ANAPLASMOSIS

Anaplasmosis, also known as yellow bag or yellow fever,

is an infectious parasitic disease of cattle caused by the
microorganism Anaplasma sp.

This parasite infects the red blood cells

It causes severe anemia, weakness, fever, lack of

appetite, depression, constipation, decreased milk
production, jaundice, abortion, and sometimes death
ETIOLOGY
The genus Anaplasma (Rickettsiales: Anaplasmataceae)
contains obligate intracellular gram-negative bacteria

A. marginale, A. centrale, A. bovis, and A. ovis, which are

pathogens of ruminants;
 A. phagocytophilum, which affects a wide range of hosts,
including humans, wildlife, and domesticated animals;
and
 A. platys, which infects dogs.
A. marginale is the type species of the genus
A. marginale - cattle, buffalo, and wild ruminants
A. ovis - sheep and goats
A. centrale (closely related to, or a subspecies of, A.
marginale) - cattle (mild anaplasmosis)
 The characteristic of pathogens of genus Anaplasma
Aetiological agent Disease Vector Infected organism Infected
or host cell
Before 2001 After 2001

Ehrlichia bovis Anaplasma Bovine Haemaphysalis sp. Ruminants farming, Emonocytes

bovis anaplasmosis Rhipicephalus sp. small mammals
Amblyomma sp.

Anaplasma Anaplasma Bovine Dermacentor sp. Small ruminants Erythrocytes

ovis ovis anaplasmosis (sheep, goats)

Anaplasma Anaplasma Bovine Ixodes sp. Ruminants farming Erythrocytes

marginale marginale anaplasmosis Dermacentor sp.

Anaplasma Anaplasma Bovine Ixodes sp. Ruminants farming Erythrocytes

centrale centrale anaplasmosis Haemaphysalis sp.
E. equi Anaplasma Human and Ixodes sp. Small ruminants Granulocyte
E. phagocyto phagocytophil animal Dermacentor sp. forming and wild,
phila um (HGA granulocytic horses, dogs,
agent) anaplasmosis humans
E. platys Anaplasma Canine cyclic Rhipicephalus Dogs Platelets
platys thrombocytope sanguineus
nia
The time of incubation of the disease depends on the
degree of infection - Last from 7 to 60 days (on average
28 days)
number of infected blood cells increases geometrically-
acute phase of the disease 70% or more erythrocytes can
be infected

Anaplasma marginale
During infection, cattle erythrocytes are phagocyted by
reticuloendothelial cells, which leads to anaemia and icterus
without haemoglobinaemia and haemoglobinuria.

A clinical picture of the disease also includes fever, weight loss,

abortions and lethargy.

Animals older than two years may even die due to the
infection.
Calves that experience the acute phase of the disease are
permanently infected with the cyclic low-level rickettsemia or
become carriers of A. marginale

Consequently in both cases they are reservoirs for the

bacteria.
Anaplasma centrale
A. centrale is a parasite in the
erythrocytes of ruminants, mainly cattle.
As opposed to A. marginale, it creates
concentrations in the central part of the
cell.
This bacterium is widely-spread
throughout the world
A. centrale is closely related to A.
marginale
A. centrale is the cause of mild anaemia
in most cases of cattle infection
 Ixodes sp

Anaplasma ovis (deer tick)

A. ovis mainly parasitizes small ruminants, i.e. sheep and

goats- live in erythrocytes- anaemia
In the case of A. ovis, bacterial inclusions are found 35–40% of
the time in the central or submarginal part of the erythrocyte
of the host, and the remaining 60–65% of the time in the
marginal part.
animals experiencing an acute phase of the disease
Depression
Debility
Marked decline in body weight
Fever
Progressive anaemia
Reduction in milk production
symptoms of the disease depend on age, on the general
condition of the animals and their breed
EPIDEMIOLOGY
Geographic Occurrence
Infection in cattle is endemic in tropical and subtropical
areas that support large populations of vectors

