COURSE TITLE: ENVIRONMENTAL EPIDEMIOLOGY

COUSE CODE: (IEC 668)

ASSIGNMENT: Write a Comprehensive term paper on the Sequelae of all the infectious

and parasitic diseases listed in the ICD 10 blocks B90-B94. For each identified diseases

describe not more than 20 lines the mode of transmission, infection patterns, pathology and

pathogenesis.

SUBMITTED BY:

OLAIYA, OLASUNKANMI OLALEKAN

REG. NUMBER: SCP16/17/H/1122

TO

LECTURER IN CHARGE: PROFESSOR I.E OFOEZIE

FACULTY OF SCIENCE, INSTITUTE OF ECOLOGY AND ENVIRONMENTAL

STUDIES,

OBAFEMI AWOLOWO UNIVERSITY, ILE-IFE

FEBRUARY, 2018
INTRODUCTION: SEQUELAE
A sequel usually used in the plural, sequelae) is a pathological condition resulting from a
disease, injury, therapy, or other trauma. Typically, a sequela is a chronic condition that is a
complication which follows a more acute condition. It is different from, but is a consequence of,
the first condition. Timewise, a sequela contrasts with a late effect, where there is a period,
sometimes as long as several decades, between the resolution of the initial condition and the
appearance of the late effect.
In general, non-medical usage, the terms sequela and sequelae mean consequence and
consequences. Chronic kidney disease, for example, is sometimes a sequela of diabetes, "chronic
constipation" or more accurately "obstipation" (that is, difficulty in passing stool) is a sequela to
an intestinal obstruction, and neck pain is common Examples and uses sequela of whiplash or
other trauma to the cervical vertebrae. Post-traumatic stress disorder may be a psychological
sequel of rape. Sequelae of traumatic brain injury include headache and dizziness, anxiety,
apathy, depression, aggression, cognitive impairments, personality changes, mania, psychosis.
Some conditions may be diagnosed retrospectively from their sequelae. An example is pleurisy.
Other examples of sequelae include those following neurological injury; including aphasia,
ataxia, hemi- and quadriplegia, and any number of other changes that may be caused by
neurological trauma. Note that these pathologies can be related to both physical and chemical
traumas, as both can cause lingering neuron damage. Rheumatic fever is a nonsuppurative
sequela of a primary infection of groups. A Streptococcus bacteria. Glomerulonephritis can also
be a sequel of Streptococcus pyogenes.
The specific classification of sequel of these diseases are listed below:
B90: Sequelea of tuberculosis e.g. chronic respiratory failure (CRF). Cor pulmonale or
chronic pulmonary inflammation
B90.0 Sequelae of central nervous system tuberculosis
B90.1 Sequelae of genitourinary tuberculosis
B90.2 Sequelae of tuberculosis of bones and joints
B90.8 Sequelae of respiratory and unspecified tuberculosis
Sequelae of tuberculosis NOS
B91 Sequelae of poliomyelitis
B92 Sequelae of leprosy
 B94 Sequelae of other and unspecified infectious and parasitic diseases
B94.0 Sequelae of trachoma
B94.1 Sequelae of viral encephalitis
B94.2 Sequelae of viral hepatitis
B94.8 Sequelae of other specified infectious and parasitic diseases
B94.9 Sequelae of unspecified infectious or parasitic disease

B90: Sequelae of tuberculosis e.g. chronic respiratory failure (CRF), cor pulmonale or chronic
pulmonary inflammation

TB is an airborne disease caused by the bacterium Mycobacterium

tuberculosis (M. tuberculosis). M. tuberculosis and seven very closely related mycobacterial
species (M. bovis, M. africanum, M. microti, M. caprae, M. pinnipedii, M. canetti and M. mungi)
together comprise what is known as the M. tuberculosis complex. Most, but not all, of these
species have been found to cause disease in humans. In the United States, the majority of TB
cases are caused by M. tuberculosis. M. tuberculosis organisms are also called tubercle bacilli.
Chronic respiratory failure is one of the most frequent causes of death in the patients of the late
sequelae of pulmonary tuberculosis. Tuberculosis is a contagious disease caused by a bacteria
infection of the lungs, which can also spread to other parts of the body, such as the brain,
kidneys, and bones. Tuberculosis also known as TB, is caused by the bacterium Mycobacterium
tuberculosis.

MODE OF TRANSMISSION: M. tuberculosis is carried in airborne

particles, called droplet nuclei, of 1– 5 microns in diameter. Infectious droplet nuclei are
generated when persons who have pulmonary or laryngeal TB disease cough, sneeze, shout, or
sing. Depending on the environment, these tiny particles can remain suspended in the air for
several hours. M. tuberculosis is transmitted through the air, not by surface contact.
Transmission occurs when a person inhales droplet nuclei containing M. tuberculosis, and the
droplet nuclei traverse the mouth or nasal passages, upper respiratory tract, and bronchi to reach
the alveoli of the lungs (When the Mycobacterium tuberculosis bacteria are able to grow,
multiply and spread, this is called active tuberculosis. People who are malnourished, have
impaired immune systems, or have chronic disease are most susceptible to developing active
tuberculosis.

