AIRBORNE/ DROPLET-

BORNE DISEASES
• Some pathogenic microorganisms can be
transmitted through the air by tiny droplets or dust
particles that are invisible to the naked eye.
• The microbe-laden droplets or particles can be
inhaled by a healthy individual and cause an
infection.
 MODE OF TRANSMISSION OF
AIRBORNE PATHOGENS
Aerosols
• Refers to a spray of
small and large droplets
which may contain
microorganisms
• It can be generated from
human sources or
environmental sources
Aerosols Generated from Human Sources
• Microorganisms that can cause respiratory
infections occur in secretions from the nose and
throat of infected individuals
• When a person coughs or sneezes, an aerosol is
expelled
• The larger droplets can be inhaled by people nearby,
or settle onto clothing and other inanimate objects
• When inhaled, usually are trapped on the moist
mucus layer covering the surfaces of the nasal cavity
and nasopharynx
• The small droplets can also be inhaled directly, but
the water in these droplets tends to evaporate
quickly, leaving droplet nuclei
• Droplet nuclei that contain living microorganisms
can remain suspended in air for hours or days,
travel long distances, and serve as continuing
source of infection
• The smaller droplets
and droplet nuclei are
less likey to be
trapped in the
nasopharynx, they
may reach the alveoli
of the lungs and be
retained there
• Macrophages in the lungs can often destroy the
microorganisms that reach the lungs
• The likelihood that pathogens can be transmitted by
droplets or droplet nuclei is greatest when people
are crowded together
this increases the number of microorganisms
expelled into air in a confined space
Aerosols Generated from Environmental Sources:
• Some human infections result from the airborne
transmission of microorganisms an environmental
source rather than from infected persons
Example:
• Legionnaire's disease
attributed to aerosol generated from the
contaminated water of air-conditioning system, and
from mist sprays used in grocery stores to keep the
vegetables fresh
Infectious Dust
• Dust containing pathogenic microorganisms
• Infectious dust may arise from human or
environmental sources
Infectious Dust Generated from Human Sources
• When a person sneezes or coughs, the large
aerosol droplets that are expelled settle on the
surfaces such as bedclothes or floor, where they
evaporate and leave a residue
• Nasal or throat secretions on a handkerchief
eventually dry, leaving a residue of mateerial
• Disturbance of these residues can generate dust
particles that may add pathogenic microorganisms
to the circulating air
• Dust-borne spread of infection is enhanced when
people move about in poorly ventilated areas
• Some pathogenic microorganisms are able to
survive for relatively long periods in dust
Infectious Dust Generated from Environmental
Sources
• Some airborne pathogens inhabit soil and are not
transmitted from person to person; instead they are
transmitted by inhaling dust arising from this soil
• Example is the fungus that causes histoplasmosis
 AAIRBORNE DISEASES CAUSED BY
BACTERIA
Streptococcal Pharyngitis
and Related
Streptococcal Diseases
• Commonly called
streptococcal sore
throat
• It is characterized by
acute inflammation of
the pharynx
• If a red skin rashes accompanes the pharyngitis,
the disease is known as scarlet fever
Causative Agent:
• Streptococcus pyrogenes (Lancefield group A)
• Causes over 90 percent of human streptococcal
infections including:
pharyngitis/scarlet fever
rheumatoid arthritis
erysipelas
impetigo contagipsum
poststreptococcal glomerulonephritis
Transmission:
• Humans are the natural reservoir of S. pyrogenes
• The organisms are carried in the nasopharynx and
are spread primarily by sneezing and coughing
• S. pyrogenes may survive for several weeks in
mucoid material expelled from the throat
Pathogenicity:
• S. pyrogenes produces a number of substances
that contribute to its infective ability:
1. The M protein of the cell wall is important because
a) it is responsible for attachment of the streptococci
to the cells of the throat
b) it is antiphagocytic
2. Stretolysin O (SLO)
a streptococcal toxin that is inactivated by oxygen
(hence the “O” in its name)
• It has the ability to kill cells by inserting its crescent
or horseshoe-shaped polymers into cell
membranes, thereby forming small holes that allow
cell contents to leak out
• SLO act mainly as a leucocidin, killing host
phagocytes
Streptolysin S
a streptococcal toxin that is oxygen-stable (hence
the “S” in its name)
• It kills leucocytes in the same manner as SLO
• It is also a hemolysin that can ß-hemolysin on
aerobically in incubated blood-agar plates
3. Some strain of S. pyrogenes produce an
erythrogenic toxin, which causes the red skin rash
characteristic of scarlet fever
• Only strain of S. pyrogenes that harbor a particular
type of bacteriophage can produce the erythrogenic
toxin
• Streptococcal pharyngitis is characterized by:
fever
enlargement of lymph nodes of the neck
red, raw, and often bleeding throat surface
• Scarlet fever is similar but is accompanied by a skin
rash that may extend to all parts of the body
appearing on the first or second day after onset of the
infection
• Both can give rise to various complications
following the primary infection such as:
Otitis media
Mastoiditis
Sinusitis
Pneumonia
Rheumatic fever
• Characterized by:
inflammation of the joints
involuntary jerking movements
pea-sized nodules that develop beneath the skin
reddened areas with raised edges on the skin
degeneration of heart valve
Acute poststreptococcal glomerulonephritis (AGN)
• Also called Bright's disease
a kidney disease that may occur within 1-3 weeks
after S. pyrogenes pharyngitis
• It is an inflammation rather than infection (probably
due to immunilogical cause)
• Sign of kidney damage is hematuria
Erysipelas
a skin infection
caused by S.
