Introduction
⇒ Bovine
anaplasmosis rickettsiales , tick borne bone disease characterized by extravascular hemolysis, anemia, jaundice and sudden death.
Synonym:
⇒ Gall Sickness
Etiology
⇒ Order:
rickettsiales
⇒ Family:
Anaplasmataceae
⇒ Genus:
Anaplasma
⇒ Species:
Anaplasma
marginale
Anaplasma centrale
⇒ Small,
pleomorphic, gram negative, obligated, intracellular organism,
⇒ Anaplasma ovis:- cause disease in sheep
and goat
Host
⇒ Anaplasma
marginale and Centrale are both seen in cattle.
⇒ Anaplasma
ovis cause disease in sheep and goat.
⇒ Calves
are more resistance to disease then older cattle, this resistance is not due to
colostrum antibody from immune Dams
⇒ Animal
become carrier after recovery
⇒ BOS indicus breed of cattle appear
to process a greater resistance to anaplasma marginale infection than bos taurus breed.
Transmission
Tick bites:
⇒ 19
different type of ticks transmitted this disease
⇒ Ixodes,
dermacentor, Rhipicephalus
Mechanical transmission
⇒ Fresh
blood from infected animals is susceptible cattle from biting flies
⇒ Blood
contaminated fomites like needles,
ear tagging, and dehorning and castration equipment
Pathogenesis
Feeding of infected blood meal by
vector
⇓
Bacteria go into midgut epithelium
cell of the tick
⇓
First bacterial application
⇓
Bacterium then migrate to and invades
the salivary gland
⇓
Second round application in salivary
gland and bacteria present in the Saliva of tick
⇓
This tick take blood meal from
healthy animal and inoculate a bacterium in body
⇓
This bacterium enter to RBCs and
formed vacuole
⇓
Bacterium and replicate by binary fission
in RBCs up to 75% RBCs can be infected in acute febrile stage
⇓
Infected RBCs identified by macrophage
in spleen lymph node liver and bone marrow
⇓
Phagocytosis of infected RBCs by
macrophages (erythrophagocytosis)
⇓
Lysis of RBCs in cytoplasm of
macrophage and releasing hemoglobin in cytoplasm
⇓
The heme group contain iron in porphyrine ring and globin chains separated
globin used in protein synthesis and
porphyrine ring oxidized
⇓
Producing delivered in and releasing
the iron biliverdin convert to
unconjugated bilirubin in excess production
⇓
Development of prehepatic or hemolytic jaundice
⇓
Free Iron into the cells bind to the
protein apoferritin, forming ferritin
Ferritin becomes oxidized and degrade
to form hemosiderin
⇓
Excessive hemosiderin laden
macrophages found in spleen liver lymph nodes and bone marrow
⇓
Spleen and liver become enlarged due
to excessive lysis of RBCs
⇓
Most body tissue become yellow is due
to jaundice
⇓
Due to excessive lysis of RBCs in
spleen liver bone marrow and lymph node there is development of extravascular
hemolysis and anemia
⇓
Secondary changes due to anemia occurs
in body.
Clinical sign
⇒ Fever
⇒ Depression
⇒ Decrease
Milk Production
⇒ Anemia
Pale Or Yellow Mucous Membrane
⇒ Dehydration
Clinical Pathology
⇒ Intraerythrocytic organism
⇒ Spherocytosis
⇒ Marked anemia so there is decrease hemoglobin pack cell volume
and RBCs
⇒ Leukocytosis with neutrophilia
Macroscopic Pathology
⇒ Pale
anemic and jaundice all tissue and carcass
⇒ Pale
and discoloration of lung
⇒ Liver
is also enlarged with round stage and gallbladder is distended with granular
bile
⇒ Spleen
is greatly enlarged and reddish in color
⇒ Urinary
bladder contains bilirubin stained urine
⇒ Bone
marrow hyperplasia
Microscopic Pathology
⇒ Hemosiderin
laden in macrophages and hemosiderosis found in many organs
Liver:-
⇒ Hemosiderin
accumulation in hepatocyte and kuffer cells
⇒ Vacuolar
degeneration
⇒ Canalicular
cholestasis
Spleen and lymph nodes:-
⇒ Congestion
⇒ Medulla
- erythophagocytosis by macrophages
Bone marrow:-
⇒ Erythroid
hyperplasia
Diagnosis
⇒ Based
on clinical sign and symptoms
⇒ Blood
smear examination
⇒ PCR
⇒ ELISA
⇒ Complement
fixation test
⇒ Indirect
fluorescent antibody test
Great information for the vet practioners
ReplyDeletevery informative dr
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