Transcript Fall Exam 2 OMSII CLIs 2015xx

Fall 2015 exam 2
OMSII CLIs
Clostridia spp.
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Pathogens:
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Gram +, anaerobic, spore-forming rods
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C. difficile (antibiotic assocaited diarrhea and pseudomembranous colitis)
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C. perfringens (gas gangrene)
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C. botulinum (botulism, “floppy baby” after honey))
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C. tetani (tetanus)
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Encounter:
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Entry:
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For wounds: gram stains and culture under anaerobic conditions
C. diff infection usually diagnosed by detecting toxins in feces
Neurotoxic clostridial infections (tetanus- SPASMOTIC PARALYIS via GABA Inhibition and botulism- FLACCID
PARALYSIS via inhibiting ACH release)
Treatment :
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Expression of disease depends on production of clostridial cytotoxins of neurotoxins
Diagnosis:
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Grow in anaerobic environment of GI or devitalized, anaerobic tissue of necrotic wound
Damage:
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Ingestion of clostridial spores in context of antibiotic therapy
Contamination of wounds with soil
Botulism can occur after ingestion of preformed clostridial neurotoxin in contaminated food (does not necessarily
change appear or taste of food)
Spread and multiplication:
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Mostly acquired from the environment
colonize mammalian colon and are returned to the environment as spores from the feces
Wound infections – surgical debridement of tissues
C. diff infection – metronidazole or vancomycin (PO only!)
Tetanus and botulism – antitoxins
Prevention:
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Sterility in canning foods to prevent contamination with C. botulinum spores
“toxoid” vaccine prevents tetanus
Proper wound management
Judicious use of antibiotics
Chlamydia spp.
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Pathogen:
○ Obligate intracellular gram-negative bacteria
Encounter:
○ Genital, ocular, respiratory infections in humans
○ Certain animal and avian isolates cause disease
Entry:
○ Sexually transmitted
○ Human-to-human droplet spread
○ Contact with infected animals
Spread:
○ Undergo unique developmental cycle within eukaryotic host cells
Multiplication:
○ 2 distinct morphological forms:
○ Elementary bodies (EB) –enfectious small extracellular infectious particles that attach to
and enter into host cells but are metabolically inert (do not grow or divide)
○ Reticulate bodies (RB) – replicate. derived from EBs after uptake by cells; larger,
intracellular, noninfectious but metabolically active forms; divide by binary fission within
membrane-bound inclusion in eukaryotic host cells
Damage:
○ Most damage related to host hypersensitivity reaction
Diagnosis:
○ PCR (genital infection) or serologic diagnosis
Treatment and prevention:
○ Chlamydiae are sensitive to macrolides, tetracyclines, and fluoroquinolones
Candida spp.
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Pathogen:
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Encounter:
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Mucosal candidiasis – adherent white plaques on oropharyngeal and vaginal mucosa (thrush); non-painful
Proliferation in warm moist areas (intertriginous candidiasis and diaper rash)
Underlying tissues are not damaged
Candidemia is dissemination which can cause microabscesses in many organs, meningitis, chorioretinitis and
vitritis, hepatosplenic abscesses, and vertebral osteomyelitis. Endocarditis on prosthetic valves.
Diagnosis:
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Main host defense in T-cell mediated immunity (protects against mucosal surfaces)
Neutrophils protect from spread through mucosa and subsequent dissemination
Damage:
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Disruption of normal flora will cause opportunistic infection
Decreased T- cell immunity allows proliferation
Neutropenia and central venous catheters
Spread and multiplication:
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Normally colonize GI tract (mouth to rectum), vagina, and skin
Most infections endogenous
Immunosuppressed (especially neutropenic and ICU patients.)
Risk factors: broad-spectrum antibiotics, renal failure requiring dialysis, central venous catheters, parenteral
nutrition
Entry:
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Round or oval yeasts that reproduce by forming buds or blastoconidia
Potential to form hyphae in vivo
C. albicans (most infections), C. glabrata (resistant to some antifungal agents), C. parapsilosis (central venous
catheter associated infections)
Scrapings of lesion show budding yeast and pseudohyphae
Blood culture for disseminated candidiasis with blood agar or Sabouraud agar (selective for fungi).
