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CANINE EHRLICHIOSIS
(E. CANIS)
Dr. Jibachha Sah
M.V.Sc, Lecturer, College of Veterinary Science,
NPI, Bhojad, Chitwan, Nepal
jibachhashah@gmil.com,00977-9845024121
Introduction
●Ehrlichiosis is a globally distributed canine vectorborne disease (CVBD) transmitted by
ticks.
●Caused by the rickettsial bacteria Ehrlichia spp., ehrlichiosis affects dogs and humans
as well as other domestic and wild animal species.
●E. canis causes canine monocytic ehrlichiosis (CME). This disease, also known as tropical
canine pancytopenia, canine rickettsiosis or canine hemorrhagic fever, was first described
in Algeria in 1935 by Donatien and Lestoquard.
Etiology
● There are two different types of leukotropic diseases that are caused by ehrlichia
bacteria in dogs.
● These are “Canine Monocytic Ehrlichiosis” caused by E. canis that is frequently
encountered, and “Canine Granulocytic Ehrlich-iosis” caused by E. ewingi.
● Ehrlichia canis (a small, Gram-negative, coccoid bacterium), which parasitizes
cytoplasm of the circulating monocytes in form of distinct clusters termed as “Morulae”
(Ristic and Holland,1993).
E. canis
Incubation period
● The incubation period of the illness is 7-21 days in general and it has three stages as acute, sub-clinical,
and chronic (Woody and Hoskins ,1991).)
Breed Susceptibility
●CME was observed in wide variety of breeds with somewhat more predisposition in Labrador
retriever followed by Pug, Rottweiler, German shepherd, Lhasa apso, Pomeranian and Gaddi.
Age susceptibility
●Age-wise prevalence of CME recorded in dogs of varying age i.e. from 3 months to 9 years with
maximum number of cases in more than 1 year age group.
Transmission/Vector
●Typically, tick nymphs or larvae are infected with E. canis after feeding on a
persistently infected dog.
● Transstadial transmission occurs to subsequent stages of the tick vector.
● A new host is infected via salivary gland secretions during blood feeding.
● Transmission of the disease has also been reported via blood trans fusion.
Zoonotic Potential
●A few decades ago, ehrlichioses were considered to only have veterinary relevance.
●The first human infection with E. chaffeensis was diagnosed in 1986 raising the
awareness of Ehrlichia spp. as zoonotic pathogens.(Maeda et al.,1987).
● The best-known Anaplasma species is A. phagocytophilum, formerly referred to as
human granulocytic ehrlichiosis (HGE) factor, E. phago - cytophila or E. equi.
● It causes granulocytic anaplasmosis in dogs and humans.
There are three phases of illness with Ehrlichiosis: acute, subclinical, and chronic.
Acute Phase
●This phase occurs 1 to 3 weeks after the host is bitten by the tick. The Ehrlichia organism is replicating in
this time period and attaching to white blood cell membranes. During the acute infection, the platelet
count will drop and an immune-mediated platelet destruction will occur.
●The acute disease is characterized by high fever, depression, lethargy, anorexia, lymphadenomegaly,
splenomegaly, epistaxis, dermal petechiae and ecchymoses.
●The dog will be listless, off food, and may have enlarged lymph nodes and/or spleens. There may be
fever and even neurologic symptoms as well, but although the dog may seem pretty sick, this phase of
infection is rarely life-threatening.
●Ophthalmological lesions are frequent and include anterior uveitis, chorioretinitis, papilledema, retinal
hemorrhage, presence of retinal perivascular infiltrates and bullous retinal detachment (Komnenou et
al. 2007).
Subclinical Phase
●In this phase, the dog appears normal. The organism has sequestered in the spleen and is
essentially hiding out there. Dogs can stay in this phase for months or even years.
●●The only hint that Ehrlichia is hiding is a somewhat reduced platelet count and/or elevated
globulin level on a blood test.
●The blood protein level on a lab report is divided into albumin (an important carrier protein) and
globulins (every other blood protein including antibodies.) Long-term stimulation of the immune
system will elevate globulins, sometimes dramatically.
