USMLE / Lektion

Microbiology

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  • Sexually transmitted diseases
    AIDS (HIV): Opportunistic infections, Kaposi sarcoma, lymphoma Chancroid (H ducreyi): Painful genital ulcer with exsudate, inguinal adenopathy Chlamydia (C trachomatis D-K): Urethritis, cervicitis, epididymitis, conjunctivitis, reactive arthritis, PID Condylomata acuminata (HPV-6, -11): Genital warts, koilocytes Genitalherpes (HSV-2): Painful penile, vulvar, or cervical vesicles and ulcers Gonorrhea: Urethritis, cervicitis, PID, prostatitis, epididymitis, arthritis, creamy purulent discharge Granuloma inguinale (Donovanosis, Klebsiella granulomatis): Painless, beefy red ulcer that bleeds readily on contact, not common in US Hepatitis B: Jaundice Lymphogranuloma venereum (C trachomatis L1-L3): Infection of lymphatics, painless genital ulcers, painful lymphadenopathy Syphilis: Primary - painless chancre, secondary - skin rashes, condyloma lata, tertiary - gummas, tabes doralis, aortitis, Argyll Robertson pupil Trichomoniasis: Vaginitis, strawberry cervix, motile in wet prep
  • Pelvic inflammatory disease
    Chlamydia trachomatis (subacute, often undiagnosed) and Neisseria gonorrhea (acute) - Cervical motion tenderness (chandelier sign), purulent cervical discharge - May include salpingitis, endometritis, hydrosalpinx, tubo-ovarian abscess- Salpingitis is risk factor for ectopic pregnancy, infertility, chronic pelvic pain, and adhesions Fitz-Hugh-Curtis syndrome: Infection of the liver capsule and "violin string" adhesions of peritoneum to liver
  • Nosocomial infections
    Aspiration (2° to mental status, old age): polymicrobial gram -, often anaerobes- Right lower lobe infiltrate or right upper/middle lobe; purulent malodorous sputum Intravascular catheters: S aureus (including MRSA), S epidermidis, Enterobacter  Mechanical ventilation: P aeruginosa, Klebsiella Renal dialysis unit: HBV, HCV Urinary catherization: E coli, Klebsiella, Proteus Water aerosoles: Legionella
  • Pleomorphic bacteria
    No cell wall - Chlamydia (Giemsa)- Rickettsia (Giemsa)- Mycoplasma (contain sterols, which do not Gram stain)- Anaplasma, Ehrlichia- Haemophilus
  • Intracellular bugs
    Obligate intracellular: Chlamydia, Coxiella, Rickettsia. - Rely on host ATP. Facultative intracellular: Neisseria, Salmonella, Brucella, Mycobacterium, Listeria, Francisella, Legionella, Yersinia pestis.
  • Type III secretion system
    Also known as "injectisome." Needle-like protein appendage facilitating direct delivery of toxins from certain gram ⊝ bacteria (eg, Pseudomonas, Salmonella, Shigella, E coli) to eukaryotic host cell.
  • Bacterial virulence factors
    These promote evasion of host immune response. Protein A: Binds Fc region of IgG. Prevents opsonization and phagocytosis.- Expressed by S aureus. IgA protease: Enzyme that cleaves IgA, allowing bacteria to adhere and to colonize mucous membranes.- Secreted by Neisseria, S pneumoniae, H influenzae type b. M protein: Helps prevent phagocytosis. Shares similar epitopes to human cellular proteins (molecular mimicry); possibly underlies the autoimmune response seen in acute rheumatic fever.- Expressed by group A streptococci.
  • Transformation
    Competent bacteria can bind and import short pieces of environmental naked bacterial chromosomal DNA (from bacterial cell lysis).  - The transfer and expression of newly transferred genes is called transformation. - A feature of many bacteria, especially S pneumoniae, H influenzae type b, and Neisseria. - Adding deoxyribonuclease degrades naked DNA, preventing transformation.
