This document discusses several emerging and re-emerging zoonoses including bovine spongiform encephalopathy (BSE or mad cow disease), American trypanosomiasis (Chagas disease), cryptosporidiosis, Ebola hemorrhagic fever, cyclosporiasis, hantavirus pulmonary syndrome (HPS), and influenza. It provides definitions, etiologies, epidemiologies, symptoms, diagnoses, and control methods for each disease. The document is presented as part of a class on emerging and re-emerging zoonoses.

1. EMERGING AND RE-EMERGING
Prajwal S.
14-M.V.M-49
ZOONOSES

2. DEFINITION
EMERGING ZOONOSES;
A zoonosis that is newly recognized or newly evolved.
Shows an increase in incidence.
Expansion in geographical host or vector range.(W.H.O)
RE EMERGING ZOONOSES
Is considered an already known disease
Shifts its geographical setting.
Expands its host range.
Significantly increases its prevalence. (O.I.E)
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3. CONTENTS
Definition
Etiology
Epidemiology
Symptoms
Diagnosis
Control and prevention
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4. BOVINE SPONGIFORM
ENCEPHELOPATHY(B.S.E)
Syn Mad Cow Disease
Fatal neurodegenerative disease (encephalopathy)
Spongy degeneration in the brain and spinal cord.
BSE has a long incubation period, about 30 months to 8
years, all breeds being equally susceptible.
Etiology
The Prion = Proteinaceous infectious particle
Nature of the transmissible agent is not well
understood.
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5. PRION
Fibril model of prion propagation
PrPC (for Common or Cellular)
PrPSc for Scrapie
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6. By www.cdc.gov/ncidod/dvrd/bse/
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7. 7 11/20/14

8. SYMPTOMS
Deteriorating behavioral
and neurological signs.
Increase in aggression.
Slowly become ataxic.
Systemic signs of disease,
Drop in milk production.
Anorexia and lethargy.
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9. DIAGNOSIS
No ante mortem testing available
Sample
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10. POST MORTEM DIAGNOSIS
Histopathology of brain tissue
Spongiform changes in
gray matter
Detection of abnormal prion protein
Differentials
Nervous ketosis,
Hypomagnesaemia, Listeriosis,
Polioencephalomalacia, Rabies,
Brain tumor, Lead poisoning
Spinal cord trauma.
z
Conti…
10 11/20/14

11. DIAGNOSIS
All are based on antibodies to detect prion protein in
tissue
Immunohistochemistry (IHC) is considered the gold
standard
Internationally recognized
Expensive, labor intensive
Rapid diagnostic tests
Western blotting, ELISA
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12. CONTROL
Feeding regulations and surveillance measures. A ban on
feeding cattle meat and bone meal
At the abattoir , the brain, spinal cord, trigeminal ganglia,
intestines, eyes and tonsils from cattle are classified as
specified risk materials, and must be disposed of
appropriately.
India has been recognized as the most secure status for
the deadly mad cow disease.(78th W.H.O general session)
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13. AMERICAN TRYPANOSOMIOSIS
syn; Chagas disease
Is a potentially life-threatening illness
Caused by the protozoan parasite, Trypanosoma cruzi (T.
cruzi).
It is found mainly in Latin America, where it is
Mostly transmitted to humans by the faeces of triatomine
bugs, known as kissing bugs
Carlos Ribeiro Justiniano Chagas, a Brazilian doctor who
discovered the disease in 1909.
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14. ETIOLOGY
Is a hemoflagellate is
found in mammalian
blood and is 15 to 20
microns in length.
•VECTOR
•TRITOMINE BUG (KISSING BUG)
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15. LIFE CYCLE

16. EPIDEMIOLOGY
Chagas disease occurs
mainly in Latin America.
This is due mainly to
population mobility
between Latin America
and the rest of the world.
TRANSMISSION
Blood transfusion
Organ donation
Congenital transmission
(from infected mother to
child)
www.cdc.gov/chagas