pyrogenes
• The skin becomes
bright-red and
swollen, especially on
the face or legs
Impetigo contagiosum
• The S. pyrogenes involved
usually are not those that
can cause pharyngitis
• Pus-filled blisters appear
most commonly on the
face and hands but may
cover the body
• They eventually develop
thick crust
• Can be transmitted by
direct contact
Puerperal fever
a stretococcal infection associated with chilbirth
it is an infection of the uterus of the mother and is a
serious and often fatal disease
• The streptococci may come from:
the patient's respiratory, genital, or
from the skin or hands of the patient or her
attendants
Laboratory Diagnosis:
• An accurate diagnosis cannot be made from clinical
information alone
• Laboratory data are required through:
isolation of microorganism and identifying it as
belonging to Lancefield group A
group A antigen directly from material on a swab of
the inflamed area through ELISA test
Treatment and Prevention:
• Penicillin is usually used since no penicillin-
resistant strains of S pyrogenes have been found
• Erythromycin is used for patients who are allergic
to penicillin
• Antibiotic treatment should be continued for some
days after the symptoms have subsided to ensure
complete elimination of the streptococci
• Chemoprophylaxis is advisable for at least 5 years
after a patient has had rheumatic fever, to prevent
recurrences
 Tuberculosis
• A slowly progressive disease of humans that often
becomes well-established before symptoms
become apparent
Causative Agents:
• Mycobacterium
tuberculosis and
Mycobacterium bovis
• The cells of M.
tuberculosis and M.
bovis are slender,
straight or curved
rods, and, like other
mycobacteria, they
exhibit acid-fast
staining
Mode of Transmission:
• M. tuberculosis is almost exclusively a prasite of
human and has airborne mode of transmission
• Usually cause pulmonary tuberculosis (lungs) but it
is capable of infecting any tissue or organ of the
body
• M. bovis is ingested rather than inhaled, causes
tuberculosis of body sites other than the lungs:
intestinal tract
lymph nodes
bones
joints
• It is a rarely found tuberculosis because of the
widespread use of milk pasteurization
• It is an important pathogen in places where raw milk
is consumed
Pathogenicity:
• PTB begins when M.
