Guava Diseases - their Symptoms, Causes
Central Institute for Subtropical Horticulture,
Rehmankhera, PO. Kakori, Lucknow-227 107, India
Abstract: Guava (Psidium guajava Linn.) an important fruit of subtropical countries is af-
fected by about 177 pathogens of which, 167 are fungal, 3 bacterial, 3 algal, 3 nematodes and
one epiphyte. Wilt is the most important disease of guava. Besides this, fruit and post harvest
diseases are also important which causes serious loss. The fruit diseases are of two types i.e.
field diseases and post harvest diseases, which develop during transit and storage. Due to it's
perishable nature number of pathogens are reported on fruits which causes different types of
rots of guava fruits. In the present communication all major diseases are described with their
symptoms, causal organisms and disease management practices.
Guava (Psidium guajava Linn.) is an important fruit of subtropical countries. It is hardy
crop and is cultivated successfully even in neglected soils. There are number of patho-
gens, mainly fungal which affect guava crop besides few bacterial, algal and some
physiological disorders or deficiencies. About 177 pathogens are reported on various
parts of guava plant or associated with guava, fruit of which, 167 are fungal, 3 bacterial,
3 algal, 3 nematodes and one epiphyte. About 91 pathogens are reported on fruits, 42
on foliage, 18 on twig, 18 on root and 17 fungi are isolated with surface wash of fruits.
These cause various diseases viz. pre and post harvest rots of fruits (dry rots, wet rots,
soft rots, sour rots, anthracnose, brown rots, ripe rots, scab, styler end rots, ring rots,
pink rots and waxy fruit rots etc.), canker, wilt, die back, defoliation, twig drying, leaf
spot, leaf blight, anthracnose, red rust, sooty mould, rust, seedling blight and damping
off etc. (Misra and Prakash, 1990). Wilt is one of the most destructive diseases of guava
in India and loss due to this disease is substantial. As the disease is of soil borne in
nature, there are limitations for the control of this disease. Other important field dis-
eases of guava are anthracnose (Gloeosporium psidii Dec1acr
canker (Pestalotia psidii Pat.), and algal leaf and fruit spot (Cephaleuros virescens
Kuntze) etc. Some twig/stem diseases which are of minor importance are twig blight
(Phomopsis psidii de Camara), stem canker and die back, drying and defoliation (Torula
stage of Hendersonula toruloidea Nattrass.). There are number of foliar pathogens
causing leaf blight and leaf spots. Leaf blight causing pathogens are Phoma jolyana,
Priozy and Morg., Alternaria alternata (Fr.) Keissler, while leaf spot causing patho-
gens are Cercospora sawada Yamamoto, Pestalotiajodhpurensis Bilgrarni and Purohit,
S.A.MH. Naqvi (ed.), Diseases of Fruits and Vegetables, Volume II, 81-119.
Kluwer Academic Publishers. Printed in the Netherlands.
Discosia hiptage Lib., Curvularia siddiqui Ahmed
Quraishi, and Pestalotiopsis
psidii (Pat.) Mordue. Leaffall caused by Phytophthora hevea,rust caused by Puccinia
psidii Wint. and spotted anthracnose caused by Sphaceloma psidii are also reported.
Among the root diseases, damping off of seedlings caused by Rhizoctonia solani
Kuhn. and root rot by Clitocybe tabascens (Scop.) Bres., are reported. Fruit rots in field
(pre harvest rots) or during transit and storage (post harvest rots) are the most serious
diseases of guava, which cause maximum loss. It can be said that due to the perishable
nature of the fruit and very short self life, guava suffers badly by different rot patho-
gens. Phytophthora, Diplodia, Phomopsis, Gloeosporium and Guignardia fruit rots
which can be classified as field rots, and further damage fruits during transit and stor-
age. Among the important storage rots, Gloeosporium psidii, Pestalotia psidii,
Phytophthora nicotianae var. parasitica Dastur, Macrophoma allahabadensis Kapoor
& Tandon, Phomopsis psidii, Geotrichum candidum Link ex Pers., Botryodiplodia
theobromae Pat., Fusarium solani (Mart.)App. & Wollenw, Pestalotiopsis psidii,
Fusarium moniliforme var. intermedium, Phytophthora citricola Sawada cause dam-
age to the fruits in various ways. Diseases due to some of the deficiencies like zinc,
magnesium, other nutritional deficiencies are also reported besides physiological dis-
orders like fruit firm rot and internal break down. Thus though the guava is hardy plant,
but it suffers by number of important diseases viz. wilt and fruit rots resulting in the
high loss of guava production in India and abroad.
Wilt of guava is one of the most important diseases of guava especially in India and
loss due to this disease is substantial. As the disease is soil borne in nature, there are
limitations in it's control. Misra and Pandey (1999b) reported that the disease is a
challenge for coming millennium as chemical control proved unsatisfactory in field.
Although, more than five decades have been passed since the disease was first re-
ported (Das Gupta and Rai, 1947), limited progress has been made in the understanding
of the disease. Comprehensive review of work has been done on wilt disease of guava
by Prakash and Misra (1993), Misra (1995), Misra and Pandey (1996), Misra (2001) and
Negi et al. (200 1).
2.1 Geographical distribution
India, wilt of guava was first reported in 1935 from Babakkarpur (Allahabad). Das
Gupta and Rai (1947) recorded the disease in a severe form in orchards of Lucknow,
while Dey (1948) reported it from Allahabad, Kanpur and Lucknow. During 1949-50,
guava trees suffered serious losses in 11 districts of UP (Anonymous, 1949, 1950).
Prasad et al., (1952) estimated that guava wilt spread rapidly to cover about 20.000 sq.
m area in UP, while, Mathur (1956) was of the view that 15-30 per cent trees inAllahabad,
Farrukhabad and Unnao districts, 5-15 per cent in Kanpur and Jaunpur and less than 5
per cent in Gorakhpur, Ballia, Hardoi, Barabanki and Varanasi districts were affected.
Edward and Srivastava (1957) reported wilt as the most serious disease threatening
guava culti vation in UP. Disease was also reported from western districts of UP (Singh
GUAVA DISEASES AND MANAGEMENT 83
and Lal, 1953), Varanasi (pandey and Dwivedi, 1985), Kaimganj (Farrukhabad), Bithoor
(Kanpur), Ganga Ghat (Unnao), Abbubakarpur (Allahabad), Lucknow, Bichpuri (Agra),
Sasni (Aligarh) (Misra and Prakash, 1986, Misra, 1987). Occurrence of wilt was also
reported from guava orchards in West Bengal (Chattopadhyay and Sen Gupta, 1955)
where it was confined to mainly in the Gangetic alluvium of Baruipur area in the district
of 24 Parganas and in the laterite zone of Jhargram and Midnapur in the districts of
Midnapur and of Kashakul in the district of Bankura (Chattopadhyay and Bhattacharjya,
1968a,b). Besides U.P. and West Bengal, the disease has also been reported to occur in
Haryana (Suhag, 1976, Mehta, 1987), Punjab (Chandra et al., 1986), Rajasthan (Katyal,
1972), Delhi state (Anonymous, 1953), Bihar (Kumar, 1993) and Andbra Pradesh (Jhooty
1984). Recently the disease was also recorded in severe form from Hatod guava
area of Indore (M.P.), India (Personal observation).
From other parts of world too, similar symptoms of wilt or the death of plants
have been reported but with different pathogens. Disease has been reported from
countries like U.S.A., Florida (Webber, 1928), Taiwan (Hsieh et
1976, Leo and Kao,
1979), Cuba (Rodriguez and Landa, 1977), South Africa (Grech, 1985), Brazil (Tokeshi et
al., 1980, Rodrigues et al., 1987), Pakistan (Ansar et al., 1994).
Singh and La1 (1953) estimated 5-15 per cent losses every year in 12 districts of U.P.,
which was around Rs. 1million during 1953.
West Bengal, it reduced the yield by 80
per cent i.e., from 113.5q / ha in healthy plantations to about 18.16-22.7q / ha in affected
orchards (Chattopadhyay and Sen Gupta, 1955). Attempt to regenerate the affected
trees failed and new seedlings or grafts planted in affected succumbed to wilt within a
very short time (Chattopadhyay and Bhattacharjya, 1968a).
Andhra Pradesh, 7,000
acres of land was under guava cultivation and disease reduced the land value to half
1984). About 150 acres of guava orchards in Punjab and 300 acres in
Haryana were uprooted during 1978-81 as these were affected by wilt (Jhooty et al.,
1984). Assessment of loss around Lucknow revealed that loss vary from 5-60 per cent
and above 5 year old guava plants are more prone to wilt incidence (Misra and Shukla,
First external symptom of the disease is the appearance of yellow colouration with
slight curling of the leaves of the terminal branches. Plants, at a later stage, show un-
thriftiness with yellow to reddish discolouration ofleaves. Subsequently, there is pre-
mature shedding of leaves. Some of the twigs become bare and fail to bring forth new
leaves or flowers and eventually dry up. Fruits of all the affected branches remain
underdeveloped, hard and stony. Later on, the entire plant becomes defoliated and
eventually dies. Usually, fifteen days are required for complete wilting but some treestake
up to one year. The finer roots show black streaks, which become prominent on remov-
ing the bark (Das Gupta and Rai, 1947). The roots also show rotting at the basal region
and the bark is easily detachable from the cortex. The cortical regions of the stem and
root show distinct discoloration and damage. Light brown discoloration is also noticed
in vascular tissues (Chattopadhyay and Bhattacharjya, 1968a,b). The pathogen attacks
young as well as old fruit bearing trees but older trees are more prone to the disease.
