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88 Cards in this Set
- Front
- Back
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hepadnaviridae
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hep B
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herpes viridae
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- herpes simplex virus type 1 - oral herpes trigeminal ganglion
- HSV 2- genital herpes sacral ganglion - varicella zoster - varicella - chicken pox zoster - shingles - latency in dorsal root ganglion - epstein bar virus - burkitts lymphoma and infectious mononucleosis inf. mononucleosis - infection of B lymphocytes burkits lymphoma - common malgnancy in african children - Cytomegalo virus - retinitis in AID S patients. - congenital - can cross placental barrier. Roseola - - rose colored rash - kaposi sarcoma ass. herpes virus - seen mostly in aids patients. |
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adenoviridae
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- cause of URTI, sore throat and conjunctivitis
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papovirida
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human papilloma visur
- warts and types 16 and 18 are ass. with cervical cancer |
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poxviridae
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- responsible for Variola (smallpox) and vaccinia (cow pox)
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parvoviridae
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- parvo - small SLAPPED FACE syndrome, causes febrile illness in children.
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retroviridae
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- have RT.
- HTLV 1 and 2 - retrovirus that likes to grom in human t cells - causes T cell lymphoma HIV 1 and 2 - kills T helper cells, the on switch of the immune system. HIV does not kill the aids patine |
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picornoviridae
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- 3 subfamilies
1. enterovirus 2. heptovirus rhinovirus |
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enterovirus
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- poliovirus - salk vaccine - injection of killed virus --> humoral immunity
- sabin oral vaccine - cell mediated immunity. produces Iga and IgG - ECHOVIRUS - summer cold like illness, childhood exanhthems, aseptic meningitis, hand foot and mouth disease - coxsackievirus - similar effects to echo virus. |
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heptovirus
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- hep a spread by fecal oral route
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rhinovirus
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cause of the common cold or URTI
immunity is type specific, and there are 115 serotypes. |
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reoviridae
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- reovirus - typically cause URTI
- Rotavirus - infectious diarrhea |
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orthomyxoviridae
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- INfluenza A and B
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paramyxoviridae
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- measles(kopliks spots) mumps rubella
- parainfluenza virus - severe childhood URTI (croup) - respiratory syncytial virus - severe urti and bronchitis in young children. |
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togaviridae
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- arthropod transmission
- unique lifecycle - vertebrate --arthropod--vertebrate |
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flaviviridae -
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arthropod transmission - febrile illness - ecephalitis --hepatitis
dengue fever, west nile, yellow fever |
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bunyaviridae
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- general features - arthropod transmission endemic in midwest USA, calfornia and LACROSSE Encephalitis./
- Hantavirus - spread among rodents |
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coronaviridae -
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URTI SARS
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calciviridae - URTI
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NOrwalk virus, cruise ships and schools have large break outs of GI illnesses due to this.
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patterns of infection
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- acute - cell host death/ symptomatic
- subacute - mild to no symptoms - latnet - may follow acute or subacute infection and reactivation is highly variable. - vuris is undetectable at this stage. intermittnet or sporadic virus production - chronic - may follow acute or subacute exposure Virus is CONTINUOUSLY produced. |
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viruses that have ass. with malignancies
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- retroviruses - HTLV 1 and 2 cause t cell lymphoma (rare)
- HPV 16 and 18 - cervical cancer - epstein barr herpesvirus - burkitts lymphoma - HEP b and c - can lead to primary hepatocellular carcinoma. Herpesvirus 8 - kaposi sarcoma - HSV 1 and 2 - HSV 1 - hither incidence of oral cancers HSV 2 - higher incidence of cervical cancers. |
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fetal teratogens virus caused
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- in first trimester interferes with cellular differentiantion and therefore has th emost profound effects.
