Research Article
Open Access
Epidemiology of Bovine Anaplasmosis
Tagesu Abdisa*
Jimma University College of Agriculture and Veterinary Medicine, School of Veterinary Medicine, Ethiopia
*Corresponding author: Tagesu Abdisa*, Roba Hasen, Tolera Tagesu, Gemechu Regea, Getachew Tadese, Jimma University, School of Veterinary Medicine,Jimma, Oromia, Ethiopia,Tel: +251933681407; Email:
@
Received: 4 February, 2019; Accepted: 8 February, 2019; Published: 19 March, 2019
Citation: Abdisa T (2019) Epidemiology of Bovine Anaplasmosis. SOJ Vet Sci 5(1): 1-6. DOI: 10.15226/2381-2907/5/1/00165
Summary
Bovine Anaplasmosis is one of the most important tick borne
diseases of ruminants worldwide causing significant economic losses
in the livestock industries due to the high morbidity and mortality in
susceptible cattle herds. The main aim of this paper is to review the
epidemiology of bovine anaplasmosis. Bovine Anaplasmosis, caused
by Anaplasma marginale, is an infectious but non-contagious disease.
The mode of transmission of Bovine anaplasmosis includes mechanical
(blood contaminated fomites (needles, ear tagging, dehorning and
castration equipment), biological (tick bites) and transplcenta (mother
to fetus). Bovine Anaplasmosis occurs in tropical and subtropical
regions worldwide. Cattle of all ages are susceptible to infection
with A. marginale, but the severity of disease increases with age. The
common clinical sign of bovine anaplsmosis includes; Fever, anorexia,
rapid loss of body condition, severe decrease in milk production, pale
and icteric mucous membranes, increased heart and respiratory rates,
muscle weakness and depression. Diagnosis of bovine Anaplasmosis
can be made by demonstration of A. marginale on stained blood
smears from clinically infected animals during the acute phase of the
disease, but it is not reliable for detecting infection in pre-symptomatic
or carrier animals. Instead of blood smears, serological demonstration
of antibodies and confirmation of antigen with molecular detection
method is more prefer than blood smear. Anaplasmosis can be
treated by administration oxytetracycline; however a carrier animal
doesn’t recover with oxytetracycline treatment. Control measures
for bovine Anaplasmosis vary with geographical location and include
maintenance of Anaplasma free herds, vector control, administration
of antibiotics and vaccination. Generally, Anaplasmosis is one of
the ricketticia diseases of bovine which decrease development of
country. Intensive acaridae application to control ticks has a number
of limitations, therefore, immunization together with strategic tick
control is recommended for exotic and crossbred cattle. Further
studies on epidemiology of bovine anaplasmosis were not conducted
in Ethiopia; therefore the researcher and Veterinarians should have to
be focused on Bovine anaplasmosis.
Keywords: Anaplasmosis, Anaplasma marginale, Bovine Rickettsia, Tick
Keywords: Anaplasmosis, Anaplasma marginale, Bovine Rickettsia, Tick
Introduction
Bovine Anaplasmosis is one of the most important tick borne
diseases of ruminants across the worldwide which causing
significant economic losses in the livestock industries in the
tropical and subtropical areas mainly due to the high morbidity
and mortality in susceptible cattle herds [1]. Bovine anaplasmosis
also known as Red water or Gall sickness which is an important
disease of cattle primarily caused by Anaplasma marginale and
it infects erythrocytes, which results to erythrophagocytosis
and subsequently anaemia [2]. The primary causative agent
is Anaplasma marginale, Gram-negative obligate intracellular
bacteria parasitizing erythrocytes [3]. It has been described in
domestic and wild animals (Cattle, Water Buffalo, Bison, African
Antelopes, White-Tailed Deer and Mule Deer); clinical disease is
most notable in cattle, but wild ruminants can become persistently
infected serving as reservoirs for infection of susceptible hosts
[1].It is an infectious but noncontiguous disease, which spread
through tick bites, mechanical transfer and/or transplacental
transmission [3].
A. phagocytophilum causes febrile disease in cattle varying from undetectable clinical signs to serious complications, including death [4]. The disease is characterized by high fever, cough, abortion, decreased milk production, and anorexia [5].
Even if, the disease is present in Ethiopia, the epidemiology of bovine anaplasmosis has not been conducted well in Ethiopia. Therefore, the main objective of this paper is to review epidemiology of Bovine Anaplasmosis.
A. phagocytophilum causes febrile disease in cattle varying from undetectable clinical signs to serious complications, including death [4]. The disease is characterized by high fever, cough, abortion, decreased milk production, and anorexia [5].
