remerging disease

1. Emerging & Re-emerging BacteriaI
Infection
Dr. Sshrutkirti Gupta
Assistant Professor
Dept. Microbiology
IIMSR
.

2. Microbes were here on earth 2 billion years
before humans arrived, learning every trick for
survival, and it is likely that they will be here 2
billion years after we depart (Krause 1998).

3. Definition of Emerging infectious
diseases
 A/c to CDC- “New, reemerging or drug-resistant
infections whose incidence in humans has
increased within the past three decades or whose
incidence threatens to increase in the near
future.”
 Infections that have newly appeared in a
population or have existed previously but are
rapidly increasing in incidence or geographic
range (Morse 1995)

4. Classification of Emerging
Infectious Diseases
 Newly emerging
 Have not previously been recognised in man.
 Re-emerging / Resurging
 Existed in the past but are now rapidly increasing either
in incidence or in geographical or human host range.
 Deliberately emerging
 Microbes are those that have been developed by man,
usually for causing bioterrorism

5. Why we are so concerned for
emerging and re-emerging
Infection?

6. Epidemics or pandemics :
 Often take a heavy toll of life .
 Rapidly spread across borders.
 Economic, developmental and security challenge.
 26 % of annual deaths worldwide.
 1,407 species of human pathogens, with 177 (13%) species
regarded as emerging or re-emerging.
 37 % of emerging and re-emerging pathogens are viruses
and prions followed by protozoa (25%) (T. Dikid et al. 2013).

7. After great advances in medical research and
antimicrobial drug discovery, technology
development, improvement in sanitation..
Why are microbes still posing such a problem?

8. Contributing Factors:
2/3rd emerging infections originate from
animals- wild & domestic.(zoonosis).
Evolution of pathogenic infectious
agent(microbial adaptation & change:
mutations).
Resistance to drugs.(MRSA)
Resistance of vectors to pesticides
(malaria).

9.  Changes in human and demographic behaviour.
 International travel and commerce.(Traveler's
diarrhea)
 War and famine.
 Ecological changes and Agricultural development.
 Placing the people in contact with a natural
reserviour or host.
Contributing Factors con…

10. Increases in the elderly populations.
Increases in children in daycare: working woman
with kids under 5 was 30% in 1970, is 75% in 2000.
Fast paced Lifestyles- increase in convenience items
and more stress.
High-risk behavior- Drug use and unprotected sex.
Urbanization-more people concentrate in cities-often
without adequate infrastructure.
Contributing Factors con…

11. Causes:
• Wrong prescribing practices
• Non-adherence by patients
• Counterfeit drugs
• Prolonged hospital admissions e.g. MRSA, VRE
Antimicrobial Drug Resistance

12.  It used to take 365 days to circumnavigates globe, now
it takes 36 hours.
 400 million people per year travel internationally.
 Increased incidence of both Tuberculosis and
Influenza transmission on long flights.
International travel and commerce

13. • Global warming-climatologists project
tempratures
to increase by 5.8°C by 21 degree .
• Elevated rainfall.(Plague)
• Increases vegetation which increases
rodents.(Lyme disease).
Climate and Weather

14.  Bioterrorism is a form of terrorism where there is
international & deliberate release of biological agent to
cause mass illness or death of people & animals.
 Biological agents are attractive instruments of terror-
easy to produce, difficult to detect, widespread panic &
civil disruption.
 Highest potential- B. anthracis, C. botulinum toxin, Y.
pestis Melliodosis.
Bioterrorism

15.  Modern mass production increased the chance of
accidental contamination and amplifies the effect of
such contamination. e.g. contamination of hamburger
meat by E. coli strains.
 New diagnostic technology lead to identification of
previously unknown microbes for known diseases e.g.
Helicobacter pylori and peptic ulcer.
Technology and Industry

16. Year Bacteria Disease
1977 Legionella pneumophilla Legionnaires disease
1977 Campylobacter jejuni Enterititis
1981 Exotoxin
producing Staph. aureus
Toxic shock syndrome, Scalded skin
syndrome
1982 E .coli 0157 :H7 Haemorrhagic colitis ,Haemolytic
uremic syndrome
1982 Borrelia burgdorferi Lyme disease
1983 Helicobacter pylori Peptic ulcer
1992 Vibrio cholerae O139 Cholera
Emerging Bacterial infection in the
world since 1975