INFECTION PATTERN, PATHOLOGY AND PATHOGENESIS

Infection occurs when a person inhales droplet nuclei containing tubercle

bacilli that reach the alveoli of the lungs. These tubercle bacilli are ingested by alveolar
macrophages; the majority of these bacilli are destroyed or inhibited. A small number may
multiply intracellularly and are released when the macrophages die. If alive, these bacilli may
spread by way of lymphatic channels or through the bloodstream to more distant tissues and
organs (including areas of the body in which TB disease is most likely to develop: regional
lymph nodes, apex of the lung, kidneys, brain, and bone). This process of dissemination primes
the immune system for a systemic response.

B90.0: Sequelae of central nervous system tuberculosis

Central nervous system (CNS) tuberculosis is a potentially life threatening

condition which is curable if the correct diagnosis is made in the early stages. Its clinical and
radiologic manifestations may mimic other infections and noninfectious neurological conditions.
Hence, familiarity with the imaging presentations of various forms of CNS tuberculosis is
essential in timely diagnosis, and thereby reducing the morbidity and mortality of this disease.

With the outbreak of acquired immunodeficiency syndrome (AIDS) and

increasing frequency of other immunocompromising conditions in recent decades, tuberculosis
has resurged and remained a major worldwide health problem. Although, Mycobacterium
tuberculosis can involve any organ, most commonly the lung, Central nervous system (CNS)
tuberculosis is the most devastating form of the disease. Approximately 5-10% of all the patients
with tuberculosis end up to 20% of patients with AIDS related tuberculosis have CNS
involvement.

MODE OF TRANSMISSION: Central Nervous System (CNS)

tuberculosis usually results from hematogenous spread, while direct spread from intra-or
extracranial focus is rare. The clinical and radiologic manifestations of CNS tuberculosis may
mimic other infectious and noninfectious neurological condtions, such as brain tumors.
 INFECTION PATTERN AND PATHOLOGY

TBM after the release of tubercle bacilli from granulomatous lesions into the
subarachnoid space, a dense gelatinous exudate forms; it is most florid in the interpeduncular
fossa and suprasellar region anteriorly, and it may extend throughout the prepontine cistern and
surround the spinal cord. This exudate envelops arteries and cranial nerves, creating a bottleneck
in the flow of cerebrospinal fluid at the level of the tentorial opening, which leads to
hydrocephalus. The exudate contains erythrocytes, neutrophils, and macrophages, followed by
lymphocytes in more mature exudates. The Rich foci typically follow the vascular pattern and
are located both in the meninges and in the brain parenchyma. Of note, Rich foci are not
preferentially distributed to the basilar areas of the brain where the exudate is typically located.

The most serious consequence of TBM, however, is the development of vasculitis in the
vessels of the circle of Willis, the vertebrobasilar system, and the perforating branches of the
middle cerebral artery, resulting in infarctions in the distribution of these vessels. Direct contact
of the exudate with the brain surface causes a border zone reaction that damages the underlying
brain tissue. Rich and McCordock ascribed most of these changes to a hypersensitivity response.

TuberculomaTuberculomas are thought to arise when tubercles in the brain parenchyma

enlarge without rupturing into the subarachnoid space. As such, they often occur in the absence
of TBM but certainly may occur along with TBM. They more commonly arise as solitary
lesions, but multiple tuberculomas are seen. Tuberculomas of the brain show a typical
granulomatous reaction consisting of epithelioid cells and giant cells mixed with predominantly
lymphocytes around a central area of caseating necrosis. Any liquefaction of the central area of
necrosis contains clear or straw-colored fluid, as opposed to pus (108).

PATHOGENESIS OF TUBERCULOSIS OF THE CENTRAL NERVOUS SYSTEM

M. tuberculosis is an aerobic, nonmotile, non-spore-forming, acid-fast bacillus (AFB)

that infects primarily humans. Its doubling time is quite slow (15 to 20 h) and requires several
weeks to grow on conventional Löwenstein-Jensen medium, where it tends to grow in parallel
groups, producing the colonial characteristic of serpentine cording. Biochemical as well as
RNA/DNA-based methods can identify M. tuberculosis from other AFB.
 The acquisition of M. tuberculosis infection occurs through the inhalation of droplet
nuclei containing the bacilli, eventually leading to deposition in the lung alveoli. Once in the
alveoli, the bacilli interact with alveolar macrophages through a multitude of different receptors.
Once these innate immune cells are triggered, numerous cytokines and chemokines are released,
the activation of a type 1 T-helper cell-mediated immune response occurs, and, ultimately, a
granuloma is formed. Early in this process, prior to the actual containment of the infection,
bacilli are filtered into draining lymph nodes, and there exists a low-level bacteremia in which
M. tuberculosis disseminates to distant sites in the body. This hematogenous seeding occurs most
frequently in regions of the body that are highly oxygenated, including the brain. A complex
interplay of host immune factors and M. tuberculosis virulence factors in the end determines
whether or not the infection is contained and whether, or to what extent, the dissemination of the
bacilli leads to clinical disease. For CNS tuberculosis, the disease begins with the development
of small tuberculous foci (Rich foci) in the brain, spinal cord, or meninges. The location of these
foci and the capacity to control them ultimately determine which form of CNS tuberculosis
occurs. CNS tuberculosis manifests itself primarily as tuberculous meningitis (TBM) and less
commonly as tubercular encephalitis, intracranial tuberculoma, or a tuberculous brain abscess.

