Infectious Endocarditis

Description Staph Aureus B-hemolytic Transmission Skin of IVDA, spread by sloppy HCW, surgical wounds infections => bacteremia Pathogenesis Clumping factor bind fibrinogen & TA binds fibronectin, a-toxin (form pore), produce tissue thromboplastin => vegetations, coagulase, protein A bind Fc of IgG inhibit phagocytosis Polysac slime (biofilms on catheter), bind fibronectin Bind fibronectin , grows in vegetations, Preexisting damage to heart valve follows dental work Symptoms FUO, murmur, fatigue (1st day dont see murmur, but 2nd day see murmur)

Staph Epidermidis (S. Mutan) Strep Viridans (Group D Strep)

Not hemolytic

Skin, prosthetic devices, IV lines (pre-mature babies), IC pt w neutropenia Human oropharynx

a-hemolytic, optochin resistant

Enterococcus

PYR test +, grow in high salt, detergent (bile), toughest bacteria Surface yeast converting to hyphae, pseudohyphae

GI, GU

Preexisting heart dis with GU or GI tract manipulations w/o prophylactic antibiotics (prostatic biopsy)

B-lactam & aminoglycoside, VRE-Vancomycin Resistant Enterococci, Hygiene Endocarditis, chorioretinitis, skin nodules

Candida

Moist skin, mucosa flora, IV drugs (heroin), invade catheters -> septicemia

Bartonella Quintana
Bartonella Henselae

G(-), fastidious (blood agar +H2O), slow growing

May or may not be culturable, in serotiters used in diagnosis

homeless (body lice)

Skin, LN, spleen & liver in IC pt

Bacillary Angiomatosis in AIDS pt, Trench Fever

Catch Scratch Dis- fever + regional adenopathy Damaged heart/prosthetic device

Coxiella Burnettii Strep Pyogenes G +, B-hemolytic, PYR + Lancefield Group A

Autoimmune disease

Endocarditis
Acute: high fever, something very virulent (Stap. Aureus) Chronic: less fever, less virulent (opportunists) IDU: Skin flora (S. aureus, S. epidermis) Contaminants from drugs (Candida in heroin) & Aspergillus Water (Pseudomonas) Oral flora (licking needles) Homeless (Bartonella Quintana)

Culture negative endocarditis:

1. 2. Bartonella Quintana or Bartonella Henselae Acute Rheumatic Fever and Rheumatic Heart Disease: Pancarditis Starts with Strep pyogenes. Pt produce Ab that cross react with some antigen on heart muscle and connective tissue a couple weeks after pharyngitis Diagnosis: high anti-streptolysin O titer (do not use anti-M protein Ab to diagnose), high ASO titer If not treated => Rheumatic heart disease => EDUCATE PT when to use prophylactic

Pericarditis
acute benin most often viral (Enteroviruse or Coxsackie) Symptoms: sharp pain (often precordial), can be mistaken for heart attack, fever if have infection

Myocarditis, Atherosclerosis & Lyme disease

Description Transmission Pathogenesis Symptoms

Coxsackie

Naked, +ssRNA (Picornaviridae)

Fecal oral, replicate in GI 1st > viremia, mainly in IC pt

Infect heart cells, triggers WBC to attack infected cells, makes Ab & WBC to attack uninfected cells (autoimmune) Life threating in babies (febrile w sudden HF)

Myocarditis: Chest pain, arrhythmia, chronic -> heart enlargement, CHF w dyspnea

Parvovirus B19 Adenoviruses T. Cruzi

ssDNA, naked dsDNA, naked Hemoflagellate C shapes in images, South & Central America poverty housing Reduvid bug, Trypomastigote is transferred in feces, either rubbed into eye or scratch, heart transplantation & transfusion Chagas disease , megacolon, megaesophagus Myocarditis

C. Diphtheria

G+ rod, non-spore forming

Bind ADP-ribosylates eukaryotic EF-2 -> no protein syn

2nd wk of disease => heart failure, Myocarditis

Chlamydophila Pneumoniae

OIP, no peptidoglycan, DFA show inclusion bodies, cant make ATP, elementary & reticular body Motile spiral-shaped w endoflagella, larger & fewer spirals than Treponemes

Respiratory route, heat shock protein

infects endothelial cells triggering inflammation, activate heat shock protein trigger plaque formation Invades skin, spreads via bloodstream to involve primarily in heart, jt, CNS, OspA (tick) => OspC (feeding on human blood)

Atherosclerosis

Borrelia Burgdorferi

Ixodes ticks, larvae & nymphs over winter on white footed mice, a

Lyme disease, erythema migrans (visit to risk area or your dog may have gone, lack of known tick bites)

Lyme Disease

Borrelia burgdorferi

Ixodes scapularis (deer tick)

Ixodes scapularis (deer tick) in North central & Eastern US
Ixodes pacificus in western US Adult Female

