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114 Cards in this Set
- Front
- Back
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CHARACTERISTICS OF VIRUSES
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GENOME = RNA OR DNA (NOT BOTH)
- need host cell 2 survive/replicate - most common cause of infxn - takes over host cell Protein coat/capsid nucleic acids lipids/carbs (sometimes) enveloped vs. not |
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VIRAL LIFE CYCLE
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1. ADSORPTION/ATTCH
2. UPTAKE/PENETRATE 3. UNCOAT 4. SYNTHESIS/REPLICATE 5. ASSEMBLE 6. RELEASE |
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+ vs - sense ss RNA viruses
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+ssRNA = mRNA
- only codes for viral RNA polymerase - purified genome alone is infectious -ssRNA virus: codes & carries viral rNA polymerase *purified rNA is NOT infectious |
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PHYSICAL/CHEMICAL AGENTS & VIRUSES
- WHAT WORKS/DOESN'T |
WORKS:
- HEAT (MOIST HEAT/AUTOCLAVE) - UV - detergents - bleach - heavy metal ions - activated glutaraldehyde (cidex) DOESN'T WORK: - ALCOHOL - CYANIDE - fluoride - ammonium compounds *cold stabilizes them* |
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TRANSMISSION in enveloped vs. nonenveloped viruses
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inhalation is most common route period:
Nonenv: Hardy bitches - resp & oral-fecal routes ENV: weak, fragile - need to stay wet: blood, semen, resp droplets, mucus, injection, organ transplants |
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HUMAN PAPILLOMAVIRUSES
HPV - assc w/ human disease - gen **only MUCOSAL HPV types cause CA** |
1ST oncogenic DNA viruses
= warts, anogenital CAs & head/neck tumors NAKED, CIRCULAR dsDNA, SMALL icosahedral capsid E6/E7: Promote cell growth; bind p53 & p105Rb - controlled by URR (noncoding DNA) Classified based on L1 gene seq homology --> then cutaneous or mucosal - L1/L2 = Late structural proteins Does NOT encode own DNA polymerase Cause Lytic infxns in permissive cells - but Latent infxns/immortalization of nonpermissive cells |
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HPV
- ACCESS - LIFE CYCLE |
1. Virus accesses basal cell layer of skin by breaks in skin
- ONLY infects BASAL CELLS 2. Uses host cell machinery to replication - as basal cell differentiate, dif tsc factors promote tsc of different viral genes *Late genes expressed only in the terminally differentiated upper layer* 3. Virus shed w/ dead cells of upper layer *viral induced growth causes warts (basal & stratum spinosum thickening) |
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HPV PATHOGENESIS
- warts/papillomas - koilocytes - immune evasion |
1. Infect 7 replicate in squamous epithelium (warts) & mucous membranes (papillomas) --> epithelial proliferation
2. Koilocytes: BIG keratinocytes w/ vacuolization & atypical/enlarged nuclei 3. Infxns remain LOCAL & regress spontaneously 2' innate/cell-mediated immunity 4. Good at immune avoidance - maintains low levels of Ag expression except in "near-dead" skin cells **immunosuppressed have it worse** |
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HPV & CA
genome integration --> malignancy p53: Controls cell cycle, activates DNA repair, induces apoptosis P105Rb: restricts entry into cell cycle (G1 checkpoint) |
HPV16 & 18: Most common culprits of Cervical CAs
- GENOME INTEGRATION - dsDNA breaks w/in E1/E2 genes (req'd for replication) - E2 normally controls E6/7 --> integration leads to deregulated control of oncogene expression = bound p53 & p105Rb = immortalization (also increased mtts) |
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HPV EPIDEMIOLOGY
- transmission - types in CA |
MOST PREVALENT STD IN THE WORLD
TRANSMISSION: - Small breaks in skin/mucosa - Sex - Delivery (laryngeal HPV) HPV 16,18 = HIGH RISK HPV 6,11 = LOW RISK 10% high risk HPV = Cervical dysplasia *no inter-species transfer of papillomavirus types* |
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CLINICAL CONSEQUENCES OF HPV INFXN
- Cutaneous Syndromes |
CUTANEOUS SYNDROMES:
1. WARTS: benign, self-limited, HPV1-4 *keratinized surfaces* 2. Epidermodysplasia Verruciformis: rare genetic *HPV5&8, "tree man" |
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CLINICAL CONSEQUENCES OF HPV INFXN
- Mucosal Syndromes |
low risk HPV 6 &11
1. Benign head/neck tumors (papillomas) *can be fatal in kids w/ laryngeal papillomatosis *HPV 16 = oropharyngeal squamous cell CA 2. ANOGENITAL WARTS: condylomata acuminata (raised & dry) vs. c. lata of syphilis (flat & wet) - squamous epithelium - rarely cancerous 3. Cervical Neoplasia - HPV 16,18,31, 45 = CIN & CA - PAP smears look for koilocytes ASCUS, LSIL, HSIL *3% of HPV infected --> Cervical CA |
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HPV VACCINES
*boys are the main ones that spread dz* |
Major capsid protein L1
--> self-assembles into virus-like particles (VLP) that are immunogenic GARDASIL: Quadrivalent vaccine - HPV 6 & 11 (wart), HPV 16,18 (CAs) - boys & girls - Prevents infxns, but not existing infxns CERVARIX: BIVALENT - HPV 16,18 + ADJUVANT - GIRLS ONLY |
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HUMAN POLYOMAVIRUSES
- GENERAL (SIMILAR TO HPV) |
BK & JC VIRUSES
- ubiquitous (usually don't cause disease) - naked, dsDNA circular Early genes: Polyoma T Ags = promote cell growth (bind p53 & p105Rb) Permissive cells = cell death (lysis) Nonpermissive = cellular transformation **ONLY REALLY A PROBLEM IN IMMUNOCOMPROMISED PEOPLE* |
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HUMAN POLYOMAVIRUSES
- PATHOGENESIS *BK -->prostate CA? *JC --> colorectal CA? *NO TX, except to tx immunosuppresion allowing reactivation* |
1. Enter through respiratory tract
2. Infect Lymphocytes & kidney cells w/ minimal CPE (asymptomatic primary infxns) BK: latent infxn in kidney JC: infects kidneys, B cells, monocyte-cells *Replication blocked in healthy people* Immunocompromised: reactivation = - BK: UTIs & viremia, renal transplant rejection - JC: CNS demyel (kills oligos), PML (progressive multifocal leukoencephalopathy) *Pregnancy can also cause reactivation of virus* |
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dsRNA VIRUSES
- replication strategy - dangers (reoviridae --> reo/rota/colti) Resp,Enteric,Orphan viruses |
