UNESCO-NIGERIA TECHNICAL &

VOCATIONAL EDUCATION
REVITALISATION PROJECT-PHASE II

NATIONAL DIPLOMA IN
SCIENCE LABORATORY TECHNOLOGY

PATHOLOGY
COURSE CODE: STB 212

YEAR 2 – SEMESTER 1

THEORY

Version 1: December 2008

 TABLE OF CONTENT
TITLE PAGE

WEEK 1: TERMINOLOGY IN PARASITOLOGY

1.1 Terminology in parasitism ………………………………………. ………………1

1.1.1 Parasitism …………………………………………………………………………1
1.1.2. Symbiosis……………………………………………………................................1
1.1.3. Commensalism…………………………………………………............................2
1.1.4 Definitive host ……………………………………………………………………2
1.1.5 Intermediate host…………………………………………………………..............2
1.1.6 Vector…………………………………………………………………………….2

WEEK 2 ADAPTATION TO PARASITE

2.1 Adaptation to parasitism…………………………………………………………4

WEEK 3 : DISEASES CAUSED BY PROTOZOANS

3.1 Disease caused by

protozoan………………………………………………………….7
3.2 Life cycle of Rhizopoda…………………………………………………………..8
3.3 Mode of infection--------------------------------------------------------------------------------
3.4 Pathogenesis--------------------------------------------------------------------------------------
-
3.5 Economic Importance of Entomoeba histolytica--------------------------------------------
--
3.6 Life cycle of Mastigophora……………………………………………………….…8
3.7 Mode of Infection of Trypanosoma gambiense---------------------------------------------
3.8 Economic Importance of Trypanosoma gambiense----------------------------------------

WEEK 4 : LIFE CYCLE OF PLASMODIUM

4.1 Mode of infection------------------------------------------------------------------------------
4.2 Economic importance of Plasmodium-------------------------------------------------------

WEEK 5 : METHOD OF CONTROL OF INFECTION BY PROTOZOANS

5.1 Entomoeba histolytica. …………………………………………..........................13

5.2 Trypanosoma gambiense ………………………………………..………..15
5.3 Plasmodium viax…………………………………………………………………15

WEEK 6 : PARASITIC PLATYHELMINTHE OF MEDICAL AND VETERINARY

IMPORTANCE

6.1 Life history and economic importance of Trematode and

cestode………...………18
6.1.1 Life history of Fasciola
hepatica…………………………………………...……….19
6.1.2 Life history of Schistosoma haematobium…………………………………….….20
 6.2 Economic importance of Schistosoma haematobium-----------------------------------
6.3 Life history of Taenia solium and Taenia saginata………………………….……..2
6.3.1 Economic importance of Taenia saginata And Taenia solium --------------------------
--

WEEK 7: MODE OF TRANSMISSION OF TREMATODE AND CESTODE

7.1 Fasciola hepatica

……………………………………………………………...22
7.2 Schistosoma haematobium………………………………………………...……….23
7.3 Taenia solium and Taenia
saginata……………………………………..………….24
7.4 Preventive\control measures against Trematode and Cestode
………………………25
7.4.1 Prevention\control of Fasciola
hepatica…………………………………………….26
7.4.2 Prevention\control of Schistosoma
haematobium……………………………..……..26
7.4.3 Prevention\control of Taenia solium and Taenia
saginata……………………...….26

WEEK 8 : DISEASED CAUSED BY NEMATODE

8.1 Life history and economic importance of nematode

………………………............30
8.1.1 Life history and economic importance of Ascaris lumbricoides
…………………...30
8.1.2 Life history and economic importance of
Hookworm……………………………..33
8.1.3 Life history and economic importance of Wuchereria
bancrofti…………………..33
8.1.4 Life history and economic importance of Onchocerca
volvulus……………...……36
8.1.5 Life history and economic importance of Dracunculus
medinensis…………….....37
8.1.6 Life history of Loa loa-----------------------------------------------------------------------
-37

WEEK : 9 MODE OF TRANSMISSION AND AGENT OF NEMATODE

9.1 Mode of transmission and agent of Ascaris lumbricoies…………………………42

9.2 Mode of transmission and agent of Hookworm-----------------------------------------43
9.3 Mode of transmission and agent of Wuchereria bancrofti…………………..…….47
9.4 Mode of transmission and agent of Onchocerca volvulus………………………..49
9.5 Mode of transmission and agent of Dracunculus medinensis…………………....50
9.6 Mode of transmission and agent of Loa loa---------------------------------------------
9.7 Method of control of nematode diseases…………………………………………56
9.7.1 Method of control of Ascaris lumbricoides………………………………………59
9.7.2 Method of control of Hookworm……………………………………………….. .66
9.7.3 Method of control of Wuchereria bancrofti…………………………………..…67
9.7.4 Method of control of Onchocerca volvulus………………………………………68
9.7.5 Method of control of Dracunculus medinensis……………………………...……7
 9.7.6 Method of control of Loa loa-----------------------------------------------------------------
71

WEEK 10: NATURE OF PLANT DISEASES THEIR TRANSMISSION AND

CONTROL

10.1 Scope of plant pathology…………………………………………

………….74
10.2 Terminology in plant
pathology………………………………………………74
10.2.1 Pathogen………. ……………………………………………………….….75
10.2.2
Parasite…………………………………………….………………….………76
10.2.3
Pathogenesis……………………………….……………………..……………..77
10.3 Nature of fungal diseases ………………………………….………………78
10.4 Nature of bacterial diseases ……………………………….……………….80
10,5 Nature of viral diseases …………………………………………….……...81
10.6 Generalize structure and life cycle of viral
particles…………………………83
10.6.1 Structure of Viruses---------------------------------------------------------------------
10.6.3 Life cycle of a virus------------------------------------------------------------------

WEEK 11: EPIDEMIOLOGY, CAUSATIVE AGENT, LIFE CYCLE AND CONTROL

OF FUNGAL DISEASES.

11.1 Black pod of

cocoa………………………………….………………………...….87
11.2 Damping off
seedling…………………...…………………………………..……87
11.3 Leaf spot of
groundnut………………..……………………………….…………87
11.4 Rust and smut of
maize…………………………………………………………..87

WEEK 12: EPIDEMIOLOGY OF BACTERIAL DISEASES.

12.1 Wilt off ------------------------------------------------------------------------------------

88
12.2 Citrus canker------------------------------------------------------------------------------
88
12.3 Bacterial spot of tomato… ……………………………………………..89

WEEK 13: EPIDEMIOLOGY OF VIRAL DISEASES.

13.1 Cassava mosaic…………………..……………………..………………91

13.2 Life history of aphids……………………..……………………………………91

13.3 Reproduction of Aphids----------------------------------------------------------------------

WEEK 14: KOCH POSTULATE OF ESTABLISHING PATHOGENECITY OF

DISEASES
 14.1 Koch
postulate……………………...…………………………………………..91

WEEK 15: PRINCIPLE OF PLANT DISEASES CONTROL

15.1
Exclution………………………………………….……………………………92
15.2 Eradication……………… …………………………………………...………92
15.3 Protection…………………………………………………………….……….93
15.4
Resistance…………………………………………………………...…………93
15.5 Application of control principle to specific plant diseases …………………..93
 WEEK 1: TERMINOLOGY IN PARASITOLOGY

1.1 Terminology in Parasitism

1.1.1 Parasitism is a type of symbiotic relationship between organisms of different

species [1]. The parasite benefits from a prolonged, close association with the host,
which is harmed. In general, parasites are much smaller than their hosts, show a high
degree of specialization for their mode of life and reproduce more quickly and in
greater numbers than their hosts. Classic examples of parasitism include the
interactions between vertebrate hosts and such diverse animals as the tapeworms,
flukes, Plasmodium species and scabs.

Fig 1.1 mite

1.1.2. Symbiosis

The term symbiosis commonly describes close and often long-term interactions between
different biological species. The term was first used in 1879 by the German mycologist,
Heinrich Anton de Bary, who defined it as: "the living together of unlike organisms".

The definition of symbiosis is in flux and the term has been applied to a wide range of
biological interactions. The symbiotic relationship may be categorized as being mutualistic,
parasitic, or commensal in nature.[4][5] Others define it more narrowly, as only those
relationships from which both organisms benefit, in which case it would be synonymous with
mutualism.

Symbiotic relationships included those associations in which one organisms lives on another
(ectosymbiosis, such as mistletoe), or where one partner lives inside another (endosymbiosis,
such as lactobacilli and other bacteria in humans or zooxanthelles in corals). Symbiotic
relationships may be either obligate, i.e., necessary to the survival of at least one of the
organisms involved, or facultative, where the relationship is beneficial but not essential to
survival of the organisms

1.
Fig 1.1.2 fish

An example of mutual symbiosis is the relationship between Ocellaris clownfish that

dwell among the tentacles of Ritteri sea anemones. The territorial fish protects the
anemone from anemone-eating fish, and in turn the stinging tentacles of the anemone
protect the clownfish from its predators (a special mucus on the clownfish protects it from
the stinging tentacles).

1.1.3 Commensalism describes a relationship between two living organisms where one
benefits and the other is not significantly harmed or helped. It is derived from the
English word commensal, meaning the sharing of food, and used of human social
interaction. The word derives from the Latin com mensa, meaning sharing a table.

1.1.4 Primary host or definitive host is a host in which the parasite reaches maturity
and, if applicable, reproduces sexually.

1.1.5 Secondary host or intermediate host is a host that harbors the parasite only for a
short transition period, during which (usually) some developmental stage is
completed. For trypanosomes, the cause of sleeping sickness, humans are the
primary host, while the tsetse fly is the secondary host. Cestodes (tapeworms) and
other parasitic flatworms have complex life-cycles, in which specific
developmental stages are completed in a sequence of several different hosts.

1.1.6 Vector is an organism that does not cause disease itself but which transmits
infection by conveying pathogens from one host to another. A classic example is
the anopheles mosquito which acts as a vector for the disease malaria by
transmitting the malaria parasite plasmodium to humans. In this case plasmodium
is harmless to the mosquito (its intermediate host) but causes the disease malaria
in humans (its definitive host).

2.
 WEEK 2 ADAPTATION TO PARASITE

2.1 Adaptation to parasitism

Parasitic adaptations are responses to features in the parasite's environment and this
environment is the body of another organism, the host. This seems to be a difficult
environment to invade but those organisms that have done so have often been very successful
both in terms of numbers of individuals and numbers of species. Blood and tissues seem to be
harder to invade than the gut, as is shown by the smaller number of blood and tissue
parasites. This is probably in part related to the difficulties of getting eggs to the outside from
sites within the host. Almost all phyla have some parasitic members (at least 50% of all
species are parasites). None of the deuterostome phyla are truely parasitic (echinoderms,
chordates, chaetognaths). Whilst amongst the protostomes, the only groups that have no
known parasitic members are the ectoprocts, endoprocts, phoronids and brachiopods.

 A characteristic feature of many parasites are organs of attachment. Despite the wide
variety of parasites there are only two trends running through the evolution of
attachment organs, the development of either hooks or suckers. Suckers occur in such
widely divergent groups as protozoa, monogeneans, digeneans, cestodes, parasitic
crustaceans and parasitic annelids. Spines and hooks are present in many parasitic
groups and the elaboration of spines or suckers or both into an eversible proboscis has
occurred in the cestodes, acanthocephalans, and the acarines (ticks). Other types of
attachment organ include claws in parasitic insects and the ctenidia (comb organ) of
fleas. Penetrative filaments occur in a number of groups of parasite (Oxyurid
nematodes, Microspora protozoans).

 In many parasites, particularly endoparasites, there is often a reduction in the CNS

and sense organs.

 In endoparasites, again there is a trend to reduce the gut and absorb nutrients through
the whole body surface.

 In those intestinal parasites, which do not absorb nutrients through the body surface,
there is usually a thick cuticle. So helminths tend either to loose their gut and absorb
nutrients through their teguments, or else retain their gut and have a thick resistant
cuticle.

 In many parasites there is a tremendous elaboration of the reproductive organs,

associated with increased gamete production. Cestodes, for example, basically consist
of a small head and neck region and the rest is serially repeated gonads. Parasites can
be described as being solely adapted for reproduction.

 Parasitic protozoa are in an essentially isosmotic environment and so lack a

contractile vacuole.

