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VIRUS Herpesvirus-1 (HSV-1) Herpesvirus-2 (HSV-2) FAMILY Alpha herpesvirus (latent in sensory neurons) Alpha herpesvirus (latent in sensory neurons) ENVELOPE STUFF TO KNOW yes IE (immediate early) proteins - bind DNA, regulate transcription E (early) - transcription factors, DNA polymerase, thymidine gD is main kinase (TK) glycoprotein; L (late) - structural proteins, glycoproteins, envelope coat gp's B, D, H, L -DNA replicates in nucleus, but envelope received in cytosol for attachment -gp's + tegument = envelope and infectivity! Pathogenesis: CTL mediated response -evades endosomes → released in infectious form! -virus migrates to sensory ganglia during primary infection, lives there until reactivation: during stress, vesicles appear again, may be due to a deficiency in IFN-γ -blisters contain multinucleated giant cells and intranuclear inclusions Receptors: heparan sulfate, Hve A,B,C,M, Nectin 1,2, Diseases: virus + immune response (although many are asymptomatic) 1. Gingivostomatitis - swollen vesicles on mucous membranes 2. Whitlow - watery finger pustule spread from primary infection 3. Keratitis - corneal infection, very common cause 4. Encephalitis - fever, personality change, focal seizures 5. Eczema herpeticum - in presence of underlying eczema Latency = transcription but no translation yes gD is main glycoprotein pathogenesis same as HSV1, just antigenically distinct (diff. gp's) genital infection, usually with self-limited meningitis Diseases: 1. neonatal infection - transplacental viral transfer, attack rate higher if mother is newly infected near time of birth (otherwise do C-section) a) skin and mucous membrane infection - skin rash, DIC if untreated b) CNS infection - fever, lethargy, seizures, CSF abnormal c) disseminated - hepatosplenomegaly, jaundice, high mortality! TREATMENT/ VACCINE immunofluorescence, culture, PCR topical acyclovir, or start IV if suspect encephalitis, even before results come back! Ribavarin no vaccine immunofluorescence, culture (24-48 hrs), PCR acyclovir, oral or IV (fam or valacyclovir is oral) no vaccine yet VIRUS Varicella-zoster virus (VZV) Cytomegalovirus Epstein-Barr virus FAMILY Alpha herpesvirus (latent in sensory neurons) ENVELOPE yes gE is main glycoprotein Beta herpesvirus yes (latent in lymphoid and other cell types gB and gH like salivary glands and the kidney) Gamma herpesvirus yes STUFF TO KNOW no asymptomatic shedding, only infectious when clinically apparent can be transmitted during pregnancy and delivery - give newborn IgG cell-mediated immune response most important Pathogenesis: inhaled virions infect respiratory mucosa -cell-cell spread only, unless talking about skin vesicles - enveloped infectious virions produced in vesicles -T lymphocytes infected, viremia ensues, get skin vesicles -virions in vesicles migrate up sensory root and are latent in ganglia only to reappear in zoster -lytic infection, regulatory protein expression nuclear; latent infection, regulatory protein expression is cytoplasmic -ORF 62 (open reading frame) protein is critical in formation of new viruses and maintenance of latent infection Receptors: heparan sulfate, mannose-6-phosphate receptor Diseases: 1. Varicella (chickenpox) in children - skin vesicles (adults are 25x more likely to have severe disease) 2. Zoster (shingles) in adults only as reactivation of latent VZV rash distributed along sensory nerve root one on side of body 3. Post-herpetic neuralgia, a rare development after zoster reactivation Pathogenesis: infection is through saliva, tears, urine, sexual contact -not airborne! no skin lesions -infectious virus can persist on table-tops → day care problem -latent in bone marrow precursors of monocytes -down-regulates MHC class I, evades immune system Diseases: 1. self-limited mono in immunocompetent patients 2. CMV infection in immunocompromised - pneumonia, fever, retinitis, colitis, lymphadenopathy, rash, encephalitis, neutropenia -reactivation common in transplant pts, AIDS pts 3. Congenital CMV - transfered during pregnancy, risk highest during 1st trimester. If acquired at birth, disease not as bad. Pathogenesis: asymptomatic people shed virus in saliva -lytic infection, tumor virus gp350 binds to -evades immune system with 1L-10 mimics, ↓ IFN, inhibits apoptosis CD21 on B -latent EBV lives in memory B cells cells Diseases: 