B90.1 Sequelae of genitourinary tuberculosis

Genitourinary tuberculosis is the second most common site of infection in

humans by Mycobacterium tuberculosis, second only to pulmonary tuberculosis. It can almost
easily be divided anatomically into:

 Renal tuberculosis (renal parenchyma, calyces and renal pelvis)

 Bladder and uteric tuberculosis
 Prostatic tuberculosis
 Scrotal tuberculosis (testes, epidydamis, seminal vesicles, ductus deferences)
 Tuberculosis pelvic inflammatory diseases
MODE OF TRANSMISSION: M. tuberculosis is carried in airborne particles, called
droplet nuclei, of 1– 5 microns in diameter. Infectious droplet nuclei are generated when
persons who have pulmonary or laryngeal TB disease cough, sneeze, shout, or sing.
 Depending on the environment, these tiny particles can remain suspended in the air for
several hours.
PATHOLOGY AND PATHOGENESIS

The most common pathogen associated with tuberculosis (TB) is Mycobacterium

tuberculosis, a strictly aerobic nonmotile bacterium. The bacterium grows slowly, dividing only
once every 24 hours, and is capable of surviving within immune cells after phagocytosis.
Uncommonly implicated pathogens include M kansasii, M fortuitum, M bovis, M avium-
intracellulare (MAI), M xenopi, M celatum. Male genital TB is usually a manifestation of the
usual pulmonary acquisition of TB. Venereal acquisition of male genital tuberculosis is unlikely,
although cases of male-to-female transmission of genital TB have been reported. Human
immunodeficiency virus (HIV) infection increases the risk for active TB and has been suggested
to increase the risk for reactivation of dormant foci; epididymal TB most commonly develops in
sexually active young men.
In very rare cases, TB epididymitis and prostatic TB have been reported following
intravesical bacille Calmette-Guérin (BCG) therapy for superficial bladder tumors, presumably
due to retrocanalicular descent of organisms from the prostatic urethra. Generally, TB prostatitis
results from hematogenous dissemination of M tuberculosis from the site of the primary
infection. Thus, previous infection with TB is the most important risk factor. Historically, 10-
12% of men with TB had pathologic evidence of prostatic involvement during autopsy. Theories
of descending spread via infected urine have been abandoned, largely in light of animal studies
demonstrating hematogenous spread and the scarcity of prostatic urethral TB in association with
prostatic parenchymal TB. Prolonged steroid use and immunosuppressive therapy may increase
the risk of reactivation of dormant foci.

B90.2 Sequelae of tuberculosis of bones and joints

Tuberculosis affects predominantly the lungs and gastrointestinal tract, but

may also infect the musculaskeletal system. There is caseating granulomatus inflammatory with
bone necrosis, resulting in the damage of bone. Extension of the TB osteomyelitis in to joint
spaces results in tuberculosis arithis. The infection crosses to the bone on the other side of the
joint.
 MODE OF TRANSMISSION: Only people who have active TB
infections can spread the TB bacteria. Coughing, sneezing, even talking can release the bacteria
into the surrounding ir, and people breathing this air can then become infected. This is more
likely to happen when living close with someone who has TB or if a room isn’t well ventilated.
Once a person is infected, the bacteria will settle in the air sacs and passages of the lungs and, in
most cases, will be contained by the immune system.

PATHOLOGY AND PATHOGENESIS

Musculoskeletal tuberculosis arises from haematogenous seeding of the bacilli soon after
the initial pulmonary infection. Osteoarticular tuberculosis usually starts as osteomyelitis in the
growth plates of bones, where the blood supply is best, and then spreads locally into the joint
spaces. Less commonly, it can occur by spreading through the lymphatic system. Joints can
become infected by activation of dormant lymphatic or blood stream areas of morbidity. In the
long bones TB originates in the epiphysis and causes tubercle formation in the marrow, with
secondary infection of the trabeculae. The joint synovium responds to the mycobacteria by
developing an inflammatory reaction, followed by formation of granulation tissue. The pannus of
granulation tissue formed then begins to erode and destroy cartilage and eventually bone, leading
to demineralization. Because TB is not a pyogenic infection, proteolytic enzymes, which destroy
peripheral cartilage, are not produced. The joint space, therefore, is preserved for a considerable
time. If allowed to progress without treatment, however, abscesses may develop in the
surrounding tissue. Since space-occupying exudates with extensive disruption of vascular supply
do not occur, sequestration of bone is rare. Therefore, bone destruction without sequestra and
with minimal new bone formation characterizes the active phase of tuberculous osteomyelitis.

