PATHOGENIC DISEASES AND PEST IN SILKWORM

 

PATHOGENIC DISEASES AND PEST

Natural silk is produced by the silkworm, which is used for many purposes. Silk thread has several uses, including parachute manufacturing, tire lining, electrical insulation, artificial blood vessels, and surgical thread. Oil can be extracted from silkworm pupa, amino acids and vitamin B2 and can be used in the pharmaceutical industry.

Overall, the silkworm industry plays an important and active role in the development of national income and stimulates the rural economy and the overall development of agriculture, forestry, animal husbandry, side-line occupations and fisheries, suprs the development of local light industry and expands trade

Silkworm disease must necessarily have a specific cause. These causes belong to various categories including biological, chemical, physical, nutritional, environmental, constitutional, etc. Among which the most important are the biological factors. The biological agents eliciting silkworm diseases are viruses, bacteria, fungi, protozoa and arthropods, all of which belong to parasitic pathogens and excepting the arthropods are infectectious agents. Moreover, many diseases of other insects can be transmitted to the silkworm, the diseases of the Lepidoptera being especially so. Also, ants, rodents, birds, wasps and spiders can do harm to silkworm larvae. Some important challenges faced in sericulture are listed below.

• The pebrine disease can infect the eggs, resulting in their death before the hatching of the larvae. Any larvae affected by this disease develop dark spots and become lethargic.
• Viral infections in the larvae may result in the shrinkage of their bodies. They may also start giving off an unpleasant odour.
• Other viral infections such as cytoplasmic polyhedrosis can cause the larvae to lose their appetites.
• The muscardine infection, caused by fungi, can cause the larvae to become extremely feeble and eventually die.
• The larvae of dermestid beetle can bore into the silkworm cocoons and eat the pupae. Silk cannot be reeled from these damaged cocoons.
• Some mites produce a toxic substance that kills silkworms
  

  
  FIG: ENVIRONMENT CONDITION INFLUNCING SILKWORM DISEASE

Most of the pathogenic microbes cause infectious disease in silkworm by invading, multiplying and spreading infection. Major disease causing pathogens of silkworm and their diseases are viruses which cause nuclear polyhedrosis, cytoplasmic polyhedrosis, viral flacherie and densonucleosis; bacteria causes bacterial flacherie, bacterial disease of the digestive tract, bacterial septicemia and bacterial toxicosis; fungi causes white, green, yellow, red muscardine, aspergillosis and microsporidiosis; protozoa cause pebrine. Disease imposed heavy losses in cocoon production.

VIRAL DISEASE

Viral diseases of silkworm pose a major problem to sericulture as they account for almost 70 percent of the total loss due to diseases. Viral diseases of silkworm comprise of inclusion and non-inclusion types. The inclusion virus diseases form typical inclusion bodies. They are nuclear polyhedrosis and Cytoplasmic polyhedrosis which can be more easily identified through ordinary

microscope. The non-inclusion type consists of Infectious flacherie and Densonucleosis which can be detected only through electron/fluorescent microscopy and serological tests.

1. GRASSERIE

The complexes of diseases caused by viruses showing jaundice-like symptoms are collectively referred to as grasserie or polyhedrosis.

According to the kind of causative viruses, location of the latter in host’s tis­sue and cell, polyhedrosis again is of 2 types:

(1) Nuclear polyhedrosis which according to recent concept is considered as grasserie and

(2) Midgut cytoplasmic polyhedrosis or Midgut nuclear poly­hedrosis.

It is one of the most serious viral diseases in tropical countries and occurs throughout the year. This disease is also known as Nuclear polyhehedrosis, Jaundice, Milky disease, Fatty degeneration and Hanging disease.

CAUSATIVE ORGANISMS

The nuclear polyhedrosis is caused by Nuclear Polyhedrosis Virus strain Bm (NPV Bm).. This DNA virus multiplies only in the nucleus of the host cells, where it forms hexagonal polyhedra which remain embedded in a proteinaceous matrix, called Polyhedral Inclusion Bodies (PIB).

