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266 Cards in this Set
- Front
- Back
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Staphylococcus aureus: characteristics in culture
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G+, cluster-forming cocci
nonmotile, non-spore forming, facultative anaerobe (prefers O2) golden colonies on blood agar Catalase positive Coagulase positive Ferments mannitol |
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Staphylococcus aureus:
pathogenically significant molecules |
Protein A - inhibits phagocytosis: binds Fc region of Ig
Ribitol techoic acid - antigen, specific to S. aureus Lipotechoic acid --> Mph -->TNF, IL-1, IL-6 a-toxin/a-hemolysin - pore-forming toxin --> osmotic lysis leukocidin/b-hemolysin - membrane damaging toxins, found in dermonecrotic lesions b-toxin - sphingomyelinase, damages membranes Coagulase - extracellular protein binds host PT: fibrinogen --> fibrin clumping factor - promotes attachment to blood clots Panton-Valentine Toxin (PVL) - exotoxin, destroys WBCs, in furuncles and hemorrhagic PNA |
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S. aureus molecules associated with endocarditis
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clumping factor A
fibronectin binding protein |
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S. aureus molecule associated with osteoarthritis
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collagen binding protein
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5 S. aureus molecules involved in avoidance of host defenses
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Protein A - inhibits phagocytosis
Coagulase - mediates fibrin formation around bacterium Hemolysins - lyse RBCs, WBCs penicillinase - disrupts beta-lactam ring a-toxin - forms transmembrane pores, osmotic lysis |
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S. aureus toxin that causes SEPTIC shock
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a-toxin
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S. aureus toxin that causes TOXIC shock
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TSST-1 (superantigen)
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2 superantigens released by S. aureus
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TSST-1
enterotoxins |
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Disease states associated with S. Aureus
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Skin and soft-tissue infections:
Bullous impetigo Scalded skin syndrome Boil/furnuncle/carbuncles Toxic shock: Fever > 39*C Diffuse "sunburned" appearance hypotension N/V/D sore throat, myalgia desquamation of palms/soles 7-10 days later Endocarditis: regurgitant murmur, petechiae, fever Food poisoning: acute N/V/D w/in 1-5 hrs Purpura fulminans Bursitis |
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What do you look for when screening for MRSA?
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PBP 2A
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Complications of S. aureus infection
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septic arthritis
osteomyelitis pyomyosistis endocarditis PNA |
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Treatment of S. aureus
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Nafcillin (IV), dicloxacillin (PO)
MRSA: Vancomycin, Clindamycin, Linezolid, Daptomycin |
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Staphylococcus epidermidis: characteristics in culture
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G+, facultatively anaerobic clusters on blood agar
Catalase positive Coagulase negative |
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Disease states associated with S. epidermidis
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nocosomial infections of prosthetic joints, heart valves, sepsis from IV lines
UTI from infection of Foleys |
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Diagnosis and treatment of S. epidermidis
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Draw blood from 2 different places and compare to rule out contamination by normal flora
Gram stain, culture, cat/coag tests Vancomycin & removal of infected prostheses |
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Streptococcus pyogenes: characteristics in culture
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G+ cocci in chains
Catalase negative Coagulase negative beta-hemalytic Glucose fermentation Bacitracin sensitive, Optichin resistant |
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Streptococcus pyogenes: pathogencially significant molecules
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M protein - inhibits complement and phagocytosis
Streptolyin O - beta-hemalytic, antigenic (ASO titer) pyrogenic exotoxin - scarlet fever, causes massive cytokine release by T cells streptokinase - lyses fibrin clots hyaluronidase - degrades proteoglycans C5a peptidase |
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What test establishes a recent but resolved S. pyogenes infection?
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ASO titer
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Anti-streptococcal antibodies are directed against what virulence factor?
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M protein
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How many M protein serotypes have been identified?
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> 80
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Disease states associated with S. pyogenes
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Streptococcal pharyngitis
Scarlet fever Skin and soft tissue infections: - Impetigo - Cellulitis - pyoderma - erysipelas - necrotizing fascitis Bacteremia TSS Resp tract infections: PNA, sinusitis Bone & joint: septic arthritis, osteomyelitis Meningitis Peritonitis |
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Describe strept throat
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inflamed tonsils and pharynx
purulent grayish-white exudate on tonsils high fever swollen cervical LNs self-limiting: 5-10days |
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Possible complications of strept throat
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peritonsillar or retropharyngeal abcesses,
acute otitis media cervical adenitis acute sinusitis rare: PNA, meningitis, bacteremia |
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Pyoderma
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pustule on extremity or face
degrades, leaves crusty area, then depigmentation |
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Erysipelas
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S. pyogenes infection of the dermis
raised, bright red-salmon rash sharp demarcation |
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cellulitis
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deep S. pyogenes infection of skin cells
produces red, swollen skin hot to the touch |
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Impetigo
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vesicular, blistered eruption
becomes crusty and flaky frequently circumoral associated with Staph & Strept |
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Necrotizing fasciitis
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direct inoculation, then follow path along fascia
associated with S. pyogenes strains with M proteins that prevent phgocytosis and allow quick migration within ONE DAY: swelling, heat, redness skin color turns blue, large blisters form skin dies, muscle may become infected |
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Scarlet Fever
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results from pyrogenic toxin produced by soem GAS
fever scarlet rash begins trunk/neck and spreads to extremities circumoral pallor beefy red pharynx and tonsils yellow-white glossal exudate, then strawberry tongue |
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Streptococcal TSS
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due to pyogenic exotoxin release
onset: myalgia, chills, severe pain at site of infection then N/V/D then hypotension, shock, organ failure |
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2 delayed antibody mediated diseases associated with S. pyogenes
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Acute Rheumatic Fever - anti-M protein Ab reactis with cardiac Ag
Acute glomerulonephritis - Ag-Ab complexes deposited in the glomeruli --> inflammation |
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Natural history of acute rheumatic fever (ARF)
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results from untreated strept throat, but NOT skin infections
anti- M protein Ab cross-reacts with cardiac Ag (Type II Autoimmunity) presentation: FACES Fever Arthritis Chorea Erythema marginatum Subcutaneous nodules repeated attacks damage endocardium & heart valves children 5-15 y/o |
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Natural history of acute glomerulonephritis
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occurs 1 week s/p S. pyogenes infection of pharynx OR skin &
can occur despite ABS tx associated with Type I M protein Ab-Ab complexes deposited in glomeruli cause infection (Type III autoimmunity) Presentation: edema, HTN 2* fluid retention, hematuria, proteinuria, decreased serum complement levels |
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Only streptococcus sensitive to bacitracin
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S. pyogenes
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Best way to culture for S. pyogenes
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Blood agar plates incubated anaerobically because they demonstrate beta-hemolysis
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Treatment of streptococci
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Penicillin (usu. amoxacillin)
Penicillin allergy --> erythromycin Impetigo treated with erythromycin to cover S. aureus risk |
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What disease is a significant risk factor specifically for GBS?