Eggs

Larva

Nymph

Stage last 3d to 4wks -Single erythema migrans (EM)at bite site, regional lymphadenopathy -Often no knowledge of tick bite 2nd Stage- w/i few days of bite to wks-months -Severe malaise, fatigue, fever, chills -Skin: multiple EMs, lesions -Neurological: meningitis, facial palsy, painful radiculopathy - Cardiac: conduction defects => myopericarditis 3rd Stage- months-years after initial bite -fatigue, prolonged arthritis attacks => CNS disease (cognitive problems), scleroderma - Ixodes co-infection - Anaplasma - Babesia 1st

Diagnosis:
-ELISA, Western blot, PCR (jt or CNS), culture-special medium (skin), NOT urine test Prevention -Tuck pant legs into socks, repellent Relapsing Fever (Orphan febrile disease) 1. Tick-borne relapsing fever (TBRF) Associated w Western US, caused by spiral-shaped bacteria, rusted cabin 1. Louse-borne relapsing fever (LBRF) Caused by Borrelia recurrentis, outbreak in Africa

White footed mice

Spirochetes

Human

Deer

Rickettisial Diseases
Organism
Rickettsia rickettsii

Descriptions
G (-), OmpA & OmpB, escape phagosome to cytoplasm, invade vascular endothelium by phogocytosis same same

Disease
Rocky Mountain spotted fever

Vector
Tick

Diagnoses
Weill-Felix rxndetecting Ab cross react w Proteus see agglutination

Symptoms
Rash on palm, sole of feet

Rickettsia typhi Rickettsia prowazeki

Endemic typhus Epidemic typhus

Flea Louse

Rashes Rashes

Orientia tsutsugamushi Ehrlichia chaffeensis

same

Scrub typhus

Chigger (mite) Tick Blood smear for round inclusion monocytes, leukopenia, thrombocytopenia Blood smear for round inclusion neutrophils,

Eschar (black scab), Asia, common cause of fever in VN war Rashes but no vasculitis, incubation 7 days

G (-), no LPS, no PG, remain in membrane bound vacuoles, dont invade endothelium cells, invade monocytes, not free in cytoplasm G (-), no LPS, no PG, dont invade vasculoendothelium, invade PMNs, not free in cytoplasm

Ehrlichiosis

Anaplasma phagocytophilum

Anaplasmosis

Tick

Rashes but no vasculitis, incubation 7 days

Immunology of Rickettsia -Ab formed but not protected so need CD8 to kill organism - INF- & TNF- activate infected endothelium to kill organism

Rocky Mountain Spotted Fever

-Elderly & black w G6PH def => severe case - 6-10h of feeding before get fever - Incubation 7 days (fever) then 3 days later dev maculopapular erythema => petechia => necrosis & gangrene

Bacterial Upper Respiratory Tract Infection

Causes Otitis Media
1. Strep Pneumoniae 2. H. Influenza 3. Moraxella Catarrhalis Inflam paranasal sinuses due to viral infection, allergies

Age Range
6 m 3 yr

Pathogenesis
Viral infection, adenovirus inflame adenoid tissue around E. Tube -> fluid acc, bacterial growth Nose blowing inc P -> push fluid & infection to sinuse Kartagener, Bronchiectasis, Immotile cilia

Diagnosis
Erythema, bulging tympanic membrane X-ray (CT scan preferred) show fluid in acute sinusitis, thickening of mem in chronic sinusitis Throat cul, Rapid Ag diag test if (-) do culture (more sensitive)

Treatment
Give Antibiotics

Sinusitis

Avoid antibiotics,

Pharyngitis

Group A Strep Pyogenes

3y 15 yr

Symptoms: Anterior cervical lymphadenopathy, sore throat, odynophagia (painful swallowing), tonsillar enlarge beefy red w white exudates Spread: resp droplets (asymp carrier) Virulences: 1. M protein antiphagocytic 2. Capsule of hyaluronic acid 3. Streptolysins O and S damage cells 4. Streptokinase lyses clots 5. Hyaluronidase spreadg factors 6. Lipoteichoic acid adhesin

Untreated, the bacteria can persist for wks

Group A Strep

Fuzzy surface due to fibrils of M protein, dense layer due to fibrinogen after exposure to plasma

Acute Rheumatic Fever (ARF) C. Diphtheria

Due to complication of Pharyngitis

M protein cross react w heart protein, see acute glomerulonephritis

Spread: resp droplet (asym carrier) Toxin: exotoxin by lysogenic phage, bind EF-2 -> prevent protein syn, myocarditis, neuropathy Fatal Diphtheria: gray, leathery pseudomembrane covers trachea, larynx, tongue => death by asphyxia

Vaccines: DTaP infant Td adult every 10 yr DT children w CI for pertussis vaccine

