Difference between revisions of "Anaplasmosis"
| (25 intermediate revisions by 4 users not shown) | |||
| Line 1: | Line 1: | ||
| − | |||
Also Known As: '''''Gall sickness''''' — '''''Gallsickness''''' — '''''Tick fever''''' (Australia) — '''''Tristeza''''' (Portugal) | Also Known As: '''''Gall sickness''''' — '''''Gallsickness''''' — '''''Tick fever''''' (Australia) — '''''Tristeza''''' (Portugal) | ||
| − | Caused by: '''''[[ | + | Caused by: '''''[[Anaplasma marginale]] — Anaplasma ovis — A. ovis — Ehrlichia bovis |
==Introduction== | ==Introduction== | ||
| − | [[File: | + | [[File:Anasmosis.jpg|thumb|200px|right|''Rickettsia'' sp. inside tick haemolymph cells (sourced from Wikimedia Commons)]] |
| − | Anaplasmosis is a ruminant disease caused by the [[:Category:Rickettsiales|'''rickettsial''']] pathogens [[ | + | Anaplasmosis is a ruminant disease caused by the [[:Category:Rickettsiales|'''rickettsial''']] pathogens ''[[Anaplasma marginale]]'', ''A. ovis'', ''A. mesaeterum'' and ''Ehrlichia bovis''. |
These rickettsial parasites reside exclusively within the '''[[erythrocytes| red blood cells]]''' of their hosts. | These rickettsial parasites reside exclusively within the '''[[erythrocytes| red blood cells]]''' of their hosts. | ||
Cattle, sheep, deer, antelope and wild ruminants can all be affected. | Cattle, sheep, deer, antelope and wild ruminants can all be affected. | ||
| − | ''A. marginale'' is usually the causative agent in cattle and wild ruminants, while ''A. ovis'' is most commonly isolated in sheep and goats. | + | [[Anaplasma marginale | ''A. marginale'']] is usually the causative agent in cattle and wild ruminants, while ''A. ovis'' is most commonly isolated in sheep and goats. |
| − | ''A. | + | ''A. central'' caused mild disease in cattle and is now the foundation for some vaccines. |
''A. mesaeterum'' is similar to ''A. ovis'' but has a lower pathogenicity. | ''A. mesaeterum'' is similar to ''A. ovis'' but has a lower pathogenicity. | ||
| Line 28: | Line 27: | ||
==Distribution== | ==Distribution== | ||
| − | Anaplasmosis occurs | + | Anaplasmosis occurs in '''tropical''' and subtropical regions, particularly South and Central America, USA, Africa, Australia and Southern Europe. This climate supports the insect and mechanical vectors required for transmission of the parasite. |
| − | + | ==Transmission and Lifecycle== | |
| + | Anaplasmosis is '''not directly contagious''' and most transmission occurs via ticks. | ||
| + | Any stage of the tick’s lifecycle can become infected with Anaplasma organisms. | ||
| + | After development within the tick, the final infective stage is within the '''salivary glands''' and is injected into the bloodstream of the host when the parasite bloodfeeds. Male ticks are more mobile and longer lived therefore may play a bigger role. | ||
| − | + | See [[Tick Disease Transmission]] for more information on ticks as disease vectors. | |
| − | + | ||
| + | Infected [[erythrocytes]] are disrupted and release bodies which can invade other erythrocytes. These bodies form vacuoles within the cytoplasmic membranes of the [[erythrocytes | red blood cells]] and then undergo binary fission to form inclusion bodies. This amplifies infection within the host and increases the likelihood of transmission when insects bloodfeed. | ||
| + | |||
| + | Other insects can be important vectors depending upon location, such as dipteran flies in the USA. | ||
Cattle that recover become persistent '''carriers''' and although clinical signs do not recrudesce, sequential ricketssial lifecycles are ongoing and therefore reinfection of insect vectors and transmission to other vulnerable animals continues. | Cattle that recover become persistent '''carriers''' and although clinical signs do not recrudesce, sequential ricketssial lifecycles are ongoing and therefore reinfection of insect vectors and transmission to other vulnerable animals continues. | ||
| Line 43: | Line 48: | ||
==Clinical Signs== | ==Clinical Signs== | ||
'''Cardiovascular''' | '''Cardiovascular''' | ||
| − | :Profound anaemia resulting in tachycardia and dyspnoea. Congestion of mucous membranes | + | :Profound anaemia resulting in tachycardia and dyspnoea. Congestion of mucous membranes. |
'''Gastrointestinal''' | '''Gastrointestinal''' | ||
| Line 49: | Line 54: | ||
'''Urinary''' | '''Urinary''' | ||
| − | : | + | :Red, brown or pink urine |
'''Neurological signs''' | '''Neurological signs''' | ||
| Line 58: | Line 63: | ||
'''Other''' | '''Other''' | ||
| − | : | + | :Swelling of the head, face and ears, general paresis/paralysis, rough hair coat |
| − | Signs are often severely exacerbated by '''exercise''' | + | Signs are often severely exacerbated by '''exercise'''. |
==Diagnosis== | ==Diagnosis== | ||
| Line 73: | Line 78: | ||
Serous effusions may be present in any body cavity. The spleen may be engorged and the kidneys congested. | Serous effusions may be present in any body cavity. The spleen may be engorged and the kidneys congested. | ||
| − | Urine is dark yellow/brown due to the presence of [[Bilirubin | bilirubin]] | + | Urine is dark yellow/brown due to the presence of [[Bilirubin | bilirubin]]. |
==Treatment== | ==Treatment== | ||
| Line 80: | Line 85: | ||
Supportive treatment such as '''blood transfusions''' and appetite stimulants in severe cases may be required. | Supportive treatment such as '''blood transfusions''' and appetite stimulants in severe cases may be required. | ||
| − | A long combined course of imidocarb and oxytetracycline can also be used to | + | A long combined course of imidocarb and oxytetracycline can also be used to eliminate the carrier state. |
==Control== | ==Control== | ||
| Line 90: | Line 95: | ||
[[Tick Control|Control of the tick vector]] is viable but expensive. | [[Tick Control|Control of the tick vector]] is viable but expensive. | ||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
==References== | ==References== | ||
<references/> | <references/> | ||
| − | + | Animal Health & Production Compendium, Anaplasmosis datasheet, accessed online 02/06/2011 @ http://www.ahpc.org/ | |
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
[[Category:Lymphoreticular and Haematopoietic Diseases - Cattle]] | [[Category:Lymphoreticular and Haematopoietic Diseases - Cattle]] | ||
| − | + | [[Category:CABI Expert Review]] | |
| − | [[Category:CABI Expert Review | + | — |
| − | |||
| − | |||
Revision as of 13:01, 3 June 2011
Also Known As: Gall sickness — Gallsickness — Tick fever (Australia) — Tristeza (Portugal)
Caused by: Anaplasma marginale — Anaplasma ovis — A. ovis — Ehrlichia bovis
Introduction
Anaplasmosis is a ruminant disease caused by the rickettsial pathogens Anaplasma marginale, A. ovis, A. mesaeterum and Ehrlichia bovis. These rickettsial parasites reside exclusively within the red blood cells of their hosts.
