Ocular Microbiology
Ocular Microbiology
Ocular Microbiology
MICROBIOLOGY
OCULAR
MICROBIOLOGY
PK Mukherjee MS
Consultant Ophthalmologist
Former Professor and Head
Upgraded Department of Ophthalmology
Pt JNM Medical College, Raipur
Chhattisgarh, India
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Ocular Microbiology
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PK Mukherjee
Preeti Bandyopadya
ACKNOWLEDGMENTS
INTRODUCTION
ii. Endoparasites that live inside the body of the host, i.e.
malarial parasites. The parasites that can not survive
without a host are called obligate parasites, i.e. toxoplasma.
A facultative parasite may exist without a host.
Opportunistic pathogens are commensals and saprophytes
that can produce disease when the body resistance is below
optimal level.
Source of Infection
1. Normal flora
Normal flora may become pathogen due to changed
immunity that may be:
i. Systemic as in AIDS
ii. Biochemical change, i.e. diabetes
iii. Indiscriminate use of antibiotic, steroid
iv. Chemotherapy and radiation.
v. Local ocular conditions like abnormal tear status, ocular
surface defect, contact lens, prolonged uses of antibiotics
or steroids are some of the examples.
2. Human beings are the commonest source of infection to others,
both systemic as well as ocular.
The mode of transmission among humans can be:
i. Inhalation: This method of transmission is commonest
mode in respiratory tract infection. The organisms may
remain suspended in the air and inhaled or may fall on
the ground and inhaled along with dust.
ii. Ingestion: This is the most frequent mode of transmission
of gastrointestinal diseases, may be water borne or food
borne.
iii. Inoculation: The organisms are virtually implanted in the
tissue following breach in the skin. The examples are
6 OCULAR MICROBIOLOGY
The eyes are sterile only for few hours after birth and then get
invaded by microorganisms.
Eyes are highly sensitive sensory organs. They have been given
adequate anatomical and physiological protection
The anatomical protection is offered by
1. Walls of orbit: The boney orbital walls surrounds the eyeball
from all sides. The wall is shorter on the lateral side, this
makes the eyes vulnerable to trauma and infection from
the lateral side.
2. Lids: The combination of tarsal plate and orbicularis form
a formidable curtain that can be activated both voluntarily
as well as reflexly. This is the commonest form of protection
from exogenous invasion by microbes.
3. The lashes: The lashes entangle the microorganism and
prevent them from entering the conjunctival sac.
4. The orbital septum prevents infection spreading from
pre-septal area to retroseptal space and vice versa.
5. The conjunctival epithelium itself is resistant to many
organisms. It had good phagotic action as well.
6. The corneal epithelium is resistant to all organisms except
Gonococcus, Meningococcus, Diphtheria, Haemphilus aegyptius
and Listeria.
7. The Descemet’s membrane also restrains organisms to go
deeper but can not stop toxins from passing through it.
8. The tear film has multiple protective functions –
i. Mechanical flushing of the conjunctiva and the cornea.
The tear production is increased manifolds as soon as
an organism finds its way on the conjunctiva or cornea.
ii. Antimicrobial action: The lysozyme and lactoferrin present
in tear have a microstatic action on many organisms. If
the level of these two fall below the critical level, there is
immediate rise of bacterial flora in the conjunctival sac.
GENERAL CONSIDERATIONS 13
Rich blood supply of the eye except the cornea and lens
makes the eye predisposed to hematogenous spread of the
infection. The meninges and cerebrospinal fluid (CSF)
transport intracranial infection to the eye. The organism
finds the paper thin walls of paranasal sinuses easy to
pass through. The retained intraocular and intraorbital
foreign bodies are a constant and common source of ocular
infection.
14 OCULAR MICROBIOLOGY
MORPHOLOGY OF BACTERIA
Size
The bacteria have variable sizes, the cocci are smaller than
bacilli. The size varies between 0.1 to 50 micron. Common
pathogens have a range between 0.5 to 2.0 micron. The large
bacteria have more complex structure than small bacteria.
The smaller bacteria are deficient in enzymes, hence they
depend more on host cells for growth and multiplication.
Shape
The bacteria are divided into two main groups as per shape,
i.e. the cocci and bacilli. The former are circular, can be spherical,
kidney-shaped or lancet-shaped. The latter are rod-shaped
in between them are Cocco bacilli which are in fact bacilli. The
spirochetes are spiral, vibrios are a comma-shaped. Some are
filamentous, i.e. actinomycetales (Figure 2.1).
