Current Status of Post Harvest Soft Rot in Vegetables: A Review
M. Ashraf Bhat,
Soft rot is one of the destructive diseases of vegetables and occurs worldwide wherever fleshy storage tissues of vegetables and ornamentals are found. It causes a greater total loss of produce than any other bacterial disease. The disease can be found on crops in the field, in transit, in storage and during marketing; resulting in great economic losses. It is primarily caused by Erwinia carotovora sub-sp. carotovora and sometimes by Erwinia carotovora sub-sp. atroseptica. The soft rot disease has a very wide host range infecting vegetable species belonging to all families. Name of the disease aroused from the characteristic soft decay of fleshy tissue which terminates into watery or slimy mass. The bacteria enters the host tissue through injuries. The decay is aggravated when high humidity is coupled with high temperature which results in fast rate of multiplication of the pathogen. For this reason much of the loss due to this disease occurs during middle of the summer. Increased amounts of pecteolytic enzymes released by the pathogen results in maceration of tissue and are of great significance to the pathogenesis of the disease. Control of the disease which includes sanitation of packing house, lowering of storage temperature and humidity, host resistance and other physical and chemical measures are discussed in detail.
December 08, 2009; Accepted: March 29, 2010;
Published: June 19, 2010
Soft rot is one of the destructive diseases of vegetables. It occurs worldwide
wherever fleshy storage tissues of vegetables and ornamentals are found. The
disease can be found on crops in the field, in transit and in storage or during
marketing resulting in great economic losses. Soft rot causes greater total
loss of produce than any other bacterial disease. Post harvest bacterial soft
rot losses have been estimated to vary between 15-30% of the harvested crop
(Agrios, 2006). Vegetables coming from the field may be already infected although
they may not yet show visible symptoms at harvest which later on may cause severe
damage because of high air temperature, humidity and poor transport management.
Erwinia carotovora subsp. carotovora and Pseudomonas fluorescens
causes the most common and most destructive soft rots Erwinia carotovora
sub sp. atroseptica is also found associated with soft rot.
The soft rot bacterium enters plant tissues primarily through wounds, often
created by insect feeding or bruising at harvest. Insects and water are effective
in spreading the bacterium. Once in the plant tissue, the bacterium produces
increasing amounts of pectolytic enzymes that break down the pectic substances
of the middle lamella causing break down and maceration of the tissues (Gupta
and Thind, 2006). Soft rot (Erwinia carotovora subsp. carotovora
(Jones) (Bergey et al., 1939) is of great importance
both in the field as well as in transit and storage, causing heavy economic
losses to various vegetables. In this study, an attempt has been made to review
the relevant available literature concerning soft rot disease in vegetables.
CAUSAL ORGANISM AND ITS MORPHOLOGICAL CULTURAL AND BIOCHEMICAL CHARACTERISTICS
Soft rot of vegetables is caused by various species of, Bacillus, Pseudomonas
and Erwinia (Agrios, 2006). Erwinia carotovora
subsp. carotovora is however considered to be one of the major soft rot
causing bacterium (CCHAU, 2002; Larka,
2004). Erwinia carotovora subsp. carotovora and Pseudomonas fluorescens
cause the most common and most destructive soft rots. Erwinia carotovora
sub-sp atroseptica may be thought of as a cool temperate variety of Erwinia
carotovora sub-sp. carotovora (Agrios, 2006).
Erwinia carotovora are straight rods, 0.5-1x1-3 microns mainly single;
motile with peritrichous flagella. Gram negative, facultatively anaerobic; catalase
positive, oxidase negative, Urease not produced by the bacterium. Acid is produced
from D (+) glucose, D (+) galactose, D(-) fructose and sucrose. Starch is not
hydrolyzed but the bacterium readily hydrolyses gelatin and pectin. Optimum
temperature for Erwinia carotovora ranges from 27-30°C maximum varies
from 32-40°C (Bradbury, 1986).
They are non pigmented and grows well in most laboratory media, produces H2S
from cystine. Reduces nitrate, some strains also produce gas but others are
anaerobic produce acid actively from various carbohydrates (Bradbury,
1986). Erwinia carotovora sub-sp atroseptica has similar properties
except its maximum temperature for growth is 35°C and shows acidic reaction
in 7 days with alpha-methylglucoside and utilizes maltose unlike Erwinia
carotovora sub-sp. carotovora (Bradbury, 1986).
Bacterium generally produces white colonies on nutrient agar and cloudy growth
in nutrient broth (Gupta and Thind, 2006).
OCCURRENCE AND SEVERITY OF THE DISEASE
Bacterial soft rot occurs world wide and causes serious diseases of vegetable
crops in the field, in transit and especially in the storage. It causes a greater
total loss of produce than any other bacterial disease (Agrios,
2006). Bacterial soft rot of vegetables has been studied since 1891 when
Halsted described it on celery (Walker, 1998). A few years later it was recorded
as injuring cabbage and other crucifers (Russel, 1898).
