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Leishmaniosis

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Clinical Signs

Natural infections with L. infantum in dogs may remain asymptomatic for long periods before clinical signs develop. But once the disease becomes patent, progression is usually rapid and death occurs within a few weeks to months. Clinically affected dogs usually exhibit one or more of nine main clinical features: 1. skin lesions, 2. loss of weight or poor appetite, 3. local or generalized lymphadenopathy, 4. ocular lesions, 5. epistaxis, 6. lameness, 7. anemia, 8. renal failure or 9. diarrhoea. No predilection of the infection for any age, breed or sex is observed, but Ferrer (1999) suggested from epidemiological data that mongrel dogs and some Spanish autochthonous breeds are more resistant. Small breeds seem to be affected less often, presumably due to their mainly indoor living. Despite high percentages of dogs that had contact in endemic areas (60 to 80%), many show no clinical signs. The incubation period also varies independent of age, sex or breed and generally takes some weeks or months up to several years. Atypical forms of canine leishmaniosis with haemostatic problems, disorders of the cardiovascular, respiratory and musculo-skeletal systems, chronic colitis, and renal failure (without any other signs) have also been described.

Clinic in 'resistant' dogs

Depending on the type of cellular immune response some dogs do not show any clinical sign or develop only cutaneous nodules at the place of inoculation, sometimes termed 'inoculation chancres'. They are usually located on the nose or ears, typical sites of sand fly bites, nodules of 1 to 3 cm, alopecic, ulcerated and crusted, non-pruritic and only mildly painful. The general appearance is that of a healthy dog, and most chancres disappear spontaneously in 1 to 6 months (Ferrer, 1999).

Clinic in 'susceptible' dogs

The incubation period may vary between one month and seven years. During this time the parasites disseminate with predilection sites in the following organs: bone marrow, lymph nodes, spleen and liver. The damage caused by the parasite is dependent on two factors:

  • direct effect onto the tissue, causing non-purulent, infectious lesions in skin, liver, gut, kidneys, eyes and bones
  • indirect damage due to the deposit of immune complexes in joints and basal membranes of the kidneys, vessels and eyes, causing vasculitis, glomerulonephritis, polyarthritis and uveitis.

With exclusion of the CNS, numerous organs can be affected thus causing different clinic. Main symptoms are weakness, reduced physical activity, skin lesions/alterations and weight loss.

The first stage, displaying with an enlargement of the popliteal lymph nodes and deterioration in the texture of the dog's coat, co-exists with seroconversion and the presence of parasites in the reticuloendothelial system. The severity of the skin lesions seems to be depending on the state of immunity of the infected animal. Ill patients generally look older due to a marked muscle atrophy, especially in the head region. Immune complex deposits in the kidneys, leading to glomerulonephritis, are seen in 32 % of all clinical cases, often associated with a severe proteinuria. Nephropathies and associated symptoms represent the main cause of death in dogs.

Table 1: Relative prevalences (%) of different symptoms of cutaneous leishmaniosis (symptoms with prevalences > 4%) (in Noli, 1999).

generalised lymphadenomegaly, symmetrical

71.2-96.1

skin lesions (see table below)

75-89

pale mucosal membranes

58-94.4

weight loss

30.7-70

fever

23-70

lethargy

18-70

anorexia

18-70

splenomegaly

15-53.3

renal insufficiency

16-32

eye lesions

16-50

epistaxis

10-37

arthropathies

4-4.6

acute form of leishmaniosis (fever,
generalised lymphadenopathy and missing skin lesions)

4

severe renal failure without other
symptoms of leishmaniosis

4

Table 2: Relative prevalences (%) of different skin lesions (in relation to all affected animals) (in Noli, 1999).

dry, exfoliative dermatitis

56-90.9

ulcers

32.8-40

periocular alopecia

18

diffuse alopecia

14

onychogryposis

24-54.5

paronchia

13.6

sterile, pustular dermatitis

1.6-13.6

nasal depigmentation

4.5

nasal / digital hyperkeratosis

4.5

non-ulcerative nodules

4.5-16.8

Cutaneous leishmaniosis in dogs

Skin lesions are the most common manifestation of CanL in dogs admitted for treatment due to the disease (Ciaramella et al., 1997; Koutinas et al., 1999). They may be seen along with other clinical signs and/or clinicopathological abnormalities, be the only reported abnormality or may be absent. Several dermatological entities have been described (Ferrer et al., 1988; Koutinas et al., 1992): (1) non-pruritic exfoliative dermatitis with or without alopecia which can be generalized or localized over the face, ears and limbs, (2) ulcerative dermatitis over bony prominences, mucocutaneous junctions, paws, ear pinnae, (3) focal or multifocal nodular dermatitis, (4) mucocutaneous proliferative dermatitis and (5) papular dermatitis (Ordeix et al., 2005; Bottero et al., 2006).