The inclusions of PIB are synthesized by the silkworm (host) machinery, independent of viral components and so, may or may not contain viral particles. In midgut polyhedrosis, the RNA Smithia virus forms polyhedra in cytoplasm in case of midgut cytoplasmic polyhedrosis or in nucleus in case of midgut nuclear polyhedrosis.

MODE OF TRANSMISSION

Nuclear polyhedrosis can be transmitted to healthy worms from infected worms by the following routes:

 ORAL

Ingestion of leaves contaminated with PIB from the dead tissue or faeces from infected worms can transmit the disease to fresh worms.

ENVIRONMENT:

High temperature, humidity, etc. may induce the spreading of this disease by transforming latent stage to virulent stage of the pathogen.

BLOCKAGE OF SPIRACLES

Contaminated leaves with formalin, exposure to camphor during rearing and blocking of spiracles by dust, Uzi fly, etc. may induce the disease.

SKIN WOUND

Skin wound may get infection from contaminated rearing bed.

Midgut polyhedrosis, on the other hand, can be transmitted through oral route or by induction due to bad environment.

SYMPTOMS

In case of nuclear polyhedrosis, the late stage of infection shows the following sym­ptoms

·         Loss of appetite,

·         Loose and shiny white skin with elevated protuberances in inter seg­mental zones,

·         Ruptured skin exuding milky-white or yellowish fluid containing polyhedra (Fig. 3.38).

·         Restless larvae usually try to leave the rearing tray and die due to exuding body fluid,

·         Infected larvae usually do not moult,

·         Body colour turns to yellow and faeces are white in colour because of accumulated polyhedra, so the name ‘jaundice’ is given to the disease.

For midgut viral infection, the worms show initially no symptoms.

The symptoms appear only in late stage and include

·         Loss of appetite,

·         Translucent cephalothorax and shrinkage of body,

·         Reduced growth,

·         Opaque midgut due to accumulation of polyhedra in cytoplasm,

·         White, loose faeces due to accumula­tion of polyhedra, and

·         Irregular moults

FIG: GRASSERIE

CONTROL MEASURE

·         Rearing environment should be hygienic with proper ventilation,

·         Sterilization of rearing room with steam or 2% formalin or bleaching powder or Resham Keed Ouzhad (RKO) or Labex,

·         Removal of dead or infected worms from rearing tray

·         Feeding the larvae with healthy leaves, and

·         Oral administration of nalidixic acid, P-aminobutyric acid etc. or topical application of imanine can control NPV to some extent.

2. INFECTIOUS FLACHERIE

Besides bacteria, Infectious Flacherie Virus (IFV), an RNA virus can also cause flacherie in the host silkworm where it forms irregular inclusions mostly in the midgut goblet cells.

MODES OF TRANSMISSION

The causative viruses enter the host midgut through oral route via ingested contaminated leaves.

SYMPTOMS

·         Shrinkage of body with transpa­rent appearance.

·         Vomiting of digestive juice.

CONTROL MEASURES

·         Feeding the larvae with healthy leaves,

·         Hygienic rearing, and

·         Disin­fection of rearing room and appliances.

3. GATTINE

This disease is also known as clear head disease because of the transparent appearance of affected worms.

CAUSATIVE AGENTS

Primary agent is some virus while Streptococcus bombycis acts as the secondary invader.

SYMPTOMS

Following secondary infections by bacteria the larvae show

·         Lack of appetite,

·         Vomiting of an alkaline, clear fluid, and

·         The ante­rior part of the alimentary canal appears transparent due to absence of any mulberry leaves and hence given the name of “Clear Head” to this disease.

CONTROL MEASURES

·         Rearing of larvae in hygienic conditions, and 

·         Disinfection of rearing place and appliances between each stage of whole rearing process.

