1) Johne's disease, also known as paratuberculosis, is a chronic, infectious disease of ruminants caused by Mycobacterium avium subspecies paratuberculosis. 2) It is characterized by chronic diarrhea and weight loss. Young calves are most susceptible to infection through ingestion of contaminated feces or milk. 3) The disease has a long incubation period, usually 2-5 years, before clinical signs appear. It causes thickening of the intestinal wall and infiltration of the intestine by macrophages containing acid-fast bacilli.

1. Presentation on
Johne’s Disease/
PARATUBERCULOSIS
Department of PATHOLOGY
U.P. Pt. Deen Dayal Upadhyay Pashu Chikitsa Vigyan Vishwavidyalaya Evam Go-Ansundhan
Sansthan,DUVASU Mathura
Suggested by :
Dr. Neeraj Gangawar
Dr. Renu Singh
Presented by :
Harshit Saxena
B.V.Sc & A.H.
Enroll. No. – V-1598/16

2. Introduction

3. What is Paratuberculosis/Johnes’s disease??
Can be defined as:
Chronic, infectious, granulomatous
enteritis of Ruminants characterised
clinically by Chronic diarrhoea and
Progressive emaciation

4. Aetiological Agent
• The aetiological agent
Mycobacterium avium subsp. paratuberculosis,
• Acid-fast organism formerly referred
to as Mycobacterium johnei
• Slower growth
• Requires the addition of an iron transport chemical
known as mycobactin when grown
in vitro
• Forms a rough colony when grown
on a solid agar medium
• Infects mammals instead of birds

5. Hosts/Species Affected
• Cattle –Economic losses
• Sheep and Goat – Much prevalent in INDIA
• Horses & Pigs – Lesions minimal or absent
• Wildlife – Deer
• Laboratory animals – Resistant
#however a model of disease reproduced in Athymic
mice
• 3 strains of M. paratuberculosis can cause disease in
cattle
• A bovine strain and 2 sheep strains are present
• Young calves more susceptible that acquire infection in
their first year

6. Animals affected with JD

7. Spread
• Faeces is the main source
Ingestion is main route(contaminated feed & water)
• Long incubation but animals excrete bacteria about 15-
18 months before clinical science appear
• Semen can also be as source
• Foetal /periparturient infection
• Green pastures
• Infection upto 30 days
• Clinical signs- 3-5 years

8. Pathogenesis

9. Ingestion of contaminated Feed & Litter by
Faeces
Localization of bacteria in Lymph node,
Tonsils & Suprapharangeal lymphnode
Penetration in the intestinal mucosa
Residing & Multiplication of bacteria in
Macrophages (intracellularly)
Growth of bacterium in macrophages &
their distribution systemically
Sustained multiplication mainly in Terminal
Ileum & Large intestine

10. Different animals behave differently giving
rise to 3 distinct groups
Infected Resistants
Intermediate
Cases28
Clinically active
Infected Resistants: Control infection rapidly develop
resistance ; Do not become shedders
Intermediate cases: intemittently shed bacteria
Clinically active: Develop clinical conditions ; organisms persist
in intestine ; become heavy shedders

12. Clinically Active
More proliferation and infiltration to
Submucosa
Decreased absorbtion & Chronic diarrhoea
with other clinical manifestation
The Bacteria via circulating macrophages reaches to various
sites particularly,
1. Uterus – Abortion
2. Mammary gland
3. Testes
4. Semen of bull
5. Foetus through placenta (Prenatal) – Congenital infection

13. Why bacteria mainly resides in Terminal Ileum???
How bacteria sustains inside Macrophages???
MAP survives by inhibiting the fusion of phagosome -
lysosome and also by ↑↑mitogen activated protein
kinase(MAPK)
MAPK help in survival by inhibiting phg-lys & decreased
Expression of IL-10 anti inflam cytokine
Due to presence of M cells over Peyer’s patches function to
pass antigens (bacteria) through to the underlying cells of the
Peyer's patch to "show" these antigens to the macrophages
and lymphocytes
Attempt to present antigen Fails & MAP flourishes

14. “Within macrophages the, the bacteria remain viable and
protected from humoral factors”
“Immunological response depend upon the stage of
infection but not the stage of clinical disease”
Initally : Cell mediated Response
Later : Humoral Response due to
dying macrophages & disease
advancement
JD -Insight through Immunology