New seedlings and grafts also show disease symptoms (Singh and Lal, 1953 and Ed-
ward, 1960b). Mainly two main symptoms are identified: (a) Slow wilt and (b) Sudden
wilt (Chakraborty and Singh, 1989).
2.4 Causal organism
The exact cause of the disease is still not fully understood but the pathogens viz.
Fusarium oxysporum f. sp. psidii (Prasad, Mehta
Lal), F. solani(Mart.)App. &
Wollenw., Macrophomina phaeseoli (Maubl.) Ashby, Rhizoctonia bataticola (Taub.)
Bulter, Cephlosporium sp. and Gliocladium roseum (Link ex Fr.) and various patho-
gens are reported by different workers may be the incitant of the disease. Prior to 1941,
wilt was considered to be caused by Cephalosporium sp. (Vestal, 1941). Dey (1948)
also invariably isolated Cephalosporium from roots of wilted plants. Das Gupta and Rai
(1947) reported the association of Fusarium sp. Later, Prasad et al. (1952)
attributed wilt due to Fusarium oxysporum (Fr.) Schl. and proposed the name Fusarium
oxysporum (Fr.) Schl. f.sp. psidii Prasad, Mehta and Lal. It was also supported by
Edward and Srivastava (1957) and Pandey and Dwivedi (1985). Edward (1960a) also
observed that F. oxysporum f. sp. psidii exist in a variety of forms, which differ in
cultural and morphological characters. Besides the involvement of above pathogens,
association of the other pathogens have also been suspected in inducing wilt disease
West Bengal, both M. phaseoli and F. solani were reported to incite wilt
either individually or in combination.
either case, the fungus first colonizes the surface of roots and then enters in
to it's epidermal cells. There after, intercellular mycelium establishes first in epidermal
cells and then spreads into cortical cells which get considerably damaged and filled up
with the mycelium. Fusarium solani enters the xylem vessels, grows inside and blocks
them. Macrophomina phaseoli first invades the phloem and destroys it. The xylem
vessels are also attacked in a few cases (Chattopadhyay and Bhattacharjya, 1968a,b,
Chattopadhyay and Sengupta, 1955). Wilt and dieback of guava are also reported to be
caused by Gloeosporium psidii Dec1acr. The fungus penetrate the petiole and attack
the young leaves which become distorted with dead areas at the margins or tips and in
severe cases, die (Tandon and Agarwal, 1954). F. oxysporum
sp. psidii penetrate
either directly through the root piliferous layer of the guava seedlings or through
openings caused by secondary roots. Hyphae are found in the xylem vessels of the
roots of the inoculated plants (Edward, 1960b). Histopathological observations made
by various workers in naturally wilted and artificially inoculated plants revealed the
presence of F. solani, F.oxysporum and M. phaseolina (Tassi) Goid. in vascular tissues
(Chattopadhyay and Bhattacharjya, 1968a,b, Edward, 1960c, Chandra Mohan, 1985,
Pandey and Dwivedi, 1985 and Sohi, 1983a,b). Gliocladium vermoesenii Corda., a
known saprophytic fungus, is also found associated with diseased plants (Chandra
Mohan, 1985). From Varanasi F.oxysporum fsp.psidii, F. solani, F. coeruleum, F.
moniliforme and Rhizoctonia solani Kuehn were also from rhizoplane as well as from
GUAVA DISEASES AND MANAGEMENT
the soil (Dwivedi, 199Ia). Cylindrocarpon lucidum Wollenw., Gliocladium virens and
Bartilinia robillardoides Tassi. caused drooping and subsequent wilting of guava
seedlings grown in Hoagland's solution on artificial testing (Misra and Pandey, 1992).
The reports from the other parts of the world are different. Similar symptoms of
wilt are reported but with different pathogens. As early as in 1928, Clitocybe tabescens
killing guava trees in Florida (USA) was reported (Webber, 1928). In Taiwan, the disease
is reported to be caused by Myxosporium psidii Corda (Hsieh et aI., 1976, Leu et aI.,
1979), while in Cuba three nematodes viz., Meloidogyne, Helicotylenchus and
Pratylenchus have been found associated (Rodriguez and Landa, 1977). In South Af-
rica, Septofusidium sp. was found associated with the rapid death of guava plants
(Grech, 1985). Tokeshi isolated Pseudomonas sp. from wilt affected plants (Tokeshi et
aI., 1980). Disease similar to wilt caused by Erwinia psidii was also observed at Sao
Paulo (Brazil) in 1982 (Rodrigues et aI., 1987). From Pakistan (Punjab) disease is re-
ported in the name of decline and Fusarium oxysporum and Colletotrichum
gloeosporioides (Glomerella cingulata) are considered associated with the disease
and are supposed to act synergistically when present together (Ansar et aI., 1994). In a
recent study Misra and Pandey (1997) and Misra and Pandey (2000a) reported that
Gliocladium roseum as a most potent pathogen, which reproduces symptom of wilt on
artificial inoculation. They also developed an inoculation technique i.e. stem hole in-
oculation technique, which reproduce the wilt symptom very quickly. Misra et al. (2003)
further reported pathogenic diversity in the cause of wilt disease of guava and advo-
cated that there may be several cause of wilt but G.roseum is a very potent as pathogen
of guava wilt.
The severity of disease is reported high at 40-60 per cent soil saturation with Fusarium
solani or Macrophomina phaseoli individually, while for both 60-80 per cent saturation
is reported optimum. The pH 6.0 is reported optimum for the development of the dis-
ease, but at pH 4.0 and 8.0 the disease decrease. Incidence of the disease is reported
less at 630 ppm N and is reported more both at higher or lower levels. Moderate to high
concentrations of phosphates (207 - 345 ppm) are effecti ve in reducing the attack. Incor-
poration of organic manure in affected soils reduce the disease and under green manur-
ing there is no incidence (Chattopadhyay and BhattacJujya, 1968b). Earlier Mehta (1951)
reported severe incidence of wilt in alkaline soils at pH ranging from 7.5 to 9.0. However,
high disease incidence is recorded in lateritic soils at pH 6.5 (Sen and Verma, 1954).
Mehta (1987) reported more disease in clay loam and sandy loam as compared to other
soil types. The wilting is observed during rainy season. It starts in August with the
largest number of plants dying in September and October. The incidence of decrease is
markedly reduced in November and it become negligible with advancing winter (Das
Gupta and Rai, 1947). Edward (l960c) observed that the disease starts in the beginning
of June but the intensity of infection and spread increases with the onset of monsoon.
The highest wilting of guava trees is, however, restricted to the month of Sep-
tember and October, beyond which the incidence reduces gradually. Suhag (1976) also
reported that soon after rainy season, in September-October, the entire tree dries up
within a period of3-4 weeks. But some times due to unknown reasons decline and death
of tree is slow and taking 6-8 months for complete collapse. Dwivedi et aI., (1990) also
found more pathogenic fungi during rainy and winter season surviving better in asso-
ciation with root bits. Studies on progressive natural wilting of guava plants during
different months were done by Misra and Pandey (1999a,d), Misra and Pandey (2000b)
revealed that maximum wilting takes place during the month of October. Some plants,
which show slight yellowing but resist wilting, start recovering from December on-
wards. On analyzing the weather data, it was revealed that higher rainfall during July-
September, maximum temperature around 31.3-33.50C and minimum temperature around
23-250C with high humidity of 76 per cent were conducive for wilt incidence. They
further found that generally two months are required for the complete wilting of plants
after the appearance of first visible symptom but some times only 16 days were required
for complete wilting.
2.6 Varietal reaction
Cultivar, Chittidar, Hafsi, Safeda Riverside, Rolf and Stone acid were reported suscep-
tible and Psidium cattleianum var. lucidium and Syzigium cumini (Jamun) resistant to
wilt (Edward, 1961). Varieties, white guava No. 6229, Clone.32-12, Webber and Popeno
from Florida (USA), Hart and Rolf from Florida but acclimatized at Allahabad, Riverside
and Rolf from California (USA), Safeda from Sri Lanka, Banarasi (Andhra strain), Dholka,
Sindh and Nasik (Bombay strain) were reported tolerant to wilt disease (Mathur and
Jain, 1960). In Taiwan, a local variety Pei-pa has been reported resistant and Psidium
friedrichsthlianum has been recommended as possible root stock (Leu and Kao, 1979).