Avoid exposure to host cell cytoplasm via nano transcription machines (basic infectious unit)
- enzymes & genomes are encased in stable, closed capsid shells dsRNA activated Host Defense Mechanisms: - Induction of apoptosis - IFN production - RNA silencing ALLLLL RNA VIRUSES (Except retro) ENCODE AN RNA-DEP RNA POLYMERASE *negative sense RNA & dsRNA must also CARRY an RNA-dep RNA pol* |
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dsRNA Replication
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dsRNA genomes are stable,
but SUCK as mRNA templates -sense strand of dsDNA --> +sense mRNA using viral RNA pol --> protein template or -sense RNA (dsRNA) made *Synthesized mRNA leaves the core to be translated - Viral proteins & +sense RNA associate together to make new cores - +sense RNA is copied w/in the cores to make dsRNA genome |
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ROTAVIRUS
- GENERAL **MAJOR CAUSE OF INFANTILE DIARRHEA & DEATH** |
Naked, segmented dsRNA, double/triple layered icosahedral protein capsids
= VERY STABLE 10-12 dsRNA segments/virion Inner capside = complete tsc system |
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ROTAVIRUS REPLICATION
*cause 50% of acute gastroenteritis* |
Inner capside = complete tsc system:
- RNA-dep RNA pol - Enzymes for 5' capping/PolyA - Replication occurs in cytoplasm; dsRNA stays in core **LOOKS like an enveloped virus** - inner capsid buds into the ER - obtains outer capsid & a membrane (which is later lost) Proteolytic Cleavage of Outer Capsid activates VIRUS - occurs in GI tract = ISVP - Lose VP7 & VP4 - VP4 MUST be cleaved so it can attach 2 sialic acid+ glycoproteins --> core is released into cytoplasm - random filling of capsids --> reassortment CELL LYSIS!! |
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ROTAVIRUS PATHOGENESIS & IMMUNITY
ubiquitous; 95% kids 3-5 yo infected - fecal-oral route - withstands drying; survives well on fomites |
LOSE WATER & IONS IN SECRETORY DIARRHEA
1. Viral replication after adsorption to columnar epithelial cell of SI villi 2. Shortened & blunt villi 3. ~ CHOLERA; prevent water reabsorption 4. WATER DIARRHEA (lose water &ions) - cytolytic & toxic effects (NSP4 = viral enterotoxin) MAJOR CAUSE OF GASTROENTERITIS (self-limiting dz) TX symptoms/dehydration |
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ROTAVIRUS VACCINES
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ROTATEQ: Oral pentavalent vacc
- five LIVE reassortant viruses ROTARIX: live, attenuated G1P8 rotavirus strain - temporarily suspended |
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COLORADO TICK FEVER
*transferred by wood tick saliva - most common tick-borne dz in US |
Reovirus family
- naked, segmented dsRNA, double layered capsid - Colivirus Infects Erythroid precursor cells & remains w/in them - prevents viral clearance - Biphasic fever NOT rocky mt spotted fever (rikettsial dz) |
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POSITIVE STRANDED RNA
- gen |
codes for (doesn't need to carry) an RNA-dep RNA POL.
Purified +SENSE RNA is INFECTIOUS (but needs a 5'cap & poly-A tail, if it doesn't already have it, before it can be translated) |
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+sense ssRNA viruses
- viruses *code for at least 1 protease & a viral RNA pol |
1. Calici: Hep E & Norwalk
2. Picorna: enteroviruses, Rhino, Heparna 3. Flavi: arboviruses, Dengue, hepaci 4. Toga: Alpha WEE EEE, Rubi 5. Retroviruses: HTLV, HIV - 2 copies 6. Corona: corona & SARS * All except corona are ICOSAHEDRAL |
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PICORNAVIRUSES
- classifications - micropathology: viremia, replication/assembly - transmission *Rhinovirus is transmitted through resp secretions* |
1. Enteroviruses: Entero / Echo / Coxsackie A & B / Polio
- enteroviruses don't really cause enteric dz 2. Rhinoviruses 3. Heparnaviruses (HepA) Small, naked icosahedral +ssRNA - very stable to bile & protease (fecal-oral) - enter cell via receptor mediated endocytosis (not fusion) - has a 5' cap & poly-A tail = immediate translation *Poly-protein is created & then cleaved by a viral protease --> different proteins - viral RNA pol makes TONS of mRNA - CELL LYSIS *Initially infect pharynx, but all (excpet rhinovirus) spreads first to Peyer's patches --> 2nd viremia to target tissues |
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PICORNAVIRUSES: NON-POLIO ENTEROVIRUSES
- CLINICAL BY DISEASE *HYPOGAMMAGLOBULINEMIA: increase risk of severe dz |
3-6 day incubation
1. Aseptic meningitis - sore, not stiff, neck - acute; recover in 3-7 days - Pathogens: Entero Strain 71, Echovirus, Coxsackie B5 - Dx: CSF WBC, RT-PCR - Report to health dept. 2. Hand/Foot/Mouth dz - Fever 3d, mouth ulcers (herpangina) - 50% blisters on hands/feet (10-14d) - Pathogens: Coxsackie A&B 3. Pleurodynia: Coxsackie B - Acute UL thoracic/pleuritic chest pain - 4d 4. Myocarditis: - Fever followed by mypoathy, big heart, heart fail - Milder infxn = pericarditis - Deadly if myocarditis - MECH: VP1 capsid protein has tropism 2 myocytes (slow replication) --> Immune response = damage - Pathogens: Coxsackie B3,A9 5. aCUTE hEMORRHAGIC CONJUNCTIVITS - Coxsackie A24, Enterovirus 70 |
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POLIO
- SYMPTOMS - PATHOGENESIS - MORTALITY - PATHOGEN = Poliovirus (1 of 3 strains); a type of picornavirus (+ssRNA, naked, icos) |
MOST ARE ASYMPTOMATIC
- Contagious 2 mo - Few non-specific illness - Rare aseptic meningitis or flaccid paralysis PATH: - Virus binds PVR/CD 155 on skeletal muscle; especially those used during viremia (use it & lose it) - Retrograde travel to AHC & kills neurons *can also travel up to Cranial nn & CNS (medulle oblongata) MORTALITY: - 2-5% KIDS, 15-30% ADULTS In Paralytic Polio: -79% improves over 6-12 mo, but remainder is permanent - 2% Bulbar paralysis: 25-75% die - 19% mixed |
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POLIO PREVENTION
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1. INACTIVATED polio vaccine
- not contagious - best choice in non-endemic areas w/ high vacc rate 2. Oral (LIVE, attenuated) vacc - contagious by stool - can spread to unimmunized (herd immunity) - IgA production better protects gut - Occasionally reverts to LIVE ACTIVE POLIO in gut - use in areas w/ low vacc rates & high risk of dz |
