Pulmonary Infectious Disease

Tory Davis, PA-C

Pneumonia What is it?

– Acute infection of the lung parenchyma, including alveolar spaces and interstitial tissue

– Alveoli fill with exudate (pus), fibrin, cells

– Usually bacterial or viral infection– May be fungi, rickettsial, yeasts, parasites

Classification of Pneumonia

“Typical” vs. “Atypical” By site of acquisition (ie where the pt

picked up the bug) By location in lung Other pt factors (such as

imunocompromised, HIV-associated, aspiration)

General Info Community acquired pneumonia

(CAP)- 2-3 million cases per year Most deadly infectious disease in US 6th leading cause of death in US 60,000 deaths annually Worldwide: leading cause of death in

children

Community Acquired Pneumonia (CAP)

Definition– Onset outside hospital or diagnosed

within 48 hours of admission in a patient who has NOT been in long-term care facility for 14d prior to symptom onset AND who does not meet the criteria for health-care associated pneumonia (HCAP)

HAP & VAP Hospital Acquired pneumonia

– New infection occurring 48 hours or longer after hospital admission

Ventilator Associated Pneumonia– 48-72 hours after endotracheal intubation

HealthCare Associated Pneumonia (HCAP)

Infection occurring within 90 days of a 2-day or longer hospitalization

In nursing home or long-term care residence Within 30 days of IV abx therapy,

chemotherapy, wound care or hemodialysis in a hospital or hemodialysis clinic

Pneumonia in any pt in contact with a multi-drug-resistant pathogen

HCAP Includes many pts who used to be

considered CAP Newer evidence suggest that pts with

HCAP are more like pts with HAP (than CAP) and may need HAP-like treatments

Other things to consider Aspiration pneumonia- who would

get this? Opportunistic organisms- such as

Pneumocystis jerovecii pneumonia (seen only in immunocompromised patients.)

Classify by Location Primarily from x-ray observation Lobar pneumonia- Entire lobe Segmental or lobular pneumonia

(segment of lobe) Bronchopneumonia- (alveoli

contiguous with bronchi) Interstitial pneumonia- (Involvement of

tissue between the alveoli)

Common Signs and Symptoms

Fever Cough sputum Dyspnea Chills/Rigors Diaphoresis Chest pain Abd pain

Pleurisy Hemoptysis Fatigue Myalgias Arthralgias Anorexia Headache

Typical Presentation

Sudden onset fevers, cough with purulent sputum, dyspnea, occasional pleuritic chest pain

Signs of consolidation, x-ray abnormalities Usually caused by more common bacteria:

– Pneumoccocus, H. influenza, etc.

Remember Clinical Assessment?

Consolidation: tactile fremitus (“Ninety-nine”)– Bronchophony (Auscultate “Ninety nine”) – sounds

like listening without stethoscope– Egophony (EA changes)– Rales (crackles)

Associated pleural effusion: tactile fremitus– Distant breath sounds– Pleural friction rub (creaking leather)

Atypical Presentation

Gradual onset, dry cough, myalgias, fatigue, sore throat, N/V, diarrhea, dyspnea

Less remarkable pulmonary exam despite abnormal x-ray findings

Organisms: Mycoplasma pneumoniae, Legionella pneumophila, Chlamydia pneumoniae, Chlamydia psittaci, Francisella tularensis, viruses

Pathogenesis Some combination of:

– Defect in normal host defenses, which include:

Cough reflex Mucociliary clearance system Immune response

– Very large infectious inoculation– Highly virulent pathogen

Mechanism of spread Most common

– Inhalation of droplets small enough to get to alveoli

– Aspiration of secretions from upper airways

Other– Hematogenous or lymphatic

dissemination– Direct spread from nearby infection

Predisposing factors URI Smoking Alcoholism – dec immune fxn and inc aspiration Institutionalization Heart failure COPD Age extremes Debility or consciousness Immunocompromise (including CRF, DM) Dysphagia

