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81 Cards in this Set
- Front
- Back
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Adenovirus
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Nonenveloped
Icosahedral ds-DNA Transmission respiratory (upper respiratory tract infections) Affects acute (upper and lower) respiratory infection |
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All Herpes Viruses
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Enveloped
Icosahedral ds-DNA Common viruses Can cause latent phase infection after earlier acute infection. Viral DNA hides in the nerve close to infection Latent disease stimulated by . . . Fever Abrasion UV light Stress |
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Human Herpes 1 Herpes Simplex Virus 1
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Causes mucosal eruptions
Eruptions on lips are called fever blisters or cold sores Found on genitalia also Latency usually follows acute infection Viral DNA is produced inside nerve cells Exposure by direct contact with infected person may induce immunity |
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Human Herpes 2 : Herpes Simplex Virus 2
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Genital eruptions due to (primarily) sexual contact
Latency usually follows w/ viral DNA in nerve cells Sheds particles 75% of the time even when lesions are absent Neonatal infections are common and may be fatal – neurological defects – spontaneous abortion Associated w/ cervical cancer (unsure of the cause) Associated with HIV |
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Human Herpes 3 : Varicella-Zoster Virus or Chicken Pox Virus
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VERY contagious
Primary infection is “Chicken Pox” Eruptions of fluid filled-vesicles over entire skin Spread by aerosol (respiratory) very contagious Reactivation is called Zoster or SHINGLES Occurs in the area of the infected nerve (unilateral) VERY PAINFUL |
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Human Herpes Virus 4: Epstein-Barr Virus (EBV)
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Causes many conditions:
Infectious Mononucleosis Sore throat Fever Swollen lymph nodes Increase in mononuclear cells Common in teens “kissing disease” Self-limiting Rarely fatal enlarged spleen Most patients are able to return to work within 3 to 4 weeks Burkett’s Lymphoma Tumors on jaw and central organs develop (full of viral capsid protein) Found in Africa Rare in US A connection to Chronic Fatigue Syndrome |
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Human Herpes Virus 5
Cytomegalovirus CMV |
Common
Most asymptomatic Mucous transmission Giant cell is characteristic Problems with fetuses and newborns Enlarged liver and spleen, neurological damage Possible hearing visually inpaired Possibly fatal |
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Human Herpes 6:
T-lymphotropic virus |
Replicated in T-lymphocytes, macrophages, salivary and gland cells
Linked to Fever in infants (105oF) and rash Multiple sclerosis 70% of MS pts test positive Brain lesions contain the virus Hodgkin lymphoma Oral carcinoma Some T-Cell lymphoma |
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Variola
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Causes “Smallpox”
Large brick-shaped enveloped virus ds-DNA Symptoms Severe fever Prostration Rash (starts 2-3 days later) Papules (bumps) Vesicles (fluid bumps) Pustules (cloudy fluid bumps) Deep scar Causes severe disfigurement and was very deadly 5-10% die Eradicated through universal immunization 1966 10-15 million die world wide 1967 WHO begins eradication 1977 last case in Somalia 1980 Eradicated |
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Papovavirus
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Includes Papillomavirus (HPV)
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Papillomavirus (HPV)
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40 types of wart-causing viruses such as “genital warts”
Nonenveloped Icosahedral circular ds-DNA All are associated with human tumors Tumors are usually benign Some cause cervical cancer |
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Picornavirus
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Morphological characteristics
Very small ss-RNA Enveloped Includes Enterovirus (gastro-intestinal) i.e. Coxsackie virus Rhinovirus (common cold) > 100 types And… Hepatitis A (more later) |
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Poliovirus is a
Picornavirus |
Spread by fecal-oral transfer
Most infections are asymptomatic and limited to GI tract. However, it can invade Central Nervous System (CNS) tissues causing . . . Meningitis (mild form in the CNS) Post-Polio Syndrome Had polio but learned to use different muscles Lose these muscles in old age Paralysis occurs |
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Bulbar-Spinal Poliomyelitis is a Picornavirus
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Worse case
Brain stem attacked |
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Rhabdovirus
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Helical virus w/ protein spikes, bullet shaped
ss-RNA Causes Rabies Spread usually by a bite of dog, rabbit, squirrel, cattle, horses, etc.,(rarely inhalation of dust with bat droppings) Virus moves along peripheral nerves to CNS May take 2 weeks to several months. Average is 8 weeks before symptoms: Difficult swallowing Nervousness Excitation Headache nausea Untreated is usually fatal in humans (only 2 exceptions in history) |
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Hepatitis
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Five viruses that cause liver disease and/or cancer
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Fibrosis
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virus infects liver cells and damages them producing scar tissue. This scar tissue replaces the liver cells.
