Fundamentals II Test 3
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- Influenza Virus
- Host: Respiratory Epithelium Attachment site: Neuraminic acid
- Mycoplasma pneumoniae
- Host: respiratory epithelium Attachment site: neuraminic acid Smallest free-livign org.; agent of walking pneumonia Lack cell wall Specialized lipid-containing cell membrane Pleiomorphic Related to gram positive Extracellular pathogen that reside in mucosal surfaces Susceptible to drying & freezing Person to Person transmission Disease: community acquired pneumonia Tracheobronchitis Role in asthma, causes wheezing
- Streptococcus mutans
- Host: Tooth enamel Attachment: bacterial glucan
- Neisseria gonorrhoeae
- Host: Uretheral epithelium Attachment: carbohydrate on host cells
- Escherichia coli
- Normal flora: O157:H7- causes disease Host: Intestinal epithelium, urinary tract, epithelium Attachment: D-mannose Coliform: measures fecal content in water
- Malaria (Plasmodium vivax)
- Host: erythrocytes Attachment: Duffy blood group antigen
- Giardia Lamblia
- Host: Duodenum & jejunum Attachment: Mannose-6-phosphate
- Diphtheria toxin
- ADP-ribosylation of host elongation factor 2-- stops protein synthesis Type of Toxin: A-B
- Cholera toxin
- ADP-ribosylation of host regulatory protein. Leads to massive fluid loss. Type: A-B
- Listeriolysin
- Escape from phagosomes Type: membrane disrupting
- Pneumolysin
- Non-protective inflammation
- Toxic Shock Toxin
- Non-protective inflammation Type of Toxin: Superantigen
- Cell Wall/ Other Toxins
- Function: inflammation & necrosis Type of Toxin: Bacterial products
- Enterobacteriaceae Common Characteristics
- Gram Negative Rods Rounded ends & straight parallel sides Colony Morphology on Sheep blood agar: 2mm colonies, dull gray Sometimes Present: hemolysis, mucoid, swarming, pigmented colonies
- E. coli UTI
- Predisposition: female anatomy, honeymoon cystitis, pregnancy, childbirth, male prostatic hypertrophy, catheterization, failure to empty bladder
- E. coli Opportunistic Infections
- Peritonitis from ruptured gut Septicemia secondary to UTI or pneumonia Wound infection
- E. coli Enteric Pathogens
- EPEC: enteropathogenic E. coli = infantile diarrhea EAEC: enteroaggregative E. coli = traveler\'s diarrhea ETEC: enterotoxigenic E. coli = traveler\'s diarrhea EHEC: enterohemorrhagic E. coli = hemolytic uremic syndrome Enteroinvasive E. coli = bacillary dysentery
- Klebsiella pneumoniae
- Lab: gram negative rods w/ capsules that exclude stain Lactose positive Nonmotile Large Capsule B-lactamase: ampicillin & carbenicillin resistant Sensitive to: Cephalosporins Predisposition: Nosocomial, respirator, age, aspiration of oral secretions, alcoholism, diabetes, chronic bronchopulm. disease Disease: pneumonia (non-purulent bloody sputum, necrosis & abscess), septicemia, UTI, meningitis
- Enterobacter cloacae E. aerogenes
- Lactose positive Nonmotile UTI- nosocomial Cephalosporinase- ampC: ampicillin & cephalothin resistant
- Proteus mirabilis P. vulgaris
- Urease positive Highly motile, swarm on plate H2S positive Infections: UTI (community acquired), wound infections, pneumonia, septicemia Resistance: tetracycline, ampicillin, cephalosporin
- Vibrio Cholerae (NOT Enterobacteriaceae)
- Causes: secretory diarrhea from adenylate cyclase activation of water & electrolyte secretion Spread: contaminated water Host protection: stomach acid; infectious dose is 10^7 organisms Cholera Toxin: B subunit binds intestinal cells; A subunit irreversibly activates adenylate cyclase Treatment: hydration
- Enterotoxigenic E.coli (ETEC)
- Causes: secretory diarrhea Labile toxin: related to cholera; does not secrete as much or grow as large of numbers; activates adenylate cyclase (incr. Na+ & Cl- permeability Stable toxin: activates guanylate cyclase; decreases Na+ & Cl- absorption Toxin coded by extragenomic plasmid DNA
- Salmonella (general)
- Salmonella typhi is most common Salmonella enterica has 2400 main species Syndromes: Enteric Fever (typhoid) Enterocolitis (food poisoning, self-limiting) Bacteremia (complication of enterocolitis) Labs: lactose negative; H2S positive
- Salmonella Enterocolitis
- Vomiting & profuse diarrhea 8-48 hrs. after infection Resolves in 3-7 days Source of Infection: water, meat, dairy, eggs, humans
- Salmonella enteric fever (typhoid fever)
- Humans are only hosts Resistance is common Pathogenesis: Ingest organisms; go through gastric acid barrier & attach to Peyer\'s patches; go through mesenteric lymph nodes, cause bacteremia Live in macrophages of liver, spleen, gallbladder, bone marrow 7-14 days later: secondary bactermia, responsible for symptoms Vaccine: Killed whole S. typhi with LPS = localized side effects Live vacine: Ty21a-- chemically mutagenized strain
