Ivermectin was the first commercially available macrolide anthelmintic. It is a semi-synthetic agent derived from the natural avermectins. It occurs as on off-white to yellowish powder and is highly lipophilic. It is very poorly soluble in water, but is soluble in propylene glycol, polyethylene glycol and vegetable oils.

Pharmacokinetics

Ivermectin is well absorbed (>90%) from GI tract after oral administration in simple stomach animals. In ruminants, absorption from GI tract is moderate (25-30%) due to inactivation of the drugs in the rumen. Parenteral administration (SC) results in higher bioavailability, but the rate of absorption is comparatively slower than that seen after oral administration. Once in circulation, ivermectin is well distributed to most tissues except the CNS. Collie breed of dogs allow more penetration of ivermectin into the CNS than other breeds or species; therefore, they are more susceptible to ivermectin toxicity. Ivermectin is partly metabolised in the liver by oxidation and is excreted in both unchanged and metabolised forms in the faeces. Ivermectin in faeces or soil degrades at a much slower rate, which has been shown to suppress larvae of some dung-breeding insects. Ivermectin has a long terminal half-life in most species (dogs = 2 days, cattle = 2-3 days, sheep = 2-7 days and swine = 0.5 day)      

Mechanism of Action

Avermectins and milbemycins act by binding to a special type of glutamate-gated Cl^--channel receptors found in susceptible nematode and arthropod nerve cells. The glutame-gated chloride channel (GluCls) are invertebrate-specific numbers of the Cys-loop family of ligand-gated ion channels present in neurons and myocytes. This binding opens the Cl^--channel triggering chloride ion influx. Increased intracellular chloride ions cause hyperpolarisation of the parasite neuron and prevent initiation or propagation of normal action potential. The net effect of avermectin is paralysis followed by death of the target parasite. In addition to paralysis, disruption of reproductive function in ticks has been elucidated with avermectins. In addition to the effect on glutamate-gated Cl^--channel receptors, avermectins bind with high affinity to GABA-gated Cl^--channels in nematodes and insects and block the transmittance of electrical activity in nerves and muscle cells. Avermectin also stimulate the release and binding of gama-aminobutyric acid (GABA) at nerve endings. The GABA-receptor mediated hyperpolarisation, however is less well defined.

Avermectin and milbemycins are not active against cestodes and trematodes presumably because these parasites lack a receptor at glutamate-gated chloride channel. The lack of toxicity in mammals is explained by absence of avermectin sensitive glutamate gated Cl^—channels in mammals and low affinity of mammalian GABA receptors to macrocyclic lactones. Further, inability of the drugs penetrate blood-brain barrier and reach CNS where the mammalian glutamate and GABA receptors are located makes the avermectin and milbemycins safe in mammals.

Development of resistance or relative unresponsiveness to avermectins action has been described in some nematodes. Alteration in genes encoding ATP-dependent P-glycoprotein transports which bind avermectins or changes in component of glutamate-gated Cl^--channel receptors are primarily associated development of drug resistance.

Clinical Uses

Ivermectin is a commonly used endectocide in veterinary medicine. It is useful against GI roundworms and lungworms in horses, ruminants and pigs and heartworms (mainly preventive) in dogs and cats. It is also used as an ectoparasiticide against mange mites, lice, grubs and horn flies.    

Adverse effects

Ivermectin has a high margin of safety (T.I. >30) in cattle. In horses, swelling and pruritus at the ventral mid-line may be seen about 24 hour after ivermectin dosing due to a hypersensitivity reaction to dead parasites. In dogs, toxicity is predominantly seen in rough-haired Collie breed but may occur in other breeds as well (e.g. Australian Shepherd and Shetland sheepdog). The increased sensitivity of some breeds of dogs is related in mutation in a gene named MDRI that encodes for the membrane pump P-glycoprotein in the blood-brain barrier. The toxic signs in dogs include mydriasis, salivation, ataxia, tremors, paresis, stupor, recumbency and coma. Dogs may also exhibit a shock-like reaction when ivermectin is used as a microfilaricide, presumably due to hypersensitivity reaction associated with dying microfilaria. Neonatal pigs are more susceptible to ivermectin toxicity presumably due to more permeability of blood-brain barrier to ivermectin. Ivermectin in birds has been associated with lethargy and anorexia. Kittens are also very sensitive.