 

BACTERIAL DISEASE

In sericulture, silkworm can be attacked by various bacteria resulting in different diseases. Bacterial disease is common in mulberry silkworm. Very hot weather and high humidity in a long time of summer are ideal conditions for arising bacterial disease. Most common bacterial diseases are as follows

1. FLACHERIE

The word “flacherie” was used to describe the flaccid condition seen in the silkworm, Bombyxmori, ailing from all sorts of dysenteries. Even now this term is widely used to describe many different diseases. Louis Pasteur separated flacherie from other silkworm diseases and attributed the disease microbial or infectious causes. According to him, owing to the extremely rapid multiplication of a large number of certain kinds of bacteria in the intestine the digestive functions of the gut were adversely giving rise to the symptoms typifying the disease. This disease generally occurs in the mature larvae.

FIG: FLACHERIE

CAUSATIVE ORGANISM

Flacherie is caused by Bacillus bombycis, B. sotto, Streptococcus bombycis, Pseudomonas aeroginosa, etc. In general, the pathogenic bacteria may attack their alimentary canal and haemolymph.

MODE OF TRANSMISSION

ORAL

Larvae when take contaminated leaves can get infection directly. The entered bacteria attack and grow in their alimentary canal. Due to bacterial growth and consequent accumulation of lactate, acetate, etc. the permeability of gut is lowered due to lowering of pH.

Then the bacteria become able to invade the haemocoel and spread the infection in whole body of larvae. The infected larvae pass bacterial spore containing stool which acts as new source of infection.

BAD REARING CONDITION

Temperature and humidity if not maintained properly in the rearing room, may enhance the growth and spreading of flacherie bacteria. Other than this poor ventilation, poor sanitation, improper bed cleaning and overcrowding of worms also transmit this disease.

SYMPTOMS

The diseased silkworms show following general symptoms

·         Lack of appetite,

·         Stunted growth,

·         Sluggish movements,

·         Soft and loose skin,

·         Shrinkage of body after moulting and these larvae usually refuse to take any food,

·         The body become dull colored to black-brown,

·         The larvae show signs of pain, convulsions and die,

·         The carcass turns black and emits foul smell

·         Swollen thorax

·         Body softened & rupture

·         Diarrhea and vomiting.

Above men­tioned symptoms help to detect about flacherie infected larvae. Besides, histopathological studies can reveal affected cylindrical cells in gut wall in case of streptococcus infection and affected goblet cell in case of Diplococcus infection.

CONTROL MEASURES

·         Optimum environmental conditions with required temperature and humidity should be maintained in the rearing place,

·         Heal­thy and quality leaves should be supplied to rearing larvae,

·         Unhealthy larvae should be discarded from rearing trays

·         Avoid overcrowding

·         Maintain optimum temperature & Relative humidity

·         Proper bed cleaning

·         Regular disinfection of rear­ing room and appliances should be done with 2% formalin.

2. SEPTICEMIA

This is a condition where bacteria multiply enormously in the blood (haemolymph) of the larvae, pupae and moths. Septicemia during the larval stage leads to larval mortality whereas the infection in pupal and moth stages leads to a large number of melted cocoons affecting the egg production in the grainages. Septicemia is one of the serious diseases infecting silkworm yield. Both gram positive and negative bacteria are reported to cause pathogenesis. The gram positive are Bacillus sp, staphylococcus aureus, streptococcus bombycis and gram negative Serratia marcenscens.

This disease is caused by the multiplication of a large number of bacteria, bacilli, streptococci and staphylococci in the haemolymph. Two major types of bacterial septicemia are generally observed, one is the black thorax septicemia caused by Bacillus sp. belonging to the family Bacillaceae of the order Eubacteriales size 1-1.5 x 3 microns, spores sub terminal, gram-positive and the other is the red septicemia or serratia septicemia caused by the bacillus Serratia marcescens Bizio size 0.6-1.0 x0.5 microns non-sporulating and gram negative. The former is more resistant to disinfectants than the latter except for lime emulsion.

