This agent affects various species of domesticated animals, characterized by high rise of temperature, generalised enlargement of lymph, depression, loss of body condition, anaemia and some other aberrant clinical signs.
Distribution
This disease has been identified as early as 1930 but its clinical importance has been assigned in 1962. The disease is widely distributed in North and South Africa, North America, Middle East, Sri Lanka and other Asian countries. The disease has been reported from India in 1982. Subsequently the disease in canine has been reported from dog in Tamil Nadu.
Ehrlichiosis in bullock and buffaloes has been reported in Tamil Nadu.
Aetiology
The disease is caused by a rickettsia known as Ehrlichia. The organisms are considered as leukocytophilic bacteria and they multiply within the cytoplasmic vacules of circulating monocytes and tissue macrophages. Earlier this organisms was thought to be protozoa. Within he cytoplasm small clusters of cocci are evident. In cattle, this disease is caused by Ehrlichia bovis, in dog the disease is caused by E. canis, in sheep E. ovina and in horse E. risticii, E. bovis, E. canis and E. ovina resemble morphologically but differ serologically.
The order – Rickettsiales; Family – Rickttsiaceae, Tribe – Ehrlichieae; Genus – Ehrlichia. But, it differs from Rickettsiae because it replicates within phagosome of the host cell where as all Rickettsia excepting C. burnetti which grow free within the cytoplasm. Other feature of it it its ultrastructure tropism for circulating leukocytes and antigenic composition. Unlike rickettsia Ehrlichia prefer glutamate to generate ATP because it has got the ability to penetrate phagosomes. From mid 1960 Ehrlichia was recognised as globally distributed pathogen. Recently, increased awareness about tick related pathogens in USA and UK raised concerned on tick bites and the zoonotic significance of it.
Susceptible Hosts
Cattle, horse, sheep, dogs are susceptible. Pigs may also suffer. Both domestic and wild canine population used to suffer and outbreak may flare up in them. Cases of human infection with E. canis has been detected in USA and the organism has been identified as E. sennsu from Japan.
Mode of Transmission
The disease is not a contagious disease and this disease is transmitted through the bites of ticks. In case of cattle various species of ticks like Amblyomma, Rhipicephalus, Hyalomma have been considered as proven vectors. In case of dog Rhipicephalus sanguineus is considered as natural vector, whereas in case of sheep Rhipicephalus evertsi has been identified as transmitting agent of this disease. It has been possible to transmit the disease experimentally in horse by parenteral inoculation of the organism.
Pathogenesis
On entry organism invade the monocytes, macrophages and epithelial cells. Monocytes multiply in number and the entire cytoplasm is filled with them. As a result of destruction of leukocytes and thrombocytes, leukopenia and thrombocytopenia take place. There is bone marrow depression and anaemia. In horse, the organism may invade the intestinal epithelial cells causing colitis and typhlitis.
Blood transfusion from infected done may also spread the diseases. After 8 to 20 days following entry of the organisms acute phase start where in the organisms multiply in the mono-nuclear leucocytes of the blood and thus spread in liver, spleen, lymph nodes. Following this, acute phase sub-clinical phase set in when the animals appear to be normal. If the immunity is strong enough the animal throw the organisms. Otherwise, chronic phase develops. The severe chronic form is attributed as tropical canine pancytopenia. There is impairment in the production of blood cells. Thrombocytopaenia is the most consistent blood abnormality. The causes for such reduction of platelets have been put forth as increased platelet consumption as a result of inflammatory changes in the blood vessel endothelium, increased splenic sequestration of platelets and immunologic destruction of platelets. In this case, dogs used to collapse due to haemorrhage or secondary infection.
Cellular immune response assumes a major role in affording protection. Due to inadequate immunogenic response dogs like GSD used to suffer more than other variety of dogs. Stress factor such as major surgery, malnutrition, pregnancy, liver disorder, canine distemper, parasites may augment the disease process.
