From the first descriptions, by Ligniers and Spitzen 1902 and the later fixation by Brumpt in 1910 to nowadays, several microorganisms have been included and excluded to the Actinobacillus type.A. mallei was traspased to Pseudomona mallei,while Bacillus nephriditis equi (Meyer 1910) turned to Shigella viscosa (Bergey 1930) to be finally described as Actinobacillus equuli (Haupt 1934).

The last incorporation has been Haemophillus pleuroneumoniae, now called Actinobacillus pleuroneumoniae.

The pathogen activity, in the veterinary area, caused by some Actinobacillus is already known. For example A.ligneriesi and A.seminis in sheep (Fontaine, 1987), A.equuli in horses ((Fontaine, 1987); A. Actinonomycetem-comitans in dog (Allaker, 1987), A.ligneriesi and A.actinoides in cattle (Fontaine, 1987), A.suis in pig (Zimmerman 1964, Fontaine 1987, Miniats 1988, Sandford 1990 and Odin 1993) and alpacas (Hill 1992).

Some of theses species still have an uncertain bacteriological classification, but there are no doubts about their increasing incidence in the industrial breeding in pigs and sheep, what makes actinobacilosis a disease needing all the attention from pathologists and zootechnitians.

II.INCIDENCE AND sanitary+ECONOMIC IMPORTANCE

The first observation are dated 1983. At first sight it seemed to be just disconneted lesions (necrosis and ear dermatitis) and symptoms (infertility and suppuration), laterly have been related with porcine actinobacilosis, pointing the existence of this disease , with an enough incidence to fix our attention.

A better control of other accute diseases (such as Aujezky, parvovirus and swine pest) allowed to observe clearly subaccute and cronic processes. This is why from 1985 the clinical picture of porcine actinobacilosis.

With the new knowledges we can assure that this disease has a high incidence (around 80%). Its sanitary importance is high because of its own pathology and because of its inmunological consequences.

Economically the effects are around 10-15% of lacting deaths and repetition increasing in 10 % and growing delays (5-10%)

III.DESCRIPTION:

1. Definition:

Porcine actinobacilosis is an infectious subaccute or chronic disease, by vertical transmission contagion in whose course limphatic ganglion from lumboaortic chain are infected. After, the dependent organic chains and finally spleen are infected. The pathogen agent is Actinobacillus suis.

2. History:

Swine actinobacilosis has been included during years as part of the antimycosis complex and thought was caused by several microorganisms (Corynebacterium, Actinobacillus ligneriesi, Bacterium pyogenes and Staphylococcus pyogenes)

The classic description (Hutyra-Marek-Manninger-Moscy-Sánchez-Garnica 1968) already linked it with amygdalas, vertebral metastasic focus, subcutaneous tissues and lungs.

Deep changes by industrialization, in breeding of swine made that during sixties and seventies, no research about actinobacilosis was made. Zimmerman studies (1964) were an exception. The pathogenic conception about the disease was starting to change, because A. Suis was considered as the responsible of septicemic processes and articular, renal and cardiac infections (Fontaine 1987)

Later on, Miniats (1988) and Sandford (1990) isolated it between 1985 and 1989 with increasing frequence, in pathogen processes including epithelial lesions similar to erysipela.

The most exact description, but without a definition of the etiology, was made by Smith, Thompson and Done (1993) under the name of Porcine dermatitis-nephropaty syndrome.

3. Location:

The porcine actinobacilosisi in its modern conception has been found in Europe ( Germany, United Kingdom, France, Italy, Spain) and America ( Canada, Venezuela and Argentine) However, the vertical transmission and the increasing interchange of reproductive animals has made the disease a world disease.

4. Ethiology:

The pathogen agent Actinobacillus suis is found in limphatic tissues ( spleen and ganglions), but can also be isolated in kidney, lungs and subcutaneous purulent nodules. The microorganism can be cultivated in liquid culture mediums cointaining spleen extract, brain-heart infussion and blood agar. In the liquid mediums there is an initial turbidity that finally sediments.

In blood agar plates there is an hemolysis although one of the two isolated strains takes around 5 days for this.

If the germ is not in pure status, its growth is masked by other microorganism with higher vitality (E. Coli, Salmonella and others).

It is pathogen for mices at doses of 0.1 ml by intraperitoneal injection after 6 hours and has cross reation with A. Ligneriesi positive serums.

It is no resitent to heat, desecation ad desinfectants.

The natural infection is produced by blood via during pregnancy causing a purulent focus in internal part of umbilicus.

5. Receptivity:

All swine breeds industrially exploted are receptive to the disease, but those breeds of quick growth are more sensitive.

The main clinical demonstration take place in extreme temperatures season.

6. Inmunity:

Because the infection is mainly in limphatic system, its inmunology is erratic.