What’s Buggin’ Ya? Community Acquired (CAP)- bacterial

– Streptococcus pneumoniae (pneumococcus) 20-60% of CAP

– Haemophilus influenzae (H. flu)– Mycoplasma pneumoniae– And a bunch of others

What’s Buggin’ Ya 2

Viral– Infants and children: major pulmonary

pathogens are VIRAL: RSV, parainfluenza, influenza A and B

– Adults: influenza A (B less often), rare varicella-zoster

Fungal: Histoplasma capsulatum, coccidiodies immitis, blastomyces dermatitidis, cryptococcus neoformans, aspergillus fumigatus, pneumocystis carinii/jerovecii

Rickettsial: primarily Coxiella burnetii

What’s Buggin’ You Worse?

HAP/HCAP– Enteric aerobic gram-negative bacilli– Pseudomonas aeruginosa– S. aureus (includng MRSA)– Oral anaerobes

HIV Infection-Associated – Pneumocystis jerovecii– M. tuberculosis– S. pneumoniae– H. influenzae

Demographics Aids Diagnosis

Influenza assoc with community outbreaks– Typical pneumonia outbreak after flu outbreak

Legionella: exposure to aerosolized water vapor (cooling systems) → outbreak

Mycoplasma in younger pts in conjugate settings (college, military), with slow transmission

Chlamydia psittaci in bird handlers, Tularemia from cute bunnies, Anthrax from pigs…

Pneumococcal pneumonia

Caused by Streptococcus pneumoniae (>80 serotypes)

Most common cause of bac-t pnu Most frequent in winter Most common in age extremes Inhaled/aspirated pneumococci lodge in

alveoli. Inflammatory process in alveolar spaces, causes accumulation of protein-rich fluid which is great growth medium for bac-t, helps them spread to nearby alveoli

Pneumococcal S & S Often preceded by URI Sudden onset with SINGLE shaking chill,

followed by fever up to 40.5º, pleurisy, cough, dyspnea

Tachypnea with RR rising to 20-45 Tachycardia P 100-140 Can have: n/v, malaise, myalgias Cough initially dry, progresses to producing

purulent, rusty or blood streaked sputum Exam may show signs of lobar consolidation or

pleural effusion (know exam signs)

Complications Progressive pneumonia Respiratory distress Septic shock Contiguous infections Bacteremia extrapulmonary

infections

Prognosis- Pneumococcus Pneumococcus accounts for 85% of lethal CAP

cases Overall, 10% mortality Poor prognostic markers:

– age <1 or >60– positive blood cx– involvement of >1 lobe– low WBC count– extrapulm complication– immunosupression– CHF– Cirrhosis– asplenia

Staphylococcal Pneumonia

2% of CAP, 10-15% of HAP/HCAP are caused by Staph aureus

Risks: age extremes, hospitalized pts, intubated, tracheostomy, immuno-suppressed, recent surgery, pts with cystic fibrosis, IVDU (who are prone to tricuspid valve endocarditis with resultant embolic pneumonia)

CXR- multiple bilateral nodular infiltrates with central cavitation

Staph Aureus S & S

Similar to pneumococcus, except:– Recurrent rigors (vs single chill)– Tissue necrosis and abscess formation– Empyema common- suspect S. aureus in

post thoracotomy empyema or an empyema complicating chest tube drainage s/p chest wall trauma

– Fulminant course with prostration

Staph Aureus prognosis Mortality 30-40%, often (but not

always) due to serious associated conditions– Can be lethal in previously healthy adult

who develops Staph superinfection after influenza

Slow response to abx, prolonged convalescence

Gram Negative Bacilli Account for <2% CAP, but the majority of

HAP/HCAP pneumonias Klebsiella, Pseudomonas aeruginosa,

Escherichia coli, Enterobacter sp, Proteus sp, Acinetobacter sp

Rare in healthy adults Seen in infants, elderly, alcoholics,

debilitated/immunocompromised hosts, esp those with neutropenia

Bronchopneumonia similar to other infections, except: very high mortality 25-50% despite abx

