Resp Bacterial Flashcards
Bacterial Resp infections (strep)
- Gram (+) cocci in chains or pairs
- Catalase (-) anaerobic
- Serology: Lancefield grouping (A-G) based on carb Ag in cell wall
- Also grouped by M-protein KEY Ag to provoke immune response
- A-Hemolytic: Green-partial hemolysis
- Pneumoniae (optochin sensitive)
- Viridans (optochin resistant)
- B-Hemolytic: Clear-complete hemo
- Pyogenes A (bacitracin sensitive)
- Agalactiae B (bacitracin resistant)
- Y-Hemolytic: No hemolysis
- Enterococcus (Faecalis/Faecium)
Strep tests
- Catalase Test:
- Superoxide dismutase splitrs O2+H2O2 into catalase & peroxidase
- Enzyme that splits Hydrogen peroxide into Water & O2
- Hydrogen peroxide by-product of resp & is LETHAL in excess
- Catalase degrades hydrogen peroxide in cell before it can get to excess
- Result=H2O2 in Free O2 (bubbles/water)
- PYR (Pyrrogutamyl aminopeptidase):
- Filter paper= L-pyrrolidonyl-β-naphthylamide (PYR). Bacterial pyrrolidonyl peptidase hydrolizes PYR=Color change
- ex. Strep Group A(+) & S.pneumoniae (-)
Strep pyogenes (GAS) General
- Gram (+) catalase (-)
- Beta hemolytic in blood agar
- Bacitracin sensitive & Group A/PYR(+)
- Reservoir: Human upper resp & skin
- Transmission: Resp droplet & P to P HIGH frequency in Winter-Spring
- Pharyngitis in children 5-15
- Capsule: Hyaluronic acid (anti-phago)
- M-protein: Ag variation used for serotype
- Binds to Fc region on IgG/IgA (anti-phag)
- Binds to collagen, fibronogen, plasminogen
- F-protein BINDS to fibronectin=Camo
- Hemolysins: Strep S & O (toxic)
- C5A peptidase: inactivates C5a
- Streptokinase: Lyses blood clots
- Streptodornases: DNAse
- Pytogenic exotoxins-Super Ags
GAS M protein Structure
- N terminal: Type specific sequence variation
- Conserved Region:
- Ag cross reacting domain w/human tissue
- Binds to human tissue
- Carb group Ag=Lancefield grouping common to certain types
Strep GAS Clinical Outline
- Pyogenic infections=Local infections
- Pharyngitis
- Otitis media
- Pneumonia
- Toxin mediated:
- Scarlet fever
- Toxic shock smdrome
- Fascitis
- Immune mediated=Untreated pyogenic
- Rheumatic fever
- Glomerulonephritis
Strep GAS Pharyngitis
- Pyogenic/Local infection
- Sudden onset no more than 3-5 days
- Sore throat, Fever, Headache
- Inflammation of pharynx/Tonsils
- Patchy exudates (not always)
- Palatal petechiae
- Tender & enlarged Ant cervical nodes
- Seen in winter or early spring
- NO COUGH
- Diagnosis: Beta-hemolytic agar, bacitracin sensitive, Catalase (-), Gram (+) cocci in chains
- Lancefield-Group A
- Rapid strep (10-15min) Ag detection-ELISA
- Throat swab (monoclonal Ab to detect the strep group A cap polysac)
Strep GAS Scarlet Fever
- Associated with Pharyngitis if left untreated=Immune mediated
- Streptococcal pyrogenic exotoxin=Super Ag causes outbreak
- Diffuse erythromatous rash ALL over body
- Fever
- Strawberry Tongue
- Skin desquamation=Peeling @ toes/fingers
Strep GAS Rheumatic Fever
- Immune mediated inflammation in heart, Joints, Blood vessels, & subcutaneous
- Type 2 hypersensitivity (Ab binds to Ag on cell surface NOT free floating)
- Immune cross reactive w/Mprotein=Mol mimicry
- Rheumatogenic Strains=1,3, 6, 18
- Appear 2-4 weeks after pharyngitis
