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135 Cards in this Set
- Front
- Back
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Parvoviruses
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Naked, icosahedral capsid
Smallest DNA viruses Single stranded DNA virus (4.7 kb) Genome is either + or - strand Host cells must be in S phase for a productive infection |
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Parvoviruses
Disease caused? |
B19 = fifth disease
(erythema infectiosum) Typical “slapped-check” rash on face lacy red rash spreads to arms and legs in children |
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B19 Epidemiology
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Disease occurs in late winter and early spring
Transmitted by respiratory droplets Most common in children ages 4-15 65% of adult population have been infected with B19 |
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Human Papillomaviruses
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dsDNA, circular genome (8 kb)
non-enveloped Classification is based on DNA sequence homology, over 100 serotypes Grouped into types A-P Cutaneous or mucosal HPV Cause warts, cervical carcinomas Encode proteins that promote cell growth |
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Human Papillomaviruses
Disease? |
Cutaneous warts
Types 1-4, on hands and feet Self-limited Resolves in 3-4 months Mucosal warts Benign head and neck tumors Laryngeal, oral, conjunctival papilloma Types 6, 11 Laryngeal can be life threatening to children -- obstructs the airways Mucosal warts Genital warts (types 6, 11) Asymptomatic Soft, flesh-colored warts that develop weeks-months after sexual contact Cervical Dysplasia (types 16, 18) Develop into cervical cancer |
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Papillomavirus infection in humans
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Infect squamous epithelium of skin (warts) or mucous membranes (genital, oral)
Induce epithelial proliferation Wart develops within 3-4 months Viral infection remains local, can regress spontaneously |
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Papillomavirus life cycle
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Virus binds to receptor
DNA is uncoated and delivered to nucleus Early genes are expressed (E6 and E7) DNA replication of viral genome Late gene expression (capsid proteins) Virus is assembled in NUCLEUS Release by cell lysis |
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How do HPVs cause warts?
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HPV genome (ds DNA)
E genes E6 and E7 -- growth promoting properties Disrupt cell growth cycle to drive cells into S phase |
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Gardasil
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Quadrivalent vaccine
L1 coat proteins from HPV 6, 11, 16, 18 Administered to females, ages 12-29 and males, ages 9 to 26 Can only PREVENT, not treat, infections |
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Adenoviruses
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ds DNA virus (36 kb)
Non-enveloped Over 100 serotypes Subgroups A-F based on DNA homology |
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Adenovirus clinical syndromes
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Pharyngitis/respiratory disease (Ad types 1-7)
Gastroenteritis and diarrhea (Ad 40, Ad 42) Conjunctivitis (multiple types) |
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Adenovirus Genome
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Early proteins promote cell growth and include a DNA polymerase, proteins that suppress host immune responses
Late proteins are capsid components |
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Adenovirus replication
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EPISOMAL -- not integrated
Early genes Cell cycle regulators and DNA polymerase E1A and E1B -- oncogenes similar to papillomavirus E6 and E7 (bind to p105-Rb and p53) Small viral RNAs to block interferon production/ PKR activation E3 proteins block CTLs, TNF actions |
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Adenovirus epidemiology
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Non-enveloped viruses
Resist drying, detergents, chlorine treatments, gastrointestinal tract enzymes Spread by respiratory route Close interactions of humans promotes spread (military barracks, day care, schools) Can be shed for prolonged periods in the feces |
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Herpesviruses
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DS DNA viruses (50-80 kb)
Enveloped ubiquitous Three groups based on tropism ( alpha, beta, gamma) Encode its own DNA polymerase (target for anti-virals) Different members of this family can cause lytic, persistent, latent and immortalizing infections |
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Herpesvirus Diseases
HSV-1-- HSV-2 -- VZV -- EBV -- CMV -- HHV-8 - |
HSV-1-- cold sores, genital lesions
HSV-2 -- genital lesions VZV -- chickenpox, shingles EBV -- mono, Burkitt’s lymphoma CMV -- infections for immunocomp. HHV-8 -- Kaposi’s sarcoma-assoc. virus |
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Herpesviruses
Life cycle... |
Infect and replicate in mucoepithelial cells
Cause disease at site of infection Establish a latent infection of the innervating neurons |
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HSV latency life cycle
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Virus travels by retrograde transport to the ganglion
“stress” reactivates virus and virus returns to initial site of infection |
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Treatment for HSV-induced warts
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No vaccine
Acyclovir, valacyclovir, penciclovir, famciclovir Deoxyguanosine analog Acyclovir works best in cells with rapidly replicating virus Not a cure |
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Acyclovir
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Inert by itself