Klebsiella pneumoniae CAP in alcoholics, common HAP Frequent abscess formation causes Friedlander’s pneumonia- affects

upper lobes, produces current jelly sputum, tissue necrosis, early abscess, and fulminant course

CXR- “bulging fissure” sign. Upper lobar consolidation with bowing fissure, also abscess and lung necrosis

Pseudomonas aeruginosa

Common VAP pathogen Seen in neutropenic, intubated, ICU or

burn unit pts, CF, AIDS High mortality CXR- microabscesses coalescing into

large abscesses

Haemophilus influenza 2nd most common cause of CAP (when

bug is ID’d) Strains containing type B polysaccharide

capsule most virulent; cause meningitis, epiglottitis, bacteremic pneumonia. Nearly gone in US due to HiB vaccine.

Non-type B strains colonize lower resp tract of pts with chronic bronchitis, implicated in exacerbations (thus abx in bronchitis in pts w/ COPD)

H. influenza Hib pneumonia usually in kids- median

age 1 year – esp if not immunized Usually proceeded by coryza Early pleural effusion in 50% In adults, presentation similar to other

bac-t pneumonias Bacteremia and empyema uncommon

Legionnaire’s Disease Pneumonia caused by Legionella pneumophilia.

Discovered in members of American Legion during 1976 convention in Philadelphia.

1-8% of CAP and 4% of lethal nosocomial cases. Occurs in late summer, early fall. Caused by aerosolization of contaminated water

source, spread by AC systems or shower heads. Risk factors: smoking, etoh abuse,

immunosuppression

Legionella

Incubation 2-10 days Prodrome resembles influenza:

malaise, fever, myalgia, headache, cough- initially non-productive, then productive of mucoid sputum

Characteristic high fever, relative bradycardia, commonly diarrhea

Less common: altered mental status

Legionella CXR shows patchy segmental or lobar

infiltrate, unilateral progressing to bilateral, often with pleural effusion. Abnormalities persist

Labs: leukocytosis, hyponatremia, hypophosphatemia, abnl LFTs

Mortality >15% in CAP, higher in hospitalized or immunosuppressed pts

Slow convalescence

Mycoplasma pneumoniae Most common pathogen in ages 5-35 “Walking pneumonia” Slow spreading epidemics due to incubation

time of 10-14 days. Spread common thru close contacts, closed populations such as military, families, PA students

Attaches to and destroys ciliated epithelial cells of respiratory tract mucosa

M. pneumoniae Initial sx are flu-like: malaise, sore throat, dry

cough with progressive severity Gradual progression (vs fast onset of

“typicals”) Coughing may be paroxysmal, produces

mucoid, mucopurulent, or blood-streaked sputum

Acute sx 1-2 weeks, then slow recovery. Often mild sx, spontaneous recovery usually- pts will recover with or without treatment

M. pnemoniae Prolonged cough due to inhibition of ciliary action Exam: unimpressive, esp compared to pt

complaint and xray findings Prognosis good. Abx tx will fever and pulm

infiltrates and recovery speed- BUT pts will continue to carry mycoplasma for weeks-

NB! Mycoplasma doesn’t have cell wall, and therefore won’t respond to abx that interfere with cell wall-go with macrolides

Chlamydia pneumoniae 5-10% of CAP and nosocomial pnu in

adults. May be provocative for asthma Resembles Mycoplasma pneumoniae

symptoms Cough, sputum, fever- most not

seriously ill, but can require admit Older kids, young adults usually

Chlamydia psittaci Bird handler’s pneumonia Clinically and antigenically distinct from C.

pneumo Atypical pneumonia transmitted to humans

by psitticine birds via inhalation of dust from feathers, excreta or by bite

Clinically similar to other “atypicals”, plus epistaxis, splenomegaly

CXR- Pneumonitis radiating from hilum

Pneumocystis jerovecii Fungal agent (previously thought to be

parasite) and previously called P. carinii

causes pnu only in immunocompromised pts

S&S: fever, dyspnea, nonproductive cough. Evolves over days to weeks

CXR- diffuse bilateral perihilar infiltrates, but 20-30% of CXR are normal

PCP/PJP and HIV/AIDS 30% of HIV+ pts get PCP/PJP as initial

AIDS defining illness Become vulnerable when CD4 count

<200 80% of AIDS pts will get PCP if not

prophylaxed, usually with TMP/SMX (Bactrim) 80/400 mg daily starting when CD4 count hits 200

