Virus Properties Replication Tansmission Pathogenesis & Immunity CM Lab Findings Treatment Prevention

& CM
Fam: Picornaviridae - ssRNA + Replicates Pleonaril:
naked in inhibits
- cytoplasm penetration of
Icosahedral aviruses
capsid VP1 intocell, must
- Cytolytic proteins be
binds to administered
receptor  in the course
VP4 of infection
release 
virion
weakned
 genome
injected by
VP1  -
RNA 
mRNA 
VP0, VP1,
VP3 are
cleaved 
capsid
Total time:
3-4 hours
Genus: Resistant Fecal-Oral PoE: URT, oropharynx, intestinal tract IgM  4x
Enterovirus to pH 3-9,  tahan asam lambung  replicate in increase
detergents, mucosa, lymphoid tissue of the tonsil, between acute
mild pharynx, M cells, Peyer patches, and and
sewage enterocytes of intestinal mucosa  concalescence
treatment, primary viremia  blood stream 
heat. reticuloendothelial of lymph nodes,
 spleen, liver  secondary replication
 secondary viremia & symptoms
*cytolytic  replicating and causing
direct damage to target cell, kecuali hep
A

secretory antibody can prevent the

initial establishment of infection in
oropharynx and GI to prevent viremic
spread to target tissue

Subtypes: 3 types Fecal-Oral Poliovirus gains access to the brain by Culture from Vaccine:
Poliovirus type 1 infecting skeletal muscle and traveling pharynx  first -Inactivated polio
paling up the innervating nerves to the brain few days vaccine (IPV),
sering (like rabies). The virus is cytolytic for *grows well in SALK
motor neuron of the anterior horn and monkey kidney -Live attenuated
brainstem tissue culture oral polio vaccine
Asymptomatic illness (90%)  limited (OPV) SABIN
in oropharynx and gut yg live virusnya
bisa keluar di
 -Abortive poliomyelitis  minor feces selama
illness, nonspecific febrile illness, beberapa minggu
headache, malaise, sore throat, dan bisa
vomiting, 3-4 days after exposure reimmunize
-Nonparalytic poliomyelitis/ aseptic people?
meningitis  progresses into CNS and Gaboleh dikasih
meninges  back pain, muscle spasm untuk org
-Paralytic polio  major illness, 3-4 imunokompromis
days after minor illness has subsided,
virus spreads from blood to anterior
horn cells of spincal cord and motor
cortex of the brain. Causing spinal
paralysis (limbs) or bulbar paralysis
(cranial nerves + respi center)
Paralytic poliomyelitis  asymmetric
flaccid paralysis with NO SENSORY
LOSS
Bulbar poliomyelitis  more severe,
involve muscle of pharynx, vocal cord,
respi  death
Postpolio syndrome  sequela of
poliomyelitis 30-40 years later, no
poliovirus but only the syndrome

Coxsackievirus Herpangina  vesicular lesions on Throat/stool

Group A posterior half of palate, tonsil, toungue, culture
severe fever, sore throat, pain on
swallowing, anorexia, vomiting
Coxsackievirus Hand Foot Mouth disease Throat/stool
A16,4,5,6,9,10,  moderate fever 1-2 days, sore throat, culture
24 mouth, mucosal vesicular lesions that
B2-5 ulcerate in the tongue, soft palate,
Echo 18, entero 17 buccal mucosa, tender erythematous
papulovesicular lesion in palm and
soles, extrimites, gluteal, perianal.
Vesicle heals w/o crusting
always associated with oral lesion
Coxsackievirus Aseptic meningitis  fever, malaise, CSF  lacks of
A & B, echo 9 headache, nausea, abdominal pain, mild neutrophil,
muscle weakness (poliomyelitis like), glucose
nuchal rigidity, petechiae, rash, normal/low,
encephalitis protein
normal/elevated,
+virus
Coxsackieviruses Rhinovirus-like common cold Throat /stool
A21, A24 & echoviruses 11  meningitis in infant culture
echoviruses 11, 20 RT PCR
Echo & Coxsackie Fever, rash, common coldlike Throat /stool
symptoms culture
Coxsackievirus group B  Body Throat /stool
B Myocarditis  older children, culture
neonates, febrile and sudden and
unexplained heart failure, cyanosis,
tachy, cardiomegaly, hepatomegaly
Pericarditis  young adults, older
persons, myocardial infarction with
fever
Pleurodynia  fever, stabbing chest
pain (2 days-2 weeks), abdominal pain
Beta cells of the pancreas  insulin-
dependent
Enterovirus 70, Incubation : 24 h Throat /stool
Coxsackievirus A24 Resolution: 1-2 weeks culture
Contagious ocular disease
 Acute hemorrhagic conjunctivitis
Subconjunctival hemorrhages
Conjunctivitis
Rhino Labile at Aerosol Common cold and URTI Sneezing Virus from nasal Nasal No vaccine karena
virus acidic pH, Objects Self limiting followed washing vasoconstrictor terlalu banyak
optimum (virus can Unable to replicate in GIT by RT PCR Inhaling hot serotype, jadi
growth survive on rhinorrhea steamed air handwashing and
temp 33C such objects Enters through Sore No antiviral disinfection
>100 for many mouth/nose/eyes  throat, no
serotypes hours) replication in nose  fever
infected cells release 3-4 days
sering kena bradykinin and histamine but cough
infants and ingusan 500-1000 and nasal
children <2 infectious virion/ml  symptoms
years runny nose may
*infection juga di URTI & persist 7-
throat 10 days
Interferon may limit
progression of infection
release of cytokines during
inflame can promote
spread of virus by
expression of ICAM-1
viral receptors
kena rhinovirus bisa
berkali2 karena serotype
banyak
nasal secretion ada IgA
dan IgM
cell mediated ga kepake
Hepatovirus
Hepatitis A
Arthropod-Borne and Rodent-Borne Viral Disease
+ssRNA (E)

