Gnarpe’s Vicious Viruses Clinical Presentation:

-dependent on serotype.
-acute respiratory infection: often fever in children 6 months to 5
Virus: Adenovirus (ds DNA) years of age - self-limiting (types 1,2,5,6)
a. nonenveloped virus, icosahedral with protruding fibers -enteric strains cause diarrhea (40 and 41).
b. ~50 serotypes, 6 subgroups -serotypes 3,4,7,14,21 often cause epidemics in military.
c. wide spectrum of disease dependent on serotype -risk for disseminated adenovirus infection in neonates.
d. latency in lymphocytes
e. replication in epithelial cells
Epidemiology:
f. infectious dose dependent on site of infection
-stable for weeks on fomites and surfaces
g. risk factor for infection: close contact, crowding
-resistant to ether
h. viral shedding varies according to strain
-nosocomial infections common.
-“Shipyard Eye”, “swimming pool conjunctivitis” or epidemic
Immune Response: keratoconjunctivitis caused by serotype 8
-high incidence in bone marrow transplant (20%) (types 34,35)
-secretory IgA, humoral IgG/IgM -worldwide distribution
-stimulates inflammatory response.

Diagnosis:
Transmission: direct, droplet and fecal-oral -collect specimens early
-virus isolation in cell culture, PCR, EM
-serology to detect IgM or 4-fold IgG titer increase.
Pathogenesis:
Complications:
-binds via fibers sticking out of the viral envelope. -disseminated and fatal infection (neonates & immunosuppr.)
-inhibition of macromolecular synthesis in host cell
-disease state caused by results of the inflammatory response.
-some types bind to MHC 1 prevent their translocation to cell Treatment and Prevention: No current vaccine. No
Pneumonia in neonates.
surface, inhibiting immune recognition. antiviral agent. Supportive treatment. Chlorination of
swimming pools and wastewater. Strict attention to asepsis
during eye exams.
Gnarpe’s Vicious Viruses Clinical Presentation:
-fever, sore throat, cough, severe respiratory distress
Virus: Avian Influenza (ss RNA) secondary to interstitial pneumonia
-can mimic SARS
-patients probably more susceptible to secondary bacterial
a. enveloped, genus Orthomyxoviridae, Influenza A infections if they survive the avian influenza
b. 8 segments of RNA -birds usually die of their infection
c. H5N1 is the most dangerous serotype at present
d. natural reservoir: birds
e. receptor is a different sialic acid molecule, to present
the virus does not readily infect humans

Diagnosis:
Immune Response and Pathogenesis: -PCR/ cell culture and serology (IgM or ↑ in IgG).
-information limited on pathogenesis and immune response
-virus can undergo Antigenic shift and Antigenic drift
- mutation in the genes coding for the glycoprotein receptors Complications:
and allowing them to more easily bind to human cells -death, secondary bacterial infection
would be disastrous
-antibodies are produced during infection, not known how Epidemiology:
protective and how long lasting -started appearing in Asia (Hong Kong 1997) as a disease of
-respiratory infection and severe lung disease even in chickens, has since then spread through Asia, the Middle
immunocompetent individuals East and has started appearing in birds in Europe
->500 people have died as of 2009 and overall mortality
mortality rate ~60%.
Transmission: bird to bird transmission may be fecal-oral.
Humans infected by direct contact with sick birds. Rare Treatment and Prevention: Vaccine not available for
documented case of person-person transmission, likely direct humans. Some resistance to influenza antivirals reported.
contact Supportive therapy important. Prevention – eradicate
infected flocks, reduce bird contact.
Gnarpe’s Vicious Viruses Clinical Presentation:
- incubation 2-12 days, usually 3-7 days
- abrupt onset, fever, headache, fatigue, nausea, vomiting,
muscle pain, rash and joint pain (similar to Dengue Fever)
Virus: Chikungunya Virus (CHIKV) - can have asymptomatic infection
a) ssRNA, enveloped, positive sense
- as with Dengue fever, can have prolonged fatigue or
b) alphavirus, family Togaviridiae
arthritis lasting weeks to months
c) several subtypes based on E1 typing
d) arthropod borne (mosquito= Aedes aegypti)
e) first detected 1952 in Tanzania, name from a local Epidemiology:
word meaning “that which bends up” refers to -primarily East Africa and Asia, especially Indian Ocean
stooped posture of patients with painful joints Reunion Island & India

Immune Response and pathogenesis:

- infection confers immunity Diagnosis:
-major histopathologic changes seen in animal models: -PCR/ serology (specific IgM by ELISA)
focal necrosis and inflammation of skeletal muscle,
followed by fibrosis and dystrophic calcification. Some
mice also showed dystrophic calcification in the joint Complications:
cartilage. -fatalities rare, associated with increased age
-fulminant hepatitis, arthritis, some neurological

Treatment and Prevention: No vaccine, no antiviral,

supportive therapy.

Transmission: Prevention: control of mosquito population. DEET

-arthropod, mosquito bites from Aedes (day biter). Same
mosquito as for Dengue and Yellow Fever
Gnarpe’s Vicious Viruses Clinical Presentation:
-upper respiratory tract infection: common cold
-up to 8% of infants hospitalized for bronchiolitis and
pneumonia have coronavirus
Virus: Coronavirus (ss RNA) -lower respiratory tract infection in military recruits
a) enveloped virus, many strains -incubation period 2 days, symptoms peak day 3 or 4.
b) common causes of animal disease, enteric strains exist
c) Coronavirus causes 10-20% of common colds SARS: fever, chills, myalgia, dry cough, headache,
d) new variant: SARS (not species specific) dizziness, sore throat, runny nose, vomiting,
diarrhea, hypoxia, pneumonia (often biphasic)
Immune response and Pathogenesis: Epidemiology: seasonality (winter/spring), 2 year intervals
-secretory IgA.
-antibodies are formed to the major structural proteins on for ordinary coronavirus, one known epidemic so far for SARS
virus, e.g. S protein, but may not be protective. Diagnosis:
-immunity short-lived.
-clinical diagnosis for “normal” coronavirus.
-SARS: PCR, cell culture and serology
*Important to differentiate from avian influenza.
Transmission: direct or droplet -Chest x-ray: progressive lung infiltrates

Complications:
Pathogenesis: “Ordinary coronavirus”: complications only seen in
-infects respiratory epithelium of upper and lower airways individuals with underlying disease, include
-uses receptors on host cells, e.g. neuraminic acid and wheezing and exacerbations of COPD
aminopeptidase N, both widespread in tissues
-enters cells by fusing host and viral membranes “SARS”: increasing age most important risk for severe
-inflammatory response causes tissue and cilia damage disease. ~15% die, ~20% develop ARDS (acute
-SARS induces violent inflammation. respiratory distress syndrome)

Treatment and Prevention:

-supportive, no good antivirals, no good vaccines yet
-prevention includes isolation of patients and use of N95
masks
Gnarpe’s Vicious Viruses Clinical Presentation:
-Type A Disease: Hand foot and mouth: vesicular viral rash
Virus: Coxsackie Virus (ssRNA) on palms of hands, soles of feet and inside the mouth.
Adults usually don’t get it as they have antibodies from their
childhood. -fever, poor appetite, runny nose and sore throat
a. Family Picornaviridae; genus enterovirus ssRNA
b. First isolated in Coxsackie NY in 1948 can appear three to five days after exposure. Blister like rash
c. GroupAandB develops 1-2 days after original symptoms.
d. Over 24 serotypes of disease
e. Type A: Hand foot and mouth disease, conjunctivitis -Type B Disease: chest pain, some of the symptoms above
f. Type B: pleurodynia “Bornholms disease”
g. Both types A and B can cause meningitis,
myocarditis and pericarditis but this is rare
Complications:
-death from myocarditis, pericarditis if not treated.
Immune Response and Pathogenicity:

Type A: Hand foot and mouth mostly caused by A16, but

also other serotypes. Specific immunity to infecting serotype,
but not to other serotypes