  • Mycobacteria
    - Mycobacterium tuberculosis (TB, often resistant to multiple drugs)- M avium-intracellulare (causes disseminated, non-TB disease in AIDS; often resistant to multiple drugs). Prophylaxis with azithromycin when CD4+ count <50 cells/mm3.- M scrofulaceum (cervical lymphadenitis in children).- M marinum (hand infection in aquarium handlers). - All mycobacterial are acid-fast organisms.- Cord factor (trehalose dimycolate) creates a "serpentine cord" appearance in virulent M tuberculosis strains; activates macrophages (promoting granuloma formation) and induces release of TNF-α.- Sulfatides (surface glycolipids) inhibit phagolysosomal fusion.
  • Neurocysticercosis
    - Ingestion of Taenia solium (pork tapeworm) eggs excreted in feces of human carriers. Presentation:- Common in Central & South America, sub-Saharan Africa, Asia- Prolonged incubation (months to years)- Seizures, focal neurologic symptoms, intracranial hypertension (CSF obstruction) Diagonisis:- CT/MRI – cysts, scolex- Eosinophilia, ↑ ESR Therapy: Albendazole
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  • Bacterial exotoxins
    Bacillus anthracis- Edema factor: Increases cAMP concentration by acting as an adenylate cyclase, causing edema & phagocyte dysfunction- Lethal factor: Zinc-dependent protease that inhibits mitogen-activated protein kinase signaling, causing apoptosis & multisystem physiologic disruption Bordatella pertussis- Pertussis toxin: Disinhibits adenylate cyclase through Gi ADP-ribosylation, increasing cAMP levels; causes edema & phagocyte dysfunction Streptococcus pyogenes- Pyrogenic exotoxin: Acts as a superantigen, inducing fever & shosk; associated with scarlet fever & streptococcal toxic shock syndrome- Streptolysin O&S: Damages erythrocyte membranes, causing β-hemolysis
  • Actinomyces israelii
    Gram ⊕, anaerobic, non-acid fast, branching rod.- Normal flora of oral and female genital tract. Presentation:- Poor dental hygiene, oral surgery (tooth extraction), local tissue inflammation (tonsillitis), comorbidities → cervicofacial actinomycosis- Intestinal surgery, foreign body ingestion → abdominal actinomycosis- Ascending infection from pelvis, associated with IUD → pelvic actinomycosis- History of aspiration, oral infection, pulmonary malignancy → thoracic actinomycosis- CNS: solitary brain abscess (Nocardia will produce multiple foci) - Generally not painful but spreads contiguously, penetrating all tissues including bone- Tissue swelling can lead to draining abscesses (sinus tracts) with 'sulfur' granules (hard yellow microcolonies)  Treatment: penicillin V and surgical draining 
  • Moraxella catarrhalis
    Gram-negative diplococcus. Close relative of Neisseria. - Reservoir: nasopharynx- Transmission: respiratory droplets Diseases:- Otitis media- Sinusitis- Bronchitis and bronchopneumonia in elderly patients with COPD Treatment: Amoxicillin and clavulanate, 2nd or 3rd-generation cephalosporins, TMP-SMX
  • Burkholderia cepacia
    Oxidase-⊕, catalase-⊕, non-fermenting, gram-negative. Transmission: Water aerosols, person-person (respiratory droplets) Diseases: Cystic fibrosis (recurrent pneumonia), CGD (pneumonia, septicemia) Treatment: TMP-SMX
  • Acinetobacter baumannii
    Oxidase-Θ, non-fermenting, aerobic, gram-negative bacilli; biofilm Transmission: Wound infection or nosocomial Diseases: Wound infection and pneumonia in military personnel Treatment: highly drug-resistant; carbapenem or polymyxin
  • Francisella tularensis
    Small gram ⊝ coccobacillus. Facultative intracellular pathogen (localized in reticuloendothelial cells); granulomatous response.- Potential biowarfare agent- Zoonosis- Reservoir: ticks, rabbits, deer, and rodents; highest in Arkansas and Missouri Transmission: - Tick bite (Dermacentor) → ulceroglandular disease, characterized by fever, ulcer at bite site, and regional lymph node enlargement and necrosis- Traumatic implantation while skinning rabbits → ulceroglandular disease- Aerosols (skinning rabbits) → pneumonia Disease: Ulceroglandular tularemia (open wound contact with rabbit blood; tick bite), pneumonic tularemia (bioterrorism; atypical pneumonia). Treatment: Streptomycin