ATP + HSV-2 thymidine kinase = acyclovir phosphate HSV DNA polymerase incorporates acyclovir into viral DNA Viral DNA synthesis inhibited |
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Varicella zoster virus clinical syndromes
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Chickenpox (lytic)
Fever, rash lasting 14 days Shingles (Latent) Severe pain in innervated areas Rash in a belt or girdle shape |
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Epstein-Barr virus
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Ultimate B cell parasite
Isolated from a B cell neoplasm (Burkitt’s lymphoma) associated with infectious mononucleosis, Hodgkin’s disease and nasopharyngeal carcinoma |
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EBV Pathogenesis
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Productive infection of B cells in the oropharynx
Virus replication, shedding in the saliva to establish a viremia Virus spreads to other B cells in the body |
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Poxviruses
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Ds DNA virus (linear)
Brick-shaped 200 kb genome Replicates in cytoplasm Expresses its own polymerase and RNA synthesis enzymes NO LATENT/PERSISTANT LIFE CYCLE |
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Human Monkeypox disease
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Same presentation and time course as smallpox, HOWEVER
Rarely passed on from human to human Only 10% mortality rate Endemic in central and western African countries Does not exist naturally in the USA |
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Molluscum contagiosum
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Pox?
Benign neoplasms (2-5 mm), pearly, central core Persist for weeks to years Direct skin-to-skin contact Children and sexually active young adults Opportunistic infection Therapy includes freezing, burning |
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Hepadnavirus
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DNA virus that infects liver
enveloped Only one member -- Hepatitis B virus Weird virus!!!!! Partially ds, circular DNA genome Virus carries a reverse transcriptase Genome can integrate into host chromosome |
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Hepatitis virus family
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Hepatitis A (RNA) -- fecal oral
Hepatitis B (DNA) -- sexual Hepatitis C (RNA) -- sexual Hepatitis D (RNA) -- sexual Hepatitis E (RNA) -- fecal oral |
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Hepatitis B (DNA)
life cycle! |
Entry into hepatocyte
Completion of dsDNA genome in cytoplasm DNA delivered to nucleus Transcription of genome 3 small mRNAs = translation into core proteins 1 large mRNA = surrounded by core proteins (-)DNA is synthesized by reverse transcriptase activity in core (-) RNA in core is degraded, (+) DNA is synthesized Core is enveloped and virus is released by exocytosis |
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Hep B and Cancer Link
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Worldwide, chronic HepB infections cause 80% of all primary liver cancers (cancer starts in the liver cells)
Primary liver cancer is the third cause of cancer death in many Asian and African countries 500,000 people die each year from primary liver cancer |
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Hepatitis B disease
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Spread by blood, sexual contact, birth
Range from acute to chronic Immune response of person determines it Acute disease = fever, rash, malaise 90-95% of people clear virus Chronic hepatitis 10% of those patients develop cirrhosis and liver failure Very close association with hepatocellular carcinoma and HBV Vaccine given to newborns Transmitted by sexual intercourse, blood, direct injection into bloodstream (needle) and birth Moves from point of entry to the liver; multiply in liver cells; genome integrates into hepatocytes Patient may be symptom-free for up to 45 days Symptoms : jaundice, malaise, anorexia |
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Envelope
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protein-phospholipid membrane from the host cell membrane (cytoplasmic or nuclear) that covers the capsid
Only some viruses are enveloped HIV, herpesviruses Enveloping occurs when the virus leaves the cell (budding) or during cell lysis Wrapping of virus particle with cellular membrane material |
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Viral Envelope glycoproteins
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Normal cellular membrane
Viral proteins are embedded in the phospholipid bilayer membrane Project outward, like spikes Mediate attachment of virus to host cell membrane |
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Non-enveloped viruses (NAKED)
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Viruses that have no envelope
Capsid without a cover Capsid proteins mediate attachment to host cell |
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Non- Enveloped Viruses
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Durable
Resistant to acid (gut), resistant to detergents and bile, remains in tact in raw sewage, stable in water Resistant to pH changes Spread by aerosol, fecal-oral route |
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Three stages of virus infection
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Attachment and Entry Into the Host Cell
Replication of Virus Genome and Synthesis of Viral Proteins Assembly and Release of nascent virions |
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DNA virus high points
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Most DNA viruses replicate in the nucleus
Temporal expression of genes DNA to mRNA to protein DNA copied to more progeny genomes Progeny genome is inserted into capsid |
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(+) single strand (SS) RNA viruses
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(+) RNA = mRNA
Can be translated immediately upon entering the cytoplasm Need an RNA-dependent RNA polymerase to replicate viral RNA Enzyme is not present in host cells Therefore, RNA virus will make its own RNA polymerase |
