Acute respiratory infection

1. RESPERATORY INFECTIONS
 SMALL POX: An acute infectious disease caused by
variola virus and clinically characterized by a
sudden onset of fever, headache, backache and
sometimes convulsions and a rash.
 Rash evolves as---- macule ---- papule---- vesicle ----
pustule ---- scab ---- scarring

2. SMALL POX
 HISTORY: Small pox was eradicated in 20th century.
 Till 1967 it was endemic in more than 33 countries.
 Last indigenous case in India occurred on May 11th 1975
in Bihar.
 April 1977: India was declared small – pox free by an
international commission for assessment of small pox
eradication. Last case of small pox occurred in
Somalia on 26 October 1977. The WHO declared on
May 8th 1980 – That small pox had been eradicated.

3. SMALLPOX ERADICATION:
 EPIDEMIOLOGICAL BASIS:
1. No known animal reservoir
 2. No long – term carrier of the virus.
 3. Life long immunity after recovery from the
disease.
 4.The diagnosis of cases is easy based on rash AND
C.F.
 5. Sub clinical cases will not transmit the disease.
 6. Vaccine highly effective, easily administered,
heat stable and confers long-term protection.
 7. International cooperation.

4. CURRENT STATUS OF VACCINATION
 On May 1980 the WHO declared that the global
eradication of small pox had been achieved.
 May 1981: the 34th world health assembly
recommended deletion of all references to
small pox, small pox vaccination and amended
international health regulations.
  Almost all member states of WHO had
officially discontinued compulsory vaccination
by 1982.

5. Small pox vaccination
 VACCINATION CAN BE INDICATED TO:
 Those who handles vaccinial virus for
vaccine production.
 Conduct research on orthopox viruses
pathogenic to man.
 WHO directly investigate human monkey
poxviruses.
 Military personal can be vaccinated for
protection against smallpox

6. SMALLPOX ERADICATION SURVEILLENCE
 1997 – marked the 20th anniversary of the
smallpox free status in India.
 Stocks are still held at govt. research centers
in Moscow and at CDC, Atlanta, Georgia, USA.
 A resolution by WHO executive board to the
world health assembly in May 1999
recommended that the stocks of virus should
be destroyed in 2002.

7. POX VIRUS DISEASE AFTER SMALLPOX ERADICATION:
 a)Accidental infection with laboratory associated
stocks.
 b) Infection with animal poxviruses.
 A) Accidental infection:
 1976 = 76 labs kept stocks of small poxvirus.
 1980 = 6 labs.
 1983 = 2 labs.
 4 members of poxviruses can produce human
infections.
 E.g. Monkey pox, Camel pox, Cowpox, Tana pox,
and Tateno pox.

8. HUMAN MONKEY POX
 A)HUMAN-INFECTIONS-WITH-ANIMAL
POXIVIRUSES:
 Two poxviruses – The monkey pox and Tanapox Viruses
are having capabilities to infect human beings.
 Monkey poxvirus is a distinct species from a
variola virus.
 SINCE 1970:
 400 patients with monkey pox infection occurred.
 -7 countries in western and central Africa. Zaire –
95%of cases.
 - Monkey pox is an infrequent and sporadic
zoonoses.

9. HUMAN MONKEY POX
 -Humans can contact monkey pox by Close
Contact with infected animals.
 - Enzootic area:
 -Dose not poses a significant health problem.
 - Genus ortho pox virus.
 - Man is an incidental host.
 I.P: – 14 days

10. HUMANMONKEY POX
 - Rash and lymphadenopathy.
 -The secondary attack rate is 15% as compare to
30 – 45% in small pox.
 - Small pox vaccination protects against
monkey pox.
 -Zaire – 1982-1983.
 The disease is now under WHO surveillance in
west and central Africa

11. TANAPOX
 TANA POX: C.F: Fever, 1-2 pustular lesions, up to
6 weeks, reservoir unknown, zoonotic disease,
east and central Africa.
 Vector – Mosquito.
 Small pox vaccination dose not give protection
against Tanapox.
 300 million vaccines and bifurcated needles are
kept as stockpile under WHO guide lines in
Geneva, Toronto and New Delhi against
smallpox