Chronic Phase
●In this phase the dog gets sick again. Up to 60
percent of dogs infected chronically with Ehrlichia
canis will have abnormal bleeding due to reduced
platelets numbers.
● Deep inflammation in the eyes called uveitis may
occur as a result of the long-term immune
stimulation.
● Neurologic effects may also be
seen. Glomerulonephritis, resulting in serious urinary
protein loss, can also result. Increased globulin levels
are almost always seen in this stage, albumin is
often low.
● Most dogs do not show the full pancytopenia
(literally reduction in all blood cell lines) but severe
cell deficiencies are associated with high mortality
rates.
uveitisUveitis in pug
Epistaxis ( bleeding from nose unilateral/bilateral
●Pale mucous membranes and weakness, bleeding and significant weight loss are common findings in
the chronic phase (Harrus and Waner 2010).
Clinical examination
Pale mucous membrane Epistaxis (Nose bleeding
Haematology analyzing and RDT at Jibachha
Veterinary hospital
●Thrombocytopenia appears around day 10 and peaks in the third week post-infection, with platelet
counts ranging from 20,000 to 52,000/µl (normal range: 20000– 450,000/µl). There can also be mild anemia and
leukopenia.
●Hypoalbuminemia, hyperglobulinemia, and hypergammaglobulinemia (mostly polyclonal (Antibody
represents a collection of antibodies from different B cells), rarely monoclonal(represents antibody from
a single antibody producing B cel)) are common in CME. Also moderate increases in alanine aminotrans -
ferase (ALT) and alkaline phosphatase (ALP) can occur due to hepatocyte damage during the acute
phase.
● Pancytopenia due to bone marrow hypoplasia is characteristic of the chronic severe form (Harrus, et
al.,1997).
● E. canis can occasionally induce a proteinlosing nephropathy as a result of immunecomplex
glomerulonephritis with consequent proteinuria and azotemia
Clinical pathology
Source;Laxmi Bai et al;2017
●Lower levels of total erythrocyte count, Hematocrit, MCH, MCHC and higher levels of MCV indicates
macrocytic, hypochrmic anemia in affected dogs. Such type of anaemia might be due to
haemorrhagic manifestation of disease (Bhardwaj 2013) owing to thrombocytopenia.
●Platelet consumption, increased splenic sequestration and decreased platelet lifespan are the
possible attributes for thrombocytopenia (Harrus et al. 1999).
●Thrombocytopenia, anemia, eosinopenia. Left deviation in neutrophils, are the hematological
signs frequently encountered in canine ehrlichiosis (Shipov et al.,2008).
●Thrombocytopenia by leading to immunological destruction of platelets (Lee pyle, 1980). and also
cause central nervous system
abnormalities in dogs.
● The most commonly observed hematological abnormalities are thrombocyto penia and
anemia(Harrus et al.,1997)
Biochemistry analyzing at Jibachha Veterinary
hospital
Abdominal USG done for organ dysfunction at Jibachha veterinary hospital
Source;Laxmi Bai et al;2017
●Increase in serum ALT, AST and alkaline phosphatase values in affected dogs, suggesting hepato-
biliary dysfunction dueinfiltration of perivascular mononuclear cells (Nair et al. 2016).
●Increased levels of AST and ALT might be due to histopathological changes in liver as a result of the
infiltration of perivascular mononuclear cells (Nair et al. 2016). Serum protein profile indicated
hypoproteinemia owing to hypoaluminemia and hypoglobunemia in affected dogs.
●The hypoalbuminemia seen in CME might be the consequence of peripheral loss of albumin to
edematous inflammatory fluids as a result of increased vascular permeability (Woody and
Hoskins 1991), blood loss, or decreased protein production due to concurrent liver disease as
suggested by elevated hepatic enzymes.
●Total bilirubin levels in affected dogs were higher as compared to healthy control which is due to
rise in indirect bilirubin levels owing to immune mediated RBC lysis. Mean urea and creatinine value
in affected dogs were higher than healthy control dogs.
●The increase in urea and creatinine values may be due to membrane-proliferative glomerulopathy
and interstitial nephritis. It has been suggested that the presence of inflammatory infiltrates rich in
lymphocytes might be responsible for immuno-pathogenesis of renal lesion in dogs with CME.