Treatment

Overdosage of ivermectin may be treated by supportive and symptomatic therapy. Intravenous administration of physostigmine may provide some relief for dogs suffering from severe ivermectin toxicity.

Contraindication and Precautions

Ivermectin should not be used in Collies or Collie-mixed breeds, unless alternative therapies are unavailable. It is not recommended for calves less than 12 weeks and puppies less than 6 week of age. The injectable products for use in cattle and swine should be given SC only; IV or IM injection is not advised. In horses, ivermectin is used only by oral route.

Drug Interaction

Ivermectin does not show interaction with commonly used drugs.   

 Cefpodoxime  is an oral third generation cephalosporin antibiotic. It is marketed as the pro-drug cefpodoxime proxetil to improve oral absorption. The oral absorption of cefpodoxime proxetil in dogs is about 60%, and half life in dogs is about 6 hours and in horses is 7 hours. 

Antibacterial Spectrum

It is less active against gram-positive cocci and more active against streptococci, Enterobacteriaceae and β-lactamase producing H. influenza. It has slightly more active against Staphylococcus aureus.

Clinical Uses

Cefpodoxime is indicated for treatment of skin and other soft tissue infections in dogs caused by susceptible bacteria.

Mechanism of Action

All cephalosporins are bactericidal. They inhibit bacterial cell wall synthesis in a manner similar to that of penicillins. However, they bind to different proteins than those required by penicillins and are less susceptible to penicillinases. Like other beta-lactam antibiotic, cephalosporins are generally considered to be more effective against actively growing bacteria.

Adverse effects

The cephalosporins are relatively non-toxic antibiotics with relatively low frequency of allergic reactions. Hypersensitivity reaction, if occurs, is similar to that produced by penicillins with manifestations of rashes, fever, esinophilia, lymphadenopathy, or full-blown anaphylaxis. About 10% of the penicillin sensitive individuals show some cross-reactivity to cephalosporins. Other adverse reactions associated with cephalosporins in animals may include GI disturbances (nausea, vomiting and diarrhoea), superinfection, pain at IM injection site and lethargy. Prolonged treatment with cephalosporins in man has been associated with interstitial nephritis, hepatitis, thrombocytopenia and neutropenia.

Contraindications and Precautions

Like Penicillins, cephalosporins are contraindicated in patients those are hypersensitive to them or penicillins. Prolonged administration of cephalosporins should be avoided in animals, particularly cats, as they may lead to anaemia or superinfection. Cephalosporins should be used with caution in pregnant animals as they cross placenta and reach foetal tissues. Dosage adjustment may be required in patients with renal insufficiency.

Drug Interactions

Drug interaction of cephalosporins are generally similar to those of penicillins. Concomitant use aminoglycosides and loop diuretics (e.g. furosemide) appears to potentiate the nephrotoxic effect of cephalosporins. Bacteriostatic agents (e.g. chloramphenicol) interfere with bactericidal action of cephalosporins, thus their concurrent administration should be avoided. Probenecid administered concurrently with cephalosporins increases and prolongs plasma level by competitively inhibiting renal tubular secretion.

Brand Name

WigShield

Enrofloxacin is a prototypical veterinary fluorinated quinolone developed exclusively for use in animals. It occurs as a pale yellow, crystalline powder that is slightly soluble in water. Enrofloxacin is related structurally to the human-approved drug ciprofloxacin, having an additional ethyl group on the piperazinyl ring. Like other quinolones, inhibition of DNA gyrase in susceptible bacteria is the primary mechanism of action.

Antimicrobial spectrum

Enrofloxacin has good activity against some gram-positive organism and many gram-negative bacilli and cocci including most species strains of Pseudomonas, Klebsiella, E.coli, Enterobacter, shigella, Camphylobacter, Salmonella, Haemophilus, Proteus, Serratia, Citrobacter, Yersinia and Vibrio. Other organisms susceptible to enrofloxacin include Brucella, Chlamydia, Staphylococcus and Mycobacterium species.