12. CHICKEN POX
 CHICKEN POX: Chicken pox or varicella is an
acute, highly infectious disease caused by
varicella zoster virus.
 It is characterized by vesicular rash
accompanied by fever and malaise. World wide in
distribution. Epidemic and endemic.
  Chicken pox – Herpes zoster (shingles)

13. EPIDEMOLOGICAL
DETERMINANTS
 AGENT FACTORS:
 a) Agent: varicella zoster virus – is also called
“Human (alpha) herpes virus 3”
 - Primary infection – Chicken pox.
 - Reactivation – herpes zoster.
 “ A painful, vesicular, pustular eruption of skin
dermatome (s) in the distribution of one or
more sensory nerves roots

14. AGENT FACTORS:CONT
 a)SOURCE OF INFECTION: A case of chicken pox.
Pharyngeal secretions and lesions of skin and
mucosa contains virus, which can be isolated from
vesicular fluid during the first 3 days of illness.
 b)INFECTIVITY: 1-2 days before the appearance of
rash and 4-5 days there after the rash. The patient
ceases to be infections once the lesions have scab
formation.

15. AGENT FACTIRS:
 SECONDARY ATTACK RATE: Chicken pox is highly
communicable.
 The secondary attack rate in house hold contacts
will be around 90%.
Host factors:
 Age: Mainly occurs in children less than 10 yrs of
age .The disease can be severe in normal adults

16. HOST FACTORS:
 a)Immunity: one-attack gives long lasting
immunity. Second attacks are rare.
  IgG antibodies persist for life and their
presence is correlated with protection against
varicella.
 The cell-mediated immunity appears to be
important in recovery from v – z infections and in
protection against the reactivation of latent v-z
virus

17. ENVIRONMENTAL FACTORS.
 a) Pregnancy: infection during pregnancy
presents a risk for the fetus and the neonate.
ENVIRONMENTAL FACTORS:
- Chicken pox shows a seasonal trend in
India.
- Occurs mainly in 1st 6 months of the year.
- Over crowding favour it’ s transmission.
infection and by droplet nuclei.
 o Most patients are infected face-to-face direct
personal contact.
 o The portal of entry of the virus is the
respiratory tract.

18. ENVIRONMENTAL FACTORS
 oVirus is heat labile so fomites may not play
any significant role.
 oContact infection plays a role when an
individual with herpes zoster is an index case.
 oVertical transmission possibility is present.
Fetus can get congenital varricella.

19. CLINICAL FEATURES:
 INCUBATIONPERIOD:
14-16 days (7-21 days is range).
 CLINICAL FEATURES:
 oCan vary from mild infection with few skin
lesions to a severe febrile illness with wide
spread rash.
 o PRE – ERUPTIVE STAGE:
 Onset is sudden with mild or moderate
fever, pain in the back, shivering and
malaise and lasts for 24 hours

20. CLINICAL FEATURES
 ERUPTIVE STAGE: In children the rash is often
the first sign.
 a)DISTRIBUTION: The rash is symmetrical
first appears on the trunk and face then
appears on extremities (CENTRIFUGAL).
 Mucosal surfaces (eg. Buccal and pharyn geal)
are generally involved, axilla may be affected
but palms and soles are not affected.
Centrifugal distribution of rash.

21. CLINICAL FEATURES
 a) RAPID EVOLUTION: stages of macule,
papule, vesicle and scab.
 - Rash will be like Due drops on a rose-petal
appearance.
 - The vesicles may form crusts with out going to
pustular stage.
 -Scabbing begins in 4-7 days after the rash.

22. CLINICAL FEATURES
 a) PLEO MORPHISM: All stages of the rash
(macule, papule, vesicle and crust) may be
seen simultaneously at one time in the same
area.
 FEVER: Exacerbations of fever with each fresh
crop of eruption

23.  SMALL POX: CHICKENPOX:
 1. Incubation: 12 days ------------ 15 days
 2. Prodromal symptoms.
Severe ------------ mild.
 3.Distribution of rash:
 a) Palms and soles involvement. A)No rash.
 B) Axilla free b)axilla affects.
 c) Extensor surfaces c) Flexor surface.
4. Rash characters tics:
a) Deep seated. A)Superficial.
b) Vesicles multi loculated b)unilocular.
& Umblicated due drops like appearance.