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POST-POLIO SYNDROME
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25%
30-40 years AFTER paralytic polio New muscle pain / weakness / new paralysis Not explained by loss of neurons w/ age - post-polio, oversized muscle motor units form - Units die by autoimmune process --> Weakness returns |
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RHINOVIRUS
virus family symptoms pathogenesis |
Picornavirus family (+ssRNA, naked, icos)
SYMPTOMS: common cold (congested, sore throat, cough) Pathogenesis: - Grows best @ 33 degrees - Less hardy than other picornas - 100serotypes with Genetic drift (immunity only lasts 18 mo) - Droplet/direct secretion contact transmission - Infected cells release BRADYKININ & HISTAMINE = RHINORRHEA ** ^ ICAM-1 exp in host cell** |
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hepatitis a
- SYMPTOMS - MICROPATH - PATHOGENESIS **CAN'T BE CULTURED* - give pt IgG - clean water is important |
Picornavirus family (+ssRNA, naked, icos); heparnavirus
Symptoms: most are asymptomatic - ABRUPT fever, anorexia, abd pain, jaundice, high ALT/AST (DARK urine) - Relapsing 6-9 mo course in 15% - Rare fulminant hepatitis MICROPATH: - STABLE AT pH 1, ether, salt water, drying, high temps, etc - USE CHLORINE, FORMALIN, UV RADIATION - only 1 species (endemic worldwide) PATH: - incubation 2-4 wks - Viremia spreas to hepatocytes, Kupffer's cells (special macros) - Slow replication (NOT CYTOTOXIC) --> T CELLS kill cells Shed in stool for 1-2 weeks prior & during disease state --> fecal-oral trans (shell fish & water) NO CARRIER STATE!!!! |
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CORONA VIRUS
- gen - DISEASES *Abs are poorly protective* |
longest, helical +ssRNA, enveloped
( only helical +ssRNA) E2 binding Glycoprotein surrounding envelope = corona *promotes cell binding/fusion* - Grows at 33-35 degrees - Viral RNA pol "jumps templates" = RECOMBO if co-infxn Diseases: - URIs - zoonotic Corona = SARS |
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CALICIVIRUS
- Norwalk Virus - Hep E |
naked, icosahedral +ssRNA virus
Calici = Norwalk Virus: - STABLE 2 drying/heat/pH3/detergent/mild chlorination - Infection of GI --> watery diarrhea (lose water & ions) - Malabsorption: blunts brush border & delays gastric emptying *can persist for months post-infxn* - Causes 45% AGE (more abd pain than rotavirus) - Virus shed for 2 weeks HEPATITIS E: 1-2 mo incubation - animal reservoir; fecal-oral trans (vertical trans too) - Self-limiting illness; mild, low mortality - No chronic carrier state - 50% of water-borne hepatitis *20% mortality in pregnant women* |
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FLAVIVIRIDAE
- gen - viruses |
Enveloped, +ssRNA, w/o capsid
Viruses bind to Fc receptor, forming non-neutralizing Abs - 2nd infxn is MUCH worse (Abs bring macros to infect) VIRUSES: - ARBOVIRUSES - Hep C (West nile, st. louis enceph, yellow fever, dengue |
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ARBOVIRUSES
- gen - viruses (families) **many are asymptomatic** |
"Arthropod Borne"
- Infect midgut --> salivary glands - Very seasonal; localized - Need a reservoir of viremic, asymptomatic individuals VIRUS FAMILIES: All env'd 1. Flavivirus: +ssRNA, binds Fc-R 2. Togavirus: + ssRNA, tight env 3. Bunya: -ssRNA, no Matrix Proteins |
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ARBOVIRUS
- MICROPATHOLOGY |
ssRNA made into dsRNA
--> activates IFN = crappy symptoms (malaise) --> Encephalitis/confusion & ^ ICP |
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ENCEPHALITIS & VIRUSES
- ENTERO VS ARBO |
ENTEROVIRUS: Very low mortality, unless <1yo
ARBOVIRUS: prevalence is age-dept - ADULTS: West Nile & St. Louis Encephalitis (flavivirus) - Children (5-18 yo): LaCrosse encephalitis (bunyavirus) - Infants (<1yo): Western/Eastern EE (togaviridae) * HIGH MORTALITY* |
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VIRUSES CAUSING HEMORRHAGIC FEVER
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1. Yellow Fever: Flavivirus
2. Dengue: Flavivirus 3. Lassa (Arenavirus) |
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DENGUE
- VIRUS FAMILY - GEN *live attenuated vaccines stop most flaviviruses EXCEPT dengue** |
Mosquitoes are viremic for life; Humans for months
- Flavivirus: Binds Fc-R Initial exposure = Cross-reacting Abs - non-neutralizing Abs bring macros to infect (crucial) Clinical: - Primary infection = Break-bone fever; high fever, headache, diffuse maculo-papular rash, back and bone pain lasting 6-7 days. - Subsequent exposure = Dengue HF, hypersensitivity --> DIC/shock, weakening, rupture of vascular walls. |
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YELLOW FEVER
*live attenuated vaccines stop most flaviviruses EXCEPT dengue** |
Similar pathogenesis as Dengue
- also an arbovirus/ flavivirus (+ssRNA, env'd, w/o capsid) Most cases are sub-clinical - Infxns can lead to Hepatitis or renal failure - Can progress to Hemorrhagic fever & heart failure Moderate mortality: 10% **High bilirubin with rising creatine in serum is suspicious** |
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HEPATITIS C
- micropath - egypt - clinical - TRANSMISSION |
NON-ARBO flavivirus (+ssRNA, env'd, no capsid)
Abs don't clear infxn; CD8+ T cells do - Hypervariable envelope gene regions = many subgroups Egypt has the highest Hep C rate (iatrogenic - anti-schistosomal serum products ) CLINICAL: 6-8 wks - More indolent/prolonged than Hep B - 10% acute infxns = jaundice/Sx - 80% infxns = CHRONIC!!! - 20% = cirrhosis - 4% = liver CA TRANSMISSION: sex, blood, IVDU, tattoo, vertical |
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TOGAVIRIDAE
- GEN - DISEASES |
icosahedral +ssRNA, tight envelope
- looks shrink wrapped 1. Arbovirus - infects infants <1yo *ENCEPHALITIS* - Eastern Equine Encephalitis (US) - Western EE (US) - Venezuelan EE (a. aegypti ltd) *many infected w/o visible dz 2. Rubella (rubivirus) |
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RUBELLA
- micopath - clinical - congenital rubella infxn (ToRCHes) *live attenuated vacc (MMR) - 1 & 5 YO *MUST REPORT TO HEALTH DEPT* |
NON-ARBO TOGAVIRUS
