Fairhurst a la chart



Fairhurst a la chart

Kendensed bacteriology notes for USMLE I

Adapted from notes by Rick Fairhurst, M.D. Ph.D., with additional corny mnemonics

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

|Diseases |Characteristics |Habitat/Transmission |Pathogenesis |Diagnosis |Treatment |Prevention |

|*Skin infections: impetigo, |Gm + cocci in |Ubiquitous in environment; normal |Enterotoxin- vomiting, diarrhea, |Gm + cocci in grapes, Catalase |Beta lactamase production|none |

|cellulitis, erysipelas, abcess, |grapes/clusters |flora of skin/nose |heat resistant, (actually released|differentiates from Strep. |is common! Use | |

|furuncle, carbuncle | | |in gut) | |methicillin, nafcillin, | |

|*Bacteremia/sepsis: hematogenous |Catalase + |Spread through lesions, fomites |TSST-1 – tampon use, wounds, |S.aureus: Beta hemolysis, |dicloxacillin | |

|spread |coagulase + | |superantigen |coagulase, Yellow (Au) pigment | | |

|*Acute endocarditis: DESTRUCTIVE | | |Exfoliatin- scalded skin | |MRSA: (Methicillin | |

|(compare to S.viridans and | | | |(coagulase causes coagulation!)|resistant S. aureus) : | |

|S.faecalis) | | |TISSUE SPREAD: | |vancomycin | |

|*Pneumonia –damaging process, | | |Alpha toxin(lechthinase)- skin | | | |

|cavitations, empyema, effusions | | |necrosis;hemolysis |Coagulase neg: | | |

|*Osteomyelitis/septic arthritis- | | |Hyaluronidase- degrades | | | |

|hematogenous and traumatic spread | | |proteoglycans |S. epidermidis: novobiocin | | |

|*Food poisoning – 1-8 hr onset, | | |Fibrinolysin- lysis fibrin clots |sensitive | | |

|vomiting, preformed toxin | | | |“sensitive skin” | | |

|*Tox shock syndrome- fever, | | |IMMUNE EVASION: | | | |

|vomiting, diarrhea, diffuse | | |Protein A- binds IgG-Fc, blocks |S. saprophyticus: | | |

|erythematous rash | | |opsonization and complement |Novobiocin resistant | | |

| | | |fixation | | | |

| | | |Coagulase- activates prothrombin | | | |

| | | |Hemolysin- destroys RBCs, PMNs, | | | |

| | | |M0s, platelets | | | |

| | | |Leukocidin- destroys WBCs | | | |

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

|Streptococcus viridans (GABHS) (nonmotile, nonsporeforming) Gm+ cocci |

|Diseases |Characteristics |Habitat/Transmission |Pathogenesis |Diagnosis |Treatment |Prevention |

|*Pharyngitis- “strep throat”, erythema, |Gm + cocci in chains or |Human throat/skin, |Hyaluronidase- degrades |All Strep are Catalase – |Penicillin to | |

|tonsillar exudate, fever |pairs |Transmission by respiratory |proteoglycans | |prevent rheumatic | |

|*Skin/soft tissue infections- impetigo, | |droplets |(TISSUE SPREAD) |Beta hemolysis and |fever. | |

|cellulitis, necrotizing fascitis |Beta-hemolytic are | |Erythrogenic toxin- scarlet fever,|Bacitracin sensitivity | | |

|*Scarlet fever- centrifugal, red rash, |classified by Lancefield | |lysogenized S.pyogenes |point to GABHS, esp with |Penicillin DOES NOT | |

|erythrogenic toxin, slap cheek, strawberry |groups (A,B,D) according | |Streptolysin 0- results in beta |inc. ASO titer. |treat post strep | |

|tongue |to C-carbohydrates | |hemolysis, target of ASO | |disease or | |

|*Tox shock syndrome- clinically like Staph TSS| | |antibodies | |enterococcus. | |

|*Rheumatic fcver- fever, myocarditis, | | | | | | |

|polyarthritis, chorea, subcutaneous nodules, | | |M protein- antibody target, but | | | |

|erythema marginatum rash. Mitral valve disease| | |inhibits complement/phagocytosis | | | |