1. Infectious mononucleosis - fever, malaise, pharyngitis, myalgias, lymphadenopathy, hepatosplenomegaly 2. Nasopharyngeal carcinoma 3. B-cell lymphoma 4. Leiomyosarcoma 5. Oral hairy leukoplakia in AIDS pts 6. X-linked lymphoproliferative disease (in males only) TREATMENT/ VACCINE culture (5-7 days) immunofluorescence PCR acyclovir, oral or IV (famciclovir or valacyclovir for elderly with zoster) vaccine is live attenuated, 85% effective - contraindicated in immunocompromised tissue culture looks inclusion bodies, immunofluorescence no acyclovir! Use ganciclovir, foscarnet, cidofovir no vaccine (+) heterophile test monospot test = Viral capsid antigen (VCA) early test EBV nuclear antigen(EBNA) late test no good treatment steroids for complications no vaccine VIRUS FAMILY ENVELOPE Kaposi Sarcoma Gamma herpesvirus yes herpes virus (HHV8) (latent in lymphoid cells) Influenza A Orthomyxoviridae yes STUFF TO KNOW only appears in immunocompromised patients strongly linked to male-male sex Pathogenesis: -pirated human genes for it's own repertoire, such as IL-6, Bcl-2, chemokine genes Disease: oncogenesis is via transformation 1. Kaposi's Sarcoma in AIDS pts 2. primary effusion lymphoma = body cavity B-cell lymphoma 3 Castleman's disease - malignant lymphoproliferative disease 8 segments of RNA, so can shift and drift! Shift causes major epidemics - if one cell infected with two strains, they can mix - not recognized by any human antibodies RNA replicates in the nucleus, which allows for easier antigenic shifting / drifting A has greatest mutation rate Virulence: -HA is hemagglutinin glycoprotein, binds sialic acid residues on host cells like RBCs sticks out of viral outer membrane; anchored by M-proteins -NA is neuraminidase protein, cleaves mucin neuraminic acid, exposing sialic acid residues beneath so HA can bind; also anchored by M-proteins -M1 protein anchors HA and NA, provides stability -M2 becomes ion channel in endosomes once endosome is acidified - acid activated -also has viral polymerase, nucleocapsid, and nonstructural proteins Pathogenesis: Tryptase Clara (protease) secreted by non-ciliated Clara cells in bronchial epithelia cleaves HA into 2 subunits, which allows fusion of virion and host cell membrane viral HA attaches to host cell and is endocytosed once endosome is acidified (via M2 in influenza A), virus uncoats viral RNA is released and transported to nucleus, mRNA is transported out of nucleus and translated; copies of RNA with ribonucleoprotein also transported out of nucleus HA and NA brought to surface of host cell and stick out, M proteins accumulate, packaged RNA is incorporated and virion buds off Disease: 1. Influenza - fever above 101˚F; myalgia, chills or malaise; cough or respiratory discharge abrupt onset, lasts for 2-4 days but some symptoms can persist for 2 weeks a) complications: pneumonia, either viral or bacterial -if viral, can be from actual influenza - lower tract involvement, can be fatal in young adults! -if bacterial, two most common infections are S. pneumo and Staph aureus - can be fatal, especially in older adults and pts with chronic medical conditions -also neurological - post-infectious encephalitis - self-limited TREATMENT/ VACCINE treat with chemo or radiotherapy no vaccine clinical symptoms, nasopharyngeal swab or rapid antigen test Amantadine, Rimantadine (interfere with viral uncoating) only for flu A; Zanamivir (inhaled-bad for asthmatics) and Oseltamivir (oral) good for A and B, work by inhibiting NA protein; Ribavarin interferes with mRNA, stops RNA polymerase 2 vaccine: injected is whole killed; inhaled is live attenuated VIRUS Influenza B FAMILY Orthomyxoviridae ENVELOPE yes STUFF TO KNOW segmented RNA , so can shift and drift no M2 protein! Pathogenesis basically same as above Disease same as above -can have myositis as complication of Influenza B TREATMENT/ VACCINE diagnosis same as above, can also use DFA neuraminidase inhibitors effective for flu A and B yes yes Influenza C Orthomyxoviridae yes segmented RNA, but not associated with significant morbidity/mortality no NA protein! No real shift associated with flu C see above for general info about influenza Parainfluenza virus Paramyxoviridae yes Disease: 1. respiratory infections that are a little milder than flu - rhinitis, pharyngitis, sinus congestion, bronchitis and flu-like symptoms 2. Croup - infection of larynx and upper