Understanding of Gallsickness in Cattle
K.H. Bulbul1, Shahnur Rahman2, I.M. Allaie3 and Z.A. Wani3
1Associate Professor, Division of Veterinary Parasitology, F.V.Sc. & A.H, SKUAST-K, Shuhama, Srinagar, J&K, 190006.
2M.V.Sc. Student, Division of Livestock Production and Management, F.V.Sc. & A.H, SKUAST-K, Shuhama, Srinagar, J&K, 190006. Corresponding e-mail:shahnurrahman134@gmail.com
3Assistant Professor, Division of Veterinary Parasitology, F.V.Sc. & A.H, SKUAST-K, Shuhama, Srinagar, J&K, 190006.
Abstract
Anaplasmosis formerly known as gallsickness in cattle is a tick borne rickettsial disease, predominantly caused by the organism Anaplasma marginale and to a lesser degree, A. centrale. The disease can be divided into four stages viz. incubation, developmental, convalescent, and carrier. The disease has a very long incubation period and clinical signs and symptoms may only occur 21 to 42 days after transmission. Fever, progressive anaemia and icterus are the main clinical manifestation of gallsickness in cattle. The animal’s body destroys red blood cells due to the immune system recognize the infected cells as abnormal and removes them, hence producing anaemia. Adult animals are more significantly affected by anaplasmosis than younger animals. The diseases can be treated with tetracycline and imidocarb and prevented with effective control measures of ticks and flies. Economic losses are due to reduced production and productvity, death loss and abortion of cattle, diagnosis and treatment costs.
Keywords: Anaplasmosis, cattle, tetracycline, control
Introduction:
Tick-borne bovine anaplasmosis is an infectious haemolytic disease caused due to destruction of the red blood cells resulting in anaemia followed by mortality (Howden et al., 2010; Kocan et al., 2010). Clinical disease is mostly found in cattle, but other ruminants including water buffalo, bison, African antelopes, and some species of deer can become persistently infected. The disease is triggered by a minute parasite, Anaplasma marginale, found in the red blood cells of infected cattle. The organism causes progressive anemia in ruminants leading to huge economic losses (Kumar et al., 2015). The transmission of the disease may be occurred in healthy animals from infected animals through tick bites or the mechanical transfer of fresh erythrocytes from biting flies or surgical equipment viz. needles, or dehorning, castration and tattooing equipment (Aubry and Geale, 2011).
Distribution:
The disease is distributed in tropical and subtropical areas worldwide including South and Central America, USA, Mexico, Caribbean, Southern Europe, Africa, Asia and Australia (Kocan and de la Fuente, 2003; Aubry and Geale, 2010). Interestingly, it is mostly scattered through most of the rainier regions of South Africa and it also occurs in cold mountainous areas such as the Drakensberg range and parts of Lesotho. As anaplasmosis is primarily transmitted by ticks, the distribution of the disease overlaps the distribution of three main tick species. Rhipicephalus decoloratus (African blue tick), Rhipicephalus microplus (Asian blue tick) and Rhipicephalus evertsi evertsi (red legged tick) are the most important vectors of the disease. These ticks are found in the coastal regions of the Western and Eastern Cape, throughout KwaZulu-Natal, Mpumalanga, Gauteng, Limpopo, North West and the eastern half of the Free State.
Transmission:
Gallsickness is primarily transmitted by ticks to animals. At least 20 different species of ticks have been reported to transmit A. marginale worldwide (Davidson and Goff, 2001; Kocan et al., 2004; Lankester et al., 2006), at least 12 species of biting flies have been shown experimentally to have the potential of mechanically transmitting A. marginale, including stable flies (Stomoxys calicitrans), eight species of tabanids (Tabanidae) and 3 species of midges (Culicidae) (Ewing, 1981; Potgieter et al., 1981; Hawkins et al., 1982). Insects such as biting flies and mosquitoes can also spread this disease to susceptible animals. In South Africa it is transmitted by 5 different tick species (Rhipicephalus decoloratus, R. microplus, R. simus, R. evertsi, Hyalomma marginatum rufipes), flies (Stomoxys calcitrans) and infected needles. The mechanical transfer of fresh blood from infected to susceptible cattle from biting flies or by blood contaminated fomites including needles, ear tagging, dehorning and castration equipment play the significant roles in transmission of the disease. Transplacental transmission of A. marginale may contribute to the epidemiology of bovine anaplasmosis in some regions.
Basically, A. marginale can be transmitted by three methods: (i) biological: infected erythrocytes are ingested by ticks; A. marginale replicates within the tick’s gut and salivary glands and is subsequently transmitted via tick saliva into uninfected ruminants; (ii) mechanical: infected erythrocytes are transferred from infected to susceptible cattle by biting flies or blood-contaminated fomites, including needles or surgical instruments, without amplification of A. marginale; and (iii) transplacental: infected erythrocytes move across the placenta in the uterus from infected cows to their offspring, without amplification of A. marginale.