Transmission: Resp secretion/droplet - infects UR tract --> lymph - Localizes in lungs, skin, placenta, joints, and kidney Virus is NOT cytolytic - Abs control viremia, causing RASH & arthralgias - cell-mediated imm also nec. CLINICAL HALLMARK: 3 days of fever, malaise (viremia) followed by 3 days of rash spreading UP AND DOWN from nape of the neck - arthralgias in adults CONGENITAL RUBELLA INFXN: - chromosomal abnormalities - Microcephaly, heart defects, cataracts, deaf - contagious; die w/in 1yr |
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CHIKUNGUNYA
so dumb |
"that which bends"
Arbovirus A. aegypti S. america, Asia & Africa Fever, headache, rash, Polyarthritis - 15% ongoing symptoms (Viral arthritis caused by togavirus (alpha & rubella), Hep B, parvo b19) |
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HEPATITIS DELTA (D)
Prevention: Hep B vacc |
SUBVIRAL PARTICLE (not really a virus)
- small circ ssRNA - self-folds & cleaves itself by ribozyme activity - only codes for 1 protein (binds RNA) - can only replicate w/ a Hep B co-infxn (no envelope protein, must be packaged in HBsAg particles) CLINICAL: - Coinfxn w/ Hep B = chronic infxn - Superinfxn w/ Hep B established = Fulminant dz --> 70% chronic infxn, 70% cirrhosis, 20% acute mortality |
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NEGATIVE SENSE SSRNA
- GEN |
NEEDS TO CODE FOR & CARRY RNA-DEP RNA POLYMERASE
- usually takes place in cytoplasm (except in orthomyxovirus) |
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ORTHOMYXOVIRUS
- GEN - CLINICAL |
enveloped, helical capsid, segmented -ssRNA
Responsible for Influenza A, B, C CLINICAL: last 3-8 days - Abrupt fever, headache, malaise, nausea + congestion/cough - IFN & cytokines contribute to symptoms - Rare lung infxns (desquamation can be severe) - Damaged cells recover 3-5 days; take 1 mo to fully recover *immunity is cell-mediated* Transmission: resp droplets/sec - Incubation: 3-5 days - Shedding: 5-10 days - only 50% have classic symptoms |
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OTHOMYXOVIRUS
- PATHOPHYS ex// H1N1 (h= hemagglutinin; n = neuraminidase) *H & N are processed in the Golgi (M2 ensures proper pH) |
PATHOPHYS:
- Membrane glycoproteins control binding *Hemagglutinin binds sialic acid = clathrin-coated endosome (no fusion) *Neuraminidase & M1 enable capsid transport --> Nucleus - M2 proton channel acidifies Endosome --> low pH causes h to refold & fuse w/ endosome membrane - Neuraminidase does its thing - Viral Assembly in the cytoplasm!! - 11 genomic segments randomly pack (specific 8 are infective) - viruses BUD OUT from apical side 8hrs post-infxn - Neuraminidase CLEAVES sialic acid of the Receptor = virion release |
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ORTHOMYXOVIRUS
- PATHOGENESIS *Ag shift/drift |
1. Neuraminidiase cleaves sialic acid in mucous --> infecting nasal cells
2. Initial resp infxn = viremia (but NO SYSTEMIC BINDING) - need T cell immunity Ag Drift: Mtts lead to diff antigenicity Ag Shift: new arrangement 2' COINFXN --> new HA/NA combo --> more serious *Influenza B only affects humans --> no Ag Shift |
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ORTHOMYXOVIRUS
- complications of influenza |
kids: OM, Bronchiolitis, croup, febrile seizures
elderly: bact. pneumonia (s. aureus) & MI rare: myocytis, encephalitis Reye's Syndrome: <21 yo - encephalopathy & liver failure |
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ORTHOMYXOVIRUS
- FLU VACCINE |
standard shot = inactivated virus
live attenuated cold nasal spray is better at making IgA *not as effective if you're older |
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SPANISH FLU
- H1N1 OF 1918 - NEW PROTEIN |
PBI-F2: viral polymerase protein
- way more viral replication - stops mitochondrial cytochrome c - apoptosis of CD8+ T cells & macros |
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PARAMYXOVIRUS
- gen - classifications |
env'd, helical capsid, -ssRNA virus
*Formation of mutinucleated giant cells/syncytia possible* - only possible when virus BUDS and FUSES directly Classifications: - Morbillivirus: Measles - Paramyxovirus: Mumps & parainflu - Pneumovirus: RSV & metapneumo GENERAL PATH: 1. G-hemagglutinin glycoproteins: cell-binding 2. F protein: env-cell fusion & cell-cell fusion --> syncytia - Cytoplasmic inclusion bodies = incomplete viral particles |
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MEASLES
- VIRUS - PATHOGENESIS - SYMPTOMS - CLINICAL *Vit A Def = blindness (2' infxn) 1% mortality (^ if malnourished) *Live, attenuated vacc* |
Morbillivirus (type of parainfluenza virus)
- G-Hemagglutinin & F protein cause binding & fusion clinical: incubation 9-10 days -MOST CONTAGIOUS DZ (>99% eff) - resp. droplets - infected are allll symptomatic - lungs --> lymph --> epithelium SYMPTOMS: Fever + 3 C's - Cough, Conjunctivitis, & Coryza (rhinorrhea) & fever - Koplik's spots: buccal mucosa (before rash) - Rash on neck; 3rd day of symptoms **Lifelong, cell-mediated immunity - T cells = rash - t cell def kids = giant cell pneumonia w/o rash (hard to identify) |
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parainfluenza / Resp Syncytial Virus / Metpneumovirus
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Paramyxovirus
- G-hem & F protein LRI occurs without anti-F Abs - young, immunocompromised - give Synagis (passive imm) to premies - Short lived immunity (virus interferes w/ T cell memory) Clinical: - ALL 3 = URI/Colds; exacerbate asthma - Parainfluenza = Laryngitis & croup (seal) - RSV & metapneumo = bronchiolitis & viral pneumonia * recurrent infections possible * |
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MUMPS
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Infects nasopharynx --> eyes --> lymph tissue --> salivary glands, pancreas, meninges, testes/ovaries
*affects glands & CNS* Clinical: most are asymptomatic - malaise, myalgias, low grade fever - parotitis men = orchitis aseptic meningitis live attenuated virus (MMR) |
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BUNYAVIRUS
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Env'd, helical capsid, segmented -ssRNA
*NO MATRIX PROTEIN* 1. Arbovirus: - LaCrosse Encephalitis (CA; children 5-16) - Riff Valley Fever (systemic) 2. Hantavirus: causes ARDS directly from inhaled rodent feces - hemorrhagic fever w/ renal syndrome |
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FILOVIRUS
- micropath - transmission |
Env'd, helical capsid, thread-like -ssRNA