- Campylobacter jejuni; C. coli (NOT enterobacteriaceae)
- Gram negative curved rod Carriers: food animals, pets Humans: from contaminated water & food (eg raw eggs, milk) Treatment: rehydration
- Enterohemorrhagic E.coli (EHEC)
- Mild diarrhea; sometimes hemorrhagic colitis 5% hemolytic uremic syndrome-- causes death Most common strain: O157:H7
- Hemolytic Uremic Syndrome
- Shiga-like toxin specific for removing single adenosine from 28S rRNA Cell loses ability to product protein Renal glomeruli are big targets for toxin Kids: kidney trouble Adults: thrombocytopenia
- Shigella
- Related to E. coli; four types All lactose negative (must lose lac operon to be virulent) Nonmotile Fermentative, no gas produced from glucose Bacillary dysentary-- oral inoculation, infects upper GI, moves from watery diarrhea to bloody-mucoid stool as organism moves from upper GI to lower colon Treatment: supportive; should give antibiotics for public health
- Shigella Epidemiology
- Humans are normal host Fingers, Feces, Food, Flies, Water Common daycare disease Sanitary facilities & handwashing can control Incidence: Group A in Mexico; Group D (Shigella sonnei) in US
- Staphylococcus
- Family: Micrococcaceae Others in fam: Stomatococcus & Micrococcus Carrier state: colonizes newborn- nares, umbilical stump, perineal area = warm, moist Adult: some colonization goes away; varies amongst individuals Characteristics: Gram positive; round colonies, nonmotile, no endospore; beta hemolytic beige; catalase positive; facultative anaerobes; heat & salt tolerant
- Coagulase Negative Staphylococci
- Non-hemolytic white colonies Some species more pathogenic than others: S. epidermidis, S. saprophyticus, S. lugdenensis, S. schleiferi Usually multi-resistant Common infections: bacteremia (endocarditis), UTI, endopthalmitis, infections w/ prosthetics (IV catheters, prosthetic joints, vascular grafts, CSF shunts)
- Staphylococcus saprophyticus
- Catalase positive Coagulase negative Novobicin resistant Rarely cultured from genitourinary tracts of asymptomatic women UTI symptoms present in 90% of women from whom S. saprophyticus cultured Honeymoon cystitis
- Coagulase Positive Staphylococci
- S. aureus is only significant pathogen Ferment mannitol IgG binding protein (protein A) Coagulase positive Cell walls have teichoic acid Common infections: bacteremia, vascular infections like endocarditis; skin & soft tissue infection like abscess; food poisoning; bone & joint infection; surgical site infections; sepsis (assoc. w/ multi organ failure) Drug resistance: penicillin, methicillin, vancomycin...
- Staphylococcal Scalded Skin Syndrome
- Mostly children Systemic symptoms = RITTER\'s disease Skin lesions due to toxins produced, not bacteria
- Toxic Shock Syndrome
- 1980\'s: New tampon that grew S. aureus S. aureus secreted TSS Nonmenstrual: seen w/ wounds Staph form is less deadly than Strep form Manifestation: fever, malaise, feeling bad, rash like sunburn After effects: desquamation esp. hands & feet Potential consequences: multi-organ failure; immune system over activation = hypotensive
- Streptocacceae
- Family that includes streptococcus and enterococcus Both form long chains Enterococci is normal in stool; strep is not Easily spread through aerosolization of S. pneumoniae in lungs or other kinds in stool
- Streptococcus General
- Beta hemolytic Lancefield groups-older classification Colonize gut Catalase negative Grow on sheep\'s blood agar Aerobic or anaerobic Enhanced growth in CO2 Antigenic/Lancefield group classification--older
- Streptococcus pyogenes- Group A
- Gram positive cocci in long chains Catalase negative Beta hemolytic- caused by Streptolysin S Bacitracin disk (A disk) susceptible PYR positive- turns red Diseases: pharyngitis can lead to rheumatic fever Skin: erysipeals, impetigo, cellulitis- can lead to glomerulonephritis Erysipelas: well demarcated Cellulitis: soft borders Pneumonia- very rare (Jim Henson) Scarlet Fever: erythematous rash w/ prominence along axillary & inguinal creases (Pastia\'s lines) Strawberry tongue Virulence Factors: M-protein- antiphagocytic, lipoteichoic acid-aids adherence to tissues, protein F- binds fibronectin; Protein G-binds Fc portion of Abs & inactivates, DNPase-kills WBC Test: 90% positive, swab, treat with antibiotics while waiting for results
- S. agalactiae
- Newborn illness; common colonizer of gut & vagina Gram positive cocci in chains Catalase negative Beta hemolytic CAMP test positive Infections in adults: immunocompromised, diabetics, alcoholics Disease: cellulitis or endocarditis or osteomyelitis