- RUbells CMV and VZV |
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control of viruses
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- physical and chemical agents
- act on lipids - envelope viruses - detergents, phenolics adn alcohols. - act on capsid protesins - heat, bleach, aldehydes adn radiation. - act on nucleic acids - most internal structures - bleach aldehyde and radiation. |
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chemotherapy
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- antivirals
- chemoprophylaxis - alpha interferon |
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antivirals
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- nucleoside analogs - mimic nucleotides but don't allow attachment of another base and inhibits DNA intermediate
- Non nucleoside RT inhibitors - inhibit reverse transcriptase - protease inhibitors - used for HIV - inhibits cleavage of polopeptide so viral proteins can't be activated. acyclovir and derivatives - interferw with DNA replicaiton of the herpes virus - non nucleoside polymerase inhibitors - used for all HERPES VIRUSES , CMV retinitis in AIDS |
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chemoprophylaxis
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- amantidine and rimantidine - effective against infl. A ONLY
- prevent penetration of the virus - administered before exposure |
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alpha interferon
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- nonspecific first defense against viral infections.
- causes flu like symptoms of malaise, chill and fever ass. with many viral infections. recombinant, alphi interferon is used therapeutically for HEP B, C and severe HSV - therapeutic doses have some toxicity. |
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vaccines
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- inactivated (subunit) vaccine
- active immuniczation - yield AB's only - influenza, HEP a and B, salk polio, rabies and HPV (gardisil) |
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live attenuated vaccines
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- actually infect you, result in HUMORAL and CELL MEDIATED IMMUNITY.
- use viral mutants - result in some limited infection without symptoms - used for sabin polio, MMR and VZV. |
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hybrid vaccines using vaccinia virus
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- imm. against a variety of viral agents in fewere immunizations.
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passive immunization
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- pre and post exposure prophylaxis
- inject anti hep a antivody before you come into contact with the virus - post exposure - HB Ig - Hep B immune globulin as well as vaccine ZIG - zoster immune globulin. |
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Herpes viridae
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- epstein barr - causes infectious mononcucleosus
is an infection of B cells also causes burkitts lymphoma signs and symptoms - edmeatous glands, splenomegaly |
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herpes simplex virus 1
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- primarily cuases oral herpes - 99% of initial infections are subclinical.
- latency in trigeminal ganglion - clinical (acute) illness is referred to as primary herpetic gingivosomatitis - typically these primary infections occur intraorally, involving the gingiva, secondary spreading to other tissues such as the buccal mucosa or tongue. may end up with extra oral spread too. - usually affect a sensory neuron = painful! - blister develops ( initally clear) - as cells die, things accumulate the fluid becomes cloudy leasds to ulcerated state where the virus is shed reoccurence typically occurs peri orally - results from reactivation of latent virus near lips and around mouth. - tingling --burning --vesicle formation rupture -- |
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herpetic whitlow
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- herpes will infect any part of the body really
- paronychia is herpes infection of the nail bed - herpetic keratoconjunctivitis - can be recurrent - patients with eczema or psoriasis are at increased risk. - immunocompromised patients - at risk for reactivation of latnetn herpes - herpes encephalitis - can move up the spinal cord to the brain. |
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tzanck smear
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- used to make the microscopic diagnosis of herpes infections
- with herpes, adjacent cells tend to fuse. |
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herpes simplex virus 2
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genital herpes; latent in the sacral ganglia
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neonatal herpes
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- 5% acquired in utero
- 10% acquired postnatally - 85% acquired during labor/ bith - greatest risk if mom becomes infected during the 3rd trimester - maternal aby provides some protection - may be localized or disseminated. |
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who is most affected by aids
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those in sub saharan africa
- over 7400 new HIV infections a day in 2008.. more than 97% are in low to middle income countries - tremendous economic impact in non industrialized countries |
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why does HIV present such a unique problem
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- antigenic hypervariability - Reverse transcriptase - makes many mistakes mutations
- as the virus replicatesin a patient antigenic variants emerge that are no longer neutralized by the body that made against the initial infecting virus. |
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goal of therapy
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- to maintain T helper cell count
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Obligatory integration of host cell DNA
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- the DNA transcript that is produced must integrate into the chormosome of the host cell. and can remain there in a non replicating state - imm. system can't get to it here
- won't be affected by chemotherapeutic agents. - intracellular nature - inaccessible by aby and CMI - aby can't enter the cell. - if non replicating, escapes detection by Tctl |
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sequestration of the virus in the cns
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- the virus also affects cells in the brain, bc of the BBB it is almost impossible to get chemotherapeutic agents to those cells.