24. SMALLPOX-CHICKENPOX
 c) Only one type of rash. c) Pleomorphism
of rash
can be seen at one time.
 D) No area of inflammation. D) Area of
inflammation
Around the rash.
 5. EVOLUTIONN OF RASH: A) Rapid,
 A). Slow. Stages of macule, pustular stage
 Papule, Vesicle and pustular may be
 Changes are present. Absent.

25. SMALLPOX-CHICKENPOX
 6)Fever:Subsides 6) Fever occurs
with appearance with each fresh
of rash ,rise again crop of rash.
in pustular stage.

26. COMPLICATIONS:
 COMPLICATIONS:
 Mild and self-limiting disease. The
mortality is less than 1% in un-complicated
cases.
 -Severe complications in Immuno
compromised patients, children and adults.
 These include Hemorrhages;
Pneumonia(HIV&PREG),ARDS
Acute cerebellar ataxia,
Reye’s syndrome.

27. COMPLICATIONS:
 Acute encephalopathy with fatty
degeneration of viscera especially liver – due to
aspirin ingestion. Reye syndrome. Common
in Children.
 -Maternal varicella during pregnancy may
cause fetal wastage, birth defects, atrophied
limbs, microcephaly , LBW,
Cataract,Chorioretinitis,deafness and
cerebrocortical atrophy.
 Hepatitis:Aminotransferase levels will be
elevated.

28. VZV IN HIV
 Multifocal encephalitis.
 Ventriculitis.
 Myeloradiculitis.
 Arteritis.
 More dermatomes involvement.
 Bell’s palsy in patients lacking antibodies to HSV.
 Ocular :Acute retinal necrosis &progressive outer
retinal necrosis.

29. LAB DIAGNOSIS
 Lab diagnosis is rarely required.Vesicle fluid
under the electronic microscope, which shows
round particles and may be used for
cultivation of the virus.
 Scrapings of floor of vesicles show multi
nucleated giant cells with giemsastaining ,
Tzanck smear or Calcoflour staining.
 DFA:Direct immunofluorescent antibody
staining or PCR of scrapings of lesions.

30. CONTROL MEASURES:
 Serology is used for epidemiological surveys:
No specific treatment.
 Control measures are like.
 a) Notifications.
 b) Isolation of cases for 6 days after onset of
rash.
 c) Disinfection of articles soiled by nose and
throat discharges.

31. PREVENTION:
 1.VARICELLA ZOSTER IMMUNOGLOBULIN (VZI):Given
with in 72 hrs of exposure. A dose of 1.25 to 5
ml given.12.5 units /kg.
 Reserved for Immuno suppression,
Contacts of acute case and newborn
contacts.
 2. VACCINE: A live attenuated vaccine
(OKA strain) developed by takashasi in
Japan.
 VZI&VACCINE SHOULD NOT BE GIVEN
CONCOMITANTLY.

32. PREVENTION:
 - Sero conversion after vaccination in healthy sero
– negative children is over 90%
 Remarks: Establish a latent infection may
produce zoster

33. TREATMENT
 ISOLATION.
 CARE GIVERS SHOULD WEAR GOWNS,
GLOVES AND MASKS.
 PRURITIS CAN BE RELIVED WITH
ANTIHISTAMINS AND CALMINE LOTION &
COLLODIAL OATMEAL BATHS.
 ANTIVIRAL TREATMENT:
 ACYCLOVIR:800mgs/5times daily.
 VALCYCLOVIR :1000 mgs /3times daily.
 FAMCICLOVIR:500mg/ 3times daily.
 Antiviral drugs reduce the severity and
shortens the duration of treatment.

35. Infections of the respiratory tract
are perhaps the most common
human ailment.
Causes discomfort, disability and
loss of time for most adults.
Substantial cause of morbidity
and mortality in young children
and the elderly.

36. Many of these infections run their
natural course in older children and
in adults without specific treatment
and without complications,
Young infants, small children, the
elderly, or persons with impaired
respiratory tract reserves, it
increases the morbidity and
mortality rates.