●Ehrlichiosis accompanied by hyperglobulinemia and thrombocytopenia leads to renal damage
and causes renal amyloidosis in dogs, and high levels of BUN and CREA are significant markers
of kidney damage (Luckschander et al.,2003).
●Dogs with ehrlichiosis showed increased levels of SGPT, SGOT and serum creatinine suggestive
of hepatic and renal involvement in the pathophysiology of the disease.
● The increase in creatinine levels may be due to immune complex-mediated glomerulonephritis
indicating renal involvement in dogs with ehrlichiosis (Srikala et al.,2010].
Diagnosis
●Traditional diagnostic techniques such as hematology, cytology, serology and isolation are valuable
diagnostic tools for CME; however, a definitive diagnosis of E. canis infection requires molecular
techniques (Harrus and Waner 2010).
●Poor sensitivity of blood smear examination might be due to low level parasitaemia that can be
detected by highly sensitive nested PCR (Lakshmanan et al. 2007).
Application of nested PCR. Lane L—gene
ruler TM 100 bp ladder, Lane 7 positive
control, Lane 6 negative control and
Lane 1–5 clinical samples(Source; Laxmi
Bai et al;2017)
Differential Diagnosis
●Anaplasmosis, canine Rocky Mountain spotted fever (another rickettsiosis), babesiosis, bartonellosis,
hepatozoonosis, and canine distemper should all be considered as possible differential diagnoses for
ehrlichiosis
Treatment
●For canine ehrlichiosis, tetracycline (22 mg/kg given every
eight hours) or doxycycline (5 mg/kg every twelve hours)
administered for four weeks is the recognized treatment.
● The specific therapy for ehrlichiosis is doxycycline (5 to
10mg/kg every 12 hours, orally, for 21 days) and/or
imidocarb dipropionate (5mg/kg, subcutaneously, with an
interval of 15 days minimum) (FISCHER, 2002).
● With regard to the tick-control, the use of fipronil on a
monthly basis has proved to be an effective prevention
and treatment for dogs in areas endemic to canine
monocytic ehrlichiosis (DAVOUST et al., 2003).
● Supportive therapy such as blood or fluid transfusions
and anabolic steroids may be required in severe cases.
Blood transfusion in serious case at jibachha
Veterinary hospital
Close monitoring of patient during fluid therapy and
serious condition using oxygen mask at Jibachha
veterinary hospital
Prevention:
●Recent studies have evaluated the efficacy of a spot-on formulation containing imidacloprid 10%
and permethrin 50% (Advantix®) to prevent tick exposure and thus E. canis infection in dogs.
Preventive efficacies of 95–100% were demonstrated in treated dogs living under natural conditions
in endemic areas(Otranto et al.,2010; Otranto et al.,2008).
References
Maeda, K., Markowitz, N., Hawley, R.C., Ristic, M., Cox, D., McDade, J.E. (1987): Human infection with Ehrlichia canis, a leukocytic rickettsia. Ne
Engl. J. Med. 316(14), 853– 856
Harrus, S., Kass, P.H., Klement, E., Waner, T. (1997): Canine monocytic ehrlichiosis: a retrospective study of 100 cases, and an epidemiologic
investigation on prognostic indicators for the disease. Vet. Rec. 141, 360–363
Harrus, S., Waner, T., Bark, H. (1997): Canine monocytic ehrlichiosis update. Compend. Contin. Educ. Pract. Vet.19, 431–444
Otranto, D., de Caprariis, D., Lia, R.P., Tarallo, V., Lorusso, V., Testini, G., Dantas-Torres, F., Latrofa, S., Diniz, P.P., Mencke, N., Maggi, R
Breitschwerdt, E.B., Capelli, G., Stanneck, D. (2010): Prevention of endemic canine vector-borne diseases using imidacloprid 10% and permethr
50% in young dogs: a longitudinal field study. Vet. Parasitol. 172(3–4), 323–332 36.