Even if, the disease is present in Ethiopia, the epidemiology of bovine anaplasmosis has not been conducted well in Ethiopia. Therefore, the main objective of this paper is to review epidemiology of Bovine Anaplasmosis.
Literature Review
Etiology
Anaplasmosis in cattle is caused mainly by Anaplasma marginale and are intra-erythrocytic microorganisms of the
order of Rickettsiales [6]. Anaplasma marginale is a tick-borne
pathogen and the causative agent of bovine anaplasmosis. A. marginale is classified in the Rickettsial order, reorganized into
two families such as Anaplasmataceae and Rickettsiaceae [7].
Anaplasma organisms are obligate intracellular Gramnegative rickettsia, found exclusively within vacuoles derived from the erythrocyte membrane, and are membrane-bound within the cytoplasm of the host cell. A. marginale persist in nature in mammalian and ticks hosts, which serve as reservoirs of infection in the bovine, A. marginale infect erythrocytes and endothelial cells [8, 9]. The genus Anaplasma includes three species that can infect ruminants, A. marginale and A. centrale in cattle as detailed in table 1. A. marginale and A. centrale infect cattle, but differ in morphology, virulence and geographical distribution [7].
Source: Rymaszewska, and Grenda (2008)
Anaplasma organisms are obligate intracellular Gramnegative rickettsia, found exclusively within vacuoles derived from the erythrocyte membrane, and are membrane-bound within the cytoplasm of the host cell. A. marginale persist in nature in mammalian and ticks hosts, which serve as reservoirs of infection in the bovine, A. marginale infect erythrocytes and endothelial cells [8, 9]. The genus Anaplasma includes three species that can infect ruminants, A. marginale and A. centrale in cattle as detailed in table 1. A. marginale and A. centrale infect cattle, but differ in morphology, virulence and geographical distribution [7].
Source: Rymaszewska, and Grenda (2008)
Table 1: The characteristic of pathogens of genus Anaplasma causative agent of Bovine anaplasmosis
Aetiological agent |
Disease |
Vector |
Infected organism or host |
|
Before 2001 |
After 2001 |
|||
Anaplasma marginale |
Anaplasma marginale |
Bovine anaplasmosis |
Ixodes spps; dermancentor spps |
Ruminnat farming |
Anaplasma central |
Anaplasma central |
Bovine anaplasmosis |
Haemaphysalis spps, Ixodes spps |
Ruminants farming |
E.equi |
Anaplasma phagocytophilum |
Human and animal granulocytic anaplsmosis |
Ixodes spps; Dermacentor spps |
Small ruminants forming an wild,horses,dogs, |
Epidemiology
Geographic distribution
Bovine anaplasmosis is the major cause of morbidity and
mortality in the tropics and subtropics, particularly in exotic
and crossbred cattle. The geographic distribution of the disease
is dependent on the density and distribution of tick vectors and
reservoir host. The distribution of Anaplasmosis may continue to
change due to the trend of global warming, which may influence
the movement of the tick hosts [10].
Host occurrence
Among domestic livestock, A. marginal infects ruminants, but
is principally pathogenic only in cattle. The pathogen has a wide
host range including various wild animals. The epidemiological
contribution of domestic and wild animals toward prevalence
of disease is insufficient due lack of further research conduction
[11]. Severity of Anaplasmosis is related to various factors such
as virulence of the strain, age-related host susceptibility and
breed resistance. Calves less than 1 year old show only mild signs
or remains asymptomatic and Cattle more than 2 years of age are
most likely to have severe, acute and potentially fatal disease. Bos
Taurus cattle appear to be more likely to develop severe, acute
disease than Bos indicus cattle [12, 13].
Calves are much more resistant to disease (although not infection) than older cattle. This resistance is not due to colostral antibody from immune dams, but they regenerate red blood cells faster than adults. In endemic areas where cattle first become infected with A marginale early in life, losses due to anaplasmosis are minimal [14, 15]. Animals that recover from the disease may remain carriers for life and becoming reservoirs for transmission to other susceptible hosts. However, these chronically infected cattle may relapse to anaplasmosis when immunosuppressed (by corticosteroids), when infected with other pathogens, or after splenectomy. Carriers serve as a reservoir for further transmission. Serious losses occur when mature cattle with no previous exposure are moved into endemic areas or under endemically unstable situations when transmission rates are insufficient to ensure that all cattle are infected before reaching the more susceptible adult age [15].
