About bacterial zoonotic disease and some of viral zoonotic disease

1. ZOONOSIS
Made By : Niteesh Kumar

2. Zoonosis has been defined as infectious diseases that are primary
infections of vertebrate animals, which can be naturally transmitted
to humans.
CLASSIFICATION : -
• Anthropozoonosis: infections transmitted to man from lower
vertebrate animals.
• Zooanthroponosis: Infections that are transmitted from man
to lower vertebrate animals.
• Amphixenoses: Infections chat are maintained in both animals and
lower vertebrate animals that may be transmitted in either
direction.

4. BACTERIAL ZOONOTIC INFECTIONS
1. Anthrax
Anthrax also called Malignant pustule, Malignant oedema, Woolsorter's disease, or
Ragpicker’s disease, is an acute infectious disease of animals caused
by Bacillus anthracis, a gram-positive, spore-forming bacillus. Spores of B.anthracis
can persist in the environment for many years in some types of soil and enter
the body through skin abrasions, inhalation or ingestion and multiply to
produce exotoxins. Anthrax is primarily a disease of herbivorous animals that
occasionally affects human.

5. Causative agent : Bacillus anthracis
 Gram positive ,
 Large rectangular rods,
 Arranged into chains,
 Non motile ,
 Capsulated and bear non bulging oval spore
 Most common agent of bioterrorism

6. Virulence Factors And Pathogenesis
1- Anthrax Toxins :- By plasmid pX01
A) Oedema Factor : Cause oedema
B) Protective Factors :- Facilitate entry of bacteria into cell.
C) Lethal Factor :- Mechanism is unknown.
2- Anthrax capsule :-
• Made up of polyglutamate
• By plasmid pX02
• Inhibit complement mediated phagocytosis.

7. Transmission
• Cutaneous mode – most common method
• Spore inhalation
• Ingestion of animals died due to animal anthrax
• By fomites – very rare
• Highest incidence in Africa , Central & Southern Asia

8. Human Anthrax
1. Cutaneous anthrax
2. Pulmonary Anthrax
3. Intestinal anthrax – Very rare and by Ingestion
Highly fatal and manifest as bloody diarrhoea.

10. Diagnosis

11. Treatment
 Ciprofloxacin + Clindamycin for 60 days
 Prophylaxis : Ciprofloxacin + Doxycycline for 60 days
Raxibacumab : Monoclonal antibodies against anthrax toxin
Vaccine :
1. Stern vaccine : Live attenuated non capsulated spore vaccine
2. Attenuated precipitated toxoid vaccine

12. Prevention
The general control measures include:
• Disposal of animal carcasses by burning or by deep
burial in lime pits.
• Decontamination ( usually by autoclaving) of animal
products.
• Protective clothing and gloves for handling potentially
infectious materials.

13. 2. PLAGUE
Plague is an infection of wild rodents transmitted from one
rodent to another and occasionally from rodents to humans
by the bites of fleas.
Causative agent : Yersinia pestis - short, pleomorphic
Gram-negative rods that can exhibit bipolar staining.
Zoonotic animal : Rodents

14. Yersinia pestis stained by Wayson Stain
(Safety Pin Appearance)

16. Pathogenesis of
Yersinia pestis

17. Clinical Features
After an incubation period of 2–7 days, there is high fever and painful
lymphadenopathy, commonly with greatly enlarged, tender nodes (buboes)
in the neck, groin, or axillae. This is the bubonic form of the disease.
Vomiting and diarrhoea may develop with the early septicemic form of disease.
Later, disseminated intravascular coagulation leads to hypotension, altered
mental status, and renal and cardiac failure. Terminally, signs of pneumonia
and meningitis can appear, and Y pestis multiplies intravascularly
and can be seen in blood smears. Primary pneumonic plague results from
Direct inhalation of organism into the lung. Patients often have a
fulminant course with chest pain, cough, haemoptysis, and
severe respiratory distress.

