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Organisms that Cause
Enterobacteriaceae (Klebsiella, E Coli, Proteus, Serratia)
Leading cause of death from an infectious disease
Risk Factors/HIgh Risk
Gram + Encapsulated
Lancent Shaped paired Cocci IN PAIRS *** This is indicative of Strep Pneu. (Know this)
No group specific carb
~ Capsule: helps prevent phagocytosis
~ IgA protease = Digest Abs (Immunoglobulin)
~ Pnemolysin = cytolytic, inhibits cilia movement & Inhibits PMN from killing bacteria
~ NEURAMINIDASE (thins secretions)
Res: Humans; 5-75% carriage; highest in preschool
Transmission: Respiratory droplet spread
Risk: Most common cause of community acquired typical pneumonias...
***Most common bacterial pathogen causing a post-influenza infection***;
alcoholics, elderly, COPD
Pneumococcal Pneumonia - Community and Nosocomial....Typical Pneumonia
Start with early symptoms of viral upper respiratory tract infection
Aspiration into lower lobes - LOBAR PNEUMONIA
Colonization of alveolar spaces
Severe shaking chills, sustained fever of 39-41 celsius
Productive cough, thin blood-tinged (rust or cherry colored) sputum, pleurisy common - leakage of erythrocytes, neutrophils, macrophages into alveoli
Rapid recovery after antimicrobial therapy
Culture of aspirate from sinus or middle ear
***Alpha-hemolysis (greenish color) due to oxidation iron in hemoglobin on BAP.
** Bile solubility test, differential diagnosis of pneumococcal from other streptococcal
infection. A broth culture of each organism is placed into tube with Ox bile.
Pneumococci dissolve in ox bile, producing a CLEAR SOLUTION. Other streptococci do not dissolve and the resulting solution is cloudy.
Microscopy, neufeld, bile solubility, optichin
- Inflammatory exudate filling alveolar spaces
Optochin susceptibility*** Optochin (ethylhydrocupreine) inihibits pneumococci but not
other α-hemolytic streptococci at low concentrations.
+ neufeld quellung for capsule ( positive for swelling)
Penicillin if susceptibile (many times pplare infected w/ penicillin resistant strains)
~ Amoxicillin, Cephalosporins
1. Polyvalent capsular vaccine (ppl over 2 & adults <65)
2. Heptavalent Pneumococcal Conjugate Vaccine (PCV7) for thoes as young as 2 months
(Typical Pneumonia (and Empyema) - Community and Nosocomial
Gram +, Cocci in clusters
PANTON VALENTINE LEUKOCIDIN (PVL): NEW VF = severe hemorrhagic pneumonia
- Hemolysin coded on a phage
coagulase, hyaluronidase, fibrinolysin
Transmission: Respiratory droplets, fomites, autoinnoculation, aspiration
1-5% of community acquired pneumonias in US
20-30% of nosocomial pneumonias
Staph Aureus Clinical Diseases:
Typical Pneumonia (and Empyema) - Community and Nosocomial
~patchy infiltrates with consolidation or ABSCESS...pocket of air
~Acute, often accompanied by empyema - accumulation of pus between membranes
~very young, aged, and patients with underlying respiratory disease
Common in patients with bacteremia or endocarditis
NECROTIZING INFECTION with rapid progression to tissue destruction and cavitation )PVL + strains)...Fever hemoptysis, leukopenia, resp distress
Inflammation of the bronchial tubes or bronchi
Caused by viruses, bacteria, parasites, smoking, chemical pollutants
Fever, cough, and sputum production
Sore throat, runny or stuffy nose, headache
Muscle aches, extreme fatigue
Acute bronchitis is almost always self limited and should not be treated with antimicrobials
Organism that cause Bronchitis
gram - pleomorphic rod appears pink on gram stain
Gram - Coccobacillus
Grows aerobically and anaerobically
Grows on Chocolate (Blood) Agar
Antibody Based Tests to identify
Respiratory droplets...present as type b strains with capsule and nontypable strains without capsule
Type B = strains assoc with meningitis, epiglotittis..
Nontypable - exacerbation of bronchitis, ottitis media
EXCLUSIVELY HUMAN PATHOGEN
Beta lactamase produces are common
Pneumonic Plague seen on___
It produces a bipolar staining of the rod - a safety pin appearance
contains methylene blue, azure A, thionin with eosin Y
Gram - rod, bipolar staining with Wright's Stain***
Zoonotic disease...RATS...southwest US and Africa
Flea bite, respiratory droplets, person to person
(flea bite = bubonic which can become pneumonic...usually fatal)****
Respiratory = straight to pneumonic
****Risk groups: Camping, hiking, hunting, fishing, occupational exposure (researchers, veterinarians), Direct Handling or inhalation of contaminated tissue or tissue fluids
Sleeping in rat/ flea infested cabins ***
What is Coagulase' importance in the Plague?
Yersinia VF - it's important in transmission from flea to man
VF of Yersinia Pestis
Plasminogen Activator protease gene
(Pla) protease gene
degrades complement C3b/C5a and fibrin clots
Protection against opsonization and clearing; dissemination
VF of Yersinia Pestis
Type 3 secretion system (YOPs)
Yersinia Outer proteins
Initiate apoptosis, disrupt actin to destroy host cell's ability to phagocytose
VF of Yersinia Pestis
fever, headache, chills, painful swollen lymph nodes (buboes) within 2 - 6 days of flea bite...rapid development of bacteremia...75% mortality if untreated...fatality rate is 14%
Can progress to Pneumonic plague
Positive blood cultures but no palpable lymphadenopathy...mortality rate is 30-50%
Rare form...spread via respiratory droplets form infected individuals...
1-3 day incubation period; person to person through aerosols
fever, malaise, cough, cp, dyspnea pulmonary signs within 1 day if untreated, >90% mortality (bloody sputum)
Primary Pneumonic Plague
Gram -, WRIGHT's STAIN (BIPOLAR STAINING BACILLI)...culture....fluorescent Ab testing...
