Medfools Bacteria chart for USMLE I, Schemes and Mind Maps for Microbiology

Medfools Bacteria chart for USMLE I, Schemes and Mind Maps for Microbiology

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Staphylococcus aureus (virulent) (nonmotile, nonsporeforming, facultative anaerobe) Gm+ cocci 1

Medfools Bacteriology a la chart for the USMLE I

Adapted from notes from UCLA., with additional corny mnemonics

Staphylococcus aureus (virulent) (nonmotile, nonsporeforming, facultative anaerobe) Gm+ cocci Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention *Skin infections: impetigo, cellulitis, erysipelas, abcess, furuncle, carbuncle *Bacteremia/sepsis: hematogenous spread *Acute endocarditis: DESTRUCTIVE (compare to S.viridans and S.faecalis) *Pneumonia –damaging process, cavitations, empyema, effusions *Osteomyelitis/septic arthritis- hematogenous and traumatic spread *Food poisoning – 1-8 hr onset, vomiting, preformed toxin *Tox shock syndrome- fever, vomiting, diarrhea, diffuse erythematous rash

Gm + cocci in grapes/clusters

Catalase + coagulase +

Ubiquitous in environment; normal flora of skin/nose

Spread through lesions, fomites

Enterotoxin- vomiting, diarrhea, heat resistant, (actually released in gut) TSST-1 – tampon use, wounds, superantigen Exfoliatin- scalded skin

TISSUE SPREAD: Alpha toxin(lechthinase)- skin necrosis;hemolysis Hyaluronidase- degrades proteoglycans Fibrinolysin- lysis fibrin clots

IMMUNE EVASION: Protein A- binds IgG-Fc, blocks opsonization and complement fixation Coagulase- activates prothrombin Hemolysin- destroys RBCs, PMNs, M0s, platelets Leukocidin- destroys WBCs

Gm + cocci in grapes, Catalase differentiates from Strep.

S.aureus: Beta hemolysis, coagulase, Yellow (Au) pigment

(coagulase causes coagulation!)

Coagulase neg:

S. epidermidis: novobiocin sensitive “sensitive skin”

S. saprophyticus: Novobiocin resistant

Beta lactamase production is common! Use methicillin, nafcillin, dicloxacillin

MRSA- vancomycin


S. epidermitis: associated w/ IV catheters, damaged/prosthetic heart valves: INSIDIOUS onset, Nosocomial, LESS virulent. Blood culture Contaminant

S. saprophyticus: Community acquired UTI in young women 2

Streptococcus viridans (GABHS) (nonmotile, nonsporeforming) Gm+ cocci Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention *Pharyngitis- “strep throat”, erythema, tonsillar exudate, fever *Skin/soft tissue infections- impetigo, cellulitis, necrotizing fascitis *Scarlet fever- centrifugal, red rash, erythrogenic toxin, slap cheek, strawberry tongue *Tox shock syndrome- clinically like Staph TSS *Rheumatic fcver- fever, myocarditis, polyarthritis, chorea, subcutaneous nodules, erythema marginatum rash. Mitral valve disease follows pharyngitis, NOT skin infections. Abs vs. bacteria cross react w/ joint and heart antigens *Acute GN- hypertension, hematuria, edema of face/ankles. Follows both pharyngitis AND skin infections. Cross reactive antigens deposited in GBM.

Gm + cocci in chains or pairs

Beta-hemolytic are classified by Lancefield groups (A,B,D) according to C- carbohydrates

Human throat/skin, Transmission by respiratory droplets

Hyaluronidase- degrades proteoglycans (TISSUE SPREAD) Erythrogenic toxin- scarlet fever, lysogenized S.pyogenes Streptolysin 0- results in beta hemolysis, target of ASO antibodies

M protein- antibody target, but inhibits complement/phagocytosis Streptokinase- converts plasminogen to plasmin, dissolves fibrin clots IgA protease


All Strep are Catalase –

Beta hemolysis and Bacitracin sensitivity point to GABHS, esp with inc. ASO titer.