18. Diagnosis

19. Treatment
 Drug of choice : Streptomycin
Along with Tetracycline for 10-14 days
Gentamicin is superior to streptomycin and currently recommended
for treatment.
 Tetracycline of Choice : Doxycycline

20. Prevention
Prevention and control of plague involves:
• Control of cases by early diagnosis, isolation and treatment of cases.
• Control of fleas by use of effective insecticides, such as DDT or
BHC (ß-hexachloro-cyclohexane)
• Control of rodents
• Chemoprophylaxis should be given to all contacts of pneumonic plague.
Doxycycline ( 100 mg twice a day) or tetracycline (500 mg 6 hourly)
is the drug of choice for prophylaxis given for 7 days.

21. 3. Brucellosis
Primarily a zoonotic disease of sheep, goat , camel. Human infection is
usually associated with occupational or domestic exposure to infected
animals or their products.
Causative agent : - Brucella melitensis
Gram –ve coccobacilli, obligate aerobe , non capsulated , non motile

22. Brucella melitensis

23. Pathogenesis and virulence factors
Infection of reticuloendothelial system by
Cell wall LPS
Type 4 secretion system
Cu-Zn superoxide dismutase.
Initial site of infection Lymphatic vessels Local lymph node
Dissemination to various organs Bacteremia

24. Transmission
By three modes –
1) Direct contact : M/C route
2) Food borne
3) Air borne : By inhalation of dust or aerosols in the infected cowshed
or slaughter houses.

25. Clinical features :
Classical triad : Fever with profuse night sweats,
Arthralgia/Arthritis
Hepatosplenomegaly
Typhoid like illness
Malta fever
Vertebral osteomyelitis and septic arthritis
Depression and lethargy with meningitis or lymphocytic
meningoencephalitis.

26. Lab diagnosis

28. Treatment
Two Regimens :-
1) Gold –Standard Regimen :
Streptomycin 1mg IM OD× 6 𝑤𝑘𝑠
Doxycycline 100mg Oral BD × 14 − 21 𝑑𝑎𝑦𝑠
2) WHO Regimen :-
Rifampin 15mg/kg Oral OD× 6 𝑤𝑘𝑠
Doxycycline 100mg Oral BD× 6 𝑤𝑘𝑠

29. Prevention & Control :
1. Persons handling the animals should use protective clothing
and gloves.
2. Pasteurisation or boiling of milk should be done.
3. Vaccination: Cattle should be vaccinated with live attenuated
Br. abortus strain 19, RB 51 for cows.
4. Unimmunized infected animals should be slaughtered.
5. Br. abortus strain 19-BA, a more attenuated variant of strain 19,
has been widely employed for human immunisation in USSR
for protection of population exposed to infection. Vaccine is given
intradermally.

30. 4. Leptospirosis
Infection caused by Leptospira interrogans is called as Weil’s disease or
leptospirosis.
Leptospira interrogans :-
1. 6-12μm× 0.1μm in size.
2. Tightly & regularly coiled with characteristic hooked ends.
3. Single endoflagellum at one end
4. Exhibit spinning &translational movements.
5. Can not seen under light microscope due to its thinness.

31. Scanning electron micrograph of Leptospira interrogans, showing the
characteristic tight coils.

32. Mode Of Transmission :-
1. Indirect contact with water, moist soil and wet surfaces
contaminated with animal urine.
2. Direct contact of urine and products of parturition ,placenta of
infected animals.
3. Direct human to human transmission does not occurs
Seasonality : Rainy and post monsoon period.
Incubation Period : 4-20 days

33. Pathogenesis
A) Septicemic phase :
Vascular damage
Penetration and invasion of tissue
B) Immune phase :
Antibodies developed
Leptospira disappear from the blood
Ab-Ag complexes are deposited in the various organs

