Summary
This book on “Human Diseases” is written with a view to meet curricular requirements of students at undergraduate and post graduate levels of Indian Universities. Diseases are illnesses impairing the normal physiological functioning of living organisms. The causative agents are virus, bacteria, protozoans, helminthes and others. The diseases chosen for this book are: measles, smallpox, chickenpox, AIDS, Ebola, Dengue, cholera, leprosy, tuberculosis, typhoid, malaria, amoebiasis, Diarrhoea, Filariasis, Cancer and Jaundice. The text describes causative agents, signs and symptoms, diagnosis, prevention, treatment, epidemiology and history of all 16 diseases. A table containing these factors has also been included for the convenience of readers to have an immediate idea about these human diseases.
Excerpt
Table Of Contents
Simani Mohanty
Research Scholar
Post Graduate Department of Zoology
Berhampur University
Berhampur-760007
Odisha, India
Bibarani Tripathy
Research Scholar
Post Graduate Department of Zoology
Berhampur University
Berhampur-760007
Odisha, India
Surya Narayan Swain
Research Scholar
Post Graduate Department of Zoology
Berhampur University
Berhampur-760007
Mrs. Bijayalaxmi Sahu
Research Scholar
Post Graduate Department of Zoology
Berhampur University
Berhampur-760007
Odisha, India
Deepika Panda
Research Scholar
Post Graduate Department of Zoology
Berhampur University
Berhampur-760007
Odisha, India
Chinmayee Panda
Research Scholar
Post Graduate Department of Zoology
Berhampur University
Berhampur-760007, Odisha, India
Table of Contents
1. MEASLES ... 1
1.1. INTRODUCTION ... 1
1.2. SYMPTOMS ... 1
1.3. COMPLICATIONS ... 2
1.4. CAUSE ... 3
1.5. MECHANISM OF INFECTION... 4
1.6. DIAGNOSIS ... 4
1.7. PREVENTION ... 4
1.8. TREATMENT ... 4
2. SMALLPOX ... 7
2.1. INTRODUCTION ... 7
2.2. SYMPTOMS ... 7
2.3. COMPLICATIONS ... 8
2.4. CAUSE ... 8
2.5. DIAGNOSIS ... 9
2.6. PREVENTION AND TREATMENT ... 10
2.6.1. SMALLPOX VACCINE ... 10
3. CHICKENPOX ... 12
3.1. INTRODUCTION ... 12
3.2. CAUSE ... 12
3.3. SYMPTOMS: ... 13
3.3.1. Before the rash appears ... 13
3.3.2. After the rash appears ... 13
3.4. COMPLICATIONS ... 13
3.5. DIAGNOSIS ... 14
3.6. PATHOPHYSIOLOGY ... 15
3.6.1. Shingles ... 15
3.7. PREVENTION ... 15
3.7.1. Hygiene measures ... 15
3.7.2. Vaccine ... 16
3.8. TREATMENT ... 16
4. AIDS ... 18
4.1. INTRODUCTION ... 18
4.2. SYMPTOMS OF HIV ... 19
4.3. SYMPTOMS OF AIDS ... 20
4.4. TRANSMISSION ... 20
4.5. DIAGNOSIS ... 21
4.5.1. Antibody test ... 21
4.5.2. Antibody/antigen test ... 22
4.5.3. Nucleic acid test (NAT) ... 22
4.6. PREVENTION ... 22
4.6.1. Sexual contact ... 22
4.6.2. Pre-exposure ... 23
4.6.3. Post-exposure ... 24
4.7. Mother-to-child ... 24
4.8. VACCINATION ... 24
4.9. TREATMENT ... 24
4.10. HIV MEDICATIONS ... 25
4.11. HIV AND AIDS: CONNECTION ... 26
5. EBOLA ... 28
5.1. INTRODUCTION ... 28
5.2. CAUSE AND AGENT ... 28
5.3. DISEASE AGENT CHARACTERISTICS ... 28
5.4. GEOGRAPHICAL DISTRIBUTION ... 29
5.4.1. RESERVOIR ... 29
5.5. PATHOGENESIS AND TRANSMISSION ... 30
5.6. SIGNS AND SYMPTOMS ... 31
5.7. DIAGNOSIS ... 31
5.8. TREATMENT ... 32
5.9. PREVENTION ... 32
6. DENGUE... 35
6.1. INTRODUCTION ... 35
6.2. ORIGIN AND HISTORY ... 35
6.3. DISTRIBUTION ... 36
6.4. STRUCTURE AND CHARACTERISTICS OF DENGUE VIRUS ... 36
6.5. REPLICATION OF DENGUE VIRUS ... 37
6.6. VECTORS OF DENGUE ... 38
6.7. HOST FACTOR ... 39
6.8. TRANSMISSION ... 39
6.9. CLINICAL PRESENTATION ... 40
6.10. SYMPTOMS ... 40
6.11. PATHOPHYSIOLOGY ... 42
6.12. DIAGNOSIS ... 42
6.12.1. Clinical laboratory findings ... 42
6.12.2. LABORATORY DIAGNOSIS ... 43
6.13. TREATMENT ... 44
6.13.1. Medication ... 44
6.13.2. Immunization ... 44
6.14. PREVENTION ... 44
7. CHOLERA ... 46
7.1. INTRODUCTION ... 46
7.2. SYMPTOMS ... 47
7.3. CAUSE ... 47
7.4. MECHANISM OF TRANSMISSION ... 48
7.5. DIAGNOSIS ... 48
7.6. TREATMENT ... 48
7.7. PREVENTION ... 49
7.8. VACCINE ... 49
8. LEPROSY ... 51
8.1. INTRODUCTION ... 51
8.2. HISTORY ... 51
8.3. GEOGRAPHICAL DISTRIBUTION ... 51
8.4. CAUSATIVE AGENT ... 52
8.5. TYPES OF LEPROSY ... 52
8.6. TRANSMISSION ... 53
8.7. SYMPTOMS ... 54
8.7.1. Symptoms caused by damage to the nerves are: ... 54
8.7.2. Symptoms caused by the disease in the mucous membranes are: ... 55
8.8. COMPLICATIONS ... 55
8.9. DIAGNOSIS ... 56
8.9.1. SKIN BIOPSY ... 56
8.9.2. SMEAR TEST ... 56
8.9.3. SEROLOGY ... 56
8.10. PREVENTION ... 56
8.11. TREATMENT ... 56
9. TUBERCULOSIS ... 59
9.1. INTRODUCTION ... 59
9.2. GEOGRAPHIC DISTRIBUTION ... 59
9.3. ORIGIN AND HISTORY ... 59
9.4. CAUSATIVE AGENT AND CNS TUBERCULOSIS ... 60
9.5. SYMPTOMS ... 60
9.6. LIFE CYCLE ... 61
9.7. TRANSMISSION ... 62
9.8. TREATMENT ... 62
9.9. TESTING FOR PULMONARY TB ... 64
9.9.1. SCREENING FOR TB ... 64
9.10. DIAGNOSIS ... 64
9.11. DIAGNOSIS OF TB IN INDIA ... 64
9.12. FLUORESCENT MICROSCOPY ... 65
9.13. PREVENTION ... 65
10. TYPHOID ... 68
10.1. INTRODUCTION ... 68
10.2. OCCURENCE ... 68
10.3. EPIDEMIOLOGY ... 69
10.4. CAUSATIVE AGENT ... 69