All clinical & culture Samples must be handled under BIOLOGICAL CONTAMINENT CONDITIONS
Supportive therapy and antibiotics
Strict respiratory isolation for 24-72 hrs after starting therapy
No vaccine...vector control
Due to what defect?
Results in what complications?
due to genetic defect in CFTR protein
Results in Faulty regulation of Na absorbtion and inability to secrete Cl
Leads to a reduction of hydration airway surfaces
Causes a Thickening of mucus...inability to clear mucus and adhesion mucus to airway surfaces
Bacteria colonizes this mucus layer and can cause respiratory disease including pneumonia
Gram - Rod; Nonfermentor; oxidase +
~ Pigments: stimulate inflammatory response
(Produces blue green pigment on colorless agar. One of the ways of distinguishing from Burkholderia spp.)
~ exotoxin A: contributes to dermatonecrosis
~exoenzymes: contribute to invasive properties
biofilms, efflux pumps
Reservior: Ubiquitous, environmental, soil, water...hospitalized patients have transient colonization
Immunocompromised; COPD, CF patients; hospitalized
Clinical Disease of Pseudomonas
Typical Pneumonia (Productive cough with purulent sputum)
Necrotizing bronchopneumonia (exotoxin A)
neutropenia patients following chemotherapy and in pateints with AIDS - shock may devleop
*****CHRONIC INFECTION OF Lower Respiratory Tract
prevalent among CF: present with chronic productive cough, anorexia (loss of appetite), wheezing, rales and tachypnea (rapid breathing).
Can also see leukocytosis
Fever, chills, severe dyspnea, cyanosis, retractions, productive cough with purulent sputum, lung abscesses, confusion - may be rapidly fatal
Diagnosis of Pseudomonas
Specimens of sputum and blood
Primary pseudomonal pneumonia - bilateral bronchopneumonia consisting of nodular infiltrates, cavitgation with or without pleural effusion...NO LOBAR PNEUMONIA
Culture and sensitivity; natural fluorescnece under UV light (blue green pigment);
oxidase positive/strict anaerobe (purple color)
lactose nonfermentor (MacConkey Agar) (turns yellow)
Oxidase test determines presence of cytochrome C oxidase...DARK BLUE WHEN OXIDIZEDGreen/blue on BAP
TX with Combo antibiotics
Multiple dotty confluent opacities particularly in middle lobes in lower lobes track liked striped pattern
Cystic fibrosis patient with pseudomonas infection
Gram negative Bacilli
Aerobic Nonfermentor...Oxidase +
NO DIFFUSABLE PIGMENTS****
Res: Colonization of variety of moist environmental surfaces
Opportunistic infection from environmental source
Patients with underlying chronic pulmonary disease
How do I differentiate Pseudomonas from Burkholderia
THE MAJOR DIFFERNCE BETWEEN PSEUDOMONAS AND
BURKHOLDERIA - Burkholderia does not produce diffusible pigments
BCSA Agar - burkholderia cepacia will grow on B.C selective agar & cause a color change in the media from red-orange -> yellow
Media inhibits growth of P. aeruginosa.
Crystal violet inhibits gm. + organisms.
Antimicrobials inhibit non B. cepacia organisms.
Burkholderia Cepacia selective agar
Cause color change in the media from red-orange -> yellow
List the main "players"
largest group of medically important gram - bacilli
Associated with aspiration/typical pneumonia in elderly and those with underlying disease, alcoholism, diabetes
1)Klebsiella (Thick Capsule, Lac +, mucoid colonies, Indole -)
2) E Coli (Lac +, Indole +, Citrate -, Simmon's Citrate Agar)
3) Proteus (Lac -, Urease +, Swarmer (rings))
4) Serratia (lipase _, Gelatinase +, produces red pigment
Gram - bacilli
typical pneumonia in elderly and those with underlying disease alcoholism, diabetes
Klebsiella (Thick Capsule, Lac +, mucoid colonies, Indole -)
E Coli (Lac +, Indole +, Citrate -, Simmon's Citrate Agar)
Proteus (Lac -, Urease +, Swarmer (rings))
Serratia (lipase _, Gelatinase +, produces red pigment
Gram - Bacilli
Large Polysaccharadie Capsule
Res: Inhabits enteric tract (flora)
Transmission: Aspiration - inhalation of respiratory droplets
Patients with underlying chornic pulmonary disease
Currant Jelly Sputum
Large polysaccharide capsule of
Klebsiella pneumoniae pneumonia.
mucoid = thick, blood tinged
produces red pigment
Above = Lipase + on left
Zone of clearing round the area of growth indicates DNase production
Take a gelatin tube and then the organism can liquify the gelatin
Necrotic destruction of alveolar spaces,
Primarily upper lobes
Bulging Fissure sign on chest x ray due to lobar consolidation
May form abscesses
Thick blood tinged sputum = "currant Jelly"****
Bacteremia ( small % but high case fatality rates)
Risks: alcoholism diabetes, immunocompromised ( lobar pneumonia)
Gram - rod...
Indole - (yellowish in vial)
Mucoid colonies form thick capsule...