17. Year Bacteria Disease
1992 Bartonella henslae Cat scratch syndrome
1994 Yersinia pestis Plague , Bubonic plague
2001 Bacillus anthracis Anthrax
2008
NDM-1resist K.
Pneumoniae
Various infection

18. Global examples of emerging and re-emerging infectious
diseases.

19. A BRIEF SURVEY OF EMERGING AND RE-EMERGING
BACTERIAL DISEASES OF PUBLIC HEALTH
IMPORTANCE IN INDIA
 Plague re-appeared in two outbreaks in Maharashtra and
Gujarat in 1994, indicating a breakdown of the public health
measures that had prevented its occurrence for several
decades.
 Leptospirosis appears to be on the increase in Kerala,
Tamilnadu and the Andaman's during the last 2 decades,
probably due to increased farming and inadequate rodent
control.
 It is suggested that Melioidosis due to the soil organism
Burkholderia pseudomallei may be prevalent in many parts

20.  Since 1991, a completely new choleragenic Vibrio
cholerae, designated 0139 has emerged in southern
India and spread to other parts of India and to
neighboring countries, setting in motion the 8th cholera
pandemic.
 Since 1990, a multi-drug resistant variety of typhoid fever
had been prevalent in many parts of India, caused by
Salmonella typhi resistant to chloramphenicol, ampicillin
and trimethoprim-sulphamethoxazole.
 Nosocomial methicillin-resistant Staphylococcus aureus
infection seems to be widely prevalent in hospitals in
many regions in India, and its prevalence seems to be on
the rise.

21. Some Example of Emerging bacterial
infection
• Legionellosis
• Meliodosis
• Helicobacter pylori
• Infection
• Lyme disease
• Rickettsia.

22. Legionellosis
• Cause: Legionella pneumophila.
• Legionella Was first recognized in 1976 when an
outbreak of pneumonia took place at a Philadelphia
hotel during American Legion Convention.
• Properties of the genus Legionella
• Gram-negative rods.
• Strictly aerobic
• Found in highly aerated, moist environments
e g. Streams.
• May parasitize certain aquatic protozoa
• Can contaminate building ventilation systems, air filters,

23.  In April 1997 &December 1998 60 pt. were admitted to
the AIIMS New Delhi with community acquired
pneumonia,15% cases positive for legionella.
 In Toranto September 2005, 127 resident of nursing
have become ill with Legionella &21 resident died with
in one week.

25. Pathogenesis of legoinella

26. Pontiac fever
 A milder infection caused by legoinella, is called Pontiac
fever.
 The symptoms of Pontiac fever are similar to those of
Legionnaires disease and usually last for 2 to 5 days.
 Incubation period about 2-10 days.
 Symptoms:-
 Fever
 Headache
 Sore throat
 Nausea and cough

27. Legionnaires disease
 It is an interstitial atypical pneumonia with incubation
period about 2-10 days.
 It is the fourth common cause of community acquired
pneumonia.
 It is characterized by non productive cough.
 Chest pain
 Fever
 Dyspnoea
 Diarrhea

28. Risk factor
 Advanced age.
 Smoking , Alcoholism .
 Immuno suppression transplantation.
 Prior Hospitalization.
 Chronic lung disease.

29. Lab Diagnosis
 Specimen:-Sputum ,Bronchial lavage Fluid, Pleural fluid
 Direct microscopy:- Gram stain-Gram negative
cocobacilli. Silver impregnation and Giemsa stain
 Direct immunofluoroscence test
 Culture:-
 (BCYE) Buffered charcoal yeast extract agar(pH 6.8-
6.9)-plate
are incubated at 37°C in 5% C02 for 3-5 Days, Colonies
Round circular with an entire edge, glistening convex
green iridescent.
 Serology ELISA
 PCR

30. MELIODOSIS
 Melioidosis is an emerging infection in India, especially in
male from rural area with diabetes and alcoholism being a
common risk factor caused by Burkholderia pseudomallei .
 B. Pseudomallei is saprophyte found in soil , water and
large number in animal reservoirs.
 B. pseudomallei was first described by Whitmore and
Krishna (1902) from a glanders like disease in human in
rangol.
 It was first discovered in north Australia in far northern
Queensland in 1962.

