Anaplasmosis

Dr PRUTHVISHREE B S
ASSISTANT PROFESSOR
DEPARTMENT OF VETERINARY MEDICINE
VETERINARY COLLEGE, HEBBAL.
Introduction
• Anaplasmosis is a vector-borne disease that affects animals
and humans worldwide.
• an obligate intracellular, Gram-negative alpha-proteobacteria
that belongs to the Anaplasmataceae family, order
Rickettsiales.
• These pathogens parasitize circulating blood cells
(erythrocytes, monocytes, granulocytes, and platelets).
• Ticks act as natural vectors for Anaplasma species and play a
key role in the biological multiplication of these bacteria in
salivary glands and guts.
Transmission
• Ixodidae ticks act as biological vectors and play an
essential role in the spread and propagation of
Anaplasma during various stages of its life cycle.
• Vertical transmission - A. platys
• Intrauterine transmission - A. phagocytophilum.
Transmission
• Trans-placental route less in occurrence in cattle usually
results in Abortion or neonatal infection.
• Mechanically by biting flies(belong to tabanus)
• Blood contaminated fomites (hypodermic needles, by
castrating, spaying and dehorning instruments, and by
blood transfusions and embryo transplants)
Development cycle of A. marginale in cattle
and ticks
Risk factors
• Age: young animals are less susceptible compared to
adults, severe form of the disease is common after 3
years of age.
• Geography: certain geography the disease occurrence is
more common, introduction of animals into endemic
areas or expansion of vector population to the previously
vector free areas.
• Economic importance: Economi c losses are due to death,
abortions, decreased production in sick or recovered
animals and cost involved in controlling of ticks and
treatment costs, exports will be affected.
Pathogenesis
• Anaplasma marginalae is obligate intracellular organism,
it enters the mature RBC’s within the host by endocytosis
and there by undergoes binary fission to produce 2 to 8
initial bodies, which comes out of the RBC by exocytosis
and these initial bodies will affect new RBC’s.
• Atleast 15% of the RBC’s should be parasitized to produce
the clinical disease.
• These parasitized RBC’s are removed by reticulo-
endothelial system with release of inflammatory
reactants leading to fever and mild to severe jaundice.
• Basically, the disease causes anemia without
haemoglobinurea!! (anemia is due to falling number of
parasitized RBC) and
• Later in the disease anti-erythrocyte antibodies
produced will further deteriorate the condition.
• Cattle that survive the disease become carriers and
serve as reservoirs of A. marginale because they
provide a source of infective blood for both mechanical
and biological transmission by ticks. They have lifelong
immunity and are resistant to clinical disease on
challenge exposure.
Clinical signs
• IP 3 to 5 weeks
• Fever is often irregularly intermittent in nature, anorexia,
pale m.m, icterus, anemia, without haemoglobinurea,
respiratory dyspnea and finally death.
• In per acute cases, affected animals often hyper-excitable
and tend to attack attendants just before death.
• Pregnant cows frequently abort.
• In convalescent bulls there may be depressed testicular
function for several months
Clinical signs
• Sheep: disease is often subclinical in nature with
anemia
• Goats: clinical picture is similar to cattle with Goats
may show hyper-excitability and may bite at inanimate
objects
PM FINDINGS
• Enlarged liver
• Thin blood
• Emaciated body condition,
• Pale mucus membranes
• Enlarged spllen with soft pulp,
• Kidney –congested,
• Reddened bone marrow –indicating increased
hemopoietic activity.
Diagnosis
• Hematology-falling erythrocyte i.e decreased TEC, Hb,with
apperence of small immature RBC’s (anisocytosis)
• Blood smear examination: Giemsa staining–ear vein smear
is preferable.
• Microscopic examination of blood or organ smears is the
most common method of identifying Anaplasma in clinically
affected animals
• Serology:(for detection of antibodies) compliment fixation
test:f or detection of carrier animals, but false–Ve can occur.
Ab titre is highest during acute phase of the disease and low
in carrier animals.
• Rapid card agglutination test: cheap and quick,
sufficiently accurate, used for herdscreening.
• Capillary tube agglutination test:
• Dot ELISA: sensitive and specific.
• Competitive inhibition ELISA:
• Nucleic probe analysis: used to detect the lowest level
of parasitaemia.
Treatment
• Blood transfusion in cases with less than 15% PCV is
necessary.
• Clinical disease:
• OTC:10mg/khg B Wt daily for 3day or long-acting OTC–
20mg/kg once
• But tetracycline treatment does-not eliminate carrier state
• Imidocarb:3mg/kg B.wt also useful in clinical cases.
• Long term protection plan: administering long-acting OTC
once in 28days for rest of the life or daily administration of
chlortetracycline in the feed @1.1mg/kg Bwt Daily.
ERLICHIOSIS
• Ehrlichiosis is induced by a group of emerging rickettsial
tick-borne pathogens of public importance that are
Gram-negative obligate intracellular bacteria of the
genus Ehrlichia, family Anaplasmataceae.
• It is also recognized as canine rickettsiosis, canine
typhus, canine hemorrhagic fever, tropical canine
pancytopenia, and tracker dog disease.
Etiology
• E. canis is the well-known etiological pathogen of canine ehrlichiosis
affecting platelets,monocytes, and granulocytes.
• E. chaffeensis is considered the main etiological agent of human
monocytic ehrlichiosis (HME), it is also reported in canines.
• In general, three Ehrlichia spp. (E. canis, E. ewingii, and E.
chaffeensis) are involved in infecting dogs
• A minimum of five different species of ticks (Amblyomma americanum,
Haemaphysalis longicornis, Rhipicephalus sanguineus, Haemaphysalis
yeni, and Dermacentor variabilis) have been identified as vectors
transmitting clinical ehrlichiosis in dogs.
• Thevectors become more potent during summer and spring seasons.
• Rhipicephalus sanguineus (the brown tick of dogs) is generally
considered the main vector responsible for canine ehrlichiosis.
Risk Factors Associated with Canine Ehrlichiosis

