Sketchy Notes - USMLE Microbiology PDF

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Sketchy Notes

MedSN 1

Bacteria Gram Positive COCCI

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Staph Aureus (+) Features: 1. 2. 3. 4. 5.

Small, yellow colonies. Beta Hemolytic Catalase Positive Coagulase positive Ferments Mannitol a. Positive (Yellow) b. Negative (Pink)

Reservoir: 1. Nasal mucosa 2. Skin

Pathogenesis: 1. Protein A a. Binds Fc portion of IgG, inhibits phagocytosis. 2. TSST-1 (Superantigen) 3. Coagulase 4. Exfolatins (Scalded skin syndrome) Diseases: 1. Postviral Pneumonia a. After influenza usually b. Patchy infiltrates on x ray 2. Abscesses 3. Septic arthritis a. Most common cause 4. Endocarditis a. Acute in nature b. Affects Tricuspid 5. Food poisoning 6. Osteomyelitis a. Most common cause 7. Toxic Shock Syndrome 8. Scalded skin Syndrome

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Treatment: 1. Nafcillin 2. Vancomycin (MRSA)

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Staph Epidermidis (+) Features: 1. 2. 3. 4. 5. 6.

Coagulase (-) Catalase (+) Urease (+) Contaminates blood cultures Makes biofilms on artificial valves Novobiocin sensitive

Reservoir: 1. Skin Diseases: 1. Affects prosthetic joints (enemy of orthopedic surgeons) 2. Endocarditis (artificial valves) Treatment: 1. Vancomycin a. Replace valves too in case of endocarditis

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Staph Saprophyticus (+) Features: 1. 2. 3. 4.

Coagulase (-) Catalase (+) Urease (+) Novobiocin resistant

Diseases: 1. UTIs in sexually active females

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Strep Pyogenes (+) (GROUP A STREP) Features: 1. Catalase negative 2. Encapsulated a. Hyaluronic acid in capsule 3. Beta hemolytic 4. Bacitracin sensitive Pathogenesis: 1. M protein a. Virulence factor for Rheumatic fever and Post streptococcal glomerulonephritis 2. Hyaluronic acid a. Not immunogenic 3. Streptococcal pyogenic exotoxin (SPE) a. SPE A, C: Scarlett fever, Toxic shock-like syndrome (TSLS) b. SPE B: Necrotizing fasciitis 4. Streptolysin O a. Hemolysin b. ASO antibodies (ASO titer) 5. Streptokinase a. Converts plasminogen to plasmin b. Breaks fibrin clots c. Spreading factor 6. DNAse Diseases:

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Divided into as follows: Impetigo Pyogenic Infections

Pharyngitis

Diseases

Cellulitis/Erysiplas Scarlet Fever Caused by SPE

TSLS Necrotizing Fascitis Rheumatic Fever

Sequelae PSGN

Pyogenic Infections: 1. Pharyngitis 2. Impetigo a. Honey-crusted lesions on skin 3. Cellulitis 4. Erysiplas a. Superficial cellulitis with well-demarcated borders b. Most common cause Caused by SPE: 1. Scarlet Fever a. Strawberry tongue b. Widespread rash that spares face 2. TSLS a. Superantigen 3. Necrotizing Fascitis a. Caused by SPE B b. Surgical emergency c. Sometimes amputation done Sequelae: 1. Rheumatic fever 2. PSGN

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Rheumatic Fever: 1. M protein (main virulence factor) a. Interferes opsonization (inhibits phagocytosis) b. Very antigenic i. Leads to immune response ii. Antibodies made against self antigens iii. The self antigen is in myosin in muscles iv. Hence, affecting heart (mitral valve) v. This process is called molecular mimicry c. If pharyngitis is immediately treated, RF doesn’t occur. d. Symptoms (JONES): i. Joints: Polyarthritis ii. : Valvular damage, myocarditis, pericarditis. iii. Nodules: Subcutaneous iv. Erythema Marginatum: Rash with thick borders v. Sydenham’s chorea: Involuntary movement of hands and face Post Streptococcal Glomerulonephritis: 2. M12 serotype 3. Symptoms: a. Dark brown (cola colored) urine b. Facial edema 4. Occurs 2 weeks after streptococcal infection

Differences between RF and PSGN Rheumatic Fever

PSGN

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Occurs after pharyngitis

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Doesn’t occur if pharyngitis is treated

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Treatment: 1. Penicillin (Beta lactam drugs)

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Can occur after pharyngitis or any other superficial infection like impetigo Occurs, no matter if the strep infection is treated or not

Strep Agalactiae (+) (GROUP B STREP) Features: 1. 2. 3. 4. 5. 6.