Cattle, sheep, deer, antelope and wild ruminants can all be affected. A. marginale is usually the causative agent in cattle and wild ruminants, while A. ovis is most commonly isolated in sheep and goats.
A. central caused mild disease in cattle and is now the foundation for some vaccines. A. mesaeterum is similar to A. ovis but has a lower pathogenicity.
This disease is notifiable to the World Organisation of Animal Health (OIE)
Signalment
The resistance of Bos indicus cattle to ticks may reduce the rate of transmission in this breed.
No other breed predilection is evident.
Maternal derived immunity in calves is followed by age related immunity, and thus animals do not appear susceptible to anaplasmosis until 9-12 months old. Exposure before this age often results in lifelong, protective immunity providing endemic stability even in the presence of disease and vectors.
No marked age vulnerability appears to exist in sheep and all ages appear to acquire disease equally although it is usually mild but is exacerbated by stress.
Distribution
Anaplasmosis occurs in tropical and subtropical regions, particularly South and Central America, USA, Africa, Australia and Southern Europe. This climate supports the insect and mechanical vectors required for transmission of the parasite.
Transmission and Lifecycle
Anaplasmosis is not directly contagious and most transmission occurs via ticks. Any stage of the tick’s lifecycle can become infected with Anaplasma organisms. After development within the tick, the final infective stage is within the salivary glands and is injected into the bloodstream of the host when the parasite bloodfeeds. Male ticks are more mobile and longer lived therefore may play a bigger role.
See Tick Disease Transmission for more information on ticks as disease vectors.
Infected erythrocytes are disrupted and release bodies which can invade other erythrocytes. These bodies form vacuoles within the cytoplasmic membranes of the red blood cells and then undergo binary fission to form inclusion bodies. This amplifies infection within the host and increases the likelihood of transmission when insects bloodfeed.
Other insects can be important vectors depending upon location, such as dipteran flies in the USA.
Cattle that recover become persistent carriers and although clinical signs do not recrudesce, sequential ricketssial lifecycles are ongoing and therefore reinfection of insect vectors and transmission to other vulnerable animals continues.
Transplacental transmission from infected dams can also occur.
Anaplasmosis is not considered zoonotic.
Clinical Signs
Cardiovascular
- Profound anaemia resulting in tachycardia and dyspnoea. Congestion of mucous membranes.
Gastrointestinal
- Anorexia and mucoid diarrhoea, rumenal atony, excess salivation.
Urinary
- Red, brown or pink urine
Neurological signs
- Shivering, fasciculations, ataxia, seizures, syncope
Reproductive
- Abortion, infertility, agalactia
Other
- Swelling of the head, face and ears, general paresis/paralysis, rough hair coat
Signs are often severely exacerbated by exercise.
Diagnosis
Identification of the organism within the erythrocytes on a thin blood smear with Giemsa staining is both uncomplicated and definitive. A positive result is deemed as >5% red blood cells infected or accompanying anaemic signs. The number of infected cells doubles every 24 - 48h and may reach 90%.
The degree of parasitaemia is much lower in sheep and goats.
Complement fixation is the current international test but it lacks sensitivity.
On post mortem, carcasses are emaciated and blood is thin and watery. Jaundice is often evident and the spleen may be engorged as a consequence of profound anaemia. Serous effusions may be present in any body cavity. The spleen may be engorged and the kidneys congested.
Urine is dark yellow/brown due to the presence of bilirubin.
Treatment
Oxytetracycline and Imidocarb are both highly effective and prompt treatment usually ensures survival for all but the most severely affected individuals. Note that imidocarb is not approved for use in some countries.
Supportive treatment such as blood transfusions and appetite stimulants in severe cases may be required.
A long combined course of imidocarb and oxytetracycline can also be used to eliminate the carrier state.
Control
Vaccines against anaplasmosis are available, all are derived from the blood of infected cattle. Both live and killed forms are available.
Detection and culling or treatment of carrier animals is essential.
Take care when performing veterinary and husbandry procedures to prevent iatrogenic transmission with contaminated instruments.
Control of the tick vector is viable but expensive.
References
Animal Health & Production Compendium, Anaplasmosis datasheet, accessed online 02/06/2011 @ http://www.ahpc.org/
—