 In parasitic insects there are often elaborate tracheal trunks, so the insect can remain
air breathing even when it is in its host.
WEEK 3 : DISEASES CAUSED BY PROTOZOANS
3.1 Life Cycle of Rhizophoda (e.g Entomoeba histolytica)

Figure 3.1 Life cycle of Entamoeba histolytica and the clinical manifestations of infection
in humans. E. histolytica is a protozoan parasite that causes amoebic colitis and liver
abscess. Its life cycle consists of two stages: cysts and trophozoites. (a) Cysts measure 10–15
m in diameter and typically contain four nuclei; (b) they are spread via the ingestion of
faecally contaminated food or water. (c) During excystation within the lumen of the small
intestine, nuclear division is followed by cytoplasmic division, giving rise to eight
trophozoites. (d) Trophozoites, which measure 10–50 m in diameter and contain a single
nucleus with a central karyosome, reside in the lumen of the caecum and large intestine,
where they adhere to the colonic mucus and epithelial layers. (e) Approximately 90% of
individuals infected with E. histolytica are asymptomatically colonised; (f) re-encystation of
the trophozoites occurs within the lumen of the colon, resulting in (g) the excretion of cysts in

the faeces and continuation of the life cycle. (h) Alternatively, the trophozoites can invade the
colonic epithelium, causing amoebic colitis (in ~10% of infected people). Amoebic dysentery
usually occurs gradually, with symptoms [such as abdominal pain and tenderness, and painful
sudden bowel evacuation (tenesmus) and diarrhoea] developing over a period of one to
several weeks, often followed by weight loss. E. histolytica can spread in the bloodstream
(haematogenously) after it has penetrated the colonic epithelium (not shown) and can
establish persistent extraintestinal infections, most commonly (i) amoebic liver abscess. Liver
abscess is overwhelmingly the most common extraintestinal manifestation of amoebiasis.
This complication is 10 times more common in adult men than in adult women. The typical
patient with amoebic liver abscess is a 20–40-year-old male with a 1–2-week history of fever
and diffuse or right, upper quadrant abdominal pain.Entamoeba histolytica is an anaerobic
parasitic protozoan, part of the genus Entamoeba.[1] Predominantly infecting humans and
other primates. E. histolytica is estimated to infect about 10% of the world's population, a
further 10% of the carriers display symptoms, so around 50 million people. Mammals such as
dogs and cats can become infected transiently, but are not thought to contribute significantly
to transmission.

3.2 Mode of infection

The active (trophozoite) stage exists only in the host and in fresh loose feces; cysts survive
outside the host in water, soils and on foods, especially under moist conditions on the latter.
The cysts are readily killed by heat and by freezing temperatures, and survive for only a few
months outside of the host.[2] When cysts are swallowed they cause infections by excysting
(releasing the trophozoite stage) in the digestive tract. The trophozoite stage is readily killed
in the environment and cannot survive passage through the acidic stomach to cause infection.

3.3 Pathogenesis

E. histolytica, as its name suggests (histo–lytic = tissue destroying), is pathogenic; infection

can lead to amoebic dysentery or amoebic liver abscess.[1] Symptoms can include fulminating
dysentery, diarrhea, weight loss, fatigue, abdominal pain, and amoebas. The amoeba can
actually 'bore' into the intestinal wall, causing lesions and intestinal symptoms, and it may
reach the blood stream. From there, it can reach different vital organs of the human body,
usually the liver, but sometimes the lungs, brain, spleen, etc. A common outcome of this
invasion of tissues is a liver abscess, which can be fatal if untreated. Ingested red blood cells
are sometimes seen in the amoeba cell cytoplasm.

3.4 Economic Importance of Entomoeba histolytica

The parasite play an important role in killing or causing death to their host by exciting
different types of pathological effects on the host.
3.5 Life Cycle of Mastigophora (e.g Trypanosoma gambiense)

Life cycle of the Trypanosoma brucei parasites.

The tsetse fly is large, brown and stealthy. While taking blood from a mammalian host, an
infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The
parasites enter the lymphatic system and pass into the bloodstream (1). Inside the host, they
transform into bloodstream trypomastigotes (2), are carried to other sites throughout the
body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by
binary fission (3). The entire life cycle of African Trypanosomes is represented by
extracellular stages. A tsetse fly becomes infected with bloodstream trypomastigotes when
taking a blood meal on an infected mammalian host (4,5). In the fly's midgut, the parasites
transform into procyclic trypomastigotes, multiply by binary fission (6), leave the midgut,
and transform into epimastigotes (7). The epimastigotes reach the fly's salivary glands and

continue multiplication by binary fission (8). The cycle in the fly

approximately 3 weeks to progress.
takes
3.6 Mode of Infection of Trypanosoma gambiense

The tsetse fly inject a metacycle trypomastigote into the skin tissue of the host and then enter
the lymphatic system and then pass into the blood stream.

3.7 Economic Importance of Trypanosoma gambiense

The parasite play an important role in killing or causing death to their host by exciting
different types of pathological effects on the host.
WEEK 4 : LIFE CYCLE OF PLASMODIUM

Figure 4 Life cycle of plasmodium

The Plasmodium genus of protozoal parasites (mainly P.falciparum, P.vivax, P.ovale, and
P.malariae) have a life cycle which is split between a vertebrate host and an insect vector.
The Plasmodium species, with the exception of P.malariae (which may affect the higher
primates) are exclusively parasites of man. The mosquito is always the vector, and is always
an Anopheline mosquito, although, out of the 380 species of Anopheline mosquito, only 60
can transmit malaria. Only female mosquitos are involved as the males do not feed on blood.
The basic life cycle of the parasite is shown below:
The spozozoites from the mosquito salivary gland are injected into the human as the
mosquito must inject anticoagulant saliva to ensure an even flowing meal. Once in the human
bloodstream, the sporozoites arrive in the liver and penetrate hepatocytes, where they remain
for 9-16 days, multiplying within the cells. Next they return to the blood and penetrate red
blood cells, in which they produce either merozoites, which reinfect the liver, or micro- and
macrogametocytes, which have no further activity within the human host. Another mosquito
arriving to feed on the blood may suck up these gametocytes into its gut, where exflagellation
of microgametocytes occurs, and the macrogametocytes are fertilized. The resulting ookinete
penetrates the wall of a cell in the midgut, where it develops into an oocyst. Sporogeny within
the oocyst produce many sporozoites and, when the oocyst ruptures, the sporozoites migrate
to the salivary gland, for injection into another host.

This highly specialised life cycle requires specialised biology on the part of the Plasmodium
species. The reason that not all mosquitos are vectors for Plasmodium parasites is that
refractory mosquitos posses substances toxic to Plasmodium within their cells . A higher
trypsin-like activity was also found in the midgut of resistant species, possibly inhibiting
ookinete development. Plasmodium parasites seem capable of adapting to any suitable
anopheline mosquito, given sufficient time and contact. Sporogeny within the mosquito are
governed by environmental temperature as Anopheline mosquitos are poikilotherms.

Once injected into the human host, all Plasmodium species will penetrate hepatocytes.
However, P.falciparum and P.malariae sporozoites trigger immediate schizogony whereas
P.ovale and P.vivax sporozoites may either trigger immediate schizogony or have a delayed
trigger, resulting in dormant hypnozoites. Some strains, such as the North Korean strain,
seem to consist of sporozoites with universally delayed triggers, so they all form long lasting
hypnozoites. P.vivax may have an incubation period of up to 10 months. Gametocytes
produced in the primary attack seem to contain all the genetic information required to create
sporozoites of several different activation times. The same seems true for gametocytes
produced in relapses where the hypnozoites become activated.

Sexual development of Plasmodium begins as the merozoites invade the erythrocytes after
their release from the liver. Within the erythrocyte, shizogony occurs to produce either more
merozoites (taking 22 1/2 hours in the case of P.berghei), or the sexual micro and
macrogametocytes (taking 26 hours). In P.falciparum, erythrocytic schizogony takes 48 hours
and gametocytosis takes 10-12 days. Normally a variable number of cycles of asexual
erythrocytiic shizogony occurs before any gametocytes are produced . The immune system
may produce antibodies to the gametocytes at this stage.

Once drawn into the mosquito, the gametocytes increase in volume and escape the
erythrocyte. Microgametes are formed by 3 mitotic divisions within the microgametocyte,
and are expelled explosively. No further changes affect the female macrogametocyte until
fertilisation where the plasmalemmas of male and female gametes fuse and the nucleus of the
microgamete enters the female cytoplasm. After fertilisation, the zygote is a motionless
globular cell, but after 18 to 24 hours it becomes elongated and motile, containing
micronemes and a pellicle. The cell invades the microvillus border, passes through the
midgut cells, and lies beneath the basement membrane. The ookinete then becomes a static
oocyst, between the basal lamina and the basement cell membrane, and bounded by a thick
plasmalemma. The chief source of nutrients is the haemolymph in which the oocyst develops.
Sporoblasts form, and sporozoites bud off.

After the cyst ruptures, the sporozoites escape into the haemocoele and migrate to and
penetrate salivary gland cells, where they lie in vacuoles for up to 59 days. These sporozoites
develop and become up to 1000 times more infective than when in the oocyst. They are more
antigenic, and bear circumsporozoite polypeptide on their plasmalemma. Sporozoite motility
is involved in their invasion of cells and escape from the salivary gland. The sporozoites are
about 12µm long and 1µm across, with a single nucleus, anterior to which lie micronemes,
and posterior to which lies ER and mitochondria. They posses a complex pellicle, which is
responsible for motility, and this pellicle contains circumsporozoite protein. The apical
penetrating region contains extensions of the microneme ducts which release an agent which
interacts with host cell plasma membrane during penetration.

A biting mosquito transfers about 10% of its sporozoite load into the capillaries or
perivascular tissue. Now the sporozoites must begin their evasion of the host defences,
possibly by binding serum proteins for 'camouflage'. Some are destroyed by macrophages, or
by antigen-specific antibodies in immune individuals, but in non-immune individuals, they
reach the hepatocytes and initiate schizogeny or become hypnozoites depending on their
delay trigger. All sporozoites have left the peripheral circulation system within 45 minutes.

4.1 Mode of infection

The disease occur when an infected female anopheline mosquito inject the sporozoite while
taking its blood meal. It can be transmitted through blood transfusion, or by using
contaminated hypodermic needle.

4.2 Economic importance of Plasmodium

The parasite play an important role in killing or causing death to their host by exciting
different types of pathological effects on the host.
WEEK 5 : METHOD OF CONTROL OF INFECTION BY
PROTOZOANS

5.1 Entomoeba histolytica

This can be control through the following method

 By personal hygiene
 Do not defecate outside latrines, toilets etc.
 Protection of food from dirt and soil; thorough washing of produce; and hand
washing.
 Food dropped on the floor should never be eaten without washing or cooking,
particularly in endemic areas. Vegetables originating from third-world countries
should always be washed thoroughly before consumption

5.2 Trypanosoma gambiense

This can be control through the following method

 It can controlled by controlling the infection. The man source of infection of

trypanosomiasis in the human patient.
 The reservoir host should be destroyed.
 Eradication of tsetse flies by using insecticides
 It can be control by treatment with pentavalent drugs such as diamidines.

5.3 Plasmodium

 It can controlled by controlling the infection.

 The reservoir host should be destroyed.

 Eradication of Mosquito lavae by using insecticide.
 By using mosquito net.
WEEK 6 : PARASITIC PLATYHELMINTHE OF MEDICAL AND
VETERINARY IMPORTANCE

6.1 Life history And Economic Importance of Trematode And cestode

6.1.1 Life history of Fasciola hepatica

Fasciola hepatica, also known as the common liver fluke or sheep liver fluke, is a
parasitic flatworm of the class Trematoda, phylum Platyhelminthes that infects liver
of various mammals, including humans. The disease caused by the fluke is called
fascioliasis (also known as fasciolosis). F. hepatica is world-wide distributed and
causes great economic losses in sheep and cattle.

Life Cycle:

In order to complete its life cycle, F. hepatica requires an aquatic snail as an intermediate
host such as Galba truncatula, in which the parasite can reproduce asexually. From the snail,
minute cercariae emerge and swim through pools of water in pasture, and encyst as
metacercariae on near-by vegetation. From here, the metacercariae are ingested by the
ruminant, or in some cases, by humans eating un-cooked foods such as water-cress. Contact
with low pH in the stomach causes the early immature juvenile to begin the process of
excystment. In the duodenum, the parasite breaks free of the metacercariae and burrows
through the intestinal lining into the peritoneal cavity. The newly excysted juvenile does not
feed at this stage, but once it finds the liver parenchyma after a period of days, feeding will
start. This immature stage in the liver tissue is the pathogenic stage, causing anaemia and
clinical signs sometimes observed in infected animals. The parasite browses on liver tissue
for a period of up to 5-6 weeks and eventually finds its way to the bile duct where it matures
into an adult and begins to produce eggs. Up to 25,000 eggs per day per fluke can be
produced, and in a light infection, up to 500,000 eggs per day can be deposited onto pasture
by a single sheep.

