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Botulism

2020-03-27T12:58:00.000+05:00

BOTULISM

Synonyms: Equine grass tetany, Equine dysautonomia, Limber neck, and Shaker foal syndrome.

INTRODUCTION AND ETIOLOGY

Introduction

Clostridium botulinum produces potent neurotoxins during their vegetative transformation.
The vegetative cells multiply rapidly and elaborate a stable and highly lethal toxins types such as B, C, and D which when ingested or absorbed by tissues develops botulism.
Preformed toxin is the main source of intoxication.
Botulism causes toxemia and flaccid paralysis in humans, animals, and birds.

Etiology

Clostridium botulinum is a spore (oval, subterminal endospores) forming, gram the positive organism appears as single/paired/short chain.

It does not grow up in animal but on decaying organic matters
Spores survive for a long time in the environment. It remains in the intestine as normal inhabitant in cattle and sheep.
Seven Antigenically distinct toxin types (A-G) are identified.
In farm animals, the disease is produced primarily by types B, C, and D.
Type-A- is present in neutral or alkaline soil.
Type–B– and E – in damp or wet soil.
Type–C- in acidic soil - subtypes Ca, Cb.
Type–D– alkaline soil.
Clostridial multiplication is inhibited at >pH 4.5.
A-E type toxins are pathogenic for mammals.

EPIDEMIOLOGY

Prevalence of infection

Spores survive in the environment for long period.
The disease is distributed worldwide, including India.

Predisposing factors

Heat and moisture favors the germination of spores.

Source of infection

The proliferation of the organism occurs in decaying vegetable or animal matters.
The toxin is stable particularly in bones.
In sheep, due to dietary deficiency of protein or net energy.
Phosphorous deficient cattle or sheep chew and ingest dead carcass, bones, debris and get the highest possible infection.
Meat and milk containing toxin causes public health hazards.

TRANSMISSION

Transmission

The spread of infection by ingestion of contaminated material or birds or blow flies are possible.
Spread of infection through injury.

Host affected

Cattle and sheep are susceptible to type C and D while horses are susceptible to type B toxin.
Pigs, dogs and cats found to be resistant.
Human is also susceptible for bolutinum toxins.

PATHOGENESIS

Pathogenesis

Botulism toxins are neurotoxins absorbed by the intestinal tract or the wound and traverse through the bloodstream to peripheral cholinergic nerve terminals and neuromuscular junction, postganglionic parasympathetic nerve endings and peripheral ganglia.
The toxin has heavy chain binds to the receptors and translocated into the cells and the light chain of the toxin blocks the release of acetylcholine at the neuromuscular junction/motor nerve endings.
Toxins produce functional flaccid paralysis.
Animal dies due to respiratory paralysis.

Types of botulism

Carrion associated botulism: Multiplication of the organism in the feed produce toxin and is mostly consumed by phosphorous deficient and protein deprived animals.
Wound botulism: The organisms produce toxins directly in the wounds.
Toxico-infectious botulism: The organism grows and produces a toxin in the alimentary tract.

Forage botulism: Most cases of botulism is associated with the ingestion of preformed toxin in forages.

CLINICAL SIGNS

Cattle and horses

The incubation period is 3-17 days.
After exposure to toxic material even within a day the clinical signs may appear.
It maybe depends on the amount of toxin released and ingested.
Toxico-infectious botulism can also be a cause for “equine grass tetany” (equine dysautonomia).

Peracute

No rise of temperature or clinical signs seen.
Animals die immediately.

Acute

One of the most important signs is the development of progressive symmetric, muscular paralysis of the limb muscles and the muscles of the jaw, tongue, throat and muscle weakness.
Paralysis starts in the mid quarters and proceed to the forequarters, followed by head and neck.
Muscle weakness, an obvious muscle tremor and fasciculation may be enough to cause limb tremor.
Colic in the horse is an important sign.
Partial or complete paralysis of muscles of locomotion.

