LEPTOSPIROSIS

INTRODUCTION It a group of zoonotic disease which is caused by spirocheates of the genus leptospira

Etiology  Originally classed as spirocheate but now bacterial. It is a filamentous motile organism which infects all animals, domestic, wildlife and humans.  All pathogenic strains of leptospira belong to one species, Leptospira interrogans of which there are many serovars.  More than 200 serovars have been indentified and several serogroups based on serological relatedness. There are many important changes based on DNA – relatedness. Many serovars infect dogs and cats but clinical disease occurs only in a few dogs.

Etiology (contd)  Majority of cases of canine leptospirosis are caused by 2 serovars, L. canicola and L. ictorohaemorrhagiae, L. Pomona and L. grippotyphosa L. autumnalis have also been reported in dogs.  The survival of the leptospires in the environment depends on 3 factors:  Soil moisture, pH (7.0) and ambient temperature ( C)

Epizootiology  Worldwide occurrence.  Dogs are more affected than cats.  Male dogs are commonly affected than females.  Dogs between 6 to 24 months are mostly affected but any age group can be affected.  Dogs are the reservoir hosts of L. canicola, L. icterohaemorrhagiae

Transmission  Leptospires are shed in urine.  Infections is usually through contamination of food, water, bedding, soil, vegetation even formites by the urine of the affected animal and ingestion of contaminated tissues.  Infections can also occur through abraded or devitalized skin, transplacental, venereal and through bite wound contamination and intact mucous membranes  Clinically recovered animals become carriers because they shed the organisms for several months or years in their urine.

Pathogenesis  After entering the body, replication takes place in tissues of non-immune animals  Host with pre-existing antibodies usually eliminate the organisms and thus becoming subclinically infected.  In the dog, highest level of infection occurs in the liver and kidneys.  The inflammation induced by the organism and toxins produced results in renal or hepatic or both renal and hepatic damages

Pathogenesis (contd.)  Clinical signs may occur 7 days post infection but with prompt treatment or immunity the animals survive.  Some animals will clear the system of the infection even without treatment which may last 2-3 weeks but may develop chronic active hepatitis or chronic renal disease.  Cats are subclinically affected.

Clinical signs  The disease can present as o peracute, o acute, o chronic o subclinical.  After the infection and entering into the body, the leptospires enter the blood they multiply and get into the target tissues, such as the liver and kidneys.

Clinical signs Acute  Characterized by o Heptatic and renal failure o Accompanied by biochemical and haemotological derangement.  Death can occur if treatment is not instituted immediately.  All age groups of non-immuned dogs can be effected but males, herding dogs, working dogs or mixed breeds are more susceptible than companion dogs.

Clinical signs Acute (contd.)  Sudden onset of fever, vomiting and diarrhea. o Vomitus may contain shred of gastric mucosa or be bile stained.  Dehydration, polydipsia, polyuria or anuria.  Anorexia, depression and weakness.  Pain in the muscles and abdominal region, kidney and liver.

Clinical signs Acute (contd.)  The visible mucous membranes may be icteric and necrotic with offensive (uremic or gangrenous) odour from the mouth.  The initial slight erosion may develop into ulcers with tendency to bleed with slightest pressure.  The edges of the tongue become ulcerated and also the tonsil.  Urine is concentrated and bile stained.  Mild to severe enteritis, soft to liquid, dark brown in colour faeces which may contain fresh or decomposed blood and mucus.  Intussusceptions is a complication. Upper respiration involvement is manifested by coughing, nasal and ocular discharges.

Clinical signs Peracute  Usually show as o anorexia: o depression, o myalgia o hyperesthesia, o vomiting, o tachypnea, o fever, pale mucous membranes and tachycardia.  Other clinical signs such as melena, epistaxis petcchial or ecchymotic haemorrhage due to thrombocytopenia and disseminated intravascular coagulation may occur.  These signs may progress to death before renal and hepatic conditions are recognized.

Clinical signs Subacute  In subacute infection, there are usually  Haemorrhagic syndromes.  Hepatic and renal diseases are usually common.  Other signs such as conjunctivitis, rhinitis, tonsillitis, cough, dyspnea, anuria or oliguria. These are very common in the acute and subacute diseases.  Recovery from the above state usually results in chronic interstitial nephritis, hepatitis, polyuria, polydipsia, weight loss, ascites and signs of hepatic encephalopathy resulting from hepatic insufficiency.  These are also seen in chronic leptospirosis.

 Fever during the initial stages becomes subnormal, towards the terminal stages  Convulsion and muscular spasms also occur during the terminal stages.  Leucocytosis manifested by neutrophilia with left shift (15,000-50,000)  When uremia occurs the WBC may be normal or subnormal.

 Aneamia may be marked by dehydration, increase in BUN in chronic cases, plasma and urine are bile stained.  The mucous membrane of the eye is injected.  The pulse is irregular.  Urinary system.  High urine specific gravity due to excess of protein in urine and renal cell casts.  Slow recovery 7 – 10 days with permanent damage to the kidneys e.g. chromic interstial nephritis.  In fatal cases animal may die within 4 days of onset of clinical signs

Diagnosis History and clinical signs Confirmed by the isolation and identification of organisms(7-10 days after onset) in the urine and plasma, confirmed through dark-ground illumination, Animal Inoculations – guinea pigs, nice and hansters (death in days) but L. canicola is much less virulent to Lab. Animals. The organisms may be present in the blood at the early stage of the disease. Serology agglutination and FAT

Treatment Antibiotic: massive dose of procaine penicillin at least 50,000 units/kg body wt. for 7 days. Streptomycin 50mg/kg body wt for 3-6 days. May be combined with penicillin. Tetracycline should be used if condition doesn’t improve. 10% sodium chloride i/v for intractable vomiting. Supportive treatment 1.For dehydration – fluid i/v 2.Diarrhea, vomiting 3.Vitamin – Food should be withheld for some days. Patient should be kept in well ventilated room.