Otranto, D., Paradies, P., Testini, G., Latrofa, M.S., Weigl, S., Mencke, N., Capariis, D., Parisi, A., Capelli, G., Stanneck, D. (2008): Application of 10
imidacloprid/50% permethrin to prevent Ehrlichia canis exposure in dogs under natural conditions. Vet. Parasitol. 153, 320–328
DAVOUST, B. et al. Assay of fipronil efficacy to prevent canine monocytic ehrlichiosis in endemic areas. Veterinary Parasitology, v.112, p.91-10
2003
FISCHER, C.A.; EVANS, T. Uveitis: ocular manifestations of systemic diseases in dogs. In: RIIS, R.C. Small animal ophthalmology secret
Philadelphia : Hanley & Belfus, 2002. Cap.29, p.184-191
Laxmi Bai,Goel,Ricky Jhambh,Pawan Kumar and V. G. Joshi,2017. Molecular prevalence and haemato-biochemical profile of
canine monocytic ehrlichiosis in dogs in and around Hisar, Haryana, IndiaJ Parasit Dis (July-Sept 41(3):647–654
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.Komnenou AA, Mylonakis ME, Kouti V, Tendoma L, Leontides L, Skountzou E, Dessiris A, Koutinas AF, Ofri R. Ocular
manifestations of natural canine monocytic ehrlichiosis (Ehrlichia canis): a retrospective study of 90 cases. Vet
Ophthalmol. 2007;10:137–142
Harrus S, Waner T, Bark H, Jongejan F, Cornelissen AW. Recent advances in determining the pathogenesis of canine
monocytic ehrlichiosis. J Clin Microbiol. 1999;37:2745–2749
Lakshmanan B, John L, Gornathinayagam S, Dhinakarraj G. Molecular detection of Ehrlichia canis from blood of naturally
infected dogs in India. Vet Archive. 2007;83:353–354.
Bhadesiya CM, Raval SK. Hematobiochemical changes in ehrlichiosis in dogs of Anand region, Gujrat. Vet
World. 2015;8(6):713–717. doi: 10.14202/vetworld.2015.713-717.
Harrus S, Waner T, Bark H, Jongejan F, Cornelissen AW. Recent advances in determining the pathogenesis of canine
monocytic ehrlichiosis. J Clin Microbiol. 1999;37:2745–2749.
Nair AD, Cheng C, Ganta CK, Sanderson MW, Alleman AR, Munderloh UG, Ganta RR. Comparative experimental infection seen in
dogs with E. canis, E. chaffensis, A. platys and A. phagocytophilum. PLoS One. 2016;11(2):e0148239. doi:
10.1371/journal.pone.0148239
Woody BJ, Hoskins JD. Ehrlichial diseases of dogs. Vet Clin North Am Small Anim Pract. 1991;21:75–98. doi: 10.1016/S0195-
5616(91)50009-7.
Shipov A, Klement E, Reuveni-Tager L, et al. Prognostic indicators for canine monocytic ehrlichiosis. Vet Parasitol.
2008;153:131-8.
Luckschander N, Kleiter M, Willmann M. Renal amyloidosis caused by Ehrlichia canis. Schweiz Arch Tierheilkd. 2003;145:482-5.
Woody B J, Hoskins J D. Ehrlichial diseases of dogs. Vet Clin North Am Small Anim Pract. 1991;21:75-98.
Lee Pyle R. Canine Ehrlichiosis. J Am Vet Med Assoc 1980; 177: 1197-1202.
Ristic, M. and Holland, C.J. (1993) Canine ehrlichiosis. In: Woldehiwet, Z. and Ristic, M., editors. Rickettsial and Chlamydial
Diseases of Domestic Animals. Pergamon Press, New York. p169-186.
Srikala, D., Satish Kumar, K., Amruth Kumar, V.V. and Tirumala Rao, D.S. (2012) Clinical and therapeutic aspects of canine
monocytic ehrlichiosis. Indian J. Vet. Med., 32(2): 109-110.