- S. pneumniae, pneumococcus
- Cause: resp. tract infections Kids: sinus or ear infections, pneumonia Pneumonia: can lead to bacteremia = meningitis, bone & joint infections Osler\'s Triad: S. pneumoniae pneumonia, endocarditis, meningitis Gram positive cocci in pairs or short chains Alpha hemolytic Optochin (P disk) susceptible Bile soluble- autolyses in bile Quellung rxn Pathology; can aspirate from upper airway to lower = pneumonia Virulence factor: capsule Vaccine: adult-23 valent polysacch- prevent invasive pneumococcus, not pneumonia Child: 7 valent conjugate vaccine (w/ diphtheria toxin)
- Strep D
- Ex: S. bovis Can cause endocarditis Ask about GI malignancy
- Viridans streptococci
- Number of species that are similar Alpha & Gamma hemolytic Human host Differentiate biochemically Cause dental carries/tooth decay, GI malignancies or endocarditis
- Enterococci
- Two species: Enterococcus faecalis-more common Enterococcus faecium- vancomycin resistance likely Live in gut- usually benign unless bowel obstruction or colon mass requires opening of gut = exposure to abdomen Catalase negative P test rules out S. pneuoniae Bile esculin test--turns black PYR positive Infections: UTI, bacteremia, endocarditis, intra-abdominal infections
- Bacillus (general)
- Most serious: anthrax Ubiquitous in soil Gram positive rods; can be gram-variable Form spores- resistant to radiation, chemicals, heat, dessication b/c has dipicolinic acid Aerobic, can be facultative Beta hemolytic Motile Large gray spreading beta hemolytic colonies Catalase Positive Note: non anthrax are not beta hemolytic or motile Common environment commensals w/ occasional opportunistic infection B. cereus are most important B. antracis- other
- Bacillus cereus
- Common in environment Cause gastroenteritis, ocular infection (self-limiting) Enterotoxins: heat stable (emetic) & heat labile (diarrheal) IV catheter-related blood stream infection, endocarditis, meningitis Usually immunocompromised, drug abusers Must distinguish between contaminant of culture or cause of infection
- Bacillus antracis
- Biological warfare Enzootic in Middle East (endemic in animals) Cutaneous: eschar is blackened area/ulcer seen on skin; caused by spores inoculating skin Respiratory: worst form, usually fatal, spores in lungs GI: swallow spores, less common Pathogenesis: Produces toxins; protein capsule (Poly D-glutamic acid); 3 component exotoxin (protective antigen-bind cells, edema factor-swelling, immune suppression, lethal factor-disrupts cell function, stimulates cytokines, kills infected cells = necrosis) Vaccine: avirulent nonencapsulated; series of injections & boosters
- Listeria monocytogenes
- Gram positive bacilli/coccobacillis (oval organism) Catalase positive Motile Esculin positive Beta hemolytic Habitat: refrigerator; multiply at 4 degrees C- food bourne Epidemiology: asymptomatic, meningitis/sepsis in immunocompromised; neonatal infections (transplacental) Genotype: determines strain similarity of seemingly related cases-restriction enzymes w/ electrophoresis Pathogenesis: low temp., facultative intracellular pathogen (in macrophages), makes hemolysin (listeriolysin)-can open RBC, asymptomatic carriage reservoir
- Erisipelothrix rhusopathiae
- Gram positive bacillus Zooontic infection-common in animals Transmission: skin wounds Occupational hazard: working w/ animals Self-limiting skin lesions w/ erythema & eruption Susceptible to antibiotics Can spread to bloodstream
- Aerobic actinomyces
- Large group: mycobacteria & corynebacteria Separated by presence or absence of mycolic acids in cell wall Corynebacteria & Nocaridea are most important Gram positive rods Catalase positive
- Corynebacterium
- Like bacillus Found: skin, commensals of skin, contaminants of culture Major example: Diphtheria-- there is vaccine Gram positive, curved pleiomorphic rods \"Chinese Letters\"; aka diphtheroids Aerobic/facultative anaerobic Grow on sheep blood agar Catalase positive Oxidase positive
- Diphtheria
- Worst Corynebacteria Spreads by respiratory droplets Causes: psuedomembrane at back of throat (suffocation) Has phospholipases to promote spread & increase vascular permeability Phage encoded toxin: interferes w/ protein synthesis by inactivating EF-2 = necrotic cells that build up to form pseudomembrane Pseudomembrane: fibrin, bacteria, epithelial & phagocytic cells Toxin-mediated: can spread to heart affecting cardiac myocytes Identified: selective cysteine-tellurite media-specific for Diph. Vaccine: toxoid, immunologically active, non virulent toxin mimic Series: DAaPT, acellular pertussis tetanus combo