- Fever, migratory polyarthritis, Erythema marginatum (Rash), Subcutaneous nodules (elbows,knees, wrists)
- Carditis (damage to heart tissue)-Assoc w/subcutaneous nodules
- Chorea (Nerve damage) uncontrollable movement of limbs/face
- Diagnosis: Ab against Steptolsin O (ASO)-Hemolysins used to ID in Titer
Strep GAS Glomerulonephritis
- Ag/Ab complex deposition (Type 3) on glomerular basement membrane
- Triggers inflammatory Rxn->tissue damage w/impairment of kidney function
- Localized skin infection & pharyngitis follows
- Takes 10-15 days after skin infection
- Symptoms:
- Hypertension
- Edema
- Hematuria (smoky unrine)
- Proteinuria
- Diagnosis: History of skin/throat infections
- Serology-Anti-ASO & Anti-DNase
Jones Criteria RF
- Diagnostic= 1 required & 2 major OR 1 required & 1 major w/2 minor
- Required: Strep infection
- ASO/Strep Ab
- Strep group A throat culture
- Recent scarlet fever
- Anti-DNA-B
- Anti-Hyaluronidase
- Major: Cariditis (mitral valve), Polyarthritis (3 days per joint w/3 weeks total), Chorea, Erythema, Subcutaneous Nodules
- Minor:
- Fever
- Arthralgia
- History of RF or RHD
- Elevated Acute phase rxns (ESR, CRP, Leukocytosis)
- Prolonged PR interval
Strep Pyogenes (GAS) Treatment
- All treatment given after (+) Rapid Ag detection test or Strep culture
- Penicillin G
- Macrolides for Penicillin Allx-Azithromycin & Erythromycin
- Prevention: NO vaccine
- Early treatment of Pharyngitis helps prevent RF
- Pts recovered from RF given monthly dose of Penicillin to prevent further infection-
- Strep
- Recurrence of RF
Strep Pneumoniae-General
- Gram (+) encapsulated, Lancet-shaped (elongated) paired w/cocci (short chains)
- Alpha hemolytic (stains green)
- Optochin & Bile sensitive
- Autolysis-Releases virulence factors
- NO lancefield type due to lack of carb in cellwall
- Reservoir: Humans nasopharyngeal more common children
- Transmission: resp droplets & aspiration of normal flora
- High risk: Children & elderly
-
Pts w/history of previous viral RT infection
- Ex. Post-influenza, asthma
- Alcoholics & smokers
- Chronic pulm disease pts
- Congestive heart failure
- Asplenic/Splenectomy pts
- <u><strong>Trauma/Meningitis</strong></u>=<em><strong>CSF leakage to nose</strong></em>
Strep Pneumoniae-Pathogenesis
- Polysaccharide capsule=Anti-phagocytic (90 serotypes)-Vaccines
- IgA proteases: Disrupts IgA activity
- Pneumolysin-O: Alpha-hemo is Cytotoxin destroys ciliated epi cells (pulm)
- Teichoic acid & peptidoglycan: Activate alternative complement (inflammation)
- Phosphrylcholine: Unique to SP=Cell wall component
- Binds to receptors of platelets activating factor (found on many cells)
- Bacteria “hide” phagocytes=Spread infection
- Pneumococcal pneum(typical)-most common cause for Community/Nosocomial
- Aburtpt onset, fever, chills, rigors, cough w/rusty sputum-Lobular pneumonia
- Otitis Media most common disease
Strep Pneumoniae-Diagnosis
- Lab Specimen: Aspirate from sinus or Middle ear, CSF, blood
- Gram stain: (+) diplococci & capsule
- Quellung test: Capsular swelling applying specific Ab (like gram stain BUT w/Ab)
- Culture: Alpha-hemolysis on Blood agar w/Optochin sensitive
- Bile solubility: Addition of Bile to culture=killing of cell (less turbid=clear)