Cause serious infections in newborns Hydrolyze hippurate (hippurate test +) Beta Hemolytic Encapsulated Bacitracin resistant CAMP test (+) a. Increasing zone of hemolysis when plated with staph aureus b. Arrowhead hemolysis

Transmission: 1. Newborn infected during birth Diseases: 1. Neonatal meningitis a. Most common cause 2. Neonatal sepsis 3. Neonatal Pneumonia Treatment: 1. Penicillin Prevention: 1. Penicillin is given intrapartum to mother tested positive for strep agalactiae infection through vaginal and rectal swab at 35 weeks of pregnancy.

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Strep Pneumoniae (+) (GROUB B STREP) Features: 1. 2. 3. 4. 5. 6.

Encapsulated (polysaccharide capsule) Alpha hemolytic Optochin sensitive Bile soluble Lancet-shaped diplocci Sickle cell (asplenia) patients are more susceptible to Encapsulated bacterial infections such as S. pneumonia

Pathogenesis: 1. Polysaccharide capsule a. Major virulence factor 2. IgA Protease a. Helps in invading mucosa b. Reduces host defenses Diseases: Diseases are given the mnemonic MOPS. S. pneumonia is #1 cause for all of these.

MOPS

Meningitis

Otitis Media

Pneumonia

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Sinusitis

Pneumonia o Lobar pneumonia o Infiltrates lower lobes o Rust colored sputum

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Treatment: 1. Macrolides (erythromycin) 2. Ceftriaxone Prevention: There are two vaccines available: 1. Adult Vaccine (PPV, pneumococcal polysaccharide vaccine) 2. Pediatric Vaccine (PCV, pneumococcal conjugate vaccine)

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Adult Vaccine 23 of most common capsular serotypes Not conjugated with protein T-cell independent response due to no protein conjugation

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Pediatric Vaccine 13 of most common serotypes Conjugated with protein T-cell response due to protein conjugation

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IgM produced

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IgG produced

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Viridans Streptococci (+) (GROUP B STREP) Features: 1. 2. 3. 4.

Non-Encapsulated Bile insoluble Optochin resistant Alpha hemolytic

Diseases: 1. Dental carries 2. Subacute infective endocarditis a. Affects already damaged heart valves b. It adheres to platelets through dextran and attacks damaged heart valves c. Most commonly involved valve is Mitral Valve i. Mitral valve common due to higher risk of following diseases in general population: 1. Mitral prolapse 2. Rheumatic Fever

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Enterococcus (+) 1. E. faecalis (more common) 2. E. faecium (more dangerous) Features: 1. Bile insoluble 2. Grow in 6.5% NaCl Diseases: Mnemonic: “do U

trees”

1. Urinary Tract Infections 2. Endocarditis 3. Biliary tree infection Treatment: 1. Vancomycin resistant enterococci a. Linezolid b. Tigecycline

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Bacteria Gram positive RODS

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Bacillus Anthracis and Baccilus Cereus(+) Features: 1. Rods in chains 2. Obligate aerobe 3. Encapsulated a. Protein capsule i. Poly D-glutamate 4. Spore forming 5. Potential biowarfare agent Pathogenesis: 1. Edema Factor (EF) a. Acts as adenylate cyclase b. Increases cAMP c. Causes fluid to move in extracellular fluid (edema) d. Leads to inhibition of host defenses e. Hence, prevents phagocytosis 2. Lethal Factor (LF) a. Kills cells by acting as a protease b. Cleaves MAP kinase i. MAP kinase is a signal transduction protein ii. It is involved in control of cell growth iii. Hence, LF causes tissue necrosis Diseases: 1. Cutaneous anthrax a. Black eschar with erythematous border 2. Pulmonary anthrax (wool sorter’s disease) a. Caused by spores that are inhaled from wool while dealing with it and they germinate in lungs. b. Presents first as non-specific pulmonary symptoms like dry cough, fever etc c. Eventually leads to mediastinal hemorrhagic lymphadenitis i. It presents as widened mediastinum on X ray Treatment: 1. Flouroquinolones 2. Doxycycline