Type B: replicates in the gut and spleen then spreads to the Epidemiology:
heart where it continues replicating and causes WBC to -worldwide distribution
move into the heart muscle where they kill virus infected -tropics: peaks in hot dry seasons; epidemics every 2-3
cells and some uninfected cells as well. yr -large WHO led program underway to eradicate
disease

Treatment and Prevention: No vaccine, Antivirals:

Transmission: fecal-oral, direct Supportive care, vitamin A supplements.
 Gnarpe’s Vicious Viruses Clinical Presentation:
Congenital:
- 7% defects at birth, 93% later in life
Virus: Cytomegalovirus (CMV, HHV-5) - brain damage, blindness, deafness, 20% die in infancy.
a) Enveloped, member of herpes family Postnatal:
b) Major role in graft versus host disease -usually asymptomatic, few cases of IM with no
c) Ubiquitous, multiple strains with cross-immunity heterophile antibodies, spontaneous recovery
d) Latency in granulocyte precursors Infection in immunocompromised:
-primary or reactivated infection
e) Incubation 3-8 weeks
-spiking fevers most common symptom
Immune response and pathogenesis: -often seen in solid organ transplant and bone marrow
-replication in many different tissue types (lung, liver, graft recipients
esophagus, colon, kidney) and immune cells (PMNL, -25% of AIDS patients develop CMV disease, most
monocytes, T-lymphocytes, B-lymphocytes) common is disseminated disease; 90% retinitis.
-formation of giant cells (cytomegaly) – “owls-eyes” Epidemiology:
-important role in GVHD, transplant rejection, congenital -worldwide
disease -infections easily spread in daycare
-virus excreted in urine for many years
Trans Tranmission: -seropositivity in developed nations ~ 40%
-seropositivity in underdeveloped nations ~70-90%.
Horiz Horizontal: droplet, direct from saliva, sexual contact, organ -greatest risks for pregnant women & organ transplants
Transplants, blood transfusions
Diagnosis:
Vertical: via placenta, breast milk. -cell culture/histological exam tissues, urine FA/EIA/PCR
-serology: CMV IgM in ongoing or recent 1° infection

Complications: See Clinical presentation.

Treatment and Prevention: No vaccine. Gancylovir.

Prophylactic treatment for immunosuppressed, e.g.
transplant patients 3-6 mo post transplant.
Gnarpe’s Vicious Viruses Clinical Presentation:
-Dengue Fever: incubation 2-15 days, fever, malaise,
chills, rash, headache, pain in back, joints, muscles and
Virus: Dengue Virus eyeballs. (“Breakbone Fever”).
-Dengue Hemorrhagic Fever (DHF): usually affects children
a) ssRNA, enveloped, positive sense
(if progression to Dengue Shock Syndrome, mortality
b) flavivirus
c) arthropod borne (mosquito = Aedes) four serotypes 40%)

Immune Response and pathogenesis: Epidemiology:

-major site of replication is macrophages/monocytes. -most tropical and subtropical areas = endemic areas (>100
-histopathology in small vessels, endothelial swelling countries)
-perivascular edema and infiltration with MNC -epidemics occur
-Dengue infection with 2nd serotype within 1-2 years can - > 50 million cases/yr (WHO) and rising
give rise to Dengue Hemorrhagic Fever
-release of cytokines and other mediators result in Diagnosis :
Incidence is increasing.
disseminated intravascular coagulation -PCR/ serology
-humoral antibodies only protective against specific
serotype Complications:
-DSS, shock, circulatory collapse and death.

Transmission: Treatment and Prevention: No vaccine, no antiviral,

-arthropod, mosquito bites from Aedes (day biter). supportive therapy.

Prevention: control of mosquito population.

Gnarpe’s Vicious Viruses Clinical Presentation:
-mostly asymptomatic in young children, but otitis media,
diarrhea, abdominal pain, URTI, IM
Virus: EBV (Epstein-Barr Virus or HHV-4) -young adults more symptomatic: “kissing disease”: fever,
a) -enveloped, member of herpes family tonsillopharyngitis, swollen glands, lymphocytosis, malaise,
b) -incubation 30-50 days fatigue, headache, ± rash, mild hepatitis, splenomegaly.
c) -latent infection in B lymphocytes
d) -host range: humans and few primates
e) -causes Infectious Mononucleosis (IM)
Epidemiology:
-worldwide, 70-95% of adults are seropositive
f) -replication in lymphoid cells of oropharynx
-clinically apparent infection greatest in 15-25 year olds.
-Burkitt’s lymphoma and nasopharyngeal cancer endemic in
Immune Response and Pathogenesis: parts of the world with concomitant high rates of malaria.
-infects B lymphocytes
-“Atypical lymphocytes” appear 1-3 weeks after infection Diagnosis:
& these are source of immuno-active substances like -serology best; heterophile antibodies (monospot) or specific
cytokines that cause the clinical symptoms antibodies (EIA)
-CD8+ important for controlling acute infection -finding of “atypical lymphocytes in peripheral blood
-associated with malignancy: Burkitt’s Lymphoma, NP-
carcinoma Complications:
-acute infection related: ampicillin rash, splenic rupture,
Transmission: airway obstruction, lymphoproliferative disorders
-direct (saliva) especially in immunocompromised
-intermittent shedding in saliva (asymptomatic carriers) -malignancies – Burkitt’s lymphoma, nasopharyngeal
carcinoma, oral hairy leukoplakia

Treatment and Prevention: No vaccine. Supportive

care.
Gnarpe’s Vicious Viruses Clinical Presentation:
-disease caused by Ebola and Marburg similar
- abrupt onset, incubation 3-16 days, severe frontal
Virus: Ebola headache, high fever
a) Enveloped, member of filoviridae family -rapid prostration with diarrhea + vomiting, conjunctivitis,
b) Name filo comes from ‘thread’ pharyngitis
c) Only found in Africa -sometimes maculopapular rash after 5-7 days when severe
d) Source? recently found in bats (Uganda) bleeding starts in the lungs, nose, gums, gastrointestinal
tract + conjunctiva
Immune response and pathogenesis: - thrombocytopenia
- death due to severe shock and blood loss between day 7-
- pantropic virus 16
- similar to Marburg virus
- infect and cause lesions in many organs, especially liver .
and spleen, causing severe degeneration and necrosis Epidemiology:
- mechanism of pathogenesis obscure - outbreaks in Africa
-damage to endothelial cells results in increased vascular - probably endemic in Sudan Zaire
permeability  hemorrhage and shock

Transmission:
- unknown, probably droplet Diagnosis:
- contact with an infected patient is necessary for infection -Biosafety level 4, high containment; virus isolation from
- normal isolation and barrier nursing methods prevent blood and autopsy tissue in cell culture
transmission -antigen tests (ELISA), PCR
-serology: significant rise in antibody

Complications: Severe shock, often death

Treatment and Prevention: No vaccine. No antiviral,

but they often try ribavirin and sometimes heparin.
Gnarpe’s Vicious Viruses Clinical Presentation:
-may be asymptomatic, symptoms increase with age.
-may be icteric (with jaundice) or non-icteric (age related)
-mild prodrome, nausea, vomiting, malaise, fever.
Virus: HAV (Hepatitis A) (ssRNA) -smokers may lose taste for tobacco.
-dark urine followed by pale or clay-colored feces, yellow
a) non-enveloped, also called “infectious hepatitis”
discoloration of the sclera, skin and mucous membranes.
b) resistant to acid, relatively stable in heat (30 min
56C), hard to grow in vitro
c) viable in dried form for several weeks at room Epidemiology:
temperature -occurs worldwide but prevalence is higher in areas with
d) one serotype, infects primates, incubation period 2-7 poor hygienic standards (most children in these areas have
weeks had Hepatitis A)
e) acute infection of liver
f) immunocompromised = immunocompetent for Diagnosis:
severity -presence of Hepatitis A virus (HAV) IgM in serum
h) no chronic carriers
Complications:
-relapsing hepatitis (resolves eventually)
Immune Response and Pathogenesis: -extrahepatic: rare, fulminant hepatitis: rare
-infection confers total immunity Epidemiology:
-serum antibody alone can confer protection
-virus not cytolytic, damage to hepatocytes may be due to -occurs worldwide but prevalence is higher in areas with
inflammation of hepatocytes resulting in spilling of poor hygienic standards.
enzymes (transaminases). -most children in these areas have had Hepatitis A.