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(+) RNA viruses
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(+) RNA = mRNA
Can be translated immediately upon entering the cytoplasm Need an RNA-dependent RNA polymerase to replicate viral RNA Not present in host cells Therefore, (+) RNA viruses will code for their own RNA pol Entire life cycle occurs in the cytoplasm No division into early v. late gene expression |
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(-) RNA viruses
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Anti-sense or (-) RNA cannot
be translated by host cell Virus packs an RNA polymerase Into its virion (-) RNA is “transcribed” into (+) RNA |
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Retrovirus Replication
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RNA genome
Retro = reverse transcriptase (RT) Enzyme that reverse transcribed RNA Into copy DNA These viruses have a DNA stage not Present in other RNA viruses They have a weird life cycle! |
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Assembly and Release of the Virion
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Release by budding (enveloped viruses)
Release by lysis (naked virus) |
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RNA viruses
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Most viral RNA replicates in cytoplasm (except for orthomyxoviruses / flu)
RNA viruses must encode an RNA-dependent RNA polymerase (-) RNA viruses carry a pre-formed RNA pol in the virion Most infections are lytic |
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+) RNA viruses
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(+) RNA = mRNA
Can be translated immediately upon entering the cytoplasm Need an RNA-dependent RNA polymerase to replicate viral RNA Enzyme is not present in host cells Therefore, (+) RNA virus will make its own RNA polymerase Potential drug target |
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Picornaviruses
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Non-enveloped
Genome resembles mRNA Single strand of (+) RNA Poly A at the 3’ end High mutation rates of genomes Spread by fecal-oral route |
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Picornavirus family:
Poliovirus Echovirus Rhinovirus Coxsackievirus Hepatitis A virus] |
Poliovirus (polio)
Echovirus (diarrhea) Rhinovirus (common cold) Coxsackievirus (mild URI or flu; hand, foot and mouth disease) Hepatitis A virus (hepatitis) Sometimes these viruses are called ENTEROVIRUSES |
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Picornavirus pathogenesis
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ENTEROVIRUSES
Target tissue determines the disease caused by the virus Transmitted by fecal-oral route Upper respir. tract, oropharynx are portals of entry Virions are resistant to bile, stomach acids |
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Picornavirus replication
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Standard method for (+) RNA virus replication
Cell surface receptor specificity differs between groups Ig superfamily, ICAM-1, CD55 |
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Enterovirus epidemiology
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(Picornavirus)
Fecal-oral route for spread Asymptomatic shedding for up to 1 month Sewage contamination results in outbreaks, also in schools and day care settings Summer is major season |
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Coxsackievirus
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(Picornavirus)
Causes hand-foot-and-mouth disease, painful blisters Meningitis, myocarditis No specific treatment Virus spreads via droplets or fecal-oral route Symptoms resolve in 2-7 days Can cause complications when pregnant mother passes it on to newborn |
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Hepatitis A virus
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(Picornavirus)
Fecal-oral route, contaminated shellfish, daycare workers and children Oral acquisition, enters bloodstream Infects liver cells (shedding in stool) Fever, fatigue, abdominal pain, jaundice or no symptoms 99% of people completely recover Hep A vaccine (killed) is available |
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Rhinovirus
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Causes the common cold
Sensitive to acids, cannot replicate in GI tract (unlike other picornaviruses) Virus enters through nose, eyes or mouth Grow best at 33C Viral replication in the nose & severity of symptoms correlate with the time and quantity of virus being shed |
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Poliovirus- disease
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paralytic polio in 0.1 to 2% of all infected people
Virus spreads from the blood to the anterior horn cells of the spinal cord Severity of paralysis depends upon the extent of neuronal infection |
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Poliovirus vaccine
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Salk vaccine (IPV)
Formalin inactivated, injected Sabin vaccine (OPV) Live attenuated, oral Inexpensive, easy to administer, almost 100% efficient Occasionally reverts to a virulent form Last natural polio case in U.S = 1979 Polio is still prevalent in third world countries |
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Calicivirus/Norovirus/Norwalk-like virus pathogenesis
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Non-enveloped
Resistant to detergents, drying and acid Transmitted by fecal-oral route, contaminated food & water Common on cruise ships Cause outbreaks of gastroenteritis Virus compromises the function of the intestinal brush border Diarrhea with nausea and vomiting for 2 days No lasting immunity |
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Coronaviridae
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(+) ss RNA genome (mRNA-like)
30 kbp is linear enveloped Sensitive to drying, but some strains can survive the gi tract Crown appearance of virion SARS, common colds |
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SARS