Penicillin to prevent rheumatic fever.

Penicillin DOES NOT treat post strep disease or enterococcus.

S. agalactiae (Group B strep) Neonatal menigitis, sepsis pneumonia

Beta-hemolytic Female urinary tract

S. faecalis (enterococcus) Subacute endocarditis, UTI “Oh crap! I’ve got Heart problems!”

Not hemolytic GI tract Grows in 6.5% NaCl

S. bovis (group D) UTI Not hemolytic GI tract Hydrolyze esculin in presence of

bile. NOT grow in 6.5% bile S. pneumoniae (pneumococcus) Lobar pneumonia, ADULT meningitis, URI (kids)

Alpha-hemolytic Nasopharynx 85 different capsular polysaccarides

Quellung rxn 23 valent vaccine, for AIDS, elderly, asplenics

S. Mutans , mitis (Viridans group) Subacute endocarditis, caries Alpha-hemolytic Oropharynx 3

Neisseria (Chocolate agar, Oxidase +, kedney bean shape) Gm- cocci N. meningitidis (meningococcus) Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention *Meningococcemia- fever, arthralgias, myalgias, petechial rash, inc. in people w/ complement deficiencies *meningitis- fever, headache, stiff neck, photophobia, inc.PMNs in CSF * Waterhouse- Friedrichsen- fever, purpura, DIC, adrenal insufficiency due to bilateral adrenal hemorrhage, shock, death (like a bad meningococcemia)

Gm – cocci kidney beans.

Thayer-Martin, chocolate agar

Airborne droplets, colonized nasopharynx, establishes carrier states in some

Polysaccharide capsule, endotoxin (LPS), IgA protease

Capsular polysaccharides are antigenic serve as markers for classification.

Ferments maltose

Presumptive diagnosis by Gm stain of petechiae or CSF

LATEX agglutination test b/c capsular polysaccharides

Penicillin or Ceftriaxone (G3)

Chemoprophylaxis with Rifampin (excreted into saliva)

Polysaccharide vaccine in military recruits.

N. gonnorhoeae (gonnococcus) (most common notifiable disease in US) Males- symptomatic dysuria, penile discharge b/c of urethritis. Leads to epididymitis, prostatitis, urethral strictures

Female- asymptomatic, vaginal discharge, dyspareunia, due to cervicitis,Infertility, PID, ectopic, tubo-ovarian abcess, perihepatitis (Fitz- Hugh-Curtis syndrome), opthalmia neonatorum

Both: Septic arthritis


Gm – cocci kidney beans.

Thayer-Martin, chocolate agar

Sexual transmission

OFTEN coexistent WITH Chlamydia AND Syphilllis (tx w/ tetracycline or chloramphenacol)

Pili/fimbriae (ANTIGENIC variation)

LPS OMPs IgA protease


Men: Gm – diplococci in PMNs

Does NOT ferment maltose

No serologic testing, no capsule!

Ceftriaxone (G3) b/c penicillinase producing N.gonnorhoeae PPNG common

Erythromycin eye drops in newborns (also protects vs. Chlamydia)

No Vaccine.

NOTE: bacterial meningitis: 0-6 months (Group B Strep, E.coli,Listeria); 6 months – 3 years (H.influenzae B), 3-15 years (N. meningitidis), >15 years (S. pneumoniae) 4

Clostridium (Anaerobic, spore-forming, with Exotoxin) Gm+ Rods C. tetani Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention Tetanus – tetany, risus sardonicus “joker smile”, exaggerated reflexes, respiratory failure

Spores, ubiquitous in soil, enter wounds and germinate in anaerobic environment of necrotic tissue

Tetanus toxin travels intra axonally to CNS, blocks release of inhibitory glycine neurotransmitter

Penicillin, ventilatory support, muscle relaxants

Tetanus immune globulin, preformed Ig

Tetanus toxoid (formaldehyde treated tox)

C. botulinum Botulism “flaccid paralysis”, descending weakness, diplopia, flaccid paralysis, resp failure. Wound botulism- spores to wounds, germinate, release toxin Infant botulism- ingestion of spores in honey- floppy baby

Spores, in soil, inadequate sterilization of canned foods. Alkaline veggies, smoked fish.