Singh et aI., (1977) reported that among 10 red-fleshed cultivars, only one of Allahabad
was found infected by Fusarium solani. Among the 15 white-fleshed cultivars, Lucknow
49 was free from the disease and in Allahabad Safeda incidence was only 4 per cent,
whereas Kerala and Behat Coconut suffer heavily (33%). None of the species, Psidium
aracae, P. cattleianum, P. cattleianum var. lucidium, P. corecium, P. cujavillus, P
quineese and Pfridichsthalanum developed wilt infection. Edward and Gaurishanker,
(1964) reported that Syzigium cumin ii, Psidium molle, P quianense, Chinese guava (P
friedrichsthalianum) and Philippine guava resistant to wilt organism. The strawberry
guava (Psidium cattleianm) is reported relatively hardy species from Reunion (Normand,
1994). In South Africa, Fan Retief, a most extensively cultivated guava variety is highly
susceptible to wilt (Preez , 1995). '
2.7 Disease management
Time to time recommendations for the control of wilt has been given by different scien-
tists. These are summarized as below:
Disease can be controlled by proper sanitation in the orchard. Wilted trees should be
uprooted, burnt and trench should be dug around the tree trunk (Mathur, 1956). While
transplanting, roots of plants should not be severely damaged. Maintenance of proper
tree vigour by timely and adequately manuring, inter-culture and irrigation enable them
GUAVA DISEASES AND MANAGEME T
to withstand infection. The pits may be treated with formalin and kept covered for about
3 days and then transplanting should be done after two weeks (Edward, 1960c).
Symptoms of the disease do not appear under green manuring and the disease
development is less when organic sources of nitrogen are used (Chattopadhyay and
Bhattacharjya, 1968b). Organic manures, oil cakes and lime also check the disease (Das
Gupta and Ghoshal, 1977). Spread of wilt could be checked byjudicious amendments of
Nand Zn (Suhag and Khera, 1986).
Good control of wilt was achieved by the application of Chaubatia paste con-
sisting of 4-oz red lead, 4 -oz CuC03and 5-oz lanolin (Anonymous, 1949). Injection of 0.1
per cent water soluble 8-Quinolinol sulphate was found to have chemotherapeutic
action against the wilt pathogen (Fusarium oxysporum f. psidii). Injection in appar-
ently healthy guava plants in a diseased area with 0.1 per cent 8- Quinolinol sulphate
provided protection against wilt for at least one year. When injected into slight wilted
plants, it was beneficial for their partial recovery (Jain, 1956). Both at Allahabad and
Lucknow, the wilt was controlled by soil treatment with 1.82 kg. lime or gypsum/tree,
although the control mechanism was not well understood (Mathur et al., 1964). Suhag,
(1976) reported that it is possible to regenerate even the worst affected trees by severe
pruning followed by a drench with 0.2 per cent either Benlate or Bavistin 4 times in a
year and spraying twice with Metasystox and Zinc sulphate. Dwivedi, (1991 b) reported
that heavy metal like Hg, Cd and Cu effectively check the growth of
psidii. In Taiwan, Carbendazim (50%), Captafol (30%) and Thiabendazole proved effec-
tive against Myxosporium psidii under laboratory experiments but failed in vivo (Leu et
1979). Disinfection of soil was achieved with DBCP at 52.8rnl 110m
sodium at 252.5ml/l Om2and control nematodes (Rodriguez and Landa, 1977). In Paki-
stan decline of guava is supposed to be caused by Fusarium oxysporum and
Colletotrichum gloeosporioides and was found to be controlled by combined use of
Topsin M sprays and the antagonists Trichoderma harzianum and Arachniotus sp.
added in soil amended with wheat straw (Ansar et al., 1994).
Use of rootstocks resistant to wilt disease could be an effective method for
control of wilt. Psidium cattleianum var. lucidium and Syzigium cuminii (Jamun) sel-
dom get attacked by the disease. Since interspecies and intergeneric graft compatibility
is there, it may be an effective way for the control of wilt disease (Edward, 1961). Misra
and Pandey (1999c) reported that though different fungicides are effective for the con-
trol of wilt pathogens in lab, but these pathogens increases it's aggressiveness, once
the effect of these fungicides diminishes in soil. Eco-friendly approach of guava wilt
control was suggested by Misra etal., (2001) where biological control, soil amendment
and intercropping were suggested. Biological control by Aspergillus niger strain AN17
(Misra et al., 2000) and by Penicillium citrinum (Prakash et al., 2002) are effective.
The disease is serious problem in Uttar Pradesh, Punjab and Karnataka. It was first
reported by Mehta during the year 1951 from Uttar Pradesh. In Karnataka disease was
reported by Rawal during 1993 (Rawal, 1993). It causes die back, twig blight, wither tip
and fruit spots. Die back phase is caused by Gloeosporium psidii resulting in the death
of plants was observed at Allahabad (Tandon and Agarwal, 1954) but this phase was
not observed at Saharanpur (Tandon and Singh, 1969). The disease is reported from
Taiwan also (Yang and Chuang, 1994).
3.1 Causal organism
Gloeosporium psidii Delacroix=Glomerella psidii (Del.) Sheld. / Colletotrichum psidii
Curzi.The disease is caused by
+Glomerell a p sidii
(Del.) Sheld. It is now calledColletotrichumpsidiiCurzi.
Brown to dark brown coloured acervuli are formed on the affected parts of the
plant. Setae and conidia are formed in the acervuli. Mycelium is intercellular, branched
and light brown in colour. Conidiophores are hyaline and small, setae are long, tapering
at the end, dark brown to black in colour. Conidia are formed at the tip of the conidio-
phores and are sickle-shaped, unicellular, hyaline measuring 11.24 x 4.5-5~ m. They
germinate by germ tube. In moist weather, acervuli appear as black dots on twigs or
fruits, which later produce pinkish spore mass. Spores are disseminatedby wind or rain
and initiate fresh infection.
3.2 Die back phase
Die back phase of anthracnose was reported from Minto Park, Allahabad, in 1952 and
the intensity of the disease varied from half dead to complete dead plant (Tandon and
The plant begins to die backwards from the top of a branch. Young shoots, leaves and
fruits are readily attacked, while they are still tender. The greenish colour of the growing
tip is changed to dark brown and later to black necrotic areas extending backwards
causing the die back. The disease is more noticeable after a period of incubation in the
infected buds and twigs. The brown spots, formed previously, change into silvery grey
and ultimately develop at the junction of the diseased and healthy parts.
The fungus develops from the infected twigs and then petiole and young leaves
are attacked. These may droop down or fall leaving the dried twigs without leaves. In
moist condition, acervuli of the fungus may be seen as black dots scattered throughout
the dead parts of the twigs (Tandon and Agarwal, 1954).
3.2.2 Disease development
After slight rain, old twigs show the symptoms of die back. In the first fortnight of
August the disease causes death of small, tender growing twigs. From August to
October the infected twigs wither and shrivel at their tips. The disease appears in
epidemic form, during August to September. It is also noticed in December after which
the older leaves and twigs remain immune from attack. During less humid weather
GUAVA DISEASES AND MANAGEMENT
conditions i.e. from January to June further progress of the disease is not there (Tandon
and Agarwal, 1954).
rainy season symptoms develop after 15-20 days of inoculation.
test inoculation without injury give negative result.
summer, even after injury, symp-
tom development fails. Thus, humidity is necessary for the growth of the organism. Old
branches resist infection. The young leaves show dead area on the margin and the tips,
which generally appear after one week of inoculation. When flowers are inoculated,
unopened buds show infection within two or three days and fail to develop. Petals turn
brown and buds fall off without opening. On inoculation of fruits, rot develop in the
ripened fruits but they never develop mummy (Tandon and Agarwal 1954).
Although complete control is not possible, the application of 3:3:50 Bordeaux mixture
and 0.22 or 0.33 per cent Perenox give encouraging results in reducing the development
of die back and mummies (Tandon and Agarwal, 1954).
3.3 Fruit and leaf infection phase
Fruit and leaf infection was reported from Saharanpur and it is generally seen in rainy
Pin-head spots are first seen on the unripe fruits which gradually enlarge measuring 5-
6 mm in diameter. They are dark brown to black in colour, sunken, circular and has
minute black stromata in the center of the lesion which produce creamy spore masses
in moist weather. Several spots coalesce to form bigger lesions. The infected area on the
unripe fruits become corky and hardy, and often develop cracks in case of severe
infection (Fig. 1). On ripe fruits, the infection causes softening of tissues and lesions
attain a diameter of 10 to 20mm (Tandon and Singh, 1969). Unopened buds and flowers
are also attacked and cause their shedding. Spread of infection is very rapid on fully
matured green fruits, whereas, young fruits do not normally get infected (Midha and
Chohan, 1968) perhaps owing to the differences in the concentration of K- ions in the
fruit tissues. On leaves, the fungus causes necrotic lesions at the tip or on the margin.
These lesions are usually ashy grey and bear fruiting bodies. The tender twigs are also
infected, which wither and die from the tip downwards giving it a wither tip appearance
(Tandon and Singh, 1969).
The leaves and stems of seedlings and new leaves, buds, flowers and fruits of grown
plants are readily infected. Tandon and Agarwal (1954) were unable to infect the green
fruits under artificial conditions and were of the opinion that the fungus remains latent
for two and half to three months and spots appear when fruits ripen. According to them
the hard tissues of young fruits prevent the fungus from growing but Tandon and
Singh (1969) were able to infect both the young and ripe guava fruits. The
disease was found to develop more rapidly at 30°C and 96.1 per cent relative humidity
both in ripe and unripe fruits.