No vaccine...multiple drug resistance through transmission of resistance plasmids (R-Plasmids); Resistant to Ampicillin...polymixin B = last resort
What does indole test do
determines the ability of bacteria to split tryptophan into indole pyruvate & ammonium... ammonium raises pH & changes color from yellow to red
Multiple drug resistance through transmission of resistance plasmids (R plasmids) inherent resistance to Ampicillin
Gram - Rod
Indole + (red in vial) (Klebsiella is -)
Lactose + (like klebsiella)
Citrate - (stays green)
EMP (Eosin Methylene Blue) agar plate (Fecal Sample)
What does Simmon's citrate agar test do?
medium contains sodium citrate and bromothymol blue (turns blue at alkaline pH)
Medium also contains ammonium salts as sole nitrogen source
Use sodium citrate and ammonium salts results in alkaline pH and converts media from green to blue color
E coli is citrate negative so color remains green... doesnt turn blue
MOTILE (Swarmer) (klebsiella = nonmotile)
Hydrogen Sulfide (H2S) +/- (turns black)
Use of Urease and hydrogen Sulfide Test
What organism is + for both
Urease Test...RED +. Yellow -
Urease converts urea to ammonia and bicarbonate...increase in pH causes solution to turn red
Hydrogen sulfide test detects presence of thiosulfate reductase...+ Black
Both seen + in Proteus
Tx Proteus Spp
IMIPENEM - 4th generation cephalosporins (cefepime), amikacin and TMP-SMX
Effecttive against 90 - 100%
(In red know this)
Serratia Marcescens differs from other enterobac...
Distinguished form other bc it has 3 specil enzymes:
Most strains resistant to several antibiotics because of the presence of R-factors on plasmids
Think AIDS pts. / Immunocpmpromised
Found mainly in environment including health care facilities....can infect resp tract...HEALTHY will be Resistant to infections
Resist to ampicillin
Lipase Test Purpose
Spirit Blue Lipase Test
Agar plate containing tributyn, a triglyceride hydrolyzable by the enzyme lipase...Bacteria secretes lipase, zone of clearing surround sample
+ lipase in serratia
- in ecoli
DNAse Assay purpose
methyl green forms a complex with intact DNA to form the green color of the medium
Serratia DNAse activity depolymerizes the DNA breaking down the methyl-green DNA complex
Colorless zone round the area of growth indicates DNase production
Which Mycobacteria cause TB
M TB - most common
M Bovis (ingest of contaminated milk)***
M Africanum - rare
M Canetti - rare
ACID FAST ROD (gram + on gram stain) (auramine-rhodamine staining - sensitive/not specific)
FAC INTRACELLULAR, slow growing
1) Produces NIACIN and & a HEAT SENSITIVE CATALASE
2) Sulfatides (cell envelope)
3)Trehalose Dymcolate (cord factor in cell wall)
4) Mycolic acid (Long Chain Fatty Acid)
as SURFACE ANTIGEN
**Disease is due to damage mediated by immune response **
Airborne transmission - 1 cough produce 3000 infectious nuclei...same as talking for 5 minutes...sneezing produces more
ONLY MODERATELY INFECTIOUS... usually due to chronic exposure
Acid Fast Rod
USE ACID FAST STAIN!!! (In red)
Who is most at risk?
Why are TB rates increasing?
Anyonfe for infection (1/3 of world)
Progression to diease depends on host factors...weakened cell mediated immunity increases risk
Who is most at risk?
Malnourished, elderly, poor
Migrants, refugees, travelers
Smokers, chronic alcoholics
Those with co-morbidity: diabetes, HIV/AIDS, silicosis
Why are TB rates increasing?
Aging populations, increase travel and migration, increasing drug resistance and increasing HIV prevalence = TB rates increasing
Clinical Disease TB
Where does initial seeding occur?
Where does replication occur?
assymptomatic or a mild flu
initial seeding occurs in middle/lower lung fields
replication in alveolar macrophages and cause macrophage death
TUBERCULE (is a lesion that may occur after primary infection )Granuloma consiss of dead cells and infected macrophage surrounded by Langerhans cells, epithelioid cells & lymphocytes
GHON COMPLEX - formed as macrophage carry organism to nearby lymph nodes causing it to swell (become calcified -> show up on chest X ray)
Progression to active disease depends on infectious dose and the host's immune competence - **organisms may remain viable in some but most people heal wihtout clincal disease** - viable = latent TB infection
primary TB disease
calcified right lung nodule with associated calcified hilar lymph node
TB Infection Process
TB inhibition of phagocytic killing by preventing acidification
2-4 weeks after infection develop
Macrophage activating response
T cell mediated activation of mac. kill TB
T cell produce INF-Y, produce cytokines
Fever and wt loss
Tissue damage response
result of DTH
Destroys unactivated mac
Granuloma Formation (Tubercules)
Growth inhibited bc of lack of oxygen and low pH
Lymph Node TB
Painless swelling of lymph nodes
Posterior cervical and supraclavicular sites
Usaully discrete and nontender in early disease but become inflamed with a fistulous tract draining caseous material in later disease
Primary Progressive or Re-Activation TB
Results from reduced T Cell Immunity
Organisms reactivate in the higher lung fields (Higher O2)
Erosion into airways to ensure high levels of O2 (obligate anaerobe)
Disease becomes contagious; sputum smear becoms acid fast
Cavitating lesions may occur
Describe disease &
Widespread "hematological" dissemination results in "shot gun pellet" or "Millet" type lesion in lung
May spread (hematogenous) to other organs including the CNS, GI tract, kidney, or almost any other organ resulting in
Due to hematogenous spread TB
YELLOWISH GRANULOMAS 1-2 mm in diameter
Choroidal tubercles in eye
Choroidal tubercles in eye
Due to hematogenous spread
Lesions are yellowish granulomas 1-2 mm in diamter
Main sites of extrapulmonary TB
More common since advent of HIV
Increase risk with advancing immunosuppression
CNS - meningitis
Lymphatics - scrofula
Disseminated - miliary TB
Bones and joints of spine (Pott's disease)
Genitourinary (urogenital TB)
Initial Phase: malaise, headache, fever, personality change...2-3 weeks later see headache, MENINGISMUS, vomiting, confusion, and focal neurologic findings
Can deteriorate into stupor or coma
Lab Diagnosis of TB
*****Microscopy: Acid fast Bacilli in sputum or other body fluid
*****Positive PPD for screening - aka TST and Mantoux Test (10 PPD Tuberculin units are injected intradermally & read 48-72 hrs later)
*****XRAY - look for tubercles, ghon complexes (swollen lymph nodes) cavitary lesions (In Red - use w/ PPD test)
Lowenstein Jensen (but takes 2-6 wks)
Routine susceptibility testing
IGRAs - interferon gamma release assays
TST and MANTOUX TEST
synonyms for PPD screening for TB
Injected intradermally and read 48-72 hours later
read by measuring induration diameter
(localized hardening of soft tissue) in millimeters. No induration should be recorded as "0 mm".