  • Brucella spp
    Small, gram-negative coccobacilli, aerobic. Facultative intracellular.- Zoonosis- Potential bioterorrism agent- Reservoir: Domestic livestock- Transmission: Unpasteurized dairy products, direct contact with the animal - Granulomatous repsonse with central necrosis Disease: Brucellosis (undulant fever)- Painful, generalized lymphadenopathy- Moldy body odor- Acute septicemias- Influenza-like symptoms, including arthralgias, anorexia, myalgia, back pain- Profuse sweating- Hepatomegaly Diagnosis: culture is hazardous; serum agglutination test (anti-LPS antibody titers) Treatment: rifampin and doxycycline minimum of 6 weeks (adults); rifampin and cotrimoxazole (children)
  • Pasteurella multocida
    Small gram ⊝ coccobacillus; facultative anaerobic. Reservoir: Mouth of many animals, especially cats and dogsTransmission: Animal bites; particularly from cat bites Disease: Cellulitis with lymphadenitis (rapidly spreading wound infections), osteomyelitis - Culture has a mouse-like odor (indole-positive species) Treatment: Amoxicillin/clavulanate for cat bites
  • Vibrio parahaemolyticus
    Reservoir: Marine life Transmission: Consumption of undercooked or raw seafood Presentation: Watery diarrhea with cramping and abdominal pain - Self-limiting- Life-threatening sepsis can occur in those with liver disease or hemochromatosis.
  • Klebsielle granulomatis
    Transmission: sexual contact Disease: Granuloma inguinale (Donovanosis)- small painless nodules that burst and ulcerate- beefy red painless genital ulcers that bleed readily on contact Diagnosis: Donovan bodies seen on Wright-Giemsa stain, bipolar staining Treatment: Doxycycline
  • Yersinia pestis
    Gram ⊝ rods with bipolar staining. Coagulase ⊝.- Reservoir: prairie dogs, chipmunks, squirrels. Western US.- Potential biowarfare agent Transmission: wild rodents flea bite → sylvatic plague (ie, Black death)- Human-to-human transmission by respiratory droplets Bubonic plague:- Rapidly increasing fever- Regional buboes (painful swollen lymph nodes)- Conjunctivitis- Leads to septicemia, DIC, necrosis of the digits, and death if untreatedPneumonic plague:- Arises from inhalation of organisms from infected individual- Highly contagious Diagnostics: cultures with Wayson stain → shows bipolar staining of bacteria (appearance of "closed safety pin"). Treatment: IV gentamycin
  • Proteus
    Gram-Θ, highly motile/"swarming motility", non-lactose-fementing, urease-positive Proteus mirabilis (90% of infections), Proteus vulgaris Reservoir: human colon and environment Pathogenesis:- Urease raises urine pH to cause kidney stones (staghorn renal calculi)- Endotoxin Diseases: UTIs, septicemia Treatment: Fluoroquinolones, TMP-SMX, or 3rd generation cephalosporin for UTIs
  • Eikenella corrodens
    Gram-negative rods; bleach-like odor Reservoir: Human oropharynxTransmission: Human bites or fist fight injuries Disease: Cellulitis Treatment: 3rd generation cephalosporins, fluoroquinolones
  • Bactericides fragilis
    Gram-negative rod. Anaerobic. Reservoir: Human colonTransmission: Endogenous from bowel defects Diseases:- Septicemia- Peritonitis (often mixed infections)- Abdominal abscess Treatment: Metronidazole, clindamycin, or cefoxitin; abscess should be drained
  • Treponema pallidum