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Coronaviridae
(+) ss RNA genome (mRNA-like) 30 kbp is linear enveloped Sensitive to drying, but some strains can survive the gi tract |
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Coronavirus pathogenesis
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Transmitted by aerosol from respiratory secretions
Replicates mostly in the URI (optimum temperature here) Mild, self-limited disease (classical “cold” or upset stomach) Mainly in infants and children, outbreaks in winter and spring |
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SARS (severe acute respiratory syndrome)
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Cornonavirus
High fever (greater than 100 F) Most patients develop pneumonia Death due to progressive respiratory failure due to alveolar damage |
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Togaviridiae
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enveloped (= toga/cloaked)
Three genera of this family Alphavirus = eastern equine, Western equine encephalitis Rubivirus = Rubella (German measles) Arterivirus (no known disease in humans) |
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Alphavirus Togaviridiae
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eastern equine, Western equine encephalitis
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Rubivirus
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Rubella (German measles)
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Rubella virus
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Togaviridiae
Respiratory virus Causes “Rubella” or “German measles” One of the five classic childhood diseases Maternal rubella infection results in severe congenital defects |
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Rubella virus pathogenesis
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Viremia spreads virus throughout body -- mild rash
Antibody prevents spread of virus to fetus (important for pregnant woman) |
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Rubella congenital infection
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If there’s no antibody, the virus can replicate in the placenta and spread to the fetal blood supply and throughout the fetus
Virus is not cytolytic, but prevents normal growth and development of cells Improper development of fetus, low birth weight, cataracts, deafness, mental retardation Fetus is at most risk until the 20th week of pregnancy |
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Rubella disease
Lab diagnosis |
Detect genome by RT-PCR
Anti-rubella-specific IgM |
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Rubella disease
Treatment, control |
No treatment
Live cold-adapted vaccine (MMR) given at 24 mos of age Prevent seronegative mothers |
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Reoviruses
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Respiratory, enteric, orphan viruses
Rotavirus = diarrhea Responsible for 50% of all hospitalized childhood diarrhea cases Ds RNA, segmented genome DOUBLE ENVELOPED |
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Rotavirus
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Reoviruses
diarrhea Responsible for 50% of all hospitalized childhood diarrhea cases Ds RNA, segmented genome DOUBLE ENVELOPED |
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Reovirus Replication
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Virus enters gi tract
Virion is partially digested in gut Loss of external capsid VP7 protein, cleavage of VP4 protein Produces the ISVP form (infectious subviral particle) VP4 binds to sialic acid Release of core into cytoplasm (contains RNA polymerase) Double stranded RNA genome is always associated with the core Transcription is in two phases Early: (-) RNA -- template for making (+) RNA; mRNA is translated Late: (+) RNA in cores -- copied to make (-) RNA in the new cores, core polymerase makes another (+) RNA for the DS RNA Assembly and release by cell lysis |
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Rotavirus
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Virus transmitted via fecal-oral route
Virus replicates in epithelial cells in small intestine TONS of viral particles produced and released Infection prevents absorption of water, resulting in diarrhea Leads to severe dehydration Extremely contagious No antiviral therapy Supportive therapy |
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Orthomyxoviridae
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(-) RNA
8 segments per virion Respiratory viruses that causes classic flu symptoms Influenza A,B,C |
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Virus binding to the host cell
(Orthomyxoviridae) |
HA binds to the cell via sialic acid moities
HA forms a spike shaped trimer Elicits protective neutralizing antibodies Mutations in HA is the cause of minor and major changes in antigenicity of a virus (epi- or pandemic) |
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Orthomyxovirus replication
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endocytosis
Fuses with vesicle membrane Proton channel formed by the M2 protein RNA goes to nucleus Viral transcriptase steals methylated cap from host mRNA and adds it to viral RNA (+) RNA is also made in nucleus, and (-) RNA is synthesized in the nucleus Assembly NA cleaves virus from host cell |
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New influenza strains causing disease (H1N1 influenza)
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Caused by antigenic shift and drift of the HA and NA flu genes
Shift = re-assortment of HA and NA genes (between animals-> pandemic) Drift = mutation of HA and NA genes Only occurs with influenza A virus; zoonotic virus |
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Reassortment
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A method to make large genetic changes in the viral genome (responsible for pandemics)
Only works with viruses that have segmented genomes (influenza) |
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How does influenza mutate?