Figure 1: Anthracnose of guava fruit
3.3.3 Varietal resistance
Apple guava (deep red fleshed), Apple shaped seedling, Behat Coconut, Red Chittidar,
Muzaffamagar, Bulandshahar, Lucknow-49 and species Psidium chinensis Lodd., P
catteleianum var. lucidium Isab. P quianense and P molle Bertol are susceptible to
anthracnose while Apple guava (light red fleshed) has moderate resistance (Tandon
and Singh, 1969). P chinensis resist leaf infection whereas P molle and Beumont are
highly susceptible and Allahabad Safeda develop heavy infection on fruits (Anony-
GUAVA DISEASES AND MANAGEMENT 91
Effective control of anthracnose can be achieved by sprays of Bordeaux mixture (3:3:50)
at 7 days interval. Copper oxychloride and cuprous oxide also significantly control
thedisease (Tandon and Singh, 1969) but Bordeaux mixture and other copper fungicides
cause russeting of fruits especially in cv. Allahabad Safeda and reduce their market
value (Sohi and Sridhar, 1969). Monthly sprays of Difolatan (0.3%) and Dithane Z-78
(0.2%) are effective in controlling the disease (Anonymous, 1974). For post harvest
treatment 20 min. dip treatment in 500 ppm tetracycline is effective (Gupta et al., 1973).
Pre treatment of sodium metabisulphite and stable bleaching powder is also effective
under in vivo conditions (Singh and Sharma, 1982). Thiabendazole and Aureofungin
are also effective (Sharma et
1983). Growth and acervulus formation are inhibited by
Thiophenate methyl, Benomyl and Thiabendazole at 5-50 ppm. Vitigram blue check
acervulus formation at 50 ppm and hyphae is restricted by boric acid (Butt et al., 1995).
Fruit canker caused by Pestalotia psidii Pat. was recorded from Bombay (Chibber,
1911) and later from Mysore (Narsirnhan, 1938, Venkatakrishniah, 1952), Thane,
Dharwar,Poona (Patel et
1950), Ponta Valley, Himachal Pradesh (Verma and Sharma,
1976) and Lucknow (Misra and Prakash, 1986).
The disease generally occurs on green fruits and rarely on leaves. The first evidence of
infection on fruit is the appearance of minute, brown or rust coloured, unbroken, circu-
lar, necrotic areas, which in advanced stage of infection, tears open the epidermis in a
circinate manner. The margin of lesion is elevated and a depressed area is noticeable
inside. The crater like appearance is more noticeable on fruits than on leaves. The
canker is confined to a very shallow area and does not penetrate deep into the flesh of
the fruit (Fig.2). In older cankers, white mycelium consisting of numerous spores are
noticeable. Canker on the green fruits of different varieties exhibit considerable differ-
ences in their appearance (Patel et al., 1950).
severe cases, raised, cankerous spots
develop in great numbers and the fruits break open to expose seeds. The infected fruits
remain underdeveloped, become hard, malformed and mummified and drop in great
numbers. Sometimes small rusty brown angular spots appear on the leaves
winter the cankerous spots are cornmon but in rainy season
minute red specks are formed (Verma and Sharma, 1976).
4.2 Causal organism
Fruit canker is caused by Pestalotia
Pat. (Chibber, 1911). Narsirnhan (1940) and
Venkatakrishniah (1952) found Colletotrichum
Sheld. and Pestalotia psidii Pat. associated with canker. Venkatakrishniah (1952) advo-
cated that Colletotrichum psidii is a general parasite and Pestalotia
is a special-
ized to guava. Both species are present on young green and mature fruitslleaves but
Pestalotia psidii is considered the real cause of canker (Patel et al., 1950). Pathogen
develops dark black and circular pycnidia on the culture media and fruits, and these
contain conidiophores and conidia. The conidia are typically 5-celled, oblong, clavate
or elliptic-fusoid, erect, hardly constricted at septa, measuring 13-31 x 5-10 urn, 3 me-
dium cells are guttulate, highly brownish; the central cell being the thickest and greatly
bulged and other cells are comparatively hyaline; the apical conical or cylindrical cell
grows out into 3 hyaline, slender, elongated appendages; the basal cell is obtuse, erect
with a small pedicel. The mycelium of young culture is sub-aerial, serrate, thin, septate,
cottony white to pinkish, irregularly branched and measuring upto 3 urn in diameter. In
old cultures, the hyphae are more or less thickened (Patel et al., 1950).
Figure 2: Fruit canker caused by pestaLotia psidii Pat.
The maximum disease occurs at 25-30
C and at high RH (Kaushik et al., 1972). The
fungus grows, profusely on different media but scanty vegetative growth occurs on
green guava decoction. Sporulation is quick and abundant on PDA and Richard's
medium. The pathogen grows vigorously at temperature between 15-30°C. Best growth
and sporulation is seen at 26°C. The fungus grows profusely on media containing
mannitol, dextrin and sucrose, fairly on maltose and salicin, poorly on ripe guava decoc-
tion, glycerol and Richard's modified agar. Best sporulation is in mannitol, dextrin and
sucrose. With different sources of nitrogen, the growth characters of P. psidii remain
GUAVA DISEASES AND MANAGEMENT 93
practically constant but the sporulation is profuse in case of potassium nitrate and
aspargin. The fungus grows in a wide range ofH-ion concentrations, but optimum pH
is 3.9-4.9 with maximum growth at pH 4.9. The spores of the fungus germinate at l
and increase with rise in temperature up to 32°C. Maximum growth is on sulphates or
cystein (Tandon, 1950). On thio-urea, growth is moderate but sulphide, dithionate and
persulphate are only feebly utilized. Addition of green fruit tissues and it's decoction
give greater stimulation to germination than the ripe fruit tissues. The fungus remains
viable in conidial stage upto 38.8°C (patel et al., 1950). Germination of spores of Pestalotia
psidii is maximum at 30°C and it do not germinate below 15°C or above 40°C
(Ramaswamy et al., 1984). The best germination medium is guava fruit extract. High RH
(98%) is required for germination.
Detached fruits, both ripe and unripe fail to reproduce symptoms. Fresh, young, green
guava fruits (undetached) inoculated after wounding give typical severe symptoms,
while in unwounded fruits symptom development take more time. Artificial infection on
leaves is generally unsuccessful. The pathogen is primarily a wound parasite (Patel et
4.5 Varietal resistance
In cv. Lucknow 49, development of canker pustule is large, more elevated and numer-
ous. On cv. Dhokla it is not well developed. On cv Sindh, the development of pustule is
insignificant and inconspicuous, while cultivar Nasik is almost immune (patel et al.,1950).
Safeda and Apple coloured are highly resistant cultivar to canker.
The spread of disease (in early stage of infection) is controlled by 3 to 4 spraying of 1
per cent Bordeaux mixture or lime sulphur (1 in 25) at 15 days interval (Venkatakrishniah,
1952). Homeopathic drugs, Kali (Potassium iodide) at potencies of 1,20, 24, 61 and 67;
Arsenic album (Arsenic oxide) at potencies of 60,65 and 82 completely inhibit spore
germination in in vitro test. Potassium iodide at potencies of 1, 20, 24 and 61 and
Arsenic oxide at potency of 60 inhibit growth of the pathogen. Fruit treated with some
of the effective potencies before inoculation do not develop rotting (Khanna and
Chandra, 1977). Leaf extract of Atadirachata indica and Ocimum sanctum inhibit the
germination of spores in vitro test. Dipping of guava fruits in these extracts before or
after inoculation is effective. Use of O. sanctum extract is recommended, as it does not
affect fruit flavour (Pandey et aI., 1983).
5. Algal leaf and fruit spot
The alga causes spots on leaves and fruits and thus reduces the photosynthetic activ-
ity of the plant. The disease does not cause severe economic loss. Ruehle (1941) re-
ported Cephaleuros virescence Kuntze., on leaves, fruits, twigs and bark of guava from
Florida. Although twig and bark infections are of little or no consequence in Florida but
leaves and fruits are severely attacked. Thirumalachar (1945) collected Cephaleuros
parasiticus from Mysore, which is responsible for blemishes of guava fruits. Yadav
(1953), reported Cephaleuros sp. on guava from Patna (Bihar). Misra and Prakash
(1986), found that the Cephaleuros virescence affect guava leaves in areas of Lucknow
and Sitapur (U.P.) and the incidence was found as high as 30 per cent.
Cephaleuros infects immature guava leaves during early spring flush. Minute, shallow
brown lesions appear on leaves, and as the disease progress, the lesions enlarge to 2-
3 mm in diameter. On leaves the spots may vary from specks to big patches. They may
be crowded or scattered. Leaf tips, margins or areas near the mid vein are most often
infected. Although the alga's zoosporangia arise from thalli on adaxial surfaces of many
host species, lesions on guava frequently extend through the entire lamina and sporan-
gia most often occur on the abaxial leaf surface. On immature fruits the lesions are
nearly black. As fruits enlarge, lesions get sunken. Cracks frequently develop on older
blemishes as a result of enlargement of fruits. Penetration of fruit is confined to several
layers of cells beneath the epidermis. Fruit lesions are usually smaller than leaf spots.
They are darkish green to brown or black in colour (Ruehle, 1941; Marlatt and Campbell,
5.2 Time of infection
Disease begins to appear from April and is more serious during May to August. In
October disease is difficult to find (Ruehle, 1941). The pathogen sporulates readily
during the period of highest rainfall (July-September) and the disease incidence is
greatest during September. In winter, symptom is not available (Marlatt and Campbell,
5.3 Causal organism
The alga, Cephaleuros virescens Kuntze.
mycoidae Karst.) occurs on wide range of
plants in South Florida. Nineteen species are listed as it's host in the vicinity of Home-
stead, Florida in 1936 (Ruehle, 1936). Ruehle (1941), reported algal leaf and fruit spot
caused by Cephaleuros virescens Kunze
mycoidea Krast) while Thirumalachar
(1945) reported that it is caused by C.parasiticus. Yadav (1953), Marlatt and Campbell
(1980 a, b) reported it to be caused by Cephaleuros spp.