Typical Pneumonia (CAP)

Symptoms: fever, cough productive of purulent (pus- yellow or green) or rusty (RBCs) sputum, dyspnea, pleuritis pain, lobar (alveolar) pattern of consolidation by x-ray, severe Diagnostics: Urinary antigen for Strep pneumoniae and Legionella sp PCR new, not routine or reliable, good for Mycoplasma Serology for Mycoplasma Defense in Lower tract: sterile, ciliated epith, cough, phagocytes, immune sys Defense in alveolar macrophage Alveolar macrophages ingest particles Fibronectin cell-cell adhesion, by attaching to both bacteria and PMNs promotes phagocytic function Surfactant bind to bacteria, fungi, viruses acting as opsonins to enhance phagocytosis by macrophages and PMNs

Prevention
-Adults > 65 need Pneumococcal Polysac vaccine (23 serotypes) - Children 2-15 m need Pneu Conjugate vaccine (7-13 serotypes) - Influenza vaccine annually - All persons > 50 w risks of COPD, HF, metabolic dis, immunodeficiencies => need to get vaccine sooner
Virulence factors Strep Pneumonia (G + cocci) 1. Capsular Polysac inhibit phagocytosis mutants lacking a capsule are avirulent 2. Surface adhesin A- attaches to epith cells of nasopharynx 3. Surface protein C binds to complement factor H inhibit C3 convertase => reducing phagocytosis 4. Pneumolysin cytotoxic, activates complement Pathogenegis -Colonization (asymptomatic) in NP for wks (no inflam of interstitium, no necrosis, no abscess form) => trachea (usually cleared by ciliary mov., impaired clearance in allergies, smoking => resp infection => alveoli (need to escape phagocytosis by hv capsule) => inh complement activation - In alveoli, bacteria proliferate, activate complement, generate cytokines, attract PMNs, and exudate into alveolar spaces by cell wall PG, lipoteichoic acid stim TLR-2 => prod cytokines - can spread to pleura => pleural effusion & emphysema 1. Fatalities Resp failure. Hypoxemia, cyanosis, labored breathing, need for mechanical ventilation Sepsis => meninges => shock w poor perfusion (brain & kidney)

2.

H. Influenza (G coccobacillus) Moraxella Catarrhalis (G cocci)

Atypical Pneumonia
Symptoms: fever, dry (non-productive) cough, interstitial infiltrates on X-ray, less severe than typical pneumonia, sputum (scanty, thin, white) X-ray show infiltrates in mildly ill outpatient Walking pneumonia Characteristics Mycoplasma Pneumonia Not visible on G stain, not culturable by routine methods, lack cell wall, 2nd most common CA pneumonia Pathogenesis No exotoxins produced. No endotoxin because there is no cell wall. Produces hydrogen peroxide, which may damage the respiratory tract. -long incubation period 2-3 wks, gradual onset of fever, malaise, dry cough -Facultative intracellular pathogens multiply in alveolar macrophage - Virulence: LPS endotoxin, flagellin, biofilm Transmission - respiratory droplets disseminated by cough (person to person) -more common in children < 3 yr, who mostly hv upper resp dis - Seasonal, winter related Diagnosis - IgM Ab, cold agglutinate or lyse RBCS

Legionella

Resistant to Cl, grow at high temp 46C, grow in free living amoeba

-Aerosols by water coolers, faucets, showers, acquire from environment - not transmitted person-to person, not contagious, year round - Host susceptibility inc: smokers, COPD, elderly, IC -person-to-person, aerosol droplets - incubation 21 days (asymptomatic) - not seasonal or winter related

-Slow growing: Ag stain, culture on charcoal yeast extract takes 3-5 days - Symptoms: about pt purulent sputum & lung consolidation by X-ray suggest S. Pneumoniae. Abdominal pain, diarrhea -Serology by microimmunofluorescence

Chlamydophila Pneumoniae

G-, LPS is truncated => not very endotoxic, OI organism req ATP, no PG -Elementary form can survive outside but d.n replicate => contagious, enters cell via endocytosis - Reticulate body- divide by fission=> disease, some will convert back to Elementary form and survive outside body G - , coccobacillus, aerobic nonfermantative, fastidious (sensitive to cold and drying),

-Male > female - adults w Ab can get reinfected - related to atherosclerosis

Bordetella Purtussi

Pertussis toxin- cAMP by ADPribosylation of G protein Cough to expel muscus Exotoxins: 1. pertussis toxin 2. Adenylate cyclate cAMP 3. Tracheal cytotoxin -> thick mucous

Vaccine effect up to 12 yr Kids 1-5 prone to infection Adhesin factors for vaccine: 1. Fimbriae 2. filamentous hemagglutinin 3. Pertussis toxoid

-Bordet Gengou agar, leukocytosis Adult need boost er every 4-6 y (for post-partum mother & other caregiver of infant