|follows pharyngitis, NOT skin infections. Abs | | |Streptokinase- converts | | | |

|vs. bacteria cross react w/ joint and heart | | |plasminogen to plasmin, dissolves | | | |

|antigens | | |fibrin clots | | | |

|*Acute GN- hypertension, hematuria, edema of | | |IgA protease | | | |

|face/ankles. Follows both pharyngitis AND skin| | | | | | |

|infections. Cross reactive antigens deposited | | |“HE’S an MSI” | | | |

|in GBM. | | | | | | |

|S. agalactiae (Group B strep) |

|Neonatal menigitis, sepsis pneumonia |Beta-hemolytic |Female urinary tract | | | | |

|S. faecalis (enterococcus) |

|Subacute endocarditis, UTI |Not hemolytic |GI tract | |Grows in 6.5% NaCl | | |

|“Oh crap! I’ve got Heart problems!” | | | | | | |

|S. bovis (group D) |

|UTI |Not hemolytic |GI tract | |Hydrolyze esculin in presence of bile. NOT | | |

| | | | |grow in 6.5% NaCl | | |

|S. pneumoniae (pneumococcus) |

|Lobar pneumonia, ADULT meningitis, URI (kids) |Alpha-hemolytic |Nasopharynx |85 different capsular |Quellung rxn | |23 valent vaccine, for AIDS, |

| | | |polysaccarides |Optochin sensitive | |elderly, asplenics |

|S. Mutans , mitis (Viridans group) |

|Subacute endocarditis, caries |Alpha-hemolytic |Oropharynx | |Optochin resistant | | |

|Neisseria (Chocolate agar, Oxidase +, kedney bean shape) Gm- cocci |

|N. meningitidis (meningococcus) |

|Diseases |Characteristics |Habitat/Transmission |Pathogenesis |Diagnosis |Treatment |Prevention |

|*Meningococcemia- fever, |Gm – cocci kidney beans. |Airborne droplets, colonized |Polysaccharide capsule, endotoxin |Ferments maltose |Penicillin or |Chemoprophylaxis with |

|arthralgias, myalgias, petechial | |nasopharynx, establishes carrier |(LPS), | |Ceftriaxone (G3) |Rifampin (excreted into |

|rash, inc. in people w/ complement |Thayer-Martin, chocolate |states in some |IgA protease |Presumptive diagnosis by Gm | |saliva) |

|deficiencies |agar | | |stain of petechiae or CSF | | |

|*meningitis- fever, headache, stiff| | |Capsular polysaccharides are | | |Polysaccharide vaccine in|

|neck, photophobia, inc.PMNs in CSF | | |antigenic serve as markers for |LATEX agglutination test b/c | |military recruits. |

|* Waterhouse-Friedrichsen- fever, | | |classification. |capsular polysaccharides | | |

|purpura, DIC, adrenal insufficiency| | | | | | |

|due to bilateral adrenal | | | | | | |

|hemorrhage, shock, death (like a | | | | | | |

|bad meningococcemia) | | | | | | |

|N. gonnorhoeae (gonnococcus) (most common notifiable disease in US) |

|Males- symptomatic dysuria, penile |NO CAPSULE |Sexual transmission |Pili/fimbriae (ANTIGENIC |Men: Gm – diplococci in PMNs |Ceftriaxone (G3) b/c|Erythromycin eye drops |

|discharge b/c of urethritis. Leads | | |variation) | |penicillinase |in newborns (also |

|to epididymitis, prostatitis, |Gm – cocci kidney beans. |OFTEN coexistent WITH | |Does NOT ferment maltose |producing |protects vs. Chlamydia) |

|urethral strictures | |Chlamydia AND Syphilllis (tx w/ |LPS | |N.gonnorhoeae | |

| |Thayer-Martin, chocolate |tetracycline or chloramphenacol) |OMPs |No serologic testing, no |PPNG common |No Vaccine. |