Botulinum toxin ingested preformed. Tox spreads in blood, to nerves blocks Ach RELEASE

Toxin can be used to Tx torticollis, blepharospasm

Antitoxin, ventilatory support

NO PENICILLIN!! Will burst cells and release toxin

Watch swollen cans!

C. perfingens Gas gangrene (myonecrosis): war wounds, septic abortions

Food poisoning- ingestion of cooking resistant spores in foods. Watery diarrhea, cramps, little vomiting

Results in crepitus- gas production and Hemolysis

Normal flora of colon and vagina

Alpha tox- lecithinase degrades cell membranes- hemolytic

Morphology, exudate smears, culture, sugar fermentation, organic acid production

Debridement, O2 gas, Penicillin

C. difficile Antibiotic associated pseudomembranous colitis- esp in hospitalized pts.

Normal flora in 3% of people

Suppression of normal flora allows overgrowth, usually by clindamycin, ampicillin, cephalosporins Exotox A (severe diarrhea Exotox B (damage to colonic mucosa)

ID C-diff tox in stool

Metronidazole- poorly absorbed orally, inc. colonic dose

Vancomycin 5

Bacillus (Aerobic, spore-forming, with Exotoxin) Gm+ Rods B. anthracis Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention Woolsorter’s disease- pulmonary anthrax, pneumonia

Large w/ square ends, nonmotile

Common in animals. Humans infected by spores on animal products (skins/hides)

Transmission through skin, GI tract, respiratory tract

Antiphagocytic capsule made of d-glutamate [only one w/ Amino acids!] (not a polysaccharide)

Tripartite anthrax toxin: protective antigen, lethal factor, edema factor. Protective factor inhibits phagocytosis.

Morphology and blood agar growth.

Penicillin Sterilization of animal products, and vaccination of animals.

Vaccine (protective antigen) for humans at risk

B. cereus Vomiting with 4 hr incubation period (like S.aureus)- heat stable toxin--

Distinguished from B. anthracis by motility and lack of capsule.

Spores on grains survive cooking and germinate when food is warmed.

Preformed heat-labile enterotoxin (like E.coli, Cholera tox) - diarrhea

Treat symptoms Avoid reheated rice

Corynebacterium diptheriae (nonmotile, nonsporeforming, Chinese) Gm+ Rods Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention Diptheria – throat inflammation, gray fibrinous exudate (pseudomembrane), airway obstruction, myocarditis, recurrent laryngeal nerve palsy

Club shaped, in palisades, Chinese characters

Polyphosphate granules stain metachromatically

Airborne droplets, colonization of throat and production of Diptheria tox.

Diptheria tox: inhibits protein syn by ADP ribosylation of eukaryotic ef-2. Toxin produced by lysogenized bacteria (like erythrogenic toxin of GABHS)

Tellurite plate, Loefller’s

Toxin assessed by animal inoculation or gel diffusion precipitin test.

Antitoxin, Penicillin to reduce transmission

Diptheria toxoid vaccine. (disease in US is iatrogenic due to innoculation by inadequately killed toxin. 6

Listeria monocytogenes (Facultative intracelluar anerobes, Non-sporeforming, tumbling motility) Gm+ Rods Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention Neonatal meningitis and sepsis, abortion, premature delivery

Gm + rods, in clumps, Chinese characters, NON- sporeforming, Tumbling distinguishes it from corynebacterium

Newborns, immunocompromised are high risk groups.

Transmitted to humans from animal feces, veggies, unpasteurized milk/cheese.