Diseases: - Ebola - Marburg Hemorrhagic fevers --> DIC Transmission: - Blood/semen for months post-recovery - mortality 20% *natural reservoir might be bats* |
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RHABDOVIRUS
- PATHOGENESIS |
Enveloped, helicocapsid, -ssRNA
RABIES 1. Zoonotic infxn (animal bite;saliva) 2. Endocytosed in clathrin pits 3. Multiplies in muscle & CT 4. Spreads to peripheral nn. 5 Retrograde travel to CNS via passive axoplasm flow 6. In CNS --> Salivary glands; rpt. LOCAL PROCESS (NO VIREMIA) - Incubation depends on distance to the CNS (ex// neck vs. toe) |
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RHABDOVIRUS
- Clinical - epidemiology - prevention |
CLINICAL:
- Fever, malaise, sore throat, vomit - Apprenhension, throat spasm (HYDROPHOBIA), agitation - LATE: salivation & perspiration *Encephalitis: seizures, hallucinate, paresthesias --> resp. paralysis EPIDEM: - Mostly BATS (other wild animals) - KEEP THE ANIMAL that bit you *check it for Negri bodies in neurons PREVENT: - Vaccinate animals - Pre-exposure vaccine: Killed vaccine (takes 14 days to make Igs) - Post-exposure Rabies Ig |
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ARENAVIRUS
- pathogenesis - transmission - clinical |
Pleomorphic Env'd, helicocapsid, segmented -ssRNA
- Virus has host RIBOSOMES = sandy (arena) PATH: - Infects macros & lymphocytes (NOT cytotoxic) - Symptoms caused by cytokines --> DIC, liver/spleen necrosis Transmission: - Regional rodents: saliva/urine/stool - Inhalation of aerosolized excreta/bodily fluids CLINICAL: - Hemorrhagic Fever Lassa - Aseptic meninigitis (LCM) assc'd with HAMSTERS |
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RETROVIRUSES
- contents |
- Duplicate copies of +ssRNA
- Icosahedral capsid - Enveloped - Enzymes: Protease & poly-protein pol *Poly-protein pol cleaved into - Integrase - RNA-Dep DNA pol (RT) **MUST CODE FOR & CARRY THESE ENZYMES** |
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RETROVIRUS LIFE CYCLE:
- tat = ^ host tsc - rev = ^ RNA proc - nef = downreg MHC-I Vif = destory APOBEC3G - blocks RT in virion |
1. binding
- gp120 to CD4 of T cells - 2' binding causes conformational change in gp120 (+gp41) = fusion (also binds to dendritic cells = CD4 & CCR5) (post-viremia, binding also to macros) 2. REVERSE TRANSCRIPTION - RT makes dsDNA - RT sucks; high mtt rate - RNA end sequences are copied 2x = LTRs 3. INTEGRATION: viral integrase - does NOT require host genes = provirus 4. Transcription - LTRs trigger host tsc w/ host RNA pol - dif splicing = dif proteins (tat = ^ host tsc; rev = ^ RNA proc; nef = downreg MHC-I; Vif = destory APOBEC3G - blocks RT) 5. Translation: - host dept. - 3 poly proteins (and reg proteins) made & cleaved 6. Latency: - Variable - integrated HIV remains in the host DNA for LIFE of the cells 7. EXIT: - Budding - Protease cleaves protein precursors = mature vireon **syncytia formation is possible via GP120) |
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HTLV 1 & 2
- pathogenesis - Clinical |
Env'd, helicocapsid, +ssRNA (duplicated), Retrovirus
- Infects CD4+ T cells & neurons in the skin - tax gene: + WBC colony-stimulating factors --> slow clonal expansion TRANSMISSION: Sex, blood, IVDU, breastmilk - HTLV1 : South Japan CLINICAL: - 5% WITH HTLV1 --> Adult T cell ALL (ATLL) --> RAPIDLY FATAL - 5% = Tropical spastic paraparesis (demyel) - HTLV-2: HAIRY CELL LEUKEMIA |
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RETROVIRUSES
- contents |
- Duplicate copies of +ssRNA
- Icosahedral capsid - Enveloped - Enzymes: Protease & poly-protein pol *Poly-protein pol cleaved into - Integrase - RNA-Dep DNA pol (RT) **MUST CODE FOR & CARRY THESE ENZYMES** |
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RETROVIRUS LIFE CYCLE:
- tat = ^ host tsc - rev = ^ RNA proc - nef = downreg MHC-I Vif = destory APOBEC3G - blocks RT in virion |
1. binding
- gp120 to CD4 of T cells - 2' binding causes conformational change in gp120 (+gp41) = fusion (also binds to dendritic cells = CD4 & CCR5) (post-viremia, binding also to macros) 2. REVERSE TRANSCRIPTION - RT makes dsDNA - RT sucks; high mtt rate - RNA end sequences are copied 2x = LTRs 3. INTEGRATION: viral integrase - does NOT require host genes = provirus 4. Transcription - LTRs trigger host tsc w/ host RNA pol - dif splicing = dif proteins (tat = ^ host tsc; rev = ^ RNA proc; nef = downreg MHC-I; Vif = destory APOBEC3G - blocks RT) 5. Translation: - host dept. - 3 poly proteins (and reg proteins) made & cleaved 6. Latency: - Variable - integrated HIV remains in the host DNA for LIFE of the cells 7. EXIT: - Budding - Protease cleaves protein precursors = mature vireon **syncytia formation is possible via GP120) |
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HTLV 1 & 2
- pathogenesis - Clinical * HTLV immunosuppression = ^ weird infxns |
Env'd, helicocapsid, +ssRNA (duplicated), Retrovirus
- Infects CD4+ T cells & neurons in the skin - tax gene = ^ IL-2 = ^ WBC --> slow clonal expansion TRANSMISSION: Sex, blood, IVDU, breastmilk - HTLV1 : South Japan CLINICAL: - 5% WITH HTLV1 --> Adult T cell ALL (ATLL) --> RAPIDLY FATAL (but takes >30 yr to dev) - 5% = Tropical spastic paraparesis (demyel) - HTLV-2: HAIRY CELL LEUKEMIA |
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HIV
- CLINICAL = 1' INFXN (aka Acute HIV syndrome) - wide dissemination of virus - seeding of lymphoid organs |
PRIMARY INFXN:
7-14d post-infxn = viremia - night sweats + low grade fever - CD8+ T cells cause DECREASED viral load - Abs to gp120/41/p24 are NON-neutralizing - RAPID decrease in CD4 T cell |
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HIV CLINICAL LATENCY
- define AIDS |
After primary infection
Can last as long as 10 years (children only 2 years) - 6 wks post-infxn, CD4 T cells REBOUND --> go through long, slow decline - Viremic load INCREASES as CD4 count is reduced (infect those cells) AIDS = CD4 count of 200cell/mL or certain # of AIDS-defining infxns (weird infxns) ------> Constitutional sympoms --> opportunistic diseases --> death |
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HIV LAB DX
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1. ELISA FOR anti-HIV Abs
- 0.1% false positives 2. Western blot confirmation of anti-HIV Abs or viral antigens *RT-PCR or proviral DNA can be used for viral load assessment - can be quantitative for mtts that effect resistance for meds |