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time course of AIDS -
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- time course in years
- t helper = t4 cells = CD4 cells - normally at 1400/microliter of blood - killed off by viral replication - immune system responds - decrease level of virus - virus continues to replicate and new mutants emerge - periodic spikes in virus production, each of hwch is neutralized by subsequent CMI - with time we kill off enough Thelper cells and new mutants will continue to emerge - immune system can't keep up adn drop in helper cell numbers. - patient experience - initial spike in viral numbers - flu like symptoms, aby is detectable in pats. blood - may fell fine for years - start to experience night sweats, diarrhea and adenopathy - leads up to opportunistic infections |
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esophogeal candidiasis
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- one of the first indicators of HIV infectinon.
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goal of therapy
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- inhibit virus replication
- can prevent drop in t helper cell numbers - can drive viral numbers below detectable levels. - side effects are quite pronounced - |
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current chemotherapeutic regimens target HIV early in the infectious stage.
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- agents - nucleoside RT inhibitors
- non nucleoside RT inhibitios - prevents the synthesis of DNA transcript - protease inhibitors - prevents post translationnal modification of HIV proteins |
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types of tests performed to detect HIV/ AIDS
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Elisa - a rapid sreening test to detect anti HIV aby in teh patients blood. Positive ELISA is followed by a western blot test
- WESTERN BLOT TEST - confirms the presence of HIV aby in the patients blood - viral load assay - used to quantify HIV RNA in the patients blood. - can gauge the effectiveness of the chemotherapy. |
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influenza abc
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- genera of orthomyxoviridae
- inf. a b and c viruses are distinguishable on the baseis of their internal nucleoprotein and matrix proteins which are specific for each viral. - influenza A virus - only one species are naturally able to infect a randg of anmila species infl. b - only infect humans c infects humans and swines. a and b are cause of seasonal epidemics. |
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external antigens
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- the external antigens H and N show more vatiation and are the subtype and strain specific antigens
- neuramidase - allows the virus to penetrate the mucous overlying the respiratory epithelium more easily. - these are used to determine the particular strain of inf. a responsible for an outbreak. - neuramidase - allows the virus to penetrate the mucous overlying the resp. epithelium more easily. - these are used to determine the particular strain of infl. a responsible for an outbreak. |
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hemagluttin protein
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- involved in attachment and membrane fusion with the infected cell.
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neuramidase protein
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- digests sialic acid (neuramic acid) with most cells have on their surface and is involved in penetration of the mucous layer in the resp. tract.
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antigenic drift
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- due to mutation
- antibodies to the H protein are the most imp. protection. - both proteins undergo antigenic drift - results in sporadic outbreaks and limited epidemics |
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antigenic shift
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- is due to reassortment
- in the case of inf.a antigenic shift periodically occurs |
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pigs have teh ability to support avian and human virus
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- human swine and human avian virus and hybrids can emerge and lead to large scale epidemics
- human avian hybrids is diff. from avian hybrid in its esae of infecting humans. |
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influenza pandemics
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- result from reassortment, new influenza virus subtypes are formed.
