarkan dengan tinja kucing
tertelan manusia.
• Kongenital: in utero melalui plasenta  bila ibunya mendapat
infeksi primer waktu ia hamil
• Laboratorium: orang yang bekerja dengan binatang percobaan
yang diinfeksi dengan T gondii, melalui jarum suntik dan alat
laboratorium lain yang terkontaminasi dengan T.gondii
• Transplantasi organ atau transfusi darah lengkap dari donor yang
menderita toksoplasmosis laten
 Siklus hidup
10. Dalam tubuh manusia, parasit membentuk kista jaringan
yang lazimnya menempati otot skeletal, myokardium,
otak, mata kista menetap seumur hidup  diagnostik
bila menemukan kista jaringan dari biopsi spesimen. atau
PCR DNA T.gondii dari cairan amnion pada infeksi
kongenital
 Patogenesis
• Kista jaringan tertelan oleh manusia  parasit terbebas
dari kista
• Bradizoit resisten terhadap pepsin  menginvasi GI tract
manusia
• Di dalam eritrosit, parasit mengalami transformasi
morfologi  jumlah takizoit invasif >>>  mencetuskan
respon lgA sekretorik spesifik parasit
• Parasit menyebar ke berbagai organ, terutama jaringan
limfatik, otot lurik, miokardium, retina, plasenta, dan
SSP bereplikasi dan menginvasi sel yang berdekatan 
kematian sel dan nekrosis fokal yang dikelilingi respon
inflamasi akut
 Patogenesis pd imunokompeten
• Respon imun thdp takizoit:
– Induksi antibodi parasit
– Aktivasi makrofag dengan perantara radikal bebas
– Produksi interferon gamma
– Stimulasi limfosit T sitotoksik
• Limfosit spesifik antigen ini mampu membunuh baik
parasit ekstraselular maupun sel target yang terinfeksi
oleh parasit
• Proses pemusnahan takizoit, kista jaringan yang
mengandung bradizoit mulai muncul, biasanya di
dalam SSP dan retina
 Patogenesis pd imunokompeten
• Infeksi menetap dengan kista yang mengandung
bradizoit  infeksi subklinis
• Kista tidak mengalami degenerasi dan ruptur di dalam
SSP
• Perkembangan kista baru  stimulus menetapnya titer
antibodi
Patogenesis pd imunokompromais
• Respon imun thdp takizoit <<< karena sistem imun
tidak baik
• Takizoit menetap penghancuran progresif 
kegagalan organ (necrotizing encephalitis, pneumonia,
dan miokarditis)
• HIV: defisiensi imun disebabkan defisiensi kuantitatif
dan kualitatif progresif dari T helper  CD4 
penurunan kadar CD4, gangguan produksi IL-12 dan
interferon gamma, serta gangguan fungsi limfosit T
sitotoksik  infeksi T.gondii
 Gambaran klinis
• Lesi di SSP dan mata berat dan permanen
• SSP  nekrosis + kalsifikasi, hidrosefalus pd bayi akibat
penyumbatan akuaduktus Sylvii karena ependimitis
• Mata retina: reaksi peradangan fokal dengan
edema dan infiltrasi leukosit  kerusakan total 
parut (sikatriks) akibat penyembuhan atrofi retina
dan koroid, disertai pigmentasi
 Infeksi akut pada pasien imunokompeten
• Dewasa: hanya 10-20% dg gejala. Sisanya asimtomatik
• Limfadenopati leher >>, kelenjar-kelenjar biasanya terpisah atau
tersebar; uk <3 cm, tidak nyeri, kekenyalannya bervariasi, tidak
bernanah
• Nyeri abdomen bila adenopati kelenjar mesentrial atau
retroperitoneal
• Korioretinitis unilateral
• Lain-lain: demam, malaise, keringat malam, nyeri otot, sakit
tenggorok, eritema makulopapular, hepatomegali, splenomegali,
atau gambaran klinis umum seperti yang disebabkan infeksi
virus
• Gejala menghilang dalam beberapa minggu atau bulan
Infeksi akut pada pasien imunokompromais

• >>> pasien HIV dg CD4 < 100

• Ensefalitis toksoplasma  gangguan mental, defisit
neurologik, sakit kepala, demam, tubuh terasa lemah,
gangguan nervus kranialis, gejala parkinson, focal
dystonia, rubral tremor, hemikorea-hemibalismus, dan
gangguan pada batang otak. Medula spinalis juga dapat
terkena dengan gejala seperti gangguan motorik dan
sensorik di daerah tungkai, gangguan berkemih dan
defekasi  Onset dari gejala biasanya subakut
• Pneumonitis  demam berkepanjangan, batuk, sesak
nafas  sulit dibedakan dg Pneumocystis carinii.
Infeksi akut pada pasien imunokompromais