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THEORIES BEHIND DECREASED CD4 T CELL COUNT IN HIV INFXN
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1. Direct cytotoxic effect by HIV
2. CD8 cell-induced apoptosis **whatever, it's still the loss of CD4 cells that leads to devastation of immunity** |
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HUMAN FUNGAL DISEASES & DEPTH OF SKIN THEY INFECT
- superficial - cutaneous - sc - systemic (opportunistic) |
A. Superficial: Pityriasis versicolor & tinea nigra
- Malassezia furfur & exophiala werneckii (dead layer) B. Cutaneous: tinea corporis/cruris/pedis/capitis/unguium - Dermatophytes: Microsporum, trichophyton, epidermophyton (epidermis) C. SC: - Sporotrichosis (rose thorns) - Chromomycosis: Copper cells (Phialophora & cladosporium) - Mycetoma: Exophiala, Madurella - Scedosporium D. Systemic: - Coccidiodes immitis - Histoplasma capsulatum - Blastomyces dermatiditis - Cryptococcus neoformas - Candida albicans (systemic & cutaneous) - Aspergillus flavus - Paracoccidioides brasilienes OPPORTUNISTIC: - Candidiasis - Aspergillosis - Mucormycosis - PCP: pneumocystis carinii |
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fungal morphology
- cell membrane - cell wall - capsule |
cell membrane:
- Ergosterol: drug target (EXCEPTION: P. carinii does NOT have ergosterol) Cell Wall: Chitin - potent antigens Capsule: polysacc - Virulence factor of C. neoformans ONLY - India ink stain |
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anti-fungals
general - anti-ergosterol |
Polyene macrolide antifungals bind ergosterol:
Amphotericin B & Nystatin - Punch HOLES in fungal cell wall - poor oral absorption Azoles & Echinocandins: - Interfere w/ ergosterol synthesis - Block CYP51 - Prevent Lanosterol --> ergosterol |
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ANTI-FUNGALS
- 6 MAJOR GROUPS & MECH |
1. Polyenes: Amphotericin B
- binds ergosterol; holes in membrane - poor absorption; give IV - AWFUL SEs 2. Anti-metabolites: Flucytosine - Converted to 5-fluorouracil by cytosine deaminase (humans don't have that enzyme) - inhibits DNA synthesis 3. Azoles - Inhibit fungal Cytochrome P450 3A-dep C 14-demethylase - can't convert lanosterol --> ergosterol - good SE profile 4. Glucan Synthesis Inhibitors: - Echinocandins & -fungins - IV - inhibit 1,3 D-glucan synthase - inhibit cell wall (chitin) 5. Allylamines: topical - except terbinafine (oral too) - inhibit squalene oxidase (inhibit ergosterol synth) 6. Others - griseofulvin: prevents fungal division; disrupts mitotic spindles |
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DIMORPHIC FUNGI
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1. Coccidoides
2. Histoplasma 3. Blastomyces 4. Paracoccidiodes 5. Sporothrix Higher temp (37 degrees) = yeast (single cells) Lower temp (25 degrees) = molds - mycelia/spores |
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fungal culture medium
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SDA: Sabourad dextrose agar
- acidic pH - nutritionally poor - inhibit bacterial growth *H. capsulatum has a hard time growing on this* |
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Tinea/Pityriasis versicolor
- fungus - morpho - where? **Malassezia & candida are ONLY commensal fungi** |
Malassezia furfur
- Multi-colored (looks dark on light skin; light on dark skin) - mainly upper body (rarely neck/face) SUPERFICIAL - only keratinized epithelium - UV light: green - KOH: "Spaghetti & meatballs" (spherical YEAST + pseudohypae) *Young adults* - tx w/ ketoconazole shampoo |
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Tinea NIGRA
- FUNGUS - WHERE? - looks like? - tx *Tx superficial fungal infxns w/ dandruff shampoo or topical imidazoles** |
Phaeoannellomyces / Exophiala wernickii
SUPERFICIAL - brown/black macules on palms - esp in third world tx: topical imidazole KOH: DARK SEPTATE HYPHAE - MOLD!! |
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DERMATOPHYTOSIS
- Microsporum canis |
Tinea capitis & corporis
- RINGWORM Colonizes stratum corneum, but DOESN'T INVADE - rings = inflamm response CATS = natural habitat Scraping: micro & macroconidia - thin septa - UVA light: blue-green |
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DERMATOPHYTOSIS
- Trichophyton rubrum |
Toe web spaces: tinea pedis
- shedding of infectious scales are infectious MORPHO: MOLD - micro & macroconidia |
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DERMATOPHYTOSIS
- EPIDERMOPHYTON FLOCOSUM |
Jock itch: tinea cruris
- tinea incognito = steroid modified tinea corporis *inappropriate use of steroid cream can shield inflamm rxns* --> when you run out of steroid cream, inflamm is 1000x worse! MOLD: - smooth walled conidia & thick walled chlamydoconidia |
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DERMATOPHYTES
- GENERAL - fungi - location - transmission - dx - tx: topical antifungals |
All dermatophytes live in stratum corneum (horny layer**
- secrete keratinase - ALL MOLDS Fungal antigens can diffuse systemically --> Dermatophytid rxns (distant vesicles) - but fungus itself is LOCALIZED (Never invades) - trigger delayed-HYP rxns: inflamm, itchy, scaly skin Microsporum: tinea capitis/corporis Trichophyton: tinea pedis Epidermophyton: tinea cruris Geophilic & zoophilic = inflamm lesions -Anthropophlic = little inflamm |
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Scedoporium apiospermum
(Pseudallescheria boydii) - where - special charac - |
Polluted water
- introduced by local trauma (cut) - SUBCUTANEOUS INFXN (can cause olecranon bursitis) MOLD: - Anamorphic or asexual state of p. boydii (filamentous fungi w/ ovoid, unicellular conidia + septate hyphae) LOOKS LIKE A BAG OF FRUIT? RESISTANT TO AMP. B |
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MYCETOMA
FUNGUS + TUMOR - causes - looks like *often in the foot* |
Causes: bacterial or fungal
A. Actinomycetes or nocardia B. Madurella mycetomatis - Exophiala jeanselmei + Sclerotia: hardened mass of hyphae within host tissue - has a dark ring, which fruit bodies/stomata/mycelia can develop Chronic infxn from inital injury to skin - multiple localized lesion |
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TX of dermatophyte infxns of hair & nails
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ORAL agents: azoles & terbinafine
(fluconazole & itraconazole) |
