Pathogenesis

1. Lecture Notes
For Level-3 Semester-2
Prepared by
Prof. Dr. Md. Rashidul Islam
Department of Plant Pathology
Bangladesh Agricultural University
Mymensingh

2.  Toxin in Pathogenesis
Toxin
A Low molecular weight microbial metabolites or substances
produced by the microorganisms that disrupt the physiological
processes of the plant by disturbing the essential metabolic
reactions at very low concentration.
a. Exo-toxins (released from the living cells)
Exotoxins are toxic substances secreted by microorganisms
and released outside the cell.
b. Endo-toxins (released from the lysed cell)
Endo-toxins are substances produced by the microorganisms
bound to the cell wall and released when the cell ruptures or
disintegrates. Toxins act directly on living protoplast

4.  Toxin-producers
 Some bacteria e.g., Pseudomonas, Burkholderia, Clavibacter,
Streptomyces, Xanthomonas
 A number of fungi: e.g. Alternaria, Ascochyta, Bipolaris, Botrytis,
Cercospora, Cochliobolus, Colletotrichum, Drechslera, Fusarium,
Phoma

5. A. Pathotoxins (Wheeler and Luke, 1963)
Those toxins which play an important causal role in disease
development and are produced by the pathogen or interaction
between host and pathogen.
Criteria for any toxin to be a pathotoxin:
 When applied on a susceptible host at low concentration,
should produce all or nearly all symptoms of the disease.
 Toxin and the pathogen should have same host range; same
resistance/ susceptibility spectrum.
 The pathogenicity of the pathogen should be correlated with
its capacity to produce the toxin.
e. g. Tabtoxin : Pseudomonas tabaci
HMT toxin: Dreschlera maydis race T
 Classification of toxins on the basis of their role in pathogenesis

6. B. Vivotoxins (Diamond & Waggoner, 1953)
Those toxins produced in the infected plant/host by the pathogen
and/or its host that function in the production of the disease.
Criteria/ characteristics of vivotoxins
 Reproducible separation of the toxin from the diseased host
 It must be characterized chemically.
 It must be able to induce of at least a part of disease syndrome
when applied on healthy plant.
 These are generally non-specific.
e. g. Fusaric acid: Fusarium spp.
Pyricularin: Pyricularia oryzae

7. C. Phytotoxins
Phytotoxins are phytotoxic substances produced by living
organism and whose role in disease is merely suspected rather
than established.
Phytotoxins are nonspecific, incite few or none of the symptoms
that are incited by the pathogen, and as happens in most cases,
show no relation between toxin production and pathogenicity.
e. g. Alternaric acid, cochliobolin
Pseudomonas syringae, P. syringae pv. tomato, and P. syringae pv.
maculicola are primarily associated with production of the
phytotoxin coronatine.

8.  On the basis of specificity to host (Scheffer, 1983)
A. Host selective/ specific toxins
B. Non- host selective/ non-specific toxins

9. A. Host Specific/ selective toxins
A host-specific or host-selective toxin is a substance produced by
a pathogenic microorganism that, at physiological concentrations,
is toxic only to the hosts of that pathogen and shows little or no
toxicity against nonsusceptible plants.
Most host-specific toxins must be present for the producing
microorganism to be able to cause disease i.e. it is essential for
pathogenicity.

10.  So far, host-specific toxins have been shown to be produced
only by certain fungi (Cochliobolus, Alternaria, Periconia,
Phyllosticta, Corynespora, and Hypoxylon), although certain
bacterial polysaccharides from Pseudomonas and Xanthomonas
have been reported to be host specific.
 20 such toxins have been recognized mainly produced by
Alternaria and Cochliobolus spp.
 Victorin
T-toxin,
 HC-toxin,
 AAL-toxin

11.  Host-Specific (selective) Toxins
• Produced by fungi
• Almost all are produced by loculoascomycetes
• Alternaria spp. and Cochliobolus spp. primarily
• First toxins characterized–AKT-toxin (Japan 1933), Victorin
(USA,1947), HC-toxin (USA,1965)
• Toxins reproduce all disease symptoms when applied to a
susceptible host
• Scheffer & Nelson- 1960’s- single genetic loci control toxin
production in Cochliobolus spp.
Cochliobolus heterostrophus – T-toxin – TOX1
C. carbonum – HC-toxin – TOX2
C. victoriae – Victorin – TOX3

12.  Victorin or HV toxin
Victoria blight of oats (cv. Victoria)-
Cochliobolus (Helminthosporium) victoriae
A host-specific toxin – victorin: a cyclic pentapeptides
 Toxin reproduces all disease symptoms when applied to a
susceptible host
 Susceptibility to toxin conferred by dominant allele at Vb locus
Victorin causes premature senescence of leaves
Host selective(specific) toxins

13. Functions of victorin
 C. victoriae infects the basal portions of susceptible oat plants
and produces a toxin that is carried to the leaves, causes a leaf
blight, and destroys the entire plant. All other oats and other plant
species tested were either immune to the fungus and to the toxin.
 The toxin not only produces all the external symptoms of the
disease induced by the pathogen, but it also produces similar
histochemical and biochemical changes in the host, such as
changes in cell wall structure, loss of electrolytes from cells,
increased respiration, and decreased growth and protein
synthesis.
 Moreover, only fungus isolates that produce the toxin in culture
are pathogenic to oats, whereas those that do not produce toxin
are nonpathogenic.