Calves are much more resistant to disease (although not infection) than older cattle. This resistance is not due to colostral antibody from immune dams, but they regenerate red blood cells faster than adults. In endemic areas where cattle first become infected with A marginale early in life, losses due to anaplasmosis are minimal [14, 15]. Animals that recover from the disease may remain carriers for life and becoming reservoirs for transmission to other susceptible hosts. However, these chronically infected cattle may relapse to anaplasmosis when immunosuppressed (by corticosteroids), when infected with other pathogens, or after splenectomy. Carriers serve as a reservoir for further transmission. Serious losses occur when mature cattle with no previous exposure are moved into endemic areas or under endemically unstable situations when transmission rates are insufficient to ensure that all cattle are infected before reaching the more susceptible adult age [15].
Source of infections
Anaplasmosis is a vector-borne and also known as yellowbag
or yellow fever. This parasite infects the red blood cells and
causes severe anemia. It is most usually spread by ticks. The tick
is considered the primary vector for this disease, and it acquires
A. marginale by feeding on infected erythrocytes in cattle. The
tick then acts as a reservoir by replicating in several tissues, but
primarily in the midgut and salivary glands, with the latter of
greater importance for transmission back to cattle [16].
Method of Transmissions
A. marginale transmission typically occurs via two different
routes, the biological pathway through mostly ticks and
mechanical pathway [9, 11, 17]. Mechanical transmission
can occur through reusing of needles, dehorners, ear taggers,
castrating knives or other surgical instruments, and tattoo
instruments [1, 18]. In mechanical transmission, the organism
is transferred 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. Bloodcontaminated
equipment, such as used vaccination needles, can
also transfer A. marginale from an infected animal to uninfected
animals [19, 20].
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. 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 [20, 21]. Transplacental transmission occurs when the organism is transmitted from dam to fetus. This transmission appears to occur during the second or third trimester of pregnancy [22, 23].
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. 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 [20, 21]. Transplacental transmission occurs when the organism is transmitted from dam to fetus. This transmission appears to occur during the second or third trimester of pregnancy [22, 23].
Risk Factors
Bos taurus breeds are not commonly affected by Anaplasmosis
because of their reistance to heavy tick infestation, however they
are more likely to develop acute Anaplasmosis than cross Zebu
breed [1]. Anaplasmosis infection is higher in female than male
animals due to hormonal disturbances, milk production, draught
power and breeding system which pose it to weakened immune
system (Setotaw et al., 2014). In temperate regions seasonal
occurrence of the disease is associated with the occurrence
of the vectors and the prevalence of Anaplasmosis is found
higher in hot and humid weather associated with the abundance
of ticks [24].
Lifecycle and Pathogenesis
Ticks acquire the rickettsia while feeding on carrier hosts
(figure1), and within the erythrocyte, the rickettsia replicates
by binary fission to form 8–12 initial bodies and exit from the
erythrocyte does not involve destruction of the host’s cell. Once
out of the host cell, the initial bodies invade new erythrocytes
in endless cycles. In the tick, the rickettsia infects midgut cells,
where there is a first cycle of replication and from here dense
Figure 1:Life cycle of A. marginale (Source: Kocan et al. 2003)
forms move to other tissues. After several rounds of replication,
dense forms travel to the salivary glands where the rickettsia is
transmitted to a new mammalian host (Rodríguez et al 2009;
Futs e et al 2003). When cattle are exposed to A. marginale, an
incubation period of 7-60 days follows depending on the infective
dose. A. marginale is a strictly intra-erythrocyte microbe and
the infected erythrocyte contains a membrane-bound inclusion,
called initial body, that each contains four to eight rickettsias [1].
Figure 1:Life cycle of A. marginale (Source: Kocan et al. 2003)
In the erythrocytes, A.marginale undergoes a cycle of
replication, and subsequently they are phagocytized by the
reticuloendothelial system to further reinvade other erythrocytes.
During this acute phase as many as 109 erythrocytes per milliliter
of blood, corresponding 70 % of all erythrocytes, can be infected
[26, 27]. The phagocytosis of erythrocytes results in mild to
severe haemolyticanaemia and icterus without hemoglobinemia
or hemoglobinuria [9, 11].
Clinical Signs
Bovine anaplasmosis have different forms of clinical phases
including; Peracute, acute, chronic and mild. Acute anaplasmosis
is most common and usually occurs in summer and fall during
peak vector season. Fever (in some), anorexia, rapid loss of body
condition, severe decrease in milk production, pale and icteric
mucous membranes, increased heart and respiratory rates,
muscle weakness and depression are common. Aggression from
cerebral anoxia is common, especially in beef cattle. Abortions
can occur in females and temporary infertility can occur in males.