37.  Inflammation of the respiratory tract anywhere from
nose to alveoli with a wide range of combination of
symptoms and signs.'
 AURI: The upper respiratory tract infections include
common cold, pharyngitis and otitis media.
 ALRI: The lower respiratory tract infections include
epiglottitis, laryngitis, laryngotracheitis, bronchitis,
bronchiolitis and pneumonia,

38.  Every year ARI in young children is responsible for an
estimated 3.9 million deaths worldwide. It is estimated
that Bangladesh, India, Indonesia and Nepal together
account for
 40 per cent of the global ARI mortality. About 90 per
cent of

39.  The ARI deaths are due to pneumonia which is usually
bacterial in origin.
 The incidence of ARI is similar in developed and
developing countries.
 Incidence of pneumonia in developed countries may
be as low as 3-4 per cent,
 Incidence in developing countries range between 20 to
30 per cent.
 This difference is due to high prevalence of
malnutrition, low birth weight and indoor air
pollution in developing countries.

40. Clinical features
The clinical features include
running nose
Cough
sore throat
difficult breathing and ear problem.
Fever

43. Classifications for cough or difficult
breathing
 SEVERE PNEUMONIA OR VERY SEVERE DISEASE
 PNEUMONIA
 NO PNEUMONIA: COUGH OR COLD.

44.  2. If the child does not have the severe classification,
look at the yellow (or second) row.

45. INFLUENZA
  Influenza is an acute respiratory tract
infection caused by influenza virus of which
there are 3 types – A, B and C.
  All known pandemics are caused by
influenza-A strains. The disease is
characterized by sudden onset of chills,
malaise, fever, muscular pains and cough.

46. PROBLEMSTATEMENT
 It occurs in all countries and affects
millions of people every year.
  It may occur in pandemics every 10-15
years due to major antigenic changes. In
between pandemics, epidemics tend to
occur. Influenza A – 2-3 yrs interval and
Influenza B- 4-7 yrs interval.
  Epidemic of influenza is characteristic.
 The unique features of influenza epidemics
are
 the suddenness with which they arise and
the speed and ease with which they spread.

47. PROBLEMSTATEMENT
  The short incubation period, large number of sub
clinical cases, high proportion of susceptible
population, short duration of immunity, and
absence OF cross immunity all contribute to its
rapid spread.
 SPORADIC CASES: extra human reservoir, latent
infection in humans is the cases.
  INFLUENZA TYPES: 3 types are present.
 A (N1 H1) virus type.
 A (H3 N2) virus type .
 B virus type
 A (H5 N1) – new influenza virus in Hong Kong –
1997.

48. EPIDEMIOLOGY
 AGENT FACTORS:
 a) Agent influenza viruses are classified
with in the family “orthomyxo viridiae”.
Three viral subtypes namely influenza type
A, type B, and type C.
  These 3 viruses are antigenic ally distinct.
 There is no cross immunity between them.
  Influenza A and B viruses – which causes
epidemics of disease.
 Both have 2 distinct surface antigens. The hem
agglutinin (H) and the neuraminadase (n)
antigens.

49. EPIDEMIOLOGY
 H -ANTIGEN:- Initiates infection following
attachment of the virus to the susceptible cells.
 N-ANTIGEN: is responsible for the release of
the virus from the infected cells.
  ANTIGENIC VARIATION:
 ANTIGENIC SHIFT: Sudden complete or major
change it is called shift.
 ANTIGENIC DRIFT: Antigenic change is
gradual over a period of time.
  Shift is due to genetic combination of human
with animal or avian virus. Provide major
antigenic change. Epidemic or pandemic.
 DRIFT:- Involves point mutation in the gene

50. AGENT
  The antigenic changes occur to a lesser
degree in the B- group influenza virus.
Influenza C appears to be antigenically stable.
 - Virus isolated in 1933.
 - Major antigenic change occurred twice.
 - 1957 (H2 N2) strain.
 - 1968 (H3 N2) strain.
 1946-1956- (H1 N1) strain

51. AGENT FACTORS
 a) RESERVOIR OF INFECTION:
 Exists in animals and birds.E.g.: swine, horses,
dogs, cats, domestic, poultry, and wild birds.
 Animal reservoirs provide new strains of influenza
virus by recombination of virus from humans,
birds and animals.
 b)SOURCE OF INFECTION: Usually a case of
influenza or sub clinical case.
 - During epidemic – many are mild and
asymptomatic . which play vital role in spread.
 -The secretions of respiratory tract are infective.
PERIOD OF COMMUNICABILITY: Virus found in
nasopharynx 1-2 days before and 1-2 days after
onset of symptoms