DONT MEASURE EYTHEMA (redness of skin)
Vaccination w/ BCG is not a contraindication for TST
(In red - know this )
Interferon gamma release assays
Interferon gamma release assays ( Use w/ ppl who have been vaccinated)
meassure how the immune system reacts to the bacteria that cause TB (cytokines released by T cells to activate macrophages)
Positive says infected
negative = unlikely
Combine test with sputum results and xrays
Acid Fast Stain...use for M TB
Appear as glowing yellow rods
counter stain = methylene blue
Classification of Tuberculin RXN
(The person's medical risk factors determine at which millimeter of induration the result is positive (5mm, 10mm, or 15mm).
A positive result indicates TB infection (past or present)
Positive result indicates TB infection (past or present)
A. 5 mm or more is positive in (imunocompromised)
HIV-positive person, recent contacts of TB case, persons with changes on CXR consistent with old healed TB, patients with organ transplants and other immunosuppressed patients
B. 10 mm or more is positive in (positive exposure) THIS IS FOR MOST PPL
Recent arrivals (<5 yrs) from high-prevalent countries, injection drug users, residents and employees of high-risk congregate settings (e.g., prisons, nursing homes, hospitals, homeless shelters, etc.), persons with clinical conditions that place them at high risk (e.g., diabetes, leukemia, etc), children <4 yrs, or children exposed to adults in high-risk categories.
C. 15 mm or more is positive in
Persons with no known risk factors for TB
Treatment of TB once infection has been demonstrated
RIFAMPIN (RIF) aka Refampicin
Tx started in children under the age of 1 if active case diagnosed in immmediate family
Anyone older who has been exposed to an active case is not treated unless a positive PPD is seen
old Tx of choice for TB (1956)
Note - Pyridoxine (Vit B6) is given to prevent INH toxicity
severe form of pneumona
Rapid transmission and high mortality
SARS - severe acute respiratory syndrome
Risk Factors and High Risk
Enveloped SS + sense RNA
Does NOT have the Hemagglutin acetylesterase glycoprotein
Res : Humans
Transmission : Person to person - respiratory droplets via cough or sneeze...virus may contaminate a surface, shed in urine, sweat, feces...unlike Corona virus which can cause the common cold
Risk: Over 50 CVD, diabetes, hepatitis and ESPECIALLY PREGNANT
Clinical Disease of SARS
Severe Acute Respiratory SYndrome
ATYPICAL PNEUMONIA (nonproductive cough)
Begins with high fever > 100.4, cough, DIFFICULTY BREATHING after initial symptoms
Discomfort, body aches
Develop a dry cough, trouble breathing & demonstrable pneumonia
No Tx to date shown to be effective
Respiratory barriers and isolation of suspected and confirmed patients
Negative pressure hospital rooms to prevent spread
Explain Coronavirus Virion
SS + stranded UNSEGMENTED RNA genome
RNA covered by nucleocapsid (N protein)
Spike glycoprotein (S) binds cellular receptor glycoprotein (AngiotensinConvertingEnzyme2 ACE2)******* & fuses viral envelope with host cell membrane
Matrix Glycoprotein (M) an envelope protein combines with S during formation virion. M-S association brings both proteins to site of viral assembly
This Virus has a glycoprotein that binds cellular receptor glycoprotein (ACE) and fuses with viral envelope with hose cell membrane
Spike glycoprotein (S) of Cornoavirus
S protein can also embed in plasma membrane and spread infection by cell-cell fusion
Also has nucleocapsid (N) protein and Matrix glycoprotein (M)
Binds to ACE receptor...what is rest of replication mechanism?
then undergoes conformation change exposing fusigenic activity
virus enters by fusion viral and celluar plasma membranes
Viral replication occurs completely in cytoplasm
Genomic RNA translated to yield polyprotein that is processed to RNA polymerase, helicase and viral proteinases
Transcription takes place in flask shaped cytoplasmic compartment
Hunter hiking in New Mexico
Fever, Headache, muscle aches, stomach ache, dizziness, chills
Hantavirus Pulmonary syndrome
Enveloped, Negative sense SS RNA, SEGMENTED
Res: Rodents (Deer Mice)
Transmission: Rodents through urine, droppings, or saliva...CAN NOT BE TRANSMITTED PERSON TO PERSON
Risk: Campers, forest rangers, woodsmen, rodent contact
CANT BE TRANSMITTED PERSON TO PERSON
infected via rodents or inhalation of aeroslized virus
List Symptoms :
HANTAVIRUS PULMONARY SYNDROME (HPS) (potentially deadly) OR
HEMORRHAGIC FEVER WITH RENAL SYNDROME (Hantaan Virus)
Rapid breathing, tachycardia, hypotension, crackles or rales on lung examination
No extreme swelling of lymph nodes (as seen w/ Bubonic plague)
EARLY = fever, headaches, muscle aches, stomach problems, dizziness, chills
LATE= 4-10 later lungs fill with fluid, sob
INTERSTITAL PULMONARY EDEMA; RESPIRATORY FAILURE, DEATH WITHIN DAYS
Class 4 labs only
ELISA (IgM or paired sera IgG)
No specific Tx
Human Herpes Virus 5
DS DNA virus Enveloped
Humans (80% are seropositive)
Congenital infection, perinatal infection, breast milk, saliva, infection in adults = sexual/transplants/transfusions
(In Red) At risk individuals, immunocompromised, AIDS, bone marrow transplant patients, people receiving chemotherapy
Clinical Disease of HHV 5
ATYPICAL PNEUMONIA IN IMMUNOCOMPROMISED (reactivation)
Fever, non-productive cough, sob (dyspnea) (All in red) ****
Often presents simultaneously with Pneumocystis Pneumonia
Congenital Infection generally assymptomatic...TORCH syndrome...retinitis/chorioretinitis
Transplant and posttransfusion infection usually assymptomatic
***Immunocomp patients - reactivation and primary infections occur
~ Interstitial pneumonia a common outcome, fatal if not treated Other manifestations: hepatitis, encephalitis, esophagitis colitis, pancreatitis, etc.