- C. jeikeium
- Corynebacteria Bacteremia in bone marrow transplant patients Multiple antibiotic resistance Susceptible: vancomycin, tetracycline
- C. urealyticum
- Corynebacteria Causes UTIs and stones Bacteria splits urea, releases ammonia, raises urine pH - calcium & magnesium to precipitate out (stones) Difficult to treat b/c antibiotics cannot reach bacteria due to stones
- Nocardia
- Filamentous gram positive bacilli Lipid in cell wall- produce partial acid fast-- retain stain under less rigorous conditions than complete acid fast Culture is slow-grows on TB media Can ID w/ PCR Ubiquitous in environment- acquired by inhalation, cutaneous inoculation Pathogenesis: Cord factor prevents phagolysosome fusion & intracellular killing in phagocytes Facultative intracellular parasites--can be chronic Produce: catalase & superoxide dismutase Disease: mostly immunocompromised- see pneumonia, lung abscesses, brain abscess/meningitis Others: cellulitis/ulcerations, mycetomas Common: respiratory manifestations
- Rhodococcus
- Gram positive Weakly acid fast bacilli Can revert to coccoid forms Common in animals & environment Opportunistic lung infections (esp. AIDS, transplants) Facultative intracellular pathogen-survives in macrophages Leads to granuloma & abscess Produces: slow-growing, mucoid salmon-colored colonies of R. equi on chocolate agar
- Tropheryma whippeli
- Actinomycete etiologic agent of Whipple\'s Disease CANNOT be cultured except in tissue culture Dx: histopathology & PCR
- Haemophilus
- Blood loving- need things from RBC to survive Gram negative coccobacilli Facultative anaerobes Non-hemolytic- cannot lyse or enter RBC Invasive strain: encapsulated Non-encapsulated: non invasive; normal flora upper resp. tract Pathogenesis: Spread by resp. aerosol, exacerbated by COPD Endogenous infection: Haem. influenza colonizes lung w/o symptoms then becomes pathogenic Virulence factor: antiphagocytic capsule; 6 capsular serotypes Type B- worst NO exotoxin Produces IgA protease- destroys Abs Produces beta-lactamase Diseases: respiratory tract infection, community acquired pneumonia, epiglottitis (stridor, drooling, fever; seen w/ X-ray; wiped out by vaccine) Vaccine: polysaccharide capsule conjugate vaccine against Type B Type A: still exists- causes otitis media, cellulitus, sinusitis, conjunctivitis
- Haemophilus Detection
- Detection: fastidious organism; grows on chocolate agar Chocolate agar: lysed RBC- releases factor X (hemin) and factor V (NAD) Satellitism test: Blood agar plate w/ haemophilus, streak S. aureus in middle; S. aureus hemolyzes RBCs so haemophilus will grow near S. aureus streak Old school test: haemophilus on agar w/ added paper strips w/ factor X, V or both- grows near both strip Specific for haemophilus influenza, not others
- Other Haemophilus
- H. ducreyi- painful genital ulcers H. aegyptius- purulent conjunctivits
- Bordatella pertussis
- Encapsulated, gram negative coccobacillus bacteria Fastidious, slow growing- difficult to culture Strict aerobe Uses amino acids NOT carbs Vaccine: almost eradicated disease Older vaccine: whole killed organisms-wears off Aka: whooping cough- caused by irritation produced in upper resp. tract by bacteria & necrosis from toxins Stages: catarrhal stage (cough, sneeze), paroxysmal, convalescent Recovery confers immunity Pathogenesis: Attach to ciliated resp. epithelium w/ adhesins, filamentous hemagglutinin (FHA), Pertussis toxin (PTx), kills resp. cells Releases factors that interfere w/ neutrophil chemotaxis Exotoxins Damage Tissues
- Pertussis Toxins
- Pertussis toxin: adherence Adenyl cyclase/hemolysin: incr. cAMP, inhibits phagocytosis & monocyte migration Lethal toxin: inflammation & local necrosis Tracheal cytotoxin: Kills resp. epith. cells; stimulates release of IL-1 Endotoxin (LPS): activates alternate complement, cytokine release
- Pertussis Detection and Prevention
- Detection: Nasopharyngeal swab Bordet-Gengou or Regan-Lowe enriched horse blood-charcoal medium-- not used Measure Ab titers Main method: detection of symptoms Prevention: Acellular vaccine- DaPT Older vaccine: did not provide specific antigens Abs to toxins stop attachment Adults: Tdap
- Legionella Pneumophila
- Fastidious Catalase-negative Facultatively intracellular Gram-negative bacillus Nonfermentative Stains poorly w/ safranin Multiple serogroups Community acquired pneumonia
- Pathogenesis of Legionellosis
