Respimicro [recovered]

24Microbial Diseases of the Respiratory System

MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

upper respiratory system

The consists of the nose, pharynx, and associated structures, such as the middle ear and auditory tubes.

Coarse hairs in the nose ciliated mucous membranes ( nose and

throat ) Lymphoid tissue, tonsils, and adenoids


lower respiratory system

consists of the larynx, trachea, bronchial tubes, and alveoli.

ciliary escalator alveolar macrophages. Respiratory mucus contains IgA antibodies.


NORMAL MICROBIOTA OF THE RESPIRATORY SYSTEM

The normal microbiota of the nasal cavity and throat can include pathogenic microorganisms.

The lower respiratory system is usually sterile because of the action of the ciliary escalator.


Upper Respiratory System Upper respiratory normal microbiota may

include pathogens

Figure 24.1MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

Microbial Diseases of the Upper Respiratory System

Laryngitis: S. pneumoniae, S. pyogenes, viruses

Tonsillitis: S. pneumoniae, S. pyogenes, viruses

Sinusitis: Bacteria Epiglottitis: H. influenzae Hib vaccine


MICROBIAL DISEASES OF THE UPPER RESPIRATORY SYSTEM

These infections may be caused by several bacteria and viruses, often in combination.

Most respiratory tract infections are self-limiting.

H. influenzae type b can cause epiglottitis.


Streptococcal Pharyngitis (Strep Throat) GAS- Streptococcus

pyogenes Resistant to

phagocytosis Streptokinases lyse

clots Streptolysins are

cytotoxic Diagnosis by indirect

agglutination/ EIA


Streptococcal Pharyngitis (Strep Throat) group A beta-hemolytic streptococci-

Streptococcus pyogenes.

Symptoms of this infection are inflammation of the mucous membrane and fever; tonsillitis and otitis media may also occur.


Streptococcal Pharyngitis (Strep Throat) Rapid diagnosis is made by enzyme

immunoassays.

Penicillin is used to treat streptococcal pharyngitis.

Immunity to streptococcal infections is type-specific.

Strep throat is usually transmitted by droplets.


Scarlet Fever Streptococcus

pyogenes Pharyngitis Erythrogenic toxin

produced by lysogenized S. pyogenes by a phage.


Scarlet Fever

Strep throat, caused by an erythrogenic toxin-producing S. pyogenes, results in scarlet fever.

starts general malaise and swelling of neck

Symptoms include a red rash, high fever, and a SPOTTED STRABERRY like red, enlarged tongue.


Diphtheria Corynebacterium diphtheriae: Gram-

positive rod pleomorphic club shape


Diphtheria Clinical

Start as sore throat and fever followed by general malaise and swelling of neck

Diphtheria (leather) tough grayish membrane of fibrin, dead tissue, and bacteria

Diphtheria toxin produced by lysogenized C. diphtheriae (highly virulent toxin)


Diphtheria


Diphtheria


Vao day nghe bai nay di ban http://nhattruongquang.0catch.com

Diphtheria A membrane can block the passage of air. Exotoxin inhibits protein synthesis, and

heart, kidney, or nerve damage may result (fatal)

minimal dissemination of the exotoxin in the bloodstream.

Antitoxin - neutralize the toxin

Antibiotics- Penicillin and Erythromycin can stop growth of the bacteria.


Diphtheria Prevented by DTaP and Td vaccine

(Diphtheria toxoid) Cutaneous diphtheria: Infected skin

wound leads to slow healing ulcer



A 15 y/o male patient have chief complaint of difficulty of breathing with associated throat pain, difficulty of swallowing and fever. Physical exam reveals inflamed pharyngeal area covered by grayish thick mucus that is adherent. Patient was noted to have an incomplete set of vaccination. Grams staining reveals gram positive bacilli with endospore.