|Female- asymptomatic, vaginal |agar | |IgA protease |capsule! | | |

|discharge, dyspareunia, due to | | | | | | |

|cervicitis, Infertility, PID, | | |NO CAPSULE! | | | |

|ectopic, tubo-ovarian abcess, | | | | | | |

|perihepatitis (Fitz-Hugh-Curtis | | | | | | |

|syndrome), opthalmia neonatorum | | | | | | |

| | | | | | | |

|Both: Septic arthritis | | | | | | |

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)

|Clostridium (Anaerobic, spore-forming, with Exotoxin) Gm+ Rods |

|C. tetani |

|Diseases |Characteristics |Habitat/Transmission |Pathogenesis |Diagnosis |Treatment |Prevention |

|Tetanus – tetany, risus sardonicus “joker | |Spores, ubiquitous in soil, enter |Tetanus toxin travels intra | |Penicillin, ventilatory |Tetanus toxoid |

|smile”, exaggerated reflexes, respiratory | |wounds and germinate in anaerobic |axonally to CNS, blocks release | |support, muscle relaxants|(formaldehyde |

|failure | |environment of necrotic tissue |of inhibitory glycine | | |treated tox) |

| | | |neurotransmitter | |Tetanus immune globulin, | |

| | | | | |preformed Ig | |

|C. botulinum |

|Botulism “flaccid paralysis”, descending | |Spores, in soil, inadequate |Botulinum toxin ingested | |Antitoxin, ventilatory |Watch swollen cans! |

|weakness, diplopia, flaccid paralysis, | |sterilization of canned foods. |preformed. Tox spreads in blood, | |support | |

|resp failure. | |Alkaline veggies, smoked fish. |to nerves blocks Ach RELEASE | | | |

|Wound botulism- spores to wounds, | | | | |NO PENICILLIN!! Will | |

|germinate, release toxin | | |Toxin can be used to Tx | |burst cells and release | |

|Infant botulism- ingestion of spores in | | |torticollis, blepharospasm | |toxin | |

|honey- floppy baby | | | | | | |

|C. perfingens |

|Gas gangrene (myonecrosis): war wounds, |Results in crepitus- gas|Normal flora of colon and vagina |Alpha tox- lecithinase degrades |Morphology, exudate smears, |Debridement, O2 gas, | |

|septic abortions |production and Hemolysis| |cell membranes- hemolytic |culture, sugar fermentation,|Penicillin | |

| | | | |organic acid production | | |

|Food poisoning- ingestion of cooking | | | | | | |

|resistant spores in foods. Watery | | | | | | |

|diarrhea, cramps, little vomiting | | | | | | |

|C. difficile |

|Antibiotic associated pseudomembranous | |Normal flora in 3% of people |Suppression of normal flora allows|ID C-diff tox in stool |Metronidazole-poorly | |

|colitis- esp in hospitalized pts. | | |overgrowth, usually by | |absorbed orally, inc. | |

| | | |clindamycin, ampicillin, | |colonic dose | |

| | | |cephalosporins | | | |

| | | |Exotox A (severe diarrhea | | | |

| | | |Exotox B (damage to colonic | |Vancomycin | |

| | | |mucosa) | | | |

|Bacillus (Aerobic, spore-forming, with Exotoxin) Gm+ Rods |

|B. anthracis |

|Diseases |Characteristics |Habitat/Transmission |Pathogenesis |Diagnosis |Treatment |Prevention |

|Woolsorter’s disease- pulmonary anthrax, |Large w/ square ends, |Common in animals. Humans infected|Antiphagocytic capsule made of |Morphology and blood agar |Penicillin |Sterilization of |

|pneumonia |nonmotile |by spores on animal products |d-glutamate [only one w/ Amino |growth. | |animal products, and|

| | |(skins/hides) |acids!] (not a polysaccharide) | | |vaccination of |

| | | | | | |animals. |

| | |Transmission through skin, GI |Tripartite anthrax toxin: | | | |

| | |tract, respiratory tract |protective antigen, lethal | | |Vaccine (protective |

| | | |factor, edema factor. Protective | | |antigen) for humans |

| | | |factor inhibits phagocytosis. | | |at risk |

|B. cereus |

|Vomiting with 4 hr incubation period (like|Distinguished from B. |Spores on grains survive cooking |Preformed heat-labile enterotoxin | |Treat symptoms |Avoid reheated rice |

