Surra (Mal De Caderas)

Surra (Mal De Caderas) is caused by trypanosoma evansi, which is the first pathogenic trypanosome to be identified  in 1880 in India.

Occurrence

• The Surra (Mal De Caderas) in South America is called as Maldecaderas or Murrina, Tibersa in camel.
• The incidence of Surra increases significantly in rainy season when there is large number of biting fly populations.
• The incidence of disease is high in dogs living around slaughter houses, which may be of peroral infection.

Host affected

• All domestic animals are susceptible but the disease is only fatal in horse, camels and dogs.

Pathogenesis

• Inoculation of metacyclic trypanosome intradermally by blood sucking flies causes local skin reaction (chancre) within the chancre metacyclic trypanosome transform into trypomastigote form, which enter the blood stream through lymphatics produce intermittent parasitemia, which causes extravascular hemolysis through erythrophagocytosis  in mononuclear pahgocytic system of   spleen, liver and lungs results in anemia, decreased haemoglobin synthesis, leukopenia and thrombocytopenia is due to immune mediated phagocytosis.
• The lymphoid enlargement and splenomegally develops associated with plasma cell hyperplasia and hypergammaglobinemia which is primarly due to an increase in IgM antibody.
• Concurrently there is a variable degree of suppression to immune response to other microbial antigen and vaccine results in immunnosuppression.
• In chronic condition lymphoid organ and spleen become shrunken due to exhaustion of their cellular element.
• Tissue damage as a result of localization and production of inflammatory reaction in skin, skeletal muscle, central nervous system and myocardium and eye.

Effect of trypanosomes on host metabolism:

1. Depletion of essential nutrients
2. Production of toxic metabolites

(1) Depletion of essential nutrients

• The motility of trypanosomes in blood depends upon adequate supplies of glucose in the host. 
• It was suggested that so much glucose was consumed by the trypanosomes results in hosts’ carbohydrate reserves became exhausted resulting in a breakdown of liver function and the onset of lethal hypoglycemia.
• The Blood sugar levels return to normal, even in fasting animals, after administration of trypanocidal drugs.
• Feeding glucose to infected animals may prolong their lives for short periods but does not prevent the onset of terminal hypoglycemia.

(2) Production of toxic metabolites

• The major end-products of glucose breakdown by trypanosomes are pyruvate and glycerol, which are readily metabolized by the host to produce a considerable amount of energy.
• Although pyruvate is readily used by host tissues, the accumulation of pyruvate in the blood is directly proportional to the numbers of parasites present.
• High concentrations of pyruvate could lead to depletion of alkali reserves, acidosis, and a lowered affinity of hemoglobin for oxygen.
• It drew attention to the dark purple colour of blood in late stages of T. brucei infections.
• It is proposed that deficient oxygenation of hemoglobin coupled with mechanical blockage of the circulation leads to death by asphyxiation.

Clinical manifestion

Horse

• Intermittent fever, progressive anemia, edema on dependent parts of the body (ventral abdomen and genitalia) and  petechial haemorrhage on the serous membrane  Dullness, listlessness, loss of body condition despite good appetite, extreme emaciation, nasal and ocular discharge, the nervous signs includes incordination, circling, staggering gait, head pressing, paraplegia, paralysis, delirium and convulsion.

Camel

• The chronic form of disease in camel is called as tibersa.
• The chronic signs exhibited for upto 3 years, reduction in milk yield and working capacity and abortion in pregnant animals.

Dog

• Intermittent fever (39°C–41°C), oedema of the head, including larynx (to be differentiated from rabies), oedema of the abdominal wall and legs, anaemia, weakness, lack of appetite leading to emaciation, sexual excitement and paresis of the hindquarters.
• Ocular signs are most often observed in dogs, with conjunctivitis, lacrimation, keratitis, corneal opacity, and/or haemorrhagic signs, which can lead to fibrin deposits in the anterior chamber of the eye, sometime parasites have been observed in ocular aqueous fluid and myocarditis has been described and can be fatal.

Cattle and buffaloe

The clinical signs occur as peracute, acute, subacute and chronic form.

Peracute form

• Convulsion and death within 2-3 hrs.

Acute form

• Dull, sleepy, staggering gait, circling, beating against wall, stamping of feet , bellowing, twitching of muscle and shivering of body, coma and death within 6-12 hrs.

Subacute and chronic form

• Emaciation, oedema, lacrimation and diarrhoea
• Mild infection occur in endemic area, signs may include irregular estrus, high rate of abortion and still birth occur in pregnant animals and poor semen quality in bulls.

Pig

• Infection is often chronic with not only intermittent fever, anaemia, loss of weight, abortion, and cutaneous rash, but also cause late nervous signs with hind leg paralysis.

Necropsy Findings

• Liver, spleen and lymph node enlarged are enlarged in acute infection.
• Non suppurative myocarditis and sometimes with hydropericarditis.
• Atrophy of lymphoid organ.

Diagnosis

(1) Identification of the agent

• Parasite detection techniques are highly specific, but their sensitivity is relatively low (i.e. the proportion of false negative).
• Early acute phase of infection- Sensitivity is high as parasites are actively multiplying in the blood in the absence of immunological control.
• Late chronic phase- during the chronic phase the sensitivity is low as, due to the immune response of the host, parasites are scanty and rarely seen in the blood.