tuberculosis lodges
within the alveoli
• The bacteria are
rapidly engulfed by
macrophages but are
not destroyed, instead
they multiply slowly
within the phagocytes
• The first evidence of
infection is the
development of a
hypersensitivity to the
bacterial after about a
month through
tubercullin test
an extract of protein
from MTB is injected into
skin
a positive test is
indicated by a red,
swollen zone (weal) at
the site of injection
within 48 hours
• If a person who has been tubercullin-negative
becomes positive, it indicates that the person has
become infected during the interim
• Although such infection often remain subclinical,
the individual should be treated with appropriate
antibiotics to ensure that clinical TB does not
develop
• In untreated TB, antibody formation is ineffective
• The only effective type of immunity is cell-mediated
immunity
develops in the infected individual, specif T
lymphocytes migrate toward the bacilli lodged in
the lungs
upon contact, these these lymphocutes release
soluble substances that attract macrophages to the
area and activate them causing increase amounts of
hydrolytic enzymes and other antibacterial
substances
after engulfing the mycobacteria, the macrophages
are able to halt the intracellular growth of the
bacteria but do not kill them (bacteriostatic)
• Eventually a small, pearl-gray nodule (tubercle)
forms
consist of mycobacteria surrounded by several
concentric layers of macrophages and an outer
layer of lymphocytes
• The MTB usually become dormant within the
tubercle and the infection remains subclinical
• Tubercullin test will continue to give positive results
• If the cell-mediated action does not develop
strongly to stop the multiplication of the MTB
the initial tubercle becomes larger and and more
tubercle develops

macrophages and lung tissues inside the enlarged
tubercle begin to die because of toxic lipids from
MTB or lack of oxygen circulation

they then fused together to form a cheeselike mass of
dead tissue

several tubercles merge to form an area large enough
to be seen on a chest x-ray

as the area of dead tissue expands, it may erode the
wall of the bronchus

the acid-fast bacilli begin to appear in the sputum with
hemoptysis

• As the disease progresses, the patient exhibits:
loss of appetite
fatigue
weight loss
night sweats
persistent worsening cough
• If able to access to the bloodstream, bacilli will be
transported to the various parts of the body causing
numerous tubercle to develop at these sites
• Death ultimately results when sufficient damage has
occurred in the lungs or other vital organs
• Reactivation tuberculosis is most prevalent today
the dormant bacilli from an old subclinical primary
infection are no longer held in check by cell-
mediated immunity and begin to proliferate
• This form of disease occurs most often in the elderly
whose resistance has been lowered by:
malnutrition
alcoholism
other stresses
• It also occurs frequently in people with AIDS
Laboratory Diagnosis:
• A tentative diagnosis of PTB can be made by
detecting acid-fast bacilli in smears of sputum
• A definite diagnosis depends upon isolating the
bacilli from the patient and identifying them as MTB
Treatment and Prevention:
• Usually treated effectively by a combination of
antimcrobial agents
• Commonly used antibiotics in combination:
isoniazid
rifampicin
pyrazinamide
ethambutol
streptomycin
para-aminosalicylic acid
• Treatment must be extended ver a year or more
because of its chronicity and slow penetration of
the chemical agents into the tubercles
• BCG vaccine is used widely throughout the world to
prevent tuberculosis
it consist of live cells of an attenuated strain of M.
bovis that was isolated in 1908 by French
microbilogists Calmette and Guérin
• Injection of harmless BCG into a tubercullin-
negative individual induces cell-mediated immunity
against tuberculosis (60-80% effective)
• BCG is not used in the United States because:
the risk of MTB infection is very low
because the recepients become tubercullin-
positive, which prevents use of tubercullin test in
early detection of individuals infected with MTB
 Legionnaires' Disease
• First described in 1976 after an outbreak of illness
at an American Legion convention in Philadelphia
• 182 persons were affected, and 29 of those died
• The cause of the outbreak remained a mystery for
months
• Microbiologist in CDC in Atlanta were able to isolate
and identify the microorganism
a small-rod shape microorganism
Causative Agent:
• Legionella
pneumophila
• More than 20 species
of Legionella has been
described and all are
pathogenic
• The best known is L.