Arrangement
Cell Wall
Flagella
Fimbriae (Pili)
Spores
Oxygen Requirement
Visualization of Bacteria
GRAM-POSITIVE COCCI
Staphylococci
Streptococci
Classification of Streptococci
Anaerobic Streptococci
GRAM-NEGATIVE COCCI
Neisseriaceae
Neisseria gonococci
Acinetobacter
Moraxella lacunata
GRAM-POSITIVE BACILLI
Corynebacterium
Corynebacterium diphtheriae
Corynebacterium xerosis
Propionibacterium acnes
Bacillus
B. cereus
Bacillus subtilis
Clostridium
The genus Clostridium contains many species but all are not
human pathogen. Only few are opportunistic pathogens. The
important pathogens are C. tetani, C. Welchii and C. botulinum.
All of them have profound systemic involvement. Ocular
involvements are rare and mostly accidental.
The organisms are gram-positive anaerobes which are
destroyed in presence of oxygen. Presence of CO2 enhances
growth. They are spore forming, the positions of the spores
are variable. It can be terminal, subterminal or central. They
are stained with ease. They show slow motility, only few are
capsulated.
All the three organisms produce lethal exotoxin.
Clostridium tetani
160°C for one hour to destroy the spores. The best method is
autoclaving at 121°C. The spores are also destroyed by iodine
and hydrogen peroxide. The spores are known to survive in
the soil for years.
The organism produces two exotoxin—Tetanolysin and
tetanospasmin, which are responsible for clinical features of
tetanus.
The ocular involvements are secondary to toxic neuritis of
cranial nerves, i.e. blepharospasm, ptosis, various extraocular
muscle palsies, internal ophthalmoplegia, supranuclear gaze palsy
and nystagmus.
Treatment
Clostridium botulinum
Mycobacteria
Mycobacterium tuberculosis
Laboratory Diagnosis
Atypical Mycobacteria
Classification
Mycobacterium leprae
The Mycobacterium leprae is found all over the world and cause
leprosy. It is also known as Hansen bacilli.
The organism is gram-positive, stain poorly with Gram’s
stain, is acid-fast but not alcohol fast. The live bacilli can be
differentiated from dead bacilli by their staining character:
54 OCULAR MICROBIOLOGY
Higher Bacteria
Actinomyces
Nocardia
GRAM-NEGATIVE BACILLI
The common gram-negative bacilli of ocular importance
belong to genera:
1. Pseudomonas
2. Haemophilus
3. Acinetobacter
4. Moraxella
5. Enterobacteriaceae
6. Brucella
7. Franciscella tularensis
Pseudomonas
Haemophilus
Acinetobactor
It is an ubiquitous organism that is found in soil and water as
saprophyte. Previously, it was not considered as an ocular
pathogen but there are frequent reports that show it as a
potential cause of endophthalmitis following lens extraction
and penetrating injury. It is an opportunistic organism that
becomes pathogen in immunocompromised persons. It is a
frequent cause of nosocomial infection.
The organism has striking similarity with Neisseria
and Moraxella. There are about seventeen geno species,
out of which the two, i.e. Mima polymorpha and Herellea
60 OCULAR MICROBIOLOGY
Moraxella
Enterobacteriaceae
Escherichia coli
Klebsiella
Proteus
Salmonella
Intestinal parasite, gram-negative, facultative anaerobic,
motile, nonsporing, grow on ordinary culture media,
ferment glucose, maltose, mannitol but not lactose or sucrose
causes conjunctivitis and corneal ulcer and it is destroyed by
heat at 60°C in 20 minutes, chlorination and pasteurization,
sensitive to ampicillin and ciprofloxacin.
Shigella
Gram-negative, aerobic, nonmotile, nonflagellate, non-
capsulated, grows on ordinary media, ferment glucose, produce
acid but no gas. Produce endotoxin and exotoxin, destroyed
by heat and phenol, sensitive to sulpha and many broad
spectrum antibiotics. Rarely causes dacryocystitis and keratitis.
BACILLI OF OCULAR INTEREST 63
Francisella tularensis
Brucella
Bordetella pertussis
Spirochetes
2. Borrelia
B. Burgdorferi
3. Leptospira
Treponema
Borrelia
Leptospira
CHLAMYDIAE
These organisms were previously thought to be viruses
because they are:
1. Intracellular obligate parasites.
2. Filterable.
3. Do not grow on cell free media.
4. Do not grow in culture media.
5. They form inclusion foreign bodies.
It was later realized that as they have following properties
they should be considered as bacteria:
1. They have a cell wall.
2. They possess both DNA and RNA.
3. They have ribosomes
4. They multiply by binary fission.
5. They are susceptible to anti microbial agent.
6. They contain metabolically active enzyme.
The organisms belong to:
Order – Chlamydiae
Family – Chlamydiaceae
Genus – Chlamydia have three species, i.e. C. trachomatis—
causing trachoma, nonspecific urethritis, cervicitis and
lymphogranuloma venerum.