Subacute

Restlessness, respiratory distress, disinclination to rise, pronounced roaring sound and persists up to 3 months in some animals.
In-coordination, stumbling, knuckling, ataxia, inability to raise or to lift the head, mydriasis, and ptosis occur early.
Difficulty to take hay for 3 weeks.
Mydriasis is prominent in type-C botulism in horses.
Sternal recumbency, turning of head-on the ground or into the flank.
Reduced tongue tone, paralysis, tongue hangs out from the mouth, difficulty in chewing, or swallow and drooling of saliva is prominent.
Depression of rumen motility and constipation present.
Paralysis of chest muscles results in terminal abdominal type respiration.
Animals is alert and consciousness until at the end or death.

Foals

Toxico-infectious botulism in foals by type-B toxin.
In young foals of up to 8 months highest prevalence occur.
The multiplication of organism in the intestine and production of toxins causes the disease called “shaker foal syndrome”.
Type–B toxin has been isolated from feces of naturally infected animals.
Muscle tremor is a prominent early sign.
If the foal walks, show stiff gait, a stilted gait, dragging of toes and drooling of saliva from mouth.
Attempts to eat hay but regurgitate it through nostrils.
Constipation occurs consistently.
Rapid progression to severe muscular weakness, prostration, loss of condition and unable to rise .
Prostrate foals are bright and alert have normal sense, pain perception, dilation of pupils with a sluggish pupillary light reflex and in later period, complete cessation of peristaltic movement.
Temperature varies from slightly elevated to depressed.
Death occurs in 72 hours after the onset of signs due to respiratory failure.

Sheep

Affected sheep do not show typical flaccid paralysis.
Stiffness while walking, in-coordination and excitability in the early stages noticed.
Head held on one side or bobbed up and down while walking (Limber neck).
Lateral switching of tail, salivation and serous, nasal discharge are common.
Terminal abdominal respiration, limb paralysis followed by rapid death.

Pigs

Affected pigs show staggering, recumbency, vomiting, pupillary dilatation, flaccid paralysis of the muscle, anorexia, and adypsia.

Dogs

In dogs, symptoms develop more quickly, within 12-36 hours after exposure to the toxin.
There is generalized weakness, paralysis which spread from the hind limbs to the forelimbs.
In addition, increased respiratory effort, facial nerve paralysis, and difficulty in swallowing.
The disease progresses to fatal respiratory failure.

Zoonosis

Botulism toxin is an agent of bio-terrorism.
Meat and milk containing toxins should not be used for human consumption.
Human get infections by eating improperly cooked meat, its products, and milk.

NECROPSY FINDING

Necropsy findings

Non-specific sub endocardial, sub epicardial hemorrhages and congestion of intestines found.
Non-specific perivascular haemorrhages in the corpus stratum, cerebellum, and cerebrum present.

DIAGNOSIS

Based on clinical signs and necropsy findings.
Demonstration of toxin in serum, feed, intestinal contents and from wounds.
In foals arterial blood analysis show acidemia, hypercapnia, hypoxemia and desaturation of Haemoglobin.
Repeated arterial blood gas analysis should be conducted during the first 48 hours of treatment.
Demonstration of spores of Cl.botulinum in the feed.
Mice: Injected with toxin and neutralized with polyvalent antitoxin.
But the sensitivity is low in mice as compared to ruminants and horses to botulism toxin.
In chronic/sub-acute condition, ELISA is used for the detection of type C and D in cattle.

Samples collection

Suspected contaminated feed material, liver, rumen contents, and serum etc.
Formalin-fixed brain.

Differential diagnosis

Ruminants

Parturient paresis in cattle.
Hypocalcemia in sheep.
Tick paralysis.
Rabies.
Organophosphate or carbomate poisoning.
Louping ill.

Horses

Equine protozoan myelitis.
Equine encephalomyelitis.
Hepatic encephalopathy.
Rabies.