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Cirrhosis
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a build up of fibrous tissue. Liver becomes hard and bumpy. Blood flow is blocked. Get back pressure in the veins (can’t get nutrients from stomach and intestine to needed cells). Varicose veins form in stomach and esophagus can burst . . . vomiting blood or passing black stools.
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Liver Cancer
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5,000 people die in the US each year related to Hepatitis B and C
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Hepatitis A
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A picornavirus (small)
ss-RNA enveloped CDC estimates: 150,000 people in US are infected each year 1/3 of US population have been infected Most recover within 6 months w/out serious health problems Transmitted: Water, food w/ fecal material (enterovirus) Fecal matter has high conc. of viruses compared to saliva or other fluids Shellfish a big problem Direct contact w/ infected person Kissing Anal sex IV needles > 40% cases are unknown causes Symptoms None or asymptomatic Symptomatic Fatigue Nausea Vomiting Liver area pain Dark urine Light colored stools Fever Jaundice due to liver damage Prevention Sanitation Hygiene Vaccine (attenuated) High risk areas Middle East South America Eastern Europe Central America Africa Southeast Asia A few areas in US with poor sanitation Day care Military Institutions for the disabled |
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Hepatitis B
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Icosahedral
ds DNA Enveloped CDC estimates: 125,000 contract the liver disease each year. 90 – 95% ADULTS fight off infection off themselves . . . develop immunity. Will always test positive & can’t give blood even though it’s cleared. 5%-10% infected are carriers (currently, ~1 million are carriers in US) Carry virus in blood > 6 mos. Usually no symptoms May clear virus on their own . . . most don’t! Have a higher risk of liver failure or cancer chronic liver disease and cancer Transmitted More infectious than HIV Direct contact w/ infected person Biting Sex IV needles Blood Body fluids Semen Vaginal secretions Saliva Open sores 3%-40% unknown (diff. due to pts. not wanting to admit) Has been found in, but not transmitted by sweat, tears, breast milk, urine, and feces Symptoms None or asymptomatic (approximately 40%, blood donation test is 1st indication Symptomatic Fatigue (lasting weeks or months) Nausea Vomiting Liver area pain Dark urine Light colored stools Fever Jaundice due to liver damage Prevention Vaccine . . . 2 + 1 booster Lasts 13 years (after that . . . ?) Hepatitis B Immune Globulin (HBIG) Pooled human plasma w/ Ab’s to Hep.B. Given right after exposure (sex, needle sticks) Successful in 70%-75% Condoms Wear gloves Cleaning blood Clean blood contaminated area w/ Bleach Don’t share razors, toothbrushes, pierced earrings Don’t share gum or pre-chew for a baby Use caution w/ body piercing & tattooing High risk Work w/ blood & blood products First aid EMT Mortician Police Dentist /hygienist Medical personnel Etc., Live in the same house with an infected person Have sex with chronically infected or carrier IV drug user > 1 sex partner Blood transfusion prior to 1975 (screen was developed at this time) Hemophilia Pt. in a long-term care facility (nursing home) Incarcerated person Bitten by infected/carrier Travel to countries w/ high incidence Treatment Interferon |
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Hepatitis C
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ssRNA, icosahedral, enveloped
Causes a current epidemic CDC estimates Four million cases in the US (1/8 the population) It is expected to triple in the next decade (partly due to increased screening) #1 reason for Liver Transplants Previously, it wasn’t regularly screened for Can’t test liver enzymes due to fluctuations Was first named and fully identified in 1989 (before then it was called “Non-A & Non B Hepatitis). Transmission Mostly we don’t know What we do know We carry virus in blood Can live in dried caked blood Body piercing Tattoos Acupuncture Nasal cocaine use Symptoms Asymptomatic usually the case Symptomatic Most infections are acute/ not chronic May have headache and fatigue (vague . . . no biggie) Affects mostly 20 – 40 year olds Prevention: see other hepatitis viruses gloves Treatment: Interferon |
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Hepatitis D
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Transmission by contaminated blood and syringes
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Hepatitis E and Hepatitis F
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Transmission by contaminated water . . . oral-fecal route
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Hepatitis G
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Unknown
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Hantavirus
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Pulmonary Disease - Pulmonary Syndrome
Transmission In the urine and feces of field mice First found in NW corner of NM in 1993. Now has been identified in 21 states Symptoms Flu-like in healthy adults Fever Abdominal pain Shortness of breath Fatal in 30% – 60% cases that proceed to later stages if the disease. |