- PCR/Latex particle agglutination: mainly used for meningitis
Strep Pneumoniae-Treatment
- Penicillin/Erythromycin for most strains w/increasing resistance to penicillin
- Resistance is NOT due to beta-lactasmase BUT mutation to penicillin binding proteins
- Ceftriaxone or Vanomycin used as alt
- Pneumo capsular vaccines used 2 types:
- Adult PPV: 23 T-cell independent polysac Ags recommended for elderly over 65 (short lived immune response)
- Pediatric PPV: 13 T-cell dependent conj diphtheria toxin for children under 5 (long lived immune response)
Haemophilus Influenza-General
- Type B most VIRULENT type causes:
- Localized infections in URT & LRT
- Bacteremia (bacteria in blood)
- **Meningitis **
- Flora=Otitis media, Sinusnitis, pneumonia
- Gram (-) pleomorphic Rod w/pink stain
- Grow on chocalate agar or on Blood agar w/Strep aureus that lysis RBCs=Satellite Growth
- Coccobacilli encapsulated w/diff types
- Requires growth factors - **Ten(hemin) & five(NAD) **
- Reservoir: Humans ONLY nasopharynx capsular type B & non-typable strains COMMON (Flora)
- High Risk: Anyone-Unvaccinated children 2-4 or children w/severe infections
Haemophilus Influenza-Virulence factors
- Polysaccharide capsule: Type B capsule made of polyribose-ribitol phosphatase (PRP)
- IgA protease-Stops IgA
- Endotoxin: Lipo-oligosacc (LOS) similar to Neisseria=Adherence, toxic to ciliated cells, Induce inflammation
- Diseases:
- Otitis media <strong>(2nd common next to <u>strep pneumo</u>) </strong>seen w/conjunctivitis
- Sinusitis
- Lower resp tract infection
- Invasive disease=<strong>Meningitis & Epiglottitis</strong>
- Children 2-4 yrs most affected-Milder in adults
Haemophilus Influenza-Epiglottitis
- Acute onset, fever, sore throat
- Dysphagia
- Dysphonia=Hoarseness
- Drooling
- Distress=Breathing problem
- Stridor=High pitched sound on inspiration
- Muffled voice
- Pharynx inflammed=Beefy cherry red, stiff, Swollen epiglottis
- Diagnosis: Lateral X-ray of neck=Thumb sign
- Laryngoscopy before intubation
Haemophilus Influenza-Treatment
- Diagnosis: culture tiny colonies=Gray on chocolate agar or streak around Staph aureus=Satellite growth
- Ag Detection-Latex agglutination-Rapid PRP capsular Ag for H.Influenza type B ONLY
- Treatment: Suspected epiglottis is considered hospital emergency
- Supportive treatment: Cricothyrotomy (between thyroid&ciricoid)
- Antibiotics: Broad spectrum cephalosporin (Severe) & amoxicillin/Doxycycline (mild)
-
Prevention: Hib vaccine-for type B capsular polysaccharide-conj diphtheria or tetanus used to make it
- Vaccine reduces carrier rate
- Chemoprophylaxis(admin of meds to help minimize spread): Rifampin eliminates carriers in HIGH risk groups by type B
Corynebacterium diphtheriae-General
- Pleomorphic, gram (+) rods, w/clubbed ends (Coryneform)
- Arranged in pairs (V & L shapes)
- Formation of granules (volutin-stain red w/methyl blue) beaded appearance
- Reservoir: Human ONLY in nasopharynx, URT, GI, Skin-Normally harmless (flora)
- Aquires toxin gene from phage=lysogenized carriers
- Transmission: Resp or P to P spread of lysogenized bacteria
- High Risk: Unvaccinated, Crowded, CHILDREN