pneumophila
aerobic Gram-negative
rod-shaped bacilli that
require amino acid
cysteine for growth
Mode of Transmission:
• It does not seem to be transmitted from person to
peron
• Humans probably acquire the organism by inhaling
aerosols generated from:
contaminated water of lakes and reservoir
contaminated water of air-conditioning cooling-
towers and condensers
contaminated shower heads and pipes of hot water
plumbing system (especially in “dead-end” system)
Pathogenicity:
• L. pneumophila can cause 2 kinds of disease:
1. Legionnaires' disease
• A severe pneumonia characterized by fever, chills,
and a dry cough
• Sometimes it is associated with:
chest pain
abdominal pain
vomiting
diarrhea
mental confusion
• The disease tends to occur most frequently in men
above the age of 50
• The fatality rate in untreated cases is 15% or higher
2. Pontiac fever
• Named after the outbreak that occurred in Pontiac,
Michigan
• It is a milder, nonfatal disease characterized by:
fever
chills
headache
dry cough
muscle pain
• This disease is self-limiting and complete recovery
without treatment occurs within a week
Laboratory Diagnosis:
• The definitive diagnosis is to isolate the bacterium
from the respiratory secretions
• Identification of the isolate as Legionella is based
mainly on its requirement for cysteine
• Flourescent antibody staining can be used to
quickly detect the bacteria in the clinical specimens
from the patient
however this method is less sensitive than the
culture method
Treatment and Prevention:
• Erythromycin is the antibiotic of choice for treatment of
Legionaires' disease
• No vaccine is available
• To eliminate Legionella bacteria from institutional
water systems:
the level of chlorination of of water supplies should be
increased
dead ends in the plumbing system should be
eliminated
hot water tanks should be heated to at least 70ºC for
72 hours
Other Airborne Diseases Caused
by Bacteria
 Pneumococcal Pneumonia
Causative Agent:
• Streptococcus pneumoniae
Gram-positive cocci in pairs, surrounded by
polysaccharide capsule that resist phagocytosis
• 84 capsular serotypes exist
• Colonies are ą-hemolytic on blood agar plate with
methylene blue
Pathogenicity:
• The major cause of bacterial pneumonia
• Fatality rate is higher in persons age 65 or older
• Symptoms include chills, fever, and chest pain
• Air sacs of the lungs fill with fluid in which
pnemoococci multiply
• Neutrophils attempt to engulf the cocci but often
hindered by the antiphagocytic bacterial capsule
• Cells make pneumolysin O
an oxygen-labile hemolysin that damages host-cell
membranes
• From the lungs the cocci may invade the
bloodstream
Treatment and Prevention:
• Penicillin is usually effective but some
pneumococcus strains are resistant to it
• A vaccine is available and consists of the purified
capsular material from 23 most frequent serotype
• Given mainly to elderly person
 Diptheria
Causative Agent:
• Corynebacterium diptheriae
• Gram-negative rods, often arranged in parallel like a
picket fence
• The cell contains metachromatic granules when
stained with methylene blue
Pathogenicity:
• Causes a localize throat infection
makes a powerful exotoxin that kills throat tissue
cells and causes and exudates to form that can
block the trachea and causes the patient to
suffocate
• The toxin also circulates in the blood and can kill the
patient by damaging the:
kidneys
nerves
especially the heart
Treatment and Prevention:
• Antitoxin is administered to neutralize the toxin
• Vaccination in infants has reduced the incidence of
diptheria dramatically
• The vaccine consists of toxoid made from diptheria
exotoxin
 Pertussis (Whooping cough)
Causative Agent:
• Bordetella pertusis
• Short Gram-negative rods
Pathogenicity:
• Bacteria attach to the surface tissue of bronchi and
cause a localized infection
• The patient develops a severe cough that ends with
a “crowing” sound, or whoop
• The coughing may be accompanied by:
vomiting
lack of oxygen in the blood
hemorrhages in the eyes, nose, and brain
Deafness and other permanent damage may occur
Traetment and Prevention:
• Erythromycin is the antibiotic of choice
• Vaccination of infants and children has generally
reduced the incidence of the disease
• The vaccine consists of killed cells B. pertussis
 Haemophilus Meningitis
Causative Agent:
• Haemophilus influenzae
Gram-negative rod that requires heme and nicotinamide
adenine dinucleotide (NAD) to grow
• Cells have a polysaccharide capsule that resist
phagocytosis
• Six capsular serotypes exist
serotype B causes nearly all cases of Haemophilus
meningitis among children
Pathogenicity:
• Haemophilus meningitis is the most frequent kind of
meningitis in children between 6 weeks and 2 years
of age
• Fatality rate in untreated cases is 90-100%
• The organisms initially grow in the nasopharynx
• An endotoxin probably helps to damage the surface
tissue, and the bacteria penetrate to reach the
underlying blood vessels
• The bacteria are then transported by the blood to the
meninges where the cause a severe inflammation
Cardinal Signs:
• Infection
fever, chills, malaise
• Increased intracranial pressure ( ICP)
headache
vomiting (projectile)
papilledema (rare)
Signs of Meningeal irritation:
• Nuchal rigidity
• (+) Brudzinki's and Kernig's signs
• Exaggerated and symmetrical DTR
• Brudzinki's Sign
Kernig's sign
• (after Waldemar Kernig
(1840–1917), a Russian
neurologist) is positive
when the thigh is flexed
at the hip and knee at 90
degree angles, and
subsequent extension in
the knee is painful
(leading to resistance).
• This may indicate
subarachnoid
hemorrhage or
meningitis.
