Sketchy Micro

  • “THE GOLDEN STAFF OF MOSES”
  • STAPH AUREUS
    • Catalase +; coagulase +; beta-hemolytic.
    • Plated on mannitol salt agar (selects for staph species).
    • Mannitol-fermenters turn bright yellow.
    • Virulence factor Protein A binds Fc portion of immunoglobulins, preventing opsonization and phagocytosis.  
    • Colonizes nares.
    • Causes: 
    • Pneumonia – bacterial infection secondary to primary viral infection (URTI); “patchy” infiltrates on CXR.   
    • Most common cause of septic arthritis.
    • Large abscesses > skin infections. 
    • Most common cause of osteomyelitis in adults.  
    • Acute bacterial endocarditis (R-sided, tricuspid valve) due to IVDU. 
    • Scalded skin syndrome by exfoliative toxin (protease). 
    • TSS (superantigen TSST -> non-specific binding of MHC Class II and T cell receptors -> overactivation -> cytokine storm. 
      • E.g., vaginal tampon, nasal packing. 
    • Rapid onset (1-8 hours) food poisoning (mayonnaise, custards, picnic foods) – vomiting > diarrhea.
    • MRSA (mercy) alters PBP for resistance against penicillin.
    • Treat MRSA with vancomycin. 

Nafcillin for methicillin-sensitive staph aureus (“Naf for Staph”).

  • STREP PYOGENES (GROUP A STREP)
    • Encapsulated (hyaluronic acid) – not immunogenic; beta-hemolytic.
    • Virulence factors: Streptolysin O lyses RBCs -> ASO antibodies for titer. Streptokinase converts plasminogen to plasmin. DNase depolymerizes DNA.
    • Can cause pyogenic infections: 
    • Impetigo (S aureus also can cause).
    • Pharyngitis (strep throat).
    • Cellulitis, erysipelas (well demarcated borders).  
    • SPE can cause: 
    • SpeA and SpeC (superantigens) cause scarlet fever – strawberry tongue, pharyngitis, wide-spread rash that spares the face. 
    • SpeA and SpeC cause TSLS mediated by super-antigen.
    • SpeB (protease) causes necrotizing fasciitis – invades fascia and spreads rapidly -> surgical emergency. 
    • Rheumatic fever only occurs following poorly treated pharyngitis.
    • Type II hypersensitivity reaction. 
    • M protein interferes with opsonization, anti-phagocytic; elicits strong humoral response (molecular mimicry).
      • Mimics myosin in heart (mitral valves -> mitral stenosis).
    • JONES criteria: 
      • Polyarthritis. 
      • Valvular damage, myocarditis, pericarditis.
      • Subcutaneous nodules on extensor surfaces, elbows, knees. 
      • Erythema marginatum. 
      • Syndenham’s chorea. 
    • PSGN occurs 2 weeks following initial strep infection e.g., pharyngitis or impetigo. 
    • Type III hypersensitivity reaction.
    • Coke colored urine.
    • Facial edema.
    • Penicillin doesn’t cure PSGN. 

Bacitracin-sensitive.

  • CLOSTRIDIUM TETANI 

    • Obligate anaerobe, spore-forming.
    • Puncture wound caused by rusty nails/barbed wire -> spores are embedded in flesh -> tetanus toxin travels retrograde and cleaves SNARE protein -> inhibits exocytosis of GABA and glycine -> Renshaw cells cant release GABA and glycine. 
    • Causes:
    • Spastic paralysis.
    • Risus sardonicus, lock jaw.  
    • Opisthothonus – powerful spasms of back muscles.  
    • Toxoid vaccine -> antibody response to toxin.

  • ESCHERICHIA COLI

    • Lactose-fermenter (pink on MacConkey agar); encapsulated (K antigen for serotyping); metallic green colonies on EMB agar; catalase +; fimbriae/pili. 
    • Causes:
    • #1 cause of UTI.
    • #1 cause of gram – sepsis via LPS endotoxin.
    • Neonatal meningitis (only if K antigen +).
    • EHEC – O157:H7 serotype associated with outbreaks; doesn’t ferment sorbitol.  
    • Associated with undercooked hamburger. 
    • Causes bloody diarrhea.
    • Shiga-like toxin – can cause HUS in children
      • Damage endothelial cells in glomerulus.
      • Platelet aggregation and decrease in platelet count.
      • Hemolysis. 
    • ETEC – heat-labile toxin increases cAMP; heat-stable toxin increases cGMP. 
    • Causes “traveler’s diarrhea” (watery), transmitted via water source e.g., recent travel to Mexico and drinking the water. 