- Clinical: Diphetheria & skin infections
Corynebacterium diphtheriae-Virulence factor
- DT-A/B exotoxin (Secreted or released)
- Inhibits Protein synthesis VIA ADP ribosylation/inactivation of EF-2
- Carried by Phage B-Lysogenized corynebacteria
- Binds to heparin-binding epidermal growth factor found on Heart/nerve cells
- DT-3 parts 1. receptor binding region, 2.Translocation region (transmembrane), 3.catalytic region(A-unit)
-
Regulation via DTxR (Fe dependent repressor protein) on chromosome=responds to tissue Fe lvls
- Low lvls = Toxin made
- High lvls = Toxin Repressed
Corynebacterium diphtheriae-Clinical
- Incubation time: 2-6 days (fever, dyspnea)
- Local inflammation: Characterized by fibrinous exudate (tough, adherent-gray/green/black) pseudomembrane over tonsils
- Exudate filled w/neutrophils, necrotic epithelial cells, erythrocytes, & bacteria w/fibrin mesh
- Difficult to detach w/o damaging underlying tissue <strong>(bleeds occur when attempted)</strong>
- Located @ pharynx = More severe due obstruction to air flow
- Bull neck appearance-enlarged Ant cervical lymph nodes w/edema of soft tissues
- Skin diphtheria-Skin ulcer if bacteria enters through skin <strong>(non-healing ulcer)</strong>
Corynebacterium diphtheriae-Clinical complications
- Toxin carried to other organs-Heart, liver, kidney = necrosis
- Myocarditis-Arrhythmias & circulatory collapse
- Nerve weakness/paralysis: Cranial nerves
- Paralysis of muscles of soft palate & pharynx=Lead to regurg of fluids through nose
- Difficulties w/vision, speech, swallowing or movement of legs & arms
- Swelling/congestion of pharyngeal/tonsilar area w/white exudate
- Perforation of soft palate-Late effect
- Skin lesions-More common & present in tropics
Corynebacterium diphtheriae-Treatment
- Poor specificity on microscopy NOT all strains produce toxin
- Culture=isolate organism w/3 medias
- Cystine-Potassium tellurite (selective NO gram (-) & flora/Grey-Black colonies 24-48hrs)
- Blood agar (small gray irreg zone & small zone of hemolysis)
- Loeffer’s serum <u>(granule formation/Stain metachromic-inorganic polyphos)</u>
- Toxin test for production-Elek test=ouchterlony (<u>bind to Ab to form immune complex</u>) Lines cross same Or PCR
- Treatment: Early admin of diphtheria antitoxin (passive immunity)
- Penicillin or erythromycin
- Resp Support
- Prevention: DPT (diphtheria, pertussis, tetanus) vaccine followed by boosters
Bordetella Pertussis-General
- Gram negative coccobacillus-capsulated
- Strict aerobic-requires enriched media (Bordet-Gengou)
- Resistant to penicillin-Added to medias to make it selective
- Reservoir- Humans only
- Transmission-Aerosol/Direct contact
- High Risk-Unvaccinated children-Increasing in adults
-
Pathogenesis-adheres & multiplies rapidly on epi surface of trachea/bronchi
- Interferes w/ciliary action
Bordetella Pertussis-Adhesins (virulence)
- Adhesins:
- FHA (filamentous hemagglutinin) & pertactin
- Both bind to:
- Integrins on ciliated cells
- CR3 on macrophages=induce phagocytosis w/o initiating oxidative death
- Result=Intracellular growth in macrophages w/protection from humoral immunity= COUGH
- It does NOT invade rather it liberates internal toxins that irritate surface cells.