• Opisthotonos
a spasm in
which the back
and extremities
arc backward so
that the body rest
on the head and
heels
Treatment and Prevention:
• Combination of ampicillin and chloramphenicol is
used for treatment
• A vaccine (HIB) is available and consists of purified
capsular polysacharide of serotype b
 Meningococcal Meningitis
Causative Agent:
• Neisseria meningitidis
Gram-negative cocci in pairs
• A polysaccharide capsule
occurs and inhibits
phagocytosis during
infection
• Serotype are based on type
capsule
A, B, C, and Y are the most
common
Pathogenicity:
• The bacteria can be harbored in the nasopharynx
without causing a disease;
• However, they may gain access to the blood stream
and be carried to the meninges, where they cause a
severe inflammation
• Patients have:
headache
fever
pain in the neck and
back
loss of alertness
sometimes skin rash
• Death can occur within
24 hours
Treatment and Prevention:
• Penicillin is the antibiotic of choice
• A vaccine is available consisting of the capsular
polysaccharide from serotypes A, C, Y, and W135
• No vaccine is available against serotype B
Airborne Diseases Caused By Viruses
 Common Cold
• A mild infection of the
upper respiratory tract
• The most prevalent
infectious disease of
humans and is
worldwide in its
distribution
Causative Agent:
• Rhinoviruses (from the Greek word rhis, “nose”)
it consist of icosahedral protein capsid which
encloses single-strand RNA
• It grow best at temperature of 33ºC instead of body
temperature of 37ºC
helps to explain why rhinoviruses are restricted to
the respiratory tract and do not invade internal
organs
• At present, there are at least 115 serotypes of
rhinoviruses
• immunity against one type does not prevent
infection by another type
Coronaviruses
• So named because large particlws of glycoprotein
project from the surface of the virions, giving the
appearance of a crown (corona)
• Have a helical nucleocapsid composed of protein
and single-stranded RNA;
• The nucleocapsid is surrounded by a lipid envelope
• Have only 2 antigenic types
• Immunity developed in response to a coronavirus
infection is relatively short-lived (1 year)
Mode of Transmission:
• The main cold-causing
viruses (rhinovirus) are
shed in high
concentration in nasal
secretions and can be
spread by aerosol
• However their main MOT
appears to be through
hand-to-hand
transmission
• Person suffering
from a cold should
wash his hands
frequently with soap
and water, especially
after disposing of
handkerchiefs
contaminated with
nasal secretions
Pathogenicity:
• Viral multiplication
occurs in the cells lining
the surface of the nasal
passages and pharynx
• Incubation period: 12 to
72 hours
cold develop as an
acute infection of the
nose, throat, sinuses,
trachea and bronchi
lasting approximately 2
to 7 days
• Symptoms include:
nasal discharge
nasal congestion
sneezing
coughing
sore or ithcy throat
hoarseness
sometimes slight
fever
• During the acute phase, large amounts of virus
appear in the nasal secretions
• Although it is a mild infection, it may affect a
patient's normal resistance to bacterial invasion of
the sinuses and the middle ear
Laboratory Diagnosis,
Treatment and Prevention:
• Usually diagnosed by its
symptoms rather than laboratory
methods
• There is no specific treatment
only supportive measures such
as:
adequate rest
warm clothing
aspirin
liberal intake of fluids
• Antibiotic has no place in the treatment for
uncomplicated cases
 Influenza
• It is common for influenza to occur as an epidemic
• Epidemic influenza or “flu” is one of the most
familiar example of airborne infection
• There are 3 antigenic types of the influenza virus:
A, B, and C
• Type A influenza commonly cause epidemics
Causative Agent:
• Influenza viruses have a core
of single-stranded RNA
contained within a helical
capsid
• The capsid is wound up to form
a rounded mass and is covered
by a lipid envelope from which
protein spikes project (H
protein)
hemaglutinins (H protein) allow
attachment of the virus to red
cells and other host cells
• It also has another
projections composed
of neuraminidase (N
protein)
this enzyme can
degrade the protective
mucus layers of mucous
membrane, allowing
attachment of the virus
to the undelying tissues
• Influenza A can be classified into subtypes on the
basis of H protein and N protein
13 major types of H proteins (H1- H13) but only 3
have been identified
9 types N protein (N1 - N9); only 2 have been
identified
• H and N protein can occur in different combination
to yield various types of influenza A viruses
Example:
• The strain that