• Korioretinitis  penurunan tajam penglihatan, nyeri pada

mata, melihat benda beterbangan, serta fotofobia. Pada
funduskopik  daerah nekrosis yang multifokal atau
bilateral.
• Gejala klinis lain yang jarang: panhipopituari dan diabetes
insipidus, gangguan gastrointestinal dengan nyeri perut,
asites, serta diare, gagal hati akut, gangguan muskuloskeletal.
• Pembesaran KGB yang kenyal, tidak nyeri, berkonfluens, dan
paling sering timbul di daerah servikal.
• Low grade fever, hepato-splenomegali dan timbul rash pada
kulit
 Diagnosis
• Diagnosis pasti toksoplasmosis akut:
menemukan takizoit dalam biopsi otak atau
sumsum tulang, cairan serebrospinal dan
ventrikel  Sulit
 Imaging
• CT Scan otak pasien Ensefalitis
toksoplasma (ET): gambaran
menyerupai cincin yang multipel
pada 70-80% kasus, letak lesi
terutama berada pada ganglia basal
dan corticomedullary junction.
• MRI: lebih baik dari CT Scan, sering
menunjukkan lesi-lesi yang tidak
terdeteksi dengan CT Scan  MRI
merupakan prosedur baku bila
memungkinkan
• Diagnosis banding dari CT scan atau
MRI: limfoma dengan lesi multipel
Penatalaksanaan
Terapi toxoplasmosis cerebri pasien HIV-AIDS
(INDONESIA)
• Terapi fase akut (6 pekan):
– Pirimetamin H1: loading 200mg (8 tablet); H2 –
selanjutnya: 2 x 25 mg (BB < 50 kg), 3 x 25 mg
(BB>50kg)
– Clindamycin 4x600mg (H1 – selanjutnya)
• Terapi maintenance:
– Setengah dosis fase akut, atau
– Kotrimoksazol 1 x 960 mg
Sampai CD4>200 selama 6 bulan
RUBELLA
 Rubella = German measles
• an acute viral infection of children and adults
that characteristically includes rash, fever, and
lymphadenopathy and has a broad spectrum
of other possible manifestations.
• Rubella during pregnancy can lead to fetal
infection, with the production of a significant
constellation of malformations (congenital
rubella syndrome) in a high proportion of
infected fetuses
 Etiology
• Rubella virus, a togavirus, does not require a vector for
transmission.
• The rubella virion is composed of an inner icosahedral capsid
of RNA and protein that is surrounded by a lipidcontaining
envelope with glycoprotein spikes and a diameter of ∼60
nm.
• incubation period is 18 days on average, with a range of 12–
23 days
• Spread in droplets shed in respiratory secretions, infects the
respiratory tract and then the bloodstream
 Clinical manifestations: postnatally acquired
infection
• adults  more severe disease  a brief prodrome of malaise, fever,
and anorexia.
• The foremost symptoms:
– posterior auricular, cervical, and suboccipital lymphadenopathy;
– Fever  may be absent entirely or may be present for only several days in
the early phase of the illness
– Rashbegins on the face and spreads down the body, maculopapular but
not confluent, sometimes accompanied by mild coryza and conjunctivitis,
and generally lasts for 3–5 days.
– A petechial exanthem on the soft palate, (Forschheimer spots).
• Complication: arthritis, most frequently involving the fingers, wrists,
and/or knees  develops as the rash is appearing and may take
several weeks to resolve.
 Diagnosis
• The isolation of rubella virus in cell cultures of throat samples,
urine, or other secretions difficult and expensive
• Polymerase chain reaction (PCR) is also useful for diagnosis 
useful when congenital rubella is suspected
• Ig M dan IgG ELISA
– Acute rubella : a fourfold or greater rise in the titer of IgG
antibodies in paired acute- and convalescent-phase serum
specimens or by the detection of rubella-specific IgM
antibodies in one serum specimen.
• Biopsied tissues and/or blood and cerebrospinal fluid have
alsobeen used for the demonstration of rubella antigens with
monoclonal antibodies and for the detection of rubella RNA
by in situ hybridization and PCR.
 Prevention and therapy
• Vaksin MMR mumps measles rubella
• There is no specific therapy for rubella. At one time,
immune globulin was used in an effort to prevent
congenital rubella when pregnant women became
infected
• However, because administration of immune
globulin did not prevent maternal viremia, this
approach was discarded. Symptom-based treatment
is given for manifestations such as fever, arthralgia,
and arthritis
CYTOMEGALOVIRUS
 Cytomegalovirus (CMV)
• a β-herpesvirus, ds-DNA, 4 species mRNA, a protein capsid, and a
lipoprotein envelope
• icosahedral symmetry, replicates in the cell nucleus, and can
cause either a lytic and productive or a latent infection
• Inducing severe birth defects, wide spectrum of disorders in older
child and adults: asymptomatic – subclinical – mononucleosis
syndrome  healthy individual – immunocompromised patients
• Transmitted in breast milk, saliva, urine, feces  required
repeated or prolonged intimate exposure
• Once infected  carries CMV for life
•
 CMV mononucleosis = heterophile antibody–
negative mononucleosis syndrome
• often involves sexually active young adults
• incubation periods: 20–60 days, the illness generally lasts for 2–6 weeks
• Prolonged high fevers, sometimes with chills, profound fatigue, and
malaise  characteristic
• Myalgias, headache, and splenomegaly.
• Exudative pharyngitis and cervical lymphadenopathy are rare
• Relative lymphocytosis in peripheral blood, with >10% atypical
lymphocytes
• Serum aminotransferase and alkaline phosphatase levels are often
moderately elevated.
• Heterophile antibodies are absent; the presence of cryoglobulins,
rheumatoid factors, cold agglutinins, and antinuclear antibodies
CMV infection in immunocompromised hosts