31. In India most cases of meliodosis are reported from Kerala ,
Tamilnadu , Maharashtra , Orissa in 2005-2010(R. gopal
krishna et al 2013).
Incidence of Meliodosis recorded for region of Alor Setar,
Kedah Malaysia(16.35per 100,000) in 2009(Muhammad R.A.
Hassan et al 2010) .

32. Types of meliodosis
Acute meliodosis:-is characterized by development of a
nodule at the site of inoculation of the bacteria in the skin. The
bacteria subsequently spread, causing secondary lymphangitis,
fever, and myalgia.
Pulmonary Infection:- manifest as mild bronchitis to severe
pneumonia. The condition is associated with high fever,
headache, chest pain.
Chronic suppurative infection:- it is associated with multiple
caseous or suppurative foci of infection in several organ
including joints, lymph nodes spleen, lungs, liver, and brain .

33.  The infection start with nonspecific lesion at the
inoculums where there can be break in the skin.
 Lead to septicaemia.
 Most common form is pulmonary infection can lead
to suppurative infection and bacteraemia.

34. Transmission:-
Contaminated water with excreta of infected animal.
Inhalation of infected aerosols.
Contaminated food , soil.
The infection also may be transmitted by the bite of
hematophagous insects.
Skin abrasion.
Pathogenesis:
The disease can manifest as acute ,sub acute and
chronic disease .
Incubation may be short as 2-3 days.
Latent infection can occur after month to year.

35. Lab diagnosis
 Specimen:-Sputum, Pleural discharge from lesion
 Direct microscopy:- Gram’s stain- Gram negative bacilli
typically exhibit a bipolar appearance.
Methylene blue stain
 Culture:-Nutrient medium, Ashdown’s medium.
 Biochemical test- Gelatin liquefaction test –positive.
 Arginine test –it utilizes arginine.

36. Helicobacter pylori
 Helicobacter pylori was isolated in1983 by Warren and
Marshall in Australia .
 It is gram’s negative rod that colonizes stomach.
 It is microaerphilic and grown in the presence of
decrease oxygen concentration(5%) and increase co2..
 It is highly motile and show cork screw motility.
 It is associated with peptic ulcer disease and gastric
carcinoma.

37. • H. pylori infection occurs worldwide.
• Prevalence varies greatly among countries and population
groups.
• 20 – 50% prevalence in middle age adults in
industrialised countries.
• More than 80% prevalence in middle age adults in
developing countries.
• In European Regions ,Clarithromycin resistance H. Pylori
was reported from Narwey 5.9%, 32.0% in Spain in 2009.
• Clarithromycin resistance were reported from India 58.8%
China 46.54% Malaysia 2.4% in 2014.

38. Site of infection

 Highly adapted organism that lives only on gastric mucosa.
 Gastric antrum is the most favoured site .
 Present in the mucus that overlies
Transmission:-
 Person to person contact .
 Fecal oral transmission.
 Oral ingestion of bacterium

39. Helicobacter pylori infection
Peptic ulcer disease
• lifetime risk 3% in US, 25% Japan.
• Eradication provides long-term cure
Gastric carcinoma
• Strong evidence of increased risk 0.1-3%
• Unclear whether eradication reduces the risk of gastric
cancer
MALT lymphoma
• 72%→ 98% of MALT lymphoma infected with H. pylori

40. Lab diagnosis
 Specimen:- Stool sample, gastric biopsy sample.
 Microscopy:- Gram stain-Gram negative bacilli
Hematoxylin –eosin stain.
 Culture :- Chocolate agar , Skirrow campylobacter
selective media.
 Biochemical test-Catalase test –positive
Oxidase test positive
Urease test positive
 Rapid urea test
 Antibody detection test by ELISA

41. Lyme Disease
 First identified in 1975 in
a group of arthritis
patients in Lyme,
Connecticut , in the
United State.
 1978 it was found to be
tick related
 1981 Borrellia burgdorferi
was identified as the
main cause of Lyme
disease

42.  It is endemic in United States, and has also been
reported from Europe, Middle-East, South-East Asia,
former Soviet Union and Australia, mainly based on
the habitat of the Ixodes ticks.
 There have been few cases reported from India,
Patial, et al. have reported a case of Lyme disease in
India by finding Borrellia in the blood smear of a 15
year old boy in Shimla.
 The Centre for Disease Control and Prevention (CDC)
carried out surveillance for Lyme disease in India 1982
and 1991.(Biju vasudevan et al in 2013).