resp. tract, coughs sound like barks Ribavarin occurs in winter months Th2 response - cell-mediated immune response most important Virulence: glycosylated surface proteins F (fusion), G, and SH mediate attachment & fusion -proteins N, L, P assc. with nucleocapsid, M (matrix) proteins, NS (nonstructural) proteins which may play a role in RNA replication Pathogenesis: inoculation is via eyes or nose, infection limited to respiratory tract -G and SH mediate attachment to host cell -F protein helps virion fuse -replication of RNA and formation of mRNA -virion assembly and budding -if lower tract involvement, atalectasis and trapped air, especially in young children -easily transmissible, reinfection is common b/c immunity is not complete Disease: 1. Bronchiolitis in infants - nasal congestion, sore throat, fever, increased RR, can see retraction of intercostal muscles (means lower tract involvement); lungs are hyperinflated -duration = 7-21 days 2. Pneumonia in adults - nasal congestion, cough - significant mortality! 20% in older pts characteristic formation of syncytia (fusion of multi-nuc giant cells) Respiratory Syncytial virus Paramyxoviridae yes no vaccine -aerosolized Ribavarin (interferes with viral RNA polymerase) can be given to high risk pts, but is teratogenic -treat high risk infants with RSV-Ig or Palivizumab (monoclonal RSV antibody) no vaccine Adenovirus Adenovirus no transmission by respiratory droplets, fecal-oral route, and direct contact outbreaks occur in crowded conditions Pathogenesis: capsid contains a fiber that helps the virus attach to host cells Diseases: -pharyngitis, conjunctivitis, cystitis, pnuemonia, gastroenteritis Ribavarin only military uses vaccine VIRUS Rhinovirus FAMILY Picornavirus ENVELOPE no uses ICAM-1 as receptor Rabies virus Rhabdovirus yes STUFF TO KNOW occurs in early fall and spring optimal growth at 33˚C, which is temperature of nose and large airways can survive on environmental surfaces for hours - efficient transmission Virulence: noncytolytic - host immune response is responsible for most of symptoms -many differect serotypes, so vaccine not really possible Pathogenesis: -virus enters via nasal or ophthalmic mucosa -replication occurs in lymphoepithelial cells in nasopharynx - no viremia -usually upper respiratory infections, but can involve lower tract -IL-8 released from infected cells causes more rhinorrhea and nasal congestion Disease: 1. Common cold! sneezing, coughing, rhinorrhea, nasal congestion, pharyngitis - 1 week -high fevers, myalgias, chills are not commonly seen -green nasal discharge not indicative of bacterial infection! color is from myeloperoxidase a) also acute sinusitis, otitis media, exacerbations of chronic bronchitis, asthma attacks transmission via bite from infected animal 100% fatal if untreated! high neuroinvasiveness, high neurovirulence Virulence: RNA encodes: L protein (polymerase) - capping, methylation P protein - transcriptional activator M protein - bridges RNA and envelope N protein - wraps the template G protein - antigenic glycoprotein spike Pathogenesis: virus enters through a break in the skin, across a mucosal surface or inhaled -virus replicates and infects muscle spindle → infects nerve to muscle, travels centrally -once it reaches the spinal cord, virus spreads to CNS with almost every neuron infected -after CNS spread, there is peripheral spread to the rest of the body (saliva, stool, etc) Disease: 1. Rabies - incubation may be 1-week to a year! biphasic a) febrile prodrome followed by excitation phase b) paralysis - paresthesias at site of bite, spasm of laryngeal muscles, coma, paralysis inevitable death Vaccine does not work if clinical symptoms have already started. TREATMENT/ VACCINE clinical symptoms treatment is symptomatic - treat with over-the-counter cold remedies not antibiotics!! no vaccine diagnosis uses RT-PCR of brain, Negri bodies in brain tissue, CSF culture, urine, saliva treatment is postexposure prophylaxis (vaccine + Rabies Ig) 2 vaccines: whole killed administered at 0, 3, 7, 14, 28 days; or passive Ig shot injected at site VIRUS Poliovirus Coxsackievirus Echovirus FAMILY Picornavirus (enterovirus) Picornavirus (enterovirus) Picornavirus (enterovirus) ENVELOPE no no no STUFF TO KNOW Pathogenesis: enteroviruses enter through GI tract from fecally contaminted material -virus replicates in submucosal lymphatic tissues in gut -virus penetrates host cells, uncoats, and releases RNA into cytoplasm -4 viral capsid proteins and 8 non-structural proteins are transcribed -inhibition of host cell protein synthesis -release not necessarily cytolytic -minor viremia in lymphatic tissue, major viremia in bloodstream -polio specifics: hematogenous spread to CNS motor and autonomic neurons (not sensory) attacks gray matter of anterior horn and motor nuclei of pons ans medulla Disease: 1. Asymptomatic - 95% 2. Abortive poliomyelitis - fever, headache, abdominal pain, anorexia - self-limited 3. Nonparalytic poliolyelitis - looks like aseptic meningitis 4. Spinal paralytic poliomyelitis - 0.1% - biphasic illness a) minor: looks like abortive polio, lasts a few days, then well for 2-5 days b) major: headache, fever, vomiting, neck stiffness, muscle pain relieved by motion results in weakness and eventually flaccid paralysis (can be 1 muscle or many) 5. Bulbar paralytic poliomyelitis - paralysis of cranial nerves, usually IX and X 6. Polioencephalitis - rare, can occur in infants; changes in mental status infections occur in late summer, early fall replication, pathogenesis and epidemiology same as polioviruses Disease: 1. Aseptic meningitis - common in children - fever, followed by headache, stiff neck, URI self-limited, all pts recover 2. Summer cold - rhinorrhea, sore throat, etc. 3. Encephalitis (rare) - lethargy, seizures, but excellent prognosis 4. Hand-Foot-and-Mouth disease - fever and vesicles in mouth, hand, feet; mouth pustules help differentiate between this and chickenpox; very contagious! 5. Herpangina - vesicular rash in oropharynx; fever, vomiting, sore throat, painful to swallow 6. Transient paralysis - flaccid paralysis 7. Epidemic pleurodynia - sharp muscular pain with spiking fevers after each paroxysm 8. Myopericarditis - inflammation of heart muscle; virus replication in myofibers → necrosis seems to attack young adults, esp. males; can lead to dilated chronic CHF 9. Neonatal myocarditis or hepatitis infections occur in late summer, early fall replication, pathogenesis and epidemiology same as polioviruses Disease: 1. Aseptic meningitis - fever, followed by headache, stiff neck, URI 2. Summer cold - rhinorrhea, sore throat, etc. 3. Chronic meningoencephalitis only in patients with defects in B-cell function - can be fatal 4. Transient paralysis 5. Acute hemorrhagic conjunctivitis - pain, swelling of eyelids - contagious, bilateral! 6. Myopericarditis - inflammation of heart muscle; virus replication in myofibers → necrosis seems to attack young adults, esp. males; can lead to dilated chronic CHF 7. Neonatal myocarditis or hepatitis TREATMENT/ VACCINE diagnosis from throat secretions in 1st week of illness; can't use CSF; serology no treatment 2 vaccines: OPV (oral) can revert to wild-type, also assc. w/ paralytic dz; IPV (inactivated) given IM as series of 4 shots CSF is clear with PMNs at first, then lymphos (glucose + protein nl) culture or PCR treat symptomatically no vaccine PCR, viral culture symptomatic treatment no vaccine VIRUS Rotavirus Rubella virus Calicivirus FAMILY Reovirus Togavirus Calicivirus Coronavirus (SARS) Coronavirus ENVELOPE no yes no yes STUFF TO KNOW segmented RNA, but major antigenic shifts don't occur infections occur during 3-4 months in winter responsible for 10-20% of all diarrheal-related deaths in children spread by fecal-oral route, resistant to stomach acid since no envelope Pathogenesis: -since ds RNA, must package own RNA polymerase to make mRNA -binds to sialic acid residues -once swallowed, infects mature villus epithelial cells of small intestine → death of cells leading to decrease in absorptive area, may result in lactase deficiency Disease: 1. Gastroenteritis - vomiting and watery diarrhea, nausea, high fever TREATMENT/ VACCINE clinical diagnosis ELISA or PCR to detect rotavirus in stool supportive treatment with fluids, don't use anti-diarrheals Rotashield vaccine pulled from US market transmission via respiratory droplets envelope contains HA (hemagglutinin) protein and F (fusion) protein Pathogenesis: virus enters via nasopharynx, replicates in regional lymph nodes -viremia follows, hematogenous spread Disease: 1. German measles - mild fevers, rash on head and neck, spreads to body resolves in 2-3 days, but contagious for 7 days 2. Congenital rubella syndrome - rubella acts as a teratogen → severe birth defects