It was in 1901 the disease was described in detail on carrots (Jones,
1901; Harrison, 1904). Since then the organism under
various names, has been observed on following additional hosts; artichoke, asparagus,
cauliflower, egg plant, pepper, potato, radish, rhubarb, tomato and turnip (Hurding
et al., 1909; Johnson and Adams, 1910).
Recently Farrar et al. (2009) reported that
lenticel rot caused by E. carotovora in potato has probably been in California
since potato production became established in Kern County in 1912, but did not
reach damaging levels until the late 1990s. soft rot in vegetables have been
reported from all over the world, Rajeh and Khlaif (2000)
reported soft rot disease caused by E. carotovora from different areas
of Jordan including Jordan valleu and upland. Togoshi et
al. (1988) gave the first report of bacterial soft rot in vegetables
grown on burnt fields in Japan. In Norway this disease has been reported to
cause serious problem in Chinese cabbage (Balvoll, 1995).
In India E. carotovora subsp. carotovora is considered to be one
of the major soft rot causing bacterium in the tropics (CCHAU,
2002; Larka, 2004). In northern India where cabbage
is grown for seed production the disease cause rotting of cabbage heads which
later on fails to through flowering shoots (Gupta and Thind,
2006). Patel et al. (1970) reported during
analysis of second major Black rot epidemics in cauliflower during 1968-69 that
stump rot in cauliflower due to E. carotovora and other associated pathogens
generally follow a severe infection of black rot. This had not been described
previously from India and occurred in nearly all fields surveyed. Occurrence
of soft rot on maturing cabbage heads were also reported from Udaipur (Rajastan)
by Chakravarti and Hegde (1972).
Soft rot disease caused by Erwinia carotovora has a very wide host range
infecting large number of vegetable species belonging to different families.
Walker, 1998 has reviewed bacterial soft rot in crucifers and reports that
if not all but many crucifers are susceptible to bacterial soft rot which include
cabbage, cauliflower, brussel sprouts, kohlrabi, turnip, radish, rape, horse
radish and rutabaga. The host range includes genera from all the plant families
of vegetables, fruits and ornamentals, nearly about sixty four plant species
are susceptible to the disease (Anonymous, 1990). Togoshi
et al. (1988) isolated 52 isolates of bacteria from 15 different
vegetable crops showing soft rot symptoms from Tsuruoka district of Japan, out
of which 36 isolated were of E. carotovora subsp. carotovora and
16 were E. carotovora subsp. atroseptica.
Phokim et al. (2006) conducted a DNA polymerase chain reaction assay
using Y1 and Y2 primers specific to amplify 434 bp pectate lyase gene (Pel)
of E. carotovora from ten different varieties of vegetables viz., cabbage,
cauliflower, Chinese cabbage, pakchoi, spinach, carrot, Chinese radish, cucumber,
tomato and asparagus. The result showed that primers Y1 and Y2 detected all
isolates and were classified as soft rot Erwinias..
Rajeh and Khlaif (2000) during a survey in different
areas in Jordan collected eighty seven isolates of bacteria from soft rot symptoms
from different vegetable crops including, cabbage, cauliflower, chard, common
mellow, Gladiolus sp., lettuce, onion, pepper, potato, spinach, sweet
melon and tomato. Upon identification it was observed that cause of soft rot
in all the vegetables is E. carotovora. Bradbury, 1986
has reviewed the host range of E. carotovora subsp. carotovora
and reported that B. chinensis ( Chinese cabbage) B.o var acephala
(kale), Cucumis sativus, Delphinum ajacis Glycine max, Helianthus
tuberosus, Lupinus sp., Phaseolus vulgaris, Nicotiane tabacum,
as its hosts while Solunum tuborosum as main host of E. carotovora
subsp. atroseptica but natural infection has also been reported for this
sub- specie on cauliflower, cabbage, iris and tomato E. carotovora have
been reportedly causing severe post harvest soft rot and stem end decay that
result in losses to bell pepper in Florida (Sherman and
There are no accurate measurements of fleshy fruits and vegetables to post
harvest bacterial soft rots. They are estimated, however to vary between 15-30%
of harvested crop (Agrios, 2006). The economic importance
of losses caused by soft rot bacteria can be very great, depending upon the
value of the crop and the severity of the attack. Although accurate estimates
of the losses are not available, they may cause up to $50 to 100x106 annually
on a world wide basis. The extent of these losses varies from country to country
and is influenced by climate, conditions of growth and storage (Perombelon
and Kelman, 1980). Walker, 1998 reported that no actual figure of losses
have been collected for all the hosts yet it probably is safe to assume that
few other phytopathogenic organisms cause a greater total loss. He also describes
the disease extremely destructive in some instances causing injury to cabbage
seed plants and often follows black rot of cabbage. Severe post harvest losses
had been reportedly incurred by bacterial soft rot or stem end decay in bell
pepper during transit and marketing (Sherman and Allen,
1983). Ceponis and Butterfield (1974) reported sever
market losses in metropolitan New York in cucumber and bell pepper which were
produced in Florida. Bacterial soft rot has been said to be the most important
single cause of wastage in stored potatoes (Harris, 1979).