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Most Influenza A infects birds (non-pathogenic)
Influenza A circulates and infects pigs Reassortment in pigs Transmission of new influenza virus to humans |
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History of H1N1/09 virus
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Enzoonotic in pigs in North America in the late 1990s
Spread to humans Virus spreads easily from human-to-human First outbreak was reported in Mexico Spread globally via travel Sequencing of virus revealed it is a triple reassortment virus Resulted from mixing of influenza virus A in pigs |
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Zanamavir and oseltamivir
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Zanamivir = Relenza
Oseltamivir = Tamiflu Neuroanidase |
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H1N1/09 Flu vaccine
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37 companies making the vaccine
majority are heat killed vaccines Produce 876 M doses per year (largely due to H5N1 preparedness) |
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Types of Flu Vaccine
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Inactivated flu virus
70-90% effective “FluMist” -- intranasal influenza vaccine using live, attenuated virus 35% effective Not for a majority of people, including hospital workers |
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Organisms found in the resident microbiota
Mouth |
Staphylococcus epidermidis and S. aureus (gram-positive,
aerobes) α-Hemolytic streptococci (gram-positive, facultatives) Streptococcus mutans (teeth), S. salivarius (teeth and tongue) (gram-positive, facultatives) Actinomyces (between teeth and gingival crevices) (gram-positive, anaerobes) Porphyromonas, Fusobacterium (gums) (gram-negative, anaerobes) Spirochetes (gums) (anaerobes) Anaerobic cocci (gums) (gram-positive, anaerobes) |
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. Organisms found in the resident microbiota
Nasopharynx |
Staphylococcus epidermidis and S. aureus (just inside
nares) (gram-positive, aerobes) Diphtheroids (gram-positive, aerobes) Occasionally Moraxella (gram-negative cocci, aerobes) and Streptococcus spp. (gram-positive, facultatives) |
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rhinitis
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Any number of viruses can cause rhinitis, but the two most important causes are rhinoviruses and coronaviruses.
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Rhinoviruses
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Rhinoviruses belong to the picornavirus family. They are nonenveloped icosahedral viruses with a nonsegmented single-strand positive sense RNA genome. The capsid consists of 4 proteins (VP1-VP4). VP1 mediates adherence to host cells and is the protein against which a protective antibody response is directed.
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Rhinoviruses attach to a host cell protein
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(ICAM-1),
involved in adhesion of host cells to each other ICAM-1 mediates the adhesion of PMNs to endothelial cells |
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symptoms of the common cold are caused by
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vasodilating effects of inflammatory mediators such as cytokines, which cause fluids from blood to accumulate in respiratory tissues.
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secondary complications
rhinovirus infections |
bacterial sinusitis or otitis media
lower respiratory tract disease and exacerbation of asthma |
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Pharyngitis
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inflammation of the pharynx and/or tonsils caused by a variety of microorganisms
most often caused by viruses |
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S. pyogenes -Pharyngitis
Complications |
acute glomerulonephritis (inflammation of the kidney) and
rheumatic heart disease (damage of the heart valves). |
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S. pyogenes
virulence factors relevant to pharyngitis Protein F |
surface protein, protein F, which mediates attachment to fibronectin molecules on pharyngeal cells- aid in colonization of the throat
Protein F also plays a role in allowing S. pyogenes to enter host cells |
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S. pyogenes
virulence factors relevant to pharyngitis M protein |
S. pyogenes is able to resist phagocytosis because it is covered with a layer of fibrillar protein structures, composed of M protein
M protein binds serum factor H better than factor Bb and thus discourages complement activation and prevents opsonization of the bacteria by C3b 80 different types of M protein |
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hyaluronic acid capsule
S. Pyrogenes virulence factors |
hyaluronic acid capsule that is identical to the hyaluronic acid in human connective tissue so as a result it is not immunogenic. Strains with such a capsule usually cause severe infections.