don't give vaccine to women during pregnancy or within 3 months of conceiving serology spread by fecal-oral route encodes 4 proteins - helicase, protease, RNA polymerase, capsid protein can withstand heat and chlorination (swimming pools, disinfectants) Pathogenesis: causes blunting of small intestinal villi, esp. jejunum -virus shedding in stool highest in first 1-2 days -extremely contagious! Disease: 1. Gastroenteritis - vomiting and diarrhea, fever, myalgias, malaise; 2-3 days then done clinical, epidemiological diagnosis; ELISA infections occur in winter and spring virulence probably due to recombination event of 2 different coronaviruses infects multiple species, cats, dogs, etc - spread by respiratory droplets and other secretions Disease: 1. SARS - 2-7 day incubation, but up to 10 days - important for sequestering possible pts a) fever - then chills, headache, malaise, maybe diarrhea b) dry cough, shortness of breath, which may rapidly progress to respiratory distress that requires mechanical assistance -CXR shows increasing infiltrates and consolidations -lymphopenia, thrombocytopenia, elevated creatinine and LFT's clinical diagnosis viral cultures and PCR being tested now; ELISA (+) after 1 month symptomatic live attenuated vaccine part of MMR supportive treatment with fluids no vaccine supportive treatment no vaccine VIRUS Human Immunodeficiency viruse (HIV) West Nile virus FAMILY Retrovirus Flaviviridae ENVELOPE STUFF TO KNOW yes carries 2 identical copies of RNA and reverse transcriptase enzyme ten billion virions are produced and destroyed each day; HIV is not latent! -gp120 amd viral set point reached at ~6 months, lose about 50 CD4 cells per year gp41 most Virulence: important -gag codes for internal structural proteins -pol codes for reverse transcriptase, protease, integrase -memory CD4 -env codes for gp120 (binds to and gp41 cells do not -tat (transcription factor) binds RNA LTR sequence to enhance transcription have viral -rev regulates export of full genomic (unspliced) RNA surface -nef down-regulates host cell MHC class I and CD4 expression, enhances release of virus proteins (nef deletion results in much slower progression of disease) -virion maturation is completed as it is budding off the host cell Pathogenesis: acute infection - dendritic cell binds HIV with DC-SIGN receptor, brings to lymph node, where extensive replication occurs -gp120 binds to CD4 and CCR5/CXCR4, then gp41 inserts into membrane and allows fusion with host cell -clinical latency for up to 10 years or more - depends on immune response, HLA type, etc Disease: 1. Acute HIV infection - fever, lymphadenopathy, macular rash, fatigue, sore throat can treat at this stage to delay onset of AIDS 2. AIDS/Opportunistic infections - usually with CD4 counts under 200, reactivations of latent dz a) TB: CD4 = 300 b) PCP: CD4 = 200 c) Toxoplasmosis: CD4 = 100 d) Cryptococcal dz: CD4 = 100 - diarrhea may be dominant symptom e) M. avium complex: CD4 = 50 - diarrhea may be dominant symptom f) CMV: CD4 = 50 g) cryptosporidium - diarrhea yes vector-borne disease - transmitted by mosquito bite, usually in late summer previously described virus, but in new location human-human transmission possible because of blood transfusions, organ transplantation, and breast-feeding single polyprotein made from RNA - encodes M (membrane), E (envelope) and many NS (nonstructural) proteins neurons don't express MHC class I, so CTL's can't kill infected neurons Pathogenesis: mosquito bite leads to viral replication in peripheral sites -viremia in blood follows, with eventual CNS invasion and disease Disease: 1. Asymptomatic - most common 2. Flu-like illness, abrupt onset with fever, headache, sore throat, rash, lymphadenopathy 3. Encephalitis - flu-like syndrome progresses to encephalitis, with changes in mental status and focal neurological abnormalities → profound muscle weakness prominent feature -neuronal apoptosis induced by virus, CSF pleocytosis -elderly at greatest risk; overall mortality ~5% TREATMENT/ VACCINE acute - use ELISA, Western blot, and RNA viral PCR AIDS - use CD4 count and RNA viral load Treatment: almost always triple combo! Resistance if less (see syllbus for combos) no vaccine clinical diagnosis and serology supportive treatment (IFN + Ribavarin in clinical trials) no vaccine yet VIRUS Dengue virus Yellow fever virus FAMILY Flaviviridae Flaviviridae ENVELOPE yes yes STUFF TO KNOW vector-borne disease - transmitted by mosquito bite, usually in late summer most common arthropod-borne viral infection; worldwide distribution in warmer climates same structure for all flaviviridae (see above) same pathogenesis as above (mosquito bite, viremia, CNS invasion) major exception - cross-protective immunity does not occur, reinfections are often worse! Diseases: 1. Dengue fever (DF) encephalitis - 2-7 day incubation period a) joint/bone pain, fever, headache, retro-orbital pain, then vomiting, respiratory symptoms b) fever, rash, lymphadenopathy, cytopenia -NO fatalities! 