STEP/Level 1 Microbiology

Modified version of Mario's deck from Quizlet

Characteristics of Staphylococcus aureus

Gram (+) cocci growing in Grape-like clusters. Catalase (+), Coagulase (+), β-hemolytic. Mannitol-fermenter --> Mannitol salt agar; secretes Protein A & Toxic Shock Syndrome Toxin-1 (TSST-1)

Protein A

Virulence Factor of Staphylococcus aureus; Binds Fc region of IgG, inhibiting complement activation & phagocytosis.

Toxic Shock Syndrome Toxin-1 (TSST-1)

Virulence Factor of Staphylococcus aureus; Simultaneously binds to MHC-II and T-cell receptors outside the antigenic grove, activating T-cells to stimulate the release of IFN-γ and IL-2.

Clinical Presentation of Staphylococcus aureus

Cellulitis, Impetigo, Abscess, Septic arthritis (most common >2yo), Osteomyelitis (most common pathogen), Toxic Shock Syndrome (TSS); Food poisoning - Nonbloody diarrhea & emesis; heat-stable enterotoxin --> Not killed by cooking; Pneumonia (often after influenza infection; also in IV drug users); Endocarditis

Treatment of Staphylococcus aureus

Oxacillin or clindamycin (penicillin allergy); vancomycin

Toxic Shock Syndrome (TSS)

Caused by S. aureus Toxin. Associated with prolonged tampon use & nasal packing. Presents with Flu-like symptoms - Fever, chills, NVD, myalgia, HA; Rash - Transient, erythematous, macular (sunburn-like); can involve medial thighs, palms, & soles; Desquamation - 1-2 weeks after onset; Septic shock --> End-organ failure. Lab Findings of ↑AST, ↑ALT, ↑Bilirubin

Characteristics of Staphylococcus epidermidis

Gram (+) cocci forming Grape-like clusters. Catalase (+), Coagulase (-), Novobiocin-sensitive, Urease (+), Mannitol-nonfermenter. Forms biofilms.

Clinical Presentation of Staphylococcus epidermidis

Infects prosthetic devices (e.g. hip arthroplasty & heart valve) and IV catheters through biofilm formation and adherence

Treatment of Staphylococcus epidermidis

Oxacillin or clindamycin (allergy); vancomycin

Characteristics of Staphylococcus saprophyticus

Gram (+) cocci forming Grape-like clusters. Catalase (+), Coagulase (-), Novobiocin-resistant, Urease (+)

Clinical Presentation of Staphylococcus saprophyticus

2nd most common cause of uncomplicated UTI in young females (preceded by E. coli).

Treatment of Staphylococcus saprophyticus

1st cephalo. (cephalexin), amoxicillin, fluoroquinolone (cipro), nitrofurantoin, TMP-SMX.

Urease

Hydrolyzes urea to ammonia & CO2 Increases pH. Predisposes to struvite (magnesium ammonium phosphate) stones. Found in Proetus, Cryptococcus, H. pylori, Nocardia, Klebsiella, S. epidermidis, & S. saprophyticus.

Characteristics of Streptococcus pneumoniae

Gram (+) lancet-shaped diplococci that Forms chains. Catalase (-), α-hemolytic, Encapsulated. Facultative anaerobe. Optochin-sensitive, Bile-soluble, IgA1 protease

Virulence Factors of Streptococcus pneumoniae

Encapsulated (polysaccaride inhibiting phagocytosis & complement fixation); IgA1 protease (cleaves IgA, promoting mucous membrane colonization)

Clinical Presentation of Streptococcus pneumoniae

Pneumonia - Rusty-colored sputum; lobar or bronchopneumonia; most common pathogen in CAP; young children (>4 weeks old), adolescents, adults, nursing home pts, IV drug users; Meningitis - Infants (1mo-2yo), children/adolescents/young adults (2yo-20s), adults, & elderly; Otitis media (most common followed by H. flu); Overwhelming Postsplenectomy Infection (OPSI) - Sepsis in pts w/ asplenia or SCD due to susceptibility to encapsulated bacteria; Sinusitis