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streptolysin O
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a pore-forming cytotoxin that kills many different cell types and contributes to the zone of β-hemolysis seen around colonies growing on a blood agar plate
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Corynebacterium diphtheriae
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best known for causing diphtheria
Another cause of pharyngitis nonmotile, gram-positive rod that colonizes the throat does not have a capsule and does not form spores produce the main virulence factor, diphtheria toxin, which acts locally on mucosal cells to produce a mat of dead tissue (pseudomembrane) toxin enters the circulation |
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Diphtheria toxin
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B subunit recognizes a glycoprotein found on many different cell types, a cell bound form of heparin binding epidermal growth factor
can attack many but not all types of host cells component of diphtheria toxin ADP-ribosylates elongation factor-2 (EF-2), a protein that is essential for host cell protein synthesis. ADP-ribosylation of EF-2 stops host cell protein synthesis and the cell dies. gene for diphtheria toxin is carried on a bacteriophage |
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Sinusitis
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same viruses that cause pharyngitis (e.g., rhinoviruses, adenoviruses, influenza viruses, and parainfluenza viruses)
Occasionally (~ 1% of cases) a secondary bacterial infection occurs. Streptococcus pneumoniae and Haemophilus influenzae |
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Otitis Media
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eustachian tube becomes blocked and drainage is prevented
initial cause is usually a viral upper respiratory infection After a few days, bacterial members of the oral microbiota move into the area S. pneumoniae and H. influenzae. Moraxella catarrhalis may also cause such infections. |
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Acute Bronchitis
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Bronchitis is defined as inflammation of the tracheobronchial tree
typically follows an upper respiratory tract infection such as rhinitis cause in about 95% of cases is one of the usual cast of viral characters such as influenza, parainfluenza, adenovirus, rhinovirus, coronavirus and respiratory syncytial virus. Rarely bacterial species cause bronchitis. The usual bacterial pathogens are Mycoplasma pneumoniae and Chlamydophila pneumoniae. |
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Pertussis
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B. pertussis, a small gram-negative coccobacillus that has complex nutritional requirements.
It is normally grown on medium containing blood. The bacteria are spread from human to human by aerosols or direct contact. The organism attaches to ciliated respiratory cells and kills them. The infected person develops a cough that can become severe enough to cause convulsions and cyanosis. The clinical symptoms of whooping cough are seen primarily in children and infants. The infected person is most contagious in the early coughing stage. |
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virulence factors of Bordetella
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Filamentous hemagglutinin, a pilus-like structure is important for specific attachment to ciliated cells.
exotoxin, pertussis toxin contains components that bind ciliated cells. contributes to the killing of ciliated cells |
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Bronchiolitis
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Respiratory syncytial virus (RSV), a member of the paramyxovirus family, is a helical enveloped virus with a nonsegmented, negative-sense, single-stranded RNA genome
responsible for the majority of severe bronchiolitis an acute lower respiratory tract infection in infants under the age of 2 years |
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Croup
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acute laryngotracheobronchitis
infection of both the upper and lower respiratory tract caused by a variety of microbes, the parainfluenza viruses are the most common causes. Parainfluenza viruses (serotypes 1, 2, 3 and 4) are also members of the paramyxovirus family so they are enveloped viruses with a nonsegmented negative-sense, single-stranded RNA genome. have neuraminidase and hemagglutinin antigenic shift does not occur because their genomes are not segmented. nonbacterial respiratory infections in infants and young children |
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Pneumonia
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caused by viruses or by bacteria
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STREPTOCOCCUS PNEUMONIAE
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gram-positive diplococcus
human-specific pathogen that is acquired by inhalation of aerosols most common cause of bacterial pneumonia , 3,000 cases of meningitis, 50,000 cases of blood stream infection, 500,000 cases of bacterial pneumonia, and 7 million cases of ear infection Resistance to ß-lactam antibiotics |
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S. pneumoniae
virulence factors |
i) an antiphagocytic capsule, of which there are at least 90 serotypes, ii) cell wall components that elicit a strong inflammatory response, iii) an intracellular toxin, iv) autolysins, and v) an extracellular protease
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MYCOPLASMA PNEUMONIAE
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M. pneumoniae causes a debilitating flu-like illness that has been called "walking pneumonia" because it is not as severe as pneumococcal pneumonia.
