ORGANISM PROPERTIES ENCOUNTER ENTRY MULTIPLICATION DAMAGE/VIRULENCE OUTCOME TREATMENT

FACTORS
Picornavirus Small, non-enveloped, Replicates in
icosahedral, (+) ssRNA cytoplasm
Enterovirus Stable at low pH Primarily human Can enter and
3 antigenic types: pathogen, survives in replicate in
poliovirus, water sources, nonprimate cells
Poliovirus coxsackievirus, destroyed by Ingestion and -Grows in oropharynx -Invades brain + spinal Inapparent infection (no Two vaccines:
(enterovirus) echovirus pasteurization infection of GI tract and intestine cord* symptoms), mild febrile 1. Killed Salk vaccine
-Can enter blood and -Anterior horn cells of illness (fever), (multivalent formalin)
spread to CNS and the spinal cord -viral meningitis, – injection
PNS destroyed (results in paralysis, 2. Live-attenuated
paralysis of limb mm.) progressive Sabin vaccine (single
Peripheral nn. also postpoliomyelitis muscle and multivalent) –
affected atrophy oral; more effective
Coxsackie virus Infects GI tract -Group A: Herpangina Ibuprofen/ Tylenol,
(enterovirus) (painful mouth blisters), topical anesthetic for
Hand, foot, mouth disease blisters
(lesions)
-Group B: Pleurodynia,
myocarditis, pericarditis
Echovirus *Most common cause of
(enterovirus – enteric viral (aseptic)
cytopathic human meningitis)
orphans)
Rhinovirus Acid-labile Enters URT by Main cause of Common
(susceptible to acid), inhalation cold*
heat stable, destroyed -Nasal discharge, cough,
at low pH headache, chills
-Usu. afebrile (no fever)
Orthomyxoviridae (-)ssRNA, enveloped, Very hardy survive Airborn droplets or Virus changes its 1)Uncomplicated -Neutralizing
helical capsid in nature contact antigenic characteristics influenza: chills, headache, antibodies against HA
-Genetic reassortment -respiratory epithelial from one epidemic to dry cough, fever, muscle and NA are
via Antigenic Shift: cells infected the next aches, malaise, anorexia, responsible for killing
major, sudden -Transcriptase (RNA fever (3 days) virus
antigenic changes polymerase) 2) Pneumonia: elderly and -Short term: 1 year
Antigenic drift: minor -Nucleoprotein: Capsid debilitated at high risk protection
antigenic changes protein -due to loss of ciliary -Neuraminidase
(point mutations) -Matrix: shell beneath clearance, phagocytic cell inhibitors should be
-3 types, based on the viral lipid envelope dysfunction, alveolar given within 2 days of
Ribonucleoprotein -Hemagglutinin*: exudate= rich bacterial symptom onset
based mainly on M attachment functions, medium -Vaccine: 2 types of
and NP proteins fuses viral envelope 3) Reye’s syndrome: influenza A and 1 type
-only type A has with host cell Acute encephalopathy of influenza B, use yearly
subtypes based on membrane children for “at risk” ppl
other proteins: 16H -Neuraminidase* -fatty degeneration of liver -FluMist (LAIV): live
and 9N (release of virions from -cause unknown (salicylate attenuated
cell) association), high mortality -TIV (trivalent): killed
virus
Coronaviruses Long helical structure, Grows in cytoplasm Infects and kills -2nd main cause of
(+) ssRNA, enveloped Limited to URT epithelial cells common cold
with viral -More nasal discharge than
glycoproteins (E2 – rhinovirus
viral receptor, E1 – -Less cough than rhino
fusion function) -SARS (severe acute
-env. Glycoproteins respiratory syndrome)
halo around virus
Paramyxoviruses (-) ssRNA, helical Transmitted by -HN: binds to host -Grows in cytoplasm -Large droplet aerosol -Croup: barking cough due
nucleoprotein capsid, respiratory secretions sialic acid receptor of host using viral transmission to infection and swelling of
-Parainfluenza: envelope with (present on surfaces RNA-dependent RNA -virus replicates in larynx