In Japan the disease has been reportedly been causing severe damage to vegetables
including cabbage (Tatsuyama, 1961; Umekawa,
1991). Soft rot is also known to cause severe damage to cabbage during distribution
under high temperature and poor transportation system in countries like Indonesia,
Malaysia and Singapore (Higashio and Yamada, 2004).
Farrar et al. (2009) observed that the potato
in Keren County, California is affected by E. carotovora subsp. carotovora
an estimated of 30% of the harvested produce is effected. They further reported
that excessive post harvest losses caused by E. carotovora subsp. carotovora
have resulted in significant losses to San Joaquin Valley. Produce buyers for
large national grocery outlets carefully scrutinize California potatoes for
sunken and rotted tissue. Unsightly rotted or discolored lenticel tissues render
the potatoes unmarketable and occasionally shipments of California potatoes
are dumped. A survey of the post-harvest fruit rot diseases of tomato was conducted
in five states of Nigeria. During severe infections, the diseases could cause
25% loss at harvest and 34% loss of the remaining product in transit, storage
and market stalls; thus giving an overall loss of about 50% of the product.
Two types of rots, soft and dry were recognised. The soft rot was found to account
for about 85% of total losses (Fajola, 1978).
Disease has much the same appearance on each host. The effected tissue becomes
soft and slimy without much discoloration, but often accomplished by an offensive
smell. Soft rot symptoms begin as small water soaked lesion, which enlarge rapidly.
The effected area becomes soft and mushy while its surface become discolored
and some what depressed tissue within effected region become slimy (Walker,
1998). However crucifer plants and onions when infected by soft rot almost
always give off a repulsive odor (Agrios, 2006). Walker (2004) in his description reports that the name of the disease aroused from
characteristic soft decay of fleshy tissue. He further reports that fleshy tissue
of storage organs have cells in a semi-dormant condition and content of carbohydrate
is high, when soft rot effects, the tissue softens, becomes watery or slimy
in consistency and as the rot progresses the water exudates from the effected
Harvest bruises, freezing injury and insect wounds are predisposing factors.
Abundant moisture at the surface of tissue where wounds are present is essential.
After infection fairly high RH is essential for progress of disease (Walker (2004)). The bacteria that cause Erwinia rot are common on the surface
of potato tubers, in soil and in surface irrigation water (Romberg
et al., 2002). Farrar et al. (2009)
reported that during the lifting and harvest of potatoes, tubers can be smeared
with soft-rot bacteria from decayed seed pieces. At the packing shed, potatoes
are first dumped into a wash tank to clean them. Surface bacteria can be pushed
into lenticels by hydrostatic (exerted by water) pressure in the wash tanks
(Bartz and Kelman, 1985). Hydrostatic pressure increases
with increasing depth of the tank. Once inside the lenticel tissue, the bacteria
multiply and cause lenticel rot. Several species of insects are known to carry
the causal organism the relation of the insect with bacterial soft rot disease
has been worked out and first reported by Leach (1926).
Johnson (1930) described the relation of cabbage maggot
and other insects to spread as well as development of soft rot in cruciferae.
Similar observations were recorded by Bonde (1939) while
working on blackleg of potato Walker, 1998 has summarized that when a high
humidity is combined with a temperature of 80°F the pathogen is capable
to cause greatest injury. The optimum temperature for its growth is 85°F
the maximum slightly over 100°F. For this reason much of the loss due to
this disease occurs during middle of the summer. Bhat et
al. (2010) also reported higher growth of pathogen at 30°C and storage
temperature ranging from 30 to 35°C as the most favourable for development
of soft rot on cabbage. Temperature in range of 30-37°C were found optimum
for soft rot development in different vegetable crop species (Farrar
et al., 2000). Raju et al. (2008)
also reported enhansment of rotting ability of the pathogen E. carotovora
subsp. carotovora at increased temperature of 20 to 30°C. They also
reported that increased RH levels enhanced rotting. The highest rotting was
recorded when radish discs were incubated at 35°C and 100%. Walker (2004)
reported that when decaying roots effected by soft rot are placed in dry atmosphere
the rot tissue dehydrated rapidly and further advancement of disease is checked
out. Kikumoto (1974) during field observations using
3 varieties of Chinese cabbage reported that disease was prevalent from early
summer to autumn and developed rapidly at high temperature the population of
Erwinia reached to high levels during mid June and remained for six months
then disappear from root zone or plant parts by following January. Clayton
(1929) had earlier reported that stump rot caused by E. carotovora
and other associated pathogens is unable to attack plants without the presence
of black rot. Similar observations were recorded by Patel
et al. (1970) during analysis of black rot epidemic in 1968-69 in
Solan, in which they observed that stump rot presumably caused by E. carotovora
generally follow severe infection of black rot. Frost injury has also been implicated
as predisposing factor for the causation of soft rot. Kapoor
(1987) reported that in valley areas of Kashmir and Himachal Pradesh where
cabbage is grown for seed production the rotting starts just after frost, chilling
after melting of snow this is because frost injury provides avenues for entry
of bacterium. Galati et al. (2005) reported that
disease becomes apparent under conditions of high soil temperature and moisture.
