Anaplasmosis, pinkeye and cowdriosis in cattle treatment and prevention

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Anaplasmosis, pinkeye and cowdriosis in cattle treatment and prevention Anaplasmosis is a disease caused by the bacterium Anaplasma phagocytophilum. These bacteria are spre Prevention
There is no vaccine to prevent anaplasmosis.

Prevent illness by preventing tick bites, preventing ticks on your pets, and preventing ticks in your yard. Ticks live in grassy, brushy, or wooded areas, or even on animals, so spending time outside camping, gardening, or hunting will bring you in close contact with ticks. Protect yourself, your family, and your pets. Here’s how:
Ticks can be active year-round, but ticks are most active during

warmer months (April-September). Series of three images showing a woman treating clothing with permethrin
Tick exposure can occur year-round, but ticks are most active during warmer months (April-September). Know which ticks are most common in your area. Before You Go Outdoors
Know where to expect ticks. Ticks live in grassy, brushy, or wooded areas, or even on animals. Spending time outside walking your dog, camping, gardening, or hunting could bring you in close contact with ticks. Many people get ticks in their own yard or neighborhood. Treat clothing and gear with products containing 0.5% permethrin. Permethrin can be used to treat boots, clothing and camping gear and remain protective through several washings. Alternatively, you can buy permethrin-treated clothing and gear. Use Environmental Protection Agency (EPA)-registered insect repellentsexternal icon containing DEET, picaridin, IR3535, Oil of Lemon Eucalyptus (OLE), para-menthane-diol (PMD), or 2-undecanone. EPA’s helpful search toolexternal icon can help you find the product that best suits your needs. Always follow product instructions. Do not use products containing OLE or PMD on children under 3 years old. Avoid Contact with Ticks
Avoid wooded and brushy areas with high grass and leaf litter. Walk in the center of trails. After You Come Indoors
Check your clothing for ticks. Ticks may be carried into the house on clothing. Any ticks that are found should be removed. Tumble dry clothes in a dryer on high heat for 10 minutes to kill ticks on dry clothing after you come indoors. If the clothes are damp, additional time may be needed. If the clothes require washing first, hot water is recommended. Cold and medium temperature water will not kill ticks. Examine gear and pets. Ticks can ride into the home on clothing and pets, then attach to a person later, so carefully examine pets, coats, and daypacks. Shower soon after being outdoors. Showering within two hours of coming indoors has been shown to reduce your risk of getting Lyme disease and may be effective in reducing the risk of other tickborne diseases. Showering may help wash off unattached ticks and it is a good opportunity to do a tick check. Check your body for ticks after being outdoors. Conduct a full body check upon return from potentially tick-infested areas, including your own backyard. Use a hand-held or full-length mirror to view all parts of your body. Check these parts of your body and your child’s body for ticks:

Under the arms
In and around the ears
Inside belly button
Back of the knees
In and around the hair
Between the legs
Around the waist

Pinkeye VaccinesFive pharmaceutical companies currently produce commercial pinkeye vaccines for M. bovis; three have con...
15/09/2022