70 OCULAR MICROBIOLOGY
Lymphogranuloma venerum
Laboratory Diagnosis
1. Serological tests
i. Fluorescein labeled monoclonal antibody
ii. Enzyme immunoassay
iii. Polymerase chain reaction
iv. ELISA
v. DNA probe
2. Isolation of C. trachomatis by yolk sac inoculation.
3. Cytology: Neutrophilic mononuclear infiltrates, presence
of Leber cells and Humbrecht cells.
74 OCULAR MICROBIOLOGY
Morphology
Classification of Viruses
1. RNA viruses
2. DNA viruses
The RNA viruses of ophthalmic interest are:
1. Measles and mumps
2. Rubella
3. HIV and AIDS
The DNA viruses of ophthalmic interest are:
1. Smallpox, molluscum
2. Herpes simplex, herpes zoster, cytomegalovirus, Epstein-
Barr virus
3. Adenovirus
4. Papovaviruses
Mutation is a characteristic of viruses of all types. It occurs
in vivo as well as tissue culture. The virus changes its
behavior, virulence and antigenic property by mutation.
Multiplication: The viruses do not multiply by binary fission.
As the viruses do not contain biosynthetic enzymes, they
have to use enzyme system of the host cells to form specific
molecule to replicate. The nucleic acid of the virus carries
the genetic information. The replication of virus is a
complicated procedure.
They can be broadly divided into following phase:
1. Adsorption
2. Penetration
3. Uncoating
4. Biosynthesis
5. Maturation
6. Release
Virus Infection
The route of infection are varied, they enter the human body
by any of the following routes:
Skin: Through cuts, abrasion
Oral: GI tract, contaminated food and drink.
Respiratory: Droplet infection
Conjunctiva: Droplet or via fomites
Sexually transmitted: HIV, AIDS
Hematogenous: By contaminated needles, bite of vector.
Transplacental: Congenital rubella
OCULAR VIROLOGY 79
Cellular Changes
Variola
Vaccinia
Molluscum Contagiosum
Herpes Virus
Diagnosis
Microscopy
Virus Isolation
Diagnosis
Cytomegalovirus
Epstein-Barr virus
Adenoviruses
Picorna Viruses
Paramyxovirus
1. Paramyxo virus:
i. Mumps
ii. Parainfluenza
iii. New castle disease
2. Morbilli virus
i. Measles virus
3. Pneumovirus—respiratory syncytial virus.
Out of these only mumps and measles have ocular
involvement.
Mumps Virus
Human beings are the only known host. The virus inflicts
mostly children. Children under six months are protected
by maternal antibodies which develop in the mother even
after a subclinical infection. The virus gives a lifelong
immunity hence second attack does not occur. The incubation
period is 16-18 days. Epidemics are common. The virus causes
hemagglutination followed by hemolysis. The organism is
killed at room temperature, formaldehyde and ultraviolet
light. The organism grows on chick embryo and human
amnion.
Diagnosis is simple on the basis of clinical presentation.
Atypical cases may require laboratory tests which consist of:
1. Demonstration of virus by immunofluorescent method.
2. Culture
3. Serology
i. Four-fold rise in antibody titre in paired serum
sample.
ii. Complement fixation test
iii. Hemagglutination inhibition test
iv. ELISA
92 OCULAR MICROBIOLOGY
Measles (Rubeola-Morbilli)
Laboratory Diagnosis
Laboratory Diagnosis
2. Tissue culture
3. Immunofluorescent with specific antibody.
4. Serology—Hemagglutination inhibition test in avian
blood.
5. ELISA for IgG and IgM.
Retrovirus
The HIV attacks those cells that have CD4 antigen. These
are helper lymphocytes, monocytes and macrophages.
Diagnosis
FUNGI
Fungi are ubiquitous organism found in soil and decaying
organic matters. Their importance as cause of disease in
plants and animals was established earlier than bacteria or
viruses. They are generally saprophytes but becomes pathogens
to cause opportunistic infection when there is a decline in the
immunity local or systemic. They are all parasites.
