MCB 102 LECTURE NOTE

Introduction
Microbiology is the scientific study of all living organisms that are too small to be visible
with the naked eye unless by the use of microscope. They are generally 1 millimetre or less in
diameter which includes bacteria, viruses, fungi, protozoa and algae, they are collectively
known as microbes. These microbes play key roles in nutrient cycling,
biodegradation/biodeterioration, food spoilage, cause of diseases, control/treatment of
diseases and also inhabit our body as normal flora.

Brief history of Microbiology

Antony van Leeuwenhoek (1632-1723) of Delft, the Netherlands. Leeuwenhoek earned his
living as a draper and haberdasher (a dealer in men's clothing and accessories) but spent
much of his spare time constructing simple microscopes composed of double convex glass
lenses held between two silver plates. His microscopes could magnify about 50 to 300 times.
In 1674 he likely observed protozoa for the first time and several years’ later bacteria. He
called these very little creatures as ‘animalcules’ he was able to observed them from
different sources, such as rainwater, pond, well water, human mouth and intestine.
Leeuwenhoek sent detailed letters describing his discoveries to the Royal Society of London.
It is clear from his descriptions that he saw both bacteria and protozoa.

Spontaneous Generation
After van Leeuwenhoek discovered the previously “invisible” world of microorganisms, the
scientific community of the time became interested in the origins of these tiny living things.
Until the second half of the nineteenth century, many scientists and philosophers believed
that some forms of life could arise spontaneously from nonliving matter; they called this
hypothetical process spontaneous generation.
1. This view finally was challenged by the Italian physician Francesco Redi (1626-1697), who
carried out a series of experiments on decaying meat and its ability to produce maggots
spontaneously. Redi placed meat in three containers. One was uncovered, a second was
covered with paper, and the third was covered with fine gauze that would exclude flies. Flies
laid their eggs on the uncovered meat and maggots developed. The other two pieces of meat
did not produce maggots spontaneously. However, flies were attracted to the gauze-covered
container and laid their eggs on the gauze; these eggs produced maggots. Thus the generation
of maggots by decaying meat resulted from the presence of fly eggs, and meat did not
spontaneously generate maggots, as previously believed.
2. In 1748 the English priest John Needham (1713-1781) reported the results of his experiments
on spontaneous generation. Needham boiled mutton broth in flasks that he then tightly closed.
Eventually many of the flasks became cloudy and contained microorganisms. He thought
organic matter contained a vital force that could confer the properties of life on nonliving
matter.
3. A few years later, the Italian priest and naturalist Lazzaro Spallanzani (1729-1799) improved
on Needham's experimental design by first sealing glass flasks that contained water and seeds.
If the sealed flasks were placed in boiling water for about 45 minutes, no growth took place as

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 long as the flasks remained sealed. He proposed that air carried germs to the culture medium
but also commented that the external air might be required for growth of animals already in the
medium. The supporters of spontaneous generation maintained that heating the air in sealed
flasks destroyed its ability to support life. Several investigators attempted to counter such
arguments.
4. Louis Pasteur (1822-1895) was the first scientist to settle the matter of spontaneous
generation. Pasteur first filtered air through cotton and found that objects resembling plant
spores had been trapped. If a piece of the cotton was placed in sterile medium after air had
been filtered through it, microbial growth occurred. Next he placed nutrient solutions in flasks,
heated their necks in a flame, and drew them out into a variety of curves. The swan-neck flasks
that he produced in this way had necks open to the atmosphere. Pasteur then boiled the
solutions for a few minutes and allowed them to cool. No growth took place even though the
contents of the flasks were exposed to the air. Pasteur pointed out that growth did not occur
because dust and germs had been trapped on the walls of the curved necks. If the necks were
broken, growth commenced immediately. Pasteur had not only resolved the controversy by
1861 but also had shown how to keep solutions sterile.

The Golden Age of Microbiology

The period from 1857 to 1914 has been appropriately named the Golden Age of
Microbiology. During this period, rapid advances, spearheaded mainly by Pasteur and Robert
Koch, led to the establishment of microbiology as a science. Some of the major events that
occurred during the Golden Age of Microbiology are:
1. Louis Pasteur a French Microbiologist, is known as the father of medical microbiology for
his immense contributions to the field of medical microbiology. He first coined the term
“microbiology” for the study of organisms of microscopic size. some of his important
contributions are: Germ theory of disease, Pasteurization, fermentation, Vaccination.
2. Robert Koch: The Founder of Koch’s Postulates. The first direct demonstration of the role of
bacteria in causing disease came from the study of anthrax by the German physician Robert
Koch (1843–1910). Koch used the criteria proposed by his former teacher, Jacob Henle
(1809–1885), to establish the relationship between B. anthracis and anthrax, and he published

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 his findings in 1876 briefly describing the scientific method he followed. He also developed
Solid medium for culture of bacteria.
3. Joseph Lister (The Pioneer of Antiseptics): Indirect evidence that microorganisms are the
agents of human disease came from the work of an English surgeon Joseph Lister (1827–
1912) on the prevention of wound infections. Lister, impressed with Pasteur’s studies on the
involvement of microorganisms in fermentation and putrefaction, developed a system of
antiseptic surgery designed to prevent microorganisms from entering wounds. Instruments
were heat sterilized and phenol was used on surgical dressings and at times sprayed over the
surgical area. The approach was remarkably successful and transformed surgery after Lister
published his findings in 1867. It also provided strong indirect evidence for the role of
microorganisms in disease because phenol, which killed bacteria, also prevented wound
infections.

General characteristics of microorganisms

There are five important groups of microorganism studied by microbiologist, these includes:
Bacteria, Fungi, Virus, Algae and protozoan.

BACTERIA
General characteristics of bacteria
1. Most are microscopic in nature
2. All bacteria are fundamentally single-celled (unicellular).
3. Bacteria are prokaryote: the genetic material (DNA) exists unbound in the cytoplasm of
the cells i.e. there is no nuclear membrane and the genetic material exist in form of
nucleoid.
4. They have three basic forms: cocci (round), bacilli (rod), and curved or spiral (coma or
spring).
5. Bacteria reproduce asexually by the process of cell division called binary fission.
6. Enzymes for cellular respiration are bound to the cell membranes.
7. The cell wall of bacteria is made up of Peptidoglycan also known as murein.
8. They have 70s ribosomes
9. Few of them are pathogens i.e. they cause diseases in plants and animals. Many bacteria
are saprophytes which means, they live on dead and decaying matter. While others are
symbiotic i.e. they live in give and take relationships with other animals

FUNGI
General characteristics of fungi
1. They are eukaryote i.e. they have true nucleus, their DNA is bound by a nuclear
membrane.
2. Fungi exist in the form of multicellular filaments or unicellular yeast form.
3. They also have ergosterols in their cell membrane
4. Possesses 80S ribosomes.
5. All fungi possess a rigid cell wall containing complex polysaccharides called chitin.
6. Most are non-motile, a feature that separates them from animals.

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7. Require organic compounds for both carbon and energy sources
8. Fungi are osmotrophic i.e. they obtain their nutrients by absorption.
9. They obtain nutrients as saprobes, which means, they live on dead and decaying matter.
10. Most are plants pathogen while other are opportunistic pathogen of humans
11. Most fungi require water and oxygen.
12. They typically reproduce asexually and/or sexually by producing spores.
13. They grow either reproductively by budding or non-reproductively by hyphal tip
elongation.

VIRUS

General characteristics of virus

1. All viruses are obligate intracellular parasites; when inside a host cell, viruses show some
of the features of a living organism, such as the ability to replicate themselves, but
outside the cell they are just inert chemical.
2. Viruses are much smaller than prokaryotic or eukaryotic cells therefore they cannot be
observed using a light microscope.
3. They have no internal cellular structure i.e. unlike cells; they have a generally simple and
static structure.
4. They contain either DNA or RNA, but not both
5. They are incapable of replication unless occupying an appropriate living host cell i.e.
they depend upon the machinery of the host cell for replication (obligate intracellular
parasites).
6. Some viruses (bacteriophages) infect prokaryotic cells, while others infect eukaryotic
cells.
7. Some viruses destroy cells, producing disease; other persists in infected cells either in a
latent or persistent state; and other may cause cellular malignant transformation.

ALGAE

General characteristics of algae

1. Algae include both microscopic unicellular members and macroscopic multicellular

organisms.
2. All algal types are eucaryotic, and therefore contain the internal organelles that is,
nuclei, mitochondria, endoplasmic reticulum, ribosomes, Golgi body, and in most
instances, chloroplasts.
3. Most algae are found in the ocean. Their locations depend on the availability of
appropriate nutrients, wavelengths of light, and surfaces on which they can grow.
4. Algae contain chlorophyll, which is necessary for photosynthesis (photoautotrophs). In
addition, many algae contain other pigments that extend the range of light waves that
can be used by these organisms for photosynthesis.

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 5. Algae lack organized vascular system and have relatively simple reproductive
structures (What distinguishes algae from other eukaryotic photosynthetic organisms
such as land plants).
6. Algae do not directly infect humans, but some produce toxins that cause paralytic
shellfish poisoning. Some of these toxins do not cause illness in the shellfish that feed
on the algae but accumulate in their tissues. When the shellfish are eaten by humans the
toxins cause nerve damage.
7. Algal cell walls are rigid and for the most part composed of cellulose, often associated
with pectin.

PROTOZOA

General characteristics of protozoa

1. Protozoa are microscopic, unicellular organisms that lack photosynthetic capability

2. They are all eukaryotic organisms.
3. Majority are free-living, the group also includes commensal forms and some extremely
important parasites of animals and humans.
4. Most protozoans are found in freshwater or marine habitats
5. One of the most characteristic structural features of protozoans is the contractile
vacuole, whose role is to pump out excess amounts of water that enter the cell by
osmosis.
6. Most protozoans have a heterotrophic mode of nutrition, typically ingesting particulate
food such as bacteria, and digesting them in phagocytic vacuoles. Since they actively
‘hunt’ their food rather than simply absorbing it across the cell surface,
7. It is not surprising that the majority of protozoans are capable of movement at least at
some stage in their life cycle, and the structural features used to achieve locomotion
(e.g. cilia, flagella) are among the characteristics used to classify the protozoans.

BACTERIAL DISEASES OF MEDICAL SIGNIFICANCE

1. STAPHYLOCOCCAL DISEASES

Staphylococcus aureus (S. aureus), the most virulent of the many staphylococcal species, has
demonstrated its versatility by remaining a major cause of morbidity and mortality despite the
availability of numerous effective antistaphylococcal antibiotics. S. aureus is capable of
causing disease through both toxin-mediated and non–toxin-mediated mechanisms. This
organism is responsible for both nosocomial and community-based infections that range from
relatively minor skin and soft tissue infections to lifethreatening systemic infections.

Microbiology and taxonomy

Staphylococci, gram-positive cocci in the family Micrococcaceae, form grapelike clusters on
Gram’s stain. These organisms are catalase-positive (unlike streptococcal species), nonmotile

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and facultatively anaerobic. They are capable of prolonged survival on environmental
surfaces in varying conditions. More than 30 staphylococcal species are pathogenic. S. aureus
is distinguished from other staphylococcal species by its production of coagulase, a surface
enzyme that converts fibrinogen to fibrin.

S. aureus infections epidemiology

S. aureus is a part of the normal human flora; healthy persons may be persistently or
transiently colonized. The rate of colonization is higher among patients with insulin-
dependent diabetes, HIV-infected patients, patients undergoing hemodialysis, and individuals
with skin damage.

The anterior nares are the most frequent site of human colonization, although the skin
(especially when damaged), vagina, axilla, perineum, and oropharynx may also be colonized.
These colonization sites serve as a reservoir of strains for future infections, and persons
colonized with S. aureus are at greater risk of subsequent infection than are uncolonized
individuals.

However, S. aureus may also be acquired from other people or from environmental
exposures. Transmission most frequently results from transient colonization of the hands of
hospital personnel, who then transfer strains from one patient to another.

Clinical Syndromes
The diseases caused by S. aureus can be divided into two groups: (a) inflammatory and (b)
toxin-mediated staphylococcal diseases.

Inflammatory staphylococcal diseases

These include the following conditions:
1. Staphylococcal skin infections include:

i. Impetigo: red sores on face and affect mainly infant and children
ii. Folliculitis: inflammation of hair follicles, tender and swollen on the neck, breast, buttocks
and face
iii. Furuncles: painful, pus-filled bump under the skin caused by infected inflamed hair
follicles
iv. Carbuncles: a group of pus filled bumps forming connected area of infection under the
skin often occur on the back of the neck, shoulders or thights,
v. Paronychia: infection of tissue adjacent to the nail, surgical wound infection, blepharitis
(eyelid inflamation), and postpartum breast infection.

2. Bacteremia and septicemia may occur from any localized lesion, especially wound
infection or as a result of intravenous drug abuse.
3. S. aureus is an important cause of acute bacterial endocarditis
4. S. aureus is the most common cause of osteomyelitis in children. The bacteria reach bone
through blood stream or by direct implantation following trauma.

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 5. S. aureus causes pneumonia in postoperative patients following viral respiratory
infection, leading to empyema; it also leads to chronic sinusitis.
6. S. aureus causes deep-seated abscesses in any organ after bacteremia.

Toxin-mediated staphylococcal diseases

These include (a) staphylococcal food poisoning, (b) staphylococcal toxic shock syndrome,
and (c) staphylococcal scalded skin syndrome.
1. Staphylococcal food poisoning: Staphylococcal food poisoning is caused by
enterotoxin. The enterotoxin is a preformed toxin, already present in the contaminated
food before consumption. Milk and milk products and animal products like fish and meat
kept at room temperature after cooking are mainly incriminated. When kept at room
temperature, the contaminating staphylococci multiply and produce toxin adequate
enough to cause food poisoning. It is a self-limiting condition characterized by nausea,
vomiting, abdominal cramps, and watery, non-bloody diarrhea.
2. Staphylococcal toxic shock syndrome: Staphylococcal toxic shock syndrome (STSS) is
caused by TSST. The STSS is an acute and potentially life-threatening condition similar
to Gram-negative sepsis and septic shock. STSS is a multisystem disease characterized
by fever, hypotension, myalgia, vomiting, diarrhea, mucosal hyperemia, and an
erythematous rash followed by desquamation of the skin, particularly on palms and soles.
3. Staphylococcal scalded skin syndrome: Staphylococcal scalded skin syndrome (SSSS)
is caused by the exfoliative toxin, exfoliatin. The condition is seen commonly in infants
and children. It is associated with extensive exfoliation of the skin, in which outer layer
of the epidermis is separated from the underlying tissue and is characterized by the
appearance of extensive bullae. These bullae when ruptured may leave behind scalded,
red, tender skin.

Prevention
Prevention of the spread of S. aureus infections in the hospital setting involves hand washing
and careful attention to appropriate isolation procedures. The use of topical antimicrobial
agents (e.g.,mupirocin) to eliminate nasal colonization with S. aureus and to prevent
subsequent infection has been investigated in a number of clinical settings. Elimination of
nasal carriage of S. aureus has reduced the incidence of infections among patients undergoing
hemodialysis and peritoneal dialysis.

2. ENTERIC (TYPHOID) FEVER

Typhoid fever, or enteric fever, is a potentially fatal multi-systemic infection produced

primarily by Salmonella typhi and to a lesser extent Salmonella paratyphi A, B and C.
Salmonella is gram negative rod, motile and part of the member of enterobacteriaceae that
can produce variety of gastrointestinal infections. The most serious of these is typhoid fever.

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 Mode of transmission
The transmission commonly occurs through food or water contaminated by faeces of ill or
asymptomatic chronic carriers. Health care workers occasionally acquire enteric fever after
exposure to infected patients or during processing of clinical specimens and cultures. Risk
factors include contaminated water or ice, flooding, food and drinks purchased from street
vendors, raw fruits and vegetables grown in fields fertilized with sewage,

Clinical manifestation of typhoid fever

The clinical manifestation of typhoid fever includes; fever that can be as high as 39 – 40oC,
weakness, stomach pain, headache, diarrhoea or constipation, cough, loss of appetite

Prevention and Control

Improvements in food handling and water/ sewage treatment. Theoretically, it is possible to
eliminate the salmonellae that cause enteric fever since they survive only in human hosts and
are spread by contaminated food and water. However, given the high prevalence of the
disease in developing countries that lack adequate sewage disposal and water treatment, this
goal is currently unrealistic.

3. SHIGELLOSIS

Etiologic agent of Shigellosis

The etiologic agent of shigellosis is Shigella dysenteriae, a gram negative, rod shape bacteria
and a member of enterobacteriaceae, the discovery of Shigella as the etiologic agent of
dysentery is attributed to the Japanese microbiologist Kiyoshi Shiga, who isolated the Shiga
bacillus (now known as Shigella dysenteriae) from patients’ stools in 1897 during a large and
devastating dysentery epidemic.