10.5. MORPHOLOGY AND STAINING ... 70
10.6. MULTIPLICATION AND PROPAGATION ... 70
10.7. SYMPTOMS ... 73
10.8. COMPLICATED FEVER ... 73
10.9. CONTAMINATION AND TRANSMISSION ... 73
10.10. DIAGNOSIS ... 74
10.11. TREATMENT ... 74
10.12. SURGERY ... 75
10.13. PREVENTION ... 75
10.14. VACCINATION ... 75
11. MALARIA ... 77
11.1. INTRODUCTION ... 77
11.2. ORIGIN AND HISTORY ... 77
11.3. GEOGRAPHICAL DISTRIBUTION ... 77
11.4. CAUSATIVE AGENT ... 78
11.5. LIFE CYCLE OF PLASMODIUM ... 79
11.6. VECTORS OF MALARIA ... 80
11.7. TRANSMISSION ... 81
11.8. SYMPTOMS ... 81
11.9. DIAGNOSIS AND TREATMENT ... 82
11.10. PRECAUTIONS ... 83
11.11. PREVENTIVE MEASURES ... 83
11.12. ANTI MALARIAL CAMPAIGN ... 84
12. AMOEBIASIS ... 86
12.1. INTRODUCTION ... 86
12.2. CAUSATIVE AGENT ... 86
12.3. LIFE CYCLE OF ENTAMOEBA HISTOLYTICA ... 86
12.4. RESERVOIR AND SOURCE ... 88
12.5. TRANSMISSION ... 88
12.5.1. Faecal-oral route ... 88
12.5.2. Oral-rectal contact ... 88
12.6. PATHOGENESIS AND PATHOLOGY ... 89
12.7. SYMPTOMS ... 90
12.8. DIAGNOSIS ... 90
12.9. TREATMENT ... 91
12.10. PREVENTION ... 91
13. DIARRHOEA ... 93
13.1. INTRODUCTION ... 93
13.2. TYPES OF DIARRHOEA ... 93
13.2.1. Secretory ... 93
13.2.2. Osmotic ... 93
13.2.3. Exudative ... 94
13.2.4. Inflammatory ... 94
13.2.5. Dysentery ... 94
13.3. DIAGNOSIS ... 95
13.4. CAUSES: ... 95
13.5. PREVENTION ... 96
13.6. TREATMENT ... 97
14. FILARIASIS ... 100
14.1. INTRODUCTION ... 100
14.2. ORIGIN AND HISTORY ... 100
14.3. CAUSATIVE AGENT ... 100
14.4. MORPHOLOGY OF THE PARASITE ... 100
14.5. LIFE CYCLE OF THE PARASITE ... 101
14.6. DISTRIBUTION ... 102
14.7. CLASSIFICATION OF DISEASE ... 102
14.8. FILARIA VECTORS ... 102
14.9. CAUSE AND MODE OF INFECTION ... 103
14.10. SYMPTOMS ... 104
14.11. BANCROFTIAN FILARIASIS ... 104
14.12. LYMPHATIC FILARIASIS (LF) ... 105
14.13. DIAGNOSIS ... 105
14.14. TREATMENT ... 106
14.15. INDIVIDUAL CHEMOTHERAPY ... 107
14.16. SURGICAL AND SUPPORTIVE TREATMENT ... 107
14.17. PREVENTION ... 107
14.18. PERSONAL PRACTICE ... 108
15. CANCER ... 109
15.1. INTRODUCTION: ... 109
15.2. WHAT IS CANCER? ... 109
15.3. GENETIC BASIS OF CANCER: ... 110
15.4. ONCOGENES AND SIGNAL TRANSDUCTION: ... 110
15.5. TUMOR SUPPRESSOR GENES: ... 111
15.6. DNA REPAIR GENES: ... 112
15.7. CELL CYCLE: ... 114
15.8. CAUSE OF CANCER: ... 115
15.9. TUMOR BIOLOGY: ... 116
15.10. SIGNS AND SYMPTOMS: ... 118
15.11. DETECTING AND DIAGNOSING CANCER: ... 118
15.12. TREATMENT ... 119
16. JAUNDICE ... 124
16.1. INTRODUCTION ... 124
16.2. SIGNS AND SYMPTOMS ... 124
16.3. TYPES OF JAUNDICE ... 125
16.3.1. Pre-hepatic ... 125
16.3.2. Hepatocellular ... 126
16.4. SYMPTOMS ... 126
16.4.1. Post-hepatic ... 127
16.4.2. Neonatal jaundice ... 128
16.5. DIFFERENTIAL DIAGNOSIS ... 128
16.6. PATHOPHYSIOLOGY ... 128
16.7. HEPATIC EVENTS ... 129
16.8. EPIDEMIOLOGY ... 129
16.8.1. DIAGNOSTIC APPROACH ... 129
TABLES
T
ABLE
14.1 ... 106
T
ABLE
15.1 ... 113
T
ABLE
15.2 ... 121
T
ABLE
16.1 ... 125
T
ABLE
16.2 ... 132
FIGURES
F
IGURE
1.1 ... 3
F
IGURE
6.1 ... 36
F
IGURE
6.2 ... 37
F
IGURE
6.3 ... 38
F
IGURE
6.4 ... 38
F
IGURE
6.5 ... 39
F
IGURE
6.6 ... 41
F
IGURE
8.1 ... 52
F
IGURE
8.2 ... 52
F
IGURE
8.3 ... 54
F
IGURE
8.4 ... 55
F
IGURE
9.1 ... 60
F
IGURE
9.2 ... 61
F
IGURE
10.1 ... 68
F
IGURE
10.2 ... 69
F
IGURE
10.3 ... 71
F
IGURE
10.4 ... 72
F
IGURE
11.1 ... 78
F
IGURE
11.2 ... 79
F
IGURE
11.3 ... 80
F
IGURE
12.1 ... 88
F
IGURE
12.2 ... 89
F
IGURE
14.1 ... 101
F
IGURE
14.2 ... 102
F
IGURE
14.3 ... 103
F
IGURE
14.4 ... 105
F
IGURE
16.1 ... 126
1
1. MEASLES
Sasmita Panda
1.1. INTRODUCTION
The first systematic description of measles, and its distinction from smallpox and
chickenpox, is credited to the Persian physician Rhazes (860932), who published The Book of
Smallpox and Measles. Measles is an endemic disease, meaning it has been continually present
in a community, and many people develop resistance. In populations not exposed to measles,
exposure to the new disease can be devastating. In 1529, a measles outbreak in Cuba killed two-
thirds of those natives who had previously survived smallpox. Two years later, measles was
responsible for the deaths of half the population of Honduras, and it had ravaged Mexico, Central
America, and the Inca civilization. Measles, or rubeola, is a viral infection of the respiratory
system. It is a very contagious disease that can spread through contact with infected mucus and
saliva. An infected person can release the infection into the air when they cough or sneeze. The
measles virus can live on surfaces for several hours. As the infected particles enter the air and
settle on surfaces, anyone within close proximity can become infected. Drinking from an
infected person's glass, or sharing eating utensils with an infected person, increases the risk of
infection. Measles is a leading cause of death in children. Of the 114,900 global deaths related to
measles in 2014, the World Health Organization (WHO) reported that most of the victims were
under the age of 5.