CAUSATIVE ORGANISM

Septicemias mainly caused by the gram positive bateria are Bacillus sp, staphylococcus aureus, streptococcus bombycis and gram negative Serratia marcenscens

MODE OF TRANSMISSION

·         Contact through wounds on skin, and

·         Oral route or intake of contaminated food can also transmit the infection

SYMPTOMS

·         Softening of body,

·         Change of body colour to brown,

·         Liquid excreta,

·         Loss of clasping power of prolegs

·         Death of larvae.

Difference in the symptoms of two diseases are that, in case of the black thorax septicemia, the blackening starts from the thorax and extends to the dorsal vessel till the whole body blackens and rots.

 In the case of red septicemia the whole body softens taking a slightly reddish tinge. Septicemias are generally acute diseases, spreading quickly, the time clasping from the time of infection to death at 28°C being about 10 hours. At higher temperature and under epidemic conditions they may die within 5-6 hours.

 

FIG: BLACK THORAX SEPTICEMIA

FIG: RED SEPTICEMIA

CONTROL MEASURES

·         Good sanitation and healthy environment should be provided,

·         Infected larvae should be removed/discarded,

·         Larvae should be handled carefully to reduce skin wounds.

3. SOTTO DISEASE

This disease is caused by the toxins released by some bioinsecticidal bacteria. This is otherwise known as bacterial toxicosis.

CAUSATIVE ORGANISM

·         Bacillus thuringiensis, bacteria widely used as a bioinsecticide, release some endotoxin thuricide that remains stored in a parasporal crystalline structure during the time of sporulation of the bacteria. This toxin, if taken by the larvae orally causes two types of responses:

·         In type I response, the larvae of B. mori stop feeding, haemo­lymph becomes alkaline and paralysis occurs within 60-80 minutes of intake. In type II response, other lepidopteran larvae only show rapid inhibition of feeding.

MODE OF TRANSMISSION

·         Oral intake of mulberry leaves contaminated with toxin-crystals can cause toxicity to the larvae. But if infected by injection to the larvae, the same bacterial toxins show no effects to the silk worm larvae.

FIG: SOTTO DISEASE

SYMPTOMS

·         Lack of appetite,

·         Sluggish movement,

·         Shrinkage of skin,

·         Diarrhea,

·         Loss of clasping power of prolegs, and

·         Death. After death the body becomes black in colour, internal organs become liquid and emit foul odour.

 

CONTROL MEASURES

·         Good sanitation, specially cleaning the room with hot water to inactivate the toxin,

·         Removal of dead / infected larvae from rearing tray,

·         Bacterial spores if detected can be destroyed by exposing to 2% formaldehyde for 3 hours or to 100°C for 5 minutes.

4. BACTERIAL DISEASE OF DIGESTIVE SYSTEM

A widely accepted theory states that silkworms become weak on and after hatching, and then their metabolism becomes inactive, causing imbalance of function. As the sterilizing power of the digestive fluid weakens, the bacteria devoured together with mulberry leaf multiply in the digestive track and take nutrition from the body of the silkworm destroying the membranous tissue of the intestine.

CAUSATIVE ORGANISM

·         Initial infection stage: Streptococci

·         Final stage(near death): Colisuchasbacillus

·         Moribund stage or corpse: ProteussuchasBacillus

 

SYMPTOMS

Not always uniform vary according to the time of occurrence, the kind of bacteria multiplying in the digestive organ, the race of the silkworm and other conditions following are the general symptoms

·         Loss of appetite,

·         Sluggishness,

·         Slow growth

·         Inelasticity of the skin

·         Softening of the body

·         Diarrhea: This suddenly afflicts the silkworms in the fourth and fifth instars, especially in the latter causing soft excrements of irregular shape. In the latter case, the excrements come out in beads mingled with membrane of the intestine.

·         Vomiting disease: Diarrhea and vomiting of fluid are observed. The body softens putrefies and shrinks as time passes. In most cases the body becomes black but sometimes it turns red owing to the presence of Bacillus prodigious or green because of Bacillus pyocyaneus. Mixed propagation of a few bacteria may show some other colours.

CONTROL MEASURES

·         Foremost requisite is to raise healthy and strong silkworms since the primary cause is the weakness of the silkworms.