43. Transmission
 It is transmitted by tick bite (ixodes ricinus).
 All three stages of tick , I.e. larval, nymphal, and adult
stage can transmit the infection.
 The incubation period varies from 7-14 days.
 It is transmitted through the skin and spread locally.
Symptoms
 Annular maculo papular lesion.
 Fever ,Chill.
 Musculoskeletal pain.
 Fatigue.

44. Lab diagnosis
 Specimen:- Skin lesion , Blood , CSF in BSK medium
(Barbour stoenner,Kelly).
 Microscopy:- Dark field microscopy.
 WBC count: Joint fluid exam.
 Serology:- ELISA, western blot for detection of IgG & IgM
antibody.
 C6 peptide IgG ELISA .

45. RICKETTSIOSIS
• Rickettsiosis consist of a spectrum of vector borne
disease caused by small Gram’s negative obligate
intracellular parasites.
Which include Epidemic Typhus, Scrub Typhus, and
spotted fever.
• Cell membrane similar to Gram (-) bacteria with LPS &
peptidoglycan.
• The organisms will not show up on Gram stain, but can
be seen with Giemsa stains.
• Will not grow on artificial media.
• Grown in embryonated eggs or tissue culture.

46.  Four confirmed case found in KGMU hospital at Lucknow in
Nov.2013,which include tick borne agent Rickettsia rickettsii, R.
conorii & R. akari.(M. Singh, Dr Jyotsna Agarwal et al2013)
 During 2010-2011, eleven outbreak were reported from
himachal pradesh in kangra, Shimla, Solan Sirmapur(Vishal
dasari et al2014.
 Two from manipur ,one each from Jammu& kashmir& North
indian state.(Vishal dasari et al (2014).
 24 cases of scrub typhus fever were seen over a period of 2
month Nov.2014 –Dec.2014in Rajasthan.
 46% positive patient. reported in south vietnam and Tiwan
respectively (Mobeen H. Rathore et al 2016).
 Rickettsial disease have been reported various part of India
namely Jammu & Kashmir, uttarakhand, Maharashtra Kerala,

47. Transmission
 Rickettsia are usually introduced into human skin by the
bite of an insect (flea or louse) & (tick or mite)
 R. Rickettsii invades the endothelial cells that line the blood
vessels
 Incubation period: 2-14 Days
 changes in the host cell phagocytosis
 bacterial surface protein

48. Pathogenesis
 Endothelial damage & vasculitis progress causing
 development of maculo papular skin rashes
 perivascular tissue necrosis
 thrombosis & ischemia
 Endothelial damage can lead to activation of clotting
system Disseminated intravascular coagulation (DIC)
 Infected cells show intracytoplasmic inclusions &
intranuclear inclusions

49.  During the first few days of incubation period
 local reaction caused by hypersensitivity to tick or vector
products
 Bacteria multiply at the site & later disseminate via
lymphatic system
 Bacteria is phagocytosed by macrophages (Ist barrier to
rickettsial multiplication)
 After 7-10 days
 organisms disseminate replicate in the nucleus or cytoplasm
of endothelial cells causing vasculitis

50. Spotted fever
 Spotted fever is caused by Rickettsia rickettsii .
 It is transmitted by various genera of tick such as
Dermacentor andersoni in USA Amblyomma
cajennense in south America.
 Transmission – by the bite of infected tick.
 Incubation period is 4 days to 14 days

51.  Symptoms: severe headache, chills, fever, and
after a fourth day, a maculopapular rash caused
by subcutaneous hemorrhaging as Rickettsia
invade the blood vessels.
 The rash begins on the upper trunk and spread
to involve the whole body except the face, palms
of the hands, and the soles of the feet.
 The disease lasts about 2 weeks and the patient
may have a prolonged convalescence.

52. Lab diagnosis
 Serology-Weil Felix test-Rickettsial antibodies detected
against proteus ox19, ox2, & oxK antigen.
 Specific antibody detection by Immunofluoroscence test,
ELISA & latex agglutination test.
 Histopathological examinations done by cutaneous
biopsy sample.
 PCR

53.  Cholera
 Plague
 Anthrax
 Tuberculosis
 Diphtheria
 MRSA
EXAMPLES OF RE-EMERGING DISEASES

54. CHOLERA
 Cholera is one of the oldest recorded infectious diseases.
 John Snow demonstrated the spread by infected water.
 Pacini in 1854, first described comma shaped bacteria.
 Robert Koch in 1883, showed the causative agent V.
Cholerae.
 Das and Gupta -2005 reported the diversity of V.
Cholerae.
 Narang et al (2008) described the changing patterns of V.
Cholerae.

