Pneumonia

Created by AshleyJ88 

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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
VF
Reservoir
Transmission
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
Diagnosis
Treatment
Prevention

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

Prevention:
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
VF
Reservoir
Transmssion
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

Neuraminidase

Strep Pneumo
Thins Secretions

Panton Valentin Leukocidin

Staph Aureus
Severe Hemorrhagic Pneumonia

Staph Aureus Clinical Diseases:

Typical Pneumonia (and Empyema) - Community and Nosocomial

ASPIRATION PNEUMONIA
~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

HEMATOGENOUS PNEUMONIA
Common in patients with bacteremia or endocarditis

NECROTIZING INFECTION with rapid progression to tissue destruction and cavitation )PVL + strains)...Fever hemoptysis, leukopenia, resp distress

Bronchitis

definition
cause (general)
symptoms

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
Transmission
Risk
Reservoir
Tx
Prevention

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

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
Reservoir
Transmission
Risk

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 ***

Coagulase
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
Diagnosis
Tx
Prevention

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

Pseudomonas

Infectious Agent
Reservoir
Transmission
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

OPPORTUNISTIC PATHOGEN

Immunocompromised; COPD, CF patients; hospitalized

Clinical Disease of Pseudomonas

Typical Pneumonia (Productive cough with purulent sputum)

ASPIRATION PNEUMONIA
Necrotizing bronchopneumonia (exotoxin A)

HEMATOGENOUS PNEUOMNIA
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
CXRs
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
Reservoir
Transmission
Risk groups
Clinical Disease

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

Typical Pseudomonas

How do I differentiate Pseudomonas from Burkholderia

THE MAJOR DIFFERNCE BETWEEN PSEUDOMONAS AND
BURKHOLDERIA - Burkholderia does not produce diffusible pigments

Burkholderia

Diagnosis

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.

BCSA Agar

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
Reservoir
Transmission
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 -)

Klebsiella

(Lac +, Indole +, Citrate -, Simmon's Citrate Agar)

E Coli

Non Lactose fermentor -
Urease +
Swarmer (rings)
Motile
Hydrogen sulfide +/-
Indole -

Proteus

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

Klebsiella
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

Pseudomonas

Klebsiella
Diagnosis
Tx
Prevention

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
(serratia)

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 +
LIPASE +
GELATINASE +

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

RED PIGMENTED

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

TB

Infectious Agent
Reservoir
Transmission

ACID FAST ROD (gram + on gram stain) (auramine-rhodamine staining - sensitive/not specific)
OBLIGATE AEROBE,
FAC INTRACELLULAR, slow growing

VF:
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 **

Humans

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

TB

USE ACID FAST STAIN!!! (In red)

Produce NIACIN and heat sensitive CATALASE

TB

TB

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?

PRIMARY
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

GHON COMPLEX

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
Necrosis

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 &
Symptoms

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

Hepatomegaly
Splenomegaly
Lymphadenopathy
Choroidal tubercles in eye

Shot Gun Pellet

Miliary TB due to widespread hematological dissemination

resembles millet seeds

Axillary Lymphadenitis

(esp common in AIDS patient)

TB

Hepatomegaly
Splenomegaly
Lymphadenopathy
meningismus
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)

CNS TB

Initial Phase: malaise, headache, fever, personality change...2-3 weeks later see headache, MENINGISMUS, vomiting, confusion, and focal neurologic findings

MENINGITIS

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)
PCR

Lowenstein Jensen (but takes 2-6 wks)
Middlebrook 7H10
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)

MEASURE HARDNESS

Vaccination w/ BCG is not a contraindication for TST

(In red - know this )

IGRAs
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
Streptomycin
ISONIAZID (INH)
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

ISONIAZID (INH)

old Tx of choice for TB (1956)

Note - Pyridoxine (Vit B6) is given to prevent INH toxicity

RIFAPENTINE

New drug for TB (1st line)

Fluroquinolones if 1st line not tolerated

Most common among homeless people in urban centers

MDR-TB

severe form of pneumona

Corona virus

Rapid transmission and high mortality

SARS - severe acute respiratory syndrome

SARS

Infectious Agent
Reservoir
Transmission
Risk Factors and High Risk

Enveloped SS + sense RNA
Nonsegmented

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

OVER 50
CVD, DIABETES, HEPATITIS
PREGNANT

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

Diarrhea

Develop a dry cough, trouble breathing & demonstrable pneumonia

Ventilator required

SARS
Prevention
Treatment

No Tx to date shown to be effective

Prevention:
Respiratory barriers and isolation of suspected and confirmed patients

Negative pressure hospital rooms to prevent spread

Close proximity humans and poultry
Civet Cat

SARS

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?

SARS

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
Bunyaviridae

Hantavirus

Family
Infectious Agent
Reservoir
Transmission
Risk Groups

Bunyaviridae

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

Enveloped
Negative Sense SS RNA
SEGMENTED

Hantavirus

(same as orthomyxovirus, influenza)

CANT BE TRANSMITTED PERSON TO PERSON

Hantavirus

infected via rodents or inhalation of aeroslized virus


Legionella Pneumophilia

h20 aersols

Hantavirus

Clinical Disease
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

Deer Mice

Hantavirus

Hantavirus

Lab Diagnosis
Tx
Prevention

Class 4 labs only
ELISA (IgM or paired sera IgG)
RT-PCR

Rodent control

No specific Tx

Cytomegalovirus (CMV)

Family
Infectious Agent
Reservoir
Transmission
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

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

TORCH syndrome

Congenital CMV infection

Diagnosis of CMV
Tx
Prevention

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*****

GANCICLOVIR

Safe sex; screeing

What causes ATYPICAL PNEUMONIA (unproductive cough)

1) Mycoplasma (walking) Pneumonia (most common)
2) Legionnaire's Disease
3) Chlamydial Pneumonia

Viral pneumonia :
Influenza
Parainfluenza
RSV (Respiratory Syncytial Virus)
Adenovirus

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

Influenza
Parainfluenza
RSV
Adenovirus

Walking Pneumonia

Mycoplasma (most common)

Pneumonia thats mild enough that youre not bedridden

Legionella Pneumophilia

Infectious Agent
Reservoir
Transmission
Risk Groups

ATYPICAL 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
(h20 aersol)

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

WHOLE THING IS IN RED

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

ATYPICAL PNEUMONIA

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

Antibiotic therapy


PONTIAC FEVER
(95% of those exposed, milder, self limiting)
1-2 day incubation...similar to influenza
NO GI TRACT MANIFESTATIONS
NO CNS manifestations

Legionella Pneumophilia

Diagnosis
TX
Prevention

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

No vaccine

Silver Impregnation Stain

Legionella Pneumophilia

BCYE

Buffered charcoal Yeast Extract Agar
Contains Iron and Cysteine

Legionella Pneumophilia

Mycoplasma Pneumoniae

Infectious Agent
Reservoir
Transmission
Risk Groups

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

VF: ***
Causes CILIOSTASIS
P1 Ag - attachment to respiratory epithelium
Hydrogen Peroxide - tissue damage

Humans

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

CILIOSTASIS

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

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
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
Reservoir
Transmission
Risk Factors

ATYPICAL PNEUMONIA

"energy parasites" obligate intracellular
Differences with viruses

Humans

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
Bronchitis
Pharyngitis
Sinusitis
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)
Hantavirus
Cytomegalovirus

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
ducts

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:

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?

Orthomyxoviridae
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
alcoholism,
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

See More

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