Download Influenza

Influenza
Respiratory virus
a. RSV
b. parinfluenza
RSV and PIV
c. human
metapneumovirus
Other Respiratory
virus
d. adenovirus
e. coronavirus
f. Picornovirus
G. Reovirade
Family: orthomyxociruses
Particle: segmented – sense rna
Surface proteins: neuraminidase (release of virus) & hemagglutin (attachment), M2 uncoats (only in type A)
Incubation: 1-4 days, viral shedding 1-5 post inf.
Spread: aerosol droplets, A- shift and drift, B- drift only
Diagnosis: culture, serology, rapid viral diagnostic test: IF, EIA, PCR
Prevention and treatment: 1. Immunization 2. Drugs
Vaccine priority: elderly, nursing homes, young kids, pregnant women, travelers
Type A: treat w. amantadine/rimatadine (block M2)
Type A & B: oseltamivir (oral, kids)/ zanamivir (inhaled) both are neuramidase inhibitor (no resistance yet)
3 conditions for pandemic: no immunity, jump b/w species, human to human transmission (bird flu h5:N1 has all but last)
Family: paramyxovirus
Particle: enveloped, non-segmented, negative sense rna
Diseases: measles, mumps, rsv, parainfluenza, metapneumovirus
Surface protein: g glycoprotein (attachment to resp. cells) & F glycoprotein (facilitate fusion)
Time: late fall/ early spring
Spread: droplets, direct contact
Incubation: 2-8 days, shedding: 1-2 wks
Symptoms: cold-like, otitis media
Infects: kids, older adults w/ chronic diseases
Diagnosis: viral isolation, viral ag test, id vRNA, serology
Prevent: close contact necessary so avoid it, no vaccine
Treatment: supportive care, ribavirin
- 2nd most common of lower respiratory tract inf. In kids
-PIV1 most common cause of croop
-serotypes: PIV1 most common
Reinfections common, but milder, chronic, old 5-10% hosp, 7% mortality
-similar to RSV
- sever illness if co-infected w. rsV
- severe disease in lung and hematopoietic cell transplants
spread: close contacts
Note: have different family than above
Particle: naked, icosahedral, ds DNA
Surface: fiber protein (attachment and internalization)
Spread: droplet, fecal oral route
Symptoms: ½ are asymptomatic, inf epithelial cells undergo necrosis & slough off; intense inflammation, latent inf may be present for yrs
Diagnosis: culture/biopsy of lower respiratory tract, direct ag assay, pcr, serology
Prevent and treatment: vaccine w/ an oral, live attenuated
Drugs: cidofovir and intravenous immunoglobulin
Particle: ss RNA, enveloped
Surface: spike protein mediates receptor binding and fusion
Symptoms: common cold
Time: fall/winter
Diagnosis: PCR, indirect IF, diagnosis clinically
Treatment: no therapy, wash hands, cover mouth
Diseases: ex. SARS
SARS
Incubation 2-7 days
Symptoms: fever, muscle ache, lower respiratory symptoms, resp failure, mortality 10-20%
Therapy: supportive
Family: rhinovirus (common cold)
Particle: small, naked ss RNA , + sense
Spread: secretions and aerosols
Time: spring/summer
Replicates: 33 degrees C, same temp as Nose, and URT
Diagnosis: clinical
Prevention & treatment: wash hands, symptomic relief
Particle: naked, segmented, double stranded RNA
Symptoms: mild URI
Diseases: reovirus (respiratory), rotavirus (GI), Colorado tick fever agent
Incidence, epidemiology, treatment- unknown
Dna virus and some important members
Poxviridie: small pox
Rna viruses and some important members
Paramyxoviridae- measles
Herpesviridae- herpes simplex types 1 and 2
.Adenoviridae- adenovirus
Polyoma viridae- jc virus
Papilloma viridae- papilloma virus
Parvoviridae- parvovirus B19
Orthomyxoviridae- influenza virus types a, b, c
Co ronaviridae- coronavirus, sars
Arenaviridae- lass fever virus
Rhabdoviridae- rabies virus
Filoviridae- ebola virus
Noroviridae- Norwalk virus
Bunyaviridae- California encephalitis virus, hemorrhagic
fever virus
Retroviridae- human immunodeficiency virus
Reovirida- rotavirus
Picornaviridae- rhinoviruses, poliovirus
Togaviridae- rubella virus
Flaviviridae- yellow fever virus
Enteric virus
Transmitted fecal oral
All acid resistant
a. Rotavirus
Particle segmented double stranded rna, non enveloped
Surface protein: induce neutralizing ab, multiple serotypes
Incubation: 1-3 days
Symptoms: most common cause of diarrhea in kids
Treatment: supportive, treat symptoms
Immunity: most sever in kids less than age 2, b/c by age 3 have anti-rotavirus ab, breast feeding protects, previous infection- gives partial protection
Vaccine: bovine reasssortment (2,4,& 6 months), and virus like particles (just protein coat)
Particle: ds DNA, no envelope
Incubation: 7-10 days
Symptoms: similar to rota, worse diarrhea less vomiting
Particle: ss RNA, positive sense, no envelop
Family: calciviridae
Incubation- 1-2 days
Symptoms: vomiting at first, diarrhea for 5 days, most common cause of non-bacterial gastroenteritis in adults