Pharmacokinetics

Enrofloxacin is well absorbed after oral administration with bioavailability of about 80% in dogs, 60% in adult horses and 40% in foals. The peak plasma concentration is attained within one hour of oral dosing. Absorption of enrofloxacin is nearly complete from IM or SC injection. It is distributed throughout the body including bone, synovial fluid, prostrate, aqueous humour and pleural fluid. It also accumulates in very high concentrations in WBCs. Enrofloxacin is eliminated primarily unchanged in urine, although up to 25% of the drugs is metabolised to active metabolite ciprofloxacin, which is subsequently metabolized to inactive metabolites. The elimination half-life of enrofloxacin in dogs and cats is approximately 4-5 hours and 6 hours, respectively.

Adverse effects

Adverse reactions to the enrofloxacin are limited. Cartilage deformities and joint growth disorders have been documented in young dogs, so it is contraindicated in growing dogs. Gastrointestinal disorders( vomiting and anorexia), crystalluria and CNS disorders (dizziness, stimulation) are similar to other fluorinated quinolones. Acute blindness has been reported in cats receiving high doses of enrofloxacin as it is retinotoxic.

Contraindications and precautions

Quinolones are contraindicated in patients hypersensitive to the group. They are not recommended in growing dogs under 12 (small medium breeds) to 18 (large breeds) months of age due to inhibition of the growth of load bearing articular cartilage. They should be used with extreme care in pregnant animals and in patients with seizures disorders. As quinolones have tendency to cause crystalluria in acid urine, animals should not be allowed to become dehydrated. Patients with renal insufficiency may require dosage adjustments to prevent drug accumulation. Quinolones should not be used in patients with a know predisposition to arrhythmias (e.g. hypokalaemia and bradycardia) or in patients those are receiving antiarrhythmic drugs or other medications which might prolongs the QTc.  

Drug Interactions

Quinolones are potent chelators of Mg⁺⁺, Ca⁺⁺, Zn⁺⁺, Fe⁺⁺, and Al⁺⁺⁺,  so products containing multivalent  cations, including sucralfate, non-systemic antacids, nutritional supplements, and multivitamin and mineral supplements taken within two or four hours of orally administered quinolones may interfere with their absorption. Probenecid is reported to block tubular secretion of some quinolones and may increase their blood levels and half-lives. Quinolones inhibit biotransformation of theophylline, resulting in its prolonged and potentially toxic levels. The combination of fluorinated quinolones with non-steroidal anti-inflammatory drugs increases the potential of fluoroquinolones to lower seizure threshold. Simultaneous use of corticosteroids has been associated with almost one-third of quinolones-associated tendon rupture in animals. A synergistic effect of quinolones with beta-lactam, aminoglycoside, clindamycin or metronidazole antibacterials has been reported.

Clinical Uses

Enrofloxacin is approved for use in dogs and cats and some other species like cattle, swine and poultry for the treatment of diseases caused by organisms susceptible to it. The treatment includes infections of skin, urinary tract and soft tissues in dogs and cats. The activity against mycoplasma suggests usefulness in respiratory diseases in cattle and enzootic pneumonia in pigs. Enrofloxacin is also recommended in most exotic animal species because of its safety and activity against a variety of pathogens.  

Brand Name

Enrox 

 Chlorphenamine (chlorpheniramine) maleate is an alkylamine H₁ receptor antagonist. Chlorpheniramine is among the most potent and most selective H₁ antagonist (relative selectivity for H₁:H₂ receptors is 15000:1). In addition to being histamine H₁ receptor antagonist, chlorphenamine has been shown to work as a serotonin-norepinephrine reuptake inhibitor(SNRI). It has less sedative effect and is not likely to produce intense drowsiness.

Pharmacokinetics

Chlorphenamine  maleate is well absorbed after oral administration, but undergoes some degree of first pass metabolism in liver. It is well distributed in body, metabolised mainly in liver and excreted both as metabolites and unchanged drug in the urine.

Mechanism of Action

The H₁ receptor antagonists do not influence formation or release of histamine, but they antagonise actions of histamine at H₁-receptor sites. These drugs block all actions of histamine except for those mediated solely by H₂-receptors. In recent years, it has been shown that these drugs are actually H₁-receptor inverse agonist rather than H₁-receptor antagonists as they stabilise the H₁-receptor in inactive state. However, the older concept still prevails and even today they are commonly called H₁-receptor antagonists. In addition to H₁ blocking action , many of these drugs tend to block muscarinic receptors and few drugs also antagonise adrenergic or serotonin receptors.  