2. Dengue Hemorrhagic fever (DHF) - dengue-like illness with thrombocytopenia and increased hematocrit - usually 2nd infection, but can be first -increased vascular permeability = ↑ TNF, IL-8, apoptotic endothelial cell death -bleeding diathesis = cytokines, vascular injury, viral antibodies to platelets -circulatory failure with GI bleeding, pulmonary edema, neurological manifestations -can lead to shock -10% fatal if untreated, less than 1% fatal if treated Reasons why re-infection is worse: pts have non-neutralizing antibodies to DF that will bind the virus, and simply target it more efficiently to the Fc receptors on macrophages, where it can replicate faster; this is called antibody-dependant immune enhancement -also, memory CD4+ and CTL's results in increased cytolysis of Dengue-infected macrophages, which results in much higher amounts of cytokines and vasoactive mediators vector-borne disease - transmitted by mosquito, usually in late summer same structure as above (flaviviridae) occurs exclusively in Africa and Americas, not Asia - no human-human transmission different mosquitos transmit different diseases - jungle yellow vs. urban yellow Pathogenesis: mosquito bits leads to replication in regional lymph nodes, followed by hematogenous dissemination and liver infection - degeneration and "Councilman bodies" caused by direct viral injury -vasoactive and inflammatory cytokines are released → hemorrhagic diatheses, shock Disease: 1. Yellow fever - 3-6 day incubation period, 3 stages of disease a) viremia - fever, chills, headache, back pain b) remission, lasts 1 day c) intoxication - jaundice, "black vomit" hematemesis, shock - no viremia -in pts with jaundice, mortality is 20-50% TREATMENT/ VACCINE clinical diagnosis supportive treatment essential for survival; Ribavarin? vaccine becoming available serology, viral culture no liver biopsy! supportive treatment; Ribavarin? live attenuated vaccine boosters given q. 10yrs VIRUS Measles virus Prions FAMILY Paramyxoviridae Prions ENVELOPE yes (different) STUFF TO KNOW transmission via respiratory droplets envelope contains HA and F proteins, virion also comes with RNA polymerase Th2 response Pathogenesis: virus infects epithelium of respiratory tract, spreads to local lymph nodes -viremia follows, hematogenous spread Disease: 1. Measles - 7-14 day incubation - fever, rhinitis, cough, conjunctivitis, photophobia Koplik spots appear in the mouth, followed by rash on head and then trunk - not contagious at this point proteinaceous infectious particles no genome, not inactivated by UV light, heat, or formaldehyde Biology: PRPc is a normal human protein on chromosome 20. Infection results in PRPsc. PRPc = It is α-helical, protease sensitive, located on cell surface PRPsc = β-sheets, protease insensitive, located in cytoplasm -insolubility b/c of protease insensitivity thought to cause storage problems and aggregation Diseases: TSE = transmissible spongiform encephalopathies 1. Kuru - spread by exposure to brains/mucous membranes of infected individuals headaches, arthralgias, neurologic disease and death within 3months - 1year 2. CJD (Creutzfeldt-Jakob disease) - can be sporadic or from infected surgical instruments vCJD = mad cow disease (variant); death within 3-6 months -looks like Alzheimer's disease, lack of coordination, dementia, motor weakness 3. Fatal familial insomnia - autonomic dysfunction and sleep disturbances thalamic, cerebellar changes 4. Gerstmann-Straussler-Scheinker (GSS) disease - autosomal dominant, progressive spinocerebellar degeneration and accumulations of plaques in cerebellum TREATMENT/ VACCINE Koplik spots are diagnostic symptomatic treatment Ribavarin? live attenuated vaccine part of MMR - 2 doses are recommended clinical syndromes, history no treatment