The pathogen extends itself between cuticle and epidermis and penetrate the
epidermal cells. The affected cells eventually die. It is also called red rust because of the
upper surface of the thallus produces erect, yellow to red filaments and fruiting bodies.
These are flat, short, closely crowded branched filaments, beneath which, there are
irregularly branched rhizoid. Most obviously fruiting bodies are consist of upright
multi-cellular filaments bearing 1-8, sharply bent pedicels. Each pedicel bears a pear
GUAVA DISEASES AND MANAGEMENT
shaped or nearly spherical sporangium, which eventually emits about 8-32 motile bi-
On guava, contrary to other hosts, no thallus is apparent on the upper leaf
surface, the lesions extend through the entire lamina soon after it appears and the
sporulation occurs on the lesion surface on the underside of the leaf (Marlatt and
Campbell 1980 a). The alga sporulates readily during the period of greatest rainfall.
5.4 Change in physiology
Among sugars, glucose and sucrose are less while fructose is more in alga infected leaf
tissues. Cellulose and pectin are also more in infected tissues while lignin content is
unaffected (Vidyasekaran and Parambaramani, 1971b). Vidyasekaran and Parambaramani
(1971 a) further noted that algal infection causes reduction in the total protein, ammonical
nitrite, amino and amide nitrogen content of guava leaves. Glutamic acid, alanine in-
creases considerably while glycine decreases sharply. The valine content is not af-
fected by algal infection.
further studies they found that algal infection increases
transpiration and decreases water content. While potassium and phosphorus content
is less in infected tissues, sodium accumulate in them. Magnesium content slightly
increase while sulphur content decreases due to infection. Among the trace element,
iron and manganese accumulate while copper decrease in diseased tissues (Vidyasekaran
and Parambaramani, 1972).
5.5 Varietal reaction
Large fruit peruvian variety of Florida is highly susceptible (Ruehle, 1941). The culti-
vars Patillo and Blitch are low disease cultivars, Ruby x Supreme 6-29 moderate disease
cultivars, Webber x Supreme and Ruby x Supreme 10-30 high disease cultivar (Marlatt
and Campbell, 1980a, b).
The control of alga can be achieved by spray of copper oxychloride (0.3%) 3-4 times at
the interval of 15 days. Spray of copper oxychloride in rainy season is more effective
(Ruehle, 1941). An ascomycetous parasite closely resembling Strigula astridiza on
Cephaleurous parasiticus can be used for controlling disease biologically (Thirumalachar,
6. Stem canker / bark canker
Stem canker of guava was reported from Patharchatta, Nainital (Rana, 1981).
Initial symptoms of the disease are longitudinal cracks in the bark on stem or branches,
which are visible during post monsoon period in October-November. Usually the dis-
ease originates from the injured bark. On scraping bark, brown to black streaks or bands
are present in the sub-cortical region. The affected bark turns dark brown to greyish
and develops large vertical cracks.
The disease spreads up and down from one branch to another and ultimately
passes on to the main trunk and upper roots. Leaves on the engirdled portions loose
their colour slowly and become purplish bronze. Completely engirdled trees decline and
die gradually in course of2-3 years.
6.2 Causal organism
The pathogen is identified as Diplodia natalensis Pole-Evans. Pycnidia are grey to
black, erumpent, globoid to irregular, ostiolate and measure 160-600 urn in diameter. The
pycnidiospores are at first hyaline, later become brown, uniseptate and striate. They are
oblong to elliptical andmeasure 19.2-32.0 x 11.8-16.0 urn (av.27.1 x 14.8 urn) (Rana, 1981).
The bark canker disease of guava has been reported from other parts of India also but
the fungus causing disease is reported as Physalospora psidii. Uppal (1936) observed
Physalospora psidii in Dholka, North Gujarat and Bombay Presidency causing a se-
vere disease of guava. Infection originates in the bark and spreads rapidly along the
stem from one branch to another resulting in desiccation, cracking, decortication and
death of the affected part, and finally of the whole tree. Numerous perithecia of the
causal organism are scattered over the dead bark.
7. Leaf blight
The disease was first reported by Sridhar and Ullasa in 1978 although it was observed
during 1975 from Hessarghatta, Bangalore, India.
First symptom of blight is the appearance of small circular spots, with dark brown
center, surrounded by a reddish margin.
advance stages, these spots gradually
enlarge and coalesce resulting in large necrotic patches and cause blightening. The
fruiting bodies (pycnidia) of the fungus appear in large numbers in the form of small,
light brown to black pin heads on the necrotic spots. Both young and old leaves are
susceptible to the infection and severely affected plants are completely defoliated
(Sridhar and Ullasa, 1978).
7.2 Causal organism
The pathogen was identified as Phomajolyana Priozy and Morg. (Sridhar and Ullasa,
8. Cercospora leaf spot
Leaf spot of guava caused by Cercospora sawada Yamamoto, was recorded from
GUAVA DISEASES AND MANAGEMENT
Mauritius (Anonymous, 1965), Nainital, India (Bose and Muller, 1967) and Annamalai
University (T.N.) (Raghunathan and Prasad, 1969). The disease is severe during De-
cember to February.
The disease appears as water soaked, brown irregular patches on the lower surface and
yellowish on the upper surface of the leaf. Old leaves are mostly and severely affected,
later curl and subsequently drop off (Raghunathan and Prasad, 1969).
8.2 Causal organism
The disease is caused by Cercospora sawadae Yamamoto. Conidia are sub-hyaline to
pale olivaceous, slightly curved, obclavate to obclavate cylindric, 1-5 septate, base
obconic, tip obtuse, measuring 3-4.2 x 18-87.4 mm. Mycelial patches are hypohyllus,
fruiting effuse, irregular, stromae lacking, conidiophores non fasciculate, arise singly
from hyphal threads, straight or slightly curved, geniculate, 2-5 septate, pale to
olivaceous brown, tip conic measuring 3-3.7 x 46 77f.UIl(Raghunathan and Prasad, 1969).
8.3 Varietal resistance
The cultivars Red flesh, White large, Luclcnow and 'Chittidar' are susceptible while the
cultivars Safeda and Seedless are resistant (Raghunathan and Prasad, 1969).
9. Pestalotia leaf spot
A new pathogenic species of Pestalotia i.e. Pestalotia jodhpurensis sp. novo Bilgrami
and Purohit, which causes leaf spot of guava was reported by Bilgrami and Purohit
9.2 Causal organism
The spots originate from the tips or the margins and gradually advance towards the
base, assuming dark brown grey colour. Fruiting pustules develop profusely on the
upper surface of the leaves. The pathogen is found constantly associated with such
This leaf spot is caused by Pestalotia jodhpurensis. The fruiting pustule of typical
pycnidium is amphigenous, globoid to ovoid, dark brown, occasionally with prominent
neck,ostiolate, 167-389 urn in diameter; conidia 5 celled, narrowly elliptical, slightly
constricted at septa, 17.55-24.30 x 3.51-5.40 um, 3 intermediate coloured cells light olive,
concolorous, 10.8-13.5 urn; upper two coloured cells usually smaller than lower most
coloured cell, apical hyaline cell short, conic bearing 2 to 3 (usually 3) setulae, 8.1-13.5
mm long; basal hyaline cell long, conic to cylindric, pedicels oblique 2.7 -7.29 IlIDlong
(Bilgrami and Purohit, 1971).
10. Curvularia leaf spot
Leaf spot of guava caused by Curvularia siddiquii Ahmed
Quraishi, was first re-
ported from Naini, Allahabad, UP, India during 1964 (Srivastava, 1963).
Dark brown spots on the leaves of guava develop during the months of September-
October. The infection is restricted only on the tips and margins in the initial stages but
subsequently the spots cover the whole leaf lamina. Defoliation is observed in case of
10.2 Causal organism
The organism is identified as Curvularia siddiquii. The hyphae are white or olive green
septate, branched, 3.0-4.0 urn wide, conidiophores light brown, variable in size, un-
branched, septate, 3.5-4.5 urn wide, conidia large, brown, curved, 4 celled, two inner
cells bigger than the distal cells measuring 27.5-39.0 x 13.5-21.0!lJl1 (av. 33.0 x 16.5!lJl1).
11. Pestalotiopsis leaf spot
Pestalotiopsis psidii (Pat.) Mordue causes violate spots formed near mid rib with
necrotic center and pycnidia are formed on the lower surface (Misra, 1987). Pestalotiopsis
versicolor (Speg.) Steyaert causing leaf spot of Anogeissus latifolia when inoculated
on guava, was also found pathogenic (Agarwal and Ganguli, 1959).
12. Rust of Guava
Rust of guava caused by Puccnia psidii Wint., was recorded first from Brazil in 1884
and Its distribution is limited to the western hemisphere in Central and South America,
Florida and the Caribbean (Anonymous, 1949). The Pathogen attacks leaves, flowers,
shoots and fruits and may cause 80 - 100
losses. P psidii has wide host range and
infects about eight genera and 25 species of plants belonging to family Myrtaceae. The
autoecious rust pathogen attacks and produces symptoms on guava, jamb (Eugenia
jambos), jaboticaba (Myrciariajaboticaba) and Eucalyptus spp.