Mode of transmission
The human intestinal tract represents the major reservoir of Shigella. Because excretion of
shigellae is greatest in the acute phase of disease, the bacteria are transmitted most efficiently
by the fecal-oral route. Most cases of shigellosis are caused by person-to-person transmission,
although some outbreaks reflect contamination of water or food. Shigella can also be
transmitted by flies and, given its capacity to survive in foodstuffs, can be a significant cause
of food-borne infection.

Clinical manifestations
The clinical manifestation of shigellosis are: fever, intestinal cramps, and frequent passage of
small, bloody, mucopurulent stools. The incubation period usually lasts 1–4 days but may be
as long as 8 days.

Prevention
Hand washing after defecation or handling of children’s feces and before handling of food is
recommended.

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4. CHOLERA

Cholera is an acute diarrheal disease that can in a matter of hours, result in profound, rapidly
progressive dehydration and death.

Etiologic agent of Cholera

The etiologic agent of cholera is Vibrio. cholerae serogroup O1. In 1992, however, a new
serogroup (O139) that causes epidemic cholera emerged on the Indian subcontinent and has
since killed thousands of people

Mode of transmission
Ingestion of water contaminated by human feces is the most common means of acquisition of
V. cholerae. Consumption of contaminated food can also contribute to spread. There is no
known animal reservoir.

Clinical manifestation
Cholera begins with the sudden onset of painless watery diarrhea that may quickly become
voluminous and is often followed shortly by vomiting. In severe cases, stool volume can
exceed 250 mL/kg in the first 24 h. If fluids and electrolytes are not replaced, hypovolemic
shock and death ensue. Fever is usually absent. Muscle cramps due to electrolyte
disturbances are common. The stool has a characteristic appearance: gray, slightly cloudy
fluid with flecks of mucus, no blood, and a somewhat sweet, inoffensive odor. It has been
called “rice-water” stool because of its resemblance to the water in which rice has been
washed.

Prevention and Control

Provision of safe water and facilities for sanitary disposal of feces, improved nutrition, and
attention to food preparation and storage in the household can significantly reduce the
incidence of cholera.
5. TUBERCULOSIS

Tuberculosis, one of the oldest diseases known to affect humans, is a major cause of death
worldwide. It usually affects the lungs, although other organs are involved in up to one-third
of cases. If properly treated, tuberculosis caused by drug-susceptible strains is curable in
virtually all cases. If untreated, the disease may be fatal within 5 years in 50–65% of cases.

Etiologic agents
Tuberculosis is caused by bacteria of the Mycobacterium tuberculosis complex which
includes Mycobacterium tuberculosis, Mycobacterium bovis, Mycobacterium bovis BCG
and Mycobacterium africanum,

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 Mode of transmission
Mycobacterium tuberculosis is most commonly transmitted from a person with infectious
pulmonary tuberculosis to others by droplet nuclei, which are aerosolized by coughing,
sneezing, or speaking. The tiny droplets dry rapidly; the smallest (5–10 µm in diameter) may
remain suspended in the air for several hours and may reach the terminal air passages when
inhaled. There may be as many as 3000 infectious nuclei per cough.

Clinical manifestations
Fatigue, weakness, weight loss, fever, night sweats. In more severe cases: chronic cough and
spitting of blood

Prevention
By far the best way to prevent tuberculosis is to diagnose and isolate infectious cases rapidly
and administer appropriate treatment until patients are rendered non-infectious and the
disease is cured. Additional strategies include BCG vaccination and treatment of persons with
latent tuberculosis infection who are at high risk of developing active disease.

6. TETANUS

Tetanus is a neurologic disorder, characterized by increased muscle tone and spasms, that is
caused by tetanospasmin, a powerful protein toxin elaborated by Clostridium tetani. Tetanus
occurs in several clinical forms, including generalized, neonatal, and localized disease.

Etiologic agent
Clostridium tetani is an anaerobic, motile, gram-positive rod. The organism is found
worldwide in soil, in the inanimate environment, in animal feces, and occasionally in human
feces. Spores may survive for years in some environments and are resistant to various
disinfectants and to boiling for 20 min. Vegetative cells, however, are easily inactivated and
are susceptible to several antibiotics, including metronidazole and penicillin. Tetanospasmin
is formed in vegetative cells.

Mode of transmission
Tetanus is common in areas where soil is cultivated, in rural areas, in warm climates, during
summer months; most cases of tetanus follow an acute injury (puncture wound, laceration,
abrasion, or other trauma). Tetanus may be acquired indoors or during outdoor activities (e.g.,
farming, gardening). Tetanus has also been associated with burns, frostbite, middle-ear
infection, surgery, abortion, childbirth, body piercing, and drug abuse (notably “skin
popping”). Recurrent tetanus has been reported.

Clinical manifestations
i. Typically, the patient first notices spasm of the mastication muscles in the jaw that limits
the opening of the mouth and it is called trismus, or lockjaw

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 ii. Dysphagia or stiffness and pain in the neck, shoulder, and back muscles appears
concurrently or soon thereafter.
iii. The subsequent involvement of other muscles produces a rigid abdomen and stiff
proximal limb muscles.
iv. Sustained contraction of the facial muscles results in a grimace (risus sardonicus), and
v. Contraction of the back muscles produces an arched back (opisthotonos).

Prevention

All partially immunized and unimmunized adults should receive vaccine, as should those
recovering from tetanus. The primary series for adults consists of three doses: the first and
second doses are given 4–8 weeks apart, and the third dose is given 6–12 months after the
second. A booster dose is required every 10 years and may be given at mid-decade ages—35,
45, and so on

7. Bacterial pneumonia

Bacterial pneumonia (from the Greek pneuma, “breath”) is a potentially fatal infection and
inflammation of the lower respiratory tract (i.e., bronchioles and alveoli) usually caused by
inhaled bacteria. Pneumonia that develops outside the hospital setting is commonly referred
to as community-acquired pneumonia. Pneumonia that develops 48 hours or later after
admission to the hospital is known as nosocomial or hospital acquired pneumonia.

Causative agent of bacterial pneumonia

Many types of bacteria can cause pneumonia which includes:

Mode of transmission
Bacteria reach the lung by one of four routes:
1. Inhalation of microorganisms that have been released into the air when an infected
individual coughs or sneezes
2. Aspiration of bacteria from the upper airways
3. Spread from contiguous infected sites
4. Hematogenous spread

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 Clinical manifestation
The illness is frequently characterized by high fever, shortness of breath (dyspnea), rapid
breathing, sharp chest pain, and a productive cough.

Prevention
Vaccine, good hygiene (washing your hands often), and quitting smoking,

8. MENINGITIS

Meningitis is an inflammation of the covering of the brain and spinal cord. It can be caused
by viruses, parasites, fungi, and bacteria. Viral meningitis is most common and the least
serious. Meningitis caused by bacteria is the most likely form of the disease to cause serious,
long-term complications. It is an uncommon disease but requires urgent treatment with
antibiotics to prevent permanent damage or death.

Causative agents of meningitis

Bacterial meningitis can be caused by multiple organisms. Two common types are
Streptococcus pneumoniae, with over 80 serogroups that can cause illness, and Neisseria
meningitidis, with five serogroups that most commonly cause meningitis.

Mode of transmission
The bacteria are spread when people exchange saliva (such as by kissing; sharing drinking
containers, utensils, or cigarettes) or when people cough or sneeze without covering their
mouth and nose. The bacteria do not cause meningitis in most people. Instead, most people
become carriers of the bacteria for days, weeks or even months. The bacteria rarely
overcome the body’s immune system and cause meningitis or another serious illness.

Clinical manifestations of bacterial meningitis

Children (over 1 year old) and adults with meningitis may have a severe headache, high
temperature, vomiting, sensitivity to bright lights, neck stiffness, and drowsiness or
confusion. In both children and adults, there may be a rash of tiny, red-purple spots. These
can occur anywhere on the body.

Prevention
Bacterial meningitis caused by Streptococcus pneumoniae and Neisseria meningitidis may be
prevented through vaccination. The vaccine which protects against Streptococcus
pneumoniae is called pneumococcal conjugate vaccine or PCV. Do not share utensils,
toothbrushes, or cigarettes. Wash your hands. Limit the number of persons you kiss. Cover
your mouth and nose when you sneeze or cough. Maintaining healthy habits, like getting
plenty of rest and not having close contact with people who are sick.

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9. URINARY TRACT INFECTION (UTI)

A urinary tract infection (UTI) is an infection in any part of the urinary system. The urinary
system includes the kidneys, ureters, bladder and urethra. Most infections involve the lower
urinary tract i.e the bladder (cystitis) and the urethra (urthritis). Women are at greater risk of
developing a UTI than are men. If an infection is limited to the bladder, it can be painful and
annoying. But serious health problems can result if a UTI spreads to the kidneys
(pyelonephritis).

Causative agents of UTI

The causative agents of UTI includes: Escherichia coli, Klebsiella pneumoniae, proteus
mirabilis, Pseudomonas aeruginosa and other gram negative rod bacteria.

Clinical manifestation of UTI

UTIs don't always cause symptoms. When they do, they may include:

1. A strong urge to urinate that doesn't go away (urgency)

2. A burning feeling when urinating (dysuria)
3. Urinating often, and passing small amounts of urine (frequency)
4. Urine that looks cloudy
5. Urine that appears red, bright pink or cola-colored - signs of blood in the urine
(hematuria)
6. Strong-smelling urine
7. Pelvic pain, in women - especially in the center of the pelvis and around the area of the
pubic bone
8. If the infection reached the kidney, the patient may experience diarrhea, nausea,
vomiting, chills, lower back pain, pain in the groin, pain in the side and fever

Prevention
These steps may help lower the risk of UTIs:

1. Drink plenty of liquids, especially water. Drinking water helps dilute the urine. That
leads to urinating more often allowing bacteria to be flushed from the urinary tract before
an infection can begin.
2. Empty your bladder soon after having sex. Also drink a full glass of water to help flush
bacteria.
3. Avoid potentially irritating feminine products. Using them in the genital area can irritate
the urethra. These products include deodorant sprays, douches and powders.

10.MYCOPLASMA

Mycoplasmas are the smallest, free living organisms; many are as small as 0.3μm in
diameter. Their most striking feature is the absence of a cell wall. Consequently,
mycoplasmas stain poorly with Gram stain, and antibiotics that inhibit cell wall

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 (peptidoglycan) synthesis (e.g., penicillins and cephalosporins) are ineffective. Their outer
surface is a flexible cell membrane; hence, these organisms can assume a variety of shapes. It
is the only bacterial membrane that contains cholesterol, a sterol usually found in eukaryotic
cell membranes. Mycoplasmas can be grown in the laboratory on artificial media, but they
have complex nutritional requirements, including several lipids. They grow slowly and
require at least 1 week to form a visible colony. The colony frequently has a characteristic
“fried egg” shape, with a raised center and a thinner outer edge.

MYCOPLASMA PNEUMONIAE
Causative agent
Mycoplasma pneumonia is cause by Mycoplasma pneumoniae, a pathogen only for humans,

Mode of transmission
The organism is transmitted by respiratory droplets.

Clinical Findings
Mycoplasma pneumonia is the most common type of atypical pneumonia. The term atypical
means that a causative bacterium cannot be isolated on routine media in the diagnostic
laboratory or that the disease does not resemble pneumococcal pneumonia. The onset of
Mycoplasma pneumonia is gradual, usually beginning with a non productive cough, sore
throat, or ear ache. Small amounts of whitish, non bloody sputum are produced.
Constitutional symptoms of fever, headache, malaise, and myalgias are pronounced. In
addition to pneumonia, M. pneumoniae also causes bronchitis.

Prevention
There is no vaccine or other specific preventive measure, but maintaining healthy habits may
be helpful

Other Mycoplasmas
Mycoplasma hominis has been implicated as an infrequent cause of pelvic inflammatory
disease. Mycoplasma genitalium causes urethritis, predominantly in men. Infections in
women are typically asymptomatic but cervicitis may occur.

11.Chlamydiae

Chlamydiae are obligate intracellular bacteria (i.e., they can grow only within cells). They
lack the ability to produce sufficient energy to grow independently and therefore can grow
only inside host cells. They have a rigid cell wall but do not have a typical peptidoglycan
layer. Their cell walls resemble those of gram negative bacteria but lack muramic acid. They
are the agents of common sexually transmitted diseases, such as urethritis and cervicitis, as
well as other infections, such as pneumonia, psittacosis, trachoma, and lymphogranuloma
venereum.

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 Spectrum of diseases
Chlamydia trachomatis causes eye (conjunctivitis, trachoma), respiratory (pneumonia), and
genital tract (urethritis, lymphogranuloma venereum) infections. C. trachomatis is the most
common bacterial cause of sexually transmitted disease. Infection with C. trachomatis is also
associated with Reiter’s syndrome, an autoimmune disease.

Chlamydia pneumoniae and Chlamydia psittaci causes pneumonia and psittacosis

respectively and are sufficiently different molecularly from C. trachomatis that they have
been reclassified into a new genus called Chlamydophila. Taxonomically, they are now
Chlamydophila pneumoniae and Chlamydophila psittaci. However, from a medical
perspective, they are still known as C. pneumoniae and C. psittaci,

Transmission
1. Chlamydia trachomatis infects only humans and is usually transmitted by close personal
contact (e.g., sexually or by passage through the birth canal). Individuals with asymptomatic
genital tract infections are an important reservoir of infection for others. In trachoma, C.
trachomatis is transmitted by finger to eye or fomite to eye contact.
2. Chlamydia pneumoniae infects only humans and is transmitted from person to person by
aerosol.

3. Chlamydia psittaci infects birds (e.g., parrots, pigeons, and poultry, and many mammals
including humans). Humans are infected primarily by inhaling organisms in airborne dry bird
feces.

Prevention
There is no vaccine against any chlamydial disease. The best preventive measure against C.
trachomatis sexually transmitted diseases is to limit transmission by safe sex practices and
prompt treatment of both the patient and the sexual partners, including persons who are
asymptomatic. Sexual contacts should be traced, and those who had contact within 60 days
should be treated. Screening of sexually active, asymptomatic young women and treatment of
those who are positive is cost effective because it may prevent PID and ectopic pregnancy.
Several types of sexually transmitted diseases are often present simultaneously. Thus,
diagnosis of one requires a search for other causative agents. Oral erythromycin given to
newborn infants of infected mothers can prevent inclusion conjunctivitis and pneumonitis
caused by C. trachomatis. Note that erythromycin ointment used to prevent neonatal
gonococcal conjunctivitis is much less effective against neonatal chlamydial conjunctivitis.
Oral erythromycin should be used.

12.Rickettsiae

Rickettsiae are obligate intracellular bacteria, they are unable to produce sufficient energy to
replicate extracellularly. Therefore, rickettsiae must be grown in cell culture, embryonated
eggs, or experimental animals. Rickettsiae divide by binary fission within the host cell and

15
are very short rods that are barely visible in the light microscope. Structurally, their cell wall
resembles that of gram negative rods, but they stain poorly with the standard Gram stain. .

They are the agents of several important diseases, namely

1. Typhus: There are several forms of typhus, namely, louse borne epidemic typhus caused
by R. prowazekii, flea borne endemic typhus caused by R. typhi, chigger borne scrub typhus
caused by Orientia tsutsugamushi, and several other quite rare forms such as flea borne
endemic typhus, also called murine typhus.
2. Spotted fevers such as Rocky Mountain spotted fever (cause by Rickettsia rickettsii), Q
fever (cause by Coxiella burnetii), ehrlichiosis (Ehrlichia chaffeensis), and anaplasmosis
(Anaplasma phagocytophilum). Other less important rickettsial diseases such as endemic and
scrub typhus occur primarily in developing countries.

Transmission
They are transmitted to humans by the bite of the arthropod (such as ticks, lice, fleas, and
mites, with the exception Coxiella burnetii, the cause of Q fever, which is transmitted by
aerosol and inhaled into the lungs). The rickettsiae circulate widely in the bloodstream
(bacteremia), infecting primarily the endothelium of the blood vessel walls. Virtually all
rickettsial diseases are zoonoses (i.e., they have an animal reservoir), with the prominent
exception of epidemic typhus, which occurs only in humans. It occurs only in humans
because the causative organism, R. prowazekii, is transmitted by the human body louse.

Clinical Findings
Rocky Mountain Spotted Fever
This disease is characterized by the acute onset of nonspecific symptoms which includes
fever, severe headache, myalgias, rash, which on the hands and feet and then moves inward
to the trunk. In addition to headache, other profound central nervous system changes such as
delirium and coma can occur.