Affected animal, who have tolerated the disease and arrived to slaughter, had positive rates tested with A. Suis antigen dyed with Gentian Violet to aglutine ill animal serum, as is usually made with brucelosis. Common dilutions are 1/10, 1/20, 1/40, 1/80, 1/160.

When in an exploitation there is as strong incidence of A. Suis, there are systematic failure in inmunitary system in front of vaccines of Aujezky, parvovirus, athrophic rhinitis and erysipela, even by using vaccines of excelent quality.

The leucocitary formula of infected animals is altered. Lymphocytes are increased while monocytes, basofiles and eosinophiles content is, usually minimmum.

Finally, is important to say that those animals positive of A. Suis were also positive when titulated with Leptospira icterohaemorraghic.

7. Pathogeny:

The infection is produced during pregnancy, leading to omphalitis and inflammation of the first lumbar pairs of the lumbo-aortic lymphatic chain. As consequence, some foetuses die , some new-born piglets are very weak and labour schedule is modified in some days.

In the following days or weeks , the infection pushes in ascendent direction to the heart, affecting succesive pairs of limphatic ganglions and organic lymphatic chains (renal, intestinal, esplenic, gastric and tracheobronchial)

With the infection of several organs petechias and vasculitis are produced, healing spontaneously or going to purulent focus specially in kidney, spleen or oviduct. As consequence, elder animals show purulent discharge in urine, infertility rate and spleen breakages increase, as well as unequal inmunitary response to vaccinations. The infection in the lumbo-aortic chain can be extended to near vertebral carcass and to the superficial lymphatic ganglions (cervical, axillary and groinal) to subcutaneous tissue and articulations.

At cardio-respiratory level the disease causes pneumonia, starting at bronchial area and extended radially to the lobes and finally, endocarditis with gelatinous intracardiac masses specially in the right part.

Externally, pigs have lesions similar to erysipela, caused by vascular and inmunitary disorders, violet colourations, in ears and snout bacause of cyanosis and pneumonia and endocarditis; tearing and dirty auditive pabillon because of extention of infection to parotidic and retropharinxitic limphatic ganglions, and also darker colour of urine.

The infection by Actinobacillus suis to the lymphatic ganglions , causes indefension to other bacterial attacks such as Bordetella, Corynebacterium, Salmonella and E. Coli

8. Anatomic alterations:

Essentially omphalitis and later umbilicus fibrosis , vasculitis in arterial small and medium branches and organic purulent focus are the characteristic anathomic alterations caused by porcine actinobacilosis.

Vasculitis affects lymphatic ganglions, spleen, kidney and skin.

Purulent focus are developed in kidney, lungs,oviducts, articulations, vertebras and subcutaneous tissues, coming from regional lymphatic ganglions.

9. Sympthoms:

The affected animals have different sympthoms, according to their age.

During lactation, umbilicus is enlarged and hardened, also litter is unequal. The delayed piglets will grow more slim and more hairy than the others.Morbility can be 20- 40 % and mortality the 3 first weeks affect almost all ill animals after a short period of diarrhoea and disnea.

In post-weaning period, the first 2-5 mm cutaneous lesions are observed and tearing starts. The most affected piglets are pale and the urine colour gets darker. Sneezes are usually. If the aortic and cardiac lesion have been developed, the ear and snout cyanosis is showed. Number of herniated and convulsive animals increases in the most affected litters.

In the fattening period, all the infected animals have already dead, but the other ones will be in chronic phase: pus in urine, subcutaneous abceses, tearing, cutaneous decamation, dirty ear, pneumonia and increasing of feed conversion index, lameness and vertebral lesions.

Reproductive animals, have the same symptomathology but adding infertility specially in first-labour due to the purulent nodules in oviduct. As they seem to have the zeal, the general diagnosis is metritis.

10. Course:

Actinobacilosis goes on subaccute form in the first ages of the animals and chronically from 40-50 kg up.

This course can be altered with acute outbreaks of consecutive diseases helped by the inmunosupression that the animal supports. The usual complications can be caused by Aujezky, parvovirus, Salmonella, Bordetella and Corynebacterium.

11. Diagnostic:

The clinical diagnostic can be wrong because of the superposition of several diseases specially at the beginning.

It is necessary to go to a serologic diagnosys as explained in part III.6 of inmunology. Is a quick and reliable test.

The microbiological test is hard due the difficulty on the A.suis growth. The culture medium must be the described in point III.4 of ethiology.

12. Forecast:

The disease is very serious, because of the mortality in first aged as per morbility ( delays, increase of feed consumption, infertilty) in the chronic phase.

The application of a drugs and vaccinal program goes to quick improvements but don’t finish with the infection, so productive parametres, fertility and other parameters on the exploitation go to normal values the inmune status of the animal is still fragile.