·         Proper incubation of eggs; Temperature and humidity should be maintained at 22°-25°C and 80-85 percent respectively.

·         Selection of suitable race: It is essential to select a race that is sturdy and resistant to adverse conditions for summer and autumn rearing

·         Feeding of good quality leaf; it is essential to feed plenty of high-quality mulberry leaves

5. COURT DISEASE

This bacterial disease is also known as Rangi in India because of the colours shown by dead larvae.

CAUSATIVE ORGANISM

·         In this disease, both larvae and pupae get infected by the bacteria Serratia marcescans and also by S. piscavotar following the primary infection with Streptococcus faecalis.

MODE OF TRANSMISSION

·         Through skin wounds and

·         Oral route.

SYMPTOMS:

·         Affected larvae are flaccid

·          Death and Following death, the body colour of larvae changes to crimson red.

CONTROL MEASURES

·         Hygienic and clean rear­ing,

·         Isolation and killing of diseased larvae and pupae and

·         Disinfection of rearing place and appliances with 2% formalin.

FUNGAL DISEASE

Fungal diseases otherwise called mycosis, is caused in the silkworm by a few parasitic fungi. Two major kinds of such disease are Muscardine and Aspergillosis. Muscardine appears in various forms and depending upon the colour of spores which cover the body of the silkworm giving a characteristic colour, they have been named as white-muscardine, green-muscardine, yellow-muscardine, blackmus cardine, red-muscardine etc. The more common muscardine diseases are, however, white and green-muscardine. In addition Aspergillosis is also found to occur. Since the silkworm attacked by a fungal disease in course of time turns hard and chalky, muscardine disease is also called Calcino.

1. MUSCARDINE

Fungal diseases of silkworm are called muscardine where the body of larvae gets mummified due to deposition of calcium oxalate and hence the disease is also called ‘calcino’.

CAUSATIVE ORGANISMS

Different fungi cause this disease but the name varies according to the colour of conidiospores, produced by them on the body of worms. Name of different muscardines and their causative fungi are given below.

White muscardine is caused by Beauveria bas- siana where the conidia are spherical or oval and spores are like white powdery specks. Black muscardine is spread by Metarrhizium arisopliae. The conidia are cylindrical and the spores are dark greenish black in colour.

The fungus Poecilomyces farinosus causes yellow muscardine, where oval to spherical spores collectively look yellow in colour. Aspergillus flavus and A. oryzel cause brown muscardine with pro­ducing spores dirty brown in colour. Red muscardine may be caused by Sorosporella uvella and Spicaria fumosorosea with their red spores.

MODES OF TRANSMISSION

CONTACT

All types of muscardine infections are transmitted through skin. However, oral transmission through ingestion of contaminated leaves and transmission through spiracles are also noticed. The fungal spores upon falling on the body surface of silkworm germinate and gradually penetrate the cuticle by mechanical and enzymatic forces. The growing hyphae then draw nourishment from host’s tissue and ultimately kill them.

The fungi then take saprophytic nutrition from the dead larvae tissue and grow mycelia as white flakes over the dead tissue. Reproductive conidiophores with characteristic colour then grow from the mycelia. Due to continuous growth of fungi-colony, and their release of calcium oxalate as metabolite, the dead tissue of host larvae becomes hard and mummified.

Yellow muscardine fungi affect the gut of larvae, while red muscardine fungi attack the body wall. In case of white, green and black muscardines, the pathogenic fungi reach the haemocoel where they spread their hyphae.

SYMPTOMS

·         Sluggish movement showing “unequal” in rearing bed,

·         Loss of appetite,

·         Coloured patches may appear around spiracles or at leg bases,

·         Body shrinks with loose cuticles,

·         Vomiting,

·         Early infected larvae do not spin, but late infected instars may spin flimsy cocoon within which the pupae die, and

·         Dead larvae may be covered with coloured spores of causative fungi or may be mummified into chalky white structure

FIG: MUSCARDINE

CONTROL MEASURES

 PROPER REARING

Rearing room and bed should be free from humidity and darkness as these can stimulate the growth of fungi. Free aeration by keeping windows and doors open or by using fan for continuous flow of air should be maintained. Temperature should be kept above 22°C. Any kind of dampness in and around rearing place is to be avoided.