- happens every 25 years. - about 3-4 happen in each century |
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spanish flu
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originated wholly in birds adn did not recombine with human flu viruses
- the virus jumped from birds to humans. - high mortality due to cytokine storms with release of increased variety and increase levels of pro inflammatory cytokines from macrophages in teh lung. - edema and hemmorage - bronchopneumonia - acute respiratory distress syndrome with necrosis |
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chemotherapy for influenza
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- zanamivir (relanza) and oseltamavir ( tamiflu)
- rimantidine and amantidine - block virus entry - used prophylactically in high risk populations - resistance is increasing. |
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hepatitis a
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- fairly common
- spread through fecal -oral route contamination of food and water. - no chronic inflammation |
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hep b
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- a killed subunit vaccine available
- passive immunization used in post exposure situation - |
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Hep D
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- is a defective virus --> actually employs Hep B capsid proteins
- only reproduces in cells that re simultaneously infected with Hep B (bc hep d can't make its own capsid Hep b vaccination also prevents Hep D infection |
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Hep C
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- the vast majority of exposurese result in chronic infection. patients remain clueless as to infectious status
- very few exposures result in chronic infection where the patient feels ill and seeks tx. - |
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prevealance of different hep.
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- most is hep a
- as more moms enter the workplace, more kids go to daycare - B is second most common - C is third most common |
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mortality of Hepatitis
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- with hep a is rare, usually has to have an underlying issue.
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chronic hep b
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- killing hepatocytes on a regular basis
- death and regeneration of liver cells due to hep b infectivity may result in an increased chance of liver cancer. |
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Hep C
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- high incidence of subclinical infections
- large number of chronic cases - death rate is much higher |
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incubation period is quite
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LONG
- symptoms have a gradual onset - nothing really indicates hepatitis until you reach jaundice and dark urine |
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why does jaundice occur
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- hepatocytes work to cln up old and damaged RBC's - the Hb needs to be broken down and reprocessed.
- if you don't have enough hepatocytes these breakdown products (bilirubin) accumulates and leads to jaundice. |
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hep a
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- RNA picornavirus - single serotype worldwide
- acute disease and asymptomatic infection - NO chronic infection- protective ab's develop in response to infection confers lifelong immunity. because there is a single serotype worldwide it makes for a very effective vaccine the younger you are during infection the more likely you are to have an asymptomatic infection. |
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clinical features of Hep a
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- incubation period - average is 30 days and range is 15-50 days
- jaundice by age group - <6 y.o. = <10% ; 6-14 = 40-50% ; > 14 y.o. = 70-80% chronic sequelae = young - acute hepatitis is defined by the development of jaundice |
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events in Hep a infection
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- we become symptomatic when we are exposed because of alpha interferon
- pain and swelling occurs because cells are killed ALT - liver enzyme - typically little to none of this in circulation - is relaeased into blood when hepatocytes are damaged. - viremia - infections process develops long before patients become symptomatic - shed in feces long before they know they are infectious - IGM - initially high and fades off as IGG comes up ALT drops and IGM drops and IGG goes up. - recovery phase - as ALT begins to drop down. |
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concentration of hep a virus in various bodlily flueds
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- feces is most common
- serum - viremia - a small amount of virus shed in saliva. |
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virus transmission
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- fecal to oral is most common route
contaminated food and water with close personal contact |
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prevention of Hep a
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- vaccination (pre exposure)
- single serotype worldwide - vaccination is good whereever you go. - will take several weeks to develop active levels of antibody (Ig) - good hygeine important - Picornaviridae - NON ENVELOPED |
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global patterns of Hep b infection
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- 45% of the worlds pop. is at high risk early childhood infections are common.
- intermediate (2-7%) 43% of global pop. - infections occur in all age groups - low - most infections occur in high risk adult groups. |
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70s abd 80s
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we saw an increase in HEP B infections.