C. albicans can be differentiated by development of germ tubes when exposed to calf serum
Treatment and prevention:
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Local antifungal topical creams/powders
Invasive/disseminated infection can be treated with systemic fungal agent fluconazole or amphotericin B
Aspergillus spp.
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Pathogen:
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Encounter:
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Presents initially as pulmonary or sinus infection
Histopathologically seen are hemorrhagic infarction and necrosis; acutely branching septate hyphae seen
invading through tissues
Invasive pulmonary aspergillosis will show fever, pleuritic chest pain, cough, hemoptysis, and dyspnea
Disseminated aspergillosis include: necrotic skin lesions and brain abscess
Diagnosis:
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Neutrophils and macrophages are main host defense
Angioinvasive fungus which can cause tissue infarction, hemorrhage, and necrosis
Damage:
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Conidia are inhaled into upper and lower respiratory tracts
After entry is germination of conidia into hyphae which then invade tissues
Spread and multiplication:
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Ubiquitous in soil, manure, and decomposing vegetation
Usual hosts are those who are neutropenic, on corticosteroids, or other immunosuppressive drugs, or
transplant recipients
Entry:
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Filamentous fungi that form mycelium of septate hyphae
Reproduce by forming conidia on aerial conidiophores
Major pathogenic species are A. fumigatus and A. flavus
Not part of normal flora of humans
Grow on Sabouraud agar
Tissue biopsy for tissue invasion
Treatment:
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Invasive aspergillosis – voriconazole, amphotericin B, or echinocandin is used
Empiric treatment often initiated based on clinical manifestations and CT scan results
Plasmodium
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Organism:
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Encounter and entry:
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Fever, chills, anemia
Can cause splenomegaly
Diagnosis:
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Sporozoite is the infectious form present in mosquitoes that is transmitted to humans
Sporozoites enter liver cells which mature, multiply, and are released as merozoites
(form that invades RBCs)
Merozoites divide and mature inside RBCs and release new infective merozoites; a
minority form gametocytes
Damage:
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Transmission through bite of infected female anopheline mosquitoes (saliva)
Spread and multiplication:
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Protozoa
Malaria caused by P. falciparum, P. vivax, P. ovale, and P. malariae
Giemsa-stain
P. vivax have Schüffner dots
Treatment:
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Chloroquine
Chloroquine resistant P. falciparum can be treated with Malarone, Coartem, quinine +
doxycycline, or quinidine
Trypanosomes
T. cruzi (Chagas disease)
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Bite of infected reduviid bug (“kissing bug”) (fecal matter)
Chancre or tissue and lymph node swelling at bite site
Most develop mild disease w/ fever, recover spontaneously, and remain asymptomatic
Small proportion develop complications 10-20 years later
○ damage to nerves in GI tract (megaesophagus, megacolon)
○ Conducting tissue in heart (right bundle branch block)
○ Heart muscle (cardiomyopathy)
Fibrosis is the hallmark of pathology
Diagnosis and treatment:
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Blood culture, positive antibody titer
Treat with nifurtimox or benznidazole
No treatments for late complications
T. Brucei (African sleeping sickness)
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Bite of infected tsetse flies (saliva)
Undergo antigenic variation of its immunodominant surface antigen (variable surface
glycoprotein)
Reservoirs are wild game animals in East Africa (takes only months to reach CNS);
humans and domestic animals in West Africa (takes years to reach CNS)
Bouts of systemic illness with fever and swollen lymph nodes; can eventually reach
brain and CNS and infect brain and spinal fluid. During each bout, undergo surface
antigen rearrangement (genetic rearrangement).
