Other Diseases.pptx

7/27/2019 Other Diseases.pptx

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Hepatitis A

Symptoms

Fatigue

Fever

Loss of appetite

Nausea

Right side abdominal

pain

Dark colored urine

and clay colored

feces

Jaundice

Symptoms

Children less than 6

years old are generally

asymptomatic

Nearly 70%

Jaundice most common

20% of adults require

hospitalization

Full recovery in about 2

months

Formally called

infectious hepatitis


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Hepatitis A

Pathogenesis

Transmission from

ingestion of

contaminated food or

water

Ingested virus reaches

liver by unknown route

Liver main site of viral

replication Only tissue know to be

damaged

Virus is released into

bile Virus laden bile eliminated

Epidemiology

Spreads via fecal-oral route

Many outbreaks originated

from restaurants

Due to infected food handler

Raw shellfish frequent source

of infection

Low socioeconomic groups

make up high percentage of

infected High risk groups include

people in day care and nursing

homes and homosexual men


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Hepatitis A

Causative Agent

Hepatitis A virus (HAV)

Small

Single stranded RNAgenome

Belongs to picornavirus

family

Given namehepatovirus

Only one serotype

Makes good target for

vaccine

Prevention and Treatment Vaccine available since 1995

Indicated for travelers todeprived regions,homosexual men, sewer

workers, and healthcareworkers

Gamma globulin containsHAV antibody, can be givento individuals that have beenexposed

Afford short term protection ifgiven within 2 weeks ofexposure


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Hepatitis B

Symptoms

Similar to hepatitis A

Symptoms for hepatitis B more

severe

Causes death in 1% to 10% ofhospitalized cases

Formerly known as serum

hepatitis

Causative Agent Hepatitis B virus (HBV)

Double stranded DNAgenome

Enveloped Part of the hepadnavirus

family

Virus contains 3 importantHBV antigens

HBsAgo Surface antigen

HBcAg

o Core antigen

HBeAg e antigen


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Hepatitis B Pathogenesis

HBV carried in liver

Mechanism of liver damageunknown Damage most likely results from immune

response

Virus replicates via reversetranscriptase Viral DNA transported to host nucleus

Host mRNA makes RNA copy RNA copy transcribed by viral reverse

transcriptase

New DNA copy is genome for new virus

New viruses bud from host cell


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Hepatitis B

Epidemiology

Progressive rise in

reported cases between

1965 and 1985

Incidence appears to have

plateaued

HBV spread mainly by

blood, blood products,

and semen Carriers are of major

importance

Often unaware of infection

Epidemiology

Risk factors for infection

include

Sharing needles

Tattooing and piercing with

contaminated instruments

Shared toothbrushes,

razors, and towels

Sexual intercourseresponsible for nearly

50% of cases in United

States


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Hepatitis B

Prevention and Treatment Vaccine approved in 1980s

New more effective vaccine available since 1986

Vaccination against HBV can help prevent liver cancer

caused by the virus Passive immunization with HBIG (hepatitis B

immune globulin) offers immediate protection

No curative treatment


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Hepatitis C

Symptoms Same as hepatitis A

and hepatitis B

Generally milder

65% are asymptomatic 25% have jaundice

Causative Agent Hepatitis C virus

Enveloped

Single stranded RNA

genome Member of flavivirus

family

Considerable genetic

variability

Virus divided intotype and subtype


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Hepatitis C Pathogenesis

Few details known

Infection transmitted via contact with infected blood

Incubation period average 6 weeks

Over 80% develop chronic infections

Virus infects the liver

Incites inflammatory and immune responses

Disease comes and goes

Individuals have times of near normalcy

10% to 20% will develop cirrhosis or liver cancer


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Hepatitis C

Epidemiology Mechanism of exposure not

always obvious

Risk factors include

Sharing toothbrush, razors,

towels Tattooing and piercing with

unclean instrument

Sharing syringes

60% of US cases due to sharing

needles

Transmission via intercoursemost likely rare

Can occur if multiple partners

Prevention and Treatment

No vaccine for HCV

Vaccination against A and B

seem to give some

protection

Avoidance of alcohol tolimit effect on liver

No satisfactory treatment

Some are helped by

interferon therapy

Often has undesirable

side effects

Interferon usually

combined with ribavirin


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AIRBORNE DISEASES


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Mumps

Acute viral illness

Preferentially attacks salivary

and parotid gland

Formerly common in United

States Now rare due to

immunization

Causative Agent

Mumps virus

Member of the paramyxovirus

family

Enveloped

Single stranded RNA genome


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Mumps Symptoms

Early symptoms Fever with loss of appetite and headache

Later symptoms Painful swelling of one or both parotid glands and spasms

Usually makes it difficult to chew and swallow

Symptoms disappear in about a week Symptoms much more severe in individuals past

puberty Post-pubertal males can suffer painful swelling of testicles

Ovarian involvement occurs in about 20% of cases

Pregnant women often miscarry


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Mumps

Pathogenesis Transmitted by inhalation of infected droplets

Long incubation period 15 to 20 days

Virus reproduces in the upper respiratory tract Virus spreads throughout body via bloodstream

Produces symptoms after infecting tissues

In salivary glands Virus multiplies in epithelium of salivary ducts

Destroys epithelium and releases virus into saliva

Inflammation produced

Inflammation responsible for symptoms and pain


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Mumps

Epidemiology Humans only natural host

Natural infection conferslifelong immunity

Virus is spread byasymptomatic individuals inhigh numbers

Virus can be present insaliva of symptomaticpersons Virus may be present for up to

a week before symptomsappear to 2 weeks after

Prevention andTreatment Prevention directed at

immunization Usually given in same

injection as measles andrubella

MMR

Immunization prevents

latent recurrentinfections

Due to only one viralserotype

No effective antiviraltreatment


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Diphtheria

Symptoms

Usually begins with mild sore throat and slight fever,

fatigue and malaise and dramatic neck swelling

Whitish membrane forms on tonsils, or in nasal cavity Most strains release diphtheria toxin

Production of toxin requires lysogenic conversion of

causative agent

Toxin is produced in low iron environments High iron repressor shuts down toxin production