Since the hemolysis is extravascular, hemoglobinuria does not
occur [13]. Peracute anaplasmosis is most common in highly
susceptible purebred animals and dairy cows and also the death
occurs within hours of the onset of clinical signs due to icterus
[28]. Chronic disease occurs in severely affected animals that
do not die. It may take weeks to months for animals to recover,
during which time production losses can be significant (decreased
calf weaning weights, infertility). Clinical signs of anaplamosis
include fever, jaundice, anorexia and lethargy, which can lead to a
dramatic decrease in milk production [28, 29].
If cattle are carefully observed, weakness may be the first clinical sign that is noticed with Anaplasmosis. Infected cattle will fall behind the rest of the herd and will not eat or drink. Cows with light skin will initially look pale around the eyes and muzzle, but later this can change to a yellowish color (jaundice). This jaun dice is due to the destruction of the blood cells and their contents being released into the blood stream. Weight loss is rapid. Cattle can become extremely aggressive if they are oxygen deprived due to the severe anemia. Oxygen deprivation can also result in abortions in pregnant cows. Constipation, high fever, and labored breathing can also be seen. The most critical period is the first 4 to 9 days after clinical signs appear [13, 30].
Signs are refusal to eat, constipation, very hard dung, panting, sudden drop in milk production, Fever (41°C), swollen abdomen, loss of balance, raised hair, animal is depressed and docile; it seeks shade. The urine may be brown but, in contrast to babesiosis, hemoglobinuria does not occur. Surviving cattle convalesce over several weeks, during which hematologic parameters gradually return to normal [14].
If cattle are carefully observed, weakness may be the first clinical sign that is noticed with Anaplasmosis. Infected cattle will fall behind the rest of the herd and will not eat or drink. Cows with light skin will initially look pale around the eyes and muzzle, but later this can change to a yellowish color (jaundice). This jaun dice is due to the destruction of the blood cells and their contents being released into the blood stream. Weight loss is rapid. Cattle can become extremely aggressive if they are oxygen deprived due to the severe anemia. Oxygen deprivation can also result in abortions in pregnant cows. Constipation, high fever, and labored breathing can also be seen. The most critical period is the first 4 to 9 days after clinical signs appear [13, 30].
Signs are refusal to eat, constipation, very hard dung, panting, sudden drop in milk production, Fever (41°C), swollen abdomen, loss of balance, raised hair, animal is depressed and docile; it seeks shade. The urine may be brown but, in contrast to babesiosis, hemoglobinuria does not occur. Surviving cattle convalesce over several weeks, during which hematologic parameters gradually return to normal [14].
Necropsy
Lesions are typical of those found in animals with anemia
due to erythrophagocytosis. The carcasses of cattle that die from
anaplasmosis are generally markedly anemic, jaundiced; watery
blood and enlarged spleen. The liver may be mottled and yelloworange.
The gallbladder is often distended and contains thick
brown or green bile (Gall sickness). Hepatic and mediastinal
lymph nodes appear brown. There are serious effusions in body
cavities, pulmonary edema, petechial hemorrhages in the epiand
endocardium. Widespread phagocytosis of erythrocytes is
evident on microscopic examination of the reticuloendothelial
organs. A significant proportion of erythrocytes are usually found
to be parasitized after death due to acute infection [14].
Diagnosis
The diagnosis of Bovine anaplasmosis is depending on clinical
history of animals and laboratory examination. The clinical
history of patient has a history of tick bites or exposure of animals
to ticks in environment, and then, after an incubation period of
2-7 days the bovine animal develops an illness of sudden onset of
muscle pains, headache, fever and a rapidly evolving severe illness
with the development of a haemorrhage state with bleeding from
the mucous membranes and petechial in the skin, associated with
thrombocytopenia and leucopenia [11].
The most commonly used laboratory method for the identification of the organism in most developing countries is microscopic examination of Giemsa stained thin blood film. However, this method cannot detect low level of rickettsiaemia as seen in infected host. In addition, in persistently infected cattle, it is difficult to differentiate the pathogen from similar structures such as Howell-Jolly bodies, Heinz bodies and staining artifacts, thus rending this method unreliable [31].