The disease is a serious threat to natural forests and plantations of Eucalyptus
spp. in both Southern Africa and Australia. Description of P psidii is provided in the
CMI description set-6 (Anonymous, 1965).
12.1 Varietal resistance
Sweet varieties, both white and red fleshed are more susceptible to the rust than the
GUAVA DISEASES AND MANAGEMENT
sour varieties. Vigorous growth varieties have high infection (Andrade, 1951).
For the control of rust, spray of 1 per cent Bordeaux mixture after winter rain is recom-
mended. ext spray is given when the tree begin their active growth, and subsequent
sprays at monthly intervals. B 03818 (a combination of Nif'l, and Zineb) 0.03 per cent is
also effective for the control of rust and is equivalent to 1 per cent Bordeaux mixture
(Andrade, 1959). The products based on chlorothalonil were the most efficient in the
control of guava rust, controlling above 85% disease ( Ferrari et aI., 1997). Fusarium
decemcellulare (Nectria rigidiuscula) is found hyperparasite on the uredospores of P.
psidii in Recife, Pernambuco, Brazil and can be used for control (Amorim et aI., 1993).
13. Damping off of seedlings
Damping off of guava is a serious disease and often responsible for enormous loss in
nurseries. The disease was reported from Saharanpur (Tandon, 1961) and Basti (Gupta,
Both pre emergence and post emergence phases of the disease are observed. In pre
emergence phase the infected seeds and seedlings show water soaked discolouration,
the seed becomes soft and ultimately rots. The affected young seedlings are killed
before they reach the soil surface. In post emergence pha e, hypocotyle at ground level
or upper leaves are discoloured into yellowish to brown colour, which spreads down-
wards and later turn soft and finally rot and constrict. The affected seedlings ultimately
topple down and die (Fig.3). Strands of mycelium may appear on the surface of the
plants under humid conditions (Tandon, 1961, Gupta, 1978).
13.2 Causal organism
The pathogen is identified a Rhizoctonia solani Kuhn. (Gupta, 1978). Tandon (1961)re-
ported seedling blight of guava caused by Rhizoctonia sp., but he did not specify the
species. He reported that the seedlings over four months old are not affected.
There are some old reports for the control of the disease. These are as follows. Good
control of the disease was achieved by Flit 406 (0.2%) or Ferbam (0.3%) (Tandon, 1961)
and with Bavistin (Carbendazim) and Brassicol (Quintozene) at 3 and 5 g/kg seed re-
spectively (Gupta, 1979). Now for the control of the disease following recommenda-
tions may be made.
i. Diseased guava seedlings and weeds should be removed and burned.
ii. Excessive use of water and close planting should be avoided as the organism is
moisture loving. Seed-beds should be prepared with proper drainage arrangement.
As the fungus survives on several hosts. Hence planting of susceptible hosts
should be avoided.
iv. Two minutes dipping of guava seeds in CaptanfThiram.
v. Drenching of soil with Copper oxychloride help in reducing the disease intensity in
14. Clistocybe root rot
Root rot caused by Clitocybe tabescens (Scop.) Bres. has been observed most fre-
Figure 3: Damping off of seedlings
quently in guava trees, killing them in old citrus grooves in various localities of Florida
(Rhoads, 1927, Webber, 1928). The disease is reported on Psidium guajava, P. molle
and Cattley guava (Rhoads, 1927, Webber, 1928 and Rhoads, 1942).
15. Phytophthora fruit rot
Fruit rot caused by Phytophthora parasitica Dastur was reported by Mitra (1929) from
Pusa, Bihar, India. He described that the disease appears in wet season (July-Septem-
ber). The disease is also reported to cause considerable losses in other States of India.
Allahabad Safeda, Banaras, Bangalore local, Red fleshed and seedless cultivars are
susceptible to the disease (Sohi and Sridhar, 1971). In Punjab, it was noticed for the first
GUAVA DISEASES AND MANAGEMENT 101
time at Ludhiana during July 1975. The incidence of the disease varied from 5-20 per
cent. The varieties, Allahabad Safeda, Apple guava, Red fleshed and pink fleshed were
found affected (Singh et al., 1976). Fruit rot of guava caused by Phytophthora nicotianae
var. parasitica Dastur, Waterhouse Syn. Phytophthora nicotianae Dastur was reported
from Haryana (Gupta et al., 1977), Poona (Rao, 1966), Bangalore (Sridhar et al., 1975,
Rawal,1993) and Cuba (Ariosa, 1982).
Fruit rot of guava caused by Phytophthora citricola Sawada was also reported
by Ko et al., in 1982 in an orchard ofWaiakea-Ukaon the island of Hawaii. Fruit hanging
close to the soil surface were found affected during rainy period. The infected area
appears grayish brown and water soaked with grayish black centre. Mature fruits ap-
pear to be less susceptible than mature green or green fruits. The distribution of disease
appear to be limited (Ko et al., 1982). The fungus is self inducing (homothallic) produc-
ing oospores in single culture.
The fruits especially affected are those, which have fallen on the ground or which hang
near the ground level or which have been placed in storage. The disease starts at styler
end. The whitish cottony growth develops very fast as the fruit ripens and is able to
cover almost the entire surface within a period of about 3-4 days during humid weather
(Fig. 4).The fruits near the soil level covered with dense foliage under high relative
humidity are most severely affected. The skin of the fruit below the whitish cottony
growth of mycelium becomes a little soft, turns light brown to dark brown and emits a
characteristic unpleasant smell. The diseased fruits generally retain their normal shape
unless they are invaded by saprophytes. These fruits either remain intact or drop off.
When the disease appears on young and half grown fruits, they shrink, turn dirty
brown to dark brown, remain hard in texture, either remain intact as mummified fruit, or
drop off (Singh, et al., 1976).
15.2 Causal organism
Phytophthora parasitica Dastur (MitraI929, Sohi and Sridhar, 1971) and Phytophthora
nicotianae var. parasitica (Singh et al. 1976. P citricola ( Ko et al., 1982) are reported
to cause guave fruit rot.
15.3 Physiological change
Phytophthora nicotianae var. parasitica infected fruits had reduced free amino acids,
sugars, ascorbic acids, phenol and orthodihydroxyphenol contents. The inverse corre-
lation between disease development and phenol and ortho-dihydroxy phenol contents
of the fruits suggests that phenols may not be involved in resistance mechanism against
this pathogen (Mathur et
1980). Rotted guava tissue always show more cellulolytic
and pectolytic activity than healthy tissue (Prasad et al., 1979).
15.4 Varietal resistance
Cultivar Lucknow-49, Banarsi Surkha, Allahabad Safeda and Mishri are highly suscep-
tible, Tehsildar is moderately susceptible and Chittidar and Apple Colour are quite
resistant (Gupta et al., 1977).
Diathane Z-78 (0.2 %) or Aureofungin (10 ppm) are reported effective in controlling the
disease, while Copper oxychloride is found toxic to the fruits (Sohi and Sridhar, 1971).
Phytophthora fruit rot
16. Dry rot
The dry rot of guava fruits was observed during 1969 at VeUayani. In some of the
infected trees more than 40 % of the fruits were infected (Rajgopalan and Wilson,
Initially the light brown spots mostly at the stalk end or at the calyx end of the fruit
few cases, infection spreads quickly and within 3-4 days entire fruit is
affected. Completely infected young and mature fruits become dark brown to almost
black in colour and ultimately dry up. A number of dry fruits can be seen on infected
trees. Numerous pycnidia of the pathogen appear as pinhead like structures on the rind
GUAVA DISEASES AND MANAGEMENT 103
of the dried fruits. (Rajgopalan and Wilson, 1972a).
16.2 Causal organism
The dry rot of guava fruit is caused by Diplodia natalensis Evans. The pycnidia of the
fungus produced on guava fruits are erumpent, more or less globose, dark coloured and
measure 175-475 x 90-185 mrn. Pycnidiospores are initially hyaline, oblong and unicellu-
lar. On maturity they become oblong to elliptical, two celled and dark brown having
longitudinal striation on the wall. They measure 21.5 to 32.2 mrnlong and 12.2 to 16.5 mrn
wide (Rajgopalan and Wilson, 1972a).
16.3 Physiological changes
Sucrose, glucose and fructose concentrations increase with the age in non-inoculated
fruits and sucrose of guava fruit is slowly hydrolyzed by D. natalensis (Ghosh et al.,
Ziride 3000 ppm controls Diplodia dry rot of guava fruits in orchards and does not
cause any phytotoxic effect on flowers and fruits of guava when it is applied at 15 days
interval (Rajgopalan and Wilson, 1972b).
17. Phomopsis rot
The disease was reported from Sagar (Rao et al., 1976). About 60 per cent of the fruits
of a plant were found affected.
The infected fruits show disease symptoms near the stalk. Under favourable environ-
mental conditions, infection centers are numerous. Lesions are dark brown, at first,
small and increase in size to 2 em diameter. The tissues soften and the entire fruit rots
within 8-12 days. The rotten fruits fall from the parent plants causing heavy loss in the
yield of the crop (Fig.5).
