Agricultural Encyclopedia of China: Sericulture Volume

Author: Chief Editor: Shi Chu / et al
Publisher:
Publication Date: 1996-12-01
Features: Excerpt: Louis Pasteur (1822–1895), a renowned French microbiologist and chemist, was born on December 27, 1822, in Dole, France, and passed away on September 23, 1895. Pasteur was celebrated for his research in stereochemistry, fermentation, and bacteriology, and made outstanding contributions to the study of silkworm diseases. In 1845, the silkworm disease caused by microsporidia broke out in the Vaucluse department of France and spread to neighboring provinces. Over the next five to six years, it spread nationwide, drastically reducing France's silk production. In 1865, Pasteur was commissioned by the Ministry of Agriculture to investigate the disease in Asia, where he spent five years identifying the pathogen of microsporidia, understanding the maternal transmission pathway, inventing the bag-style seed collection method, and eliminating diseased female moths to prevent the disease, effectively saving France's silk industry. In 1870, he published Studies on Silkworm Diseases, documenting the history of silkworm diseases in France and Italy, which became a classic work on the study of microsporidia and softening disease. The bag-style seed collection principle developed by Pasteur is still used in many countries today. (Jiang Youlong)
Brazilian Sericulture (Sericulture in Brazil) Since 1920, Italian and Japanese immigrants began to develop sericulture in Brazil. By 1928, the annual silk production reached 192 tons, and by 1938, it increased to 403 tons. During World War II, due to smooth silk exports, the silk industry developed rapidly. In 1946, silk cocoon production rose to 6,000 tons, and silk production exceeded 600 tons. After the war, the sharp decline in silk prices led to the destruction of mulberry trees by Brazilian silk farmers and the closure of silk factories. By 1948, annual silk cocoon production dropped to less than 500 tons. Later, as Japanese silk exports reversed from export to import, Japanese immigrants and some Japanese silk enterprises began investing in sericulture in Brazil, and by 1953, annual silk cocoon production rebounded to 2,501 tons. From the 1950s to the 1960s, Brazil's annual silk cocoon production remained roughly between 1,023 and 1,500 tons. In 1970, Brazil had 11,021 hectares of mulberry plantations, 1,400 silk farmers, with an average annual silk cocoon production of 1.48 tons per household: 19 kilograms of silk cocoon production per 10 hectares of mulberry; an annual silk cocoon production of 2,650 tons, and silk production of 342 tons. In 1979, mulberry plantations expanded to 40,000 hectares, with a total silk cocoon production of 8,700 tons, silk production of 1,146 tons, and over 3,000 silk farmers. In 1981, silk cocoon production reached 8,547 tons, and silk production was 1,330 tons. Silk consumption is primarily domestic, with silk exports accounting for only 12–13% of total silk production. The main silk-producing regions in Brazil are S?o Paulo, Paraná, Mato Grosso do Sul, Minas Gerais, Goiás, and the Federal District. Sericulture is also produced in other areas. Silk-producing regions are generally located between 15° and 25° South latitude, with a focus near the Tropic of Capricorn. The climate in Brazilian silk-producing regions is subtropical monsoon humid and tropical grassland, with warm temperatures year-round. Average temperatures in January are 20–25°C, and in July, they are around 20°C. Annual rainfall ranges from 1,000 to 2,000 millimeters. Brazil's silkworm rearing season starts in September and ends in June of the following year, with 7–8 rearing cycles. Brazil's original mulberry varieties are "Caraplecha" and its selected variant "Sanpu." Cuttings are a distinctive feature of Brazilian mulberry cultivation, with cuttings sprouting within one month and growing to about 1 meter tall in three months. The first harvest of leaves can be taken after 8–10 months. The planting distance for mulberry trees is 2.8–3.0 meters between rows and 0.8–1.0 meters between plants, suitable for mechanical field operations. The yield of mulberry leaves per unit area is generally low. Silkworm eggs are supplied by silk production companies as "greening eggs" (the day before hatching). Silk farmers practice small silkworm rearing together and large silkworm rearing with strip mulberry leaves, with three to four feedings per day. Brazil currently has two silk factories with 12 sets of automatic reeling machines and 200 other reeling machines. (Liu Shixian)
White Muscardine (Whitemuscardine) A common fungal parasitic silkworm disease caused by Beauveria bassiana invading the silkworm body through the skin. The disease is named after the dried, hardened bodies of infected silkworms covered with white conidia. White muscardine is widely distributed, especially in warm and humid regions, where it is common during all stages of spring and summer-autumn silkworm rearing. Records of white muscardine can be found in the Shen Nong Herbal Classic. The Agricultural Book of Chen Fu (1149 AD) from the Song Dynasty mentions "white, salty in taste." In 1835, Italian botanist Agottino Bassi experimentally proved that white muscardine is an infectious silkworm disease caused by a fungal parasite. In the 1950s, China, Japan, and other silk-producing countries tested and promoted agents such as bleaching powder anti-muscardine powder, Ceresan anti-muscardine powder, and Selexan anti-muscardine powder, effectively controlling the harm caused