55. •Vibrio cholerae O139, a new serogroup was associated with
this epidemic cholera
• India in 1992 starting in southern peninsular India and
spreading both inland and along coast line of Bay of Bengal.

56.  Genus Vibrio
 Cause: Vibrio cholerae
 Gram-negative curved bacteria
 comma-shaped
 facultatively anaerobic
 Normal flora in many animals
 Notable Pathogenic Species
 Vibrio cholerae
 Vibrio parahaemolyticus
 Vibrio cholerae o139

57. Transmission:-
 Contaminated food.
 Contaminated water.
Symptoms:-
 Sudden onset of painless watery diarrhea
 Rice water stool
 Vomiting may be present
 Muscle cramps

58. Laboratory diagnosis
 Specimen:- watery stool , or rectal swab.
 Direct microscopy:- Gram negative rods short curved
comma shaped .
Hanging drop demonstrate darting motility.
 Culture:-Bile salt agar TCBS agar, Monsur'sTaurocholate
tellurite agar
 Biochemical identification:- catalase test –positive
Oxidase test- positive Indole (+) citrate (+/-) urease (-)
TSI- A/A H2S (-)
 Cholera red reaction (+)
 Serotyping- To differentiate Ogawa, Inaba &Hikojima
serotype of serogroup.
 Anti microbial susceptibility test.

59.  Plague is a zoonotic disease ,caused by
Yersinia pestis.
 Plague epidemic have occurred in Africa ,
Asia & America.
 Yersinia pestis was isolated by Alexander
yersin in 1894 in Hong Kong.
 plague in human can occur either by the bite
of infected rat flea flea: Xenopsylla cheopis.
 It is transmitted by close contact with infected
tissue ,body fluid or direct inhalation of
bacteria.
 Plague occur in three forms:-
1. Bubonic plague
2. Pneumonic plague
3. Septicemic plague
PLAGUE

60.  Out break of bubonic plague were reported in Beed- Latur
district of Maharashtra. sept.1994. Out break of pneumonic
plague was reported in surat and Guajrat and Maharashtra
6000 suspected cases and 60 death were reported in these
outbreak.
 In 2002 Ashort outbreak were reported Rohru at near Shimla.
 61 cases of plague reported in United state in 2003.
 In 2004 Uttar kashi Localized outbreak of bubonic plague was
reported from dangud village of Uttarkashi district Uttaranchal.
 During 2006 13 cases were reported in 2006 in state Mexico &
Taxas(T. Dikid et al 2013.)

61. Source of infection
 Infected wild rodent.
 Rat flea.
 Cases of Pneumonic plague.
Transmission:-
 Bite of infected rat flea.
 Direct contact of infected tissue of infected animal.
 Droplet inhalation from cases of Pneumonic Plague.

62. Laboratory diagnosis
 Specimen:- Pus or fluid aspirated from buboes , sputum
&blood
 Direct microscopy:- Gram’s negative oval coccobacilli
with round end surrounded by capsule.
 Way son stain –Bipolar safety pin appearance.
 Culture:- Blood agar nonhemolytic &dark brown
pigmented due to absorption of hemin pigment.
 Nutrient broth :- granular turbidity with surface pellicle
formed later.
 Biochemical reaction:- Catalase (+) Oxidase(-) MR(+)
 Molecular method:- PCR
 Serology- ELISA ,DIRECT immunofluoroscence test

63. Anthrax
 From the Greek word anthrakos for coal.
 Caused by spores.
 Primarily a disease of domesticated & wild animals.
 Natural reservoir soil.
 Does not depend on an animal reservoir making it
hard to eradicate.
 Cannot be regularly cultivated from soils where there
is an absence of endemic anthrax.
 Occurs sporadically throughout US.

64.  2010-11, anthrax was reported in Osmanabad
district. In 2011-12, it was reported in Pune,
Jalgaon, Ahamad nagar and Beed districts.
 In august 2011 2% cases reported a cluster of
cutaneous Anthrax cases to the Andhra
pradesh.(R.reddy et al2012).