Prevalence rates as high as nearly 80% have been

reported in cattle and 40% in buffalo
Infection occurs more sporadically in temperate- climate
areas where vectors are seasonal
Source of infection
The source of infection is always the blood of an infected
animal.
Recovery from acute infection results in persistent infection
characterized by repetitive cycles of rickettsemia.
Persistent carriers are the reservoir for herd infection
Transmission is biologically by ticks but can also occur
transplacentally
Mechanical transmission is by biting flies or blood
contaminated fomites
 Methods of Transmission
1. Hematophagous Insect Transmission
 ticks in the family Ixodidae and flies in the family
Tabanidae
 the one-host Rhipicephalus spp. are of major
importance in tropical and subtropical regions
2. Iatrogenic Transmission
3. Transplacental Transmission

Rhipicephalus spp Dermacentor spp

There appears to be no developmental sequence of
Anaplasma spp. in flying insects.

Tabanids are efficient mechanical vectors and can

transmit infection for 2 hours after feeding.

Sucking lice (Haematopinus spp. and Linognathus spp.)

have been identified as potential vectors of anaplasmosis
in cattle, goats, and buffalo.
Iatrogenic Transmission
Anaplasmosis may also be spread mechanically by
Infected hypodermic needles
By castrating
Spaying
Tattooing
Ear-tagging
Dehorning instruments
By blood transfusions
Embryo transplants
Transplacental Transmission
Intrauterine infection also occurs in cattle but much less
frequently in field
Abortion, neonatal infection, and fatal congenital
infection have also been reported.

In ewes intrauterine infection appears to occur with ease

in experimental cases, provided the ewe is exposed
during the latter two-thirds of pregnancy.
Animal and Environmental Risk Factors
Breed
 Bos indicus, Bos taurus, and their crosses have equal
susceptibility to infection and B. indicus are not as
commonly affected
 black or red coat colour have a higher risk of infection than
those with white coats in regions where biting flies are the
insect vectors
Nutritional Status
Age at Infection
Season
Geographic Region
Nutritional Status
Clinical disease is less severe in cattle on a low plane of
nutrition.
devitalizing environmental influences, particularly
shortage of feed, and the presence of other diseases
result in the development of acute anaplasmosis
Age at Infection
major determinant of the severity of clinical disease.
Young calves are less susceptible to infection with A.
marginale than older cattle and, when infected, are less
susceptible to clinical disease.
Infection between 6 months and 3 years of age has increasing risk
of clinical illness.
Animals infected for the first time after 3 years of age are
commonly affected by a peracute and fatal form of the disease
Clinical disease occurs where
introduction of susceptible animals into endemic areas
or the expansion of the vector population into previously free
areas or into the interface between endemic and nonendemic
regions.

Case-fatality rates are usually high in outbreaks,

mortality rate varies widely depending on susceptibility and may
be 50% or more in cattle introduced to enzootic areas.
PATHOGENESIS
Anaplasma are obligate intraerythrocytic bacteria
They infect mature erythrocytes by an endocytic process
Inside the erythrocyte, bacterial reproduction occurs - produce two to
eight infective initial bodies that leave by exocytosis to infect other
erythrocytes
Depending on the strain and the susceptibility of the host, from 10% to
90% of erythrocytes may be infected in the acute stage of the disease
At least 15% have to be infected before there is clinical disease
release of acute-phase inflammatory reactants and the consequent
development of fever
Continued erythrocyte destruction occurs, resulting in the
development of mild to severe anemia and icterus without
hemoglobinemia or hemoglobinuria
If the animal recovers from the initial acute attack, the disease
goes into the subacute and chronic phase.