TREATMENT

Early administration of antitoxin before complete recumbency.
Supportive therapy includes fluid therapy, parenteral feeding, nasal in-sufflation with oxygen and mechanical ventilation.
Although it is expensive, a single dose of specific or polyvalent antiserum administrated early in the course with 30,000IU for a foal and 70,000IU for adult horses may increase the survival rate.
Antimicrobials for treating secondary complications such as aspiration pneumonia.
Avoid the use of drugs that may deplete the neuromuscular junction of acetylcholine such as neostigmine and that procaine penicillin, tetracyclines, aminoglycosides potentiate neuromuscular weakness.
Muzzling is essential to prevent aspiration pneumonia.
Frequent turning to prevent the development of muscle necrosis and decubital ulcers.

PREVENTION AND CONTROL

Prevention

In enzootic area animals vaccinated with type-specific combined C and D toxoid for occasions at bi-weekly intervals.
Stocks should be rigorously vaccinated with a toxoid on 3 occasions at 2 weeks intervals.
Carrion verses non-carrion associated botulism is an important factor when considering prophylactic vaccination program.

Control

Hygienic disposal of carcasses.
In horses as the disease is sporadic caused by accidental contamination of food and water must be curtailed.
Range animals - supplementation of feeds with phosphorous and/or protein.

Anthrax

2020-03-24T17:49:00.002+05:00

ANTHRAX

Synonyms

Splenic fever, Milzbrand, Charbon, Wool sorters disease, and Malignant carbuncle.

Introduction

It is a peracute, acute and septicaemic disease of cattle and sheep leading to sudden death.
The extensive enlargement of the spleen given this disease the name splenic fever.
It is a zoonotic disease spread from infected animals to human during processing of wool and hides.

Etiology

Bacillus anthracis is a pathogenic strain causing anthrax in both human and animals.
It is a non-motile, capsulated, aerobic, spore-forming, gram-positive, organism.
Appears as straight, very large rod-shaped, arranged in a small short chain.
The organism has two virulent factors such as a capsule containing poly D-glutamic acid, which resists the phagocytosis induced by the host immune cells and is coded by the virulent plasmid pxo2, and the triple toxins such as edema factor-1, lethal factor-11, and the protective antigen factor- 111 and these are coded by the plasmid pXo1.

The organism produces spores when exposed to the external environment and can live for a prolonged period outside the host in the environment.

EPIDEMIOLOGY

Prevalence of infection

The disease is reported to be recognized from sub-Saharan Africa and has worldwide distribution.
The prevalence of the disease depends upon the nature of the soil and climatic condition, because, the climatic parameter helps to forecast the “anthrax year”.
If the infection is restricted to a particular area is called as “anthrax belts” or enzootic region. During heavy and prolonged rainfall, following a draught, or dry summer, in warm weather and in the temperature at which (>60F /15 ° C) formation of spores, vegetative proliferation with the production of disease or the outbreak occurs.
In African countries, every summer with heavy rainfall is followed by a devastating occurrence of anthrax.
In India this is enzootic.

Economic impact

Mortality, reduced milk yield and the expenses incurred for vaccination leads to severe economic loss.

Predisposing factors

pH of the infected soil, infected wool, materials, hides and other materials.
In wet soil, and in stagnant water spores are concentrated and suspended.
Alkaline soil (pH 9.0) under warm climate preserves the organism to develop anthrax but acid soil destroys the organism.
Blood transfusion may also spread the disease.
Contaminated bone meal, pasture contaminated with tannery effluents, fodders grew on infected soil, turning up of soil, blood and other discharges from infected animals are a major source of infection.
Calcium rich alluvial soil, organic and poorly drained soils have the risk of causing endemic infection.

· Source of infection

· Contaminated soil, environment, infected excretions and secretions from animals.

TRANSMISSION

Transmission

Ingestion, inhalation and contamination of the wound by spores are the prime modes of spread.
Injury to oral mucosa permits the invasion of the organism.
Inhalation plays a less important role in animals contrast to more spread in human being and is responsible for causing wool sorters disease.
Mechanical transmission through Tabanid fly bite occurs.

Host affected

Cattle and sheep are highly susceptible as compared to goats and horses.
Human is less susceptible than cattle.
Pigs, dogs and cats are relatively resistant.
But once affected the case fatality rate is high in farm animals and pigs.
Hippopotamus, cape buffalo and elephants die in large numbers due to anthrax.
Persons working in wool and hide industries are mostly affected.
Predators acts as a carrier for this infection.