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diabetes mellitus
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Streptococcus pneumoniae: characteristics in culture
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G+, encapsulated, lancet shaped diplococci
Catalase negative alpha-hemolytic facultative anaerobe Bacitracin resistant, optichin sensitive No Lancefield grouping |
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Streptococcus pneumoniae: pathogenically significant molecules
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Polysaccharide capsule - interferes with C3b deposition
Pneumococcal Surface Protein A - interferes with complement deposition Autolysin - degrade peptidogycan Pneumolysin - pore-forming toxin released on lysis of bacteria Neuraminidase - cleaves sialic acid |
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How many antigenic serotypes of the S. pneumoniae polysaccharide capsule have been identified?
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> 90
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Which S. pneumoniae enzyme is specifically toxic to the ciliated cells of the cochlea
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pneumolysin
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Passage of pneumococci up Eustacian tube mediated by _____
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Migration in Eustacian tube - neuraminidase (cochlear toxicity mediated by pneumolysin)
Neuraminidase cleaves sialic acid in host mucin, glycolipids, glycoproteins |
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Functions of pneumolysin
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transmembrane pore-forming toxin
direct effect on phagocytes, suppresses host immune response stimulates cytokines disrupts cilia --> resp. & cochlear toxicity in conjunction with H2O2 --> NO (vasodilation, hypotention) |
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Pneumococci associate with cells that produce a ____-containing surfactant
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Pneumococci associate with cells that produce a CHOLINE-containing surfactant
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Stages of Pneumococcal lung infection
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1st stage: impairment of host clearance mechanisms + phagocytosis inhibition by capsule allows multiplication in alveoli
2nd stage: organisms disintigrate via autolysins and release pneumolysins that cause cell injury. Initial growth produces outpouring of serous edema fluid, then PMNs and RBcs 3rd stage: Lung increases in weight due to fluid accumulation in single lobe of a lung (LOBAR PNA) 4th stage: PMNs predominate lesion until bactera stop growing, then Mph replace and resolution ensues. Lesions resolve without permanent structural damage |
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Presentation of pneumococcal PNA
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ABRUPT onset:
shaking chills fever pleuritic CP hemoptysis SOB CXR: lobar consolidation s/ tx: symptoms continue 5-10 days until crisis and abatement most common complication: pleural effusion |
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S. pneumoniae is the most common cause of which four disease states?
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PNA
Otitis media Sinusitis Meningitis |
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S. pneumoniae sinusitis
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Eustachian tube congestion 2* viral infection common
usu. limited to ethmoid and maxillary sinus in kids > 5 y/o Sinus mucosal swelling * ostia obstruction, followed by purulent discharge + cough |
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Treatment of pneumococcal infections
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Penicillin still drug of choice
If resistant, erythromycin, vancomycin, quinolones Community S. pneumoniae - azithromycin + 3rd gen cephalosporin |
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Pneumococcus vaccines
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Adult - polysaccharide vaccine of 23 most common serotypes
Infants - protein-conjugate vaccine of 7 most common serotypes |
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Bacillus anthracis: characteristics on culture
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G+, large, sporeforming rod
nonmotile, nonhemolytic ordinary mutrient medium catalase positive metabolically active |
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How is the capsule of B. anthracis unique?
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Protein, NOT polysaccharide capsule
D-glutamate of single Ag type like polysaccharide capsules, it is antiphagocytic |
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B. anthracis: 3 components of exotoxin complex
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Edema Factor (EF) - active A subunit (adenylate cyclase)
Protective antigen (PA) - promotes entry of EF Lethal factor (LF) - Z2+ methalloprotease inactivates protein kinase |
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Functions of B. anthracis exotoxin complex
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EF - calmodulin-dependent AC
increases cAMP --> PMN impairment, massive edema PA - promotes entry of EF into phagocytes LF - metalloprotease, inactivates protein kinase stimulates Mph to release TNF, IL-1 --> contribute to DEATH |
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Natural history of cutaneous anthrax
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begins as pruritic papule, enlarges w/in 1-2 days
--> ulcer surrounded by satellite bulbus with edematous halo 2-3 cm diameter round, regular raised edge nonpainful regional lymphadenopathy ulcer --> black eschar w/in 7-10 days lesions on neck may cause swelling, stridor and asphyxiation |
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Inhalation anthrax signs and symptoms
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widened mediastinum
low-grade fever non-productive cough may improve temporarily before rapidly deteriorating --> hemorrhagic mediastinitis usually fatal |
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Septicemic anthrax
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aka: black blood
internal organs become darkly colored w/ widespread petechiae & hemorrhage anthrax bacilli multiply in blood to outnumber RBCs most cases follow inhalaltion anthrax |
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Distinguishing sign of anthrax meningitis
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Cardinal's cap - hemorrhagic leptomeningitis
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Infectious routes of anthrax
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Inhalation of spores from...
grazers & their products ("woolgatherer's ds") NOT human-to-human NOT from viable bacteria |
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Pseudomonas aeruginosa: characteristics on culture
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G-, motile rod
aerobic minimal nutritional requirements blue-green pigment fruity odor oxidase positive |
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True or False: P. aeruginosa is an opportunistic pathogen?