Typhus
Typhus begins with the sudden onset of chills, fever, headache, and other influenza like
symptoms approximately 1 to 3 weeks after the louse bite occurs. Between the fifth and ninth
days after the onset of symptoms, a maculopapular rash begins on the trunk and spreads
peripherally. The rash becomes petechial and spreads over the entire body but spares the face,
palms, and soles. Signs of severe meningoencephalitis, including delirium and coma, begin
with the rash and continue into the second and third weeks. In untreated cases, death occurs
from peripheral vascular collapse or from bacterial pneumonia.

Prevention
Prevention of many of these diseases is based on reducing exposure to the arthropod vector
by wearing protective clothing and using insect repellent. Frequent examination of the skin
for ticks is important in preventing Rocky Mountain spotted fever; the tick must be attached
for several hours to transmit the disease. There is no vaccine against Rocky Mountain spotted
fever. Prophylactic antibiotics are not recommended in the asymptomatic person bitten by a

16
 tick. Prevention of typhus is based on personal hygiene and “delousing” with DDT. A typhus
vaccine containing formalin killed R. prowazekii organisms is effective and useful in the
military during war time.

13.TREPONEMA

Three genera of spirochetes cause human infection: (1) Treponema, which causes syphilis
and the nonvenereal treponematoses (2) Borrelia, which causes Lyme disease and relapsing
fever and (3) Leptospira, which causes leptospirosis. Spirochetes are thin walled, flexible,
spiral rods. They are motile through the undulation of axial filaments that lie under the outer
sheath. Treponemes and leptospirae are so thin that they are seen only by dark field
microscopy, silver impregnation, or immunofluorescence. Borreliae are larger, accept Giemsa
and other blood stains, and can be seen in the standard light microscope.

Treponema Pallidum
Treponema pallidum causes syphilis. T. pallidum has not been grown on bacteriologic media
or in cell culture. Nonpathogenic treponemes, which are part of the normal flora of human
mucous membranes, can be cultured. T. pallidum grows very slowly. The medical importance
of that fact is that antibiotics must be present at an effective level for several weeks to kill the
organisms and cure the disease.

Transmission
T. pallidum is transmitted from spirochete containing lesions of skin or mucous membranes
(e.g., genitalia, mouth, and anus) of an infected person to other persons by intimate contact. It
can also be transmitted from pregnant women to their fetuses. Rarely, blood for transfusions
collected during early syphilis is also infectious. T. pallidum is a human organism only. There
is no animal reservoir.

Clinical Findings
Stages of syphilis include:
1. Primary syphilis, the spirochetes multiply at the site of inoculation, and a local, non tender
ulcer (chancre) usually forms in 2 to 10 weeks. The ulcer heals spontaneously, but
spirochetes spread widely via the bloodstream (bacteremia) to many organs.
2. Secondary syphilis, between one to three months later, the lesions of secondary syphilis may
occur. These often appear as a maculopapular rash, notably on the palms and soles, or as
moist papules on skin and mucous membranes (mucous patches). Moist lesions on the
genitals are called condylomata lata. These lesions are rich in spirochetes and are highly
infectious, but they also heal spontaneously. Patchy alopecia also occurs. Constitutional
symptoms of secondary syphilis include low grade fever, malaise, anorexia, weight loss,
headache, myalgias, and generalized lymphadenopathy. Pharyngitis, meningitis, nephritis,
and hepatitis may also occur. In some individuals, the symptoms of the primary and
secondary stages may not occur, and yet the disease may progress.

17
 About one third of these early (primary and secondary) syphilis cases will “cure” themselves,
without treatment. Another third remain latent (i.e., no lesions appear, but positive serologic
tests indicate continuing infection). The latent period can be divided into early and late
stages. In the early latent period, which can last for 1 or 2 years after the secondary stage, the
symptoms of secondary syphilis can reappear and patients can infect others.
3. Tertiary syphilis may show granulomas (gummas), especially of skin and bones; central
nervous system involvement, also known as neurosyphilis (e.g., tabes, paresis); or
cardiovascular lesions (e.g., aortitis, aneurysm of the ascending aorta). In tertiary lesions,
treponemes are rarely seen. T. pallidum also causes congenital syphilis. The organism is
transmitted across the placenta, typically after the third month of pregnancy, and fetal
infection can occur.

Prevention
Prevention depends on early diagnosis and adequate treatment, use of condoms,
administration of antibiotic after suspected exposure, and serologic follow up of infected
individuals and their contacts. To prevent congenital syphilis, all pregnant women should be
screened by using a treponemal test such as FTAABS. The presence of any sexually
transmitted disease makes testing for syphilis mandatory, because several different infections
are often transmitted simultaneously. There is no vaccine against syphilis.

14.BORDETELLAE
There are several species of Bordetella. Bordetella pertussis, a highly communicable and
important pathogen of humans, causes whooping cough (pertussis). Bordetella parapertussis
can cause a similar disease. Bordetella bronchiseptica (Bordetella bronchicanis) causes
diseases in animals, such as kennel cough in dogs and snuffles in rabbits, and only
occasionally causes respiratory disease and bacteremia in humans, primarily in
immunocompromised hosts. Bordetella avium causes turkey coryza and is a rare cause of
respiratory illness in humans. Newer species and their disease associations include Bordetella
hinzii (bacteremia, respiratory illness, arthritis), Bordetella holmesii (bacteremia among
immunosuppressed patients), and Bordetella trematum (wound infections and otitis media).

Bordetella pertussis
The organisms are minute gram-negative coccobacilli resembling H influenzae. With
toluidine blue stain, bipolar metachromatic granules can be demonstrated. A capsule is
present. The organism is a strict aerobe and it is oxidase and catalase positive but nitrate,
citrate, and urea negative, the results of which are useful for differentiating among the other
species of bordetellae. It does not require X and V factors on subculture. Hemolysis of blood-
containing medium is associated with virulent B pertussis.

Mode of transmission
The source of infection is usually a patient in the early catarrhal stage of the disease. The
organism is transmitted via droplet when infected patient cough or sneeze. Communicability

18
is high, ranging from 30–90%. Most cases occur in children younger than age 5 years; most
deaths occur in the first year of life.

Clinical Findings
After an incubation period of about 2 weeks, the “catarrhal stage” develops, with mild
coughing and sneezing. During this stage, large numbers of organisms are sprayed in
droplets, and the patient is highly infectious but not very ill. During the “paroxysmal” stage,
the cough develops its explosive character and the characteristic “whoop” upon inhalation.
This leads to rapid exhaustion and may be associated with vomiting, cyanosis, and
convulsions. The “whoop” and major complications occur predominantly in infants;
paroxysmal coughing predominates in older children and adults. Convalescence is slow. B
pertussis is a common cause of prolonged (4–6 weeks) cough in adults. Rarely, whooping
cough is followed by the serious and potentially fatal complication of encephalitis. Several
types of adenovirus and Chlamydia pneumoniae can produce a clinical picture resembling
that caused by B pertussis.

Prevention
Prevention of whooping cough rests mainly on adequate active immunization of all infants
and good personal hygiene.

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FUNGI
The fungi are eukaryotic organisms and they differ from the bacteria, which are prokaryotic
organisms, in many ways. The fungi possess rigid cell walls made up of characteristic cell
structures called chitin.

Structural morphology of fungi

Fungi exist in two fundamental forms; the mould form and yeast form.
Moulds: are fungi that grow in a long, branched, threadlike filaments of cells called hyphae
( s., hypha; Greek hyphe, web) that form a tangled mass called a mycelium (pl., mycelia).

Yeasts:
A yeast is a unicellular fungus with a single nucleus that reproduces either asexually by
budding and transverse division or sexually through spore formation. Each bud that separates
can grow into a new cell, and some group together to form colonies. Generally yeast cells are
larger than bacteria and are commonly spherical to egg-shaped. They lack flagella and cilia
but have most other eukaryotic organelles. In some cases, as the cells buds the buds fail to
detach and elongate thus forming a chain of elongated hyphae like filament called
pseudohyphae. This property is seen in Candida albicans. Some yeast such as Cryptococcus
and the yeast form of Blastomyces dermatatidis produce polysaccharide capsule.

Dimorphic fungi: are fungi that can grow in either yeast or a mold phase, depending on
environmental conditions. Several human pathogens demonstrate dimorphism; they grow in
the mold form in their environmental reservoir and in culture at ambient temperatures, but
convert to the yeast or some other form in infected tissue. For most, it is possible to
manipulate the cultural conditions to demonstrate both yeast and mold phases in vitro. Yeast

20
phase growth requires conditions similar to those of the parasitic in vivo environment, such
as 35 to 37°C incubation and enriched medium. Mold growth requires minimal nutrients and
ambient temperatures (22°C to 25°C).

Examples of molds: Examples of yeast: Examples of dimorphic fungi:

1. Aspergillus niger, 1. Cryptococcus 1. Candida albicans
2. Epidermophyton neuformans 2. Blastomyces dermatitidis
floccosum 2. Saccharomyces 3. Histoplasma capsulatum
3. Microsporum cerevisiae 4. Sporothrix schenckii
audouinii 5. Paracoccidiodes
4. Mucor indicus brasilliensis
5. Rhizopus oryzae 6. Coccidioides immitis
6. Trichophyton (changes to spherule of
concentricum enospores not yeast)
7. Penicillium notatum

Reproduction in fungi

Fungi are capable of both sexual and asexual reproduction.

Asexual Reproduction

Fungi reproduce asexually by fragmentation, budding, or producing spores.

i. Mycelial fragmentation: occurs when a fungal mycelium separates into pieces with each
component growing into a separate mycelium.
ii. Budding: during budding, a bulge forms on the side of the cell, the nucleus divides
mitotically, and the bud ultimately detaches itself from the mother cell.
iii. Producing spores: the most common mode of asexual reproduction is through the
formation of asexual spores, which are produced by one parent only (through mitosis) and
are genetically identical to that parent. Spores allow fungi to expand their distribution and
colonize new environments. They may be released from the parent thallus, either outside
or within a special reproductive sac called a sporangium (enclosure or cell where spores
are formed). Asexual Spores come in a number of morphological types: Conidia,
Sporangiospores, Arthrospores. Blastospores:

Sexual Reproduction

Sexual reproduction introduces genetic variation into a population of fungi. In fungi, sexual
reproduction often occurs in response to adverse environmental conditions. Two mating types
are produced. When both mating types are present in the same mycelium, it is called
homothallic, or self-fertile. Heterothallic mycelia require two different, but compatible,
mycelia to reproduce sexually.

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 Although there are many variations in fungal sexual reproduction, all include the following
three stages.

i. Plasmogamy (literally, "marriage or union of cytoplasm"): two haploid cells fuse, leading
to a dikaryotic stage where two haploid nuclei coexist in a single cell.
ii. Karyogamy ("nuclear marriage"): the haploid nuclei fuse to form a diploid zygote
nucleus.
iii. Meoisis: meiosis takes place in the gametangia (singular, gametangium) organs, in
which gametes of different mating types are generated. At this stage, spores are
disseminated into the environment.

FUNGAL DISEASES OF MEDICAL SIGNIFICANCE

1. Vaginal Candidiasis
Candidiasis is an infection caused by a yeast called Candida albicans. Candida normally lives
on skin and inside the body such as in the mouth, throat, gut, and vagina, without causing any
problems. Candida can cause an infection if conditions change inside the vagina to encourage
its growth. Things like hormones, medicines, or changes in the immune system can make
infection more likely. The common term for candidiasis in the vagina is a vaginal yeast
infection. Other names for this infection are vaginal candidiasis, vulvovaginal candidiasis, or
candidal vaginitis.

Symptoms
The symptoms of vaginal candidiasis include: Vaginal itching or soreness, pain during sexual
intercourse, pain or discomfort when urinating, abnormal vaginal discharge. Vaginal
candidiasis is often mild. However, some women can develop severe infections involving
redness, swelling, and cracks in the wall of the vagina.

Risk factors of vaginal candidiasis

Vaginal candidiasis is common. Women who are more likely to get vaginal candidiasis
include those who: are pregnant, use of hormonal contraceptives (for example, birth control
pills), have diabetes, have a weakened immune system (for example, due to HIV infection or
medicines such as steroids and chemotherapy) and taking or have recently taken antibiotics

Prevention of vaginal candidiasis

Wearing cotton underwear might help reduce the chances of getting a yeast infection. Taking
antibiotics can lead to vaginal candidiasis, so take these medicines only when prescribed and
exactly as your healthcare provider tells you.

2. Aspergillosis
Aspergillosis is an infection caused by Aspergillus, a common mold that lives indoors and
outdoors. Most people breathe in Aspergillus spores every day without getting sick. However,
people with weakened immune systems or lung diseases are at a higher risk of developing

22
 health problems due to Aspergillus. The types of health problems caused
by Aspergillus include allergic reactions, lung infections, and infections in other organs.

Causes of Aspergillosis
There are approximately 180 species of Aspergillus, but fewer than 40 of them are known to
cause infections in humans. Aspergillus fumigatus is the most common cause of
human Aspergillus infections. Other common species include A. flavus, A. terreus, and A.
niger.

Symptoms of Aspergillosis
The different types of aspergillosis can cause different symptoms.

The symptoms of allergic bronchopulmonary aspergillosis (ABPA) are similar to asthma

symptoms, including: Wheezing, shortness of breath, cough, Fever (in rare cases)

Symptoms of allergic Aspergillus sinusitis include: Stuffiness, runny nose, headache,

reduced ability to smell

Symptoms of an aspergilloma (“fungus ball”) include: Cough, coughing up blood, shortness

of breath

Symptoms of chronic pulmonary aspergillosis include: Weight loss, cough, coughing up

blood, Fatigue, Shortness of breath

Risk factors of aspergillosis

The different types of aspergillosis affect different groups of people.

i. Allergic bronchopulmonary aspergillosis (ABPA) most often occurs in people who

have cystic fibrosis or asthma.
ii. Aspergillomas usually affect people who have other lung diseases like tuberculosis.
iii. Chronic pulmonary aspergillosis typically occurs in people who have other lung
diseases, including tuberculosis, chronic obstructive pulmonary disease (COPD), or
sarcoidosis.
iv. Invasive aspergillosis affects people who have weakened immune systems, such as
people who have had a stem cell transplant or organ transplant, are getting chemotherapy
for cancer, or are taking high doses of corticosteroids. Invasive aspergillosis has been
described among hospitalized patients with severe influenza.

Prevention of aspergillosis
It’s difficult to avoid breathing in Aspergillus spores because the fungus is common in the
environment. For people who have weakened immune systems, there may be some ways to
lower the chances of developing a severe Aspergillus infection.

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 1. Protect yourself from the environment.

i. Try to avoid areas with a lot of dust like construction or excavation sites. If you can’t avoid
these areas, wear an N95 respirator (a type of face mask) while you’re there.

ii. Avoid activities that involve close contact to soil or dust, such as yard work or gardening.

iv. Wear gloves when handling materials such as soil, moss, or manure.

v. To reduce the chances of developing a skin infection, clean skin injuries well with soap
and clean water, especially if they have been exposed to soil or dust.

2. Antifungal medication. If you are at high risk for developing invasive aspergillosis (for
example, if you’ve had an organ transplant or a stem cell transplant), your healthcare provider
may prescribe medication to prevent aspergillosis.

3. Testing for early infection. Some high-risk patients may benefit from blood tests to detect
invasive aspergillosis.

3. Blastomycosis
Blastomycosis is an infection caused by a fungus called Blastomyces dermatitidis. The
fungus lives in the environment, particularly in moist soil and in decomposing matter such as
wood and leaves. People can get blastomycosis after breathing in the microscopic fungal
spores from the air. Although most people who breathe in the spores don’t get sick, some
people will develop symptoms like fever and cough, and the infection can sometimes become
serious if it is not treated.

Symptoms of Blastomycosis
Fever is a common symptom of blastomycosis. Approximately half of people who are
infected with the fungus Blastomyces will show symptoms. The symptoms of blastomycosis
are often similar to the symptoms of other lung infections, and can include: Fever, Cough,
Night sweats, Muscle aches or joint pain, Weight loss, Chest pain, Fatigue (extreme
tiredness)

Risk factors of blastomycosis

Anyone can get blastomycosis if they’ve been in an area where Blastomyces lives in the
environment. People who participate in outdoor activities that expose them to wooded areas
(such as forestry work, hunting, and camping) in these areas may be at higher risk for getting
blastomycosis. People who have weakened immune systems may be more likely to develop
severe blastomycosis than people who are otherwise healthy. Blastomycosis can’t spread
between people or between people and animals.