17. SIGNS AND SYMPTOMS
Acute phase ( 2 months after infection)
Fever, headache, enlarged lymph glands, pallor, muscle
pain, difficulty in breathing, swelling and abdominal or
chest pain.
Chronic phase
Cardiac disorders
Digestive disorders(typically enlargement of the
esophagus or colon)
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18. DIAGNOSIS
Microscopic examination of fresh anticoagulated blood, or
its Buffy coat, for motile parasites; or by preparation of
thin and thick blood smears stained with Giemsa, for direct
visualization of parasites.
Complement fixation
Indirect hemagglutination
Indirect fluorescence assays
Radioimmunoassay, and ELISA
Polymerase chain reaction
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19. CRYPTOSPORIDIOSIS
Is a protozoan disease caused by Cryptosporidium.
It affects the intestines and is typically an acute short-term
infection.
It is spread through the fecal-oral route, contaminated
water .
Symptom is self-limiting diarrhea in people with intact
immune systems. In immunocompromised individuals,
the symptoms are particularly severe and often fatal.
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20. ETIOLOGY
Micrograph showing cryptosporidiosis.
The cryptosporidium are the small, round bodies in
apical vacuoles on the surface of the epithelium.
H&E stain (Colonic biopsy)
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21. EPIDEMIOLOGY
Transmission
People who swim regularly in pools with insufficient
sanitation
Child care workers
Parents of infected children
People who take care of other people with
cryptosporidiosis
International travelers
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22. Conti….
People, including swimmers, who swallow water from
contaminated sources
People who handle infected cattle
Backpackers, hikers, and campers who drink
unfiltered, untreated water
People exposed to human feces through sexual contact

23. LIFE CYCLE
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24. DIAGNOSIS
Diagnosis of
cryptosporidiosis is
made by stool samples
Acid-fast staining,
Direct fluorescent
antibody [DFA]
Enzyme immunoassays
for detection of
Cryptosporidium sp.
antigens Cryptosporidium oocysts in a modified acid-fast stain.
(CDC Photo; DPDx)
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25. DIFFRENTIAL DIAGNOSIS
Amebiasis
Campylobacter Infections
Cyclospora
Cytomegalovirus Colitis
Escherichia Coli Infections
Gastroenteritis, Viral
Giardiasis
Isosporiasis
Salmonellosis
Shigellosis
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26. PREVENTION & CONTROL
Practice Good Hygiene Everywhere
At recreational water venues (pools, interactive
fountains, lakes, ocean)
Minimize contact with the feces of all animals
Immunocompromised persons don’t handle suspected
samples
Avoid close contact with any person or animal that has
cryptosporidiosis.
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27. EBOLA HEAMORREGIC FEVER
Ebola hemorrhagic fever (Ebola virus disease) is a severe,
often-fatal disease caused by infection with a species of
Ebola virus.
 The first Ebola virus species was discovered in 1976 in
what is now the Democratic Republic of the Congo near the
Ebola River.
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28. ETIOLOGY
Ebola belongs to a
family of viruses
entitled Filoviridae,
 and is commonly
classified as a viral
hemorrhagic fever
(CDC, 2002).
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29. Filovirus virions are characterized by having one
molecule of single stranded, negative-sense RNA, as
well as their unique "U" shaped structures (CDC, 2002).
RNA viruses, whose survival is dependent on an animal
reservoir.
Viral hemorrhagic fever commonly describes a multiple
organ systems of the body are affected as well as
extensive internal bleeding.
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30. EPIDEMIOLOGY
Ebola Outbreaks
1976-2014
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31. TRANSMISSION
Ebola is spread through direct contact (through broken
skin or mucous membranes in, for example, the eyes,
nose, or mouth)
Blood or body fluids (including but not limited to urine,
saliva, sweat, feces, vomit, breast milk, and semen) of a
person who is sick with Ebola
Objects (like needles and syringes) that have been
contaminated with the virus
Infected fruit bats or primates (apes and monkeys)
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32. LIFE CYCLE
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33. SYMPTOMS
Nausea and vomiting
Diarrhea (may be bloody)
Red eyes
Raised rash
Chest pain and cough
Stomach pain
Severe weight loss
Bleeding, usually from the eyes,
and bruising
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34. Total Cases CDC
Updated: August 19, 2014
Suspected and Confirmed Case Count: 2240
Suspected Case Deaths: 1229
Laboratory Confirmed Cases: 1383
WHO
18 Aug 2014
Total confirmed, probable, and suspect cases and deaths
from Ebola virus disease :
Cases: 2473
Deaths: 1350.
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35. DIAGNOSIS
Timeline of Infection Diagnostic tests available
Within a few days after symptoms
begin · Antigen-capture enzyme-linked
immunosorbent assay (ELISA)
testing
· IgM ELISA
· Polymerase chain reaction
(PCR)
· Virus isolation
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36. PREVENTION
Avoid contact with bats and
nonhuman primates or
blood, fluids, and raw meat
prepared from these
animals.
Wear appropriate PPE.
Isolate patients with Ebola
from other patients.
Avoid direct contact with
the bodies of people who
have died from Ebola.
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37. CYCLOSPORIOSIS
Caused by protozoan
Cyclospora cayetanensis
Pathogen transmitted by feces
and contaminated fruits and
vegetables.
It is not spread from person to
person
Hazard for travelers by being
a cause of diarrhea.
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38. ETIOLOGY
Is a coccidia parasite that
emerged in the last decade
as an important enteric
pathogen
Cyclospora cayetanensis oocysts
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39. 39 11/20/14