The degree of anemia varies widely in young cattle up to 3

years of age but is always severe in adults and in
splenectomized animals.

carriers for life and serve as reservoirs of A. marginale -provide

a source of infective blood for both mechanical and biological
transmission by ticks
Carrier animals have cycles of parasitemia
CLINICAL FINDINGS
Cattle
In most cases the disease is subacute, especially in young
animals.
Rectal temperature rises rather slowly and rarely to above 40.5°
C (105° F)
It may remain elevated or fluctuate with irregular periods of fever
and normal temperature alternating for several days to 2 weeks.
Anorexia is seldom complete
Death can occur at this stage, but many survive in an emaciated
condition, and their fertility is impaired.
The mucous membranes are jaundiced and show marked pallor,
particularly after the acute stage is passed, but there is no
hemoglobinuria.
Peracute cases, with a sudden onset of high fever,
anemia, icterus, severe dyspnea, and death, often within
24 hours, are not uncommon in adult dairy cows.
Affected animals are often hyperexcitable
Pregnant cows frequently abort
Sheep and Goats
In sheep and goats, infection is usually subclinical
But in some cases, particularly in goats, a severe anemia
may occur, and a clinical picture similar to that found in
cattle may be seen- most frequent with concurrent
disease
Goats may show hyperexcitability and may bite at
inanimate objects
The anemia not completely resolved in 3 to 4 months.
CLINICAL PATHOLOGY
Hematology
Erythrocyte destruction may be so severe that the erythrocyte
count is reduced to 1.5 million/μL.
Immature red cells are common at this stage, and their
presence is considered to be a favorable sign
The small dot-like bacteria are discernible at the periphery of
up to 10% of the red cells in subacute cases, but in peracute
cases more than 50% of the cells may be infected
A. ovis are usually situated at the periphery of erythrocytes,
but as many as 40% of infested cells may show submarginal
organisms
Reticulocytosis and basophilic stippling are usually evident
A rapid lateral flow assay (LFA) has been developed that
is a useful tool for screening cattle moving from an area
with infection to a disease-free area
Molecular methods
CFT
CELISA
NECROPSY FINDINGS

The most obvious findings are

Emaciation
Pallor of the tissues
Thin, watery blood
Mild jaundice
Liver - enlarged and orange.
Kidneys – congested and myocardial haemorrhages
Spleen - enlarged, with a soft pulp
Bone-marrow cavity – reddened by increased hematopoietic
tissue in acute cases
Postmortem identification of A. marginale can be established
by staining blood smears with Giemsa
Peripheral blood is superior to organ smears
Brain smears - unsatisfactory.
The technique is applicable to fetuses suspected of being
aborted as a result of infection with Anaplasma spp
Differential diagnosis
Babesiosis – there will be haemglobinuria
(because in anaplasmosis haemolysis is extravascular)
Theileriosis – lymph node enlargement
TREATMENT
Oxytetracycline (6 to 10 mg/kg IM daily for 3 days, or 20
mg/kg IM single dose) /22mg/kg IV
Imidocarb (5 mg/kg IM twice, 7 days apart)
Enrofloxacin (12.5 mg/kg SC twice, 48 hours apart)
Concurrent administration of estradiol cypionate (14.3 mg/kg
BW IM) - improve the rate of recovery by reducing
rickettsemia during treatment.
Blood transfusions are indicated in animals with a PCV less
than 15%.
CONTROL AND PREVENTION MEASURES
1) Maintenance of Anaplasma- free herds through import
and movement control, testing, and elimination of
carrier cattle
2) Vector control
3) Prevention of iatrogenic transmission
4) Administration of antibiotics
5) Preimmunization with live vaccines and immunization
with killed vaccines
Outbreaks
If an outbreak does occur, affected animals should be
treated vigorously and in-contact animals vaccinated
and/or placed on a regimen of prolonged tetracycline
protection
Prolonged treatment regimens can be used to provide
protection to cattle in seasonal risk periods of
transmission.
Vaccination
Live or killed vaccines are there

Both types use A. marginale or A. centrale from infected

bovine erythrocytes, - both types induce protective
immunity that reduces or prevents clinical disease,
neither prevents from persistently infected
Killed Vaccines
Killed A. marginale are usually in an adjuvant vehicle.

The vaccine requires two doses, 4 weeks apart, with the

last dose given at least 2 weeks before the vector season.

Subsequently, booster doses should be given 2 weeks

before the next vector season.