6.1.2 Life history of Schistosoma haematobium

Schistosomiasis (also known as bilharzia, bilharziosis or snail fever) is a parasitic disease

caused by several species of fluke of the genus Schistosoma. It is most commonly found in
Asia, Africa, and South America, especially in areas with water that is contaminated with
freshwater snails, which may carry the parasite. The disease affects many people in
developing countries, particularly children who may acquire the disease by swimming or
playing in infected water.[1] Although it has a low mortality rate, schistosomiasis often is a
chronic illness that can damage internal organs and, in children, impair growth and cognitive
development.[1] The urinary form of schistosomiasis is associated with increased risks for
bladder cancer in adults.[1]Schistosomiasis is the second most socioeconomically devastating
disease after malaria.[1]

Schistosomiasis is known as bilharzia or bilharziosis in many countries, after Theodor

Bilharz, who first described the cause of urinary schistosomiasis in 1851. The first doctor
who described the entire disease cycle was Pirajá da Silva in 1908.

Life cycle of Schistosoma haematobium, S. mansoni and S. japonicum

Fig 6.2
Schistosomes have a typical trematode vertebrate-invertebrate lifecycle, with humans being
the definitive host. The life cycles of all five human schistosomes are broadly similar:
parasite eggs are released into the environment from infected individuals, hatching on contact
with fresh water to release the free-swimming miracidium. Miracidia infect fresh-water snails
by penetrating the snail's foot. After infection, close to the site of penetration, the miracidium
transforms into a primary (mother) sporocyst. Germ cells within the primary sporocyst will
then begin dividing to produce secondary (daughter) sporocysts, which migrate to the snail's
hepatopancreas. Once at the hepatopancreas, germ cells within the secondary sporocyst begin
to divide again, this time producing thousands of new parasites, known as cercariae, which
are the larvae capable of infecting mammals.

Cercariae emerge daily from the snail host in a circadian rhythm, dependent on ambient
temperature and light. Young cercariae are highly mobile, alternating between vigorous
upward movement and sinking to maintain their position in the water. Cercarial activity is
particularly stimulated by water turbulence, by shadows and by chemicals found on human
skin. Penetration of the human skin occurs after the cercaria have attached to and explored
the skin. The parasite secretes enzymes that break down the skin's protein to enable
penetration of the cercarial head through the skin. As the cercaria penetrates the skin it
transforms into a migrating schistosomulum stage.

The newly transformed schistosomulum may remain in the skin for 2 days before locating a
post-capillary venule; from here the schistosomulum travels to the lungs where it undergoes
further developmental changes necessary for subsequent migration to the liver. Eight to ten
days after penetration of the skin, the parasite migrates to the liver sinusoids. S. japonicum
migrates more quickly than S. mansoni, and usually reaches the liver within 8 days of
penetration. Juvenile S. mansoni and S. japonicum worms develop an oral sucker after
arriving at the liver, and it is during this period that the parasite begins to feed on red blood
cells. The nearly-mature worms pair, with the longer female worm residing in the
gynaecophoric channel of the shorter male. Adult worms are about 10 mm long. Worm pairs
of S. mansoni and S. japonicum relocate to the mesenteric or rectal veins. S. haematobium
schistosomula ultimately migrate from the liver to the perivesical venous plexus of the
bladder, ureters, and kidneys through the hemorrhoidal plexus.

Parasites reach maturity in six to eight weeks, at which time they begin to produce eggs.
Adult S. mansoni pairs residing in the mesenteric vessels may produce up to 300 eggs per day
during their reproductive lives. S. japonicum may produce up to 3000 eggs per day. Many of
the eggs pass through the walls of the blood vessels, and through the intestinal wall, to be
passed out of the body in faeces. S. haematobium eggs pass through the ureteral or bladder
wall and into the urine. Only mature eggs are capable of crossing into the digestive tract,
possibly through the release of proteolytic enzymes, but also as a function of host immune
response, which fosters local tissue ulceration. Up to half the eggs released by the worm pairs
become trapped in the mesenteric veins, or will be washed back into the liver, where they will
become lodged. Worm pairs can live in the body for an average of four and a half years, but
may persist up to 20 years.

Trapped eggs mature normally, secreting antigens that elicit a vigorous immune response.
The eggs themselves do not damage the body. Rather it is the cellular infiltration resultant
from the immune response that causes the pathology classically associated with
schistosomiasis.

6.2 Economic importance of Schistosoma haematobium

Continue exposure may result in urethral deformation and bladder calcification. And also
it can result into death or loss of productivity of the individual to himself and the society.

Schistosoma haematobium is the cause of schistosomiasis also known as Bilharzia. Hosts of

the parasite are humans. Schistosomiasis affects 200 million people worldwide and is
considered one the most serious pathogenic infections today.

Schistosoma haematobium is pathogenic to humans and causes blood in the and urine and
sometimes in the stool. Persons affected by S. haematobium may also develop cough, fever,
skin inflammation, and tenderness of the liver because the spined eggs attach to vital organs
and cause tissue degeneration. Later stages of the disease may be characterized by the
swelling and damaging of the bladder, liver, and other organs. The eggs of Schistosoma
haematobium can clog the bladder neck and cause infection. Many researchers have also
observed damage on other body structures. Chronic schistosomiasis raises the incidence of
bladder cancer in many Middle Eastern countries.

Drugs are available to cure Schistomiasis although the treatment process is long and
unpleasant. Praziquantel is the leading drug in America In other nations, including Africa,
Trichlorfon is administered. Unfortunately once the bladder wall is infested with eggs and
feeding Schistosomes, prognosis is poor and the chances of surviving are slim.

6.3 Life history of Taenia solium and Taenia saginata

Taenia saginata, also known as Taeniarhynchus saginata or the Beef tapeworm, is a

parasite of both cattle and humans, but which can only reproduce asexually in humans.
Taenia saginata occurs where cattle are raised by infected humans maintaining poor hygine,
human feces is improperly disposed of, meat inspection programs are poor, and where meat is
eaten without proper cooking. The disease is relatively common in Africa, some parts of
Eastern Europe, the Philippines, Mexico, and Latin America.[1]

Taenia saginata are normally 3m to 5m in length, but it can become very large, over 20m in
some situations. It does not have a rostellum or scolex armature. The scolex is composed of 4
powerful suckers. The segments are made up of mature and gravid proglottid. The mature
proglottid contains the uterus (unbranched), ovary, genital pore, tapeworm).

Life Cycle

Fig 6.3.1 Life cycle of Taenia saginata and Taenia solium

Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata or Taenia
solium. Humans are the only definitive hosts for T. saginata and T. solium. Eggs or gravid
proglottids are passed with feces ; the eggs can survive for days to months in the
environment. Cattle (T. saginata) and pigs (T. solium) become infected by ingesting
vegetation contaminated with eggs or gravid proglottids . In the animal's intestine, the
oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where
they develop into cysticerci. A cysticercus can survive for several years in the animal.
Humans become infected by ingesting raw or undercooked infected meat . In the human
intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive
for years. The adult tapeworms attach to the small intestine by their scolex and reside in
the small intestine . Length of adult worms is usually 5 m or less for T. saginata (however
it may reach up to 25 m) and 2 to 7 m for T. solium. The adults produce proglottids which
mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in
the stool (approximately 6 per day). T. saginata adults usually have 1,000 to 2,000
proglottids, while T. solium adults have an average of 1,000 proglottids. The eggs contained
in the gravid proglottids are released after the proglottids are passed with the feces. T.
saginata may produce up to 100,000 and T. solium may produce 50,000 eggs per proglottid
respectively.

6.3.1 Economic importance of Taenia saginata And Taenia solium .

Taenia saginata and Taenia solium are the two taeniids of greatest economic and
medical importance, causing bovine and porcine cysticercosis and taeniasis in
humans. In addition, T. solium eggs can infect humans, often giving rise to fatal
neurocysticercosis. Infections with these cestodes are therefore a serious public health
problem in areas of endemicity. In addition, an increase in the number of cases in
areas of nonendemicity has been observed in recent years.
 WEEK 7 : MODE OF TRANSMISSION OF TREMATODE AND
CESTODE

7.1 Fasciola hepatica

This can be transmitted through faecally contaminated vegetables, food and water
7.2 Schistosoma haematobium

This can be transmitted through faecally contaminated vegetables, food and water

7.3 Taenia solium and Taenia saginata

This can be transmitted by eating improperly cooked meat, fish, or vegetable.

7.4 Prevention and control of trematode and cestode

7.4.1 Prevention\control of Fasciola hepatica

 Prevention includes; use of toilet facilities; safe excreta disposal;

protection of food from dirt and soil; thorough washing of produce; and hand
washing.
 Food dropped on the floor should never be eaten without washing or
cooking, particularly in endemic areas. Vegetables originating from third-world
countries should always be washed thoroughly before consumption
 Treatment with drug of choice such as triclabendazole, a member of the
benzimidazole family of anthelmintics. The drug works by preventing the
polymerization of the molecule tubulin into the cytoskeletal structures,
microtubules. However, resistance of F. hepatica to triclabendazole has already
been recorded in Australia[1] and Ireland.[2] Artemether has been shown to be
effective in a rat model of fascioliasis

7.4.2 Prevention and control of Schistosoma haematobium

Prevention is best accomplished by eliminating the water-dwelling snails which are the
natural reservoir of the disease. Acrolein, copper sulfate, and niclosamide can be used for this
purpose. Recent studies have suggested that snail populations can be controlled by the
introduction or augmentation of existing crayfish populations; as with all ecological
interventions, however, this technique must be approached with caution.

Individuals can guard against schistosomiasis infection by avoiding bodies of water known or
likely to harbor the carrier snails.

Schistosomiasis is readily treated using a single oral dose of the drug praziquantel annually.[2]
As with other major parasitic diseases, there is ongoing and extensive research into
developing a vaccine that will prevent the parasite from completing its life cycle in humans.
7.4.3 Prevention\control of Taenia solium and Taenia saginata

The best way to prevent infection with tapeworms is to eliminate the exposure of livestock
to the tapeworm eggs by properly disposing of human feces. The next best strategy is to
thoroughly cook or freeze all meat and fish before it is eaten to prevent consumption of live
tapeworm larvae in infected samples. Larval cysts in pork and beef are killed by moderate
temperatures of 150°F (65°C) or if frozen for at least 12 hours. Proper cooking of
freshwater fish could also eliminate the possibility of human infection with the fish
tapeworm. Freezing fresh fish for 24 hours will also kill the larval form.

People who raise sheep or horses should have these animals checked regularly by a
veterinarian and dewormed if necessary.

The Centers for Disease Control and Prevention (CDC) recommends that people traveling
abroad should wash their hands with soap and water before handling food; should wash and
peel all raw vegetables and fruits before eating; and should drink only bottled or boiled water,
or carbonated drinks in cans or bottles.
 WEEK 8 : DISEASED CAUSED BY NEMATODE

8.1 Life history and economic importance of nematode

8.1.1 Life history and economic importance of Ascaris lumbricoides

Ascariasis is a human disease caused by the parasitic roundworm Ascaris lumbricoides.

Perhaps as many as one quarter of the world's people are infected, and ascariasis is
particularly prevalent in tropical regions and in areas of poor hygiene. Other species of the
genus Ascaris are parasitic and can cause disease in domestic animals.

Infection occurs through ingestion of food contaminated with feces containing Ascaris eggs.
The larvae hatch, burrow through the intestine, reach the lungs, and finally migrate up the
respiratory tract. From there they are then reswallowed and mature in the intestine, growing
up to 30 cm (12 in.) in length and anchoring themselves to the intestinal wall.

Infections are usually asymptomatic, especially if the number of worms is small. They may
however be accompanied by inflammation, fever, and diarrhea, and serious problems may
develop if the worms migrate to other parts of the body. Prevalence

Roughly 1.5 billion individuals are infected with this worm, primarily in Africa and Asia.
Ascariasis is endemic in the United States including Gulf Coast; in Nigeria and in Southeast
Asia. One study indicated that the prevalence of ascariasis in the United States at about 4
million (2%) [8]. In a survey of a rural Nova Scotia community, 28.1% of 431 individuals
tested were positive for Ascaris, all of them being under age 20, while all 276 tested in
metropolitan Halifax were negative[3]. Deposition of ova (eggs) in sewage hints at the degree
of ascariasis incidence. A 1978 study showed about 75% of all sewage sludge samples
sampled in United States urban catchments contained Ascaris ova, with rates as high as 5 to
100 eggs per litre. In Frankfort, Indiana, 87.5% of the sludge samples were positive with
Ascaris, Toxocara, Trichuris, and hookworm. In Macon, Georgia, one of the 13 soil samples
tested positive for Ascaris .Municipal wastewater in Riyadh, Saudi Arabia detected over 100
eggs per litre of wastewater [4] and in Czechoslovakia was as high as 240-1050 eggs per litre
[5]
.