Family : Togaviridae
Genus : Alphavirus
 Envelope surrounding the particle contains 2 glycoproteins
 Persistent infection in all mosquitoes/ other blood feeding arthropods
 All alphaviruses are antigenically related
 Inactivated by acid, heat, lipid solvents, detergents, bleach, phenol, 70% alcohol. Formaldehyde
 Replicate in cytoplasma and mature by budding nucleocapsids through the plasma membrane
 HI, ELISA, and immunofluorescence test  define 8 antigenic complexes/serotypes  western equine encephalitis, eastern equine
encephalitis, Venezuelan equine encephalitis, Semliki Forest virus

Family : Flaviviridae
Genus : Flavivirus
 Antigenically related
 Sama kaya toga
 Replicate in the cytpplasm, and particle assembly occurs in the intracellular vesicles
 Proliferation of intracellular membranes is a characteristic of flavivirus infected cells
  Neutralization test  bedain serotype

Pathogenesis and Pathology

 Multiplication occurs in myeloid and lymphoid cells or in vascular endothelium
 Multiplication in CNS depends on the ability of the virus to pas BBB  widespread neuronal degeneration occurs in all arbovirus
induced encephalitis  infants and elderly adults are most susceptible
 Equine encephalitis in horse  first phase  minor illness, virus multiplies in non-neural tissue and present in blood
second phase  major illness, virus multiplies in brain cells

Clinical findings
 Incubation  4-21 days
 Flu like illness, encephalitis, severe bad headache, chills, fever, nausea, vomiting, generalized pains, and malaise
 24-48 hours after  drowsiness  stuporous
 mental confusion, tremors, convulsions, and coma develop in severe cases
 fever lasts 4-10 days
 Japanese B encephalitis paling parah 80% mati
 Bisa ada sequelae  paralysis, aphasia, cerebellar signs

Lab Diagnosis
 Virus in blood  early infection, before symptoms
 PCR  find RNA
 Neutralizing and Hemagglutination-inibiting antibodies  detectable within a few days after onset of illness
 IgM 4x rise by ELISA  serum or CSF taken soon after onset and second sample 2-3 weeks later
 After a single infection by one member of the group, antibodies to other member may also appear
Immunity
 Immunity permanent after a single infection
 Humoral and cellular immune response are important for protection
Tick-Borne Encephalitis Ixodes ricinus,I. persulcatus animal,human Europe,Rusia,China Encephalitis
Treatment and Control
 Biological control
 Avoid mosquitoes
 Vaccine for horses not humans
 Vaccine for humans  killed virus and attenuated live virus Japanese B encephalitis

Arbovirus Host-Vector Transmission Cycles

Female culex mosquitoes  birds/mammals yang terinfeksi virus ↔ infected mosquitoes (seumur hidup)  gigit human/horse (dead end host)
artinya tdk kontribusi dalam penularan virus
*mosquito-bird-mosquito St. Louis encephalitis, West Nile virus, Japanese B encephalitis
*swine  Japanese B encephalitis
Alphavirus
Chikungunya virus
 Flaviviridae