Only Gm+ with LPS Infects monocytes and induces granulomas. Listeriolysin O punches holes in cells

Gm+ rods, beta hemolysis, motility

Ampicillin No vaccine 7


Note: Not all gram negative enterics belong to Enterobacteriaciae family: 1) colonic location 2) facultative anaerobes 3)ferment glucose, 4)oxidase negative, and 5)reduce nitrates to nitrites. ALL are members here EXCEPT: Vibrio, Campylobacter, Helicobacter, Pseudomonas, Bacteriodes. (“Vile People Can’t Be Happy”) As a group, Enterobacteriaciae are often normal flora. Pathogenisis is by endotoxin/LPS, exotoxins. O (Outer polysaccharides), H (flagHella), K (Kapsular polysaccharides) are important antigens. Inoculation on MacConkey’s or Eosin-Methylene Blue (EMB) agar differentiates family members by lactose fermenting ability. Fermenters are pink-purple, non-fermenters are colorless. Also keep an eye on motility.

ENTERIC (Intestinal AND non-Intestinal disease) Gm- Rods E. coli (Enterobacteriaciae) Diseases Character Hab/Trans Pathogenesis Diagnosis Treatment Prevent Most common UTI, Gm- sepsis, traveller’s diarrhea. 2nd most common cause of Neonatal meningitis. Enterotoxigenic strains: Do NOT invade! heat labile enterotox binds GM1 ganglioside receptor, activates adenylate cyclase via ADPribosylation of G protein. (like Cholera tox) Watery diarrhea. Enterohemorragic: verotoxin inhibits 60s ribosome (like Shigella)Bloody diarrhea. 0157:H7 type causes hemolytic-uremic syndrome (anemia, thrombocytopenia, renal failure) associated w/ fast food outbreaks Enteroinvasive: factor mediated invasion of epithelial cells, sepsis. Bloody diarrhea with WBCs.

As other enterobacteria ciae family

Normal flora, but need virulence factors to cause disease.

Pathogenisis by pilus and enterotox, capsule, and endotoxin.

Serotype ID by O,H,K antigens

Ferments lactose, unlike Salmonella, Shigella

G3 Cephalosporin No vaccine

Salmonella (Enerobacteriaciae) S. enteritidiscauses gasteroenteritis via Cholera like tox. Large inoculum needed. (Peptic acid kills) Tx symptoms. S.typhi –Typhoid fever, init by asymptomatic infection of gut phagocytes and dissemination to liver, Gall bladder (carrier state), Fever, RLQ abdominal pain, rose spots. Tx Cipro or ceftriaxone. S. cholerae-suis- Gm- sepsis. Esp patients with Sickle cell (risk for osteomyelitis b/c func. Asplenia)

As other enterobacteria ciae family

Normal flora of animals. Contamination food, poultry / eggs

K anitgen/Vi antigen Flagella antigenic variation

Does NOT ferment lactose. Production of H2S gas distinguish from Shigella.

S. typhi- by Cipro or ceftriaxone

Hand washing, cooking, water chlorination 8

ENTERIC (INTESTIAL disease) Gm- Rods Shigella (Enterobacteriaciae) Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention Enterocolitis (dysentary) by S.dysentariae, S.sonnei, S. flexneri, S. boydii


Small innoculum <100 bugs

Not normal flora. Humans only host. 4Fs: fingers flied food feces (fecal- oral)

Distal ileal and colonic mucosal invasion and cell death. Does NOT enter bloodstream (unlike Salmonella)

NO H2S gas, nonmotile. Non lactose fermenting on EMB, MacConkey’s agar

PMNs in smear w/ fever suggest invasive bug.

Fluid replacement, avoid antiperistaltic drugs which prolong excretion of organism.

Vibrio (Not Enterobacteriaciae) Cholera - Massive watery diarrhea (Rice water stool) like enterotoxic E.coli

V.parahemolyticus is a marine bug in contaminated raw seafood. Japan

Comma shaped, single flagella. Large innoculum needed.

Infects humans only, transmission by fecal- oral.