caused the worlwide
human “Asian flu”
epidemic in 1957 was
the A(H2N2) subtype
• The strain that
caused the “Hong
Kong flu” epidemic in
1968 was of A(H3N2)
subtype
• Recovery from influenza will confer a degree of
active natural immunity
• However, antibodies formed from by a host
population against one antigenic subtype of
influenza A do not protect against other subtypes
which may develop by mutation
Mode of Transmission:
• Large amount of
influenza virus are
present in the respiratory
secretions of infected
patients
• It can be transmitted by
aerosols and fomites
Fomites:
• inanimate objects that harbor pathogenic
microorganism
• A single infected person can transmit the virus to a
large number of susceptible persons, accounting to
the “explosive” nature of epidemics
Laboratory Diagnosis:
• Inoculation into culture of specimens from
respiratory secretions and nasal and throat swabs
Pathogenicity:
• Viral multiplication is usually restricted to the
tissues in the respiratory tract
• The death and sloughing of the linings of the
mucous membrane may be responsible for many of
the symptoms:
nasal congestion
increased respiratory secretions
• Influenza is
characterized by:
clear nasal discharge
fever and chills
headache
muscle pain
sore throat
coughing
marked weakness and
exhaustion (fatigue
and body malaise)
• Patient with influenza, body temperature usually
rises rapidly to 100 to 104ºF (37.8 - 41ºC) within 12
hours of the onset of symptoms
common cold is accompanied with slight fever only
• Fever usually lasts 3 days, but it can persist for up
to 8 days
• Influenza causes a decreased resistance to infection
by other microbial pathogens, and there is tendency
to develop a secondary pneumonia caused by
bacteria
• Many deaths attributed to influenza are due to
secondary infections
Treatment and Prevetion:
Uncomplicated cases:
• Supportive measures such as bed rest
• Amantidine:
can only shorten the duration of influenza up to
50%, but it can not cure
• Active immunization with vaccine consisting of
formaldehyde-inactivated strain is presently the
most effective prevention
• Live attenuated influenza virus vaccine is usually
75% effective
have greater immunogenic properties
based on previous year's virus
made from chicken embryos and must not be given
to people hypersensitive to eggs, feathers, or
chicken
it is not recommended to pregnant women during
first trimester (although not proven harmful to the
fetus)
• Maximum protection requires annual immunization, since
the protective immunity lasts only 3 - 6 months
• It is particularly important that high-risk individuals receive
immunization before the beginning of the “flu season”
each year:
elderly
health workers
 Varicella (Chickenpox)
Causative Agent:
• A common, acute, and highly contagious infection
caused by the herpesvirus varicella zoster (V-Z)
• The same virus that, in latent stage, causes herpes
zoster (Shingles)
• It can occur at any age, but it's most common in 2-8
years old
Mode of Transmission:
• Chickenpox is transmitted by direct contact
(primarily with resoiratory secretion; less often with
skin lesions) and indirect contact through the air
• Incubation period: 14-17 days
• It is probably communicable from 1 day before the
lesions erupt to 6 days after vesicles form
• most contagious in the early stage of eruption of
skin lesions
Pathogenicity:
• The virus multiplies in
the respiratory tract
and regional lymph
nodes, reaches the
blood and spreads to
all parts of the body
• Most children recover completely
• Potentially fatal complications may affect children
receiving corticosteroids, immunosuppressant
agents, those with leukemia, other neoplasm, or
immunodeficiency disorders
Prodromal Phase
• Patient has slight fever, body malaise, and anorexia
• Within 24 hours:
the rash begins as crops of small, erythematous
macule on trunk or scalp that progress to papules

then clear vesicles on an erythematous base (the so-
called “dewdrop on a rose petal”)

the vesicles become cloudy and break easily, then
scabs form
• The rash spreads to the
face and, rarely to the
extrmities
• New vesicles continue to
appear for 3-4 days, so
the rash contains a
combination of red
papules, vesicles, and
scabs in various stages
• Occasionally, it also produces shallow ulcers on the
mouth, conjunctivae, and genitalia
• Severe pruritus with this rash may provoke
persistent scratching, which can lead to infection,
scarring, impetigo, furuncles, and cellulitis
Herpes-Zoster (Shingles)
Variola (Small pox)
Laboratory Diagnosis:
• Diagnosed by characteristic clinical signs and