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True
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Pseudomonas aeruginosa: pathogenically significant molecules
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LPS - toxicity, attachment to epithelial cells
Sialic acid & N-acetylglucosamine - receptors Elastase - cleaves IgA, IgG, collagen, complement, fibronectin, respiratory epithelium Alkaline protease - inferferes w/ fibrin formation, inactivates IFNy & TNFa Exotoxin A - EF-2 inactivation by ADP-ribosylation, inhibits protein synthesis |
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P. aeruginosa is the leading cause of mortality for patients with what disease?
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cystic fibrosis
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Antibodies for P. aeruginosa are directed primarily against what virulence factor?
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LPS
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Disease states associated with P. aeruginosa
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PNA
Otitis externa (swimmer's ear) UTIs Bacteremia Endocarditis CNS infections Eye infections Bone & Joint infections Skin & Soft tissue infections |
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Presentation of otitis externa
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pain
pruritus ear discharge pain worsened with traction on pinna common cause of chronic otitis media malignant otitis externa: EAM inflamed, TM obscured by edema, local LN involvement |
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Most common sites of bone/joint involvement in P. aeruginosa infection
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vertebral column
pelvis sternoclavicular joint |
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2 stereotypic P. aeruginosa skin & soft tissue infections
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burn wound infections
- black or discolored - systemic symptoms: ---temp dysregulation, ---ALOC, ---hypotenion, ---oliguria ---ileus ---decreased WBCs Ecthyma gangrenosum lesions - hemorrhagic and necrotic w/ surr erythema - characteristic of P. aeruginosa - axialla, groin, perianal area |
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Histologic hallmark of Pseudomonas PNA & pathogenesis
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hemorrhagic destruction of lungs
from elastase attacking elastin in the lungs & blood vessels |
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What is Exotoxin A?
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Exotoxin of P. aeruginosa
EF-2 inhibiting toxin (via ribosylation of ADP) inhibits protein synthesis --> cell death enters cell via receptor-mediated endocytosis, internalized in low pH vesicle |
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Natural history of pseudomonas eye infections
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colonizes ocular epithelium via fimbrial attachment to sialic acid receptors
elastase, alkaline protease, exotoxin A --> rapid destruction --> loss of entire eye symptoms: lide edema, conjunctival erythema & chemosis severe mucopurulent discharge adherent to underlying corneal ulcer |
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Treatment for pseudomonal...
Endocarditis, bacteremia - PNA - Meningitis - UTI - |
Pseudomonal ...
Endocarditis, bacteremia - aminoglycoside + extended-spectrum penicillin OR cephalosporin PNA - beta-lactam + aminoglycoside Meningitis - ceftriaxone or ceftazidime (3rd gen w/ CNS penetration) UTI - aminoglycoside OR quinolones |
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Mycobacterium tuberculosis: culturing characteristics
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slim, strongly acid fast rod
stains w/ irregular beading obligate aerobe grows at 37C, but not at R.T. Lowenstein-Jensen medium very slow growth produces large amounts of niacin |
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Mycobacterium tuberculsosis: pathogenically significant molecules
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Antigens:
cord factor sulfatides Wax D Cell wall struture: mycolic acids LAM |
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Function of cord factor
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M. tuberculosis
inhibits PMN migration damages mitochondria --> TNF --> rapid weight loss |
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Function of sulfatides
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M. tuberculosis
inhibit phagosome-lysosome fusion |
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Function of Wax D
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M. tuberculosis
mycoside acts as adjuvant may activate CMI |
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LAM
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cell wall component of M. tuberculosis
binds alveolar macrophages via surface fibronectin, mannos or complement receptors modulates cytokine production downregulates aspects of T cell function including Ag presentation |
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Natural history of initial TB infection
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inhaled droplets containing M. tuberculosis deposited in peripheral alveoli
- usu. well-ventilated middle & lower lobes engulfed by alveolar macrophages bacteria multiply until macrophage bursts some bacteria-laden macrophages transported to hilar lymph nodes - may disseminate from LNs |
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Describe tubercle that results from contained, initial TB infection
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microscopic granuloma with
- multinucleate giant cells - many epitheloid cells - surrounding collar lymphocytes & fibroblasts may be caseous necrosis at granuloma center |
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Lesions of reactivation TB
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in areas of relatively high O2 tension & low lymph drainage
spreading, coalescing tubercles w/ many bacilli large areas caseous necrosis wall of a small bronchus often involved small blood vessels frequently eroded |
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Immune responses to TB
DTH develops against ... CMI develops against... timeline |
DTH against tuberculoprotein
CMI against M. tuberculosis 2-6 weeks after primary infection, in both cases |
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Development of CMI against M. tuberculosis
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T cells recognize mycobacterial Ag complexes on surface of infected Mph
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Pathogenesis of caseous necrosis in TB infection
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DTH to tuberculoprotein mobilizes Mph to site of bacilli deposition
DTH & Mph --> local tissue destruction --> caseous necrosis |
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Signs and symptoms of pumonary TB
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productive cough
fever weight loss hemoptysis CP night sweats |
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Manifestations of reactivation TB
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Pulmonary
Meningitis Pott disease Arthritis (single joint, usu. hips/knees) Genitourinary Gastrointestinal Scrofula (lymphadenitis - usu. SCM) Cutaneous (lupus vulgaris) Sterile Pyuria |
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What does PPD measure?