34. Clinical Stages of Leptospirosis
Mild Anicteric Febrile Illness Weil’s Disease
In 90% patients
Biphasic
Mild form of leptospirosis
In 10% patients
May not be biphasic.
Severe and fulminant form of
disease

35. Lab Diagnosis

36. Treatment
Mild Leptospirosis Severe Leptospirosis
Oral Doxycycline
100mg BD × 7 𝑑𝑎𝑦𝑠
Alternative - Amoxicillin
Penicillin
1.5M units IV , four times a
day× 7 𝑑𝑎𝑦𝑠
Alternative – Ceftriaxone
or Cefotaxime

37. Prevention And Control :
1. Rodent control
2. Avoidance of swimming in contaminated places
3. Health education
4. General sanitation approach including proper waste disposal.
5. SPIROLEPT Vaccine – Sub cutaneous dose of 1ml each at 15 days
interval , 3rd dose 4-6th month after 1st dose followed biannual
revaccination . It is a whole cell vaccine containing specific serovars
of Leptospira.

38. 5.Salmonellosis
Salmonellosis is disease caused by members of the genus Salmonella.
Salmonellosis is of two type :-
1. Typhoidal Salmonellosis
2. Non Typhoidal Salmonellosis (NTS)
Since we are talking about zoonotic disease, Only NTS is zoonotic so
later on we discuss only about NTS , not about typhoidal salmonellosis.

39. Non Typhoidal Salmonella
Causative Agents : Salmonella typhimurium, S. Heidelberg
S. enteritidis, S. Newport, S. javiana, S. Dulbin
Gram negative bacilli
Transmission : Animal food product-borne
Seasonality : Rainy season in tropical climates;
Summer periods in temperate climates

40. Pathogenesis
Entry through epithelial cells ( M cells ) lining the intestinal mucosa
Entry into macrophages
Survival inside the macrophage
Primary Bacteremia
Spread
Secondary Bacteremia

41. Clinical Manifestations
I. Gastroenteritis
II. Bacteremia
III. Endovascular infections
IV. Intra abdominal infections
V. NTS meningitis
VI. UTI
VII. Pulmonary infections
VIII.Reactive arthritis
IX. Salmonella osteomyelitis

42. Treatment
On Milder cases : Fluid Replacement Therapy
ON severe case : Antibiotics are given i.e. Ciprofloxacin and Ceftriaxone

43. 6. Bovine Tuberculosis
Bovine tuberculosis is a chronic bacterial disease of cattle that
occasionally affects other species of mammals. This disease is a
significant zoonosis that can spread to humans, typically by the
inhalation of aerosols or the ingestion of unpasteurized milk.
Causative agent : Mycobacterium bovis
Non motile, non sporing, non capsulated, weakly gram positive,
Rod shaped obligate aerobic bacteria which show acid fastness.
G+C content of DNA is 61-71 mol%.

44. Transmission of M. bovis
1: Infection by contaminated
materials;
2: Infection by aerosol;
3: Infection by ingestion of
derivative products;
4: Vertical transmission;
5: Horizontal transmission;
6: Infection by predation.

46. Clinical features

47. Lab diagnosis

49. Treatment

51. 7.Endemic (Murine) Typhus
Endemic typhus caused by Reckettsia typhi infection.
Small non motile Gram negative coccobacilli with some common properties :
1) Obligate intracellular organism .
2) Not cultivable in artificial media.
3) Transmitted by arthropod vectors.

53. Vector : Rat flea ( Xenopsylla cheopsis) – M/C
Cat flea ( Ctenocephalides) - Rarely
Mode of transmission : Flea bite
Reservoir : Rodents
Rattus rattus
Rattus norvigecus
Geographical Distribution :- Warm areas specially coastal areas.

54. Clinical Manifestations
• Incubation period : 1-2 wks.
1) Rash on upper trunk on 5th days later on become generalised.
2) Fever
3) Headache , anorexia
4) Myalgia
5) Mental confusion & coma
6) Interstitial pneumonitis
Symptoms are similar to epidemic typhus but milder and rarely fatal.