14.  T-toxin
• Produced by Helminthosporium maydis race T (Cochliobolus
heterostrophus race T). Single genetic locus is involved in
toxin production.
• Southern Corn Leaf Blight
• Toxin is a polyketide secondary metabolite.
• Toxin causes swelling, uncoupling of oxidative
phosphorylation, stimulation of respiration, leakage of Ca2+
and NAD in mitochondria.

15. Functions of T toxin
 T toxin does not seem to be necessary for the pathogenicity
of C. heterostrophus race T, but it increases the virulence of
the pathogen.
 The pores cause loss of mitochondrial integrity, i.e., loss of
selective permeability of the mitochondrial membrane, and
disease.

16. Symptoms caused by host-selective T toxin, on a corn plant
produced by race T of the fungus Cochliobolus
(Helminthosporium) heterostrophus and its toxin.

17.  HC-toxin
• Produced by Race 1 of Cochliobolus carbonum
(Helminthosporium carbonum)-causes Northern Leaf blight
of Corn.
• It is a cyclic peptide
• Mode of action may be different than T-toxin - inhibiting
defense reactions rather than causing cell death
 This is the only toxin, so far, for which the biochemical and
molecular genetic basis of resistance against the toxin is
understood.
• Hm1 was the first plant resistance gene to be cloned and
characterized in 1992 by Johal & Briggs Science 258: 985.
• Hm1 encodes a NADPH-dependent reductase enzyme (HC-
toxin reductase - HCTR) that detoxify the toxin

18. Functions of HC toxin
HC toxin is not actually toxic in itself, but rather acts as a
virulence factor by preventing initiation of the changes in gene
expression that are necessary for the establishment of induced
defense responses, i.e., it acts as a suppressor of defense
responses.

19. Northern corn leaf spot symptoms caused by the fungus
Cochliobolus carbonum and its toxin, HC toxin, on corn.

20.  Alternaria toxins
 Produced by closely related Alternaria spp., Alternaria alternata.
Several pathotypes of Alternaria alternata attack different host
plants and on each they produce one of several multiple forms of
related compounds that are several pathotypes of Alternaria
alternata attack different host plants and on each they produce one
of several multiple forms of related compounds.
• All are low molecular weight, secondary metabolites and are
structurally similar .
 Some of the toxins and the hosts on which they are produced and
affect are
 AK toxin causing black spot on Japanese peat fruit
 AAL toxin causing stem canker on tomato,
 AF toxin on strawberry,
 AM toxin on apple,
 ACT toxin on tangerine,
 ACL toxin on rough lemon, and
 HS toxin on sugar cane.

21. AKT-toxin
AF-toxin
ACT-toxin
 One specific genotype of each host is susceptible to toxin - very
narrow host range
• Tangerine pathotype – ACT-toxin
• Strawberry pathotype – AF-toxin
• Japanese pear pathotype – AKT-toxin

22. Functions of AM Toxin
 The AM toxin causes plasma membranes of susceptible cells
to develop invaginations, and cells show a significant loss of
electrolytes.
 The AM toxin also causes rapid loss of chlorophyll.

23. Fruit spots on Japanese pear
caused by one of the strains
of the fungus Alternaria
alternata and its toxin, AK
toxin.
Leaf spots caused by the AM
toxin produced by another
strain of the fungus A. alternata
and its toxin, AM toxin, on
apple leaves.

24. Pathogen Name of the toxin Disease/Hosts
Periconia circinata Peritoxin (PC toxin) Sorghum root
rot
Mycosphaerella (Phyllosticta)
zeae-maydis
PM toxin (T toxin) Leaf blight of
corn
Pyrenophora tritici-repentis Ptr toxin Tan spot of
tomato
Corynespora cassiicola CC toxin Target Spot
A. brassicae destruxin B Alternaria leaf
spot
Other Host-Specific Toxins

25. B. Non-Specific/ selective
Several toxic substances produced by phytopathogenic
microorganisms have been shown to produce all or part of the
disease syndrome not only on the host plant, but also on other
species of plants that are not normally attacked by the pathogen in
nature. Such toxins, called nonhost-specific or nonhost-selective
toxins.
 Non-specific toxins affect the protoplast of many unrelated plant
species in addition to the main host of the pathogen producing the
toxins.
 These toxins affect virulence of the pathogen but are not essential
for pathogenicity.
e.g. Tab toxin, phseolotoxin, tentoxin, cercosporin

26. Non host selective (non-specific) toxins
Tabtoxin
 Produced by Pseudomonas syringae pv. tabaci causes wild fire
disease in tobacco.
 Tab toxin is a dipeptide composed of amino acid threonine and
tabtoxinine
 Also by other strains of pv. tabaci in other hosts like bean and
soybean, also by other attacking oat, maize and coffee.
 Toxin producing strains cause necrotic spots on leaves
surrounded by yellow halo.