Pinkeye Vaccines
Five pharmaceutical companies currently produce commercial pinkeye vaccines for M. bovis; three have conditionally licensed commercial vaccines for M. bovoculi. Studies have shown that vaccination with M. bovis does not protect against M. bovoculi, and vaccination with M. bovoculi does not protect against M. bovis. Herds vaccinated with M. bovoculi vaccine have broken with IBK due to M. bovis. A prevention program with vaccines that target both M. bovis and M. bovoculi involves vaccinating with each product separately on the same day.
Since different strains of Moraxella are found in different vaccines, some vaccines may be more effective in a particular herd than another. Follow label directions! Some products recommend vaccine not be given to calves earlier than 2, 3 or 5 months of age. Some require a booster the first year the vaccine is given, others do not. Dosage itself varies between products. Some are available in combo with blackleg.
All IBK vaccines must be given 3-6 weeks ahead of the traditional summer IBK season as it takes time to develop protective immunity. Work with your veterinarian to determine how often to booster vaccines when dealing with winter pinkeye.
Current whole cell Moraxella bacterins have potential endotoxin concerns, and produce systemic IgG, which may not provide enough local eye immunity. Only piliated strains of Moraxella bovis have been proven to produce IBK in cattle and these appendages have antigenic and immunogenic properties. Moraxella bovis also produces a toxin and a hemolysin. Vaccines created from these antigenic components might create better immunity with fewer side effects (Prieto et al).
On-farm IBK pathogens can vary from year to year and therefore, treatments and vaccines used prior may fail. Find out what you are dealing with when your herd’s incidence of IBK is too high or response to treatment is poor. Culturing and antibiotic sensitivity testing takes the guess work out of treatment and helps to make sure treatments makes sense. Knowing which organism is involved allows evaluation of vaccine choices.
Those Pesky Face Flies!
Face flies have economic and health impacts to cattle. Twelve to fourteen flies per face decreases grazing time one hour per day. 20 – 200 per face is considered a heavy population and causes a lot of annoyance as cows cluster under shade. Mechanical transmission of diseases and active fly feeding causes further damage to eye tissue. Normal eye and nasal secretions attract face flies that feed on secretions. Face flies are not blood feeders like horn flies.
When talking about flies spreading IBK, our focus is on Musca autumnalis. The Musca fly family includes houseflies and stable flies; but neither swarm on faces like face flies do. Darker than a house fly, the adult face fly is 3/8 inch long. It’s a summer fly, feeding on secretions near the muzzle and eyes during bright sunny days. Face flies are strong fliers that can travel several miles. Face flies do not enter darkened barns or stables during the summer months. In the fall, however, they enter buildings and overwinter indoors in a state of hibernation.
Face flies are more active during hotter days, awake and feeding in bright warm sunlight, resting and not feeding during the night. Removal of decomposing feed, manure, bedding to reduce house and stable fly populations does not help for face flies as eggs are laid in freshly deposited manure (less than 15 min old). Control of face flies is achieved by regular application of insecticides to animals’ face and fly breeding sites (fresh manure).
Feeding fly larvicide may kill emerging face fly larvae in freshly deposited manure. Tetrachlorvinphos (RabonÒ) is an oral feed-through product and is labeled for face flies. To be an effective oral larvicide, it must be dosed to the weights of the animals, be consistently consumed every day, and fed throughout the entire fly season. Remember face flies are summer flies, so think about adding larvicidal products to feed beginning in July, perhaps when grass is less lush, and cattle are more likely to consume supplemental feed.
Using organophosphate or permethrin in sprays can be helpful to repel face flies. When using dust bags or oilers, make sure to hang them low enough so cattle can lift and rub them with their head. Place them where cattle are forced to use them, above the waterer, cross- over lanes, doorways or hung along the feeder wagon or bale feeder.
Insecticidal ear tags are labeled primarily for horn flies, some have face fly indications. Use as label directs. Adults usually need one in each ear; the calf usually needs one tag. Tag the calf too, as the calf will receive the flies repelled from the cow’s tags, and the calf is more susceptible to IBK.
Insecticide resistance develops, so switch tag ingredients between seasons. Check the label’s duration of activity and wait to apply tags so active ingredient is present when you need it. Face flies are a summer fly, especially active during the hotter days of July and August. Timely remove tags. Leaving them in leads to sub-therapeutic dosing which creates resistance.
Some pour-on parasiticides are labeled for horn flies. Horn flies are active blood feeders, obtaining the therapeutic ingredient from poured cattle. No pour-on products are specifically labeled for face flies. Some are labeled for stable and house flies which are in the same fly family as face flies, but passage of the ingredient into fresh manure has not been proven to be an effective face fly larvicide.
According to “Face Fly Biology and Management”, from the West Virginia Extension Service, face flies are attacked by parasitic nematodes, and immature stages of both horn flies and face flies are attacked by predaceous mites, predaceous beetles, and parasitoids.
Manure competitors such as dung beetles also limit fly populations by removing and burying cattle dung before immature flies can complete their development. Adult flies are attacked by predaceous yellow dung flies, and face flies are occasionally attacked by pathogenic fungi.
In spite of the diversity and importance of natural enemies of face flies and horn flies, methods are not known for exploiting these biological control agents in pest management programs. Parasitoid releases for house fly and stable fly control are not effective against pasture face flies.
Face and horn flies can travel for miles, so control is difficult when your neighbor’s flies are not being controlled. You may have more problems with flies when your neighbor is using repellant methods and you are not.