40. EPIDEMIOLOGY
Initially tropical and subtropical regions, occurrences
of Cyclosporiasis are becoming more frequent in North
America according to the (CDC).
There were 11 documented cases U.S. government public
health agency, of Cyclospora infection outbreaks in the
U.S. and Canada since the 1990s.
CDC recorded 1,110 laboratory-confirmed sporadic
instances of Cyclosporiasis. As of August 2, 2013
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41. SYMPTOMS
Watery diarrhea (most
common)
Loss of appetite
Weight loss
Cramping
Bloating
Increased gas
Nausea
Fatigue
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42. DIAGNOSIS
Examining stool specimens.
Acid-fast staining, are often used to
make Cyclospora oocysts more visible under the
microscope.
UV fluorescence microscope shows stool containing the
parasite the parasite appears blue or green against a black
background.
 Polymerase chain reaction (PCR).
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43. CONTROL
Avoiding food or water that may have been
contaminated with feces is the best way to prevent
cyclosporiasis.
Treatment with chlorine or iodine is unlikely to
kill Cyclospora oocysts.
 No vaccine for cyclosporiasis is available.
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44. HANTAVIRUS PULMONARY
SYNDROME (HPS)
Is a severe, sometimes fatal, respiratory disease in
humans caused by infection with a hantavirus.
Contact with rodents that carry hantavirus is at
risk of HPS.
Rodent infestation in and around the home
remains the primary risk.
Even healthy individuals are at risk for HPS
infection if exposed to the virus.
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45. ETIOLOGY
Transmission electron micrograph of the Sin Nombre Hantavirus
Negative sense single stranded R.N.A virus
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46. EPIDEMIOLOGY
TRANSMISSION; Aerosolized rodent excreta still remains
the only known way the virus is transmitted to humans.
The hispid cotton rat,
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47. Case report in U.S.A
 December 31, 2013, a total of 637 have been reported in
the United States.
 Out of606 cases occurred from 1993-onward,
Thirty-six percent of all reported cases have resulted in
death.
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48. 48 11/20/14

49. SYMPTOMS
Fever
Cough
Myalgia
Headache
Lethargy
Shortness-of-breath
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50. DIAGNOSIS
Early diagnosis is difficult confused with influenza.
History of potential rural rodent exposure, together with
shortness of breath, would be strongly suggestive of HPS
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51. PREVENTION AND CONTROL
Rodent control primary prevention strategy.
Eliminating contact with rodents in the
workplace.
Closed storage sheds and cabins are often ideal
sites for rodent infestations.
Wear a mask while cleaning such areas to avoid
inhalation of aerosolized rodent secretions.
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52. INFLUENZA
syn ;flu
Is an infectious disease of birds and mammals caused by
R.N.A viruses of the family Orthomyxoviridae
the influenza viruses.
The most common symptoms are chills, fever, runny
nose, sore throat, muscle pains, headache, coughing,
weakness and general discomfort.
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53. ETIOLOGY
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54. Classification influenza viruses are
Influenza virus A
Influenza virus B
Influenza virus C
The serotypes that have been confirmed in humans,
ordered by the number of known human pandemic
deaths, are:
•H1N1, which caused Spanish Flu in 1918,
and Swine Flu in 2009
Conti..
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55. •H7N7, H2N2, which caused Asian Flu in 1957
•H3N2, which caused Hong Kong Flu in 1968
•H5N1, which caused Bird Flu in 2004
•H1N7which has unusual zoonotic potential
•H1N2 endemic in humans, pigs and birds
•H9N2
•H7N2
•H7N3
•H10N7
•H7N9
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56. ANTIGENIC SHIFT AND DRIFT
•Antigenic shift subtype having a mixture of the
surface antigens of the two or more original strains.
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57. Antigenic drift viruses that involves the accumulation of
mutations within the genes that code for antibody-binding
sites.
New strain of virus particles which cannot be inhibited as
effectively by the antibodies
Easier for the virus to spread throughout a partially
immune population.
Antigenic drift occurs in both influenza A and influenza
B viruses.
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58. EPIDEMIOLOGY
Transmission
Infected person coughs, infected droplets get into the air.
Hands contaminated with influenza viruses.
Seasonal epidemics and disease burden
In temperate climates, seasonal epidemics occur mainly
during winter while in tropical regions, influenza may
occur throughout the year, causing outbreaks more
irregularly.
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59. http://www.who.int/entity/influenza/surveillance_monitoring/updates/2014_10_20_influenza_59 11/20/14