- Binds C3 receptor on macrophages, taken up Evade binding to phagolysosome & multiply Fill up macrophage & kill it Produce enzymes that damage lung tissue Causes acute purulent pneumonia & absesses Primary affect: elderly, immunosuppressed NO person to person, but point source Culture: buffered charcoal yeast extract agar & cysteine medium Hard to grow
- Legionella Detection
- Silver staining of histopath. specimens of lung biopsy Direct fluorescent antibody (poor sensitivity) Urine polysaccharide antigen-- will ONLY pick up Legionella pneumonia Serotology (IFA)-paired sera required; retrospective dx PCR- currently evolving
- Legionnaire\'s Disease
- Community acquired pneumonia Point source outbreak More common in north Diarrhea is associated symptom Found in older men w/ COPD, immunosuppressed, transplant recipients Higher occurrence in summer NO vaccine
- Moraxella catarrhalis
- Common cause of community acquired resp. infections Otisis media, sinusitis, bronchitis, pneumonia Carried in upper resp. tract of healthy children Most strains: produce beta lactamase-- main virulence factor Gram negative coccus
- Pathogenesis of Mycoplasma
- Attaches to resp. epithelium w/ P1 Testing looks for Abs to P1 Danamages tissue w/ peroxide & hemolysin Affects beating of cilia Stimulates cytokine cascade Self-limited, NO acute fever or chills No vaccine b/c changes its antigen Exotoxin recently described similar to pertussis ADP ribosyl transferase that causes vacuolation & ciliostatis of epith.
- Mycoplasma Detection
- Grow on specialized enriched agar; takes 3 weeks Metabolizes glucose Small genome Fastidious Lab looks for IgG for mycoplasma PCR Increased occurrence of antibiotic resistance
- Mycoplasmas (in addition to pneumoniae)
- Genital Mycoplasmas: M. hominis M. genitalium Ureaplasma species Found in lower urogenital tract Cause opportunistic infections Disease: Nongonococcal urethritis: ureaplasma & M. genitalium Urinary calculi: ureaplasma (b/c splits urea) Pelvic inflammatory disease/cervicitis: M. genitalium & M. hominis Premature delivery: ureaplasma infection; causes oxygen damage in lung due to incr. oxygen demand, spontaneous abortion, postpartum fever Septic arthritis in Ab deficient: ureaplasma
- Detection of genital mycoplasmas & ureaplasma
- M. hominis & ureaplasmas grow rapidly in specialized medium but they are fastidious Serology is NOT useful M. genitalium is slow growing PCR used
- Brucella
- Bioterrorism Small gram negative coccobacillus Intracellular pathogen Fastidious Slow growing Pass to humans through food direct contact Most common strain: B. melitensis Intermittent, undulating fevers of unknown origin bone marrow & blood cultures are preferred
- Francisella tularensis
- Causes: tularemia (rabbit fever) Tick-bourne Midwest Enters skin Causes ulcer Vaccine: use is rare
- Mycobacteria
- Acid fast stain Do not know species w/o further testing Staining: defined by mycolic acids- unable to be decolorized by acid fast solution Contains waxes Obligate aerobes Slow groing (eg TB) Not designed to be pathogens Usually infect immunocompromised Live in amoeba or human macrophages
- Bacterial Cell Walls
- Gram positive: thick peptidoglycan layer Gram negative: thin peptidoglycan layer, outer membrane Mycobacterium: complex cell wall, outer membrane w/ mycolic acids, waxes, lipoarabinomannan (LAM), galactomannan
- Mycobacterium tuberculosis
- Origin of Koch\'s postulates Humans are only natural host TB does NOT transmit easily; requires high degree of contact High prevalence: Zambia & Namibia (also high rates of AIDS) Transmission: respiratory droplets (infectious load: 5-200 droplets) Pathogenesis: inhaled, go to middle lung, phagocytosed by macrophage, set up tubercle & infect Process: latent disease- inhaled, middle lobe of lung, hilar & peribronchiolar lymph nodes, lymphohematogenous dissemination, finally immune system kicks off Forms tubercles, walls off infection, as granuloma grows, caseous necrosis occurs and eventual dystrophic calcification (Ghon complex)
- TB prevention
- Decrease exposure Air exchange to reduce organisms in air UV irradiation Chemoprophylaxis: after positive skin test- must rule out disease first then give Isoniazid (6-9 mo.) BCG vaccine: can give positive skin test up to 10 yrs. after- against primary disease only
- Environmental Resistance of M. tuberculosis
- Survives drying Resistant to many disinfectants like alcohol Susceptible to: UV irradiation (does not penetrate plastic), chlorine & phenols, pasteurization, High Efficiency Particulate Air Filters
- Diagnosis of Tuberculosis