Clinical Uses

Chlorphenamine maleate is one of the most commonly used antihistamines in small-animal veterinary practice. It is commonly used as premedication for drugs which may induce an anaphylactic reaction(e.g. cytotoxic drugs), to control pruritis in allergic skin disorders, and in behavior modification programmes. Although not generally approved as an antidepressant or anti-anxiety medication, chlorphenamine appears to have these properties as well. Chlorphenamine is often combined with phenylpropanolamine to form an allergy medication with both antihistamine and decongestant properties. It is also combined with cough suppressant dextromethorphan to produce antiallergic and antitussive effects.

Adverse effects

Important adverse effects of chlorphenamine include CNS depression and GI disturbances.

Mechanism of Acion 

The non-steroidal anti-inflammatory drugs act primarily by inhibiting the synthesis of prostaglandins, the mediators involved in nociception and pathogenesis of inflammation and fever.  These drugs block the cyclooxygenase (COX) enzyme either reversibly (e.g. most NSAIDs) or irreversibly (e.g. aspirin) causing inhibition of synthesis of prostaglandins (PGs), prostacyclin (PGI₂) and thromboxane A₂ (TXA₂). This mechanism of action was elucidated by John Vane (1927-2004), who received a Nobel Price for this work in 1982. Cyclooxygenase enzyme occurred in two isozymes: cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). The COX-1 is a constitutive enzyme and is considered to be necessary for normal homeostasis, while COX-2 is mainly inducible (induced by cytokines such as IL-1 in inflammation) and is considered to be associated with inflammation and pain. Most of NSAIDs inhibit both COX-1 and  COX-2 non-selectively, although ratio for the inhibition of COX-1 : COX-2 varies widely being high for aspirin, phenylbutazone and piroxicam, and low for naproxen, carpofen and meloxicam. Some newer NSAIDs (e.g. celecoxib, rofecoxib and firocoxib) selectively inhibit COX-2. The relatively bulky structure of COX-2 inhibitors prevents COX-1 inhibition by steric hindrance. Most of the toxic effects (e.g. GI irritation, retinotoxicity and interference with clotting mechanism) of non-selective inhibitors of COX-1 and COX-2 are due to inhibition of COX-1, while desirable anti-inflammatory and analgesic actions are attributable to blockade of COX-2 also has some constitutive functions associated with renal, nerve, brain, ovaries, uterus and bones; therefore the associated side effects with these system may not be completely eliminated with selective COX-2 inhibitors.

Other proposed mechanisms of action for some NSAIDs include inhibition of neutrophils function, blockade of oxygen radical production, stabilization of lysosomal enzymes, antagonism of bradykinin release, modulation of nitric oxide synthesis, alteration of signal transduction mechanisms, or inhibition of metalloproteinase activity. Some NSAIDs (e.g. aspirin) are reported to influence cytokines production. Non-steriodal anti-inflammatory drugs (except licofelone), however, do not inhibit lipoxgenase production and hence do not suppress leukotrienes formation; rather there may be more formation of leukotrienes due to more availability of arachidonic acid substrate.

Analgesia

Non-steroidal anti-inflammatory drugs produce analgesic effect mainly by inhibiting production of prostaglandins and by decreasing sensitisation of pain receptors to noxious stimuli. Prostaglandins (mainly PGE₂ and PGI₂ ) sensitize the nociceptive  afferent nerve terminals to mediators like bradykinin, cytokines (e.g. TNF-α, IL-1 and IL-8)  and some other algesic agents, so that even a small concentrationof algesic agent produces intense pain. The capacity of prostaglandins to sensitize pain receptors to mechanical stimuli appears to result from lowering  of the threshold of the polymodal nociceptors of C-fibers. Non-steroidal anti-inflammatory drugs are, therefore, mainly effective against those types of pain in which prostaglandins act to sensitize nociceptors, namely pain associated with inflammation or tissue damage. NSAIDs do not affect the hyperalgesic or the pain caused by direct action of prostaglandins. Some agents (e.g. aspirin) may also depress pain stimuli at subcortical site (thalamus and hypothalamus).

