NOTES

NOTES
TOGAVIRUSES

MICROBE OVERVIEW
▪ Pathogenic viruses in Togaviridae family
▪ Capsid symmetry: icosahedral
▪ RNA structure: linear, positive polarity

EASTERN EQUINE ENCEPHALITIS

VIRUS (EEEV)
osms.it/eastern-equine-encephalitis

Coquillettidia, Culex) to bridge between

PATHOLOGY & CAUSES infected birds, humans
▫ Infected mosquito bite → 4–10 day
▪ Highly pathogenic; causes central nervous incubation period → prodromal period
system illness in humans, horses (equines) → neurological symptom development
▪ Genus: Alphavirus occurs rarely
▪ Spherical, approx. 69nm diameter
(including glycoprotein spikes)
RISK FACTORS
▪ Enveloped, single-stranded, positive-sense
▪ Rural residence; living in/visiting woodland
RNA genome
habitats, swampy areas
▪ Glycoproteins associated with
▪ Outdoor occupation/recreational activity
neurovirulence, cellular apoptosis
▪ Potential bioterrorism agent use (aerosol
route) COMPLICATIONS
▪ Range ▪ Encephalitis; cerebral edema; coma;
▫ Atlantic, Gulf-coast states in eastern residual brain damage (mild–severe, esp.
USA young children); death (some)
▪ Four lineages
▫ Group I: endemic in North America, SIGNS & SYMPTOMS
Caribbean (causes most human disease)
▫ Groups IIA, IIB, III: primarily cause ▪ May be asymptomatic
equine illness in Central, South America
▪ Prodromal period: high fever, headache,
▪ Viral life-cycle: wild birds, Culiseta nausea, vomiting
melanura mosquito (enzootic vector)
▪ Neurologic presentation: cranial nerve
▫ C. melanura rarely bites humans palsy, seizure, stupor → coma
▫ Human transmission requires other ▪ Infants: fever, bulging fontanel, generalized
mosquito species (e.g. Aedes, flaccid/spastic paralysis

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 DIAGNOSIS TREATMENT
DIAGNOSTIC IMAGING ▪ No specific treatment

MRI
▪ Focal lesions in basal ganglia, thalamus, MEDICATIONS
brainstem ▪ Supportive: anticonvulsants,
corticosteroids (↓ inflammation)

LAB RESULTS
▪ Leukocytosis; left shift
OTHER INTERVENTIONS
▪ Supportive: IV fluid, respiratory support,
▪ Hyponatremia
monitor intracranial pressure
▪ Serology
▪ Prevention
▫ IgM antibody presence
▫ Insect repellent (DEET, picaridin,
▪ Cerebrospinal fluid (CSF) examination IR3535, oil of lemon eucalyptus)
▪ Lymphocytic pleocytosis, ↑ neutrophils; ▫ Protective clothing
↑ protein; IgM antibodies (assay); virus
▫ Vector control
isolation

OTHER DIAGNOSTICS
Electroencephalography (EEG)
▪ Generalized slowing; disorganized pattern

RUBELLA VIRUS
osms.it/rubella-virus
node viral replication → viremia →
PATHOLOGY & CAUSES maculopapular rash eruption → rash
resolution (approx. two days)
▪ Highly communicable virus → German ▫ Contagious via virus shedding before,
measles after rash appears
▪ Enveloped, positive-sense, single-stranded ▫ ↑ contagiousness during rash eruption
RNA virus
▪ Spreads transplacentally
▪ Family: Togaviridae
▪ Genus: Rubivirus
▪ Three structural proteins
RISK FACTORS
▪ Unvaccinated
▫ C: capsid protein surrounding virion
RNA ▪ Travel (especially abroad)
▫ E1, E2: glycosylated proteins forming ▪ Contact with febrile rash individuals
transmembrane antigenic sites
▪ Humans are the only natural hosts COMPLICATIONS
▪ Transmission: droplet inhalation/direct ▪ Thrombocytopenic purpura
contact with infectious nasopharyngeal ▪ Encephalitis (rare)
secretion ▪ If infected during pregnancy: congenital
▪ Viral contact → 12–23 day incubation rubella syndrome (CRS)
→ nasopharyngeal cell, regional lymph