- AFB smear- negative or positive reported in 24 hrs. (use fluorescent stain) TB smear: shows red organisms in stain Skin test: Mantoux test, can show exposure to other mycobacteria Larger the swelling around area of test, more positive dx of TB Chest radiograph AFB culture Culture prep: digest sputum w/ mycolytic agent (eg NaOH), decontaminant w/ 2-3% NaOH; concentrate, acid fast stain, cultivate in solid (egg or agar) or liquid (automated) media, wait 8 weeks If TB grown, MUST send off for susceptibilities
- Quantiferon- Gold Standard
- IFN-gamma release assay Three tubes: No antigen, TB antigen, Mitogen Blood collected & put in tubes Mitogen releases all IFN-gamma = measure of possible rxn Antigens used are not in BCG vaccine- can differentiate b/t vaccine & actual TB
- TB Risk Factors
- AIDS w/ CD4 less than 400 Iatrogenic immunosuppression (eg TNF-alpha inhibitors, steroids) Age Pregnancy Alcoholism/malnutrition Diabetes Genetics
- Types of TB
- Primary: infected, develop fulminant disease Adult/reactivation: upper lobes of lungs where more oxygen Miliary: partial immunity resulting in partial control = multiple granulomas throughout body Cold abscess: develops slowly Addison\'s disease: disease of adrenal glands = adrenal insufficiency
- TB disease morphology & colony morphology
- Disease: caseous necrosis, cavity can form after cleared, where organisms becomes aerosolized Lab: M. tuberculosis - crunchy
- M. gordonae
- Common in water Not pathogen Pigmented
- M. kansasii
- Photochromagen Non-pigmented colonies but turns bright yellow in light
- M. marinum
- Photochromagen Associated w/ fish, water, fishermen Lesion that marches up arm Can lead to amputation of fingers If grown in dark- not pigmented Shown to light: bright yellow
- M. scrofulaceum
- Granulomatous cervical lymphadenitis in children
- M. fortuitum
- Rapid grower Skin infections Pulmonary diseases Esp. CF & lung transplants
- M. leprae
- Hansen\'s disease Humans & armadillos Transmission: inhalation or skin contact w/ contaminated resp. secretions of lepromatous patients Incubation: 3 mo. to 3 yrs. Dx: does not grow in artificial media Grows in nude, immunocompromised, mice or armadillo AFB stain of nasal secretions Leprominin test- skin test Tx: dapsone & rifampcin (at least 1 yr. treatment) Prevention: isolation of leper, vaccines in development
- Tuberculoid Leprosy
- Intact cell-mediated response to M. leprae Grow in nerves in cooler parts of body; cause nerve damage; form granulomas Not in tissue often Cutaneous loss of sensation: discolored skin, loss of digits as result of loss of sensation (stupid choices) Non-progressive disease
- Lepromatous Leprosy
- Depressed cell-mediated response Bacteremia w/ localization in nerves & skin High number of organisms Less nerve function loss Also involves: testes, spleen, liver Leonin facies Acid fast tissue stain Different organisms Coller areas of skin loaded w/ different species
- Aerobic bacteria
- Have to have oxygen Ex: pseudomonas
- Microaerophilic
- Cannot grow under atmospheric oxygen; must have reduced oxgygen Ex: Campylobacter
- Capnophilic bacteria
- Require Co2 Ex: fastidious bacteria like Neisseria gonorrhea & Haemophilus influenza
- Facultative bacteri
- Have enzymes that can produce energy in absence or presence of oxygen Have machinery to use oxygen and will use O2 first b/c more ATP is made
- Anaerobic bacteria
- Some are obligate Others are aerotolerant (can withstand some oxygen) Lack cytochrome systems, superoxide dismutase and/or catalase Categories: gram positive or negative Rods or cocci Ex: gram negative rods- part of normal flora, opportunists Gram positive- also vary; part of normal flora Most infections are MIXED Will often see abscess formation Habitat: mutliple, can be aspirated, oral cavity (esp. with poor dental hygiene), colon (disruption: pelvic inflammatory disease, endometritis), foot & decubitis ulcers
- Oral hygiene and bacteria
- Can see Fusobacterium (long, pointy rods), Treponema (thin, wavy), Bacteroides If don\'t clean mouth, crypts close up; byproducts of metabolism cause problems Vigorous teeth brushing produces bacterial shower-- requires prophylaxis for mitral valve prolapse or heart valve problems
- Gram Negative Bacilli
- Most common & important Genera: Bacteroides Prevotella Porphyromonas Live above or below diaphragm Most important groups: Bacteroids fragilis (colon), Prevotella melaninogenica (oral cavity) Others: Prevotella bivia & P. disiens colonize female genital tract Again, anaerobic infection is characterized by abscess formation & mixed bacteria
- Necrotizing Fascitis
- Associated w/ Strep and Bacteroides fragilis Once established, must be debrided Lots of necrosis & tissue destruction Some tx w/ hyperbaric chambers
- Fusobacterium