Antipyresis

Normal body temperature is regulated by a centre in the hypothalamus, which ensures a balance between the heat loss and heat production. During infection ( also tissue damage, inflammation or other disease states), there is enhanced generation of cytokines like interleukins (e.g. IL-1β and IL-6), interferons and tumour necrosis factor (TNF-α) which include PGs production, especially PGE₂ , in and near hypothalamic area. The PGE₂ via increase in cyclic AMP triggers the hypothalamus to elevate the set point at which body temperature is regulated resulting in fever. Cytokines either directly or indirectly through induction of PGs (mostly) stimulate also the vasomotor centre in the CNS resulting in sympathetic nerve stimulation, peripheral vasoconstriction, decrease in heat dissipation or fever. Non-steroidal anti-inflammatory drugs apparently reset the ‘set point or thermostat’ and also increase heat loss through peripheral vasodilatation by inhibiting synthesis of prostaglandins. Non-steroidal anti-inflammatory drugs do not influence body temperature when it is elevated by factor such as exercise or rise in ambient temperature. The NSAIDs reduce body temperature in fever, but do not cause hypothermia in normothermic individuals.

Anti-inflammatory effect

Inflammation is a complex process that occurs due to participation of a large number of vasoactive, chemotactic and proliferative factors at different stages. Prostaglandins, leukotrienes, platelet activating factor, cytokines and other mediators are released by a host of mechanical, thermal, chemical, bacterial and other insults which contribute to the genesis of inflammation. Although PGs do not appear to have direct effects on vascular permeability and inflammation, PGE₂ and PGI₂ markedly enhance oedema formation and leucocyte infiltration

 Meloxicam is a recently developed congener of piroxicam that exhibits anti-inflammatory, antipyretic and analgesic activities. Meloxicam has greater in vivo inhibitory action against the inducible COX-2, which is implicated in the inflammatory response than COX-1. In animal studies, a COX-2:COX-1 selectively of 11-14 times has been measured. Accordingly, the anti-inflammatory efficacy of meloxicam has been found to be similar to piroxicam, while GI and renal side effects are significantly less. The elimination half-life of meloxicam is reported to be shorter in horses (~3 hours) and pigs (4 hours), while it is longer in dogs (12-36 hours), cattle (~13 hours) and man (20 hours). Oral absorption is almost complete in dogs when administered with food.

Clinical Uses

In veterinary medicine, meloxicam is used mainly in dogs for relieving pain and inflammation associated with osteoarthritis and synovitis. It is also used as an antipyretic in dogs and cats. In pigs, meloxicam has been recommended for the treatment of mastitis-metritis-agalctia syndrome. In horses, meloxicam is for treating pain and inflammation associated with surgery. It is also used for treatment of some other condition such as mastitis in cattle and diarrhoea in calves.

Adverse effects

Meloxicam has fewer gastrointestinal side effects than piroxicam and perhaps other NSAIDs which are not COX-2 selective. However, similar to other NSAIDs, gastrointestinal toxicity (inappetance, vomiting, and diarrhoea), and bleeding may occur after prolonged use or in high doses.

Precautions

Meloxicam use should be avoided for treatment of diarrhoea in calves less than one week of age and in cats less than 2 kg body-weight. Meloxicam is mostly given by addition to food or soon after feeding.

 Cefotaxime is a semi-synthetic antibiotic that is considered as the prototype of the third-generation cephalosporins. It has relatively wide spectrum of activity. It generally has good coverage against most Gram-negative bacteria. It is also effective against most Gram-positive cocci except for Entercoccus. It is active against penicillin-resistant strains of streptococcus pneumonia. However, it is not so active on anaerobes particularly Bacteriodes fragilis, Pseudomonas aeruginosa and Staphylococcus aureus. It is highly resistant to many, but not all, bacteria β-lactamases.

Pharmacokinetics

Cefotaxime sodium is not appreciably absorbed after oral administration and must be given parenterally. After IM OR SC injection, cefotaxime is well absorbed(>90%) and distributed into body fluids and tissues. It is partially metabolized in vivo to desacetylcefotaxime, which is less active than the parent compound. The desacetylcefotaxime may act synergistically with parent compound against some susceptible bacteria. The desacetylcefotaxime is further metabolized to inactive metabolites which along with unmetabolised cefotaxime are excreted in the urine. The plasma half-life of cefotaxime is about 45-60 minutes in dogs and cats, but the deacetylated metabolite may permit longer dosing intervals in some cases.

Mechanism of Action

All cephalosporins are bactericidal. They inhibit bacterial cell wall synthesis in a manner similar to that of penicillins. However, they bind to different proteins than those required by penicillins and are less susceptible to penicillinases. Like other beta-lactam antibiotic, cephalosporins are generally considered to be more effective against actively growing bacteria.