PATHOGENESIS

Discharges and materials containing anthrax bacilli when exposed to air, spores are produced.
The spores are very resistant in the external environment but the un-germinated spores are considered not harmful it becomes a vegetative form inside the host.
The organism is resistant to phagocytosis due to the presence of poly D glutamic acid-containing capsule, and triple toxin factors such as edema factor-I, lethal factor-II and protective antigen-III.
Primarily, spores proliferate in the regional draining lymph nodes, subsequently, travels via lymphatic vessels and reach the bloodstream and cause septicemia followed by massive invasion into all body tissues.
The lethal toxin of B.anthracis causes edema, tissue damage, and death as a result of shock, acute renal failure, and terminal anoxia. The blockage of capillaries initiating death is commonly known as the “Log Jam” theory.
As per the evidence, at least 3x106 bacteria/ml blood is necessary for causing death.
In pigs, localization of the organism occurs in the lymph nodes of the throat following invasion through the upper part of the digestive tract eventually lead to fatal septicemia.
Shock acute renal failure and terminal anoxia lead to death.

CLINICAL SIGNS AND ZOONOSIS

Cattle and sheep

Peracute form

Sudden death without any premonitory signs. Upon close observation following signs will be seen.
Fever, muscle tremor, dyspnoea, congestion of mucous membranes are noticed.
Animal collapses and die due to terminal convulsions.
After death, oozing of blood from nostrils, mouth, anus and vulva is noticed.

Acute form

Incubation period of the disease is 1-2 weeks.
The course of this form is about 48 hours.
Fever (42°C), severe depression, listlessness, congestion, and hemorrhage of the deep mucous membrane, increased heart rate, and rapid respiration observed.
Affected cattle with mouth breathing due to oxygen hunger.
Abortion, the decrease in milk yield, blood-stained or deep yellow color milk, diarrhea, local edema of the tongue, throat, sternum, perineum and flank occur.

Pigs

Acutely and sub-acutely infected animals show high temperature, appears dull, anorectic with distinct inflammatory edema in throat and face.
Painless swelling causes obstruction which leads to swallowing and respiration difficulty.
Blood stained froth present at the mouth.
Petechial hemorrhages of skin, dysentery without any edema of throat occurs.

Pulmonary form

In baby pigs, it develops lobar pneumonia and exudative pleurisy through inhalation of dust which leads to death in a day or two.
Occasionally, affected individuals may be alive for several days after infection.

Horse

Always horses are affected with acute infection by ingestion and lead to septicemia, enteritis, and colic.
Painful, edematous and subcutaneous swellings appear in the throat over the lower neck, the floor of the thorax, abdomen, prepuce and mammary gland.
There is a high fever, severe depression, dyspnoea due to swelling of the throat or colic due to intestinal irritation.
The course of the disease is about 48-96hours.

Zoonosis

It is a fatal disease of human beings.
B.anthracis is an agent of bioterrorism and listed as category A disease by OIE.

Occupational hazard by inhalation of spores occurs mostly while sorting out wool and processing of hides.

NECROPSY FINDINGS

Absence of rigor mortis with gaseous decomposition, quick assumption of the characteristic sawhorse posture.
Un-clotted tarry colored blood oozes out through natural orifices.
There is a soft and enlarged spleen with a blackberry jam consistency and is an important feature of anthrax.
The carcass suspicious of anthrax should not be opened before confirmation made by peripheral blood smear examination.

In horses and pigs enlargement of local lymph nodes, lesions in the soft tissues of the neck and pharynx are important and it is called a pharyngeal form of anthrax.