Mucinase aided colonization of small intestine, bipartite enterotox: binds GM1 gangliosides on enterocyte, ADP- ribosylation of G protein. (like ETEC)

Diagnosis clinically in endemic areas: Asia, Africa, Latin America.

Oral rehydration No effective vaccine.

Campylobacter (Not Enterobacteriaciae) More frequently causes enterocolitis than Salmonella or Shigella. Can cause bloody diarrhea

Comma or S- shaped, Microaerophilic, urease negative

Domestic animals via fecal oral, unpasteurized milk

Probably enterotoxin

Blood agar w/antibiotics, C.jejunigrows at 42C, produces oxidase, nalidixix acid sensitive C.intestinalis grows at 25C, oxidase neg, resistant to nalidixic acid

Antibiotics No Vaccine

Helicobacter pylori (Not Enterobacteriaciae) Gastritis, peptic ulcer, risk factor Gastric carcinoma

Urease + (protects from stomach acid)

Fecal-oral. Attaches to gastric mucosa, mediated by NH3 production, host inflammatory response

Bismuth sulfate, tetracycline, metronidazole

No vaccine. 9


Klebsiella-Enterobacter-Serratia (Enterobacteriaciae) Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention Opportunistic pathogens cause UTI, pneumonia, usually nosocomial Klebsiella is nonmotile, with capsule, mucoid colony appearance. Klebsiella pneumo renowned for severity, bloody “currant jelly” sputum, lung cavitations. Serratia-bright red pigment. Nosocomial- Ab resistant

All ferment Lactose

K.pneumoniae, E.cloacae, S.marcescens difficult to distinguish clinically

Large intestine, soil water Ferment lactose on EMB, MacConkey’s agar

No vaccine

Proteus-Providencia-Morganella (Enterobacteriaciae) Community and nosocomial UTI, b/c high motility

(important species: Proteus mirabilis, Proteus vularis Providencia rettgretii M. morganii )

Non lactose fermenting, urease + (alkalinizes urine)

Only enterobac that makes phenylalanine deaminase

Large intestine, soil water Swarming appearance on blood agar. Use antigens from Rickettsiae cross react with Proteus.

P.mirabilis is indole neg unlike others of this group.

No vaccine

Pseudomonas (Not Enterobacteriaciae) P aeruginosa: opportunistic, nosocomial:Pneumonia, osteomyelitis, burn infections, sepsis, UTI, endocarditis, malignant otitis externa, corneal infections. P. cepacia colonizes CF patients

Strict aerobe, Not glucose fermenting, Not reduce nitrates, oxidase +

Normal flora of colon. Exotox like C.diptheriae (ADP- reibosylation)

Produces pyocyanin, pyoverdin

Highly resistant. Combo pipercillin, ticarcillin and aminoglycoside. Ceftazidime

Bacteroides fragilis (Not Enterobacteriaciae) Peritoneal abscesses. Growth favored by growth w/ facultative anaerobes to exhause local oxygen

Anaerobic, non sporeforming, non LPS, polysaccharide capsule. No exotox, No LPS

Predominant flora of colon. NOT communicable. Exits colon via break in mucosa (Chronic disease, PID, trauma)

Polysaccharide capsule provides virulence factor

Treat as mixed infection. Clindamycin, or metronidazole

No Vaccine

www 10

RESPIRATORY Gm- Rods H. Influenzae (chocolate agar w/ heme and NAD) Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention Leading cause of meningitis in kids. Peak at 6m to 1 yr. (decline in maternal IgG, inability of infants to mount attack vs. polysaccharide capsule)

Fatal epiglottitis by type B influenzae.

Coccobacillus w/ polysaccharide Capsule

Upper respiratory tract, respiratory droplets

ONLY encapsulated forms like type B cause invasive disease. Nonencapsulated cause URI, pneumonia in pts with preexisting lung disease (COPD). IgA protease,

Chocolate agar, w/ heme and NAD.