Clinical Uses

Cefotaxime is used for infections of the respiratory tract, skin, bones, joints, urogenital system, meningitis and septicemia. In Veterinary medicine, cefotaxime sodium is primarly used in the treatment of gram-negative meningitis in small animals. It is also used in other veterinary species when an injectable third-generation cephalosporin is indicated.

Adverse effects

The cephalosporins are relatively non-toxic antibiotics with relatively low frequency of allergic reactions. Hypersensitivity reaction, if occurs, is similar to that produced by penicillins with manifestations of rashes, fever, esinophilia, lymphadenopathy, or full-blown anaphylaxis. About 10% of the penicillin sensitive individuals show some cross-reactivity to cephalosporins. Other adverse reactions associated with cephalosporins in animals may include GI disturbances (nausea, vomiting and diarrhoea), superinfection, pain at IM injection site and lethargy. Prolonged treatment with cephalosporins in man has been associated with interstitial nephritis, hepatitis, thrombocytopenia and neutropenia.

Contraindications and Precautions

Like Penicillins, cephalosporins are contraindicated in patients those are hypersensitive to them or penicillins. Prolonged administration of cephalosporins should be avoided in animals, particularly cats, as they may lead to anaemia or superinfection. Cephalosporins should be used with caution in pregnant animals as they cross placenta and reach foetal tissues. Dosage adjustment may be required in patients with renal insufficiency.

Drug Interactions

Drug interaction of cephalosporins are generally similar to those of penicillins. Concomitant use aminoglycosides and loop diuretics (e.g. furosemide) appears to potentiate the nephrotoxic effect of cephalosporins. Bacteriostatic agents (e.g. chloramphenicol) interfere with bactericidal action of cephalosporins, thus their concurrent administration should be avoided. Probenecid administered concurrently with cephalosporins increases and prolongs plasma level by competitively inhibiting renal tubular secretion.

Brand Names

Taxim

 

Affected animal - Female goat

History - The goat had this symptoms, after parturition.

SYMPTOMS

    1.The muscles are contracted.

    2.The third eyelid droops.

    3.Lock jaw, saliva drools.

    4.The animal falls and it cannot rise again.

    5.Neck show opisthotonous or orthotonus.

    6.The fore legs are extended stiffly forward and the hind legs backward.

PATHOLOGICAL CONDITION

     The pathological condition of the symptoms mentioned above for the goat was TETANUS. 

     Tetanus(synonym - Lockjaw) is a highly fatal infectious disease caused by the exotoxin of clostridium tetani, a gram positive, sporulating  anaerobe. The spore are terminal giving the organism a drum stick appearance.

SUSCEPTIBILITY

     Horse and mules are more susceptible. Sheep, goat, dogs and swine may also be infected. Mice, rabbits, guinea pigs and rats are susceptible. Cattle are least susceptible. Birds are resistance.

ROUTES OF INFECTION

     Wound infection, surgical wound, deep punctured wound(horse gathered nail), particularly, are more conducive for the growth of the organism affording anaerobic environment. Wounds that occur during shearing, docking, and parturition in females and through the umbilical vein in young. The organism is voided with the dung and so it is found normally in the soil and stables.

PATHOGENESIS

     The spores that enter a wound require certain favourable conditions to vegetate and liberate the toxin. When necrosis or hemorrhage or other aerobic and pyogenic bacteria are present, producing anaerobiasis, the spores vegetate. The organisms liberate the toxin locally. This toxin consists of three components.

    1. a hemolysin - tetanolysin, which is not of much importance.

    2. a neurotoxin - tetanospasmin, Which is responsible for the nervous symptoms.

    3. A fibrinolysin, which is not very potent.

The toxin is absorbed by the axons of the peripheral nerves. It passes with the intercellular fluid along the interneural spaces  centripetally to the neurones of the spinal cord and the brain. This passage centripetally is brought about by the pressure exerted during muscular contraction. The toxin may reach the CNS by way of blood also. The exact action of the toxin on the nervous system is not known. The tetanus toxin gets fixed to a substance called PROTAGON in the nervous tissue. The protagon is a complex made up of cerebroside plus oligosaccharides like N-acetyl galactosamine and galactose. It acts on the inhibitory synapses interfering with the action of the inhibitory transmitter thus producing spastic action. The toxin causes hyperirritability responsible for the tetanic spasms.