Transmission: Treatment and Prevention: Active immunization

-fecal-oral, person to person, contaminated water and with inactivated virus, passive immunization with pooled
shellfish human IgG, no antivirals, supportive therapy
Gnarpe’s Vicious Viruses Clinical Presentation:
-acute infection: asymptomatic to cholestatic hepatitis with
Jaundice
Virus: HBV (Hepatitis B Virus) -prodrome of myalgia, arthralgias usual
a) dsDNA, enveloped -chronic infection: usually symptoms due to chronic liver
b) envelope contains HBsAg disease.
c) humans only host Epidemiology:
d) incubation period 6 wks-6 mo., average 10 wks
-worldwide incidence
e) chronicity large problem
-primarily STI in developed world
f) virus has reverse transcriptase
-high incidence among HIV+, drug abusers, hemodialysis
g) three forms of antigen made of HBsAg: tubular,
patients etc (high rates in SE Asia, Africa, & E. Europe
small spherical and large spherical (Dane) - transmission from mother to child common
-infants highest chance of becoming chronic carriers
Immune Response:
-first humoral antibody HBcAb (core antibody), then Diagnosis:
HBsAb, HBeAb (can use for diagnosis and follow-up) Serology, PCR for HBV DNA.
-infectivity of patients shown by HBeAg in blood or
HBV-DNA Complications:
-cell mediated immunity important for eradication of Liver cancer.
HBV in treated patients.
Transmission: Treatment and Prevention: Lamuvidine (antiviral).
-direct – sexual contact and by blood-products Growing resistance to drug. Vaccine very good, produced in
-vertical via placenta yeast. Infants born to HBV+ mothers should get active
vaccine and passive immunization at birth.
Pathogenesis: Passive immunization with HBIg. Interferon used for
-chronic infection in liver major factor for development of chronic carriers, but relapse quickly when drug
liver cancer, mechanism not understood, inflammation? discontinued.
-viral replication not directly toxic to cells.
Gnarpe’s Vicious Viruses Clinical Presentation:
-fatigue, spider nevi in head and neck area
-few symptoms until end stage liver disease.
Virus: HCV (Hepatitis C Virus)
a) ssRNA virus, enveloped Epidemiology:
b) 6 serological types -200 to 400 million carriers worldwide
c) 5 main genotypes 1a,1b,2,3a,4a -15-20,000 new cases/yr in Canada
d) earlier called non-A, non-B hepatitis -most transmission through IV drug use (sharing needles)
e) flavivirus family -can have several genotypes at the same time.
f) chronicity a problem
g) HCV proteins synthesized as one polyprotein
Diagnosis:
Immune response: -serology
-humoral antibodies and cell-mediated immunity important. -PCR for HCV-RNA in blood
-many quasi-species of virus present, making target -genotyping to guide therapy
more difficult to control. -elevated liver enzymes with low platelet counts and low
signal liver failure
Transmission:
-blood products, vertical transmission, low risk sexual spread
Complications:
Pathogenesis: -liver cirrhosis, liver cancer, chronic hepatitis.
-not well characterized, virus grows only in vivo. - major reason for need for liver transplants
-development of chronic hepatitis with inflammatory
infiltrates, mainly lymphocytes and macrophages, leads to
necrosis of tissue
-large lipid droplets in cytoplasm of infected hepatocytes Treatment and Prevention:
-hepatitis develops to fibrosis, cirrhosis + liver cancer
-20% of patients develop cirrhosis after 20 years of chronic No vaccine. Chemotherapy with ribavirin and interferon.
carriage Variable success dependent on serological type.
-pathogenesis dependent on genotype (Type 1 not easily
treated).
Gnarpe’s Vicious Viruses Clinical Presentation:
-acute infection: asymptomatic to cholestatic hepatitis with
jaundice, subclinical infections common, especially in
Virus: HEV (Hepatitis E Virus) children
a) ssRNA, nonenveloped, small virus with spikes -no chronic infection
b) calicivirus- like (hepevirus) -carrier state not known
c) incubation period 6 wks
Epidemiology:
d) one serotype but four distinct genotypes (1 +2 in
-infection usually acquired in adolescence or adulthood
humans and 3+4 in animals like swine) -pregnant women in third trimester most at risk for serious
disease (mortality rate jumps from 0.9-4.0% to 20%)
-high prevalence in underdeveloped countries of Central and
East Asia, Africa and Mexico but globally causes <1% of all
Hepatitis disease
Immune Response:
-antibodies are formed to the virus but little is as yet Diagnosis:
known about humoral and cell mediated immunity Serology, EIA tests for IgM antibody. RT-PCR.
-self-limiting disease Not routinely available.

Transmission: Complications:
-vehicle, fecal-oral, water-borne Death in pregnant women
-animals likely reservoir, >95% of swine infected in
endemic areas
Treatment and Prevention: Water treatment. No
vaccine yet available. No antiviral therapy available. Liver
Pathogenesis: transplant may be necessary where possible in fulminant
-pathogenesis resembles Hepatitis A virus
disease states.
-viral replication not directly toxic to cells but damage may
be due to inflammatory response
Gnarpe’s Vicious Viruses Clinical Presentation:
-most infections are likely asymptomatic.
Exanthema subitum (ES) or “Roseola” or “Sixth Disease” in
children 6-18 mo.: high fever (40ºC) for 2-3 days, when
Virus: HHV-6 and HHV-7 fever drops, rash begins (maculopapular) and lasts 1-2 days.
a) Enveloped, members of the herpes family
-drowsiness, irritability common, rash first on neck, behind
b) Latency
ears and back, spreads to scalp and torso.
c) Associated with a variety of disorders
Adult disease: ill-defined as yet. Can cause IM.
d) HHV-6 and 7 primary infection in infancy (roseola)
-association with connective tissue diseases,
e) Lymphoproliferative disorders in adults
lymphomas, immune suppression
-infections reactivate after liver transplants.
Immune Response and Pathogenesis:
-HHV-6 replicates predominantly in CD4+ lymphocytes
and NK cells Epidemiology:
-HHV-7 similar to HHV-6 -HHV-6: High seroprevalence in children (90% of 3 yo)
-not much known about these viruses. -HHV-7: High seroprevalence in children < 5 years (95% )
-worldwide

Diagnosis:
Transmission: -Clinical diagnosis based on symptoms in children
-unknown, likely respiratory secretions and direct. -Serology in adults or PCR/culture using blood lymphocytes.

Complications: See Clinical Presentation, much is

unknown for both HHV-6 and HHV-7.