In Western Australia, bacterial soft rot is seasonal it is most severe under
warm, wet conditions (summer and autumn) and it is usually not a problem under
cooler weather conditions. Excess nitrogen fertilization and irrigation have
both been associated with increased susceptibility to bacterial soft rot, as
excess fertility or water promotes more succulent tissues, making the fruit
more susceptible to physical damage during harvest and handling (Annonymous,
Production of enzymes: Enzymes that hydrolyze the middle lamella of
host tissue in the development of soft rot were studied in great detail by Jones
(1901) and referred the enzymes as pectinase. He reported that action of
this enzyme produced by bacteria is to dissolve middle lamella, which serves
to cement the adjacent cell walls together and thus to loosen the cells from
one another. The by product of the bacterial growth also set ex-osmosis of liquid
containing sugar and salts from within the cells to inter cellular spaces, where
it un-doughtily serve as a source of food for further bacterial growth. The
continuation of this process accounts for the watery condition and for the loss
of consistency of the decayed tissue. Jones (1901) showed
clearly that the pathogenic action was actually brought by the diffusion of
enzymes in advance of bacteria and the later were really saprophytic upon the
hydrolyzed lamella and ex-osmoses material. When soft rot bacteria enter wounds
they feed and multiply at first on the liquid released by the broken cells on
the wound surface then they produce increased amounts of pecteolytic enzymes
that break down pectic substance of middle lamella and bring about maceration
of tissue. Bacteria continue to move and multiply in intercellular spaces; as
a result cells plasmolyse, collapse and die in the intercellular spaces, while
their enzymes advance ahead of them and prepare the tissue for invasion. The
epidermis of most tissue is not attacked by the bacteria; however cracks are
usually present and the slimy mass extrude through them (Agrios,
The capacity to produce pectic enzymes is wide spread in bacteria. According
to most of the workers pectic enzymes which are currently known are, pectinestraces
(PE or PME) and polygalacturonases (PG), pectinestraces or pectin methylestraces
catalyse the hydrolysis of methyl ester groups of pectinic acid to methyl alcohol.
It is of interest that rate of cleavage of α 1, 4 bond of pectic substances
is enhanced by removal of methoxy group and this is illustrated by the fact
that endopolygalacturonase prefers de-methylated pectin (Bateman
and Miller, 1966; Mehrotra and Aggarwal, 2003).
Polygalacturonases or pectic glycosidase are chain splitting enzymes which
break the links between adjacent galacturonic acid units in pectic substances
this occurs by hydrolytic mechanism (hydrolases) or an eliminative mechanism
(lyases) (Mehrotra and Aggarwal, 2003). There had been
some confusion about chain splitting enzymes of pertinacious material; Wood
(1960) followed the classification followed by Denim
and Phaff (1957) who distinguished between the polygalacturonases (PG) which
prefer Pectic acid of the de-esterified parts of pectinic acid as substrates
and Pectin Methyl Galacturonases (PMG) which prefer the esterified chain parts.
They further distinguished these polygalacturonases according to weather they
cause cleavage in glycosidic linkage at random by an endo-type of polygalacturonases
or polymethyl galacturonases, or by an exo-type of action in which the end linkages
Albersheim et al. (1969) made a significant
advance by discovering pectin transeliminase (PTE) which split the pectin chain
by a transeliminative mechanism. This enzyme breaks the glycosidic linkage of
pectin at C4, accompanied by simultaneous elimination of H+ and C5. Protopectinases
are thought to attack protopectin which is a native substance in cell wall,
although the pectinases are widely used for macerating activity (Mehrotra and Aggarwal, 2003). Denim and Phatf (1957) devised a new
system of classification where the macerating principal was shown to be associated
with chain splitting enzymes polygalacturonases (PG and PME) Maceration of plant
tissue has been associated with hydrolases and lyases which degrade the alpha
1-4 linkages in the galacturonic acid polymer of pectin substance in a random
manner (Mehrotra and Aggarwal, 2003).
The work done by McDendon (1974),on purified pectin
enzymes suggests that macerating enzymes are not of only one type. Brown
(1965), Bateman and Miller (1966) emphasized that
the non specific term macerating enzyme should be retained but all macerating
enzymes which have been purified and identified till date have proven to be
pectic enzymes (Mehrotra and Aggarwal, 2003).
There has been considerable variation among the isolates of Erwinia
with respect to their pectinenzyme activites, Gregg (1952)
suggested that the quantitative pathogenic superiority in potato tuber of E.
carotovora was compared with two other strains associated with production
of greater quantity of pecteolytic enzymes. Phokim et
al. (2006) while assessing disease severity of Erwinia sp. by
determining the activity of tissue macerating enzymes; pectate lyase, polygalacturonases,
cellulose and protease with spectrometer and measuring the area of soft rot
symptom on Chinese cabbage after artificial inoculation found out that Erwinia
isolate from carrot was the most severe because it produced higher macerating
enzymes and macerated plant tissue with highest soft rot area in comparison
to other soft rot Erwinias isolated from other 10 varieties of vegetables.