Treatment of Streptococcus pneumoniae

Penicillin, 3rd cephalo. (ceftriaxone). If Allergy, Macrolide (23S rRNA of 50S)

Encapsulated Bacteria (Polysaccharide)

Inhibits phagocytosis, complement fixation, & antibody-dependent killing mechanisms. Cannot be presented to T-cells. Has to be opsonized and then cleared by spleen. Used for vaccination. Found in Pseudomonas, S. pneumoniae, H. flu, N. meningitidis, E. coli, Salmonella, Klebsiella, & GBS.

IgA Protease

Cleaves mucosal IgA --> Adherence & colonization of mucous membranes. Found in Neisseria spp., H. flu, S. pneumoniae, & Proteus

Characteristics of Viridans Streptococci (S. mutans, S. mitis, S. sanguinis)

Gram (+) cocci that Forms chains. Catalase (-), α-hemolytic. Facultative anaerobe. Optochin-resistant, Bile-insoluble

Clinical Presentation of S. mutans, S. mitis, & S. sanguinis

Dental caries, Subacute bacterial endocarditis; Forms biofilms

Treatment of S. mutans, S. mitis, & S. sanguinis

Penicillin, 3rd cephalo. (ceftriaxone); If Allergy, Macrolide (23S rRNA of 50S)

Characteristics of Streptococcus pyogenes [GAS]

Gram (+) cocci that Forms chains; Catalase (-), β-hemolytic, Encapsulated. Facultative anaerobe, Bacitracin-sensitive. Pyrrolidonyl arylamidase [PYR] (+)

Erythrogenic exotoxin A/B/C

Virulence Factor of Streptococcus pyogenes [GAS]. Binds to T-cell receptors & MHC-II on APCs, releasing large amounts of TNF-α, IL-1, IL-2, and IFN-γ --> Scarlet fever.

Streptococcal pyrogenic exotoxins

Virulence Factor of Streptococcus pyogenes [GAS]. Similar to erythrogenic

Streptolysin O

Virulence Factor of Streptococcus pyogenes [GAS]. Degrades cell membranes, mainly of RBCs --> β-hemolysis

DNase

Virulence Factor of Streptococcus pyogenes [GAS]. Destroys neutrophils --> Potentiates infection and transmission

Streptokinase

Virulence Factor of Streptococcus pyogenes [GAS]. Catalyzes the conversion of plasminogen to plasmin --> Thrombolysis.

Hyaluronic acid capsule

Virulence Factor of Streptococcus pyogenes [GAS]. Inhibits phagocytosis.

M protein

Virulence Factor of Streptococcus pyogenes [GAS]. Prevents opsonization by C3b (First Aid says phagocytosis). Structurally similar to human myosin --> Acute rheumatic fever.

Clinical Presentation of Streptococcus pyogenes [GAS]

Pharyngitis (can progress to rheumatic fever), Tonsillitis (can progress to rheumatic fever), Peritonsillar abscess, Otitis media

Clinical Presentation of Streptococcus pyogenes [GAS]; (Pyogenic)

Impetigo: “Honey-crusted” lesions, erythematous papules/pustules. Nonbullous --> (-) Nikolsky sign. Highly contagious. Regional lymphadenopathy; Erysipelas: Superficial skin infection of upper dermis and superficial lymphatics. Sudden-onset, tender, sharply demarcated, erythematous, edematous, warm patches and plaques. Most commonly lower limbs; Cellulitis; Necrotizing fasciitis

Clinical Presentation of Streptococcus pyogenes [GAS] (Toxigenic)

Scarlet fever: Induced by erythrogenic exotoxin A. Flushed face w/ circumoral pallor, strawberry tongue, blanching sandpaper-like rash that spreads from neck --> trunk & extremities but spares palms & soles, fever, pharyngeal erythema, and LAD; toxic shock-like syndrome (TSS)

Acute Rheumatic Fever

Develops after Streptococcus pyogenes [GAS] pharyngitis or tonsillitis. Type II hypersensitivity rxn to M protein. Early valvular regurgitation --> Late valvular stenosis (mitral > aortic >> tricuspid).