    Thin spirochete with periplasmic flagella. Obligate pathogen. Pathogenesis: Endarteritis resulting in lesions. Primary (10 days to 3 months after exposure):- Nontender chancre; clearn, indurated edge; heals spontanouslyin 3-6 weeks- Diagnosis: Dark-field or fluorescent microscopy of lesion Secondary (1 to 3 months later):- Maculopapular (copper-colored) rash, diffuse, includes palms and soles, patchy alopecia. - Condylomata lata: flat, wartlike perianal and mucous membrane lesions; highly infectious- Diagnosis: Serology nonspecific and specific; both positive Latent: No symptoms but positive serology. Tertiary (30% of untreated, years later):- Gummas (syphilitic granulomas), aortitis, CNS inflammation- Diagnosis: Serology: specific tests Serology – two types of antibody:1. Nontreponemal antibody (=reagin) screening tests- Ab binds to cardiolipin- Very sensitive but not specific; confirm with FTA-ABS- Examples: VDRL, RPR, ART2. Specific tests for treponemal antibody- Earliest antibodies; bind to spirochetes- More specific- FTA-ABS most widely used test - Benzathine penicillin (long-acting form) for primary and secondary syphilis; penicillin G for congenital and late syphilis
  • Borrelia burgdorferi
    Spirochetes, microaerophilic Reservoir: white-footed mice (nymphs) and white-tailed deer (adult ticks)Transmission: By Ixodes (deer) ticks and nymphs Pathogenesis: Invades skin and spreads via the bloodstream to involve primarily the heart, joints, and CNS. Arthritis is caused by immune complexes. Lyme disease- Stage 1 (3 days to 1 month): Target rash- Stage 2 (days to weeks later): Fatigue, chills and fever, headache, muscle and joint pain, swollen lymph nodes, secondary annular skin lesions- Stage 3 (months to years): Bell palsy, headache, meningitis, extreme fatigue, conjunctivitis, palpitations, arrhythmias, myocarditis, pericarditis. Arthritis, most common in knees. Diagnosis:- Serodiagnosis by ELISA - Western blot for confirmation Treatment: Doxycycline, amoxicillin, or azithromycin/clarithromycin (primary). Ceftriaxone for secondary. Doxycycline or ceftriaxone for arthritis.
  • Chlamydia trachomatis
    Obligate intracellular bacterium; cannot make ATP. Found in cells as replicating reticulate bodies. Inactive, extracellular elementary bodies. Not seen on Gram stain. Peptidoglycan layer lacks muramic acid. Reservoir: Human genital tract and eyes.Transmission: Sexual contact and at birth; trachoma is transmitted by hand-to-eye contact. Pathogenesis: Infection of nonciliated epithelial cells leads to granulomatous response. STDs:- Serotypes D-K- Nongonococcal urethritis, cervicitis, PID- Inclusion conjunctivitis and pneumonia in neonates/infants (stacatto cough)Lymphogranuloma venereum:- Serotypes L1, 2, 3, prevalent in Africa, Asia, South America- Painless shallow ulcers followed weeks later by swollen, painful lymph nodes ("buboes")- Tertiary: ulcers, fistulas, genital elephantiasisTrachoma:- Preventable infectious blindness: serotypes A, B, C- Follicular conjunctivitis leading to conjunctival scarring, and inturned eyelashes leading to corneal scarring and blindness Treatment: doxycycline or azithromycine- Erythromycin is effective in infected mothers to prevent neonatal disease
  • Ehrlichia chaffeensis
    Gram-negative bacilli, obligate intracellular bacteria of mononuclear or granulocytic phagocytes.- Reservoir: white tail deer- Transmission: Bite of the lone star tick (Ambylomma) Disease:- Similar to Rocky Mountain spotted fever but generally without rash- May cause renal failure and GI bleeding- Morulae – mulberry-like structures inside infected cells Diagnosis:- Leukopenia, thrombocytopenia- Giemsa-stained blood film: Morulae – mulberry-like structures inside infected cells- Serology Treament: doxycycline
  • Phage-coded pathogenic factors
    - Cholera toxin - O antigen of Salmonella - Botulinum toxin - Erythrogenic exotoxins of Streptococcus pyogenes - Diphtheria toxin - Shiga toxin
  • Fungal morphology
