204 terms


Block 4
Typical Pneumonia
Organisms that Cause
Streptococcus Pneumo
Staph Auereus
Pseudomonas aeruginosa
Burkholderia Cepacia
Enterobacteriaceae (Klebsiella, E Coli, Proteus, Serratia)

Leading cause of death from an infectious disease
Strep Pneumo

Infectious Agent
Risk Factors/HIgh Risk
Pneumococcal Pneumonia

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
Most common cause of community acquired typical pneumonias
Strep Pneumoniae
Most common bacterial pathogen causing a post-influenza infections
Strep Pneumoniae
Strep Pneumo

Cliinical Disease
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
Pneumococcal Pneumonia
Strep Pneumoniae
Strep Pneumo
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
Staph Aureus

Clinical Disease
Infectious Agent
Risk Factors
(Typical Pneumonia (and Empyema) - Community and Nosocomial

Gram +, Cocci in clusters

Catalase/Coagulase +

PANTON VALENTINE LEUKOCIDIN (PVL): NEW VF = severe hemorrhagic pneumonia
- Hemolysin coded on a phage

coagulase, hyaluronidase, fibrinolysin

Res: Humans

Transmission: Respiratory droplets, fomites, autoinnoculation, aspiration

1-5% of community acquired pneumonias in US
20-30% of nosocomial pneumonias
Strep Pneumo
Thins Secretions
Panton Valentin Leukocidin
Staph Aureus
Severe Hemorrhagic Pneumonia
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

cause (general)
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
Haemophilus Influenza

gram - pleomorphic rod appears pink on gram stain
Haemophilius Influenza

Infectious Agent
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


Beta lactamase produces are common

Hib vaccine
Yersinia Pestis
Pneumonic Plague
Pneumonic Plague seen on___
Wright's Stain

It produces a bipolar staining of the rod - a safety pin appearance

contains methylene blue, azure A, thionin with eosin Y
Yersinia Pestis

Infectious Agent
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 ***
Plasminogen Activator
Type 3 Secretion System (YOPs)
VF of Yersinia Pestis
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%
Bubonic Plague
Yersinia Pestis

Can progress to Pneumonic plague
Positive blood cultures but no palpable lymphadenopathy...mortality rate is 30-50%
Septicemic Plague
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

quick progression
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
Cystic Fibrosis

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

Infectious Agent
Risk Groups
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

Common Symptoms
Fever, chills, severe dyspnea, cyanosis, retractions, productive cough with purulent sputum, lung abscesses, confusion - may be rapidly fatal
What is Typical Pneumonia Definition?
Productive cough with purulent sputum
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
Burkholderia Spp

Infectious Agent
Risk groups
Clinical Disease
Gram negative Bacilli
Aerobic Nonfermentor...Oxidase +

Res: Colonization of variety of moist environmental surfaces

Opportunistic infection from environmental source

Patients with underlying chronic pulmonary disease

Typical Pseudomonas
How do I differentiate Pseudomonas from Burkholderia
BURKHOLDERIA - Burkholderia does not produce diffusible pigments

NO 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
Family Enterobacteriacae:
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
Biochemical Tests (API (20E)), EnteroTube) are used to identify
Family Enterobacteriacae
Gram - bacilli
typical pneumonia in elderly and those with underlying disease alcoholism, diabetes
Family enterobacteriae

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
Klebsiella Pneumoniae

Infectious Agent
Risk Factors
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
Mucoid Colonies
Large polysaccharide capsule of
Klebsiella pneumoniae pneumonia.

mucoid = thick, blood tinged
(Thick Capsule, Lac +, mucoid colonies, Indole -)
(Lac +, Indole +, Citrate -, Simmon's Citrate Agar)
E Coli
Non Lactose fermentor -
Urease +
Swarmer (rings)
Hydrogen sulfide +/-
Indole -
lipase +
Gelatinase +
Dnase +
produces red pigment
Serratia marcescens

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
Clinical Disease
Typical Pneumonia

Necrotic destruction of alveolar spaces,

cavity formation

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)
Bulging Fissure
sign on chest x ray due to lobar consolidation
Klebsiella Pneumo
No Lobar Pneumonia
Gram - rod...
Lactose +
Indole - (yellowish in vial)
Mucoid colonies form thick capsule...
NON motile
oxidase -

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
Klebsiella pneumonia
E Coli