DIAGNOSIS

Diagnosis

Based on clinical signs and necropsy findings.
Isolation and identification of the organism.
Haematological and blood chemistry examinations should not be conducted because of the risk for human exposure.
The square-ended blue bacilli (chain) with metachromatic pink capsule detected by microscopic examination after staining with ripened polychrome methylene blue stain is called as 'McFadyean's reaction'.
In early stages bacilli may not be present in the blood, so, culture can be done or the materials like infected fluid can be injected into guinea pigs would give proper diagnostic results.
Fluorescent antibody technique using monoclonal antibody can be done to detect the disease.
In decomposed carcass vegetative bacilli may not be present, in such a condition diagnosis is difficult so that the protective antigen is detected by the immuno-chromatography test. It has high specificity but does not give positive results in recently vaccinated cattle.
Isolation of bacilli from infected soil is difficult but real-time quantitative PCR and Nested PCR have been found highly sensitive.
In human cutaneous anthrax is diagnosed by Immunohistochemical detection of the bacilli in the skin biopsies.
Gelatin stab culture: The growth resembles an 'inverted fir tree appearance' with slow liquefaction commencing from the top.
Nutrient agar media: The 5% blood agar show 'medusa head colonies'.

	B.anthracis Gram stain. Cells : Squared end Endospores: Ellipsoidal shape, Central in the sporangium. Spores are highly refractile to light and resistant to staining.
	B. anthracis Incubation at 5% CO2 tension increase the production of poly-D-glutamyl acid production by capsule thereby mucoid colonies.

	B. anthracis McFadyean's reaction: Cells in short chains with plenty of disintegrated capsular material. White blood cells stained blue.
	B.anthracis: Medusa Head Colonies.
	Anthrax Spore Vaccine It is a nonpathogenic, nonencapsulated variant vaccine strain Sterne 34F2 of B. anthracis spore vaccine in saponin, in India.

Ascoli's test: To demonstrate the antigen in the severely decayed carcass and the skin in which tube containing positive serum is overlayed with suspected sample develops a white precipitation ring at the junction of the two liquids.

Sample collection

Unopened carcass, blood, edema fluid in sealed leak-proof containers and direct smear from the tip of the ears.
In live animals, the organism may be detected in a stained peripheral blood smear, edema fluid, lymph node needle puncture smear, amputated tail or ears and jugular vein aspiration etc.
If anthrax is suspected then shipping of diagnostic samples via air or courier is not permitted.

Differential diagnosis

Lightening strike.
Peracute blackleg.
Malignant edema.
Bacillary hemoglobinuria.
Hypomagnesemia.

TREATMENT

Treatment

Recovery occurs when the infection is identified in the early stages and treated with penicillin 20,000 IU /kg BW twice daily for 3 days.
Streptomycin 8-10g/day in two divided doses IM for cattle is effective.
Oxytetracycline 5-10mg /kg/day IV or IM can be given.

Antiserum is given daily for 5 days, however, itis expensive.

BLACK QUARTER

2020-02-10T23:03:00.003+05:00

BLACK QUARTER

Synonyms : Symptomatic Anthrax, Quarter ill, Black leg, Emphysematous gangrene.

Introduction

It is an acute ,infectious, and fatal disease of cattle, sheep and goats. It spreads rapidly following heavy rainfall.

Affected animals develop skeletal muscle damage, severe gangrenous, necrotizing, emphysematous myositis and a fatal systemic toxaemia.

Etiology

Black Quarter (BQ) is caused by Clostridium chauvoei.
It is a gram positive, spore forming, rod shaped bacteria measuring 0.6µ in dia and 3-8µ in length.
It is a toxin producing anaerobic bacterium.
Spores produced by this organism persists in soil for many years and is highly resistant to disinfectants, dryness and hot.
Spores can withstand 120 degree Celsius for 10 minutes.
The name C. chauvoei came after the Professor J.A.B. Chauveau, a French bacteriologist.
There are 23 strains of C.chauvoei identified so far around the world.
Both natural and accidental hosts are supposed to be affected by these strains.
In India - Strain 49 - used in BQ vaccine production .

Predisposing factors

Occasional outbreak: Damage to tissues caused by administration of formalized vaccines, accidental injury of muscle and injury made by chemical agents.
Cattle: Digging of soil spreads the infection.
Alternate hot and dry seasons followed by heavy rainfall favors the dispersion of spores for long distance.
Turning up of soil expose the spores to the top surface.