For this purpose, anhydrated lime can be kept in the corner of rearing room. All rearing appliances along with leaf-food should be kept free from extra moisture. During moulting, new bed should be kept thin and old newspaper can be kept below the bed to prevent mus­cardine infection during wet season.

DISINFECTION

For preparing disinfected rearing beds, 0.4% formalinised husk can be used for the beds of I and II instars; 0.5% for II and III instars, 0.6% for IV and 0.8% for V instar. The ratio of diluted formalin and burnt husk is usually kept 1:10 (v/v).

After each bed cleaning and during moulting, a mixture of dithane-M45 and kaoline can be applied on silkworm to prevent the germination of fungal spores if present on body surface of larvae. Again, for every 100 layings, 3-4 kg of Resham Keed Ouzhad (RKO) can be spread on the worms after each moulting and 30 minutes before the larvae resume feeding.

Labex, a mixture of lime and bleaching powder has anti-muscardine and grasserie effects and can improve larval growth and commercial characters as well. This mixture taken in muslin cloth can be spread directly on silkworm in each instar at a recommended dosage of 4 gm/ 0.1 nr of rearing tray.

Other chemicals used as contact disinfectants for muscardine include benzoic acid, aliband, chemi-chlon, benzoalkonium chloride, mixture of ceresan and lime, etc. Burning of 20-30 gm of sulphur/m³ area of rearing space is very effective to prevent growth of muscardine fungi.

REMOVAL OF INFECTED LARVAE

Infected larvae if detected should be removed immediately from rearing tray before the formation of conidiospores on them. Infected larvae may be kept in 2% formalin to kill the spores or buried in deep pits.

CLEANING THE REARING BED

Litter from the infected bed should be removed immediately after detection of infection and be dumped in deep pits and burnt.

CARE IN BETWEEN REARING

The rearing room and appliances should be disinfected immediately after muscardine infection before the next rearing. These should also be kept dry during the period between rearing.

PROTOZOAN DISEASE

Protozoa which are injurious to silkworm are the parasitic ones belonging to the class Microsporidia and genera Nosema, Pleistophora and Thelohania the major protozoan disease of the silkworm is the pebrine disease, so named due to the appearance of black peppery patches following infection.

1. PEBRINE

Pebrine is a chronic and disastrous disease of the silkworm. It was responsible for the sudden collapse of the silkworm industry of both France and Italy in 1865. Even though the fight against this disease in all the sericulture countries is going on since more than 100 years, the disease is not yet eliminated.

However, it has been kept under check by following the techniques of strict mother moth examination for the supply of disease free silkworm eggs, in addition to disinfection and hygienic rearing. Though the disease is under reasonable control, it appears sporadically due to infected seed and persisting secondary contamination in the rearing house.

 

 

CAUSATIVE ORGANISM

Pebrine is caused by the protozoan Nosema bombycis that has several strains of which most virulents are NIK-2r. NIK-3h and NIK-4m in India. The protozoa pass its life cycle through 2 stages.

MODES OF TRANSMISSION:

The disease is transmi­tted to silkworm in three different ways

 ORAL

Spores liberated through the faeces of infected worms or through dead larvae, contaminate the mulberry leaves given in rearing bed. Such leaves when taken by other larvae, they get infected.

Again, eggs may be contaminated by such faecal matter or dead tissues containing the spores during the time of oviposition or after oviposition. The newly hatched larvae who take part of chorion of such contaminated eggs may get infection.

 

 

CONTACT

Larvae may get infection through their skin from the rearing bed contaminated with Nosema spore containing faecal matter or dead tissues

TRANSOVARIAL

If infection occurs in 5^th instar stage, the adult moth normally emerges through pupal stage. However, the spores of Nosema ingested then sporulate within the oocyte and pass on to the eggs. Thus, the egg itself acquires infection from the layers (mother) and hatches into primary infected larvae.