24
 Prevention of blastomycosis
There is no vaccine to prevent blastomycosis, and it may not be possible to completely avoid
being exposed to the fungus that causes blastomycosis in areas where it is common. People
who have weakened immune systems may want to consider avoiding activities that involve
disrupting soil in these areas.

4. Cryptococcus neoformans Infection

Cryptococcus neoformans is a fungus that lives in the environment throughout the world.
People can become infected with C. neoformans after breathing in the microscopic fungus,
although most people who are exposed to the fungus never get sick from it. C.
neoformans infections are rare in people who are otherwise healthy; most cases occur in
people who have weakened immune systems, particularly those who have advanced
HIV/AIDS.

Symptoms of C. neoformans Infection

C. neoformans usually infects the lungs or the central nervous system (the brain and spinal
cord), but it can also affect other parts of the body. The symptoms of the infection depend on
the parts of the body that are affected.

Lung infection: C. neoformans infection in the lungs can cause a pneumonia-like illness. The
symptoms are often similar to those of many other illnesses, and can include: Cough,
shortness of breath, chest pain and Fever

In the brain (cryptococcal meningitis): Cryptococcal meningitis is an infection caused by the

fungus Cryptococcus after it spreads from the lungs to the brain. The symptoms of
cryptococcal meningitis include: Headache, fever, neck pain, nausea, vomiting, Sensitivity to
light and Confusion or changes in behaviour

Risk factors of C. neoformans Infection

C. neoformans infections are rare among people who are otherwise healthy. Most cases of C.
neoformans infection occur in people who have weakened immune systems , such as people
who have advanced HIV/AIDS, have had an organ transplant, or are taking corticosteroids,
medications to treat rheumatoid arthritis, or other medications that weaken the immune
system.

Prevention of C. neoformans infection

It’s difficult to avoid breathing in C. neoformans because it’s thought to be common in the
environment. Prevention of disease cause by C. neoformans can be done by detecting silent
cryptococcal infections in people who have HIV/AIDS. One approach to prevent
cryptococcal meningitis is called “targeted screening.” Research suggests that C.
neoformans is able to live in the body undetected, especially when a person’s immune system
is weaker than normal. In a targeted screening program, a simple blood test is used to detect
cryptococcal antigen (an indicator of cryptococcal infection) in HIV-infected patients before
they begin taking antiretroviral treatment (ART). A patient who tests positive for

25
 cryptococcal antigen can take fluconazole, an antifungal medication, to fight off the silent
fungal infection and prevent it from developing into life-threatening meningitis.

5. Mycetoma
Mycetoma is a disease caused by certain types of bacteria and fungi found in soil and water.
These bacteria and fungi may enter the body through a break in the skin, often on a person’s
foot. The resulting infection causes firm, usually painless but debilitating masses under the
skin that can eventually affect the underlying bone. Mycetoma can be caused by bacteria
(actinomycetoma) or fungi (eumycetoma). Mycetoma affects people of all ages and is more
common in men. This disease primarily affects poorer people in rural regions of Africa, Latin
America, and Asia that are located near the equator and have dry climates. People affected by
mycetoma often live in remote areas where they have limited access to healthcare and
medications. Mycetoma can cause severe physical disabilities that can force people to stop
working and cause stigma.

Transmission
The bacteria and fungi that cause mycetoma live in soil and water. These germs can enter the
body through wounds or other small skin injuries, like a thorn prick. It is not known why
some people develop mycetoma and others do not, but aspects of the environment and living
conditions are likely involved. Mycetoma does not spread between people.

Symptoms
Symptoms are similar for bacterial and fungal mycetoma. Both appear as firm, painless
masses under the skin. These masses usually appear on a person’s foot but can form
anywhere on the body. The mycetoma masses start small, but over time they can grow larger,
develop oozing sores, and cause the affected limb to become deformed or unusable. If
mycetoma is not treated or if treatment fails, it can spread to other areas of the body. Long-
term mycetoma can eventually destroy the underlying muscle and bone.

Risk factors of mycetoma

Mycetoma is a health problem in equatorial regions of Africa, Latin America, and Asia
known as the “mycetoma belt.” Fungal mycetoma (eumycetoma) is the most common type in
Africa, while bacterial mycetoma (actinomycetoma) causes most cases in South and Central
America and some Asian countries. Mycetoma affects people of all ages and is more
common in men. Many people with mycetoma work in agricultural jobs, such as farmers and
livestock herders.

Prevention of Mycetoma
Wearing shoes might prevent injuries that can lead to mycetoma. Shoes protect the feet while
someone is walking or working outside in areas where the germs that cause mycetoma are
common in water and soil. Early detection and treatment, before symptoms cause serious
effects, can reduce disabilities from mycetoma and may cure the condition.

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6. Mucormycosis
Mucormycosis (previously called zygomycosis) is a serious but rare fungal infection caused by
a group of molds called mucormycetes. These molds live throughout the environment.
Mucormycosis mainly affects people who have health problems or take medicines that lower
the body’s ability to fight germs and sickness. It most commonly affects the sinuses or the lungs
after inhaling fungal spores from the air. It can also occur on the skin after a cut, burn, or other
type of skin injury.

Cause of mucormycosis
Several different types of fungi can cause mucormycosis. These fungi are called
mucormycetes and belong to the scientific order Mucorales. The most common types that
cause mucormycosis are Rhizopus species and Mucor species.

Symptoms of Mucormycosis
The symptoms of mucormycosis depend on where in the body the fungus is growing.

Symptoms of rhinocerebral (sinus and brain) mucormycosis include: One-sided facial

swelling, headache, nasal or sinus congestion, black lesions on nasal bridge or upper inside of
mouth that quickly become more severe and fever

Symptoms of pulmonary (lung) mucormycosis include: Fever, Cough, Chest pain and
Shortness of breath

Cutaneous (skin) mucormycosis can look like blisters or ulcers, and the infected area may
turn black. Other symptoms include pain, warmth, excessive redness, or swelling around a
wound.

Symptoms of gastrointestinal mucormycosis include: Abdominal pain, nausea and vomiting

and gastrointestinal bleeding

Risk factors of mucormycosis

Mucormycosis is rare, but it’s more common among people who have health problems or
take medicines that lower the body’s ability to fight germs and sickness. Certain groups of
people are more likely to get mucormycosis: Diabetes, especially with diabetic ketoacidosis,
cancer, organ transplant, stem cell transplant, neutropenia (low number of white blood cells),
long-term corticosteroid use, injection drug use, too much iron in the body (iron overload or
hemochromatosis), skin injury due to surgery, burns, or wounds and prematurity and low
birth weight (for neonatal gastrointestinal mucormycosis)

Prevention of mucormycosis
There is no vaccine to prevent mucormycosis. For people who have weakened immune
systems, there may be some ways to lower the chances of developing mucormycosis such as
protecting yourself from the environment and use of antifungal medication.

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7. Pneumocystis pneumonia
pneumonia (PCP) is a serious infection caused by the fungus Pneumocystis jirovecii. Most
people who get PCP have a medical condition that weakens their immune system, like
HIV/AIDS, or take medicines (such as corticosteroids) that lower the body’s ability to fight
germs and sickness.

Transmission Pneumocystis pneumonia

PCP spreads from person to person through the air. Some healthy adults can carry
the Pneumocystis fungus in their lungs without having symptoms, and it can spread to other
people, including those with weakened immune systems.

Symptoms
The symptoms of PCP can develop over several days or weeks and include: fever, cough,
difficulty breathing, chest pain, chills, atigue (tiredness)

Risk factors of Pneumocystis pneumonia

Most people who get PCP have weakened immune systems, meaning that their bodies don’t
fight infections well. About 30-40% of people who get PCP have HIV/AIDS. The other
people who get PCP are usually taking medicine (such as corticosteroids) that lowers the
body’s ability to fight germs or sickness or have other medical conditions, such as: Chronic
lung diseases, Cancer, Solid organ or stem cell transplant and Inflammatory diseases or
autoimmune diseases (for example, lupus or rheumatoid arthritis)

Prevention of pneumocystis pneumonia

There is no vaccine to prevent PCP. A healthcare provider might prescribe medicine to
prevent PCP for people who are more likely to develop the disease. The medicine most
commonly used to prevent PCP is called trimethoprim/sulfamethoxazole (TMP/SMX), which
is also known as co-trimoxazole.

28
MEDICAL PARASITOLOGY

Parasitology: is the scientific study of parasites, their hosts and relationship between them.

Parasite: is a living organism that lives in or on another living organism of different species
called the host, where it obtained food, shelter and other necessities of life and living at the
expense of the host who gained nothing.

Types of Parasites

1. Ectoparasite: This is a parasitic organism that lives on the outer surface of its host,
e.g. lice, ticks, mites etc.
2. Endoparasites: These are parasites that live inside the body of their host, e.g.
Entamoeba histolytica.
3. Obligate Parasite: This parasite is completely dependent on the host during a
segment or all of its life cycle, e.g. Plasmodium spp.
4. Facultative parasite: This is an organism that exhibits both parasitic and non-
parasitic modes of living and hence does not absolutely depend on the parasitic way
of life, but is capable of adapting to it if placed on a host. E.g. Naegleria fowleri
5. Accidental parasite: when a parasite attacks an unnatural host and survives. E.g.
Hymenolepis diminuta (rat tapeworm).

Types of Host

1. Definitive host: a host that harbors a parasite in the adult stage or where the parasite
undergoes a sexual method of reproduction.
2. Intermediate host: harbours the larval stages of the parasite or an asexual cycle of
development takes place. In some cases, larval development is completed in two
different intermediate hosts, referred to as first and second intermediate hosts.
3. Reservoir host: a host that makes the parasite available for the transmission to
another host and is usually not affected by the infection.
4. Natural host: a host that is naturally infected with certain species of parasite.
5. Accidental host: a host that is under normal circumstances not infected with the
parasite.

General classification of parasites of medical importance

Parasites of medical importance come under the kingdom protista and animalia which
includes:
1. Protozoa: are microscopic single-celled eukaroytes belonging to the kingdom protista. The
body wall is covered by cell membrane. Its cytoplasm is made up of ectoplasm and
endoplasm. The nucleus is usually single but may be double or multiple. Reproduction can
be asexual (e.g. binary fission, schizogony, endodyogeny) or sexual (e.g. gametogony).
Protozoa can be divided into the following groups:

1. Amoebae: Has pseudopodia as a mean of locomotion:

Amoebae of medical importance:

29
 i. Amoeba in the large intestine: Entamoeba histolytica
ii. Free-living amoebae in CNS and eye: Naegleria, Acanthamoeba

2. Flagellates: Has flagella as organ of locomotion:

Flagellates of medical importance:
i. Hemoflagellates: Trypanosoma, Leishmania
ii. Gastrointestinal: Giardia lamblia
iii. Urogenital: Trichomonas vaginalis

3. Apicomplexa: Has a structure called apical complex which serves as the organ of
attachment to host cells.
Apicomplexa of medical importance:
i. Blood: Plasmodium, Babesia
ii. Tissue: Toxoplasma gondii, Sarcocystis
iii. Gastrointestinal: Cryptosporidium, Cystoisospora, Cyclospora

4. Ciliate: Has cilia for locomotion

Ciliate of medical importance:
Gastrointestinal: Balantidium coli

2. Helminths
Helminths are metazoa which are macroscopic, multicellular worms possessing well
differentiated tissues and complex organs belonging to the kingdom animalia. They are
bilaterally symmetrical (divisible into symmetrical halves). Body of helminths has a cuticle
or integument which is the outer covering. Most helminths require more than 1 intermediate
host for completion of their life cycle. Helminths unlike protozoa do not multiply in the
human.

Helminths are classified into 2 phyla:

i. Nemathelminthes possess a cylindrical body with a body cavity. Alimentary canal is

complete with absence of suckers and they are sexually differentiated. Nematodes belong
to phylum Nemathelminthes They can be classified based on the following:
(a) Intestinal nematodes: soil transmitted helminths (STH), which includes;
Round worm (Ascaris lumbricoides, Trichuris trichiura, Strongyloides stercoralis)
Hookworms (Ancyclostoma duedenale, Necatot americanus)
(b) Intestinal nematodes: non soil transmitted
Pinworm (Enterobius vermicularis, Trichinella spiralis)
Filarial worms (Wucherieria bancrofti, Brugia melayi, Loa loa, Onchocerca
volvulus)

ii. Platyhelminthes: Platyhelminthes possess a body which is flattened dorsoventrally with

absence of body cavity. Alimentary canal is absent or rudimentary. Suckers are present
and most of the worms are hermaphrodite. Platyhelminthes includes:
(a). Cestodes (tape worm) eg. Taenia
(b). Trematodes (flukes): there are different types of flukes depending on the infection
site in the host, these includes; blood flukes (Schistosoma haematobium, Schistosoma
mansoni, Schistosoma japonicum), liver flukes (Clonorchis sinensis, Fasciola hepatica),
intestinal flukes (Fasciolopsis buski), lung flukes (Paragonimus westermani)

30
Parasites of medical importance

1. Entamoeba histolytica

Distribution
Entamoeba histolytica is the causative agent of amoebiasis, it has a worldwide prevalence,
especially where sanitation is poor and is more common in developing countries of the
tropics. Majority of cases are asymptomatic.

Habitat
Entamoeba histolytica is found in the human colon.

Morphology
Entamoeba histolytica occurs in 2 forms i.e trophozoite and cyst

Life Cycle
(1) The cysts (usually found in formed stools) and trophozoites (in loose stools) are passed
out in faeces of infected human.
(2) Cysts are ingested via contaminated food or water.
(3) In the intestine, the cysts undergo excystation and form trophozoites
(4). As the trophozoite passes down the intestine, it undergoes encystations and is excreted in
the faeces.

Pathogenesis and Clinical Features

Entamoeba histolytica causes intestinal and extraintestinal amoebiasis. The lumen-dwelling
amoebae do not cause any illness. They cause disease only when trophozoites invade the
intestinal tissues where they cause ulcer. The clinical manifestations are diarrhoea, abdominal
symptoms and dysentery. This may resemble bacillary dysentery.

Prevention and Control

1. Boil drinking water
2. Wash fruits and vegetables in clean water before eating
3. Detection and treatment of carriers and prohibit them from food handling
4. Health education

2. Giardia lamblia (also referred to as Giardia duodenalis or Giardia intestinalis) is the

causative agent of giardiasis and is the only common pathogenic protozoan found in the
duodenum and jejunum of humans.

Morphology
Giardia exists in two forms: the trophozoite and the cyst forms.

Life cycle
1. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral
route (hands or fomites)
2. In the small intestine, excystation releases trophozoites (each cyst produces 2
trophozoites).
3. Trophozoites multiply by longitudinal binary fission remaining in the lumen of the
proximal small bowel where they can be free or attached to the mucosa by a ventral
sucking disk .

31
4. Encystation occurs as the parasites transit toward the colon.
5. Both cysts and trophozoites can be found in the feces. The cyst is the stage found most
commonly in non-diarrheal feces (The cysts are hardy, can survive several months in cold
water.) and trophozoites are found in the diarrheal stools. Because the cysts are infectious
when passed in the stool or shortly afterward, person-to-person transmission is possible.

Transmission
Humans are infected by ingestion of fecally contaminated water or food containing giardia
cysts or by direct fecal contamination, as may occur in day care centers, refugee camps, and
institutions, or during oral–anal sex.

Clinical features
Giardia infection can cause a variety of intestinal symptoms, which include: Anorexia,
Flatulence (gas), nausea, vomiting, stomach or abdominal cramps, Watery (non bloody), foul-
smelling diarrhea, Greasy stools that tend to float, dehydration (loss of fluids)
.
Treatment
For asymptomatic carriers and diseased patients the drug of choice is quinacrine
hydrochloride or metronidazole.

Prevention
1. Asymptomatic reservoirs of infection should be identified & treated.
2. Avoidance of contaminated food and water.
4. Proper waste disposal and use of latrine.

3. Trichomonas vaginalis

Distribution
It is distributed worldwide.

Habitat
In human, it lives mainly in the vagina and cervix of females. In males, it occurs mainly in
the anterior urethra. It causes trichomoniasis.

Morphology
It only exists in the trophozoite stage.

Life Cycle
(1) Trophozoites live in the vagina and cervix and may also be found in urethra and urinary
bladder in females. In males, it occurs mainly in the anterior urethra, but may also be found in
the prostate.
(2) Trophozoites multiply by longitudinal binary fission.
(3) Trophozoites in vagina or orifice of urethra can be found in the vaginal and prostatic
secretions and urine. Life cycle of T. vaginalis is completed in a human host. There is no
cystic stage.