Corynebacteria (Genus Corynebacterium)• Aerobic or facultatively anaerobic

• Small, pleomorphic (club-shaped), gram-positive bacilli short chains (“V” or “Y” configurations) or in clumps resembling “Chinese letters”

• Cells contain metachromatic granules

• Lipid-rich cell wall contains meso -diaminopimelic acid

OTITIS MEDIA

infection of the middle ear, primarily in infants and young children

three manifestations• acute otitis media• chronic otitis media• otitis media with effusion

A. Symptoms - fever, pain in the ear, dulled hearing.

Otitis Media S. pneumoniae (35%) H. influenzae (20-30%) M. catarrhalis (10-15%) S. pyogenes (8-10%) S. aureus (1-2%)

RSV Affects 85% of children before age 3, and

estimated 8 million cases/ year


Otitis Media

Treated with broad-spectrum antibiotics Amoxicillin

Incidence of S. pneumoniae reduced by vaccine


Otitis Media

Earache, or otitis media, can occur as a complication of nose and throat infections.

Pus accumulation causes pressure on the eardrum causes inflammation and pain.

Often in children because of shorter and more horizontal eustachian tube


B. DIAGNOSIS –

1. clinical presentation of fever and pain, especially following an URT infection such as a cold

2. otoscopic examination to see inflammation and/or fluid (pus); also loss of mobility with air pressure

6.

• swelling and blockage • cyclic pattern of damage• discomfort - pressure and blocked nasal passages

Common cold Rhinoviruses (50%) Coronaviruses (15-20%)


The Common Cold

Any one of approximately 200 different viruses can cause the common cold; rhinoviruses cause about 50% of all colds.

Immunity is based on the ration of Ig A antibodies


The Common Cold

Symptoms Sneezing nasal secretions congestion.

Sinus infections, lower respiratory tract infections, laryngitis, and otitis media can occur as complications of a cold.


The Common Cold

Colds are most often transmitted by indirect contact.

Rhinoviruses grow best slightly below body temperature.

The incidence of colds increases during cold weather

Antibodies are produced against the specific viruses.


Microbial Diseases of the Lower Respiratory System

Bacteria, viruses, and fungi cause

Bronchitis Bronchiolitis Pneumonia


Lower Respiratory System The ciliary escalator keeps the lower

respiratory system sterile.


Pertussis (Whooping Cough) Bordetella pertussis:

Gram-negative coccobacillus

Capsule Tracheal cytotoxin of cell

wall damaged ciliated cells

Pertussis toxin produces systemic disease

Prevented by DTaP vaccine (acellular Pertussis cell fragments)


Man is only natural host; obligate parasites of man

Disease is highly communicable (highly infectious)

Children under one year at highest risk, but prevalence increasing in older children and adults

Epidemiology of Bordetella pertussis Infection

Whooping cough

Inhalation of aerosols

Adhere to ciliated epithelial cells (FHA, Pili)

Toxin production

Damage to mucosal cells(TCT, Ptx, Acase, LPS?)

Act on neurons(Ptx, Acase, LPS)

Paroxysmal cough

Whooping cough

Symptoms Severe coughing, spasms, inspiratory

whoop Lymphocytosis

Stages of disease Catarrhal -> Paroxysmal -> Convalescent

Spread--highly contagious Inhalation or direct contact with secretion

Usually self-limiting Neurological sequelae Secondary respiratory infections Secondary aspiration pneumoniae

leading cause of death

Pertussis (Whooping Cough)



.


Initial stage of pertussis

resembles a cold and is called the catarrhal

stage.

Paroxysmal (second)

stage

accumulation of mucus

in the trachea and

bronchi causes deep

coughs

Convalescence (third)

stage

can last for months

Clinical Progression of Pertussis

Most infectious, but generally not yet diagnosed

Inflammation of respiratory mucosal memb.

,or death

Laboratory Culture, Prevention & Treatment of Bordetella

Treatment with erythromycin

Nonmotile Fastidious and slow-growing

· Requires nicotinamide and charcoal, starch, blood, or albumin

· Requires prolonged growth · Isolated on modified Bordet-Gengou agar


Laboratory diagnosis is based on isolation of the bacteria on enrichment and selective media, followed by serological tests.

Regular immunization for children has decreased the incidence of pertussis.