low-grade fever, headache, malaise, and a persistent cough. short duration but in some cases can last up to 3 weeks. generally limited to the lung and does not become systemic M. pneumoniae does not have LPS, LTA, or the peptidoglycan fragments |
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CHLAMYDOPHILA PNEUMONIAE
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relatively newly discovered cause of primary interstitial pneumonia
obligate intracellular parasites with a gram-negative cell wall and gram-negative type LPS, but no peptidoglycan. include sore throat, low-grade fever and a persistent cough. |
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LEGIONELLA PNEUMOPHILA
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a gram-negative motile rod with complex nutritional requirements,
incidence of L. pneumophila pneumonia has increased dramatically in recent years because of the installation of air-conditioning systems i most likely to develop in people with underlying conditions that impair airway defenses. |
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L. pneumophila virulence factor
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ability to grow inside macrophages
L. pneumophila also produces a phospholipase and a metalloprotease with hemolytic activity. These enzymes could contribute to lung damage. |
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Influenza
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orthomyxovirus family. It has a helical capsid and an envelope. The genome is negative sense, single stranded RNA consisting of 8 segments. The envelope contains two glycoproteins, hemagglutinin (H) and neuraminidase (N). The H protein mediates attachment of the virus to sialic acid residues on the host cell surface. Antibodies to H protein block this interaction.
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Amantidine and rimantidine
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two antivirals used to prevent and treat seasonal influenza, act by binding to M protein and inhibiting the uncoating process
only effective if given within the first 48 hr and they are only effective against influenza A, not influenza B |
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How does influenza virus cause death?
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In some people, however, the virus can move into the lungs and cause destruction of lung tissue. This appears to be the case for pandemic H1N1. In this situation death is due to reduced ability of the lungs to introduce oxygen into the blood and remove carbon dioxide. Moreover, extensive tissue destruction is usually accompanied by massive release of cytokines
most common cause of deaths associated with influenza is a secondary bacterial infection of the lung, i.e., bacterial pneumonia. |
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Tuberculosis
lungs? |
Mycobacterium tuberculosis
M. tuberculosis enters the lungs on aerosols, it is ingested by alveolar macrophages. However, M. tuberculosis can survive and grow in macrophages. |
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M. tuberculosis
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rod that has a gram-positive cytoplasmic membrane and a peptidoglycan cell wall. In addition to peptidoglycan, there are lipoarabinomannans and lipomannans, which are embedded in the cytoplasmic membrane and extend outward from the bacterial surface, and arabinogalactan and mycolic acids, which are attached to the peptidoglycan.
Mycobacteria do not destain with the acid-alcohol and are therefore termed acid-fast. Mycolic acids are found only in a few groups of bacteria, including Mycobacterium spp. and Corynebacterium spp. Mycolic acids and other mycobacterial cell wall components stimulate antibody production and are the active ingredients in Freund's adjuvant. During an infection, mycolic acids may contribute to the strong antibody response seen in some people. Antibodies have no protective effect because M. tuberculosis is able to grow in macrophages and is resistant to killing by complement. High antibody titers to mycobacterial antigens are actually correlated with the more serious form of the disease |
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M. tuberculosis
virulence factor |
ability to survive and grow in macrophages
binds directly to macrophage surface protein CR3, the normal receptor for iC3b Binding is followed by internalization of the bacteria in a vesicle. The internalized bacteria reduce the oxidative burst of the macrophage and reduce IL-12 production, which leads to suppression of the Th1 response. Although antibodies are useless in controlling TB, the Th1-stimulated cell-mediated response, especially the activated macrophage response, is critical. |
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M. tuberculosis
The Th1 response can also be inhibited |
Lipoarabinomannans of the mycobacterial cell wall inhibit activation of T helper cells. Th1 cells produce gamma-interferon, which is necessary for activation of macrophages. High enough levels of lipoarabinomannans shed in an infected lung may thus delay activation of macrophages and protect the bacteria from this protective host response.
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Isoniazid and ethionamide
Ethambutol |
by inhibiting mycolic acid synthesis
Ethambutol is thought to inhibit carbohydrate metabolism |
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HISTOPLASMA, COCCIDIOIDES, BLASTOMYCES
CRYPTOCOCCUS |
these fungi are usually described as dimorphic, i.e., fungi that exist in the mycelial form in the environment and in the yeast form in the human body
Cryptococcus has traditionally been considered to be a yeast, but some species have now been shown to have a mycelial |
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Location:
Blastomyces Histoplasma Cryptococcus Coccidioides |
most abundant in the southeastern and north¬eastern U.S.