Microscopic examination of Giemsa-stained thin and thick blood films is critical to distinguish anaplasmosis from babesiosis and other conditions that result in anemia and jaundice, such as leptospirosis and theileriosis [32]. Blood sample is taken to anticoagulant vacutainer tube from jugular vein of bovine animals for hematologic testing. Then, the blood is examined by Giemsa staining of thin blood films and thus Anaplasma spss appears as dense, homogeneously staining blue-purple inclusions 0.3–1 μm in diameter. Anaplasma marginale inclusion is usually located toward the margin of the infected erythrocyte, whereas A. centrale inclusion bodies are located more centrally [32]. Even if Anaplasma infections usually are persistent, it may be undetectable by microscopy after the acute phase. Thus, for detection of pre-symptomatic and persistently infected animals serological method seems more reliable. The only way to diagnose of the presence of the causative organism is to demonstrate it, either by presence in blood smears or by molecular diagnostics. The golden standard is to inoculate blood from a suspected animal into a spleenectomized calf. This procedure is followed by multiple blood-smear examination every 2nd–3rd week for the presence of the pathogen. This method is very expensive and raises welfare issues (OIE, 2012)
Chronically infected carriers may be identified with a fair degree of accuracy by serologic testing using the msp5 ELISA, complement fixation, or card agglutination tests. Nucleic acid– based detection methods are most useful, because species and strain differentiation tests may not detect carrier levels. At necropsy, thin blood films of liver, kidney, spleen, lungs, and peripheral blood should be prepared for microscopic examination [32].
The most commonly used laboratory method for the identification of the organism in most developing countries is microscopic examination of Giemsa stained thin blood film. However, this method cannot detect low level of rickettsiaemia as seen in infected host. In addition, in persistently infected cattle, it is difficult to differentiate the pathogen from similar structures such as Howell-Jolly bodies, Heinz bodies and staining artifacts, thus rending this method unreliable [31].
Microscopic examination of Giemsa-stained thin and thick blood films is critical to distinguish anaplasmosis from babesiosis and other conditions that result in anemia and jaundice, such as leptospirosis and theileriosis [32]. Blood sample is taken to anticoagulant vacutainer tube from jugular vein of bovine animals for hematologic testing. Then, the blood is examined by Giemsa staining of thin blood films and thus Anaplasma spss appears as dense, homogeneously staining blue-purple inclusions 0.3–1 μm in diameter. Anaplasma marginale inclusion is usually located toward the margin of the infected erythrocyte, whereas A. centrale inclusion bodies are located more centrally [32]. Even if Anaplasma infections usually are persistent, it may be undetectable by microscopy after the acute phase. Thus, for detection of pre-symptomatic and persistently infected animals serological method seems more reliable. The only way to diagnose of the presence of the causative organism is to demonstrate it, either by presence in blood smears or by molecular diagnostics. The golden standard is to inoculate blood from a suspected animal into a spleenectomized calf. This procedure is followed by multiple blood-smear examination every 2nd–3rd week for the presence of the pathogen. This method is very expensive and raises welfare issues (OIE, 2012)
Chronically infected carriers may be identified with a fair degree of accuracy by serologic testing using the msp5 ELISA, complement fixation, or card agglutination tests. Nucleic acid– based detection methods are most useful, because species and strain differentiation tests may not detect carrier levels. At necropsy, thin blood films of liver, kidney, spleen, lungs, and peripheral blood should be prepared for microscopic examination [32].
Treatment
In the carrier phase, animals that have recovered from
Anaplasmosis become persistent carriers of the organism.
The benefit of the carrier state is that the animal has life-long
immunity and rarely shows clinical disease again, but it does
serve as a reservoir of the organism within the herd. Because
of the latter, elimination of carrier animals through either
culling or chemo sterilization has been attempted [26]. Chemo
sterilization involves the use of antimicrobials. Until recently,
it was believed chemo sterilization could be achieved with
repeated administration of injectable oxytetracycline, but new
studies show this method to be ineffective [33, 34]. The longterm
feeding of chlortetracycline has been proposed as an option,
but this strategy is not 100 percent effective and requires feeding
chlortetracycline in an unapproved manner, which is unlawful
[20, 40].
Prevention and Control
Control measures currently available for tick-borne diseases
include the use of acaricides for reduction or tick populations,
specific chemotherapy, chemoprophylaxis, controlled exposure
and vaccination. These measures limit losses caused by ticks
and the diseases they transmit [27]. Control measures for
bovine anaplasmosis vary with geographical location and
include maintenance of Anaplasma‐free herds, vector control,
administration of antibiotics and vaccination [11]. For effective
control of anaplasmosis, early diagnosis and treatment is
essential, while continuous screening should be practiced to
control the disease. The strategies commonly employed to
control Anaplasmosis are minimizing transmission, use of feed
antimicrobials, and vaccination [13, 32].
To minimize transmission, control of arthropod vectors such as ticks and horse flies is recommended when feasible. Several sprays pour on and fly tag products are approved for tick control, but control of biting flies can be more difficult and may require the use of alternative methods. Finally, eliminating carrier animals from the herd and testing new animals may be warranted in some cases. The benefits versus risk of an Anaplasmosis-free herd in a region where the disease is common, along with the costs associated with testing and eliminating carrier animals would need to be considered [35]. Control measures implemented vary with geographic location, and depend on availability, cost, and the feasibility of application. Vaccination has been an effective means of preventing outbreaks of anaplasmosis, but these vaccines, live and inactivated, are dependent on bovine blood as the source of infection or antigen [35, 36].