Ascariasis can often be measured by examining food for ova. In one field study in
Marrakech, Morocco, where raw sewage is used to fertilize crop fields, Ascaris eggs were
detected at the rate of 0.18 eggs/kg in potatoes, 0.27 eggs/kg in turnip, 4.63 eggs/kg in mint,
0.7 eggs/kg in carrots, and 1.64 eggs/kg in radish[6]. A similar study in the same area showed
that 73% of children working on these farms were infected with helminths, particularly
Ascaris, probably as a result of exposure to the raw sewage.
 Life cycle

Adult worms (1) live in the lumen of the small intestine. A female may produce
approximately 200,000 eggs per day, which are passed with the feces (2). Unfertilized eggs
may be ingested but are not infective. Fertile eggs embryonate and become infective after 18
days to several weeks (3), depending on the environmental conditions (optimum: moist,
warm, shaded soil). After infective eggs are swallowed (4), the larvae hatch (5), invade the
intestinal mucosa, and are carried via the portal, then systemic circulation and/or lymphatics
to the lungs . The larvae mature further in the lungs (6) (10 to 14 days), penetrate the alveolar
walls, ascend the bronchial tree to the throat, and are swallowed (7). Upon reaching the small
intestine, they develop into adult worms (8). Between 2 and 3 months are required from
ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2
years.
First appearance of eggs in stools is 60-70 days. In larval ascariasis, symptoms occur 4-16
days after infection. The final symptoms are gastrointestinal discomfort, colic and vomiting,
fever; observation of live worms in stools. Some patients may have pulmonary symptoms or
neurological disorders during migration of the larvae. However there are generally few or no
symptoms. A bolus of worms may obstruct the intestine; migrating larvae may cause
pneumonitis and eosinophilia.

Adult worms (1) live in the lumen of the small intestine. A female may produce
approximately 200,000 eggs per day, which are passed with the feces (2). Unfertilized eggs
may be ingested but are not infective. Fertile eggs embryonate and become infective after 18
days to several weeks (3), depending on the environmental conditions (optimum: moist,
warm, shaded soil). After infective eggs are swallowed (4), the larvae hatch (5), invade the
intestinal mucosa, and are carried via the portal, then systemic circulation and/or lymphatics
to the lungs . The larvae mature further in the lungs (6) (10 to 14 days), penetrate the alveolar
walls, ascend the bronchial tree to the throat, and are swallowed (7). Upon reaching the small
intestine, they develop into adult worms (8). Between 2 and 3 months are required from
ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2
years.

First appearance of eggs in stools is 60-70 days. In larval ascariasis, symptoms occur 4-16
days after infection. The final symptoms are gastrointestinal discomfort, colic and vomiting,
fever; observation of live worms in stools. Some patients may have pulmonary symptoms or
neurological disorders during migration of the larvae. However there are generally few or no
symptoms. A bolus of worms may obstruct the intestine; migrating larvae may cause
pneumonitis and eosinophilia.

Symptoms

Patients can remain asymptomatic for very long periods of time. As larval stages travel
through the body, they may cause visceral damage, peritonitis and inflammation, enlargement
of the liver or spleen, toxicity, and pneumonia. A heavy worm infestation may cause
nutritional deficiency; other complications, sometimes fatal, include obstruction of the bowel
by a bolus of worms (observed particularly in children) and obstruction of the bile or
pancreatic duct. More than 796 Ascaris lumbricoides worms weighing 550 g [19 ounces]
were recovered at autopsy from a 2-year-old South African girl. The worms had caused
torsion and gangrene of the ileum, which was interpreted as the cause of death.[9]

Ascaris takes most of its nutrients from the partially digested host food in the intestine. There
is limited evidence that it can also pierce the intestinal mucous membrane and feed on blood,
but this is not its usual source of nutrition.[10] As a result, Ascaris infection does not produce
the anemia associated with some other roundworm infections.
8.1.2 Life history and economic importance of Hookworm

The hookworm is a parasitic nematode worm that lives in the small intestine of its host,
which may be a mammal such as a dog, cat, or human. Two species of hookworms
commonly infect humans, Ancylostoma duodenale and Necator americanus. Necator
americanus predominates in the Americas, Sub-Saharan Africa, Southeast Asia, China, and
Indonesia, while A. duodenale predominates in the Middle East, North Africa, India and
(formerly) in southern Europe. Hookworms are thought to infect 800 million people
worldwide. The A. braziliense and A. tubaeforme species infect cats, while A. caninum infects
dogs. Uncinaria stenocephala infects both dogs and cats.

Hookworms are much smaller than the large roundworm, Ascaris lumbricoides, and the
complications of tissue migration and mechanical obstruction so frequently observed with
roundworm infestation are less frequent in hookworm infestation. The most significant risk of
hookworm infection is anemia, secondary to loss of iron (and protein) in the gut. The worms
suck blood voraciously and damage the mucosa. However, the blood loss in the stools is
occult blood loss (not visibly apparent).

Ankylostomiasis, alternatively spelled anchylostomiasis and also called helminthiasis,

"miners' anaemia", "tunnel disease", "brickmaker's anaemia" and "Egyptian chlorosis",
is the disease caused by hookworms. It is caused when hookworms, present in large numbers,
produce an iron deficiency anemia by voraciously sucking blood from the host's intestinal
walls. The name is derived from Greek ancylo "crooked, bent" and stoma "mouth."

Hookworm is a leading cause of maternal and child morbidity in the developing countries of
the tropics and subtropics. In susceptible children hookworms cause intellectual, cognitive
and growth retardation, intrauterine growth retardation, prematurity, and low birth weight
among newborns born to infected mothers. Hookworm infection is rarely fatal, but anemia
can be significant in the heavily infected individual

Pathology

Most individuals with hookworm infection have no symptoms. Generally, very high loads of
the parasite coupled with poor nutrition (inadequate intake of protein and iron) eventually
lead to anemia.

The disease was linked to nematode worms (Ankylostoma duodenalis) from one-third to half
an inch long in the intestine chiefly through the labours of Theodor Bilharz and Griesinger in
Egypt (1854).
The symptoms can be linked to inflammation in the gut stimulated by feeding hookworms,
such as nausea, abdominal pain and intermittent diarrhea, and to progressive anemia in
prolonged disease: capricious appetite, pica (or dirt-eating), obstinate constipation followed
by diarrhea, palpitations, thready pulse, coldness of the skin, pallor of the mucous
membranes, fatigue and weakness, shortness of breath and in cases running a fatal course,
dysentery, hemorrhages and edema.

Blood tests in early infection often show a rise in numbers of eosinophils, a type of white
blood cell that is preferentially stimulated by worm infections in tissues (large numbers of
eosinophils are also present in the local inflammatory response). Falling blood hemoglobin
levels will be seen in cases of prolonged infection with anemia.

In contrast to most intestinal helminthiases, where the heaviest parasitic loads tend to occur in
children, hookworm prevalence and intensity can be higher among adult males. The
explanation for this is that hookworm infection tends to be occupational, so that plantation
workers, coalminers and other groups maintain a high prevalence of infection among
themselves by contaminating their work environment. However, in most endemic areas, adult
women are the most severely affected by anemia, mainly because they have much higher
physiological needs for iron (menstruation, repeated pregnancy), but also because
customarily they have access to much poorer food than the men.

An interesting consequence of this in the case of Ancylostoma duodenale infection is

translactational transmission of infection: the skin-invasive larvae of this species do not all
immediately pass through the lungs and on into the gut, but spread around the body via the
circulation, to become dormant inside muscle fibers. In a pregnant woman, after childbirth
some or all of these larvae are stimulated to re-enter the circulation (presumably by sudden
hormonal changes), then to pass into the mammary glands, so that the newborn baby can
receive a large dose of infective larvae through its mother's milk. This accounts for otherwise
inexplicable cases of very heavy, even fatal, hookworm infections in children a month or so
of age, in places such as China, India and northern Australia. (An identical phenomenon is
much more commonly seen with Ancylostoma caninum infections in dogs, where the
newborn pups can even die of hemorrhaging from their intestines caused by massive numbers
of feeding hookworms. This also reflects the close evolutionary link between the human and
canine parasites, which probably have a common ancestor dating back to when humans and
dogs first started living closely together.)

Hookworm therapy to treat a number of these diseases is currently in the trial stage at the
University.[6] Some people, including Dr. David Pritchard of the University of Nottingham,
and Jasper Lawrence of Autoimmune Therapies, have independently infected themselves
with hookworms and reported positive results.[7]
 Life cycle

See the image for the biological life cycle of the hookworms where it thrives in warm earth
where temperatures are over 18°C. They exist primarily in sandy or loamy soil and cannot
live in clay or muck. Rainfall averages must be more than 1000 mm (40 inches) a year. Only
if these conditions exist can the eggs hatch. Infective larvae of Necator americanus can
survive at higher temperatures, whereas those of Ancylostoma duodenale are better adapted to
cooler climates. Generally, they live for only a few weeks at most under natural conditions,
and die almost immediately on exposure to direct sunlight or desiccation.

Infection of the host is by the larvae, not the eggs. While A. duodenale can be ingested, the
usual method of infection is through the skin; this is commonly caused by walking barefoot
through areas contaminated with fecal matter. The larvae are able to penetrate the skin of the
foot, and once inside the body, they migrate through the vascular system to the lungs, and
from there up the trachea, and are swallowed. They then pass down the esophagus and enter
the digestive system, finishing their journey in the intestine, where the larvae mature into
adult worms.

Once in the host gut, Necator tends to cause a prolonged infection, generally 1–5 years (many
die within a year or two of infecting), though some adult worms have been recorded to live
for 15 years or more. On the other hand, Ancylostoma adults are short lived, surviving on
average for only about 6 months. However, infection can be prolonged because dormant
larvae can be "recruited" sequentially from tissue "stores" (see Pathology, above) over many
years, to replace expired adult worms. This can give rise to seasonal fluctuations in infection
prevalence and intensity (apart from normal seasonal variations in transmission).

They mate inside the host, females laying up to 30,000 eggs per day and some 18 to 54
million eggs during their lifetime, which pass out in feces. Because it takes 5–7 weeks for
adult worms to mature, mate and produce eggs, in the early stages of very heavy infection,
acute symptoms might occur without any eggs being detected in the patient's feces. This can
make diagnosis very difficult.
Symptoms

There are no specific symptoms or signs of hookworm infection. As mentioned above, they
arise from a combination of intestinal inflammation and progressive iron/protein-deficiency
anemia. Larval invasion of the skin might give rise to intense, local itching, usually on the
foot or lower leg, which can be followed by lesions that look like insect bites, can blister
("ground itch"), and last for a week or more. Animal hookworm larvae on penetrating
humans may produce a creeping eruption called cutaneous larva migrans. The larvae migrate
in tortous tunnels in between stratum germinativum and stratum corneum of the skin, causing
serpigenous vesicular lesions. With advancing movement of the larvae, the rear protions of
the lesions become dry and crusty. The lesions are typically intensely pruritic. Coughing,
chest pain, wheezing, and fever will sometimes be experienced by people who have been
exposed to very large numbers of larvae. Epigastric pains, indigestion, nausea vomiting,
constipation, and diarrhea can occur early or in later stages as well, although gastrointestional
symptoms tend to improve with time. Signs of advanced severe infection are those of anemia
and protein deficiency, including emaciation, cardiac failure and abdominal distension with
ascites.

Diagnosis

Hookworm egg

Diagnosis depends on finding characteristic worm eggs on microscopic examination of the

stools, although this is not possible in early infection. The eggs are oval or elliptical,
measuring 60µm by 40µm, colourless , not bile stained and with a thin transparent hyaline
shell membrane. When released by the worm in the intestine, the egg contains an
unsegmented ovum. During its passage down the intestine, the ovum develops and thus the
eggs passed in feces have a segmented ovum, usually with 4 to 8 blastomeres. As the eggs of
both Ancylostoma and Necator (and most other hookworm species) are indistinguishable, to
identify the genus, they must be cultured in the lab to allow larvae to hatch out. If the fecal

sample is left for a day or more under tropical conditions, the larvae will have hatched out, so
eggs might no longer be evident. In such a case, it is essential to distinguish hookworms from
Strongyloides larvae, as infection with the latter has more serious implications and requires
different management. The larvae of the two hookworm species can also be distinguished
microscopically, although this would not be done routinely, but usually for research purposes.
Adult worms are rarely seen (except via endoscopy, surgery or autopsy), but if found, would
allow definitive identification of the species.
Treatment

The hookworm can be treated with local cryotherapy when it is still in the skin.

Albendazole is effective both in the intestinal stage and during the stage the parasite is still
migrating under the skin.