Low iron repressor removed, toxin production begins


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Diphtheria

Causative Agent

Corynebacterium

diphtheria

Variably shaped Gram-positive

Non-spore forming

Certain strains produce

diphtheria toxin


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Diphtheria

Pathogenesis

Little invasive ability

Exotoxin released into bloodstream

Results in damage to heart, nerves and kidneys

Diphtheria toxin

Released from bacteria in inactive form

Cleaved into A and B chains

B attaches to host cell membrane and enters

through endocytosis A chain becomes active enzyme that inhibits

proteins synthesis

Small amount of enzyme inactivates large

population of cells which explains potency


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Diphtheria

Epidemiology Humans are primary reservoir

Spread by air

Acquired through inhalation

Sources of infection include Carriers who recovered from infection

Asymptomatic cases

People with active disease

Contaminated fomites Bacterium can be carried in chronic skin ulcer

Cutaneous diphtheria


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Diphtheria Prevention

Disease results primarilyfrom toxin absorption

Not microbial invasion

Prevention directed at

immunization DPT - Neutralize toxin

Immunity wanes afterchildhood

Booster immunizationshould be given every 10

years

Treatment Effectiveness depends on

early antiserum treatment

Delay in treatment may befatal

Antibiotics are given toeliminate bacteria

Penicillin and erythromycin

Stops transmission ofdisease

No effect on absorbed toxin

Even in presence oftreatment 1 in 10 patients die


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Pneumococcal Pneumonia

Symptoms

Cough - Fever

Chest pain - Sputum production

Runny nose and upper respiratory congestion precedeabove symptoms

Chest pain is aggravated with each breath and by

cough

Resulting pain causes breathing to become shallow and rapid

Causes skin to become dusky colored due to poor oxygenation

Symptoms abate in individuals who survive within 7 to

10 days without treatment


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Causative Agent

Streptococcus pnuemoniae

Gram-positive

Diplococci

Thick polysaccharide capsule

Capsule responsible for virulence

o 80 different types ofS.

pneumoniae based on

capsular antigen


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Pathogenesis

Infection develops when bacteria are inhaled into

alveoli

Causes inflammatory response in lung Bacterial capsule interferes with phagocytosis

Pneumococci that enter bloodstream are responsible

for three often fatal complications

Septicemia

Endocarditis

Meningitis

Recovery is usually complete

Most bacterial strains do not destroy lung tissue


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Epidemiology 30% of healthy individuals carry encapsulated strain

in their throat

Bacterial rarely reach lung due to mucociliary escalator

Risk of pneumonia rises when escalator is destroyed Underlying disease and age also increase risk of disease


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Prevention and Treatment Prevention is aided by vaccine

Gives immunity to 23 strains

Conjugate vaccine against 7 types is available for infants

Antibiotic treatment is generally successful if givenearly

Penicillin and erythromycin

More strains are becoming antibiotic resistant


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Klebsiella Pneumonia

Symptoms Most symptoms are undistinguishable from

pneumoncoccal pneumonia; they include

Cough

Fever Chest pain

Other symptoms include

Repeated chills

Red gelatinous sputum 50% to 80% mortality in untreated patients

These patients tend to die sooner than with other

pneumonia


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Causative Agent

Several species of

Klebsiella cause

pneumonia

Primary cause

Klebsiella pneumoniae

Gram-negative

Bacillus

Encapsulated


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Pathogenesis

Organism colonizes mouth and throat

Carried to the lung with inspired air or mucus

Survival in the lung is aided by capsule Interferes with phagocytosis

Specifically interfering with complement protein C3b

Organism causes tissue death

Leads to formation of lung abscess

Infection in bloodstream leads to abscess in other

tissues


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Epidemiology Part of the normal flora of the intestine in small

population

Colonization of mouth and throat is more common in

debilitated individuals Especially in institutional settings

Prevention and Treatment No specific prevention measures

Disinfect environment Make sure medical equipment in sterile

Use antimicrobials only when necessary Help to control antimicrobial resistance


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Mycoplasmal Pneumonia

Symptoms Onset is typically gradual First symptoms include

Fever, headache, musclepain, fatigue

Later symptoms are Dry cough and

mucoid sputum

Causative Agent

Mycoplasma pneumoniae Small Deformed bacterial lacking cell wall

Slow growing Aerobic Colonies have a distinctive fried egg appearance


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Pathogenesis Small infecting dose

Organism attaches to receptors on epithelium

Attachment interferes with ciliated cell action

Ciliated cells slough off

Inflammation initiates thickening of bronchial and

alveolar walls

Causes difficulty in breathing


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Epidemiology Bacterial are spread by aerosolized droplets from

respiratory secretions

Survive for long periods in secretions

Aids in transmissionAccounts for approximately one-fifth of bacterial

pneumonias

Peak incidence in young people

Immunity is not permanent


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Prevention and Treatment No practical prevention

Avoid crowding in schools and military facilities

Particularly dormitories and recruit barracks

Antibiotic treatment is successful Penicillins and other cell wall synthesis inhibitors are ineffectual

Antibiotics of choice are tetracycline and erythromycin

Must be given early

Both are bacteriostatic

o Will only inhibit growth, not kill organism


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Psittacosis (Ornithosis)

Comes from birds and fowl and the organism iscalled Chlamydophila psittacithat form

elementary bodies

It is a form of pneumonia that causes fever,

headache, and chills and if it affect the nervoussystem it leads to disorientation and delirium


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Chlamydial pneumonia

caused by Chlamydophila pneumoniae withclinical manifestations similar to mycoplasma

pneumonia and transmitted via the respiratory

route

Treated with tetracycline


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Whooping Cough

Symptoms Runny nose followed by bouts of uncontrollable

coughing

Termed paroxymal coughing

Severe cough can cause rupture of small blood vessels inthe eyes

Coughing spasm followed by characteristic whoop

Sound made by the forceful inspiration of air

Vomiting and seizure may occur


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Whooping Cough

Causative Agent

Bordetella pertussis

Small

Encapsulated

Strictly aerobic

Gram-negative

Bacillus

Does not survive long

periods outside the host


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Whooping Cough

Pathogenesis Enters respiratory tract with inspired air and attaches to

ciliated cells

Organism colonizes structures of the upper and lower

respiratory tract Mucus secretion increases which causes ciliary action

to decrease

Cough reflex is only mechanism for clearing secretions


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Whooping Cough

Pathogenesis

B. pertussis produces numerous toxic

products

Pertussis toxin - A-B toxin

B portion attaches to cell surface

A portion enters cell and inactivates

regulation of cAMP

o Causes increased mucus formation

o Decreases phagocytic killing

Invasive adenylate cyclase

Increases production of cAMP

Increased mucus formation


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Whooping Cough

Epidemiology Spreads via infected respiratory droplets

Most infectious during runny nose period

Number of organisms decrease with onset of cough

Classically disease of infants Milder forms are seen in older children and adults

Often overlooked a persistent cold

Fosters transmission


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Whooping Cough

Prevention

Directed at vaccination of

infants

Prevents disease in 70% of

individuals

Pertussis vaccine combined

with diphtheria and tetanus

toxoids (DPT)