Pinkeye antibiotic treatmentTreatment outcomes are highly variable and the act of treatment itself can further spread th...
15/09/2022

Pinkeye antibiotic treatment
Treatment outcomes are highly variable and the act of treatment itself can further spread the disease. IBK is reported to have a 98% spontaneous recovery and eye loss occurs in 2 per 100 animals. However, when herds break with IBK , the attack rates can be 20 -100% with an average 44% herd prevalence rate. The veterinary community agrees that promptly isolating affected animals is important for controlling IBK and providing relief from sunlight aids in recovery. Stabling affected cattle, applying eye patches or suturing the eyelids are all beneficial.
Two antibiotics, Tetracycline and Tulathromycin (Draxxin) are labeled to treat pinkeye. Extra-label drug use (ELDU) of Florfenicol (Nuflor) and Ceftiofur (Excede) has been reported. Chlortetracycline pellets (CTC) have been used for calf IBK metaphylaxis and CTC is only available with a veterinary feed directive. All antibiotic use will require slaughter withdrawal times.
ELDU involving sub-conjunctival injections (often are sub- palpebral, placed under inner surface of the eye lid) using penicillin have antidotal evidence of effectiveness. Sub-conjunctival/sub-palpebral injections have caused violative residues at slaughter markets. Topical antibiotic ophthalmic ointments may be helpful (benzathine cloxacillin).
Moraxella bovoculi appears to be less sensitive to commonly used antibiotics. Often times a mixed infection of Moraxella bovis and M. bovoculi fails clinical treatment, and then when tested, a drug resistant M. bovoculi is isolated. Generally, clinical signs due to Moraxella respond to antibiotics when caught early. Cases that fail to respond are often due to Mycoplasma or IBR.
Viral IBR may cause conjunctivitis. The resulting corneal involvement is usually located along the outer edge of the eye, not in the center like that of IBK. Calves born with eye infection may be the result of periparturient infection with IBR (or BVD). IBR is not nearly as common as was once thought. Even with careful diagnostics, labs often fail to find IBR; however, if you are having tough cases, test for it. Boost herd IBR immunity when you suspect IBR; but do not vaccinate with modified live IBR vaccines (MLV) during an IBK outbreak. IBK infected cattle are immune stressed and could develop IBR from MLV use in this instance.
Recovery from IBK is not immediate. Damage to the cornea and conjunctiva may continue after all bacteria are dead. It takes time for the eye to heal. If the cornea is scarred badly enough, it may never completely clear. Blindness or reduced eyesight in the affected

Preventing traditional summer pinkeye in cattle involves eliminating the many eye irritations listed in this report. Ide...
15/09/2022

Preventing traditional summer pinkeye in cattle involves eliminating the many eye irritations listed in this report. Identifying and taking steps to resolve physical hazards in your operation, including face fly control, may be more effective than pinkeye vaccinations. Offer protection from the sunlight by providing adequately sized shade and allow cattle to graze at night when face flies are not active. Make sure mineral consumption is adequate months before the pinkeye season. Selenium, copper, and zinc are vital for maintaining eye health. Be vigilant and immediately isolate the first case of pinkeye. Seek a veterinary diagnosis. Develop a treatment and prevention plan with input from your veterinarian.