- Secondary invaders: staph, H.Influenza lead to bacterial pneumonia
Bordetella Pertussis-Virulence factors
- Pertussis Toxin (Ptx)-Ab type toxin
- ADP ribosylation of G protein=Increase cAMP lvls
- Increased resp secretion/mucus made
- Inhibits signal transduction by cytokine receptors
- Interfere signals from cell surface receptors to intracellular mediator sustems
- Interfere w/chemotaxis of lymph/neutophils & phagocytosis <strong>(increase WBC)</strong>
-
Tracheal cytotoxin (peptidoclygan)
- Interferes w/DNA synth, kills clilated resp cells
- Adenylate cyclase toxin/hemolysin: Secreted by bacteria, absorbed by host cells, & activated to convert ATP to cAMP
- Impairs chemotaxis=Inhibit phagocytosis
Bordetella Pertussis-Clinical
- Incubation 7-10 days NO symptoms
-
Catarrhal: 1-2 weeks=Inflammation mucous membranes nose and throat
- Highly contagious
- Best time to culture
- Paroxysmal: 2-4 weeks=destruction of ciliated epithelium, impairment of mucous clearing, whooping w/series of coughs vomiting, leukocytosis “sudden attacks”
-
Convalescent: 3-4 weeks (+)=secondary complications lack of oxygen supply: Pneumonia, seizures, encephalopathy & diminished cough (recovering)
- Possible stage for super infection
Bordetella Pertussis-Diagnosis
- Microscopy: Fluorescent Ab on aspirated specimens (false + high)
- Specimen: Calcium alginate swabs
- Culture: Not very sensitive
-
Bordet Gengou (Potato/Blood/glycerol agar w/High amount of blood 20-30%)
- Nicotinic acid + to support growth
- charcoal & Starch + to remove FA
- Molecular method: PCR
- Serology: ELISA-titers against pertussis to Hemagglutinin using acute/Convalescent serum (blood from recovering pt)
Bordetella Pertussis-Treatment
- Macrolides: Erythromycin or Azithromycin for early stage
- Treatment of dehydration & Low O2 for late stage-Steroids for babies/elderly
- Prevention & control:
- DPT vaccine (diphteria, pertussis, tetanus)
- Whole cell inactivated=80-85% effective w/SE
- DaPT vaccine-Multivalent acellular vaccine effective w/less SE
- Made up of several purified proteins, pertussis, hemagglutinin, peractin, fimbriae (contains @ least 2)-Booster needed
- Main immunogen is pertussis-engineered by intro 2 AA to inactivate enzyme activity
- Erythromycin prophylaxis-in young children prevent relaspse-In catarrhal stage shorten length/severity
Moraxella Catarrhalis-General
- Large # of gram(-) rod/bean shaped cocci attached or residing w/in PMNs in sputum
- Neisseriaceae family=Oxidase +(cyto C-electron transfer chain)
- Does NOT ferment glucose, maltose, sucrose
- Reservoir: Pharyngeal flora in children/adults
- High Risk: Children/elderly & may be combo infection w/other pathogen=Lower resp tract infection
- Clinical: Otitis media, sinusitis=Children & Bronchitis, pneumonia=Elderly
- Diagnosis-Gram stain
- Treatment-Beta lactamase(+)=Penicillin resistant
- Ampicillin/Clavulanate(Augmentin-beta inhibitor) 2nd or 3rd gen cephalosporins
Klebsiella Pneumoniae (General)
- Gram (-) rods, Faculative anaerobe
- **Lactose fermenter on MacConkey **
- Enteronacteriaciae=Non-motile, Oxidase <em><strong>(cyto-c</strong></em>) & Indole (reduction of trytophane) negative
- High Mucoid colonies due to LARGE cap
- Reservior: Part of normal flora GI & URT
- Transmission: endogenous, aspiration/inhalation of resp droplets.