Spinal TB is the most common form of skeletal system TB, comprising 50% of all cases.

Wherever the primary site of TB infection is, it travels by subligamentous spread in the spine, as
well as into paravertebral spaces and adjacent soft tissue. It causes osteonecrosis characterized by
loss of the exracellular matrix of vertebral bone and collapse of the vertebrae. The bone is
devitalized by an exotoxin produced by the acid-fast bacilli. The anterior portions of two or more
contiguous vertebrae are involved owing to haematogenous spread through one arteria
intervertebralis feeding two adjacent vertebrae. The spinal cord may become involved either by
compression by bony elements and/or expanding abscess; or direct involvement of cord and
leptomeninges by granulation tissue. Neurological deficits are usually more symmetrical and
more gradual in onset than those resulting from other pathologies. The spinal TB can involve
vertebral bodies at two or three different sites and these are referred to as “skipped lesions”.

B90.9 Sequelae of respiratory and unspecified tuberculosis

Sequelae of tuberculosis NOS

Sequelae of respiratory and unspecified tuberculosis is a causes of death

classified under the ICD-10 Code. Certain infectious and parasitic diseases reported to have
killed or cause of death. Hence, the mode of transmission, infection patterns, pathology and
pathogenesis are as the same as the Sequelae of central nervous system tuberculosis.

B91: Sequelae of poliomyelitis

Post polio Syndrome (PPS, or post-poliomyelitis syndrome or post-polio sequelae) is a

condition that affects approximately 25 to40% of people who have previously survives an acute
attack of poliomyelitis-a viral infection of the nervous system-after the initial infection.
Symptoms include acute or increased muscular weakness, pain in the muscles, and fatigue. The
same symptoms may also occur years after nonparalytic polio (NPP) infection. Poliomyelitis is a
viral disease that can affect nerves and can lead to partial or full paralysis. It is caused by
infection with the poliovirus which can be spread by direct person-to-person contact, by contact
with infected mucus or phlegm from the nose or mouth, or by contact with infected feces. There
are three basic patterns of polio infection: subclinical infections, nonparalytic, and paralytic.
Symptoms vary based on the pattern of infection and can range from asymptomatic with
subclinical poliomyelitis to partial or full paralysis. Treatment is aimed at controlling symptoms
while the infection runs its course. Since the development of the polio vaccine, the incidence of
the disease has been greatly reduced. The prognosis depends on the form of the disease
(subclinical, nonparalytic, or paralytic) and the site affected.

MODE OF TRANSMISSION: Polio virus is highly communicable. The

time between infection and onset of paralysis (incubation period) is 10-21 days (range 4-35
days). Transmission is primarily person to person via the faecal oral route, i.e. the poliovirus
multiplies in the intestines and is spread through the faeces. The virus is intestinally excreted to
one month or more after infection.

Communicability of infected children is highest just prior to the onset of

paralysis and during the first two weeks after paralysis occurs. The virus spreads rapidly and
transmission is usually widespread by the time of paralysis onset. There is no term carrier state in
normal children.

PATHOLOGY AND PATHOGENESIS OF POLIOMYELITIS

The virus enters through the mouth, and primary multi-plication of the virus occurs at the
site of implantation in the pharynx and gastrointestinal tract. The virus is usually present in the
throat and in the stool before the onset of illness. One week after onset there is fewer viruses in
the throat, but virus continues to be excreted in the stool for several weeks (CDC, 2012c).
Poliovirus replication occurs in the alimentary tract, followed by a primary, transient presence of
viremia. The virus invades local lymphoid tissue, enters the bloodstream, and then may infect
cells of the central nervous system. Replication of poliovirus in motor neurons of the anterior
horn and brain stem results in cell destruc-tion and causes the typical manifestations of
poliomyelitis (CDC, 2011).

Approximately 4%–8% of polio infections consist of a minor, nonspecific illness without

clinical or laboratory evidence of central nervous system invasion. This clinical presentation is
known as abortive poliomyelitis, and is characterized by complete recovery in less than a week.
The spread and replication of the virus in other sites such as brown fat, reticuloendothelial tissue,
and muscle causes secondary viremia and leads to the development of minor symptoms. Three
syndromes observed with this form of poliovirus infection are upper respiratory tract infection
(sore throat and fever), gastrointes-tinal disturbances (nausea, vomiting, abdominal pain,
consti-pation or, rarely, diarrhea), and influenza-like illness. These syndromes are
indistinguishable from other viral illnesses (CDC, 2012c).