In case of anemia, iron supplementation can cause relief symptoms of iron deficiency anemia.
However, as red blood cell levels are restored, shortage of other essentials such as folic acid
or vitamin B12 may develop, so this might also be supplemented.

8.1.3 Life history and economic importance of Wuchereria bancrofti

Wuchereria bancrofti is a parasitic filarial nematode worm spread by a mosquito vector. It is

one of the three parasites that cause lymphatic filariasis. Named for Otto Wucherer and
Joseph Bancroft, it affects over 120 million people, primarily in Africa, South America, and
other tropical and sub-tropical countries. Elephantiasis can result if the infection is left
untreated. Limited treatment modalities exist and no vaccines have been developed.

W. bancrofti carry out their life cycle in two hosts. Human beings serve as the definitive host
and mosquitoes as their intermediate hosts. The adult parasites reside in the lymphatics. They
are viviparous. The first stage larvae are known as microfilariae. The microfilaria are present
in the circulation. The microfilaria migrate between the deep and the peripheral circulation.
During the day they are present in the deep veins and during the night the migrate to the
peripheral circulation. Next, the worm is transferred into a vector; the most common vectors
are the mosquito species: Culex, Anopheles, Mansonia, and Aedes. Inside their second host, it
matures into motile larvae. When its current host feeds, and it is egested into the blood stream
of its new human host. The larvae moves to the lymph nodes, predominantly in the legs and
genital area, and develops into adult worm over the course of a year. By this time, an adult
female can produce microfilariae itself.
 Life Cycle of Wuchereria bancrofti:

Different species of the following genera of mosquitoes are vectors of W. bancrofti filariasis
depending on geographical distribution. Among them are: Culex (C. annulirostris, C.
bitaeniorhynchus, C. quinquefasciatus, and C. pipiens); Anopheles (A. arabinensis, A.
bancroftii, A. farauti, A. funestus, A. gambiae, A. koliensis, A. melas, A. merus, A. punctulatus
and A. wellcomei); Aedes (A. aegypti, A. aquasalis, A. bellator, A. cooki, A. darlingi, A. kochi,
A. polynesiensis, A. pseudoscutellaris, A. rotumae, A. scapularis, and A. vigilax); Mansonia
(M. pseudotitillans, M. uniformis); Coquillettidia (C. juxtamansonia). During a blood meal,
an infected mosquito introduces third-stage filarial larvae onto the skin of the human host,
where they penetrate into the bite wound . They develop in adults that commonly reside in
the lymphatics . The female worms measure 80 to 100 mm in length and 0.24 to 0.30 mm
in diameter, while the males measure about 40 mm by .1 mm. Adults produce microfilariae
measuring 244 to 296 μm by 7.5 to 10 μm, which are sheathed and have nocturnal
periodicity, except the South Pacific microfilariae which have the absence of marked
periodicity. The microfilariae migrate into lymph and blood channels moving actively
through lymph and blood . A mosquito ingests the microfilariae during a blood meal .
After ingestion, the microfilariae lose their sheaths and some of them work their way through

the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the
thoracic muscles . There the microfilariae develop into first-stage larvae and
subsequently into third-stage infective larvae . The third-stage infective larvae migrate
through the hemocoel to the mosquito's prosbocis and can infect another human when the
mosquito takes a blood meal .

8.1.4 Life history and economic importance of Onchocerca volvulus

Onchocerciasis (pronounced /ˈɒnkoʊsɝːˈsaɪəsɨs/ or /ˈɒnkoʊsɝːˈkaɪəsɨs/),[1] also known as

river blindness, is the world's second leading infectious cause of blindness. It is caused by
Onchocerca volvulus, a nematode that can live for up to fifteen years in the human body.[2] It
is transmitted to people through the bite of a black fly. The worms spread throughout the
body, and when they die, they cause intense itching and a strong immune system response
that can destroy nearby tissue, such as the eye.[3]

The primary treatment is a drug, ivermectin. For best effect, entire communities are treated at
the same time. A single dose may kill first-stage larvae (microfilariae) in infected people and
prevent transmission for many months in the remaining population.[4]

About 18 million people are currently infected with this parasite; approximately 300,000
have been irreversibly blinded by it.[5]

Life cycle

The life cycle of O. volvulus begins when a parasitised female black fly of the genus
Simulium takes a blood meal. The microfilariae form of the parasite found in the dermis of
the host is ingested by the black fly. Here the microfilariae then penetrates the gut and
migrates to thoracic flight muscles of the black fly, entering its first larval phase (J1.). After
maturing into J2, the second larval phase, it migrates to the proboscis where it can be found in
the saliva. Saliva containing stage three (J3S.) O. volvulus larvae passes into the blood of the
host. From here the larvae migrate to the subcutaneous tissue where they form nodules and
then mature into adult worms over a period of six to twelve months. After maturation, the
smaller adult males migrate from nodules to subcutaneous tissue where they mate with the
larger adult females, which then produce between 1,000 and 3,000 microfilariae per day. The
normal adult worm lifespan is up to fifteen years. The eggs mature internally to form stage
one microfilariae, which are released from the female's body one at a time and remain in the
subcutaneous tissue.

These stage one microfilariae are taken up by black flies upon a blood meal, in which they
mature over the course of one to three weeks to stage three larvae, thereby completing the life
cycle. Humans are the only definitive host for O. volvulus. The normal microfilariae lifespan
is 1-2 years.

8.1.5 Life history and economic importance of Dracunculus medinensis

Dracunculiasis, more commonly known as Guinea worm disease (GWD) or Medina

Worm, is a parasitic infection caused by the nematode, Dracunculus medinensis. The name,
dracunculiasis, is derived from the Latin "affliction with little dragons."[1] The common name
"Guinea worm" appeared after Europeans first saw the disease on the Guinea coast of West
Africa in the 17th century.[2] The painful, burning sensation experienced by the infected
patient has led to the disease being called ―the fiery serpent.‖ Once prevalent in 20 nations in
Asia and Africa, the disease remains endemic in only five countries in Sub-Saharan Africa. It
is hoped that Guinea worm disease will be the first parasitic disease to be eradicated and the
first disease in history eradicated through behavior change, without the use of vaccines or a
cure.[3] Guinea worm disease is only contracted when a person drinks stagnant water
contaminated with the larvae of the Guinea worm. There is no animal or environmental
reservoir of D.medinensis. The infection must pass through humans each year.[3]

Life cycle

The life cycle of Dracunculus medinensis.

Guinea worm disease thrives in some of the world’s poorest areas, particularly those with
limited or no access to clean water.[4] In these areas stagnant water sources may host
microscopic, fresh-water arthropods known as copepods ("water fleas"), which carry the
larvae of the Guinea worm.

The larvae develop for approximately two weeks inside the copepods.[2] At this stage the
larvae can cause Guinea worm disease if the infected copepods are not filtered from drinking
water.[2] The male Guinea worm is typically much smaller (1.2–2.9 centimeters, 0.5-1.1
inches long) than the female, which, as an adult, can grow to between 2 and 3 feet (0.91 m)
long and be as thick as a spaghetti noodle.[2][4]

Once inside the body stomach acid digests the water flea, but not the Guinea worm larvae
sheltered inside.[2] These larvae find their way to the body cavity where the female mates
with a male Guinea worm.[2] This takes place approximately 3 months after infection.[2] The
male worm dies after mating and is absorbed.[2]

The female, which now contains larvae, burrows into the deeper connective tissues or
adjacent to long bones or joints of the extremities.[2]

Approximately one year after the infection began the worm attempts to leave the body by
creating a blister in the human host’s skin—usually on a person’s lower extremities like a leg
or foot.[5]

This blister causes a very painful burning sensation as the worm emerges. Within 72 hours
the blister ruptures, exposing one end of the emergent worm.

Infected persons often immerse the affected limb in water to relieve this burning sensation.
Once the blister or open sore is submerged in water the adult female releases hundreds of
thousands of Guinea worm larvae, contaminating the water supply.

During the next several days the female worm is capable of releasing more larvae whenever it
comes in contact with water. These larvae contaminate the water supply and are eaten by
copepods, thereby repeating the life-cycle of the disease. Infected copepods can only live in
the water for 2 to 3 weeks if they are not ingested by a person. Infection does not create
immunity, so people can repeatedly experience Guinea worm disease throughout their lives.[4]

In drier areas just below the Sahara desert cases of the disease often emerge during the rainy
seasons, which for many agricultural communities is also the planting or harvesting season.
Elsewhere the emerging worms are more prevalent during the dry season, when scarce
surface water is most polluted. Guinea worm disease outbreaks can cause serious disruption
to local food supplies and school attendance (see Social and economic impact section).[4]

8.2 Economic Importance of Dracunculus medinensis

The pain caused by the worm’s emergence—which typically occurs during planting and
harvesting seasons—prevents many people from working or attending school for as long as 3
months. In heavily burdened agricultural villages fewer people are able to tend their fields or
livestock, resulting in food shortages and lower earnings.[13][3] A study in southeastern
Nigeria, for example, found that rice farmers in a small area lost US$20 million in just one
year due to outbreaks of Guinea worm disease.[3]

8.1.6 Life history of Loa loa:

The vector for Loa loa filariasis are flies from two species of the genus Chrysops, C. silacea
and C. dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies)
introduces third-stage filarial larvae onto the skin of the human host, where they penetrate
into the bite wound . The larvae develop into adults that commonly reside in subcutaneous
tissue . The female worms measure 40 to 70 mm in length and 0.5 mm in diameter, while
the males measure 30 to 34 mm in length and 0.35 to 0.43 mm in diameter. Adults produce
microfilariae measuring 250 to 300 μm by 6 to 8 μm, which are sheathed and have diurnal
periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During
the day they are found in peripheral blood, but during the noncirculation phase, they are
found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion,
the microfilariae lose their sheaths and migrate from the fly's midgut through the hemocoel to
the thoracic muscles of the arthropod . There the microfilariae develop into first-stage
larvae and subsequently into third-stage infective larvae . The third-stage infective
larvae migrate to the fly's proboscis and can infect another human when the fly takes a
blood meal .
WEEK 9 MODE OF TRANSMISSION AND AGENT OF NEMATODE

9.1 Mode of transmission and agent of Ascaris lumbricoies

transmission is from soil and vegetation on which fecal matter containing eggs has been
deposited. Ingestion of infective eggs from soil contaminated with human feces or
transmission and contaminated vegetables and water is the primary route of infection.
Intimate contact with pets which have been in contact with contaminated soil may result in
infection, while pets which are infested themselves by a different type of roundworm can
cause infection with that type of worm (Toxocara canis, etc) as occasionally occurs with
groomers.Transmission also comes through municipal recycling of wastewater into crop
fields. This is quite common in emerging industrial economies, and poses serious risks for not
only local crop sales but also exports of contaminated vegetables.

9.2 Mode of transmission and agent of Hookworm

The infective larvae of the parasite enter the human body through the skin, reach the blood
stream, and then migrate to the site where they can mature and reproduce.

9.3 Mode of transmission and agent of Wuchereria bancrofti

an infected mosquito introduces third-stage filarial larvae onto the skin of the human host,
where they penetrate into the bite wound. They develop in adults that commonly reside in
the lymphatics.

9.4 Mode of transmission and agent of Onchocerca volvolus

when a parasitised female black fly of the genus Simulium takes a blood meal. The
microfilariae form of the parasite found in the dermis of the host is ingested by the black fly.
Here the microfilariae then penetrates the gut and migrates to thoracic flight muscles of the
black fly.

9.5 Mode of transmission and agent of Loa loa

During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage
filarial larvae onto the skin of the hum an host, where they penetrate into the bite wound.

9.6 Mode of transmission and agent of Dracunculus medinensis.

Guinea worm disease is only contracted when a person drinks stagnant water contaminated
with the larvae of the Guinea worm.
9.7 Method of control of nematode

9.7.1 Method of control of Ascaris lumbricoides

 Mebendazole (Vermox) (C16H13N3O2). Causes slow immobilization and death of the

worms by selectively and irreversibly blocking uptake of glucose and other nutrients
in susceptible adult intestine where helminths dwell. Oral dosage is 100 mg 12 hourly
for 3 days.
 Piperazine (C4H10N2.C6H10O4). A flaccid paralyzing agent that causes a blocking
response of ascaris muscle to acetylcholine. The narcotizing effect immobilizes the
worm, which prevents migration when treatment is accomplished with weak drugs
such as thiabendazole. If used by itself it causes the worm to be passed out in the
feces. Dosage is 75 mg/kg (max 3.5 g) as a single oral dose.
 Pyrantel pamoate (Antiminth, Pin-Rid, Pin-X) (C11H14N2S.C23H16O6) Depolarizes
ganglionic block of nicotinic neuromuscular transmission, resulting in spastic
paralysis of the worm. Spastic (tetanic) paralyzing agents, in particular pyrantel
pamoate, may induce complete intestinal obstruction in a heavy worm load. Dosage is
11 mg/kg not to exceed 1 g as a single dose.
 Albendazole (C12H15N3O2S) A broad-spectrum antihelminthic agent that decreases
ATP production in the worm, causing energy depletion, immobilization, and finally
death. Dosage is 400 mg given as single oral dose (contraindicated during pregnancy
and children under 2 years).
 Thiabendazole. This may cause migration of the worm into the esophagus, so it is
usually combined with piperazine.