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infection seen in dogs with E. canis, E. chaffensis, A. platys and A. phagocytophilum. PLoS One 11(2):e0148239
Canine ehrlichiosis - Dr. Jibachha Sah,M.V.Sc,Lecturer

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  • 1. CANINE EHRLICHIOSIS (E. CANIS) Dr. Jibachha Sah M.V.Sc, Lecturer, College of Veterinary Science, NPI, Bhojad, Chitwan, Nepal jibachhashah@gmil.com,00977-9845024121
  • 2. Introduction ●Ehrlichiosis is a globally distributed canine vectorborne disease (CVBD) transmitted by ticks. ●Caused by the rickettsial bacteria Ehrlichia spp., ehrlichiosis affects dogs and humans as well as other domestic and wild animal species. ●E. canis causes canine monocytic ehrlichiosis (CME). This disease, also known as tropical canine pancytopenia, canine rickettsiosis or canine hemorrhagic fever, was first described in Algeria in 1935 by Donatien and Lestoquard.
  • 3. Etiology ● There are two different types of leukotropic diseases that are caused by ehrlichia bacteria in dogs. ● These are “Canine Monocytic Ehrlichiosis” caused by E. canis that is frequently encountered, and “Canine Granulocytic Ehrlich-iosis” caused by E. ewingi. ● Ehrlichia canis (a small, Gram-negative, coccoid bacterium), which parasitizes cytoplasm of the circulating monocytes in form of distinct clusters termed as “Morulae” (Ristic and Holland,1993).
  • 5. Incubation period ● The incubation period of the illness is 7-21 days in general and it has three stages as acute, sub-clinical, and chronic (Woody and Hoskins ,1991).) Breed Susceptibility ●CME was observed in wide variety of breeds with somewhat more predisposition in Labrador retriever followed by Pug, Rottweiler, German shepherd, Lhasa apso, Pomeranian and Gaddi. Age susceptibility ●Age-wise prevalence of CME recorded in dogs of varying age i.e. from 3 months to 9 years with maximum number of cases in more than 1 year age group.
  • 6. Transmission/Vector ●Typically, tick nymphs or larvae are infected with E. canis after feeding on a persistently infected dog. ● Transstadial transmission occurs to subsequent stages of the tick vector. ● A new host is infected via salivary gland secretions during blood feeding. ● Transmission of the disease has also been reported via blood trans fusion.
  • 7.
  • 8. Zoonotic Potential ●A few decades ago, ehrlichioses were considered to only have veterinary relevance. ●The first human infection with E. chaffeensis was diagnosed in 1986 raising the awareness of Ehrlichia spp. as zoonotic pathogens.(Maeda et al.,1987). ● The best-known Anaplasma species is A. phagocytophilum, formerly referred to as human granulocytic ehrlichiosis (HGE) factor, E. phago - cytophila or E. equi. ● It causes granulocytic anaplasmosis in dogs and humans.
  • 9. There are three phases of illness with Ehrlichiosis: acute, subclinical, and chronic. Acute Phase ●This phase occurs 1 to 3 weeks after the host is bitten by the tick. The Ehrlichia organism is replicating in this time period and attaching to white blood cell membranes. During the acute infection, the platelet count will drop and an immune-mediated platelet destruction will occur. ●The acute disease is characterized by high fever, depression, lethargy, anorexia, lymphadenomegaly, splenomegaly, epistaxis, dermal petechiae and ecchymoses. ●The dog will be listless, off food, and may have enlarged lymph nodes and/or spleens. There may be fever and even neurologic symptoms as well, but although the dog may seem pretty sick, this phase of infection is rarely life-threatening. ●Ophthalmological lesions are frequent and include anterior uveitis, chorioretinitis, papilledema, retinal hemorrhage, presence of retinal perivascular infiltrates and bullous retinal detachment (Komnenou et al. 2007).
  • 10. Subclinical Phase ●In this phase, the dog appears normal. The organism has sequestered in the spleen and is essentially hiding out there. Dogs can stay in this phase for months or even years. ●●The only hint that Ehrlichia is hiding is a somewhat reduced platelet count and/or elevated globulin level on a blood test. ●The blood protein level on a lab report is divided into albumin (an important carrier protein) and globulins (every other blood protein including antibodies.) Long-term stimulation of the immune system will elevate globulins, sometimes dramatically.