Injections given at 6

weeks, 4,6,and 18 months

Treatment Erythromycin is

effective at reducing

symptoms if given

earlyAntibiotic usually

eliminates bacteria

from respiratory

secretions


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Tuberculosis

Symptoms Chronic illness

Symptoms include Slight fever with night sweats

Progressive weight loss Chronic productive cough

Sputum often bloodstreaked

Causative Agent Mycobacterium

tuberculosis

Gram-positive cell wall

type

Slender bacillus Acid fast due to mycolic

acid in cell wall

Slow growing

Generation time 12 hours

or more Resists most prevention

methods of control


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Tuberculosis

Pathogenesis

Usually contracted by inhalation of airborne organisms

Bacteria are taken up by pulmonary macrophages in the

lungs

Resists destruction within phagocyte

Organism prevents the fusion of phagosome with lysosomes;

allows multiplication in protected vacuole


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Tuberculosis

Pathogenesis Organisms are carried to lymph nodes

About 2 weeks post infection intense immune reactionoccurs Macrophages fuse together to make large multinucleated cell

Macrophages and lymphocytes surround large cell This is an effort to wall off infected tissue

Activated macrophages release into infected tissue Causes death of tissue resulting in formation of cheesy

material


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Tuberculosis

Epidemiology

Estimated 10 million

Americans infected

Rate highest among non-

white, elderly poor people

Small infecting dose

As little as ten inhaled

organisms

Factors important intransmission

Frequency of coughing,

adequacy of ventilation,

degree of crowding


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Tuberculosis

Epidemiology

Tuberculin test used to detect

those infected

Small amount of tuberculosis

antigen is injected under the skin

Injection site becomes red and

firm if infected

Positive test does not indicate

active disease


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Tuberculosis

Prevention Vaccination for

tuberculosis widely usedin many parts of the world

Vaccine known as Bacillusof Calmette and Gurin

BCG derived frommycobacterium bovis

Gives partial immunityagainst tuberculosis

Vaccine not given inUnited States because it

eliminates use oftuberculin test asdiagnostic tool

Treatment Antibiotic treatment is given in

cases of active tuberculosis

Two or more medications aregiven together to reduce potential

antimicrobial resistance Antimicrobials include

Rifampin and Isoniazid (INH)

o Both target actively growingorganisms and metabolicallyinactive intracellular organisms

Therapy is pronged Lasting at least 6 months


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Chickenpox

Popular name for varicella

One of the most common

rashes among children

Incidence declined due to

vaccine

Produces a latent

infection that becomes

reactive after recovery of

initial illness shingles


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Chickenpox

Symptoms Most cases are mild and recovery uneventful

Symptoms more severe in older children and adults

20% of adults develop pneumonia

Skin rash appears on back of head, face and mouth Rash is diagnostic

Rash progresses from red spots called macules to small bumps

called papuales to small blisters called vesicles to pus filled

blisters called pustules

Lesions itch and appear at different times Healing begins after pustules break and crust over

Varicella infection major threat to newborn

May lead to congenital varicella syndrome

Immunocompromised patients are also at higher risk


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Chickenpox

Symptoms

Sequella of virus infection include

Shingles or herpes zoster

Caused by reactivation of dormant virus

Characterized by rash around waist

Reyes Syndrome

Condition evident by vomiting and coma

Predominantly seen in children 5 to 15

o Characterized by liver and brain

damage

Mortality around 30% Evidence suggests aspirin therapy

increases risk


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Chickenpox

Causative Agent Varicella-zoster virus

Member of herpes virus family

Medium sized enveloped virus

Double-stranded DNA genome


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Chickenpox

Pathogenesis

Virus enters through respiratory route

Replicates and moves to the skin via blood stream

Infects living layers of skin and moves to adjacent cells

Skin lesions appear

Infected cells swell and lyse

Release virus to enter sensory nerves

Occurrence of shingles correlates with decline in cell

mediated immunity

Latent virus within nerve cell replicates and is carried to the skin

Lesions are produced


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Chickenpox

EpidemiologyAnnual incidence once estimated in the several millions

but declined due to vaccine

Disease transmitted by respiratory secretions and skin

lesions Incidences increase in winter and spring

Due to close contact

Viral incubation period approximately 2 weeks Infective 1 to 2 days before rash until blisters crust over

Persistence in the body allows survival of isolated viralpopulations


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Chickenpox

Prevention and Treatment

Prevention directed at vaccination

Attenuated vaccine licensed in 1995

Recommended for healthy individuals 12 months and older

Immunization should be done before 13th birthday due tolikelihood of increased complications

Should not be given during pregnancy or 3 months prior to

pregnancy

Immunocompromised patients should avoid vaccine

o Can be partially protected by passive immunity via injection

of zoster immune globulin (ZIG)


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Measles

A.k.a hard measles

and red measles

Common names for

rubeola Dramatic reduction in

measles cases within

twentieth century

Due to effectiveimmunization programs


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Measles

Symptoms Begins with fever, runny nose, cough, red weepy eyes

Fine rash appears within a few days

Appears first on forehead, then spreads to rest of body

Symptoms generally disappear within 1 week

Many cases complicated by secondary infections

Pneumonia and earaches are most common secondary

conditions

Less common complications include encephalitis and subacutesclerosing panencehalitis (SSPE)


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Measles

Causative Agent Rubeola virus

Pleomorphic, medium sized, enveloped

Enevlope contains projections

One for viral attachement to host One for fusion with host membrane

Single-stranded RNA genome

Belongs to paramyxovirus family


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Measles

Pathogenesis Infection via respiratory route

Virus replicates in epithelium of upper respiratory

tract

Spreads to lymph nodes Further replication takes place here

Spreads to all parts of the body


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Measles

Pathogenesis Infected mucous

membranes importantdiagnostic sign

Membranes covered withKoplik spots

White spots seen in back ofthroat opposite molars

Infected membranes mayexplain increased

susceptability to secondaryinfection

Especially to middle ear andlungs


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Measles

Pathogenesis Skin rash is due to effects of virus replication within

skin cells

Rash also due to cellular immune response to viral

antigens in the skin


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Measles

Epidemiology Humans are only natural host

Virus spread by respiratory droplets

Before routine immunization, over 99% of population

infected Vaccine resulted in decline of annual cases

Measles are no longer endemic in United States


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Measles

Epidemiology Outbreaks still occur and are due to non- immune

populations

Populations include

Children too young to be vaccinated Preschool children never vaccinated

Children and adults inadequately vaccinated

Persons not vaccinated for religious or medical reasons


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Measles

Prevention and Treatment Prevention directed to vaccination

Vaccine is usually given in conjuction with mumps and

rubella vaccine

MMR

No antiviral treatment exists for rubeola infection


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German Measles

German measles and

three day measles are

common names for

rubella Typically mild

Often unrecognized

Difficult to diagnose

Significant infection in

pregnant women


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German Measles

Symptoms Slight fever with mild cold symptoms

Enlarged lymph nodes behind ears and back of

neck

Faint rash on face Rash consists of light pink spots

Adults commonly complain of joint pain

Symptoms last only a few days

Joint pain may last up to 3 weeks


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German Measles

Causative Agent Rubella virus

Member of togavirus family

Small, enveloped

Single-stranded RNA genome


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German Measles

Pathogenesis Enters body via respiratory route

Virus multiplies in nasopharynx, then enters

bloodstream

Causes sustained viremia

Blood transports virus to body tissues

Immunity develops against viral antigens

Resulting antigen-antibody complex most likely responsible

for rash and joint pain


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German Measles

Epidemiology

Humans are only natural host

Disease is highly contagious

Less so than measles (rubeola)

