Infeksi Virus Multi-sistem-

7/23/2019 Infeksi Virus Multi-sistem-

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INFEKSI VIRUS

MULTI-SISTEM

Riyani Wikaningrum

Bag. Mikrobiologi

Fakultas Kedokteran Univ. Yarsi


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Penyakit Infeksi berdasar Sistem


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Infeksi Multi-sistem

Vector-borne

Zoonosis

Fever of Unknown Origin (FUO) Infection of the compromised host


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Vector Borne Disease

Arboviruses are arthropod-borne viruses

Arbovirus replicate in: Vascular endothelium

CNS Skin and Muscle

Arbovirus infection: Yellow fever

Dengue fever Arbovirus encephalitis

Arbovirus and hemorrhagic fever


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Yellow Fever

Yellow fever virus is transmitted bymosquitoes and is restricted to Africa,Central and South America and the

Caribbean Clinical features of yellow fever may be

mild, but liver damage can prove fatal

The diagnosis is usually clinical, there isno specific treatment, but there is avaccine


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Dengue Fever

Dengue virus is transmitted by mosquitoes

and occurs in southeast Asia, the Pacific

area, India and the Caribbean

Dengue fever may be complicated by

dengue hemorrhagic fever shock

syndrome

There is no antiviral therapy or vaccine for

dengue fever


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Arbovirus Enchephalitis

The encephalitic arboviruses only

occasionally cause encephalitis


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Zoonosis

Some multisystem infections in man

are animal diseases (i.e. zoonoses)

Viral Haemorrhagic Fever caused by:

Arenaviruses

Filoviruses

Bunyaviruses

Flaviviruses


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ARENAVIRUS INFECTIONS

Arenaviruses are transmitted to humans inrodent excreta

Arenavirus infection is diagnosed byserology, virus isolation or viral genome

detection Lymphocytic choriomeningitis virus occurs

worldwide

Lassa fever virus is an arenavirus thatinfects a bush rat in parts of west Africa


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KOREAN HEMORRHAGIC FEVER

The Hantaan virus causes Korean

hemorrhagic fever and infects rodents


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MARBURG AND EBOLA

HEMORRHAGIC FEVERS


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Outbreaks

1976- First Major

Outbreak (ZEBOV)

1976- Sudan(SEBOV)

Occur Sporadically

www.cdc.govfor

more information
http://www.cdc.gov/http://www.cdc.gov/


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Where does Ebola hide?

2002- Fruit Bats

Antibodies against

Ebola

Ebola Gene sequences

in liver and spleen

Fruit bats do not show

any symptoms

Best candidate to be

the reservoir

More research needs to

be done


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Clinical Observations

Incubation period:2-21 days

Stage I (unspecific):

-Extreme asthenia (body weakness)

-diarrhea, nausea and vomiting, anorexia

abdominal pain

- headaches

- arthralgia (neuralgic pain in joints)

- myalgia (muscular pain or tenderness), back pain

- mucosal redness of the oral cavity, dysphagia (difficulty inswallowing)

- conjunctivitis.- rash all over body except in face

** If the patients dont recover gradually at this point, there is a highprobability that the disease will progress to the second phase,resulting in complications which eventually lead to death (Mupapa et

al., 1999).


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Stage II (Specific):

- Hemorrhage

- neuropsychiatric abnormalities- anuria (the absence of urine formation)

- hiccups

- tachypnea (rapid breathing).

** Patients who progressed to phase two EHF almost always die.(Ndambi et al., 1999)

Late Complications:

-Arthralgia

- ocular diseases (ocular pain, photophobia andhyperlacrimation)- hearing loss

- unilateral orchitis( inflammation of one or both of the testes)

** These conditions are usually relieved with the treatment of 1%

atropine and steroids


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Epidemiology Ebola Hemorrhagic Fever was first found in 1976

It struck two countries within that year a. Sudanin a town called Nzara

b. Zaire, now known as the Democratic Republic ofCongo

In these two instances the mortality rate wasbetween

5090%

Following those epidemics, Ebola hit Africa in manyother instances the worst yet being in the year 2000

when it struck Uganda infecting more than 400people.