respiratory infection hemagglutinin (HN), of erythrocytes and polymerase epithelial cells of
-Respiratory syncytial neuraminidase (NA), cells of URT); allows -Fusion (F) protein nasopharynx
virus: respiratory and fusion adsorption and fusion causes host cells to -carried to lower
infection glycoproteins of virion membrane fuse together into respiratory tract by
-Mumps: systemic with host cell multinucleated giant secretions
disease with parotitis -different from ortho membrane cells (syncytia)
predominating in that Hemagglutinin -NA: cleaves
-Measles (rubeola): and neuraminidase neuraminic acid in
generalized are part of the same mucin, disrupting
exanthematous (skin glycoprotein mucin barrier
eruption/rash) -Possess Fusion covering mucosal
disease Protein that causes epithelial cells and
infected host cells to exposing sialic acid
fuse together into receptors
multinucleated giant
cells (syncytial cells)
Respiratory Aerosol transmission Inhalation Virus replicates in -Immediate Type 1 *Most important cause of -Ribavirin (guanosine
syncytial virus epithelial cells of the hypersensitivity (IgE) LOWER respiratory tract analog—antiviral)
nasopharynx, then -Bronchopneumonia illnesses in Infants and
spreads to LRT with sloughing of younger children
bronchiolar epithelium, -Pharyngitis
monocyte infiltration -Rhinitis
and abundant mucus -Bronchitis, bronchiolitis,
secretion pneumonia
-Most RSV infections are
symptomatic
-Incubation ~4 days
-More severe and
infectious than common
cold
Measles (Rubeola) Humans – natural host Inhalation, local -Initially replicates in -Rash: spreads from Typical measles: Infection or Live
virus replication of virus in respiratory epithelial Forehead feet and prodromal fever, vaccine gives life-long
respiratory tract, tissues coalesces sneezing/other cold immunity! (MMR)
spread to lymphatic -Primary viremia: -Red or reddish-brown, symptoms, red eyes,
system and blood virus spreads thru continues for many days Koplik’s spots in buccal
which seeds the blood to lymphoid (7-10) mucosa: white spot with
epithelial surfaces of tissue and -disappears from head red base
the body reticuloendothelial to feet as well -secondary invader:
-CNS involvement system (aka bronchopneumonia, otitis
uncommon mononuclear media
phagocyte system) -encephalitis
contact with -Secondary viremia: Atypical measles: no
conjunctiva body rash due to T rash/unusual rash,
cells interacting with -Occurs in individuals who
virus have received Killed
-Formation of measles vaccine as chidren
multinucleated giant -Killed vaccine= no Fusion
cells in lymphoid protein incomplete
tissue protection
Rubella (German Togaviridae Inhalation -Forchheimer’s spots -Vaccine (MMR)
measles) (+)ssRNA, icosahedral, Congenital** (red) on soft palate -Antibodies rise
enveloped -Rash, mild upper quickly after rash
respiratory symptoms, -Life-long immunity
lymph gland with excellent Live,
-Milder than measles attenuated vaccine
-Pink or light red rashes
that disappear in 3 days
-Lymphadenopathy
(swelling of nodes)*
-Complications: possible
fetus malformation, esp. in
women during 1st trimester
of pregnancy
Mumps Person-to-person -Primary replication Epithelial cell -1/3 of cases subclinical Live attenuated
transmission occurs in nasal or destruction (usually (no symptoms) vaccine
- Humans: natural upper respiratory self-limiting) -Prodrome
host tract epithelial cells (malaise/anorexia)
-Viremia to salivary followed by rapid
glands (parotid); enlargement of parotid
testes and ovaries are (parotitis) and salivary
secondary targets glands (single or bilateral)
-Orchitis: testes infection
-Aseptic (Viral)
meningitis: 15% of all
post-infectious
encephalitis cases are
called by the mumps virus