52. HOST FACTORS
 a) AGE AND SEX: Influenza affects all ages and
both sexes children will be a link in
transmission chain.
 -Mortality rates are more during epidemics in
aged, children < 18 months and people with
diabetic or chronic heart disease, kidney and
respiratory ailments.
 B)HUMAN MOBILITY: Important factor in spread

53. HOST FACTORS
 a)IMMUNITY: Antibodies are important in
influenza immunity.
 Antibody to H neutralizes the virus; Antibody
to N modifies the infection. Secretary
antibodies develop in the R.T. after infection
and will be mainly of Ig G.
 - Antibodies appear in about 7 days after an
attack and reach a maximum level in about 2
weeks. After 8-12 months the antibodies drop
to pre infection level.

54. EPIDEMIOLOGY
 ENVERONMENTAL FACTORS:
 a) SEASON: winter months in N.H, winter
or rainy season in S.H. In India – epidemics
have often occurred in summer.
 b)OVERCROWDING: Enhances
transmission. Attack rate high in schools,
institutions, ships and industries.
 MODE OF TRANSIMMISION:
 Person to person by drop let infection or
droplet nuclei created by sneezing;
coughing or talking, The portal of entry is
R.T.

55. PATHOGENESIS &C.F:
 I.P: 18-72 hours.
 PATHOGENESIS-AND-CLINICAL
FEATURES:
 Enters the R.T – causes inflammation and
necrosis of superficial epithelium of
tracheal and bronchial mucosa followed by
secondary bacterial infection.
 No viraemia. Fever, chills, aches and pains,
coughing and general weakness fever lasts 1-50
days. Common complication – pneumonia

56. LABORATORY DIAGNOSIS
 LABORATORY DIOGNOSIS:
 a)VIRUS ISOLATION: Naso pharyngeal
secretions are best specimens. Virus can be
detected by indirect fluorescent antibody
technique egg inoculation is required for
virus isolation and antigenic analysis.
 b) PAIRED SERA: Two sera specimens
should be examined – one specimen and 5th
day: 2nd one 10-14 days
 - In C.F. antibodies are 4 fold or greater rise
in titer – is diagnostic.
 - Six pairs of sera should be examined from
one locality.

57. VIRUS ISOLATION
 IN INDIA: Influenza virus isolation can be
done by
 1.Influenza center, Pasteur institute coonoor.
 2. Haffkine institute; Mumbai.
 3. School of tropical medicine, Kolkata.
 4. AIMS.
 5. A.F.M.C.Poona (pune).

58. PREVENTION
 Prevention:
 - Good environment
 - Health education.
 -Immunization – two weeks before epidemic.
 -Vaccination – recommended in select groups,
elderly, industrial workers, public servants,
 Chronic and severely ill

59. PREVENTION
 a) KILLED VACINES: Vaccine strains are
grown in allontoic cavity of developing
chick embryos, harvesting, purified and
killed by formalin or beta propiolactones.
 - One dose of vaccine contains 15
micrograms of HA. 0.5ml given S.C
 - 2ND doses with 4 weeks interval should be
given.
 - Protective value of the vaccines between
70-90% revaccination on annual basis.
 Fever, local inflammation and rarely
G.B.syndrome

60. VACCINATION
 a) LIVE VACINES: Nose drops.
 b) Newer vaccines:
 1. Split virus vaccine sub-virion vaccine.
 2. Neuraminidase specific vaccine.
 Recombinant vaccine

61. TREATMENT
 ANTIVIRAL DRUGS:
 ANTIVIRAL DRUGS HAVE BEEN TRIED FOR
THE PROPHYLAXIS AND TRATMENT OF
INFLUENZA TYPE-A INFECTIONS.
 1.AMANTIDINE& 2.RIMANTIDINE:
 BOTH DRUGS CAN BE USED IN
PROPHYLAXIS & TREATMENT OF
INFLUENZA TYPE-A INFECTIONS.100mg
TWICE A DAY FOR 3-5 DAYS.