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”
-----------------------
“Hememmm Chocolaaate!”
[pic]
H.Simpson
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