Disease Pathogenesis & Pathology Clinical Findings Lab Findings Immunity Tx Prevention
Yellow Mosquitoe bites  multiples in Incubation: 3-6 days Immunohistochemistry, Neutralizing No antiviral Mosquito
Fever skin  local lymph nodes, liver, Fever, chills, headaches, ELISA, PCR  first 4 antibodies  drug abatement
spleen, kidney, bone marrow, dizziness, myalgia, backache days after onset on blood develop 1 week into
myocardium (persist for days)  nausea, vomiting, the illness and 17D strain of
*virus present in blood during bradycardia ELISA  IgM antibodies responsible for viral yellow fever
early infection (viremic and source of appear during the 1st week clearance and virus live-virus
Lesion in particular organ infection for mosquitoes) of illness complete protection vaccine
 Liver & kidney  necrotic 15% patients  severe  from the disease CI:
lesions fever, jaundice, renal failure, Confirmation with: infant <9mo
 Spleen, lymph nodes, hemorrhagic manifestations Neutralizing antibody  pregnancy
heart  degenerative (black vomitus)  between acute and egg allergies
 Hemorrhage and hepatorenal failure convalescent phase with postvaccinal
*infection may be so mild 4x rise encephalitis 
circulatory collapse
*no sequelae  die/recover occurred in
 Myocardium  shock infants
Acute, febrile, liver and renal
dysfunction, hemorrhage

Dengue 4 serotype  antigen beda-beda Incubation: 4-7 days NS-1  (+) day 1-3 Bedain 4 serotype Supportive Vaccine untuk
(Breakbone walaupun 1 serotype Prodromal symptoms  Primary infection pake molecular- by fluid anak
fever) Asian genotype (DEN 2)  lebih malaise, chills, headache IgM  (+) day 4, cek day based assays dan replacement
virulent Back, joints, muscles, eyeball 5-7 neutralization tests therapy
Dengue hemorrhagic fever/ pain IgG  (+) day 7-9
dengue shock syndrome  occur Fever : 2-7 days Second infection
usally in children with passively Day 3  turun IgM  (+) day 4
acquired or pervious infection Day 5-8  rise again
with a diff serotype of virus Jadi saddleback form Bahaya kalo IgM dan IgG
Myalgia and deep bone pain (+)
 -Increased vascular permeability Rash
with plasma leakage into Day 3/4  1-5 days RTPCR
interstitial spaces associated with Lymph nodes enlarged
increased levels of vasoactive Self limiting
cytokines Convalescence (recovery) 
monocyte are the major target in take weeks
blood for dengue virus infection
second infection with type 2 after Initial phase
type 1  high risk for severe -temp >38.5C
disease -mild hemorrhagic
manifestation  petechiae,
second infection lebih parah bruising
karena virus-antibody complexes -palpable liver
sudah terbentuk beberapa hari
setelah second infection dan non Critical phase
neutralizing bikin jumlah sel -children and young adult 
mononuclear lebih banyak dan karena imun masih bgs
diikuti pelepasan sitokin, -systemic vascular leak
mediator vasoaktif, dan syndrome
procoagulan sehingga mengarah -hemorrhagic manifestation
ke DIC -DIC (cowo)
Recovery phase
-reverting spontaneously to a
normal level after approx. 48-
72 h
Japanese Mild (fever and headache) or without apparent symptoms Serum/CSF No cure JE immunization
encephalitis Treatment is 4 types
1 in 250 infections results in severe clinical illness
focused on inactivated
Severe disease by rapid onset of high fever, headache, neck relieving mouse brain-
stiffness, disorientation, coma, seizures, spastic paralysis and severe derived
ultimately death clinical signs vaccines,
and inactivated Vero
supporting cell-derived
the patient to vaccines, live
 Of those who survive 20%–30% suffer permanent intellectual, overcome the attenuated
infection vaccines, and
behavioural or neurological problems such as paralysis, recurrent
live recombinant
seizures or the inability to speak vaccines.

St. Louis Most persons infected with SLEV No treatment Stay away from
encephalitis have no apparent illness. Just mosquitoes
supportive
Initial symptoms ill, fever,
headache, nausea, vomiting, and
tiredness. Severe neuroinvasive
disease (often involving
encephalitis, an inflammation of
the brain) occurs more
commonly in older adults. In rare
cases, long-term disability or
death can result.