Papoviridae: -Naked icosahedral -Transmission is by -Must first infect the Common warts: Cidofovir: inhibits
Human Papilloma -ds circular DNA Direct contact with Basal cells*, then Types 1, 2, 4, 7 DNA synthesis
Virus -over 150 types infected individuals rises to the surface Genital: 6, 11, 16, 18
(sexual contact) or but continues to Cervix cancer: 16, 18 Vaccines:
with contaminated multiply in the prickle *note overlap Gardisil: types 6, 11,
surfaces (fomites) such layer *boards TQ 16, 18
as communal Cervarix: 16, 18
bathroom floors
Viral Hepatitis -Other viruses can Acute:Hep A, B, C, D, E Inflammation and necrosis -IFN treatment is the
(general) cause hepatitis, but Chronic: B, C, D of liver cells only anti-viral
they often involve *Boards TQ -Lethargy, loss of appetite, treatment
other organ systems nausea, vomiting,
such as skin abdominal pain, jaundice
(Epstien-Barr, (bilirubin build-up)
Cytomegalovirus,
Rubella, Rubeola,
Mumps, Adenovirus,
Coxsackie)
In immunosuppressed
and neonates, Herpes
simplex virus and
Varicella-Zoster can
produce a
disseminated
infection with hepatic
involvement
Hepatitis A PicoRNAviridae family Transmitted by -Acute only Vaccinations for A + B
-Enterovirus genera Ingestion (also Hep -Necrosis of hepatocytes: recommended for at
-Unusually Stable: E!) virus growth risk adults
resistant to ether, -15-40 days incubation -GI stress, weakness, fever, -Immune serum
chlorine, merthiolate, jaundice, slow recovery, globulin
survive 60 C for hours relapses common.
-Destroyed @ 100 C -No chronic carrier state
for 30 mins by (B, C, D are chronic)
autoclaving or by
treatment with
ethylene oxide
Hepatitis B HepaDNAviridae Transmitted HBsAg: present on HBsAg= Disease -Similar to Hep A, but
(Serum Hepatitis) family Parenterally (that the surface of the (acute or chronic: if more severe
-dsDNA which occurs outside large 42 nm Dane over 6 months) -GI distress, weakness,
-circular DNA, but one of the alimentary tract, Particle (HBV) Anti-HBsAg= fever, slow recovery,
strand not fully closed such as in Immune, cure, no relapses common
-enveloped subcutaneous, HBcAg: Hep B Core active disease -Incubation 60-160
-helical capsid intravenous, antigen present within IgM Anti-HBcAg= days
-More stable than intramuscular, and Dane particle New infection
most viruses (0.0004- intrasternal injections) IgG Anti-HBcAg= Old Chronic Hep B:
0.000001 ml of -B-D: parenterally HBeAg: internal Ag, infection Measurement of
infected blood can -A, E: enterally important for HBsAg positive for 6
transmit disease) -Transmission by measuring Infectivity HBeAg= High months or longer*
-Has DNA polymerase sexual contact and Potential (aka infectivity, virus Active protection:
with Reverse from mother to fetus Epsilon) going wild vaccine
Transcriptase -Use serology to Anti-HBeAg= low -Interferons
activity identify what stage of infectivity
disease you are in

Hepatitis C Flaviviridae family Transmitted Most common cause of Lab: Serological test
(Non-A, Non-B (+)ssRNA Parenterally and Chronic Hepatitis * for HCV or antibodies
Transfusion -Enveloped Sexual contact -Most common cause of
Associated) -Primarily transmitted Posttransfusion Hepatitis Treatment:
by blood now Interferons
-Oral sex can cause it -Clinically Mild
to be enterally -HCV disease resembles
transmitted acute HBV infections
-a Chronic carrier state
also exists
Delta Hepatitis: Deltavirus group Co-infection with HBV -Can cause acute or chronic
(HDV) Defective virus hepatitis
(-) ssRNA -Defective: Requires HBV
for replication (only infects
patients who are HBsAg+)
Hepatitis E: -Calciviridae family Transmitted by -Acute hepatitis only (also
(Enterically (+)ssRNA Ingestion (enteral) Hep A)
transmitted) (eg. contaminated
water supply)