Paralytic polio is classified into three types, depending on the level of involvement.
Spinal polio is most common, and during 1969–1979, accounted for 79% of paralytic cases. It is
characterized by asymmetric paralysis that most often involves the legs. Bulbar polio leads to
weakness of muscles innervated by cranial nerves and accounted for 2% of cases during this
period. Bulbospinal polio, a combination of bulbar and spinal paralysis, accounted for 19% of
cases. The death-to-case ratio for paralytic polio is generally 2%–5% among children and up to
15%–30% for adults (depending on age). It increases to 25%–75% with bulbar involvement
(CDC, 2012c).

B92: Sequelae of leprosy

Leprosy (Hansen’s Diseases) is a chronic infection caused by the acid-fast,

rod shaped bacillus Mycobacterium leprae. Leprosy can be considered 2 connected diseases that
primary affect superficial tissues, especially the skin and peripheral nerves. Initially, a
mycobacterial infection causes a wide array of cellular Immune responses. These immunologic
events then elicit the second part of the disease, a peripheral neuropathy with potentially long
term consequences.

The social and psychological effects of leprosy, as well as its highly visible debilities and
sequelae have resulted in a historical stigma associated with leprosy. To minimize the prejudice
against those with leprosy, the condition is also known as Hansen disease, name after G.A.
Hansen, who is credited with the 1873 discovery of M.leprae. This mycobacterium grows
extremely slowly and has not been successfully cultured in vitro.

MODE OF TRANSMISSION: Leprosy results from exposure of a person to a case of

leprosy, it is important to note that prolonged contact with the person is necessary. Casual
contact does not cause leprosy. This contact may be direct (e.g. skin to skin) or indirect (e.g.
contact with soil, and fomites such as contaminated clothes and linen). Leprosy has a long
incubation period, an average of about three to five years. The nose is a major portal of exit of
organisms of a person affected by leprosy. Some cases of leprosy harbor millions of
Mycobacterium leprae in their nasal mucosa which are discharged when they sneeze or blow the
nose. The bacilli can also exit through ulcerated or broken skin of bacteriologically positive
cases of leprosy. Leprosy results from exposure of a person to a case of leprosy, it is important to
note that prolonged contact with the person is necessary. Casual contact does not cause leprosy.
This contact may be direct (e.g. skin to skin) or indirect (e.g. contact with soil, and fomites such
as contaminated clothes and linen). Leprosy has a long incubation period, an average of about
three to five years. The nose is a major portal of exit of organisms of a person affected by
leprosy. Some cases of leprosy harbor millions of Mycobacterium leprae in their nasal mucosa
which are discharged when they sneeze or blow the nose. The bacilli can also exit through
ulcerated or broken skin of bacteriologically positive cases of leprosy.

It is generally agreed that people who harbor a large number of organisms, as their
immune system cannot get rid of them, are the most important source of infection in the
community. Among household contacts lepromatous cases, a varying proportion – roughly about
5 to 10% – is expected to show signs of leprosy within five years. This occurs despite treatment
of the case, as the person usually harbors the organisms before exhibiting clinical signs and
symptoms. Leprosy occurs more commonly in males than in females in most regions of the
world. Leprosy is not particularly a disease of children as was once believed.

INFECTION PATTERN, PATHOLOGY AND PATHOGENESIS OF LEPROSY

Leprosy can manifest in different forms, depending on the host response to
the organism. Individuals who have a vigorous cellular immune response to M leprae have the
tuberculoid form of the disease that usually involves the skin and peripheral nerves. The number
of skin lesions is limited, and they tend to be dry and hypoesthetic. Nerve involvement is usually
asymmetric. This form of the disease is also referred to as paucibacillary leprosy because of the
low number of bacteria in the skin lesions (i.e., < 5 skin lesions, with absence of organisms on
smear). Results of skin tests with antigen from killed organisms are positive in these individuals.

Individuals with minimal cellular immune response have the lepromatous form of the
disease, which is characterized by extensive skin involvement. Skin lesions are often described
as infiltrated nodules and plaques, and nerve involvement tends to be symmetric in distribution.
The organism grows best at 27-30°C; therefore, skin lesions tend to develop in the cooler areas
of the body, with sparing of the groin, axilla, and scalp. This form of the disease is also referred
to as multibacillary leprosy because of the large number of bacteria found in the lesions (ie, >6
lesions, with possible visualization of bacilli on smear). Results of skin tests with antigen from
killed organisms are nonreactive. Patients may also present with features of both categories;
however, over time, they usually evolve to one or the other (indeterminate or borderline leprosy).
Interestingly, most individuals who are exposed to leprosy never develop the disease.
 B94.0 Sequelae of trachoma

Trachoma is the most common infections cause of blindness in the world

and is due to recurrent ochlar infection with Chlamydia trachomatis. Repeat infection with this
organism leads to conjunctiva inflammation and scarring, trichiasis, and ultimately blinding
corneal opacificstion. The infection causes a roughening of the inner surface of the eyelids. This
roughening can lead to pain in the eyes, breakdown of the outer surface or cornea of the eys and
eventual blindness. Untreated, repeated trachoma infections can results in a form of permanent
blindness when eyelids turn inward.