For an effective vaccination program, the herd owner should follow these recommendations: the initial vaccination (1st year) consists of 2 doses given 4 weeks apart, scheduled so that the second dose is given at least 2 weeks or more before the vector season begins. The following year, a booster should be administered two weeks or more before the next vector season. After the first booster, additional boosters should be administered at least every other year to provide adequate protection. Identification of Anaplasmosis carriers, by testing, could constitute an appreciable savings in heavily infected herds because vaccination of the carriers is unnecessary. A positive test reaction resulting from vaccination cannot be differentiated from the positive reaction caused by the natural infection [36].
To minimize transmission, control of arthropod vectors such as ticks and horse flies is recommended when feasible. Several sprays pour on and fly tag products are approved for tick control, but control of biting flies can be more difficult and may require the use of alternative methods. Finally, eliminating carrier animals from the herd and testing new animals may be warranted in some cases. The benefits versus risk of an Anaplasmosis-free herd in a region where the disease is common, along with the costs associated with testing and eliminating carrier animals would need to be considered [35]. Control measures implemented vary with geographic location, and depend on availability, cost, and the feasibility of application. Vaccination has been an effective means of preventing outbreaks of anaplasmosis, but these vaccines, live and inactivated, are dependent on bovine blood as the source of infection or antigen [35, 36].
For an effective vaccination program, the herd owner should follow these recommendations: the initial vaccination (1st year) consists of 2 doses given 4 weeks apart, scheduled so that the second dose is given at least 2 weeks or more before the vector season begins. The following year, a booster should be administered two weeks or more before the next vector season. After the first booster, additional boosters should be administered at least every other year to provide adequate protection. Identification of Anaplasmosis carriers, by testing, could constitute an appreciable savings in heavily infected herds because vaccination of the carriers is unnecessary. A positive test reaction resulting from vaccination cannot be differentiated from the positive reaction caused by the natural infection [36].
Economic Impacts
Bovine anaplasmosis cause great economic losses in
developing countries where it is highly endemic. Economic losses
are due to reduced production, decreased weight gain, treatment
costs, bull infertility, death loss and abortion [26]. Costs are
incurred from mortality, loss of milk and meat production, control
measures (acaricides treatments, vaccines, and chemotherapy),
and its impact on international cattle trade (Bock et al., 2004).
Anaplasmosis has also the grave socioeconomic consequences
often leading to trade restrictions both locally and internationally
[38].
Bovine Anaplasmosis Status in Ethiopia
The Bovine analasmosis has been reported in Ethiopia,
however further studies were not conducted as well. As reported
that the prevalence of Bovine anaplasmosis was 6.8% in Jimma
town and its surrounding [39]. Other studies have not been
conducted to expose Bovine anaplasosis in Ethiopia.
Conculsion and Recommendations
Bovine anaplasmosis is one of the overwhelming infectious
diseases in cattle industry which cause diminishes socioeconomic
of developing country. It is caused by intracellular rickettisia
microorganisms. Bovine anaplasmosis have the behavior of self
limit in blood of animals this lead persistence carrier of cattle,
thus it is so difficult to treat this disease with antibiotics. It is
better to prevent and control future outbreaks and the spread
of Anaplasmosis to naive herds than treatment. Problems
of acaridae resistance, chemical residues in food and the
environment and the unsuitability of tick resistant cattle for all
production systems make the current situation unsatisfactory
and require the development of absolute control through effective
vaccine. Generally, Anaplasmosis is one of the rickettisia diseases
of bovine which decrease development of country by reducing
number of animal production and productivity. Therefore, in
line with the above conclusions; the following recommendations
were forwarded:
→ The government should monitor the use of potentially drugs and conserve foreign exchange.
→ Intensive acaridae application to control ticks has a number of limitations, therefore, immunization together with strategic tick control is recommended for exotic and crossbred cattle.
→ The researcher need to study Bovine anaplsmosis and its control in Ethiopia
→ The veterinarian ought to aware the community how to prevent bovine anaplasmosis.
→ The government should monitor the use of potentially drugs and conserve foreign exchange.
→ Intensive acaridae application to control ticks has a number of limitations, therefore, immunization together with strategic tick control is recommended for exotic and crossbred cattle.
→ The researcher need to study Bovine anaplsmosis and its control in Ethiopia
→ The veterinarian ought to aware the community how to prevent bovine anaplasmosis.