- vaccines in early 80's - - in 90s started immunizing newborns shortly after birth. - OSHA - hep b for all immunizations for employees at risk. |
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hep b clinical features
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- incubation period is 60-90 days
range is 45-180 days - clinical illness jaundice - <5 yo <10% - > 5 y.o. 30-50% - acute case fatality rate - .5-1% - chronic infection - <5 y.o. - 30-90% ; > 5 y.o. 2-10% - premature mortality from chronic liver disease - 15-25% |
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infection routes
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- anicteric (subacute) no jaundice
- 90% recover - 10% become asymptomatic chronic carriers - 10% develop acute disease - 90% of these recover - chronic active hepatitis leading to cirrhosis, hepatocellular carcinoma - chronic persistant hepatitis - fulmitant hepatitis |
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HBV antigen and antibodies
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- hep b surface antigen - HBsAg with corresponding antibody being anti HBs
- HBcAg - hepatitis B core antigen anti Hbc antibocy. - HBsag this is the only antibody that is protective - current vaccine creates a recombinant form. of the hep b surface antigen HBcAG antibody is anti Hbac - proteins that facilitate tight packaging inside capsule - anti Hbc IgM is important diagnostically IGg tells you if therei s a chronic infection or not. In the presence of anti HbC it confirms presence. - HbE ag - is there when virus replication is at its maxiumum - ots of virus = surface antigen and HbeAg positive. - more likely to be in chronic hep. situation - important prognostically (prediction) |
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HBV angn and aby
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- anti Hbs - protective and indicates ummunity and recovery
- anti Hbc, igm with HBsag - confirms current infection anti Hbc Igg with Hbsag - confirms chronic infection - anti HBe - indicates an improving prognosis. |
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acute hep b infection with recovery
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- paek of surface agn production indicates peak of virus replication
- sx develop gradually at peak, pts. become jaundiced - anti Hbc - confirms presence and prognosis is improving because HBsag is reducing in number. - around 24 weeks surface antigen is nearly gone, there is a gap between hbsag and anti Hbs this is known as the surface antigen convalescent window. - during this time patients are potentially infectious. - even a few months before we see anti HBs appear. - which indicates immunity or recovery - |
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how to distinguish between successfully immunized and recovered patients
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- successfully imminized - anti HBs
- infected and recovered - anti HBs, anti Hbe and anti HBc Anti Hbe indicates improving prognosis and anti HBc igm confirms presence of infections. |
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progression to chronic hep. b virus infection
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- chronic infection is defined by persistance of surface antigen beyond 6 mos.
- heavy chain switch - IgM anti Hbc persists but IGm disappears. - patients prognosis is improved - may recover to the point of being physcally well - chronic persistent - are reminded every so often of disease state - chronic active - continuously symptomatic. |
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HBV modes of transmission
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- sexual
immunoprophylaxis - can be acitve and passive simultaneously (inject with Hep B Ig and vaccine simultaneously) - perenteral - mom is a chronic carrier - intervene within hours of birith with hep b ig and vaccine - consequences of being infected as an infant - high incidence of subclinical and chronic infection. risk of developing cirrhosis and liver cancer goes up a lot. - parenteral - exposure through skin and mucous membranes. |
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concetration of Hep b in diff. body fluids
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- high in blood serum and wound exudates
- moderate in semen, baginal fluid and saliva - low in urine, feces, sweat, tears and breast milk. |
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hepatitis c infection descriptions
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- the vast majority of Hep c infections do not result in jaundice majority become chronic
- many dif. serological types - almost impossible to make a vaccine - high rate of subacute infections makes management quite difficult. |
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risk factors for hep b infections
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- IV drug use is the highest
- can be sexually transmitted - transfusions |
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clinical features of Hep C infections
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- incubation period - avg. is 6-7 weeks and range is 2-26 weeks
acute illness - mild <20% - fatality rate - low - chronic infection - 60-85% cirrhosis - 20% mortality is 3% |
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risk factors ass. wth transmission of HCV
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- illegal injection drug use
- transfusion or transplant from infected donor - occupational exposure to blood - iatrogenic (unsafe injections) - birth to HCV infected mothers - sexual household exposure to anti HCV positve ontact - multiple sex partners - iatrogenic - |