However, these infected eggs hatch in very low percentage and the hatched out larvae usually die before reaching 3^rd instar. These larvae act as the source of secondary infection for other larvae through their faeces or dead tissues.

These larvae, form weak cocoons and exhibit pebrine symptoms and may die during or after spinning. Thus, they serve as source of tertiary infection to other 5^th instar larvae which may spin and may even live up to the adult stage.

 

FIG: PEBRINE

SYMPTOMS

EGG

Infected eggs do not show firm attachment with the egg card due to improper deposition of glue. These eggs are pale yellow in colour and may fail to hatch.

LARVAE

Primary infected larvae usually die before exhibiting any typical symptoms. Larvae having secondary or tertiary infections may show- different symptoms like loss of appetite, ‘unequals’ appearance due to slow and irregular growth; clean worm symptom that arises due to irregular and incomplete moulting, black pepper-like spots on the body, irregular brown patches due to dead hypodermal cells, spitting and wasting silk instead of spinning the cocoon, etc.

Infected larvae also pass soft faeces and often die after spinning without pupating.

PUPA

Live infected pupa if present inside the cocoon, may show black, swollen body with black spots on sides of abdomen.

ADULT MOTH

Pebrine infected adult moths show black spot on abdomen, deformed antennae, unstretched, and discoloured wings. Females usually lay eggs in irregular, loose heaps. Scales fall off easily from the body of pebrine infected moths.

DETECTION OF PEBRINE

Pebrine at any stage of silkworm life cycle can be detected by observing the above mentioned symptoms. Besides, microscopic observation of homogenate / fluid from dead tissues, faecal pellets can indicate the presence of infective spores of Nosema. Again, by advanced immune enzymatic methods, presence of pebrine spores can be detected quickly.

 

CONTROL MEASURES

·         In grainages only diseases free layings (DFLs) will be allowed for rearing.

·         Diseased larvae if detected in rearing tray/bed should immediately be removed and burnt. All rearing appliances including the rearing room then should be disinfected with 4-5% formalin solution or by spreading bleaching powder,

·         Adult moths showing symptoms of pebrine should not be undertaken for any sericulture processes.

·         For disinfection of rearing accessories, other agents like Benomyl. Bavistin, Bengard, etc. can be used instead of routine formalin/bleaching powder.

Besides, the above preventive/corrective measures, it has been reported that immersing of the silkworm eggs in hot water, high temperature treatment of the pupae, dipping of the eggs in hot hydrochloric acid minimize the incidence of pebrine. Chemotherapy of Nosema infection has been reported through a number of antimicrosporidian drugs like fumagillin, benomyl, bengard, bavistin, ethyl and methyl thiophanate and some of their analogues with positive results, but

preventive methods have always been found to be better than the curative measures.

UZI FLY (SILKWORM PEST)

The uzifly, Exoristabombycisis a serious parasitoid of the silkworm, Bombyxmori, causing 10-15% damage to the silkworm cocoons. The adult Uzi fly is blackish grey in colour. It is bigger than the common Housefly, Musca domestica and is more efficient in flight. It has four longitudinal black stripes on the dorsum of the thorax and three cross-wise stripes on the abdomen. Male are 11.9 mm to 12.00 mm and the female 10.20 mm to 10.40 mm in length. Width varies from 3.60 to 3.90 mm. Wing span is about 10 mm and the wings are covered with dark grey hairs. Eyes are chocolate brown in colour. The lateral margins of the abdomen are covered with bristles, which are thicker and longer in males than in females. Males can be easily distinguished from the females by the presence of external genitalia (pinkish brown in colour) at the tip of the abdomen on the ventral side and well developed tips of the legs (tarsal pads).