13. Treatment:

The causing agent A.suis is sensitive to betalactamic antibiotic and to quinolons. Amoxycillin, aztreonan, nalidixic acid and enrofloxanin are particularly active. Their parenteral application have short term effects so it is preferable to give them by oral route mixed with feed. The treatment by oral administration is longer at decreasing doses, parallelly to the sympthoms remision ( tearing, ears epithelial descamation, urine colour)

14. Profilaxis

The pharmacological treatment must be together with an active profilaxis by A.suis bacterines application.

These bacterines must no be applyed until 4 to 6 weeks after the treatment start.

Is is adviceable for these bacterines to include also consecutive germs: Bordetella bronchiseptica, salmonella, Corynebacterium an also A. Pleuroneuminiae.

Due to the inmunitary fragility it is necessary to do quarterly serological analysis to reproductive animals to know the status of the given protection.

This work in collaboration between a clinic and an analyst give excellent results allowing to act precisely and quickly.

The pasive profilaxis, based in the intramuscular injection of blood or serum from inmunized animals have also apported good results but no lasting. The same happens with autohemotherapy.

IV. CONCLUSION:

1. Porcine actinobacilosis is caused by Actinobacillus suis, and it is a subacute and chronical disease of high incidence, economical importance and vertical transmission.

2. Due to infection of lymphatic ganglions and spleen, the disease has negative effects in inmunitary status and leads and increase of consequent pathology (Bordetella, Salmonella and Corynebacterium)

3. The clinical picture changes according to the age of the animal but finally brings dermatitis, nephritis, reproductive alterations and cardiopathy.

4. The antygen helps to control sanitary status of reproductive animals and new-coming animals to the exploitation.

5. The use of drugs together with bacterines help to control correctly actinobacilosis and its consequences.

BIBLIOGRAFY

1. ALLAKER, R.P et al (1994). Prevalence of Eikenella corrodens and Actinobacillus actinomycetem comitans in the dental plaque of dogs. Veterinary Record 134 (26) 519-520.

2. BRUMPT E. (1910). Precis de Parasitologie. 1º Edition. Masson et Cie. Paris.

3. BURROWS L.L.; LO R.Y.C (1992). Molecular characterization o fan RTX toxin determinant from Actinobacillus suis. Infection and immunity 60 (6) 2166-2173.

4. DEVENISH J. et al. (1989). Immunoserological comparison of 104-Kilodalton proteins associated with hemolysis and histolisis in Actinobacillus pleuropneumoniae, Actinobacillus suis Pasteurella haemolytica and Escherichia coli. Infection and Immunity. 57(10)3210-3213.

5. ELAD, D. et al. (1991). Actinobacillus suis-like organismo in a mare-first report in Israel anda brief review of the literature. Israel Journal of Veterinar medicine 46(3)102-106.

6. FONTAINE, M. (1987). Vademecum du Veterinaire XV Edition. Cap. III pag. 1117. editions Vigot. Paris.

7. HILLF.I.; JOHNSTONE A.C (1992). Actinobacilosis in an Alpaca (Lama pacos). New Zealand Veterinary Journal 40( 1) 28-30.

8. HUTYRA et al. (1968). Patología y Terapeutica especiales de los animales domésticos 2ª edición. Tomo I: Enfermedades infecciosas crónicas pág. 744-760. ed. Labor. Barcelona.

9. LIGNIERES J.; SPITZ G. (1902). L’actinobacillose Bull. Soc. Centr. Med. Vet. 20:487-535, 546-565.

10. LIGNIERESJ.; SPITZ G. (1902). Contribución al estudio de infecciones conocidas bajo el nombre actinomicosis: Actinobacilosis. Bol. Agr. Ganad. Buenos Aires 2:169-230.

11. MINIATS O.P. et al (1988). Actinobacillus suis septicaemia in an SPF-Swineherd-a case report. Proceedings International Pig Veterinary Society 10th Congress pag. 158. Rio de Janeiro.

12. MINIATS O.P et al. (1989). Actinobacillus suis septicemia in mature swine two outbreakers resembling erisipelas. Canadian Veterinay Journal 30 (12) 943-947.

13. SANDFORD S.E et al. (1990). Actinobacillus suis infection in pigs in Southwestern Ontario. Canadian Veterinary Journal 31 (6) 443-447.

14. SANDFORDE (1990). Erisipelas Lookalike in High Health heards. Pig International 20 (11) 31.

15. SMITH W.J et al. (1993). Dermatitis-nephropathysyndrome of pigs. Veterinary Record 2 (132) 47.

16. ODINM.; HELIE P (1993). Actinobacillus suis in Swine in Southwestern Quebec. Canadian Veterinary Journal 34 (10) 634.

17. SIMMERMANNT. (1946). Untersuchungenüberdie Actinobazillose des Schweines. DeutTicraerztlwochenschr 71:457-461.