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DTH to tuberculoprotein
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Chemotherapeutic agents for TB
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Isoniazid
ethambutol rifampin pyrazinamide streptomycin |
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Vaccine for TB is called...
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BCG vaccine
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Hemophilus influenzae: characteristics on culture
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Gram negative rod: aerobic or facultative
Requires hematin (X) and NAD (V) - only grows on chocolate agar Oxidase positive Ampicillin resistance (transmitted by plasmid) |
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Hemophilus influenzae: pathogenically significant components
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polysaccharide capsule (type B)
attachment pili IgA protease endotoxin - toxic to ciliated respiratory cells |
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Primary agent of immunity
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T-cell independent, anti-capsular Ab
- infants protected by mom's Ab - natural levels lowest btw 3 mo - 2 yrs |
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Disease states associated with HiB
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Meningitis
Cellulitis Epiglottitis PNA Pericarditis Septic arthritis Occult bacteremia Neonatal infections Otitis media, conjunctivitis with nonencapsulated forms H. influenzae |
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Cellulitis characteristic of HiB
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raise, indurated, tender area with indistinct margins
mostly on head and neck, particularly buccal and preseptal areas |
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HiB PNA presentation
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mostly indistinguishable from other bacterial PNAs, except:
INSIDIOUS ONSET fever, cough, purulent sputum production CXR: often, more pleural and pericardial involvement than other bacterial PNAs |
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HiB is normal flora where?
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nasopharynx in 20-80% of people
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Most common manifestation of HiB?
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Meningitis
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Peds HiB meningitis presentation
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ALOC
fever HA photophobia |
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HiB is noteably resistant to which antibiotic?
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ampicillin
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Treatment of HiB
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3rd generation cephalosproins - usu. cefotaxime or ceftriaxone b/c of meningitis risk
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Legionella pneumophilla: characteristics on culture
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Gram negative, aerobic rod
catalase positive oxidase positive requires charcoal buffered yeast w/ iron & cysteine (CBYE) slow growth GROUND GLASS appearance |
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Legionella pneumophilla: pathogenically significant components
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pili and flagella - attachment
LPS OMP - binds C3, facilitates uptake Cu-Zn superoxide dismutase catalase DOT-ICM type IV secretion RNase phospholipase A (PLA) phospholipase C (PLC) |
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Pathogenesis of Legionnaire's disease
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attacks alveoli & terminal bronchioles
survivies and replicates in Mph - enters Mph using OMP to bind C3 - Cu-Zn superoxide dismutase & catalase protects against ROS - DOT/ICM type IV secretion inhibits phagolysosome fusion - extracts Fe3+ from intracellular transferrin Causes multifocal, necrotizing PNA |
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Pontiac fever
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resembles acute influenze
fever, chills, myalgia may hav cough, runny nose, sore throat **NO PNA** |
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Legionnaire's disease
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severe, toxic PNA
fever < 39*C cough - dry or productive CP - pleuritic or nonpleuritic bradycardia encephalopathy: HA, lethargy, AMS N/V/D AP: pancreatitis, peritonitis myalgia hypotension acute renal failure |
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Spread of Legionella
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inhalation of aerosolized water containing bacteria or infected amoebae
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RFs for Legionnaire's ds:
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older age
smoking chronic lung disease |
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Imaging signs charactersitic of Legionnaire's disease
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rapidly progressive asymmetrical infiltrates
unilateral lower lobes |
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Treatment of Legionnaire's disease
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doxycycline, azithromycin, macrolides, quinolones
fluoroquinolone in severe disease |
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Disinfection for Legionella
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superheating of water
installation of Cu-Ag ionization units NOT chlorine |
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Escherichia coli: 3 variable antigens
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O antigen: LPS
K antigen: cell surface polysaccharides H antigens: peritrichous flagella |
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Escherichia coli pili
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type 1 pili
- most strains express - binds mannose residues P pili - bind GU epithelial cells pili that bind intestinal epithelium CFA - colonization factor antigens BFB - bundle-forming pili |
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Escherichia coli toxins
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a-hemolysin: pore-forming toxin, osmotic lysis
Shiga-like toxin: AB toxin, blocks protein synthesis Labile Toxin (LT): AB toxin --> H2O accumulation in bowel Stable Toxin (ST) bings GP receptor --> H2O accumulation in bowel |
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Antibodies develop against what components of E. coli?
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Stable toxin
Labile toxin |
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Form of E. coli that causes UTIs
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UPEC
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UPEC causes what 3 disease states?