• All dog breeds are susceptible to canine monocytic ehrlichiosis

(CME). Siberian Huskies and German Shepherds are more
prone to exhibit severe clinical symptoms.
• No predisposition of sex in disease occurrence
(some published literature has detected increased
seroreactivity in males).
• high disease prevalence in older dogs.
• Dogs living outdoors are more prone to have ehrlichiosis
• Dogs living in non-sanitized enclosures with tick
infestations are at risk of getting E. canis infection.
Transmission Cycle
• Brown dog tick (Rhipicephalus sanguineus) carries the
pathogen from infected dog through blood meal
during the acute phase of disease.
• After the blood meal, E. canis resides in the salivary
glands and midgut of the carrier tick and it then
spreads the pathogen to another healthy dog via its
salivary glands during subsequent feeding.
• Trans-stadial transmission is well-established in which
the larval stage of tick becomes infected with E. canis,
which can pass the bacteria to the next two stages (nymph
and adult) and spread the pathogen during blood meals.
Pathogenicity
• Peptidoglycan and lipopolysaccharide are absent in the
cell wall of this bacterium which may help the bacteria
in resisting the host’s immune response.
• The lack of complex inner structures, which permits the
production of sugars. The main energy source of this
bacterium are amino acids.
Clinical signs
• The principal host cell targets for E. canis and E. chaffeensis are
agranulocytes, while E. ewingii mainly targets the
granulocytic white blood cells.
• IP- 1-3 weeks.
• Acute phase- 2 to 4 weeks and if the animal survives, the signs
vanish even without chemotherapeutic treatment.
• some dogs become subclinical carriers after improvement and
may become an important source of infection for months and
years.
• some subclinically infected dogs may proceed to the chronic
stage, which is the most fatal form of the disease, and which
cannot be differentiated from the acute phase in clinical settings
because most of the clinical manifestations are non-specific.
hypoplasia of bone marrow and severe pancytopenia will confirm
the presence of the chronic phase.
Clinical signs
• Fever, pale mucosa due to anemia, lymphadenomegaly,
bleeding disorders, hepatomegaly, lethargy, petechial
and ecchymotic hemorrhages, vasculitis, and extended
bleeding period during estrus.
• less common signs- diarrhea, exercise intolerance,
neonatal death or abortion, vomiting, and mucopurulent
or serous nasal and ocular discharge.
• Bleeding tendencies more frequent and severe in the
chronic form of CME.
Clinical pathology
• Severe drop in platelet count or thrombocytopenia is the
principal abnormality in canine ehrlichiosis.
• Decrease in total red blood cell count, pack cell volume
(PCV), and platelet count while noticeable increases in
basophil count.
• Blood urea nitrogen (BUN) and creatinine levels-elevated.
• Anemia is mostly non-regenerative along with
lymphopenia, monocytosis, thrombocytopathy,
hyperproteinemia, hypergammaglobulinemia,
hypoalbuminemia and hyperglobulinemia,
• Values of neutrophils are inconsistent and both
neutrophilia and neutropenia have been detected based
on the phase of the severity.
• The chronic form- aplastic pancytopenia, granular
lymphocytosis, mild elevation in liver enzymes, and
renal azotemia.
Histopathology
• Edema of the subcutaneous layer, ascites, anemia, jaundice,
and emaciation.
• Cuffing of the lymphatic fluid in the cerebellum and brain is
occasionally seen.
• Lungs of infected animals display vasculitis and interstitial
pneumonia.
• Additionally, a flabby heart and whole heart dilatation can
also be found.
• Grossly, the most frequent signs include apparent
splenomegaly, multifocal lymph node necrosis, and
widespread lymadenopathy
Diagnosis

• Microcopy- In blood smears, detection of ehrlichial

organisms in the form of morulae is only in 4–6% of cases.
• In the acute form, the presence of E. canis morulae in
mononuclear leukocytes using buffy coat, spleen,
cerebrospinal fluid, and bone marrow provides a definitive
diagnosis.
• Bone marrow cytology- differentiate myelosuppressive and
non-myelosuppressive canine ehrlichiosis.
• Extremely insensitive in the chronic and subclinical phases
and unable to differentiate ehrlichial species.
• Requires a lot of expertise.
• Serology- Immunofluorescence antibody test (IFAT)
and enzyme-linked immunosorbent assay (ELISA)
• IFAT is considered the gold standard test by OIE for the
diagnosis of Ehrlichia.
• Molecular diagnosis
• PCR
• RT-PCR
Treatment
• Doxycycline (semi-synthetic tetracycline) is approved as
the first-line treatment of choice.
• Ideal dose rate and duration of doxycycline is 10 mg/kg
once (per os) daily or 5 mg/kg twice (orally) daily
minimum for four weeks.
• Doxycycline is considered safe and does not cause
discoloration of enamel.
• Vomiting is the second most common side effect.
• Prolonged use of doxycycline can damage hepatocytes, so
if the liver enzymes increase, treatment must be paused.