The fungi differ from bacteria and viruses in many ways.
The peculiarities of the fungi are:
1. They are said to be plants of lower order without leaves,
branches and roots.
2. They do not contain chlorophyll, depend upon
decaying organic matter for nutrition.
3. The fungi contain rigid cell wall made up of
polysaccharide and chitin.
4. They have cytoplasmic membrane that contain sterol.
5. They are eukaryotes, i.e. contain true nuclei with
nuclear membrane, paired chromosomes, mitochon-
dria, ribosome and food reserve.
6. They may be unicellular or multicellular.
7. Pleomorphism is common.
8. The cells show various types of specialization.
9. They propagate asexually, bisexually or by combined
methods.
10. The organisms are gram-positive, some are acid-fast.
11. Some fungi show agglutination.
12. Some fungi cause complement fixation reaction.
13. Fungi can produce endotoxin.
14. Hypersensitization to fungi is well established.
15. Fungi are not known to cause epidemics. They cause
chronic diseases both local and systemic. Some of the
systemic infections can be fatal.
OCULAR MYCOLOGY 101
Wet Preparation
Other Methods
Culture of Fungi
CLASSIFICATION OF FUNGI
The fungi belong to Phyllum thallophyta. The phyllum
contains two groups, i.e. algae and fungi. The former contain
chlorophyll and are not known to cause human infection.
The fungi are again divided into Pseudomycetes and Eumycetes,
the true fungi. The pseudomycetes are now considered to
be higher bacteria. The eumycetes can either be with septate
hyphae or without septate hyphae.
Blastomyces
Candida (Monilia)
Coccidioides
Dermatophytes
Histoplasma
Mucor
brain from the paranasal sinuses and from the orbit. It is invariably
a fatal disease.
Rhinosporidium
INTRODUCTION
Parasites as causative agents of diseases were known from
the days of Hippocrates. The modern study of human
parasitology started with discovery of microscope by Antony
Van Leeunhoek in the year 1683 and study of Echinococcosis
by Hartmann in 1685.
It is essential to know some terms used in parasitology to
understand the life cycle and mode of transmission of
diseases caused by various parasite.
Parasites are the living organism that live in/on a host
that provides nutrition to the organism and protects it also.
The organism that harbors the parasite is called the host.
Parasitism is the association in which the parasite gets the
benefit at the cost of the host. In such a situation, it is the
host that suffers the injury. Parasitism exists in some bacteria,
viruses, protozoa and helminths. The host offers resistance
to the injury done by the parasite and there may be some
adaptation (tolerance) to this.
The term free living parasite denotes a parasite which
lives independent of the host, i.e. Acanthamoeba, Naegleria
and hookworm.
The term mutualism denotes a situation where both the
host as well as the parasite derive benefit from each other.
The arrangement is best seen in plants, i.e. mutualism
between rhizobium bacteria and leguminous plants.
Lichens are formed by mutualism between algae and
fungi. This process is not seen in human parasitology.
In symbiosis, the host and the parasite both depend on
each other to thrive, one can not live without the other. If
the parasite derives benefit without causing harm to the host,
the condition is called commensalism. The parasites involved
are called commensals. They live on superfluous fluid or
OCULAR PARASITOLOGY 123
Types of Hosts
The hosts are divided into two types, each with a definite
purpose:
1. Definitive host is a host that harbors the adult stage of
parasite or where the parasite uses the sexual method of
reproduction. Man is the definitive host in malaria,
Echinococcus, Toxoplasma gondi.
2. Intermediate host is the host in which the larval form lives
or the asexual replication takes place. In some parasites
the larval developments are completed in two
intermediate hosts which are called first and second
intermediate hosts.
Vectors are arthropods that transmit the parasites to host.
The vectors in which the parasites multiply are called
biological vectors in contrast to mechanical vectors in which
the parasites do not multiply, i.e. housefly is a mechanical
vector for amoebiasis and trachoma.
Zoonosis is a parasitic disease that is primarily a disease
of vertebrate animals but can be transmitted to humans to
produce disease. The examples are Leishmaniasis, Try-
pansomiasis and Echinococcus.
Zoonanthroponosis is an infection where human beings
are incidental hosts and serve as an essential link in the life
cycle of the beef or the pork tapeworm.
Anthroponosis refers to parasitic infection that are solely
seen in humans, i.e. filarial.