    Hyphae = filamentous cellular units of molds and mushrooms- Nonseptate hyphae = Broad hyphae with irregular width, broad angle of branching, no cross walls (eg, Mucor, Rhizopus spp)- Septate hyphae = Width is fairly regular, with cross walls (eg, Tinea, Aspergillus) Yeasts = single celled (round to oval) fungi Dimorphic fungi = Fungi able to convert from hyphal to yeast (eg, Histoplasma, Blastomyces, Coccidioides, Sporothrix) Pseudohyphae = Hyphae with constriction at each septum (Candida) Spore types- Conidia = Asexual spores- Blastoconidia = "Buds" on yeast- Spherules and endospores (Coccidioides): Spores inside the spherules
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  • Nocardia
    Gram ⊕ rod (beading or branching), partially acid-fast, aerobic.- Ubiquitous in soil - Trasmission via spore inhalation or traumatic inoculation into skin- Immunocompromised or elderly patients Symptoms:- Bronchopneumonia in immunocompromised – can mimic tuberculosis but with ⊝ PPD- CNS involvement – brain abscess- Cutaneous involvement in immunocompetent– cellulitis, nodules, abscesses Treatment: Trimethropim-sulfamethoxazole, surgical drainage of abscesses
  • Bacterial structures
    Flagellum: Proteins. MotilityPilus/fimbria: Glycoprotein. Mediate adhesion of bacteria to cell surface; sex pilus forms during conjugation. Spore: Keratin-like coat; dipicolinic acid; peptidoglycan, DNA. Gram ⊕ only. Survival: resist dehydration, heat chemicals.Capsule: Organized, discrete polysaccharide layer (except poly-D-glutamate on B anthracis). Protects against phagocytosis.Glycocalyx: Loose network of polysaccharides. Mediates adherence to surfaces, especially foreign surfaces (eg, indwelling catheters).Outer membrane: Outer leaflet: contains endotoxin (LPS, LOS). Embedded proteins: porins and other outer membrane proteins (OMPs). Inner leaflet: phospholipids. Gram ⊝ only. Endotoxin: lipid A induces TNF and IL-1; antigenic O polysaccharide component. Most OMPs are antigenic. Porins: transport across outer membrane.Periplasm: Space between cytoplasmic membrane and outer membrane in gram ⊝ bacteria. (Peptidoglycan in middle.) Accumulates component exiting gram ⊝ cells, including hydrolytic enzymes (eg, β-lactamases).Cell wall: Peptidoglycan is a sugar backbown with peptide side chains cross-linked by transpeptidase. Net-like structure gives rigid support, protects against osmotic pressure change.Cytoplasmic membrane: Phospholipid bilayer sac with embedded proteins (eg, penicillin-binding proteins [PBPs]) and other enzymes. Lipoteichoic acids (gram ⊕ only) extend from membrane to exterior. Site of oxidative and transport enzymes; PBPs involved in cell wall synthesis. Lipoteichoic acids induce TNF-α and IL-1.
  • Catalase-positive organisms
    Catalase degrades H2O2 into H2O and bubbles of O2 before it can be converted to microbicidal products by the enzyme myeloperoxidase. People with chronic granulomatous disease (NADPH oxidase deficiency) have recurrent infections with certain catalase ⊕ organisms. - Nocardia, Pseudomonas aeruginosa, Listeria, Aspergillus, Candida, Cryptococcus, Staphylococci, Burkholderia, Enterobacteriacae (E coli, Salmonella, Shigella, Serratia, Klebsiella, Yersinia, Proteus)
  • Anaerobes
    Examples include Clostridium, Bacteroides, Fusobacterium, and Actinomyces israelii. They lack catalase and/or superoxide dismutase and are thus susceptible to oxidative damage. Generally foul smelling (short-chain fatty acids), are difficult to culture, and produce gas in tissue (CO2 and H2). Anaerobes are normal flora in GI tract, typically pathogenic elsewhere. Aminoglycosides are ineffective against anaerobes because these antibiotics require O2 to enter into bacterial cell.
  • Encapsulated bacteria
    - Pseudomonas aeruginosa- Streptococcus pneumoniae- Haemophilus influenzae type b- Neisseria meningitidis- E coli- Salmonella- Klebsiella- Group B Strep Are opsonized, and then cleared by spleen.Their capsules serve as an antiphagocytic virulence factor.Capsular polysaccharide + protein conjugate serves as an antigen in vaccines.