- High risk: Chonic lung disease, alcoholism, diabetes, resp equipment (MEN)
-
Virulence: Capsule-Antiphago
- Endotoxin(LPS)= Inflammation leads to Septic shock
Klebsiella Pneumoniae (Clinical)
- Presents: Typical pneumonia (productive)=hospital/community
- Upper lobes w/50% mortality
- Necrotic destruction of alveolar spaces=Cavity formation
- Sputum THICK & Blood tinged jelly
- Complications: Septicemia (bacteria in blood) or UTI
- Diagnosis: Sputum w/gram stain <strong>(BIG CAPSULES)</strong>
- Pink colonies on **MacConkey-Lactose **
- Treatment: Antibiotic resistance, even vancomycin resistance
Pseudomonas Aeruginosa (General)
- Gram (-) rod in pairs, Oxidase (+) non-fermenter (aerobic)
-
Makes pigments:
- Pyocyanin (blue
- Pyoverdin (yellow/green)
- Some strains have Cap, slime layer, mucoid colonies
- Fruity grape-like oder
- Beta Hemolytic
-
Reservoir: Uniquitous (everywhere)-moist/wet sources, AC towers, Respirators, soil, disinfectant sol=Requires minimal nutrition
- Normal flora in some people
- High risk: Oppurtunistic: immunocomprimised (COPD, CF) hospitalized pts, Mech ventilation, or Pts on Broad spec antibio
Pseudomonas Aeruginosa (Pathogenesis)
- Several virulence factors, adhesions, toxin, exoenzymes
- Adhesins=Pili, LPS, capsule
- Exotoxin A=A-B exo in single protein-ADP ribosyltransferase reacts w/EF-2=Inhibit protein synthesis (diphtheria toxin)
- Pigments: Pyocyanin (blue) activates O2 radicals (ROI) attracts WBCs-Destruction of tissues
- Phopholipase=Digests lecithin leads to cell lysis
- Capsule/slime layer=Creates Biofilm (some strains)
- Most common cause of nosocomial pneumonia can be fatal <strong>(necrotizing bronchopneumonia)</strong>
Pseudomonas Aeruginosa (Clinical)
- Virulence facts must work TOGETHER to cause disease
- Typical pneumonia: Tracheobronchitis w/pneumonia=Necrotizing
- Biofilm formation found in CF pts
- Comprimised neutrophils fail to clear bacteria=Population grows
- Exo toxin A produced once pop reaches quarum sensing (biofilm)=slimey mucous
- Bacteremia/Endocarditis: Leads to shock
- Otitis media & externa (swimmer’s ear)
- Skin: Burn wounds or Folliculitis (hot tub)
- Eye infection: Trauma (contact lens)
- UTI: Hospital w/catheters
Pseudomonas Aeruginosa (Diagnosis)
- Culture on blood agar or enteric MacConkey=Grey colonies (non-lactose)
- Oxidase (+)=Presence of Cyto C (remove electrons)
- On colorles media makes Blue, green-yellow
- Mucoid colonies=Frutiy order
- Treat: Multidrug resistant due inherent resistance
- Combo of antibiotics-Anti-pseudomonal beta lactams + aminoglycosides or fluorquinolones
- Prevention: Hospital control * CL- of Hot tubs
Burkholderia Cepacia
- *Nine species *
- Gram (-) bacilli, aerobic non-fermenter, Oxidase (+)
- Does NOT product diffusible pigments
- Reservoir: Moist envrioments like Pseudomonas
- Transmission: Inhalation
- High Risk: Oppurtunistic pathogen (CPD, CF, Chronic granulomatous disease)
- Weak & NOT pathogenic in healthy people
- Typical pneumonia & UTI in catherized pts
- Diagnosis: isolated from sputum/catheters put in Blood agar or w/**polymyxin for which it is resistant **
- Treat: less resistant to Antibiotics - Trimethoprium sulfa
- Prevent by cleaning resp equipment BUT it is ubiquitous=hard to control
Acinetobater Baumannii
- Gram(-) coccobacilli (small rods), Non-motile
- Aerobic (oxidase negative) & Highly resistant to antibio (some are completely Immune)
- Reservoir: Ubiquitous (pseudomonas)-VERY resitant to enviroment dryness
- Normal flora oropharyngeal
- Transmission: Inhalation, trauma to skin, Hospital setting
- High Risk: Opportunistic-Pts
- w/resp vent
- Catherized pts (urine dialysis)
- Surgery or trauma
- Broad spectrum antibiotics
- Presents as typical pneumonia, UTI, septecemia, Infections in aged & ICU pts
- Soft tissue infections=Gun shot wound (Iraq Bacillus)
Legionella Pneumophilia (Legionnaire’s disease)
- Gram (-) bacilli (pleomorphic) HARD to stain-Silver impregnation
- Fastidious growth (Needs nutrition) Cysteince/Iron
- Special medium-BCYE (buffered charcoal yeast extract agar)-Charcoal neutralize FAs
- Reservoir: Aquatic, Survives in amoebae(Natural water), cooling towers, Showers, water misters, hot tubs, decorative fountains.