60. SYMPTOMS
Fever and extreme coldness
Cough
Nasal congestion
Runny nose
Sneezing
Body aches, especially joints and throat
Fatigue
Headache
Irritated, watering eyes
Reddened eyes, skin (especially face), mouth, throat and nose
Petechial rash
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61. DIAGNOSIS
Samples for influenza testing include nasopharyngeal or
nasal swab, and nasal wash or aspirate
Viral culture
Serology
Rapid antigen testing
Polymerase chain reaction (PCR)
Immunofluorescence assays
Rapid molecular assays
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62. PREVENTION
The most effective way to prevent the disease and/or severe
outcomes from the illness is vaccination. Safe and effective
vaccines are available and have been used for more than 60
years. Among healthy adults, influenza vaccine can provide
reasonable protection. However among the elderly,
influenza vaccine may be less effective in preventing illness
but may reduce severity of disease and incidence of
complications and deaths.
BY W.H.O.
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63. Vaccination is especially important for people at higher
risk of serious influenza complications, and for people
who live with or care for high risk individuals.
Three types of inactivated vaccines, the
Whole virus vaccines,
Split virus vaccines,
Subunit vaccines
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64. METHICILLIN-RESISTANT
Staphylococcus aureus
Methicillin-resistant Staphylococcus aureus (MRSA) is
a bacteria that is resistant to many antibiotics.
In the community, most MRSA infections are skin
infections.
In medical facilities, MRSA causes life-threatening
bloodstream infections, pneumonia and surgical site
infections.
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65. ETIOLOGY
It is a Bacteria
Family:
Staphylococcaceae
Genus:
Staphylococcus
Species: S. aureus
Staphylococcus aureus
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66. EPIDEMIOLOGY
Some risk factors include:
Recurrent skin diseases or open wounds
Long-term illness or long-term dialysis patient
Surgery
Contact with other persons with MRSA infection
Recent antibiotic use
Live in crowded settings
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67. LESION
cutaneous abscess on the foot
post packing
cutaneous abscess on the hand,
67 11/20/14

68. DIAGNOSIS
Samples from blood,
urine, sputum or other body-fluid
samples
Quantitative PCR :procedures
which are employed in clinical
laboratories for quickly
detecting and identifying
MRSA strains Mueller Hinton agar showing MRSA
resistant to oxacillin disk
68 11/20/14

69. Conti…
Rapid latex agglutination test detects the PBP2a
protein. PBP2a is a variant penicillin-binding
protein that imparts the ability of S. aureus to be
resistant to oxacillin.
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70. PREVENTION
Screening programs
Surface sanitizing
Hand washing
Proper disposal of hospital gowns
Used paper hospital gowns are associated with MRSA
hospital infections, which could be avoided by proper
disposal
Isolation
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71.  Restricting antibiotic use
Glycopeptides, cephalosporins and in
particular quinolones are associated with an increased
risk of colonization of MRSA.
Reducing use of antibiotic classes that promote MRSA
colonization, especially fluoroquinolones, is
recommended in current guideline.
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72. REFRENCES
Sherikar A.T.,Bachhil V.N.& Thapliyal D.S.
(Eds.),for ICARGovt. Of India Textbook of
Elements of Veterinary Public Health
www.who.org
www.cdc.gov
www.oie.org
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73. 73 11/20/14