1.2. SYMPTOMS
Measles is an infection caused by the rubeola virus. Symptoms will appear about 9 to 11
days after initial infection. Its symptoms always include fever and at least one of the three Cs:
· Cough
· Coryza, or runny nose
· Conjunctivitis
· Symptoms may include:
· Runny nose
· Dry hacking cough
· Conjunctivitis, or swollen eyelids and inflamed eyes
· Watery eyes
· Photophobia, or sensitivity to light
· Sneezing
· A reddish-brown rash
2
· Koplik's spots or very small greyish-white spots with bluish-white centers in the mouth,
insides of cheeks, and throat.
· Generalized body aches
There is often a fever. This can range from mild severe, up to 40.6 degrees Centigrade. It can
last several days, and it may fall and then rise again when the rash appears.The reddish-brown
rash appears around 3 to 4 days after initial symptoms. This can last for over a week.The rash
usually starts behind the ears and spreads over the head and neck. After a couple of days, it
spreads to the rest of the body, including the legs. As the spots grow, they often join
together.Most childhood rashes are not measles, but a child should see a doctor if:
A parent suspects the child may have measles
Symptoms do not improve, or they get worse
The fever rises to above 38 degrees Centigrade
Other symptoms resolve, but the fever persists
1.3. COMPLICATIONS
The measles vaccine is widely available and is said to have dropped global rates of measles
by over 75 percent. Complications from measles are fairly common. Some can be serious. People
most at risk are patients with a weak immune system, such as those with HIV, AIDS, leukemia,
or a vitamin deficiency, very young children, and adults over the age of 20 years. Older people
are more likely to have complications than healthy children over the age of 5 years.
Complications can include:
· Diarrhoea
· Vomiting
· Eye infection
· Respiratory tract infections, such as laryngitis and bronchitis
· Difficulty in breathing
· Ear infections, which can lead to permanent hearing loss
· Febrile seizures
Patients with a weakened immune system who have measles are more susceptible to bacterial
pneumonia. This can be fatal if not treated. The following less common complications are also
possible:
· Hepatitis: Liver complications can occur in adults and in children who are taking
some medications.
· Encephalitis: This affects around 1 in every 1,000 patients with measles. It is an
inflammation of the brain that can sometimes be fatal. It may occur soon after
measles, or several years later.
3
· Thrombocytopenia, or low platelet count, affects the blood's ability to clot. The
patient may bruise easily.
· Squint: Eye nerves and eye muscles may be affected.
· Complications that are very rare but possible include:
· Neuritis, an infection of the optic nerve that can lead to vision loss
· Heart complications
· Subacute sclerosing panencephalitis (SSPE): A brain disease that can affect 2 in every
100,000 people, months or years after measles infection. Convulsions, motor
abnormalities, cognitive issues, and death can occur.
· Other nervous system complications include toxic encephalopathy, retrobulbar
neuritis, transverse myelitis, and ascending myelitis.
· Measles during pregnancy can lead to miscarriage, early delivery, or low birth
weight. A woman who is planning to become pregnant and has not been vaccinated
should ask her doctor for advice.
1.4. CAUSE
Figure 1.1
An electron micrograph of the measles virus.
Source: www.healthline.com
Measles is caused by infection with the rubeola virus. The virus lives in the mucus of the
nose and throat of an infected child or adult. The disease is contagious for 4 days before the rash
appears, and it continues to be contagious for about 4 to 5 days after.
Infection spreads through:
· Physical contact with an infected person
· Being near infected people if they cough or sneeze
· Touching a surface that has infected droplets of mucus and then putting fingers into
the mouth, or rubbing the nose or eyes. The virus remains active on an object for 2
hours.
4
1.5. MECHANISM OF INFECTION
As soon as the virus enters the body, it multiplies in the back of the throat, lungs and the
lymphatic system. It later infects and replicates in the urinary tract, eyes, blood vessels and
central nervous system. The virus takes 1 to 3 weeks to establish itself, but symptoms appear
between 9 and 11 days after initial infection. Anyone who has never been infected or vaccinated
is likely to become ill if they breathe in infected droplets or are in close physical contact with an
infected person. Approximately 90% of people who are not immune will develop measles if they
share a house with an infected person.
1.6. DIAGNOSIS
Measles gives people with it a fever. A doctor can normally diagnose measles by looking at
the signs and symptoms. A blood test will confirm the presence of the rubeola virus. In most
countries, measles is a notifiable disease. The doctor has to notify the authorities of any
suspected cases. If the patient is a child, the doctor will also notify the school. A child with
measles should not return to school until at least 5 days after the rash appears.
Laboratory testing
Alternatively, laboratory diagnosis of measles can be done with confirmation of positive
measles IgM antibodies or isolation of measles virus RNA from respiratory specimens. For
people unable to have their blood drawn, saliva can be collected for salivary measles-specific
IgA testing. Positive contact with other patients known to have measles adds strong
epidemiological evidence to the diagnosis. Any contact with an infected person, including semen
through sex, saliva, or mucus, can cause infection.
1.7. PREVENTION
Immunizations can help prevent a measles outbreak. The MMR vaccine is a three-in-one
vaccination that can protect from the measles, mumps, and rubella (German measles). Children
can receive their first MMR vaccination at 12 months, or sooner if traveling internationally, and
their second dose between the ages of 4 and 6. Adults who have never received an immunization
can request the vaccine from their doctor. If a family member contracts the measles virus, limit
interaction with others. This includes staying home from school or work and avoiding social
activities. An individual cannot get measles more than once.
1.8. TREATMENT
There is no specific treatment. If there are no complications, the doctor will recommend rest
and plenty of fluids to prevent dehydration. Symptoms usually go away within 7 to 10 days.
The following measures may help:
5
· If the child's temperature is high, they should be kept cool, but not too cold. Tylenol
or ibuprofen can help control fever, aches, and pains. Children under 16 years should
not take aspirin. A doctor will advise about acetaminophen dosage, as too much can
harm the child, especially the liver.
· People should avoid smoking near the child.
· Sunglasses, keeping the lights dim or the room darkened may enhance comfort levels,
as measles increases sensitivity to light.