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Bacillus Cereus (+) Same features as bacillus anthrax. It causes food poisoning (vomiting and diarrhea after eating reheated rice)

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Clostridium Tetani (+) Features: 1. Anaerobe 2. Spore-forming Reservoir: 1. Soil 2. Rusted Nails Transmission: 1. Punctured wound/trauma Diseases: It causes spastic paralysis. 2 important diseases are: 1. Risus Sardonicus (evil grin) or Lock Jaw Syndrome 2. Opisthotonus (exaggerated arching of back) Pathogenesis: 1. Spores germinate in tissue and produce tetanus toxin which moves retrograde to CNS 2. Name of toxin is tetanospasmin a. Acts as protease b. Cleaves SNARE protein i. It leads to prevention of exocytosis of neurotransmitters in synapse 1. Neurotransmitters are GABA and glycine a. GABA and glycine are released from Renshaw cells Prevention: 1. Toxoid vaccine a. Conjugated with protein to increase immune response b. It is a vaccine to toxin, not organism.

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Clostridium Botulinum (+) Features: 1. Spore-forming 2. Obligate anaerobe Transmission: 1. Improperly canned food (in adults) 2. Honey (in infants) Pathogenesis: 1. Adults: a. Toxin absorbed by gut b. Cleaves SNARE protein c. Leads to prevention of exocytosis of Ach in the synapse d. Leads to flaccid paralysis 2. Infants: a. Infants don’t have normal intestinal flora to outcompete any ingested botulinum spore like adults do b. Ingestion of honey leads to spore going into gut where the spore produces the toxin c. Leads to flaccid paralysis Diseases: 1. In adults: a. Flaccid paralysis i. Descending ii. Early symptoms include ptosis and diplopia 2. In Infants: a. Floppy Baby Syndrome i. More common than adult botulism

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Clostridium Difficile (+) Features: 1. Nosocomial infection 2. Spore-forming 3. Obligate anaerobe Diseases: 1. Clindamycin-associated diarrhea 2. Colitis 3. Pseudomembranous colitis Pathogenesis: 1. Exotoxin A a. Attaches to brush border of intestine b. Causes inflammation and cell death c. Leads to watery diarrhea 2. Exotoxin B a. Disrupts cytoskeleton by depolymerizing actin b. Also leads to production of yellowish gray exudate which forms a pseudomembrane that covers colonic mucosa Lab Diagnosis: 1. Visualize pseudomembrane a. Histologically b. Endoscopically 2. Stool examination for toxin a. Toxin causes the disease, not the organism Treatment: 1. Metronidazole 2. Vancomycin

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Clostridium Perfringens (+) Features: 1. 2. 3. 4.

Obligate Anaerobe Spore-forming Double zone of hemolysis on Blood Agar Presentation with a. Motorcycle accidents b. Deep wounds in military combat

Reservoir: 1. Spores in soil Diseases: Two diseases: 1. Gas gangrene a. Gas is produced by organism under the infected tissue when it consumes carbohydrates b. The underlying mechanism is related to Alpha toxin i. This toxin is a lecithinase ii. This means it lyses lechithin in cell membranes and disrupts them iii. If it disrupts RBC membrane, it causes hemolysis (this is the reason behind double zone of hemolysis on blood agar) c. Crepitus or crackles are heard on palpation 2. Food Poisoning a. Due to ingestion of large amount of spores b. Spores germinate in the gut and release toxin i. This is unlike other microbes which germinate OUTSIDE the gut (e.g C. botulinum in canned food, bacillus cereus in reheated rice etc) Treatment: 1. Gas gangrene: a. IV Penicillin G 2. Food Poisoning: a. Self resolving