MODE OF TRANSMISSION: Trachoma is caused by Chlamydia trachomatis,

serotypes (serovars) A, B, and C. It is spread by direct contact with eye, nose, and throat
secretions from affected individuals, or contact with fomites (inanimate objects that carry
infectious agents), such as towels and/or washcloths, that have had similar contact with these
secretions. Flies can also be a route of mechanical transmission. Untreated, repeated trachoma
infections result in entropion—, the inward turning of the eyelids, which may result in blindness
due to damage to the cornea. Children are the most susceptible to infection due to their tendency
to get dirty easily, but the blinding effects or more severe symptoms are often not felt until
adulthood. Blinding endemic trachoma occurs in areas with poor personal and family hygiene.
Many factors are indirectly linked to the presence of trachoma including lack of water, absence
of latrines or toilets, poverty in general, flies, close proximity to cattle, crowding, and so forth.
However, the final common pathway seems to be the presence of dirty faces in children,
facilitating the frequent exchange of infected ocular discharge from one child’s face to another.
Most transmission of trachoma occurs within the family.
PATHOLOGY AND PATHOGENESIS

Trachoma is caused by four ocular serotypes of Chalmydia trachomatis: A, B, Ba and C.

Infection with genitalserotypes D to K can cause isolated episodes of ophthalmia neonatorum in
infants or inclusion conjunctivitis in adults and do not generally lead to blindness. Blindness
from trachoma is due to recurrent episodes of active infection. The initial infection is con􀃗ned to
the conjunctival epithelium and triggers an immune response. Repeat infections with subsequent
In ammatory responses results in tissue destruction, scarring, cicatricial entropion with trichiasis,
and corneal opacication from lashes rubbing against the cornea.
 B94.1 Sequelae of viral encephalitis

MODE OF TRANSMISSION

A viral infection of the brain which is usually transmitted to man as an incidental

terminal host. The arbovirus encephalitides are zoonoses, with the virus surviving in infection
cycles involving biting arthropods and various vertebrates, especially birds and rodents. Some of
the common encephalitides:
 Eastern Equine Encephalitis (mosquito borne)
 Western Equine Encephalitis (mosquito borne)
 Venezuelan Equine Encephalitis (mosquito borne)
 St. Louis Encephalitis (mosquito borne)
 Japanese B Encephalitis (mosquito borne)
 Murray Valley Encephalitis (mosquito borne)
 California Encephalitis (mosquito borne)
 Tick-Borne Encephalitis
 Herpesvirus Encephalitis (person to person contact)

PATHOLOGY AND PATHOGENESIS

In infections with arboviruses, an initial viremia is followed by localization in the central

nervous system. In fatal cases, there is little histopathologic change outside the nervous system,
possibly excepting renal involvement in St. Louis encephalitis. On gross examination, there are
varying degrees of meningitis, cerebral edema, congestion, and hemorrhage in the brain.
Microscopic examination confirms a leptomeningitis with round-cell infiltration, small
hemorrhages with perivascular cuffing, and nodules of leukocytes or microglial cells. Neuronal
damage is seen as chromatolysis and neuronophagia. Areas of necrosis may be extensive
especially in Eastern equine encephalitis, Japanese B encephalitis, and the Far Eastern form of
tick-borne encephalitis. In patients who survive the initial illness, there are varying degrees of
repair, which may include calcification. The pattern of distribution of lesions in the brain is
rarely sufficiently specific to enable the identification of the infecting virus. However, the lesions
in Eastern equine encephalitis are concentrated in the cortex, in Western equine encephalitis in
the basal nuclei, and in St. Louis encephalitis in substantia nigra, thalamus, pons, cerebellum,
cortex, bulb, and anterior horn cells. European forms of tickborne encephalitis, including louping
ill, commonly show a polioencephalomyelitis, with extensive involvement of the anterior horn
cells mimicking poliomyelitis pathologically and clinically.

Herpesvirus encephalitis in infants may be part of a general infection that produces focal
necrotic lesions with typical intranuclear inclusions in many organs. In the adult and in some
children, lesions are confined to the brain. Necrotic foci may be macroscopically evident as
softening. Inclusion bodies are readily found in the margins of areas of necrosis; focal
perivascular infiltration and neuronal damage is evident. The temporal cortex and pons are
commonly involved, but the lesions may be widespread.

B94.2 Sequelae of viral hepatitis

Viral hepatitis is liver inflammation due to a viral infection. It may present

in acute (recent infection, relatively rapid onset) or chronic forms. The most common causes of
viral hepatitis are the five unrelated hepatotropic viruses Hepatitis A, Hepatitis B,Hepatitis C,
Hepatitis D, and Hepatitis E.