Sources of infection

Organism present in decomposed carcass of black leg affected animals and persists in soil for long period.
Sheep: Infection mostly spreads via wound developing during shearing, lambing, castration, docking and navel infection etc., hence, it is called as traumatic BQ.
Inhabitation: Organism exists as normal inhabitant in spleen, liver and alimentary tract of healthy animals and thus the animals may excrete the organisms through their feces.

Transmission

It is transmitted by ingestion, inhalation of spores and absorption of toxins through wound.
Wound contamination by spores especially in sheep and goats is possible.

Host affected

The disease is highly fatal in cattle.
Cattle, 6 months to 2 years and well-nourished are mostly affected.
In sheep all age groups are susceptible.
It is reported also in deer, elephant and horses.

Pathogenesis

Black quarter is a soil borne infection.
Spores ingested would be taken via alimentary mucosa and then distributed to tissues and skeletal muscles via the circulation.
Some of the spores in the muscles are destroyed by phagocytosis and others remain latent for at least several weeks.
Mostly, the organism affects muscles of loin, shoulder and gluteal muscle.
There is necrosis of the muscles and blood capillaries. Gases used to accumulate within the muscle fibres due to fermentation.
If animals consume the preformed toxins while grazing, ingested toxins is directly absorbed and spread along the systemic circulation which leads to fatal toxaemia.
C.septicum is a potent exotoxin producer as compared to C.chauvoei because virulent form of C.chauvoei only able to produce exotoxin. These exotoxin is responsible for the development of edema and pulmonary congestion.
Toxins causes damage to leucocytes, platelets which leads to leucopenia and thrombocytopenia.
Toxins released by the organism produces a severe necrotizing myositis in skeletal muscles and a systemic toxaemia followed by death.

Clinical Findings

Cattle

(1)Peracute form

Affected animals show sudden death.

(2)Acute form

Incubation period is 2 to 5 days.
Disease follows a rapid and fatal course of infection following ingestion of preformed toxins.
Fever may be as high as 106 or 108°F (41°C) but not common, marked depression, anorexia and ruminal tympany.
Prominent swelling on the upper part of the affected limbs leads to marked lameness.
Swelling of throat, tongue and protrusion of the tongue
Swellings are hot and painful in the early stage and become cold and painless later..
Edema, emphysema, crepitation of affected heavy muscles on thigh with muscle stiffness.
Discolored, gangrenous to black, dry and cracked skin.
Increased pulse rate 100 to 120 per minute with labored breathing.
Death follows in 12 to 36 hours of infection.
Cattle with cardiac myositis are found dead.
A thin sanguineous fluid containing bubbles of gas from affected sites.

Sheep

No palpable crepitation swelling as in cattle.
Stiff gait, disinclined to move, severe lameness either unilateral or bilateral.
Painful walking, discoloration of skin with no necrosis and gangrene.
Extensive local lesion in vulva and vagina occurs through skin wounds.
Head swelling leads to hemoptysis, high fever, anorexia, loss of appetite, depression and quick death.
Short course of the disease, dyspnea and recumbancy in 3 to 4 days occurs.

Horses

Pectoral edema, stiff gait and incoordination is recorded (ataxia).

Diagnosis

Based on clinical signs and necropsy findings.
Isolation of organism by culture of heart blood, peritoneal fluid, muscles and liver is important for both Cl.chauvoei and Cl.septicum.
Muscle bundle separation by gas.
Tube agglutination test, counter immuno electrophoresis, double immuno diffusion test used to detect humoral antibody, Immunofluorescence, Fluorescent antibody test to detect antigen.
Biological inoculation: Filtrate containing spores obtained from infected animals heated at 60°C for 30 minutes and injected one ml into glutial muscle of guinea pig leads to death in 48hrs.

Sample collection

Muscle samples should be collected in an air tight container.
Air dried impression smears obtained from surface of freshly cut lesion for bacteriology, 10% formalin fixed samples from suspected muscles for histopathology.
Impression smears of heart blood and liver examination shows numerous gram positive sub terminal spores.

