Microbiology Flashcards
intravascular sources of bacteremia
- transient: MCC teeth brushing
-
continuous: IE and other endovascular infections where there is a constant low level of bacteria being seeded over time→ biofilm
- mycotic aneurysm: damage to endothelial cells lining arteries→ seeding
- suppurative thrombophlebitis: damage to endothelial cells lining vein→ clot and seeding of clot by organisms
extravascular sources of bacteremia
bacteria enter blood stream through lymphatic sysmte from another side of infection
-
intermittent: MCC of sepsis; often associated with extravascular infection that provides portal of entry for bacteria
- usually coagulase(-) staph, S. aureus, candida
how much bacteria/mL can lead to septic shock?
1 bacterium/10mL of blood can lead to septic shock
- 3 cultures/24 hrs increases liklihood of picking up organism
- kids: tolerate more bacteria so it will probably show up with less culturing
sepsis
bacteremia with associated clinical manifestations:
- fever and shaking chills OR v. low temp
- decreased urination
- rapid pulse and RR
- N/V/D
- confusion esp. in elderly
severe sepsis
sepsis and associated organ dysfunction with:
- hypotension (systolic <90, MAP <70 that can be reversed with volume or vasopressors)
- confusion
- oliguria
- hypoxia not explained by respiratory disease
- met. acidosis
- DIC: protein C inhibits plasminogen activor inhibitor→decreased coagulation cascade
- hepatic dysfunction not explained by liver disease
septic shock
sepsis and hypotension requiring vasopressors despite fluid resuscitation
- perfusion abnormalities may include lactic acidosis, oliuria, AMS, acute lung injury
SIRS
whole body inflammatory state without proven source of infection
- TLR4 recognizes gram(-) LPS→ cytokine storm (TNFa, IL-1, IL-6)
- variation in number of acyl chains in lipid A can impact signaling through TLR4 and dramatically alter the host response
procalcitonin
differentiates infectious vs. noninfectious SIRS
- <0.5ng/mL: low risk for progression to severe sepsis/shock
- 0.5-2ng/mL: sepsis should be considered
- >2ng/mL: high risk for pression to severe sepsis/shock
malaria
- caused by 4 distinct species of protozoans
- p. falciparum is most lethal and MC strain in africa
- p. vivax: MC strain worldwide
- Duffy antigen on RBCs in erythrocyte receor for p. vivax (absence prevents p. vivax malaria)
- HbS, HbC, and thalassemias provide protection
cyclic pattern of malaria symptoms
- cold stage: lysis of RBC→ feeling of intesne cold for 15-60 mins
- hot stage: circulating merozoites and immune response→ intense heat, dry burning skin, throbbing headage for 2-6 hours
- sweating stage: merozoates are infecting other RBCs→ produse sweating, decling temp, exhaustion for 2-4 hours
recrudescence of malaria
parasitemia falls below detectable levels and then later increases to a detectible parasitemia
relapse of malaria
sporozoites invade hepatocytes, develop into schizonts and may or may not be observed in circulation; individual may be asymptomatic
p. falciparum
more acute and severe than malaria caused by other plasmodium species
-
PfEMP-1: receptor on 100% of RBCs enabling infection of all RBCs (other parasites have less access)
- cerebral malaria: sticking of RBCs along BBB→ poor oxygenation
- placental malaria: infected RBCs sequester in maternal circulation of placenta
trypanosome cruzi
chronic parasitic infection transmitted by reduviid bug→ chagas disease
- not intracellular; chronically can infect heart, colon, esophagus
- romana sign (inflammed eye)
leishmaniasis
sand fly regurgitation→ multiplication in histocytes; comes in cutaneous (MC), mucocutanous, and visceral forms
toxoplasmosis gondii
leading cause of death attributed to foodborne illness in US; 60 million carry parasite but few are symptomatic
- detection with toxo-specific antibodies, inteprete whether it is new or reccurant infection