FIG: UZI FLY

LIFE CYCLE OF UZIFLY

• A female lays 500 - 600 eggs during her life time (18 - 22 days), each day laying about 20-30 eggs.
• Eggs hatch in 48 - 60 hours.
• The Maggot after hatching from the egg immediately pierces into silkworm body using the pro-thoracic hook attached to the mouth. The place of entry of maggot into silkworm body develops a black scar.
• The maggot feeds on the silkworm tissues for 5-7 days during which time it moults twice. The maggot comes out of silkworm body by creating an opening on the body(integument) and spends 12-20 hours time as post-feeding (post- parasitic) maggot and becomes pupa in dark places like cracks, crevices, corners of the rearing house, loose soil, etc
• Adult uzifly emerges from the pupa after 10 to 12 days.
• Life cycle is completed in 17-22 days.
• Adult fly survives for 10 - 18 days (males) and 18-22 days (females).
• Adult fly feeds on pollen, rotten fruits, nectar, etc.

PERIOD OF OCCURRENCE

• In the southern sericulture belt (Karnataka, Andhra Pradesh and TamilNadu), the uzi fly is prevalent throughout the year. In other parts of the country, it does not prevail throughout the year because of discontinuous rearing of silkworm and environmental extremities.
• Maximum infestation is recorded during rainy season followed by winter.
• The infestation is least during summer months.

SYMPTOMS OF INFESTATION OF UZIFLY

• Uzi maggot-infected silkworm shows black spots on their body surface at the place of maggot entry
• Loss of weight due to continuous loss of fat bodies and other tissues
• Stop feeding
• Proneness to other bacterial or viral infections
• Sluggish movement

FACTORS RESPONSIBLE FOR THE OUTBREAK OF UZIFLY

• Large scale and overlapping rearing of host (silkworm).
• Favourable climatic conditions (temperature range of 20 – 30°C and relative humidity of 60 – 90%) facilitates continuous host / silkworm rearing which in turn helps the host availability.
• Increased adult (uzifly) longevity.
• Higher egg production and egg hatchability.
• Reduced activity of the natural enemies like parasitoids, predators and pathogens in nature.

MANAGEMENT AND CONTROL MEASURES OF UZIFLY

Various management methods have been evolved for the suppression of the uzifly incidence. These are classified as

a)      Cultural / Mechanical

b)      Exclusion

c)      Physical

d)     Chemical

e)      Biological

f)       Legislative/Quarantine

a) CULTURAL/ MECHANICAL

• Silkworm rearing in a village should be conducted at a time by all farmers.
• A minimum gap of 20 days should be maintained between the two silkworm rearings.
• The cracks and crevices on the rearing house floor must be kept closed.
• Collection and destruction of uzi infested silkworm larvae.
• Collection and destruction of uzi maggots and pupae from rearing house, grainage, cocoon market and reeling establishment.
• Collection and destruction of adult uzi fly.

b) EXCLUSION

• Use nylon net enclosure to the rearing stand
• Fix wire mesh to windows and doors
• Provide a small ante-room at the entrance of rearing house. Cover the individual rearing tray with nylon net.

 c) PHYSICAL

• Keep uzitrap solution in white trays near doors and windows (3 ft above ground level) both inside and outside the rearing house to trap adult uzi fly.

d) CHEMICAL

• Spray / dust the ovicides like uzicide / uzipowder to kill the uzi eggs laid on silkworm body.
• Spray 2% bleaching powder solution on the body of silkworm larvae to detach / kill the uzi egg.

e) BIOLOGICAL CONTROL

• Release of Nesolynx thymus by keeping parasitised pupae ready for emergence on 2nd day after keeping packets (50 ml x 2 packets/100 dfls) on second day of fifth instar of silkworm rearing.
• Shifting of the parasitised pupa packets to places where mountages with silkworms are kept spinning

f)  LEGISLATIVE/QUARANTINE

• Avoid transportation of uzi infested cocoons from infested area to new area.

The above management methods when applied individually do not keep the pest incidence below the economic injury level (5%). Hence, an Integrated Pest Management (IPM) package is developed for the suppression of the pest by selecting a few effective management strategies listed above.