Fungal Pneumonia
Characteristics Histoplasma Capsulatum
Bird or bat droppings along riverbeds, dimorphic fungus (envir: hyphae, body: yeast), facultative intracellular parasite in reticuloendothelial cells (RES) Decaying wood, dimorphic fungus

Location
Eastern Great Lakes, Ohio, Mississippi, Missouri River beds

Diseases
Chronic Cavitation Disseminated- mucous mem (more in certain HLA serotyes Blacks, Filipinos, N. American)

Symptoms
Hepatosplenomegaly, Hilar lymphadenopathy

Diagnosis
Peripheral blood cultures since it circulates in (RES)

Blastomyces Dermatitidis Coccidioides Immitis

SE seaboard, up to Canada

Chronic - Coin lesions Disseminated cutaneous surfaces Chronic Cavitation Disseminated- mucous mem (2nd and 3rd trimesters) (more in certain HLA serotyes Blacks, Filipinos, N. American)

Blastomycosis: greater tendency not to self-resolve so tx is common Coccidioidomycosis: problem in AIDS & cancer pt in endemic area from infection or reactivation

Granulomatous nodules on skin

Hyphae breaking up into barrel shaped arthroconidia, spherules w endospores

Desert sand in/from SW US (CA, Arizona, NM, TX, Nevada)

No lab culture Dangerous

Commons: Not contagious from person to person, environmental form Symptoms: Acute: fever, chills, headache, myalgia, arthralgia, cough (non-productive), chest pain, difficult breathing, erythema nodosum ( a positive prognostic sign bc immune sys is working well) No URT (except some hoarseness w Histo) Chronic: slow progression like TB w expanding lesions, wt loss, night sweats Disseminated: any where in the body Diagnosis: Travel history, timing, other family members (non contagious) Specimen: Sputa, bronchoalveolar lavage fluid (BALF), skin test for all 3

Map of Fungal Pneumonias

Blasto Blasto Histo/ Blasto

Cocci

Blasto Blasto

US only

Opportunistic Pulmonary Fungi

Characteristics Aspergillus Fumigatus Hyaphae, Septate, filamentous fungus (monomorphic), spores airborne, ceiling tiles, moldy food, compost piles, dichotomously branching filaments Pathogenesis - in transplant pt (heart & liver) - spore land on nasal mucosa, colonize surface, sporulate => seed lungs - grow into blood vessels -> infarct => pul hemorrhage Diseases 1. Invasive pul aspergillosis infection in IC pt 2. Fungus balls growing free in old TB cavities 3. Allergic Bronchopulmonary Aspergillosis where agent is growing mucous plugs in lungs of asthamtic pt w allergies including Aspergillus 4. Farmers lung (allergy) Meningitis (headache, mental confusion, fever in IC pts) Subcutaneous infections - traumatic implantation by puncture w thorns, twigs, slivers ( d.n disseminate to lungs from sub Q) Pulmonary dis in urban homeless alcoholics = alcoholic rose garden sleepers disease, like TB Esp in AIDS: fever, dyspnea, hypoxemia no culture or serology Acid fast stain Diagnosis High IgE levels

Cryptococcus Neoformans Sporothrix Schenckii

Encapsulated yeast (monomorphic), soil enriched w pigeon droppings Grow in plants (rose)

culture India Ink

Pneumocystis Jiroveci (P. carinii) Non-tuberculous Mycobacteria (Mycobacterium Kansasii & avium) Actinomyces Israeli

Yeast

Soil organism- can aerosolize or get into water, rare, less virulent in IC hosts, occur mostly in IC pt (AIDS), not transmitted person to person Anaerobic G + , non-spore forming, branching rods

Disseminated dis in AIDS, esp w MAC, by blood to liver, spleen, LN, intestine, BM w large # of bacilli in tissue Person w poor hygiene lack of brushing, or visit to dentist, person who aspirate like alcoholics, seizure pts, No spread from person-to-person, environ form, dev slowly over wks in contrast to acute pneumonia Colonizes endotracheal tube, forms biofilm , + P ventilator blows bacteria into alveoli , sec alginate in lung of CF pt

Pneumonia, multifocal bronchiectasis, small nodules

Rare now bc sensitive to penicillin and other antibiotics Chest wall mass from extension of infection from lung and pleura thr IC space Long abscess, extend to adjacent tissues like chest wall abscess, brain abscess Ventilator Associated Pneumonia (VAP) P. aeruginosa, Acinetobacter, S. Aureus, Klebsiella Pneumonia, Enterobacter Aerogenes

Anaerobic media for culture

Nocardia Asteroides Pseudomonas Aeruginosa

G + bacilli w branching, aerobic, acid-fast G - , motile bacillus, opportunist in burn wounds, CF

Blood agar showing white colonies at 48h