|S.aureus)- heat stable toxin-- |anthracis by motility |and germinate when food is |(like E.coli, Cholera tox) - | | | |

| |and lack of capsule. |warmed. |diarrhea | | | |

| | | | | | | |

|Corynebacterium diptheriae (nonmotile, nonsporeforming, Chinese) Gm+ Rods |

|Diseases |Characteristics |Habitat/Transmission |Pathogenesis |Diagnosis |Treatment |Prevention |

|Diptheria – throat inflammation, |Club shaped, in palisades, |Airborne droplets, colonization of|Diptheria tox: inhibits protein |Tellurite plate, Loefller’s |Antitoxin, |Diptheria toxoid vaccine. |

|gray fibrinous exudate |Chinese characters |throat and production of Diptheria|syn by ADP ribosylation of | |Penicillin to |(disease in US is |

|(pseudomembrane), airway | |tox. |eukaryotic ef-2. Toxin produced by|Toxin assessed by animal |reduce transmission|iatrogenic due to |

|obstruction, myocarditis, recurrent|Polyphosphate granules | |lysogenized bacteria (like |inoculation or gel diffusion | |innoculation by |

|laryngeal nerve palsy |stain metachromatically | |erythrogenic toxin of GABHS) |precipitin test. | |inadequately killed toxin. |

|Listeria monocytogenes (Facultative intracelluar anerobes, Non-sporeforming, tumbling motility) Gm+ Rods |

|Diseases |Characteristics |Habitat/Transmission |Pathogenesis |Diagnosis |Treatment |Prevention |

|Neonatal meningitis and sepsis, |Gm + rods, in clumps, |Newborns, immunocompromised are |Only Gm+ with LPS |Gm+ rods, beta hemolysis, |Ampicillin |No vaccine |

|abortion, premature delivery |Chinese characters, |high risk groups. |Infects monocytes and induces |motility | | |

| |NON-sporeforming, Tumbling | |granulomas. Listeriolysin O | | | |

| |distinguishes it from |Transmitted to humans from animal |punches holes in cells | | | |

| |corynebacterium |feces, veggies, unpasteurized | | | | |

| | |milk/cheese. | | | | |

ENTERIC GRAM NEGATIVE RODS

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 |As other |Normal flora, but need|Pathogenisis by pilus and |Ferments lactose, unlike |G3 Cephalosporin |No vaccine |

|most common cause of Neonatal meningitis. |enterobacteriaciae |virulence factors to |enterotox, capsule, and |Salmonella, Shigella | | |

|Enterotoxigenic strains: Do NOT invade! heat labile |family |cause disease. |endotoxin. | | | |

|enterotox binds GM1 ganglioside receptor, activates | | | | | | |

|adenylate cyclase via ADPribosylation of G protein. (like | | |Serotype ID by O,H,K antigens | | | |

|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. | | | | | | |

|Salmonella (Enerobacteriaciae) |

|S. enteritidis causes gasteroenteritis via Cholera like |As other |Normal flora of |K anitgen/Vi antigen |Does NOT ferment lactose. |S. typhi- by Cipro or |Hand washing, |

|tox. Large inoculum needed. (Peptic acid kills) Tx |enterobacteriaciae |animals. |Flagella antigenic variation |Production of H2S gas distinguish|ceftriaxone |cooking, water |

|symptoms. |family |Contamination food, | |from Shigella. | |chlorination |

|S.typhi –Typhoid fever, init by asymptomatic infection of | |poultry / eggs | | | | |

|gut phagocytes and dissemination to liver, Gall bladder | | | |Motile (THINK swimming salmon) | | |

|(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) | | | | | | |

|ENTERIC (INTESTIAL disease) Gm- Rods |

|Shigella (Enterobacteriaciae) |

|Diseases |Characteristics |Habitat/Transmission |Pathogenesis |Diagnosis |Treatment |Prevention |

|Enterocolitis (dysentary) by |Nonmotile |Not normal flora. Humans only |Distal ileal and colonic mucosal |NO H2S gas, nonmotile. Non |Fluid replacement, avoid | |