  • Urease-positive organisms
    - Proteus- Cryptococcus- H pylori- Ureaplasma- Nocardia- Klebsiella- S epidermidis- S saphrophyticus Urease hydrolyzes urea to release ammonia and CO2 → ↑ pH. Predisposes to struvite (ammonium magnesium phosphate) stones, particularly Proteus.
  • Pigment-producing bacteria
    Actinomyces israelii – yellow "sulfur" granules, which are composed of filaments of bacteria. S aureus – yellow pigment. P aeruginosa – blue-green pigment (pyocyanin and pyoverdin). Serratia marcescens – red pigment.
  • In vivo biofilm-producing bacteria
    S epidermidis – Catheter and prosthetic device infections Viridans streptococci (S mutans, S sanguinis) – Dental plaques, infective endocarditis P aeruginosa – Respiratory tree colonization in patients with cystic fibrosis, ventilator-associated pneumonia. Contact lens-associated keratitis. Nontypeable (unencapsulated) H influenzae – Otitis media
  • Conjugatino
    F+ x F-: F+ plasmid contains genes required for sex pilus and conjugation. Bacteria without this plasmid are termed F-. Sex pilus on F+ bacterium contacts F- bacterium. A single strand of plasmid DNA is transferred across the conjugal bridge ("mating bridge"). No transfer of chromosomal DNA. Hfr x F-: F+ plasmid can become incorporated into bacterial chromosomal DNA, termed high-frequence recombination (Hfr) cell. Transfer or leading part of plasmid and a few flanking chromosomal genes. High-frequency recombination may integrate some of those bacterial genes. Recipient cell remains F- but now may have new bacterial genes.
  • Transduction
    Generalized: A packaging "error." Lytic phage infects bacterium, leading to cleavage of bacterial DNA. Parts of bacterial chromosomal DNA may become packaged in phage capsid. Phage infects another bacterium, transferring these genes. Specialized: An "excision" event. Lysogenic phage infects bacterium; viral DNA incorporates into bacterial chromosome. When phage DNA is excised, flanking bacterial genes may be excised with it. DNA is packaged into phage capsid and infect another bacterium.Genes for the following 5 bacterial toxins are encoded in a lysogenic phage (ABCD's): Group A strep erythrogenic toxin, Botulinum toxin, Cholera toxin, Diphtheria toxin, Shiga toxin.
  • Transposition
    Segment of DNA (eg, transposon) that can "jump" (copy/excise and reinsert) from one location to another, can transfer genes from plasmid to chromosome and vice versa. This is a critical process in creating plasmids with multiple antibiotic resistance which can be transferred across species lines. Eg, Tn1546 carrying vanA gene from vancomycin-resistant Enterococcus to S aureus).
  • Spore-forming bacteria
    Some bacteria can form spores when nutrients are limited.Spores lack metabolic activity.Spores are highly resistant to heat and chemicals. Most autoclave to kill spores by steaming at 121°C for 15 minutes. Chlorine and hydrogen peroxide are sporicidal. Iodine/iodophors may be sporicidalCore contains dipicolinic acid. Bacillus anthracis – AnthraxBacillus cereus – Food poisoningClostridium botulinum – BotulinismClostridium difficile – Pseudomembranous colitisClostridium perfringens – Gas gangreneClostridium tetani – Tetanus
  • Main features of exotoxins and endotoxins
    Exotoxins:- Source: Certain species of gram ⊕ and gram ⊝ bacteria- Secreted from cell: Yes- Chemistry: Polypeptide- Location of genes: Plasmid or bacteriophage- Adverse effects: High (fatal dose on the order of 1 µg)- Antigenicity: Induces high-titer antibodies called antitoxins- Vaccines: Toxoids used as vaccines- Heat stability: Destroyed rapidly at 60°C (except staphylococcal exotoxin and E coli heat-stable toxin)- Typical diseases: Tetanus, botulism, diphtheria Endotoxins:- Source: Outer cell membrane of most gram ⊝ bacteria- Secreted from cell: No- Chemistry: Lipid A component of LPS (structural part of bacteria; released when lysed)- Location of genes: Bacterial chromosome- Adverse effects: Low (fatal dose on the order of hundreds of micrograms)- Clinical effects: Fever, shock (hypotension), DIC- Mode of action: Induces TNF, IL-1, and IL-6- Antigenicity: Poorly antigenic- Vaccines: No toxoids formed and no vaccine available- Heat stability: Stable at 100°C for 1 hr- Typical diseases: Meningococcemia; sepsis by ⊝ gram rods