- Resistant to Cl- Can grow @ 45 C
- Transmission: inhalation of aerosol & water NO person to person
- High risk: Middle age or older=immunocomprimised <strong>(alcoholics, smokers, COPD, diabetes, transplant pts)</strong>
Legionella Pneumophilia (Pathogenesis)
- Faculative intracellular of alveolar macrophage, monocytes, & epithelial
- C3B deposition facilitate phagocytosis
- NO fusion of phagosome/lysosome=Avoid intracellular killing (survive inside macrophage)
- Infected macrophage-Make inflammatory cytokines=Robust inflammatory response
- Diagnosis: Direct fluorescent Ab or silver staining
- Culture on BCYE w/cysteine&iron
- Urine Ag Test: BEST method specific for LPS Ag
- Ab Rxn: ELISA or indirect fluorescent Ab test = Lvl of 1:128 or more (+)
Legionella Pneumophilia (Clinical)
- Pontiac Fever: Flu-like symptoms
- Incubation time=1/2 dats & lasts 2/5 days
- Fever, chills, myalgia, malaise, headache
- No pneumonia
- Possible Hypersensitivity rxn
- No Antibiotic treatment
- Legion Disease: Atypical pneumonia
- Incubation time=2/10 days
- Male middle age (smoking, drinking, underlying pulm disease)
- Sever Toxic pneumonia-Rapid onset w/flu-like symptoms, high fever, chest pain DRY cough
- Patchy interstitial infiltration w/tendency to develop into conslidation w/micro-abcess
- Progress to multi-organ failure
- Mortality 75% in immunocomprimised
Legionella Pneumophilia (treatment)
- Antibiotic must be able to penetrate HUMAN cells
- Macrolides-Azithromycin or Clarithromycin
- Fluoroquinolones-Cipro or Levo
- Control-
- ID Source & eliminate
- Hyperchlorination & elevated water temp
- Replace shower heads
- Stop water mists on vegetables
- Copper-silver ionization of water supply
Mycoplasma Pneumoniae (general)
- Cell-wall less=Pleomorphic
- Sterol in cell membrane
- Smallest free living organism (extracellular)
- Requires cholesterol in culture
- Lives in Human Resp Tract
- Infected by aerosol spread w/in Close people - Incucation 1-4 weeks
- High Risk: Teenagers/Young adults
- Outbreaks occur in military & colleges
- Adhesion: Surface P1 binds to sialic acid on ciliated resp epi cells
- Tissue damage: Produce hydrogen peroxide-Superoxide radicals & cytolytic enzymes=Killing cells/Destroying ciliary action
Mycoplasma Pneumoniae (Clinical)
- Incubation time 2-3 weeks
- Pharyngitis
- Tracheobronchitis-Low grade fever w/Dry cough
- Pneumonia-Atypical-walking w/low grade fever, patchy broncho-Dry cough
- Complications: Hemolytic anemia & Neurologic Due to MP binds to sialic acid glycoproteins on RBCs
- Treatment: Beta-lactam antibios
- Tetracycline, erythromycin & quinolones
- Mulberry colonies or Fried egg colonies
Mycoplasma Pneumoniae (diagnosis)
- Specimen from bronchial washings (NO sputum produced)
- Mulberry colony on A8 agar enriched media w/animal serum (cholesterol) & antibios to inhibit bacteria=Grow SLOW up to 6 weeks
-
Cold aggutinin-IgM Ab bind to Ag on erythrocytes of O blood @ 4 C
- Can be preformed @ bed side takes mins
- For children under 12 not a good test
- Serology-ELISA 4 fold increase (1:128) detect Ab against P1 Ag