Treatment and Prevention: No vaccines. Treatment

unknown but in vitro data suggest that gancyclovir or
valcyclovir may be effective.
Gnarpe’s Vicious Viruses Clinical Presentation:
-acute HIV: fatigue, rash, headache, nausea, night sweats,
lymphadenopathy
Virus: HIV (Human Immunodeficiency Virus) -progresses with chronic diarrhea, severe opportunistic
a) ssRNA, enveloped, 2 strands infections or neoplasms like Kaposi’s sarcoma
b) carries reverse transcriptase for replication -clinical disease is usually ~10 years after exposure,
c) integrates into host cell DNA (provirus) untreated death follows in about 2 years.
d) infect cells of the immune system
e) two distinct types: HIV-1 and HIV-2 Epidemiology:
f) 11 subtypes or clades of HIV-1, 6 of HIV-2 -worldwide distribution
g) origin likely from SIV (simian virus) “rabere” = to rave - most common spread via heterosexual contact
-first recognized in 1981 among homosexual men in USA.
Immune Response and Pathogenesis:
-both humoral and cell-mediated responses
-antibodies to viral antigens develop soon after infection,
response pattern changes as disease progresses Diagnosis:
-envelope glycoprotein antibodies remain (gp41,120,160) -serology and HIV-RNA PCR used routinely
antibodies to core (p24) antigen disappear. -serology: EIA (screening). Positive tests confirmed by
-virus targets T-helper cells and attaches to CD4+ receptor Western Blot (gp41, gp120, gp160, p24)
plus a chemokine receptor. CD4+ infected have a shorter -viral load important for monitoring therapy.
lifespan and die, causing a decrease in ratio CD4/CD8.
-Some monocytes also have CD4+ and are susceptible to
infection Complications:
- virus mutates quickly (no proof-reading) – quasi species -neurological disease: dementia
and humoral immunity does not keep up with the changes -myriad of opportunistic infections, death.
-patients susceptible to opportunistic infections due to lack
of functional immune system
Treatment and Prevention: Prevention: use of barriers,
abstinence. No vaccine. Antivirals: HAART therapy – cocktail
Transmission: of drugs used to prevent rapid development of resistance.
-bloodborne, sexual transmission
Gnarpe’s Vicious Viruses Clinical Presentation:
-many different types of warts depending on the genotype
-three major types of cutaneous warts:
Virus: HPV (Papillomavirus or “Wart” virus) deep plantar
a) ds DNA, nonenveloped common warts
b) cannot be grown in vitro flat warts (often found in vagina/cervix)
c) some genotypes have oncogenic potential -usually resolve in 1-5 years
d) primarily infect the squamous epithelium -anogenital warts:
e) typed by genotyping, >100 types condylomata acuminata: often short broad shaft, ugly +
f). incubation periods different for different types irregular in shape
-respiratory papillomatosis in children infected at birth

Immune Response: Epidemiology:

-humoral antibodies produced but have limited effect -endemic worldwide, no epidemics reported
-cell mediated immunity important to restrict infections. -HPV-16 most common genital HPV & most often causes
cancer.

Diagnosis:
Transmission: direct -clinical – painting of cervix with acetic acid to visualize
-can type warts via molecular methods like PCR (genotype)
Pathogenesis:
-tropism for epithelial cells of skin and mucous membranes Complications:
-some integration into host cell DNA in cancer cells -Cancer, disseminated and fatal infection in neonates and
-virus causes proliferation of cells, usually causing benign Immunosuppressed, psychosocial problems.
“tumours” Treatment and Prevention: Vaccine for HPV 6,11,16,
-type 16 and 18 associated with cervical and penile cancer 18. (Gardasil) No good antiviral agent. Interferon is
-viral gene products E6 and E7 interact with tumor sometimes used in respiratory cases. Usual treatment is
suppressor genes e.g. p53 and Rb107 and interfere with cell destroying lesions with physical or chemical means (liquid
cycle regulation. nitrogen, salicylic acid, Podophyllin benzoin tincture, etc)
Gnarpe’s Vicious Viruses Clinical Presentation:
-General symptoms: painful and/or itchy vesicles, primary
infection usually accompanied by some systemic
Virus: HSV (Herpes simplex 1 and 2) symptoms, eg nausea, swollen glands, fever or meningitis
(HSV-2)
a. enveloped, large dsDNA viruses -Orofacial infection: most HSV 1, cold sores, primary
b. replicate in nucleus of host cell infection usually in childhood. Trigeminal nerve latency –
c. lytic, incubation 1 week recurrent lesions in 20-40%. HSV keratitis is a major cause
d. latency after primary infection of blindness in adults.
e. HSV 1 and HSV 2 closely related -Skin Infections: often manifeset as eczema herpeticum.
f. HSV 1 usually infects above waist; HSV 2 Herpes gladitorium, Herpes whitlow
below waist -Genital infection: most HSV 2, most acquired sexually, 1
infection often aseptic meningitis, more prone to reoccur
Immune Response and Pathogenesis:
than HSV1. Latency in dorsal root ganglia. Risk for
-virus enters abraded skin or mucosa infecting babies during birth. Outcome dependent on site of
-viral infection results in multinucleated giant cells infection.
(syncytia) and inflammation in dermis
-cell lysis causes release of vascular fluid to dermis Epidemiology:
(vesicles which become pustular with healing). -worldwide distribution of both HSV 1 and HSV 2.
-specific host defense mechanisms develop 7-10 days
-humoral antibodies not protective Diagnosis:
-cell mediated immunity important; immunocompromised -most often clinical, DFA/PCR/EIA/cell culture
get more severe disease
-latency in sensory nerve ganglia Complications: encephalitis/disseminated viral infection in
neonates

Transmission: direct contact Treatment and Prevention: No vaccine, acyclovir,

valcyclovir IV for disseminated infection, otherwise oral or
topical. Resistance to drug through mutation of TK
(thymidine kinase) gene.
Gnarpe’s Vicious Viruses Clinical Presentation:
-severe acute respiratory illness
- interstitial pneumonitis
Virus: Hanta -sudden onset, starts with cough and muscle pains
a) Enveloped, member of bunyavirus family -dyspnoea, tachycardia, pulmonary edema, pleural
b) Arthropod borne or from rodent excreta effusion, hypotension
c) CNS infections and pulmonary infections (HPS) - blood clotting impaired
d) At least 6 species .

Immune response and pathogenesis:

-HPS: characterized by interstitial pneumonitis with Epidemiology:
edema and infiltration by MNC
-HPS in Southwest USA (Four Corners Disease) and
-blood clotting is impaired but severe hemorrhage is not
around Edmonton in Canada (highest rate in Canada)
an important feature of the disease
-death due to respiratory failure

Transmission: Diagnosis:
- droplet/direct contact with rodent excreta (spring
-cell culture, PCR
cleaning perhaps not a good idea without protection!)
- suspected to occasionally spread from person to person -serology for specific IgM or rising titers of IgG

Complications: Severe shock, often death

Treatment and Prevention: No vaccine. No antiviral,
but they often try ribavirin. Supportive care important
Gnarpe’s Vicious Viruses Clinical Presentation:
-usually mild, cause of acute respiratory infection in
children
Human Metapneumovirus (hMPV) (ssRNA) -may cause an influenza like illness in adults
a. Enveloped, paramyxovirus -sore throat, malaise, cough, fever, coryza, lower RT
b. first isolated in 2001in Holland symptoms may present
c. found worldwide in all ages, important cause of
lower respiratory tract infection in children < 2 yr, Diagnosis:
similar to RSV -PCR, serology
d. major proportion of hospitalizations for lower
respiratory tract infection in children Complications:
-otitis, sinusitis, bronchitis, croup – similar to RSV
Immune response
-secretory IgA, humoral IgG and IgM
-cell mediated responses develop before antibodies
and are important for termination of infection Epidemiology:
-commonly community acquired
Transmission: - causes most disease in <2 yr, elderly and
-droplet and direct immunocompromised.
- peak incidence in temperate climate: winter in tropical
Pathogenesis: areas year-round

-thought to be similar to RSV, trial attempts to make a Treatment and Prevention: No vaccine.
vaccine resulted in the same outcome : enhanced disease Supportive care.
instead of protection
- studies are undergoing with animal models, (cotton rat)
Gnarpe’s Vicious Viruses Clinical Presentation:
-Influenza A: classical influenza croup, vomiting, diarrhea
and myositis in children
Influenza A (Seasonal Flu) (ssRNA)
a. enveloped, segmented genome (A has 8 RNA)
b. antigenic drift and shift
c. Many subtypes based on typing of H and N Diagnosis:
d. M2 protein forms a pore in the virus -detection of viral antigens/PCR/cell culture