  • α-hemolytic bacteria
    Gram ⊕ cocci. Partial reduction of hemoglobin causes greenish or brownish color without clearing around growth on blood agar.  - Streptococcus pneumoniae (catalase ⊝ and optochin sensitive)- Viridans streptococci (catalase ⊝ and optochin resistant)
  • β-hemolytic bacteria
    Gram ⊕ cocci. Complete lysis of RBCs → clear area surrounding colony on blood agar.  - Staphylococcus aureus (catalase and coagulase ⊕)- Streptococcus pyogenes – group A strep (catalase ⊝ and bacitracin sensitive)- Streptococcus agalactiae – group B strep (catalase ⊝ and bacitracin resistant)
  • Lactose-fermenting enteric bacteria
    Fermentation of lactose → pink colonies on MacConkey agar. Fast-fermenters:- E coli- Klebsiella- Enterobacter Slow-fermenters:- Citrobacter- Serratia - E coli produces β-galactosidase, which breaks down lactose into glucose and galactose.- EMB agar – lactose fermenters grow as purple/black colonies. E coli grows colonies with a green sheen.
  • Escherichia coli
    Gram ⊝ rod, fast lactose-fermenter, indole ⊕ (ability to convert tryptophan to indole; distinguishes from Enterobacter cloacae). - Fimbriae – cystitis and pyelonephritis (P-pili)- K capsule – pneumonia, neonatal meningitis- LPS endotoxin – septic shock. Enteroinvasive E coli: Microbe invades the intestinal mucosa and causes necrosis and inflammation. Invasive dysentery. Clinical manifestations similar to Shigella. Enterotoxigenic E coli: Produces heat-labile (activation of adenylate cyclase → ↑ cAMP → ↑ Cl- secretion) and heat-stable (activation of guanylate cyclase → ↑ cGMP → ↓ NaCl reabsorption) enterotoxins. No inflammation or invasion. Traveler's diarrhea (watery). Enteropathogenic E coli: No toxin produced. Adheres to apical surface, flattens villi, prevents absorption. Diarrhea, usually in children. Enterohemorrhagic E coli: O157:H7 is most common serotype in US. Often transmitted via undercooked meat, raw leafy vegetables. Shiga-like toxin → cleaves adenine from rRNA → inactivation of the 60S subunit → protein synthesis inhibited → necrosis and inflammation of the GI mucosa. Causes hemolytic-uremic syndrome: triad of anemia, thrombocytopenia, and acute renal failure due to microthrombi forming on damaged endothelium → mechanical hemolysis, platelet consumption, and ↓ renal blood flow. Dysentery (toxin alone causes necrosis and inflammation). Does not ferment sorbitol (vs other E coli).
  • Bartonella spp
    Gram ⊝ rod, facultative intracellular, microaerophile. Bartonella henselae- Reservoir: Cats are asymptomatic carriers- Cat scratch disease: one or more 5-10mm large, erythematous, non-tender papules or vesicles develop approx. 4-6 days after exposure. Swollen, tender lymphadenopathy.- In HIV patients: bacillary angiomatosis: One or more red, flesh-colored or colorless papules and nodules that bleed easily Bartonella quintana- Reservoir: Humans (the louse is usually the vector)- Trench fever (five-day fever)
  • Borrelia recurrentis
    Transmission via louse (recurrent due to variable surface antigens). Relapsing fever
  • Tinea (pityriasis) versicolor
    Caused by Malassezia spp, a yeast-like fungus (not a dermatophyte despite being called tinea). Degradation of lipids produces acids that damage melanocytes and cause hypopigmented, hyperpigmented, and/or pink patches.- Less pruritic than dermatophytes. Can occur at any time of year, but more common in summer (hot, humid weather). - "Spaghetti and meatballs" appearance on microscopy. Treatment: selenium sulfide, topical and/or oral antifungal medications.