Mode of transmission
The trophozoite is transmitted directly from person to person. Sexual transmission is the
usual mode of infection. Trichomoniasis often coexists with other sexually transmitted

32
diseases; like candidiasis, gonorrhoea, syphillis, or human immunodeficiency virus (HIV).
Babies may acquire infection during birth from infected mothers. Fomites such as towels
have been implicated in transmission.

Clinical Features
The infection can range from mild irritation to severe inflammation. Infection is often
asymptomatic, particularly in males, although some may develop urethritis, epididymitis and
prostatitis. In females, it may produce severe itching in the genital area with foul smelling
yellowish green frothy discharge, dysuria, burning sensation when urination and dyspareunia.
Cervical erosion is common. The incubation period is 4 days to 4 weeks.

Treatment
Treatment of both sexual partners is recommended. Metronidazole is the drug of choice (250
mg 3 times daily for 10 days). In pregnancy, metronidazole is safe to be given in second and
third trimesters.

Prevention and Control

1. Treatment of sexual partner
2. Patients should be advised to abstain from sexual intercourse until they and their partners
have completed treatment and follow-up

4 Trypanosomes

There are two distinct types of human trypanosomes:

(1) Trypanosoma brucei complex (Trypanosoma brucei rhodesiense and Trypanosoma brucei
gambiense): which causes sleeping sickness (African trypanosomiasis)
(2) Trypanosoma cruzi which causes Chagas disease (American trypanosomiasis)

Trypanosoma brucei gambiense

Distribution
It is endemic in scattered foci in West and Central Africa. The principal vectors are Glossina
palpalis and Glossina tachynoides (riverine tsetse flies).

Habitat
Trypanosomes live in human and other vertebrate hosts. From the blood, they invade regional
lymph nodes and finally CNS.

Morphology
1. In vertebrate host Trypomastigote form, which is highly pleomorphic (long slender form,
stumpy short broad form and an intermediate form)
2. In vector (tsetse fly) Occurs in 2 forms:
(a) Epimastigotes (b) Metacyclic trypomastigotes

Life Cycle
(1) Tsetse fly (the invertebrate host) takes a blood meal and injects the infective metacyclic
trypomastigotes.
(2) Injected metacyclic trypomastigotes transform into trypomastigotes and are carried to
other sites via blood stream.
(3) Trypomastigotes multiply by binary fission.

33
(4) Trypomastigotes are found in blood extracellular.
(5) Trypomastigotes in the blood are ingested by tsetse fly and transform into procyclic
trypomastigotes in the midgut of the fly
(6). Procyclic trypomastigotes transform into epimastigotes before transforming into
metacyclic trypomastigotes in the fly’s salivary gland. Modes of transmission are via bite of
infected tsetse fly and congenital transmission. It is endemic in scattered foci in West and
Central Africa.

Clinical Features
Trypanosoma brucei gambiense causes African trypanosomiasis (West African sleeping
sickness). The illness is chronic and can persist for many years. A painless chancre appears
on the skin at the site of bite by tsetse fly, followed by fever, chills, rash, anaemia and weight
loss. Invasion of CNS occurs after several months later and is marked by increasing
headache, mental dullness, apathy and daytime sleepiness. The patient may fall into coma
followed by death from other infections and physical weakness

Trypanosoma cruzi

Distribution
It is limited to South and Central America and it causes Chagas’ disease, which is a zoonotic
disease.

Habitat
In human, trypomastigotes are in the blood and amastigotes are in tissue.

Morphology
In humans, Trypanosoma cruzi exists in 2 forms, amastigote and trypomastigote.

Life Cycle
Trypanosoma cruzi completes its life cycle in 2 hosts. Human is the vertebrate host. Its
invertebrate host (vector) is reduviid bug or triatomid bug (Triatoma infestans, Rhodnius
prolixus and Panstrongylus megistus). Its reservoir hosts are armadillos, cats, dogs and pigs.
The infective stage to human is metacyclic trypomastigotes which are found in faeces of
reduviid bugs. This bug defaecates while feeding. The parasite enters human at the biting site.
Transmission of infection to human and other reservoir hosts takes place when mucus
membranes, conjunctiva, or wound on the surface of the skin is contaminated by faeces of the
bug containing metacyclic trypomastigotes. Other modes of transmission are blood
transfusion, organ transplantation and vertical transmission.

Clinical Features
The incubation period of T. cruzi in human is 1–2 weeks. The disease manifests in acute and
chronic forms.

1. Acute Chagas’ disease

Acute phase occurs soon after infection and may last for 1–4 months. It is seen often in
children under 2 years of age. First sign appears within a week after invasion of parasite.
‘Chagoma’ is the subcutaneous lesion occurring at the site of inoculation. Inoculation of the
parasite in conjunctiva causes unilateral, painless oedema of periorbital tissues known as
Romana’s sign. This is a classical finding in acute Chagas’ disease. There may be generalized

34
infection with fever, lymphadenopathy and hepatosplenomegaly. The patient may die of
acute myocarditis and meningoencephalitis. Usually within 4–8 weeks, acute signs and
symptoms resolve. Then, patient progresses into asymptomatic or chronic phase of T. cruzi
infection.

2. Chronic Chagas’ disease

The chronic form is found in adults and older children and becomes apparent years or even
decades after the initial infection. In chronic phase, T. cruzi produces inflammatory response,
cellular destruction and fibrosis of muscles and nerves which can present with cardiac
myopathy, megaoesophagus and megacolon.

Prevention and Control

1. Insecticide to control the vector bug
2. Insect repellant and use of insect netting
3. Improvement in housing to eliminate breeding places of bugs

5 Malaria Parasites

Causative agents of human malaria:

1. Plasmodium vivax
2. Plasmodium falciparum
3. Plasmodium malariae
4. Plasmodium ovale
5. Plasmodium knowlesi

Habitat
In human, the parasites are found in the erythrocytes and hepatocytes.

Transmission
Modes of transmission are via bite of infected Anopheles mosquito, blood transfusion,
congenital transmission and shared syringes.

Life Cycle
Malaria parasite completes its life cycle in 2 hosts. Its definitive host is the female Anopheles
mosquito.

1. Human cycle (schizogony) Humans acquire infection from the bites of infective female
Anopheles mosquito. The sporozoites, which are the infective forms of the parasite, are
present in the salivary gland of the mosquito. They are injected into blood capillaries when
the mosquito takes a blood meal. The sporozoites circulate in the blood stream and enter
the liver parenchymal cells (hepatocytes).
2. There, the sporozoites mature into schizonts.
3. The schizonts rupture and release merozoites. This initial replication in the liver is called
the exoerythrocytic cycle.
4. Merozoites infect RBCs. There, the parasite multiplies asexually (called the erythrocytic
cycle). The merozoites develop into ring-stage trophozoites.
5. Some then mature into schizonts. The schizonts rupture, releasing merozoites
6. Some trophozoites differentiate into gametocytes.
7. During a blood meal, an Anopheles mosquito ingests the male (microgametocytes) and
female (macrogametocytes) gametocytes, beginning the sporogonic cycle.

35
8. In the mosquito’s stomach, the microgametes penetrate the macrogametes, producing
zygotes.
9. The zygotes become motile and elongated, developing into ookinetes.
10. The ookinetes invade the midgut wall of the mosquito where they develop into oocysts.
11. The oocysts grow, rupture, and release sporozoites, which travel to the mosquito’s salivary
glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life
cycle.

Clinical Features
The disease process in malaria occurs due to local or systemic response of the host to parasite
antigens. The typical presentation of malaria is periodic bouts of fever with chills, rigors,
headache, nausea, and vomiting. Anaemia is caused by rupture of infected red blood cells.
Cerebral malaria is the most serious complication of P. falciparum infection.

Prevention and Control

1. Chemoprophylaxis provides effective protection for travellers visiting endemic areas. The
drugs recommended are proguanil, chloroquine or mefloquine weekly or doxycycline daily.
Prophylaxis should begin 1 week before travelling and be continued while in the endemic
area and for 4–6 weeks after departure from endemic area.
2. Vector Control Strategies
(a) The spraying of the indoor surfaces of house with residual insecticides
(b) Insecticide treated bed nets (ITN)
(c) Use of repellants, protective clothing, mosquito coils and screening of house
3. Anti-larval Measures

6. Ascaris lumbricoides
Common name: roundworm

Distribution
It is distributed worldwide mainly in the tropics and subtropics.

Habitat
Adult worms live in the lumen of the small intestine.

Life Cycle
(1) The adult male and female worms live in the lumen of the small intestine of human.
(2) The female worm produces both fertilized and unfertilized eggs which are passed out in
faeces.
(3) In the soil, the fertilized egg undergoes development to the infective stage.
(4) Human acquires infection via ingestion of the infective eggs.
(5) In the intestine, the eggs hatch into larvae.
(6) The larvae penetrate the mucosa of the small intestine and enter the portal circulation and
are carried to the heart and lungs.
(7) In the lungs, the larvae rupture out of the alveolar capillaries into the alveolar space and
crawl up the bronchiole, bronchi, trachea and pharynx. They are swallowed back into the
intestine where they develop into adults in about 3 months.

Clinical Features
Clinical manifestations of ascariasis are caused by the migrating larvae and the adult worms.
The larval migration causes allergic reaction. The initial exposure to larvae during the lung
36
migration phase is usually asymptomatic, except when the larval load is heavy. When
reinfection occurs, there may be infiltration of eosinophils and macrophages. Loeffler’s
syndrome is characterized by low-grade fever, cough, wheezing, dyspnea. The sputum may
contain larvae. Loeffler’s syndrome seen in ascariasis is also known as ascaris pneumonitis.
The pulmonary clinical features subside in 1 or 2 weeks after infection.
.
Prevention and Control
1. Proper faecal disposal
2. Wash fruits and vegetables before consumption
3. Personal hygiene
4. Treatment of infected persons

7. Taenia saginata and Taenia solium

Common name
Taenia saginata Beef tapeworm
Taenia solium Pork tapeworm

Distribution
Taenia saginata and Taenia solium have a worldwide distribution.

Habitat
The adult worms of both T. saginata and T. solium live in the small intestine of human.

Life Cycle
(1) Eggs or gravid proglottids in faeces of infected humans are passed out.
(2) Cattle (T. saginata) and pigs (T. solium) become infected by ingesting vegetation
contaminated by eggs or gravid proglottids.
(3) Eggs hatch into oncospheres (larval form) and then penetrate intestinal wall and circulate
to muscles to develop into cysticerci.
(4) Humans acquire infection by ingesting raw or undercooked infected meat containing the
larvae.
(5) Adults develop in the small intestine of human and scolex attaches to the mucosa of the
small intestine.

Clinical Features
Intestinal taeniasis can be caused by both T. saginata and T. solium. It is mostly
asymptomatic. In symptomatic infection, patient presents with vague abdominal discomfort,
indigestion, nausea, diarrhoea and weight loss. Cases of acute intestinal obstruction and acute
appendicitis have been reported. Cysticercosis is caused by larval stage (cysticecus
cellulosae) of T. solium.

Prevention and control

1. Proper cooking of beef and pork
2. Proper sanitation
3. Personal hygiene
4. Avoid eating raw vegetables grown in polluted soil to prevent from acquiring cysticercosis
5. Treatment of cases with taeniasis solium as they can develop cysticercosis due to
autoinfection.

37
 8. Blood Flukes
Schistosoma haematobium

Distribution
Schistosoma haematobium is endemic in most parts of Africa and West Asia.

Habitat
The adult worms live in the vesical and pelvic venous plexuses of humans.

Life Cycle
(1) The eggs are passed in urine (S. haematobium) and in faeces (S. mansoni and S.
japonicum) from infected humans.
(2) Eggs hatch in water releasing miracidia.
(3) Miracidia penetrate tissue of freshwater snail (intermediate host).
(4) Sporocysts develop in snail.
(5) Free swimming cercariae are released by snail into water.
(6) Cercariae penetrate skin of human.
(7) Cercariae lose their tails during penetration and become schistosomulae.
(8) The schistosomulae are carried in blood circulation and migrate to portal blood in liver
and mature into adults.
(9) Paired adult worms migrate to venous plexus of bladder (S. haematobium) or mesenteric
venules (S. mansoni and S. japonicum) where the female lay their eggs.

Clinical Features
Cercarial dermatitis presents with transient itching and petechial lesions at the site of entry of
the cercariae, more often seen in visitors to endemic areas than among locals who may be
immune due to repeated exposure. Acute systemic schistosomiasis may cause Katayama
fever which presents with leucocytosis, eosinophilia and hepatosplenomegaly. Clinical
features during oviposition include painless terminal haematuria. Haematuria is initially
microscopic, but become gross in heavy infection. Patients develop frequency of micturition
with burning sensation.

Symptoms of schistosomiasis mansoni are mainly intestinal. Patients develop colicky

abdominal pain and dysentery, which may persist intermittently for many years. The eggs
deposited in the intestinal wall of colon and rectum, cause inflammatory reactions causing
granulomas, hyperplasia and followed by fibrosis. Eggs that are carried through portal
circulation to the liver may cause hepatosplenomegaly, periportal fibrosis and portal
hypertension.

Treatment
Praziquantel (40 mg/kg/day orally in 2 divided doses for 1 day) is the drug of choice.
Metrifonate is the alternative drug.

Prevention and Control

1. Proper disposal of urine and faeces
2. Treatment of infected persons
3. Avoid swimming, bathing and washing in snail-infested water
4. Control of snails

38
Summary Note

MCB 102

2022

1
Viruses are ultramicroscopic bits of genetic material (DNA or RNA) enclosed in a protein shell
and, sometimes, a membranous envelope. Viruses have no metabolism; therefore, it is difficult to
use drugs to interfere with their structures or activities. Viruses multiply in living cells and use the
chemical machinery of the cells for their own purpose. Often, they destroy the cells in the process
of replicating.

Virus classification

Viruses are not classified as part of any of the three domains. Viruses are not composed of cells,
and they use the anabolic machinery within living host cells to multiply. A viral genome can direct
biosynthesis inside a host cell, and some viral genomes can become incorporated into the host
genome. The ecological niche of a virus is its specific host cell, so viruses may be more closely
related to their hosts than to other viruses. The International Committee on Taxonomy of Viruses
defines a viral species as a population of viruses with similar characteristics (includ ing
morphology, genes, and enzymes) that occupy a particular ecological niche. Therefore, viruses are
classified based on;

1. Classification based on disease: classification of viruses according to the nature of the

disease with which they are associated. However, most viruses either do not cause disease

2
 or cause a disease that we do not recognize because of a lack of understanding of the host.
Similarly, a single virus can cause more than one type of disease; a good example of this
is a varicella- zoster virus, which causes chickenpox in a first infection but when reactivated
later in life causes shingles.
2. Classification based on host organism: classification based on parasitic nature of the
virus-host interaction. Some viruses are very restricted in their host range, infecting only
one species, such as the hepatitis B virus infecting humans and so a designation based on
the host is appropriate. However, others may infect a small range of hosts, such as
poliovirus, which can infect various primates, and the designation here must reflect this
rather than name a single species and can replicate both within plant and insects species.
3. Classification based on viral particle morphology: a classification groups based on the
observed particle shape or morphology. If the virion is nonenveloped, three morphologica l
categories are defined, isometric, filamentous, and complex. Isometric viruses appear
approximately spherical but are icosahedrons. Filamentous viruses have a simple, helical,
morphology. The complex viruses are those, which do not neatly fit within the other two
categories. However, knowing the shape of a virus particle does not allow us to predict
anything about the biology, pathology, or molecular biology of similarly shaped viruses.
Thus, two viruses with very similar morphologies may differ in all of their other
fundamental characteristics.
4. Classification based on viral nucleic acids (Baltimore Classification): a classifica tio n
scheme, which encompasses all viruses, based on the nature of their genomes, and their
modes of replication and gene expression. In the Baltimore scheme, viruses are grouped
according to the mechanism of mRNA synthesis, which they employ.

3
1. Classification based on taxonomy: The International Committee on Taxonomy of
Viruses (ICTV), first founded in the late 1960s, has established a taxonomic classifica tio n
scheme for viruses. In assigning a virus to a taxonomic group, the ICTV considers a range
of characteristics. These include host range (eukaryote or prokaryote, animal, plant, etc.),
morphological features of the virion (enveloped, the shape of capsid or nucleocapsid, etc.),
and nature of the genome nucleic acid (DNA or RNA, single-stranded or double-stranded,
positive or negative sense, etc.).

4
5
Host Parasite Relationship

Infection and Disease

A delicate relationship exists between pathogenic microorganisms and body defenses. When the
defenses resist the pathogens, the body remains healthy. However, when the pathogens overcome
the defenses, the result is disease. Once disease has been established, the infected individual may
suffer temporary or permanent damage or may experience death. The outcome depends upon many
factors attending the episode of disease.