- in newborn: chorioretinitis, hydrocephalus, intracranial calcifications; highest risk of transmission in 3rd trimester; most babies do not initially show signs but develop disabilities later
- in immunocompromised: leading cause of focal CNS disease in AIDS; eye disease (retinochoroiditis) can result rom congenital infection or infection after birth→ white fluffy patches on fundoscopy
borrelia
- spirochetes that are large enough to see with microscope
- b. burgdorferi (lyme dsease)
- relapsing fever
borrelia burgdorferi
- lyme disease; vectored by deer ticks, requires 24 hours to transmit
- serolog: confirms exposure but not disease and not promptly
- stage 1: flulike with erythema migrans
- stage 2: musculoskeletal and/or neurologic symptoms
- stage 3: additional neurologic symptons, post-lyme syndrome with lingering neurological sequlae
- treat: amoxicillin or doxy for 10-30 days (lingering symptoms are due to damage, not bacteria)
- potential for jarisch-herxheimer rxn
relapsing fever
- louse or tick borne (louse is more severe, tick is more likely in US)
- borrelia immediately enter bloodstream→ repeated rounds of bacteremia and clean up by IL-10→ spirochetes vary surface antigens
- repeated high fevers with wellperiods between
- diagnosis: peripheral blood smear (spirochetes visible during febrile periods)
- treatment: tetracycline (Jarisch-Herxheimer rxn)
rickettsia
- small cocci to short-rods transferred by arthropod vectors
- obligate intracellular parasite (grown in vitro in tissue culture)
- reproduce by binary fission
- Omp A&B, T4SS, phospholipase A1, ActA
- diagnose with immunochemical staining
- rocky mountain spotted fever
- typhus
- treat: doxy (even kids); chloramphenicol for pregnany and allergic patients
rocky mountain spotted fever
- rickettsial disease spread by dog ticks and mice
- eschar at tick site (mediterranean spotted fever also has this)
- pitecheal rash on extremities that spreads towards trunk
- treatment: doxy
typhus
- humans are normal host and reservoir; body louse as vector
- abrupt onset of fever/chills and unremitting headache
- Brill-Zinsser Disease: recrudescent form of epidemic typhus (maay be seen in geriatrics who had typhus in WWII)
- treatment: doxy (even for small children)
ehrlichia
- human monocytic ehrlichiosis: tiny gram (-) obligcate intracellular parasite that replicate in WBC
- severe headache, fever/shaking, chills one week after tick bite
- morulae on blood smear
- treatment: doxy (even for children)
anaplasmosis
causes human monocytic anapalsmosis (similar to erlichiosis, obligate intracellular parasite that survives and mulltiplies in early endosome of WBC)
S. aureus
- gram+ coagulase+ (doesn’t spread)
- virulence factors: protein A, capsule, toxins (exfoliatin, TSS)
- surface lesions
- impetigo: due to mix of s. aureus and s. pyrogenes; mupiricin ointment
- exfoliating rash of TSS
- scalded skin syndrome due to exfolatin (no infection at site just circulating toxin)
- furunculitis: bacterial infection of hair follicles and sweat glands; abcess drainage and antibiotics
s. epidermidis
- gram+ coagulase(-) novobiocin sensitive
- surface lesions: infection piercings→ biofilm with chronic low grade infection (Au, Ag less likely to cause infection)
- no treatment except for removal of piercing/catheter (organism is protected in biofilm)
streptococci
- subcutaneous infection: cellulitis/erysipelas: usually due to s. pyogenes, can spread (coagulase -) and break down tissues
- deep skin: necrotizing fascitis: usually group A strep with high proteases; mysterious etiology (infects healthy individuals), rapidly spreading
- post strep glomerulonephritis: 3-4 wks s/p strep skin infection with specific M protein-types; lesions are sterile (no treatment)
scabies
- mites→ scabies: itching due to delayed hypersensitivity reaction
- treat with topical steroids (itch) and malathion (antimite)