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Human Immunodeficiency Virus (HIV)
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Retrovirus
Subfamily “Lentiviruses” contains HIV-1 and HIV-2 These viruses differ genomically and biologically HIV-1 is the more aggressive disease Icosahedral enveloped with spikes ss RNA Capsid contains: ss RNA 3 + genes env – envelope gag – inner core protein pol – polymerase Enzymes Reverse Transcriptase - functions as . . . All around DNA polymerase Protease Cuts new viral proteins to their proper size . Integrase allows the viral DNA intermediate to be incorporated into host cell chromosomal DNA. Cycle HIV Replication: Attachment Spikes (w/ gp41) are specific and attaches to: CD4 proteins on Helper T-lymphocytes Macrophages Monocytes Dendritic cells Uncoating Viral RNA is exposed Viral reverse transcriptase makes dsDNA (replicative intermediate) Viral dsDNA may then be integrated into the host DNA (integrase) Virus may remain latent or produce more viral particles Progeny virus RNA and mRNA are made by host cell RNA polymerase from the dsDNA intermediate. Viral proteins originate from the mRNA. Assembly of the proteins with viral RNA produces new viruses except for the envelope which is acquired when the viruses leave the host cell. Release Buds out of the host cell Outcome Helper T-lyphocytes become depleted and pt. progresses towards immunodeficiency May take as long as 10 years to develop into AIDS Acquired Immunodeficiency Syndrome Transmission Sexual contact Homosexual Heterosexual Easier transmission with anal intercourse or with ulcerous V.D. Contaminated blood Blood products Injection equipment In utero Infected mothers pass on virus to children Symptoms Lymphadenopathy Weight loss Fatigue Other Opportunistic pathogens Cryptococcus neoformans fungi from pigeons/soil pulmonary infection-pneumonia brain/meninges - meningitis Candida albicans Pneumoncystis carinii Fungi cysts/spores? Normal in lungs Others Dementia Kaposi’s sarcoma (cutaneous neoplasm) Lab identification Low lymphocyte count Ab’s to HIV – Western Blot Others Prevention and Treatment Monitor blood for contamination “safe sex” whatever! Abstinence … good luck! Nucleic Acid analogs Azidothymidine (AZT) Dideoxyinosine (ddi) Reverse transcriptase inhibitors Protease inhibitors Integrase inhibitors Combination of nucleic acid analogs and integrase inhibitors appear promising |
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SARS - Severe Acute Respiratory Syndrome
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Coronavirus
ssRNA enveloped Helical/Pleomorphic Respiratory Colds Low grade fever Common in animals |
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Orthomyxoviridae
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Enveloped; pleomorphic and filamentous forms occur; spherical, or filamentous;
Divided into two genera: Influenza A viruses In humans, pigs, birds, and horses. Haemagglutinin (HA) – the larger protein is an essential virulence factor Neuraminidase (NA) – the smaller protein is responsible for the transport of the virus into and out of cells. Influenza B viruses Only humans Influenza C viruses Only humans |
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Human Influenza
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Transmitted
Respiratory Disease Contagious 1 day before symptoms Symptoms fever (usually high) headache extreme tiredness dry cough sore throat runny or stuffy nose muscle aches Stomach symptoms, such as nausea, vomiting, and diarrhea, also can occur but are more common in children than adults ~5% to 20% of the population gets the flu More than 200,000 people are hospitalized from flu complications ~36,000 people die from flu. CDC, September 28 , 2005 Prevention/Treatment Antivirals approved for treatment of influenza A viruses Amantadine, Rimantadine Zanamivir first neuraminidase inhibitor available for clinical use and is effective against both influenza A and B. Oseltamivir Neurominidase inhibitor Vaccine Sigh! |
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Spanish Flu
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First Wave
Spring 1817 infants and aged Second/Thirst Wave Spring 1818 20 yrs - 40yrs Mortality rate was 2.5% - 5% previous influenza epidemics are usually less than 0.1% 20% affected Symptoms Cyanosis Severe obstruction of the lungs Coughing up blood Hemorrhaging suffocation Some military doctors injected severely afflicted patients with blood or blood plasma from people who had recovered from the flu |
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Human Influenza A
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RNA genome (genetic material) split into 8 segments.
If two different viral types infect the same cell, then segments from both types can get jumbled together (they reassort) as the new virus particles are assembled. Antigenic Shift (antigenic drift is minor changes) The new viral strain can emerge that contain a mixture of the parental genes and has the potential to spread rapidly. |
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Avian influenza, influenza A (H5N1)
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Morphology