Histoplasma is found mainly in the middle U.S., and is most abundant in areas like chicken coops that are contaminated with bird feces. Cryptococcus is also found most commonly in soil contaminated with bird feces, but is not as geographically localized Coccidioides is found mainly in the southwestern U.S. in sandy soils |
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PNEUMOCYSTIS JIROVECI
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fungal pathogen/yeast
In the lung, the trophozoite form of P. jiroveci associates tightly with lung cells (pneumocytes). Proliferation of the trophozoites in the lung results in destruction of cells lining the alveoli, damage to pneumocytes, and elicitation of an eosinophilic host response Perhaps enzymes released by the eosinophils digest lung cell surfaces and contribute to the foamy exudate and "honey-comb" appearance of lung tissue that is the hallmark of the disease |
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ASPERGILLOSIS
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Aspergillus species are best known as producers of aflatoxins, but Aspergillus spp. can also cause oral and lung infections
a fungus that does not assume the yeast form can cause serious disease In the lung, the fungi grow in the mycelial form and cause damage both because they evoke a tissue-damaging host cell-mediated response and also because growth of the mycelial mat causes tissue damage. These mats (also called fungus balls) usually form in a lung cavity resulting from some previous infection (e.g., tuberculosis or histoplasmosis |
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Hepatitis A
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transmitted person-to-person by ingestion of contaminated food or water or through direct contact with an infectious person
he disease can be prevented by vaccination Symptoms typically appear 2 to 6 weeks, (the incubation period), after the initial infection |
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Hepatitis A- life cycle
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HAV enters the bloodstream through the epithelium of the oropharynx or intestine
fecal-oral route ingestion of shellfish cultivated in polluted water is associated with a high risk of infection The blood carries the virus to its target, the liver, where it multiplies within hepatocytes and Kupffer cells (liver macrophages). Virions are secreted into the bile and released in stool. HAV is excreted in large quantities approximately 11 days prior to appearance of symptoms or anti-HAV IgM antibodies in the blood Within the liver hepatocytes the RNA genome is released from the protein coat and is translated by the cell's own ribosomes. Unlike other members of the Picornaviruses this virus requires an intact eukaryote initiating factor 4G (eIF4G) for the initiation of translation |
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Hepatitis virus (HAV)
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a Picornavirus; it is non-enveloped and contains a single-stranded RNA packaged in a protein shell.
There is only one serotype of the virus, but multiple genotypes exist |
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Hepatitis B
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serum hepatitis
exposure to infectious blood or body fluids liver inflammation, vomiting, jaundice and rarely, death. Chronic hepatitis B may eventually cause liver cirrhosis and liver cancer—a fatal disease with very poor response to current chemotherapy. The infection is preventable by vaccination. |
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Hepatitis B virus
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hepadnavirus—hepa from hepatotrophic and dna because it is a DNA virus[7]—and it has a circular genome composed of partially double-stranded DNA. The viruses replicate through an RNA intermediate form by reverse transcription, and in this respect they are similar to retroviruses.[8] Although replication takes place in the liver, the virus spreads to the blood where virus-specific proteins and their corresponding antibodies are found in infected people.
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genome of HBV
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The genome of HBV is made of circular DNA, but it is unusual because the DNA is not fully double-stranded. One end of the full length strand is linked to the viral DNA polymerase
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Hepatitis C
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chronic infection can progress to scarring of the liver (fibrosis), and advanced scarring (cirrhosis)
In some cases, those with cirrhosis will go on to develop liver failure or other complications of cirrhosis, including liver cancer spread by blood-to-blood contact. No vaccine against hepatitis C is currently available. |
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Acute hepatitis C
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decreased appetite, fatigue, abdominal pain, jaundice, itching, and flu-like symptoms. Hep C genotypes 2A and 3A have the highest cure rates, at 81% and 74% respectively.
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Chronic hepatitis C
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roughly one-third progress to liver cirrhosis in less than 20 years
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hepatitis C virus
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small (50 nm in size), enveloped, single-stranded, positive sense RNA virus. It is the only known member of the hepacivirus genus in the family Flaviviridae. There are six major genotypes of the hepatitis C virus, which are indicated numerically (e.g., genotype 1, genotype 2, etc.).
heterosexual vaginal intercourse is thought to be a rare means of transmission of hepatitis C infection |
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Hepatitis D,
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disease caused by a small circular enveloped RNA virus.
HDV is considered to be a subviral satellite because it can propagate only in the presence of the Hepatitis B virus (HBV) |
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HDV genome
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enveloped negative sense, single-stranded, closed circular RNA
Because of a nucleotide sequence that is 70% self-complementary, the HDV genome forms a partially double stranded RNA structure that is described as rod-like |
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Hepatitis E
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EV is a positive-sense single-stranded RNA icosahedral virus with a 7.5 kilobase genome
HEV has a fecal-oral transmission route The virus itself is a small non-enveloped particle. is a polyadenylated single-strand RNA molecule that contains three discontinuous and partially overlapping open reading frames |