The scientific study of disease is called pathology, from the Greek “pathos” meaning suffering.
Pathology is concerned with the cause of disease, called the etiology (the agent of disease is
the etiologic agent). It also deals with pathogenesis, the manner in which a disease develops.
Pathology is also concerned with the structural and functional changes brought about by the
disease in tissues.

The terms infection and disease do not have identical meaning. Infection refers to an invasion of
body tissues by microorganisms; disease is a change from the state of good health resulting from
a microbial population living in the tissues. Infection may occur without disease. For example, the
flora of microorganisms always present on the body's skin is a type of infection but not disease

The normal flora

The normal flora is the population of microorganisms found where the body tissues interface with
the environment. Much of the normal flora is permanent, but some portions are transient.
The transient flora is present for a time and then disappears. Various types of relationships exist
between the normal flora and the body. The general name of a relationship is symbiosis, a term
that means living together. In some cases, the symbiosis is further identified as a commensalis m,
when one-organism benefits and the other remain unaffected. A type of symbios is
called mutualism exists when both organisms benefit one another. A symbios is
called parasitism develops when one organism damages the other.

6
Opportunistic organisms

Certain organisms of the normal flora are opportunistic. Opportunistic organisms are potentially
pathogenic organisms that normally do not cause disease. However, in a compromised host, the
organisms may see “opportunity” to invade the tissues. An example occurs in individuals who
have AIDS. Opportunistic organisms such as Pneumocystis carinii invade the lung tissues and
cause a lethal pneumonia.

Knowing How Infectious Disease Spreads

Infectious diseases are those caused by microorganisms. In order to relate a particular organism to
a particular disease, Koch's postulates must be fulfilled. First devised by Robert Koch in the
1870s, Koch's postulates are a series of procedures for identifying the cause of a particular disease .

Koch’s four postulates are:

1. The organism causing the disease can be found in sick individuals but not in healthy ones.
2. The organism can be isolated and grown in pure culture.
3. The organism must cause the disease when it is introduced into a healthy animal.
4. The organism must be recovered from the infected animal and shown to be the same as the
organism that was introduced.

Symptoms and signs

An infection is the successful colonization of a host by a microorganism. Infections can lead to

disease, which causes signs and symptoms resulting in a deviation from the normal structure or
functioning of the host. Microorganisms that can cause disease are known as pathogens. The signs
of disease are objective and measurable, and can be directly observed by a clinician. Vital signs,
which are used to measure the body’s basic functions, include body temperature (normally 37 °C
[98.6 °F]), heart rate (normally 60–100 beats per minute), breathing rate (normally 12–18 breaths
per minute), and blood pressure (normally between 90/60 and 120/80 mm Hg). Changes in any of
the body’s vital signs may be indicative of disease. For example, having a fever (a body
temperature significantly higher than 37 °C or 98.6 °F) is a sign of disease because it can be
measured. In addition to changes in vital signs, other observable conditions may be considered

7
signs of disease. For example, the presence of antibodies in a patient’s serum (the liquid portion
of blood that lacks clotting factors) can be observed and measured through blood tests and,
therefore, can be considered a sign. However, it is important to note that the presence of antibodies
is not always a sign of an active disease. Antibodies can remain in the body long after an infectio n
has resolved; also, they may develop in response to a pathogen that is in the body but not currently
causing disease. Unlike signs, symptoms of disease are subjective. Symptoms are felt or
experienced by the patient, but they cannot be clinically confirmed or objectively measured.
Examples of symptoms include nausea, loss of appetite, and pain. Such symptoms are important
to consider when diagnosing disease, but they are subject to memory bias and are difficult to
measure precisely.

Incidence and prevalence

The incidence of a disease refers to the percent of a population that contracts it over a particular
period. The prevalence of a disease, by contrast, is the percentage of a population having the
disease at a particular time. When a disease occurs only occasionally, it is called a sporadic
disease. A disease present in a population at all times is an endemic disease. A disease that breaks
out in a population in a short period is an epidemic disease, and an epidemic disease occurring
throughout the world is a pandemic disease.

Types of disease

Diseases can be defined in terms of their severity and duration. An acute disease occurs rapidly
and lasts a short time, while a chronic disease develops slowly and lasts a long time. Influenza is
an acute disease, while tuberculosis is a chronic disease. A subacute disease is a disease that has
vague symptoms and lasts a relatively long time. A latent disease remains inactive in a host for a
time and then becomes active. Infectious diseases may also be described as primary diseases or
secondary diseases. A primary disease is the first illness that occurs, and a secondary disease is
due to an opportunistic microorganism, often a normal resident, after the body's defenses have
weakened.

8
Classifications of Disease

An infectious disease is any disease caused by the direct effect of a pathogen. A pathogen may be
cellular (bacteria, parasites, and fungi) or acellular (viruses, viroids, and prions). Some infectio us
diseases are also communicable, meaning they are capable of being spread from person to person
through either direct or indirect mechanisms. Some infectious communicable diseases are also
considered contagious diseases, meaning they are easily spread from person to person. Not all
contagious diseases are equally so; the degree to which a disease is contagious usually depends on
how the pathogen is transmitted. For example, measles is a highly contagious viral disease that
can be transmitted when an infected person coughs or sneezes and an uninfected person breathes
in droplets containing the virus. Gonorrhea is not as contagious as measles because transmiss io n
of the pathogen (Neisseria gonorrhoeae) requires close intimate contact (usually sexual) between
an infected person and an uninfected person.

Diseases that are contracted as the result of a medical procedure are known as iatrogenic diseases.
Iatrogenic diseases can occur after procedures involving wound treatments, catheterization, or
surgery if the wound or surgical site becomes contaminated. For example, an individual treated for
a skin wound might acquire necrotizing fasciitis (an aggressive, “flesh-eating” disease) if bandages
or other dressings became contaminated by Clostridium perfringe ns or one of several other bacteria
that can cause this condition.

Diseases acquired in hospital settings are known as nosocomial diseases. Several factors
contribute to the prevalence and severity of nosocomial diseases. First, sick patients bring
numerous pathogens into hospitals, and some of these pathogens can be transmitted easily via
improperly sterilized medical equipment, bed sheets, call buttons, door handles, or by clinicia ns,
nurses, or therapists who do not wash their hands before touching a patient. Second, many hospital
patients have weakened immune systems, making them more susceptible to infectio ns.
Compounding this, the prevalence of antibiotics in hospital settings can select for drug-resista nt
bacteria that can cause very serious infectio ns that are difficult to treat.

Certain infectious diseases are not transmitted between humans directly but can be transmitted
from animals to humans. Such a disease is called zoonotic disease (or zoonosis). According to
WHO, a zoonosis is a disease that occurs when a pathogen is transferred from a vertebrate animal
to a human; however, sometimes the term is defined more broadly to include diseases transmitted

9
by all animals (including invertebrates). For example, rabies is a viral zoonotic disease spread from
animals to humans through bites and contact with infected saliva. Many other zoonotic diseases
rely on insects or other arthropods for transmission. Examples include yellow fever (transmitted
through the bite of mosquitoes infected with yellow fever virus) and Rocky Mountain spotted fever
(transmitted through the bite of ticks infected with Rickettsia rickettsii).

In contrast to communicable infectious diseases, a noncommunicable infectious disease is not

spread from one person to another. One example is tetanus, caused by Clostridium tetani, a
bacterium that produces endospores that can survive in the soil for many years. This disease is
typically only transmitted through contact with a skin wound; it cannot be passed from an infected
person to another person. Similarly, Legionnaires disease is caused by Legionella pneumophila, a
bacterium that lives within amoebae in moist locations like water-cooling towers. An individ ua l
may contract Legionnaires disease via contact with the contaminated water, but once infected, the
individual cannot pass the pathogen to other individuals. In addition to the wide variety of
noncommunicable infectious diseases, noninfectious diseases (those not caused by pathogens) are
an important cause of morbidity and mortality worldwide.

Modes of disease transmission

 When a disease remains in a population, a source of pathogens called a reservoir of

infection exists within the population. The reservoir can be human, animal, or nonliving,
such as the soil. A human reservoir who has had the disease and recovered but continues
to shed infectious organisms is called a carrier. Animal diseases spread to humans are
called zoonoses.
 Among the principal routes of transmission of disease are contact, vectors, and
vehicles. Contact can be direct or indirect. Direct transmission occurs from person to
person by such things as touching, kissing, and sexual intercourse. Indire ct
transmission occurs when a nonliving object is intermediary between two humans.
 A lifeless object known as a fomite is often involved in disease transmission. The object
may be a towel, cup, or eating utensil. Transmission can also be effected by droplet nuclei,
bits of mucus and saliva that spread between individuals.

10
  Vectors are living things. Arthropods such as mosquitoes, flies, and ticks may carry
pathogens on their body parts, in which case they are mechanical vectors. If the arthropod
is infected and transmits the organism in its saliva or feces, it is a biological vector.
 Vehicles are lifeless objects such as food, water, and air. Water may be contaminated by
human feces, while food is often contaminated by pathogens from the soil. Air can be a
vehicle for transmission for droplet nuclei in such diseases as tuberculosis and common
colds.
 In order for infection to be transmitted, microorganisms must leave the body through a
portal of exit, which can be the intestine, mouth, or skin surface. Generally, the portal of
exit is the same as the infected body part. Organisms enter the new individual through
a portal of entry.

Disease patterns

 When a disease develops in an individual, a recognized set of periods can be identified.

The first period is the period of incubation, the time between the entry of the parasite into
the host and the appearance of symptoms.
 The next period is the prodrome period. This period is accompanied by mild symptoms
such as aches, fever, and early signs of disease.
 Next comes the period of illness, when the disease is most acute. Signs and symptoms are
most apparent, and each disease has its own characteristic appearance. The body's immune
system is activated during this period, and specific defense is critical to recovery.
 The final periods are the periods of decline and convalescence. The period of decline is
one in which the signs and symptoms subside, and during the period of convalescence,
the person returns to normal. After the disease has abated, the immune system continues to
produce antimicrobial factors that will ensure long-term immunity.

Infectious diseases can be contagious during all five of the periods of disease. Which periods of
disease are more likely to associated with transmissibility of an infection depends upon the disease,
the pathogen, and the mechanisms by which the disease develops and progresses. For example,
with meningitis (infection of the lining of brain), the periods of infectivity depend on the type of
pathogen causing the infection. Patients with bacterial meningitis are contagious during the

11
incubation period for up to a week before the onset of the prodromal period, whereas patients with
viral meningitis become contagious when the first signs and symptoms of the prodromal period
appear. With many viral diseases associated with rashes (e.g., chickenpox, measles, rubella,
roseola), patients are contagious during the incubation period up to a week before the rash
develops. In contrast, with many respiratory infections (e.g., colds, influenza, diphtheria, strep
throat, and pertussis) the patient becomes contagious with the onset of the prodromal period.
Depending upon the pathogen, the disease, and the individual infected, transmission can still occur
during the periods of decline, convalescence, and even long after signs and symptoms of the
disease disappear. For example, an individual recovering from a diarrheal disease may continue to
carry and shed the pathogen in feces for some time, posing a risk of transmission to others through
direct contact or indirect contact (e.g., through-contaminated objects or food).

12
Pathogenicity and Virulence

The ability of a microbial agent to cause disease is called pathogenicity, and the degree to which
an organism is pathogenic is called virulence. Virulence is a continuum. On one end of the
spectrum are organisms that are avirulent (not harmful) and on the other are organisms that are
highly virulent. Highly virulent pathogens will almost always lead to a disease state when
introduced to the body, and some may even cause multi-organ and body system failure in healthy
individuals. Less virulent pathogens may cause an initial infection, but may not always cause
severe illness. Pathogens with low virulence would more likely result in mild signs and symptoms
of disease, such as low-grade fever, headache, or muscle aches. Some individuals might even be
asymptomatic.

An example of a highly virulent microorganism is Bacillus anthracis, the pathogen responsible

for anthrax. B. anthracis can produce different forms of disease, depending on the route of
transmission (e.g., cutaneous injection, inhalation, ingestion). The most serious form of anthrax is
inhalation anthrax. After B. anthracis spores are inhaled, they germinate. An active infectio n
develops and the bacteria release potent toxins that cause edema (fluid buildup in tissues), hypoxia
(a condition preventing oxygen from reaching tissues), and necrosis (cell death and inflammatio n).
Signs and symptoms of inhalation anthrax include high fever, difficulty breathing, vomiting and
coughing up blood, and severe chest pains suggestive of a heart attack. With inhalation anthrax,
the toxins and bacteria enter the bloodstream, which can lead to multi-organ failure and death of
the patient. If a gene (or genes) involved in pathogenesis is inactivated, the bacteria become less
virulent or nonpathogenic.

Virulence of a pathogen can be quantified using controlled experiments with laboratory animals.
Two important indicators of virulence are the median infectious dose (ID ) and the median lethal
dose (LD ), both of which are typically determined experimentally using animal models.
Contributing Factors

Infectious disease results from a competition for supremacy between the parasite and the host. If
the parasite overcomes the host, there is a change in the general state of good health and disease

13
develops. Several contributing factors are involved in the establishment of infectious disease.
These factors determine whether the infecting organism will survive in the body.

1. Portals of entry: In order for a pathogen to gain access to the host, the pathogen must pass
through a portal of entry. One of the most common portals of entry is the mucous
membranes, especially those of the respiratory, gastrointestinal, and urogenital tracts.
Another important portal of entry is the skin. Penetration of the skin occurs during a wound
or by a hair follicle. When microorganisms penetrate below the skin, the portal of entry is
said to be the parenteral route.
2. Dose: The dose of an organism refers to the number of microorganisms required to
establish an infection. For some diseases, such as typhoid fever, the dose is a few hundred
bacteria. For other diseases, such as cholera, the dose may be several million bacteria. The
ID is the number of pathogen cells or virions required to cause active infection in 50% of
inoculated animals. The LD is the number of pathogenic cells, virions, or amount of toxin
required to kill 50% of infected animals. To calculate these values, each group of anima ls
is inoculated with one of a range of known numbers of pathogen cells or virions. In graphs
like the one shown below, the percentage of animals that have been infected (for ID ) or
killed (for LD ) is plotted against the concentration of pathogen inoculated.

14
 3. Invasiveness: Invasiveness is a property that encourages disease because it refers to the
ability of pathogens to penetrate into the tissues. Those organisms that cause intestina l
ulcers, such as Entamoeba histolytica, penetrate the tissue effectively. Tissue invasio n
often begins with adherence, the ability of pathogens to attach to the tissue by using
structures such as pili. The presence of a capsule or glycocalyx encourages adherence
because they are composed of sticky materials.

Pathogenic Viruses

 Because viruses lack metabolic capabilities, they rely on other means for overcoming body
defenses and causing disease. Viruses avoid body defenses by multiplying within host
cells, where antibodies and other components of the immune system cannot reach them.
 The effect occurring in host cells during viral invasion is referred to as the cytopathic
effect. The cytopathic effect can develop when the virus alters the metabolism of the cell
and prevents it from producing essential cellular components.
 Alternatively, the virus may induce cells to cling together in a large mass called
a syncytium. In some cases, the virus causes the cell's lysosomes to release enzymes which
then destroy the cell.

The virulence of viruses is not well defined. A number of factors contribute to the virule nce
(pathogenicity) of a particular strain of virus.

A. Ability to enter the cell

B. Ability to grow within the cell
C. Ability to combat host defense mechanisms
D. Ability to produce temporary or permanent damage in the host via:
1. Cell lysis
2. Production of toxic substances
3. Cell transformation
4. Induction of formation of substances, which are not specified by the viral genome, but are
apparently cellular products normally not produced by the cell.
E.Induction of structural alterations in the host cell

 Nuclear (including chromosomal)

 Cytoplasmic

15
Some viruses enter host tissues directly by trauma or insect bite, but most infections start on the
mucous membranes of the respiratory and alimentary tracts. To initiate infection, virus particles
must first survive on these mucous-covered membranes in the presence of viral and non-viral
commensals. Subsequently, to replicate, the virus must enter host cells either in the mucous
membrane itself or in tissues farther afield after penetration through the surface membrane.
Replication in mucous membrane cells can produce the disease effects directly as in respiratory
diseases, but sometimes it provides a staging post for subsequent damaging replication in another
site, e.g., polio virus replicates first in the alimentary tract cells and ultimately in anterior horn
cells of the spinal cord.

What is the Immune system?

When microbes attack our bodies, we defend ourselves by utilizing our various mechanisms of
immunity. Immunity, also called resistance, is the ability to ward off disease caused by microbes
or their products and to protect against environmental agents such as pollen, chemicals, and animal
dander. Lack of immunity is referred to as susceptibility.