Post-Op/ Post-traumatic Hypoventilation Poor diaphragmatic excursion Impaired cough reflex Bronchospasm Dehydration Combine to cause retention of

bronchial secretions, segmental atelectasis, and ultimately pnu

Aspiration

3 syndromes from aspiration– Chemical pneumonitis (when aspirated material is

directly toxic, i.e. gastric acid)– Mechanical obstruction (“So you inhale a

meatball…”)– Bacterial pneumonia caused by anaerobic bacteria

colonizing oropharynx. CXR will show infiltrate in whatever lung

segment was dependant at time of aspiration.

Workup Hx and PE – good psx hx CXR- PA and Lateral CBC with diff BMP (glucose and lytes) Liver function tests (LFTs)

– Remember CMP=BMP+LFTs Renal function Pulse ox &/or ABG

What else? Consider EKG, HIV test If immunocompromised pt, consider

other causes: fungal, viral, TB, PCP Flu season: rapid flu test with back-up

culture

PORT severity index Prediction model for prognosis of CAP Scoring system based on 19 variables

– Demographics– Comorbid disease– PE Findings– Lab findings

PSI Risk stratification for death from all

causes in next 30 days– Class I (by algorithm) LOW (outpt tx)– Class II 70 points LOW (outpt tx)– Class III 71-90 points LOW (consider

admit)– Class IV 91-130 MODERATE (admit,

maybe intermediate care)– Class V >130 HIGH (likely ICU)

Other Admission Considerations

Virulence of organism if known (S. aureus) Support at home and functional status Ability to comply with medications Ability to afford treatment Immune status Multilobar involvement Follow-up Clinical judgment paramount

Drugs Tx with abx usually initiated before ID

of causative agent, then modified Outpatient tx usually empiric (= guided

by practical experience) Often institutions have rotating

schedule of 1st choice abx Treat pneumococcus PLUS other

likely bugs

Antibiotics for Pneumonia Choose least-toxic, most cost-effective,

narrowest spectrum possible Penicillin was mainstay anti-pneumococcal

– BUT 40% resistance in many locales– If you know resistance rates in your community, can

consider its use IDSA Guidelines for outpts:

– Macrolide (e.g. azithromycin, clarithromycin)– Doxycycline– Fluoroquinolone: (levofloxacin, moxifloxacin,

gatifloxacin)

IDSA Antibiotics for Pneumonia

Hospitalized pts:– Fluoroquinolone, or– Ceftriaxone (or cefotaxime) plus macrolide

ICU pts:– Fluoroquinolone or macrolide plus

ceftriaxone or cefotaxime or ampicillin-sulbactam or piperacillin-tazobactam

Antibiotics

Switch to oral Abx when clinically stable

Afebrile 8 hrs, nl resp rate, reduced oxygen requirement, wbc

Fluoroquinolones same bioavailability (IV and oral)

Treat for 7 to 14 days total

Other Therapies IV fluids Oxygen Incentive spirometry Anti-pyretics like acetaminophen Cough suppressants and mucolytics Chest physical therapy PT/OT and consider rehab hospital

Preventing Pneumonia Infection control: handwashing,

cleaning, gloves, isolate if indicated, treat promptly

Chemoprophylaxis: antivirals during flu outbreaks, TMP-SMZ for PCP prevention

Vaccinations Aspiration precautions Incentive spirometry post-op

Follow up Consider repeat CXR in 4-6 weeks to

demonstrate resolution of imaging findings.