Pinkeye (infectious bovine kerato-conjunctivitis, or IBK) is a bacterial infection of the eye that causes inflammation a...
15/09/2022

Pinkeye (infectious bovine kerato-conjunctivitis, or IBK) is a bacterial infection of the eye that causes inflammation and, in severe cases, temporary or permanent blindness. Most cattle producers will be familiar with pinkeye, but may not know how best to treat it and minimise its spread within a herd.

Heartwater is an infectious, noncontagious, tickborne rickettsial disease of ruminants. The disease is seen only in area...
15/09/2022

Heartwater is an infectious, noncontagious, tickborne rickettsial disease of ruminants. The disease is seen only in areas infested by ticks of the genus Amblyomma. These include regions of Africa south of the Sahara and the islands of the Comores, Zanzibar, Madagascar, Sao Tomé, Réunion, and Mauritius. Heartwater was introduced to the Caribbean, and it and its vector (A variegatum) are endemic on the islands of Guadeloupe and Antigua. A variegatum, but not the rickettsia, has since spread to several other islands despite attempts at eradication. Possible spread to the mainland threatens the livestock industry of regions from northern South America to Central America and the southern USA. In heartwater endemic areas in southern Africa, it is estimated that mortalities due to the disease are more than double those due to bacillary hemoglobinuria (red water, see Bacillary Hemoglobinuria in Animals) and anaplasmosis ( see Anaplasmosis in Ruminants) combined. Cattle, sheep, goats, and some antelope species are susceptible to heartwater. In endemic areas, some animals and tortoises may become subclinically infected and act as reservoirs. Indigenous African cattle breeds (Bos indicus), especially those with years of natural selection, appear more resistant to clinical heartwater than B ta**us breeds.
Etiology and Transmission:
The causative organism is an obligate intracellular parasite, previously known as Cowdria ruminantium. Molecular evidence led to reclassification of several organisms in the order Rickettsiales, and it is now classified as Ehrlichia ruminantium. Under natural conditions, E ruminantium is transmitted by Amblyomma ticks. These three-host ticks become infected during either the larval or nymphal stages and transmit the infection during one of the subsequent stages (transstadial transmission). The progeny of an infected female tick are most probably not infective (ie, there is no epidemiologically significant transovarial transmission). This and the fact that ticks are indiscriminate feeders probably play a role in the low infection rate in tick populations.
E ruminantium can be propagated experimentally by serial passage, either by inoculating infective blood into, or by feeding infected nymphal or adult stages of a vector tick on, susceptible animals. The organism can also be propagated in tissue culture, most reliably in endothelial cells, but also in primary neutrophil cultures and macrophage cell lines. At room temperature, infective material loses its infectivity within a few hours, but the organism, together with suitable cryoprotectants, may be viably preserved in liquid nitrogen for years.
Immunity to heartwater appears to be chiefly, if not exclusively, cell mediated, because spleen cells from an immune donor inoculated into susceptible recipients protects, whereas serum from an immune donor fails to protect recipients when challenged. There is no, or only partial, cross-protection between different stocks (strains) of E ruminantium. Most of these stocks are infective for, but cannot be serially passaged in, mice; however, a few are pathogenic to mice infected by the IV route.
Pathogenesis:
The pathogenesis of heartwater has not been elucidated; however, the tick probably infects the host via organisms in the saliva or regurgitated gut content while feeding. Replication of the E ruminantium organisms in the tick probably occurs in the intestinal epithelium and is significantly amplified. Once in the host, the organisms may replicate first within the regional lymph nodes with subsequent dissemination via the bloodstream to invade endothelial cells of blood vessels elsewhere in the body. In domestic ruminants, there does seem to be a predilection for endothelial cells of the brain. Organisms can often be found in colonies (commonly but mistakenly referred to as morulas) within the cytoplasm of endothelial cells. Colonies can vary in size, as can the organisms that reside in them. Generally, small-sized organisms are found in larger colonies and vice versa. The smaller organisms are usually referred to as elementary bodies and represent the infective stage, the larger organisms as reticulated bodies and the proliferative stage, and those in between as intermediate bodies.
During the febrile stage, and for a short while thereafter, the blood of infected animals is infective to susceptible animals if subinoculated. Signs and lesions are associated with functional injury to the vascular endothelium, resulting in increased vascular permeability without recognizable histopathologic or even ultrastructural pathology. The concomitant fluid effusion into tissues and body cavities precipitates a fall in arterial pressure and general circulatory failure. The lesions in peracute and acute cases are hydrothorax, hydropericardium, edema and congestion of the lungs and brain, splenomegaly, petechiae and ecchymoses on mucosal and serosal surfaces, and occasionally hemorrhage into the GI tract, particularly the abomasum. The typically straw-colored effusions are high in large-molecular-weight proteins, including fibrinogen; hence, this fluid readily clots on exposure to air. The amount of effusion seen, particularly in body cavities, is not necessarily proportionate to the concentration of parasitic colonies detected in endothelial cells.
The clinical signs are dramatic in the peracute and acute forms. In peracute cases, animals may drop dead within a few hours of developing a fever, sometimes without any apparent clinical signs; others display an exaggerated respiratory distress and/or paroxysmal convulsions. In the acute form, animals often show anorexia and depression along with congested and friable mucous membranes. Respiratory distress slowly develops along with nervous signs such as a hyperaesthesia, a high-stepping stiff gait, exaggerated blinking, and chewing movements. Terminally, prostration with bouts of opisthotonus; “pedaling,” “thrashing,” or stiffening of the limbs; and convulsions are seen. Diarrhea is seen occasionally. In subacute cases, the signs are less marked and CNS involvement is inconsistent.
Diagnosis:
In clinical cases, heartwater must be differentiated from a wide range of infectious and noninfectious diseases, especially plant poisonings, that manifest with CNS signs. In acute clinical cases in endemic areas, clinical signs alone may suggest the etiology, but demonstration of colonies of organisms in the cytoplasm of capillary endothelial cells is necessary for a definitive diagnosis. Traditionally, this is done with “squash” smears of cerebral or cerebellar gray matter stained with Romanowsky-type stains. Low concentration Giemsa stain developed for 30 min gives the best color differentiation and batch-to-batch consistency. Organisms in autolyzed material lose their stainability, and diagnosis then becomes difficult.