  • 11. Chronic Phase ●In this phase the dog gets sick again. Up to 60 percent of dogs infected chronically with Ehrlichia canis will have abnormal bleeding due to reduced platelets numbers. ● Deep inflammation in the eyes called uveitis may occur as a result of the long-term immune stimulation. ● Neurologic effects may also be seen. Glomerulonephritis, resulting in serious urinary protein loss, can also result. Increased globulin levels are almost always seen in this stage, albumin is often low. ● Most dogs do not show the full pancytopenia (literally reduction in all blood cell lines) but severe cell deficiencies are associated with high mortality rates. uveitisUveitis in pug Epistaxis ( bleeding from nose unilateral/bilateral
  • 12. ●Pale mucous membranes and weakness, bleeding and significant weight loss are common findings in the chronic phase (Harrus and Waner 2010).
  • 14. Pale mucous membrane Epistaxis (Nose bleeding
  • 15. Haematology analyzing and RDT at Jibachha Veterinary hospital
  • 16. ●Thrombocytopenia appears around day 10 and peaks in the third week post-infection, with platelet counts ranging from 20,000 to 52,000/µl (normal range: 20000– 450,000/µl). There can also be mild anemia and leukopenia. ●Hypoalbuminemia, hyperglobulinemia, and hypergammaglobulinemia (mostly polyclonal (Antibody represents a collection of antibodies from different B cells), rarely monoclonal(represents antibody from a single antibody producing B cel)) are common in CME. Also moderate increases in alanine aminotrans - ferase (ALT) and alkaline phosphatase (ALP) can occur due to hepatocyte damage during the acute phase. ● Pancytopenia due to bone marrow hypoplasia is characteristic of the chronic severe form (Harrus, et al.,1997). ● E. canis can occasionally induce a proteinlosing nephropathy as a result of immunecomplex glomerulonephritis with consequent proteinuria and azotemia Clinical pathology
  • 17.
  • 19. ●Lower levels of total erythrocyte count, Hematocrit, MCH, MCHC and higher levels of MCV indicates macrocytic, hypochrmic anemia in affected dogs. Such type of anaemia might be due to haemorrhagic manifestation of disease (Bhardwaj 2013) owing to thrombocytopenia. ●Platelet consumption, increased splenic sequestration and decreased platelet lifespan are the possible attributes for thrombocytopenia (Harrus et al. 1999). ●Thrombocytopenia, anemia, eosinopenia. Left deviation in neutrophils, are the hematological signs frequently encountered in canine ehrlichiosis (Shipov et al.,2008). ●Thrombocytopenia by leading to immunological destruction of platelets (Lee pyle, 1980). and also cause central nervous system abnormalities in dogs. ● The most commonly observed hematological abnormalities are thrombocyto penia and anemia(Harrus et al.,1997)
  • 20.
  • 21. Biochemistry analyzing at Jibachha Veterinary hospital
  • 22. Abdominal USG done for organ dysfunction at Jibachha veterinary hospital
  • 24. ●Increase in serum ALT, AST and alkaline phosphatase values in affected dogs, suggesting hepato- biliary dysfunction dueinfiltration of perivascular mononuclear cells (Nair et al. 2016). ●Increased levels of AST and ALT might be due to histopathological changes in liver as a result of the infiltration of perivascular mononuclear cells (Nair et al. 2016). Serum protein profile indicated hypoproteinemia owing to hypoaluminemia and hypoglobunemia in affected dogs. ●The hypoalbuminemia seen in CME might be the consequence of peripheral loss of albumin to edematous inflammatory fluids as a result of increased vascular permeability (Woody and Hoskins 1991), blood loss, or decreased protein production due to concurrent liver disease as suggested by elevated hepatic enzymes. ●Total bilirubin levels in affected dogs were higher as compared to healthy control which is due to rise in indirect bilirubin levels owing to immune mediated RBC lysis. Mean urea and creatinine value in affected dogs were higher than healthy control dogs.
