Anaplasmosis (Gall Sickness)

Anaplasmosis (Gall Sickness) is a rickettsial disease affecting cattle, sheep and goats including wild ruminants and has been characterized by anaemia, jaundice and haemoglobinemia without the evidence of haemoglobinuria.

Etiology

All outbreak and clinical disease in Anaplasmosis (Gall Sickness) is caused mainly by a virulent Anaplasma marginale followed by a less virulent A. centrale. Anaplasma is an obligate, intra-erythrocytic parasite.

A. phagocytophilum has been recently reported in cattle and man.

• A. marginale and A.centrale: cattle and wild ruminants.
• A. ovis: sheep and goats ( will not infect cattle).
• A. centrale: sheep and goats (closely related to A.marginale cause mild anaplasmosis in cattle).

Epidemiology

Prevalence of infection

• A. marginale in cattle is endemic, occurs in most tropical and sub-tropical countries and is sporadic in temperate countries.
• A. centrale is prevalent in South Africa, Australia, South America, South East Asia, Middle East Asia and Middle East.

Source of infection

• Source of infection is always blood.
• Recovery from acute infection leads to carrier infection status and is characterized by repetitive cycle of rickettsemia.
• And the persistent carrier becomes the reservoir for infection.

Economic impacts

• Death, abortion, loss of production in sick, recovered animals and cost associated with preventive measures.

Transmission

• The disease has been transmitted mechanically/biologically by arthropod vectors.
• There are 19 different ticks have been found capable of transmitting A. marginale.
• Boophilus, a one host tick (male ticks) are serving as a reservoir for infection.
• A. centrale is transmitted by a multi-host tick, Rhiphicephalus, Dermacentor parasitizes deer and cattle Spread of infection occurs from animal to animal by insect vectors. E.g. Ixodidae, Tabanidae (mechanical vector) In addition to the vectors disease also spread by blood transfusion.
• Transtadial transmissions are usual mode of transmission Transplacental (intra uterine) transmission is possible.
• Latrogenic transmission occurs through hypodermic needles, castration, spaying, dehorning instruments, blood transfusions, and embryo transplants.

Host affected

• Cattle, sheep and goats, and wild ruminants are affected.
• Animals under low plane of nutrition are susceptible to anaplasmosis.
• All age group of cattle are infected, although, young calves are less susceptible as compared to adult cattlefor A. marginale.
• Animals infected after the age of 3 years may suffer from per acute fatal form of disease.

Pathogenesis

• Anaplasmosis (Gall Sickness) is caused by an obligate, intra-erythrocytic parasite.
• The organism undergoes a complex development cycle within the gut cells of biological vectors (ticks) after a blood feeding from the infected hosts.
• The infective stage is transferred from gut to the salivary gland of the ticks and has been transmitted to the animal hosts during their next feeding.
• The organism infect mainly the mature red blood cells (mRBC) by an endo-cytosis process.
• The organism reproduce by binary fission and form 2-8 infective initial bodies which leave the cells and infect other RBCs by means of exo-cytosis.
• The number of infected RBC doubles each day for upto 10 days and may be visible by microscopic examination and then follows latency within 2-6 weeks after infection.
• Ten to ninety percent of the RBCs parasitized in acute stage, amongst 15% might have been parasitized before the cattle becoming clinically diseased.
• Within the reticulo-endothelial systems the parasitized RBC is removed by phagocytosis which release acute phase inflammatory reactants.
• However, continued destruction of RBCs results in development of fever, mild to severe anaemia, icterus without haemoglobinuria.
• The degree of anaemia depends on the proportion of RBC parasitized.
• The first appearance of anaplasma in the blood coincides with a fall in the haematocrit value and reduced RBC numbers and the appearance of immature RBCs.
• In acutely infected cases, fever and death occurs shortly after this phase.
• Case fatality rate ranges from 29-49%. Recovered animals emaciated and there is prolonged convalescence.
• In recovered animals from initial acute attack, parasitic invasion of mature RBC occur but only with limited intensity.
• Degree of anaemia is severe in adult cattle than in young.
• Infected animals become carrier/reservoir.
• A. marginale affected cattle develop prolonged immunity and is not protective immune response.
• Cattle and ticks infected with one genotype of A.marginale avoid getting infection caused by other genotype and herds of cattle in endemic areas are called as Phenomenon of Infection Exclusion.

Clinical Signs

Per acute form

• Sudden onset of high fever, anaemia, icterus, severe dyspnoea and death in 24 hours is common in adults cattle.
• Acute form Incubation period is 3-4weeks with tick borne infection.
• Pregnant cows frequently abort, In convalescent bulls, there may be depression in testicular function for several months.

Sub clinical form

• Most sub acute cases seen in young animals.
• Rectal temperature increase slowly and rarely reaches 40.5 ° C, fever (irregular period) for 2 weeks (altered), complete anorexia followed by death.
• Survivors of infection have emaciation, impaired fertility, jaundiced mucous membrane, markedly pale after an acute stage but there is no haemoglobinuria.
• Usually disease is sub clinical in goats, clinical signs are as similar to cattle.
• Severe disease in goats show hyper excitability.
• Not completely resolved from anaemia atleast for 3-4months.

Necropsy Findings

• Anaemia, hamoglobinuria, icterus, submucosal haemorrhages, dark, swollen, multifocal petichial and echymotic haemorrhages in kidney.
• Infiltration with interstitial cells, swollen, pale, and friable liver with focal necrosis.
• Liver is mottle and yellow orange in color.
• The gall bladder is often enlarged and contains thick brown or green bile.
• Ophthalmitis, uveitis, conjunctival suffusion and moon blindness for 2-8 months period.

Diagnosis

• Based on clinical signs and necropsy findings.
• Identification of organisms.
• Diff Quik staining of blood smears is as accurate as Giemsa and detects the organism in less than 15 sec.
• The organism appears as dense, rounded and intra-erythrocytic bodies (0.3-1.0µm in dia) and has been found on or nearer the margin of the RBC.
• Blood for the (thin smears must be prepared) smears should be collected from jugular veins and/or large blood vessels.
• Molecular diagnosis by PCR.
• Competitive ELISA, Indirect ELISA, Dot ELISA, Card Agglutination test and Capillary tube agglutination test.
• Indirect Fluorescent Antibody test and Complement Fixation test.

Differential diagnosis

• Babesiosis
• Borreliosis
• Trypanosomiasis
• Theileriosis
• Bacillary haemoglobinuria
• Leptospirosis
• Post-parturient haemoglobinuria
• Poisoning

Treatment

• Treatment Inj.Tetracycline 10-15mg/kg bw for 10–15 days, for i/v or i/m.
• Chlortetracycline 10 mg/kg bw, bolus for 30-60days.
• Long Acting Oxytetracycline deep intra muscular, two doses at 3 – 7 days intervals.
• Imidocarb 3 mg/kg bw s/c into two equal daily doses.

Prevention

• Live and killed vaccines containing infected RBCs of A. marginale are in use in some endemic countries.

Control

• Tick and fly control can be done using acaricides.