Similar observations were recorded by Zaki et al.
Smith and Bartz (1990) isolated thirty seven strains
of soft rot Erwinias and they found significant differences among the strains
for aggressiveness in tuber and fruits, but the relative aggressiveness on one
host were not always associated with the pathogenicity in the other host.
A number of measures like through cleaning of storage house with formaldehyde (1 pint in 100 gallons of water) or copper sulphate (1 pound in 5 gallons of water), sorting out of any bruises or diseased vegetables and only perfect ones should be stored. It is further suggested to have sufficient ventilation to keep the humidity of air reasonably low, at the same time temperature should be as nearly 32°F, as possible. The trouble may be eliminated partly by long rotations with crops that are immune, as corn, cereals and grasses. In certain cases it may be practical to destroy the insects that may aid in disseminating the bacterium, or injure the host. Reporters also suggests that provisions should be made to control bruising at harvest, healing of wounds and drying of surface (Walker, 1998).
If diseased material had been stored previously in store house, such stores should be sweaped clean and thoroughly sprayed from celing to floor with a disinfectant solution like sodium hypo chloride (1000 to 1900 ppm), sodium o-phenylphenate (0.1 to 0.3%), calcium hypochlorite (700 to 5000 ppm), peracetic acid (3000 ppm) and disinfecting of tools by dipping in 70% alcohol, or 5% Formaldehyde solution (Anonymous, 1990).
Tanaka and Kikumoto (1976) reported no elongated lesions
development when detached Chinese cabbage leaves were exposed to 30% R.H. for
less then two hours at 24- 27°C before inoculation, they reported host cells
were dead in lesions in both dried and non dried leaves Growth and movement
of E. carotovora subsp. carotovora was inhibited in the dried
leaves compared with that in non dried ones. In the dried leaves they reported
no out flow of host cell contents or flow of water from living to dead cells
and failure of development of lesions due to localization of bacteria in incubated
area. Higashio and Yamada, 2004 during a study recognized
drying as one of the simple factors to control soft rot. They further reported
that drying cut end contributes greatly to control and keeping cabbage indoors
for more then one day after the harvest was a more easy and simple way to prevent
occurrences of soft rot in cabbage.
The appearance of soft rot symptoms in storage or in transit can be delayed
by holding plants and produce at a temperature of 4° to 6°. Low temperature
do not prevent bacterial infections, but slow down bacterial soft rot (Anonymous, 1990). Few varieties have resistance to soft rot and no variety is immune (Agrios, 2006). However number of workers have reported more or less degree of susceptibility.
Walker, 1998 reported that among forty verities of turnip that were tested
for comparative susceptibility nearly all showed some rotting, the Jersey navel
being the only one listed immune.
Kikumoto (1984) reported the number of bacterial cells
recovered from inoculated sited of lesions being constantly higher in susceptible
cultivars of Chinese cabbage.
Hot water treatment is recognized as a simple and easy technique to control
the disease and insect damage and is already been put to practical use in many
foreign countries (Gonzalez-Aguilar, 1999; Miura,
2001). However in a study conducted by Higashio and
Yamada, 2004 found no suppressive effect by dipping cabbage heads in hot
water having temperature of 50°C. They found that in certain cases rot was
promoted and concluded that lethal temperatures for soft rot bacterium was more
then used in their study. Similar conclusions were made by Tasuyama (1961) during
their studies on soft rot disease on Chinese cabbage.
As per Farrar et al. (2009) There are no effective
chemical controls for any of the soft-rot Erwinias. As per Galati
et al. (2005) chlorination is only recommended if carrots break down,
because the disease occurs only under certain conditions. He suggested the use
of sodium or calcium hypochlorite as the source of chlorine. Chlorination should
take place after dirt and debris is removed from the carrot root. Chlorine quickly
loses effectiveness when soil, leaves or diseased roots are present in the water,
soit is important to check chlorine concentrations and pH often. Washing water
should be changed as often as practical. However reportedly there are limitations
to chlorination. Chlorination acts as a preventative measure only. If there
is already disease, decay or injury in the field, chlorine will help limit spread
of soft rot in storage. The disinfectant activity of a chlorines solution is
determined by its pH, lower the pH greater the amount of hypochlorus acid available
for disinfection. However vegetables and fruits are damaged by low pH chlorine
solutions (Anonymous, 1990). In Japan hypochlorus acid
is the only chemical used to disinfect fresh vegetables and is being used to
control microorganisms in shredded vegetables (Ishigaro,
2002). In the study conducted by Higashio and Yamada,
2004, reported only a certain degree of soft rot suppression after hypochlorus
acid application during post harvest management of disease. They further reported
that effect on hypochlorus acid treatment did not occur at high humidity conditions.
They stored the cabbage under various degrees of dryness after harvest and found
that by keeping heads indoors for more then one day after the harvest had good
effect in control of soft rot, which they attributed to healing of injuries
of cabbage head which they receive at the time of harvest because it is thought
that soft rot bacterium dose not enter a plant without a wound.