TUBERCULOSIS

Situationer

Leading causes of death world wide Up to a half of world’s population

infected, 95% in developing countries 8 million people get TB every year

(WHO fact sheet 2007)

Philippines ranks 4th for # of TB cases worldwide, highest # per head in SEA

2/3 of Filipinos with TB

(DOH, 2007)

Rex Karl S. Teoxon, R.N, M.D 46

PTB

Mycobacterium tubercle, acid fast bacilli

Airborne/droplets Pott’s disease – thoracolumbar Milliary TB – kidney, liver, lungs



Morphology

Mycobacterium tuberculosis Thin straight rods, 0.4 x 3 µm Acid-fast organisms

Mycobacterial cell wall components Lipids (mycolic acids) Proteins Polysaccharides

TB symptoms

1. Cough with two weeks or more2. Sputum expectoration3. Fever4. Significant weight loss5. Hemoptysis6. Chest and/or back pains


SIGNS AND SYMPTOMS

Wt loss, night sweats, low fever, non productive to productive cough, anorexia, Pleural effusion and hypoxemia, cervical lymphadenopathy

Tuberculosis Mycobacterium

tuberculosis: Acid-fast rod; transmitted from human to human.

M. bovis: <1% U.S. cases, not transmitted from human to human.

M. avium-intracellulare complex infects people with late stage HIV infection.


Tuberculosis Mycobacterium tuberculosis

Acid fast-lipid, wax Slow growth (nutrient permeability) Resist to detergent and common antibiotics

A leading cause of death by infectious disease 50% population infected, 3m death/yr Reemergence in 1980 (AIDS, homeless, immigrants)

Diagnose PPD test Chest X-ray Sputum smear (for acid-fast bacilli) Sputum culture

Diagnosis

Sputum culture Slow, 13 hour generation time, takes weeks

Acid-fast stainingSkin test (PPD)DNA hybridization PCR (16s rRNA)Bacteriophage


PPD – ID

macrophages in skin take up Ag and deliver it to T cells

T cells move to skin site, release lymphokines

activate macrophages and in 48-72 hrs, skin becomes indurated

- > 10 mm is (+)


DIAGNOSIS

Chest x ray - cavitary lesion

Sputum exam Sputum culture

Stages of disease Primary infection

Asymptomatic to flu-like 3-5% develop TB Tubercle (granulomatous response)

Reactivation (active TB) Years later, 10% experience

LRT disease (pneumonia) Disseminated miliary TB

Almost everywhere AIDS and antibiotic resistance

Stages of pathogenesis

Encounter - respiratory droplet Entry - direct inhalation into LRT

(ID=10) SPREAD - alveoli, but can spread

throughout body seeding many tissues Multiplication

Grows in phagosome of macrophage Strict aerobe Very slow in culture (24 hr doubling time)

Evade defenses Inhibits phagolysosomal fusion

Tuberculosis

Tuberculosis is caused by Mycobacterium tuberculosis.

Large amounts of lipids in the cell wall account for the bacterium’s acid-fast characteristic as well as its resistance to dryingnd disinfectants.


Tuberculosis

M. tuberculosis may be ingested by alveolar macrophages; if not killed, the bacteria reproduce in the macrophages.


Tuberculosis

Lesions formed by M. tuberculosis are called tubercles

Dead macrophages and bacteria form the caseous lesion that might calcify and appear in an X ray as a Ghon’s complex.


Tuberculosis Liquefaction of the

caseous lesion results in a tuberculous cavity in which M. tuberculosis can grow.


Tuberculosis New foci of

infection can develop when a caseous lesion ruptures and releases bacteria into blood or lymph vessels; this is called miliary tuberculosis.


M. tuberculosis Damage

Host response to bacteria (cell-mediated immunity) Glycolipids (Freund adjuvant)

Spread to new hosts Contagious by droplet, resistant to drying

Vaccine - BCG Causes people to become PPD+, not very effective Infect AIDS

Treatment Unusual set of antibiotics (isoniazid, ethambutol,

rifampin) High mutation rate

Tuberculosis

Miliary tuberculosis is characterized by weight loss, coughing, and loss of vigor.