In mechanical transmission, the organism is transmitted by blood-contaminated mouthparts of biting flies or by blood-contaminated equipment. Horse flies are capable of transmitting the organism and may remain mechanically infective for up to two hours after feeding on an infected animal (Hawkins et al., 1982). The blood-contaminated equipment, such as used vaccination needles, can also transmit A. marginale from an infected animal to uninfected susceptible animals. Biological transmission occurs through ticks. Once a tick acquires the organism through a blood meal, the organism infects the tick’s gut cells and completes part of its life cycle (Scoles et al., 2008). Over time, other tissues within the tick, including salivary glands, become infected. When a tick feeds on cattle, it transmits the organism through its saliva. Ticks can develop persistent infections and, with their intermittent feeding, can transmit the organism to multiple animals within the herd and nearby herds. Transplacental transmission occurs when the organism is transmitted from dam to foetus (Salabarria and Pino, 1988; Grau et al., 2013). This transmission appears to occur during the second or third trimester of pregnancy.
Pathogenesis:
Anaplasma spp. is transmitted to the animals from an infected tick through its saliva when it attaches to the animal. Once in the bloodstream, the Anaplasma organisms penetrate the red blood cells (RBC) and twitch to multiply. The number of infected RBCs doubles every 24-48 hours (Radostits et al., 2007). The incubation period varies but is usually between 3-4 weeks after tick bite transmission took place (Radostits et al., 2007). Once the RBCs are infected, they become foreign to the body and are removed by the liver, spleen and lymph nodes. The infected RBCs are broken down and anaemia starts to develop. Animals can lose up to 70 % of their RBCs (De Vos et al., 2004). Anaemia normally becomes noticeable once the animal has lost 40-50 % of the RBCs. The animal’s mucous membranes (gums, eyes and inner layer of the vulva or preputium) are therefore first pale, before it turns into the more common yellow colour. The yellow colour originates from the broken down haemoglobin (red blood cell pigment) in the liver. The immune systems recognizes the infected cells as abnormal and removes them, thereby creating anaemia. Anemia results when the animal’s body destroys red blood cells faster than it can produce new ones, which can lead to death.
Clinical signs:
The severity of disease is associated with the age of the animals. Cattle of all ages may become infected with anaplasmosis, but the severity of illness increases with age (De Vos et al., 2004; Radostits et al., 2007). Calves less than 6 months of age seldom show enough signs to indicate that they are infected, Cattle 6 months to 3 years of age become increasingly ill, and more deaths occur with advancing age. After 3 years of age, 30 to 50 percent of cattle with clinical anaplasmosis die if untreated (Radostits et al., 2007). The severity of disease is related to the number of infected red blood cells and subsequent red blood cell loss. Affected animals show continuous/fluctuating fever >40°C (although in later stages of disease it will disappear), depression, inappetance, weight loss, anaemia, jaundice, severe dyspnea, rumen stasis and constipation (Soulsby, 1982; Richey and Palmer, 1990; Bhatia et al., 2010). A severe drop in milk production in dairy animals and pregnant animals may abort. Death often occurs within 24 hours in adult dairy cows (Soulsby, 1982; Bhatia et al., 2010). Animals that survive have a convalescence period of several months to regain their former condition. Severe anemia can cause temporary infertility in bulls.
In mild cases, animals may exhibit symptoms such as elevated temperature, depression and pale mucous membranes. In severe cases, animals may be jaundiced, the most obvious symptom of which is a yellow tinge to the mucous membranes around the eyes; exhibit severe depression or nervousness; and eventually die. In herds that are not closely monitored, the first sign of Anaplasmosis may be dead animals.
Stages of anaplasmosis:
Anaplasmosis can be divided into four stages: incubation, developmental, convalescent, and carrier. These stages and the symptoms associated with them are summarized below.
Incubation stage
The incubation stage starts with the introduction of A. marginale and lasts until 1.0% of the RBCs of infected animal are infected. The average ranges of incubation stage are 3 to 8 weeks, but wide variations have been documented. The variation of the incubation stage directly depends to the number of organisms introduced into the animal. After attaining entry into the susceptible animal, Anaplasma spp. slowly reproduces in RBCs during this phase. During this period the animal remains healthy and shows no signs of being infected. Finally, after the parasite has reproduced many times and established itself in the RBCs of the animal, the body attempts to destroy the parasite.