Opportunity to address risk factors, possibly modify them

Great time for intervention with smokers

Acute Bronchitis

What is it? Inflammation of tracheobronchial tree Usually infectious, but can also be

irritant Often occurs in relation to other

respiratory illness (ie common cold) 5% of US population dx with bronchitis

yearly Tends to be self-limited

Bronchitis is not pneumonia

– Infection of bronchial tree by similar organisms but no parenchymal infection

Cough, sputum, upper respiratory symptoms

No lung findings except wheeze, nl xray

– Usually viral infection, rarely bacterial (* see Pertussis)

Pathogenesis Infectious

– Viral: adenovirus, influenza, parainfluenza, rhinovirus

– Bacterial: chlamydia, pertussis Noninfectious

– GERD– Irritant– Asthmatic

Risk Factors for Infectious Bronchitis

Recent URI Recent LRI Smoker Lung compromise, ie: COPD

Symptoms Cough (+/- purulent) Fever Malaise Nasal congestion +/- rhinorrhea Sore throat Looks a lot like a cold so far…

More sx Wheeze Dyspnea Chest pain-costochondritis

inflammation from coughing so much (press on it by sternum to elicit pain)

Myalgia/arthralgia

Physical exam No uniform description Can be normal exam +/- wheeze/rhonchi No signs of consolidation

– Because if there IS consolidation, it’s NOT bronchitis

DDX Asthma COPD Bronchiolitis Croup Pneumonia Bronchiectasis

Influenza TB Cancer Foreign body URI Sinusitis

Work up Thorough history PE CXR? – can r/o pneumonia if you can’t

do it with hx and PE

Treatment Generally aimed at symptoms: Analgesics Antipyretic Anti-inflammatory Antitussives Expectorants Bronchodilators

“but my doc always gives me….”

In immunocompetent individuals, no abx needed. BUT 80% get them.

Who should get abx? Moderate-severe COPD Asthma…maybe Immunocompromised pts Suspected pertussis

NB! <5% of bronchitis pts will develop pneumonia.

“Prophylactic” antibiotics will NOT decrease incidence of pneumonia

ABX Macrolides effective against

mycoplasma chlamydial organisms and B. pertussis– Erythromycin, Clarithromycin,

Azithromycin Also tetracyclines, tmp/smx (Bactrim),

and cefditoren (Spectracef)

Prevention Stop smoking Influenza vaccines Stop smoking Tdap vaccine Stop smoking Cover that cough Stop smoking Pneumococcal vaccine And WASH YOUR HANDS

Pertussis

Pertussis aka whooping cough Classic: at least 21 days of cough illness

with paroxysms, associated whoops or post-tussis vomiting

Bordatella Pertussis: highly contagious gram neg bac-t in respiratory tract, spread by direct contact with secretions

Incubation 7-10 days

Pertussis Phases Catarrhal (1-2 weeks) Looks like

URI, rhinorrhea, sneezing, fever, occasional cough

Paroxysmal-severe spasms of quick, short, coughs like a machine gun without breathing in between coughs. Gagging and gasping. After cough spasm, pts strain to inhale, making high-pitched whooping sound. May be followed by vomiting and exhaustion

Convalescent- Gradual recovery

Pertussis Nearly eradicated in 70s (1,000 cases in

1976), now increased incidence (11,000 in 2007)

Waning immunity, under-vaccination Infants at greatest risk for complications:

apnea, pneumonia, seizures, brain damage, cerebral hemorrhage

Milder disease in older children can contribute to spread

Diagnosis Hx PE Culture respiratory secretions Elevated white count with

lymphocytosis

Treatment Macrolides for 5 days: erythromycin,

clarithromycin, azithromycin. (2nd line: TMP/SMX) Treat EARLY, treat often, treat contacts to reduce spread

If no abx (ie pt refuses), then no contact with other humans for 21 days. No work, school, daycare, etc.

Fluids (IV prn) O2 Sedatives

Prevention Vaccination with DTaP (kiddos) and

Tdap (adolescents and adults) Handwashing Prophylactic abx to close contacts to

prevent spread

Tuberculosis Infection with Mycobacterium

tuberculosis Most commonly attacks the lungs (as

pulmonary TB) but can also affect the CNS, the lymphatics, the circulatory system, the genitourinary system, bones, joints and skin.