|S.dysentariae, S.sonnei, S. flexneri, S. | |host. 4Fs: fingers flies food |invasion and cell death. Does NOT|lactose fermenting on EMB, |antiperistaltic drugs | |

|boydii |Small innoculum 35 y.o.) |

| |acid walls |mycobacteria at expense of bystander cell |virulence factor (mycoside= 2 |hr after injection (DTH | | |

| | |damage. Result: necrotic host cells, viable |mycolic acids + disaccharide) |rxn.) |Protracted tx b/c: |Live attenuated |

| | |mycobacteria. Walled off w/ giant cells, | | |intracellular life |M.bovis (BCG) |

| | |fibroblasts, collagen, calcification to form | |Note: candida and mumps as|cycle, granuloma blocks|induces some |

| | |granuloma or tubercle. This 1’ infection = | |controls in immunocomp. |penetration of drug, |protective |

| | |Ghon focus on CXR (when including Ca tubercles| | |metabolically inactive |immunity. |

| | |in perihilar lymph nodes = Ghon complex.) | |Acid fast stain. NaOH |mycobac persist in | |

| | |Reactivation prefers upper lobe (obligate | |concentrate on |lesion | |

| | |aerobe) of lung. Reactivation can infect any | |Lowenstein-Jensen medium. | | |

| | |organ. Cervical LN (scrofula),spine (Pott’s | |Slow culture, 6-8 wks. | | |

| | |disease.) | |Niacin production | | |

|M. avium- intracellulare |

|Clincal TB indistinguishable from M |Atypical mycobacterium |Found in water, soil, not pathogenic in| | |Azithromycin |Macrolide prophylax|

|tuberculosis in AIDS. | |guinea pigs (infects birds) | | |Clarithromycin |when CD4 count < 50|

|M. leprae |

|Leprosy- preferential growth in < 37C, skin, |Never has been |Brazil, India, Sudan |Intracellular replication (skin| |Rifampin |Prophylax exposed |

|superficial nerves. |grown in lab. | |histiocytes, endothelial cells,| |Dapsone |persons with |

|Tuberculoid- good cellular immune response, few | |Humans only natural hosts. Mouse |Schwann cells) | |Up to 2 years! |Dapsone. |

|AFB, granulomas, positive lepromin skin test. | |footpad and armadillo growth only. | | | | |

|Anethetized skin lesions and thickened superficial | |Transmission by nasal secretions, skin | | | | |

|nerves. | |lesions to persons with prolonged | | | | |

|Lepromatous- poor cellular immune response, lots of| |contact w/pts. | | | | |

|organisms, foamy histiocytes, negative lepromin | | | | | | |

|skin test (poor response.) Skin lesions, lion | | | | | | |

|facies. Skin anesthesia, bone resorption, skin | | | | | | |

|thickening, disfiguring. | | | | | | |

|ACTINOMYCETES Gm- Branching Rods |

|A. israelii |

|Diseases |Characteristics |Habitat/Transmission |Pathogenesis |Diagnosis |Treatment |Prevention |

|Actinomycosis- hard non-tender |Aanerobic Gm-branching rods|Normal anaerobic flora oral |Invasion after local trauma (risk |Anaerobic Gm-branching rods, |Penicillin |No vaccine |

|swelling, drains pus through sinus.| |cavity/GI tract. Not communicable.|factor for anaerobic growth) |sulfur granules in pus | | |

|(abscess that spreads to neck, | | | | | | |

|chest, abdomen.) | | | | | | |

|Nocardia asteroides (Acid Fast Branching) |

|Nocardiosis- pneumonia that |Aerobic Gm- branching rods.|Soil, NOT normal flora | |Acid fast branching, NO sulfur,|Bactrim (trimethorprim + |No vaccine |

|progresses to abscess formation, | | | |aerobic |sulfamethoxazole) | |

|sinus tract drainage, dissemination| | | | | | |

|to brain/kidney (immunosuppressed) | | | | | | |

|Mycoplasma pneumoniae (No cell wall, poor gm stain) Small free living organism |

|Diseases |Characteristics |Habitat/Transmission |Pathogenesis |Diagnosis |Treatment |Prevention |