  • V. CHOLERAE, V. PARAHAEMOLYTICUS, V. VULNIFICUS  

    • Comma-shaped; fecal-oral transmission due to poor sanitation; grows in alkali environment (acid-labile); oxidase +.
    • Doesn’t invade mucosa, uses fimbriae to attach -> enterotoxin -> activates Gs -> activates AC -> increases cAMP -> secretion of water into intestinal lumen.  
    • V. cholerae is endemic to developing countries.
    • Causes profuse (10-20L) rice watery diarrhea.  
    • Treatment: Oral rehydration with electrolytes. 
    • V. vulnificus, V. parahaemolyticus associated with raw seafood. 

  • HAEMOPHILUS INFLUENZAE 

    • Coccobaccilary shape.
    • Plate on chocolate agar plus factor V (NAD+) and X (hematin).
    • Aerosol transmission.
    • Causes:
    • Pneumonia.
    • Epiglottitis (cherry red epiglottis), inspiratory stridor, drooling.
    • Otitis media.
    • Meningitis (capsular form, type B).
    • Sepsis and septic arthritis in specnectomized, SCD patients.
    • Vaccine for type B capsule (polysaccharide conjugated to diphtheria toxoid) administered between 2-18 months of age.
    • Use beta-lactam antibiotic, ceftriaxone.
    • Rifampin prophylaxis for close contacts. 

  • MYCOBACTERIUM LEPRAE 

    • Thrives in cool temperatures, reservoir is armadillo (cooler core body temperature); AFB; facultative intracellular; thin rods. 
    • Causes: Leprosy = Hansen’s disease
    • Tuberculoid leprosy
    • Th 1 cells – cell-mediated immunity. 
    • Lepromin skin test +.
    • Dapsone and rifampin for 6 months. 
    • Lepromatous leprosy – classical presentation 
    • Th2 cells – humoral response.
    • Bacteria not contained in macrophages. 
    • Human to human transmission. 
    • Stocking glove neuropathy. Poorly demarcated lesions on extensor surfaces – large amounts of bacteria in the lesions. Profound facial deformity – leonine facies, loss of eyebrows, saddle-node deformity. 

Dapsone and rifampin plus clofazimine for 2-5 years, deformities and neuropathies may not be reversible.

  • BORRELIA BURGDORFERI
    • Can be visualized on light microscopy with Wright and Giemsa stain due to size.
    • Larvae feasts on white-footed mouse (main reservoir); white tail deer is obligatory host; humans are incidental dead-end hosts.
    • Northeastern US: NH, CT.
    • Causes: Lyme disease – Ixodes tick-borne disease.
    • 1. Erythema chronica migrans (bull’s eye rash) occurs within 1 month of tick bite, flu-like symptoms (fever and chills).
    • 2. Heart block caused by myocarditis; bilateral facial nerve palsy (Bell’s).
    • 3. Arthritis of large joints (migratory polyarthritis); memory difficulty/cognitive slowing/lymphocytic meningitis (encephalopathy).

Start treatment quickly: doxycycline; ceftriaxone for later stages. 

  • MYCOPLASMA PNEUMONIAE

    • No cell walls -> no gram stain.
    • Sterol in cell membrane for stabilization and flexibility.
    • Plate on Eaton’s agar (not routinely used).
    • Cold agglutinin test may be + due to IgM -> can lyse RBCs.
    • Associated with young adults (<30y) in areas of close contact e.g., military recruits.
    • Causes:
    • Atypical (“walking”) pneumonia (can’t isolate/culture, clinically asymptomatic).
    • CXR shows patchy infiltrate. Looks worse than presenting patient.
    • Treat with erythromycin, azithromycin. 

  • RICKETTSIA SPP.

    • Obligate intracellular (can’t produce NAD+ or CoA); weak gram – so poor gram staining; coccobacillary shape, Giemsa staining.
    • Weil-Felix test – uses Proteus vulgaris antigens that will cross-react with a patient’s serum antibodies against Rickettsia. 
    • Causes:
    • Headache
    • Fever
    • Vasculitis plus rash.
    • Treatment: doxycycline for all. 

  • RICKETTSIA RICKETTSII

    • Obligate intracellular (NAD+ and CoA provided by eukaryotic host); poor gram staining; Giemsa stain. 
    • Dermacentor (dog) tick bite.
    • Causes: RMSF
    • Rash starts 2-14 days following tick bite.
    • Rash moves from distal (early) extremities to proximal (later). 
    • Headache, fever, myalgias. 
    • Treat with doxycycline.