9.7.2 Method of control of Hookworm

The infective larvae develop and survive in an environment of damp dirt, particularly sandy
and loamy soil. They cannot survive in clay or muck. The main lines of precaution are those
dictated by sanitary science:

 Do not defecate outside latrines, toilets etc.

 Do not use human excrement or raw sewage as manure/fertilizer in agriculture
 Deworm pet dogs — canine and feline hookworms rarely develop to adulthood in
humans (Ancylostoma caninum, the common dog hookworm, occasionally develops
into an adult to cause eosinophilic enteritis in people), but their invasive larvae can
cause an itchy rash called cutaneous larva migrans.

Moxidectin has been released in the United States as part of Advantage Multi (imidacloprid +
moxidectin) Topical Solution for dogs and cats. It utilizes moxidectin for control and
prevention of roundworms, hookworms, heartworms, and whipworms.

In the late 1800s and early 1900s, many Mississippians were plagued by hookworms. They
did not have indoor plumbing or proper sanitation facilities. As a result, hookworms, spread
by fecal contamination of the environment, were very prevalent (as well as other diseases
caused by lack of sanitation).
9.7.3 Method of control of Wuchereria bancrofti

The parasite's severe symptoms can be avoided by cleansing the skin, surgery, or the use of
therapeutic drugs, such as Diethylcarbamazine(DEC), ivermectin, or albendazole. The drug
of choice however, is DEC, which can eliminate the microfilariae from the blood and also kill
the adult worms with a dosage of 6 mg/kg semiannually or annually. A treatment that
includes ivermectin with DEC or albendazole is more effective than each drug alone.
Protection is similar to that of other mosquito spread illnesses; one can use barriers both
physical (a mosquito net), chemical (insect repellent), or mass chemotherapy′ as a method to
control the spreading of the disease.

9.7.4 Method of control of Onchocerca volvulus

The treatment for onchocerciasis is ivermectin (Mectizan); infected people can be treated
once every twelve months. The drug paralyses the microfilariae and prevents them from
causing itching. In addition, while the drug does not kill the adult worm, it does prevent them
from producing additional offspring. The drug therefore prevents both morbidity and
transmission. Additionally, Doxycycline can be added to the treatment regimen to kill the
endosymbiotic bacteria, Wolbachia. This adjunct therapy has been shown to significantly
lower microfilarial loads in the host and may have activity against the adult worms choice
however, is DEC, which can eliminate the microfilariae from the blood and also kill the adult
worms with a dosage of 6 mg/kg semiannually or annually. A treatment that includes
ivermectin with DEC or albendazole is more effective than each drug alone. Protection is
similar to that of other mosquito spread illnesses; one can use barriers both physical (a
mosquito net), chemical (insect repellent), or mass chemotherapy′ as a method to control the
spreading of the disease.

9.7.5 Method of control of Dracunculus medinensis

Guinea worm disease can only be transmitted from drinking contaminated water. Educating
people to follow simple control measures can completely prevent illness and eliminate
transmission of the disease, leading to the disease’s eradication:

 Drink only water from underground sources free from contamination, such as a
borehole or hand-dug wells.
 Prevent persons with an emerging Guinea worm from entering ponds and wells used
for drinking water.
 Always filter drinking water, using a fine-mesh cloth filter like nylon, to remove the
Guinea worm-containing water fleas.
 Water sources can be treated with an approved larvicide that kills water fleas, such as
Abate, without posing a great risk to humans or other wildlife.[6]
 Communities can be provided with new safe sources of drinking water or have
dysfunctional ones repaired.

The ancient symbol of medicine, the staff of Asklepios, is believed to also represent the
treatment of Guinea worm still used today.
There is no vaccine or medicine to treat or prevent Guinea worm disease. Once a Guinea
worm emerges a person must wrap the live worm around a piece of gauze or a stick to extract
it from the body. This long, painful process that can take up to a month.[3] This is the same
treatment that is noted in the famous ancient Egyptian medical text, the Ebers papyrus from
1550 B.C..[2] Some people have said that extracting a Guinea worm feels like they are being
stabbed or that the afflicted area is on fire.[7][8]Although Guinea worm disease is usually not
fatal, the wound where the worm emerges could develop a secondary bacterial infection such
as tetanus, which may be life-threatening—a concern in endemic areas where there is
typically limited or no access to health care.[9] Analgesics can be used to help reduce swelling
and pain and antibiotic ointments can help prevent secondary infections at the wound site.[4]

9.7.6 Method of control of Loa loa

infected people can be treated once every twelve months. The drug paralyses the
microfilariae and prevents them from causing itching. In addition, while the drug does not kill
the adult worm, it does prevent them from producing additional offspring. The drug therefore

prevents both morbidity and transmission. Additionally, Doxycycline can be

added to the treatment regimen to kill the endosymbiotic bacteria, Wolbachia. This adjunct
therapy has been shown to significantly lower microfilarial loads in the host and may have
activity against the adult worms choice however, is DEC, which can eliminate the
microfilariae from the blood and also kill the adult worms with a dosage of 6 mg/kg
semiannually or annually. A treatment that includes ivermectin with DEC or albendazole is
more effective than each drug alone.
WEEK 10: NATURE OF PLANT DISEASES THEIR TRANSMISSION
AND CONTROL

10.1 Scope of plant diseases

Plant Pathology is defined as the study of the organisms and environmental conditions that
cause disease in plants, the mechanisms by which this occurs, the interactions between these
causal agents and the plant (effects on plant growth, yield and quality), and the methods of
managing or controlling plant disease. It also interfaces knowledge from other scientific
fields such as mycology, microbiology, virology, biochemistry, bio-informatics, etc.Plant
pathology (also called phytopathology) is the scientific study of plant diseases caused by
pathogens (infectious diseases) and environmental conditions (physiological factors).
Organisms that cause infectious disease include fungi, oomycetes, bacteria, viruses, viroids,
virus-like organisms, phytoplasmas, protozoa, nematodes and parasitic plants. Not included
are insects, mites, vertebrate or other pests that affect plant health by consumption of plant
tissues. Plant pathology also involves the study of the identification, etiology, disease cycle,
economic impact, epidemiology, how plant diseases affect humans and animals, pathosystem
genetics and management of plant diseases.

10.2 Terminology in plant pathology

10.2.1 Pathogen is a biological agent that causes disease or illness to its host.[1] The term
pathogen is derived from the Greek "that which produces suffering." There are several
substrates and pathways whereby pathogens can invade a host; the principal pathways have
different episodic time frames, but soil contamination has the longest or most persistent
potential for harboring a pathogen.

10.2.2 Parasite lives in a close relationship with another organism, its host, and causes it
harm. The parasite is dependent on its host for its life functions. For example, viruses are
common parasites. The parasite has to be in its host to live, grow, and multiply. Parasites
rarely kill their hosts. A common, well-known type of a parasite is a hookworm. It is
possible for humans or their pets to get them. Hookworms attach themselves in the lining of
the small intestine, and cause diseases, and malnutrition as well, as they eat the nutrients and
keep them from going to the host.
 Here, we'll be talking about a different type of parasite, called a parasitoid. The parasitoid
Encarsia pergandiella is a tiny wasp that lays its eggs in developing whiteflies. The wasp
larva eventually kills the whitefly, and then emerges as free-living adults. This is why it is
said that the wasps are parasitic. If you have ever seen Aliens, the developing aliens are
parasitoids. Parasitods are different from normal parasites because they kill their hosts when
they develop.

10.2.3 Pathogenesis

The term pathogenesis means step by step development of a disease due to a series of
changes in the structure and /or function of a cell/tissue/organ being caused by a microbial ,
chemical or physical agent.The pathogenesis of a disease is the mechanism by which an
etiological factor causes the disease. The term can also be used to describe the development
of the disease, such as acute, chronic and recurrent. The word comes from the Greek pathos,
"disease", and genesis, "creation".

Types of pathogenesis include microbial infection, inflammation, malignancy and tissue

breakdown.

Most diseases are caused by multiple pathogenetical processes together. For example, certain
cancers arise from dysfunction of the immune system (skin tumors and lymphoma after a
renal transplant, which requires immunosuppression).

Often, a potential etiology is identified by epidemiological observations before a pathological

link can be drawn between the cause and the disease
10.3 Nature of Fungi disease

Figure 10.3 Powdery mildew, a Biotrophic Fungus

Fiogure 10.3 Rice blast, a necrotrophic fungus

The majority of phytopathogenic fungi belong to the Ascomycetes and the Basidiomycetes.

The fungi reproduce both sexually and asexually via the production of spores. These spores
may be spread long distances by air or water, or they may be soil borne. Many soil borne
spores, normally zoospores and capable of living saprotrophically, carrying out the first part
of their lifecycle in the soil.

Fungal diseases can be controlled through the use of fungicides in agriculture, however new
races of fungi often evolve that are resistant to various fungicides.

10.4 Nature of Bacteria Diseases

Fig 10.4 Crown gall disease caused by Agrobacterium

Most bacteria that are associated with plants are actually saprotrophic, and do no harm to the
plant itself. However, a small number, around 100 species, are able to cause disease.[2]
Bacterial diseases are much more prevalent in sub-tropical and tropical regions of the world.

Most plant pathogenic bacteria are rod shaped (bacilli). In order to be able to colonise the
plant they have specific pathogenicity factors. There are 4 main bacterial pathogenicity
factors:

1. Cell wall degrading enzymes - used to break down the plant cell wall in order to release
the nutrients inside. Used by pathogens such as Erwinia to cause soft rot.

2. Toxins These can be non-host specific, and damage all plants, or host specific and only
cause damage on a host plant.

3. Phytohormones - for example Agrobacterium changes the level of Auxin to cause

tumours.

4. Exopolysaccharides - these are produced by bacteria and block xylem vessels, often
leading to the death of the plant.

10.5 Nature of Viral Diseases

There are many types of plant virus, and some are even asymptomatic. Normally plant
viruses only cause a loss of yield. Therefore it is not economically viable to try to control
them, the exception being when they infect perennial species, such as fruit trees.

Most plant viruses have small, single stranded RNA genomes. These genomes may only
encode 3 or 4 proteins: a replicase, a coat protein, a movement protein to allow cell to cell
movement and sometimes a protein that allows transmission by a vector.

Plant viruses must be transmitted from plant to plant by a vector. This is normally an insect,
but some fungi, nematodes and protozoa have been shown to be viral vectors.

10.6 Structure and life cycle of viral diseases

10.6.1 Structure of Viruses

Although all viruses are extremely small, they vary in size and organisation. Generally,
viruses vary in diameter or length from 20 – 200 nm, with the largest viruses actually being
bigger than the smallest cells (bacteria and mycoplasmas).

Most viruses are either rod shaped or roughly spherical. They contain a nucleic acid core
surrounded by a specific arrangement of protein molecules, which form a coat known as the
capsid. The proteins of the capsid are positioned either to form a helical pattern (when the
virus is rod-like) or an isometric pattern making the virus appear like a polyhedron. Viruses
causing diseases like chicken pox or the common cold have polyhedral capsids. Helical
capsids tend to be found amongst viruses that affect plant cells and bacteria, for example the
tobacco mosaic virus that infects the leaves of the tobacco plant. In many animal viruses and
in some plant viruses, a lipoprotein envelope protects the capsid (for example with the herpes
virus).

10.6.3 Life cycle of a virus

Isolated from other living tissue viruses show no metabolism and cannot reproduce. Viral
reproduction requires a host cell; in its simplest form, it follows the following pattern. One or
more viruses attach to specific sites on the host cell. Following attachment, the viral nucleic
acid is inserted through the plasma membrane and into the host’s cytoplasm. Once inside the
host cell, the viral nucleic acid changes the metabolism of the host so that new parts of the
virus are formed. These viral components assemble in the cell to form new viruses, which
either burst from the host cell causing cell lysis or bud from the host cell, which does not lyse
the host cell. The viral life cycle then repeats itself.

On some occasions and only with certain viruses, the injected nucleic acid does not trigger
the production of new viruses. Instead, the viral nucleic acid is incorporated into the host’s
DNA. The host cell continues to behave in its normal way. However every time the host cell
duplicates, so does the incorporated viral nucleic acid. But eventually the incorporated viral
nucleic acid will begin to direct the replication of new viruses.
WEEK 11 : EPIDEMIOLOGY, CAUSATIVE AGENT, LIFE CYCLE
AND CONTROL OF FUNGAL DISEASES.