|“Walking pneumonia” (dry |Smallest free living |Respiratory droplets. Attaches but|Pathogenic only for humans. |Elevated titer of cold |Erythromycin |No vaccine |

|nonproductive cough, horrible CXR, |organism, no cell wall so |does NOT invade respiratory | |agglutinins or specific |Tetracycline | |

|generally feel well) Most common |poor gm stain, resists |epithelium, like B.pertussis. |Arrests cilliary motion, induces |anitbodies | | |

|pneumonia in young adults (college |penicillins, | |epithelial cell necrosis. Cross | | | |

|students). |cephalosporins. Cell | |reactive antigens induce anti RBC | | | |

| |membrane has chol which are| |autoantibodies (cold agglutinins.)| | | |

| |not in other bacteria. | | | | | |

| |“Fried egg” colonies on | | | | | |

| |Eaton’s agar. (“Eat Fried | | | | | |

| |Eggs w/ chol”) | | | | | |

|SPIROCHETES Thin walled , flexible, spiral rods |

|Treptonema pallidum |

|Diseases |Characteristics |Habitat/Trans |Pathogenesis |Diagnosis |Treatment |Prevention |

|1’ syphillis – 6 wks post infection, highly infectious, nontender |Thin-walled flexible |Human genital tract |Immunopathogenesis |Darkfield microscopy in early |Early disease by |Prophylax in sexual |

|chancre, many organisms, “cures” in 6 weeks |spiral rods, tight | |mediated by |lesions; VDRL, RPR for |single injection of |contacts. |

|2’ syphillis – 6 wks post chancre healing, spriochetes |spiral | |inflammatory cell |screening, and monitoring |bezathine penicillin | |

|disseminates to organs (hepatitis), maculopapular lesions on | | |infiltrates, |response to therapy. High |G. |No vaccine |

|palms, soles oral mucosa. Condoloma latum may arise. Noninfectious| | |granuloma |sensitivity, low specificity. | | |

|stage, serology positive, 66% resolve in 6 wks, 33% go to 3’. | | |formation, vascular|VDRL titers decline as |Erythromycin | |

|3’ syphilllis – six years later, reactivation, bone and skin | | |proliferation |syphillis is treated. | | |

|granulomas (gummas), aortic aneurysm , meingitis, circle o Willis | | | | | | |

|infarcts, tabes dorsalis (post column/dorsal root damage, loss of | | | |Use FTA-ABS test to rule out | | |

|vibration, pain, temp, position sense) Treptonemes rare in these | | | |false positive VDRL, RPR. | | |

|lesions. | | | |FTA-ABS turns positive earliest| | |

|Congenital syphillis- transmitted to fetus AFTER 1st trimester. | | | |in the disease. | | |

|Stillbirth, fetal abnormalities | | | | | | |

|Borrelia burgdorferi (most common vector borne disease in US) |

|Lyme disease- 1) Erythema chronicum migrans, spreading circular |Big, spirals |White footed mouse reservoir, |Bloodstream spread |Darkfield microscopy w/ |Doxycycline |Stay out of the |

|red rash w/ clear center at bite appears 10 days post bite, lasts | |deer tick Ixodes as vector | |Giemsa stain |Amoxicillin |woods! |

|4 wks. 2) Myocarditis- pericarditis, meningitis, cranial nerve | | | | | | |

|palsy 3) arthritis in large joints, chronic progressive CNS | | | |Diagnose w/ ELISA antibody| | |

|involvement | | | | | | |

|Borrelia recurrentis |

|Relapsing fever- chills, headache, multiple organ dysfunction |Big spirals |Human hosts, rodent reservoir,| |Large spirochetes in |Doxycycline | |

| | |human body louse vector | |Giemsa blood smears. No | | |

| | | | |serology | | |

|Leptospira interrogans |

|Leptospiriosis- fever, chills, headache to meningitis. Also Weil’s|Tight coils |Transmission by swimming/ |Penetrates abraded |Tightly coiled spirochetes|Penicillin | |

|disease- (infectious jaundice) –hepatitis, renal failure, alt | |contaminated food, water. Water, |skin. |by darkfield, rise in |Doxycycline | |