Enveloped, Spherical helical 8 stranded RNA Jumped species Thailand November 2003. Chicken cholera? South Korea December 2003, avian flu’. Thailand January 23, 2004 first human case of ‘avian-flu’ confirmed Vietnam followed, 2004, Symptoms Fever, malaise, myalgia, sore, throat and cough are found in most of the patients Persistent high fever is an useful sign. Life threatening viral pneumonia and respiratory distress syndrome multiorgan failure 65% mortality (1.6 billion) Treatment Amantadine (rapid viral resistance) Rimantadine (rapid viral resistance) Zanamivir (approved for treatment of persons aged >7 years) first neuraminidase inhibitor available for clinical use and is effective against both influenza A and B. Oseltamivir (approved for treatment of persons aged >1 year) neuraminidase inhibitor Tamilflu Neuropsychiatric events |
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Noroviruses
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Like Norwalk
genus Norovirus, family Caliciviridae single-stranded RNA nonenveloped viruses cause acute gastroenteritis in humans incubation period is between 24 and 48 hours transmitted primarily through the fecal-oral route |
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Symptoms
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a change in body function
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Syndrome
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a collection of symptoms that accompany a disease
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Etiology
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the cause of the disease
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Epidemiology
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the study of when and where disease occurs
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Incidence
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number of people in a population at a particular time who develop a disease
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Prevalence
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total number of people in a population who have developed the disease (both old and new cases)
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Sporadic disease
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occurs occasionally
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Endemic disease
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a disease consistently in a particular area (malaria, cold)
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Epidemic disease
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many people in a population acquire the disease during a short period of time (flu epidemic)
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Pandemic disease
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an epidemic disease occurring worldwide
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Extent of Host Involvement
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Subclinical Infection vs. Clinical Infection
Localized Infection Generalized Infection (systemic or disseminated infection) |
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Bacteremia
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Presence of bacteria in the blood
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Septicemia
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Bacterial are multiplying in the blood
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Viremia
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Presence of viruses in the blood
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Toxemia
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Presence of toxins in the blood
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Primary Illness
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Acute infection
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Secondary Illness
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Opportunistic infection
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Nosocomial infection
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Infection acquired during a hospital stay
Microbe availability Compromised hosts (patients) Easily transmitted by staff |
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Zoonotic
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A disease transmitted between animals and humans
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Contact Transmission of Disease
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Fomite
Normal Microbiota(Flora) Transient Microbiota (Flora) |
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Chronic
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Disease occurs slowly and stays with you for a long time, it may reoccur
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Acute
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Symptoms appear quick and only last for a short time
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Prions
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disease-causing variants of normal proteins produced in nerve cells (and a few others)
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PrPc (Prion Protein cellular) normal "healthy" prions
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RNA that codes for PrPc is produced in the nucleus and exits via the nuclear pore.