Complications:
Immune response -otitis, sinusitis, bronchitis, croup
-secretory IgA, humoral IgG and IgM -exacerbations of preexisting chronic diseases
-cell mediated responses develop before antibodies -Reyes syndrome, myositis
and are important for termination of infection

Transmission: Epidemiology:
-droplet and direct -commonly community acquired, also nosocomial
outbreaks
Pathogenesis: - secondary bacterial pneumonia relatively common.
-Influenza A thought to originate from birds
-initial site of replication is the respiratory mucosa
-uses sialic acid residues on host cells to attach Treatment and Prevention: Vaccine for Influenza A
-disease is due to inflammation causing respiratory given yearly.
epithelial cell and cilia damage; symptoms due to release of Amantadine acts on the M2 protein. Neuraminidase
cytokines from mononuclear cells etc. inhibitors (e.g. tamiflu) act to help viral particles escape
from the cell.
Gnarpe’s Vicious Viruses Clinical Presentation:
-fever, cough, sore throat, runny or stuffy nose, body aches,
headache, chills and fatigue, some diarrhea and vomiting.
Influenza A (H1N1 “Swine” flu) (ssRNA)
a. enveloped, segmented genome (A has 8 RNA)
b. new combination of genes in this strain; genes from Diagnosis:
flu viruses that normally circulate in pigs in Europe -detection of viral antigens/PCR/cell culture
and Asia + avian strain genes + human strain genes
c. antigenic drift and shift possible
Complications:
-otitis, sinusitis, bronchitis, croup
Immune response -exacerbations of preexisting chronic diseases
-secretory IgA, humoral IgG and IgM -Reyes syndrome (with aspirin use)
-cell mediated responses develop before antibodies -death, respiratory distress, secondary infection
and are important for termination of infection
Epidemiology:
Transmission: - community acquired, nosocomial outbreaks probable
-droplet and direct, suspicion of airborne routes - secondary bacterial pneumonia relatively common.
- (pregnant women ↑ risk), >65 years, <5 years, any age
Pathogenesis: with a chronic illness
-Influenza A “swine flu” disease of pigs - very rapid spread worldwide
- New strain not found in pigs of North America Treatment and Prevention: Vaccine undergoing
-initial site of replication is the respiratory mucosa
human trials; will be given together with the seasonal
-uses sialic acid residues on host cells to attach
vaccine if possible, otherwise both separately.
-disease is due to inflammation causing respiratory
Neuraminidase inhibitors (e.g. tamiflu) recommended;
epithelial cell and cilia damage; symptoms due to release of
surveillance of susceptibility important. Most effective
cytokines from mononuclear cells etc.
within 48 hours of symptoms. Amantidine resistant.
Gnarpe’s Vicious Viruses Clinical Presentation:
-Influenza B: classical influenza croup, vomiting, diarrhea
and myositis in children
Influenza B & Influenza C (ssRNA) -Influenza C: common cold, febrile bronchitis, coryza,
a. enveloped, segmented genome (B has 8, C has 7) cough
b. both can cause classical influenza
c. antigenic drift can occur both, but no shift Diagnosis:
d. Influenza C is more antigenically stable, no -detection of viral antigens/PCR/cell culture
subtypes, one glycoprotein (HN)
e. Influenza B has no M2 protein, but has H and N
Complications:
Immune response -otitis, sinusitis, bronchitis, croup
-secretory IgA, humoral IgG and IgM -exacerbations of preexisting chronic diseases
-cell mediated responses develop before antibodies -Reyes syndrome, myositis (especially Influenza B)
and are important for termination of infection

Transmission: Epidemiology:
-droplet and direct -commonly community acquired, also nosocomial
outbreaks
Pathogenesis: - secondary bacterial pneumonia.
-Influenza B and C are primarily human pathogens, but B
can infect seals, dogs, cats and swine, and C infects swine
-initial site of replication is the respiratory mucosa Treatment and Prevention: Vaccine for Influenza B
-“B” uses sialic acid residues on host cells, C uses another given yearly with Influenza A types. No vaccine for
related structure Influenza C.
-disease is due to inflammation causing respiratory Amantadine does not work for Influenza B as it does not
epithelial cell and cilia damage; symptoms due to release of have M2 protein. Neuraminidase inhibitors (e.g. tamiflu)
cytokines from mononuclear cells etc. effective.
Gnarpe’s Vicious Viruses Clinical Presentation:
-classical measles: respiratory symptoms, malaise, fever,
Virus: Measles (Rubeola) (ss RNA) conjunctivitis, photophobia, myalgia, Koplik’s spots on
buccal mucosa, rash = maculopapular
a. enveloped, only one serotype -atypical measles: measles in immunocompromised: no
b. H and F glycoproteins rash, severe, progressive and often fatal, may present as
c. closely related to rinderpest and distemper viruses pneumonia or encephalitis.
d. humans only natural host, natural infection via
respiratory tract Diagnosis:
e. rare subclinical disease -PCR and cell culture
f. most contagious of childhood rash diseases -serology: IgM titer or 4-fold rise in IgG
g. 14 day incubation -clinical diagnosis suffices in endemic areas
h. cellular receptor CD46 found on all polarized
epithelial cells Complications:
i. -secondary bacterial infections.
Immune Response and Pathogenicity: -otitis, pneumonia, diarrhea, encephalitis.
-humoral antibodies detectable in serum on day 1 of rash, -keratitis in children with vitamin A deficiency
peak at 3-4 weeks; IgG remains for life, H ab are protective -sub-acute sclerosing panencephalitis: rare, late (5-
-formation of “giant cells” due to fusion of membranes, 15 years after infection) and fatal.
contain inclusions
-Koplik’s spots in mouth: manifestation of rash on buccal
Epidemiology:
-worldwide distribution, no latent or persistent infections
surfaces
-endemic in large unimmunized populations
-cell mediated immunity necessary for resolution of
-tropics: peaks in hot dry seasons; epidemics every 2-3 yr
infection, rash is due to CMI
-large WHO led program underway to eradicate disease
-immunosuppression common result of measles: humoral
and CMI affected up to a year after infection.
Treatment and Prevention: Vaccine: live attenuated,
Transmission: airborne part of the MMR vaccine; Antivirals: none. Supportive
care.
Gnarpe’s Vicious Viruses Clinical Presentation:
-short prodrome: fever, malaise, headache, ear pain
salivary gland pain and swelling
Virus: Mumps (ssRNA) -maternal mumps: 1st trimester  spontaneous abortion,
2 + 3 trimester no congenital effects
a. enveloped, one antigenic type
b. envelope contains M (matrix protein), HN, F protein Diagnosis:
c. bind to neuraminic receptors on host cells -clinical diagnosis most common
d. most infections are asymptomatic -if needed PCR/ cell culture & serology (IgM or rise IgG).
e. incubation 18 d, most contagious before clinical
onset
Complications:
Immune Response and Pathogenesis: -epididymo-orchitis in 25-40% of adult males, usually
-secretory IgA appears in saliva within 4-5 days unilateral, can rarely lead to sterility
-mumps specific IgM detectable in serum 10-12 d after -oophoritis in 5% of adult females, sterility rare
onset, IgG peaks at 3-4 weeks - mumps-associated pancreatitis
-immunity permanent due to HN antibodies. -migratory polyarthritis (resolves spontaneously)
-cell mediated immunity: cytotoxic lymphs destroy infected -sensorineural hearing loss
host cells (disastrous in brain) -mumps meningitis is common
-mumps virus binds to sialic acid residues on host cells
-mumps parotitis: diffuse edema with mononuclear cell Epidemiology:
Infiltration -disease of school-aged children in susceptible populations
-mumps orchitis: virus replicates in seminiferous tubules -world-wide distribution
leukocyte infiltration, hemorrhagic interstitial -was endemic in N.A. prior to vaccine release in 1967
edemaswelling in closed space results in pain and -rare to see mumps in infants <6 mo of age (passive ab’s)
vascular insufficiencyinfarction, scarring, fibrosis.
Treatment and Prevention: Attenuated vaccine, part
of MMR. Cases of mumps should be isolated to prevent
Transmission: droplet spread. No antivirals, supportive therapy.
Gnarpe’s Vicious Viruses Clinical Presentation:
-violent, sudden acute onset of diarrhea, nausea and
vomiting (projectile)
Virus: Norovirus (ss RNA) (earlier Norwalk) -headache, abdominal cramps, chills, fever
-self-limiting disease usually lasting 12-48 hours
a. Non-enveloped small virus, Caliciviridae -infants especially susceptible to dehydration
b. causes epidemic gastroenteritis
c. incubation period 10-51 hours, NO PRODROME
d. cannot be cultivated in vitro
e. may be responsible for 90% of food-borne illness Epidemiology:
f. >5 serotypes and many subtypes -highly infectious disease
-attack rates ~50-80%
-nosocomial infections common
Immune Response and Pathogenesis: - ~20% of population do not get the disease (carriage status
-immune response not well defined unknown)
-may be some limited protection for a short period of time -asymptomatic carriage common, sometimes for weeks
after an infection after an infection
-shortening of intestinal villi, inflammation in lamina -food borne outbreaks common
propria -cruise ship outbreaks.
-gastric emptying delayed vomiting
-receptor may be the H type 1 histo-blood group antigen
(secretors).
Treatment and Prevention: No vaccine, no antiviral,
supportive therapy (fluids and electrolytes)
Transmission:
-fecal-oral, direct
-virus lives on surfaces for several days
Gnarpe’s Vicious Viruses Clinical Presentation:
-croup: (laryngotracheobronchitis) usually in 6-18 mo,
fever, hoarseness, seal-like barking cough
Virus: Parainfluenza Virus (ss RNA) -bronchiolitis: infants < 1 year, fever, wheezing, tachypnea,
rales
a. enveloped virus, 4 serotypes -pneumonia: children and immunocompromised adults
b. antigenically stable, genome not segmented -infection/adults: nonspecific upper respiratory infection
c. HN (hemagglutinin/neuraminidase) and F (fusion)
-infection in immunocompromised: serious, fatal disease
glycoproteins
d. serotypes 1-3 cause infections in infants and
children, serotype 4 adults
e. PIV 1 = CROUP
f. PIV 3 = bronchiolitis + pneumonia Epidemiology:
-common community acquired infection
Immune Response and Pathogenicity: -PIV 1,2 = biennual outbreaks in the fall
-reinfection common -PIV 3 = endemic, sporadic year round
-neonates have maternal IgG but this is not protective
-infant IgA neutralizes poorly; poor F antibody responses, -
Diagnosis:
leads to reinfection. In adults, secretory IgA protects from -Detection of viral antigen (DFA), PCR, cell culture
reinfection for few months.
-replication is limited to respiratory epithelium Complications:
-fusion protein (F) important for virus infectivity -otitis media: most common complication
-pathogenesis similar to RSV (inflam + tissue damage) -acute sinusitis
-croup is characterized by respiratory obstruction (swelling) -secondary bacterial pneumonia (Strep & Staph)