· If there is crustiness around the eyes, gently clean with a warm, damp cloth.
· Cough medicines will not relieve a measles cough. Humidifiers or placing a bowl of
water in the room may help. If the child is over 12 months, a glass of warm water
with a teaspoon of lemon juice and two teaspoons of honey may help. Do not give
honey to infants.
· A fever can lead to dehydration, so the child should drink plenty of fluids.
· A child who is in the contagious stage should stay away from school and avoid close
contact with others, especially those who are not immunized or have never had
measles.
· Those with a vitamin A deficiency and children under 2 years who have measles may
benefit from vitamin A supplements. These can help prevent complications, but they
should only be taken with a doctor's agreement.
· Antibiotics will not help against the measles virus, but they may sometimes be
prescribed if an additional bacterial infection develops.
REFERENCES
· Baxby D (1997). "Classic Paper: Henry Koplik. The diagnosis of the invasion of
measles from a study of the exanthema as it appears on the buccal membrane".
Reviews in Medical Virology. 7 (2): 714.
· Biesbroeck L, Sidbury R (November 2013). "Viral exanthems: an update".
Dermatologic therapy. 26 (6): 4338.
· GBD 2015 Mortality and Causes of Death, Collaborators. (8 October 2016). "Global,
regional, and national life expectancy, all-cause mortality, and cause-specific
mortality for 249 causes of death, 19802015: a systematic analysis for the Global
Burden of Disease Study 2015.". Lancet (London, England). 388 (10053): 1459
1544.
· Kabra, SK; Lodhra, R (14 August 2013). "Antibiotics for preventing complications in
children with measles". Cochrane Database of Systematic Reviews. 8: CD001477.
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· Ludlow M, McQuaid S, Milner D, de Swart RL, Duprex WP (January 2015).
"Pathological consequences of systemic measles virus infection". The Journal of
pathology. 235 (2): 25365.
· Perry RT, Halsey NA (May 1, 2004). "The Clinical Significance of Measles: A
Review". The Journal of Infectious Diseases. 189 (S1): S416.
· Sabella C (2010). "Measles: Not just a childhood rash". Cleveland Clinic Journal of
Medicine. 77 (3): 207213.
· Sension MG, Quinn TC, Markowitz LE, Linnan MJ, Jones TS, Francis HL, Nzilambi
N, Duma MN, Ryder RW (1988). "Measles in hospitalized African children with
human immunodeficiency virus". American Journal of Diseases of Children (1960).
142 (12): 12712.
7
2. SMALLPOX
Sasmita Panda
2.1. INTRODUCTION
Smallpox is an extremely contagious and deadly viral disease caused by Variola virus for
which there is no known cure. The last known case occurred in the United States in 1949 and due
to worldwide vaccination programs, this disease has been completely eradicated. Smallpox is
also known as variola. Since the time of ancient Egypt, smallpox has proven to be one of the
most devastating diseases to humankind. Widespread smallpox epidemics and huge death tolls
fill the pages of our history books. The first smallpox vaccine was created in 1758. However, the
disease continued to infect and kill people on a widespread basis for another 200 years. The
World Health Organization (WHO) implemented a strict vaccination standard in order to slow
the infection rate. The last known natural case occurred in 1977 in Somalia. By 1980, the WHO
declared that smallpox had been completely eradicated, although Government and health
agencies still have stashes of smallpox virus for research purposes. People no longer receive
routine smallpox vaccinations. The smallpox vaccine can have potentially fatal side effects, so
only the people who are at high risk of exposure get the vaccine.
2.2. SYMPTOMS
Historical accounts show that when someone was infected with the smallpox virus, they had
no symptoms for between seven and 17 days. However, once the incubation period (or virus
development phase) was over, the following flu-like symptoms occurred:
· High fever
· Chills
· Headache
· Severe back pain
· Abdominal pain
· Vomiting
These symptoms would go away within two to three days. Then the patient would feel better.
However, just as the patient started to feel better, a rash would appear. The rash started on the
face and then spread to the hands, forearms, and the main part of the body. The person would be
highly contagious until the rash disappeared.
Within two days of appearance, the rash would develop into abscesses that filled with fluid
and pus. The abscesses would break open and scab over. The scabs would eventually fall off,
leaving pit mark scars. Until the scabs fell off, the person remained contagious.
8
2.3. COMPLICATIONS
Complications of smallpox arise most commonly in the respiratory system and range from
simple bronchitis to fatal pneumonia. Respiratory complications tend to develop on about the
eighth day of the illness and can be either viral or bacterial in origin. Secondary bacterial
infection of the skin is a relatively uncommon complication of smallpox. When this occurs, the
fever usually remains elevated.
Other complications include encephalitis (1 in 500 patients), which is more common in adults
and may cause temporary disability; permanent pitted scars, most notably on the face; and
complications involving the eyes (2 percent of all cases). Pustules can form on the eyelid,
conjunctiva, and cornea, leading to complications such as conjunctivitis, keratitis, corneal ulcer,
iritis, iridocyclitis, and optic atrophy. Blindness results in approximately 35 percent to 40 percent
of eyes affected with keratitis and corneal ulcer. Haemorrhagic smallpox can cause
subconjunctival and retinal haemorrhages. In 2 to 5 percent of young children with smallpox,
virions reach the joints and bone, causing osteomyelitis variolosa. Lesions are symmetrical, most
common in the elbows, tibia, and fibula, and characteristically cause separation of an epiphysis
and marked periosteal reactions. Swollen joints limit movement, and arthritis may lead to limb
deformities, ankylosis, malformed bones, flail joints, and stubby fingers.
2.4. CAUSE
One of the reasons smallpox was so dangerous and deadly is because it's an airborne disease.
Airborne diseases tend to spread fast. Coughing, sneezing, or direct contact with any bodily
fluids could spread the smallpox virus. In addition, sharing contaminated clothing or bedding
could lead to infection.
TYPES OF SMALLPOX
There were two common and two rare forms of smallpox. The two common forms were
known as variola minor and variola major. Variola minor was a less fatal type of smallpox. The
Centers for Disease Control and Prevention (CDC) estimate that only 1 percent of those infected
died. However, it was less common than variola major. The CDC estimates that 90 percent of
smallpox cases were variola major. Historically, this type of smallpox killed 30 percent of those
infected. The two rare forms of smallpox were known as haemorrhagic and malignant. Both of
these rare forms of smallpox carried a very high fatality rate. Hemorrhagic smallpox caused
organs to leak blood into the mucous membranes and skin. Malignant smallpox lesions did not
develop into pustules or pus-filled bumps on the skin. Instead, they remained soft and flat
throughout the entire illness.