Poststreptococcal Glomerulonephritis

2-4w after S. pyogenes [GAS] impetigo, pharyngitis, or tonsillitis. Presents with Nephritic syndrome --> Hematuria, proteinuria, HTN, & edema. **Type III** hypersensitivity rxn (Ag-Ab immune complexes deposit w/n glomerular basement membrane & activate complement).

Pathology of Poststreptococcal Glomerulonephritis

Light Microscopy = Enlarged & hypercellular glomeruli.
Immunofluorescence = Granular ("starry sky") appearance due to IgG, IgM, & C3 along GBM & mesangium.
Electron Microscopy = "Subepithelial humps" (immune complexes between epithelial cell layer & GBM).

Characteristics of Streptococcus agalactiae [GBS]

Gram (+) cocci that Forms chains; Catalase (-), β-hemolytic, Encapsulated. Facultative anaerobe. Bacitracin-resistant, Pyrrolidonyl arylamidase [PYR] (-). CAMP factor: Enlarges the hemolysis area in a culture formed by S. aureus; Hippurate (+)

Clinical Presentation of Streptococcus agalactiae [GBS]

Neonatal meningitis (<6m), Neonatal pneumonia (<4w), Neonatal sepsis; Colonizes vagina --> Screen at 35-37w. Typically asymptomatic in adults.

Treatment of Streptococcus agalactiae [GBS]

Treatment: Penicillin, 1st cephalo., 2nd cephalo. If Allergy, Clindamycin (lincosamide; 50S)

Characteristics of Streptococcus gallolyticus

Gram (+) cocci, Forms chains, Catalase (-), β-hemolytic/γ-hemolytic. Facultative anaerobe. Grows in bile (but not 6.5% NaCl)

Clinical Presentation of Streptococcus gallolyticus

Endocarditis --> ↑ Risk of colorectal carcinoma; Bacteremia

Treatment of Streptococcus gallolyticus

Penicillin or 3rd cephalo. + gentamicin (aminoglycoside; 30S)

Characteristics of Enterococcus faecium & E. faecalis

Gram (+) diplococci that Forms chains. α-hemolytic/γ-hemolytic; Facultative anaerobe, Pyrrolidonyl arylamidase [PYR] (+). Grows in bile & 6.5% NaCl. Normal colonic flora.

Clinical Presentation of Enterococcus faecium & E. faecalis

Often occurs after GI/GU procedure: UTI, Cholecystitis, Endocarditis

Treatment of Enterococcus faecium & E. faecalis

Ampicillin (inherent cephalo. & penicillin resistance) or (if Allergy) Vancomycin

Treatment of Vancomycin-resistant enterococcus (VRE)

Nosocomial infections --> Linezolid (oxazolidinones; 23S rRNA of 50S) or daptomycin (lipopeptide; incorporates K+ channel pores to depolarize cell membranes)

Characteristics of Clostridioides difficile

Gram (+) rod, Spore-forming, Obligate anaerobe, Toxin A (enterotoxin) & Toxin B (cytotoxin) damage enterocytes and cause watery diarrhea.