Chlamydiaceae (general)
- Under another family Clamydiopilia (Psittaci & Pneumoniae)-Non-STD
- “Energy Parasites”-Use ATP produced by host cell
- Obligate intracellular parasites w/o host cell ATP they cannot make their own
- Cannot grow w/o culture-Has cell wall BUT lacks muramic acid (sugar acid)
- NO Gram stain
- Biphasic growth cycle:
- Elementary body=Infectous stage (metab inactive comes from outside-In)
- Reticulate Body=Metab active-replicate inside cell & convery EB to RB-Lyse cell
Chlamydophilia Pneumoniae (general)
- Reservoir: Human RT
- High risk: most cases are asymptomatic or *present w/Pharyngitis *
- Elderly
- Pathogenesis: Intracellular growth infects-
- Macrophages
- Endothelial cells
- Coronary artery
- Smooth muscle
- Presents:
- Pharyngitis
- Sinusitis
- Bronchitis
- Atypical pneumonia (mycoplasma)
- Linked to atherosclerosis, Alzheimer’s, asthma, & reactive arthritis
Chlamydophilia Pneumoniae (Diagnosis)
- Difficult to diagnose
- Culture: Grow on HE-p2 cell line (not common)
- DFA staining to detect inclusion bodies (stain green)
- Serology: Best method-Microimmunofluorescence or comp fix test
- Detect IgM or 2x increase of IgG
- Treat: Reaccurance of symptoms tends to happen so 2-3 weeks treatment recommended
- Doxycycline, fluoroquinolones, erythromycin
Chlamydophilia psittaci
- Reservoir: Birds (farmhand working on turkey farm) present in tissue, feces, urine of bird (sick/healthy)
- Transmission: Aero via dust w/resp secretions/handling of avian feces
- NO person to person
- Pathogenesis: Parrot fever/Ornithosis
- Atypical pneumonia
- Bronchitis/Pharyngitis/Sinusitis
- Severe cases spread to Multi system
- Diagnosis: Serology 4x increase comp fixation or micro immuno
- Treatment: Doxycycline, macrolides, fluoroquinolones
- Treat imported birds w/chlortetracycline
Bacillus Anthracis (general)
- Large gram (+) spore forming bacilli
- Chain formation
- Aerobic spore former-Poly glutamic acid capsule (not a protein=NO gram stain)
- Reservoir: Ubiquitous around the world (soils/animals)
- Transmission: Disease of **herbivores aquire pathogen by grazing **
- Humans infected by contact w/animals
- Entry-injured skin, inhalation, ingestion
- High risk: Farm hands, vets, tanners, taxidermists
- Diagnosis: Resp secretions, Pus on skin, or Blood
- Culture: Blood agar-non/hemo w/white-grey rough colonies (rounded glass appearance)
- PCR best diagnosis
Bacillus Anthracis (Clinical)
- Virulence:
- Poly-glutamate cap (non-phago)
- Anthrax: A-B toxin coded by genes on plasmids
- PA (protective Ag), EF (edema Ag), LF (lethal factor)
- PA=Binding unit-entry <strong>(bind multi-system)</strong>
- EF=Adenylate cyclase increase cAMP=edema
- LF=Zn dependent protease inhibits kinases-Cell death
- Skin: entry through wound, black necrotic center w/raised edematous edges
- GI: RARE in humans, High mortality
- Inhalation(wool sorter’s): incubation 2+ months, alveolar macrophage engulf spores-carry to mediastinal lymph
- Massive chest edema, hemorrhagic (widened mediastinum), bacteremia/toxemia=Cyanosis-shock-death w/in 3 days (meningeal symtptoms)