Spread facilitated by: low infectious dose, prolonged shedding, stable in environment, great strain diversity, no induction of lasting/protective immunity,
asymptomatic infection
Family: astrovirade
Particle: ss RNA, + sense, no envelope
Transmission: contaminated food
Incubation: 1-2 days
- common in young children
Family: picornavirade
Particle: ss RNA, + sense, no envelope
Disease ez. Polio, coxsackie virus a & b, echovirus
- very common infectious agent
symptoms: infectious, frequently asymptomatic
Incubation: 2-10 days
infection result in serotype specific immunity
Clinical outcomes: asymptomatic (90-95%), minor illness (uri, gi upset flu)- 4-8%, 1-2% nonparalytic poliomyelitis, 1-2 paralytic mylelitis
Types of Paralytic poliomyelitis: a. spinal form (asymmetric legs), b. bulbar form (cranial nerves) c. bulbospinal (combination
Post polio syndrome: not infectious process, detoriate of functional abilities
Vaccine: 1. inactivated poliovirus vaccine (salk: IPV)- no paralysis 2. Live, attenuated, oral poliovirus (sabin:OPV)- better mucosa Immune Response
IN USA we use IPV
Elimination: humans is the only natural reservoirs
Non specific febrile illness, meningitis, hand foot, and moth disease, acute myocarditis, and pericaraditis, disseminated infection in the neonate (acquired
perinatally form mother)- may be fatal
b. Enteric adenovirus
c. Norwalk like and
sappor like
d. astroviurs
e. Enterviorus also
include members of
picornavirade
1. Polio virus
Other Syndromes due
to enterovirus
infections
Example of viral attachment proteins
Virus family
Virus
Adenoviridae
Adenovirus
Herpesviridae
Herpes simplex virus
Retroviridae
Murine leukemia virus
Viral attachment protein
Fiber protein
gD and gB
Gp70
Example of virus receptors
Virus
Epstein barr virus
Human immunodeficiency virus
Herpes simplex virus
Target cell
B lympocyte
Helper t cells
Epithelial cells
receptor
C3 complement receptor (cr2)
Cd4 molecule
Heparin sulfate
Herpes Viruses
HSV 1 and HSV 2
Varicella-zoster
virus (HHV3)
CMV (hhv5)
HHV6
HHV7
EPSTEIN BARR
VIRUS (HHV4)
HHV* (Kaposi
sarcoma)
HSV-1- oral, involves trigeminal ganglion (most fatalities b/c encephalitis, etc
HSV-2- genital, sacral ganglions, newborns get type II in birth canal- can be fatal
Pathogenesis: enter via lesionlymph nodecell enlarge, develop intranuclear inclusion w/ margination of chromatin  vesiculate and fluid
ulcer close to mucosa cutaneous junction, get vesicles at high viral load, crusting when viral load decreases
ID: 1. Restriction endonucleases and then dna fingerprint 2. Neutralizing ab (tzank test) 3. Exam proteins: elisa assay
Latency: herpes is forever, reactivation causes (fever, sun, stress, menestration),
a recurrent lesion may be reminiscent of the primary lesion but more restricted in size severity and duration of outbreak
Varicella- ubiquitous in childhood (2nd attacks uncommon) zoster: represent reactivation of VZV latent in dorsal root ganglia (freq. immunocompromised_
Transmission—probably respiratory droplets early in varicella; slight risk for vertical transmission (especially in 1 st trimester)
Pathology—latency w/in sensory dorsal root ganglia; often reactivated after 50yo or immunocompromised to cause zoster
Infection of conjunctivae or URI  replication in lymph nodes  primary viremia (by 4-6d)  replication in liver & spleen  secondary viremia
 infection of skin (vesicular rash, by 14d)
Presentation—fever & pruritic rash (maculopapules  vesicles  pustules  scabs in varying stages, localized to head & trunk, self-limiting)
Complications—bacterial superinfection (group A strep); pneumonia; encephalitis or meningitis; Reye syndrome (aspirin in children)
Congenital varicella—vertical transmission thru maternal viremia causing scarring, eye abnormalities & abnormal limbs
Zoster—unilateral rash; complications of post-herpetic neuralgia (elderly), eye damage from CNV infection; encephalitis
Ramsay-Hunt syndrome—reactivation of zoster in geniculate ganglion of ear canal resulting in facial palsy, loss of taste
Diagnosis—characteristic rash; immunofluorescent staining of Ag; culture; known exposure; serology; PCR to detect viral DNA
Treatment— Varicella: symptomatic therapy (Tylenol not aspirin), adults (acyclovir and foscarnet)
Zoster: elderly- acyclovir, valacyclovir, sorivudine, immunocompromised (iv acyclovir)
Prevention: vaccine- effective against varicells, effective against zoster and PHN (given to pts 60+ old, reduce incidence and severity of zoster
Varicella-zoster immunoglobulin (VZIG)- passive immunization, most eff. before lesion occur, immunocompromised, pregnant women, infants up to 2wks
1.
