G⁺ bacilli, non-spore forming, motile (tumbles), catalase + 

Causes flu like symptoms in pregnant women and can be passed to unborn children, resulting in miscarriage. Also causes meningitis in newborns.

listeriosis - meningitis and sepsis in neonates and the immunocompromised

Tx: ampicillin (or penicillin w/ or w/o gentamicin (aminoglycoside); TMP-SMX

Often resistant to cephalosporin, macrolides, and tetracycline

more than 100 species, some are opportunistic 

Corynebacterium diptheriae is the major human pathogen

G⁺ cocci in clusters, catalase + & coagulase +

Toxic reactions: Food poisoning (enterotoxin), scalded skin syndrome (exfoliatin), toxic shock syndrome (superantigen, hypvolemia); superantigen → cytokine storm and possible death

Infection: Carbuncle/furuncle, impetigo, endocarditis, osteomylitis, pneumonia (secondary post-viral superinfection), cellulitis, meningitis, septic arthritis, wound infections

penicillin (most strains are resistant)

methicillin, nafcillin, oxacillin

MRSA (carries SCCmec element): vancomycin

tricuspid valve endocartitis in IV drug users

α-toxin -  archetypal β-barrel pore-forming membrane-damaging cytotoxin

Protein A - prevents opsinization

leading cause of poliomyelitis in children 

G⁺ cocci in clusters, catalase + & coagulase - (CoNS)

novobiocin sensitive 

infection on indwelling medical devices (implants and catheters), endocarditis of mechanical heart valves

vancomycin 

(resistant to penicillins and cephalosporins) 

Neutropenic patients are the most susceptible 

Can lead to bacteremia (sepsis)

Skin flora can contaminate blood cultures

G⁺ cocci in clusters, catalase + & coagulase - (CoNS)

novobiocin resistant

community acquired UTI

TMP-SMX (Bactrim, Sulfatrim, and Bactrim DS)

G⁺ cocci in chains, catalase + & coagulase - (CoNS), β hemolytic, bacitracin sensitive; aka, Group A Strep

Toxin mediated: Scarlet Fever, TSS/TSLS, necrosis

Infectious: pharyngitis, skin infections (pyoderma (impetigo), erysipelas, and cellulitis)

Immune-mediated: Glomerulonephritis, Rheumatic Fever (Symptom management)

Penicillin G, clindamycin (TSS, to prevent SF toxin), cephalosporin, erythromycin, surgery and debridement

Treatment of pharyngitis is mandatory to prevent complications (eg, immune or toxin mediated responses, especially rheumatic fever). ASO titre can help predict rheumatic fever or GNitis

Virulence factors:

M protein: antiphagocytic, adhesive 

(involved in rheumatic fever) 

Lipoteichoic acid: binding to epithelial cells

F protein: adherance to epithelial cells

Streptolysins, O and S: lyse WBC, RBC, and platelets, promote spread

Streptokinase: lyse clots, promote spread

TST: superantigen

Encapsulated (Hyaluronic Acid)

pyogenic exotoxin A - Scarlet Fever

G⁺ cocci in clusters, catalase + & coagulase - (CoNS), β hemolytic, bacitracin resistant, hippurate +, CAMP +; aka, Group B Strep

meningitis, pneumonia (especially in neonates)

Most common form of meningitis in newborns

Culture swaps from vaginal and rectum and 35 weeks to test for group B strep; give intrapartum PCN if +

encapsulated bacterium 

G⁺ cocci in chains, catalase - grows in 40% bile, but susceptible to 6.5% NaCl; aka, Group D Strep

Low-grade fever and signs of endocarditis

Penicillin

Normal inhabitant of the lower GI tract, can penetrate the epithelium via lesions (eg. colon cancer or inflammed bowel)

G⁺ diplococci (lancet or football shaped), catalase - α hemolytic, bile-escullin negative, optochin sensitive; aka, pneumococci, "Quellung reaction", "rust-colored sputum"

meningitis, otitis media, lobular pneumonia, sinusitis & sepsis (bacteremia)

rare: osteomyelitis, septic arthritis, endocarditis

penicillin or celphalosporins, amoxicillin, fluoroquinolones, macrolides

vanocmycin if meningitis

Pneumovax: vaccine with capsular polysaccharides

Normal flora

Major cause of community acquired pneumonia

Asplenic pts are unable to remove Ab-coated organism (give Pneumovax)

Phosphorylcholine (binding) is unique to S. pneumoniae

IgA proteases contribute to virulence

PCN resistance by altering PCN binding proteins

G⁺ cocci in chains, catalase -, α hemolytic, bile-escullin negative (bile resistant), optochin resistant; aka, viridan streptococci

Quellung reaction

dental caries (mutans), brain or abdominal abscesses (intermedius), Subacute Bacterial Endocarditis (SBE)

penicilllin G

SBE: viridian streptococci and enterococci colonize valves previously damage by group A strep (Rheumatic fever)

Blood cultures of S. intermedius often indicates the presence of abscesses

dextrans allow adherence 

G⁺ bacilli, spore forming, aerobic, non-motile

malignant cutaneous pustules (black, surrounded by red border), dysentery, or inhalation anthrax

parenteral penicillin G, anti-PA vaccine (military)

fluoroquinolones (ciprofloxacin, levofloxacin, and moxifloxacin) and doxycycline 

Found in wool and goat skin.