ALL IN RED
Often presents simultaneously with Pneumocystis Pneumonia
CMV- HHV5 - atypical pneumonia
Decreased oxygen levels in the blood (hypoxemia) in association with CMV pneumonia often predicts a fatal outcome
Diagnosis of CMV
PCR, DFA, Serology
OWL's EYE : Enlarged cells contain
Intranuclear and intracytoplasmic inclusions ****
CMV infected lung epithelial cells are larger than uninfected and have both nuclear (owl's eyes) and cytoplasmic blue inclusions*****
Safe sex; screeing
What causes ATYPICAL PNEUMONIA (unproductive cough)
1) Mycoplasma (walking) Pneumonia (most common)
2) Legionnaire's Disease
3) Chlamydial Pneumonia
Viral pneumonia :
RSV (Respiratory Syncytial Virus)
General signs and symptoms of atypical pneumonia
Most commonly caused by mycoplasma, legionairres, chlamydia or viruses
1) General flu-like symptoms often occur first...fatigue, fever, weakness, headache, nasal discharge, sore throat, earache
2) Vague pain under and around the breastbone may occur...severe chest pain associated with typical bacterial pneumonia is uncommon
3) Severe hacking cough but it usually does not produce sputum at 1st
Severe hacking cough but it usually does not produce sputum
what organisms are you thinking
Mycoplasma (walking) Pneumonia
Gram - (stain poorly) bacillus
Fastidious growth - iron salts and cysteine
Intracellular Parasite (alveolar macrophage and monocytes but no fusion between phagosome and lysosome)
Res: Aquatic Habitat - Parasitizes amoebae
Survives elevated temperatures and many disinfectants (chlorine) - whirlpools, saunas, showers, etc
Transmission: through inhalation of aerosols (air conditioning)
No Person to person transmission
Middle age or > 55, immunocompromised
alcoholics, smokers, COPD, diabetes
WHOLE THING IS IN RED
Aquatic Habitat (whirlpools, saunas, showers) survives in cholrine
unchlorinated pools - adenovirus
(alveolar macrophage and monocytes - but no fusion between phagosome and lysosome)
Milder, self limiting
No GI tract manifestations
NO CNS manifestations
LEGIONNAIRES DISEASE (In Red)
(5% of those exposed, oppoortunistic with risk factors)
2-10 day incubation
Fever, chills, early in infection can have initial non-productive cough, myalgia, malaise, fatigue, anorexia, headache, chest pain, watery diarrhea, abdominal pain, nausea and vomiting.
Chest examination can show rales.
Can develop mild cough which is moderately productive and streaked with blood.
Can develop pneumonia, difficulty breathing, and pleural effusion (some lung abscess); renal failure
Somnolence (drowyness), delirium, confusion
(95% of those exposed, milder, self limiting)
1-2 day incubation...similar to influenza
NO GI TRACT MANIFESTATIONS
NO CNS manifestations
SILVER IMPREGNATION STAIN
direct fluorescent antibody (DFA); nucleic acid probes; serology; antigen in urine (**Red)
Growth on Buffered Charcoal Yeast Extract Agar (BCYE) * containing increased amounts of iron and cysteine (*Red)
Treatment: Azithromycin or levofloxacin in nosocomial or immunocompromised
Erthyromycin or tetracycline for community acquired
Cell Wall Less...ROD...cholesterol like molecule in plasma membrane, growth media contains serum***
P1 Ag - attachment to respiratory epithelium
Hydrogen Peroxide - tissue damage
Person to Person Transmission by contact with resp secretions
Leading cause of pneumonia in school-age children and young adults...outbreaks occur in crowded military and institutional college settings
reduction or ceasing ciliary beat - explains non-productive cough
Pneumonia in school age children and young adults...crowded military and institutional college settings
ATYPICAL PNEUMONIA (All in Red)
Walking Pneumonia - not bedridden
2-3 week incubation - then lasts ~ 2+ weeks) fever, cough (nonproductive), malaise, headache
Chest auscultation - Scattered rhonchi, Localized rales
Wheezing ( Usually absent in other Bacterial Pneumonia; more common with
May see RAYNAUD PHENOMONON due to cold agglutinins
Fatal in sickle cell patients
Persistent cough is common during convalescence
Pneumonia associated with Raynaud PHenomonon (due to cold agglutinins)
Culture : colonies on agar have a MULBERRY APPEARANCE - requires cholesterol supplementation
Cold Agglutination -> causes Raynaud's
IgM antibodies bind I antigen on erythrocytes at 4 celsius...not sensitive
"energy parasites" obligate intracellular
Differences with viruses
Present with pharyngitis..Elderly at risk for clinical pulmonary disease
Infections tend to recur so prolonged treatment
Rarely causes death
Bilateral infiltrates on xray
May be associated with atherosclerotic vascular disease, alzheimers, asthma and reactive arthritis
What are the Viruses for Lower Respiratory Infections
~Viruses (Atypical pneumonia)
Influenza (including Avian Flu)
Atypical tend to have no or clear sputum
What are the Bacterial Pneumonias (secondary to Influenza) for Lower Respiratory Infections
~ Bacterial Pneumonia secondary to Influenza
Tend to have sputum
What are the Two major classifications of Pneumonia?