Transmission: respiratory droplets Treatment and Prevention: No vaccine yet, no

specific anti-viral, supportive therapy important
Gnarpe’s Vicious Viruses Clinical Presentation:
-asymptomatic infection is most common
-symptomatic disease:
Virus: Parvovirus B19 “Fifth Disease” or “Erythema infectiosum”
a) ss DNA virus, non-enveloped -mild rash disease (slapped cheek disease) and lacy
b) only human parvovirus (species specific) rash on trunk +extremities, most common in school
c) replicates in red cell precursors (with nuclei) age children
d) small (18-26 nm) -child is afebrile or mild illness 1-4 days before rash
e) very resistant to inactivation (pH, heat) -adult females may have arthralgias/arthritis
Transient aplastic crisis (TAC): lytic infection of RBC
precursors, temporary shutdown of hematopoeisis –
Immune Response: dangerous if there is an underlying condition e.g. sickle
-primarily humoral, IgG and IgM, neutralizing antibodies cell disease. Drop in Hb by 30% or more. Self-limiting,
-persistent infection in immunocompromised resolution 7-10 days after onset. Fetal death if pregnant.
-rash is at least partially immune-complex mediated. B19 in immunocompromised: can be life-threatening
-development of chronic infection and anemia.

Transmission: probably droplet by respiratory route Epidemiology:

-worldwide, primarily in school children

Pathogenesis: Diagnosis:
-replication of parvoviruses require cellular functions -serology: IgM antibodies diagnostic, PCR
expressed only during the S phase of cell division; requires -clinical symptoms
actively dividing cells
-B19 attaches to nucleated red blood cells by a globoside or
“P” antigen, is internalized and migrates to the nucleus
Treatment and Prevention: No vaccine, no antiviral.
where it replicates Hand hygiene most important for prevention.
-virus lyses cells- results in anemia.
Gnarpe’s Vicious Viruses Clinical Presentation: 90% asymptomatic.
a. abortive poliomyelitis: most common, minor illness with fever,
malaise, drowsiness, headache, nausea, vomiting, constipation,
Virus: Polio virus (ss RNA, positive sense) sore throat. Recovery complete and rapid ( ~ 2 days)
a. non-enveloped, three serotypes b. non-paralytic poliomyelitis: (aseptic meningitis)- stiffness and
b. 90% of wild-type infections are asymptomatic pain in neck and back. Illness lasts 2-10 days, recovery is
c. human only natural host complete
d. have an “infectious” genome (act directly as mRNA) c. paralytic polio: major illness, flaccid paralysis -can be
e. acid stable, poliovirus receptor: pvr permanent. First symptoms are severe myalgia in one limb,
f. incubation period usually 7-14 days motor or sensory nerve problem, transient or permanent
g. no permanent carriers weakness, develops more often in pregnant women
d. post-polio syndrome: occurs in same muscle groups many
Immune Response and Pathogenesis: decades later (PPS). ) Children have fewer residual effects than
-immune response both humoral and cell –mediated newline adolescents or adults).
-humoral response may be most important
-neutralizing antibodies appear early in disease Epidemiology:
-virus enters via the mouth, infects tonsils, cervical lymph -worldwide distribution where there are no vaccine programs
nodes in neck and M (microfold) cells overlaying Peyer’s -year round in tropics, summer in temperate climates
Patches in intestine -case-fatality rate variable, highest in older patients
-CNS invaded via circulating blood with virus -children more susceptible to infection but less complications
-polio can also spread along axons of nerve cells to CNS -WHO has targeted polio for eradication
-anterior horn cells of the spinal cord are preferentially
infected. Inflammation is secondary to attack on nerve cells.
Diagnosis: Isolation of virus from throat or rectal swabs in cell
culture, electron microscopy, PCR. Serology with paired specimens
Transmission: fecal-oral
Complications:
Treatment and Prevention: Vaccines available. -due to paralytic polio (spinal/bulbar or both)
Transmission:
IPV: fecal-oral
Salk, recommended by WHO, has all three type of virus. Need -bulbar polio: paralysis of respiratory muscles
boosters -Spinal polio: 30% affect lower limbs
OPV: Sabin, good vaccine eliciting mucosal immunity, but can -PPS (post-polio syndrome): 25% with paralytic polio who
revert to wild type and cause disease in immunocompromised Recover
No antivirals. Supportive therapy.
- polio caused by vaccine strains (eg. Nigeria)
.
Gnarpe’s Vicious Viruses Clinical Presentation:
-range from inapparent symptoms to severe life-threatening
respiratory failure
-can cause death
Virus: RSV (ssRNA) -first symptom wheezing
a. Respiratory Syncytial Virus
-fever in ~50%
b. major cause of disease in children
-pneumonia more common <6 mo of age
c. two types, A and B. (A more prevalent)
-prematurity greatest risk factor
d. infects humans and primates
e. enveloped virus, incubation 5-6 days
Epidemiology:
Immune Response and Pathogenesis: - NA: epidemics every winter, usually Dec-Apr, sporadic
-replication in respiratory epithelium cases year round
-causes ciliary dysfunction -worldwide distribution.
-formation of giant multi-nucleated cells (syncytia)
-secretory IgA important for protection from infection; Diagnosis:
babies cannot make IgA! - DFA/EIA/Culture/PCR
-cell mediated immunity important for disease resolution
- DFA most practical for rapid diagnosis
-pathogenesis is mediated by inflammation
-no difference in disease severity between A and B subtypes
Complications:
-bronchiolitis, interstitial pneumonia, secondary bacterial
Transmission: infections
-direct
-virus viable on surfaces for ~24 hr Treatment and Prevention: No antiviral (no good
-adults need very large dose of virus to become ill evidence for ribavirin which is sometimes used anyway), no
-infants only need small dose to cause infection. good vaccine. Supportive therapy
**** Monoclonal antibody for prevention in premature
infants = Synagis® (lasts 30 days)
Gnarpe’s Vicious Viruses Clinical Presentation:
Prodromal: systemic viral infection symptoms – fever,
headache, malaise. Change in personality and cognition, pain
Virus: Rabies at bite site.
a) ssRNA, enveloped, Rhabdovirus, bullet-shaped Neurologic: two forms – furious and paralytic. Furious form
b) primary reservoir: carnivorous species (80%) presents with hydrophobia, delirium, agitation,
-rats, foxes, skunks, raccoons, coyotes and bats seizures, ends with coma and death. Paralytic form (20%) –
c) zoonotic disease, usually no human to human spread no hydrophobia, initial symptoms are ascending paralysis,
d) fatal disease, long incubation (few days to 19 years) limb weakness, end result coma then death.
e) “rabies” from the Latin “rabere” = to rave
Epidemiology:
-worldwide distribution except isolated islands, Scandinavia
Immune Response: and Australia. 112 countries reported cases in 1998.
-humoral antibodies produced do not affect disease -infections in animals
-patients who develop cellular immunity tend to develop
encephalitic form of disease and die sooner than those with Diagnosis:
the paralytic form. -detection of viral antigen or virus RNA in brain tissue,
touch preparation of corneal cells or nuchal biopsy
Transmission: bite of rabid animal, transplanted organs -postmortem using brain tissue DFA/PCR/histology