40% of infected people fail to develop symptoms

These individuals can spread virus

Infectious 7 days before appearance of rash to 7 days

after


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German Measles

Prevention and Treatment Vaccination with attenuated rubella virus vaccine

Administered at 12 months and boostered at 4 to 6 years of age

Produces long-lasting immunity in 95% of recipients

Vaccine not given to pregnant women due to potentialcomplications

Women are advised not to become pregnant for 28 days postvaccination

Vaccine has significantly reduced incidence in UnitedStates


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SARS

Severe Acute Respiratory Syndrome is stillconsidered a relatively rare disease, with 8,273

cases as of 2003.

Signs and symptoms

Initial symptoms are flu-like and may include fever,myalgia, lethargy symptoms, cough, sore throat,

and othernonspecific symptoms.

The only symptom common to all patients appears

to be a fever above 38 C (100 F). Shortness of breath may occur later.

The patient has symptoms as with a cold in the first

stage, but later on they resemble influenza.

Diagnosis
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Diagnosis

A chest X-ray showing increased opacity in both lungs

indicative of pneumonia.

SARS may be suspectedin a patient who has:

Any of the symptoms, including a fever of 38 C (100 F)

or higher, and

Either a history of:

Contact (sexual or casual, including tattoos) with someone with a

diagnosis of SARS within the last 10 days OR

Travel to any of the regions identified by the World Health

Organization (WHO) as areas with recent local transmission of

SARS (affected regions as of 10 May 2003 were parts of China,Hong Kong, Singapore and the province of Ontario, Canada).

A probable case of SARS has the above findings


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Aprobable case of SARS has the above findings

plus positive chest X-ray findings ofatypical

pneumonia orrespiratory distress syndrome.

The chest X-ray (CXR) appearance of SARS isvariable. There is no pathognomonic appearance of

SARS, but is commonly felt to be abnormal with

patchy infiltrates in any part of the lungs. The initial

CXR may be clear.

Treatment
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Antibiotics are ineffective, as SARS is a viraldisease. Treatment of SARS is largely supportive

with antipyretics, supplemental oxygen andmechanical ventilation as needed.

Suspected cases of SARS must be isolated,preferably in negative pressure rooms, withcomplete barrier nursing precautions taken for any

necessary contact with these patients.

Some of the more serious damage in SARS may bedue to the body's own immune system reacting inwhat is known as cytokine storm (also known as

cytokine cascade and hypercytokinemia is apotentially fatal immune reaction consisting of apositive feedback loop between cytokines andimmune cells, with highly elevated levels of variouscytokines).
http://en.wikipedia.org/wiki/Antibiotichttp://en.wikipedia.org/wiki/Antipyretichttp://en.wikipedia.org/wiki/Negative_room_pressurehttp://en.wikipedia.org/wiki/Cytokine_stormhttp://en.wikipedia.org/wiki/Positive_feedback_loophttp://en.wikipedia.org/wiki/Cytokinehttp://en.wikipedia.org/wiki/Immune_cellhttp://en.wikipedia.org/wiki/Immune_cellhttp://en.wikipedia.org/wiki/Cytokinehttp://en.wikipedia.org/wiki/Positive_feedback_loophttp://en.wikipedia.org/wiki/Cytokine_stormhttp://en.wikipedia.org/wiki/Negative_room_pressurehttp://en.wikipedia.org/wiki/Antipyretichttp://en.wikipedia.org/wiki/Antibiotic


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VECTOR-BONE DISEASES

M l i


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Malaria Symptoms

flu-like Includes fever, headache and pain in the joints and

muscles

Generally begin 2 weeks post infection

Transmission via bite of infected mosquito Symptom pattern changes after 2 to 3 weeks

Fall into three categories

Cold phase abruptly feels cold and develops shaking

Hot phase follows cold phase

o Temperature rises steeply reaching 104F Wet phase follows hot phase

o temperature falls and drenching sweat occurs

Malaria


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Malaria

Causative agent

Human malaria caused by

four species of genus

Plasmodium

P. vivax, P. falciparum, P.

malatiae, P. ovale Infectious form of parasite

injected via mosquito

Carried by bloodstream to

liver Infects cells of liver

Thousands of offspring released

to produce infection in

erythrocytes

M l i


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Malaria

Pathogenesis Characteristic feature

Recurrent bouts of fever followed by times of wellness

Caused by erythrocytic cycle of growth and release of offspring

Each species has different incubation periods, degrees

of severity and preferred host age and range Spleen enlarges to cope with large amount of foreign

material and abnormal RBC Common cause of splenic rupture

Parasites cause anemia by destroying red RBC and

converting iron from hemoglobin to no-usable form Stimulates immune system

Overworked immune system fails and immunodeficiencydevelops

M l i


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Malaria

Epidemiology Once common in both temperate and tropical areas

Now dominantly disease of warm climate

Eliminated from continental U.S. in late 1940s

Mosquitoes of genusAnopheles are biological vectors

Infected mosquitoes and humans constitute reservoir Transmission via mosquitoes, blood transfusion and

sharing of syringes


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M l i


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Malaria

Prevention and Treatment Treatment is complicated

Due to different stages of mosquito life cycle

Chloroquine

Effective against erythrocyte stage Will not cure liver infection

Primaquine and tafenoquine

Generally effective against exoerythrocyte stage and certain

species gametocytes


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DENGUE FEVER Dengue fever is a disease caused by a family of

viruses that are transmitted by mosquitoes (Aedes

aegypti & Aedes albopictus).

Symptoms such as headache, fever, exhaustion,

severe joint and muscle pain, swollen glands(lymphadenopathy), and rash.

The presence (the "dengue triad") of fever, rash, and

headache (and other pains) is particularly

characteristic of dengue fever. Other signs of dengue fever include bleeding gums,

severe pain behind the eyes, and red palms and

soles.