Background

Among communicable diseases, 2nd leading cause of death worldwide.

Prevalence: 2 billion Incidence: 8 million Mortality: 2 million people yearly 20-40% of world population is infected 15 million people infected in US

Mycobacterium tuberculosis

Non-motile pleomorphic rod Highly resistant to desiccation Very slow growing- generation time

12-18 hours (vs 20 min for E. coli)

Pathophysiology Aerosol transmission: cough, sneeze,

speak or sing One cough→ 3000 infective droplets 10 bacilli can initiate pulmonary infection In alveoli, taken up by alveolar macrophage,

then on to the nodes, and to organs- 80% of disease is in lung, but can affect ANY organ

Risk Minority: 2/3 of cases Indigent: 300x risk of national average HIV+ : 200-400% increase risk Other high risk groups: hospital

employee, inner city resident, nursing home resident, alcoholic, incarcerated, illicit drug users, travel to endemic area

LTBI vs Active Disease

Two forms- distinct Latent TB Infection- pt is infected

with M. tuberculosis, but is NOT sick, NOT infectious

Active Disease- Pt is infected, sick, and contagious

2-8 weeks after inoculation, +PPD caused by cell-mediated immunity and hypersensitivity reaction

90-95% primary infections are unrecognized

10-30% of healthy pts will proceed directly to active disease (up to 50 % if MDR- TB)

The rest will have latent infection. No symptoms, non-infectious. Can convert to active ANY time.

Stages Primary or initial infection- often leaves

nodular scars called Simon foci in one/both lungs.– Simon foci provide “seeds” for reactivation

Latent or dormant infection Can convert to active later Can be treated to decrease risk/likelihood of

conversion

Active TB Either direct from initial infection, or

reactivated latent infection Symptomatic Infectious Must be treated to decrease mortality

and spread Increasingly RESISTANT to treatment

– MDR-TB– XDR-TB

Classic Symptoms of Active TB

Productive cough Hemoptysis Fever Weakness

Anorexia Weight loss Night sweats Malaise

Physical Findings Fever Cachexia Hypoxia Tachycardia Lymphadenopathy Abnormal lung sounds- post-tussive

rales

Extrapulmonary Symptoms

Skin Kidney Bone Brain More common with decreased immune

function

Lab

Presence of acid-fast bacteria in sputum is a rapid presumptive positive

Definitive dx from sputum cx or DNA/RNA amplification demonstrating M tuberculosis

Culture takes weeks

PPD/Mantoux Test 0.1ml intradermal purified protein

derivative Area of INDURATION (NOT erythema)

seen 48-72h after placement I said INDURATION, not erythema Measure transverse to long axis of arm Expressed in mm- and a lack of

induration is written as 0 mm, not “neg”

False Neg PPD 20% of active cases Cancer/recent chemo Anergy Drugs (steroids) AIDS Recent live attenuated

virus vaccines (so place PPD same day or 6 weeks after vax)

Concurrent infection Metabolic

derangement (CRF) Lymphoid disease Stress (surgery, burn,

graft-vs-host) Distant primary

infection- role for 2-step testing, “booster reaction”

Population Based PPD Criteria

>5 mm: HIV +, abnl CXR, recent TB contact

>10 mm: IVDU, nursing home, jail, minority groups, age < 4, DM, CRF

>15 mm: no risk factors Positives are reportable to state False positives may occur in persons

with previous BCG vaccine This will be on boards!