Clinical Presentation of Clostridioides difficile

Post-antibiotics course (clindamycin, ampicillin, cephalosporins, fluoroquinolones); Symptoms of Watery, malodorous diarrhea (>3/day), abd. pain (cramping) & tenderness, fever, dehydration. May progress to pseudomembranous colitis. Fulminant/severe infection: Paralytic ileus, toxic megacolon, shock

Treatment of Clostridioides difficile

Vancomycin (oral), or metronidazole (nitroimidazole; DNA-damaging free radicals)

Characteristics of Clostridium tetani

Gram (+) drumstick-shaped rod. Spore-forming, Obligate anaerobe. Uses Tetanospasmin & Tetanolysin (proteases that cleave SNARE proteins involved in neurotransmission)

Tetanospasmin

Exotoxin of Clostridium tetani that spreads by retrograde axonal transport to CNS. Blocks release of GABA & glycine, causing tonic-clonic spasms & autonomic instability

Tetanolysin

Exotoxin of Clostridium tetani that causes hemolytic effects.

Clinical Presentation of Clostridium tetani

Tetanus, Spastic paralysis; Trismus = Lockjaw; Risus sardonicus = Raised eyebrow & open grin; Opisthotonos = Spasm of spinal extensors --> Arched back

Treatment of Clostridium tetani

Penicillin G, or metronidazole (nitroimidazole; DNA-damaging free radicals)

Characteristics of Clostridium botulinum

Gram (+) club-shaped rod. Spore-forming; Has flagella; Obligate anaerobe. Uses Botulinum toxin

Botulinum toxin

Exotoxin of Clostridium botulinum; Heat-labile toxin that damage SNARE proteins. Prevents ACh release at neuromuscular junction, inducing flaccid muscle paralysis.

Clinical Presentation of Clostridium botulinum

Infection via ingestion or wounds --> Neuroparalysis (w/o sensory deficits) and/or GI symptoms; Flaccid muscle paralysis that descends caudally & is symmetrical; Ptosis; Ophthalmoplegia (paralysis of EO muscles) --> Diplopia, mydriasis, loss of accommodation; Dysphagia, dysarthria; Dyspnea (w/ respiratory involvement); NV followed by constipation.

Treatment of Clostridium botulinum

Botulism immune globulin (infantile) or antitoxin (adult).

Wound botulism

Clostridium botulinum infection found in IV drug users

Floppy baby syndrome

Infantile botulism. Ingestion of spores (honey or juice) --> Constipation (often first symptom), hypotonia, poor feeding, ptosis, descending palsy.

Foodborne botulism

Poorly pasteurized canned food (may appear to be "bulging" due to bacterial gas production), such as vegetables in spore contaminated soil.

Characteristics of Clostridium perfringens

Gram (+) club-shaped rod. Spore-forming; Does not have flagella; Obligate anaerobe, has α-toxin

α-toxin

Exotoxin of Clostridium perfringens; Lecithinase, a phospholipase, causes myonecrosis (gas gangrene) & hemolysis.

Myonecrosis (gas gangrene)

Clinical Presentation of Clostridium perfringens; Severe pain, bullae, edema, soft tissue crepitus, hematogenous spread leading to septic shock and multiorgan failure.

Food poisoning/Enterocolitis

Clinical Presentation of Clostridium perfringens; Poorly cooked or unrefrigerated spore-contaminated food (e.g. meat, legumes) --> 10-12hr incubation --> Abdominal cramping & watery diarrhea that resolve in <24hrs.

Treatment of Clostridium perfringens

Piperacillin-tazobactam + clindamycin (lincosamide; 50S)

Characteristics of Listeria monocytogenes

Gram (+) rod. Has flagella --> Tumbling motility; Facultative anaerobe, Facultative intracellular. Cold resistance. Actin rocket tail & Listeriolysin O

Actin rocket tail

Virulence Factor of Listeria monocytogenes. Allows intracellular movement & cell-to-cell spread for evading antibodies

Listeriolysin O

Virulence Factor of Listeria monocytogenes. Generates pores in phagosomes, allowing its escape into cytoplasm.

Clinical Presentation of Listeria monocytogenes

Listeriosis; Meningitis or sepsis in immunocompromised pts, neonates (0-6m), and elderly; Amnionitis, spontaneous abortion, or sepsis in pregos.