TRANSMISSION
Smallpox is an airborne viral disease mainly spread by direct and fairly prolonged face-to-
face contact between people. Smallpox patients became contagious once the first sores appeared
9
in their mouth and throat (early rash stage). They spread the virus when they coughed or sneezed
and droplets from their nose or mouth spread to other people. They remained contagious until
their last smallpox scab fell off. These scabs and the fluid found in the patient's sores also
contained the variola virus. The virus can spread through these materials or through the objects
contaminated by them, such as bedding or clothing. People who cared for smallpox patients and
washed their bedding or clothing had to wear gloves and take care to not get infected. Rarely,
smallpox has spread through the air in enclosed settings, such as a building (airborne route).
Smallpox can be spread by humans only. Scientists have no evidence that smallpox can be
spread by insects or animals.
2.5. DIAGNOSIS
Smallpox is defined as an illness with acute onset of fever equal to or greater than 38.3 °C
(101 °F) followed by a rash characterized by firm, deep seated vesicles or pustules in the same
stage of development without other apparent cause. If a clinical case is observed, smallpox is
confirmed using laboratory tests.
Microscopically, pox viruses produce characteristic cytoplasmic inclusions, the most
important of which are known as Guarnieri bodies, and are the sites of viral replication.
Guarnieri bodies are readily identified in skin biopsies stained with hematoxylin and eosin, and
appear as pink blobs. They are found in virtually all pox virus infections but the absence of
Guarnieri bodies cannot be used to rule out smallpox. The diagnosis of an orthopox virus
infection can also be made rapidly by electron microscopic examination of pustular fluid or
scabs. However, all orthopox viruses exhibit identical brick-shaped virions by electron
microscopy. However, if particles with the characteristic morphology of herpes viruses are seen
this will eliminate smallpox and other orthopox virus infections.
Definitive laboratory identification of variola virus involves growing the virus on
chorioallantoic membrane (part of a chicken embryo) and examining the resulting pock lesions
under defined temperature conditions. Strains may be characterized by polymerase chain reaction
(PCR) and restriction fragment length polymorphism (RFLP) analysis. Serologic tests and
enzyme linked immunosorbent assays (ELISA), which measure variola virus-specific
immunoglobulin and antigen have also been developed to assist in the diagnosis of infection.
Chickenpox was commonly confused with smallpox in the immediate post-eradication era.
Chickenpox and smallpox can be distinguished by several methods. Unlike smallpox,
chickenpox does not usually affect the palms and soles. Additionally, chickenpox pustules are of
varying size due to variations in the timing of pustule eruption: smallpox pustules are all very
nearly the same size since the viral effect progresses more uniformly. A variety of laboratory
methods are available for detecting chickenpox in evaluation of suspected smallpox cases.
10
2.6. PREVENTION AND TREATMENT
There is no proven treatment for smallpox disease, but some antiviral drugs may help treat it
or prevent it from getting worse. There also is a vaccine to protect people from smallpox. If there
were a smallpox outbreak, health officials would use the smallpox vaccine to control it.
2.6.1. SMALLPOX VACCINE
Before contact with the virus, the vaccine can protect you from getting sick.
Within 3 days of being exposed to the virus, the vaccine might protect you from getting the
disease. If you still get the disease, you might get much less sick than an unvaccinated person
would.
Within 4 to 7 days of being exposed to the virus, the vaccine likely gives you some
protection from the disease. If you still get the disease, you might not get as sick as an
unvaccinated person would.
Once an individual have developed the smallpox rash, the vaccine will not protect him.
Currently, the smallpox vaccine is not available to the general public because smallpox has been
eradicated, and the virus no longer exists in nature.
REFERENCES
· Barquet N, Domingo P (15 October 1997). "Smallpox: the triumph over the most
terrible of the ministers of death". Annals of Internal Medicine. 127 (8 Pt 1): 63542.
· Bray M, Roy CJ (2004). "Antiviral prophylaxis of smallpox". J. Antimicrob.
Chemother. 54 (1): 15.
· Dubochet J, Adrian M, Richter K, Garces J, Wittek R (1994). "Structure of
intracellular mature vaccinia virus observed by cryoelectron microscopy". J. Virol. 68
(3): 193541.
· Duggan AT, Perdomo MF, Piombino-Mascali D, Marciniak S, Poinar D, Emery MV,
Buchmann JP, Duchêne S, Jankauskas R, Humphreys M, Golding GB, Southon J,
Devault A, Rouillard JM, Sahl JW, Dutour O, Hedman K, Sajantila A, Smith GL,
Holmes EC, Poinar HN. "17th Century Variola Virus Reveals the Recent History of
Smallpox". Curr Biol. 26: 34073412.
· Elizabeth A. Fenn. "Biological Warfare in Eighteenth-Century North America:
Beyond Jeffery Amherst", The Journal of American History, Vol. 86, No. 4 (March
2000), pp. 15521580.
· Esposito JJ, Sammons SA, Frace AM, Olsen-Rasmussen M, et al. (August 2006).
"Genome sequence diversity and clues to the evolution of variola (smallpox) virus".
Science. 313 (5788): 80712.
11
· Fenner, Frank (1988). "Development of the Global Smallpox Eradication
Programme" (PDF). Smallpox and Its Eradication (History of International Public
Health, No. 6). Geneva: World Health Organization. pp. 366418.
· Henderson DA, Inglesby TV, Bartlett JG, Ascher MS, Eitzen E, Jahrling PB, Hauer J,
Layton M, McDade J, Osterholm MT, O'Toole T, Parker G, Perl T, Russell PK, Tonat
K (1999). "Smallpox as a biological weapon: medical and public health management.
Working Group on Civilian Biodefense". JAMA. 281 (22): 212737.
· Hughes AL, Irausquin S, Friedman R (2010). "The evolutionary biology of pox
viruses". Infection, Genetics and Evolution. 10 (1): 5059.
· Jezek Z, Hardjotanojo W, Rangaraj AG (1981). "Facial scarring after varicella. A
comparison between variola major and variola minor". Am. J. Epidemiol. 114 (6):
798803.
· Rodrigues BA (1975). "Smallpox eradication in the Americas". Bull Pan Am Health
Organ. 9 (1): 5368.
· Ryan KJ, Ray CG, eds. (2004). Sherris Medical Microbiology (4th ed.). McGraw
Hill. pp. 5258. ISBN 0-8385-8529-9.
· Shchelkunov SN (December 2011). "Emergence and reemergence of smallpox: the
need for development of a new generation smallpox vaccine". Vaccine. 29 Suppl 4:
D4953.
· Tognotti E. (June 2010). "The eradication of smallpox, a success story for modern
medicine and public health: What lessons for the future?" (PDF). J Infect Dev Ctries.
4 (5): 264266.
· Wujastyk, Dominik. (1995). "Medicine in India," in Oriental Medicine: An Illustrated
Guide to the Asian Arts of Healing, 1938. Edited by Serindia Publications. London:
Serindia Publications. ISBN 0-906026-36-9. p. 29.