Chemotherapy usually involves 3 or 4 drugs taken for at least 6 months; multidrug-resistant M. tuberculosis is becoming prevalent.


Tuberculosis

Positive tuberculin skin test an active case of TB prior infection vaccination immunity to the disease

Induration and reddening at inoculation site within 48hours.

Most accurate- Mantoux test


Tuberculosis Laboratory diagnosis is based on the

presence of acid-fast bacilli and isolation of the bacteria, which requires incubation (3-6weeks) of up to 8 weeks (Lowenstein-Jensen Agar)


PPD Tuberculosis Skin Test Criteria

PPD = Purified Protein Derivative from M. tuberculosis




Chest X-Ray of Patient with Active Pulmonary

Tuberculosis

Tuberculosis

Mycobacterium bovis causes bovine tuberculosis transmitted to humans by unpasteurized

milk. affect the bones or lymphatic system. BCG vaccine -a live, avirulent culture of M.

bovis

M. avium-intracellulare complex infects patients in the late stages of HIV


Tuberculosis Treatment of tuberculosis: Prolonged

treatment with multiple antibiotics. Vaccines: BCG, live, avirulent M. bovis;

not widely used in United States.


Tuberculosis



MANAGEMENT

short course – 6-9 months long course – 9-12 months DOTS- direct observe treatment short

course Case finding Home meds (members of the family) Referrals Follow-up short course – 6-9 months long course – 9-12 months


MANAGEMENT

Follow-up * 2 wks after medications – non

communicable 3 successive (-) sputum - non communicable rifampicin - prophylactic


CATEGORIES OF TB

category I (new PTB) - (+) sputum

category II (relapse)

category III (PTB case) - (-) sputum


TREATMENT: CATEGORY 1 - NEW PTB, (+) SPUTUM

GIVE RIPE 2 MONTHS, MAINTENANCE OF RI 4 MONTHS

CATEGORY 2 - PREVIOUSLY TREATED WITH RELAPSESGIVE RIPES 1ST 2 MONTHS, REPS 1 MONTH, MAINTENANCE RIE 5 MONTHS

CATEGORY 3 - NEW PTB (-) SPUTUM FOR 3XGIVE RIP 2 MONTHS, MAINTENACE RI 2 MONTHS

* IF RESISTANT TO DRUGS GIVE ADDITIONAL MONTH/S AS PRESCRIBED


MDT side effects

r-orange urine i-neuritis and hepatitis p-hyperuricemia e-impairment of vision s-8th cranial nerve damage

AFB SMEAR REPORTING GUIDELINE, DOH

NATIONAL TUBERCULOSIS CONTROL PROGRAM (2001)

Emilio M. Ramirez, MD

National Tuberculosis Control Program (2001) prevent transmission of tubercle bacilli

to a healthy person

Goal: Reduce TB mortality and prevalence through early case detection and treatment

Target: identify at least 70% of new smear (+) cases, cure at least 85% TB patients discovered

Strategy: DOTS (directly observed treatment short course chemotheapy)

Sputum Collection Schedule forDIAGNOSIS

SPOT EARLY MORNING

SPOT

Day 1

First specimen -

collected at the time of consultation or as soon as TB symptomatic is identified.

Day 2

Second specimen

Collected in the morning by the TB symptomatic when he/she is due to submit the specimen to the health center.

Third specimen

Collected at the time the TB symptomatic comes back to the health facility to submit the second specimen.

Ideal sputum specimen?

MACROSCOPIC- Yellowish- Mucopurulent- Cheesy material

When to collect another set of 3 sputum specimens?

When the diagnosis for the sputum microscopy examination is doubtful.

When the patient fails to complete his sputum collection within two weeks from the time of the previous collection.

Ideal sputum specimen?