124 OCULAR MICROBIOLOGY
Reservoir
Types of Parasites
PROTOZOA
Acanthameba
Toxoplasma
The tissue cysts are formed within the host cell and contain
thousands of spore like organisms. As they multiply slowly,
they are called bradyzoites. They stain with periodic acid-
Schiff stain (PAS). The cyst wall stain with silver stain. They
persist in every tissue including brain, muscles, liver and
ingested by carnivores, they get infected. There is hardly any
difference in morphology of tachyzoites and bradyzoites. The
conversion from tachyzoites to bradyzoites is a defense
mechanism. The latter linger in the host for years. They cause
chronic infection and can transmit the disease. The cyst wall
is destroyed by digestive fluid after the cyst has been ingested.
OCULAR PARASITOLOGY 135
Oocytes (Sporozoites)
They are formed only in feline intestine. The cat is the only
animal in which the organism has sexual cycle comprising
of microgametes (male) and macrogametocytes (female) leading
to formation of zygote that is surrounded by wall of the
oocyte. The cat sheds the oocytes for about 5-7 days. Only,
after which there are no oocytes in cat feces. The freshly passed
oocytes are not infective. They develop infectious status in soil
and water after few days. The freshly passed oocyte in cats
feces contains a sporoblast that develops into the sporocytes.
A mature oocyte contains two sporocytes, each contain four
sporozoites (Figure 7.5).
Diagnosis
Differential Diagnosis
6. ELISA IgM
7. IgM immunosorbent agglutination test
8. Immuno Blot
9. Western Blot
10. PCR
11. TORCH
Demonstration of Organism
Microsporidia
Treatment
Pneumocystis carinii
Ocular Involvement
Metazoa
Phylum metazoan contains all multicellular animals
including helminths.
The helminths are:
1. Multicellular.
2. Bilaterally symmetric.
3. Have three germ layers.
The helminths that cause diseases in humans are:
1. Nematodes (Roundworm)
OCULAR PARASITOLOGY 143
2. Cestodes (Flatworms)
3. Trematodes
Only nematodes and cestodes cause ocular lesions.
Nematodes
Toxocara
The organism has two types of life cycle, i.e. in dogs and in
humans. In dogs, the stage differ in adult dogs/bitches and
puppies.
The adult dogs get the infection in two ways:
1. Ingestion of ova in contaminated food
2. Ingestion of larva in infected meat.
In adult dogs the ova develops in third stage larvae in the
intestine. The third stage larvae are liberated in intestine
and penetrate intestinal musculature to reach the circulation.
After some months the larvae get encysted and lie dormant
without developing further.
In pregnant bitches the picture is different. The encysted
larvae are activated to migrate through the placenta to the
developing puppy. By the time the puppies are borne, they
already have third stage larvae. The larvae pass into the gut
and pass the ova in feces.
The life cycle in humans is similar to those seen in adult
dogs. The third stage larvae in the gut penetrate the mucosa
of the intestine and are carried to distant organs by blood,
i.e. eyes, liver, lungs, brain and subcutaneous tissue. The
organism encysts in the tissue and forms a granuloma which
is the main pathological feature of the disease.
The nematode larva may wander aimlessly in various
tissues causing a condition known as larval migrans that could
be cutaneous larval migrans or visceral larval migrans.
Nematodes other than toxocara also produce cutaneous
larval migrans. Toxocara generally causes visceral larval
migrans. The term ocular larval migrans is used to denote
ocular involvement.
The other causes of cutaneous larval migrans are:
1. Human ankylostoma
146 OCULAR MICROBIOLOGY
Diagnosis
Systemic Toxocariasis is difficult to diagnosis. The diagnosis
is based on exclusion and high index of suspicion. Ocular
Toxocariasis and visceral larval migrans do not co-exist.
Ophthalmic larval margins (OLM) is seen in older children,
they may have history of visceral larval migrans (VML) few
years ago. These children have eosinophilia due to lack of
active systemic infection. The diagnosis is confirmatory.
ELISA for toxocara antigen a serum titre of 1:32 is suggestive
of VLM while a titre of 1:8 is suggestive of OLM Antibody
titre is higher in aqueous than in serum.
OCULAR PARASITOLOGY 147
Treatment
Systemic toxocariasis is treated by oral albandazole,
thiabendazole.