ReferencesTop
- Kocan A.A (2003). Ticks and Tick-Transmitted Diseases in Oklahoma. Department of Veterinary Parasitology, Microbiology and Public Health. College of Veterinary Medicine, Oklahoma State University, Stillwater, Oklahoma 7:4078.
- Bitrus AA, Jesse FFA, Abba Y, Pei JLX, Peter ID and Hambali IU. Seroprevalence of anaplasmosis in dairy cattle from peninsular Malaysia. Adv. Anim. Vet. Sci, 2018; 6: 70-74.
- Rymaszewska A, Grenda S. Bacteria of the genus Anaplasma–characteristics of Anaplasma and their vectors a review. Vet Med, 2008; 53: 573-584.
- Setotaw T, Regassa F, Zeru F, Kahsay G, Epidemiological significance of major hemoparasites of ruminants in and around Debre-Zeit, Central Ethiopia. Journal of Parasitology and Vector Biology, 2014; 6(2): 16-22.
- Woldehiwet Z, Braun U, Regula G, Staerk KDC, Lutz H. Serologiccross-reactivity between Anaplasma marginale and Anaplasma phagocytophilum.Clinical and diagnostic laboratory immunology, 2005; 12:1177–83.
- Abba Y, Jesse FAJ, Sadiq M, Ibrahim HH, Chung ELT and Bitrus AA. Clinical management and gross pathological findings of a severe anaplamosis in a dairy cow. J. Adv. Vet. Anim. Res. 2016; 3: 195-199. Doi: 10.5455/javar.2016.c150
- DumlerJS, BarbetAF, BekkerCP, DaschGA, PalmerGH and RaySC. Reorganization of genera in the family’s Rickettsiaceae and Anaplasmataceae in the order Rickettsiales: Unification of some species of Ehrlichia with Anaplasma, Cowdria with Ehrlichia and Ehrlichia with Neorickettsia, descriptions of six new species combinations and designation of Ehrlichia equi and “HGE agent” as subjective synonyms of Ehrlichia phagocytophila. International Journal of Systematic and Evolutionary Microbiology; 2001; 51:2145-2165. Doi: 10.1099/00207713-51-6-2145
- Carreño AD, Alleman AR, Barbet AF, Palmer GH, Noh SM, Johnson CM. In vivo endothelial cell infection by Anaplasma marginale. Veterinary Pathology,2007; 44:116-118
- Kocan KM, J de la Fuente, Blouin EF, Coetzee JF, Ewing SA. The natural history of Anaplasma marginale,”Veterinary Parasitology,2010; 167:95–107
- Singh H, Haque M, Singh NK, Rath SS. Molecular detection of Anaplasmamarginaleinfection in carrier cattle. Ticks tick-borne Dis. 2012 3: 55-58. Doi: 10.1016/j.ttbdis.2011.10.002
- Aubry P, Geale DW. A review of bovine anaplasmosis. Transboundary and emerging diseases, 2011; 58(1):1-30. Doi: 10.1111/j.1865-1682.2010.01173.x
- http://veterinarynews.dvm360.com/preventing-bovine-anaplasmosis
- Smith BP (2015). Large animal internal medicine, 5th Edition. St.Louis, MO: Mosby. 1054-1056
- https://www.msdvetmanual.com/circulatory-system/blood-parasites/anaplasmosis
- Coetzee JF, Harvery N, Hausmann D. Anaplasmosis: Update on diagnostic, control, and treatment approaches for improved disease management. In Proceedings of a Veterinary Roundtable, Alpharma Animal Health,2010;1–19
- Rodr´ıguez SD, Garc´ıa Ortiz M, Jim´enez Ocampo R, Vega y Murgu´ıa C. “Molecular epidemiology of bovine anaplasmosis with a particular focus in Mexico,” Infection,Genetics and Evolution,2009;9:1092–1101. Doi: 10.1016/j.meegid.2009.09.007
- Whittier WD, N Currin, JF. Currin. Anaplasmosis in beef cattle, irginia Cooperative Extension publication. 2005
- http:// beef2live.com/story-cattle-farmers-should-watch-anaplasmosis-0-133684
- Hawkins JA, JN Love, RJ Hidalgo. Mechanical transmission of anaplasmosis by tabanids (Diptera: Tabanidae). American Journal of Veterinary Research, 1982; 43(4): 732–734.