Anthrax toxin:

Protective Antigen (PA) - binds

Edema Factor (EF) - ↑ adenylate cyclase activity

Lethal Factor (LF) - causes cell death, inhibits MAP Kinases and causes necrosis

G⁺ bacilli, spore forming, aerobic, motile

food poisoning, eye infections (?)

symptom management (toxin from reheated food)

also found in soil

G⁺ cocci in chains or pairs, catalase -, variable hemolysis, grows in 40% bile and 6.5% NaCl aka. Group D enterococci 

UTI, biliary tract infection

can become systemic and colonize heart valves (endocarditis)

ampicillin, or vancomycin + aminoglycosides (synergistic)

VRE: linezolid, daptomycin, tigacycline

Biofilms

Frequent complication of biliary/hepatic surgery or indwelling catheters 

2nd most common cause of nosocmial infections in US due to high resistance

Thin G⁺ bacilli

localized skin infections

generalized cutaneous infections

septicemia w/ possible endocarditis

Penicillin, cephalosporins, erythromycin, clindamycin

Resistant to: sulfonamides, amnioglycosides, vancomycin

Zoonotic - butchers, zookeepers, etc. are at higher risk

G⁺ pleomorphic bacilli, non-spore-forming, non-motile, "Chinese letter" appearance, black colonies on potassium tellurite, Loeffler's medium, Elek's test demonstrates presence of toxin

C. diptheriae: diphtheria (complications: myocarditis), cutaneous diphtheria papule progressing to ulcer

colonizes: Respiratory tract, GI, GU, and skin

C. jeikeium: bacteremia

C. urealyticum: urease, UTIs, stones

DTaP (prevention)

antitoxin, PCN, erythromycin

asymptomatic normal flora

only cells infected with a specific lysogenic phage carry the toxin, EF-2 (elongation factor 2) which inhibits protein synthesis (activated by ribosylation) 

Bullneck

Psuedomembrane (scraping causes bleeding)

demylenates nerves in posterior pharynx 

death due to myocarditis

Acid-fast bacilli (mycolic acids), non-motile, obligate aerobe, grows on Lownstein-Jensen agar

Primary infection: middle lobes

Reactivated infection: upper lobes

wasting, fever, bloody sputum

RIPES: rifampin, isoniazid (INH), pyrazinamide, ethambutol, streptomycin prophylaxis

Second line drugs: cell wall inhibitor (cycloserine, ethionamide), aminoglycosides (streptomycin, amikacin, kanamycin, cepreomycin), antimetabolite (para-aminosalicylic acid), fluoroquinolones (levoflloxacin, moxafloxacin, gatifloxacin)

Last line of defense: cllofazimine, bedaquiline

Oppurtunistic

Wax-mycolic acid coat, thick peptidoglycan layer, cell membrane

Multidrug-resistant

cord factor - sulfatides prevent fusion with lysosomes 

latent infections reactivates in 5% of cases (usually immune compromised), within macrophages

millet infection is potentially lethal 

Pott's disease (when TB affects the bones)

γ interferon for pts with vaccine 

exposure to M. bovis can cross react with skin test

Ghan focus - initial infection site (peripheral lung)

Thin acid-fast bacilli, non-motile, obligate aerobe, grows at low temps, phenolase +

Tuberculoid: hypopigmented hairless lesion (TH1 reaction)

Lepromatous: diffuse granuloma, "saddle nose", neuropathy (TH2 reaction)

Dapsone and rifamipin for 6 months (lepromatous, plus clofazimine for 2-5 years)

Carried by armadillos, or spread by contact or inhalation

M. avium in immunocompromised only 

M. marinum with seawater contamination (granuloma)

G⁺ beaded filaments, wealky acid fast (mycolic acid), obligate aerobe, urease +

pneumonia, abscesses in kidney & brain

TMP-SMX, surgical drainage

CNS: TMP-SMX + cephalosporin or imipenem

Frequently found in soil

Infections are most common in immuncompromised patients

Mycobacterium avium complex

 M. avium & intracellulare

 avium - possible Crohn's disease or pulmonary disease

intracellulare - pulmonary disease in immunocompetent hosts

acquired through contaminated oral intake

dissemination widespread in immunocompromised patients

macrolide (clarithromycin, azithromycin), plus rifamycin (rifampin, rifabutin) and ethambutol

Prophylaxis: clarithromycin or azithromycin 

G- coccobacilli, grown on chocoate agar

pneumonia, epiglottitis, otitis media, meningitis (encapsulated Type B strain), sepsis and septic arthritis in asplenic patients 

Vaccine available for Type B strain capsule with diptheria toxin, given at 2-18 months. β lactam, ceftriaxone, rifampin 