55. Treatment
• Doxycycline
100mg Oral BD× 1 − 5 𝑑𝑎𝑦𝑠

56. 8.Tularaemia
Infection caused by Francisella tularensis , primarily a plague like disease of
rodents and other small animals. It is a small Gram negative coccobacilli with
Bipolar appearance, non motile and capsulated. It is weakly catalase positive,
H₂S positive and oxidase negative.
Four subspecies are :-
Tularensis : Most common , Most virulent , Found in North America
Holarctica : Found in North America.
Novicida : Found in North America.
Mediasiatica : Found in central Asia.

57. Francisella tularensis bacteria (blue) infecting a macrophage (yellow)

58. Epidemiology
• Transmission :
1) Interaction with biting 0r blood sucking insects.
2) Contact with wild or domestic infected animals
3) Ingestion of contaminated water or food
4) Inhalation of infective aerosols.
• Source :
Contaminated environments , insects, carrier animals.

60. Clinical Manifestations
1) Ulceroglandular tularemia
2) Pulmonary tularemia
3) Oropharyngeal tularemia
4) Oculoglandular tularemia
5) Typhoid like illness
6) Agent of Bioterrorism

61. Lab Diagnosis
Culture : Isolation is very difficult.
BCG Agar and CHAB Agar are used.
Blue-grey , round, smooth, slightly mucoid colonies with small
zone of alfa haemolysis.
Antibody detection
PCR Assay

62. Treatment
Gentamycin – DOC
5mg/kg for 7-10 days
Doxycycline/Ciprofloxacin – Alternatives

63. 9. Rabies
Rabies virus causes a rapidly progressive , acute infectious disease of
the central nervous system in human and animals transmitted from
another rabid animal. It is always almost fatal.

64. Streat Rabies Virus Fixed Rabies Vaccine
Freshly isolated Isolated after serial intracerebral passage in
rabbits/cell lines
Produce Negri body Don’t produce Negri body
Affect salivary gland Don’t affect salivary gland
Pathogenic Non pathogenic
Incubation period : 20-
90 days
4-6 days
Produce disease Used for vaccine

67. Clinical Manifestations
Prodromal Phase Acute Neurogenic Phase Coma and
death
Last for 2-10 days Encephalitic type (80% Patients)
Paralytic type (20% Patients)
Coma leads to
death within
10 days.
Fever, anorexia, malaise,
nausea, photophobia, sore
throat
Encephalitic/Furious type – Hyperexcitability,
Lucid interval, Hydrophobia , Aerophobia,
Sympathetic dysfunction
Paraesthesia, pain , pruritis
around the wound site
Paralytic/Dumb type – In partially vaccinated
people ; Flaccid paralysis often begins in
the bitten limb and progressing to quadriparesis
with facial paralysis.

68. Treatment
No specific treatment.
Symptomatic treatment may prolong life but the outcome is almost
always fatal.

69. 10.Yellow Fever
Yellow fever is an acute , febrile illness ; severe cases are characterised
by liver dysfunction which leads to jaundice , renal dysfunction and
Haemorrhage with high mortality. It is RNA virus (an arbovirus) disease
that are transmitted by bite of Aedes aegypti.
Yellow fever is endemic to West Africa and Central south America . Yellow
fever has not invaded India yet.

70. Transmission :
Vector : Tiger mosquito or Aedes aegypti
Transmission cycle : 1) Jungle cycle – In btw monkeys & forest mosquitoes
2) Urban Cycle – In btw humans & Aedes aegypti.
Period of Communicability :
1) Man – During first 3-4 days of illness
2) Aedes – After 8-10 days till the death.