RNA then passes along ribosomes attached to the rough ER. PrPc is formed in the rough ER and then progresses up through the Golgi. At the Golgi, vesicles containing PrPc bud off and travel to the cell surface. Vesicles fuse with the cell membrane and discharge their cargo The cellular proteins come to sit on the exterior of the cell. |
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PrPsc the bad protein particle
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PrPc goes bad when it encounters PrPsc prions.
(sc stands for scrapie) Causes normal proteins change shape PrPsc accumulates in the cell. PrPsc vesicles may also travel to the Golgi and intercept PrPc that is being processed there. PrPc might be switched to PrPsc at various points in and on the cell. Prions enter the brain along the axons of neurons. Probably by a flow of prion-filled vesicles. Another route of entry could be the blood, probably in immune cells. Prions cause fatal neurological diseases Produces vaculoles in the brain |
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Prions – Proteinaceous Infectious Particle
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Symptoms
Loss of motor control Dementia paralysis Wasting Eventually death (pneumonia) |
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spongiform encephalopathies
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Diseases caused by prions
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Types of Spongiform
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Mad Cow Disease (BSE, Bovine Spongiform Encephalophathy)– 1987 Great Britain
Scrapie – sheep Sheep scrape against fences and trees until raw CWD (chronic wasting disease) - muledeer, elk Kuru – Human tribes in New Guinea Cannibal ritual Creutzfeldt-Jakob Disease (CJD) rare human disease 200 cases per year in the US Probable genetic link or contact with tissues of infected people (tissue grafts) |
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Virology
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the study of viruses
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Viruses
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Latin = Poison
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General Viral Characteristics
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Noncellular & Submicroscopic
10 - 100 X’s smaller than most bacteria. Obligate intracellular parasites Lack energy-generating systems Lacks machinery to synthesize macromolecules Very limited enzymatic capabilities Do carry own genetic information! Contains DNA or RNA, not both May be single-stranded (ss) or double-stranded (ds) only contains 3-100 genes Not sensitive to normal antibiotics |
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“Virion”
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mature, infectious, complete viral particles (NA + protein coat)
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Capsid
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Protein Coat
Made up of individual subunits called “capsomeres” Capsomeres are made up of one or few kinds of protein molecules Functions to protect genetic info. Functions in attachment to host cells |
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Envelope
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Lipid envelope found on some viruses
Acquired from passing through host cell membrane Enveloped viruses lose infectivity if envelope is destroyed |
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Paplomeres or spikes
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Found on some viruses
Often used for attachment |
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Helical
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Cylinder w/ identical capsomeres in a spiral arrangement
nucleic acid coiled inside |
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Icosahedral or cubic
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20-sided figure, each side equilateral D
Often appear to be spherical |
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Virus: Structure
Three Basic Shapes |
Helical
Icosahedral or cubic Complex or combined They can also be pleomorphic |
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Viruses: Cultivation
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Cannot be grown on artificial medium
Many can be grown on tissue culture Grow host cells in a monolayer Inoculate and look for “cytopathic” effects On cells attached to beads in a bioreactor Some need embryonic eggs Some need intact animals/organisms Example Polio (1955 – 1961) Viruses grown in monkey’s liver cells Viruses killed (Salk) with formulin Problem Formulin doesn’t kill the SV40 simian virus SV40 has oncogenic properties note: Sabin vaccine = live formula 1963 |