But besides these skin lesions occurring along with a L. infantum/L. chagasi infection, dogs can also be infected with pathogenic agents of cutaneous leishmaniosis (in man). Generally, human cutaneous leishmaniosis (CL)/oriental sore may be anthroponotic, caused by L. tropica (in Asia) or L. peruviana, or zoonotic, caused by L. tropica (host: hyrax) (in Africa), L. major (host: gerbil), L. aethiopica, L. mexicana (respectively L. mexicana complex: L. mexicana, L. amazonensis, L. venezuelensis), L. amazonensis, L. panamensis, L. guyanensis or L. braziliensis (respectively L. braziliensis complex: L. braziliensis, L. panamensis, L. guyanensis). In CL, amastigotes multiply in lesions at the inoculation site, typically on the arms, legs, face or ears. Lesions are nodular or ulcerative, single or multiple. The typical lesion is a chronic 2-5 cm ulcer with indurated margins. Self-healing times are ≤5 months (L. major), ≤8 months (L. mexicana) and in ~1 year (L. tropica and L. braziliensis). Old World CL clinical features in man differ between and within regions. A 'classical' lesion starts as a nodule at the site of inoculation. A crust develops centrally, which may fall off exposing an ulcer which heals gradually, leaving a depressed scar with altered pigment. Satellite nodules at the edge of the lesion are common (WHO, 1990). New World CL has a wide variety of clinical manifestations (WHO, 1990). In endemic areas some forms are titled specifically.

L. braziliensis, L. peruviana and L. panamensis are frequently found in dogs as non-fatal cutaneous infections (Miles et al., 1999). L. braziliensis here is the main causative agent of cutaneous leishmaniosis in dogs in South America (Reithinger and Davies, 1999). Most of the dogs infected by L. braziliensis live in rural areas and they may present single cutaneous or mucosal lesions (Madeira et al., 2005). Dogs have been suspected to play a role in the domestic transmission cycle of L. braziliensis and L. peruviana in some areas of South America, but there is only circumstantial evidence supporting this hypothesis (Reithinger and Davies, 1999). In fact, the role of dogs in the maintenance of these parasites is probably minor (Dantas-Torres, 2007). A summary of CL pathogens detected in dogs in South America is listed in Table 3.

Table 3: Leishmania species causing CL infecting dogs in South America (modified after Dantas-Torres, 2009)

Species

Disease form

Suspected/proven vectorsa

Geographical distribution

L. braziliensis

Cutaneous

Lu. whitmani, among other

Argentina, Bolivia, Brazil, Colombia, Peru, Venezuela

L. mexicana

Cutaneous

Lu. ayachuchensis

Ecuador

L. panamensi

Cutaneous

Lu. trapido

Colombia, Ecuador

L. peruviana

Cutaneous

Lu. peruensis, Lu. verrucarum

Peru

L. pifanoi

Cutaneous

Unknown

Ecuador

aLutzomyia spp. that have been suspected to be involved in the transmission of Leishmania spp. to dogs in South America. Further information on the phlebotomine sand flies have been implicated as vectors of Leishmania spp. in this region can be found elsewhere (Lainson and Shaw, 2005; Young and Duncan, 1994).

Concomitant diseases

Probably due to a weakened cellular immunity infected dogs often suffer under accompanying diseases such as demodicosis and dermatophytosis. Concomitant infestation with other ectoparasites, especially ticks, lead to pathogen transmission (e.g. ehrlichiosis). Further concomitant diseases can be hepatozoonosis,  and cryptococcosis. Generally, co-infection can alter clinical signs, duration of disease and the chances for successful treatment dramatically (Roura, 2007; Oliva, 2007).

   

References

  • Bottero, E., Poggi, M., Viglione, M.: Lesioni papulari indotte da Leishmania spp. in cani giovani. Veterinaria 1, 2006, 33-36
  • Ciaramella, P., Oliva, G., Luna, R.D., Gradoni, L., Ambrosio, R., Cortese, L., Scalone, A., Persechino, A.: A retrospective clinical study of canine leishmaniasis in 150 dogs naturally infected by Leishmania infantum. Vet. Rec. 141, 1997, 539-543
  • Dantas-Torres, F.: The role of dogs as reservoirs of Leishmania parasites, with emphasis on Leishmania (Leishmania) infantum and Leishmania (Viannia) braziliensis. Vet. Parasitol. 149, 2007, 139-146
  • Dantas-Torres, F.: Canine leishmaniosis in South America. Parasites & Vectors 2(Suppl 1), 2009, S1 doi:10.1186/1756-3305-2-S1-S1
  • Ferrer, L., Rabanal, R., Fondevila, D., Ramos, J.A., Domingo, M.: Skin lesions in canine leishmaniasis. J. Small Anim. Pract. 29, 1988, 381-388
  • Ferrer, L.M.: Clinical aspects of canine leishmaniasis. In: Killick-Kendrick, R. (ed.): Canine leishmaniasis: An update. Proceedings of the Int. Can. Leishm. Forum, Barcelona, Spain, Intervet Int., Boxmeer, The Netherlands, 1999, 6-10
  • Koutinas, A.F., Scott, D.W., Kontos, V., Lekkas, S.: Skin lesions in canine leishmaniasis (Kala-Azar): a clinical and histopathological study on 22 spontaneous cases in Greece. Vet. Dermatol. 3, 1992, 121-130
  • Koutinas, A.F., Polizopoulou, Z.S., Saridomichelakis, M.N., Argyriadis, D., Fytianou, A., Plevraki, K.G.: Clinical considerations on canine visceral leishmaniasis in Greece: a retrospective study of 158 cases (1989-1996). J. Am. Anim. Hosp. Assoc. 35, 1999, 376-383
  • Lainson, R., Shaw, J.J.: New World leishmaniasis. In: Cox, F.E.G., Kreier, J.P., Wakelin, D. (eds.): Topley & Wilson’s Microbiology and Microbial Infections, Parasitology. 2005, Arnold, London, pp. 313-349
  • Madeira, M.F., Schubach, A.O., Schubach, T.M., Serra, C.M., Pereira, S.A., Figueiredo, F.B., Confort, E.M., Quintella, L.P., Marzochi, M.C.: Is Leishmania

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