For the “brain squash smear,” a piece of gray matter (~3 × 3 mm) is macerated between two microscope slides; the softened material is then spread like a blood smear with the material pushed rather than pulled along. A slight lifting of the spreader slide about every 5–10 mm creates several thick ridges across the slide, from which capillaries are arranged straight and parallel in the thin sections of the smear for easier examination. The endothelial cells of all the capillaries on a smear should be carefully scrutinized for presence of the dark purple colonies made up of clusters of individual organisms (granules) of E ruminantium. The size of the granules can vary between animals, or smears from the same animal, or even between colonies on the same smear, but is usually uniform within a particular colony.
Using immunoperoxidase staining methods, a definitive diagnosis can be made on any formalin-fixed tissue samples, even from autolyzed carcasses. The contrasting color makes the search for and identification of the rickettsial colonies much quicker, although the substructure of the colonies should be identified before the diagnosis is confirmed. Because of the nature of the test, false-positive reactions may arise with some closely related organisms. On brain squash smears, Chlamydia pecorum can be confused with E ruminantium, but histopathology or the immunoperoxidase technique allow differentiation. Serodiagnosis of animals previously exposed to the disease, ie, recovered from subclinical or clinical infection, still poses problems. Several tests are in use, including several indirect fluorescent antibody and ELISA tests. All serologic tests, including an ELISA that uses recombinant antigen, are plagued by cross-reactions with sera from animals infected with one of several Ehrlichia or Anaplasma organisms (false positive) and the fact that immune cattle on repeated exposure may become seronegative (false negative). DNA probes, available at research institutions, can be used together with PCR technology. A combination of a pCS20 probe and probes to 16S ribosomal RNA of several of the stocks are used routinely to examine samples from animals when permits for movement of animals from endemic to nonendemic areas are required. Real-time PCR has also come into use.
Treatment, Control, and Prevention:
Oxytetracycline at 10 mg/kg/day, IM, or doxycycline at 2 mg/kg/day will usually effect a cure if administered early in the course of heartwater infection. A higher dosage of oxytetracycline (20 mg/kg) is usually required if treatment begins late during the febrile reaction or when clinical signs are evident. In such cases, the first treatment should preferably be given slowly IV. A minimum of three daily doses should be given regardless of temperature; if fever persists, oxytetracycline treatment should continue for a fourth and fifth day. If the fever still does not abate, a potentiated sulfonamide at 15 mg/kg/day, IM, has been successful. The withdrawal times for milk and meat after treatment with doxycycline, short- or long-acting oxytetracycline, and sulfonamides must be observed based on local regulations.
Corticosteroids have been used as supportive therapy (prednisolone 1 mg/kg, IM), although there is debate as to the effectiveness and rationale for their use.
Diazepam may be required to control convulsions.
Affected animals must be kept quiet in a cool area with soft bedding and be totally undisturbed; any stimulation can preempt a convulsive episode and subsequent death.
Vaccination can help with the control of heartwater; however, it is neither easily administered nor monitored and gives variable to no cross-protection to the various E ruminantium stocks. The “infection and treatment method” for immunization is in use in southern Africa, where infected sheep blood containing fully virulent organisms of the Ball 3 stock is used for infection, followed by monitoring of re**al temperature and antibiotic therapy after a fever develops. In certain circumstances, the “controlled” infection is followed by preventive “block treatment” without temperature recording (cattle on day 14 [susceptible B ta**us breeds] or day 16 [for the more resistant B indicus breeds], sheep and Angora goats on day 11, and Boer and crossbreed goats on day 12). Young calves (