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Viruses: Control
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Chemical Agents
Phenol - denatures capsid proteins Formaldehyde - good for vaccine preparation Hypochlorite – bleach 70-90% EtOH, not the best Lipid solvents, for enveloped viruses Physical Agents Heating to 50-70oC for 1 hour Freezing doesn’t work Radiation (X-rays & UV light effective |
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Viruses: Classification
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Based on:
Type of Nucleic acid (NA), 4 types: Double-stranded DNA (ds-DNA) Single-stranded DNA (ss-DNA) Double-stranded RNA (ds-RNA) Single-stranded RNA (ss-RNA) Structure of capsid Site of Replication Host Range Type of Transmission |
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Viruses: Multiplication of Bacteriophages (Lytic Cycle)
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T-even Bacteriophage Lytic Cycle
ATTACHMENT (Adsorption) to Host Cell Due to chance collisions Virus binds to host cell receptor sites PENETRATION Phage tail releases lysozyme to enter bacterial cell Sheath contracts and tail is driven through cell wall DNA is released into the bacterial cell BIOSYNTHESIS (Replication) of Viral Subunits. Host DNA is degraded Viral DNA in the cytoplasm is transcribed and translated Phage initially uses hosts nucleotides, ribosomes, enzymes and amino acids Host cell makes: new enzymes (if needed) to replicate viral NA new viral NA new viral structural proteins MATURATION- Reassembly of viruses Put together from pools of subunits made by host cell RELEASE OF VIRUSES Viruses lyse out of host cell NA is incorporated (recombined) into the host DNA |
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Viruses: Replication in animal cells
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ATTACHMENT (Adsorption) to host cell
Most have very narrow host range Virus binds to host cell receptor sites *this stage determines what cells can be infected. Virus receptors located on Spikes Envelope of enveloped viruses Capsid PENETRATION Different mechanisms Many are engulfed by an endocytosis process Many enveloped viruses fuse their envelope with host cell cytoplasmic membrane UNCOATING - removal of protein coat & release of NA Usually involves degradation by proteolytic enzymes provided by host cells BIOSYNTHESIS (Replication) of Viral Subunits. Method depends on type of NA Some types require special enzymes (see notes on bacteriophages) Reassembly of viruses Put together from pools of subunits made by host cell Not very efficient - many empty capsids released RELEASE OF VIRUSES Some by lysis of host cell Enveloped viruses usually “bud” out Effects of Viruses on Host: “Cytopathic Effects (CPE)” = visible changes due to viral infection Formation of “Inclusion Bodies” Aggregates of viral components or cell debris May be useful diagnosis tool Formation of “Giant Cells” = large multi-nucleated host cells “Plaque Formation” in tissue cultures |
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Viruses: Infection outcomes
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Cell destruction
cell death & lysis large # viruses released usually causes acute-type disease Persistence of Virus in Host Cell host cell usually not killed both viral & cell macromolecules make viruses may be released gradually may cause chronic infection i.e. Hepatitis may cause latent (hidden) infection i.e. Herpes simplex may cause autoimmune disorders Host Cell Transformation Integration of viral NA into host cell DNA Causes a nonproductive infection - new viruses not made Integrated NA may carry or turn on a existing tumor-causing genes or “oncogenes” in a normal cell. This cell changes and is called “transformed!” Viral Oncogenes and CANCER Interferon Production Excreted by infected cells Interacts with membranes on adjacent cells Shuts down viral protein synthesis “Nonspecific” - protects against all viruses May be artificially induced Potential role in antitumor therapy More later |
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Biotechnology
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“any alteration of organisms, cells or biological molecules to achieve specific practical goals”
Selective breeding Genetic engineering |
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Genetic engineering
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Watson and Crick 1953, explained the DNA molecule. Since that time, efforts have been make to manipulate genes.
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Genetic Recombination
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taking a gene from one DNA molecule and tagging it on to another. Genetic info. is mixed
DNA can be added to the genome of another organisms |