  • 25. ●The increase in urea and creatinine values may be due to membrane-proliferative glomerulopathy and interstitial nephritis. It has been suggested that the presence of inflammatory infiltrates rich in lymphocytes might be responsible for immuno-pathogenesis of renal lesion in dogs with CME. ●Ehrlichiosis accompanied by hyperglobulinemia and thrombocytopenia leads to renal damage and causes renal amyloidosis in dogs, and high levels of BUN and CREA are significant markers of kidney damage (Luckschander et al.,2003). ●Dogs with ehrlichiosis showed increased levels of SGPT, SGOT and serum creatinine suggestive of hepatic and renal involvement in the pathophysiology of the disease. ● The increase in creatinine levels may be due to immune complex-mediated glomerulonephritis indicating renal involvement in dogs with ehrlichiosis (Srikala et al.,2010].
  • 26. Diagnosis ●Traditional diagnostic techniques such as hematology, cytology, serology and isolation are valuable diagnostic tools for CME; however, a definitive diagnosis of E. canis infection requires molecular techniques (Harrus and Waner 2010). ●Poor sensitivity of blood smear examination might be due to low level parasitaemia that can be detected by highly sensitive nested PCR (Lakshmanan et al. 2007). Application of nested PCR. Lane L—gene ruler TM 100 bp ladder, Lane 7 positive control, Lane 6 negative control and Lane 1–5 clinical samples(Source; Laxmi Bai et al;2017)
  • 27. Differential Diagnosis ●Anaplasmosis, canine Rocky Mountain spotted fever (another rickettsiosis), babesiosis, bartonellosis, hepatozoonosis, and canine distemper should all be considered as possible differential diagnoses for ehrlichiosis
  • 28. Treatment ●For canine ehrlichiosis, tetracycline (22 mg/kg given every eight hours) or doxycycline (5 mg/kg every twelve hours) administered for four weeks is the recognized treatment. ● The specific therapy for ehrlichiosis is doxycycline (5 to 10mg/kg every 12 hours, orally, for 21 days) and/or imidocarb dipropionate (5mg/kg, subcutaneously, with an interval of 15 days minimum) (FISCHER, 2002). ● With regard to the tick-control, the use of fipronil on a monthly basis has proved to be an effective prevention and treatment for dogs in areas endemic to canine monocytic ehrlichiosis (DAVOUST et al., 2003). ● Supportive therapy such as blood or fluid transfusions and anabolic steroids may be required in severe cases. Blood transfusion in serious case at jibachha Veterinary hospital
  • 29. Close monitoring of patient during fluid therapy and serious condition using oxygen mask at Jibachha veterinary hospital
  • 30. Prevention: ●Recent studies have evaluated the efficacy of a spot-on formulation containing imidacloprid 10% and permethrin 50% (Advantix®) to prevent tick exposure and thus E. canis infection in dogs. Preventive efficacies of 95–100% were demonstrated in treated dogs living under natural conditions in endemic areas(Otranto et al.,2010; Otranto et al.,2008).
  • 31. References Maeda, K., Markowitz, N., Hawley, R.C., Ristic, M., Cox, D., McDade, J.E. (1987): Human infection with Ehrlichia canis, a leukocytic rickettsia. Ne Engl. J. Med. 316(14), 853– 856 Harrus, S., Kass, P.H., Klement, E., Waner, T. (1997): Canine monocytic ehrlichiosis: a retrospective study of 100 cases, and an epidemiologic investigation on prognostic indicators for the disease. Vet. Rec. 141, 360–363 Harrus, S., Waner, T., Bark, H. (1997): Canine monocytic ehrlichiosis update. Compend. Contin. Educ. Pract. Vet.19, 431–444 Otranto, D., de Caprariis, D., Lia, R.P., Tarallo, V., Lorusso, V., Testini, G., Dantas-Torres, F., Latrofa, S., Diniz, P.P., Mencke, N., Maggi, R Breitschwerdt, E.B., Capelli, G., Stanneck, D. (2010): Prevention of endemic canine vector-borne diseases using imidacloprid 10% and permethr 50% in young dogs: a longitudinal field study. Vet. Parasitol. 