17.2 Causal organism
The disease is caused by Phomopsis destructum Rao, Agarwal
Sakesena. The colony
is white forming zones in the medium. Mycelium thin walled, hyaline, branched, sep-
tate; pycnidia dark coloured, leathery to carbonaceous, ovoid, thick walled, formed
generally in 20 days old culture, 300-600 mrn diameter. Sporogenous cells hyaline, simple,
rarely branched, phialidic enteroblastic, arising directly from the innermost layer of cells
lining the pycnidial cavity. Fungus produces two types of spores, stylospore long,
slender, often curved
In in vitro tests, griseofulvin was found very effective in completely inhibiting the
mycelial growth at 22 ppm while auriofungin and nystatin inhibited it at 100ppm. Tetra-
cycline and Chloramphenicol are also effective (Rao and Agarwal, 1976a,b). Phenolic
compounds, alpha-naphthol 50 ppm and guaicol250 ppm cause complete inhibition of
mycelial growth of P psidii (Khare et al., 1994)
18. Guignardia fruit rot
Figure 5 : Styler end rot caused by Phomopsis psidii de Camara.
Guignardia fruit rot of guava was recorded on variety Beaumont in transit as well as in
field from Bangalore during the year 1980 (Ullasa and Rawal, 1984).
Symptoms develop as minute depressed or flattend spots on the ripening fruits. In
these spots, fungus develops in a concentric manner. Several spots later coalesce and
form bigger lesions. On fruit, no fruiting structure is seen. On PDA fungus produces
both ascigenous as well as pycnidial stage after 10 days of incubation under laboratory
conditions. Typical symptoms appear after 6-8 days of inoculation (Ullasa and Rawal,
1984). Misra and Prakash (1986) described formation of circular black spots on the
GUAVA DISEASES AND MANAGEMENT 105
surface of ripe fruits due to this fungus.
18.2 Causal organism
The fungus was identified as a new species i.e. Guignardia psidii,Ullasa and Rawal
(Ullasa and Rawal, 1984). G. psidii was also isolated on guava fruit from Rehmankhera,
Lucknow (Misra, 1987). Colonies on PDA are greenish grey which become bluish black
with abundant aerial mycelium. Reverse in plate dark grey to black, submerged myce-
lium consists of green to brownish black hyphae are seen (Ullasa and Rawal, 1984).
Anthracnose fruit rot of guava is reported from Mysore, Bangalore, Karnataka
(Narsimhan, 1938, Venkatakrishniah, 1952), Agra, Allahabad and Lucknow, U'P (Mehta,
1951, Tandon and Agarwal, 1954, Misra and Prakash, 1986).
Gloeosporium psidii remains in dormant conditions in the young infected fruits and
subsequently it resumes activity and causes rot when the fruit starts ripening
(TandonandAgarwal, 1954). Non susceptibility of the young guava fruits is due to the
hardness of the fruit. On Ripe fruits many small, shallow, water soaked lesions are
produced on the surface of fruits and with age they enlarge and become depressed.
Subsequently they coalesce to form large spots, irregular in shape and size and under
humid conditions they develop salmon coloured spore masses at the center (Srivastava
and Tandon, 1969a). Anthracnose caused by G psidii is also common at Lucknow but
in winter crop symptoms do not develop well as compared to rainy season crop (Misra
and Prakash, 1986).
19.2 Causal organism
Anthracnose of guava fruit is caused by Gloeosporium psidii Declacr
sp. , Colletotrichum accutatum. The growth of the pathogen increases with the amount
of glucose in the basal medium. Absence of nitrogen source from the basal medium
reduces the growth of the fungus by about 75 per cent, but the different concentrations
do not affect the growth, provided the amount of glucose is kept constant. The growth
is best with fructose/glucose (f/g) ratio of 0.5 at pH 4.0, a condition present
in the mature green guava fruits wherein the pathogen causes maximum damage. With
the fig ratio of 1.5, 2.0 or 2.5 the growth is significantly less, a condition present in the
young guava fruit wherein only incipient infection results (Midha and Chohan, 1968).
G. psidii grows significantly better on any combination of galactose, raffinose and
sorbitol. Mannitol, along with raffinose, support excellent growth of G.psidii. Excellent
sporulation of G. psidii is observed on a combination of all the four carbon substances.
Gloeosporium psidii produces maximum amount of pectinolytic enzymes in potato
yeast extract medium. The optimum temperature for enzyme production is 20
mum enzyme production is noted at pH 5.0 and maximum activity at pH 4.5. The opti-
mum range of CIN ratio for enzyme production is 35-52 (Midha and Chohan, 1967).
CoLLetotrichum sp. isolated from different fruits are either pathogenic only to their
original host or to several hosts (Yang and Chuang, 1994).CoLLetotrichum acutatum-
a new fruit rotting pathogen of guava was reported from Assam. In Assam 90% of the
stored guava fruit rot in 5-10 days due to this fungus (Das and Bose, 1993).
Storage at lODCprevents decay but when guava fruits are brought back to room tem-
perature the decay is enhanced. Higher temperature favours decay (Bhargava et al.,
1965). The cultivar Allahabad safeda i classified susceptible, Chittidar as moderately
susceptible and Apple guava as resistant to G. psidii (Singh and Bhargava, 1977a,b).
Pestalotia fruit rot of guava is caused by two species of Pestalotia i.e. Pestalotia
psidii Pat. and P. olivacea Guba.
20.1 Pestalotia psidii
The disease is reported from Allahabad, Lucknow and Hissar (Srivastava and Tandon,
1969a, Misra and Prakash, 1986, Kaushik etal., 1970). Misra and Prakash (1986) found
the incidence of canker 10-1S per cerit at Rehmankhera, Lucknow.
The disease begins in the form of brownish discolouration, which becomes russet
coloured after a week. As the spots enlarge, their central region become slightly de-
pressed and subsequently minute, single or gregarious black acervuli with viscoid
spore masses appear on the infected region (Fig.6). In partially rotted fruits, the margin
of infected tissue appears ochraceous buff in the colour (Srivastava and Tandon, 1969).
P.psidii is pathogenic on guava when fruits are injured (Kaushik et al., 1970). When
fruits are stored at 100°C and brought back to room temperature, the decay is enhanced
(Bhargava et al., 1965). Higher temperature favours decay by P.psidii. Canker of ripe
fruits, require a humid atmosphere, having higher temperature (2S-3S°C) and relative
humidity (80-100%) for causing maximum disease development.
20.1.3 Physiological changes
Sucrose, glucose and fructose concentration increase with age in non inoculated fruits.
Sucrose in guava is completely hydrolized by P.psidii in 6 days (Ghosh et al., 1964).
GUAVA DISEASES AND MANAGEMENT 107
The infected fruits preserved at low temperature and dry atmosphere can be protected
from the incidence of the disease. Post harvest wash with aureofungin (200 ppm) can
also protect cent per cent guava fruits for
days from the canker caused by P psidii
1972). Allahabad Safeda was classified as susceptible, Chittidar as
moderately susceptible and Apple guava as resistant to P psidii (Singh and Bhargava,
20.2 Pestalotia olivacea Guba
Disease was reported from Kurukshetra (Dhingra and Mehrotra, 1980).
6: Fruit rot due to Pestalotia
In this rot, infection on fruits start in the form of brownish coloured watery lesions,
which later on changes to russet coloured spots. White fluffy growth along with black
pin head like acervuli make it's appearance after one week (Dhingra and Mehrotra,
20.2.2 Causal organism
The colony of the pathogen Pestalotia olivacea Guba is white, hyphae hyaline, branched,
septate 2.5-3.5 nun wide; conidia 4-5 cell varied coloured with 2 end cells on either side
hyaline and conical, next cells light brown and middle cells dark brown with thick wall
and septa. Conidia 2.5-32.5 x 4.5-6.0 nun. Setulae 2-3 on either side of the conidia at-
tached to hyaline cells by a short pedicel, thread like pointed ends, 23-25 nun long
(Dhingra and Mehrotra, 1980).
Pestalotia cruenta Syd. causing fruit rot of Indian gooseberry (Phyllanthus
emblica L.) was found pathogenic on guava also (Tandon and Srivastava, 1964).
21. Stylar end rot
The stylar end rot of guava fruits is caused by Phomopsis sp. has been recorded in the
vicinity of Lucknow and pathogenicity was proved in in vivo and in vitro test. Wound-
ing favours the infection (Rai, 1956). Later, it was considered to be caused by Phomopsis
psidii de Camara (Srivastava and Tandon, 1969a). The disease is also reported from
The first visible symptom of the disease is the discoloration in the region lying just
below and adjoining the persistent calyx. The discolouration area gradually increases
in size and turn dark brown. Later the affected area becomes soft. Along with the
discolouration of epicarp, the mesocarp tissue also shows discolouration and the dis-
eased area is marked by being pulpy and light brown in colour in contrast to the bright
white colour of the healthy area of the mesocarp. At an advanced stage due to disorga-
nization of the inner affected tissues, size of the fruit shrinks and concentric wrinkles
develop on the skin. Finally the whole fruit is affected and is covered with pycnidia. At
all stages of development of the disease the affected tissue show abundant fungal
hypahe which are mostly intercellular (Rai, 1956).