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CHROMOBLASTOMYCOSIS
- fungi - looks like - where? - dx LITTLE KID PLAYING WITH ROTTING WOOD - GETS PUNCTURED *initial lesion = violet wart-like lesion |
SUBCUTANEOUS INFXN
- Copper colored soil saprophytes (Phialophora & Cladosporium & Fonsecaea) "copper penny" cells - form rounded sclerotic bodies in tissue - CAULIFLOWER WARTS - takes a while to develop (mos) dx: KOH - copper colored sclerotic bodies tx: Itraconazole + local excision |
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fungal YEASTS
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1. Mallassezia: tinea versicolor
2. Candida 3. Cryptococcus 3. Pneumocystis |
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Sporotrichosis
- fungus - looks like - dx - tx |
Sporothrix schenckii
(very tricksy - hides on rose thorns) SUBCUTANEOUS INFXN - dimorphic - 25 deg: oval conidia (flower) + branched hyphae (thready) - 37 deg: cigar budding yeast Presentation: SC nodules (esp hands/ft) - slow local infxn - 2' nodules = along lymphatic tracts tx: Oral Pot. iodide (pot roses) - antifungals: amp B, itraconazole **Also in cats |
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systemic fungal infections
- disease process (similar to TB) - clinical presentations - dx *Histoplasma & BLASTomyces endemic to areas draining into Mississippi |
Inhaled spores (from natural habitat)
(NOT transmitted from person2person = TB) - Grow as yeast cells inside human (Local infxn) - Disseminates into blood Clinical presentations: 1. Asymptomatic: most pts 2. Pneumonia: mild - granulomas + calcifications like TB - small group = severe or chronic cavitary pneumonia 3. Disseminated - rarely; only in immmunocompromised DX: 1. Biopsy 2. Examine w/ silver stain for yeast (or SDA or blood agar) - skin tests are not that great - serum is better - urine histoplasma Ag test can help tx: itraconazole or amp B req'd for MOs in severe pts. |
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Histoplasma, Blastomyces, & Coccidioides
- similarities to TB - contrasts to TB |
LIKE TB:
1. inhaled, primary lung infxn 2. Range of severity 3. Lung granulomas, calcifications, and/or cavitations 4. Can disseminate via blod 5. Skin test like PPD (Antigenic skin preps - coccidioidin, etc) UNLIKE TB: - No person-person transmission - Via spores (NOT acid-fast bacteria) *Histoplasma = NONencapsulated - bird & bat droppings Blastomyces: soil & rotten wood |
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DIFFERENTIAL DX OF MENINGITITS
- purulent vs nonpurulent - CSF glucose |
1. Purulent = Bacterial
- High WBC - Low Glucose - High protein 2. Nonpurulent: Aseptic - normal WBC A. CSF glucose normal = viral B. CSF glucose LOW = systemic fungal or tuberculosis |
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SYSTEMIC MYCOSES:
MORPHOLOGY |
1. histoplasma: unencapsulated
- hijacks macros 2. Blastomyces: - Double contoured wall - figure 8 nucleus 3. Paracoccidioides: - circumferential buds: star/cartwheel 4. Coccidiodes: Spherules w/ endospores 5. Cryptococus: fried eggs in tissue |
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COCCIDIOIDOMYCOSIS
- disease process - risk factors - dx |
Starts as lung infxn
--> disseminates to skin - lung lesions scar = coccidioidoma RISKS: - black, filipino, native & mexican americans - pregnant women - Blood type A & AB aka VALLEY FEVER (chronic necrotizing mycotic infxn) - serological test: precipiating IgM Ab **resistant to fluconazole?* |
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HISTOPLASMOSIS
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southeast, mid-atlantic US
- bird & bat droppings Small, unencapsulated - phagocytized by giant cells in alveoli - spores replicate inside & travel to bone & organs via macros **AIDS-defining illness - can be confused w/ miliary TB - resolves spontaneously - can cause lung scar (histoplasmoma) Chronic infxn: tx w/ oral itraconazole *Can discolor skin if disseminated* |
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BLASTOMYOSIS
- looks like? - diff - where? |
Systemic
dimorphic - yeast cells: broad-based buding, double walled, figure 8 nucleus SE & central US, africa, & mexico - soil & birds (soil & rotten wood) - super rare, but worst to get (most cases = chronic disseminated dz) Males: females = 10:1 - takes a loooong time to show up tx: oral potassium iodide Skin lesions: can look like pyoderma gangrenosum or squamous cell CA |
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PARACOCCIDIOIDOMYCOSIS
- AKA - WHERE? - MEN VS WOMEN |
YEAST
- multiple synchronized daughter cells (looks like flower) aka S. American blastomycosis - Rural/agricultural areas - bats & armadillos Active infxn more common in MALES - P. brasiliensis has estrogen receptors --> inhibit yeast formation |
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CRYPTOCOCCOSIS
- fungus - where - major manifestation *major damage is due to space-occupying abscess; NOT inflamm* DX: India ink stain (50%) - Cryptococcal Ag test (capsule) - cx to confirm dx |
Cryptococcus Neoformans
- encapsulated yeast cells - fried eggs - india ink or muscarine stain - pigeon poo Spores are inhaled --> Brain = MENINGITIS (low csf glucose); develops slowly - only in impaired cell-immunity - AIDS pts might NOT have inflamm CNS rxn - Multiple cryptococcomas (masses) on MRI - Poor prognosis = 2' cutaneous infxns (can preceed dx of disseminated dz) Pulmonary lesions are usu. asymptomatic & increase risk of dissemination **MCC OF FUNGAL MENINGITIS** |
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CANDIDA ALBICANS
(CANDIDIASIS) - normal vs. immune compromised Risk factors: multiple abx, central catheters, neutropenia, hemodialysis, DM |
NORMAL:
1. Oral thrush - hard to take off - reddish base 2. Vaginitis - Abx, birth control, period, pregnancy 3. Diaper Rash - warm most areas IMMUNOCOMPROMISED: 1. Esophagitis - burning substernal pain; worse w/ swallowing 2. Disseminated - Retina: fluffy white pathes - blood c+ is ALWAYS ABNORMAL (candida is normal in urine, sputum & stool) DX: - KOH skin scrapings - Stains/cultures of biopsies tissue or blood - Blood test: beta-D-glucan (cell wall) DIFF: Candida & cryptococcus colonies look the same in cx - Cryptococcus = phenol oxidase; turns BIRDSEED AGAR BROWN |
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ASPERGILLUS FLAVUS (OPPORTUNIST)