|mental status, hemorrhage. | |soil contaminated by urine of | |antibody titer | | |

| | |infected rats, livestock, pets. | | | | |

| | |Sewage workers, farmers at high | | | | |

| | |risk. | | | | |

|CHLAMYDIAE Obligate Intracellular Parasites |

|C. trachomatis |

|Diseases |Character |Habitat/Transmission |Pathogenesis |Diagnosis |Treatment |Prevention |

|Types A-C cause trachoma, chronic conjuctivitis esp. |15 serotypes |Humans only, sexual contact, |Obligate intracellular |Giemsa of conjuntival |Treat like mixed | |

|Asia, Aftrica. Leading cause of preventable blindness.| |passage through birth canal. |parasites (require host ATP) , |scraping |infection w/ | |

|Inflammation, scar retraction, eyelashes scratch | |Finger-fomite-eye contact. |inert elementary body enters | |ceftriaxone (G3), | |

|cornea, lead to bacteria superinfection, blindness. | | |cell, inhibits phagolysosome | |doxycycline | |

|Types D-K – genital tract infections- nongonococcal | |Dirty towels. |fusion, reorganizes into | | | |

|urethritis (NGU), PID, infertility, ctopic, | | |metabolically active reticulate| | | |

|tuboovarian abscess, peritonitis, perihepatits | | |body. Undergoes binary fission | | | |

|(Fitz-hugh-curtis), neonatal inclusion conjunctivitis | | |to produce daughter elementary | | | |

|(erythromycin prophylax), pneumonitis. Clinically like| | |bodies. | | | |

|gonorrhea. | | | | | | |

|Types L1-L3 cause Lymphogranuloma venereum, tender | | | | | | |

|lesions on genitalia, draining lymph nodes | | | | | | |

|C. psittaci |

|Atypical pneumonia, psittacosis | |Infects birds/ mammals. Inhaled | | | | |

| | |from dry bird crap or feathers | | | | |

|C. pneumoniae |

|Atypical pneumonia, dry nonproductive cough, lack of | |Respiratory droplets | | | | |

|physical findings, diffuse infiltrates on CXR | | | | | | |

|RICKETTSIAE Obligate Intracellular Parasites, short rods wk gram stain |

|Rickettsiae rickettsii (Zoonose, w/vector bug, Weil-Felix postitive, Tx: Tetracycline) |

|Diseases |Characteristics |Habitat/Transmission |Pathogenesis |Diagnosis |Treatment |Prevention |

|Rocky Mountain Spotted Fever- fever, |Accounts for 95% of |SE coast, dog tick, humans as dead |Obligate intracellular |Weil-felix |Tetracycline | |

|headache, macular rash, petechiae, moves |rickettsiae disease |end hosts, no person-person |parasites, divide by binary | | | |

|from hands/feet to trunk (centripetal) | |transmission. |fission. | | | |

|Rickettsiae prowazekii (vector bug, Weil-Felix positive, Tx: Tetracycline) |

|Endemic typhus- sudden influenza like | |Person-person by human body louse. | |Weil-felix |Tetracycline | |

|symptoms, maculopapular rash spreads | |Humans obilgatory part of life | | | | |

|peripherally from trunk, spares face, | |cycle. | | | | |

|palms, soles, meningoencephalitis may | | | | | | |

|ensue | |Asia/ Africa | | | | |

|R. typhi (Zoonose, w/vector bug, Weil-Felix positive, Tx: Tetracycline) |

|Endemic typhus, milder, not occur in | |Fleas | |Weil-felix |Tetracycline |Control rat, flea |

|epidemics | | | | | |poplulations |

|Coxiella burnetti (Zoonose, Weil-felix negative, Tx: Tetracycline) |

|Q fever- fever, headache, flu-like | |Aerosol from cattle and sheep | | |Tetracycline |Milk pasteurization |

|symptoms. Can proceed to atypical | |bodily fluids | | | |and vaccine |

|pneumonia, hepatitis. Rash is RARE | | | | | | |

“Carol Burnet is Qte (cute) b/c she has NO rash”

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“Hememmm Chocolaaate!”

[pic]

H.Simpson

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