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▫ ↑ risk of miscarriage, fetal death, ▫ Reverse transcription-PCR (rubella virus

stillbirth RNA performed on amniotic fluid)
▫ CRS: A ToRCHeS (see mnemonic)
infection; ↑ first trimester risk; OTHER DIAGNOSTICS
extramedullary hematopoiesis
▪ Clinical diagnosis
(“blueberry muffin” rash), cataract, heart
defect, hearing impairment, intellectual ▪ High suspicion index
disability ▫ Febrile rash, unvaccinated status

MNEMONIC: ToRCHeS TREATMENT

Perinatal infections passed
from mother to child ▪ No specific antiviral therapy
Toxoplasmosis, toxoplasma
gondii OTHER INTERVENTIONS
Other infections ▪ Infection control measures
Rubella ▫ Prompt isolation for seven days after
Cytomegalovirus rash development
Herpes Simplex virus-2/ ▪ Vaccine: live-attenuated measles-mumps-
neonatal herpes simplex rubella (MMR)/measles-mumps-rubella-
varicella (MMRV)
▫ First dose: 12–15 months old
SIGNS & SYMPTOMS ▫ Second dose: 4–6 years old

▪ Maculopapular rash
▫ Pink/light red macules: coalesce to form
evenly-colored desquamating rash
▫ Initially: face → generalized rash within
24 hours
▫ Duration: three days
▪ Lymphadenopathy; primarily posterior
auricular/suboccipital lymph
▪ Low-grade fever
▪ Mild nonexudative conjunctivitis
▪ Forchheimer spots on soft palate
▪ Arthralgias
▪ Orchitis
▪ Asymptomatic (half of cases)

DIAGNOSIS
LAB RESULTS
▪ Polymerase chain reaction (PCR) testing/
molecular typing
▫ Throat, nasal, urine specimens
▪ Serologic testing
▫ Enzyme immunoassay (EIA) detects
rubella-specific IgM antibodies Figure 101.1 A child with rubella showing a
characteristic maculopapular, erythematous
▪ Pregnancy
rash.

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VIRUS (WEE)
osms.it/western-equine-encephalitis

COMPLICATIONS
PATHOLOGY & CAUSES ▪ Encephalitis, coma, respiratory failure,
death
▪ Causes central nervous system illness in
▪ Infants: intellectual disability, cerebellar
humans, horses (equines)
damage, spastic paralysis, developmental
▪ Genus Alphavirus delay
▪ Spherical, approx. 69nm diameter
(including glycoprotein spikes)
▪ Enveloped, single-stranded, positive-sense SIGNS & SYMPTOMS
RNA genome
▪ Contain glycoproteins associated with ▪ Neurological manifestations
neurovirulence, cellular apoptosis ▫ Generalized weakness; somnolence;
▪ Range: most commonly US states, hand, tongue, lip tremor; cranial nerve
Canadian provinces west of Mississippi palsy; motor weakness; ↓ deep tendon
River reflexes
▪ Virus life-cycle: wild birds, other ▪ Infants: poor feeding, fussiness, fever,
vertebrates, Culex tarsalis mosquito vomiting, tense/bulging fontanelle
(enzootic vector)
▫ Culex tarsalis (another human vector)
▪ Potential bioterrorism agent use (aerosol
DIAGNOSIS
route)
LAB RESULTS
▪ Infected mosquito bite → 2–10 day
incubation period → sudden onset of ▪ Serology
severe headache, fever/chills, dizziness, ▫ Enzyme-linked immunosorbent assay
chills, myalgias, malaise, tremor, irritability, (ELISA): IgM antibodies
photophobia, neck stiffness → rapid ▫ Hemagglutination-inhibition,
neurological manifestation development → neutralizing antibody presence
recovery ▪ CSF
▫ Most adults: no residual neurological ▫ ELISA: IgM antibodies
effects ▫ Lymphocytic pleocytosis
▫ Infants, children: ↑ long-term neurologic ▫ ↑ protein
sequelae risk

RISK FACTORS TREATMENT

▪ Most cases June–September
▪ No specific treatment
▪ Bimodal age pattern: < one year; ↑ risk in
elderly
▪ Biologically-female MEDICATIONS
▪ Rural residence ▪ Supportive: anticonvulsants, corticosteroids
▪ Outdoor occupation/recreational activity

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OTHER INTERVENTIONS
Prevention
▪ Insect repellent (DEET, picaridin, IR3535, oil
of lemon eucalyptus)
▪ Protective clothing
▪ Vector control

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