04/08/2022

Bovine anaplasmosis caused by Anaplasma marginale, an intra erythrocytic rickettsial organism transmitted by ticks, or mechanically by biting flies or blood-contaminated fomites. A. marginale invades and multiplies within mature erythrocytes and during acute anaplasmosis, rickettsemia levels may exceed 109 infected erythrocytes per ml (Kieser et al. 1990). Clinical signs include fever, anaemia, weakness, constipation, jaundice, loss of appetite, dehydration, depression, laboured breathing, abortion in pregnant animals and often death Anaemia and icterus are usually observed without haemoglobinaemia and haemoglobinuria as in place of intravascular haemolysis, extra vascular erthrophagocytosis occurs in disease. In severely affected animals urine often becomes dark brown due to the presence of bile pigments. While comparing parasitaemia with haemolytic indices, positive correlation has been observed in level of parasitaemia and mean corpuscular fragility in naturally infected crossbred cattle. Degenerative changes are observed in different organs due to hypoxic conditions created by anemia. Further changes may be due to immunological reactions produced by parasite. Very few published reports are available in literature on histopathological changes in bovine anaplasmosis. Here in this communication gross and histopathological changes observed in various organs of an animal died of clinical anaplasmosis are recorded.

04/08/2022

Anaplasmosis is a vector-borne, infectious blood disease in cattle caused by the rickesttsial parasites Anaplasma marginale and Anaplasma centrale. It is also known as yellow-bag or yellow-fever.
This parasite infects the red blood cells and causes severe anemia. It is most usually spread by ticks.
Symptoms
Anemia
Fever
Weight loss
Breathlessness
Jaundice
Uncoordinated movements
Abortion
Death
Treatment
Tetracycline is often used for clinical anaplasmosis. However it cannot be used in every country.
General supportive care is also important for anemic animals. Blood transfusions are of limited benefit.
The incubation time for the disease to develop varies from two weeks to over three months, but averages three to four weeks. Adult cattle are more susceptible to infection than calves.
The disease is generally mild in calves under a year of age, rarely fatal in cattle up to two years of age, sometimes fatal in animals up to three years of age, and often fatal in older cattle.
Once an animal recovers from infection, either naturally or with normal therapy, it will usually remain a carrier of the disease for life. Carriers show no sign of the disease but act as sources of infection for other susceptible cattle.
Prevention
Typically, cases of anaplasmosis increase in late summer and fall as insect vectors increase. Therefore, control of vectors is key to preventing 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.
Chlortetracycline also known as CTC can reduce the risk of anaplasmosis. A consistent intake of the correct amount of mineral is crucial to a anaplasmosis prevention programme. CTC is available in medicated feed, free choice salt-mineral mixes or medicated blocks.

04/08/2022

Anaplasmosis is a blood cell parasite of cattle with a worldwide distribution, but the disease is most common in tropical and subtropical areas. Anaplasma marginale is the most common organism involved in cattle, and it is transmitted through the bite of Dermacentor spp. ticks or tabanid flies, as well as through the use of blood-contaminated instruments. As a result, transmission is highest during heavy tick and fly seasons. Severe outbreaks of the disease can occur when naïve animals are moved into an endemic area or carrier animals are moved into a herd in a nonendemic area. Death losses in such herds can approach 50%. Mature cattle are the most susceptible to severe clinical signs of the disease while cattle under six months of age generally show no signs.
The Anaplasma organism invades the red blood cells of infected cattle and the spleen destroys the infected cells. As a result, infected animals become anemic, weak, lethargic, go off feed, and run a fever. The mucous membranes become pale and possibly yellow from the waste products of red blood cell destruction. A characteristic of anaplasmosis, however, is that the urine will not be red or brown as with “redwater” or leptospirosis. The packed cell volume of severely infected cattle can get extremely low making these animals prone to die with minimal exertion. Acute death and abortion have also been associated with some outbreaks of anaplasmosis.
Animals showing signs from anaplasmosis should be treated with appropriate antibiotics as soon as possible. Some animals are anemic to the point that a blood transfusion may be indicated. For animals in which standard antibiotic dosage therapy is successful in curbing clinical signs of infection, a carrier state will persist. Carrier animals will be immune to further disease from anaplasmosis and may be desirable in endemic areas. More intensive antibiotic therapy is sometimes administered in an effort to eliminate the carrier state with mixed results.
In endemic areas, control of the disease can be achieved with daily low-level antibiotic therapy in the feed during the vector season. Control of ticks and flies as well as proper cleaning and disinfection of dehorning, tagging, and injection equipment and supplies is also helpful in reducing the spread of this disease. A few vaccines are available for anaplasmosis, but consideration should be made for using these vaccines in late gestation due to the possibility of neonatal isoerythrolysis in calves born to vaccinated cows.
Preliminary diagnosis of anaplasmosis can be made based on the clinical signs of anemia and fever. The Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) offers multiple tests to detect Anaplasma marginale that vary from very simple (direct examination of blood) to complex (ELISA and PCR). Veterinary assistance in suspected cases of anaplasmosis is very helpful in diagnosis, treatment, and control of this disease.

04/08/2022

Anaplasmosis is an infectious parasitic disease of cattle caused by the rickettsial pathogen Anaplasma marginale. This organism multiplies in the bloodstream where it invades red blood cells, which are then destroyed by the animal’s immune system. Anemia results when the animal’s body destroys red blood cells faster than it can produce new ones, which can lead to death.

The disease occurs around the world and is endemic in many parts of California. It is very costly to producers in terms of cattle losses, reduced productivity, and reproductive disorders, with the impact estimated in the millions of dollars in California alone.