by white muscardine. The pathogen, Beauveria bassiana (Balsamo) Vuillemin, belongs to the Beauveria genus of the Moniliaceae family. Its life cycle consists of three stages: conidia, vegetative hyphae, and aerial hyphae. Reproductive structures are conidia, which are colorless, spherical or oval-shaped, with dimensions of approximately 2.5–4.5 × 2.3–4.0 micrometers. When conidia cluster together, they appear white. After germination, conidia invade the silkworm body and develop into vegetative hyphae. Vegetative hyphae are filamentous, 2.3–3.6 micrometers wide, with septa, and can branch. During growth, vegetative hyphae form oval-shaped short hyphae (cylindrical sporangia) at their tips or sides. Short hyphae measure 5.6–16.8 × 2.8–3.08 micrometers and float in the blood. Soon, one or both ends of the short hyphae elongate into vegetative hyphae, while new short hyphae form on the new hyphae and spread throughout the body via blood circulation (Figure 1). After the silkworm dies, hyphae grow vigorously in various tissues, particularly in fat tissue, Malpighian tubules, silk glands, nerve balls, and muscle tissue, while growth in the digestive tract is less. After 1–2 days, vegetative hyphae grow out of the body to form aerial hyphae. Aerial hyphae also have septa and can branch. Many conidiophores grow singly or in clusters on the aerial hyphae, often at right angles to the hyphae. Conidiophores are bottle-shaped, wider at the base and narrower at the tip, with a sawtooth-like bend at the tip. Each bend extends into a short stalk, on which conidia are formed. Mature conidia are clustered in grape-like chains on the aerial hyphae (Figure 1). Beauveria bassiana secretes toxins during its growth. These toxins are cyclic polypeptide compounds, with several types identified. Among them, beauvericin II is highly toxic to silkworms, being a cyclic tetrapeptide. Artificial diets for 4th instar silkworms containing 4–8 ppm of beauvericin II can cause death. These toxins have a cation-chelating effect, significantly altering the anion concentration in silkworm tissues, which is one reason for rapid death. In addition to toxins, octahedral calcium oxalate crystals can be observed in the blood of infected silkworms. Among various hardening fungi, Beauveria bassiana is the most pathogenic to silkworms, with rapid onset. Beauveria bassiana conidia can survive for about 5 months to 1 year in shaded outdoor environments or soil. At temperatures below 10°C, they can survive for 3 years, and at -20°C, for up to 4 years. Under direct sunlight (32–33°C), they lose pathogenicity within 5 hours. Compared to Aspergillus species, they are much more susceptible to disinfectants. Immersion in 1–3% formaldehyde solution for 10 minutes, 0.2% effective chlorine bleaching powder solution for 5 minutes, 0.1% mercury chloride solution for 2 minutes, and 70% alcohol for 1 minute can inactivate them.
Transmission White muscardine is primarily transmitted through direct contact with the body surface, with secondary transmission via injuries. Conidia covering the bodies of infected silkworms are easily detached and lightweight, dispersing with the wind. When conidia enter the silkworm's nest and adhere to its body surface, under suitable temperature and humidity conditions, they begin to germinate within 6–8 hours, swelling and forming 1–2 germ tubes. Germ tubes secrete proteases, lipases, and chitinases. These enzymes collectively degrade the body surface at the site of infection, allowing the germ tubes to penetrate the body surface through mechanical pressure from their elongation and growth (Figure 2). The optimal temperature for Beauveria bassiana conidia to germinate and develop is 24–28°C. Below 5°C or above 33°C, germination and development do not occur. Under optimal temperatures, germination requires a relative humidity of over 75%. Higher humidity leads to higher germination rates. In sericulture production, the temperature and humidity in the silkworm nest are highly suitable for the germination and development of Beauveria bassiana conidia. If Beauveria bassiana conidia are ingested by silkworms, they cannot germinate in the digestive fluid and are excreted with feces, causing no harm. Infections occurring in the late 5th instar often result in death after spinning cocoons or pupating. Larvae or pupae that die in cocoons due to dry rearing conditions, low water content, and body hardening undergo significant shrinkage and drying, resulting in dry and light cocoons.
Symptoms Initially, infected silkworms appear normal. One day before death, numerous oily or dark brown spots appear on their body surface. The spots appear randomly and are irregularly shaped, caused by the degradation of the chitinous cuticle due to fungal invasion. When the amount of pathogen is low, the appearance of spots decreases or disappears entirely (Figure 3). Soon, infected silkworms lose appetite rapidly, accompanied by diarrhea and fluid discharge, and approach death. At this stage, if blood is examined under a microscope, numerous germ tubes can be observed, and the blood appears slightly turbid. Infected silkworms die within 3–7 days, with smaller silkworms dying faster and larger silkworms dying more slowly. Early infection in the 5th instar leads to death in the late 5th instar, during reeling, or within the cocoon. The bodies of infected silkworms gradually harden due to the development of the parasite. After 1–2 days, hyphae and conidia grow, and if left naturally for a certain period, many needle-like crystals will precipitate from the body.