Hermans rash


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Dengue is prevalent throughout the tropics andsubtropics.


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p

Dengue goes by other names, including "breakbone" or"dandy fever." Victims of dengue often have contortionsdue to the intense joint and muscle pain, hence the namebreakbone fever.

Because dengue fever is caused by a virus, there is nospecific medicine or antibiotic to treat it. For typicaldengue fever, the treatment is purely concerned withrelief of the symptoms (symptomatic).

The acute phase of the illness with fever and myalgiaslasts about one to two weeks.

Dengue hemorrhagic fever (DHF) is a specific syndromethat tends to affect children under 10 years of age. Itcauses headache, fever, rash, abdominal pain,

hemorrhage (bleeding) including petechiae (small red orpurple splotches or blisters under the skin), epistaxis gumbleeding, melena and easy bruising and all possiblesigns of hemorrhage. This form of dengue fever can belife-threatening and can progress to the most severe form

of the illness, dengue shock syndrome where circulatory
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The prevention of dengue fever requires controlor eradication of the mosquitoes carrying the

virus that causes dengue.

There is currently no vaccine available for dengue

fever.


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ZOONOTIC DISEASES

Rabies


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Rabies Symptoms

Fever Head and muscle ache

Sore throat

Fatigue

Nausea Tingling or twitching at

site of viral entry Characteristic symptom

Early symptoms begin 1 to 2

months post infection Progress rapidly to secondary

symptoms of

Encephalitis, agitation,confusion, hallucinations,

seizure, increased sensitivity tolight and touch

Body temperature rises withincreased salivation and difficultyswallowing

Results in frothing of mouth

Hydrophobia occurs in 50% ofcases

Coma develops

About 50% of patients die within4 days

Rabies


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Rabies Causative agent

Rabies virus Member of rhabdovirus family

Sticking bullet shape

Enveloped, single-stranded RNA genome

Pathogenesis

Mode of transmission primarily via salivaof rabid animal

Usually due to bite or abrasion

Can be contacted via inhalation

Virus multiples in muscle cells at site ofinfection

Virus reaches brain via infected nerve

Virus multiplies extensively in brain

Negri bodies form at sites of replication

Rabies


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Rabies

Epidemiology Widespread in wild animals

5,000 cases reported annually inUnited States

Skunks, raccoons and bats

considered chief reservoir Raccoons most infected

Almost all human cases due tocontact with infected bats

Zero to 4 reported cases in

U.S annually Only 25% have history of dog

bite

Long incubation period of virusmake history unreliable

R bi


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Rabies Prevention and Treatment

Wash wound immediately and thoroughly Use soap and water and apply antiseptic

Risk of developing rabies from bite of rabid dog isapproximately 30% Risk can be lowered considerably if vaccine is administered as

soon as possible after exposure

Presumably vaccine provokes better immune response

Bitten individual should receive series of 5 injections atwound site and intramuscularly Shots should be given even if biting animal presumed to be

rabid

No effective treatment for rabies Only six known survivors of disease

Anthrax


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is an acute disease caused by the bacterium Bacillusanthracis.

Most forms of the disease are lethal, and it affects bothhumans and animals.

There are effective vaccines against anthrax, and someforms of the disease respond well to antibiotic treatment.

Anthrax commonly infects wild and domesticatedherbivorous mammals that ingest or inhale the spores

while grazing. Ingestion is thought to be the most commonroute by which herbivores contract anthrax.

Carnivores living in the same environment may becomeinfected by consuming infected animals.

Diseased animals can spread anthrax to humans, either by

direct contact (e.g., inoculation of infected blood to brokenskin) or by consumption of a diseased animal's flesh.

Anthrax spores can be produced in vitro and used as abiological weapon. Anthrax does not spread directly fromone infected animal or person to another; it is spread byspores. These spores can be transported by clothing or

shoes. The body of an animal that had active anthrax at

Signs and symptoms
http://en.wikipedia.org/wiki/Acute_(medicine)http://en.wikipedia.org/wiki/Bacillus_anthracishttp://en.wikipedia.org/wiki/Bacillus_anthracishttp://en.wikipedia.org/wiki/In_vitrohttp://en.wikipedia.org/wiki/Biological_weaponhttp://en.wikipedia.org/wiki/Biological_weaponhttp://en.wikipedia.org/wiki/In_vitrohttp://en.wikipedia.org/wiki/Bacillus_anthracishttp://en.wikipedia.org/wiki/Bacillus_anthracishttp://en.wikipedia.org/wiki/Acute_(medicine)


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g y p

Pulmonary

Respiratory infection in humans initially presents

with cold orflu-like symptoms for several days,followed by severe (and often fatal) respiratory

collapse. Historical mortality was 92%, but, when

treated early (seen in the 2001 anthrax attacks),

observed mortality was 45%. Distinguishing pulmonary anthrax from more

common causes of respiratory illness is essential to

avoiding delays in diagnosis and thereby improving

outcomes.

Illness progressing to the fulminant phase has a

97% mortality regardless of treatment.

A lethal infection is reported to result from inhalation

of about 10,00020,000 spores, though this dose

varies amon host s ecies.
http://en.wikipedia.org/wiki/Common_coldhttp://en.wikipedia.org/wiki/Flu-like_symptomshttp://en.wikipedia.org/wiki/2001_anthrax_attackshttp://en.wikipedia.org/wiki/Fulminanthttp://en.wikipedia.org/wiki/Fulminanthttp://en.wikipedia.org/wiki/2001_anthrax_attackshttp://en.wikipedia.org/wiki/Flu-like_symptomshttp://en.wikipedia.org/wiki/Flu-like_symptomshttp://en.wikipedia.org/wiki/Flu-like_symptomshttp://en.wikipedia.org/wiki/Common_cold


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Inhalational anthrax is also known as Woolsorters' orRagpickers' disease. These professions were more

susceptible to the disease due to their exposure to

infected animal products. Other practices associated

with exposure include the slicing up of animal horns

for the manufacture of buttons, the handling of hair

bristles used for the manufacturing of brushes, and

the handling of animal skins. Whether these animal

skins came from animals that died of the disease or

from animals that had simply laid on ground withspores on it is unknown. This mode of infection is

used as a bioweapon.


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Inhalational anthrax is also known as Woolsorters'or Ragpickers' disease. These professions were

more susceptible to the disease due to their

exposure to infected animal products.

Other practices associated with exposure include

the slicing up of animal horns for the manufacture of

buttons, the handling of hair bristles used for the

manufacturing of brushes, and the handling of

animal skins. Whether these animal skins came

from animals that died of the disease or fromanimals that had simply laid on ground with spores

on it is unknown.