Differential diagnosis

Malignant edema.
Anthrax.
Lightening stroke.
Bacillary haemoglobinuria.

Dairy Books

2020-01-31T23:11:00.001+05:00

What is Downer Cow Syndrome

2020-01-26T01:16:00.000+05:00

What is Downer Cow Syndrome

Cox (1982) proposed that downer cow was any cow which was down in sternal recumbency for more than 24 hours without evidence of a systemic involvement.
Blood et al. (1983) defined the downer cow syndrome is a condition occurring following parturient paresis, characterised clinically by prolonged recumbency even after 2 successive infusions with calcium.
Allen and Davies (1981) suggested that downer syndrome occurred as a result of one of the combination of the factors like milk fever, hypophosphataemia, fat cow syndrome, excessive protein intake, Vitamin E & Selenium deficiency, recumbency due to trauma and malnutrition.
Jonsson (1983) suggested that downer syndrome occurred as a result of one of combination of the factors like muscular injuries, nerve injuries, persistent hypocalcaemia, persistent hypophosphataemia, myocardosis, hepatosis, septic mastitis and other factors.
Jonsson (1983) also observed that 65% cases of injuries of muscles, nerves and hind limbs terminate as downers.
Fenwick (1969) observed that there was definite increase in number of downers and deaths with decreasing potassium concentration.

One of the most challenging problem for Veterinarians is management of recumbent/ downer animals. Prolonged recumbency due to inadequately treated and unresponsive hypocalcaemia is one of the common causes of downers syndrome.

Clinical Signs

The cow may show bright and alert with normal appetite, defecation and urination. Milk production may be reduced.
All the physiological and clinical parameter may be within normal range at the time of presentation such as body temperature 100.5 F, heart rate 56 per minute, pulse rate 66 per minute and respiratory rate 21 breaths per minute.
Cow may show in sternal recumbency and frequently try to get up. She may unable to put up weight on hindquarters.
Cow may able to stand with some assistance by lifting the tail and head or with the help of wooden sticks below thorax and abdomen with precaution to avoid any injury to udder.
All the limbs may be checked for sensitivity to pain by pricking with a needle to rule out nerve paralysis. All the fore limbs and hind limbs may show sensitivity to pain.

Prevention

excellent nutritional management
Adequate bedding in calving area, stalls
prompt treatment of milk fever to avoid prolonged recumbency
Monitor treated cows closely for 24-48 hrs. post-treatment
Prevent trauma
Supervise parturition & provide appropriate assistance to avoid prolonged calving

Prognosis

Prognosis frequently guarded & depends on:

Cause of recumbency

Duration of recumbency

Prognosis mostly found is

Mortality 20-67%

Many die within 7-10 days due to sepsis or shock

33 % recover between 3-30 days

May continue treatment if no obvious physical abnormalities, bright, eating, and continued attempts to rise.

Helping the cow rise:

On every day of the recumbency, an attempt should be made to bring the cow to its feet. Several simple but effective techniques can be tried.

In one method, the clinician stands with feet pressed under the cow at a point below the scapulohumeral joint. A sharp blow is delivered by driving the knees into the muscle mass below and caudal to the scapula. This method must not be used on the thoracic wall unprotected by the muscle mass to avoid fracturing the ribs. If the animal struggles to rise, an assistant should grasp the root of the tailhead with both hands and lift. Lifting on any other part of the tail may cause damage.

The value of hip clamps is controversial. Their proper use requires experience, skill, and a delicate touch. Continual use causes trauma and pain that is counterproductive. The forelimbs support 60 per cent of a cow’s weight and, therefore, the use of a canvas sling under the sternum is almost mandatory for consistent success.

Even if the cow does not stand, the lifted position provides an opportunity to manipulate the limbs, auscultate for crepitation, and perform vaginal and rectal examinations.