Complications: Fatal disease - death.

Pathogenesis:
-neurotropic virus, spread via peripheral nerves to CNS Treatment and Prevention: No antiviral therapy.
-proliferation in CNS, then spread back to tissues Vaccine available, rabies immunoglobulin available. Washing
-travels via nerve axons (sensory neurons) bite with soap and water immediately after a bite reduces
-much is still unknown about pathogenesis, cytokines do transmission to ~20%. Control of rabies in the wild: use of
appear to play a role vaccines in “bait”.
-Negri bodies (inclusions) seen in cytoplasm of some cells
contain viral nucleocapsids)- used in histologic diagnosis
Gnarpe’s Vicious Viruses Clinical Presentation:
-typical symptoms: sore throat, sneezing, runny nose (coryza)
Virus: Rhinovirus (RNA, picornavirus) -sometimes low grade fever, sometimes cough
a. species specific (humans and primates), nonenveloped -symptoms usually peak in 2 days and infection usually
b. ”Grows” best at 33C, receptor: 90% ICAM-1, 10% LDL resolves in one week
c. Acid-labile, >113 serotypes
d. stress not important for acquiring the virus, but may be
Epidemiology:
for developing symptomatic disease
e. immunosuppressed =immunocompetent (susceptibility) -spread worldwide
f. shedding peaks at 2-3 days after symptoms have begun -epidemic cycles in temperate countries
-endemic year round in tropics
Immune Response:
Diagnosis:
-secretory IgA important for clearance -clinical, based on symptoms
-serum antibodies not too helpful -large number of types
-cell mediated immune response important for disease
resolution and pathology of disease Complications:
-2 bacterial infection (acute sinusitis, otitis media)
Transmission: direct -precipitation of asthma in children> 2 yrs
-exacerbations of chronic bronchitis
Pathogenesis:
-ICAM-1 receptor in plasma membrane of respiratory
epithelial cells; this, and preference for growth at 33C and Treatment and Prevention: No vaccine, no antiviral
sensitivity to stomach acid restricts disease activity to the – Hand Hygiene Important!
upper respiratory tract.
-clinical symptoms are due to inflammation and release of
inflammatory mediators e.g. histamine, cytokines
a. dilation of blood vessels
b. transudation of plasma
c. secretion of seromucous glands and goblet cells
stimulation of cough and sneezing reflexes
Gnarpe’s Vicious Viruses Clinical Presentation:
-acute gastroenteritis: sudden onset of vomiting, watery
diarrhea for ~5 days and fever
Virus: Rotavirus (ds RNA) -50% asymptomatic infections
a. non-enveloped, genome in 11 segments
b. most important cause of infantile gastroenteritis
worldwide Epidemiology:
c. three major groups (A, B, C) and many subtypes -most common cause of diarrhea in infants <2 years in
d. animal and human group A viruses can reassort both developed and underdeveloped countries
e. incubation period ~48 hours. -Group A is most important cause of endemic disease in
f. stable in pH 3.0 to 9.0 N.A.
g. use a variety of cellular receptors -Group B causes outbreaks in China
-Group C causes sporadic cases

Immune Response and Pathogenesis:

-gastric acid of adults inactivates rotavirus: infants have pH Diagnosis:
and are thus susceptible -detection of virus in stool by EIA, electron microscopy,
-low pH protects from infection better than IgA RT-PCR, cell culture
-IgA is produced locally but has a short half life -serology not practical.
reinfection common
-rotavirus infects mature enterocytes on the tips of small
intestinal villi
Complications:
-dehydration can lead to death (most common cause of
Theory of pathogenicity: NSP4 protein induces secretory
infant death in underdeveloped countries)
diarrhea, malabsorption due to shortened +atrophied villi,
effect on enteric nervous system -prolonged infection in immunocompromised
-malnutrition and prematurity are risk factors.

Transmission: fecal-oral Treatment and Prevention: Vaccine: oral and IPV;

Rotarix® & RotaTeq®. No antivirals, supportive therapy.
 Clinical Presentation:
Gnarpe’s Vicious Viruses -50% of all childhood primary rubella cases subclinical
Postnatal rubella: usually benign, children no prodrome,
adults 1-5 days, lymphadenopathy, low-grade fever, mild
Virus: Rubella (ss RNA) conjunctivitis, headache, sore throat, malaise, chills, cough,
a. also known as “German Measles” coryza “3-day rash”, often itchy, starts on face
b. enveloped, one serotype, humans only host (maculopapular)
c. E1 (hemagglutinin) and E2 glycoproteins Congenital rubella: Severe manifestations – dependent on
d. 16-18 days incubation stage of pregnancy affected (worse in early stages, 1 st
trimester because fetus develops eyes, heart etc).
a. transient sequalae: rash, hepatosplenomegaly, jaundice,
Immune Response and Pathogenesis: pulmonary involvement, meningo-encephalitis,
-humoral IgM antibodies appear within 2-3 days of rash onset radiographic abnormalities
-humoral IgG antibodies peak 2-4 weeks later b. permanent effects: hearing loss, abnormalities of
-cell mediated responses detectable 1 week before antibody cardiovascular system, cataracts, retinopathy, mental
response retardation motor disabilities
-congenitally infected may have ↓ lymphocyte function c. delayed effects: endocrinopathies, deafness, eye damage,
-initial replication in nasopharyngeal respiratory epithelium vascular problems
lymph  viremic spread Epidemiology:
-rash develops 16-18 days post infection -worldwide distribution
-congenital rubella: virus causes direct cellular damage -seasonality: temperate climates disease in Mar, Apr & May.
resulting in perivasculitis of placenta, edema, fibrosis &
necrosis of chorionic villi. Affected organs hypoplastic. Diagnosis:
-majority of infections diagnosed serologically: IgM or 4-
Transmission: respiratory droplet (unless vertical fold titer rise in IgG
infection) -isolation of virus in cell culture, PCR can also be done
Treatment and Prevention: Attenuated vaccine part Complications:
of MMR. Good efficacy. No antiviral available. Postnatal rubella: Arthritis and arthralgias Neurologic effects:
Supportive therapy. encephalitis Hemorrhagic: transient depression in platelets
Congenital rubella: As above (clinical presentations)
Gnarpe’s Vicious Viruses Clinical Presentation:
-two major clinical types: variola major & variola minor
Virus: Smallpox (Variola) Variola major: case fatality 20-30%, onset of disease is
a) Orthopoxvirus, ds DNA, enveloped acute: fever, malaise, headache, backache, rash 4 days
b) largest virus, code for 150-300 proteins later, first in mouth, then face, forearms and hands.
c) replicate in cytoplasm using own enzymes Macular rash→ papular→ vesicular→ pustular
d) first virus to be “eradicated” (1977) -pustules dry up in 8-9 days unless 2 ° infected.
e) human only host, one serotype - all lesions in same stage unlike chickenpox