15. Type 3 (Immune
complex) Reaction:
Contribute to intestinal
lesions of Johne’s
disease
Type 1&3 reactions
occuring in intestinal
mucosa may lead to
increased outflow of
fluid & diarrhoea
Later stages of disease:
Anergy
No immune response
Irreversible functional
inactivation of disease

16. Clinical Signs
• The disease has long incubation period of 2 years or
more , most common in age group of 2-6 years in
cattle
• Signs & Lesions encompasses intestinal tract, lymph
node & genitals
• Cattle: Rapid development of symptoms due to
quick loss of protein ; hypoproteinemia ; wasting ;
Oedema
• Sheep: Compensatory mechanism of protein
operates development of sign occur after failure of
mechanism thus slow development of clinical signs

18. •Emaciation&Submandibular
oedema
•Fall in milk
•Absence of fever withToxiemia
•Normal Appetite but excessive
thirst
•Faeces soft thin without smell
•Diarrhoea may be continuous or intermittent without blood
epithelial debris and mucus
•Sporadic breakdown
Cattle

19. Sheep
• Shedding of wool
• Mild & controlled diarrhoea
• Emaciation
• Anorexia
• Loss of characteristic pellet
texture of faeces
Goat
Same as Sheep but with
more depression & Dyspnoea

20. Lesions
• Most common site - Terminal part of the Ileum
• Other places – large intestine & mesentric lymph node,
liver, spleen, lungs, kidneys, uterus, placenta, nonmesentric
lymph node
MICROSCOPICALLY
• Lamina Propria of Mucosa infiltrated with
closely packed large epitheloid cells
• The cells have foamy cytoplasm
& multinucleated
• Submucosa also infiltrated
• Mucosae muscularis ; and Muscular layer
are intact

21. Histopathology of the terminal
ileum from asymptomatic sheep.
(a) Ziehl-Neelsen stain for acid-
fast bacteria (× 250) showing the
absence of mycobacteria. (b) H&E
stained low power (×250) and (c)
high power (×400) show normal
histology.

22. IMPRESSION SMEARS OF LESIONS→ZEAL NEELSEN
STAIN → large no. of Acid fast rod shaped organisms
appear in cytoplasm of Epitheloid cells
High power magnification photomicrograph
of a Ziehl-Neelsen acid-fast stained
histopathology section of the bovine ileum

23. Secondary histopathological changes
•Oedema of intestinal mucosa :
Local interference of circulation
•Nest of neutrophills
•Increased Eosinophills
•Absence of Caseous Necrosis, Nodule formation &
Calcification- Cattle
•Sheep Goat Wild-Ruminants show these lesions

24. • Affected intestinal wall thickened oedematous
• Mucosal epitheium:
Closely packed Rugae
• Rugae due to villi thickening:
#Corrugated appearance does not appear when
intestine is streched
Gross Appearance

25. Ovine JD
Caseous
Lymphadenitis

26. Disease in Ruminant is not zoonotic
• Accidental innoculation of bacterin used for
vaccination : Potential occupational hazard
• Needle stick exposure to bacteria
• Exposure depend on frequency of doses
administered
Zoonotic Implication

27. Diagnosis

28. 1. Studying lesions
• Epitheloid cells containing Acid Fast bacilli :Impression
smears or section of mucosa & submucosa
Mucosal scrapings taken from Rectum
2. Bacteriological Examination of Faeces
• Faecal culture : most reliable index in Cattle
• 100% specific 100% sensitive on herd basis
• Identification of bacteria even 1-3 years before development
of clinical signs

29. 3.Serological tests : Intradermal johnin test
CFT : Complement fixation test
ELISA
AGID
LAM-ELISA : Lipoarabinomannan antigen enzyme linked
immunosorbent assay
D-AGID : Protein-D Agar gel immunodiffusion test

30. Differential Diagnosis with TB
Tuberculosis – Nodule formation, Fibrosis, Necrosis,
Calcification
Paratuberculosis – Above conditions are altogether
absent in cattle
Sheep and Goat can show these in mild form and
diffused thus tough to differentiate

31. •Misdirected immune response due to host modulation by
MAP leads to establishment of this debilitating disease.
• Inhibition phagosomal maturation, reduced apoptosis of
infected cells & reduced MHC II expression are responsible for
Invasion and persistence of MAP
•Understanding the pathogenesis becomes important for JD
since there is no efficient vaccine available
•Thus, better understanding of the pathogenesis help in
development of more effective vaccine and diagnostic to
MAPantigen & test for quick and accurate diagnosis
Conclusion

32. Thank you!!! for your
patience hearing
Any Questions…..