Supporting the downer cow:

It is vital that recumbent cows be provided with clean water at all times. A shallow rubber feed bowl prevents spillage. If the cow does not drink, she must be given fluid therapy either by drench or parenterally. Every effort must be made to roll the cow from one side onto the other every 3 hr. If this is not done, the weight of the cow results in ischemia in the muscles of the hindlimb. This pathology precedes various myopathies and may precipitate the compartment syndrome.

Protection from the elements is essential. Rain and wind can reduce body temperature considerably and worsen shock if present. A windbreak of straw bales is vital. Straw bedding should be provided to help insulate the cow from the ground. A recumbent cow does not require a warm environment; however, in a cold environment, an inactive animal can gradually succumb to hypothermia.

The downer cows most difficult to treat are those that do not try to eat. A cow that salivates on its feed will not eat it later. Rather than being offered large amounts of feed, the cow should be tempted with sweet hay. This should be cleared away every 30 min if not accepted. Placing bitter-tasting weeds such as ivy or dandelion in the mouth may provoke salivation and an interest in eating. Lettuce and cabbage leaves are accepted by some cows. In extreme cases, the cow can be drenched with rumen contents. Sometimes drenching with a thin gruel to which powdered ginger and/or gentian has been added can be helpful.

Rabies

2019-12-04T21:06:00.002+05:00

Rabies

The best known and most important member of the Rhabdoviridae is rabies virus, a Lyssavirus (Greek lyssa ,rage or fury).
This viral infection, which affects the central nervous system of most mammals including humans, is invariably fatal.
Most clinical cases are due to infection with rabies virus (genotype 1).
Classical rabies caused by genotype 1 lyssavirus is endemic on continental land masses with the exception of Australia and Antarctica.

Epidemiology

Two epidemiologically important infectious cycles are recognized.

1. urban rabies in dogs

2. sylvatic rabies in wildlife.

• More than 95% of human cases are the result of bites from rabid dogs.

• Although virus may be transmitted through scratching and licking, transmission usually occurs through bites.

• Infected animals may excrete virus in their saliva for some time before the onset of clinical signs.

Pathogenesis

• Following introduction into the tissues, virus enters peripheral nerve endings. There may be limited replication locally in myocytes or other tissue cells.

• The virus is transported to the central nervous system by retrograde axoplasmic flow and becomes widely disseminated in nervous tissue by intra - axonal spread.

• Although rabies viral antigens are highly immunogenic, immune detection is delayed because intracellular transport prevents contact with the cells of the immune system in the early stages of infection.

• Clinical signs develop following neuronal damage caused by viral replication.

• Virus spreads centrifugally within nerve cell processes and is released at axon terminals where it infects many non – nervous tissues including the salivary glands.

Clinical signs

• The incubation period (Normally 3 to 8 weeks), which is highly variable and can be of many months duration, is influenced by various factors including

Ø host species

Ø virus strain

Ø The quantity of virus in the inoculum

Ø The site of introduction of the virus.

• The clinical course in domestic carnivores, which usually lasts for days, may encompass prodromal, furious (excitative) and dumb (paralytic) phases.

• In the prodromal phase, affected animals are often confused and disorientated; wild animals may lose their natural fear of humans.

• The furious phase is characterized by an increase in aggressiveness and hyper excitability, and there is a tendency to bite at inanimate objects and at other animals. Affected animals may roam over long distances.

• In dumb rabies, muscle weakness, difficulty in swallowing, profuse salivation and dropping of the jaw are the usual features.

Diagnosis

• History

• Signs and symptoms

• Clinical examination

• Ante mortem diagnostic tests for rabies are not generally used except in humans where saliva is examined by PCR.

• Rabies virus is particularly abundant in Ammon ’ s Horn of the hippocampus, cerebrum, cerebellum and medulla.

• The preferred method of diagnosis is the direct fluorescent antibody test (FAT) on acetone – fixed brain tissue smears.

•CSF (cerebrospinal fluid)analysis.

•Negri bodies

Negri bodies are eosinophilic, sharply outlined inclusion bodies found in the cytoplasm of nerve cells containing the virus of rabies.

They consist of ribonucleic protein produced by the viruses.

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