(2) Parasite detection technique

1. Wet  films examination  (Blood or lymph from lymph node biopsy): These are made by placing a droplet of blood or lymph (about 2 μl) on a clean microscope slide and covering with a cover-slip (22 × 22 mm). The blood is examined microscopically. The Trypanosomes can be recognised by their movement among the red blood cells (RBCs).
2. Thick  films (prepared from blood or lymph taken from lymph node biopsy): These are made by placing a drop of blood (5–10 μl) on a clean microscope slide and spreading it over an area of approximately 2 cm in diameter, the film is air dried and  dehaemoglobinised by immersion in distilled water for a few seconds and dried before staining.  The dry smear should be stained with Giemsa stain for 30 minutes and examined microscopically for general morphology of trypanosomes.
3. Thin smear films (prepared from blood or lymph taken from lymph node biopsy): Thin blood smears are made by placing a small drop of blood (about 5 μl). The thin blood smear is prepared in the shape of bullet, air dry the smear and stained with giemsa stain, examined under microscopically to identify the species of trypanosomes.
4. Microhaematocrit centrifugation technique (Woo method): Fresh, usually ear vein blood (about 70 μl) is collected into heparinised capillary tube and sealed it and centrifuged at 9000 rpm for 5minutes. The plasma/white blood cell interface (buffy coat) is examined by slowly rotating the tube. Trypanosome movement can first be detected using the ×10 objective lens with reduced condenser or with phase contrast microscope or compound microscope. This is sensitive technique than wet flim examination.
5. Examination of body fluids like Cerebrospinal fluid and aqueous humour for trypanosomes

(3) Chemical tests

• To detect the changes in the chemical composition of the blood produced by alteration of protein (albumin and globulin in serum).
• Non-specific and less reliable.
• Mercuric chloride test, Formal gel test, thymol turbidity test are commonly used for camels.

• (a) Mercury chloride test
  • Take 1 ml of 1:30,000 solution of mercuric chloride in test tube.
  • Add drop of  serum.
  • Development of white precipitate within few seconds considered positive.
• (b) Formol gel test
  • Take 1 ml of serum in test tube.
  • Add 2-3 drops of formalin.
  • Shake well and allow to stand.
  • Formation of gel within 2-3 hours considered positive.
• (c) Thymol turbidity test
  • Take 1 ml of  aquous thymol (1:100-1:2000 in test tube.
  • Add drop of  inactivated serum (56^o C for 30 minutes).
  • White turbidity within few minutes considered positive.
• (d) Stilbamide test- Reliable test for diagnosis of surra in bovines in India
  • Take about 0.5-2.5 ml of 10% solution of stilbamide.
  • Add drop of suspected  inactivated serum (56^o C for 30 minutes).
  • Development of coagulant and settle down in 1 or 2 minutes and dissolve in 5-10 minutes considered positive.

(4) Other diagnosis ways

1. Isolation of trypanosomes in NNN Medium (Novy MacNeal Nicolle Medium)
2. Mice inoculation tests: About 0.5 ml of suspected blood or lymph aspirate inoculated intraperitoneally in the mice, heavy parasitemia found in 2-3 days of post infection
3. Immunodiagnostic tests: IFAT, CFT, ELISA & IHA are most reliable tests.
4. Molecular diagnosis by PCR in blood
5. Allergic tests (doubtful): About 1.0 ml antigen is injected at the side of the neck with a 2^nd dose 48 hours after first dose. Infected cases show no painful edematous, uninfected animal possess circumscribed hard nodular swelling. Accuracy lacking in this test.

Differential Diagnosis

• Theileriasis
• Anaplasmosis
• Rabies

Treatment

1. Antrycide prosalt (Triquin): Combination of Quinapyramine sulphate (Methyl sulphate) and Quinapyramine chloride (Methyl chloride) at 7.4 mg/ kg body weight  or 3.5 g in 15 ml distilled water given subcutaneously for chemoprophylaxis.Protection aganist trypanosomes occur 2-3 months only.
2. Suramins: Sulphonated naphthalamines (Nagolol) is curative.
   • Effective against T. evansi, T. brucei, T. equiperdum.
   • Cattle: 0.5 g/45 kg body weight followed by half dose after 2 weeks, I/V
   • Horse: 4 g/45 kg body weight as single dose, I/V
   • Camel: 1-2 g/100 kg body weight as single dose I/V
   • Dog: 3.5 ml, 10% solution followed by 2^nd dose at 3-4 weeks interval, I/V
3. Diamidines: Diminazene aceturate (Berenil) is curative at 3.5 mg/kg body weight S/C or I/M
   • Very effective against T. congolense and less effective against T. evansi, T. brucei ,  in bovines, ovines and caprines
   • Dog and camels react to dogs; resistance may occur to the drug
4. Phenanthiridine compounds:
   • Homidium bromide and Homidium chloride at 1-2% solution at 1 gm/kg body weight, I/M route against T. congolense and T.vivax but not against T. evansi
   • Pyrithridium bromide at 4 % solution at 2mg/kg body weight, S/C or I/M against T.congolense and T.vivax
   • Isometamidium chloride – 0.5 mg/kg body weight, deep I/M route against T. simiae in pigs.

Control

Control is difficult and the factors responsible for the wide spread existence are:

• Latent cases of cattle and buffalo
• wild animals act as reservoir
• Drug resistant strains
• Wide spread prevalence of vectors

The Control program consists of:

• Disposal of manures properly
• Proper drainage
• Regular spraying of insecticides: Sprinkling of kerosene oil over water in ponds, ditches, streams or insecticides to kill adults and aquatic larvae
• Removal of moist beddings, hay, dung from stable
• Keeping animals clean by regular grooming
• Segregation of sick animals from healthy during outbreak in fly -proof shed
• Identification of endemic areas by regular examination of blood for trypanosome sp for implementation of preventive measures
• Rearing of trypanotolerant animals e.g N-Dama cattle