West nile No symptoms, kadang demam Supportive No vaccine

virus 1% fatal

Tickborne Initial symptoms  flu, fever, Supportive

encephalitis headache, malaise, muscle
pain
(last for 8 days and make a
full recovery)
second stage  changes in
mental state, such as
confusion, drowsiness/
disorientation, seizures,
photophobia, being unable to
speak paralysis
bisa sembuh total
Fam: Bunyaviridae
 Fam: Bunyaviridae
 Transmitted by arthropods
 -ssRNA, envelope
 sensitive to heat, detergents, formaldehyde, love pH,
 hemaglutinating
 La Crosse virus  major cause of encephalitis and aseptic meningitis in Midwest children
 Disease Vector Clinical Findings Tx Prevention
Sandfly fever Female Phlebotomus Tempat gigitan  small All patients recover no Insect repellents during
papatasii that feed at night itching papules that persist specific treatment for the the night and insecticides
(phlebovirus) for 5 days disease. Pain killers and
fluid replacement may be
useful
Incubation : 3-6 days
Virus found in the blood
briefly near the time of
onset
Headache, malaise,
nausea, fever,
photophobia, stiffness of
the neck and back,
abdominal pain,
leukopenia

Rift Valley Fever Aedes sp Mild febrile illness and

(phlebovirus) Or by contact with
infected animal
blood/body fluid
always recovery
Complication  renitis,
encephalitis, and
hemorrhagic fever,
permanent loss of vision

Rodent-Borne Hemorrhagic Fevers

Disease Vector Clinical Findings Tx Prevention

Hemorrhagic fever with Urban rats Acute viral infection that Supportive Rodents control and
renal syndrome cause interstitial nephritis protection from exposure
(HFRS)  acute renal to rodent droppings and
insufficiency and renal contaminated material
Hantaan, Dobrava, Seoul failure
viruses
 Hantavirus Pulmonary Peromycus maniculatus Severe respiratory illness Maintenance of adequate Rodent control
Syndrome (deer mouse)  Sin Respiratory distress oxygen and support of
(HPS) Nombre Virus syndrome hemodynamic functioning
Ribavirin
novel hanta-virus ( Sin Lab test:
Nombre Virus), New - RT-PCR
York virus, Black Creek - ELISA  IgM
Canal virus, Bayou virus (acute), IgG (acute
and convalescent)

Arenavirus Disease
 2 ssRNA
 Large envelope
 Clarissfication WHO  Old world viruses (Lassa virus) and New world viruses
 Group A (Pichinde virus), Group B (Macupho virus)
 Each virus associated with a single rodent
 Human disease  Lassa, Junin, Machupo, Guanarito, Sabia, Whitewater, Arroyo, and lymphocytic choriomeningitis
 Transmitted by rodent hosts  milk, saliva, and urine
 Replication involving ribosome and does not cause cytopathic effect

Disease Vector Clinical Findings Tx Prevention

Lassa fever Mastomys natalensis Incubation: 1-3 weeks Ribavirin Rodent control
(house rat) Gradual with fever, No vaccine
vomiting, and back and
human-human in hospital chest pain
Very high fever, mouth
ulcers, severe muscle
aches, skin rash with
hemorrhages, pneumonia,
and heart and kidney
damage
Complication 
permanent deafness
Fatal in pregnant woman
 fetal death
Diagnosis:
ELISA  IgM and IgG
RT-PCR

South American Calomys musculinus Junin virus produces

Hemorrhagic Fever (Junin) humoral and cell mediated
Junin (Argentine) paling immunodepression 
sering bikin hemorrhagic Calomys callosus death related to an
Machupo (Macchupo) inability to initiate a cell
Guanarito  Venezuelan mediated immune
Sabia response
Lymphocytic Mus musculus Incubation: 1-2 weeks and
Choriomeningitis (wild house mouse) illness 1-3 weeks sembuh
Acute disease  aseptic
mother-fetus meningitis/ mild systemic
influenza like illness
 Filovirus Diseases
 -ssRNA , envelope
 Marbug virus
 Ebola virus  Zaire, Sudan, Reston, Ivory Coast
 Highly virulent

Disease Vector Clinical Findings Tx Prevention

African Hemorrhagic Cercopitheus aethiops Incubation: 3-9 days (M) Supportive
Fevers (M) 2-21 days (E) Maintaining renal function
(Marbug and Ebola fever, headache, sore and electrolyte balance
viruses) Staff contact with patients throat, and muscle pain. and combating
blood/excreta (E), sangat Followed by abdominal hemorrhage and shock
Ebola Zaire. The most communicable disease pain, vomiting, diarrhea,
highly virulent subtype rash, internal & external
of Ebola Epidemiologists have bleeding  shock and
tested bats, monkeys death
(Macaca fascicularis), immunosuppressive 
Ebola Sudan. An impaired humoral immune
extremely pathogenic spiders and ticks for
responses
subtype. the virus, but have not high titers of virus:
been able to acquire -kidneys
Ebola Reston originated definitive data. -liver
in Asia -spleen
and was brought to Reservoir  rodents and -lungs
bats -blood
the U.S. by infected
Monkey ga termasuk
macaques imported soalnya kalo kena mati death in 7-8 days (E)
from the Phillippines. juga Lab findings:
-ELISA
-RTPCR
Ebola-Tai. A new
strain which appeared
in 1994