12
3. CHICKENPOX
Sasmita Panda
3.1. INTRODUCTION
Chickenpox is an airborne disease which spreads easily through the coughs and sneezes of an
infected person. It may be spread from one to two days before the rash appears until all lesions
have crusted over. It may also spread through contact with the blisters. Those with shingles may
spread chickenpox to those who are not immune through contact with the blisters. The disease
can usually be diagnosed based on the presenting symptom; however, in unusual cases it may be
confirmed by polymerase chain reaction (PCR) testing of the blister fluid or scabs. Testing for
antibodies may be done to determine if a person is or is not immune. People usually only get the
disease once. Although reinfections by the virus occur, these reinfections usually do not cause
any symptoms.
The varicella vaccine has resulted in a decrease in the number of cases and complications
from the disease. It protects about 70 to 90 percent of people from disease with a greater benefit
for severe disease. Routine immunization of children is recommended in many countries.
Immunization within three days of exposure may improve outcomes in children. Treatment of
those infected may include calamine lotion to help with itching, keeping the fingernails short to
decrease injury from scratching, and the use of paracetamol (acetaminophen) to help with fevers.
For those at increased risk of complications antiviral medication such as aciclovir are
recommended. Chickenpox occurs in all parts of the world. As of 2013 140 million cases of
chickenpox and herpes zoster occurred. Before routine immunization the number of cases
occurring each year was similar to the number of people born. Since immunization the number of
infections in the United States has decreased nearly 90%. In 2015 chickenpox resulted in 6,400
deaths globally down from 8,900 in 1990. Death occurs in about 1 per 60,000 cases.
Chickenpox was not separated from smallpox until the late 19th century. In 1888 its connection
to shingles was determined. The first documented use of the term chicken pox was in 1658.
Various explanations have been suggested for the use of "chicken" in the name, one being the
relative mildness of the disease. Humans are the only known animal that the disease affects
naturally. However, chickenpox has been caused in other animals, such as primates, including
chimpanzees and gorillas.
3.2. CAUSE
Chickenpox, also known as varicella, is a highly contagious disease caused by the initial
infection with varicella zoster virus (VZV). The disease results in a characteristic skin rash that
forms small, itchy blisters, which eventually scab over. It usually starts on the chest, back, and
face then spreads to the rest of the body. Other symptoms may include fever, feeling tired, and
13
headaches. Symptoms usually last for five to ten days. Complications may occasionally include
pneumonia, inflammation of the brain, or bacterial infections of the skin among others. The
disease is often more severe in adults than children. Symptoms begin ten to twenty-one days
after exposure to the virus.
3.3. SYMPTOMS
The following are common chickenpox symptoms:
3.3.1. Before the rash appears
· A general feeling of being unwell (malaise).
· Fever (usually worse in adults than children)
· Aching muscles.
· Loss of appetite.
· Sometimes there may be a feeling of nausea.
3.3.2. After the rash appears
· Rash - its severity varies considerably. Some patients may have just a few spots,
while others are covered all over the body.
· Spots - the spots, which develop in clusters, generally appear on the face, limbs,
chest, and stomach.
· Blisters - initially, there are small red spots that itch a lot. They then develop into
spots with blisters on top - these can become very itchy.
· Clouding - within about 48 hours, the blisters cloud over and start drying out (a crust
develops).
· Healing - within about 10 days, the crusts fall off on their own.
· During the whole cycle, new waves of spots can appear - in such cases, the patient
might have different clusters of spots at varying stages of itchiness, dryness, and
crustiness.
3.4. COMPLICATIONS
Most healthy individuals make a full recovery, as is the case with a cold or flu - just by
resting and drinking plenty of fluids. A small percentage of patients have more severe symptoms
such as,
the skin around the spots or blisters becomes painful and red
there are breathing difficulties
PREGNANCY AND NEONATES
During pregnancy the dangers to the fetus associated with a primary VZV infection are
greater in the first six months. In the third trimester, the mother is more likely to have severe
14
symptoms. For pregnant women, antibodies produced as a result of immunization or previous
infection are transferred via the placenta to the foetus. Women who are immune to chickenpox
cannot become infected and do not need to be concerned about it for themselves or their infant
during pregnancy.
Varicella infection in pregnant women could lead to spread via the placenta and infection of
the foetus. If infection occurs during the first 28 weeks of gestation, this can lead to foetal
varicella syndrome (also known as congenital varicella syndrome). Effects on the foetus can
range in severity from underdeveloped toes and fingers to severe anal and bladder malformation.
Possible problems include:
Damage to brain: encephalitis, microcephaly, hydrocephaly, aplasia of brain
Damage to the eye: optic stalk, optic cup, and lens vesicles, microphthalmia, cataracts,
chorioretinitis, optic atrophy
Other neurological disorder: damage to cervical and lumbosacral spinal cord, motor/sensory
deficits, absent deep tendon reflexes, anisocoria/Horner's syndrome
Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter
dysfunction
Skin disorders: (cicatricial) skin lesions, hypopigmentation
Infection late in gestation or immediately following birth is referred to as "neonatal
varicella". Maternal infection is associated with premature delivery. The risk of the baby
developing the disease is greatest following exposure to infection in the period 7 days before
delivery and up to 8 days following the birth. The baby may also be exposed to the virus via
infectious siblings or other contacts, but this is of less concern if the mother is immune.
Newborns who develop symptoms are at a high risk of pneumonia and other serious
complications of the disease.
3.5. DIAGNOSIS
The diagnosis of chickenpox is primarily based on the signs and symptoms, with typical
early symptoms followed by a characteristic rash. Confirmation of the diagnosis is by
examination of the fluid within the vesicles of the rash, or by testing blood for evidence of an
acute immunologic response. Vesicular fluid can be examined with a Tzanck smear, or better by
testing for direct fluorescent antibody. The fluid can also be "cultured", whereby attempts are
made to grow the virus from a fluid sample. Blood tests can be used to identify a response to
acute infection (IgM) or previous infection and subsequent immunity (IgG). Prenatal diagnosis
of fetal varicella infection can be performed using ultrasound, though a delay of 5 weeks
following primary maternal infection is advised. A PCR (DNA) test of the mother's amniotic
fluid can also be performed, though the risk of spontaneous abortion due to the amniocentesis
procedure is higher than the risk of the baby's developing fetal varicella syndrome.
15
3.6. PATHOPHYSIOLOGY
Exposure to VZV in a healthy child initiates the production of host immunoglobulin G (IgG),
immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies; IgG antibodies persist for
life and confer immunity. Cell-mediated immune responses are also important in limiting the
scope and the duration of primary varicella infection. After primary infection, VZV is
hypothesized to spread from mucosal and epidermal lesions to local sensory nerves. VZV then
remains latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results in
the clinically distinct syndrome of herpes zoster (i.e., shingles), postherpetic neuralgia, and
sometimes Ramsay Hunt syndrome type II. Varicella zoster can affect the arteries in the neck
and head, producing stroke, either during childhood, or after a latency period of many years.