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Corynebacterium Diphtheriae (+) Features: 1. Club-shaped (V or Y formation) 2. Contains metachromatic granules a. These dye red with aniline dye b. Rest of the cell stays blue Transmission: 1. Respiratory droplets Pathogenesis: 1. Diphtheria toxin has two components a. A subunit is active b. B subunit is binding 2. Toxin causes ADP ribosylation of elongation factor 2 (EF-2) a. This leads to inhibition of ribosomal function and hence, inhibition of protein synthesis b. Also, it leads to production of dirty gray exudate which forms a pseudomembrane on oropharynx mucosa Diseases: 1. Diphtheria has following characteristics a. Pseudomembrane i. May spread to larynx and trachea and cause airway obstruction ii. May also cause lymphadenopathy (Bull’s neck) 2. Cardiotoxicity a. Myocarditis b. Arrhythmia c. Heart block 3. Local Paralysis: a. Starts in posterior pharynx (Myelin damage) b. May lead to other cranial nerve deficits c. Mechanism involves attack of toxin on myelin sheath of nerve fibres Lab Diagnosis: 1. Swab pseudomembrane on following: a. Tellurite agar b. Loeffler’s medium 2. Elek’s test a. To differentiate between toxic and non-toxic strains i. In vitro assay on filter paper that has anti-toxin 22

ii. If toxin binds, there is a reaction and the test is positive i.e. the strain is toxic Prevention: 1. Toxoid vaccine a. Inactivated exotoxin conjugated with protein to increase immune response b. Powerful IgG response c. Often given with vaccines of Clostridium tetani and acellular pertussis (DTaP) Treatment: 1. Passive immunity (Antitoxin)

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Listeria Monocytogenes (+) Features: 1. 2. 3. 4.

Facultative intracellular Cold growth Beta Hemolytic Motile a. Extracellular motility: tumbling motility due to flagella b. Intracellular motility: actin rocket motility, rapidly polymerizes actin against bacterial wall and propels itself in the opposite direction 5. Catalase (+)

Reservoir: 1. Unpasteurized milk 2. Soft cheese Diseases: 1. Listeriosis a. Common in pregnancy i. May lead to early termination or disease in newborn 2. Meningitis a. Neonatal i. 3rd most common cause b. Elderly and immunocompromised Treatment: 1. Ampicillin

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Actinomyces Israelii (+) Features: 1. Branching rods 2. Obligate anaerobe Reservoir: 1. Normal flora of oral cavity Diseases: 1. Cervicofacial actinomyces infection a. Following dental trauma b. Slow course i. Start as a lump on jaw (tissue swelling) ii. Formation of abscess iii. Appearance of sinus tracts iv. These tracts drain infection site through skin v. Thick yellow pus is observed (yellow color is due to sulphur granules in it) Treatment: 1. Penicillin G 2. Surgical drainage

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Nocardia (+) Features: 1. 2. 3. 4. 5. 6.

Catalase (+) Urease (+) Branching/filamentous rods Obligate aerobe Infects men more than women Weakly acid fast a. Carbofuschin stain is taken up if the cell wall has mycolic acid i. Mycolic acid is long chain fatty acid with two tails

Reservoir: 1. Soil Diseases: Mostly affects immunocompromised patients. There are 3 main sites of infection:   

Pulmonary CNS Cutaneous

1. Pulmonary Nocardiosis a. Presents as pneumonia and lung abscesses b. Associated with cavitary lesions c. It can disseminate i. Affinity for neural tissue ii. Hence, can cause brain abscesses 2. CNS a. Brain abscesses 3. Cutaneous a. Starts with traumatic implantation b. Indurated lesions c. Inflammatory reaction Treatment: 1. Sulfonamides

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Gram Negative COCCI

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Neisseria (-) (General Overview) Features: 1. 2. 3. 4. 5.

Diplococci Oxidase (+) Growth on chocolate agar Growth on VPN agar/ Thayer Martin agar Deficiency of C5 to C9 causes patients to be unable to make MAC complex that kills Neisseria and hence leads to increase in infections. 6. Neisseria has IgA protease which helps it to spread to mucosal surfaces 7. Pilli of Neisseria show antigenic variation and hence can evade our immune system

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Neisseria Meningitidis (-) Features: Refer to the general overview. The features specific for N. meningitidis are: 1. Ferments maltose, apart from glucose 2. Encapsulated a. Polysaccharide capsule inhibits phagocytosis b. 4 strains on basis of capsule i. A ii. B (most common in US) iii. C iv. D 3. Sickle cell anemic and asplenic patients are susceptible to infections Transmission: 1. Respiratory droplets; first colonizes nasopharynx Pathogenesis: Divided into 3 phases: 1st Phase: 1. Colonization of nasopharynx 2. Invasion and spread into blood 3. Severe inflammatory response a. Response is generated by lipooligosaccharide protein 2nd Phase: 1. 2. 3. 4.