This mode of infection is used as a bioweapon.

Gastrointestinal


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Gastrointestinal

in humans is most often caused by consuming anthrax-

infected meat and is characterized by serious

gastrointestinal difficulty, vomiting of blood, severediarrhea, acute inflammation of the intestinal tract, and loss

of appetite

Lesions have been found in the intestines and in the

mouth and throat. After the bacterium invades the bowel

system, it spreads through the bloodstream throughout the

body, while also continuing to make toxins.

Gastrointestinal infections can be treated but usually result

in fatality rates of 25% to 60%, depending upon how soon

treatment commences. This form of anthrax is the rarest form.

An outbreak of anthrax among humans who had eaten

meat from a dead carabao was reported in Cagayan

province in the Philippines in early 2010, with over 400

cases of illness and at least two fatalities.[

Cutaneous presents as a boil like skin lesion that eventually forms


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presents as a boil-like skin lesion that eventually formsan ulcer with a black center (eschar). The black escharoften shows up as a large, painless necrotic ulcer

(beginning as an irritating and itchy skin lesion or blisterthat is dark and usually concentrated as a black dot,somewhat resembling bread mold) at the site ofinfection.

In general, cutaneous infections form within the site ofspore penetration between 2 and 5 days afterexposure. Unlike bruises or most other lesions,cutaneous anthrax infections normally do not causepain.

caused when Bacillus anthracis spores enter throughcuts on the skin. This form of Anthrax is found mostcommonly when humans handle infected animalsand/or animal products (e.g., the hide of an animalused to make drums).

Cutaneous anthrax is rarely fatal if treated,because the


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Prevention Vaccines


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Currently administered human anthrax vaccines include acellular(USA) and live spore (Russia) varieties. All currently used anthraxvaccines show considerable local and general reactogenicity

(erythema, induration, soreness, fever) and serious adversereactions occur in about 1% of recipients. The American product,BioThrax, is licensed by the FDA and was formerly administered ina six-dose primary series at 0, 2, 4 weeks and 6, 12, 18 months,with annual boosters to maintain immunity. In 2008, the FDAapproved omitting the week 2 dose, resulting in the currently

recommended five-dose series. New second-generation vaccinescurrently being researched include recombinant live vaccines andrecombinant sub-unit vaccines.

Prophylaxis Delays of only a few days may make the disease untreatable and

treatment should be started even without symptoms if possiblecontamination or exposure is suspected. Animals with anthraxoften just die without any apparent symptoms. Initial symptomsmay resemble a common coldsore throat, mild fever, muscleaches and malaise. After a few days, the symptoms may progressto severe breathing problems and shock and ultimately death.Death can occur from about two days to a month after exposure

with deaths apparently peaking at about 8 days after exposure.

Treatment

Effective decontamination of people can be accomplished by a


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p p p ythorough wash-down with antimicrobial effective soap and water.Waste water should be treated with bleach or other anti-microbialagent. Effective decontamination of articles can be accomplished by

boiling contaminated articles in water for 30 minutes or longer.Chlorine bleach is ineffective in destroying spores and vegetativecells on surfaces, though formaldehyde is effective. Burning clothingis very effective in destroying spores. After decontamination, there isno need to immunize, treat, or isolate contacts of persons ill withanthrax unless they were also exposed to the same source ofinfection.

Antibiotics

Early antibiotic treatment of anthrax is essentialdelay significantlylessens chances for survival.

Treatment for anthrax infection and other bacterial infections includeslarge doses of intravenous and oral antibiotics, such as

fluoroquinolones (like ciprofloxacin), doxycycline, erythromycin,vancomycin, or penicillin. FDA-approved agents include ciprofloxacin,doxycycline, and penicillin.

In possible cases of inhalation anthrax, early antibiotic prophylaxistreatment is crucial to prevent possible death.

In May 2009, a new drug, raxibacumab (brand name ABthrax)

intended for emergency treatment of inhaled anthrax.

and-mouth disease (Aphthae


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epizoot icae) is an infectious and sometimes fatal viral disease that

affects cloven-hoofed animals, including domestic and wildbovids. The virus causes a high fever for two or threedays, followed by blisters inside the mouth and on the feetthat may rupture and cause lameness.

Humans can be infected with foot-and-mouth disease

through contact with infected animals, but this is extremelyrare. Because the virus that causes FMD is sensitive tostomach acid, it cannot spread to humans via consumptionof infected meat, except in the mouth before the meat isswallowed.

Symptoms of FMD in humans include malaise, fever,

vomiting, red ulcerative lesions (surface-eroding damagedspots) of the oral tissues, and sometimes vesicular lesions(small blisters) of the skin.

Another viral disease with similar symptoms, hand, footand mouth disease, occurs more frequently in humans,especially in young children; the cause, Coxsackie A virus,

is different from FMDV. Coxsackie viruses belong to the

H d F t d M th Di


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Hand, Foot and Mouth Disease is a viral infection characterized by fever and a typical rash

most frequently seen on the palms of the hands, soles of thefeet, and inside the mouth. It should not be confused with foot(hoof) and mouth disease that affects cattle, sheep, andswine.

Initial symptoms of mild fever (101 F-102 F) and malaise are

followed within one or two days by a characteristic rash. Small(2 mm-3 mm) red spots that quickly develop into small blisters(vesicles) appear on the palms, soles, and oral cavity. Thegums, tongue, and inner cheek are most commonly involved.The foot lesions may also involve the lower calf region andrarely may appear on the buttocks. Oral lesions are

commonly associated with a sore throat and diminishedappetite.

HFM is caused by several members of the enterovirus familyof viruses. The most common cause is Coxsackie virus A-16;less frequently enterovirus 71 is the infectious agent. Theclinical manifestations of routine HFM are the same

regardless of the responsible virus. However, patients


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How is hand foot and mouth disease spread?

HFM i d t b di t t t ith


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HFM is spread person to person by direct contact with

the infecting virus (either Coxsackie virus A-16 or less

commonly enterovirus 71). These viruses are mostcommonly found in the nasal and throat regions but also

in the blister fluid or stool of infected individuals. Infected

individuals are most contagious during the first week of

their illness. HFM cannot be contracted from pets or

animals.

The viruses that cause HFM may remain in the person's

respiratory or intestinal tract for several weeks to months

after all symptoms have resolved. It is possible,

therefore, to transmit the infection even though theformally ill individual has completely recovered. Some

individuals (most commonly adults) may exhibit no

symptoms during their infection but may unwittingly

transmit the illness to those (commonly infants and

How does hand foot and mouth disease affect

pregnancy and the baby?


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pregnancy and the baby?

Commonly HFM is an illness of children less than

10 years of age; adults generally were exposedduring childhood and maintain a natural immunity.