MICROSCOPIC- greater than 25

wbc/LPO, 5 wbc/OIO

- Presence of alveolar macrophage, dust cells

AFB STAINING

DIRECT SMEAR EXAMINATION(Flow Chart)

SMEARINGSPREADING

DRYING

FIXATION

STAININGINITIAL STAINING

HEATING

WASHING

DECOLORIZATION

WASHING

COUNTER-STAINING

WASHING

DRYING

MICROSCOPIC OBSERVATION

RECORDING & REPORTING

DIRECT SMEAR PREPARATION

LABELING THE SLIDES

Write down the identification number of the sputum specimen on the end of a clean glass slide.

SMEARING

SPREADING

With a coconut midrib, fish out one (1) loopful of purulent, solid particles of the sputum.

Spread the sputum evenly on the slide, approximately 2 x 3 cm

in size.

A Good Smear

Poor/too thick Good Poor/too thin

SMEARING

DRYING

Allow the smear to dry completely at room temperature. Do not dry it under the sun or over the flame.

Place used midribs in a bottle with alcohol and sand mixture or Lysol, or in a plastic containers and burn them later.

SMEARING

FIXATION

Fix the smear by passing it through the flame of an alcohol lamp 2 to 3 times, about 2-3 seconds each.

Heat the back of smeared surface of the slide. Never scorch the smear.

STAINING

FIXATION

Fix the smear by passing it through the flame of an alcohol lamp 2 to 3 times, about 2-3 seconds each.

Heat the back of smeared surface of the slide. Never scorch the smear.

STAINING

INITIAL STAINING

Arrange the slides on the staining bridge consecutively.

Pour carbol fuchsin solution covering the whole surface of the slide.

STAINING

HEATING OF THE SLIDE

Heat the slide using an alcohol lamp or spirit cotton in a stick ‘till steam comes off from the stain.

Do not boil and do not allow the stain to dry. Leave it for five minutes.

STAINING

WASHING OF THE SLIDE Tilt the slide to drain off excess stain.

Wash the staining solution off with a gentle stream of running water.

STAINING

DECOLOURIZATION

Tilt the slide to drain off excess rinse water.

Cover the whole slide with 3% hydrochloric acid-ethanol and leave it until solution runs clear.

Staining

WASHING OF THE SLIDE

Wash the slide with a gentle stream of running water.

Tilt the slide to drain off excess rinse water.

Staining

COUNTERSTAINING

Pour 0.1% methylene blue to cover the whole surface of the smear and leave for 5-10 seconds.

Tilt the slide to drain off excess methylene blue.

Staining

WASHING AND DRYING

Wash the slide with a gentle stream of running water.

Tilt and place the slide on the slide rack to dry in the air.

Don’t place under the sun to dry.

SMEAR READING PROPER SCANNING

Horizontal Scanning

Vertical Scanning

IMPROPER SCANNING

Zigzag Scanning

3 cm

AFB OBSERVATION

Single/parallel form

Clump form

Coccoid form

Scratches on the slide

MICROSCOPIC OBSERVATION OF AFB IN PROPERLY AND IMPROPERLY STAINED SMEAR

PROPER STAINING INSUFFICIENT HEATING

UNDERDECOLORIZED INTENSELY COUNTERSTAINED

National Standard Reporting Scale (2001)

No AFB seen in 300 visual fields 0

1-9 AFB/ 100 visual fields (x1000) +n

10-99 AFB/ 100 visual fields (x1000) 1+

1-10 AFB/ OIF in at least 50 visual fields 2+

>10 AFB/ OIF in at least 20 visual fields 3+

INTERPRETATION OF LAB RESULTS

POSITIVE - if all or at least two of the three

specimens are positive

NEGATIVE - if all (3) specimens are negative

DOUBTFUL - if one of the three specimens is positive (sputum examination should be repeated)

Bacterial Pneumonias

Typical pneumonia is caused by S. pneumoniae.

Atypical pneumonias are caused by other microorganisms.