Mills et al. (2006) tested several salt compounds
as inhibitors of Erwinia carotovora subsp. atroseptica and Erwinia
carotovora subsp. carotovora causing bacterial soft rot of potato.
In-vitro studies with sodium metabisulphate, propyl paraben, alum, potassium
sorbate, calcium propionate and copper sulphate pentahydrate showed that they
were completely inhibitory at lowest concentration (0.002M). They further reported
that as preventive disease control measures, tubers treated only with alum,
aluminum acetate, calcium propionate, sodium bicarbonate sodium hypochlorite
or copper sulphate pentahydrate resulted in less soft rot then untreated control,
while as for curative disease control measures tubers treated with only alum,
aluminum acetate, sodium hypochlorite, or copper sulphate pentahydrate resulted
in significantly less soft rot then untreated control.
During a study conducted by Sherman and Allen (1983)
on post harvest soft rot in bell pepper stored in jumble packed waxed corrugated
cartons, reveals that inoculation with Erwinia greatly increased decay. This
fact underscores the need for strict sanitation measures during pepper harvesting
and handling procedures. Chlorination of vegetable packing house water gave
conflicting results as washing with water alone before packing was as effective
as washing with (150 ppm concentration). They further reported vacuum cooling
of bell pepper was beneficial in reducing bacterial soft rot during storage
In Indonesia cement in which main constituent being calcium hydroxide application
at the cut end was introduced to control soft rot (Tasuyama, 1961). The efficacy
of cement was also confirmed by Higashio and Yamada, 2004 who evaluated various
calcium chemicals like calcium hydroxide, calcium carbonate, calcium sulphate
dehydrate, calcium phosphate tribasic, calcium dihydrogen phosphate monohydrate
and calcium hydrogen phosphate along with cement. Calcium proved effective,
however some chemicals showed a tendency to promote soft rot despite being calcium
compounds. Because of which they considered that the effect of cement application
was caused by the interception of bacteria at wounds rather then any physical
function of calcium.
Harris (1979) while testing five chemicals against
soft rot to batches of wounded potato tubers by dipping in a 1.5g Lit-1.
solution for 1 min reported, 5-nitro-8-hydroxyquinone as most effective in reducing
rotting. 8-hydroxyquinoline, SD740823AX and chlorine dioxide also gave some
control, while El badyne had no significant effect. However during in vivo tests
El badyne and chlorine dioxide were less effective.
Not much work has been so far conducted to control bacterial soft rot by antibiotics.
However certain reports pertaining to control of soft rot disease are those
of, Kapoor (1999) who has recommended streptocycline
in combination with copper oxychloride for control of this disease. He also
reported that cruciferous like cauliflower seed crop and curd rot have been
reportedly under check by the application of chloramphenical + captofol (1:2).
Mazzucchi and Svampa (1972) have reported that in green
house test using inoculated courgette seedlings, antibiotic preparations based
on streptomycin and / or tetracycline gave the best control of E. carotovora
while copper compounds and a few experimental compounds gave a partial control.
Good calcium fertility management in the field also reduces postharvest Erwinia
losses. Calcium is integral to maintaining cell-wall rigidity and it counters
the activity of soft-rot Erwinia enzymes, which degrade the cell walls (Farrar
et al., 2009). They further reported antimicrobial agents such as
peroxyacetic acid and hydrogen peroxide, applied as a final rinse in the packing
process, are effective in reducing the tuber surface populations of soft-rot
organisms, resulting in less postharvest loss to Erwinia rot.
Agrios, G.N., 2006. Bacterial Soft Rots. 5th Edn., Academic Press, San Diego.
Albersheim, P., T.M. Jones and P.D. English, 1969. Biochemistry of cell wall in relation to infective procures. Ann. Rev. Phytopathol., 7: 171-194.
Annonymous, 2006. Post harvest decay of bell pepper. Bacterial Soft Rot. http://www.highlandfresh.net/tb_pepper_intro.html.
Anonymous, 1990. Bacterial soft rot of vegetables fruits and ornamentals. Report on Plant Disease RPD No. 943. Department of Crop Science University of Illions. http://ipm.illinois.edu/diseases/rpds/943.pdf.
Balvoll, G., 1995. Introduction of Chinese cabbage in Norway: Problems and possibilities. J. Vegetable Crop Prod., 1: 3-18.
Bartz, J.A. and A. Kelman, 1985. Infiltration of sentinels of potato tubers by Erwinia carotovora sub sp. Caratovora under hydrostatic pressure in relation to bacterial soft rot. Plant Dis., 69: 69-74.
Bateman, D.F. and R.L. Millar, 1966. Pectic enzymes in tissue degradation. Ann. Rev. Phytopathol., 4: 119-146.
Bergey, D.H., F.C. Harrison, R.S. Bread, B.W. Hammer and F.M. Huntoon, 1939. Bergey`s Manual of Determinative Bacteriology. Williams and Wilkins, Baltimore.
Bhat, K.A., S.D. Masoodi, N.A. Bhat, M.Ahmad, M.Y. Zargar, S.A. Mir and M. Ashraf-Bhat, 2010. Studies on the effect of temperature on the development of soft rot of cabbage (Brassica oleracea var capitata) caused by Erwinia carotovora subsp. J. Phytopathol., 2: 64-67.