Treatment of Listeria monocytogenes

Ampicillin or penicillin G

Granulomatosis infantiseptica

Clinical Presentation of Listeria monocytogenes; Transplacental TORCH infection --> Disseminated abscesses, respiratory distress, skin lesions developed in utero.

Listeriosis

Clinical Presentation of Listeria monocytogenes; Ingestion of contaminated food (primarily raw milk but also cold deli meat) that can lead to either Mild, self-limiting flu-like illness (fever, HA, BAs, malaise) or gastroenteritis (watery diarrhea) in immunocompetent adults.

Characteristics of Corynebacterium diphtheriae

Gram (+) club-shaped rod in angular arrangements. Facultative anaerobe. Neisser stain & Löffler medium --> Metachromatic granules (red & blue). Elek test (+) for toxin. Cystine-tellurite agar --> Black colonies. Uses Diphtheria toxin

Diphtheria toxin

Exotoxin of Corynebacterium diphtheriae. Inhibits protein synthesis via ADP-ribosylation of elongation factor 2 (EF-2) --> Leads to necrosis in pharyngeal, cardiac, and CNS tissue.

Clinical Presentation of Corynebacterium diphtheriae

Diphtheria; Pseudomembranous pharyngitis; "Bull's neck"; Myocarditis & arrhythmias (systemic dissemination); Reversible polyneuropathy (systemic dissemination) --> Soft palate paresis, ophthalmoplegia (Strabismus due to paresis/paralysis of 1+ extraocular muscles), limb palsy, diaphragmatic palsy

Treatment of Corynebacterium diphtheriae

Macrolide (23 rRNA of 50WS) or Penicillin G

"Bull's neck"

Clinical Presentation of Corynebacterium diphtheriae; Cervical LAD & soft tissue swelling that can lead to airway obstruction.

Pseudomembranous pharyngitis

Clinical Presentation of Corynebacterium diphtheriae. Grayish-white membrane on posterior pharyngeal wall and/or tonsils. Heavy bleeding when attempting to scrape off.

Characteristics of Bacillus anthracis

Gram (+) bamboo-shaped rod. Spore-forming. Medusa head: Colonies show a halo of projections. Has Polypeptide capsule and Anthrax toxin (Protective Antigen, Lethal Factor, & Edema Factor)

Anthrax Toxin

Exotoxin of Bacillus anthracis. Protective Antigen. Lethal Factor: Inhibits MAP kinase --> Macrophage apoptosis. Edema Factor: Binds to calmodulin & gains adenylate cyclase activity, increasing cAMP --> Cellular edema.

Clinical Presentation of Bacillus anthracis

Cutaneous anthrax: Painless papule surrounded by vesicles --> Ulcer w/ surrounding edema & black eschar (necrotic but painless) --> (Uncommon) bacteremia & death; Pulmonary anthrax: Inhalation of spores --> Flu-like symptoms initially --> Fever, pulmonary hemorrhage, mediastinitis w/ widened mediastinum on CXR, septic shock.

Treatment of Bacillus anthracis

Ciprofloxacin (fluoroquinolone; inhibits DNA topoisomerase IV) [or penicillin G] + clindamycin (lincosamide; 50S) [or linezolid]. Add meropenem for meningitis.

Characteristics of Bacillus cereus

Gram (+) rod. Spore-forming. Facultative anaerobe. Cereulide (Enterotoxin I) = Emesis. Enterotoxin II = Diarrhea

Clinical Presentation of Bacillus cereus

Reheated rice syndrome: Spores survive cooking rice. Keeping rice warm leads to spore germination & enterotoxin formation. Emetic type: NV w/n 1-5 hrs. Diarrheal type: Watery diarrhea & abdominal pain w/n 8-18 hrs.