- Gram Negative Bacilli Pleiomorphic Not uniform Can be sole agent (can be seen in an empyema (pulmonary infection w/ effusion) Disease: Lemierre\'s Syndrome Colonies: nondescript Strict anaerobes
- Lemierre\'s Syndrome
- Fusobacterium in oral cavity High mortality rate Essential jugular vein thrombosis Organism gets into tissue all the way down to jugular vein High mortality rate
- Non spore-forming Gram positive Bacilli
- Ex: Actinomyces Actinomyces israelii is most common Slow growing Difficult to grow Cross tissue planes Have sulfur granules: microcolonies of organism encased in host material, visible to eye, Seen in draining sinuses, Typically yellow Cause oral, respiratory, and female genital tract infections
- Dacryocystitis
- Prior to or w/o Hib vaccine, Haemophilus influenza B infection would occur in peds around eye but caused by Actinomyces Sulfur granules clog tear ducts- once removed, infection disappears
- Classic Actinomycosis
- \"lumpy jaw\" Face is asymmetric, swollen on one side Also can see (in specific patient), an abscess tooth (bone & root are degraded) See sulfur granules When crushed, reveals thin, branching, gram positive rods Note: sulfur granules can be caused by some fungi too
- Actinomyces israelii
- Non-spore forming Gram positive bacilli Rods seem to branch off of each other Slow growing
- Prpionibacterium
- Non-spore Gram positive bacilli Could be cause of acne Don\'t usually cause infection Can contaminate blood culture
- Lactobacilli
- Non-spore Gram positive bacilli Positive role: maintain acidity of vagina Serves as defense
- Clostridia diseases
- C. botulinum- botulism C. tetani- tetanus C. difficile- antibiotic-associated diarrhea C. septicum
- Clostridia perfringens
- Rectangular, gram positive rods Makes spores (within cell, do not bulge) Double zone beta hemolysis (toxins destroy membranes but other toxins don\'t completely hemolyze, so double zone) Nagler test: Egg yolk agar; One side w/ antitoxin, the other w/ no toxin--place bacteria, see if toxin is neutralized Causes: gas gangrene (myonecrosis) Tx: requires debridement Also causes: soft tissue infections (cellulitis, myonecrosis), food poisoning, necrotizing enteritis Various types, each associated w/ different toxins All types have alpha toxin phospholipase C- chews up membranes Destroys tissue & turns it into hydrogen & CO2 Form gas pockets in skin Can be lethal
- Clostridium tetani
- Active infection where toxin produced in vivo Causes: tetanospasm from blockage of inhibitor nerve transmitters resulting in spastic paralysis Get constant firing of motor neurons Produce A-B toxins: A attaches, cell internalizes it, enzymes cleave two components & other part becomes active Glycine & Gaba (inhibitor transmitters) are affected Recovery: cells must be regenerated Dx: sardonic smile; rigidity Spores are made; seen in microscope as bigger end (like lollipop) Tx: human plasma w/ high conc. of anti-tetanus Ab to neutralize toxin and then add penicillin (order is important)
- Clostridium botulinum
- Toxin is preformed Causes flaccid paralysis so can\'t fire motor neurons Progressive Eventually diaphragm does not work Select agent; requires license for lab Food bourne toxin associates w/ other proteins in meal to prevent lysis/degradation in stomach In vivo production only seen in infant botulism
- Clostridium difficile
- Mostly hospitalized patients Antibiotic-assoc. diarrhea Very resistant Toxins produced cause diarrhea Causes pseudomembranous colitis (extreme)- can see plaques on colon Plaques preceded by diarrhea; associated w/ clindamycin use Test: often, diarrhea treated by Metronidazole (anti-anaerobe) or Vancomycin (second line)
- Pathogenesis of Clostrida
- Pathogenesis: synergy b/t Clostridia & facultative organisms in an abscess b/c facultative reduces oxygen = better environment for anaerobe Capsule = antiphagocytic Toxin production
- Diagnosis of anaerobic infection
- Clinical sign: foul smell from short chain fatty acid byproducts of anaerobic metabolism Proximity to mucosal surface Gas in tissue Abscess formation Gram stain: often shows MIXED infection Culture: should aspirate abscess Media: complex but often use aminoglycosides to suppress facultative organisms that may be present b/c anaerobes are not susceptible Grow in absence of O2
- Anaerobic containers
- Hydrogen generators w/ catalyst Add plates, water & catalyst turn hydrogen and any oxygen into water
- Anaerobe chamber
- Very extreme Filled w/ hydrogen gas Air lock Catalyst takes care of any oxygen Everything must be done inside chamber
- Anaerobic tests and treatment