- Reinbold JB, JF Coetzee, LC Hollis, JS Nickell, CM Riegel, JA Christopher, RR Ganta. Comparison of iatrogenic transmission of Anaplasma marginale in Holstein steers via needle and needle-free injection techniques. American Journal of Veterinary Research, 2010, 71(10): 1178–1188
- Scoles GA, JA Miller, LD Foil. Comparison of the efficiency of biological transmission of Anaplasma marginale (Rickettsiales: Anaplasmataceae) by Dermacentor andersoni Stiles (Acari: Ixodidae) with mechanical transmission by the horse fly, Tabanus fuscicostatus Hine (Diptera: Muscidae). Journal of Medical Entomology, 2008; 45(1): 109–114
- Salabarria FF, R Pino. Vertical transmission of Anaplasma marginale in cows affected in late pregnancy. Revista Cubana de Ciencias Veterinarias, 1988; 19: 179–182
- Grau HE, NA Cunha Filho, FG Pappen, NA Farias. Transplacental transmission of Anaplasma marginale in beef cattle chronically infected in southern Brazil. Revista Brasileira de Parasitologia Veterinária, 2013; 22(2): 189–193. Doi: 10.1590/S1984-29612013000200038
- Sajid M, R Siddique S, Khan Z, Iqbal, M Khan. Prevalence and risk factors of Anaplasmosis in cattle and buffalo populations of district Khanewal, Punjab, Pakistan. Global Veterinaria, 2014; 12: 146-153.
- Futse JE, Ueti MW, Knowles DP and Palmer GH. Transmission of Anaplasma marginale by Boophilus Microplus: Retention of vector competence in the absence of vector-pathogen interaction. Journal of Clinical Microbiology,2003;41:3829-3834
- Kocan KM, J De la Fuente, AA Guglielmone, RD Mel´endez. Antigens and alternatives for control of Anaplasma marginale infection in cattle, Clinical Microbiology Reviews,2003;16:698–712,
- Kocan KM, de la Fuente J, and Blouin EF. Advances toward understanding the molecular biology of the Anaplasma-tick interface. Frontiers in Bioscience,2008;13:7032-7045
- Kocan KM, J de la Fuente, DL Step, EF Blouin, JF Coetzee, KM Simpson, SG Genova, MJ Boileau. Current challenges of the management and epidemiology of bovine anaplasmosis. The Bovine Practitioner, 2010; 44 (2): 93:102.
- http://www.thecattlesite.com/diseaseinfo/255/anaplasmosis/
- Richey, E.J (1992). Bovine Anaplasmosis, American Association of Bovine Practitioners, Proceedings No. 24
- Noaman V, Shayan P. Comparison of microscopy and PCR-RFLP for detection of Anaplasmamarginale in carrier cattle. Iran. J. Microbiol. 2010; 2: 89–94.
- Coetzee JF. New developments in the diagnosis and treatment of bovine anaplasmosis. In Proceedings Academy of Veterinary Consultants Summer Meeting, 2013; 27–34.
- Coetzee JF, MD Apley, KM Kocan, FR, J Van Donkersgoed. Comparison of three oxytetracycline regimens for the treatment of persistent Anaplasma marginale infections in beef cattle. Veterinary Parasitology, 2005; 127(1): 61–73.
- Wallace JO, LC Hollis, CD Reinhardt, JF Coetzee, TT Marston. Failure to eliminate the Anaplasma marginale carrier state in beef cows following multiple treatments with long-acting injectable oxytetracycline. The Bovine Practitioner, 2007; 41: 84–87.
- Kocan K M, Blouin EF, Barbet AF. Anaplasmosis control: past, present, and future. Annals of the New York Academy of Sciences, 2000 916(1), 501-509.
- Radostits OM, Gay CC, Hinchcliff KW, Constable PD. Veterinary Medicine. A Textbook of the Diseases of Cattle, Horses, Sheep, Pigs and Goats. 10th ed. London: WB Saunders, 2007; 1455–1459.
- Bock RE, de Vos AJ, Kingston TG, McLellan DJ. Effect of breed of cattle onInnate resistance to infection with Babesiabovis, B bigemina and Anaplasmamarginale.Australian veterinary journal, 1997; 75:337–40.
- Reinbold JB, JF Coetzee, KR Sirigireddy, RR Ganta. Detection of Anaplasma marginale and A. phagocytophilum in bovine peripheral blood samples by duplex real-time reverse transcriptase PCR assay, Journal of Clinical Microbiology,2010;48:2424–2432,Doi: 10.1128/JCM.02405-09
- Abdela N, Ibrahim N, Begna F. Prevalence, risk factors and vectors identification of bovine anaplasmosis and babesiosis in and around Jimma town, Southwestern Ethiopia. Acta tropica, 2018; 177: 9-18. Doi: 10.1016/j.actatropica.2017.09.010