Immune Response: Epidemiology:

-neutralizing humoral antibodies after about 1 week, not -smallpox is eradicated but other poxviruses are not:
specific to any particular type of poxvirus (cross-reactive) Monkeypox, Molluscum contagiosum, etc.
-cell-mediated immunity probably more important than
humoral response. Diagnosis:
-Clinical presentation
- DFA/PCR/culture for confirmation.
Transmission: respiratory droplets
Complications:
-death
Pathogenesis: -hemorrhagic smallpox: most common in pregnant women
-viral entry via respiratory tract, multiplication in lymph
-flat-type smallpox: intense viremia and slow development of
tissue, transient viremia, infection of RE cells, 2 skin lesions (majority of infections fatal)
multiplication leading to more intense viremia and skin -secondary bacterial infections are the most common
lesions complication and most common cause of death due to
-cells contain many inclusions, infiltrate has mononuclear development of sepsis.
cells. Cell membranes coalesce and form giant cells that
become filled with fluid, white cells and debris.
-all layers of skin involved and scarring is common Treatment and Prevention: Vaccine (vaccinia =
-skin pustules easily become contaminated and 2 ° infected cowpox, closely related virus), no good antiviral.
Gnarpe’s Vicious Viruses Clinical Presentation:
Chickenpox: usually self-limited systemic infection, fever,
pruritic rash (5 days). Children rapid onset, adults 1-2 days
Virus: Varicella-Zoster (VZV or HHV-3) prodrome. Rash spreads on neck and head, less on extremities.
a) enveloped, member of herpes family, one serotype
All stages of lesions present simultaneously.
b) etiological agent of chicken pox and shingles
Zoster: usually begins as a localized skin eruption often close
c) usually infects children, remains latent until
to dorsal root ganglia. Characterized by confluent rash and
reactivated to shingles
pain which can start before rash. Untreated rash lasts 2-5 wks
d) limited host range- primates
Epidemiology:
Immune Response: -worldwide, higher rate of infection in tropics. One of the
-both humoral and cell-mediated immunity most contagious diseases, attack rate 80-90%.
-humoral antibodies 4-8 wks after infection -Zoster usually in older individuals.
-cell mediated has major role in immunity; suppression of
CMI leads to reactivation of virus
Diagnosis:
-clinical presentation, can use DFA/PCR/Cell culture
-immunological memory is good
-serology limited for diagnose, good for assessing immunity
-predominant cell in vesicles is neutrophil
- Zoster: acute inflammatory changes in ganglion – cell lysis Complications:
PHN (post herpetic neuralgia): 25-50% of patients >50 yrs,
pain can be permanent. Encephalitis in 0.5%. Complications
Transmission: airborne
in immunosuppressed: hemorrhagic lesions, encephalitis, 
Pathogenesis: spread and severity of lesions.
Neonatal: abortion, otherwise severe embryopathy. Infection
-VZV enters via respiratory tract of mother last 3 weeks of pregnancy: disseminated varicella
-two viremic phases: first delivers virus to RE system, of fetus with multiple organ involvement, mortality 30%.
second to skin, causing rash
-multinucleated cells (syncytia) and nuclear inclusions Treatment and Prevention: Active or passive immunization.
-Zoster: acute inflammatory changes in ganglion with extra- Active: live attenuated virus. Passive: VZIG = varicella
vasation of blood and destruction of ganglion cells, zoster immunoglobulin good for up to 3 days post exposure.
Prevention: isolation procedures. Antivirals: acyclovir +
inflammation of ganglion sheath. analogues, treatment must start within 2-3 days of shingles
debut to prevent PHN. Foscarnet for resistant strains.
Gnarpe’s Vicious Viruses Clinical Presentation:
-most asymptomatic
Virus: West Nile Virus (ss RNA) -15-20% of infected individuals get symptoms 3-15 days
after bite: fever, headache, body aches, sometimes rash,
swollen lymph glands
a. enveloped, genus Flaviviridae -development of encephalitis in ~1% of affected: high
b. belongs to Japanese Antigenic Complex virus family fever, headache, neck stiffness, stupor, disorientation,
c. small, 40-60, arthropod borne coma, seizure, convulsions, paralysis, muscle weakness,
d. natural reservoir: birds, especially crow and magpie numbness, difficulty moving
e. most infections are asymptomatic
f. emergence of a new viral subtype causing latest
outbreak in N. America
Diagnosis:
Immune Response and Pathogenesis: -PCR/ cell culture and serology (IgM or rise in
-WNV first isolated in the West Nile Province of Uganda in IgG).
1937
- outbreaks in Egypt, Israel, S.Africa, Asia, Europe and NA Complications:
in humans and horses -polio-like paralysis
-virus causing the N. American outbreak that is ongoing has -long term neurological effects in 50% of those with WNV
been recently been found to have mutations that have made neurological syndrome
it more pathogenic
-this recent strain is neurotropic and has been causing
polio-like syndromes Epidemiology:
-elicits both CMI and humoral response, vaccine available
-birds have brought WNV from New England and New
for horses based on production of neutralizing antibodies York state over the continent to the west
- only province that does not yet have WNV is BC

Treatment and Prevention: No vaccine, no antivirals,

Transmission: arthropod borne, mosquito bites supportive therapy. Prevention – use repellents with DEET
Gnarpe’s Vicious Viruses Clinical Presentation:
-high fever, hemorrhaging, jaundice, shock
.
Virus: Yellow Fever
a) Enveloped, member of Flaviviridae family
b) Name flavor means “yellow” Epidemiology:
c) Only found in S. America and sub-Saharan Africa -two cycles: urban or sylvan(endemic)
d) Monkeys are natural reservoir -Sylvan: virus maintained in monkey population
e) Arthropod borne -forest workers and others who are in the forest
are at risk
Immune response and pathogenesis: -infection of humans in this cycle leads to the
-some cross-immunity with Dengue, such as Dengue and Urban cycle and epidemics can occur
Yellow Fever are never found in the same population -Urban: Aedes mosquito breeds around human habitation
-growth of virus in liver causes the symptoms of disease and is widespread in the warmer areas of the world
-virus also replicates in other organs, eg kidney and heart -last case of Yellow Fever in USA 1905
and causes hemorrhaging -serious difficulties building Panama Canal due to
-neutralizing antibodies good protection against disease infestation with Yellow Fever carrying mosquitoes

Transmission:
- arthropod borne – bite of an Aedes/Haemogogus Diagnosis:
Mosquito (day biters) -clinical presentation, travel history
-mosquito bites monkey, takes in virus then bites human -specialized labs: PCR, serology
and delivers virus

Complications: Severe shock, death in 20-50% of illness

Treatment and Prevention: Good vaccine, since

1949. No antiviral, supportive care indicated.