ACUTE ANGLES! - rxns - morpho *fumigatus = fungal ball RISK FACTORS: COPD, Smoking, prev. lung damage |
Radiating Spores are ubiquitous
- Hyphae branch @ 45 degrees 1. Allergic Broncho-Pulmonary Aspergillosis (ABPA) - inhalation = IgE --> Type 1 HYP - Also type 4 HYP & lung infiltrates 2. Aspergilloma - infxn in preformed lung cavities (prev. injury) - (aspergillus fungal ball) - sx 3. Invasive Aspergillosis - bloody sputum *Aspiration of aspergillus = ASTHMA TOXINS: AFLATOXIN - penauts, grains, rice 1/2 of CAs in Africa = liver CAs |
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MUCORMYCOSIS
right angles! - causes - risk factors - where? |
Mucor & Rhizopus = also branched hyphae
- branch at 90 degrees - no septae - invade nasal mucosa *mainly affect diabetics, organ transplant, or hematologic malignancy *Decaying vegetation; OPPORTUNIST* |
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PNEUMOCYSTIS CARINII/JROVECI
opportunist! lives in the lung - special - manifestations |
NO ERGOSTEROL
- Can't tx w/ azoles or ampho B - rarely seen outside AIDS pts Silver stain = "deflated ball" PNEUMONIA: - PCP = AIDS defining illness - ground-glass pattern - multiple BL masses |
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FUNGAL TOXINS
(mycotoxisns) |
1. Aspergillus flavus - sunflower
- Aflatoxin: hepatocarcinogenesis - no refridgeration 2. Stachybotrys chartarum - toxic house mold - grows on wet cellulose 3. Amantia species - neurotoxic mushrooms |
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FUNGI-LIKE BACTERIA
- DIFFERENTIATE - tx is a SN-AP *actinomycetes = most misdx'd dz (neoplasm) - males more likely to get *Nocardia is NOT normal flora (while actinomyces IS) |
BOTH GRAM+, BEADED FILAMENTS
1. Actinomycetes - prokaryotes - mycelia-like - water & soil saprophytes - NOT acid fast; obligate anerobe - Yellow sulfur granules - surrounded by PMNs = Abscesses in mouth & GI tract & Draining sinus tracts NOCARDIA asteroides & brasiliensis - weakly acid fast - obligate aerobe = pneumonia & kidney/brain abscesses - soil - mycolic acid cell wall --> intracell --> Caseous granulomas - also causes mycetoma |
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INFECTIVE ENDOCARDITIS
- valves involed - organisms & valve type **FEVER is often seen with IE** + heart murmur + peripheral manifestations |
Mitral > aortic > tricuspid > pulmonic
1. Streptococcus: 32% native valve (CAquired) 2. Enterococcus 3. S. Aureus - esp in IVDU & native valves - Catheter-assc'd bacteremia S. Viridans: subacute disease in non-IVDU & congenital valve lesions S. Bovis: assc'd with colon CA - need to do colonoscopy |
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PERIPHERAL MANIFESTATIONS OF IE
+ complications - presentation in young adults |
1. Clubbing
- esp in dz of long duration 2. Splinter hemorrhages 3. Petechiae (conjuctivae, buccal mucosa, palate, ext) 4. Osler's nodes: - small painful nodules on finter/toe pads 5. Janeways' lesions - hemorrhagic, macular PAINLESS - more common in staph endocarditis 6. Roth's spots: pale retinal lesions COMPLICATIONS: 1. CHF = MC COD *Febrile stroke in young person = IE (neuro deficits & fever) - also major embolisms & renal involvement |
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DUKE CRITERIA FOR DX OF IE
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2 major criteria
OR 1 major criterion & 3 MINOR OR 5 minor MAJOR CRITERIA: + typical Blood cx, + TEE MINOR: - Predisposition, fever, vasc, immunologic, microbiologic evidence |
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IE & ECHOCARDIOGRAPHY
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1. tRANSESOPHAGEAL (TEE) = BEST
95% sensitivity Gold Std 2. Transthoracic: 60% sens; 95% spec. |
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INDICATIONS FOR <3 SURGICAL INTERVENTION IN PTS W/ ENDOCARDITIS
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1. perivalvular extn of infxn
2. Poorly responive s. aureus IE involving Aortic or mitral valve 3. Large hypermobile vegetations w/ high risk of embolism 4. Persistent unexplained fever in cx-neg native valve endocarditis 5. Poorly responsive or relapsed endocarditis 2' highly abx-resistant enterococci or gram neg bacilli |
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WHEN TO GIVE ABX PROPHYLAXIS IN DENTAL PTS
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ALL dental procedures that manipulate gingiva or perforate oral mucosa in patient WITH:
1. Prosthetic <3 valve 2. Previous IE 3. Congenital <3 dz 4. <3 Transplant (developed <3 valvulopathy) |
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STAPH AUREUS BACTEREMIA
- DEFINITIONS (CA vs. HA; complicated vs uncomplicated) RISK FACTORS: Prostheses (IV catheters) & IVDU ALL CASES OF SAB SHOULD BE MANAGED AS MRSA until proven otherwise - vanco |
Community-Acquired
- bloodstream infxn dx'd within 3 days of admission (or FEVER W/IN 3 DAYS) HEALTHCARE-ACQUIRED (HA) - Bloodstream infxn dx'd >3 days after admission Uncomplicated: - bloodstream infxn & fever resolve w/in 3 days of removal of intravascular hardware (or other source of infxn) Complicated - infxn & fever PERSISTS >3 days despite removal of intravascular hardware or other infxn - look for deep seated source of infxn! |
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IVDU & IE
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Can look like pneumonia
(fever, BL infiltrates, fresh tract marks, fast HR) IE of trcisupid valve --> pneumonia |
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WHO NEEDS PROPHYLACTIC ABX?
- MVP / PROSTEHETIC VALVE / PREVIOUS IE - what abx to give? |
MVP = NO
Prosthetic valve & previous IE = yes A. unable to take oral meds - ampicillin or cefazolin or ceftraixone B. allergic to penicillins or amp - Ceph or clinda or azithro/clinda C. Allergic & unalbe to take oral meds - Cefazolin or Ceftriaxone - or Clindamycin (IM OR IV) |
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QUESTIONS FROM CARDIAC MICRO
1. IVDU + IE = what bact? 2. Who do you give proph abx to? - what kind? 3. S. bovis in IE = look for? 4. What's dif bw complicated & uncomplicated baceremia |
1. S. aureus: IVDU + IE
2. Prosthetic <3 valve, Previous IE, CHD, <3 transplant w/ cardiac valvulopathy - amox 3. S. bovis --> colon CA 4. THREE DAY CUTOFF - resolving symptoms - look 4 deep seated infxn **TEE > TTE |
