Ehrlichiosis is a tick-borne disease caused by Ehrlichia canis, a rickettsial organism. E. canis infects monocytes and forms clusters called morulae. It is transmitted by the brown dog tick Rhipicephalus sanguineus. Clinical signs include fever, lethargy, anorexia, thrombocytopenia, and hemorrhaging. Diagnosis involves identifying morulae in blood smears, serology tests, or PCR. Treatment is doxycycline for 3-4 weeks. Prevention focuses on tick control and chemoprophylaxis with tetracyclines.

1. KARNATAKA VETERINARY,
ANIMAL & FISHERIES
SCIENCE UNIVERSITY, BIDAR.
VETERINARY COLLEGE,
SHIMOGA
To :
Dr. Maltesh
Asst professor
Dept of MEDICINE

2. INTRODUCTION
Canine Ehrlichiosis (Canine monocytic
Ehrlichiosis)
 It is at tick borne disease caused by
Erhlichia species.
 Dr Ehrlichia described this organism
 Hence it was name as Erhlichia sps.

3. Characteristics of E canis
 They are gram negative.
 pleomorphic coccobacilli rickettia.
 Obligatory intracellular .
 Ecanis usually appears in monocytes as a cluster of
organism called as MORULAE.
 .

4.  Etiology
 EHRLICHIA CANIS
 They are richkettsial organism.
{ They are intermediate between VIRUSES and BACTERIA.}
 E canis is transmitted by the brown dog
tick, Rhipicephalus sanguineus.

7.  Experimentally it can also be transmitted by Dermacentor
variabilis.

8.  Host for this disease is members of cinidae
family{fox , jackel , dog etc}.
 German shepherd dogs are most susceptible.

9. Epidemiology
 It has world wide distribution including Asia ,Africa
and America.
 Australia is free of E.Canis.

10.  Transmission:-
 Ticks aquired Ecanis while feeding on infected dog.
 this ticks carrying Ecanis transmit to other Dogs upon
feeding on them.

12.  PATHOGENESIS :-
 Host get infection through tick bite
 E.canis enters into host
 Ecanis adhere to membrane of Monocytes


13.  through endocytosis enters into the cell

 Divide by binary fission
 They form morulae

14. 
 Release of organism through rupture of morulae
 They spread to adjacent cells through cytoplasmic
projections
 Spread throughout the body

15.  There includes three phases :-
 Acute phase
 Persistence subclinical infection
 Severe chronic phase

16.  Once the organism enters the body causes ACUTE
PHASE.
 Which is characterised by :-
 Upto 4 weeks
 Fever,
• Severe Thrombocytopenia

17.  During this time the platelet count will drop due
an immune-mediated platelet destruction .
 The dog will be listless, off food, and may have
enlarged lymph nodes.
 Most dogs clear the organism if they are treated in this
stage.
 but those that do not receive adequate treatment will
go on to the next phase.

18.  SUBCLINICAL PHASE:
 In this phase, the dog appears normal.
 The organism has sequestered in the spleen .
 Dogs can stay in this phase for months or even years.
 Intermittent fever ,mild Thrombocytopenia and
anaemia.

19.  CHRONIC PHASE:
 Charecterised by :-
 Severe pancytopenia { due to bone marrow
Hyperplasia}.
 Fever , wide spread petechia and edema.
 Death due to secondary bacterial infection .

20.  CLINICAL SIGNS:-
 There are no signs of the subclinical phase.
 Fever , Anorexia , lethargy ,weight loss.

21.  Epitaxis ,

22.  Petechial haemorrage

23. OCULAR SIGNS :-
Retinal haemorrhage,retinal detachment {due to
Hyphema }

24.  Neurologic effects may also be seen.{due to meningeal
bleeding}
 Glomeruloneprhitis, resulting in serious urinary
protein loss, can also result.
 Increased globulin levels are also seen.

25.  POST MORTAM LESIONS :-
 Petechial haemorrhage seen on serosal surface of
organs like lungs ,kidney ,brain, nasal cavity GI tract.
 Generalised Lymphadenomegaly , splenomegaly and
Hepatomegaly

26.  Postmortem Lesions:
 During the acute or self-limiting phase of E
canis infections, lesions generally are nonspecific,
 but splenomegaly is common.
 Histologically, there is lymphoreticular hyperplasia
and lymphocytic and plasmacytic perivascular cuffing

27.  . In chronic cases:-
 these lesions may be accompanied by widespread
hemorrhage and
 increased mononuclear cell infiltration in perivascular
regions of many organs.

28.  DIAGNOSIS:-
 Clinical examination
 Hemotology and Serum biochemistry
 {Thrombocytopenia and Hypo albuminaemia and
hyperglobulinaemia}.
 Dot ELISA kit @field level
 Molecular test –PCR
• Serological test {FAT-flouroscent antibody technique }-
which is widely used.

29.  Blood smear examination { to find MORULA in
Monocytes}.

30. • Diagnosis canaiso be made by looking under
a microscope of a blood smear for the presence of
the ehrlichia morulae,
• which sometimes can be seen as
intracytoplasmic inclusion bodies within a white blood
cell

31.  TREATMENT:-
Doxycycline(5-10mg /kg/day) {PO/IV} for 21-25 days.
 OXYTETRACYCLIN –( 5-10 /Kg /day){I/V} for 21-25 days.
 Supportive therapy ( in anaemia ) – Blood transfusion if Hb
concentration is <4%.
 short term (2-7days)therapy with low immunosuppressive
doses of Glucocorticoides{1-2mg /kg prednisolone,PO}
 This may be beneficial early in the treatment period when
severe Thrombocytopenia is present.

32. Prevention:-
Tick control is the most effective method of prevention.
No vaccinesn are available.
Chemoprophylaxis by using tetracylin @6.6mg /kg .
Precautions should be taken while tranfusion of blood.