Increased capillary permeability Leakage of fluid in extracellular space Hypovolemia Shock a. Maximum peripheral vasoconstriction due to shock i. Less blood to adrenal gland causes its infarction. This is called Waterhouse Friedrichsen syndrome ii. This infarction leads to exaggeration of present symptoms

3rd Phase: 1. Petechial rash a. Due to thrombocytopenia

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b. If the petechial rash increases to ecchymoses, this means the disease is progressing to DIC Prevention: 1. Vaccine a. Contains the capsule of N. meningitidis strains b. Doesn’t include capsule for strain B 2. Prophylaxis of rifampin given to close contacts Treatment: 1. Ceftriaxone

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Neisseria Gonorrhoeae (-) Features: Refer to general overview. Other features specific to it are: 1. Sexually transmitted infection 2. Facultative intracellular a. Invades PMN lymphocytes 3. NOT encapsulated Diseases: Following are common to males and females: 1. Asymmetric polyarthritis a. Commonly affects knees 2. White purulent discharge from penis or vagina Diseases specific to males or females are given below: In Males: 1. Urethritis 2. Prostatitis In Females: 1. Pelvic inflammatory disease (PID) a. Leads to: i. Infertility ii. Ectopic pregnancy b. Can spread to peritoneum (Fritz Hugh Curtis Syndrome) i. Can cause adhesions that form to capsule of liver ii. These adhesions are called Violin String Adhesions Congenital: 1. Purulent conjunctivitis a. Starts within first 5 days of birth b. Different from chlamydial neonatal conjunctivitis which starts after a week after birth Treatment: 1. Ceftriaxone 2. Assume co-infection with chlamydia: a. Macrolides b. Doxycylcine 31

Gram Negative RODS

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Klebsiella, Serratia, Enterobacter (-) Common Features: 1. Nosocomial infections 2. Cause: a. Pneumonia b. UTIs 3. Ferment Lactose a. All lactose fermenters give pink colonies on McConkey agar 4. Multi drug resistant infections Features of Enterobacter: 1. Motile Features of Serratia: 1. Motile 2. Red pigment when cultured Features of Klebsiella: 1. Three A’s: a. Alcoholics b. Abscesses c. Aspirations 2. Currant Jelly Sputum on coughing 3. Immotile 4. Encapsulated 5. Urease (+)

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Salmonella Enteritidis (-) Features: 1. 2. 3. 4. 5.

Motile Encapsulated Black colonies on Hektoen Agar Acid labile Facultative intracellular a. Within Macrophages 6. Type 3 secretion system

Reservoir: 1. Chicken Transmission: 1. Eating undercooked chicken Diseases: 1. Inflammatory diarrhea

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Salmonella Typhi (-) Features: 1. 2. 3. 4. 5.

Motile Black colonies on Hektoen Agar Encapsulated Acid labile Facultative intracellular a. Within macrophages 6. Rose-colored macules

Reservoir: 1. Gallbladder of chronic patients Diseases: 1. Typhoid fever (enteric fever) a. Rose-colored macules 2. “Pea soup” diarrhea 3. Osteomyelitis in sickle cell patients a. #1 cause Prevention: 1. Live attenuated vaccine Treatment: 1. Flouroquinolones a. Ciprofloxacin

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Shigella (-) Features: 1. 2. 3. 4. 5.

Green colonies on Hektoen Agar Immotile Facultative intracellular Acid stable Type 3 secretion system

Pathogenesis: 1. Invades M cells in pyer’s patches 2. Escapes phagolysosome 3. Uses host actin filaments intracellularly to propel itself Diseases: 1. Bloody Diarrhea a. Shigella causes production of cytokines when it attacks the enterocytes i. Leads to severe inflammation of mucosa ii. Eventually leads to bloody diarrhea 2. Shigellosis (Dysentery) a. Caused by S. dysenteriae b. Shiga toxin binds to 60S subunit of ribosomes c. S. dysenteriae produces shiga toxin which can lead to hemolytic uremic syndrome (HUS) in patients ...