The immune system is the complex network of organs, cells, and proteins that protects the body
against infections. This defense system proceeds via the recognition and processing of foreign
substances. The network consists of the lymphatic system, complement system, spleen, thymus,
bone marrow, and cells (WBCs, B cells, T cells).
First-line defenses keep pathogens on the outside or neutralize them before infection begins. The
skin, mucous membranes, and certain antimicrobial substances are part of these defenses.

Second-line defenses slow or contain infections when first-line defenses fail. They include
proteins that produce inflammation, fever that enhances cytokine activity, and phagocytes and NK
cells, which attack and destroy cancer cells and virus-infected cells.

Third-line defenses include lymphocytes, shown in the table below, that target specific pathogens
for destruction when the second-line defenses do not contain infections. It includes a memory
component that allows the body to more effectively responds to that same pathogen in the future.

Innate and Adaptive

Innate immunity refers to defenses that are present at birth. The nonspecific arm of the immune
system with which an individual is born is termed innate immunity (also called natural immunity).
16
They are always available to provide rapid responses to protect us against disease. Innate immunity
does not involve recognition of a specific microbe. Further, innate immunity has no memory
response, that is, a more rapid and stronger immune reaction to the same microbe later. Innate
immunity first-line defenses include skin and mucous membranes, and the second-line defenses
include natural killer cells, phagocytes, inflammation, fever, and antimicrobial substances. Innate
immune responses represent immunity’s early-warning system and are designed to prevent
microbes from gaining access into the body and to help eliminate those that do gain access.

The components of the innate immune system based on innate immunity development include:

Physiological barriers: These components include the epithelial lining of the skin, mucous
membrane, and physical parameters like temperature, pH, and barriers like enzymes, antimicrob ia l
peptides, cytokines, etc.

 Anatomical barriers: Being non-specific, many components have pattern recognition in

which receptors referred to as pattern recognition receptors (PRRs) can recognize unique
molecules present within microbes called pathogen-associated molecular patterns
(PAMPs).
 Phagocytosis: The foreign body is ingested by specialized cells called phagocytes in an
endocytosis process. Phagosomes are formed when these foreign bodies are ingested,
which is a vacuole surrounding these bodies. Later on, the lysosome present within the
phagocytes fuses with the phagosome, forming a phagolysosome. The release of lytic
enzymes present in lysosome eventually lyses the infectious agent hence clearing the
infection.
 Inflammatory Reactions: Inflammatory reactions are induced with four cardinal features
when host tissue is damaged. These features include calor (temperature rise), dolor (pain),
rubor (redness), and tumor (swelling). Histamines, proinflammatory cytokines, defensins,
and kinins are mediators of inflammatory reactions.

17
Innate immunity in an individual is also influenced by other factors, such as:

 Age: Very old people and young ones are more susceptible to infections when compared
to adults.
 Hormonal level: Any individual under corticosteroid hormone treatment is more
susceptible to infection. Likewise, hormonal disorders like hypothyroidism, diabetes
mellitus, etc., can make the individual more prone to infections.
 Nutritional status: Nutritional status of the host, like deficiency of vitamins and proteins,
makes an individual more susceptible to infections.
Significance of innate immunity
 Physical and chemical barriers prevent the entry of foreign materials.
 If the infection is established, a cascade of complement reactions and phagocytosis helps
clearance of the infecting agents.
 It activates the adaptive immune system by the release of cytokines and antigen
presentation.

Adaptive immunity is based on a specific response to a specific microbe once a microbe has
breached the innate immunity defenses. It adjusts to handle a particular microbe. Unlike innate
immunity, adaptive immunity is slower to respond, but it does have a memory component that
allows the body to more effectively targets the same pathogens in the future. Adaptive immunity
involves lymphocytes (a type of white blood cell) called T cells (T lymphocytes) and B cells (B-
lymphocytes). The mediators of acquired infection include:

 Humoral immunity: Serum proteins called antibodies produced by B cells mediate this type
of immunity. The humoral immune response protects the body against extracellular
infections. Activation and differentiation of B cells into antibody-secreting plasma cells
occur when these extracellular antigens are recognized by body cells, especially helper T
cells.
 Cellular immunity: The immune response in cellular immunity is mediated by T cells.
Cellular immunity protects the body against intracellular infections. The initial step in
cellular immune response involves recognizing the antigen by phagocytes, then sensitiza tio n
of cytotoxic T cells, and, finally, releasing cytokines in response to that antigen. In case of a

18
 repeated encounter with the same antigen, memory T cells made during initial exposure act
by a faster and more potent response.
Significance of Acquired (Adaptive) Immunity
 Antigen-specific antibodies help to neutralize the infection.
 Immunological memory is developed in the form of memory B cells, which respond
immediately upon the re-exposure to the specific infectious agent.
 T helper cells help in the activation of other immune cells.
 Cytotoxic T cells destroy cells infected with viruses and tumor cells.
 Regulatory T cells suppress immune response when required, preventing body cells from
unwanted self-attack.

Body Lines of Defense- Innate and Acquired Immunity

The immune system comprises a complex network of immune cells that work in synergy with
proteins such as cytokines in order to combat pathogenic invaders such as bacteria, viruses, fungi,
parasitic worms, abnormal cells, etc. They have a unique ability to distinguish self-molecules from
non-self-molecules except in some diseased conditions such as autoimmune diseases. The ability
to distinguish self from non-self is based on the unique Major Histocompatibility Complex
(MHC) protein that an individual’s all body cells possess on their surface, except for identica l
twins. There are two types of MHC proteins: MHC I and MHC II in which MHC I differentiate
the body’s own cells from foreign cells or pathogens and displays antigen on the surface of the cell
however, MHC II is present in immune cells called antigen-presenting cells (APC) along with
MHC I and these display phagocytosed microbe on the cell surface. MHC proteins are absent in
red blood cells.
Innate and Acquired Defense Systems
There are two types of body responses against invaders:

Innate (Natural/Non-specific response) and Acquired (Adaptive/Specific) responses.

 Innate responses occur to same extent no matter how many times the pathogen is exposed while
acquired responses are improved with the repeated subsequent exposure to foreign particles.
 Innate responses employ phagocytic cells such as neutrophils, monocytes and macrophages, and
Natural Killer (NK) cells. However, adaptive responses involve antigen-specific B and T
cells or antigen-presenting cells (APCs).

19
 Innate responses respond immediately to the foreign attack while adaptive take a longer time
to react.
 Innate responses fight against all invaders, hence termed as non-specific and acquired responses
fight against specific types of invaders, specific.
 Innate response comprises of the first and second line of defense and acquired response
includes the third line of defense.
1. First Line of Defense
 It is also known as an outside defense system.
 Physical, chemical, and biological defenses form the first line of defense against the
invasion of pathogens and these do not function independently and can overlap based on
their functions.
i) Physical defenses: These include physical barriers and mechanical defenses, which block the
entry point of pathogens such as intact skin and mucus.
 Skin has three layers: the epidermis, the dermis, and the hypodermis. The topmost layer,
the epidermis is packed with keratin along with dead skin cells. These dead cells are
frequently being shed and replaced. The keratin is highly water-resistant and mechanica lly
tough hence, resists microbial growth.
 Nasal hairs filter air contaminated with microbes, dust, and dirt while microscopic
cilia lining the respiratory tract, sweep mucus and trap particles inhaled towards body
openings where they can be removed from the body.
 Mucous membranes lining respiratory, urinary, and reproductive tracts, produce mucus,
a slimy substance that traps foreign particles and directs them out of the body by
mechanical actions such as shedding, coughing, peristalsis, and flushing of bodily fluids
(e.g. urination, tears)
ii) Chemical defenses comprise chemicals and enzymes in body fluids, a variety of plasma protein
mediators, cytokines, antimicrobial peptides, inflammation- eliciting mediators that destroys
pathogens on the outer body surface, at body opening, and on inner body linings.
 Sweat, tears, mucus, and saliva contain enzymes that kill pathogens. Lysozyme, an
enzyme found in tears, perspiration, and saliva can break down the cell walls of bacteria
and kill them. Likewise, secretory IgA function in a similar manner by attacking
peptidoglycans in the cell wall of bacteria. Antimicrobial peptides (AMPs) include

20
 dermcidin, cathelicidin, defensins, histatins, and bacteriocins. AMPs are produced in
response to pathogens on the skin
 Cerumen or earwax contains fatty acids thereby lowering the pH between 3 and 5, it
protects the auditory canal from foreign particles like microbes.
 Gastric juice (pH 2-3) is highly acidic in nature and those pathogens that enter the stomach
through the oral cavity or nasal tract are destroyed by it.
 Urine flow, acidic in pH, kills microbes and direct out of the urethra.
 Serum (unsaturated fatty acids) reduce water loss as well as inhibit microbial growth
however, it is found to have certain compounds that facilitate to provide nutrition for
certain microbes.
iii) Biological defenses are provided by living microorganisms that are friendly and beneficial
This resident natural flora resides on our skin, in our bowel, and in other places such as the mouth,
gut, reproductive part, etc. These prevent pathogen adherence and their colonization by creating
an acidic environment with the help of fermentation of sugars to acids, occupying available cellular
binding sites and competing with them for available nutrients. Thus, resident normal microbiota
also contributes to chemical defenses as they produce bacteriocins that perform the antibacter ia l
activity.
2. Second Line of Defense
The second line of defense is also known as the immune system. When the first line of defense is
broken, the second line of defense within our body ‘kicks’ in and gets activated i.e. when the
pathogens successfully win the battle against barriers from the first line of defense, they are next
encountered by the second line. This mechanism involves the participation of mainly immune cells
mainly white blood cells (leucocytes) such as phagocytes, NK cells, dendritic cells, mast cells, and
complement proteins to recognize and eliminate any non-specific pathogen entered into the body.
There is no immunological memory.

Phagocytes (eating cells) and their relatives

 Basophils: These account for merely 1% of WBCs. These are known for their
inflammatory response associated with asthma and allergies as when they are stimulated,
they release heparin and histamine.
 Mast cells: These exhibit functional similarities with basophils although these reside
within tissues. They show inflammatory response because of activation with differe nt

21
 inflammatory mediators, and antigens. It releases granules that include inflamma tor y
histamine once it recognizes pathogens.
 Monocytes: These are related to scavenging and are known as “garbage trucks” or
“vacuum cleaners” of the immune system. These comprise around 2-6% of WBCs in the
blood. These cells form the largest among WBCs. They differentiate into macrophages and
dendritic cells after leaving the circulation into tissues in response to inflammation.
 Macrophages: These engulf and digest pathogens lacking specific surface proteins to
healthy body cells, such as cancerous cells, microbes, cellular debris, etc., and are found in
the tissues and organs. They release regulatory factors such as interferons, interleuk ins,
etc., and a wide array of chemicals including enzymes, and complement proteins. These
active T cells and hence, the adaptive immune system by acting as “antigen-presenting
cells” as these processes engulfed antigens and present them to T cells.
 Dendritic cells: These are differentiated from monocytes present in the tissues located in
contact with the external environment such as skin, nose, lungs, etc. These cells link innate
immunity and adaptive immunity. Once they find foreign particles, they migrate to lymph
nodes where they present the antigen and interact with T cells and B cells that initiate an
adaptive immune response. These are named dendritic in the sense that they have their
cellular morphology in the form of a “tree-like” structure.
 Neutrophils: These are the first immune cells to respond to intruders and form
approximately 65% of WBCs. They squeeze out through capillaries into the site of
infection as well as send out signals to alert other immune cells. Thus, these are also known
as ‘patrol tissue’. Once they are released from bone marrow, they have a short life span of
about only eight hours.
 Natural Killer (NK) cells: These are the only cytotoxic lymphocytes belonging to the
innate immune system and respond rapidly to virus-infected cells or tumor cells without
any priming or prior activation. Thus, these are best known for their “natural” killing ability
subsequently, help to detect and control early signs of cancer.
Mechanism of the second line of defense
 With the invasion of the pathogen at the entry site, neutrophils come into action to engulf
and destroy them.

22
  If they evade the action of neutrophils, then macrophages and dendritic cells go into battle,
which helps to phagocytose and present antigens to T cells. Different internal defense
includes phagocytosis, NK cells, inflammatory response, fever, and the compleme nt
system in the second line of defense.
 Different cytokines are released by immune cells as well as infected cells, which amplify
the quantity of cytokine secretion.
 This triggers an inflammatory response, capillary dilation, and increased permeability of
the capillary wall.
 Macrophages are involved in the resolution of the inflamed site and clearing up cellular
debris.
 Cytokines also increase the core body temperature resulting in fever. This increased
temperature inhibits microbial growth and speeds up recovery and repair processes.
 NK cells detect viral infested cells or cancerous cells thereby inducing apoptosis. Simila r ly,
different complement proteins found in the blood serum, are attracted to pathogens tagged
with the adaptive immune system.
 A cascade of binding of complement proteins to pathogens coats the pathogen that serves
as a marker to detect the presence of a pathogen in phagocytes and their digestion by the
phagocytosis process.
3. Third Line of Defense
The third line of defense is also known as the adaptive immune system, which is not acquired by
birth but during the lifetime. These target only specific pathogens and build long-lasting immunity,
strong immune response, and immunological memory. It takes a long time to develop innate
immunity as lag time occurs between exposure and maximal response. However, on repeated
exposure to the same antigen, these respond quickly to eliminate. It works to identify, destroy and
remember principles. It gets activated only when pathogens pass the first and second line of
defense. Different cells involved in the third line of defense are antigen-presenting cells (APC), B
lymphocytes, and T lymphocytes.

Lymphocytes comprise T cells, B cells, and NK cells, which make up 20-30% of WBCs and are
found in the lymph hence named lymphocytes. Among them, T and B cells are components of
adaptive immune response while NK cells are of the innate immune response as aforementio ned.
Humoral and cell-mediated immune responses are part of this defense.

23
Humoral or antibody-mediated immune response
B cells participate in antibody-mediated response where B cells in contact with a pathogen, are
activated and produce antibodies that are released into the bloodstream. Notation ‘B’ cell was
derived after the experiment conducted by Max Cooper in the 1960s to study the function of B
cells where he demonstrated that antibody production was completely abrogated in irradiated
chicken after surgical removal of the Bursa of Fabricius: the primary site of B cell development in
birds. They originate and mature both in the bone marrow. B cells express diverse antigen-spec if ic
molecules on their outer surface that helps in antigen detection. Thus, when naive B cells encounter
an antigen in the lymphatic system, these undergo clonal expansion and some clones differentiate
into Memory B cells and Plasma B cells (Plasma cells / Plasmocytes / Effector B cells).

 Plasma B cells: These secrete antibodies also called immunoglobulins (Igs).

 Memory B cells: They provide the immune system with long-lasting memory.
Mechanism of antibody-mediated immune response
 On exposure of B cells with its receptor to its matching antigen, it internalizes the antigen,
digests it, and displays its fragments on its surface bound to unique MHC II molecules.

 This complex attracts mature matching helper T cells, which secrete cytokines,
interleukins, etc. Thus, produced secretions help in turn stimulate mitosis in B cells and
their multiplication.

 Some B cells mature into plasma and memory cells. Antibodies secreted by plasma cells
attach to antigens forming antigen-antibody complexes, which are later cleared off by
complement cascade, neutralization, agglutination, precipitation, etc.

Cell-mediated immune response

This immune response is driven by T lymphocytes, APCs such as macrophages, B cells, and
dendritic cells, and various cytokines. It does not use antibodies. It mostly kills viruses and
cancerous cells. There are 4 types of T lymphocytes: T-helper cells, T-killer cells, T-suppressor
cells, and T-memory cells.

 TH /T helper cells (CD4+): These cells secrete cytokines, which stimulate cell division of B
cells and its maturation into plasma and memory cells, activation of macrophages to bring
about phagocytosis, and clonal expansion of TH cells.

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  Tc (T- killer/cytotoxic) cells (CD8+): These cells trigger the destruction of the pathogen’s
DNA by secreting cytotoxin or creating holes in the pathogen’s cell membrane by perforin.
This results in cell lysis or apoptosis.
 T-suppressor cells/Treg/Regulatory T cells: This form the part of the self-check built- in
mechanism inside the body to prevent excessive immune reactions by shutting down T cell-
mediated immunity once the pathogen has been defeated and helps to prevent autoimmune
diseases.
 T-memory cells: The population of these cells increases only after their initial exposure to
an antigen. If the same antigen presents itself again, they are triggered to convert themselves
into cytotoxic T cells and kill the pathogen.
Mechanism of cell-mediated immune response
 When APCs present antigenic fragments on its surface attached with MHC II protein, naïve
T cells interact with MHC II- Ag complex with its T cell receptor (TCR) as well as several
costimulatory interactions take place.
 They start a cross talk with each other where APCs release interleukins while on the other
hand; T cells secrete cytokines and interferons, which induce their differentiation into
subsets of effector T cells.
 T cell secretes IL-1 that signals activation of helper T cells and IL-2, which results in the
proliferation of cytotoxic T cells and B cells.
 These are associated with not only promoting cellular immunity but also humoral immunity
indirectly as TH cells stimulate B cells and their differentiation into plasma and memory
cells.
 TC cells secrete cytotoxin and perforins that destroy pathogens or infected cells.