usually does not require laboratory tests
• However, the virus can be isolated from vesicular
fluid within the first 3 - 4 days of the rash
• Giemsa stain distinguishes V-Z from vaccinia-
variola viruses
• Serum contains antibodies 7 days after onset
Treatment and Prevention:
• Patient must remainin strict isolationuntil all the
vesicles and most of the scabs disappear
usually for 1 week after the onset of the rash
• Children can go back to school, however, if just a
few scabs remain because at this stage chickenpox
is no longer contagious
• Congenital chickenpox requires no isolation
• Genrally, treatment consists of the following:
local or systemic antipruritus
cool bicarbonate of soda baths
calamine lotion
diphenhydramine or another antihistamine
antibiotics if bacterial infection develops
• Salicylates are contraindicated because of their link
to Reye's syndrome
• Susceptible children may need special treatment
• Varicella-zoster immune
globulin when given up
to 72 hours after
exposure to varicella
may provide passive
immunity
• Acyclovir may:
slow vesicle formation
speed skin healing
control the systemic
spread of infection
 Rubeola (Measles)
Causative Agent:
• Rubeola virus, a paramyxovirus
• Also known as measles or morbili, is an acute,
highly contagious paramyxovirus infection
• It is one of the most common and the most serious
of all childhood diseases
Mode of Transmission:
• Measles is spread by direct contact or by
contaminated airborne respiratory droplets
• The portal of entry is the upper respiratory tract
Pathogenicity:
• The virus multiplies in the respiratory and in the
conjunctiva in the eye in the early course of the
disease
• It is then disseminated by the blood to the intestinal
tract, urinary tract, skin, and CNS
• Incubation period: 8 - 14 days
Prodromal Phase:
• Beginning about 11 days after exposure to the virus
• This pahse lasts from 4 - 5 days
• Initial symptoms begin and greatest communicability
occurs:
fever
photophobia
malaise
anorexia
conjunctivitis
coryza
hoarseness and hacking cough
• At the end of the
prodrome, Koplik's
spots (hallmark of
measles) appear
these spots look like
tiny, bluish gray
specks surrounded by
red halo
they appear on the
oral mucosa opposite
to the molars and
ocassionally bleed
• About 5 days after Koplik's spot appear:
temperature rises sharply
spots slough off
a slightly pruritic rash appear
• This characteristic rash starts as faint macules
behind the ears and on the neck and cheeks
• These macule become papular and erythematous,
rapidly spreading over the entire face  neck 
eyelids  arms  chest  back and abdomen 
thighs
• When these rash reach the feet (2 to 3 days later), it
begins to fade in the same sequence it appeared,
leaving a brownish discoloration that disappears in
7 - 10 days
• The disease climax occurs 2 - 3 days after the rash
appears and is marked by:
temperature of 103º F to 105º F (39.4º to 40.6º C)
severe cough
rhinorrhea
puffy, red eyes
• About 5 days after the rash appears, other
symptoms disappear and communicability ends
Laboratory Diagnosis:
• Measles reults into distinctive clinical features,
especially the pathognomonic Koplik's spots
• Mild measles may resemble:
rubella
roseola infantum
enterovirus infection
toxoplasmosis
drug eruption
• Lab tests are required for a differential diagnosis
• If necessary, measles virus may be isolated from
the blood, nasopharyngeal secretions and urine
during the febrile period
• Serum antibodies appear within 3 days after the
onset of the rash and reach peak titers 2 and 4
weeks later
Treatment and Prevention:
• Therapy consist of:
bed rest and EOF
relief of symptoms
respiratory isolation throughout the communicable
period
vaporizers and warm environment help reduce
respiratory irritation
antipyretics and TSB to reduce fever
• Prevention: immunization of AMV
 Rubella (German Measles)
Causative Agent:
• Rubella virus, a togavirus
Pathogenicity:
• Rubella is a highly contagious but mild disease
unrelated to common measles (rubeola)
• After initial multiplication in the URT, the virus
becomes distributed by the blood to the lymph
nodes and joints
Symptoms:
fever
swollen lymph
nodes
maculopapular rash
that spreads rapidly,
often covering the
trunk and
extremities within
hours
• Small red, petechial
macules on the soft palate
(Forschheimer spots) may
precede or accompany rash
• By the end of the 2nd day,
the facial rash begins to
fade
• The rash generally
disappears on the 3rd day
• The rapid appearance and
disappearance of the
rubella rash distinguish it
from rubeola