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UTI
polynephritis neonatal meningitis |
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pathogensis of UTIs by UPEC
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access bladder thru minor trauma or mechanical effect of sex
adhesion to uroepithelium by P pili a-hemolysin --> cell damage, inflammation Type I pili --> periurethral & bladder colonization |
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Symptoms of UTI
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dysuria
increase urinary frequency |
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Symptoms of polynephritis
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dysuria
increased urinary frequency fever flank pain |
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Leading cause of community acquired and nocosomial UTI in the US
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E. coli
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Treatment for E. coli UTIs
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Bactrim
quinolones |
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Escherichia coli: characteristics on culture
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Gram negative, facultative anaerobes
occur singly or in pairs grows readily on simple media ferments lactose - purple on MacConkey ferments glucose oxidase negative |
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Neisseria gonorrhoeae: characteristics on culture
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Gram negative diplococcus
intracellular aerobic grows well only on chocolate agar, requires CO2 supplementation oxidase positive |
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Neisseria gonorrhoeae: antigenic characteristics
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Pili - Ag variation, adhesion, prevent phagocytosis
OMP: antigenic - porins & Opa LOS: endotoxin, sialyzation blocks C3b depotision Rmp: targets for blocking Ab IgA protease: escape from muscosal IgA |
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Pathogenesis of N. gonorrhoeae infection
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attach to nonciliated epithelial cells w/ pili, Opa, LOS
Invasion by parasite-directed endocytosis trancytose through basal mb to submucosa In submucosa - scavenge iron from transferrin & lactoferrin - pili & Opa prevent phagocytosis - LOS sialyation prevents C3b deposition - Rmp binds IgG s/ signaling phagocytes - upregulation of catalase Bacteria remain localized, causing inflammation and local injury Ag variation prevents immunity |
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Signs & symptoms of PID
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increased vaginal discharge or purulent urethral discharge
dysuria lower abdominal pain, usually bilateral cervical motion tenderness adnexal tenderness intermenstrual bleeding |
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Fitz-Hugh-Curtis syndrome
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acute perihepatitis with direct extension of G/C from uterine tube to liver capsule & overlying peritoneum
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Most common manifestation of gonorrhea in males
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urethritis
s/s: burning with urination, serous discharge |
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Classic presentation of arthritis dermatitis syndrome
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caused by N. Gonorrhoeae - 2nd stage DGI
joint/tendon pain migratory polyarthralgia, esp. knees, elbows, distal joints tenosynovitis, esp. of wrist or Achilles tendon dermatitis lesions peripheral - maculopapular to pustular - often hemorrhagic - 4 - 50 in number |
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Describe gram smears characteristic of N. gonorrhoeae
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multiple pairs G- dipplococci w/in PMNs
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Treatment of gonorrhea
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3rd generation cephalosporins
- ceftriazone (IM) - cefixime (PO) Fluoroquinolones, azithromycin & doxycycline |
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Chlamydia
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see First Aid flashcards
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Candida albicans: characteristics on culture
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4-6 microns
budding, round or oval yeast cells Sabouraud's agar |
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Candida endophthalmitis signs
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white cotton ball espanding on retina or floating free in viteous humor
can lead to blindness |
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HIV genome type
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diploid RNA genome
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4 layers surrounding HIV genome
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nucleocapsid (virally encoded)
matrix protein envelope proteins (gp120, gp41) membrane (from host cell) |
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3 HIV-specific proteins essential for viral replication
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reverse transcriptase (RT)
protease (PR) integrase (IN) |
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HIV: viral entry
- virion attachment protein - cellular receptor - cell cocreceptors - fusion protein (viral) |
Viral entry of HIV:
viron attachment protein - gp120 cellular receptor - CD4 cell coreceptors - CCR5, CXCR4 fusion protein - gp41 |
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Can HIV infect cells that lack CD4?
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YES
e.g.: fibroblasts, certain brain cells |
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HIV viral RNA replication
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Reverse transcriptase copies RNA --> dsDNA
dsDNA integrates randomly into host genome dsDNA replicates with host genome (provirus) Provirus controls transcription via host RNA polymerase RNase H activity degrades original RNA genome viral RT error prone - 1 or 2 errors per replication |
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Retroviral genes & proteins encoded
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Gag - structural proteins
Pol - reverse transcriptase, integrase Env - gp41, gp120 |
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HIV accessory proteins:
tat & rev |
promote viral gene expression
tat acts on host RNA polymerase rev acts on mRNA splicing |
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HIV accessory proteins:
Nef |
Nef enhances virus production & infectivity
interferense w/ immune recognition internalizes and downgrades CD4 & MHC I |
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HIV accessory proteins:
Vpu |
Vpu targes destruction of CD4 in ER
promotes release of virions from infected cell |
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Significance of infected macrophages in HIV disease
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HIV replicates in macrophages
infected macrophages participate in breakdown of BBB |
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Ways HIV kills CD4+ cells
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Directly: lyses during virion exit
Indirectly: -- killing of uninfected cells during cell fusion -- autoimmune processes oponize & phagocytose -- ADCC directed at gp120 |
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Characteristics of HIV disease
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Persistent, generalized lymphadenopathy
Oral lesions: thrush, hairy leukoplakia, pharyngitis Skin rash Anemia, thrombocytopenia Neurologic (usu. 2* to opportunistic ds) |
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Oral hairy leukoplasia
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seen in HIV+ patients
usu. CD4+ count 200-500/uL results from EBV infection filamentous white lesions along lateral borders of tongue |
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Type of anemia occuring most often in HIV+ patients
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hypoproliferative anemia
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6 neurologic infections 2* HIV infection
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toxoplasmosis
cryptococcus CMV TB syphillis Human T cell Leukemia Virus type I |
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HIV drug that causes myopathy
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AZT (aka: zidovudine)
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Neurologic manifestations of HIV, not due to opportunistic ds or neoplasm
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aseptic meningitis
mononeuritisi multiplex (necrotizing arteritis of peripheral nerves) myopathy |
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Problems with ELISA testing
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highly sensitive - many false positives
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Confirmatory HIV test
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Western Blot
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Describe HSV
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Large, enveloped dsDNA virus
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Can HSV infect non-dividing cells?
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YES!
codes many replication enzymes |
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Histologic changes during acute HSV infections
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multinucleated giant cells
degneration of epithelial cells, focal necrosis intranuclear inclusion bodies |
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Immune response to HSV characterized INITIALLY by...
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PMNs
then mononuclear infiltrate |
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HSV is HELD AT BAY via the _____ response
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CMI
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Which HSV episode is worse, initial or recurrent?
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initial
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What does HSV genome do in host nucleus?
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circularize
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How does HSV spread?