172(3–4), 323–332 36. Otranto, D., Paradies, P., Testini, G., Latrofa, M.S., Weigl, S., Mencke, N., Capariis, D., Parisi, A., Capelli, G., Stanneck, D. (2008): Application of 10 imidacloprid/50% permethrin to prevent Ehrlichia canis exposure in dogs under natural conditions. Vet. Parasitol. 153, 320–328 DAVOUST, B. et al. Assay of fipronil efficacy to prevent canine monocytic ehrlichiosis in endemic areas. Veterinary Parasitology, v.112, p.91-10 2003 FISCHER, C.A.; EVANS, T. Uveitis: ocular manifestations of systemic diseases in dogs. In: RIIS, R.C. Small animal ophthalmology secret Philadelphia : Hanley & Belfus, 2002. Cap.29, p.184-191 Laxmi Bai,Goel,Ricky Jhambh,Pawan Kumar and V. G. Joshi,2017. Molecular prevalence and haemato-biochemical profile of canine monocytic ehrlichiosis in dogs in and around Hisar, Haryana, IndiaJ Parasit Dis (July-Sept 41(3):647–654
  • 32. . .Komnenou AA, Mylonakis ME, Kouti V, Tendoma L, Leontides L, Skountzou E, Dessiris A, Koutinas AF, Ofri R. Ocular manifestations of natural canine monocytic ehrlichiosis (Ehrlichia canis): a retrospective study of 90 cases. Vet Ophthalmol. 2007;10:137–142 Harrus S, Waner T, Bark H, Jongejan F, Cornelissen AW. Recent advances in determining the pathogenesis of canine monocytic ehrlichiosis. J Clin Microbiol. 1999;37:2745–2749 Lakshmanan B, John L, Gornathinayagam S, Dhinakarraj G. Molecular detection of Ehrlichia canis from blood of naturally infected dogs in India. Vet Archive. 2007;83:353–354. Bhadesiya CM, Raval SK. Hematobiochemical changes in ehrlichiosis in dogs of Anand region, Gujrat. Vet World. 2015;8(6):713–717. doi: 10.14202/vetworld.2015.713-717. Harrus S, Waner T, Bark H, Jongejan F, Cornelissen AW. Recent advances in determining the pathogenesis of canine monocytic ehrlichiosis. J Clin Microbiol. 1999;37:2745–2749. Nair AD, Cheng C, Ganta CK, Sanderson MW, Alleman AR, Munderloh UG, Ganta RR. Comparative experimental infection seen in dogs with E. canis, E. chaffensis, A. platys and A. phagocytophilum. PLoS One. 2016;11(2):e0148239. doi: 10.1371/journal.pone.0148239
  • 33. Woody BJ, Hoskins JD. Ehrlichial diseases of dogs. Vet Clin North Am Small Anim Pract. 1991;21:75–98. doi: 10.1016/S0195- 5616(91)50009-7. Shipov A, Klement E, Reuveni-Tager L, et al. Prognostic indicators for canine monocytic ehrlichiosis. Vet Parasitol. 2008;153:131-8. Luckschander N, Kleiter M, Willmann M. Renal amyloidosis caused by Ehrlichia canis. Schweiz Arch Tierheilkd. 2003;145:482-5. Woody B J, Hoskins J D. Ehrlichial diseases of dogs. Vet Clin North Am Small Anim Pract. 1991;21:75-98. Lee Pyle R. Canine Ehrlichiosis. J Am Vet Med Assoc 1980; 177: 1197-1202. Ristic, M. and Holland, C.J. (1993) Canine ehrlichiosis. In: Woldehiwet, Z. and Ristic, M., editors. Rickettsial and Chlamydial Diseases of Domestic Animals. Pergamon Press, New York. p169-186. Srikala, D., Satish Kumar, K., Amruth Kumar, V.V. and Tirumala Rao, D.S. (2012) Clinical and therapeutic aspects of canine monocytic ehrlichiosis. Indian J. Vet. Med., 32(2): 109-110. Nair AD, Cheng C, Ganta CK, Sanderson MW, Alleman AR, Munderloh UG, Ganta RR (2016) Comparative experimental infection seen in dogs with E. canis, E. chaffensis, A. platys and A. phagocytophilum. PLoS One 11(2):e0148239