Information regarding fetal exposure to HFM during

pregnancy is limited. No solid evidence exists that

maternal enterovirus infection is associated with

complications such as spontaneous abortion or

congenital defects.

However, should a baby be born to a mother with

active HFM symptoms, the risk of neonatal infection

is high. Typically, such newborns have a mildillness.

Rarely, overwhelming infection involving vital

organs such as liver, heart, and brain can be lethal.

What is the course of hand foot and mouth

disease?


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disease?

The illness is characteristically self-limited and is

usually resolved within a week, particularly when due toits most common cause, Coxsackie virus A-16.

In those outbreaks due to enterovirus 71, the illness

may be more severe with complications such as viral

meningitis and encephalitis and paralytic disease.As a rule, HFM is generally a mild and self-limited

illness.

How is hand foot and mouth disease diagnosed?

Usually, the diagnosis of HFM is made on acombination of clinical history and characteristic

physical findings. Laboratory confirmation is rarely

necessary unless severe complications develop.

What is the treatment for hand foot and mouth

Bi d fl (A i fl /A i I f )


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Bird flu (Avian flu/Avian Infuenza) is caused by a type of influenza virus that rarely

infects humans. But when bird flu does strike humans,it's often deadly. More than half the people whobecome infected with bird flu die of the disease.

In recent years, outbreaks of bird flu have occurred in

Asia, Africa and parts of Europe. Most people whohave developed symptoms of bird flu have had closecontact with sick birds. In a few cases, bird flu haspassed from one person to another.

Health officials worry that a global outbreak could

occur if a bird flu virus mutates into a form thattransmits more easily from person to person.Researchers are working on vaccines to help protectpeople from bird flu.

Signs and symptoms of bird flu typically begin within twoto five days of infection In most cases they resemble


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to five days of infection. In most cases, they resemblethose of conventional influenza, including: Cough

Fever

Sore throat

Muscle aches

Some people also experience nausea, vomiting or diarrhea.

And in a few cases, a mild eye infection (conjunctivitis) is theonly indication of the disease.

When to see a doctorSee your doctor immediately if you develop a fever, coughand body aches, and have recently traveled to a part of

the world where bird flu occurs. Be sure to let your doctorknow if you visited any farms or open-air markets.

Causes


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Bird flu occurs naturally in wild waterfowl and can

spread into domestic poultry, such as chickens, turkeys,

ducks and geese. The disease is transmitted via contactwith an infected bird's feces, or secretions from its nose,

mouth or eyes.

Open-air markets, where eggs and birds are sold in

crowded and unsanitary conditions, are hotbeds ofinfection and can spread the disease into the wider

community.

According to the Food and Drug Administration, bird flu

cannot be transmitted by eating properly cooked poultrymeat or eggs from infected birds. Poultry meat is safe to

eat if it's been cooked to an internal temperature of 165

F (74 C). Eggs should be cooked until the yolk and

white are firm.

People with bird flu may develop life-threateningcomplications including:


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complications, including: Pneumonia

Collapsed lung

Respiratory failure

Kidney dysfunction

Heart problems

Although bird flu kills more than half the people itinfects, the number of fatalities is still low becauseso few people have had bird flu. According to theWorld Health Organization, a few hundred peoplehave died of bird flu since 2003.

In contrast, the Centers for Disease Control andPrevention estimates that seasonal influenza isresponsible for thousands of deaths each year in theUnited States alone.

Laboratory testsSamples of fluids from your nose or throat can be testedf id f bi d fl i Th l t b


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for evidence of bird flu virus. These samples must betaken within the first few days after symptoms appear.Depending upon the type of test, results can take weeksor just a few hours.

Imaging testsX-rays may be useful in assessing the condition of yourlungs, which can help determine the proper diagnosisand the best treatment options for your signs and

symptoms. Treatments and drugs

MedicationsMany influenza viruses have become resistant to the effectsof a category of antiviral drugs that includes amantadine and

rimantadine. Health officials recommend the use ofoseltamivir (Tamiflu) and possibly zanamivir (Relenza)instead.

These drugs must be taken within two days after theappearance of symptoms, something that may provelogistically difficult on a worldwide scale, even if there were

enough to go around. Because they're in short supply, it's

Prevention Bird flu vaccine


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The Food and Drug Administration has approved one vaccine toprevent infection with one strain of H5N1 bird flu viru sto the

public intended to help protect adults ages 18 to 64 and couldbe used early in such an outbreak to provide limited protectionuntil another vaccine designed to protect against the specificform of the virus causing the outbreak is developed andproduced.

Recommendations for travelersIf you're traveling to Southeast Asia or to any region with birdflu outbreaks, consider these public healthrecommendations: Avoid domesticated birds. If possible, avoid rural areas, small

farms and open-air markets. Wash your hands. This is one of the simplest and best ways to

prevent infections of all kinds. Use an alcohol-based handsanitizer containing at least 60 percent alcohol when you travel.

Ask about a flu shot. Before traveling, ask your doctor about a

flu shot. It won't protect you specifically from bird flu, but it may


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Poultry and egg productsBecause heat destroys avian viruses, cooked poultryisn't a health threat. Even so, it's best to takeprecautions when handling and preparing poultry, whichmay be contaminated with salmonella or other harmfulbacteria.

Avoid cross-contamination. Use hot, soapy water towash cutting boards, utensils and all surfaces that havecome into contact with raw poultry.

Cook thoroughly. Cook chicken until the juices runclear, and it reaches a minimum internal temperature of

165 F (74 C). Steer clear of raw eggs. Because eggshells are often

contaminated with bird droppings, avoid foodscontaining raw or undercooked eggs.

Mad Cow Disease


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Bovine spongiform encephalopathy (BSE)is a fatal

neurodegenerative disease (encephalopathy) in cattle

that causes a spongy degeneration in the brain andspinal cord.

BSE has a long incubation period, about 30 months to

8 years, usually affecting adult cattle at a peak age onset

of four to five years, all breeds being equally susceptible. easily transmitted to human beings by eating food

contaminated with the brain, spinal cord or digestive tract

of infected carcasses.

However, it should also be noted that the infectiousagent, although most highly concentrated in nervous

tissue, can be found in virtually all tissues throughout the

body, including blood.

In humans, it is known as new variant CreutzfeldtJakob

The infectious agent in BSE is believed to be a specifictype of misfolded protein called a prion. Prions are not


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yp p pdestroyed even if the beef or material containing them iscooked or heat-treated.

In the first few months, vCJD is "dominated" bypsychiatric symptoms. In this early stage, patientscommonly suffered from personality changes such aswithdrawal, anxiety, depression and insomnia.