65. Anthrax Infection & Spread
 May be spread by streams, insects, wild animals, birds,
contaminated wastes
 Animals infected by soil borne spores in food & water or bites
from certain insects
 Humans can be infected when in contact with flesh, bones,
hides, hair.
 nonindustrial or industrial
 cutaneous & inhalational most common
 Risk of natural infection 1/100,000

66. Lab diagnosis
 Specimen:- Pus ,Sputum, CSF blood.
 Direct microscopy:- Gram’s stain Gram positive ,large
rectangular bacilli
 McFadyean’s reaction:- polymorphous purple capsule
surrounded by blue bacilli.
 Direct immunofluoroscence test .
 Culture- Nutrient agar – medusa head appearance.
 Gelatin stab agar- Inverted fir tree appearance.
 Solid medium with penicillin:- string of pearl colonies.
 Antibody detection by ELISA .
 Molecular method:- PCR detecting specific gene.

67. Cause: Mycobacterium tuberculosis.
 Properties of the genus Mycobacterium:-
 Acid-fast rods.
 Grow slowly; some species are difficult to culture
 Several species;
some found in soil and among skin flora
 Major pathogenic species:
 Mycobacterium tuberculosis
 Mycobacterium avium-intracellulare
 Mycobacterium leprae
 Multidrug resistance tuberculosis
TUBERCULOSIS

68.  Tuberculosis is one of the oldest disease of mankind, and
major cause of death world wide.
 Tuberculosis is classified as pulmonary and extra pulmonary .
• PULMONARY TUBERCULOSIS(PTB) accounts for 80% of
all cases of tuberculosis.
• EPTB result from haematogenous dissemination of tubercle
bacilli to various organ.
• EPTB constitute about 20-50%of all cases of
tuberculosis.During 2005-2007.
• 36% 0f MDRTB detected&56%of XDRTB cases reported in
united state(Roger detel et al 2016).

69. Transmission
 Airborne Contact Prolonged Exposure.
 Occasionally via skin contact
or wounds.
 Inhalation of droplet nuclei.
 Consumption of unpasteurized milk.
 Swallowing of sputum.

70. Lab diagnosis
 Specimen collection
 Direct microscopy by acid fast staining
 Conventional culture media –takes 6-8 weeks
 Automated culture media – takes 2-3 weeks
 Biochemical identification
 Serology
 Molecular methods

71. Diphtheria
Properties of the Genus Corynebacterium
 Gram-positive rods; non-spore forming
 Coryneform (diphtheroid) arrangement
 “Snapping division”
 Met achromatic Granules
 Several different species
 Frequently found in soil & in the skin flora
 Only virulent strains of Corynebacterium
diphtheriae
are considered pathogenic

72.  Diphtheria outbreak were reported in two village of Northern
Karnataka in South India in may 2011.(Mahantesh et al2014).
 The National Health Profiles released by the Government of
India reported 3812, 3977, 3529, 3123 and 3485 cases of
diphtheria respectively from 2007 to 2011.
 Hyderabad and Pondicherry in South India (CBHI, 2011;
Sharma et al., 2007; Dravid & Joshi, 2008; Nath & Mahanta,
2010; Sashikala et al., 2011).
 The recent report of National Health Profiles released by the
Government of India (CBHI, 2012) in 2012 showed that the
number of reported cases of diphtheria in Karnataka increased
from 0 in 2010 to 217 during 2012 |(V Parande et al 2014).

73. Transmission & Symptoms
 Airborne; contact with infected persons
 Upper Respiratory Infection
 Pseudo membrane Formation
 May Spread into Bloodstream
 Cardiovascular damage

74. Lab Diagnosis
 Specimen:- Throat swab
 Direct smear :- Gram’s stain Club shape gram-positive
bacilli.
 Albert stain:- green bacilli with bluish black met
achromatic granules.
 Culture medium :- Blood agar- colony appear as small
circular white some time hemolytic
 Loeffler's serum slope colony appear small ,circular
glistening and white.
 PTA agar black colour colony
 Biochemical test- Pyrazinamidase Catalase (+) Oxidase
(-)
 Elek’s gel precipitation test-

75. MRSA
 Methicillin resistant is S. aureus is mediated by a
chromosomally coded gene called mec A gene which
alters penicillin binding protein present on S. aureus cell
membrane to PBP-2a.
 PBP is essential protein needed for cell wall synthesis
of bacteria. Beta lactam drugs bind and inhibit this
protein, there by inhibit the cell wall synthesis.
 The altered PBP 2a of MRSA strains has less affinity for
beta lactum antibiotics; hence, MRSA strains are
resistance to all beta lactum antibiotics.