Lobar pneumonia

bronchopneumoniaMICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera


Pneumonias

Sign/ symptoms

High fever DOB Chest pain Productive cough




Calculation of PSI score*Factor Result PSI score

Patient age 66 years + 66

Specified coexisting illness No 0

Signs on examination

Confusion Yes + 20

Respiratory rate 28 per min 0

Systolic blood pressure 140 mmHg 0

Temperature 38°C 0

Pulse rate 120 bpm 0

Results of investigations

Serum urea level 17 mmol/L + 20

Serum sodium level 136 mmol/L 0

Serum glucose level 19.6 mmol/L + 10

Haematocrit 40% 0

O2 saturation 86% + 10

pH 7.36 0

Pleural effusion No 0

Total 126

* If results of blood tests cannot be obtained rapidly (eg, in remote areas), risk can be determined without the PSI score (see Box 3). In this case, presence of diabetes, respiratory rate > 20 per minute, confusion and multilobar disease on x-ray would have suggested that the patient was at significantly increased risk of death.


http://www.mja.com.au/public/issues/176_07_010402/joh10289_fm.html


Mortality within 30 days according to PSI risk class19

http://www.mja.com.au/public/issues/176_07_010402/joh10289_fm.html

Pneumomoccal Pneumonia Streptococcus

pneumoniae: Gram-positive encapsulated diplococci

Diagnosis is by culturing bacteria.

Penicillin

Fluoroquinolones is drug of

choice.Figure 24.13MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

Pneumococcal pneumonia(Streptococcus pneumoniae)

Gram-positive diplococcus Encapsulated (>80 serotypes)

Susceptible population Elderly Previously ill Phagocytic dysfunction (e.g., asplenic, sickle

cell)

Also cause meningitis, otitis media Sensitive to optichin; autolysis by bile

Pneumococcal Pneumonia

The bacteria can be identified

alpha-hemolysins, inhibition by

optochin, bile solubility serological tests.


120

Not optochin sensitive

optochin sensitive

Identification

Pneumococcal Pneumonia

Symptoms Fever breathing difficulty chest pain rust-colored sputum.

A vaccine consists of purified capsular material from 23 serotypes of S. pneumoniae.


Stages of pathogenesis Encounter - humans only, by respiratory

droplet

Entry - colonization of the oropharynx, aspiration into lung (pneumonia)

Spread (extracellular) Pneumonia - blood culture can be positive Meningitis - penetration of mucous membrane Otitis media- eustachian tube to middle ear

Multiplication Grows well in serous fluid in alveoli space

Evade defenses Capsule--antiphagocytic sIgA protease

Haemophilus Influenzae Pneumonia

Gram-negative coccobacillus Alcoholism, poor nutrition, cancer, or

diabetes are predisposing factors. Second-generation cephalosporins


Mycoplasmal Pneumonia

Mycoplasma pneumoniae causes mycoplasmal pneumonia; it is an endemic disease.

Young adults and children Symptoms persist for 3 weeks and

longer (low fever, cough and headaches)

PRIMARY ATYPICAL/ WALKING PNEUMONIA


Mycoplasmal Pneumonia

M. pneumoniae produces small “fried-egg” colonies after two weeks’ incubation on enriched media containing horse serum and yeast extract.

Diagnosis is by PCR or serological tests.


Atypical (walking) pneumonia Mycoplasma pneumonia

Lacks peptidoglycan --lactam resistant

Disease primarily in young adults Encounter - inhalation from human Entry - restricted to mucosal surface

Terminal adhesin protein (P1)

Multiplication - require sterols Damage

Inflammation Damage and desquamation of ciliated epithelium

Treatments Erythromycin, doxycycline, tetracyline

Model for mycoplasma pathogenesis in the lungs

Legionellosis

The disease is caused by the aerobic gram-negative rod Legionella pneumophila.

High fever 40.5C, cough and general pneumonia symptoms

The bacterium can grow in water, such as air-conditioning cooling towers, and then be disseminated in the air.


Legionnaire's disease/Pontiac Fever Legionella pneumophila

Gram-negative rod Stains irregularly Silver stain

Disease Pontiac Fever - flu-like in anyone (1968)

Fever muscular ache and cough(self limiting) Legionnaire's disease - pneumonia

Primarily in middle aged to older men who heavy smoker and drinker or chronically ill

1976 American Legion Convention in Philadelphia ( toll 182 cases/29 death)

L. pneumophila

Legionellosis

This pneumonia does not appear to be transmitted from person to person.

