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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
Escape from phagosomes Type: membrane disrupting
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
Non-spore Gram positive bacilli Could be cause of acne Don\'t usually cause infection Can contaminate blood culture
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)
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
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%
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)
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
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

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