3.6.1. Shingles
Chickenpox and shingles are caused by the same virus. Shingles occurs when the varicella
zoster virus from a previous case of chicken pox becomes active again. A person who has never
had chickenpox or was never vaccinated can catch chickenpox from someone with shingles.
However, you cannot get shingles from somebody with chickenpox.
Complications of shingles can include:
Postherpetic neuralgia - pain from shingles lasts long after the blisters have gone.
Vision loss - from eye infections caused shingles in the area.
Neurological problems - due to inflammation in the brain.
Skin infections - more likely if blisters are not treated correctly.
Shingles affects one in five adults infected with chickenpox as children, especially those who
are immune-suppressed, particularly from cancer, HIV, or other conditions. Stress can bring on
shingles as well, although scientists are still researching the connection. Shingles are most
commonly found in adults over the age of 60 who were diagnosed with chickenpox when they
were under the age of 1.
3.7. PREVENTION
3.7.1. Hygiene measures
The spread of chickenpox can be prevented by isolating affected individuals. Contagion is by
exposure to respiratory droplets, or direct contact with lesions, within a period lasting from three
days before the onset of the rash, to four days after the onset of the rash. The chickenpox virus is
susceptible to disinfectants, notably chlorine bleach (i.e., sodium hypochlorite). Like all
enveloped viruses, it is sensitive to desiccation, heat and detergents.
16
3.7.2. Vaccine
The chickenpox vaccine prevents chickenpox in 90 percent of children who receive it. The shot
should be given when a child is between 12 and 15 months of age. A booster is given between 4
and 6 years of age. Older children and adults who have not been vaccinated or exposed may
receive catch-up doses of the vaccine. As chickenpox tends to be more severe in older patients,
parents who did not previously vaccinate may opt to have the shots given later.
People who are unable to receive the vaccine can try to avoid the virus by limiting contact with
infected people. This can be difficult, as chickenpox can't be identified by blisters until it has been
contagious for days.
3.8. TREATMENT
Chickenpox generally resolves within a week or two without treatment - there is no medication
or treatment to "cure" it. A vaccine is available for varicella. For children, 2 doses of the varicella
vaccine (one given at 12-15 months and one given at age 4-6) are 90 percent effective at
preventing chickenpox. A doctor may prescribe or advise on how to reduce symptoms of itchiness
and discomfort, and also on how to prevent the infection from spreading to other people.
Pain or fever - Tylenol (acetaminophen) may help with symptoms of high temperature and/or
pain. It is important to follow the instructions provided by the manufacturer. Aspirin containing
products should NOT be used for chickenpox as this can lead to complications. Pregnant women
can take acetaminophen (Tylenol) at any time during their pregnancy.
Avoiding dehydration - the patient should drink plenty of fluids, preferably water, to prevent
dehydration. Some doctors recommend sugar-free popsicles or Pedialyte for children who are not
drinking enough.
Mouth soreness - sugar-free popsicles help ease symptoms of soreness if there are spots in the
mouth. Salty or spicy foods should be avoided. If chewing is painful, soup might be a good option;
make sure it is not too hot.
Itchiness - although itchiness can become severe and the urge to scratch may seem impossible
to control, it is important to keep scratching down to a minimum to prevent future scarring of the
skin. The following may help a child with chickenpox:
· Keep fingernails as short as possible.
· Keep fingernails clean at all times.
· Place mittens or even socks over the child's hands when they go to sleep so that any
attempt at scratching during the night does not cut the skin.
· Calamine lotions or oatmeal baths may help reduce symptoms of itching.
· Make sure the patient wears only loose clothing.
Antiviral medication It may be prescribed to pregnant females, adults if a diagnosis is
made early enough, newborns, and patients with weakened immune systems. An example
17
of such a drug is Acyclovir. This medication works best if it is given within 24 hours of
developing symptoms. Acyclovir reduces the severity of symptoms but does not cure the
disease.
REFERENCES
· Askalan R, Laughlin S, Mayank S, Chan A, MacGregor D, Andrew M, Curtis R,
Meaney B, deVeber G (June 2001). "Chickenpox and stroke in childhood: a study of
frequency and causation". Stroke. 32 (6): 125762.
· Boussault P, Boralevi F, Labbe L, Sarlangue J, Taïeb A, Leaute-Labreze C (2007).
"Chronic varicella-zoster skin infection complicating the congenital varicella
syndrome". Pediatr Dermatol. 24 (4): 42932.
· Breuer J (2010). "VZV molecular epidemiology". Current Topics in Microbiology
and Immunology. 342: 1542.
· Flatt, A; Breuer, J (September 2012). "Varicella vaccines.". British medical bulletin.
103 (1): 11527.
· Heuchan AM, Isaacs D (19 March 2001). "The management of varicella-zoster virus
exposure and infection in pregnancy and the newborn period. Australasian Subgroup
in Paediatric Infectious Diseases of the Australasian Society for Infectious Diseases.".
The Medical journal of Australia. 174 (6): 28892.
· Kanbayashi Y, Onishi K, Fukazawa K, Okamoto K, Ueno H, Takagi T, Hosokawa T
(2012). "Predictive Factors for Postherpetic Neuralgia Using Ordered Logistic
Regression Analysis". The Clinical Journal of Pain. 28 (8): 712714.
· Macartney, K; Heywood, A; McIntyre, P (23 June 2014). "Vaccines for post-
exposure prophylaxis against varicella (chickenpox) in children and adults.". The
Cochrane database of systematic reviews. 6: CD001833.
· Matsuo T, Koyama M, Matsuo N (July 1990). "Acute retinal necrosis as a novel
complication of chickenpox in adults". Br J Ophthalmol. 74 (7): 4434.
· Nagel MA, Cohrs RJ, Mahalingam R, Wellish MC, Forghani B, Schiller A, Safdieh JE,
Kamenkovich E, Ostrow LW, Levy M, Greenberg B, Russman AN, Katzan I, Gardner
CJ, Häusler M, Nau R, Saraya T, Wada H, Goto H, de Martino M, Ueno M, Brown
WD, Terborg C, Gilden DH (March 2008). "The varicella zoster virus vasculopathies:
clinical, CSF, imaging, and virologic features.". Neurology. 70: 85360.
· Pino Rivero V, González Palomino A, Pantoja Hernández CG, Mora Santos ME,
Trinidad Ramos G, Blasco Huelva A (2006). "Ramsay-Hunt syndrome associated to
unilateral recurrential paralysis". Anales otorrinolaringologicos ibero-americanos. 33
(5): 489494.
18
4. AIDS
G. K. Panigrahi
4.1. INTRODUCTION
HIV is a virus that enters your body and begins to destroy T cells. T cells are needed in order
to fight infections. HIV spreads through bodily fluids that include: blood, semen, vaginal and
rectal fluids, breast milk.