76. Mode of Transmission
 It is transmitted by contact with a person who has
MRSA infection or is colonized with the organism.
 Hands of the health care workers is the most common
mode of transmission from patient to patient.

77. Factors that Facilitate Transmission
Cleanliness
Contaminated Surfaces
and Shared Items
Compromised Skin
Antimicrobial use

78. What are the

79.  Surveillance at national, regional, global level
 Epidemiological
 Laboratory
 Ecological
 Anthropological
 Investigation and early control measures
 Implement prevention measures
 Behavioural, political, environmental
 Monitoring, evaluation
Key tasks in dealing with emerging
diseases

80. Generic model of the organization of a rapid research response to an
emerging infectious disease.

81. Global
National
Regional
Synergy
Key tasks - carried out by

82. Infectious
diseases
Public
Health
Telecom. &
Informatics
Epidemio-
logy
International
field
experience
Laboratory Information
management
Multiple expertise needed

83.  Strong National disease surveillance and control programmes.
 Global networks of centres, organisations and individuals to
monitor diseases.
 Rapid information exchange through electronic links to guide
policies, international collaboration, trade and travel.
 Effective national and international preparedness, and rapid
response to contain epidemics of international importance.
WHO’s vision for the 21st Century

84.  Surveillance standards
 “Integrated” national surveillance systems
 Outbreak surveillance, verification and response
 Field epidemiology training
 Laboratory strengthening
WHO’s approach to surveillance

85.  Strengthening surveillance and rapid response mechanisms
 Complying with International Health Regulations (IHR)
 Building capacity in epidemiology
 Strengthening of laboratory and networks
 Research and development
 Information sharing and partnerships
Combating emerging infections: strategies
and response capacities in India

86. Strengthening surveillance and rapid
response mechanisms:
1994 Central Council Of Health And Family Welfare
1995 State and District level epidemiological units
1996 National Apical Advisory Committee
1997 National Surveillence Programme on Communicable
Diseases
1999 Technical advisory group
2004 Integrated Disease Surveillance Project (101 district)

87. IDSP (Integral disease servivelence project)
 Augment surveillance activities and response mechanisms –
epidemiologists and microbiologists.
 Cover all States and districts each district now has a surveillance
unit and a rapid response team (RRT) to quickly manage .
 IT connectivity established .
Complying with International Health Regulations (IHR) :
 (2005) 194 member countries .
 Aim : prevention of disease spread across borders.
 India ; implements various provisions ,enhance national and global
public health security by preventing and responding to acute public
health risks.

88. Research and development:
 (2007)The Government of India created a new Department of Health
Research in Ministry of Health and Family Welfare.
 Provide technical support : epidemics and natural calamities
&development of tools for prevention.
 Specific programmes : identification of agent; diagnostic tests; case
management modules and preventive strategies; establishment of
laboratories.
 The Indian Council of Medical Research (ICMR) body : formulation,
coordination and promotion of biomedical research
 Information sharing and partnerships: NCDC

89.  PARK’S Textbook of PREVENTIVE AND SOCIAL MEDICINE.
 T. Dikid, S.K. Jain Emerging & re-emerging infections in India: An
overview Indian J Med Res 138, July.
 Mortada H. F. El-Shabrawi et al
 Subhash Chandra Parija text book of micro biology and immunology.
 Anantha narayan and Paniker’s text book of microbiology
 R . Gopalkrishna Melioidosis : An Emerging Infection in India 2013
 Pullab ray Vikas goutam & Rachna singh MRSA in developing &
developed countries :Implication &solution.
 Muhammad RA Hassan, Edwin Michael. Incidence, risk factors and
clinical epidemiology of melioidosis: a complex socio-ecological
emerging infectious disease in the Alor Setar region of Kedah,
Malaysia Infectious Diseases2010.
 Choudhry R Dhawan B. incidence of Legionella pneumophila: a
prospective study in a tertiary care hospital in India.
REFERENCES