HEPATITIS A
Hepatitis A or infectious jaundice is caused by hepatitis A virus (HAV), a picornavirus
transmitted by the fecal-oral route often associated with ingestion of contaminated food. It causes
an acute form of hepatitis and does not have a chronic stage. The patient's immune system makes
antibodies against HAV that confer immunity against future infection. People with hepatitis A
are advised to rest, stay hydrated and avoid alcohol. A vaccine is available that will prevent HAV
infection for up to 10 years. Hepatitis A can be spread through personal contact, consumption of
raw sea food or drinking contaminated water. This occurs primarily in third world countries.
Strict personal hygiene and the avoidance of raw and unpeeled foods can help prevent an
infection. Infected people excrete HAV with their faeces two weeks before and one week after
the appearance of jaundice. The time between the infection and the start of the illness averages
28 days (ranging from 15 to 50 days), and most recover fully within 2 months, although
approximately 15% ofsufferers may experience continuous or relapsing symptoms from six
months to a year following initial diagnosis.
HEPATITIS B
Hepatitis B is caused by hepatitis B virus, a hepadnavirus that can cause both acute and chronic
hepatitis. Chronic hepatitis develops in the 15% of adults who are unable to eliminate the virus
after an initial infection. Identified methods of transmission include blood (blood transfusion,
now rare), unsanitary tattoos, sexually (through sexual intercourseor through contact with blood
or bodily fluids), or via mother to child by breast feeding[ (minimal evidence of transplacental
crossing). However, in about half of cases the source of infection cannot be determined. Blood
contact can occur by sharing syringes in intravenous drug use, shaving accessories such as razor
blades, or touching wounds on infected persons. Needle-exchange programmes have been
created in many countries as a form of prevention. Patients with chronic hepatitis B have
antibodies against hepatitis B, but these antibodies are not enough to clear the infection of the
affected liver cells. The continued production of virus combined with antibodies is a likely cause
of the immune complex disease seen in these patients. A vaccine is available that will prevent
infection from hepatitis B for life. Hepatitis B infections result in 500,000 to 1,200,000 deaths
per year worldwide due to the complications of chronic hepatitis, cirrhosis, and hepatocellular
carcinoma. Hepatitis B is endemic in a number of (mainly South-East Asian) countries, making
cirrhosis and hepatocellular carcinoma big killers.
HEPATITIS C
Hepatitis C (originally "non-A non-B hepatitis") is caused by hepatitis C virus (HCV), an RNA
virus that is a member of the Flaviviridae family. HCV can be transmitted through contact with
blood (including through sexual contact if the two parties' blood is mixed) and can also cross the
placenta. Hepatitis C usually leads to chronic hepatitis, culminating in cirrhosis in some people.
It usually remains asymptomatic for decades. Patients with hepatitis C are susceptible to severe
hepatitis if they contract either hepatitis A or B, so all persons with hepatitis C should be
immunized against hepatitis A and hepatitis B if they are not already immune, and avoid alcohol.
HCV viral levels can be reduced to undetectable levels by a combination of interferon and the
antiviral drug ribavirin. The genotype of the virus is the primary determinant of the rate of
response to this treatment regimen, with genotype 1 being the most resistant. Hepatitis C is the
most common chronic blood-borne infection in the United States.
HEPATITIS D
The Hepatitis D virus (HDV) or hepatitis delta agent is similar to a viroid as it can only
propagate in the presence of the hepatitis B virus.
HEPATITIS E
The Hepatitis E virus (HEV), from the Hepeviridae family, produces symptoms similar to
hepatitis A, although it can take a fulminant course in some patients, particularly pregnant
women; chronic infections may occur in immune-compromised patients. It is more prevalent in
the Indian subcontinent.

Hepatitis can progress to, or be complicated by other diseases. Some of these diseases,
like fibrosis and cirrhosis, are very common. Fortunately, other complications like liver failure
are usually prevented. Ten possible complications linked with hepatitis.
ACUTE LIVER FAILURE
Acute liver failure (also called fulminant hepatic failure, or fulminant hepatitis in the most
serious forms) is a rapidly developing medical emergency caused by cells of the liver being
injured so quickly that the liver cannot repair itself fast enough. Such an event can cause the liver
to stop working altogether, resulting in problems in other areas of the body.
Liver failure is a serious, but uncommon, complication of hepatitis. Doctors use different
terms to describe variations of liver failure, such as fulminant liver failure, fulminant hepatic
failure or acute liver failure. Basically, the liver no longer functions and this leads to the body
shutting down, and eventually, death. There are many specific causes of liver failure, but in
general, failure results when the liver is so damaged that it is unable to keep up with the body's
needs.
Acute liver failure is different from acute hepatitis in that parts of the liver begin to die or
no longer work. Because the liver is such a vital part of the body, when it is damaged, other
organs are affected, too. The brain is one of the more important organs affected during liver
failure and injury to it results in a condition called encephalopathy.
MODE OF TRASMISSION
The exact cause of FHF is unknown. The following may increase your risk:
 Autoimmune diseases may cause your body to attack and damage your liver cells.
 Cancer metastasis is when cancer has spread and reached your liver from other parts of
your body.