Typical pneumonia: Productive cough - generally associated with extracellular microbes
(most bacteria live extracellularly/ outside of cells)
Atypical pneumonia: Non productive cough - usually associated with intracellular pathogens (including viruses)
What is the most common type of pneumonia?
Community-Acquired Pneumonia (CAP) - most common type of pneumonia - infection occurs outside of hospitals and other health care settings.
Most people get CAP by breathing in germs (especially while sleeping) that live in the mouth, nose, or throat.
Most cases occur during the winter.
About 4 million people get this form of pneumonia each year. About 1 out of every 5 people who has CAP needs to be treated in a hospital.
Note ppl can also get pneumonia in a health care setting such as nursing homes etc ... Health care Associated Pneumonia
What are the Pulmonary Host Defenses
Upper Airways : mucociliary apparatus,
anatomy/turbinates bone in nose that maximizes flow of air over cilia,
Oropharynx: saliva, sloughing of epithelial cells, normal flora, complement
Conducting Airways (trachea, bronchi)
Lower Respiratory Tract (terminal airways, alveoli)
cough, epiglottic reflexes,
sharp-angled branching of airways,
IgG, IgM, IgA,
Airway surface liquid (lysozyme, lactoferrin (acts against infection), secretory leukocyte proteinase inhibitor (elastase inhibitor prevents destruction of epithelial cells)
List the specific Host Defenses of the Lower Respiratory Tract
Lower Respiratory Tract (terminal airways, alveoli) -
- alveolar lining fluid (surfactant facilitates breathing and prevents fluid in alveoli),
- immunoglobulin, complement, Cytokines, Alveolar macrophages, PMNs, Cell mediated immunity
- iron-binding proteins ( we have very little iron in the body)
What is Consolidation?
(induration) of lung due
cellular exudate (fluid and
pus) in alveolii and ajoining
Aspiration pneumonia: follows aspiration of oral or gastric contents into lungs
Occurs when you accidentally inhale food, drink, vomit, or saliva from your mouth into your lungs. This usually happens when something disturbs your normal gag reflex, such as a brain injury, swallowing problem, or excessive use of alcohol or drugs.
Aspiration pneumonias cause changes in the chest x-ray that can be seen six to 24 hours after inhalation. Symptoms include respiratory distress indicated by grunting, cough, and fever after the aspiration of hydrocarbons, foreign substances, or bodily fluids. Symptoms may develop in minutes or hours depending on the volume and nature of the aspirated substance.
Aspiration pneumonia can cause pus to form in a cavity in the lung. This is called a lung abscess.
Lobar pneumonia: pulmonary consolidation demarcated by border of segment or lobe
Congestion is the earliest stage of lobar pneumonia, characterized by extensive serous exudation, vascular engorgement, and rapid bacterial proliferation.
The next stage is called red hepatization, reflecting the liverlike appearance of the consolidated lung: Airspaces are filled with polymorphonuclear cells, vascular congestion occurs, and movement of RBCs causes a reddish discoloration on gross examination.
The next stage is gray hepatization, in which an accumulation of fibrin is associated with inflammatory WBCs and RBCs in various stages of disintegration, and alveolar spaces are packed with an inflammatory exudate.
The final stage is resolution, characterized by resorption of the exudate.
In December, a seventy year old presents with fever, headache, chills, myalgia, malaise, nonproductive cough, and sore throat.
What could cause the illness?
When does Hospital-Acquired Pneumonia (HAP) normally occur?
What increases risk of getting HAP?
Infection occurs during a hospital stay for another illness
New pulmonary infiltrate that occurs after approximately *one week of hospitalization* and that resembles a bacterial pneumonia on the chest radiograph
Higher risk if on a mechanical ventilator
HAP tends to be more serious than CommunityAP - b/c patient is already sick and defense mechanisms against infection are often impaired.
What Risk factors predispose people to hospital-acquired pneumonia
immunosuppression from medications or diseases,
recent illness, and
risk of aspiration
List the Bacterial Atypical Pneumonia
Bacterial Atypical Pneumonia
Legionella pneumophila (exposure contaminated air conditioners, cooling towers)
List the Parasitic Pneumonia
What is characteristic of them?
(IgE and eosinophils elevated)
:A single episode of shaking chills followed by fever
:Chest pain when breathing
Severe abdominal pain
:Cough, which may be dry at first, but eventually produces phlegm (sputum)
:Nausea, vomiting, and muscle aches
:Feel suddenly worse after a cold or the flu
Bacterial pneumonias develop very quickly
1)Chest pain when breathing is on the side of the infected lung).
2)Severe abdominal pain sometimes occurs in people with pneumonia in the lower lobes of the lung
3)Cough, which may be dry at first, but eventually produces phlegm (sputum) - check for low squamous epithelial cells
Potentially Serious Symptoms of Typical Pneumonia
Potentially Serious Symptoms
Rapid breathing and heartbeat
Shortness of breath with normal daily activities
get them to a hospital!
Blood in sputum
Bluish-toned (cyanotic) skin
Labored and heavy breathing
Mental confusion or reduced mental function in the elderly
Rapid heart rate
Emergency Symptoms of pneumonia indicating a medical emergency
Blood in the sputum could be indicative of TB
Weight loss - coupled w/ night sweats could be indicative of TB
how do symptoms of pneumonia in the elderly present ?
Fewer or different symptoms than younger people.
Symptoms may come on much more slowly.
An elderly person who experiences even a minor cough and weakness for more than a day should seek medical help. Some elderly people may be confused, lethargic, and show general deterioration
Auscultation - lung sounds - In pneumonia, as air passes through mucous and fluids in the lungs, it creates clicking rattling or crackling sounds called rales and rhonchi (wheezing or low pitched, snoring like sounds). Strongly suspect pneumonia if rales are heard on one side of the chest and while the patient is lying down.
tap lightly on the person's chest
Percussion - tap lightly on the person's chest - A dull thud instead of a hollow drum-like sound may indicate that the lung has become firm and inelastic from inflammation, called consolidation; or that fluid may be collecting in between the layers of the lung membrane, called pleural effusion.