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cell to cell transfer (avoids circulating Ig)
intraneuronally via axons (--> infection of sensory and autonomic ganglia) |
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Herpetic whitlow
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infection of finger or nail area (HSV-1)
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Herpetic keratitis
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common cause corneal damage/blindess
involves conjunctiva & cornea HSV-1 |
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HSV Encephalitis
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Rare, but most common cause of viral encephalitis
reactivation of latent HSV in trigeminal nerve root + extension of lytic infection to temporoparietal area of brain |
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Disseminated Herpes
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in immunocompromised patients
extensive mucocutaneous infections organ involvement |
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Acute herpetic gingivostomatitis
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primary HSV-1 infection
children 6mo-5yrs Presenation -- abrupt onset -- high fever -- gingivitis -- vesicular lesions on oral mucosa |
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Acute perpetic pharyngotonsilitis
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oropharyngeal, primary HSV-1 infection
adults Presentation -- fever -- malaise -- HA -- sore throat -- vesicles rupture --> ulcerative lesions w/ grayish exudates on pharynx & tonsils |
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Herpes labialis
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most common manifestation of recurrent HSV-1
pain, burning, tingling, red papules then tiny, thin-walled, intraepidermal vesicles vesicles become pustular and ulcerate |
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Primary genital herpes
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HSV-1 or HSV-2
asymptomatic in most patients ds in women more severe than in men Presentation: -- fever, HA, malaise, myalgia -- local pain, itching, dysuria, discharge, lymphadenopathy -- ulcerative lesions |
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Recurrent genital herpes is preceded by a prodrome of...
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tenderness, pain and burning
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Recurrent genital herpes is more common with which strain?
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HSV-2
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Vesicles and ulcers are more painful in recurrent genital herpes for which sex?
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women
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Diagnosis of HSV
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culture - inoculating other cell lines with infectious secretions or lesions
HSV-1 and -2 differentiated by staining virus-infected cells with type-specific monoclonal Ab Enzyme immunoassays and IF - rapid and sensitive |
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Treatment of HSV
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Acyclovir
nucleoside analog converted by herpes TK --> monophosphate --> triphosphate --> viral DNA polymerase inhibition |
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New drugs for recurrent genital herpes
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Valacyclovir and Famicyclovir
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VZV structure
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enveloped dsDNA virus
has own envelope glycoproteins (unlike HSV) |
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what histologic effects to HSV and VZV share?
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multinucleated giant cells
intranuclear eosinophilic inclusion bodies |
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VZV grows best in...
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human diploid fibroblast cells
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VZV infection of the URT is followed by
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replication in regionsal LNs & 1* viremia
1* infection in reticuloendothelial system 2* viremia associated with T cells After 2* viremia, skin infection, then host immune response |
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Latency of VZV occurs in what structures?
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sensory ganglia
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What prevents REINFECTION of VZV?
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circulating Ab
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What controls REACTIVATION of VZV?
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CMI
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Manifestations of VZV infection
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chickenpox
herpes zoster (shingles) zoster multiplex zoster xine herpete myelitis Rasay-Hunt syndrome Keratitis |
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Chickenpox
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generalized vesicular rash
--- back of head and ears --- spread to neck, face, trunk, proximal extremities --- mucous membrane involvement --- fever early in disease course --- lesions appear in DIFFERENT stages of evolution |
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Herpes zoster
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vesicular eruption along dermatome, usually unilateral
postherpetic neuralgia common complication in older adults |
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Zoster sine herpete
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VZV infection reactivates without causing cutaneous vesicles
severe dermatomal PAIN, possible motor weakness and possible hypersthesia |
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Ramsay-Hunt syndrome
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VZV reactivation in geniculate ganglion
peripheral facial palsy pain in ear and face vesicles in external ear canal |
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Treatment of VZV
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Acyclovir (ages <18 yrs)
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Pox virus structure
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large, brick-shaped or ovoid, dsDNA virions
complex structure! |
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Where does pox virus replication occur?
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cytoplasm
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effects of pox virus on host cell function
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sweithc from cellular to viral protein synthesis
changes in cell membrane permeability cytolysis |
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Gaurnieri's bodies
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eosinophilic inclusions in cytoplasm
indicates small pox |
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pathogenesis of smallpox infection
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virus infects macrophages
migrates and multiples in LNs multiplies in spleen, BM, LNs --> 2* viremia fever & toxemia passes from WBCs to small vessels of dermis and throat mucosa initial onse to fenanthem and exanthem (pt is infectious) |
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Clinical characteristics of smallpox
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centriFUGAL rash: more lesions on limbs than trunk: palms/sores common
initial lesions vesicular (do not disappear with pressure) raised papules fill with thick, opaque fluid with central depression severe HAs and spinal pain |
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Borrelia Burgdorferi: characteristics on staining
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long, slender spirochete with multiple axial flagella
Giemsa or Wright stains |
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Borrelia Burgdorferi: pathogenically significant components
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OspC in mammals (antigenic); OspA in ticks
adhesins LPS - different from usual Gneg |
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How is B. burdorferi LPS unique?
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inflammatory properties
survives considerable periods in tissues may contribute to arthritis |
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Describe modulated immune responses of Lyme disease patients
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inhibition of mononuclear & NK cell function
decreased lymphocyte prolifeeration decreased cytokine production |
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Antibody to B. burgdoferi develops against what component?