The newest cases 2014


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Transmission

contracted

through contact

of any infected

individuals bodyfluids

Ebola HF prevention

poster used in Kikwit

outbreak.


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Controlling the spread of Ebola Hospitals must follow precautionary methods, such as:

1. wearing gloves

2. isolating infected individuals

3. practicing nurse barrier techniques

4. proper sterilization and disposal of all equipment

Burials must be done correctly

1. no washing or touching carcass

2. put into body bags and bury outside city

Report any questionable illness to officials


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Ebola Subtypes

Ebola-Zaire

(ZEBOV)

Ebola-Sudan(SEBOV)

Ebola Ivory-Coast

(ICEBOV)

Ebola-Reston

(REBOV)


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MOLECULAR STRUCTURE

Characterization of the virus Order: Mononegavirales

Family: Filoviridae

Genus: Ebolavirus

Species: Ebola-Zaire, Ebola-Sudan, Ebola-Cote d-Ivoire,Ebola-Reston

Morphology under electron microscope filamentous, enveloped RNA virus

approx. 19 kb in length (1 kb = 1000 RNAbases/nucleotides) or 60-80 nm in diameter

single-stranded, linear, non-segmented

negative-sense RNA (encoded in a 3 to 5 direction)

appears to have spikes due to glycoprotein on

outside membrane


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Structure of Ebola genome and proteins

Transcribed into 8 sub-genomic mRNA proteins: 7structural and 1 nonstructural

7 structural proteins: nucleoprotein (NP)

4 viral/virion proteins (VP35, VP40, VP30, VP24) glycoprotein (GP)

RNA-dependent RNA polymerase (L protein)

NP, VP35, VP30, L protein: required for transcription &

replication

VP40, GP, VP24: associated with the membrane


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Viral Multi-System InfectionMucocutaneous Lessions


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Patogenesis

Infeksi HSV & VZV


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Manifestasi Infeksi HSV


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Manifestasi

Infeksi VZV


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SMALLPOX atau VARIOLA


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Smallpox (variola)

caused by a poxvirus

No animal reservoir

spread from person to person by

contact with skin lesions via the respiratory tract

The disease was severe, with a generalizedrash and was fatal in up to 40% of cases

Officially eradicated December 1979Effective vaccine


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MORBILLI atau MEASLES (RUBEOLA)

Kopliks spots


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MORBILLI atau MEASLES (RUBEOLA)

Measles outbreaks occur every few years inunvaccinated populations

Clinical features of measles include respiratorysymptoms, Koplik's spots and a rash

Measles rash results from a cell-mediatedimmune response

Complications of measles are particularly likely

among children in developing countries Measles is usually diagnosed clinically; there is

no antiviral treatment, but there is a vaccine


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RUBELLA (GERMAN MEASLES)

Rubella virus infection causes a

multisystem infection, but its main impact

is on the fetus

Rubella is diagnosed serologically; there is

no treatment, but there is a vaccine


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Rubella (German Measles)

Togavirus single-stranded RNA

one serotype

It is transmitted bydroplet infection

less contagious than

measles, but more so

than mumps Vaccine available

(MMR)

Clinical consequences of rubella virus


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Clinical consequences of rubella virus

invasion of different body tissues

Site of virus

growth

Result Comment

Respiratory

tract

Virus shedding but

symptoms minimal (mild

sore throat, coryza,

cough)

Patient infectious 5 days

before to 3 days after

symptoms

Skin Rash Often fleeting, atypical;

immunopathology involved

(Ag-Ab complexes)

Lymph nodes Lymphadenopathy More common in posterior

triangle of neck or behindear

Joints Mild arthralgia, arthritis Immunopathology involved

(circulating immune

complexes)

Placenta/fetus Placentitis, fetal damage Congenital rubella


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The pathogenesis of rubella:

Rubella is generally a very mild

often subclinical infection Arthritis

major impact when it infects the fetus


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Organ involvement and effects in

congenital rubella

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Infeksi Virus Multi-sistem-