Outline of Clinical Signs
- Weakness
- Laboured breathing
- Pneumonia
- Arthritis
- Nasal discharge
- Depression
- Anorexia
- Polyuria
- Head tremors
- Neck pain
- Bleeding tendency
- Retinal haemorrhage
- Rash
- Spontaneous bleeding
- Swollen lymph nodes
- Cough
- Fatigue
- Intermittent fever
- Muscle wasting
- Eye discharge
- Weight loss
- Polydypsia
- Incontinenence
- Seizure
- Back pain
- Pallor
- Skin bleeding
- Epistaxis
- Swelling of legs
- Tendered abdomen
Lesions
Subcutaneous oedema, fluid in the peritoneal cavity and thoracic cavity, enlarged spleen and lymph node are the main changes. Haemorrhage in the liver and kidney as well as alimentary tract are seen. Signs of haemorrhage may be evident in many organs including joints and eyes.
Diagnosis
Ante mortem diagnosis is difficult. Diagnosis is to be made based on history, clinical signs and detection of organisms in the cytoplasm of circulating monocytes. Peripheral blood examination with Giemsa stain is preferred. Histopathologically organisms may be observed in the stained section.
Various serological tests, like indirect immunofluorescence anti body and ELISA have been suggested since many a time detection of the organisms in peripheral blood cell is not possible.
PCR is rapid and sensitive test.
Blood biochemical changes include hypoalbuminemia, hyperglobulinaemia and hypergammaglobulinemia.
Differential Diagnosis
Disease has to be differentiated from other haemoprotozoan infection specially Babesiosis, Theileriosis and Anaplasmosis. Canine ehrlichiosis should be differentiated from canine distemper and auto immune haemolytic anaemia. Equine ehrlichiosis should be differentiated from Salmonellosis, Colitis-X, etc.
Treatment
Broad spectrum antibiotic like oxytetracycline has been found to yield spectacular result and is considered to be the drug of choice. Drug may be given through intravenous route.
Dogs suffering from uraemic condition should not be given tetracycline since it is a nephrotoxic drug but in that case doxycycline may be used. 5-10 mg/kg body weight for 6 weeks period. Imidocarb dipropionate has been suggested against canine ehrlichiosis.
Supportive therapy with fluid and blood should be made. Vitamin B complex and haematinic preparations may be extended. Intensive fluid therapy should be made in diarrhoeic patient. Vitamin K is to be supplemented. Blood transfusion may be warranted.
Control
Recovered animal may remain as carrier and therefore he animal from endemic area should not be introduced in a new herd. Sometimes the disease may appear in outbreak proportion and therefore all precautions should be taken to minimize the spread of the disease by controlling the vector population. In dog, tick collar may be applied to cut down the tick population. All out measures should be taken to remove the tick from the body of the animal.
An inactivated whole cell adjuvanted vaccine is recommended.
Zoonotic Aspects
The disease has got public health importance. First recorded in 1950 from a 25 year boy in Japan. The disease in man manifests in three forms.
(a) Sennetsu Ehrlichiosis: In Japan, this form is also known as glandular fever, infection, mono-nucleosis and Hyuganetsu disease. The disease manifests as acute febrile illness along with lethargy. There is lymphadenopathy. Tetracycline works well.
(b) Human Monocytic Ehrlichiosis (HME): This disease was first reported in 1987 and the aetiology of it was determined as Ehrlichia chaffeensis in 1991. The tick was considered to be the vector of the disease. The disease is ascribed as non-specific febrile condition. In addition to fever, headaches is common. Severe complications which may result is fatal renal failure and encephalopathy. Other features which may be appreciated is malaise, nausea, vomiting, myalgia, chills and loss of appetite. Blood picture shows leukopenia, thrombocytopaenia and serum hepatic enzyme level.
(c) Human Granulocytic Ehrlichiosis (HGE): It was first reported from USA. Morulae were noted in granulocytes. DNA product amplified by PCR showed that the agent responsible to is Ehrlichia phagocytophilia and E. equi. Clinical symptoms reveal fibrile illness, headache, myalgia. Laboratory findings denote thrombocytopaenia, leucopoenia and elevated liver enzymes. History of tick bite is always evident. The disease on occasion may turn fatal. Tetracycline and Doxycycline gave satisfactory response.