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OspC
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Primary lesion of Lyme disease
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begins in first month after tick bite
lasts ~4 weeks macule/papule at site of bite -- expands to annular lesion with raised, red border & central clearing "bull's eye" expanding bull's eye ring "erythema migrans" |
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Symptoms concurrent with primary lesion of Lyme disease
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fever
fatigue myalgia HA joint pain mild neck stiffness |
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Secondary lesions of Lyme disease
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erythema migrans at sites other than that of tick bite
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2nd stage of Lyme disease
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Cardiac involvement
-- conduction abnormalities -- myocarditis Neurological -- Bell's palsy -- fluctuating meningitis -- peripheral neuropathy |
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Arthritis of Lyme disease
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usu. large joints
may become chronic w/ erosion of bone and cartilage |
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Treatment for Lyme disease
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doxycycline & amoxicillin
for neurological involvement: ceftriaxone or Penicillin G |
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Enterobacter spp.: morphology
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big bacteria with parallel sides & rounded ends
range from large coccobacilli to elongated, filamentous rods non-spore-forming |
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Enterobacter spp.: antigenic characteristics
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Gram negative
O antigen: LPS K antigen: polysaccharide capsule H antigen: petrichous flagella |
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Enterobacter spp.: characteristics on culture
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grow readily on simple media
facultatively anaerobic rapid growth ferment glucose reduce nitrates to nitrites oxidase negative |
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Enterobacter toxins
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endotoxin: LPS
exotoxins: proteins produced by E. coli, Shigella, Yersinia |
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Enterobacter spp. that are normal flora
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E. coli
Klebsiella Proteus |
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Diagnosing Enterobacter spp.
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Culture,
esp. with indicator media, e.g.: MacConkey agar |
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Common E. Coli
Type of pili - Type of capsule - Type of hemolysis - Type of lesion - Transmission - Opportunistic? |
Common E. coli
> 150 types O, H, K antigens Type 1b pili K1 capsule alpha-hemolysis inflammatory lesion transmitted from adjacent flora opportunistic |
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Shigella: disease states
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acute inflammatory colitis & diarrhea
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Shigella: classic dysentery syndrome triad
|
cramps
painful straining to pass stool (tenesmus) frequent, small volume, bloody, mucoid discharge |
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Most Shigella-associated diarrhea in U.S.
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watery with leukocytosis
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Shigella: constitutional symptoms
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fever
malaise anorexia myalgia most cases resolve 3-5 days |
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Shigella spp. causing most severe disease
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More severe - S. flexneri
MOST severe - S. dysenteriae type 1 (Shiga bacillus) |
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Shigella: diagnosis
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Culture with selective media:
- Hektoen enteric agar (inhibits facultative flora) slide agglutination with O group specific antisera |
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Shigella: treatment
|
Bactrim
If resistant, quinolones & 3rd generation cephalosporins |
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Salmonella: 2 important species
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S. enterica
S. typhi |
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S. enterica serotypes differ by...?
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H antigen (via phase variation)
host range |
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Where are S. enterica infections most common?
|
In industrialized countries as a result of food handling. Especially associated with poultry/eggs.
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S. enterica: pathogenesis
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ingested cells pass stomach acid,
swim through intestinal mucous layer, reach enterocytes & M cells pili - adherence to bowel membrane ruffles - drastically alter architecture on contact with M cells - engulf bacterium in endocytic vacuole to allow trancytosis inflammatory response in lamina propria bacteria phagocytosed by macrophages cause apoptosis of captor cell may cause local infection of intestinal mucosa & submucosa may enter bloodstream on contact with M cells, membrane ruffles dramatically alter normal architecture |
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Salmonellosis: 4 clinical patterns
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gastroenteritis
bacteriemia enteric fever asymptomatic carrier |
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Salmonella: gastroenteritis
|
begins 24-48 hours s/p ingestion
N/V/D with abdominal cramping predominant sign: diarrhea - 3-4 days - may be mild to dysentery-like fever in 50% of patients usually resolves spontaneously within 1 week |
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Salmonella: bacteremia
|
can be associated with gastroenteritis
common & severe in AIDS pts - septic shock, death may lead to metastatic colonization - atherosclerotic plaques, CA sites, meninges - bone -- usually long bones - sites of trauma - sickle cell injury --- skeletal prostheses |
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Salmonella: enteric fever
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multiorgan system infection
prolonged fever, sustained bacteremia profound involvement RES, esp. mesenteric LNs, liver, spleen fever rises stepwise over 72 hours relatively slow pulse at odds with fever faint rash (rose spots) - abdomen and chest for 1st few days constipation (1/3 pts have diarrhea) endotoxic complications hemorrhagic perforations through intestinal wall |
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Endotoxic complications of salmonellosis enteric fever
|
myocarditis
encephalopathy DIC |
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Most important complication of salmonellosis enteric fever
|
Hemorrhagic perforation through wall of terminal ileum
- at site of necrotic Peyer's patches - sometimes through proximal colon - usu. s/p 2 weeks disease |
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Salmonella: treatment
|