QuantiFERON®-TB Gold Test

Whole blood test to detect both latent and active TB

One visit/one sample testing Results in 24 hrs No reader bias Not affected by BCG vaccine

Imaging Pos CXR trumps neg PPD, but neg

CXR doesn’t r/o active TB Classic xray of active TB shows

lesions in:– Post RUL– Apicoposterior LUL– Apical segments of LLL

Differential Asthma Pneumonia Influenza CA HIV/AIDS ARDS

Pneumothorax Pleural effusion MAC

(mycobacterium avian complex)

Treatment Therapeutic principles:

1. Must use multiple drugs to which M. tuberculosis is susceptible

2. Must be taken regularly

3. Must have sufficient duration to resolve the illness

Treatment: Active TB Isolation Negative pressure rooms Mask- N95 Abx - First dose decreases bacillary

load 10 fold 2 weeks decreases load 100-fold 4 wk tx plus 3 neg sputum smears

means pt is no longer infectious

Tx: Daily Regimen Initial 4 drug regimen

– INH (isoniazid) 300 mg po q day Hepatitis, rash, GI upset, neuropathy Co-administer pyridoxine (vitamin B6)

– RIF (rifampin) 600 mg po q day GI upset, rash, orange body fluids, hepatitis

– PZA (pyrazinamide) 2 g po q day Hepatotoxicity, rash, GI upset

– ETB (ethambutol) 2 g po q day Optic neuritis

Daily Regimen Drop ETB if cx favorable Drop ETB and PZA after 2 mo if

decreased symptoms and nl smear

6 month total Compliance ~ 60%.

Denver Protocol DOT 91% compliance First 2 weeks: DAILY INH 300mg, RIF

600 mg, PZA 2g, streptomycin 1g Next 6 weeks, Same doses, 2 x/week Next 18 weeks: INH & RIF 2x/wk

Relapse comparable to daily protocol (1.6%)

Exceptions HIV+ tx to 9 months min Pregnant- tx 9 months, daily INH, RIF,

ETB. OK to breastfeed Meningitis- add dexamethasone MDR TB- 7 (yup, seven) drug daily

protocol, DOT essential. There are organisms resistant to SEVEN drugs. What then? XDR-TB

Latent infection +PPD or QFT-G Neg CXR No signs/symptoms of active disease In healthy adult, 1% per year

conversion to active HIV+ person has 10% per year

conversion

Latent Infection Tx INH 300 qd x 12 m has 75% risk

reduction for converting to active disease

INH 300 qd x 6 m (65% RR) INH 900 2x/wk for 12 m

Seasonal Influenza Respiratory illness usually occurring in

epidemic form in Oct- April, epidemics in US q 2-3 years

Caused by strains of influenza virus (an orthomyxovirus)

Annually in US:– Affects 5-20% of population– Results in 200k hospitalizations for

complications– Causes 36,000 deaths

Tell me you already know this...

Influenza has 2 surface glycoproteins to allow virus to attach to and infect hosts

HA- hemagglutinin-to fuse to host membrane

NA- neuraminidase- enzyme to allow dispersion of new budding viruses

Mutations of HA or NA drift Exchange of entire gene segments (usually

between human flu and animal flu) shift

Influenza: Acute S&S Chills, fever to 39.5C Sudden onset myalgias- worse in

back and legs Prominent HA with photophobia and

retrobulbar aching Sore throat, retrosternal burning +/- coryza Nonproductive cough

Later on… Lower respiratory symptoms become

dominant with persistent productive cough Acute symptoms and fever resolve in about

3 days Weakness, diaphoresis and fatigue can

persist for weeks Secondary bacterial pneumonia suggested

by recurrence of symptoms in 2nd week

Transmission Droplet nuclei (not large particle aerosol like

the common cold.) Rare fomite transmission. Cough or sneeze Incubation average 48 hours (range 1-4 days) Infectious for

– 1 d before sx onset to 5 d after (Adults)– 1 d before to 10d after (Kiddos)– Several days before sx +10d after (Wee kiddos)– Immunocompromised folks can shed virus for

weeks to months

Complications Bacterial pneumonia Purulent bronchitis Otitis media Sinusitis Dehydration Worsening of chronic medical

illnesses, ie: CHF, DM, asthma

Rarer complications Encephalopathy Myocarditis Pericarditis Rhabdomyolysis Reye’s Syndrome- (fatty liver with

encephalopathy) no ASA for children under 18

Diagnosis Good history, incl knowledge of current local

trends. – As of October 3, 2009, 99% of circulating influenza

viruses in the United States were 2009 H1N1 influenza PE: febrile, tachycardic, flushed face, pharyngeal,

tonsillar and soft and hard palates injected without exudate. Conjunctival injection. Usually normal lung exam. No signs of consolidation.