72. Clinical Features :-
• Incubation period ; 3-6 days
1) Fever, chills, headache , dizziness, myalgia,
2) Relative bradycardia, nausea , vomiting
3) Haemorrhagic manifestations
4) Platelet dysfunction
5) Hepatitis
6) Renal dysfunction
7) Encephalitis

74. Laboratory Diagnosis
Serology : IgM ELISA can be done after 3 days of onset of symptoms.
It is not specific.
Molecular Method : rt-PCR for NS5 region of Viral RNA within
10 days of onset of symptoms.
Histopathology : Mind zonal necrosis of liver , Presence of Torres
bodies and Councilman bodies.
.

75. Treatment & Prevention
1) Hospitalisation , supportive care
2) Fluid replacement , NSAIDs , Symptomatic Treatment
I. Use of mosquito net.
II. Yellow fever 17D Vaccine : – Live attenuated vaccine

76. 11.Japanese Encephalitis
Japanese B encephalitis is the leading cause of viral encephalitis in Asia
Including India. It is the inflammation of brain due to Group B Arbo virus
transmitted by bite of Culex mosquitoes. It is directly affect to the central
nervous system and may cause severe complications

77. Agent
Group B Arbo virus in the family of Flaviviridae
Domestic pigs and wild birds (especially herons) are reservoirs
of the virus.
Season : Rainy season
Age : 85% patients are below 15 yrs

79. Vector : Culex tritaeniorhynchus , Culex vishnui
Transmission cycle :

80. Clinical Manifestations
• In symptomatic patients the disease manifests in three phases:
1) Prodromal phase: before CNS entry by the virus
- fever, G.I. disturbances, headache, malaise, etc
2) Acute Encephalitic phase: After CNS entry by the virus
- rapid onset of high fever, neck stiffness, seizures, spastic
paralysis and death
3) Recovery phase: complete or partial recovery with neurological
deficits, cranial nerve palsies occurs

81. Laboratory Diagnosis :
Detection of JE specific IgM antibody in serum.
Detection of JE virus specific envelope (E) gene in reverse
transcriptase PCR.

82. Treatment
• No specific antiviral medicine available for JE
• Clinical management is supportive
• Fluid and electrolyte balance is a must during the acute phase of the
disease
• Seizure management is necessary
• Airway management is crucial.
Vaccine prophylaxis for JE by :-
A) Live attenuated SA 14-14-2 vaccine
B) Inactivated vaccine (Nakayama & Beijing strain)

83. 12.Kyasunar Forest Disease
Kyasunar Forest disease was first recognised in 1957 in SHIMOGA
district of Karnataka state in South INDIA. KFD is a febrile disease
associated with haemorrhage caused by Kyasunar forest disease
virus, a member of virus family of arbovirus & flavivirus and transmitted
to man by bite of infected ticks . Local inhabitants called
the disease ‘monkey disease’ because of its association with dead
monkeys.

84. Epidemiology
Vector : Hard tick ( Haemaphysalis spinigera ) is the main vector but
more than 15 species of ticks are involved in transmission.
Transmission : By bite of infected ticks
Human to human transmission not seen.
Host :- Monkey , rodents , squirrels.
Season : - Dry months ( January – June)
Situation in India :- Five endemic district in Karnataka
Shimoga , North Kannada, South Kannada , Chikkmangaluru , Udupi

86. Clinical Manifestations :
Incubation period : 3-8 days
First Stage( Haemorrhagic Fever ) Second Stage
Acute high fever, Malaise, Frontal
headache,
Haemorrhagic symptoms
GIT Disturbance
Meningoencephalitis
may occur7-21 days
after the first stage.

87. Lab Diagnosis
1) IgM antibody detection by ELISA.
2) Viral RNA ( NS-5 non coding region ) detection by nested RT-PCR.

88. Treatment & Prevention
There is no specific treatment for KFD, but early hospitalization
and supportive therapy is important.
Supportive therapy includes the maintenance of hydration and
usual precaution for patient with bleeding disorders
Vaccine is also available. Inactivated chick embryo tissue culture
Vaccine developed by NIV, Pune.

89. Thank You