Direct Link |
Bonde, R., 1939. The role of insects in dissemination of potato back leg and seed picae decay. J. Agric. Res., 59: 889-917.
Bradbury, J.F., 1986. Guide to Plant Pathogenic Bacteria. CAB International Mycological Institute, New York, USA., ISBN-13: 9780000000972, Pages: 332.
Brown, W., 1965. Toxins and cell wall dissolving enxymes in relation to plant disease. Ann. Rev. Phytopathol., 3: 1-18.
CCHAU, 2002. Studies on recently occurring bacterial diseases of various crops in Haryana. Technical Report. Chowdhery Cheran Singh Heryana Agricultural University, Hisar, India, pp: 4-6.
Ceponis, M.J. and J.E. Butterfield, 1974. Market losses in Florida cucumber and bell pepper in metropolitan New York. Plant Dis. Rep., 58: 553-560.
Chakravarti, B.P. and S.V. Hegde, 1972. Occurance of bacterial soft rot in black rot effected cabbage plantws in Udaipur Rajastan. Indian Phytopathol., 25: 118-122.
Clayton, E.E., 1929. Studies on the black rot or blight disease of cauliflowers. N.Y. State Agric. Exp. Station Bull., 576: 4-4.
Denim, A.L. and H.J. Phaff, 1957. Recent advances in the enzymatic hydrolysis of pectic substances. Wallerstein Labs. Commun., 20: 119-140.
Fajola, A.O., 1978. The post harvest fruit rot of tomato (Lycopersicum esculentum) in Nigeria. Nahrung Food, 23: 105-109.
Farrar, J.J., J.J. Nunez and R.M. Davis, 2000. Influence of soil saturation and temperature on Erwinia chrysanthemi soft rot of carrot. Plant Dis., 84: 665-668.
CrossRef | Direct Link |
Farrar, J.J., J.J. Nunez and R.M. Davis, 2009. Losses due to lenticel rot are an increasing concern for Karen county potato growers. California Agric., 63: 127-130.
Galati, A., A. McKay and S.C. Tan, 2005. Minimising post harvest losses of carrots. Farmnote No. 75/95. Department of Agriculture and Food. Government of Western Australia, South Perth.
Gonzalez-Aguilar, A.G., 1999. Storage quality of bell pepper pretreated with hot water and polythene packing. J. Food Q., 22: 287-299.
Gregg, M., 1952. Studies in the physiology of parasistism XVII. Enxyme secretion by strains of bacterium carotovorum and other pathogens in relation to parasitic vigor. Ann. Bot., 16: 235-250.
Gupta, S.K. and T.S. Thind, 2006. Diseases of Cruciferous Vegetables. Scientific Publishers, India, pp: 170-185.
Harris, R.I., 1979. Chemical control of bacterial soft rot of wounded potatoes. Potato Res., 22: 245-249.
Harrison, F.C., 1904. A bacterial disease of cauliflower and allied plants. Ontairo Agric. Exp. Station Bull., 137: 1-32.
Higashio, H. and M. Yamada, 2004. Control of soft rot after harvest of cabbage in Indonesia. JARQ, 38: 175-178.
Hurding, H.A., W.J. Morse and L.R. Jones, 1909. The bacterial soft rot of certain vegetables. N. Y. Agric. Exp. Station Technical Bull., 11: 251-368.
Ishigaro, A., 2002. The Reality of the Washing Sterilization of Shredded Vegetables. In: Katto Yasai Jitsumu Handbook (Business Handbook of Shredded Vegetables), Hasegawa, Y. (Ed.). Science Forum, Tokyo, pp: 163-173.
Johnson, D.E., 1930. The relation of cabbage maggot and other insects to the spread and development of soft rot of cruciferae. Phytopathology, 20: 857-872.
Johnson, T. and J. Adams, 1910. Bacterial rot in turnip and other brassicas in reland. Econ. Proc. R. Soc. Dublin, 2: 1-7.
Jones, L.R., 1901. A soft rot of carrot and other vegetable caused by Bacillus carotororus. Victoria Agric. Exp. Station Ann. Rep., 13: 299-332.
Kapoor, K.S., 1987. Bacterial soft rot (Brwinia carotovora) of cabbage. Plant Dis., 71: 861-861.
Kapoor, K.S., 1999. Fungal and Bacterial Diseases of Crucifers. In: Diseases of Horticultural Crops: Vegetables, Ornamentals and Mushrooms, Verma, L.R. and R.C. Sherma (Eds.). Indus Publishing Co., New Delhi.
Kikumoto, T., 1974. The role of Chinese cabbage culture in seasonal trends in the populations of the soft rot bacteria in soil. Bull. Inst. Agric. Res. Tohoku Univ., 25: 125-137.
Kikumoto, T., 1984. Ecological studies on the soft rot bacteria of vegetables. Bull. Inst. Agric. Res., 35: 63-73.