INCUBATION PERIOD

      One to three weeks. 

LESIONS

      No characteristic lesions are found.

DIAGNOSIS

      There are no tests to confirm a diagnosis. The organism is local and does not become septicemic. Symptoms alone are helpful.

 

 

 The following nutrient is not dietary essential for dogs *

·         Fat

·         Protein

·         Vitamin

·         Carbohydrate

 

Which among the following is a Non-ruminant *

·         Deer

·         Guar

·         Zebra

·         Girafee

 

Rhinoceros is a *

·         Carnivore

·         Fore gut fermenter

·         Hind gut fermenter

·         Ruminant

 

Daily feed intake(grams) in laboratory mice under normal condition is *

·         15 to 20

·         2 to 5

·         5 to 10

·         10 to 15

 

Feather pecking in birds is due to *

·         Deficiency of protein

·         Excess of protein

·         Deficiency of fibre

·         Excess of fibre

 

Which among the GI Tract part is larger in horse *

·         Small Intestine

·         Stomach

·         Oesophagus

·         Large Intestine

 

Net energy requirement (Kcal) for maintenance per kg metabolic body weight in layers is *

·         62

·         72

·         82

·         92

 

Example of Methyl Donor is *

·         Betaine

·         Inulin

·         Bentonite

·         Monensin

 

Thumps is due to *

·         Copper deficiency

·         Iron deficiency

·         Thiamine toxicity

·         Iodine toxicity

 

Cat is *

·         Grainivore

·         None of the above

·         Obligate carnivore

·         Herbibore

 

Colic in horse is due to *

·         Low fat intake

·         High forage intake

·         High protein intake

·         High grain intake

 

Which among the following is Omnivore *

·         Fox

·         Ferret

·         Monkey

·         Gangaroo

 

Ideal Feed Conversion Ration in broiler chicken is *

·         3 : 1

·         1.6 : 1

·         2 : 1

·         1 : 1

 

Big head disease in horse is caused by *

·         All the above

·         High Phosphorus intake

·         Low Calcium in the diet

·         High bran intake

 

Dry matter intake in adult horse for maintenance is *

·         4 - 6 % of its body weight

·         0.5 - 1.5 % of its body weight

·         3-4 % of its body weight

·         1.5 - 2.5 % % of its body weight

 

Calcium to Available phosphorus ratio to be maintained in Layer Phase I ration is *

·         5 : 1

·         2 : 1

·         7.5 : 1

·         10 : 1

 

The material added as source of protein in pure diet for laboratory animal is *

·         Carboxy methyl cellulose

·         Starch

·         Casein

·         Sucrose

 

Ideal protein concept is based on requirement of essential amino acids in proportion with *

·         Threonine

·         Tryptophan

·         Methionine

·         Lysine

 

Parakeratosis in swine is due to deficiency of *

·         Zinc

·         Copper

·         Pantothenic acid

·         Iodine

 

Gall bladder is an essential organ for fat digestion in horse *

·         True

·         False

 

Cheapest ration for pig is swill feed *

·         True

·         False

 

Caecotrophy is the practice of consuming hard faecal material in rabbits *

·         True

·         False

 

Reptiles are mostly carnivores in nature *

·         True

·         False

 

Elephant is a ruminant and hind gut fermenter *

·         True

·         False

 

Birds can taste four primary flavours as human with considerably higher acuity *

·         True

·         False

 

Vitamin C plays major role in collagen synthesis in body of chicken

·         True

·         False

 

Fibre digestion takes place in the later part of intestine in horses *

·         True

·         False

 

Maximum permissible level of Aflatoxin B1 in poultry feed is 20 mg/kg feed *

·         True

·         False

 

Taurine is dietary essential fatty acid for cats *

·         True

·         False

 

Match the following I *

·         Soya bean meal         -  Lysine

·         Groundnut oil cake    -  Arginine

·         Wheat                        -  Biotin

·         Encephalomalacia     -  Tocopherol

·         Curled toe paralysis  -  Riboflavin

 

Match the following II *

·         Vitamin A                  -  Cat

·         Founder                     -  Horse

·         Creep feed                -  Piglet

·         Omnivore                  -  Bear         

·         Hind gut fermenter   -  Guineapig