- Quick tests: Aminoglycoside growth splitting bile esculin, which grows on bile Gram stain Tx: Varies Abscesses are drained; cannot just be treated w/ antibiotics Mixed infections require a cocktail Aminoglycosides are NOT effective Antitoxins & antibiotics if active infection vs. intoxication
- Anerobic susceptibility Testing
- Not routinely done Predictable One method: plastic strip w/ gradient of antibiotic Highest conc. to lowest, at arrow is the MIC (min. inhibitory concentration) of that antibiotic for that organism-- not done practically Annual anti-biogram: summary of susceptibility patterns of organisms that also includes aggregate (eg x% of C. perfringens are susceptible to Cefoxitin)
- Rickettsia
- Includes rickettsia group which has rocky mountain spotted fever and the typhus group Targets endothelial cells Hallmarks: Rash, fever, headache (due to CNS involvement), thrombocytopenia and neutropenia Dx: serological Tx: Doxycycline
- Ehrlichia
- Part of Rickettsial family Targets WBC Hallmarks: some rash, fever, headache, neutropenia & thrombocytopenia Dx: serology Tx: Doxycyline
- Epidemiology of Rickettsiosis
- Worldwide US: focus on RMSF Others include: American Boutonneuse Fever, Ehrlichiosis, Q Fever, Murine typhus Geography is important Tick-bourne, only certain types Highest rates of RMSF: southeast, spread by the Lone Star Tick and the Western Blacklegged Tick (west coast) Mostly in spring & summer b/c ticks don\'t do well in winter
- Rickettsia rickettsii
- Small, gram negative pleiomorphic obligate intracellular parasite Causes RMSF Life cycle in tick: go through ovary and have transovarial passage to wind up in gut of tick Not common Unlikely in winter Chances increase in: children, men, whites, dog exposure, wood activities Pathogenesis: contact w/ infected tick that must bite you, digest tissue to get to blood, and deposit R. rickettsii Hallmarks: Perivascular infiltration w/ mononuclear cells, vascular necrosis, microinfarcts, thrombosis Symptoms: incubation of 7 days; macular, papular, petechial rash, history of tick bite, fever, malaise, headache, myalgia, vomiting & abdominal pain, CNS problems (encephalitis which causes confusion, lethargy, seizures, coma or death)
- Diagnosis of RMSF
- Lab: normal or decreased WBC, increased bands (immature cells), anemia, thrombocytopenia Natural history: left untreated, can die in 1-2 wks and death is 3-4 times more likely without antibiotics Dx: Serological tests- IFA, agglutination test, Weil-Felix test (outdated) but relies on Ab production Lab: Immunofluorescence or immunoperoxidase staining of biopsy specimen (fresh or formaldehyde fixed), sensitive not that great & decreases w/ antibiotic therapy but specificity is 100%
- Ehrlichiosis
- Family of rickettsial type disease Targets WBCs Rates highest in spring & summer Clinical presentation: RMSF w/o rash Short incubation time Human monocytic ehrlichiosis or human granulocytic ehrlichiosis- details not ctriical Mortality is high untreated Dx: serology; PCR for research Tx:Doxycycline Classification: Anaplasmataceae family that is divided into Neorickettsia, Anaplasama & Ehrlichia
- Q Fever
- Caused by Coxiella burnetii (rickettsial disease)
- Spirochetes
- Different from rickettsia Includes: Treponema pallidum- syphilis Leptospira- Leptospirosis Borrelia- Relapsing Fevers Borrelia burgdorferi- Lyme Disease Spirillim minus- Rate Bite Fever
- Pathogenic Treponemas
- Diseases caused SYPHILIS Developing nations, esp SE Asia- yaws N. Africa: T. pallidum endemicum- endemic syphilis Pinta
- Syphilis
- Spiral bacteria, too thin for gram stain, so identified by dark field microscopy Mortality caused by cardiovascular & neurological disease Congenitally transmitted & life-threatening to children born to infected mothers Antibiotics have greatly decreased rates US- highest syphilis rate of developed country; Alabama is #2 Highest rates in times of social upheaval & esp. in minorities Rates increase in people of ages that are sexually active & in men Infection: invades blood vessels, infects bl. vessels, causes lesions First stage: infection of bl. vessels at site of invasion (see genital ulcers, painless) Tissue reacts & dies, causes inflammatory response Second Stage: bacteria disseminate throughout body, infecting bl. vessels (hallmark is rash of syphilis in places of lower temp. due to leaky bl. vessels), will resolve w/o therapy & enter latent phase
- Syphilis: Dx
- CANNOT be cultured Serological test used Two stage testing strategy used to eliminate false positives Serology of untreated syphilis: height of titer usually corresponds w/ disease; important in treating & managing patients Tx: Penicillin, still has not developed resistance