People with mad cow disease can have very serious

signs and symptoms, muscle stiffness, involuntary musclemovements, dementia, and seizures.

The only way to definitively diagnose any human priondisease is to examine the brain tissue itself.

Treatment

No treatment is available to slow down or stop theprogression of mad cow disease or other prion infections.

What Is the Prognosis? Mad cow disease is fatal. The incubation period for disease

related to exposure to infected tissues varies between 1.5years and more than 30 years.

Swine Flu (Swine Influenza) Is a respiratory disease caused by viruses (influenza viruses) that


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p y y ( )infect the respiratory tract of pigs, resulting in nasal secretions, abarking cough, decreased appetite, and listless behavior. Swine fluproduces most of the same symptoms in pigs as human flu produces

in people. Swine flu can last about one to two weeks in pigs that survive. Swine

influenza virus was first isolated from pigs in 1930 in the U.S. and hasbeen recognized by pork producers and veterinarians to causeinfections in pigs worldwide.

In a number of instances, people have developed the swine fluinfection when they are closely associated with pigs (for example,farmers, pork processors), and likewise, pig populations haveoccasionally been infected with the human flu infection. In mostinstances, the cross-species infections (swine virus to man; human fluvirus to pigs) have remained in local areas and have not causednational or worldwide infections in either pigs or humans.

Unfortunately, this cross-species situation with influenza viruses hashad the potential to change. Investigators think the 2009 swine flustrain, first seen in Mexico, should be termed novel H1N1 flu since itis mainly found infecting people and exhibits two main surfaceantigens, H1 (hemagglutinin type 1) and N1 (neuraminidase type1).Recent investigations show the eight RNA strands from novel H1N1flu have one strand derived from human flu strains, two from avianbird strains and five from swine strains. Swine flu is transmitted

What are the symptoms of swine flu (H1N1)?

Symptoms of swine flu are similar to most influenza


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Symptoms of swine flu are similar to most influenzainfections: fever (100 F or greater), cough, nasalsecretions, fatigue, and headache, with fatigue beingreported in most infected individuals. Some patients alsoget nausea, vomiting, and diarrhea. In Mexico, many ofthe initial patients infected with H1N1 influenza wereyoung adults, which made some investigators speculate

that a strong immune response, as seen in youngpeople, may cause some collateral tissue damage.

Some patients develop severe respiratory symptomsand need respiratory support (such as a ventilator tobreathe for the patient). Patients can get pneumonia

(bacterial secondary infection) if the viral infectionpersists, and some can develop seizures. Death oftenoccurs from secondary bacterial infection of the lungs;appropriate antibiotics need to be used in these patients.The usual mortality (death) rate for typical influenza A is

about 0.1%,

How is swine flu (H1N1) diagnosed?

Swine flu is presumptively diagnosed clinically by the


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Swine flu is presumptively diagnosed clinically by the

patient's history of association with people known to have

the disease and their symptoms listed above. Usually, a quick test (for example, nasopharyngeal swab

sample) is done to see if the patient is infected with

influenza A or B virus.

The test can be negative (no flu infection) or positive for type

A and B. If the test is positive for type B, the flu is not likely

to be swine flu (H1N1). If it is positive for type A, the person

could have a conventional flu strain or swine flu (H1N1).

However, the accuracy of these tests has been challenged

In 2010, the FDA approved a commercially available testthat could detect H1N1 within four hours. Most of these

rapid tests are based on PCR technology.

Swine flu (H1N1) is definitively diagnosed by identifying

the particular antigens associated with the virus type.

What treatment is available for swine flu (H1N1)?

The best treatment for influenza infections in humans


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The best treatment for influenza infections in humans

is prevention by vaccination.

The first vaccine released in early October 2009 was anasal spray vaccine that was approved for use in

healthy individuals ages 2 through 49.

The injectable vaccine, made from killed H1N1,

became available in the second week of October 2009.This vaccine was approved for use in ages 6 months to

the elderly, including pregnant females.

Almost all vaccines have some side effects. Common

side effects of H1N1 vaccines are typical of flu vaccines

and are as follows:

Flu shot: Soreness, redness, minor swelling at the shot site,

muscle aches, low grade fever, and nausea do not usually last

more than about 24 hours.

Nasal spray: runny nose, low-grade fever, vomiting, headache,

The nasal spray vaccine contains live virus that have

been altered to hinder its ability to replicate in human


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been altered to hinder its ability to replicate in human

tissue.

People with a suppressed immune system shouldnot get vaccinated with the nasal spray.

Also, most vaccines that contain flu viral particles are

cultivated in eggs, so individuals with an allergy to

eggs should not get the vaccine unless tested andadvised by their doctor that they are cleared to

obtain it.

Like all vaccines, rare events may occur in some

rare cases (for example, swelling, weakness, or

shortness of breath). If any symptoms like these

develop, the person should see a physician

immediately.

Two antiviral agents have been reported to helpprevent or reduce the effects of swine flu. They are


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p yzanamivir(Relenza) and oseltamivir(Tamiflu), bothof which are also used to prevent or reduce influenza

A and B symptoms.

These drugs should not be used indiscriminately,because viral resistance to them can and hasoccurred.

Also, they are not recommended if the flu symptomsalready have been present for 48 hours or more,although hospitalized patients may still be treatedpast the 48-hour guideline.

Severe infections in some patients may requireadditional supportive measures such as ventilationsupport and treatment of other infections likepneumonia that can occur in patients with a severeflu infection.
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What are the risk factors for swine flu (H1N1)?

Vaccination to prevent influenza is particularly


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acc at o to p e e t ue a s pa t cu a y

important for people who are at increased risk for

severe complications from influenza or at higher riskfor influenza-related doctor or hospital visits.

all children 6 months to 4 years (59 months) of age;

all people 50 years of age and older;

adults and children who have chronic pulmonary(including asthma) or cardiovascular (except isolated

hypertension), renal, hepatic, neurological, hematologic,

or metabolic disorders (including diabetes mellitus);

people who have immunosuppression (includingimmunosuppression caused by medications or by HIV);

women who are or will be pregnant during the influenza

season;

children and adolescents (6 months to 18 years of age)

who are receiving long-term aspirin therapy and who


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g g y

might be at risk for experiencing Reye's syndrome after

influenza virus infection;

residents of nursing homes and other long-term-care

facilities;

American Indians/Alaska natives;

people who are morbidly obese (BMI 40);

health care professionals (doctors, nurses, health care

personnel treating patients);

household contacts and caregivers of children under 5

years of age and adults 50 years of age and older, with

particular emphasis on vaccinating contacts of children

less than 6 months age;

household contacts and caregivers of people with

medical conditions that put them at higher risk for

severe com lications from influenza.


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