27. Functions of tabtoxin
 The toxin as such is not toxic but in the cell it get hydrolysed
and release aminoacid tabtoxinine which is toxic.
 It acts by inhibiting/inactivating the enzyme glutamine
synthetase and uncoupling of phosphorylation and
photorespiration, destroy the thylakoid membrane of the
chloroplast thus causes chlorosis and then necrosis.
 It reduces the ability of the plant to respond actively to the
bacterium.

28. Symptoms caused by
nonhost-selective toxins.
Symptoms of young tobacco leaves
showing spots caused by the bacterium
Pseudomonas syringae pv. tabaci.

29.  Phseolotoxin
Produced by Pseudomonas syringae pv. phaseolicola causes
halo blight of bean.
Functions
 Toxin causes growth reduction of newly expanding leaves,
disruption of apical dominance, and accumulation of the amino
acid ornithine.
 It interferes with lipid synthesis, change the permeability of
membranes, and result in the accumulation of large starch grains
in the chloroplasts.
 Phaseolotoxin plays a major role in the virulence of the
pathogen by interfering with or breaking the disease resistance
of the host toward not only the halo blight bacterium, but also
several other fungal, bacterial, and viral pathogens.

30. Leaf spots and halos caused by phaseolotoxin produced by the
bacterium Pseudomonas phaseolicola, the cause of halo blight of
bean.

31. Tentoxin
It is produced by Alternaria alternata (A. tenuis)
Functions
 It causes leaf spots and chlorosis
 It is cyclic tetrapeptide that bind to and inactivate the protein
(chloroplast-coupling factor) involved in energy transfer into
chloroplast.
 It also inhibits phosphorylation of ADP to ATP leading to
disruption of chlorophyll synthesis.
 It puts stress on the host plant with events that lead to
chlorosis and suppressing host resistance mechanisms, tend
to enhance the virulence of the pathogen.

32. Leaf spots and chlorosis caused by the Alternaria alternata toxin.

33.  Cercosporin
 Produced by Cercospora spp. and other fungi causes leaf spot
disease
 This toxin is activated by light and become toxic to plants by
generating activated species if oxygen (single O); the activated O
destroy the host membrance and provide nutrients to pathogen,
 It is photosensitizing perylenequinone that absorb light energy

34. Leaf spots on zinnia (A) and gray leaf spots on corn (B)
caused by the photosensitizing toxin cercosporin, produced
by different species of the fungus Cercospora

35.  Fusarium toxins
 Marticin: pathooxin produced by Fusarium oxysporum f sp. pisi
– pea wilt; have nepthazarin; red pigmented compounds
 Fusric acid: Vivotoxin, chemically 5-n- butyl-picolinic aacid
produced by many spp of Fusairim: Fusarium oxysporum f sp.
Batatis (sweet potato); cubense (banana); lini (Linseed);
lycopersici (Tomato); vasinfectum (Cotton)
 Lycomarasmin: Fusarium oxysporum f sp. lycopersici

36.  Pyricularin
Pyricularia oryzae - rice blast
Exist in two froms: α-picolinic acid and pyricularin
 Toxic to conidial germination, however, the fungus
produces a pyricualrin binding protein (copper oxidase) that
binds with pyricularic and destroy the fungitoxicity but not
the phytotoxicity.
 It affect respiration and growth at low concentration but
inhibit at high concentration.

37.  Effect of toxins on host tissue
 Changes cell permeability
 Disruption of normal metabolic activity
 Loss of salts from protoplasm increases
 Respiration -tab toxinine
 Uncoupling of oxidative phosphorylation-victorin
 Inhibition of host enzyme - tabtoxin inhibit normal host enzymes
 Affect cellular transport system e.g. H+/K+ exchange at the cell
membrane
 Other mechanisms:
interfere with growth regulatory system e.g. inhibition of root
growth ( F. moniliforme)

38. Other non specific toxins include
Fumaric acid : Rhizopus spp.
Oxalic acid: Sclerotinia, Sclerotium spp.
Alternaric acid: Alternaira spp.
Ophiobolin: Cochliobolus spp.
Pyricularin: Magnaporthe grisea
Lycomarasmin: F. oxysporum in tomato