11.1 Damping off seedling

11.1.1 Epidemiology of damping off diseases

The Pythium species that infect these plants are ubiquitous in soil. They will cause a disease
because environmental conditions are favourable, not as a result of the spread of the pathogen
into a new area. Water movement, through irrigation or rain splash can however disperse
active zoospores. Plants are generally most susceptible to Pythium when the conditions are
unfavourable for plant growth such as unfavourable temperature, excessive moisture, low
light or poor nutrient availability.
Each Pythium species is favoured by different conditions. P. ultimum and P. debaryanum
inhabit cool (10-15°C), moist soil as saprophytes on crop residues. Other Pythium root rots,
such as those caused by P. aphanidermatum, P. irregulare, P. sylvaticum and P. myriotylum
occur in warm (25-36°C), moist soil. Moist soil is conducive to disease development because
the low oxygen level encourages the release of exudates from seeds. These exudates stimulate
the growth of Pythium species towards the emerging plant tissue. As seedlings continue to
grow, the risk of plant death from post-emergence damping off decreases.
Pythium survives in the soil by saprophytic growth or by forming resting spores such as
oospores, hyphal swellings, chlamydospores and encysted zoospores. The spores are
stimulated to germinate by nutrients such as those in seed and root exudates.

11.1.2 Causative agent.

P. ultimum, P. aphanidermatum, P. myriotylum Drechs., P. debaryanum and P. irregulare

Buisman cause damping off and root rot diseases. Those hosts susceptible to Pythium root rot
include cucurbits (melon, squash, cucumber, watermelon and pumpkin), onion, lettuce,
beans, mungbeans, soybeans, maize, potatoes, coffee, pineapple and sugarcane. The seedlings
of many plant species are susceptible to damping off.
11.1.3 Life cycle of damping off diseases

Pythium belongs to the order Peronosporales within the class Oomycetes. Pythium produces
a white, fast-growing mycelium ,which produces sporangia. The sporangia can germinate
directly by producing one to several germ tubes, or hyphae with vesicles at the end form.
From the vesicles, 100 or more zoospores are released, they form cysts and then germination
occurs. The germ tubes that are produced upon germination can penetrate host tissue to
initiate infection or produce another vesicle to continue the zoospore life cycle. Club-shaped
antheridia produced in the mycelium develop germ tubes which enter the spherical oogonia
and fertilisation occurs. The wall of the oogonium thickens to form an oospore. From the
oospores come sporangia and the cycle repeats.

11.1.4 Control

Soil with large populations of fungi and other organisms suppress both the saprophytic and
pathogenic activity of Pythium species. The addition of organic matter may contribute to soil
microbial populations.

Minimising periods of excessive soil moisture are essential for controlling Pythium diseases.
Improve the drainage of the seed raising beds by planting on raised beds and if symptoms are
present only irrigate for short periods on alternate plant beds to maintain plant growth.

11.1.5 Symptoms

Damping off of seedlings is expressed as cotyledon and leaf chlorosis, then a watery rot
appears in the taproot and hypocotyl at or near the soil line. When the roots decompose, the
stele is left intact to leave only a white strand, which is followed by seedling death. On
soybean seedlings P. ultimum Trow causes a wet rot, where P. debaryanum Hesse causes
small, black dry lesions on the cotyledons. Plants with damaged root systems may continue to
grow, but can appear stunted to varying degrees.
When onion plants are infected after the seedling stage they are stunted and the leaves yellow
from tip to base.

In root rot of mature plants, feeder roots die, then lesions up to 2 cm long develop on the
lateral roots. The size of the lesions increase, the plant shows aboveground symptoms of wilt,
chlorosis and necrosis and the disease then spreads along the runners. In cucurbit root rots,
fruit is then exposed to sunburn and the quality is reduced.

P. aphanidermatum (Edson) Fitzp. causes a rot of maize stalks at the internode just above the
soil line at the time of tasselling. The diseased area is brown, soft, wet and collapsed. The
stalks may be twisted. Plants may remain green for a few weeks after being infected, as the
vascular tissue is not affected.
A watery wound rot of potatoes occurs upon invasion of wound sites by P. ultimum and P.
debaryanum. Infected tissue is spongy, wet, discoloured and may have cavities.

11.2 Blight of Potato and Tomato

blight is a very common disease of both potato and tomato. It causes leaf spots and tuber
blight on potato, and leaf spots, fruit rot and stem lesions on tomato. The disease can occur
over a wide range of climatic conditions and can be very destructive if left uncontrolled, often
resulting in complete defoliation of plants. In contrast to the name, it rarely develops early,
but usually appears on mature foliage.

11.2.1 Life cycle

On leaves of both crops, the first symptoms usually appear on older leaves and consist of
small, irregular, dark brown to black, dead spots ranging in size from a pinpoint to 1/2 inch in
diameter. As the spots enlarge, concentric rings may form as a result of irregular growth
patterns by the organism in the leaf tissue. This gives the lesion a characteristic "target-spot"
or "bull's eye" appearance. There is often a narrow, yellow halo around each spot and lesions
are usually bordered by veins. When spots are numerous, they may grow together, causing
infected leaves to turn yellow and die. Usually the oldest leaves become infected first and
they dry up and drop from the plant as the disease progresses up the main stem.
On tomato, stem infections can occur at any age resulting in small, dark, slightly sunken areas
that enlarge to form circular or elongated spots with lighter-colored centers. Concentric
markings, similar to those on leaves, often develop on stem lesions. If infested seed are used
to start tomato transplants, seedlings may damp off soon after emergence. When large lesions
develop at the ground line on stems of transplants or seedlings, the plants may become
girdled, a condition known as "collar rot." Such plants may die when set in the field or, if
stems are weakened, may break over early in the season. Some plants may survive with
reduced root systems if portions of stems above the canker develop roots where they contact
the soil. Such plants, however, usually produce few or no fruits. Stem lesions are much less
common and destructive on potato.

Blossom drop and spotting of fruit stems, along with loss of young fruit, may occur when
early blight attacks tomatoes in the flowering stage. On older fruits, early blight causes dark,
leathery sunken spots, usually at the point of stem attachment. These spots may enlarge to
involve the entire upper portion of the fruit, often showing concentric markings like those on
leaves. Affected areas may be covered with velvety black masses of spores. Fruits can also be
infected in the green or ripe stage through growth cracks and other wounds. Infected fruits
often drop before they reach maturity.

On potato tubers, early blight results in surface lesions that appear a little darker than adjacent
healthy skin. Lesions are usually slightly sunken, circular or irregular, and vary in size up to
3/4 inch in diameter. There is usually a well defined and sometimes slightly raised margin
between healthy and diseased tissue. Internally, the tissue shows a brown to black corky, dry
rot, usually not more than 1/4 to 3/8 inch deep. Deep cracks may form in older lesions. Tuber
infection is uncommon under Ohio conditions.

11.2.2 Causal Organism

Early blight is caused by the fungus, Alternaria solani, which survives in infected leaf or stem
tissues on or in the soil. This fungus is universally present in fields where these crops have
been grown. It can also be carried on tomato seed and in potato tubers. Spores form on
infested plant debris at the soil surface or on active lesions over a fairly wide temperature
range, especially under alternating wet and dry conditions. They are easily carried by air
currents, windblown soil, splashing rain, and irrigation water. Infection of susceptible leaf or
stem tissues occurs in warm, humid weather with heavy dews or rain. Early blight can
develop quite rapidly in mid to late season and is more severe when plants are stressed by
poor nutrition, drought, or other pests. Infection of potato tubers occurs through natural
openings on the skin or through injuries. Tubers may come in contact with spores during
harvest and lesions may continue to develop in storage.

11.2.3 Control

1. Use a crop rotation that includes potatoes or tomatoes only every third or fourth year
to allow infested plant debris to decompose in the soil. Rotations with small grains,
corn or legumes are preferable.
2. Use tillage practices such as fall plowing that bury all plant refuse.
3. Select cultivars that have a lower susceptibility to early blight.
4. Use certified disease-free tomato seed and transplants.
5. If producing tomato transplants, disinfest soil in plant beds and control humidity in
cold frames or greenhouses. Practice good sanitation throughout the transplant
production operation.
6. Use appropriate measures to control weeds and volunteer potatoes and tomatoes in
production areas.
7. Maintain fertility at optimal levels-nitrogen and phosphorus deficiency can increase
susceptibility to early blight.
8. Time applications of overhead irrigation to allow plants to dry before nightfall.
9. Although the above measures are important to minimize infection, it is usually
necessary to apply fungicide sprays to fully protect plants from early blight.
Applications to tomato are usually begun 2-3 weeks following emergence or soon
after transplanting if a calendar schedule is followed. Timing of fungicides can also be
made using the TOM-CAST system. For potatoes, fungicide applications should be
initiated when plants begin to flower. Thorough coverage is important. Adjust
equipment for good vine penetration. For current fungicide recommendations and a
description of the TOM-CAST system consult the Ohio Vegetable Production Guide
(OSU Extension Bulletin 672).

Bacterial leaf blight (caused by the bacterium Erwinia stewartii is more of a problem with
sweet corn than it is with field corn; however, it can be a problem with certain hybrids. The
symptoms are short to long, irregular, pale green to yellow streaks in the leaves ( Fig. 17).
The streaked areas, which die and become straw-colored, originate from feeding marks of the
corn flea beetle. Sometimes entire leaves die and dry up. When leaves die prematurely, yield
is reduced and weakened plants become more susceptible to stalk rots.

The bacteria overwinter in corn flea beetles, which also spread the bacteria. Although insect
control is important in controlling this disease in sweet corn, it is not a sound practice for
field corn producers. Resistance to the disease, which is available in many hybrids, is the
preferred method of control.

in maize

Smuts are not as common as rusts, and usually attack the plant's reproductive components
rather than the leaves or stems.
Boil smut (Ustilago saydis) attacks any above-ground growing part of the plant to form
blisters or galls containing black spores. Mature galls can grow as large as 20 cm in
diameter. Spores can be spread by wind, seed, clothes or farm machinery, and can survive in
the soil for many years. Ensure good hygiene and treat seed with registered fungicide.

Head smut (Sphacelotheca reiliana) infects the young seedling, then grows through the
plant, replacing reproductive tissues (ears and/or tassels) with masses of spores. Distortion is
common, and leafy structures may replace the plant's flowering components. The fungus
survives in the soil, and may also be seed-borne. Cool weather and dry seedbed conditions
favour this disease. Plant resistant varieties, or avoid early planting of susceptible varieties.

See Head smut photo.

WEEK 12: EPIDEMIOLOGY OF BACTERIAL DISEASES.

12.1 Epidemiology of wilt off Diseases

Hibiscus wilt disease is no different from wilts that affect many ornamental plants. It is
caused by fungi with such intimidating names as Fusarium oxysporum and Verticillium. This
disease is often referred to as "root rot" but that is a misunderstanding of the problem. What
is actually happening is that pathogenic fungi are rapidly reproducing in the soil mix of the
pot and entering the plant through the roots. The roots of infected plants do not show any
"rot" except possibly in the late stages of the disease - if the plant survives that long. Once
inside the hibiscus, the fungi disrupt the plant's capillary system, preventing water and
nutrients from circulating normally.

12.2 Epidemiology of citrus canker

Citrus canker is a disease affecting citrus species that is caused by the bacterium
Xanthomonas axonopodis. Infection causes lesions on the leaves, stems, and fruit of citrus
trees, including lime, oranges, and grapefruit. While not harmful to humans, canker
significantly affects the vitality of citrus trees, causing leaves and fruit to drop prematurely; a
fruit infected with canker is safe to eat but too unsightly to be sold.

The disease, which is believed to have originated in South East Asia, is extremely persistent
when it becomes established in an area. Citrus orchards have been destroyed in attempts to
eradicate the disease. Australia, Brazil and the United States are currently suffering from
canker outbreaks. Citrus canker affects all types of citrus, including oranges, sour oranges,
grapefruit, tangerines, lemons and limes. Canker causes the citrus tree to continually decline
in health and fruit production. Ultimately, the tree will produce no fruit at all

Fig 12.2 Lesions on leaves

Plants infected with citrus canker have characteristic lesions on leaves, stems, and fruit with
raised, brown, water-soaked margins, usually with a yellow halo or ring effect around the
lesion. Older lesions have a corky appearance, still in many cases retaining the halo effect.
The bacterium propagates in lesions in leaves, stems, and fruit. The lesions ooze bacterial
cells that, when dispersed by windblown rain, can spread to other plants in the area. Infection
may spread further by hurricanes. The disease can also be spread by from contaminated
equipment, and by transport of infected or apparently healthy plants. Due to latency of the
disease, a plant may appear to be healthy, but actually be infected.