The first few weeks after infection is called the acute infection stage. During this time the
virus rapidly reproduces. Your immune system responds by producing HIV antibodies. Many
people experience temporary flu-like symptoms during this stage. Even without symptoms, HIV
is highly contagious during this time. After the first month or so, HIV enters the clinical latency
stage. This stage can last from a few years to a few decades. Progression can be slowed with
antiretroviral therapy. Some people have symptoms. Many people do not, but it's still
contagious. As the virus progresses, you're left with fewer T cells. This makes you more
susceptible to disease, infection, and infection-related cancers. HIV is a lifetime condition with
no cure. Medical care, including antiretroviral therapy, can help manage HIV and prevent AIDS.
Without treatment, HIV is likely to advance to AIDS. At that point, the immune system is too
weak to fight off life-threatening disease and infection. Untreated, life expectancy with AIDS is
about three years. It is estimated that 1.1 million Americans are currently living with HIV. And
one in five don't know it.
AIDS is a disease caused by HIV. It's the most advanced stage of HIV. But just because you
have HIV doesn't mean you'll develop AIDS. HIV destroys T cells called CD4 cells. These cells
help your immune system fight infections. Healthy adults generally have a CD4 count of 800 to
1,000 per cubic millimeter. If you have HIV and your CD4 count falls below 200 per cubic
millimeter, you will be diagnosed with AIDS. One can also be diagnosed with AIDS if one have
HIV and develop an opportunistic infection that is rare in people who don't have HIV. AIDS
weakens your immune system to the point where it can no longer fight off most diseases and
infections.
In addition, women with HIV are at increased risk of:
· vaginal yeast infections and other vaginal infections, including bacterial vaginosis
· sexually transmitted diseases (STDs) such as gonorrhea, chlamydia, and
trichomoniasis
· pelvic inflammatory disease (PID)
· infection of the reproductive organs and menstrual cycle changes
· human papilloma virus (HPV), which can cause genital warts and lead to cervical
cancer
19
· Another gender difference is that women are less likely than men to notice small
spots or other changes to their genitals.
· HIV can be transmitted to your baby during pregnancy. The virus can also be passed
to your baby through breast milk. If your doctor knows you have HIV, treatment can
lower the risk of passing the virus on to your child to less than 2 percent.
4.2. SYMPTOMS OF HIV
Some people infected with HIV are asymptomatic at first. Most people experience symptoms
in the first month or two after becoming infected. That's because your immune system is reacting
to the virus as it rapidly reproduces.
This early stage is called acute stage. Symptoms are similar to those of the flu and may last
anywhere from a few days to several weeks. These include:
· Fever
· Swollen lymph glands
· General aches and pains
During the first few months of infection, an HIV test may provide a false-negative result.
This is because it takes time for the immune system to build up enough antibodies to be detected
in a blood test. But the virus is active and highly contagious during this time.
The clinical latent infection, or chronic stage of HIV, can last from a few years to a few
decades. During this time the virus is still reproducing, but at lower levels. Some people have
few, if any, symptoms. Others may have many symptoms. As the disease progresses, other
symptoms may include:
· Swollen lymph nodes
· Recurrent fevers
· Fatigue
· Aches and pains
· Nausea, vomiting
· Diarrhoea
· Weight loss
· Skin rashes
· Oral yeast infections or other infections
· Shingles
· Symptoms may come and go or progress rapidly. Even if no symptoms, an individual
can still transmit the virus to others.
20
4.3. SYMPTOMS OF AIDS
With the use of antiretroviral therapy, chronic HIV can last several decades. Without
treatment, HIV can be expected to progress to AIDS sooner. By that time, the immune system is
quite damaged and has a hard time fighting off infection and disease. Symptoms of AIDS can
include:
· Recurrent fever
· Chronic swollen lymph glands, especially of the armpits, neck, and groin
· Chronic fatigue
· Night sweats
· Dark splotches under the skin or inside the mouth, nose, or eyelids
· Sores, spots, or lesions of the mouth and tongue, genitals, or anus
· Bumps, lesions, or rashes of the skin
· Recurrent or chronic diarrhoea
· Rapid weight loss
· Neurologic problems such as difficulty concentrating, memory loss, and confusion
· Anxiety and depression
· An individual with a weakened immune system has an increased risk of pneumonia
and other opportunistic infections. Other potential complications of AIDS include:
· Candidiasis.
· Tuberculosis.
· Cytomegalo virus (CMV), a type of herpes virus.
· Cryptococcal meningitis.
· Toxoplasmosis, and infection caused by a parasite.
· Cryptosporidiosis, an infection caused by an intestinal parasite.
· Cancer, including Kaposi's sarcoma (KS) and lymphoma and
· Kidney disease.
· Antiviral medications can help control the virus. Treatment for other infections and
complications of AIDS must be tailored to an individual needs.
4.4. TRANSMISSION
HIV does not play favorites. Anyone can become infected. The virus is transmitted in bodily
fluids that include:
· Blood
· Semen
· Vaginal and rectal fluids
· Breast milk
21
Some of the ways HIV is spread from person to person include:
· Having unprotected sex with an infected person. This is the most common route of
transmission
· Sharing needles, syringes, and other items for injection drug use with an infected
person
· Passing it on to an unborn child if the mother is HIV-positive
· Passing it on to a baby through breast milk if the mother is HIV-positive
· Being exposed to infected fluids, usually through needle sticks.
· Having a blood transfusion or organ and tissue transplant can also transmit the virus.
But rigorous testing for HIV in blood ensures that this is very rare in the United
States.
· It's theoretically possible, but considered extremely rare, for HIV to spread via:
· Oral sex
· Being bitten by an infected person
· Contact between broken skin, wounds, or mucous membranes and HIV-infected
blood or fluids
HIV does NOT spread through:
· Skin-to-skin contact
· Hugging, shaking hands, or kissing
· Air or water
· Eating or drinking items, including drinking fountains
· Saliva, tears, or sweat (unless mixed with blood from an infected person)
· Sharing a toilet, towels, or bedding
· Mosquitoes or other insects
4.5. DIAGNOSIS
4.5.1. Antibody test
Between 21 and 84 days after infection, about 97 percent of people will develop detectable
HIV antibodies, which can be found in the blood or saliva.
There's no preparation necessary for blood tests or mouth swabs. Some tests provide results
in 30 minutes or less and can be performed in a doctor's office or clinic. There are also home test
kits available:
· Oral Quick HIV Test: An oral swab provides results in as little as 20 minutes.
· Home Access HIV-1 Test System: After pricking your finger, you send a blood
sample to a licensed laboratory. You can remain anonymous and call for results the
next business day.
Details
- Pages
- Type of Edition
- Erstausgabe
- Year
- 2017
- ISBN (PDF)
- 9783960676744
- ISBN (Softcover)
- 9783960671749
- File size
- 11.8 MB
- Language
- English
- Publication date
- 2017 (July)
- Keywords
- Illness measles smallpox chickenpox AIDS Ebola Dengue cholera leprosy tuberculosis typhoid malaria amoebiasis Diarrhoea Filariasis Cancer Jaundice Disease Symptoms Diagnosis India