Bacterial culture, FA tests, and DNA probes are used for laboratory diagnosis.

Prevention : Copper Ionizing procedure Treatment : Erythromycin, some

macrolides like Azithromycin


Psittacosis (Ornithosis)

Chlamydophila psittaci – gram negative intracellular bacteria and is transmitted by contact with contaminated droppings and exudates of fowl.

Elementary bodies allow the bacteria to survive outside a host.

s/sx: fever, headache , chills, some with delirium and disorientation


Psittacosis (Ornithosis)

Commercial bird handlers are most susceptible to this disease.

The bacteria are isolated in embryonated eggs, mice, or cell culture; identification is based on FA staining.

Tx: Tetracycline


Chlamydial Pneumonia

Chlamydophila pneumoniae causes pneumonia; it is transmitted from person to person.

Atherosclerosis-deposition of fats on arteries

s/sx resemble mycoplasma pneumonia Tetracycline is used for treatment.


Q Fever

Obligately parasitic, intracellular Coxiella burnetii causes Q fever or X fever

The disease is usually transmitted to humans through unpasteurized milk or inhalation of aerosols in dairy barns, cattle tick bites

Laboratory diagnosis is made with the culture of bacteria in embryonated eggs or cell culture.


Q Fever

Wide range of clinical symptoms 60% asymptomatic s/sx: High fever, muscle ache, headache

and coughing Hepatitis and endocarditis (persist for

months) Tx: Doxycycline , Chloroquine


Melioidosis

Melioidosis, glanders disease (horses) caused by Burkholderia pseudomallei

transmitted by inhalation, ingestion, or through puncture wounds.

Symptoms include pneumonia, sepsis, and encephalitis.

Tx: Ceftazidime


Disease Symptoms

Streptococcal pharyngitis Pharyngitis and tonsillitis

Scarlet fever Rash and fever

Diphtheria Membrane across throat

Whooping cough Paroxysmal coughing

Tuberculosis Tubercles, weight loss, and coughing

Pneumococcal pneumonia Reddish lungs, fever

H. influenzae pneumonia Similar to pneumococcal pneumonia

Chamydial pneumonia Low fever, cough, and headache

Legionellosis Fever and cough


Disease Symptoms

Psittacosis Fever and headache

Q fever Chills and chest pain

Epiglottitis Inflamed, abscessed epiglottis

Melioidosis Delayed-onset pneumonia


Diagnostic

Gram-positive cocci

Catalase-positive Staphylococcus aureusBeta-hemolytic Streptococcus pyogenesAlpha-hemolytic S. pneumoniae


Gram-positive rods Not acid-fast Corynebacterium

diphtheriaeAcid-fast Mycobacterium

tuberculosis

Gram-negative cocci Moraxella catarrhalis


a. Streptococcus pneumoniae

b. Haemophilus influenzae -

c. Moraxella catarrhalis -

Gram-negative rodsAerobes

Coccobacilli Bordetella pertussisRods

Grow on nutrient agar Burkholderia pseudomalleiRequire special media Legionella pneumophila

Facultative anaerobesCoccobacilli Haemophilus influenzae

IntracellularElementary bodies Chlamydophila psittaciNo elementary bodies Coxiella burnetii

Wall-less Mycoplasma pneumoniae


Viral Pneumonia

A number of viruses can cause pneumonia as a complication of infections such as influenza.

The etiologies are not usually identified in a clinical laboratory because of the difficulty in isolating and identifying viruses.


Respiratory Syncytial Virus (RSV) RSV is the most common cause of

pneumonia in infants 2-6months Life threatening- tx Ribavirin and

Palizumab Coughing, wheezing last more than a

week, fever by bacterial infection


Influenza Hemagglutinin (H)

spikes used for attachment to host cells.

Neuraminidase (N) spikes used to release virus from cell.


Influenza Antigenic shift

Changes in H and N spikes Probably due to genetic recombination

between different strains infecting the same cell

Antigenic drift Mutations in genes encoding H or N spikes May involve only 1 amino acid. Allows virus to avoid mucosal IgA antibodies.