Anaplasmosis is the most prevalent tick-transmitted disease of U.S. cattle. Hard-shell ticks (Dermacentor spp. in the U.S.) can harbor A. marginale in their tissues and infect cattle during feeding. The disease can be spread via blood from an infected or carrier animal to a susceptible animal by biting insects, such as mosquitoes and stable flies. The organism can also be transmitted through contaminated equipment during routine management practices including vaccination, castration, ear tagging, tattooing, and dehorning. This route is often responsible for cases that occur outside of the normal vector season or in areas where tick vectors are absent. Wild ruminants such as deer (primarily black-tailed deer in CA) and elk can carry the disease and act as reservoirs of infection where grazing areas are shared by free-ranging ruminants and cattle.

All cattle are susceptible to infection, but factors such as age at time of infection, breed, strain virulence and abundance of ticks and other vectors influence the development of clinical disease. Disease severity is greater in older cattle, but cattle can be infected at any age. Once an animal is infected and survives the disease, it develops long-term immunity. However, it also becomes a carrier that can be a source for transmission to other cattle.

What are the clinical signs of anaplasmosis?
Calves that are less than 1 year old usually show no clinical signs, but can become lifelong carriers. Clinical signs increase in severity in older cattle. Cattle up to 2 years of age show moderately severe signs, and those over 2 years of age often become very ill (about half die in the absence of early treatment).

The main signs of anaplasmosis are fever, jaundice and anorexia. Additional clinical signs may include progressive anemia (pale gums and eyes), weakness, inappetence, loss of coordination, aggression, difficulty breathing, rapid pulse, decreased milk production, brown urine, and sudden death. Pregnant cows may abort, and severe anemia can cause temporary infertility in bulls.

How is anaplasmosis diagnosed?
A tentative diagnosis of anaplasmosis can be made based on geographic location, season, and clinical signs. However, additional testing is required to confirm a diagnosis. The organism is visible at the microscopic level 2-6 weeks after transmission and can be identified by testing of blood samples. Serologic testing, including msp5 ELISA, complement fixation, card agglutination tests, and PCR-based testing is often required in later stages of the disease when the bacteria may be present in lower numbers.

How is anaplasmosis treated?
Anaplasmosis in cattle is commonly treated with tetracycline antibiotics (tetracycline, chlortetracycline, oxytetracyline), which are most effective in the early stages of the disease. Clearance of carrier animals through antibiotic treatment has been reported but requires multiple doses over long periods. Blood transfusions may be required in severely affected animals.

What is the prognosis for anaplasmosis?
The prognosis for anaplasmosis is dependent upon a variety of factors. Generally, the younger the animal is at the time of infection, the better the prognosis.

How can anaplasmosis be prevented?
The potential for significant economic losses makes anaplasmosis prevention an important part of herd health management. Prevention measures vary with geographic location and prevention of the disease is complicated by many factors.

Vector control is one approach to prevention, but it is not practical in many locations.
Vaccines are available in many countries, but none are USDA approved for use in the United States. An experimental killed vaccine is distributed under permit by the state of California; it is available through the California Cattlemen’s Association. Vaccination does not prevent cattle from being infected, but it may prevent clinical disease. It is also important to note that it takes time for cattle to be protected after vaccination and management plans should be adjusted accordingly. As with naturally infected animals, vaccinated animals can become carriers and contribute to the further spread of the organism. A number of factors should be considered prior to vaccination. The location of the herd is important in terms of the known presence of tick vectors, as well as natural reservoirs of the disease such as deer. It is also important to evaluate the risk to the herd from the introduction of new cattle that may be carriers. The importation of cattle infected with Anaplasma, or in some cases vaccinated against Anaplasma, is not allowed in some states and countries.
Ensure new bulls and replacement cows and heifers are vaccinated or were raised in areas with anaplasmosis. This ensures they are protected if they are brought into areas with increased risk of exposure.
Young cattle (< 2 years of age) can be moved to pastures with high infection prevalence. This increases the chance that they will be infected and avoid severe disease as adults.
It is important to discuss decisions with your veterinarian to ensure proper management based on location and other factors.

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