Characteristics of Tropheryma whipplei

Gram (+) rod. Intracellular (macrophages). Periodic acid-Schiff (PAS) stain (+) for infected foamy macrophages in intestinal lamina propria (biopsy). Non-acid-fast

Clinical Presentation of Tropheryma whipplei

Whipple disease: Most commonly occurs in >40yo males exposed to sewage. Four cardinal symptoms of Arthralgias (migratory of large joints; often first symptom), Weight loss, Diarrhea/steatorrhea (malabsorption disorder), Abdominal pain (colicky). May also present w/ Dermatologic hyperpigmentation, Fever, LAD, AMS, Respiratory symptoms, Endocarditis

Treatment of Tropheryma whipplei

-2 weeks IV ceftriaxone + 1 year of SMP-TMX (Inhibits folate synthesis, dihydropteroate synthase, & DHFR)

Characteristics of Neisseria meningitidis

Gram (-) diplococci. Aerobe, Polysaccharide capsule, Facultative intracellular. Grows in Thayer-Martin agar. Maltose & glucose fermenter. IgA1 Protease, Lipooligosaccharide (LOS), & Adhesins

Clinical Presentation of Neisseria meningitidis

Meningitis; ↑↑ Opening pressure / ↑ PMNs / ↑ Protein / ↓ Glucose; Meningoencephalitis, Meningococcemia, Waterhouse-Friderichsen syndrome, Non-blanching petechial rash; Hypoaldosteronism --> Hyponatremia, hyperkalemia, hypotension, metabolic acidosis.; Hypocortisolism --> hypoglycemia, fatigue, NVD. Elevated ACTH --> Hyperpigmentation; DIC = ↓ platelets / ↑ bleeding time, PT, PTT

Clinical Presentation of Meningitis

Neck stiffness, cutaneous petechiae (trunk & lower limbs), fever, hypotension, tachycardia. Brudzinski (neck flexion) & Kernig (hip flexion + knee extension) signs. Close quarters environments (dorms & barracks).

Meningoencephalitis

Inflammation of brain parenchyma. Focal neurologic signs, seizures, AMS.

Waterhouse-Friderichsen syndrome

Acute primary adrenal insufficiency caused by adrenal hemorrhage.

Meningococcemia

Systemic infection, often occurs w/ meningitis. High fever, organ failure, and petechial/purpuric rash.

Treatment of Neisseria meningitidis

3rd cephalo. (ceftriaxone) or penicillin G. Prophylaxis (Only close contacts) with Ciprofloxacin (fluoroquinolone; , rifampin, OR ceftriaxone)

Characteristics of Neisseria gonorrhoeae

Gram (-) diplococci. Aerobe. NO capsule. Facultative intracellular (often w/n neutrophils). Grows on Thayer-Martin agar. Maltose fermenter, Glucose nonfermenter; has IgA1 Protease, Lipooligosaccharide (LOS), & Adhesins

Gonorrhea

STD Presentation of Neisseria gonorrhoeae; Mucopurulent, yellow, malodorous discharge; dysuria; bleeding & pain during pelvic exam. Cervicitis in females. Urethritis/prostatitis/epididymitis/orchitis in males (latter two --> scrotal pain & swelling). No lesions or LAD.

Pelvic Inflammatory Disease

STD Presentation of Neisseria gonorrhoeae; Cervical motion tenderness, adnexal tenderness, fever, pelvic pain, abd. pain, NV, dyspareunia, menorrhagia --> Ectopic pregnancy, infertility.

Fitz-Hugh-Curtis syndrome

STD Presentation of Neisseria gonorrhoeae; PID progresses to perihepatitis (infection & inflammation of liver capsule). RUQ pain & violin string adhesions.

Clinical Presentation of Neisseria gonorrhoeae (Non-Sexual)

Neonatal conjunctivitis (Occurs 2-5 days after birth)

5)Purulent gonococcal arthritis (septic arthritis); Arthritis-dermatitis syndrome, Polyarthralgia (Transient, asymmetrical arthritis), Tenosynovitis, Dermatitis