Thelazia
Thelazia is a small, thin nematode, life cycle and mode of
transmission is not well established. The two common species
that have ocular manifestations are Thelazia californiensis and
Thelazia callipaeda. The adultworm usually resides in the
conjunctival sac, lacrimal sac and lacrimal duct of many
animals and birds. The definite hosts are suspected to be dogs,
cats, horses. The intermediate host is fly of genera mucosa
and fannia. Human beings are accidental hosts. The probable
mode of transmission is by flies which lay the eggs in the
conjunctival sac where they mature to become adultworms
and can be seen moving in the conjunctival sac or in the
subconjunctival space. They may penetrate the cornea or
sclera and become intraocular. The intraocular parasite may
be seen freely moving in the aqueous and mistaken for other
worms. They must be differentiated from Dirofilaria,
Burgiamalayi and Wuchereria bancrofti. Death of the worm
causes severe allergic reaction, hence it is better to remove
the live worm from AC than to use antihelmenthic drugs.
Trichinella
Trichinella is a intestinal nematode of pigs and many other
domestic and wild animals found all over the world. It is an
148 OCULAR MICROBIOLOGY
Laboratory Diagnosis
Treatment
Baylis ascaris
Tissue Nematodes
Onchocerca
LARVAE
When the fly bites an infected warm blood host it sucks the
microfilariae. The microfilariae stay in the gut of the fly for
about 20 hours after that they enter the thorax from where
they go to the mouth parts of the fly and await a chance to
be deposited in the definitive host. An infected fly may have
200-250 third stage larvae in it.
The female fly S. damnosum lays eggs on the rocks or plants
in running, rapid flowing well oxygenated clear water where
they are converted to puppa, cocoon and adult fly in
succession in two to three weeks. An adult fly has lifespan
of about four weeks during which it feeds on warm blood
four to five times. Only the female flies cause and spread
the disease.
Diagnosis
Management
Loa Loa
Diagnosis
Management
1. Vector control.
2. Use of fly repellents.
3. Covering the body as far as possible.
4. Chemotherapy by diethyl carbamazine which is
filariaecidal as well as larvaecidal.
5. The subconjunctival worm is removed under local
anesthesia by snipping the conjunctiva over the worm.
Wuchereria bancrofti
A B
Figures 7.9A and B: Histopathological section showing Wuchereria
bancrofti in high and low power. (Courtesy: Prof V Sudarshan)
Ocular Involvements
Management
1. Vector control.
2. Protection from mosquito bite by use of mosquito nets,
use of mosquito repellents.
OCULAR PARASITOLOGY 159
Treatment
Dirofilaria
A B
Figures 7.11A and B: Dirofilaria—histopathological section showing
parasite in tissue and parasite seen in high power magnification.
(Courtesy: Reproduced with permission of editor IJO)
160 OCULAR MICROBIOLOGY
Management
Gnathostoma spinigerum
The Cestodes
Cysticercus
Human Cysticercosis
Treatment
Life Cycle
The life cycle is in two hosts, i.e. the definitive hosts are dogs
and other canines and the intermediate hosts are sheep, goat,
cattle or other herbivorous animals. The humans are accidental
intermediate hosts in whom the parasite reaches a dead end.
170 OCULAR MICROBIOLOGY
The eggs of Echincocci are the infective stage for the human
beings.
Human beings acquire the infective form from the dogs
either as in contaminated food or drink or through
contaminated hands that have been fondling infected dogs.
The ingested eggs release the embryo in the duodenum
of humans. The embryos penetrate the intestinal mucosa to
reach the portal circulation and reach the liver. Most of the
embryos are filtered in the liver. The next organs where the
embryos settle are the lungs. Other organs are also seeded
by the embryos. The embryos are converted to hydatid cyst
in these organs. It takes few months to years for the cyst to
develop in these organs.
Ocular Involvement
Diagnosis
Management
The dogs or other canines are the definitive hosts, the sheep
and other herbivores are intermediate hosts. Humans beings
are accidental intermediate hosts.
Life cycle resemble that of cysticercus. The intermediate host
acquires the disease by feeding on grass contaminated by
feces of dogs that contains the infective eggs. Human beings
get infected accidentally.
The Ovo onchospores hatch in the gut of the sheep and
penetrate the gut wall to reach systemic circulation that
carries them to distant organs including the eyes. The
common sites are brain and the spinal cord where they
develop into coenurus or the bladder that has multiple
scoleces. The carnivore which is definitive host gets the
infection by eating dead herbivore with coenurus. The
systemic presentation of coenurosis is that of space
occupying lesion of the brain or the spinal cord.
The ocular manifestations are similar to cysticercosis but
less frequent. They include subconjunctival cysts, cyst in AC
or vitreous, and orbit. There may be associated eosinophilia.
Brain scan shows intracranial cyst. CT, MRI and ocular ultra-
sonography helps to locate intraorbital and intraocular
coenurus. The dead coenurus causes uveitis.