• Common viral pathogen complicating organ transplantation

 variety of syndromes: fever and leukopenia, hepatitis,
pneumonitis, esophagitis, gastritis, colitis, and retinitis
• Important pathogen in patients with advanced HIV
infection  causes retinitis or disseminated disease,
particularly when peripheral-blood CD4+T-cell counts fall
below 50–100/µL
• Prolonged fever, malaise, anorexia, fatigue, night sweats,
and arthralgias or myalgias
• Liver function abnormalities, leukopenia,
thrombocytopenia, and atypical lymphocytosis
CMV infection in immunocompromised hosts

• Lung CMV involvement:

– Tachypnea, hypoxia, and unproductive cough
– Ro thorax: bilateral interstitial or reticulonodular infiltrates that
begin in the periphery of the lower lobes and spread centrally and
superiorly (often); localized segmental, nodular, or alveolar
patterns (less common)
• Gastrointestinal CMV involvement:
– Ulcers of the esophagus, stomach, small intestine, or colon
bleeding or perforation
– May lead to exacerbations of underlying ulcerative colitis
– Hepatitis (after liver transplantation), acalculous cholecystitis,
adrenalitis
CMV infection in immunocompromised hosts

• CMV retinitis
– Cause blindness
– Early lesions consist of small, opaque, white areas
of granular retinal necrosis that spread in a
centrifugal manner and are later accompanied by
hemorrhages, vessel sheathing, and retinal edema
• CMV meningoencephalitis  rare
• CMV subacute progressive polyradiculopathy
 reversible
 Diagnosis
• Virus excretion or viremia is readily detected by
culture of appropriate specimens on human
fibroblast monolayers  better predictor of acute
infection
• PCR detection of CMV DNA
• Detection of CMV-specific IgM is sometimes useful in
the diagnosis of recent or active infection  An
increased antibody level may not be detectable for
up to 4 weeks after primary infection, and titers
often remain high for years after infection
 Prevention of CMV infection in high risk
patients
• The use of blood from seronegative donors or of blood
that has been frozen, thawed, and deglycerolized
• Matching of organ or bone marrow transplants by
CMV serology, with exclusive use of organs from
seronegative donors in seronegative recipients
• Both live attenuated and CMV subunit vaccines have
been evaluated, but neither is close to approval for
general use.
• CMV immune or hyperimmune globulin
 Treatment
• CMV retinitis:
– a 14- to 21-day induction course
• Ganciclovir: 5 mg/kg IV twice daily
• Valganciclovir: 900 mg twice daily
– Prolonged maintenance therapy
• Ganciclovir:5 mg/kg daily or 6 mg/kg 5 days per week;
• Valganciclovir: 900 mg once daily
– Discontinuation of maintenance therapy should be
considered in patients with AIDS who, while receiving
ART have a sustained (>6-month) increase in CD4+ >100–
150/µL
Thanks