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Vaccines

A vaccine is a medical preparation given to provide immunity from a disease. Vaccines use a
variety of different substances ranging from dead microorganisms to genetically engineered
antigens to defend the body against potentially harmful microorganisms.
Effective vaccines change the immune system by promoting the development of antibodies that
can quickly and effectively attack disease-causing microorganisms when it enters the body,
preventing disease development.
A vaccine may contain live-attenuated or killed microorganisms or parts or products from them
capable of stimulating a specific immune response comprised of protective antibodies and T-cell
immunity.
A vaccine should stimulate a sufficient number of memory T and B lymphocytes to yield effector T
cells and antibody-producing B cells from memory cells.
The viral vaccines should also be able to stimulate high titers of neutralizing antibodies.
Injection of a vaccine into a nonimmune subject induces active immunity against the modified
pathogens.
Vaccination is immunization against infectious disease through the administration of vaccines for
the production of active (protective) immunity in humans or other animals.

How do vaccines work in the immune system

 Vaccines are biological preparations that are made up of killed or attenuated pathogens (virus
or bacteria) or part of the surface of the antigen.
 The preparation is made in such a way that it can not cause disease on its own, but it helps
the body to develop a memory type of immunity. This means that if an individual encounters
or is infected by the same pathogen (whose part has been used to prepare the vaccine), the
immunity will ‘remember’ and induce a more vigorous immune response against the
pathogen.
 Initially, the innate immune response (primary response) elicited on the first encounter with
a pathogen, is normally slow and that is why one will display symptoms of the disease before

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 the immune system can elicit a reaction to kill the pathogen, and therefore the body develops
an adaptive immune response (secondary response) through specialized immune cells which
counter the pathogen and create a long-lasting memory.
 Therefore, vaccination or the introduction of a vaccine into the body will have a similar kind
of immune reaction (secondary response) only that it will bypass the slow initial response
but enables the body to acquire immunity (from the vaccine). In other words, the vaccine
tricks the body to believe that it has the disease, and therefore, is able to fight the disease.
This makes the body able to kill the pathogen before it can have the chance to cause disease
due to memory that is created from vaccination.

Generally, vaccine works as follows:

Administration of a vaccine which contains antigens for a specific disease or pathogen. Identifica tio n
and recognition of the antigen in the vaccine as foreign, by the immune system. Development of
antibodies by the immune system to neutralize the antigens. Storage of these immune effector
antibodies as memory antibodies for future response in case an individual is exposed to the live
pathogen or disease. Vaccines are given to prevent and eventually wipe out diseases. When a vaccine
is given to a significant portion of the population, it protects those who receive the vaccine as well
as those who cannot receive the vaccine. This concept is called “herd immunity.” When a high
percentage of the population is vaccinated and immune to a disease, they do not get sick — so there
is no one to spread the disease to others. This herd immunity protects the unvaccinated population
from contagious (spread from person to person) diseases for which there is a vaccine.

Vaccine types can broadly be classified into three groups:

Many vaccines that were developed early consist of an entire pathogen that is either killed
(inactivated) or weakened (attenuated) so that they cannot cause disease. They are known as whole -
organism vaccines. These vaccines elicit strong protective immune responses and many vaccines
used today are prepared in this manner, but not all disease-causing microbes can be effective ly
targeted with a whole-organism vaccine.
1. Inactivated (Killed) Vaccine
 These were produced by killing the pathogen (bacteria, virus, or other pathogens) with
chemicals or heat, or radiation.

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  The killed pathogen can not cause disease, and this means that they do not replicate in the
host’s body.
 Advantage: These vaccines are stable and safer than the live attenuated vaccines
 Disadvantage: The major disadvantage of this type of vaccine is that it elicits a weaker
immune response and therefore, it requires more vaccine dosages and a booster dose as well,
to confer protective immunity.
 Examples of Inactivated Vaccines include poliomyelitis (sulk vaccine), rabies, typhoid,
cholera, pertussis, pneumococcal, rabies, hepatitis B, and influenza vaccines.
2. Live-attenuated vaccines
 These vaccines were developed in the 1950s when advances in tissue culture techniques were
developed.
 These vaccines are prepared from a whole organism, by weakening their pathogenicity so
that they can not cause disease but can induce an immune response, hence the
term attenuation.
 These vaccines elicit strong immune responses because they are similar to the actual disease
pathogen and hence they confer a life-long immunity after only one or two doses, therefore
they are very effective.
 They are also relatively easy to create for certain viruses, but difficult to produce for more
complex pathogens like bacteria and parasites.
 Disadvantages: There is a remote chance that the weakened germ can mutate or revert to its
full strength and cause disease.
 Live attenuated vaccines should not be given to individuals with weakened or damaged
immune systems.
 To maintain potency, live attenuated vaccines require refrigeration and protection from light.
 Examples include Measles/Mumps/Rubella (MMR) and Influenza Vaccine Live, Intranasal
(FluMist®), Polio (Sabin vaccine), Rotavirus, Tuberculosis, Varicella, and Yellow fever.
 The attenuated strain of Mycobacterium bovis called Bacillus Calmette- Guérin (BCG) was
developed by growing M. bovis on a medium containing increasing concentrations of bile.
After 13 years, this strain had adapted to growth in strong bile and had become sufficie ntly
attenuated that it was suitable as a vaccine for tuberculosis.
3. Chimeric vaccine

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  The evolution of modern genetic engineering techniques has enabled the creation of
chimeric viruses, which contain genetic information from one viral particle and display the
biological properties of different parent viruses.
 An NIAID-developed live-attenuated chimeric vaccine consisting of a dengue virus
backbone with Zika virus surface proteins is undergoing early-stage testing in humans.
Subunit vaccines
These are vaccines that are prepared by using components or antigens of the pathogen. These
components can stimulate the immune system to elicit appropriate immune responses.
They are also known as acellular vaccines because they do not contain a whole cell, but just part
of a cell of the bacteria or virus.
Some of the subunit vaccines produced to prevent bacterial infections are based on the
polysaccharides or sugars that form the outer coating of many bacteria. Therefore, there are
subtypes of subunit vaccines as follows:

1. Polysaccharide Vaccine
 Some microbes contain a polysaccharide (sugar) capsule which they use for protection and
evading the human immune defences, especially in infants and young children.
 Therefore, these are vaccines that are prepared using the sugar molecules, and
polysaccharides from the outer layer of a bacteria or virus.
 They create a response against the molecules in the pathogen’s capsule. Normally these
molecules are small hence they are not immunogenic (can not induce an immune response
on their own).
 Hence, they tend to be ineffective in infants and young children between 18-24 months, and
they induce a short-term immunity associated with slow immune responses and slow
activation, and it does not increase antibody levels and it does not create an immune memory.
 Therefore, these sugar molecules are chemically linked to carrier proteins and work similar ly
to conjugate vaccines.
 Examples of polysaccharide vaccines include Meningococcal disease caused by Neisseria
meningitides groups A, C, W135, and Y, as well as Pneumococcal disease.
2. Conjugated Vaccines
 These vaccines are prepared by linking the polysaccharides or sugar molecules on the outer
layer of the bacteria to a carrier protein antigen or toxoid from the same microbe.

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  The polysaccharide coating disguises a bacterium’s antigens so that the immature immune
systems of infants and younger children cannot recognize or respond to them.
 Conjugate vaccines get around this problem through the linkage of polysaccharides with a
protein.
 This formulation greatly increased the ability of the immune systems of young children to
recognize the polysaccharide and develop immunity.
 The vaccine that protects against Haemophilus influenzae type B (Hib) is a conjugate
vaccine.
 Today, conjugate vaccines are also available to protect against pneumococcal and
meningococcal infections.
3. Toxoid Vaccines
 These vaccines are prepared from inactivated toxins, by treating the toxins with formalin, a
solution of formaldehyde, and sterilized water.
 This process of inactivation of toxins is known as detoxification and the resultant inactive
toxin is known as a toxoid.
 Detoxification makes the toxins safe to use.
 The toxins used for the preparation of toxoids are obtained from the bacteria that secrete the
illness-causing toxins.
 This means that when the host body receives the harmless toxoid. the immune system adapts
by learning how to fight off the natural bacterial toxin responsible for causing illness, by
producing antibodies that lock onto and block the toxin.
 Examples of toxoid vaccines include diphtheria and tetanus toxoid vaccines.
4. Recombinant Protein Vaccines
 After the start of the generic engineering era, recombinant DNA technology also evolved.
This is where DNA from two or more sources is combined. This technology harnessed the
development of recombinant protein vaccines.
 For recombinant vaccines to induce immunity against a pathogen, they have to be
administered along with an adjuvant or expresses by a plasmid or harmless bacterial or viral
vectors.
 Production of these recombinant protein vaccines involves the insertion of DNA encoding
an antigen such as a bacterial surface protein, which stimulates an immune response in

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 bacterial or mammalian cells, expressing the antigen in these cells, and then the antigen is
purified from them.
 Recombinant protein vaccines allow the avoidance of several potential concerns raised by
vaccines based on purified macromolecules. For example, the presence of contaminants in
vaccines after purification may cause potential harm to the host.
 The production of recombinant vaccines also allows the production of sufficient quantities
of purified antigenic components.
 The classical example of a recombinant protein vaccine currently in use in humans is
the vaccine against hepatitis B. The vaccine antigen is a hepatitis B virus protein produced
by yeast cells into which the genetic code for the viral protein has been inserted.
 Vaccines that are also used to prevent human papillomavirus (HPV) infections are also
based on the recombinant protein antigens, by preparing from the proteins of the outer shell
of HPV, which form particles that almost resemble the virus.
 The virus-like particles (VLPs) prompt an immune response that is similar to that elicited
by the natural virus, and they are non-infectious since they do not contain the genetic
materials that the virus needs to replicate inside the cells.
5. Nanoparticle vaccines
 This vaccine development was based on a strategy to present protein subunit antigens into
the immune system.
 The NIAID has also designed a universal flu vaccine, an experimental vaccine with the
protein ferritin which can self-assemble into microscopic pieces known as nanoparticles that
display a protein antigen.
 A nanoparticle-based influenza experimental vaccine is also being evaluated in human trials
(early stages).
 This new technology of vaccine delivery is also being evaluated and assessed for the
development of vaccines against MERS coronavirus, respiratory syncytial virus (RSV), and
Epstein-Barr virus.

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Nucleic acid vaccine
These are vaccines designed to aim at introducing the genetic materials that code the antigen or
the antigen that is aimed at inducing an immune response, enabling the host cells to use the genetic
materials to produce the antigens. The advantages of the nucleic acid vaccine approach include:
1. stimulating a broad long-term immune response
2. excellent vaccine stability
3. ease of large-scale vaccine manufacture
4. rapid production
5. reduces potential risks of working with the live pathogen
6. encoding only the key antigen without including other proteins
Some of the known nucleic acid vaccines models include:

1. DNA plasmid vaccines

 These are vaccines that are composed of a small circular piece of DNA known as a plasmid.
The plasmid carries genes that encode proteins from the pathogen of interest.
 Experimental DNA plasmid vaccines have been designed by the National Institute of Allergy
and Infection Disease (NIAID) to address some viral disease threats including SARS
coronavirus (SARS-CoV) in 2003, H5N1 avian influenza in 2005, H1N1 pandemic influe nza
in 2009, and Zika virus in 2016.
2. mRNA vaccines
 mRNA is an intermediary between DNA and protein. Recent technological advances have
developed mRNA vaccines overcoming the instability issues of mRNA and its delivery into
the cells, with encouraging results.
 Some experimental mRNA vaccines have been designed to protect mice and monkeys
against Zika virus infection and administered in a single dose.
3. Recombinant vector vaccine
 These are vaccines designed as vectors or carriers using harmless viruses or bacteria and they
introduce the genetic material into cells.
 Majorly these vaccines are designed and approved for use to protect animals from infectio us
diseases, including rabies and distemper, but some have been developed to protect humans
from viruses such as HIV, Zika virus, and Ebola virus.

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Viruses of medical importance

1. There are 20 families of viruses that are defined by chemical type of nucleic acid,
capsid symmetry, presence or absence of an envelope, number of capsomeres,
physical type of nucleic acid and number of genes.
2. The Family Parvoviridae, all members of which have linear single-stranded DNA
as their chromosome, includes the B11 virus, the agent of fifth disease, bone
marrow aplasia and polyarthralgia.
3. The Family Papovaviridae, whose members have circular double-stranded DNA
without gaps as their chromosome, includes the agents of warts, nephritis and
progressive multifocal leukoencephalopathy.
4. The Family Adenoviridae, members of which contain linear double-stranded DNA
as their chromosome, includes the agents of acute respiratory disease (ARD), the
common cold, acute hemorrhagic cystitis, epidemic keratoconjunctivitis,
gastroenteritis and hepatitis.
5. The Family Herpesviridae, members of which contain linear double-stranded DNA
as their chromosome, includes the agents of gingiva stomatitis, herpes genita lis,
herpes labialis, herpes gladiatorum, encephalitis, keratoconjunctivitis, chickenpox,
shingles, infectious mononucleosis, Burkitt's lymphoma, oropharyngeal carcinoma,
cytomegalovirus mononucleosis, cytomegalic inclusion disease, exanthema
subitum and Kaposi's sarcoma.
6. The Family Poxviridae, members of which contain linear double-stranded DNA as
their chromosome, includes the agents of smallpox, Monkeypox, vaccinia, cowpox,
pseudocowpox and molluscum contagium.
7. The Family Hepadnaviridae, members of which contain circular double-strand
DNA with gaps as their chromosome, includes the agent of hepatitis B (serum
hepatitis or long-term hepatitis).
8. The Family Picornaviridae, members of which contain linear single-stranded RNA
as their chromosome, includes the agents of polio, herpangina, aseptic meningitis,
the common cold, epidemic myalgia, hand-foot-mouth disease, myocarditis,
pericarditis, Boston exanthem, cerebellar ataxia, pneumonitis and hepatitis A
(infectious hepatitis or short-term hepatitis).

34
9. The Family Caliciviridae, members of which contain linear single-stranded RNA
as their chromosome, includes the agents of summer diarrhea and hepatitis E
(endemic hepatitis).
10. The Family Reoviridae, members of which contain linear segmented double -
stranded RNA as their chromosome, the agents of Colorado tick fever and winter
diarrhea. 11. The Family Togaviridae, members of which contain linear single -
stranded RNA as their chromosome, includes the agents of rubella, eastern equine
encephalitis and western equine encephalitis.
11. The Family Flaviviridae, members of which contain linear single-stranded RNA as
their chromosome, includes the agents of yellow fever, St. Louis encephalitis,
hepatitis G and dengue.
12. The Family Arenaviridae, members of which contain linear segmented single -
stranded RNA as their chromosome, includes the agent of lymphoc ytic
choriomeningitis.
13. The Family Coronaviridae, members of which contain linear single-stranded RNA
as their chromosome, includes the agent of the common cold.
14. The Family Retroviridae, members of which contain segmented linear single
stranded RNA as their chromosome, includes the agents of human T-cell lympho ma
and acquired immunodeficiency syndrome (AIDS).
15. The Family Bunyaviridae, members of which contain segmented linear single -
stranded RNA as their chromosome, includes the agents of California encephalitis
and Hantavirus pulmonary syndrome.
16. The Family Orthomyxoviridae, members of which contain segmented linear single -
stranded RNA as their chromosome, includes the agent of influenza.
17. The Family Paramyxoviridae, members of which contain segmented linear single -
stranded RNA as their chromosome, includes the agents of parainfluenza, mumps,
measles (rubeola), subacute sclerosing panencephalitis and respiratory syncytia l
disease.
18. The Family Rhabdoviridae, members of which contain linear single-stranded RNA
as their chromosome, includes the agents of vesicular stomatitis and rabies.

35
19. The Family Filoviridae, members of which contain linear single-stranded RNA as
their chromosome, includes agents of acute hemorrhagic fever.
20. Arboviruses are those transmitted by arthropods (insects, mites, ticks, lice).
21. Oncoviruses are those, which cause cancer.
22. Unclassified viruses include those causing hepatitis C, hepatitis D, astrovirus -
associated acute gastroenteritis and torovirus-associated enteritis.

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