There is no specific treatment. Praziquantel 50 mg/kg/
day in divided dose for a fortnight may be tried. Surgical
removal when possible is the best option.
are winged. The number of legs vary between six to ten. When
winged they may have single pair of wings or may have two
wings on each side. Most of them have antennae.
Classification of Arthropods
1. Mechanical transmission:
Trachoma, infective conjunctivitis by domestic flies, the
vectors involved is not a part of life cycle of the parasite.
174 OCULAR MICROBIOLOGY
2. Biological transmission:
The vector is an integral part of life cycle of the parasite.
i. Only multiplication in vector, i.e. plague (no ocular
involvement)
ii. Development in vector—Wuchereria in mosquito
iii. Multiplication and development in vector
iv. Depositing eggs in the conjunctiva or wound, i.e.
myiasis.
176 OCULAR MICROBIOLOGY
INTRODUCTION
COLLECTION OF SPECIMENS
To culture the material both solid and liquid media are used.
The solid media are inoculated by spreading the material in
shape of letter C, which stands for cornea, at the same time
letters R or L may be streaked away from C to demarcate the
side R for right and L for left.
Traditionally, any growth outside these letter are considered
to be the contaminants. The solid media are streaked lightly
without cutting the surface. In case of liquid media the spatula
containing the material is swirled in the liquid.
Most commonly used stains are Gram’s stain and Giemsa
stains.
Gram’s stain is used for bacteria, fungi and Acanthameba.
Giemsa stain is used for bacteria and Acanthameba. It is
also used for inclusion bodies of Chlamydia.
Less commonly used stains are:
• Ziehl-Neelson for modified kinyouns media
180 OCULAR MICROBIOLOGY
A B C
2. Chocolate agar
3. Nutrient agar
4. Brain-heart infusion broth
5. Thioglycollate broth
6. Sabouraud’s agar
7. Potatodextrose agar
8. Lowenstein-Jensen medium (Figure 8.2).
Drug Resistance
This is used to find out the most useful antibiotic that destroys
the organism in therapeutic dose in expected time. It also
finds out the drugs to which the organism is absolutely
resistance.
There are two commonly used methods. They are:
i. Disk diffusion method
ii. Tube dilution method.
BIBLIOGRAPHY
74. Savitri Sharma, Kunimoto DY, Garg P, Rao GN. Trend in antibiotic
resistance of corneal pathogens. Ind Jr Oph 1999;47:95-100.
75. Schaumberg OD, Snow KK, Dana MR. The epidemic of
acanthameba keratitis, where do we stand, Corne 1998;17:3-10.
76. Schmidt GP, Roberts LS. Foundation of parasitology, (3rd edn)
CV Mosby, St Louis, 1085.
77. Sharma Savitri. Ocular microbiology, Arvind eye hospital, Maduri.
78. Sheeja Susan John, Shobhana G Mohan. Conjunctiva oculos-
poridiosis with scleral thinning and staphyloma formation. Ind Jr
Op 2005;53:272-74.
79. Sorsby A. Modern ophthalmology, Vol. 2, (1st edn) Buttorworth,
London, 1963.
80. Steinret R. Current therapy for bacterial keratitis and bacterial
conjunctivitis, Am J Oph 1991;112:105-45.
81. Strickland GT. Hunter’s tropical medicine and emerging infectious
disease (8th edn) WB Saunders Company, Philadelphia, 2000.
82. Subodh BNR, Dash S, Chakrawarty D, Mishra DP, Senapali U:
Ocular sporganosis. JIMA 2006;104:52;9-530.
83. Thamesis RR, Foster CS. Ocular syphilis, Ophthalmology 1990;
97:1281-87.
84. WHO. Future approach to trachoma control. A report of a global
scientific meeting. Geneva WHO/PBL/96, 56.
85. WHO. Primary health care level management of trachoma. Geneva
WHO/PBL/93, 33.
86. WHO Expert Committee on Leprosy. Seventh Report, WHO Tech.
Rep. Sr. 1998;874.
87. WHO Expert Committee report on Leprosy. Sixth report, WHO
Tech Rep Sr 1988;768.
88. WHO stydy group. Chemotherapy of leprosy, WHO technical
report, Series No. 84, Geneva 1994.
89. Wilson GS, Miles AA. Topley and Wilson’s principles of
bacteriology and immunity (4th edn), William and Wilkins,
Baltimore, 1955.