Lab Diagnosis
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
Proteus Spp
Lab Diagnosis
Gram -
MOTILE (Swarmer) (klebsiella = nonmotile)
Hydrogen Sulfide (H2S) +/- (turns black)
Urease +
Indole -
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:

DNAse +

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
Gelatinase +
Serratia = +

(Salmonella = neg)
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 Microti
M Canetti - rare
Myobacteria that doesnt cause TB
M Avium Complex

Infectious Agent
ACID FAST ROD (gram + on gram stain) (auramine-rhodamine staining - sensitive/not specific)


2) Sulfatides (cell envelope)
3)Trehalose Dymcolate (cord factor in cell wall)
4) Mycolic acid (Long Chain Fatty Acid)

**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
Obligate Aerobe
Facultative Intracellular
Slow Growing

Produce NIACIN and heat sensitive CATALASE

Risk Factors
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
Primary 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
What is the difference between Latent TB infection and TB Disease
TST test = skin test for DTH
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
Miliary Tuberculosis

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
*Extra-Pulmonary TB*

Due to hematogenous spread TB

YELLOWISH GRANULOMAS 1-2 mm in diameter

Choroidal tubercles in eye
Shot Gun Pellet
Miliary TB due to widespread hematological dissemination

resembles millet seeds
Axillary Lymphadenitis

(esp common in AIDS patient)
Choroidal tubercles in eye
Miliary TB

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
Pleura -
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)
Middlebrook 7H10
Routine susceptibility testing

IGRAs - interferon gamma release assays
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
Ziehl Neelsen
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
6-12 months
RIFAMPIN (RIF) aka Refampicin

RIFAPENTINE, flouroqinolones

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
New drug for TB (1st line)

Fluroquinolones if 1st line not tolerated
Most common among homeless people in urban centers
severe form of pneumona

Corona virus

Rapid transmission and high mortality
SARS - severe acute respiratory syndrome

Infectious Agent
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
+ SS RNA Enveloped - Nonsegmented
SARS - coronavirus
Risk factors/high risk population for SARS
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

Ventilator required
No Tx to date shown to be effective

Respiratory barriers and isolation of suspected and confirmed patients

Negative pressure hospital rooms to prevent spread
Close proximity humans and poultry
Civet Cat
Explain Coronavirus Virion
Cubic symmetery

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
Rodent Droppings
Fever, Headache, muscle aches, stomach ache, dizziness, chills
Hantavirus Pulmonary syndrome

Infectious Agent
Risk Groups

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
Negative Sense SS RNA

(same as orthomyxovirus, influenza)

infected via rodents or inhalation of aeroslized virus

Legionella Pneumophilia

h20 aersols

Clinical Disease
List Symptoms :


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

Deer Mice

Lab Diagnosis
Class 4 labs only
ELISA (IgM or paired sera IgG)

Rodent control

No specific Tx
Cytomegalovirus (CMV)

Infectious Agent
Risk Factors
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

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.
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
TORCH syndrome
Congenital CMV infection
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
Atypical Pneumonia

Mycoplasma (walking) Pneumonia
Legionnaire's Disease
Chlamydial Pneumonia

Walking Pneumonia
Mycoplasma (most common)

Pneumonia thats mild enough that youre not bedridden
Legionella Pneumophilia

Infectious Agent
Risk Groups

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
(h20 aersol)

Middle age or > 55, immunocompromised
alcoholics, smokers, COPD, diabetes

Fastidious growth - iron salts and cysteine
Legionella Pneumophilia
Aquatic Habitat (whirlpools, saunas, showers) survives in cholrine
Legionella Pneumophilia

unchlorinated pools - adenovirus
Intracellular Parasite
Legionella Pneumophilia
(alveolar macrophage and monocytes - but no fusion between phagosome and lysosome)
Pontiac Fever
Legionella Pneumophilia

Milder, self limiting
No GI tract manifestations
NO CNS manifestations
Legionella Pneumophilia

Clinical Disease

(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

Antibiotic therapy

(95% of those exposed, milder, self limiting)
1-2 day incubation...similar to influenza
NO CNS manifestations
Legionella Pneumophilia

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

No vaccine
Silver Impregnation Stain
Legionella Pneumophilia
Buffered charcoal Yeast Extract Agar
Contains Iron and Cysteine