Chloramphenicol in developing countries
Ampicillin & Bactrim in U.S. 3rd generation cephalosporins & quinolones if severe/resistant |
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Yersinia: most important species
|
Y. pestis
Y. pseudotuberculosis Y. enterocolitica |
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Yersinia: pathogenesis
(not Y. pestis) |
invade M cells of Peyer's patches
- invasin binds integrins on cell surface - OMPs create contact secretion system, inject bacteria into host cell - cytotoxic events disrupt host cell function - replicate in RES cells, delay CMI response - formation of microabcesses - destruction of Peyer's patches & mesenteric LNs |
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Yersinia: virulence factors
(not Y. pestis) |
Invasin - binds integrins on surface of host cells
Yersinia OMPs (Yops) - major effector proteins - contact secretion system - allows infection of host cell PAI - Fe scavenging siderophore - enhance capacity replicate in RES |
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Yersinia: disease
|
acute mesenteric lymphadenitis
- mimics acute appendicitis - fever, abdominal pain |
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Y. enterocolitis disease
|
enterocolitis: fever, diarrhea, abdominal pain
enteric fever terminal ileus polyarthritic syndrome |
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|
Yersinia: treatment
|
diarrhea - hydration (self-limiting)
Y. pseudotuberculosis: ampicillin, cephalosporins, aminoglycosides, tetracyclines Y. enterocolitica - produces beta-lactamases - aminoglycosides, tetracyclines only |
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Brucella: characteristics on culture
|
G(-)
small coccobacillus nonmotile, non-spore-forming, non-acid fast 2 major antigenic variants: A&M (+) catalase (+) oxidase (+) urease (-) sugar fermentation |
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Brucella: reservoirs
|
zoonotic bacterium
cattle, swine, goats no human-to-human transmission |
|
|
Biggest factor in brucellosis prevention
|
pasteurizing milk
|
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|
Brucella: pathogenesis
|
facultative intracellular parasite of epithelial cells and professional phagocytes
penetrates skin and mucous membranes enters and multiplies in liver sinusoids, spleen, BM, other RES cells survival in host: - suppresses myeloperoxidase system - inhibits phagosome-lysosome fusion - impairs monocyte cytokine production Disease development: - small granulomas - bacteremia 2* release from RES cells |
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|
Brucella: immunity
|
control of disease - CMI
development of T-helper cell response associated with elimination of Brucella from macrophages |
|
|
Brucella: disease
|
Malaise, chills, high fever 7-21 days s/p infection
drenching sweats in late afternoon, evening fever: periodic, undulant, spikes at night - may last up to 2 years chronic illness: body aches, HA, anorexia <25% patients have RES enlargement, but splenomegaly most common localized infection: lung, bone, brain, heart, GU system |
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|
Brucella: diagnosis
|
isolation from blood or biopsy of liver, BM, LNs
cultures in 2-5 days, up to 2-4 weeks serologic tests - lower titers may reflect previous disease |
|
|
Brucella: treatment
|
doxycycline
may take 2-7 days to break fever |
|
|
Histoplasmosis: epidemiology
|
limited to endemic area
in soil associated with bat & bird droppings not transmitted human-to-human |
|
|
Histoplasmosis: pathogenesis
|
mode of infection: inhalation of mold microconidia
primary infection pulmonary mold develops into yeast in host readily phagocytosed by Mph & PMNs - conidia attach to CD18 integrin receptors - survive in phagocytes - catpure Fe & Ca from Mph - elevates phagolysosomal pH continued growth thru lymphatic spread - develop primary lesions --- similar to TB --- form calcified nodes |
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|
Histoplasmosis: hallmark infection
|
infection of LNs, spleen, BM, other RES
with intracellular growth in macrophages |
|
|
Histoplasmosis: immunity
|
CMI
delayed hypersensitivity skin test to mycelial antigen (histoplasmin) CD4+ T cell mediates lasting immunity |
|
|
Histoplasmosis: acute clinical presentation
|
vast majority caes asymptomatic or self-limiting fever & cough
xray: usu. (-), sometimes mediatstinal lymphadenopathy or slight pulmonary infiltrates (can mimic lung CA) histoplasmin skin test (+) s/p 3 weeks |
|
|
Histoplasmosis: disseminated disease
|
febrile illness with enlarged RES organs
involvement of CNS, skin, GI tract, adrenals painless ulcers on mucous membrane chronic may cause Addison's disease |
|
|
Histoplasmosis: diagnosis
|
blood and BM exam with special stains
culture required for firm diagnosis enzyme immunoassay (EIA) detects circulating antigen |
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|
Histoplasmosis: treatment
|
usually resolves spontaneously
Amphotericin B & itraconozole when treatment indicated |
|
|
Coccidioides immitis: morphology
|
dimorphic fungus: mold and SPHERULE
spherule - develops from invagination of fungal membrane and production of new cell wall - forms large multicompartmental structure endospores - compartments differentiate into uninucleate structures with thin walls C. immitus grows only as mold when not in living tissue, regardless of temperature septate hyphae produce thick-walled, barrel-shaped arthroconidia |
|
|
Coccidioides: pathogenesis
|
inhaled arthroconidia lodge in terminal bronchioles
outer wall of arthroconidia - antiphagocytic proteases attack host collagen, elastin, immunoglobulin |
|
|
Coccidioides: immunity
|
CMI
endospores destroyed only by cytokine-activated macrophages Ab production inversely related to disease progress |
|
|
Coccidioides: disease
|
> 50% asymptomatic
Valley Fever: - 1-3 weeks s/p infection - malaise, dry cough, fever - arthralgia - lasts 2-6 weeks - disseminated disease may cause meningitis |
|
|
Coccidioides meningitis: CSF findings
|
mononuclear cells predominate cell count
many PMNs often present |
|
|
Coccidioides: diagnosis
|
direct examination with KOH
skin and serological tests coccidioidin skin test remains (+) for life IgM in acute infection IgG coupled to complement quantitates disease |
|
|
Coccidioides: treatment
|
Amphotericin B in progressive disease
|
|
|
Sporothrix: general characteristics
|
S. schenckii
subcutaneous fungi dimorphic yeast - cigar-shaped, 2-5 mm cell wall L-rhamnose - unique component - complexes with mannose infectious form: mold - thin septate hyphae - produces clusters of conidia |
|
|
Sporothrix: epidemiology
|
ubiquitous saprophyte: hay, moss, soil, decaying vegetation
infection via traumatic inoculation exposure largely occupational |
|
|
Sporothrix: pathogenesis
|
both conidia and yeast bind ECM fibronectin, laminin, collagen
local multiplication --> acute pyogenic and granulomatous inflammation melanin production --> resistance to oxidative killing infection spreads along lymphatic drainage routes few organisms found in human lesions |
|
|
Sporothrix: immunity
|
CMI
|
|
|
Sporothrix: disease
|
skin lesion begins as painless papule
- wks - months s/p inoculation - papule enlarges & ulcerates draining lymph channels usu. thickened pustular or firm nodules around 1* SOI once ulcerated, lesions become chronic constitutional symptoms unusual bones, eyes, lungs, CNS < 1% all cases |
|
|
Sporothrix: treatment
|
cutaneous - saturated solution potassium iodide (SSKI)
systemic - amphotericin B or azoles |