21.2 Causal organism
The disease is considered to be caused by Phomopsis psidii de Camara (Srivastava
and Tandon, 1969a). The fungus produces dark carbonaceous pycnidia on rotting
fruits and also in culture. Under moist conditions, masses of spores ooze out from these
pycnidia through the ostiole. Pycnidia are ovoid and thick walled. They measure be-
tween 140 to 400nun in diameter. Conidia are ovate to elongate, hyaline varying between
5-9 x 2.5-4.0 nun. Stylospores long, slender, curved and vary between 16-30 x 0.8-1.411
m. The fungus requires a minimum temperature for growth near lOoC, an optimum near
25°C and maximum of about 35°C (Rai, 1956). Change in amino acid, organic acid, sugar
and ascorbic acid contents of infected fruit of guava with Phomopsis psidii is noticed
(Lal et al., 1985).
Alpha-naphthol (50ppm) and guaicol (250ppm) cause complete inhibition of mycelial
GUAVA DISEASES AND MANAGEMENT 100
growth of Ppsidii and fruit treated with this do not show disease symptom (Khare et
22. Sour rot
A fruit rot of guava caused by Geotrichum candidum Link ex Pers. was first recorded
from Nagpur in October, 1974 and it's pathogenicity was proved on wounded ripe
guava fruits. Mandarin orange, lemon, lime, sweet orange, banana, apple, tomato, grape
vine, watermelon, muskmelon, cucumber fruits and tubers of potato were found to
develop symptom on artificial inoculation (Shankhapal and Hatwalne, 1976).
23. Soft watery rot
It is one of the most common widely occurring disease of guava in India. This disease
was recorded in India by Edward et al., (1964), Srivastava and Tandon (1969a, 1969b)
and Patel and Pathak (1995) from Allahabad and Udaipur. Adisa (1985) reported it from
Nigeria and grouped it into soft rot causing organism and recognized the disease of
The infection starts as a brownish discolouration mostly at the stem end and it gradu-
ally proceeds downwards in an irregular wavy manner. Finally the whole fruit may get
involved. In advanced cases numerous small pycnidia are produced over the entire
surface of the fruit. The rot produced by the pathogen is soft and watery.
23.2 Causal organism
Soft watery rot of guava is caused by Botryodiplodia theobromae Pat. The optimum
temperature for the growth of the pycnidia production of B. theobromae is 25°C, but
conidial germination is maximum at 30°C but at 10°C the spores do not germinate
(Srivastava and Tandon, 1969b, Patel and Pathak, 1995). No rotting takes place upto 10
days, if fruits are stored at 1O-15°e (Srivastava and Tandon, 1969b). Storage at 10°C
prevent decay but when guava stored at 10°C and brought back to room temperature,
the decay is enhanced (Bhargava et al., 1965). Germination of spore is highest at 100 per
cent R.H. and lowest at 30 per cent R.H. (Patel and Pathak, 1995).
23.3 Physiological changes
As a result of Botryodiplodia infection many amino acids 'decrease due to their utiliza-
tion but occasionally some amino acids increase in infected tissues due to proteolysis
of host proteins. Due to infection sugar content decreases considerably (Srivastava,
1969). Inoculation of fruits with B. theobromae, reduce protein content, vitamin C,
tartaric, citric and malic acids. Succinic acid appears in inoculated fruit and reducing
sugar are abundant in inoculated fruits (Adisa, 1983).
Captan is found effective (Srivastava and Tandon, 1971). Homeopathic drug arsenic
oxide is effective against B. theobromae (Kehri and Chandra, 1986).
23.5 Varietal resistance
Variety Safeda and Apple coloured are susceptible while Pear Shaped is moderately
susceptible (Srivastava and Tandon, 1969 b).
24. Aspergillus soft rot
Aspergillus soft rot is caused by several species of Aspergillus of which A.awamori,
A. wentii and A.niger are important.
24.1 Aspergillus awamori Nakazawa
Soft rot of guava caused by Aspergillus awamori was reported from Allahabad (Lal et
1980). Unlike other Aspergillus rots, which are mainly responsible for the post
harvest decay, this disease occurs on unripe fruits and results in to-IS per cent loss.
The disease spreads as small circular water soaked spot, which enlarge and become
russet brown colour with age. The diseased lesion becomes soft in middle and later
develops warm sepia to clove brown coloured conidial heads surrounded by a white
circular ring mixed with citron yellow coloured fungus mycelia. The disease spreads on
the whole fruit with a black mouldy growth. The fruit rots completely within 10-12 days
and soft pulpy tissue emits a fermented odour. Pricked fruits develop usual symptoms.
High humidity and temperature greatly favour development of disease. However very
young green fruits fail to show any soft rot symptoms.
Guava fruit treated with Bavistin (Carbendazim) and Saprol (Triforine) at 1250 ppm as
pre inoculation treatment completely check the rot (Arya et al., 1981).
24.2 Aspergillus wentii Wehmer.
The infection starts as discoloured area. The spot later turns pulpy and yellow brown.
The infected portion shows maceration of the tissues. Optimum temperature and R.H.
for the development of fungus is 35°C and 70% respectively (Gupta et al., 1979).
GUAVA DISEASES AND MANAGEMENT
24.3 Aspergillus niger
The fungus develops brownish soft spots, which advance in size and depth, eventually
become blackish in colour. There is some shrinkage and the fruit consequently reduces
in size. An intensive maceration of tissue results into oozing of yellow brown watery
secretion mixed with spores and emission of disagreeable odour. Optimum RH is 70 per
cent (Gupta et aI., 1979). With the increase in the incubation period, the Vitamin C
content of both healthy and infected fruit tissue decreases but the rate of decline in the
healthy fruit is much less than in infected ones (Singh and Tandon, 1971). Adisa (1985)
reported soft rot caused by A. niger from igeria also.
24.4 Biochemical studies
Aflotoxin production in guava fruit by Aspergillus spp. is recorded. Aspergillus flavus
Link and A. parasitic us Speare, produce 0.563 and 0.257 ppm of aflotoxin B Ion guava
fruits respectively. These fungi also cause considerable loss in the quantity of total
reducing and non-reducing sugars, protein and ascorbic acid. Maximum decrease in
sugar content is due to the infection with A.
whereas, maximum depletion
in protein and ascorbic acid contents is caused by A.jlavus. Increase of 85 and 78 per
cent in phenol content is recorded in fruit due to infection with A.jlavus and A. parasiticus
respectively (Singh and Sinha, 1983).
The fungus develops brownish soft spots, which advance in size and depth, even-
tually become blackish in colour. There is some shrinkage and the fruit consequently
reduces in size. An intensive maceration of tissue results into oozing of yellow brown
watery secretion mixed with spores and emission of disagreeable odour. Optimum RH is
70 per cent (Gupta et al., 1979). With the increase in the incubation period, the Vitamin
C content of both healthy and infected fruit tissue decreases but the rate of decline in
the healthy fruit is much less than in infected ones (Singh and Tandon, 1971). Adisa
(1985) reported soft rot caused by A. niger from Nigeria also.
Misra (1987) reported fruit rot due to Pestalotiopsis psidii from Rehmankhera, Lucknow.
It causes reddish or brown yellow superficial spots, which cover about 50 per cent,
surface of the fruit and cause soft rotting. Disease is also reported from Bangalore
26. Fusarial rot
Adisa (1985), reported rot of guava from Nigeria by Fusarium equiseti (Corda) Sacco
and F oxysporum Schlecht., while Misra (1987) reported F moniliforme var. intermedium
causing large dark spot with cracking of epidermal tissue from Rehmankhera, Lucknow.
Fruit rot of guava caused by Rhizopus stolonifer (Ehrenb. ex. Fr.) Lind. was first re-
ported by Ooka from Kauai in 1980 (Ooka, 1980). He observed soft rot affecting mature
green to fully ripe fruits in orchard of Kauai island during 1978 and proved it's pathoge-
nicity. Adisa (1985) reported Rhizopus stolonifer and R. oryzae Went.
Nigeria causing soft rot. In early stage of disease development the lesions appear oily
and water soaked. The lesion margins are distinct and the lesions are slightly sunken at
the margin. The rapidly extending lesions reduce the fruit flesh to a semi solid state in a
The epidermis generally remains intact. Aerial hyphae develop at the point of
infection. Although development is not extensive, it rapidly extends over the lesion and
covers it with a sparse white to grey mycelium. White sporangiophores and sporangia
develop which later turn black, where the aerial hyphae contact the surface. sporangio-
phores and sporangia develop more densely at breaks that may occur in the epidermis
of the affected area and at the point of infection. Infected fruits remain attached to the
tree until they are manually dislodged or fall in the course of natural maturation. Rhizo-
pus rot is easily distinguished from Mucor rot in the field. Mucor rotted fruits are
covered with abundant yellow mycelia and sporangia and Rhizopus rotted fruit show
comparatively sparse aerial mycelium with dark grey to black sporangiophores and
sporangia (Ooka, 1980).
28. Mucor fruit rot
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in 1977 from island of Hawaii and Kauai. Even upto 80 per cent of mature green
fruits on trees were found infected. The pathogenicity was also proved by artificial
inoculation. The infected areas show water soaked lesions, which develop within a
week and the entire fruit is covered with yellowish, fuzzy mass of fungal fruiting bodies
and mycelia. Diseased fruits also give off and yeasty odour. The disease affects the
yield of marketable fruits to considerable degree. It was found that the disease devel-
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