Quellung rxn

Rifampin prevents meningitis and transmission from close contacts b/c secreted into saliva better than Ampicillin

HIB vaccine of capsular polysaccharide conjugated to carrier protein.

Legionella pneumophilia (Cysteine and Iron agar) Atypical pneumonia with high fever, nonproductive cough( differentiate from Mycoplasma, influenza, psittacosis, Q fever)

Poor gm stain Airborne from water sources. Smoking EtOH, Immunosuppressed are at risk.

High concentration

Error! No table of figures entries found.of cysteine and iron. Urine antigen test. Suspect when inc. PMNs with no organisms!

Erythromycin (also good for Mycoplasma)

Disinfect water sources

Bordetella pertussis (Bordet-genou agar) Whooping cough-acute tracheobronchitis with URI symptoms, paroxysmal hacking cough 1-4 wks, copious mucus

Small gm- rods Airborn droplets (highly contagious)

Polysaccharide capsule and pili are essential for virulence. Does NOT invade. Pertussis tox (ADP-ribosylation), and tracheal cytotoxin.

Culture on Bordet- genou agar. Ab agglutination, stain

Erythromycin reduces complications, doesn’t change clinical course. Resp tract already damaged.

Killed B.pertussis vaccine 2,4,6 months, Boosters at age 1, school. Acellular vax for booster only.

“Hmmmm Chocolaaate!”


.medfo 11

ZOONTIC Gm- Rods Brucella (virulent, facultative intracellular, tx: aminoglycoside) Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention Brucellosis- influenza like syndrome w/ undulating fever(higher during day, lower at night). Lymphadenopathy, H/Smegaly, no boboes/ulcers.

Small gm- rods Animal reserviors: B melitensisi (goats/sheep) B. abortus (cattle) B. suis (pigs) Non pasteurized milk products(travelers), through skin (meat packers, vets, farmers)

Organisms localize in RES. Persist in macrophages, induce granulomas

Serology, biochemistry

Antibiotics Animal vaccination, pasteurization.

No Human vaccine.

Francisella tularensis (virulent, facultative intracellular, tx: aminoglycoside) Tularemia- influenza like syndrome w/ ulceroglandular lesions (hole in skin, black base, swollen LN, draining pus)

Small gm- rods Ubiquitous in US in wide variety of animals. Tick/mite vectors. Humans as accidental dead end hosts by bites or animal skin handling.

Enters through skin, localizes in RES. Persist in macrophages, induce granulomas

Serology Streptomycin Live attenuated vaccine (like BCG)

Yersinia pestis (virulent, facultative intracellular, tx: aminoglycoside) Plague- Hematogenous spread results in fever myalgias, hemorrhage. Also septic shock, pneumonia.

Small gm- rods with bipolar stain

Endemic in prairie dogs in US, 99% cases in SE Asia. Rats/flease in urban centers. Also wound- person respiratory droplets.

Bacteria spread to regional LN, enlarged tender buboes.

Immunoflorescence Antibiotics Quarantine.

No Vaccine.

Pasteurella multocida Cellulitis rapid onset at bite site. Osteomyelitis as complication. Sutures predispose to infection

Small gm- rods Normal flora of dogs and cats. Transmitted to humans by animal bite.

Presumptive Dx by rapid onset cellulitis at animal bite.

Penicillin Ampicillin prophylax. 12

MYCOBACTERIA (Obligate aerobe, facultative intracellular organisms) Acid Fast Rods M. tuberculosis Diseases Character Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention Tuberculosis: chronic low grade fever, night sweats, productive cough, hemoptysis, weight loss. Elderly, immunocomp, malnourished at risk.

Obligate aerobe, intracellular, infect M0, persist for years. Mycolic acid walls

Only infects humans. Respiratory aerosol. Infects M0s in mid/lower lobes, init granuloma formation, widely disseminate the infection. T cells help M0 kill some intracellular mycobacteria at expense of bystander cell damage. Result: necrotic host cells, viable mycobacteria. Walled off w/ giant cells, fibroblasts, collagen, calcification to form granuloma or tubercle. This 1’ infection = Ghon focus on CXR (when including Ca tubercles in perihilar lymph nodes = Ghon complex.) Reactivation prefers upper lobe (obligate aerobe) of lung. Reactivation can infect any organ. Cervical LN (scrofula),spine (Pott’s disease.)