What tests may be ordered to help diagnosis of Pneumonia
:Chest x-rays - indicates extent lung involvement.
:Different types of pneumonia may have different patterns on x-ray.
:Blood and sputum cultures and/or serology to ID causative agent
:A lung biopsy may be performed in severe cases.
remove and analyze fluid from the pleura - Any accumulation of fluid between the layers of the pleura is called a pleural effusion.
to see inside the lung - Viewing the wind-pipe and major airways for pus, abnormal mucous, or other problems.
measures the amount of air you breathe -helps to determine how well the lungs are functioning.
Influenza Virus -
How many strains?
What ones are important?
when do epidemics usually occur?
Three strains Influenza A, B, C
Influenza A main cause human disease
Influenza B virus causes outbreaks that are generally less severe than influenza A
Influenza C generally causes more mild disease and is only a minor cause of disease in humans. Can be associated with flu in children.
Epidemics= winter months
Incubation time: 18-72 hours
man influenza virus generally only causes mortality in children and the elderly
In uncomplicated influenza the acute phase is generally over in 2-5 days. Most patients recover in 1 week but cough may persist for 1-2 weeks
When is the shedding of Influenza virus is maximal ?
Maximal on the 2nd day of exposure and generally has ceased by 6-7 day after 1st exposure.
What are the problems posed by flu virus? (4)
1. Wide host range
2. Rapid exchange genetic material- Ag shift
3. Respiratory spread
4. Rapid spread—air travel
Its genome dosen't consist of 1 piece of RNA - it consists of 8 pieces of RNA - it is the reason why we need to get a new shot every year...it's a segmented genome
What are the Reservoirs of Influenza Virus
Avian species carry strains of influenza virus with all different types of envelope proteins (Hemagglutinase HA and Neuraminase NA) that determine infectivity
Avian: does not generally recognize human receptors
Pigs serve as mixing vessels for influenza virus since they have receptors for both human and avian strains of virus
Avian influenza virus only rarely directly infects humans - takes a large dose (frequently w/ a 60% mortality rate when it does )
Not usually spread human to human
Avian is a special form of H5N1 it doesnt recognize humans however the pig has receptors for the avian and human virus
Influenza Virus - what kind of genome?
What does it allow for?
Influenza Virus has a segmented genome
Mixing of segments allows antigenic shift when more than one type virus infects a cell.
Transmission of Influenza Virus
Transmission - aerosol droplets, fomites, respiratory
The shedding of virus is maximal on the 2nd day of exposure and generally has ceased by 6-7 day after 1st exposure.
Detection of Influenza Virus:
Usually just self limiting but if we need to detect we'll use :
Tissue culture or on chick embryos
Immunofluorescence using anti-influenza Ab
Hemagglutinin inhibition, complement fixation or ELISA (Enzyme Linked Immunosorbant Assay)
Pathogenesis of influenza
1. Local upper respiratory tract infection kills mucous secreting, ciliated and other epithelial cells
2. NA cleaves mucous allowing more cellular infections.
3. Viremia and subsequent cytokine release responsible for myalgias (muscular aches)
4. If it is carried to the lungs, causes desquamation of epithelium in bronchi and alveoli.
What is Clinical disease/ symptoms of Influenza
Fever of 101.5ºF or higher and muscle aches(myalgias)
Clear nasal discharge (but no nasal obstruction)
(coryza = runny nose)
Clinical Diagnosis Influenza
Nasal swabs for rapid antigen detection - EIA; DFA ( they are best if you can freeze them - the virus doesn't do too well at room temp)
Serum antibodies by hemagglutination inhibition (HAI ) and EIA for type
(see slide for additional processes)
Treatment of Influenza
Treatment: Early treatment of influenza: Begin within 48 hours of illness onset, Duration: 5 days with one of the following:
Amantadine,Rimantadine: viral M2 ion channel inhibitors. Activity only against influenza A viruses
**Neuraminidase inhibitors: Activity against influenza A and B viruses
Tamiflu (Oseltamivir): - neuraminidase inhibitor - blocks viral budding) - against both A and B viruses
viral M2 ion channel inhibitors. Activity only against influenza A viruses
neuraminidase inhibitor - blocks viral budding) - against both A and B viruses
**Neuraminidase inhibitors: Activity against influenza A and B viruses
Tamiflu (Oseltamivir): - know both names
Prevention - Influenza
2 types of vaccines:
The "flu shot"— an inactivated vaccine (containing killed virus)
Approved for use in people older than 6 months, including healthy people and people with chronic medical conditions.
The nasal-spray flu vaccine — live, weakened flu viruses that do not cause the flu
(sometimes called LAIV for "live attenuated influenza vaccine" or FluMist®). LAIV (FluMist®)
Approved for use in healthy* people 2-49 years of age† who are not pregnant
Common Features Avian Influenza
fever, cough, dyspnea, cyanosis, rales, bilaterial pulmonary infiltrates, lymphopenia and increased aminotransferases
Sputum can be scanty but bloody
Initial radiographic findings diffuse, multifocal or patchy infiltrates; interstitial infiltrates, segmental or lobular consolidation
Note:Fatality rate is 60%
Incubation period following exposure to infected poultry in 7 days or less - often 2-5 days
cyanosis, tachycardia, tachypnea (rapid breathing) and diffuse rales.
Symptoms of ARDS
Note Avian Influenza can progress to Acute Respiratory Distress Syndrome
~ Progression to respiratory failure is associated with diffuse ground-glass infiltrates apparent in Xrays
~ Mechanical ventilation is generally required
~ Most patients require sedation to facilitate mechanical ventilation
What is the treatment for ARDS?
Treatment with neuraminidase inhibitor oseltamivir (Tamiflu, neuraminidase inhibitor) is recommended.
Due to drug resistance amantadine and rimantadine (M2 channel inhibitors) is not recommended.