Factor 5 (nicotenamide added to chocolate agar)

aerosol

G⁺ weakly acid fast bacilli with possible rudimentary branching; revert to coccoid forms after 14-18 hours growth in lab

oppurtunistic facultative intracellular organism that survives within macrophages

Localized infections: extended spectrum macrolide (azrithromycin, clarithromycin) or fluoroquinolone (levofloxacin)

Disseminated infections: two or more antibiotics such as vanc, imipenem, aminoglycosides, fluoroquinolones, rifampicin

not PCN or cephalosporins (cell wall synthesis is modified)

50% fatality in immunocompromise

20% fatality in immunocompetent

suppurative - purulent

cutaneous localized pyogenic  infections: carbuncles/furncles, staphylococcal wound infection

systemic: pneumonia/empyema, osteomyelitis, septic arthritis, bacteremia, endocarditis

caused by Staphyococcus aureus (tampons or surgery) Streptococcus pyogenes (skin infections)

Presents as fever, hypotension and diffuse erythematous rash

potentially fatal

purpura fulminans: virulent form of TSS with larger purpuric skin lesion, fever, and disseminated intravascular coagulation 

caused by Staphylococcus aureus (SSSS)

skin wound or cutting umbilicus in neonates. exfoliative toxins ETA & ETB are produced

potentially fatal

large, erythematous (or indurated) swollen area on diabetic patient

follicular involvement

Cause by S. pyogenes

pharyngitis + "sandpaper" rash (spares face), "strawberry tongue" within first 2 days, desquamation of palms and soles after rash subsides 

Extoxins A (TSLS), B (protease, related to necrosis) & C (TSLS)

 S. pyogenes pharyngitis left untreated in children my develop into rheumatic fever through an autoimmune cross-reaction between anti-strepococcal antibodies and antigens naturally present in the joints and heart tissue

Permanent endocardial damage (esp. mitral stenosis) which may present as murmur years later

J♥NES: Joints (polyarthritis), heart problems (valvular damage, myocarditis, pericarditis), nodules (f-arm, elbows, knees), erythema marginatum, sydenham's chorea (involuntary movements, esp. hands and face)

 Immune response to S. pyogenes pharyngitis or impetigo can cause deposits of immune complexes on the glomerular basement membranes resulting in glomerular inflammation which develops 2-3 weeks after infection.

Hematuria (dark brown urine), hypertension, periorbital edema

Complete recovery likely. Treat with PCN.

S. pyogenes is introduced to the investing fascia by trauma or surgery. 

Extoxin B released → rapid necrosis along fascial planes w/o damage to muscles

Enterotoxin A - food poisoning

B - pseudomembranous enterocolitis

C & D - milk products

ETA - heat stable, phage associated

ETB - heat liable, plasmid associated 

both are proteases

Inhibits RNA synthesis

crosses BBB (debated)

orange/red urine, tears, or sweat

speed up CYP450 (birth control)

mutation in rpoB gene encoding the β-subunit of DNAD-RNAP 

avoid giving with HIV protease inhibitors 

inhibits sythesis of mycolic acids, activated by KatG; works on actively growing bacteria best

penetrates BBB

Asian and Native American decent may need higher doses (metabolized more quickly)

supplement with vitamin B₆ to prevent neurotoxic effects

monitor for hepatotoxicity; stop drug if hepatitis develops

inhibits CYP450; affects phenytoin,carbamazepine  and warfarin

mutation of katG gene

active only against mycobacteria; mechanism of action not completely understood, but thought to involve cell membrane metabolism and transport functions

causes hyperuricemia may provoke arthritis

avoid during pregnancy

inhibits mycobacterial arabinosyl transferase 

resistance emerges rapidly if used alone

can lead to red-green colorblindness at high doses

few adverse reactions with other drugs

oxazolidones

bacteriostatic "drug of last resort"

streptogamin

"drug of last resort" against MRSA

Pyoderma (Impetigo)

Streptococcus pyogenes

Erysipeals

signs of systemic infection: fever, chills, etc

Streptococcus pyogenes

Necrotizing Fascitis with bulllae (fatal)

Streptococcus pyogenes

M. scrofulaceum

Localized lymph node infection

surgical removal

M. marinum

cutaneous infections associated with exposure to water (salt or fresh)

rifampin, ethambutol, claritrhromycin

"aquarium owners disease" 

M. kansasii

photochromagen

pulmonary disease

Treat like Tb 

M. fortuitum & abscessus

Deep subcutaneous infection that may disseminate

trauma or iatrogenic 

Stapylococcal Cytoxins

α

β

δ

γ

α - pore forming

β - heat-labile

δ - cytolytic surfactant

γ - rapid cell death of neutorphils

Virulence Factors:

Staphylococcus aureus

influenza

group A Strep

IgA proteases

Sa: Protein A

hemagglutin (facilitates cellular entry)

M protein and streptokinase

Streptococcus pneumonia, Haemophilus influenzae type B, & Neisseria spp.