Mycolic acids confer acid fastness. WaxD is active ingredient in Freund’s adjuvant. Cord factor is virulence factor (mycoside= 2 mycolic acids + disaccharide)

PPD tests for prior exposure or to BCG vax. Positive test if both redness, induration 48-72 hr after injection (DTH rxn.)

Note: candida and mumps as controls in immunocomp.

Acid fast stain. NaOH concentrate on Lowenstein- Jensen medium. Slow culture, 6-8 wks. Niacin production

Prolonged, multiple Tx. (INH, rifampin, pyrazinamide, ehtambutol)

Protracted tx b/c: intracellular life cycle, granuloma blocks penetration of drug, metabolically inactive mycobac persist in lesion

Chemoproph ylax w/ INH (watch hepatotox in people >35 y.o.)

Live attenuated M.bovis (BCG) induces some protective immunity.

M. avium- intracellulare Clincal TB indistinguishable from M tuberculosis in AIDS.

Atypical mycobacterium

Found in water, soil, not pathogenic in guinea pigs (infects birds)

Azithromycin Clarithromycin

Macrolide prophylax when CD4 count < 50

M. leprae Leprosy- preferential growth in < 37C, skin, superficial nerves. Tuberculoid- good cellular immune response, few AFB, granulomas, positive lepromin skin test. Anethetized skin lesions and thickened superficial nerves. Lepromatous- poor cellular immune response, lots of organisms, foamy histiocytes, negative lepromin skin test (poor response.) Skin lesions, lion facies. Skin anesthesia, bone resorption, skin thickening, disfiguring.

Never has been grown in lab.

Brazil, India, Sudan

Humans only natural hosts. Mouse footpad and armadillo growth only. Transmission by nasal secretions, skin lesions to persons with prolonged contact w/pts.

Intracellular replication (skin histiocytes, endothelial cells, Schwann cells)

RifampinDapsone Up to 2 years!

Prophylax exposed persons with Dapsone. 13

ACTINOMYCETES Gm- Branching Rods A. israelii Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention Actinomycosis- hard non- tender swelling, drains pus through sinus. (abscess that spreads to neck, chest, abdomen.)

Aanerobic Gm- branching rods

Normal anaerobic flora oral cavity/GI tract. Not communicable.

Invasion after local trauma (risk factor for anaerobic growth)

Anaerobic Gm- branching rods, sulfur granules in pus

Penicillin No vaccine

Nocardia asteroides (Acid Fast Branching) Nocardiosis- pneumonia that progresses to abscess formation, sinus tract drainage, dissemination to brain/kidney (immunosuppressed)

Aerobic Gm- branching rods.

Soil, NOT normal flora Acid fastbranching, NO sulfur, aerobic

Bactrim (trimethorprim + sulfamethoxazole)

No vaccine

Mycoplasma pneumoniae (No cell wall, poor gm stain) Small free living organism Diseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention “Walking pneumonia” (dry nonproductive cough, horrible CST, generally feel well) Most common pneumonia in young adults (college students).

Smallest free living organism, no cell wall so poor gm stain, resists penicillins, cephalosporins. Cell membrane has chol which are not in other bacteria. “Fried egg” colonies on Eaton’s agar. (“Eat Fried Eggs w/ chol”)

Respiratory droplets. Attaches but does NOT invade respiratory epithelium, like B.pertussis.

Pathogenic only for humans.

Arrests cilliary motion, induces epithelial cell necrosis. Cross reactive antigens induce anti RBC autoantibodies (cold agglutinins.)

Elevated titer of cold agglutinins or specific anitbodies

Erythromycin Tetracycline

No vaccine

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