Treatment:
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eflornithine
Adenovirus
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Pathogens:
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Encounter:
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Evade antiviral host defenses (prevent host cells from expressing MHC proteins,
mediate resistance to TNF, abrogate interferon response, and antigenic diversity)
Infection can be fatal in immunocompormised
Diagnosis:
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Temporal regulation of gene expression dependent upon viral regulatory genes
Employ both virally encoded and host proteins in the replication process
Damage:
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Most often cause mild infection of respiratory and GI systems
Severe infections can cause keratoconjunctivitis and acute, severe pneumonia
Replication:
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Initial site of replication in most cases is probably oropharynx
Spread:
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Respiratory serotypes: exposure to aerosols or infected fluids (saliva)
Enteric types: contamination with fecal matter
Entry:
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Large, nonenveloped, DNA viruses with icosahedral symmetry
Recognition of clinical features
Lab Dx not typically done except life-threatening situations (PCR)
Treatment/Prevention:
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No vaccine available
No antiviral drug
Influenza virus
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Pathogen:
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Segmented negative-sense RNAs
3 types: A, B, and C (type A can infect animals)
Possess hemagglutinin (HA) and neuraminidase (NA) as major surface
antigens
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antigenic drift is caused by yearly accumulation of mutations in HA and NA
Antigenic shift results from acquisition of a novel HA and NA by the virus
Encounter: influenza occurs in epidemics and pandemics in the winter
(seasonality) [Oct-April Peak incidence in December. ]
Entry: person-to-person and respiratory droplets that infect URT and LRT
Spread: cell infection initiated by attachment of the viral HA to sialic acidcontaining glycoproteins or glycolipids and subsequent uptake into an
endocytic vesicle
Replication: gene transcription and RNA replication occur in the nucleus
Damage: causes clinical symptoms, including common cold, pharyngitis,
tracheobronchitis, and bronchiolitis or croup in children
Diagnosis: virus isolation from sputum and nose/throat swabs; rapid
diagnostic tests available
Treatment/Prevention:
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rimantadine and amantadine (inhibit viral uncoating after uptake) These are NA inhibitors (inhibit viral release from infected cell and cause
aggregation of viral particles). So it won’t help symptomatic patients.
Vaccines: inactivated vaccine or the live, attenuated, cold-adapted vaccine
Human Papilloma Virus
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Non enveloped, Double stranded, Circular
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Soo many serotypes
Encounter/Entry: direct skin to skin contact ie sex;
enters break in skin and sets in the basal layer of skin
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Oncogenic properties
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Since it is non enveloped, it may live on inanimate objects.
Respiratory papillomatous: Vertical transmission during birth;rare
E6- combines with p53- Induces Ubiquitylation proteolysis pathway and
inhibits tumor suppression
E7- combines with Rb – prevents Rb exerting its normal check on cell
proliferation
Damage: Warts or Cancer
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Warts-(serotypes 6, 11)
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Cancer
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CIN, cervical cancer (most commonly 16, 18)
Diagnosis:
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Condyloma Accuminata
Warts- causing Verrucous finger like projections
Cancer- shows atypia (Koilocytes),
Treatment/Prevention:
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Surgical excision
Cryotherapy
Immunomodulators- Imiquimod
Or it disappears on its on… via cell mediated response
Quad Valent Vaccine – 6/11/16/18 serotype protection. Uses “ capsid
like” proteins
Haemophilus influenzae
• Gram-negative, small rod, nutritionally fastidious [Grows on chocolate agar or
on blood with another bacteria that can breakdown blood and provide nutrients]
• Multiple types, only type B has a capsule. It is esp associated with meningitis and there is a vaccine
for just that type]
• Encounter: Throat, inhalation, hand contact
• Pathogenic mechanism: Inflammation facilitated by resistance to
phagocytosis (capsule), endotoxin, IgA1 protease, pili, outer membrane
protein
• Typical Dz: Meningitis (infants, 3mo-2y) w/ sequelae, respiratory
infx/COPD exacerbation, cellulitis, epiglottitis [thumbprint sign]
From FA:
• Culture on chocolate agar (requires factor V(NAD+) and X (hematin) for
growth)
• Vaccine: conjugated polysaccharide vaccine [against type B], given
between 2-18 months
Klebsiella Pneumoniae
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*** very little mention in the book***
Pathogen:
Gram Negative Rod, enteric
Spread: Typically seen in Community Acquired Pneumonia, Hospital
Acquired Pneumonia ;
Common Case scenario: chronic alcoholic or Diabetic who aspirates and
makes current jelly sputum
Damage: Polysaccharide capsules- causing mucoid colonies
Diagnosis: Xray: Shows FOCAL lobar consolidation
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4 A’s of KlebsiellA:
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Aspiration pneumonia
Abscess in lungs and liver
Alcoholics
di-A-betics