Clinical alone low sensitivity and specificity Check some labs?

Better living thru nasopharyngeal swabs

Rapid testing (30 min)-often performed in office. Vary in types of flu detected, ability to distinguish types, also in specimen type needed. Know your lab!

Viral culture, esp to f/u negative rapid test when clinical suspicion is high. Results in 3 to 10 days

Also available: immunofluorescence, EIA, PCR. Use of serology reserved for public health/research.

Treat ‘em Conservative tx: rest, fluids, acetominophen

for fever, headache, myalgia, cough suppressant prn.

NB- NO ASA for children!! (Why?) Monitor for complications Antivirals: effective in sx duration, severity,

also to contagion. Ideally initiate tx within 2 d of sx onset, duration of tx 5 days– Currently reserving antivirals for ill, high-risk folks

with H1N1

Antivirals

Oseltamavir (Tamiflu)- seasonal and H1N1 Zanamavir (Relenza)- seasonal and H1N1 Amantidine and rimantidine- Only effective

against influenza A. Rapidly developing resistance to these drugs, so use of these agents is currently NOT advised. Awaiting reestablishment of susceptibility.

PREVENTION Vaccinations Chemoprophylaxis with antivirals (70-

90% effective) Handwashing- soap and water or

waterless alcohol based Education Fingers out of nose, eyes, mouth Good respiratory hygiene Avoid sick people if you’re well, and

well people if you’re sick

The Flu Shot Trivalent inactivated vaccine-

–Killed viruses- 2 A strains, and a B

– Representative of the influenza strains predicted to circulate

New vaccine yearly. Usually one strain changes. Available thimerosal-free

This year’s model A/Brisbane/59/2007(H1N1)-like virus A/Brisbane/10/2007 (H3N2)-like virus B/Brisbane/60/2008-like virus

Too early to tell if we got it right! Also, attention and data is all about

H1N1

Vaccine If well matched to circulating strains,

vaccine can decrease risk of flu 70-90% in healthy adults and 66-90% in children

Can be 30-70% effective in preventing hospitalization for pneumonia in elderly

Decrease risk of death from influenza by 80% in elderly people in nursing homes

Even poorly matched vax can provide cross-protection

Other option: LAIV Live attentuated influenza vaccine Nasal spray LIVE virus, weakened Only for healthy, non-preg people

ages 5-49

Who gets flu shot? People at risk for complications: kids

6 months to 19 years, pregnant women, age over 50, residents of LTC facilities or nursing homes, those with chronic medical conditions (see next slide), healthcare workers

Folks who live with/care for the above Anyone who wants to risk of flu

Chronic Medical Conditions

Pulmonary ds (incl asthma and any other disease that can compromise respiratory function)

Cardiovascular ds (except HTN) Renal ds Hepatic ds Hematologic ds Metabolic ds (including diabetes!) Immunosuppressed folks

NO SHOT for you Severe egg allergy Hx of severe reaction to a flu vax Hx Guillain Barre Syndrome Age <6 months Currently moderately ill with fever

– Fine to give to pt w/ low-grade fever

Influenza vaccine factoids Production starts in January Usually available in October and after Works by provoking immune response

and antibody development Effective in about 2 weeks. Immunity

lasts months to a year

Pandemics 1918- Spanish influenza. Killed 40-50

million people worldwide. 1957- Asian Influenza (2 million dead) 1968- Hong Kong Influenza (1 million) 2009- H1N1 Swine Flu ????- Avian Influenza. WHO conservative

estimate of about 7.4 million deaths. Pandemic within 3 months of evolution of virus to easily transmissible state. Are we ready?