ubiquitous virus that can cause dz in individuals with immature or malfunctioning immune systems
epidemiology: 70% of adults are seropositive, site of latency may be peripheral blood mononuclear cells, monocytes
clinical manifestations: asymptomatic most common, mononucleosis, congenital (most common in us)- .5-1%,
Congenital symptomatic at birth—ONLY 1% of fetal infections; 20% die during infancy or suffer brain damage, 80% hearing, vision loss or mental
Congenital asymptomatic at birth—may develop hearing defects or impaired intelligence
Immunocompromised:Transplant recipients (leukopenia & hepatitis); BM recipients (pneumonitis); AIDS (25% developed CMV infection before HAART)
Diagnosis: pcr, ag detection, serology
Transmission—shed in saliva, semen, vaginal secretions & breast milk w/o clinical symptoms; blood transfusion (1-5%) & transplantation (60-80%), vertical
transmission or horizontally
Prevention—blood & transplant screening; prophylactic therapy for bone marrow & solid organ transplant patients
Treatment—NONE in normal persons; antivirals drug therapy in immunocompromised, iv ganciclovir in neonates
Is the causative agent of roseola infantum
Two variants a (lymphoproliferative disease or aids & b (roseola infantum
Epidemiology: up to 70% of people acquire hhv-6 during 1st yr of life
Manifestations: roseola infantum (benign dz of children, fever which subsides w/ rash (no-puiritic, slightly elevated, blanches) liver dsy, febrile seizures,
mono in adults, can be isolated from cd4 cells, transplant pts- present in 50%, febrile syndrome, bone marrow suppression
Diagnosis; easily detected in peripheral blood during febrile phase of disease: (culture virus), IFA, western blot, elisa, and pcr (x-reactive w HH&
Treatment: ganciclovir and foscarnet
Acquired during 3rd year of life
Disease: roseola infantum?, can be isolated from saliva, may have two variant
Diagnosis: pcr on pbmc and throat swabs or culture virus, IFA, western blot, Elisa
Treatment: ganciclovir and foscarnet
Two strains: ebv-1, ebv-2,, highly conserved, diff in genes to maintain latency (ebna’s), 90:10 ratio in usa, 50:50 in Africa
Epidemiology: widely disseminated, spread by intimate contact, primary inf are subclinical and inapparant, 90-95% worldwide
Spread: infection probably begins in epithelial cells of the oropharynx and spreads to b-cells in adjacent lymph tissues, early stages (10% of b cells affect)
Clinical manifestation: infectious mono (self limiting, atypical lympocytes (nk and t cells), heterophile ab, (rash if treated w. ampicilin
Primary infection in infants and children is frequently asymptomatic
Malignancies: burkitts lymphoma (in jaw), post transplant lymphproliferate disorder (b-cells), HIV associated (non-Hodgkin’s, and oral hairy leukoplakia),
Hodgkin’s disease, nasopharyngeal carcinoma, t cell lymphoma
Diagnosis: presence of atypical lymphocytes, ant-ebv ab, heterophile ab
Transmission: primary through saliva (low titer virus is detectable for life in saliva, sporadic replication of virus in epithelial cells of oropharynx
Treatment: supportive care (non steroidal anti-inflammatory), oral leukoplakia responds to acyclovir
associated w/ KS b/c vDBA found in ks
epidemiology: seroprevalence is 10-20, endemic places 32-100%
Clinical manifestation: KS- tumor(multiple cells or pluripotent precursor), proliferation of spindle shaped cells,& irregular slit-like vascular channels, inflamm
infiltrate of lymphocytes and macrophages, tumor appear fist on skin
Non-Aids KS: classic (elderly), immunosuppresion (may appear upon withdrawal of IS therapy, poss graft rej, lesions may recur, endemic (common Africa
Aids KS: spread from skin to viscera, male homosexual & bisexual aids (20x more likely), viremia associate w/ ks
Associated primary effusion lymphoma (PEL)- aka non-Hodgkin’s- no solid tumor mass, primary in visceral body cavities
Multicentric castleman’s disease(MCD)- atypical lymphoproliferative disorder, generalized lymphoid hyperplasia
Diagnosis: detection of viral DNA (PCR or southern blot), elisa or IFA serum
Transmission: sex, needle sharing, in endemic areas(nonsexual, horizontal spread), organ transplant (3-8% of all post transplant tumors
Treatment: KS- radiation & chemo, excision, IFN, lowering or removal of immunosuppressive therapy – sirolimus (rapamycin), may have antiviral action
HAART lowers incidence of KS and may cause remission of KS
Ganciclovir for mcd, foscarnet and cidfovir