Developmental stage
Most of the clinical characteristics signs appear in the developmental stage and this stage usually last from 4 to 9 days. Clinical signs begin to be expressed about half- way through this phase. The body of the infected animals destroys the parasites along with the RBCs resulting in reduced RBCs hence animals show signs of clinical anemia. The body temperature will commonly rise to 104° to 107°F (40° to 41°C), and a rapid decrease in milk production will occur in lactating cows. Cattle producers first notice the anaemic, then becomes weak and lags behind the herd. It refuses to eat or drink water. The skin becomes pale around the eyes and on the muzzle, lips, and teats. Later, the animal may show constipation, excitement, rapid weight loss, and yellow tinged skin. The animal may fall or lie down and be unable to rise. Affected cattle either die or begin a recovery 1 to 4 days after the first signs of the disease.
Convalescent Stage
Cattle that survive the clinical disease lose body weight, abort calves, and recover slowly over a period of 2- 3 months. This is known as the convalescent stage, which lasts until normal blood values return. This stage is differentiated from the developmental stage by an increase in the production of RBCs (erythropoiesis) in the peripheral blood, shown in an increase in haemoglobin levels and high total white blood cell counts, among other characteristics. Death losses normally occur during the late developmental stage or early convalescent stage.
Carrier stage
The cattle recover from anaplasmosis remain reservoirs or carriers of the disease for the other susceptible animals if the animals is inadequately treated. An animal will not exhibit any clinical signs associated with the persistent low-level anaplasmosis in carrier stage. Nevertheless, the blood from these recovered animals will cause anaplasmosis if introduced into susceptible cattle. Carriers very rarely become ill with anaplasmosis a second time. Unidentified carriers in a herd are the most likely source of infection for future outbreaks of the disease.
Diagnosis:
A tentative diagnosis of gallsickness can be made based on geographic location, season and clinical signs. However, the confirmatory diagnosis can be done by detecting the organism at the microscopic blood smear examination 2-6 weeks after transmission (Soulsby, 1982; Bhatia, 2010). If, anaplasmosis is suspected, a blood smear should be taken from the tip of either the ear or the tail of the sick animals. Serological test including msp5 ELISA, complement fixation, card agglutination tests, and PCR-based test is helpful to diagnose the later stages of the disease when the organisms may be present in lower numbers.
Treatment:
It is advisable to treat the animals as soon as possible when they show signs symptoms and to keep the animals calm and refrain from driving them over long distances. Animals diagnosed with gallsickness can be treated with two recognised active ingredients tetracycline or imidocarb injections according to the manufacturer’s guidelines. Treatment with any of these two drugs does not cause sterilization of the infection. Anaplasmosis in cattle is commonly treated with tetracycline antibiotics (tetracycline, chlortetracycline, oxytetracyline), which are most effective in the early stages of the disease. Supportive treatment is also recommended i.e. Vitamin B complex & Rumix. Recovered animals will stay lifelong carriers of the parasites and relapses can occur. Slow administrations of blood transfusion are also effective to treat the animals Bhatia (2010). Clearance of carrier animals through antibiotic treatment has been reported but requires multiple doses over long periods.
Control and prevention:
The control of gallsickness depends on 2 strategies i.e. tick control and vaccination. However most appropriate control and prevention measures include (a) maintenance of Anaplasma-free herds through import and movement control, testing, and elimination of carrier cattle; (b) vector control (Kocan et al., 2003); (iii) prevention of iatrogenic transmission; (iv) administration of antibiotics; and (v) preimmunization with live vaccines and immunization with killed vaccines(Aubry and Geale, 2011). Testing the animals twice at approximately 3-week interval before entering the herd would also decrease the risk of introducing a false-negative animal into a negative herd, as long as there is no possibility of infection between the two tests (Aubry and Geale, 2011). Typically, cases of anaplasmosis increase in late summer and fall as insect vectors increase. Therefore, control of vectors is key to prevent anaplasmosis. If necessary herd treatment with oxytetracycline injection every 3 to 4 weeks during high risk times may be necessary will prevent clinical disease but animals can become carriers (Kumar et al., 2015). As most parts of endemic areas of the world to Anaplasma, it is advisable to sustain a stable disease situation to prevent large losses. Allowing calves natural exposure to tick borne diseases during the period when they are naturally resistant or protected by passive maternal immunity, will increase the antibody levels against these diseases. If this is not possible, all calves less than 6 months of age should be vaccinated with the Anaplasma vaccine to ensure immunity. Prevent the chance of anaplasmosis by controlling ticks and flies by dipping animals with suitable acaricides and insecticides.
Conclusion:
Anaplasmosis is an economically important disease of cattle which can be treated with oxytetracycline. Various serological and molecular tests are used to diagnose anaplasomosis. Control measures for bovine anaplasmosis vary with geographical location and include maintenance of Anaplasma-free herds, vector control, administration of antibiotics and vaccination.
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