Citrus canker bacteria can enter through a plant's stomata or through wounds on leaves or
other green parts. In most cases, younger leaves are considered to be the most susceptible.
Also, damage caused by Citrus Leaf Miner larvae (Phyllocnistis citrella) can be sites for
infection to occur. Within a controlled laboratory setting, symptoms can appear in 14 days
following inoculation into a susceptible host. In the field environment, the time for symptoms
to appear and be clearly discernible from other foliar diseases varies; it may be on the order
of several months after infection. Lower temperature increases the latency of the disease.
Citrus canker bacteria can stay viable in old lesions and other plant surfaces for several
months.

Fig 12.2 Citrus canker lesions on fruit.

Detection

The disease can be detected in orchards and on fruit by the appearance of lesions. Early
detection is critical in quarantine situations. Bacteria can be tested for pathogenicity by
inoculating multiple citrus species with the bacterium. Additional diagnostic tests (antibody
detection, fatty-acid profiling, and genetic procedures using polymerase chain reaction (PCR)
can be conducted to confirm diagnosis and may help to identify the particular canker strain.

Control

Citrus canker outbreaks are prevented and managed in a number of ways. In countries that do
not have canker, the disease is prevented from entering the country by quarantine measures.
In countries with new outbreaks, eradication programs that are started soon after the disease
has been discovered have been successful; such programs rely on destruction of affected
orchards. When eradication has been unsuccessful and the disease has become established,
management options include replacing susceptible citrus cultivars with resistant cultivars,
applying preventive sprays of copper-based bactericides, and destroying infected trees and all
surrounding trees within an appropriate radius.
 12.3 Epidemiology of Bacterial spot of Tomato

The major sources of infection for these bacteria are thought to be seed and infected crop
debris. Like the bacterial speck pathogen, they also may be present on volunteer tomato
plants and on the surfaces of contaminated equipment (farm machinery, racks, greenhouse
structures, tools). The bacteria are spread primarily by splashing water and wind-driven rain
or mists produced during storms. In the field, spread by equipment or workers is probably of
lesser importance than it is in the greenhouse, unless wounds are being opened up at the same
time, as in a pruning operation or when plants are injured by a cultivator.

Figure 12.3: Bacterial spot lesions on tomato fruit and under sepals.

Figure 12.3: Bacterial spot lesions on foliage and young bacterial spot lesions on fruit. Some
bacterial spot lesions initially have a whitish appearance, similar to a bacterial canker lesion.

Bacteria enter the plant through natural openings (stomates and hydathodes) or wounds
caused by wind-driven soil, insects or mechanical damage (handling, wind whipping, high
pressure sprayers).
WEEK 13: EPIDEMIOLOGY OF VIRAL DISEASES.

13.1 Epidemiology of cassava mosaic disease.

CMGs are transmitted either through planting infected stem cuttings or by the whitefly vector
Bemisia tabaci (Genn.). In a newly planted cassava crop, CMD is spread from plants infected
through the cutting to neighbouring healthy plants by whiteflies. Surrounding CMD diseased
cassava fields are usually more important sources of infection for newly planted cassava
crops than plants that sprout diseased within the field. Epidemic conditions may result where
there is a high incidence of severe CMD coupled with high whitefly populations. These
conditions have been characteristic of the pandemic of severe CMD that has spread through
East and Central Africa during the 1990s.

13.2 Life history of aphids

13.3 Reproduction of Aphids

Figure 13.3 Aphid giving birth to live young

Some aphid species have unusual and complex reproductive adaptations, while others have
fairly simple reproduction. Adaptations include having both sexual and asexual reproduction,
creation of eggs or live nymphs and switches between woody and herbaceous types of host
plant at different times of the year.[3][16]

Many aphids undergo cyclical parthenogenesis. In the spring and summer, mostly or only
females are present in the population. The overwintering eggs that hatch in the spring result
in females, called fundatrices. Reproduction is typically parthenogenetic and viviparous.
Females undergo a modified meiosis that results in eggs that are genetically identical to their
mother (parthenogenetic). The embryos develop within the mothers' ovarioles, which then
give live birth to first instar female nymphs (viviparous). The offspring resemble their parent
in every way except size, and are called virginoparae.

This process iterates throughout the summer, producing multiple generations that typically
live 20 to 40 days. Thus one female hatched in spring may produce many billions of
descendants. For example, some species of cabbage aphids (like Brevicoryne brassicae) can
produce up to 41 generations of females, or more than 1.5 x 1027 offspring if they all live.

In autumn, aphids undergo sexual, oviparous reproduction. A change in photoperiod and

temperature, or perhaps a lower food quantity or quality, causes females to
parthenogenetically produce sexual females and males. The males are genetically identical to
their mothers except that they have one less sex chromosome. These sexual aphids may lack
wings or even mouthparts. Sexual females and males mate, and females lay eggs that develop
outside the mother. The eggs endure the winter and emerge as winged or wingless females
the following spring. This is, for example, the life cycle of the rose aphid (Aphis rosae),
which may be considered typical of the family. However in warm environments, such as a in
the tropics or in a glasshouse or greenhouse, aphids may go on reproducing asexually for
many years.

Some species produce winged females in the summer, sometimes in response to low food
quality or quantity. The winged females migrate to start new colonies on a new plant, often of
quite a different kind. For example, the apple aphid (Aphis mali), after producing many
generations of apterous females on its typical food-plant, gives rise to winged forms which
fly away and settle on grass or corn-stalks.

Some aphids have telescoping generations. That is, the parthenogenetic, viviparous female
has a daughter within her, who is already parthenogenetically producing her own daughter.
Thus a female's diet can affect the body size and birth rate of more than one generation
(daughters and granddaughters).
WEEK 14: KOCH POSTULATE OF ESTABLISHING PATHOGENECITY OF
DISEASES

14.1 Koch's postulates are four criteria designed to establish a causal relationship between a
causative microbe and a disease. The postulates were formulated by Robert Koch and
Friedrich Loeffler in 1884 and refined and published by Koch in 1890. Koch applied the
postulates to establish the etiology of anthrax and tuberculosis, but they have been
generalized to other diseases.

Koch's postulates are:

1. The microorganism must be found in abundance in all organisms suffering from the
disease, but not in healthy organisms.
2. The microorganism must be isolated from a diseased organism and grown in pure
culture.
3. The cultured microorganism should cause disease when introduced into a healthy
organism.
4. The microorganism must be reisolated from the inoculated, diseased experimental
host and identified as being identical to the original specific causative agent.
WEEK 15: PRINCIPLE OF PLANT DISEASES CONTROL

15.1 Exclusion This includes quarantines, inspections, and certification. Plant

material is examined to prevent entry of a disease that does not already occur in a
particular country, state, or geographic area. The most notable use of this method is in
California. As you cross the state border, you must stop at an agricultural inspection
station because they screen for fresh fruit, vegetables, and plants coming from areas
known to have certain diseases (or insects). There are many quarantines on importing
plant materials into the country as well as into the Pacific Northwest. For example,
several grape viruses, Dutch elm disease, chestnut blight, eastern filbert blight, azalea
flower spot, rust-susceptible varieties of barberry, mahonia (Oregon grape) or
mahoberberis, and several peach viruses all are quarantined to prevent import into
Oregon.Quarantines are effective but may not always protect an industry. Quarantines
on the movement of Corylus sp. infected with eastern filbert blight into the Pacific
Northwest from the east coast were effective for more than a century. In 1972, an
infection center was discovered in Washington and has since moved into major
production areas of Oregon.

15.2 Eradication When a plant is infected or an area is infested with a plant

pathogen, eradication can eliminate or reduce the disease threat. Rotation, sanitation,
heat treatment, eliminating the alternate host, and certain chemicals can be used to
reduce or eliminate diseases. Crop rotation is a common method in both commercial
agriculture and home gardens. It is necessary to know the pathogen and its host range.
Rotation reduces soil populations of fungi or nematodes only if nonhost plants are
used.

Removing plant debris (sanitation) is important where pathogens may overwinter.

Raking leaves, removing rotted fruit, picking up old vines, and pruning out dead wood
or canes all are part of sanitation. Once collected, dispose of debris by burning,
burying, or hot composting. If you decide to compost, it must be done correctly or
completely or you will not benefit from your efforts. Field burning is another method
of sanitation which destroys grass stubble where plant pathogens may overwinter.

Rusts are a group of fungi that can complete their life cycle on two or more different
hosts. Eliminating an alternate host may help reduce pressure from these diseases.
Heat treatment is usually used to eliminate viruses from propagation material.

Certain chemicals can be used to eliminate infections or infestations. Soil can be

fumigated to reduce populations of certain fungi and nematodes. Lime sulfur is used
during the dormant season to denature and kill fungal fruiting bodies or spores. Some
fungicides have kickback activity, meaning that infections of some fungi can be
stopped if the chemical is applied within a few days after the infection has started.

15.3 Protection Protection is treating a healthy plant before it becomes diseased.

There are both biological and chemical means of protection. One of the most
successful biological protections has been the use of a bacterium to protect against a
 bacterial disease known as crown gall. The roots of a seedling or nursery plant are
merely dipped into a suspension of a commercial preparation of the bacterium prior to
planting.Chemical protection is one of the most widely used means of control. Some
fungicides (such as copper and sulfur products) are allowed for use under several
"organic" growing guidelines. Many fungicides are on the market but few can be
obtained easily by the homeowner. It is necessary to know the disease cycle and host
susceptibility to get good control using fungicides. Proper timing, coverage, and
selection of fungicides is also needed.

15.4 Resistance Resistance is a term sometimes mistakenly used interchangeably or

in conjunction with "immunity," "tolerance," and "susceptibility." These terms
describe the inherent genetic makeup of the plant and thus its reaction to plant
pathogens. Resistance and its opposite, susceptibility, are levels or degrees of a plant's
reaction. Some cultivars of a plant can be more or less resistant (or susceptible) than
another cultivar. Resistant cultivars can still become diseased but not as much as (or
more than) another. If a plant does not ever become diseased, then the term "immune"
can be used. Tolerance describes a plant (usually a food crop) that may become
diseased but produces yields similar to a healthy plant.Lists of resistant plants can be
found in many texts and seed catalogues. Planning ahead is essential and planting
resistant cultivars is the easiest means of disease control.Knowing what diseases a
plant is susceptible or resistant to can help in the diagnostic process. One can
eliminate possibilities by knowing which diseases are likely to occur.

15.5 Application of control principle to specific plant diseases

 Breeding for Resistance to Plant Viruses

 Control of Plant Virus Diseases by Cross-protection of Virus Infection in Crops
Through Breeding Plants for Vector Resistance: Biochemical and molecular
approaches
 Biochemistry of Resistance to Plant Viruses
 Protein and Replicase-mediated Resistance to Plant Viruses
 Antisense RNA and Ribozyme-mediated Resistance to Plant Viruses
 Satellite RNA-mediated Resistance to Plant Viruses: Are the Ecological Risks Well
Assessed?
 Alternative Strategies for Engineering Virus Resistance in Plants
 Controlling Mosaic Virus Diseases Under Field Conditions by Using Multiple-gene
Strategies in Transgenic Plants Special topics related to resistance
 Releasing Genetically Engineered Virus Resistant Crops - Risk Assessment
 Antiviral Substances of Plant Origin Resistance to Plant Viruses: an Overview

Control of Vectors

 Forecasting Aphid-borne Virus Diseases

 Chemical Control of Insect and Nematode Vectors of Plant Viruses
 Chemical Control of Fungal Vectors of Plant Viruses

Elimination

 Heat Treatment of Perennial Plants to Eliminate Phytoplasmas, Viruses, and Viroids

While Maintaining Plant Survival
  Virus Elimination by Meristem Tip Culture and Tip Micrografting

Disease Control

The five basic principles of plant disease control are: exclusion, avoidance, eradication,
protection, and resistance. These principles work at federal, state, county, and personal levels.

Avoidance If the disease does occur in your area, there may be techniques to avoid disease
development. Choice of planting site, time of planting, storage conditions, or avoiding
wounds are a few of these techniques. Phytophthora root rots can be avoided by not planting
in heavy, poorly drained soils. Planting later in the year when soils are dryer and warmer will
avoid some damping-off diseases common to many vegetables. Wounding can cause entry
points for pathogens or weaken a plant to the point that it cannot defend itself. Avoiding
wounds also helps to control the crown gall bacterium which needs an injury to begin the
infection process. Planting certified virus-free stock is a good way to avoid virus-related
diseases.

Good horticultural practices such as proper fertility, pruning, watering, and proper training
will go a long way to help control plant diseases.