Influenza Serotypes A: Causes most epidemics, H3N2, H1N1,

H2N2

B: Moderate, local outbreaks C: Mild disease


Influenza

Deaths during epidemic - secondary bacterial infections.

Multivalent vaccines for the elderly and other high-risk groups.

Amantadine and rimantadine are effective prophylactic and curative drugs

Zanamivir and oseltamivir


152

SARS

Coronavirus Severe acute respiratory syndrome

IP: 2-7 days

MOT: respiratory droplet/person to person contact

153

RISK FACTORS

history of recent travel to China, Hong Kong, or Taiwan or close contact w/ ill persons with a hx of recent travel to such areas, OR

Is employed in an occupation at particular risk for SARS exposure, i.e. healthcare worker with direct patient contact or a worker in a laboratory that contains live SARS, OR

Is part of a cluster of cases of atypical pneumonia without an alternative diagnosis

154

SIGNS AND SYMPTOMS

fever, chills, rigors, myalgia, headache, diarrhea, sore throat, rhinorrhea

2-7 days after onset of illness - shortness of breath and/or dry cough

155

DIAGNOSIS

viral culture PCR serologic testing

Mgmt: supportive




Upper Respiratory System

Common cold Coronaviruses Sneezing, excessive nasal secretions, congestion

Lower Respiratory System

Viral pneumonia Several viruses Fever, shortness of breath, chest pains

Influenza Influenzavirus Chills, fever, headache, muscular pains

RSV Respiratorysyncytial virus

Coughing, wheezing

Amantadine is used to treat influenza. Palivizumab, for life-threatening RSV.


FUNGAL DISEASES OF THE LOWER RESPIRATORY SYSTEM Fungal spores are easily inhaled; they

may germinate in the lower respiratory tract.

The incidence of fungal diseases has been increasing in recent years.

The mycoses in the sections below can be treated with amphotericin B.


Histoplasmosis Histoplasma capsulatum, dimorphic

fungus


Histoplasmosis

Resembles Tuberculosis Histoplasma capsulatum causes a

subclinical respiratory infection that only occasionally progresses to a severe, generalized disease.


Histoplasmosis Transmitted by airborne conidia from soil and

thru bird droppings Diagnosis by culturing fungus Treatment: Amphotericin B or Itraconizole


Coccidioidomycosis Coccidioides immitis- dimorphic fungi


Coccidioidomycosis

Valley Fever or San Joaquin Fever s/sx- fever, coughing and weigth loss Most cases are subclinical, but when

there are predisposing factors such as fatigue and poor nutrition, a progressive disease resembling tuberculosis can result.


Coccidioidomycosis Transmitted by

airborne arthrospores

Diagnosis by serological tests or DNA probe

Treatment: Amphotericin B

Also Ketoconazole, Itraconazole


Pneumocystis Pneumonia Pneumocystis

jiroveci (P. carinii) is found in healthy human lungs.

Pneumonia occurs in newly infected infants and immunosuppressed individuals.

Treatment: Timethoprim-sulfamethoxazole Figure

24.22aMICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

Pneumocystis Pneumonia

P. jiroveci causes disease in immunosuppressed patients.

Site - lining of alveoli DOC Trimetophrim -Sulfamethoxazole


Pneumocystis


Blastomycosis Blastomyces dermatitidis, dimorphic fungus Found in soil Can cause extensive tissue destruction,

cutaneous lesions Treatment: Amphotericin B


Blastomycosis (North American Blastomycosis) The infection begins in the lungs and can

spread to cause extensive abscesses.


Other Fungi Involved in Respiratory Disease Opportunistic fungi can cause

respiratory disease in immunosuppressed hosts, especially when large numbers of spores are inhaled.


Mucor indicus

Opportunistic Fungi Involved in Respiratory Disease

Aspergillus Rhizopus Mucor

Figures 12.2b, 12.4MICROPARA- RESPIRATORY INFECTIONby Dr Sonnie Talavera

Health & Medicine

Respimicro [recovered]