Legionella Pneumophilia
Mycoplasma Pneumoniae

Infectious Agent
Risk Groups
Cell Wall Less...ROD...cholesterol like molecule in plasma membrane, growth media contains serum***

VF: ***
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
Mycoplasma Pneumoniae
reduction or ceasing ciliary beat - explains non-productive cough
P1 Antigen
attachment to resp epithelium

Mycoplasma Pneumo

Also think H2O2, Ciliostasis
Pneumonia in school age children and young adults...crowded military and institutional college settings
Mycoplasma Pneumoniae
Clinical Disease

Mycoplasma Pneumoniae
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
Viral Pneumonia)

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)
Walking pneumonia
Mycoplasma Pneumonia
Mycoplasma Pneumonia

Lab Diagnosis
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
Mulberry Appearance
Requires cholesterol supplementation
Mycoplasma Pneumonia
can be Fatal in patients with Sickle cell
Mycoplasma Pneumoniae
Chlamydophila Pneumoniae

Infectious Agent
Risk Factors

"energy parasites" obligate intracellular
Differences with viruses


Respiratory droplets

Present with pharyngitis..Elderly at risk for clinical pulmonary disease

Infections tend to recur so prolonged treatment
energy parasites
obligate intracellular

Chlamydophila Pneumoniae
Chlamydophila Pneumoniae

Clinical Disease
Atypical Pneumonia
Rarely causes death
Bilateral infiltrates on xray
May be associated with atherosclerotic vascular disease, alzheimers, asthma and reactive arthritis
Chlamydophila Pneumoniae
What are the Viruses for Lower Respiratory Infections
~State organisms
~Viruses (Atypical pneumonia)
Influenza (including Avian Flu)
Coronavirus (SARS)

Atypical tend to have no or clear sputum
What are the Bacterial Pneumonias (secondary to Influenza) for Lower Respiratory Infections
~State organisms
~ Bacterial Pneumonia secondary to Influenza
Streptococcus pneumonia
Haemophilus Influenza
Staphlylococcus aureus

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,
IgA secretion

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,
mucociliary apparatus,
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),
- fibronectin,
- immunoglobulin, complement, Cytokines, Alveolar macrophages, PMNs, Cell mediated immunity
- iron-binding proteins ( we have very little iron in the body)
What is Consolidation?
Increased firmness
(induration) of lung due
to inflammatory
cellular exudate (fluid and
pus) in alveolii and ajoining
Aspiration pneumonia
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:
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.
Bronchopneumonia: patchy consolidation around the larger airways
Double pneumonia
Double pneumonia: This refers to pneumonia that affects both lobes of the lungs
In December, a seventy year old presents with fever, headache, chills, myalgia, malaise, nonproductive cough, and sore throat.
What could cause the illness?
Influenza Virus
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
Risk factors
older age,
immunosuppression from medications or diseases,
recent illness, and
risk of aspiration
List the Bacterial Atypical Pneumonia
Bacterial Atypical Pneumonia
Mycoplasma pneumophila
Legionella pneumophila (exposure contaminated air conditioners, cooling towers)
Chlamydophila pneumoniae
List the Parasitic Pneumonia
What is characteristic of them?
Parasitic Pneumonia
Ascaris lumbricoides
Strongyloides sercoralis
Paragonimus westermani

(IgE and eosinophils elevated)
:High Fever
: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
Typical Pneumonia

added points:
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
Purulent sputum indicative
bacterial infection
Clear sputum indicative of
viral disease
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
Weight loss
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
clicking rattling or crackling sounds called
wheezing or low pitched, snoring like sounds
lung sounds
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?
Incubation time?
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
Migration birds

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)
Sore throat
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
Viral pneumonia
Lobar pneumonia
Aspirational Pneumonia
Interstitial Pneumonia (tissue & space around air sac)
Top = Normal Lung
Bottom = Lung w/ Consolidation
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)
Haemophilus influenza
Staphylococcus aureus

Note there was purulent sputum - think bacterial pneumonia

Factors favoring bacterial pneumonia
Previous influenza infection
Elderly patient
Purulent sputum
Consoludation in X-ray
Staph Aureus


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
Psudomonas aeruginosa
Staphlococcus aureus
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)
How do we test for TB?
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)

INH isoniazid,
RIF refampin (also known as refampicin), EMB ethambutol,
PZA Pyrazinamide
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
SARS doesn't have this enzyme :
(HE) Hemagglutin acetylesterase glycoprotein