Larka, B.S., 2004. Integrated approach for the management of soft rot (Pectobacterium carotovorum sub-sp. carotovorum) of radish (Raphanus sativus) seed crop. Haryana J. Agron., 20: 128-129.
Leach, J.G., 1926. The relation of seed corn maggot (Phorbia fuseiceps Zett.) to the spread and development of potato black leg in minnebta. Phytopathology, 16: 149-176.
Mazzucchi, U. and G. Svampa, 1972. Trials on control of Erwinia carotovora, the causal agent in soft rot of vegetables. First contribution. Informatore Fitopatologico, 22: 10-10.
McDendon, J.H., 1974. Evidence for the pectic nature of the middle lamelle at potato tuber cell walls based on chromatography of macerating enzymes. Am. J. Bot., 51: 628-633.
Mehrotra, R.S. and A. Aggarwal, 2003. Pectic Enymes. Tata McGraw Will Publishers, West Patel Negar, New Delhi, pp: 72-75.
Mills, A.A.S., H.W. Plat and R.A.R. Hurta, 2006. Sensitivity of Erwinia spp. to salt compounds in vitro and their effect on the development of soft rot in potato tubers in storage. Post Harvest Biol. Technol., 41: 208-214.
Miura, K., 2001. Shinpen Yasai Engei Handbook. In: Vegetable Gardening Handbook, Nishi, S. (Eds.). Yokendo Co. Ltd., Tokyo, pp: 163-173.
Patel, P.N., B.M. Trivedi, S.S. Rekhi, P.A. Town and Y.P. Rao, 1970. Black rot and stump rot in cauliflower seed crops in India. FAO Plant Prot. Bull., 18: 136-141.
Perombelon, M.C.M. and A. Kelman, 1980. Ecology of the soft rot Erwinias. Ann. Rev. Phytopathol., 18: 361-387.
Phokim, C., P. Jitareerat, S. Photchanachai and S. Cheevadhanarak, 2006. Detection and classification of soft rot Erwinia of vegetables in Thailand by DNA polymerase chain reaction. Proc. 4th Int. Conf. Managing Q. Chains Acta-Hortic., 712: 917-925.
Direct Link |
Rajeh, O.N. and H. Khlaif, 2000. Soft rot disease of vegetables in Jordan; host range, reaction of some potato cultivars to the infection and effect of planting date. Dirasat Agric. Sci., 27: 149-157.
Direct Link |
Raju, M.R.B., V. Pal and I. Jalali, 2008. Inoculation method of Pectobacterium carotovorum sub sp. carotovorum and factors influencing development of bacterial soft rot in Radish. J. Mycol. Plant Pathol., 38: 311-315.
Romberg, M.K., R.M., Davis, J.J. Nunez and J.J. Farrar, 2002. Sources and prevention of Erwinia early drying of potato in Karen country. California Phytopathol., 92: S70-S70.
Russel, H.L., 1998. A bacterial rot of cabbage and allied plants. Wisconqen Agric. Exp. Station Bull., 65: 1-39.
Sherman, M. and J.J. Allen, 1983. Impact of post harvest handling process on soft rot decay of bell pepper. Proc. Florida State Hortic. Soc., 96: 320-322.
Direct Link |
Smith, C. and J.A. Bartz, 1990. Variation in the pathogenicity and aggressiveness of strains of Erwince carotovora sub sp. Carutoura isolated from different hosts. Plant Dis., 74: 505-509.
Tanaka, T. and T. Kikumoto, 1976. Inhibition of growth and movement of soft rot bacteria by lowering the water content in the leaf tissue of Chinese Cabbage. Bull. Inst. Agric. Res., 27: 89-101.
Tatsuyama, H., 1961. Studies on soft rot disease of Chinese cabbage caused by Frwinia aroideae (Towns) Hall. Bull. Inst. Agric. Res., 13: 221-345.
Togoshi, J., S. Takahashi and Y. Shibata, 1988. Bacterial soft rot in red turnip Brassica compertris L. (rapifera group) cv. Atsumi-kabu, grown in burnt fields. Annu. Phytopathol. Soc. Japan, 54: 616-619.
Umekawa, M., 1991. Bacterial Soft Rot of Cabbage. In: Bacterial Crop Disease in Japan-A Guide for Diagnoses and Control, Tabei, H. (Ed.). Japan Plant Protection Association, Japan, pp: 215-216.
Walker, J.C. 1998. Bacterial Soft Rots of Carrot. Discovery Publishing House, New Delhi, pp: 78.
Walker, J.C., 2004. Bacterial Soft Rot. In: Manual of Vegetable Plant Diseases, Chupp, C. (Ed.). Shristi Book Distributors, New Delhi.
Wood, R.K.S., 1960. Pectic and celhlolytic enzymes in plant disease. Ann. Rev. Physiol., 11: 299-322.
Zaki, M.M., S.A.Z. Mahmohd and F.G. Fawzi, 1978. Enzymatic activities of soft rot bacteria in relation to pathogenesis. Proceedings of the 1st Conference on Biological Aspects of Sandi Arabia, Jan. 15-17, University of Riyad, pp: 325-336.