192 OCULAR MICROBIOLOGY
BIBLIOGRAPHY
74. Savitri Sharma, Kunimoto DY, Garg P, Rao GN. Trend in antibiotic
resistance of corneal pathogens. Ind Jr Oph 1999;47:95-100.
75. Schaumberg OD, Snow KK, Dana MR. The epidemic of
acanthameba keratitis, where do we stand, Corne 1998;17:3-10.
76. Schmidt GP, Roberts LS. Foundation of parasitology, (3rd edn)
CV Mosby, St Louis, 1085.
77. Sharma Savitri. Ocular microbiology, Arvind eye hospital, Maduri.
78. Sheeja Susan John, Shobhana G Mohan. Conjunctiva oculos-
poridiosis with scleral thinning and staphyloma formation. Ind Jr
Op 2005;53:272-74.
79. Sorsby A. Modern ophthalmology, Vol. 2, (1st edn) Buttorworth,
London, 1963.
80. Steinret R. Current therapy for bacterial keratitis and bacterial
conjunctivitis, Am J Oph 1991;112:105-45.
81. Strickland GT. Hunter’s tropical medicine and emerging infectious
disease (8th edn) WB Saunders Company, Philadelphia, 2000.
82. Subodh BNR, Dash S, Chakrawarty D, Mishra DP, Senapali U:
Ocular sporganosis. JIMA 2006;104:52;9-530.
83. Thamesis RR, Foster CS. Ocular syphilis, Ophthalmology 1990;
97:1281-87.
84. WHO. Future approach to trachoma control. A report of a global
scientific meeting. Geneva WHO/PBL/96, 56.
85. WHO. Primary health care level management of trachoma. Geneva
WHO/PBL/93, 33.
86. WHO Expert Committee on Leprosy. Seventh Report, WHO Tech.
Rep. Sr. 1998;874.
87. WHO Expert Committee report on Leprosy. Sixth report, WHO
Tech Rep Sr 1988;768.
88. WHO stydy group. Chemotherapy of leprosy, WHO technical
report, Series No. 84, Geneva 1994.
89. Wilson GS, Miles AA. Topley and Wilson’s principles of
bacteriology and immunity (4th edn), William and Wilkins,
Baltimore, 1955.
INDEX
A Carriers 3
Actinomyces 55 Cestodes 161
Adenoviruses 87 Chlamydiae 69
Adherence 8 Clostridium 46
Anthrax 45 Collection of specimens 176
Ascomycetes 104 Commensals 4, 10
Aspergillus 104 Conjunctival swab 178
Atypical mycobacteria 52 Corneal scrapping 178
Corynebacterium 40
B Cross-infection 2
Bacteria 16 Culture for microbes 181
classification 20, 21 Culture of material 179
morphology 16 Cysticercus 163
arrangement 17 Cytomegalovirus 85
capsule 18
D
cell wall 17
fimbriae pili 18 Deuteromycetes 104
flagella 18 Dimorphic fungi 104
shape 16 Dirofilaria 159
size 16 DNA viruses 80
spores 19 pox viruses 80
oxygen requirement 19 variola 80
visualization 20 Dog tapeworm 168
Baylis ascaris 149 Dracunculus medinensis 160
Bell’s phenomenon 13 Drug resistance 189
Blastomyces 106
E
Blink reflex 13
Bordetella pertussis 64 Echinococcus 168
Borrelia 67 Endoparasite 5
Branhamella catarrhalis 35 Endotoxins 8
Enterobacteriaceae 60
C Epstein-Barr virus 86
Candida monilia 106 Escherichia 60
Capsule 18 Fimbriae 18
198 OCULAR MICROBIOLOGY
S Treponema 65
Salmonella 62 Trichinella 147
Saprophytes 3, 10 Tube dilution method 190
Secondary infection 2 Type of carriers 3
Shigella 62
V
Source of infection 5
Spirochetes 64 Vaccinia 81
Spores 19 Varicella zoster virus 84
Staining methods 22 Virulence 9
Staphylococci 26 Virus isolation 84
Streptococci 29 Viruses 74
T cellular changes 79
classification 76
Taenia multiceps coenurus 171
cultivation 77
classification 173
mode of transmission 173 diagnosis of viral disease 79
Thelazia 147 infection 78
Toxocara 144 morphology 75
Toxoplasma 131 multiplication 77
demonstration of organism W
138
diagnosis 137 Welchii (perfringens) 47
differential diagnosis 137 Wuchereria bancrofti 156
oocytes sporozoites 135
Y
route of infection 137
tissue cysts cytozoites 134 Yeasts 103