 A viral infection may cause hepatitis. Hepatitis causes your liver to get inflamed
(swollen). Hepatitis can lead to FHF.

 Herbal supplements or medicines such as acetaminophen may cause FHF.

Acetaminophen is used for fever or pain. If more than the recommended dosage of this
medicine is taken, it may damage your liver. Certain herbal and diet supplements may
also lead to FHF.

 Other diseases such as Wilson disease or Reye syndrome may cause FHF. Heart failure,
heat stroke, and blood vessel diseases such as Budd-Chiari syndrome can also cause FHF.
Women with acute fatty liver during pregnancy are also at risk for FHF.
 REFERENCES
American Thoracic Society and CDC. Diagnostic standards and classification of
tuberculosis in adults and children. Am J Respir Crit Care Med 2000; 161 (4): 1376– 1395.
http://ajrccm.atsjournals.org/cgi/reprint/161/4/1376

CDC. Essential components of a tuberculosis prevention and control program:

Recommendations of the Advisory Council for the Elimination of Tuberculosis. MMWR 1995;
44 (No. RR-11).www.cdc.gov/mmwr/preview/mmwrhtml/00038823.htm

CDC. Extensively drug-resistant tuberculosis— United States, 1993– 2006. MMWR

2007; 56 (11): 250– 3. www.cdc.gov/mmwr/preview/mmwrhtml/mm5611a3.htm

.A. Bernaerts, F. M. Vanhoenacker, P. M. Parizel et al., “Tuberculosis of the central

nervous system: overview of neuroradiological findings,” European Radiology, vol. 13, no. 8,
pp. 1876–1890, 2003. View at Publisher · View at Google Scholar · View at PubMed · View at
Scopus2.J. Berenguer, S. Moreno, F. Laguna et al., “Tuberculous meningitis in patients infected
with the human immunodeficiency virus,” The New England Journal of Medicine, vol. 326, no.
10, pp. 668–672, 1992. View at Publisher · View at Google Scholar · View at PubMed · View at

Scopus3.J. E. Vidal, A. C. P. de Oliveira, F. B. Filho et al., “Tuberculous brain abscess in

AIDS patients: report of three cases and literature review,” International Journal of Infectious
Diseases, vol. 9, no. 4, pp. 201–207, 2005. View at Publisher · View at Google Scholar · View at
PubMed · View at Scopus

Krambovitis, E., M. B. McIllmurray, P. E. Lock, W. Hendrickse, and H. Holzel. 1984.

Rapid diagnosis of tuberculous meningitis by latex particle agglutination. Lancet ii:1229-1231.
FREE 1994:360Medline

Lee, B. W., J. A. Tan, S. C. Wong, C. B. Tan, H. K. Yap, P. S. Low, J. N. Chia, and J. S.

Tay. 1994. DNA amplification by the polymerase chain reaction for the rapid diagnosis of
tuberculous meningitis. Comparison of protocols involving three mycobacterial DNA sequences,
IS6110, 65 kDa antigen, and MPB64. J. Neurol. Sci. 123:173-179. 681

Lees, A. J., A. F. MacLeod, and J. Marshall. 1980. Cerebral tuberculomas developing

during treatment of tuberculous meningitis. Lancet i:1208-1211.
 Swanner, Yann A. Meunier ; with contributions from Michael Hole, Takudzwa Shumba
& B.J. (2014). Tropical diseases : apractical guide for medical practitioners and students
(https://books.google.com/books?id=ZWcGAQAAQBAJ&pg=PT22
Oxford: Oxford University Press, USA. p. 199. ISBN 9780199997909. Archived
(https://web.archive.org/web/20170908222538/https://books.google.com/books?id=ZWcGAQA
AQBAJ&pg=PT222) from the original on 2017-09-08.
"Blinding Trachoma Fact sheet N°382"
(http://www.who.int/mediacentre/factsheets/fs382/en/). World Health Organization. November
2013. Archived (https://web.archive.org/web/20140314061724/http:/www.who.int/mediacentr
e/factsheets/fs382/en/) from the original on 14 March 2014. Retrieved 14 March 2014.
Jung YY, Kim JK, Cho KS. Genitourinary tuberculosis: comprehensive cross-sectional
imaging. AJR Am J Roentgenol. 2005;184 (1): 143-50. AJR Am J Roentgenol (full text) -
Pubmed citation

"sequela: definition of sequela in Oxford dictionary (British & World English) (US)" .
www.oxforddictionaries.com. Retrieved 2014-10-30.

"sequela: definition of sequela in Oxford dictionary (American English) (US)" .

www.oxforddictionaries.com. Retrieved 2014-10-30.