Intravenous zanamivir and peramivir (neuraminidase inhibitors) are under development and may be considered as alternatives in case of oseltamivir resistance in the future
Avian influenza (H5N1) vaccine
Who should not receive it?
Avian influenza (H5N1) vaccine exists
Contains chicken , egg and porcine protein
Use with caution for patients with history of Guillain-Barre Syndrome
Use with caution for elderly immunocompromised, children or pregnant women
Pt was sick ... After 3 days the patients symptoms began to subside
After a week the symptoms of pneumonia reappeared with:
Fever and cough
Production of purulent sputum
Consolidation in X-ray
What Pathogenic Organisms do you suspect ?
Bacteria most likely involved
Streptococcus pneumonia (pneumococcus)
Note there was purulent sputum - think bacterial pneumonia
Factors favoring bacterial pneumonia
Previous influenza infection
Consoludation in X-ray
Treatment & Control
beta hemolysis (complete lysis rbcs) on blood agar
Catalase + and Coagulase +
Catalase test - catalase causes the decomposition of hydrogen peroxide to water and oxygen producing gas.
Coagulase test-Coagulase reacts with prothrombin in plasma
and enables the enzyme protease to convert fibrinogen to fibrin.
This results in coagulation and clotting.
Treatment: Penicillin, Amoxicillin; Methicillin; Vancomycin for methicillin resistant (MRSA outbreaks in hospitals can be epidemic)
Control: Isolate patients and staff carrying epidemic strains, e.g. MRSA Patients treated to eradicate carriage of MRSA.
A 65 year old patient initially develops uncomplicated influenza infection. However, a week later he develops fever, cough, and produces a purulent sputum. Lobular pneumonia with consolidation is apparent on chest X-ray. On culture the organism is alpha hemolytic on blood agar. A gram positive, lancet shaped cocci in pairs is isolated from a sputum sample.
What organism do you suspect?
What further tests would you run to confirm your diagnosis
How would you treat the patient?
What organism do you suspect? Steptococcus pneumonia
What further tests would you run to confirm your diagnosis? Bile solubility, optochin susceptibility, Neufeld/Quelling reaction
How would you treat the patient? Penicillin (if susceptible), Amoxicillin, Cephalosporins
Question stems includes a CF patient with bacterial pneumonia
What organisms should be in our differential?
Most likely organisms
Burkholderia (B. cepacia)
One of the ways of distinguishing Pseudomonas aeruginosa from Burkholderia spp.
Pseudomonas aeruginosa Produces blue green pigment on colorless agar.
Burkholderia pseudomallei Treatment:
Treatment: B. pseudomallei- intensive antibiotic treatment should be
initiated early with ceftazidine, Meropenem or Imipenem (more
neurological side effects than meropenem.
A patient resides in a slum apartment in Phoenix Arizona which is rat and flea infested. He develops fever, headache and chills. He also has enlarged painful lymph nodes. A biopsy reveals a gram negative rod.
What pathogen do you suspect?
What tests would you order next?
What are some of the virulence factors for the pathogen?
How would you treat the patient?
What pathogen do you suspect? Yersinia Pestis (plague)
What test would you order next? Wright's stain, PCR, ELISA
What are some of the virulence factors for the pathogen? Coagulase, Plasminogen activator, Type III secretion system
How would you treat the patient? Supportive therapy and antibiotics (Streptomycin, gentamicin, tetracycline, doxycycline,choramphenicol)
EMB (Eosin Methylene Blue) agar
EMB is both selective and differential media
contains EOSIN and METHYLENE BLUE dyes which inhibit the growth of gram-positive bacteria and
SELECTS the growth of GRAM NEGATIVE bacteria
contains LACTOSE, which DIFFERENTIATES non-enteric bacteria based on thier ability to ferment lactose
Results:Lactose fermenting bacteria yield colored colonies
E.coli colonies appear blue black with green metallic
When do we NOT treat an E Coli infection w/ antibiotics ?
Instead what should we use?
Treating E. coli infections with antibiotics => in severe shock => death.
bacterium's toxin is released when the cell dies
If killed enteric bacteria can release lipid A => endotoxin release => cytokine release => depress the vascular system and produce shock
Instead use bacteriostatic agent.
May use with caution: ampicillin, cephalosporins at doses that are bacteriostatic
Symptoms of TB
Fever, night sweats, weight loss, anorexia (lack of appetite), malaise, and weakness.
Pneumonia. X-rays results can vary from small infiltrates to extensive cavitary disease
Chronic nonproductive sputum at first and later productive with purulent sputum.
Bloody sputum can appear as disease progresses
Extensive disease can produce dyspnea (shortness of breath) and rarely Respiratory Distress Syndrome
Rales can be present during inspiration.
Rhonchi can also be present
(All in Red)
A 60 year old man who is a smoker and an alcoholic presents with a productive cough.
A gram negative organism is isolated that swarms on an agar plate.
What organism do you suspect?
What tests would you order next?
How would you treat the illness?
What organism do you suspect? Proteus spp.
What tests would you order next? Urease, Indole
How would you treat the illness? Imipenem, amikacin, TMP-SMX
What drugs are preferred for initial, emperic treatment of TB to avoid drug resistance?
How long will we administer these?
4 Drugs - for 6 - 9 months (sometimes up to 12 months)
RIF refampin (also known as refampicin), EMB ethambutol,
A 30 year old AIDS patient presents with malaise, headache, fever and personality changes.
What primary disease do you suspect?
What secondary complication has developed?
What further tests would you do?
What primary disease do you
suspect? Milinary TB
What secondary complication
has developed? CNS TB
What further tests would you
do? Skin test, sputum smear for
acid fast bacteria, interferon-gamma
release test, PCR, culture.
What is the take home message for SARS virus antigenicity ?
The polymerase jumps during the transcription process and can jump to an animal message just as easily as it can jump to a human receptor
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